Smoking duration, respiratory symptoms, and COPD in adults aged ≥45 years with a smoking history

PubMed Central

Liu, Yong; Pleasants, Roy A; Croft, Janet B; Wheaton, Anne G; Heidari, Khosrow; Malarcher, Ann M; Ohar, Jill A; Kraft, Monica; Mannino, David M; Strange, Charlie

2015-01-01

Background The purpose of this study was to assess the relationship of smoking duration with respiratory symptoms and history of chronic obstructive pulmonary disease (COPD) in the South Carolina Behavioral Risk Factor Surveillance System survey in 2012. Methods Data from 4,135 adults aged ≥45 years with a smoking history were analyzed using multivariable logistic regression that accounted for sex, age, race/ethnicity, education, and current smoking status, as well as the complex sampling design. Results The distribution of smoking duration ranged from 19.2% (1–9 years) to 36.2% (≥30 years). Among 1,454 respondents who had smoked for ≥30 years, 58.3% were current smokers, 25.0% had frequent productive cough, 11.2% had frequent shortness of breath, 16.7% strongly agreed that shortness of breath affected physical activity, and 25.6% had been diagnosed with COPD. Prevalence of COPD and each respiratory symptom was lower among former smokers who quit ≥10 years earlier compared with current smokers. Smoking duration had a linear relationship with COPD (P<0.001) and all three respiratory symptoms (P<0.001) after adjusting for smoking status and other covariates. While COPD prevalence increased with prolonged smoking duration in both men and women, women had a higher age-adjusted prevalence of COPD in the 1–9 years, 20–29 years, and ≥30 years duration periods. Conclusion These state population data confirm that prolonged tobacco use is associated with respiratory symptoms and COPD after controlling for current smoking behavior. PMID:26229460

Effect of nicotine, cotinine and cigarette smoke extract on the neutrophil respiratory burst.

PubMed

Matthews, John B; Chen, Fa-Ming; Milward, Michael R; Wright, Helen J; Carter, Kevin; McDonagh, Anna; Chapple, Iain L C

2011-03-01

To determine the effect of nicotine, cotinine and cigarette smoke extract (CSE) on the neutrophil respiratory burst and their effect on activation of the nuclear factor-κB (NFκB) pathway in oral epithelium. Neutrophils from periodontally healthy individuals were treated with nicotine, cotinine and CSE before stimulation with Fusobacterium nucleatum, IgG-opsonized Staphylococcus aureus and Escherichia coli lipopolysaccharide. Total and extracellular reactive oxygen species (ROS) generation was determined by luminol/isoluminol chemiluminescence. Activation of NFκB in oral epithelial cells was determined by immunocytochemistry. Smoke extract alone caused increased neutrophil extracellular isoluminol-dependent chemiluminescence, not detectable with luminol. However, pre-treatment with smoke extract reduced both total and extracellular ROS generation in response to all stimuli. Nicotine and cotinine had no effect on the neutrophil respiratory burst. Smoke extract, nicotine and cotinine did not induce oral epithelial cell NFκB activation. These data demonstrate that smoke extract reduces the ability of neutrophils to generate ROS after stimulation with F. nucleatum and IgG-opsonized S. aureus but, at high concentrations, stimulates extracellular ROS generation. During periodontitis, cigarette smoking may differentially affect neutrophil function, generally preventing elimination of periodontal pathogens but, in heavy smokers, also stimulating ROS release and oxidative stress mediated tissue damage. © 2011 John Wiley & Sons A/S.

Respiratory response to cigarette smoking among adolescent smokers: a pilot study.

PubMed

Prokhorov, A V; Emmons, K M; Pallonen, U E; Tsoh, J Y

1996-01-01

Because cigarette smoking affects the respiratory system earlier than many other systems of the human body, an attempt was made to identify objective and subjective respiratory problems among adolescent smokers. Two studies based on a pulmonary function test (PFT), respiratory symptom assessment, and other smoking-related variables were undertaken. Study 1 involved cigarette smokers (N = 18, 22% males, mean age 18.7 years) from a freshman college class who participated in an acute smoking experiment that involved performing a PFT before and after smoking a single cigarette. Study 2 was performed on a combined group of vocational-technical high school students and freshman college students (N = 44, 48% males, mean age 17.8 years) where PFT parameters, respiratory symptoms, and smoking-related health vulnerability were assessed among smokers vs nonsmokers. In Study 1, the average reduction across PFT parameters was 4.4% and the mean estimated lung age increased from 27.15 to 29.84 years. In Study 2, a consistent trend toward reduction of PFT values among smokers vs nonsmokers was observed; the mean forced expiratory volume in 1 sec/forced vital capacity ratio (90.51% vs 94.59%), peak expiratory flow rate (80.32% vs 92.06%), and flow rate of 50% of forced vital capacity (88.39% vs 102.81%) differed significantly. Significant differences in respiratory symptoms were also observed among smokers vs nonsmokers. The beginning of respiratory health disorders can be identified among adolescent smokers. These findings might provide important clues on how to improve outcomes from health care provider-based adolescent smoking cessation counseling.

RESPIRATORY SYMPTOMS AND SMOKING HABITS OF SENIOR INDUSTRIAL STAFF

PubMed Central

Meadows, Susan H.; Wood, C. H.; Schilling, R. S. F.

1965-01-01

The prevalence of respiratory symptoms and the smoking habits of 224 industrial `executives' aged 30 to 69 years in Social Classes I and II were ascertained by means of the Medical Research Council's questionnaire on respiratory symptoms; 31% had persistent cough, 25% had persistent phlegm, and 21% were short of breath on hurrying or going up a hill; 9% had had one or more chest illnesses in the past three years lasting for about a week, and 4% had `chronic bronchitis'—defined as persistent phlegm and one or more chest illnesses in the past three years; 67% were smokers, 21% smoking more than 25 cigarettes (or equivalent tobacco) per day; another 20% had stopped smoking. The prevalence of cough, phlegm, and breathlessness was closely related to smoking habit. Data for those aged 40 to 59 years are compared with that obtained from London Transport Board workers and a sample of the population studied by the College of General Practitioners. The latter was further analysed and suggests that the prevalence of cough and phlegm is more closely related to the amount smoked than to social class. The prevalence of chest illness is probably more closely related to social class and less to the amount smoked. It is suggested that, although smoking may initiate irritative respiratory symptoms, the precursors of bronchitis, additional factors are important in causing progression to disabling or fatal chronic bronchitis. PMID:14278803

Smoking cessation treatment by Dutch respiratory nurses: reported practice, attitudes and perceived effectiveness.

PubMed

Kotz, D; van Litsenburg, W; van Duurling, R; van Schayck, C P; Wesseling, G J

2008-01-01

To describe Dutch respiratory nurses' current smoking cessation practices, attitudes and beliefs, and to compare these with a survey from the year 2000, before the national introduction of a protocol for the treatment of nicotine and tobacco addiction (the L-MIS protocol). Questionnaire survey among all 413 registered respiratory nurses in the Netherlands in 2006. The response rate was 62%. Seventy-seven percent of the respondents reported to have "fairly good" or "good" knowledge of all steps of the L-MIS protocol. Seven out of 10 behavioural techniques for smoking cessation from the protocol were used by more than 94% of the respondents. Seventy-four percent of the respiratory nurses recommended the use of either nicotine replacement therapy (70%) or bupropion (44%). Almost two-thirds (65% of 254) perceived lack of patient's motivation as the most important barrier for smoking cessation treatment; a four-fold increase compared to the year 2000. We conclude that respiratory nurses are compliant with the L-MIS protocol. They offer intensive support and use behavioural techniques for smoking cessation more frequently than evidence-based pharmacological aids for smoking cessation. Perceived lack of patient's motivation forms the most important threat to respiratory nurses' future smoking cessation activities. International guidelines acknowledge that respiratory patients have a more urgent need to stop smoking but have more difficulty doing so. They should be offered the most intensive smoking cessation counselling in combination with pharmacotherapy. This kind of counselling may be more feasible for respiratory nurses than for physicians who often lack time. Their efforts could be increased by reimbursing pharmacological aids for smoking cessation and by developing simple tools to systematically assess motivation to quit and psychiatric co-morbidity in smoking patients.

Prevalence and impact of active and passive cigarette smoking in acute respiratory distress syndrome.

PubMed

Hsieh, S Jean; Zhuo, Hanjing; Benowitz, Neal L; Thompson, B Taylor; Liu, Kathleen D; Matthay, Michael A; Calfee, Carolyn S

2014-09-01

Cigarette smoke exposure has recently been found to be associated with increased susceptibility to trauma- and transfusion-associated acute respiratory distress syndrome. We sought to determine 1) the incidence of cigarette smoke exposure in a diverse multicenter sample of acute respiratory distress syndrome patients and 2) whether cigarette smoke exposure is associated with severity of lung injury and mortality in acute respiratory distress syndrome. Analysis of the Albuterol for the Treatment of Acute Lung Injury and Omega Acute Respiratory Distress Syndrome Network studies. Acute Respiratory Distress Syndrome Network hospitals. Three hundred eighty-one patients with acute respiratory distress syndrome. None. 4-(Methylnitrosamino)-1-(3-pyridyl)-1-butanol, a validated tobacco-specific marker, was measured in urine samples from subjects enrolled in two National Heart, Lung, and Blood Institute Acute Respiratory Distress Syndrome Network randomized controlled trials. Urine 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol levels were consistent with active smoking in 36% of acute respiratory distress syndrome patients and with passive smoking in 41% of nonsmokers (vs 20% and 40% in general population, respectively). Patients with 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol levels in the active smoking range were younger and had a higher incidence of alcohol misuse, fewer comorbidities, lower severity of illness, and less septic shock at enrollment compared with patients with undetectable 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol levels. Despite this lower severity of illness, the severity of lung injury did not significantly differ based on biomarker-determined smoking status. Cigarette smoke exposure was not significantly associated with death after adjusting for differences in age, alcohol use, comorbidities, and severity of illness. In this first multicenter study of biomarker-determined cigarette smoke exposure in acute respiratory distress syndrome patients

Simvastatin inhibits smoke-induced airway epithelial injury: implications for COPD therapy.

PubMed

Davis, Benjamin B; Zeki, Amir A; Bratt, Jennifer M; Wang, Lei; Filosto, Simone; Walby, William F; Kenyon, Nicholas J; Goldkorn, Tzipora; Schelegle, Edward S; Pinkerton, Kent E

2013-08-01

Chronic obstructive pulmonary disease (COPD) is the third leading cause of death. The statin drugs may have therapeutic potential in respiratory diseases such as COPD, but whether they prevent bronchial epithelial injury is unknown. We hypothesised that simvastatin attenuates acute tobacco smoke-induced neutrophilic lung inflammation and airway epithelial injury. Spontaneously hypertensive rats were given simvastatin (20 mg·kg(-1) i.p.) daily for either 7 days prior to tobacco smoke exposure and during 3 days of smoke exposure, or only during tobacco smoke exposure. Pretreatment with simvastatin prior to and continued throughout smoke exposure reduced the total influx of leukocytes, neutrophils and macrophages into the lung and airways. Simvastatin attenuated tobacco smoke-induced cellular infiltration into lung parenchymal and airway subepithelial and interstitial spaces. 1 week of simvastatin pretreatment almost completely prevented smoke-induced denudation of the airway epithelial layer, while simvastatin given only concurrently with the smoke exposure had no effect. Simvastatin may be a novel adjunctive therapy for smoke-induced lung diseases, such as COPD. Given the need for statin pretreatment there may be a critical process of conditioning that is necessary for statins' anti-inflammatory effects. Future work is needed to elucidate the mechanisms of this statin protective effect.

Effects of ambient air pollution and environmental tobacco smoke on respiratory health of non-smoking women in Hong Kong.

PubMed

Wong, C M; Hu, Z G; Lam, T H; Hedley, A J; Peters, J

1999-10-01

Two-thirds of complaints received by the Hong Kong Environmental Protection Department in 1988 were related to poor air quality. In July 1990 legislation was implemented to reduce fuel sulphur levels. The intervention led to a reduction in respiratory symptoms and bronchial hyperresponsiveness of primary school children. The objectives of this study were to investigate the differences in respiratory health between non-smoking women living in the more polluted district (Kwai Tsing) and those living in the less polluted district (Southern); to assess the impact of the government air quality intervention; and to study the effect of environmental tobacco smoke on respiratory health in non-smoking women in both districts. A total of 3405 non-smoking women, aged 36.5 years (standard deviation = 3.0), from two districts with good and poor air quality respectively before the intervention were followed yearly from 1989 to 1991. Binary latent variable modelling was used to summarize the six respiratory symptoms and to estimate the effects of risk factors. In 1989, living in the polluted district was associated with poor respiratory health (odds ratio [OR] = 1.55, 95% confidence interval [CI]: 1.11-2.17, P < 0.01). After the intervention, in the polluted district only, sulphur dioxide levels fell by up to 80% and sulphate concentrations in respirable particulates by 38%. Between 1989 and 1990-1991, there was no significantly greater decline (P > 0.241) in the more polluted compared with the less polluted district for poor respiratory health. In 1989, the effects on poor respiratory health for exposure to two or more categories of smokers relative to none in the home (OR = 1.80, 95% CI: 1.15-2.83, P < 0.01) were higher but not significantly than those for living in polluted relative to less polluted district (95% CI of the two effects overlapping each other). Environmental tobacco smoke (ETS) and outdoor air pollution had independent adverse effects on respiratory health of

Chronic Respiratory Symptoms and Lung Function in Agricultural Workers - Influence of Exposure Duration and Smoking.

PubMed

Stoleski, Saso; Minov, Jordan; Mijakoski, Dragan; Karadzinska-Bislimovska, Jovanka

2015-03-15

Job exposure in agricultural workers often leads to respiratory impairment. To assess the influence of exposure duration and smoking on chronic respiratory symptoms and ventilatory capacity in agricultural workers. A cross-sectional study covered 75 agricultural workers, compared with an equal number of office workers matched by age, exposure duration and smoking status. Standardized questionnaire was used to obtain data on chronic respiratory symptoms, job and smoking history. Lung functional testing was performed by spirometry. The prevalence of respiratory symptoms was higher in agricultural workers, with significant difference for cough (P = 0.034), and dyspnea (P = 0.028). Chronic respiratory symptoms among agricultural workers were significantly associated with duration of exposure (P < 0.05) and daily smoking (P < 0.01), as well as with daily smoking in controls (P < 0.01). The average values of spirometric parameters in exposed workers were significantly different for MEF50 (P = 0.002), MEF75 (P = 0.000), and MEF25-75 (P = 0.049). Obstructive changes in small airways in exposed workers were strongly related to exposure duration (P < 0.05) and smoking (P < 0.01). Agricultural workers with job exposure more than 15 years had more expressed adverse respiratory symptoms and lung function decline. The results confirmed the influence of agricultural exposure and daily smoking on chronic respiratory symptoms and airflow limitation, primarily targeting the small airways.

Positive impact of the Portuguese smoking law on respiratory health of restaurant workers.

PubMed

Madureira, Joana; Mendes, Ana; Almeida, Sofia; Teixeira, João Paulo

2012-01-01

The impact of smoke-free law on the respiratory and sensory symptoms among restaurant workers was evaluated. Fifty-two workers in 10 Portuguese restaurants were interviewed before and 2 years after implementation of the smoke-free law. A significant reduction in self-reported workplace environmental tobacco smoke (ETS) exposure was observed after the enforcement of the law, as well as a marked reduction in adverse respiratory and sensory symptoms such as dry, itching, irritated, or watery eyes, nasal problems, and sore or dry throat or cough, between pre- and post-ban. This study demonstrates that the smoking ban was effective in diminishing the exposure symptoms among workers and consequently in improving their respiratory health. These observations may have implications for policymakers and legislators in other countries currently considering the nature and extent of their smoke-free workplace legislation.

Implementation of smoke-free legislation in Malaysia: are adolescents protected from respiratory health effects?

PubMed

Zulkifli, Aziemah; Abidin, Najihah Zainol; Abidin, Emilia Zainal; Hashim, Zailina; Rahman, Anita Abd; Rasdi, Irniza; Syed Ismail, Sharifah Norkhadijah; Semple, Sean

2014-01-01

This study aimed to examine the relationship between respiratory health of Malaysian adolescents with secondhand smoke (SHS) exposure and smoke-free legislation (SFL) implementation. A total of 898 students from 21 schools across comprehensive- and partial-SFL states were recruited. SHS exposures and respiratory symptoms were assessed via questionnaire. Prenatal and postnatal SHS exposure information was obtained from parental-completed questionnaire. The prevalence of respiratory symptoms was: 11.9% ever wheeze, 5.6% current wheeze, 22.3% exercise-induced wheeze, 12.4% nocturnal cough, and 13.1% self-reported asthma. SHS exposure was most frequently reported in restaurants. Hierarchical logistic regression indicates living in a comprehensive-SFL state was not associated with a lower risk of reporting asthma symptoms. SHS exposure in public transport was linked to increased risk for wheeze (Adjusted Odds Ratio (AOR) 16.6; 95%confidence interval (CI), 2.69-101.7) and current wheezing (AOR 24.6; 95%CI, 3.53-171.8). Adolescents continue to be exposed to SHS in a range of public venues in both comprehensive- and partial-SFL states. Respiratory symptoms are common among those reporting SHS exposure on public transportation. Non-compliance with SFL appears to be frequent in many venues across Malaysia and enforcement should be given priority in order to reduce exposure.

Impact of the Spanish Smoking Law on Exposure to Second-Hand Smoke and Respiratory Health in Hospitality Workers: A Cohort Study

PubMed Central

Fernández, Esteve; Fu, Marcela; Pascual, José A.; López, María J.; Pérez-Ríos, Mónica; Schiaffino, Anna; Martínez-Sánchez, Jose M.; Ariza, Carles; Saltó, Esteve; Nebot, Manel

2009-01-01

Background A smoke-free law came into effect in Spain on 1st January 2006, affecting all enclosed workplaces except hospitality venues, whose proprietors can choose among totally a smoke-free policy, a partial restriction with designated smoking areas, or no restriction on smoking on the premises. We aimed to evaluate the impact of the law among hospitality workers by assessing second-hand smoke (SHS) exposure and the frequency of respiratory symptoms before and one year after the ban. Methods and Finding We formed a baseline cohort of 431 hospitality workers in Spain and 45 workers in Portugal and Andorra. Of them, 318 (66.8%) were successfully followed up 12 months after the ban, and 137 nonsmokers were included in this analysis. We obtained self-reported exposure to SHS and the presence of respiratory symptoms, and collected saliva samples for cotinine measurement. Salivary cotinine decreased by 55.6% after the ban among nonsmoker workers in venues where smoking was totally prohibited (from median of 1.6 ng/ml before to 0.5 ng/ml, p<0.01). Cotinine concentration decreased by 27.6% (p = 0.068) among workers in venues with designated smoking areas, and by 10.7% (p = 0.475) among workers in venues where smoking was allowed. In Portugal and Andorra, no differences between cotinine concentration were found before (1.2 ng/ml) and after the ban (1.2 ng/ml). In Spain, reported respiratory symptom declined significantly (by 71.9%; p<0.05) among workers in venues that became smoke-free. After adjustment for potential confounders, salivary cotinine and respiratory symptoms decreased significantly among workers in Spanish hospitality venues where smoking was totally banned. Conclusions Among nonsmoker hospitality workers in bars and restaurants where smoking was allowed, exposure to SHS after the ban remained similar to pre-law levels. The partial restrictions on smoking in Spanish hospitality venues do not sufficiently protect hospitality workers against SHS or its

Impact of the Spanish smoking law on exposure to second-hand smoke and respiratory health in hospitality workers: a cohort study.

PubMed

Fernández, Esteve; Fu, Marcela; Pascual, José A; López, María J; Pérez-Ríos, Mónica; Schiaffino, Anna; Martínez-Sánchez, Jose M; Ariza, Carles; Saltó, Esteve; Nebot, Manel

2009-01-01

A smoke-free law came into effect in Spain on 1st January 2006, affecting all enclosed workplaces except hospitality venues, whose proprietors can choose among totally a smoke-free policy, a partial restriction with designated smoking areas, or no restriction on smoking on the premises. We aimed to evaluate the impact of the law among hospitality workers by assessing second-hand smoke (SHS) exposure and the frequency of respiratory symptoms before and one year after the ban. We formed a baseline cohort of 431 hospitality workers in Spain and 45 workers in Portugal and Andorra. Of them, 318 (66.8%) were successfully followed up 12 months after the ban, and 137 nonsmokers were included in this analysis. We obtained self-reported exposure to SHS and the presence of respiratory symptoms, and collected saliva samples for cotinine measurement. Salivary cotinine decreased by 55.6% after the ban among nonsmoker workers in venues where smoking was totally prohibited (from median of 1.6 ng/ml before to 0.5 ng/ml, p<0.01). Cotinine concentration decreased by 27.6% (p = 0.068) among workers in venues with designated smoking areas, and by 10.7% (p = 0.475) among workers in venues where smoking was allowed. In Portugal and Andorra, no differences between cotinine concentration were found before (1.2 ng/ml) and after the ban (1.2 ng/ml). In Spain, reported respiratory symptom declined significantly (by 71.9%; p<0.05) among workers in venues that became smoke-free. After adjustment for potential confounders, salivary cotinine and respiratory symptoms decreased significantly among workers in Spanish hospitality venues where smoking was totally banned. Among nonsmoker hospitality workers in bars and restaurants where smoking was allowed, exposure to SHS after the ban remained similar to pre-law levels. The partial restrictions on smoking in Spanish hospitality venues do not sufficiently protect hospitality workers against SHS or its consequences for respiratory health.

How beneficial is vaping cannabis to respiratory health compared to smoking?

PubMed

Tashkin, Donald P

2015-11-01

While vaping cannabis reduces respiratory exposure to toxic particulates in cannabis smoke, the resultant reduction in clinically evident harms to lung health is probably smaller than that likely to result from substituting e-cigarettes for smoked tobacco due to the comparatively greater harms of tobacco than cannabis smoking to lung health.

Respiratory symptoms following wildfire smoke exposure: airway size as a susceptibility factor.

PubMed

Mirabelli, Maria C; Künzli, Nino; Avol, Edward; Gilliland, Frank D; Gauderman, W James; McConnell, Rob; Peters, John M

2009-05-01

Associations between exposure to smoke during wildfire events and respiratory symptoms are well documented, but the role of airway size remains unclear. We conducted this analysis to assess whether small airway size modifies these relationships. We analyzed data from 465 nonasthmatic 16- to 19-year-old participants in the Children's Health Study. Following an outbreak of wildfires in 2003, each student completed a questionnaire about smoke exposure, dry and wet cough, wheezing, and eye symptoms. We used log-binomial regression to evaluate associations between smoke exposure and fire-related health symptoms, and to assess modification of the associations by airway size. As a marker of airway size, we used the ratio of maximum midexpiratory flow to forced vital capacity. Forty percent (186 of 465) of this population (including students from 11 of 12 surveyed communities) reported the odor of wildfire smoke at home. We observed increased respiratory and eye symptoms with increasing frequency of wildfire smoke exposure. Associations between smoke exposure and having any of 4 respiratory symptoms were stronger in the lowest quartile of the lung function ratio (eg, fire smoke 6+ days: prevalence ratio: 3.8; 95% confidence interval (CI = 2.0-7.2), compared with the remaining quartiles (fire smoke 6+ days: prevalence ratio = 2.0; 1.2-3.2). Analysis of individual symptoms suggests that this interaction may be strongest for effects on wheezing. Small airways may serve as a marker of susceptibility to effects of wildfire smoke. Future studies should investigate the role of airway size for more common exposures and should include persons with asthma.

Passive cigarette smoke, coal heating, and respiratory symptoms of nonsmoking women in China

DOE Office of Scientific and Technical Information (OSTI.GOV)

Pope, C.A. III; Xu, X.

1993-09-01

In this study the authors evaluated data from a sample of 973 never-smoking women, ages 20-40, who worked in three similar textile mills in Anhui Province, China. They compared prevalence rates of respiratory symptoms across homes with and without coal heating and homes with different numbers of smokers. Multiple logistic regression models that controlled for age, job title, and mill of employment were also estimated. Respiratory symptoms were associated with combined exposure to passive cigarette smoke and coal heating. Effects of passive cigarette smoke and coal heating on respiratory symptoms appeared to be nearly additive, suggesting a dose-response relationship betweenmore » respiratory symptoms and home indoor air pollution from these two sources. The prevalence of chest illness, cough, phlegm, and shortness of breath (but not wheeze) was significantly elevated for women living in homes with both smokers and coal heating.« less

Respiratory function in healthy ever-smokers is impaired by smoking habits in a dose-dependent manner.

PubMed

Osanai, Shinobu; Ogasa, Toshiyuki; Sumitomo, Kazuhiro; Hasebe, Naoyuki

2018-01-01

There is limited information about the respiratory function of ever-smokers without lung disorders. We sought to assess the effects of smoking habits on respiratory function in subjects without lung disorders. Subjects were recruited from among patients without any evidence of respiratory disorders who visited rural primary care clinics. Each participant was asked to answer a questionnaire that included questions smoking history. Their forced vital capacity (FVC) and forced expiratory volume in one second (FEV1) were measured. We analyzed 802 subjects (364 men and 438 women). The means of the lambda-mu-sigma method derived z-score of FEV1 (zFEV1) both in current-smokers and ex-smokers were lower than that in never-smokers. The mean zFEV1 in the ever-smokers with more than 30 pack-years of smoking history were lower than that in the ever-smokers with less smoking history. Univariate analysis showed that there were significant negative correlations between pack-years and zFEV1 both in the ex-smokers and current-smokers. There was no significant correlation between the duration of smoking cessation and zFEV1 in the ex-smokers. Our data suggests that respiratory function in healthy ever-smokers is decreased based on smoking habits in a dose-dependent manner. Even after a long period of smoking cessation, the decreased respiratory function seems to be maintained in ex-smokers. Copyright © 2017 The Japanese Respiratory Society. Published by Elsevier B.V. All rights reserved.

Menthol attenuates respiratory irritation and elevates blood cotinine in cigarette smoke exposed mice.

PubMed

Ha, Michael A; Smith, Gregory J; Cichocki, Joseph A; Fan, Lu; Liu, Yi-Shiuan; Caceres, Ana I; Jordt, Sven Eric; Morris, John B

2015-01-01

Addition of menthol to cigarettes may be associated with increased initiation of smoking. The potential mechanisms underlying this association are not known. Menthol, likely due to its effects on cold-sensing peripheral sensory neurons, is known to inhibit the sensation of irritation elicited by respiratory irritants. However, it remains unclear whether menthol modulates cigarette smoke irritancy and nicotine absorption during initial exposures to cigarettes, thereby facilitating smoking initiation. Using plethysmography in a C57Bl/6J mouse model, we examined the effects of L-menthol, the menthol isomer added to cigarettes, on the respiratory sensory irritation response to primary smoke irritants (acrolein and cyclohexanone) and smoke of Kentucky reference 2R4 cigarettes. We also studied L-menthol's effect on blood levels of the nicotine metabolite, cotinine, immediately after exposure to cigarette smoke. L-menthol suppressed the irritation response to acrolein with an apparent IC₅₀ of 4 ppm. Suppression was observed even at acrolein levels well above those necessary to produce a maximal response. Cigarette smoke, at exposure levels of 10 mg/m³ or higher, caused an immediate and marked sensory irritation response in mice. This response was significantly suppressed by L-menthol even at smoke concentrations as high as 300 mg/m³. Counterirritation by L-menthol was abolished by treatment with a selective inhibitor of Transient Receptor Potential Melastatin 8 (TRPM8), the neuronal cold/menthol receptor. Inclusion of menthol in the cigarette smoke resulted in roughly a 1.5-fold increase in plasma cotinine levels over those observed in mice exposed to smoke without added menthol. These findings document that, L-menthol, through TRPM8, is a strong suppressor of respiratory irritation responses, even during highly noxious exposures to cigarette smoke or smoke irritants, and increases blood cotinine. Therefore, L-menthol, as a cigarette additive, may promote smoking

Menthol Attenuates Respiratory Irritation and Elevates Blood Cotinine in Cigarette Smoke Exposed Mice

PubMed Central

Ha, Michael A.; Smith, Gregory J.; Cichocki, Joseph A.; Fan, Lu; Liu, Yi-Shiuan; Caceres, Ana I.; Jordt, Sven Eric; Morris, John B.

2015-01-01

Addition of menthol to cigarettes may be associated with increased initiation of smoking. The potential mechanisms underlying this association are not known. Menthol, likely due to its effects on cold-sensing peripheral sensory neurons, is known to inhibit the sensation of irritation elicited by respiratory irritants. However, it remains unclear whether menthol modulates cigarette smoke irritancy and nicotine absorption during initial exposures to cigarettes, thereby facilitating smoking initiation. Using plethysmography in a C57Bl/6J mouse model, we examined the effects of L-menthol, the menthol isomer added to cigarettes, on the respiratory sensory irritation response to primary smoke irritants (acrolein and cyclohexanone) and smoke of Kentucky reference 2R4 cigarettes. We also studied L-menthol’s effect on blood levels of the nicotine metabolite, cotinine, immediately after exposure to cigarette smoke. L-menthol suppressed the irritation response to acrolein with an apparent IC₅₀ of 4 ppm. Suppression was observed even at acrolein levels well above those necessary to produce a maximal response. Cigarette smoke, at exposure levels of 10 mg/m³ or higher, caused an immediate and marked sensory irritation response in mice. This response was significantly suppressed by L-menthol even at smoke concentrations as high as 300 mg/m³. Counterirritation by L-menthol was abolished by treatment with a selective inhibitor of Transient Receptor Potential Melastatin 8 (TRPM8), the neuronal cold/menthol receptor. Inclusion of menthol in the cigarette smoke resulted in roughly a 1.5-fold increase in plasma cotinine levels over those observed in mice exposed to smoke without added menthol. These findings document that, L-menthol, through TRPM8, is a strong suppressor of respiratory irritation responses, even during highly noxious exposures to cigarette smoke or smoke irritants, and increases blood cotinine. Therefore, L-menthol, as a cigarette additive, may promote smoking

Trends in respiratory morbidity of children in relation to their passive smoking exposure.

PubMed

Kukla, Lubomír; Hrubá, Drahoslava; Tyrlík, Mojmír

2006-12-01

Exposure of children to passive smoking is significantly associated with respiratory morbidity. Youngest children between 0-2 years are harmed in the most significant way, while, together with the growing age a decrease is observed of prevalence of respiratory diseases and influence of passive smoking. During repeated investigations of children from European Longitudinal Study of Pregnancy and Childhood (ELSPAC) it was assessed, whether and how in the period from the birth to five years of age varied the rate of children exposed to environment filled with smoke and what were the differences in the frequency of diseases among the groups of children with different exposure level. Some selected characteristics of health were chosen from documentation provided in the 6th, 18th month and 5 years of children's age and processed in four children groups that differ in smoking behaviour of their mothers. The differences were statistically assessed in SPSS programme. In all compared age categories were children of smoking mothers more often exposed to stay in environment filled with smoke: children of middle and heavy smokers more, children of light smokers less. In all groups of smoking mothers, children were more often protected from exposure to passive smoking in the age of six months than after they reached 18 months and 5 years of age: differences were mostly statistically significant on the level of 1% of significance. Attending the kindergarten presents significant protecting factor for five years old children: they are more exposed during weekends than on week days (p < 0.001, resp. p < 0.01). Both respiratory symptomatology and morbidity were highly significantly increased in previous life periods of those children, whose mothers smoked. At the age of five, life in smoking household causes more frequent incidence of asthmatic symptomatology: wheezing and apnoe, and higher prevalence of allergies against home and pollen dust with breathlessness and wheezing as well

Biomass Smoke Exposure Enhances Rhinovirus-Induced Inflammation in Primary Lung Fibroblasts

PubMed Central

Capistrano, Sarah J.; Zakarya, Razia; Chen, Hui; Oliver, Brian G.

2016-01-01

Biomass smoke is one of the major air pollutants and contributors of household air pollution worldwide. More than 3 billion people use biomass fuels for cooking and heating, while other sources of exposure are from the occurrence of bushfires and occupational conditions. Persistent biomass smoke exposure has been associated with acute lower respiratory infection (ALRI) as a major environmental risk factor. Children under the age of five years are the most susceptible in developing severe ALRI, which accounts for 940,000 deaths globally. Around 90% of cases are attributed to viral infections, such as influenza, adenovirus, and rhinovirus. Although several epidemiological studies have generated substantial evidence of the association of biomass smoke and respiratory infections, the underlying mechanism is still unknown. Using an in vitro model, primary human lung fibroblasts were stimulated with biomass smoke extract (BME), specifically investigating hardwood and softwood types, and human rhinovirus-16 for 24 h. Production of pro-inflammatory mediators, such as IL-6 and IL-8, were measured via ELISA. Firstly, we found that hardwood and softwood smoke extract (1%) up-regulate IL-6 and IL-8 release (p ≤ 0.05). In addition, human rhinovirus-16 further increased biomass smoke-induced IL-8 in fibroblasts, in comparison to the two stimulatory agents alone. We also investigated the effect of biomass smoke on viral susceptibility by measuring viral load, and found no significant changes between BME exposed and non-exposed infected fibroblasts. Activated signaling pathways for IL-6 and IL-8 production by BME stimulation were examined using signaling pathway inhibitors. p38 MAPK inhibitor SB239063 significantly attenuated IL-6 and IL-8 release the most (p ≤ 0.05). This study demonstrated that biomass smoke can modulate rhinovirus-induced inflammation during infection, which can alter the severity of the disease. The mechanism by which biomass smoke exposure increases

Biomass Smoke Exposure Enhances Rhinovirus-Induced Inflammation in Primary Lung Fibroblasts.

PubMed

Capistrano, Sarah J; Zakarya, Razia; Chen, Hui; Oliver, Brian G

2016-08-25

Biomass smoke is one of the major air pollutants and contributors of household air pollution worldwide. More than 3 billion people use biomass fuels for cooking and heating, while other sources of exposure are from the occurrence of bushfires and occupational conditions. Persistent biomass smoke exposure has been associated with acute lower respiratory infection (ALRI) as a major environmental risk factor. Children under the age of five years are the most susceptible in developing severe ALRI, which accounts for 940,000 deaths globally. Around 90% of cases are attributed to viral infections, such as influenza, adenovirus, and rhinovirus. Although several epidemiological studies have generated substantial evidence of the association of biomass smoke and respiratory infections, the underlying mechanism is still unknown. Using an in vitro model, primary human lung fibroblasts were stimulated with biomass smoke extract (BME), specifically investigating hardwood and softwood types, and human rhinovirus-16 for 24 h. Production of pro-inflammatory mediators, such as IL-6 and IL-8, were measured via ELISA. Firstly, we found that hardwood and softwood smoke extract (1%) up-regulate IL-6 and IL-8 release (p ≤ 0.05). In addition, human rhinovirus-16 further increased biomass smoke-induced IL-8 in fibroblasts, in comparison to the two stimulatory agents alone. We also investigated the effect of biomass smoke on viral susceptibility by measuring viral load, and found no significant changes between BME exposed and non-exposed infected fibroblasts. Activated signaling pathways for IL-6 and IL-8 production by BME stimulation were examined using signaling pathway inhibitors. p38 MAPK inhibitor SB239063 significantly attenuated IL-6 and IL-8 release the most (p ≤ 0.05). This study demonstrated that biomass smoke can modulate rhinovirus-induced inflammation during infection, which can alter the severity of the disease. The mechanism by which biomass smoke exposure increases

Respiratory infections and pneumonia: potential benefits of switching from smoking to vaping.

PubMed

Campagna, Davide; Amaradio, Maria Domenica; Sands, Mark F; Polosa, Riccardo

2016-01-01

Abstaining from tobacco smoking is likely to lower the risk of respiratory infections and pneumonia. Unfortunately, quitting smoking is not easy. Electronic cigarettes (ECs) are emerging as an attractive long-term alternative nicotine source to conventional cigarettes and are being adopted by smokers who wish to reduce or quit cigarette consumption. Also, given that the propylene glycol in EC aerosols is a potent bactericidal agent, switching from smoking to regular vaping is likely to produce additional lung health benefits. Here, we critically address some of the concerns arising from regular EC use in relation to lung health, including respiratory infections and pneumonia. In conclusion, smokers who quit by switching to regular ECs use can reduce risk and reverse harm from tobacco smoking. Innovation in the e-vapour category is likely not only to further minimise residual health risks, but also to maximise health benefits.

[Influence of smoking and industrial air pollutants on respiratory health of nickel industry workers].

PubMed

Shilov, V V; Siurin, S A

2015-01-01

Studies covered respiratory health of 1530 workers of nickel industry, among which were 796 (52.0%) smokers. Findings are that tobacco smoke combined with nickel industry hazards cause potentized negative effects in respiratory organs, with earlier and more frequent chronic bronchitis. For isolated influence of these factors, chronic bronchitis risk is higher from exposure to tobacco smoke vs. occupational hazards (OR = 2.48; DI 1.49-4.13). Chronic obstructive lung disease development in nickel industry workers is caused by smoking. Industrial air pollutants appeared to have no potentizing effect on COLD formation, as well as on toxic pneumosclerosis formation.

Smoking p66Shc knocked out mice develop respiratory bronchiolitis with fibrosis but not emphysema.

PubMed

Lunghi, Benedetta; De Cunto, Giovanna; Cavarra, Eleonora; Fineschi, Silvia; Bartalesi, Barbara; Lungarella, Giuseppe; Lucattelli, Monica

2015-01-01

The adaptor protein p66Shc regulates intracellular oxidant levels through the modulation of a forkhead-related transcription factor (FOXO3a). The genetic ablation of p66Shc (p66Shc-/-) renders mice resistant to oxidative stress and p53-dependent apoptosis. We investigated whether p66Shc ablation in mice modifies lung cellular and molecular responses to cigarette smoke (CS) exposure. No differences between wild type (WT) and p66Shc-/- mice were observed in terms of inflammation and oxidant burden after acute CS exposure; however,p66Shc ablation modifies specific features of chronic inflammation induced by repeated exposure to CS. Unlike WT mice, p66Shc-/- mice did not develop emphysema, showing protection toward oxidative damage to DNA and apoptosis as revealed by a trivial 8-hydroxyguanosine staining and faint TUNEL and caspase-3 positivity on alveolar epithelial cells. Unexpectedly, CS exposure in p66Shc-/- mice resulted in respiratory bronchiolitis with fibrosis in surrounded alveoli. Respiratory bronchiolitis was characterized by peribronchiolar infiltrates of lymphocytes and histiocytes, accumulation of ageing pigmented macrophages within and around bronchioles, and peribronchiolar fibrosis. The blockage of apoptosis interferes with the macrophage "clearance" from alveolar spaces, favouring the accumulation of aging macrophages into alveoli and the progressive accumulation of iron pigment in long-lived senescent cells. The presence of areas of interstitial and alveolar fibrosis in peripheral parenchyma often accompanied the bronchiolar changes. Macrophages from smoking p66Shc-/- mice elaborate M2 cytokines (i.e., IL-4 and IL-13) and enzymes (i.e., chitinase and arginase I), which can promote TGF-beta expression, collagen deposition, and fibrosis in the surrounding areas. We demonstrate here that resistance to oxidative stress and p53-dependent apoptosis can modify tissue responses to CS caused by chronic inflammation without influencing early inflammatory

Future respiratory hospital admissions from wildfire smoke under climate change in the Western US

NASA Astrophysics Data System (ADS)

Coco Liu, Jia; Mickley, Loretta J.; Sulprizio, Melissa P.; Yue, Xu; Peng, Roger D.; Dominici, Francesca; Bell, Michelle L.

2016-12-01

Background. Wildfires are anticipated to be more frequent and intense under climate change. As a result, wildfires may emit more air pollutants that can harm health in communities in the future. The health impacts of wildfire smoke under climate change are largely unknown. Methods. We linked projections of future levels of fine particulate matter (PM2.5) specifically from wildfire smoke under the A1B climate change scenario using the GEOS-Chem model for 2046-2051, present-day estimates of hospital admission impacts from wildfire smoke, and future population projections to estimate the change in respiratory hospital admissions for persons ≥65 years by county (n = 561) from wildfire PM2.5 under climate change in the Western US. Results. The increase in intense wildfire smoke days from climate change would result in an estimated 178 (95% confidence interval: 6.2, 361) additional respiratory hospital admissions in the Western US, accounting for estimated future increase in the elderly population. Climate change is estimated to impose an additional 4990 high-pollution smoke days. Central Colorado, Washington and southern California are estimated to experience the highest percentage increase in respiratory admissions from wildfire smoke under climate change. Conclusion. Although the increase in number of respiratory admissions from wildfire smoke seems modest, these results provide important scientific evidence of an often-ignored aspect of wildfire impact, and information on their anticipated spatial distribution. Wildfires can cause serious social burdens such as property damage and suppression cost, but can also raise health problems. The results provide information that can be incorporated into development of environmental and health policies in response to climate change. Climate change adaptation policies could incorporate scientific evidence on health risks from natural disasters such as wildfires.

Early childhood predictors of early onset of smoking: a birth prospective study.

PubMed

Hayatbakhsh, Reza; Mamun, Abdullah A; Williams, Gail M; O'Callaghan, Michael J; Najman, Jake M

2013-10-01

Early onset of smoking is associated with subsequent abuse of other substances and development of negative health outcomes. This study aimed to examine early life predictors of onset of smoking in an Australian young cohort. Data were from the Mater Hospital and University of Queensland Study of Pregnancy (MUSP), a population-based prospective birth cohort study (1981-2012). The present study is based on a cohort of 3714 young adults who self-reported smoking status and age of onset of smoking at the 21-year follow-up. Of these, data were available for 3039 on early childhood factors collected between the baseline and 14-year follow-up of the study. Of 3714 young adults, 49.6% (49.9% males and 49.3% females) reported having ever smoked cigarettes. For those who had ever smoked, mean and median ages at first smoke were 15.5 and 16.0years, respectively. In multivariate Cox proportional hazard analysis mother's education, change in maternal marital status, maternal cigarette smoking and alcohol consumption, maternal depression and child externalizing when the child was 5years statistically significantly predicted early onset of smoking. The data suggest that individuals exposed to personal and environmental risk factors during the early stage of childhood are at increased risk of initiation to cigarette smoking at an earlier age. Identification of the pathways of association between these early life factors and initiation to cigarette smoking may help reduce risk of tobacco smoking in adolescents and its adverse consequences. Copyright © 2013 Elsevier Ltd. All rights reserved.

Glass fibers and vapor phase components of cigarette smoke as cofactors in experimental respiratory tract carcinogenesis.

PubMed

Feron, V J; Kuper, C F; Spit, B J; Reuzel, P G; Woutersen, R A

1985-01-01

Syrian golden hamsters were given intratracheal instillations of glass fibers with or without BP suspended in saline, once a fortnight for 52 weeks; the experiment was terminated at week 85. No tumors of the respiratory tract were observed in hamsters treated with glass fibers alone. There was no indication that glass fibers enhanced the development of respiratory tract tumors induced by BP. In another study Syrian golden hamsters were exposed to fresh air or to a mixture of 4 major vapor phase components of cigarette smoke, viz. isoprene (800----700 ppm), methyl chloride (1000----900 ppm), methyl nitrite (200----190 ppm) and acetaldehyde (1400----1200 ppm) for a period of at most 23 months. Some of the animals were also given repeated intratracheal instillations of BP or norharman in saline. Laryngeal tumors were found in 7/31 male and 6/32 female hamsters exposed only to the vapor mixture, whereas no laryngeal tumors occurred in controls. The tumor response of the larynx most probably has to be ascribed entirely to the action of acetaldehyde. Simultaneous treatment with norharman or BP did not affect the tumor response of the larynx. Acetaldehyde may occur in the vapor phase of cigarette smoke at levels up to 2000 ppm. Chronic inhalation exposure of rats to acetaldehyde at levels of 0 (controls), 750, 1500 or 3000----1000 ppm resulted in a high incidence of nasal carcinomas, both squamous cell carcinomas of the respiratory epithelium and adenocarcinomas of the olfactory epithelium. It was discussed that acetaldehyde may significantly contribute to the induction of bronchogenic cancer by cigarette smoke in man. No evidence was obtained for a role of isoprene, methyl chloride or methyl nitrite in the induction of lung cancer by cigarette smoke.

Association between respiratory tract diseases and secondhand smoke exposure among never smoking flight attendants: a cross-sectional survey

PubMed Central

Ebbert, Jon O; Croghan, Ivana T; Schroeder, Darrell R; Murawski, Judith; Hurt, Richard D

2007-01-01

Background Little is known about long-term adverse health consequences experienced by flight attendants exposed to secondhand smoke (SHS) during the time smoking was allowed on airplanes. We undertook this study to evaluate the association between accumulated flight time in smoky airplane cabins and respiratory tract diseases in a cohort of never smoking flight attendants. Methods We conducted a mailed survey in a cohort of flight attendants. Of 15,000 mailed questionnaires, 2053 (14%) were completed and returned. We excluded respondents with a personal history of smoking (n = 748) and non smokers with a history of respiratory tract diseases before the age of 18 years (n = 298). The remaining 1007 respondents form the study sample. Results The overall study sample was predominantly white (86%) and female (89%), with a mean age of 54 years. Overall, 69.7% of the respondents were diagnosed with at least one respiratory tract disease. Among these respondents, 43.4% reported a diagnosis of sinusitis, 40.3% allergies, 30.8% bronchitis, 23.2% middle ear infections, 13.6% asthma, 13.4% hay fever, 12.5% pneumonia, and 2.0% chronic obstructive pulmonary disease. More hours in a smoky cabin were observed to be significantly associated with sinusitis (OR = 1.21; p = 0.024), middle ear infections (OR = 1.30; p = 0.006), and asthma (OR = 1.26; p = 0.042). Conclusion We observed a significant association between hours of smoky cabin exposure and self-reported reported sinusitis, middle ear infections, and asthma. Our findings suggest a dose-response between duration of SHS exposure and diseases of the respiratory tract. Our findings add additional evidence to the growing body of knowledge supporting the need for widespread implementation of clean indoor air policies to decrease the risk of adverse health consequences experienced by never smokers exposed to SHS. PMID:17897468

Fentanyl-induced respiratory depression is attenuated in pregnant patients

PubMed Central

Sun, Jie; Yu, Min; Fang, Yin; Ding, Zhengnian

2017-01-01

Background Respiratory depression is a complication of intravenous fentanyl administration. The effect of pregnancy on respiratory depression following opioid administration is unclear. This study investigated the effect of pregnancy on fentanyl-induced respiratory depression. Patients and methods Female patients were divided into three groups (n=20 per group): control group (non-pregnant and scheduled for laparoscopic surgery), early pregnancy group (pregnant for 45–60 days and scheduled for abortion), and postpartum group (5–7 days postpartum scheduled for complete curettage of uterine cavity). All patients received an intravenous infusion of fentanyl 2 μg/kg. Respiratory rate (RR), end-tidal pressure of carbon dioxide (PETCO2), and pulse oxygen saturation (SpO2) were recorded continuously from just before fentanyl infusion to 15 min after commencing infusion. Plasma levels of progesterone were measured. Results SpO2 levels in the early pregnancy and postpartum groups were significantly higher and the levels of RR and PETCO2 were significantly lower than the control group. RR and SpO2 levels were significantly decreased in all groups, whereas PETCO2 was significantly increased after fentanyl infusion. The rates of RR increase and SpO2 decrease were significantly faster in the control group than in the other groups. The lowest SpO2 after intravenous fentanyl administration was significantly positively correlated with plasma progesterone levels. Conclusion Pregnancy improves fentanyl-induced respiratory depression, which may be associated with the increased levels of plasma progesterone. PMID:29200828

Effects of a smoke-free law on hair nicotine and respiratory symptoms of restaurant and bar workers.

PubMed

Hahn, Ellen J; Rayens, Mary Kay; York, Nancy; Okoli, Chizimuzo T C; Zhang, Mei; Dignan, Mark; Al-Delaimy, Wael K

2006-09-01

Bar and restaurant workers' exposure to secondhand smoke (SHS) was compared before and 3 and 6 months after implementation of a smoke-free ordinance. Hair nicotine, self-reported exposure to SHS, and respiratory symptoms were assessed on 105 smoking and nonsmoking workers from randomly selected establishments in Lexington, Kentucky. Thirty-eight percent were current smokers with more than half smoking 10 or fewer cigarettes per day. Workers provided a hair sample at baseline and at the 3-month interview. There was a significant decline in hair nicotine 3 months postlaw when controlling for cigarettes smoked per day. Bar workers showed a significantly larger decline in hair nicotine compared with restaurant workers. The only significant decline in SHS exposure was in the workplace and other public places. Regardless of smoking status, respiratory symptoms declined significantly postlaw. Hospitality workers demonstrated significant declines in hair nicotine and respiratory symptoms after the law. Comprehensive smoke-free laws can provide the greatest protection to bar workers who are the most vulnerable to SHS exposure at work.

Respiratory tract deposition efficiencies: evaluation of effects from smoke released in the Cerro Grande forest fire.

PubMed

Schöllnberger, H; Aden, J; Scott, B R

2002-01-01

Forest-fire smoke inhaled by humans can cause various health effects. This smoke contains toxic chemicals and naturally occurring radionuclides. In northern New Mexico, a large wildfire occurred in May 2000. Known as the Cerro Grande Fire, it devastated the town of Los Alamos and damaged Los Alamos National Laboratory (LANL). Residents were concerned about the possible dissemination of radionuclides from LANL via smoke from the fire. To evaluate potential health effects of inhaling radionuclides contained in the smoke from the Cerro Grande Fire, it was first necessary to evaluate how much smoke would deposit in the human respiratory tract. The purpose of this study was to evaluate respiratory-tract deposition efficiencies of airborne forest-fire smoke for persons of different ages exposed while inside their homes. Potential non-radiological health effects of a forest fire are reviewed. The deposition efficiencies presented can be used to evaluate in-home smoke deposition in the respiratory tract and expected radionuclide intake related to forest fires. The impact of smoke exposure on firemen fighting a forest fire is quantitatively discussed and compared. They primarily inhaled forest-fire smoke while outdoors where the smoke concentration was much higher than inside. Radionuclides released at the LANL site via the Cerro Grande Fire were restricted to naturally occurring radionuclides from burning trees and vegetation. Radiation doses from inhaled airborne radionuclides to individuals inside and outside the Los Alamos area were likely very small.

Early diagnosis based on clinical history and BALF for successful management of smoking-induced acute eosinophilic pneumonia without unnecessary antibiotic usage: a case report.

PubMed

Song, Jee In; Kim, Yang-Ki; Hwang, Jung Hwa; Yang, Hyeon-Jong

2016-01-01

Acute eosinophilic pneumonia (AEP) is a rapid onset and severe respiratory illness characterized by acute febrile respiratory insufficiency, eosinophilic infiltration in the lungs and unique findings on chest imaging. Difficulty in differentiating from other respiratory distress caused by community-acquired pneumonia may result in a delayed diagnosis or treatment with empirical antibiotics. Sixteen-year-old boy who developed AEP with marked eosinophilia in bronchoalveolar lavage fluid (BALF, 36.6%), decreased diffusion capacity of the lung for carbon monoxide (62%) and unique radiological findings. Although he initially denied tobacco use, on repeated thorough clinical history questioning, he eventually admitted beginning smoking 19 days before the onset of symptoms with gradually increasing frequency. His symptoms resolved quickly without use of antibiotics after cessation of tobacco and treatment with corticosteroids. Careful clinical history taking regarding tobacco use combined with early examination of BALF and recognition of unique radiological findings are critical for proper management of AEP.

[Influence of parental smoking on pediatric hospitalization for respiratory illness among children aged less than 2 years].

PubMed

Pardo Crespo , M R; Pérez Iglesias , R; Llorca, J; Rodrigo Calabia , E; Alvarez Granda , L; Delgado Rodríguez, M

2000-10-01

To determine whether parental smoking increased the risk of hospitalization among children aged less than 2 years. Case-reference study conducted from April 1995-May 1996. The group of cases was composed of 40% of all the children aged 2 years or less years admitted to our hospital (n=392). The reference population was composed of 15% of the live newborns in the same the hospital (n=493). The information was obtained by face-to-face interview after delivery in both populations and by telephone interview or postal survey and was completed in the reference population one year after delivery. Maternal smoking increased the risk of hospitalization for lower respiratory illness (adjusted RR - 1.79; 95% CI = 1.03-3.11). Moreover, the risk of hospitalization for upper or lower respiratory illness, lower respiratory illness and bronchiolitis was increased when the mother smoked more than 19 cigarettes per day. The results were adjusted for confounding factors such as prenatal age, ethnic group, maternal education, social class, breastfeeding and hospitalization of the newborn. Parental smoking, specifically maternal smoking, affects children's health, increasing the risk of hospitalization for respiratory illness in the first 2 years of life.

Clinically important respiratory effects of dust exposure and smoking in British coal miners

DOE Office of Scientific and Technical Information (OSTI.GOV)

Marine, W.M.; Gurr, D.; Jacobsen, M.

A unique data set of 3380 British coal miners has been reanalyzed with major focus on nonpneumoconiotic respiratory conditions. The aim was to assess the independent contribution of smoking and exposure to respirable dust to clinically significant measures of respiratory dysfunction. Exposure to coal-mine dust was monitored over a 10-yr period. Medical surveys provided estimates of prior dust exposure and recorded respiratory symptoms. Each man's FEV1 was compared with the level predicted for his age and height by an internally derived prediction equation for FEV1. Four respiratory indices were considered at the end of the 10-yr period: FEV1 less thanmore » 80%, chronic bronchitis, chronic bronchitis with FEV1 less than 80%, and FEV1 less than 65%. Results were uniformly incorporated into logistic regression equations for each condition. The equations include coefficients for age, dust, and when indicated, an interaction term for age and dust. Dust-related increases in prevalence of each of the 4 conditions were statistically significant and were similar for smokers and nonsmokers at the mean age (47 yr). There was no evidence that smoking potentiates the effect of exposure to dust. Estimates of prevalences at the mean age of all 4 measures of respiratory dysfunction were greater in smokers. At intermediate and high dust exposure the prevalence of the 4 conditions in nonsmokers approached the prevalence in smokers at hypothetically zero dust exposure. Both smoking and dust exposure can cause clinically important respiratory dysfunction and their separate contributions to obstructive airway disease in coal miners appear to be additive.« less

Effect of a smoking ban on respiratory health in nonsmoking hospitality workers: a prospective cohort study.

PubMed

Rajkumar, Sarah; Stolz, Daiana; Hammer, Jürg; Moeller, Alexander; Bauer, Georg F; Huynh, Cong Khanh; Röösli, Martin

2014-10-01

The aim of this study was to examine the effect of a smoking ban on lung function, fractional exhaled nitric oxide, and respiratory symptoms in nonsmoking hospitality workers. Secondhand smoke exposure at the workplace, spirometry, and fractional exhaled nitric oxide were measured in 92 nonsmoking hospitality workers before as well as twice after a smoking ban. At baseline, secondhand smoke-exposed hospitality workers had lung function values significantly below the population average. After the smoking ban, the covariate-adjusted odds ratio for cough was 0.59 (95% confidence interval, 0.36 to 0.93) and for chronic bronchitis 0.75 (95% confidence interval, 0.55 to 1.02) compared with the preban period. The below-average lung function before the smoking ban indicates chronic damages from long-term exposure. Respiratory symptoms such as cough decreased within 12 months after the ban.

Antenatal Determinants of Bronchopulmonary Dysplasia and Late Respiratory Disease in Preterm Infants.

PubMed

Morrow, Lindsey A; Wagner, Brandie D; Ingram, David A; Poindexter, Brenda B; Schibler, Kurt; Cotten, C Michael; Dagle, John; Sontag, Marci K; Mourani, Peter M; Abman, Steven H

2017-08-01

Mechanisms contributing to chronic lung disease after preterm birth are incompletely understood. To identify antenatal risk factors associated with increased risk for bronchopulmonary dysplasia (BPD) and respiratory disease during early childhood after preterm birth, we performed a prospective, longitudinal study of 587 preterm infants with gestational age less than 34 weeks and birth weights between 500 and 1,250 g. Data collected included perinatal information and assessments during the neonatal intensive care unit admission and longitudinal follow-up by questionnaire until 2 years of age. After adjusting for covariates, we found that maternal smoking prior to preterm birth increased the odds of having an infant with BPD by twofold (P = 0.02). Maternal smoking was associated with prolonged mechanical ventilation and respiratory support during the neonatal intensive care unit admission. Preexisting hypertension was associated with a twofold (P = 0.04) increase in odds for BPD. Lower gestational age and birth weight z-scores were associated with BPD. Preterm infants who were exposed to maternal smoking had higher rates of late respiratory disease during childhood. Twenty-two percent of infants diagnosed with BPD and 34% of preterm infants without BPD had no clinical signs of late respiratory disease during early childhood. We conclude that maternal smoking and hypertension increase the odds for developing BPD after preterm birth, and that maternal smoking is strongly associated with increased odds for late respiratory morbidities during early childhood. These findings suggest that in addition to the BPD diagnosis at 36 weeks, other factors modulate late respiratory outcomes during childhood. We speculate that measures to reduce maternal smoking not only will lower the risk for preterm birth but also will improve late respiratory morbidities after preterm birth.

Respiratory Health Effects of Passive Smoking: Lung Cancer and Other Disorders

EPA Pesticide Factsheets

This page contains a PDF version of the Respiratory Health Effects of Passive Smoking report and also a pdf version of an overview of progress made in reducing exposure to secondsmoke in the past 25 years.

Association between secondhand smoking in the home and respiratory morbidity in preschool children.

PubMed

Sigaud, Cecília Helena de Siqueira; Castanheira, Ana Barbara de Couto; Costa, Priscila

2016-01-01

Identifying the prevalence of secondhand smoking in the home and its association with morbidity and hospitalization from respiratory causes in preschool children. This is a cross-sectional study conducted in five early childhood education centers at a public university in São Paulo. Sample size calculation was performed and the participants were randomly determined. Data were collected through questionnaires completed by family members or caregivers of 215 children. Chi-square and Student's t-test were used for the statistical analysis, using a 0.05 significance level. The prevalence of secondhand smoke in the household was 15.3%. Bivariate analysis revealed that secondhand smoke in the household was associated with the occurrence of rapid breathing, subdiaphragmatic retractions in the past three months, and treated ear infections/otitis. A low prevalence of secondhand smoking in the home was found. Secondhand smoke was associated with a higher prevalence of respiratory symptoms and morbidity. Identificar a prevalência de tabagismo passivo em domicílio e verificar sua associação com morbidades e hospitalização por causas respiratórias em crianças pré-escolares. Trata-se de estudo transversal conduzido em cinco centros de educação infantil de uma universidade pública de São Paulo. Foi realizado cálculo de tamanho amostral, e a seleção dos participantes foi feita por sorteio. Os dados foram coletados por meio de questionários preenchidos pelos familiares ou cuidadores de 215 crianças. Na análise estatística foram empregados os testes Qui-quadrado e t-Student, considerando-se um nível de significância de 0,05. A prevalência de tabagismo passivo em domicílio foi de 15,3%. Verificou-se na análise bivariada que o tabagismo passivo em domicílio esteve associado à ocorrência de respiração rápida, retração subdiafragmática nos últimos três meses, e otite tratada. Verificou-se uma baixa prevalência de tabagismo passivo domiciliar. O

Driving kids to smoke? Children's reported exposure to smoke in cars and early smoking initiation.

PubMed

Glover, Marewa; Scragg, Robert; Min, Sandar; Kira, Anette; Nosa, Vili; McCool, Judith; Bullen, Chris

2011-11-01

The health risks associated with second hand smoke (SHS) are well-known. However, little is known about exposure to SHS in cars and risk of smoking uptake. This paper investigates the association between pre-adolescents reported exposure to smoking in cars and prevalence of early stage smoking activity. Data from Keeping Kids Smokefree baseline surveys of students were used to investigate smoking status and reported exposure to smoking in cars. Log binomial regression analyses were used to investigate if reported exposure to SHS in cars was associated with smoking prevalence. 83% of 5676 students invited took part. After controlling for all variables reported exposure to smoking in cars and homes were significantly associated with increased risk of initiated smoking (RR 1.87, 95% CI 1.43-2.44, and RR 1.5, 95% CI 1.13-1.97, respectively). Exposure to smoking in cars was substantially and significantly associated with risk of current smoking (RR 3.21, 95% CI 1.45-7.08). Early smoking uptake is associated with students' reported exposure to smoking in cars which confirms the importance of protecting children from SHS. Smoking in cars is under parental control and therefore modifiable. Moreover, children's reports of SHlS exposure offer a simple way of identifying families who can be targeted for tobacco control interventions. Copyright © 2011 Elsevier Ltd. All rights reserved.

Smoking status in parents of children hospitalized with a diagnosis of respiratory system disorders

PubMed Central

Cinar, Nursan; Dede, Cemile; Cevahir, Reyhan; Sevimli, Döndü

2010-01-01

The purpose of this study was to investigate the relationship between the statuses of hospitalized children with diagnosis of respiratory tract disease with cigarette use in the parents. This descriptive study was conducted in a Gowerment Hospital in the Sakarya city center in Turkey between June 2007 and June 2008. The inclusion criterion was willingness of families with children hospitalized due to diagnosis of respiratory disease to particípate in the study. Data were collected from 345 parents using the questionnaire prepared by researchers. In our study parental smoking was observed in 42.3% of fathers, 7.8% mothers and for 20.9% both parents were smoking. It was found that the hospitalization rates were more than two times higher in children diagnosed with pneumonia and bronchitis and three times higher in children hospitalized for asthma whose parents smoke at home compared to those whose parents are non-smokers. Health care professionals who take care of children need to discuss the harmful effects of smoking and the importance of reducing childhood exposure to secondhand smoke; parents should be educated and encouraged not to smoke. PMID:21108615

The effect of passive exposure to tobacco smoke on perioperative respiratory complications and the duration of recovery.

PubMed

Simsek, Esen; Karaman, Yucel; Gonullu, Mustafa; Tekgul, Zeki; Cakmak, Meltem

2016-01-01

The incidence of perioperative respiratory complications and postoperative care unit recovery time investigated in patients with passive tobacco smoke exposure according to the degree of exposure. Total 270 patients ranging in age from 18 to 60 years with the ASA physical status I or II exposed and not exposed to passive tobacco smoke received general anesthesia for various elective surgical operations evaluated for the study. Patients divided into two groups as exposed and non-exposed to passive tobacco smoke, those exposed to passive smoke are also divided into two groups according to the degree of exposure. Patients taken to the postoperative care unit (PACU) at the end of the operation and monitorized until Modified Aldrete's Scores became 9 and more. Respiratory complications evaluated and recorded in intraoperative and postoperative period. A total of 251 patients were enrolled; 63 (25.1%) patients had airway complications, 11 (4.4%) had complications intraoperatively and 52 (20.7%) patients had complications postoperatively. There has been found significant relation with passive tobacco smoke exposure and high incidences of perioperative and postoperative respiratory complications. The risk of cough, desaturation and hypersecretion complications were found to be increased depending on the degree of exposure. There was significant relation between the degree of passive smoke exposure and the duration of PACU stay. Passive tobacco smoke exposed general anesthesia receiving patients also regarding to the degree of exposure having high rates of perioperative respiratory complications and prolongation of PACU stays when compared with unexposed patients. Copyright © 2015 Sociedade Brasileira de Anestesiologia. Published by Elsevier Editora Ltda. All rights reserved.

[The effect of passive exposure to tobacco smoke on perioperative respiratory complications and the duration of recovery].

PubMed

Simsek, Esen; Karaman, Yucel; Gonullu, Mustafa; Tekgul, Zeki; Cakmak, Meltem

2016-01-01

The incidence of perioperative respiratory complications and postoperative care unit recovery time investigated in patients with passive tobacco smoke exposure according to the degree of exposure. Total 270 patients ranging in age from 18 to 60 years with the ASA physical status I or II exposed and not exposed to passive tobacco smoke received general anesthesia for various elective surgical operations evaluated for the study. Patients divided into two groups as exposed and non-exposed to passive tobacco smoke, those exposed to passive smoke are also divided into two groups according to the degree of exposure. Patients taken to the postoperative care unit (PACU) at the end of the operation and monitorized until Modified Aldrete's Scores became 9 and more. Respiratory complications evaluated and recorded in intraoperative and postoperative period. A total of 251 patients were enrolled; 63 (25.1%) patients had airway complications, 11 (4.4%) had complications intraoperatively and 52 (20.7%) patients had complications postoperatively. There has been found significant relation with passive tobacco smoke exposure and high incidences of perioperative and postoperative respiratory complications. The risk of cough, desaturation and hypersecretion complications were found to be increased depending on the degree of exposure. There was significant relation between the degree of passive smoke exposure and the duration of PACU stay. Passive tobacco smoke exposed general anesthesia receiving patients also regarding to the degree of exposure having high rates of perioperative respiratory complications and prolongation of PACU stays when compared with unexposed patients. Copyright © 2015 Sociedade Brasileira de Anestesiologia. Publicado por Elsevier Editora Ltda. All rights reserved.

Toxicological impact of waterpipe smoking and flavorings in the oral cavity and respiratory system.

PubMed

Javed, Fawad; ALHarthi, Shatha Subhi; BinShabaib, Munerah Saleh; Gajendra, Sangeeta; Romanos, Georgios E; Rahman, Irfan

2017-08-01

Waterpipe smoking (WS), an emerging trend has major health concerns. It is prevalent worldwide as a recreational activity both indoors and outdoors. The aim of this review was to assess the impact of waterpipe smoke on the oral and respiratory system (oral cavity and pulmonary tissues). A number of studies have shown that periodontal health status is compromised in waterpipe smokers when compared with nonsmokers. Some studies have associated WS with oral premalignant and malignant lesions; however, due to the poor quality of these studies, the presented outcomes should be interpreted with caution. Although cigarette smoking has been considered as a potential risk factor for dental caries; there are no studies in indexed literature that have shown an association to exist between dental caries and WS. Inhaled waterpipe smoke imposes oxidative stress and inflammatory responses and compromises the ventilatory capacity of the lungs and may lead to an increased risk of decline in lung function. WS may cause oral and pulmonary diseases, such as periodontal disease and chronic obstructive airway disease, respectively. The association between WS and development of dental caries and oral pre-cancer and their relationships with chronic airways disease requires investigations. This review discusses the current evidence of waterpipe smoke effects on the oral health and respiratory system based on basic and clinical science and provides future directions for research and regulatory science on how WS can affect the oral cavity and the respiratory/pulmonary system.

Reductions in cardiovascular, cerebrovascular, and respiratory mortality following the national irish smoking ban: interrupted time-series analysis.

PubMed

Stallings-Smith, Sericea; Zeka, Ariana; Goodman, Pat; Kabir, Zubair; Clancy, Luke

2013-01-01

Previous studies have shown decreases in cardiovascular mortality following the implementation of comprehensive smoking bans. It is not known whether cerebrovascular or respiratory mortality decreases post-ban. On March 29, 2004, the Republic of Ireland became the first country in the world to implement a national workplace smoking ban. The aim of this study was to assess the effect of this policy on all-cause and cause-specific, non-trauma mortality. A time-series epidemiologic assessment was conducted, utilizing Poisson regression to examine weekly age and gender-standardized rates for 215,878 non-trauma deaths in the Irish population, ages ≥35 years. The study period was from January 1, 2000, to December 31, 2007, with a post-ban follow-up of 3.75 years. All models were adjusted for time trend, season, influenza, and smoking prevalence. Following ban implementation, an immediate 13% decrease in all-cause mortality (RR: 0.87; 95% CI: 0.76-0.99), a 26% reduction in ischemic heart disease (IHD) (RR: 0.74; 95% CI: 0.63-0.88), a 32% reduction in stroke (RR: 0.68; 95% CI: 0.54-0.85), and a 38% reduction in chronic obstructive pulmonary disease (COPD) (RR: 0.62; 95% CI: 0.46-0.83) mortality was observed. Post-ban reductions in IHD, stroke, and COPD mortalities were seen in ages ≥65 years, but not in ages 35-64 years. COPD mortality reductions were found only in females (RR: 0.47; 95% CI: 0.32-0.70). Post-ban annual trend reductions were not detected for any smoking-related causes of death. Unadjusted estimates indicate that 3,726 (95% CI: 2,305-4,629) smoking-related deaths were likely prevented post-ban. Mortality decreases were primarily due to reductions in passive smoking. The national Irish smoking ban was associated with immediate reductions in early mortality. Importantly, post-ban risk differences did not change with a longer follow-up period. This study corroborates previous evidence for cardiovascular causes, and is the first to demonstrate reductions in

Smoke Exposure Exacerbates an Ethanol-Induced Defect in Mucociliary Clearance of Streptococcus pneumoniae

PubMed Central

Vander Top, Elizabeth A.; Wyatt, Todd A.; Gentry-Nielsen, Martha J.

2005-01-01

Background Alcoholics and smokers are particularly susceptible to pulmonary infections caused by Streptococcus pneumoniae, the pneumococcus. Infection begins when pneumococci colonizing the nasopharynx are aspirated into the lower respiratory tract. The major host defense against this movement is the mucociliary clearance apparatus. Both cigarette smoke and ethanol (EtOH) exposure alter ciliary beating and protein kinase activity in the respiratory mucosa in vitro, but their effects on bacterial clearance in the intact animal have not been determined. Methods Male Sprague-Dawley rats were exposed twice daily for 12 weeks to either the smoke generated from 30 cigarettes (smoke-exposed) or room air (sham-exposed). For the last five weeks of smoke exposure, the rats were fed Lieber-DeCarli liquid diets containing 0%, 16%, 26% or 36% EtOH calories. The rats then were infected intranasally with S. pneumoniae, and movement of the organisms into the lower respiratory tract was quantified by plate counts of the trachea and lungs four hours later. Ciliary beat frequency (CBF) analysis was performed on tracheal ring explants from each animal before and after stimulation with the β-agonist isoproterenol, and tracheal epithelial cell protein kinase C (PKC) activity was measured. Results Ingestion of any of the EtOH-containing diets resulted in a dose-dependent increase in movement of S. pneumoniae into the rats’ lungs. This EtOH-induced defect was augmented further by concurrent smoke exposure, although smoke exposure alone had little effect on S. pneumoniae movement. Smoke, but not EtOH exposure, activated tracheal epithelial cell PKC. Increased movement of organisms into lungs correlated with a decrease in CBF, and loss of the ciliary response to isoproterenol. Conclusion EtOH ingestion in our model facilitates movement of S. pneumoniae into rats’ lungs, a phenomenon exacerbated by concurrent smoke exposure. Furthermore, the organism’s movement into the lungs

Respiratory symptoms in Lancashire textile weavers.

PubMed

Raza, S N; Fletcher, A M; Pickering, C A; Niven, R M; Faragher, E B

1999-08-01

To investigate a large population of cotton textile weavers for reported respiratory symptoms relative to occupational factors, smoking, and exposure to dust. Cotton processing is known to produce a respiratory disease known as byssinosis particularly in the early processes of cotton spinning. Relatively little is known about the respiratory health of the cotton weavers who produce cloth from spun cotton. By the time cotton is woven many of the original contaminants have been removed. 1295 operatives from a target population of 1428 were given an interviewer led respiratory questionnaire. The presence of upper and lower respiratory tract symptoms were sought and the work relatedness of these symptoms determined by a stem questionnaire design. Also occupational and demographic details were obtained and spirometry and personal dust sampling performed. Byssinosis was present in only four people (0.3%). Chronic bronchitis had a moderate overall prevalence of about 6% and was related predominantly to smoking. There were several other work related respiratory symptoms (persistent cough 3.9%, chronic production of phlegm 3.6%, chest tightness 4.8%, wheezing 5.4%, and breathlessness 2.3%). All of these were predicted predominantly by smoking (either past or present), with no consistent independent effect of exposure to dust. Work related eye and nasal symptoms were more common (10.4% and 16.9% respectively). Byssinosis is a rare respiratory symptom in cotton weaving. Other work related respiratory symptoms were reported but their presence was predominantly related to smoking with no consistent effects of exposure to dust.

Cigarette Smoke Exposure and the Acute Respiratory Distress Syndrome

PubMed Central

Calfee, Carolyn S.; Matthay, Michael A.; Kangelaris, Kirsten N.; Siew, Edward D.; Janz, David R; Bernard, Gordon R.; May, Addison K; Jacob, Peyton; Havel, Christopher; Benowitz, Neal L.; Ware, Lorraine B.

2016-01-01

Objective The association between cigarette smoke exposure and the acute respiratory distress syndrome (ARDS) in patients with the most common ARDS risk factors of sepsis, pneumonia, and aspiration has not been well-studied. The goal of this study was to test the association between biomarker-confirmed cigarette smoking and ARDS in a diverse cohort. Design, Setting, Patients We obtained smoking histories and measured urine NNAL (a biomarker of cigarette smoke exposure) in 426 patients with ARDS risk factors (excluding trauma and transfusion) in a prospective cohort of critically ill patients at a single tertiary care center and tested the association between smoking and ARDS. Interventions None. Measurements and Main Results The association between cigarette smoke exposure and ARDS differed based on ARDS risk factor (p<0.02 for interaction). In patients with non-pulmonary sepsis as the primary ARDS risk factor (n=212), 39% of those with ARDS were current smokers by history, compared with 22% of those without ARDS (odds ratio 2.28 (95% CI 1.24–4.18); p=0.007). Likewise, cigarette smoke exposure as measured by urine NNAL was significantly associated with ARDS in this group. The increased risk of ARDS in non-pulmonary sepsis was restricted to patients with NNAL levels consistent with active smoking and was robust to adjustment for other ARDS predictors. Cigarette smoke exposure as measured by history or NNAL was not associated with ARDS in patients with other risk factors (e.g. pneumonia, aspiration). Conclusions Cigarette smoking measured both by history and by biomarker is associated with an increased risk of ARDS in patients with non-pulmonary sepsis. This finding has important implications for tobacco product regulation and for understanding the pathogenesis of ARDS. PMID:26010690

Smoke-induced seed germination in California chaparral

USGS Publications Warehouse

Keeley, J.E.; Fotheringham, C.J.

1998-01-01

The California chaparral community has a rich flora of species with different mechanisms for cuing germination to postfire conditions. Heat shock triggers germination of certain species but has no stimulatory effect on a great many other postfire species that are chemically stimulated by combustion products. Previous reports have shown that charred wood will induce germination, and here we report that smoke also induces germination in these same species. Smoke is highly effective, often inducing 100% germination in deeply dormant seed populations with 0% control germination. Smoke induces germination both directly and indirectly by aqueous or gaseous transfer from soil to seeds. Neither nitrate nor ammonium ions were effective in stimulating germination of smoke-stimulated species, nor were most of the quantitatively important gases generated by biomass smoke. Nitrogen dioxide, however, was very effective at inducing germination in Caulanthus heterophyllus (Brassicaceae), Emmenanthe penduliflora (Hydrophyllaceae), Phacelia grandiflora (Hydrophyllaceae), and Silene multinervia (Caryophyllaceae). Three species, Dendromecon rigida (Papaveraceae), Dicentra chrysantha, and Trichostema lanatum (Lamiaceae), failed to germinate unless smoke treatment was coupled with prior treatment of 1 yr soil storage. Smoke-stimulated germination was found in 25 chaparral species, representing 11 families, none of which were families known for heat-shock-stimulated germination. Seeds of smoke-stimulated species have many analogous characteristics that separate them from most heat-shock-stimulated seeds, including: (1) outer seed coats that are highly textured, (2) a poorly developed outer cuticle, (3) absence of a dense palisade tissue in the seed coat, and (4) a subdermal membrane that is semipermeable, allowing water passage but blocking entry of large (molecular mass > 500) solutes. Tentative evidence suggests that permeability characteristics of this subdermal layer are altered by

Acute respiratory and cardiovascular admissions after a public smoking ban in Geneva, Switzerland.

PubMed

Humair, Jean-Paul; Garin, Nicolas; Gerstel, Eric; Carballo, Sebastian; Carballo, David; Keller, Pierre-Frédéric; Guessous, Idris

2014-01-01

Many countries have introduced legislations for public smoking bans to reduce the harmful effects of exposure to tobacco smoke. Smoking bans cause significant reductions in admissions for acute coronary syndromes but their impact on respiratory diseases is unclear. In Geneva, Switzerland, two popular votes led to a stepwise implementation of a state smoking ban in public places, with a temporary suspension. This study evaluated the effect of this smoking ban on hospitalisations for acute respiratory and cardiovascular diseases. This before and after intervention study was conducted at the University Hospitals of Geneva, Switzerland, across 4 periods with different smoking legislations. It included 5,345 patients with a first hospitalisation for acute coronary syndrome, ischemic stroke, acute exacerbation of chronic obstructive pulmonary disease, pneumonia and acute asthma. The main outcomes were the incidence rate ratios (IRR) of admissions for each diagnosis after the final ban compared to the pre-ban period and adjusted for age, gender, season, influenza epidemic and secular trend. Hospitalisations for acute exacerbation of chronic obstructive pulmonary disease significantly decreased over the 4 periods and were lowest after the final ban (IRR=0.54 [95%CI: 0.42-0.68]). We observed a trend in reduced admissions for acute coronary syndromes (IRR=0.90 [95%CI: 0.80-1.00]). Admissions for ischemic stroke, asthma and pneumonia did not significantly change. A legislative smoking ban was followed by a strong decrease in hospitalisations for acute exacerbation of chronic obstructive pulmonary disease and a trend for reduced admissions for acute coronary syndrome. Smoking bans are likely to be very beneficial for patients with chronic obstructive pulmonary disease.

Acute Respiratory and Cardiovascular Admissions after a Public Smoking Ban in Geneva, Switzerland

PubMed Central

Humair, Jean-Paul; Garin, Nicolas; Gerstel, Eric; Carballo, Sebastian; Carballo, David; Keller, Pierre-Frédéric; Guessous, Idris

2014-01-01

Background Many countries have introduced legislations for public smoking bans to reduce the harmful effects of exposure to tobacco smoke. Smoking bans cause significant reductions in admissions for acute coronary syndromes but their impact on respiratory diseases is unclear. In Geneva, Switzerland, two popular votes led to a stepwise implementation of a state smoking ban in public places, with a temporary suspension. This study evaluated the effect of this smoking ban on hospitalisations for acute respiratory and cardiovascular diseases. Methods This before and after intervention study was conducted at the University Hospitals of Geneva, Switzerland, across 4 periods with different smoking legislations. It included 5,345 patients with a first hospitalisation for acute coronary syndrome, ischemic stroke, acute exacerbation of chronic obstructive pulmonary disease, pneumonia and acute asthma. The main outcomes were the incidence rate ratios (IRR) of admissions for each diagnosis after the final ban compared to the pre-ban period and adjusted for age, gender, season, influenza epidemic and secular trend. Results Hospitalisations for acute exacerbation of chronic obstructive pulmonary disease significantly decreased over the 4 periods and were lowest after the final ban (IRR = 0.54 [95%CI: 0.42–0.68]). We observed a trend in reduced admissions for acute coronary syndromes (IRR = 0.90 [95%CI: 0.80–1.00]). Admissions for ischemic stroke, asthma and pneumonia did not significantly change. Conclusions A legislative smoking ban was followed by a strong decrease in hospitalisations for acute exacerbation of chronic obstructive pulmonary disease and a trend for reduced admissions for acute coronary syndrome. Smoking bans are likely to be very beneficial for patients with chronic obstructive pulmonary disease. PMID:24599156

[Impact of the legislation for smoke-free workplaces on respiratory health in hospitality workers--review of epidemiological studies].

PubMed

Polańska, Kinga; Hanke, Wojciech; Konieczko, Katarzyna

2011-01-01

Environmental tobacco smoke exposure (ETS) is a significant risk factor for the development of many diseases, including lung cancer, lower respiratory tract infections, asthma and eye, throat and nasal irritations. Hospitality workers form an occupational group with high exposure to ETS in their workplace. Taking into account the health consequences of ETS exposure and high prevalence of exposure in public places, including workplaces, many countries have implemented the smoking ban that prohibits or restricts smoking in workplaces, including restaurants and bars. The epidemiological studies have indicated a significant reduction in the exposure level after implementation of the smoking ban. Most studies have also indicated a significant reduction in respiratory and sensory symptoms. The impact of the smoking ban on the lung function measurements is still not clear.

Effects of cooking fuel smoke on respiratory symptoms and lung function in semi-rural women in Cameroon

PubMed Central

Mbatchou Ngahane, Bertrand Hugo; Afane Ze, Emmanuel; Chebu, Cyrille; Mapoure, Njankouo Yacouba; Temfack, Elvis; Nganda, Malea; Luma, Namme Henry

2015-01-01

Background: Indoor air pollution is a major health problem in the developing world. In sub-Saharan Africa more than 90% of people rely on biomass to meet their domestic energy demands. Pollution from biomass fuel ranks 10th among preventable risk factors contributing to the global burden of diseases. Objectives: The present study aimed to determine the prevalence of respiratory symptoms and the factors associated with reduced lung function in a population of women exposed to cooking fuel smoke. Methods: A cross-sectional study was conducted in a semi-rural area in Cameroon. We compared forced respiratory volume between women using wood (n = 145) and women using alternative sources of energy (n = 155) for cooking. Results: Chronic bronchitis was found in 7·6% of the wood smoke group and 0·6% in the alternative fuels group. We observed two cases of airflow obstruction in the wood smoke group. Factors associated with lung function impairment were chronic bronchitis, use of wood as cooking fuel, age, and height. Conclusion: Respiratory symptoms and reduced lung function are more pronounced among women using wood as cooking fuel. Improved stoves technology should be developed to reduce the effects of wood smoke on respiratory health. PMID:25384259

Determinants of smoking-induced deprivation in China

PubMed Central

Yao, Tingting; Huang, Jidong; Sung, Hai-Yen; Ong, Michael K; Mao, Zhengzhong; Jiang, Yuan; Fong, Geoffrey T; Max, Wendy

2015-01-01

Objective Spending on cigarettes may deprive households of other items like food. The goal of this study was to examine the prevalence of and factors associated with this smoking-induced deprivation among adult smokers in China. Methods The data came from waves 1–3 of the International Tobacco Control (ITC) China Survey, conducted from 2006 to 2009 among urban adults aged 18 years or older in China. We focus on the samples of current smokers from six cities (N=7981). Smoking-induced deprivation was measured with the survey question, “In the last six months, have you spent money on cigarettes that you knew would be better spent on household essentials like food?” We examined whether sociodemographic factors, smoking intensity and price paid per pack of cigarettes were associated with smoking-induced deprivation using generalised estimating equations modelling. Findings 7.3% of smokers reported smoking-induced deprivation due to purchasing cigarettes. Low-income and middle-income smokers were more likely to have smoking-induced deprivation compared with high-income smokers (adjusted OR (AOR)=2.06, 95% CI 1.32 to 2.31; AOR=1.44, 95% CI 1.10 to 1.69); smokers living in Shenyang (AOR=1.68, 95% CI 1.25 to 2.24) and Yinchuan (AOR=2.50, 95% CI 1.89 to 3.32) were more likely to have smoking-induced deprivation compared with smokers living in Beijing. Retired smokers were less likely to have smoking-induced deprivation compared with employed smokers (AOR=0.67, 95% CI 0.52 to 0.87). There was no statistically significant relationship between smoking intensity, price paid per pack of cigarettes and smoking-induced deprivation. Conclusions Our findings indicate that certain groups of smokers in China acknowledge spending money on cigarettes that could be better spent on household essentials. Tobacco control policies that reduce smoking in China may improve household living standards by reducing smoking-induced deprivation. PMID:24827978

Genetics Home Reference: hereditary myopathy with early respiratory failure

MedlinePlus

... Home Health Conditions HMERF Hereditary myopathy with early respiratory failure Printable PDF Open All Close All Enable ... expand/collapse boxes. Description Hereditary myopathy with early respiratory failure ( HMERF ) is an inherited muscle disease that ...

The effect of exposure to biomass smoke on respiratory symptoms in adult rural and urban Nepalese populations.

PubMed

Kurmi, Om P; Semple, Sean; Devereux, Graham S; Gaihre, Santosh; Lam, Kin Bong Hubert; Sadhra, Steven; Steiner, Markus F C; Simkhada, Padam; Smith, William C S; Ayres, Jon G

2014-11-06

Half of the world's population is exposed to household air pollution from biomass burning. This study aimed to assess the relationship between respiratory symptoms and biomass smoke exposure in rural and urban Nepal. A cross-sectional study of adults (16+ years) in a rural population (n = 846) exposed to biomass smoke and a non-exposed urban population (n = 802) in Nepal. A validated questionnaire was used along with measures of indoor air quality (PM2.5 and CO) and outdoor PM2.5. Both men and women exposed to biomass smoke reported more respiratory symptoms compared to those exposed to clean fuel. Women exposed to biomass were more likely to complain of ever wheeze (32.0 % vs. 23.5%; p = 0.004) and breathlessness (17.8% vs. 12.0%, p = 0.017) compared to males with tobacco smoking being a major risk factor. Chronic cough was similar in both the biomass and non-biomass smoke exposed groups whereas chronic phlegm was reported less frequently by participants exposed to biomass smoke. Higher PM2.5 levels (≥2 SDs of the 24-hour mean) were associated with breathlessness (OR = 2.10, 95% CI 1.47, 2.99) and wheeze (1.76, 1.37, 2.26). The study suggests that while those exposed to biomass smoke had higher prevalence of respiratory symptoms, urban dwellers (who were exposed to higher ambient air pollution) were more at risk of having productive cough.

Accounting for risk and responsibility associated with smoking among mothers of children with respiratory illness.

PubMed

Coxhead, Lauren; Rhodes, Tim

2006-01-01

Contemporary public health discourses construct individuals as rational, responsible and knowledgeable, and thus promote a self-controlled prudent response to risk. In the context of evidence emphasising risks to children's health associated with passive smoking, mothers of children with respiratory illness may knowingly place their children at increased risk should they continue to smoke in their presence. Drawing on an analysis of depth qualitative interview accounts with mothers who smoke and whose young child was recently admitted to hospital with respiratory illness, this study describes mothers' constructions of risk and responsibility associated with their smoking. Three forms of accounting style were identified: 'stories of acceptability'; 'denial of agency'; and 'reflections of guilt'. 'Stories of acceptability' either positioned the risk of passive smoking as contained and controlled to an acceptable level, or disputed the level of risk that passive smoke posed. 'Denial of agency' drew on discourses of addiction and shared responsibility to exonerate the mother of responsibility or blame. 'Reflections of guilt' were presented when contradictions arose within accounts, particularly in relation to discussions of agency and rationality in decision-making. The study illustrates how constructions of moral responsibility, especially in relation to being a 'good mother', framed mothers' accounts of smoking in the face of risk. The study concludes that far greater consideration be given to the way in which mothers rationalise their smoking to others if paediatric doctors are to foster risk reduction practices associated with passive smoking more effectively.

Socioeconomic Disparities in Smoking Behavior and Early Smoking Initiation Among Men in Malawi.

PubMed

Yaya, Sanni; Bishwajit, Ghose; Shah, Vaibhav; Ekholuenetale, Michael

2017-01-01

Tobacco smoking is a growing concern for health care systems as it is projected to become the leading cause of death in the developing world. Knowledge of how smoking behavior differs across socioeconomic groups is crucial for designing effective preventive policies and alleviating the disparities. The aim of this study was to report the prevalence of (1) smoking status, (2) early smoking initiation, and (3) association with socioeconomic status (SES) of the 2 among Malawian men. Cross-sectional data on 1693 men aged between 15 and 49 years were collected from the latest 2013-2014 Multiple Indicator Cluster Survey in Malawi. Educational qualification and wealth index quintile were used as the indicators of SES. Outcome variables were smoking status, first age of smoking being below 18 years, and ever using any form of smokeless tobacco products. Multiple logistic regression models were used to see the contribution of SES to smoking status and early smoking initiation. Mean age of the sample population was 33.23 years (SD: 8.25). Prevalence of smoking, early initiation, and ever using any form of smokeless tobacco were, respectively, 46.6%, 33.7%, and 6%. Compared with men who had higher education, those who had no formal education, primary-level, and secondary-level qualification had, respectively, 21% (adjusted odds ratio [AOR] = 1.209; 95% confidence interval [CI] = 0.498-2.935), 40% (AOR = 1.4; 95% CI = 0.647-3.029), and 26% (AOR = 1.256; 95% CI = 0.593-2.661) higher odds of being a smoker. Those who had no formal education were 2.7 times (AOR = 2.734; 95% CI = 1.123-6.653) as likely to try smoking before reaching 18 years of age. Compared with the richest, those in the lowest wealth quintile had 32% lower odds (AOR = 0.676; 95% CI = 0.455-1.006) of early onset of smoking, 63% lower odds (AOR = 0.372; 95% CI = 0.201-0.690) of trying other tobacco products. Addressing the socioeconomic disparities could play

Socioeconomic Disparities in Smoking Behavior and Early Smoking Initiation Among Men in Malawi

PubMed Central

Yaya, Sanni; Bishwajit, Ghose; Shah, Vaibhav; Ekholuenetale, Michael

2017-01-01

Background: Tobacco smoking is a growing concern for health care systems as it is projected to become the leading cause of death in the developing world. Knowledge of how smoking behavior differs across socioeconomic groups is crucial for designing effective preventive policies and alleviating the disparities. The aim of this study was to report the prevalence of (1) smoking status, (2) early smoking initiation, and (3) association with socioeconomic status (SES) of the 2 among Malawian men. Methods: Cross-sectional data on 1693 men aged between 15 and 49 years were collected from the latest 2013-2014 Multiple Indicator Cluster Survey in Malawi. Educational qualification and wealth index quintile were used as the indicators of SES. Outcome variables were smoking status, first age of smoking being below 18 years, and ever using any form of smokeless tobacco products. Multiple logistic regression models were used to see the contribution of SES to smoking status and early smoking initiation. Results: Mean age of the sample population was 33.23 years (SD: 8.25). Prevalence of smoking, early initiation, and ever using any form of smokeless tobacco were, respectively, 46.6%, 33.7%, and 6%. Compared with men who had higher education, those who had no formal education, primary-level, and secondary-level qualification had, respectively, 21% (adjusted odds ratio [AOR] = 1.209; 95% confidence interval [CI] = 0.498-2.935), 40% (AOR = 1.4; 95% CI = 0.647-3.029), and 26% (AOR = 1.256; 95% CI = 0.593-2.661) higher odds of being a smoker. Those who had no formal education were 2.7 times (AOR = 2.734; 95% CI = 1.123-6.653) as likely to try smoking before reaching 18 years of age. Compared with the richest, those in the lowest wealth quintile had 32% lower odds (AOR = 0.676; 95% CI = 0.455-1.006) of early onset of smoking, 63% lower odds (AOR = 0.372; 95% CI = 0.201-0.690) of trying other tobacco products. Conclusions

A cross-sectional study of secondhand smoke exposure and respiratory symptoms in non-current smokers in the U.S. trucking industry: SHS exposure and respiratory symptoms.

PubMed

Laden, Francine; Chiu, Yueh-Hsiu; Garshick, Eric; Hammond, S Katharine; Hart, Jaime E

2013-02-01

Previous studies have suggested associations of adult exposures to secondhand smoke (SHS) with respiratory symptoms, but no study has focused on blue-collar industrial environments. We assessed the association between SHS and respiratory symptoms in 1,562 non-current smoking U.S. trucking industry workers. Information on SHS exposure and respiratory health was obtained by questionnaire. Multiple logistic regression analyses were used to assess the associations of recent and lifetime exposures to SHS with chronic phlegm, chronic cough, and any wheeze, defined by American Thoracic Society criteria. In analyses adjusted for age, gender, race, childhood SHS exposure, former smoking, pack-years of smoking and years since quitting, body mass index, job title, region of the country, and urban residence, recent exposures to SHS were associated with all three respiratory symptoms (odds ratio (OR) = 1.46; 95% confidence interval (CI) = 1.00-2.13) for chronic cough, 1.55 (95% CI = 1.08-2.21) for chronic phlegm, and 1.76 (95% CI = 1.41-2.21) for any wheeze). Workplace exposure was the most important recent exposure. Childhood exposure to SHS was also associated with all three symptoms, but only statistically significantly for chronic phlegm (OR = 1.84; 95% CI = 1.24-2.75). Additional years of living with a smoker were associated with an increased risk, but there was no evidence of a dose-response, except for chronic phlegm. In this group of trucking industry workers, childhood and recent exposures to SHS were related to respiratory symptoms.

A cross-sectional study of secondhand smoke exposure and respiratory symptoms in non-current smokers in the U.S. trucking industry: SHS exposure and respiratory symptoms

PubMed Central

2013-01-01

Background Previous studies have suggested associations of adult exposures to secondhand smoke (SHS) with respiratory symptoms, but no study has focused on blue-collar industrial environments. We assessed the association between SHS and respiratory symptoms in 1,562 non-current smoking U.S. trucking industry workers. Methods Information on SHS exposure and respiratory health was obtained by questionnaire. Multiple logistic regression analyses were used to assess the associations of recent and lifetime exposures to SHS with chronic phlegm, chronic cough, and any wheeze, defined by American Thoracic Society criteria. Results In analyses adjusted for age, gender, race, childhood SHS exposure, former smoking, pack-years of smoking and years since quitting, body mass index, job title, region of the country, and urban residence, recent exposures to SHS were associated with all three respiratory symptoms (odds ratio (OR) = 1.46; 95% confidence interval (CI) = 1.00-2.13) for chronic cough, 1.55 (95% CI = 1.08-2.21) for chronic phlegm, and 1.76 (95% CI = 1.41-2.21) for any wheeze). Workplace exposure was the most important recent exposure. Childhood exposure to SHS was also associated with all three symptoms, but only statistically significantly for chronic phlegm (OR = 1.84; 95% CI = 1.24-2.75). Additional years of living with a smoker were associated with an increased risk, but there was no evidence of a dose–response, except for chronic phlegm. Conclusions In this group of trucking industry workers, childhood and recent exposures to SHS were related to respiratory symptoms. PMID:23368999

Chronic inhalation of carbon monoxide: effects on the respiratory and cardiovascular system at doses corresponding to tobacco smoking.

PubMed

Sørhaug, Sveinung; Steinshamn, Sigurd; Nilsen, Odd G; Waldum, Helge L

2006-12-07

Carbon monoxide (CO) is a dangerous poison in high concentrations, but the long-term effects of low doses of CO, as in the gaseous component of tobacco smoke, are not well known. The aims of our study were to evaluate the long-term effects of inhaled CO on the respiratory and cardiovascular system at doses corresponding to tobacco smoking and its effect on tumourigenesis and pulmonary neuroendocrine (NE) cells. Female Wistar rats were exposed to either CO (200 ppm) for 20 h/day (n=51) or air (n=26) for 72 weeks. Carboxyhaemoglobin was 14.7+/-0.3% in CO exposed animals and 0.3+/-0.1% in controls. In the lungs, no signs of pathology similar to that associated with cigarette smoking were observed, and no differences in number of pulmonary NE cells were observed between the groups. Chronic CO inhalation induced a 20% weight increase of the right ventricle (p=0.001) and a 14% weight increase of the left ventricle and interventricular septum (p<0.001). Histological examination of the myocardium did not reveal any signs of scarring. In the aorta and femoral artery, no signs of atherosclerosis were observed in CO exposed rats. No exposure related carcinogenic effects were observed. Spontaneous tumours were identified in 29% of CO exposed animals and in 28% of the controls. Our results suggest that low dose CO exposure is probably not responsible for the respiratory pathology associated with tobacco smoking. The effects on the cardiovascular system seem to involve myocardial hypertrophy, but not atherogenesis.

Reductions in Cardiovascular, Cerebrovascular, and Respiratory Mortality following the National Irish Smoking Ban: Interrupted Time-Series Analysis

PubMed Central

Stallings-Smith, Sericea; Zeka, Ariana; Goodman, Pat; Kabir, Zubair; Clancy, Luke

2013-01-01

Background Previous studies have shown decreases in cardiovascular mortality following the implementation of comprehensive smoking bans. It is not known whether cerebrovascular or respiratory mortality decreases post-ban. On March 29, 2004, the Republic of Ireland became the first country in the world to implement a national workplace smoking ban. The aim of this study was to assess the effect of this policy on all-cause and cause-specific, non-trauma mortality. Methods A time-series epidemiologic assessment was conducted, utilizing Poisson regression to examine weekly age and gender-standardized rates for 215,878 non-trauma deaths in the Irish population, ages ≥35 years. The study period was from January 1, 2000, to December 31, 2007, with a post-ban follow-up of 3.75 years. All models were adjusted for time trend, season, influenza, and smoking prevalence. Results Following ban implementation, an immediate 13% decrease in all-cause mortality (RR: 0.87; 95% CI: 0.76–0.99), a 26% reduction in ischemic heart disease (IHD) (RR: 0.74; 95% CI: 0.63–0.88), a 32% reduction in stroke (RR: 0.68; 95% CI: 0.54–0.85), and a 38% reduction in chronic obstructive pulmonary disease (COPD) (RR: 0.62; 95% CI: 0.46–0.83) mortality was observed. Post-ban reductions in IHD, stroke, and COPD mortalities were seen in ages ≥65 years, but not in ages 35–64 years. COPD mortality reductions were found only in females (RR: 0.47; 95% CI: 0.32–0.70). Post-ban annual trend reductions were not detected for any smoking-related causes of death. Unadjusted estimates indicate that 3,726 (95% CI: 2,305–4,629) smoking-related deaths were likely prevented post-ban. Mortality decreases were primarily due to reductions in passive smoking. Conclusions The national Irish smoking ban was associated with immediate reductions in early mortality. Importantly, post-ban risk differences did not change with a longer follow-up period. This study corroborates previous evidence for cardiovascular

Determinants of smoking-induced deprivation in China.

PubMed

Yao, Tingting; Huang, Jidong; Sung, Hai-Yen; Ong, Michael K; Mao, Zhengzhong; Jiang, Yuan; Fong, Geoffrey T; Max, Wendy

2015-11-01

Spending on cigarettes may deprive households of other items like food. The goal of this study was to examine the prevalence of and factors associated with this smoking-induced deprivation among adult smokers in China. The data came from Waves 1-3 of the International Tobacco Control (ITC) China Survey, conducted from 2006 to 2009 among urban adults aged 18 years or older in China. We focus on the samples of current smokers from six cities (N=7981). Smoking-induced deprivation was measured with the survey question, "In the last six months, have you spent money on cigarettes that you knew would be better spent on household essentials like food?" We examined whether sociodemographic factors, smoking intensity and price paid per pack of cigarettes were associated with smoking-induced deprivation using generalised estimating equations modelling. 7.3% of smokers reported smoking-induced deprivation due to purchasing cigarettes. Low-income and middle-income smokers were more likely to have smoking-induced deprivation compared with high-income smokers (adjusted OR (AOR)=2.06, 95% CI 1.32 to 2.31; AOR=1.44, 95% CI 1.10 to 1.69); smokers living in Shenyang (AOR=1.68, 95% CI 1.25 to 2.24) and Yinchuan (AOR=2.50, 95% CI 1.89 to 3.32) were more likely to have smoking-induced deprivation compared with smokers living in Beijing. Retired smokers were less likely to have smoking-induced deprivation compared with employed smokers (AOR=0.67, 95% CI 0.52 to 0.87). There was no statistically significant relationship between smoking intensity, price paid per pack of cigarettes and smoking-induced deprivation. Our findings indicate that certain groups of smokers in China acknowledge spending money on cigarettes that could be better spent on household essentials. Tobacco control policies that reduce smoking in China may improve household living standards by reducing smoking-induced deprivation. Published by the BMJ Publishing Group Limited. For permission to use (where not already

Hereditary myopathies with early respiratory insufficiency in adults.

PubMed

Naddaf, Elie; Milone, Margherita

2017-11-01

Hereditary myopathies with early respiratory insufficiency as a predominant feature of the clinical phenotype are uncommon and underestimated in adults. We reviewed the clinical and laboratory data of patients with hereditary myopathies who demonstrated early respiratory insufficiency before the need for ambulatory assistance. Only patients with disease-causing mutations or a specific histopathological diagnosis were included. Patients with cardiomyopathy were excluded. We identified 22 patients; half had isolated respiratory symptoms at onset. The diagnosis of the myopathy was often delayed, resulting in delayed ventilatory support. The most common myopathies were adult-onset Pompe disease, myofibrillar myopathy, multi-minicore disease, and myotonic dystrophy type 1. Single cases of laminopathy, MELAS (mitochondrial encephalomyopathy with lactic acidosis and strokelike events), centronuclear myopathy, and cytoplasmic body myopathy were identified. We highlighted the most common hereditary myopathies associated with early respiratory insufficiency as the predominant clinical feature, and underscored the importance of a timely diagnosis for patient care. Muscle Nerve 56: 881-886, 2017. © 2017 Wiley Periodicals, Inc.

Final data of an Italian multicentric survey about counseling for smoking cessation in patients with diagnosis of a respiratory disease.

PubMed

Capelletto, Enrica; Rapetti, Simonetta Grazia; Demichelis, Sara; Galetta, Domenico; Catino, Annamaria; Ricci, Donata; Moretti, Anna Maria; Bria, Emilio; Pilotto, Sara; Bruno, Arianna; Valmadre, Giuseppe; Bandelli, Gian Piero; Trisolini, Rocco; Gianetta, Martina; Pacchiana, Maria Vittoria; Vallone, Stefania; Novello, Silvia

2018-03-01

Smoking is the major risk factor for cancer and several respiratory diseases. Quitting smoking at any point of life may increase the effectiveness of treatments and improve prognosis of patients with any pulmonary disease, including lung cancer. However, few institutions in Europe offer to patients adequate counseling for smoking cessation. Aim of this study was to investigate the level of counseling for smoking cessation offered by healthcare professionals to patients and their appreciation towards the intervention itself. Between January 2013 and February 2016, 490 patients, diagnosed with a respiratory diseases, were prospectively evaluated with an anonymous survey developed by WALCE (Women Against Lung Cancer in Europe). The majority of patients enrolled (76%) declared to have stopped smoking after the diagnosis of a respiratory disease, 17% to smoke less, 7% to continue smoking. Patients who reported to have never received any counseling for smoking cessation were 38%. Almost 73% of the other patients reported a positive judgment about the quality of healthcare's intervention. Despite these favorable considerations, 83% of patients have disclosed they simply quit smoking overnight without help, 5% have used electronic cigarettes, 5% nicotine replacement treatments, 4% dedicated books, 3% have attended a referral clinic. Considering all the smoking-related side effects, greater efforts should be made in order to better support patients in smoking cessation. Smoking should be considered as a real physical disorder and similar surveys should be encouraged with the aim to fight the 'stigma' of smoking that still exists among patients. © 2017 John Wiley & Sons Ltd.

Respiratory physiology during early life.

PubMed

Stocks, J

1999-08-01

Despite the rapid adaptation to extrauterine life, the respiratory system of an infant is not simply a miniaturized version of that of an adult, since the rapid somatic growth that occurs during the first year of life is accompanied by major developmental changes in respiratory physiology. The highly compliant chest wall of the infant results in relatively low transpulmonary pressures at end expiration with increased tendency of the small peripheral airways to close during tidal breathing. This not only impairs gas exchange and ventilation-perfusion balance, particularly in dependent parts of the lung, but, together with the small absolute size of the airways, renders the infant and young child particularly susceptible to airway obstruction. Premature airways are highly compliant structures compared with those of mature newborns or adults. This increased compliance can cause airway collapse, resulting in increased airways resistance, flow limitation, poor gas exchange and increased work of breathing. Although there is clear evidence that airway reactivity is present from birth, its role in wheezing lower respiratory tract illnesses in young infants may be overshadowed by pre-existing abnormalities of airway geometry and lung mechanics, or by pathological changes such as airway oedema and mucus hypersecretion. Attempts to assess age-related changes in airway reactivity or response to aerosol therapy in the very young is confounded by changes in breathing patterns and the fact that infants are preferential nose breathers. There is increasing evidence that pre-existing abnormalities of respiratory function, associated with adverse events during foetal life (including maternal smoking during pregnancy), and familial predisposition to wheezing are important determinants of wheezing illnesses during the first years of life. This emphasizes the need to identify and minimize any factors that threaten the normal development of the lung during this critical period if

Substance P and neutral endopeptidase in development of acute respiratory distress syndrome following fire smoke inhalation.

PubMed

Wong, Simon S; Sun, Nina N; Lantz, R Clark; Witten, Mark L

2004-10-01

To characterize the tachykininergic effects in fire smoke (FS)-induced acute respiratory distress syndrome (ARDS), we designed a series of studies in rats. Initially, 20 min of FS inhalation induced a significant increase of substance P (SP) in bronchoalveolar lavage fluid (BALF) at 1 h and persisted for 24 h after insult. Conversely, FS disrupted 51.4, 55.6, 46.3, and 43.0% enzymatic activity of neutral endopeptidase (NEP, a primary hydrolyzing enzyme for SP) 1, 6, 12, and 24 h after insult, respectively. Immunolabeling density of NEP in the airway epithelium largely disappeared 1 h after insult due to acute cell damage and shedding. These changes were also accompanied by extensive influx of albumin and granulocytes/lymphocytes in BALF. Furthermore, levels of BALF SP and tissue NEP activity dose dependently increased and decreased, respectively, following 0, low (10 min), and high (20 min) levels of FS inhalation. However, neither the time-course nor the dose-response study observed a significant change in the highest affinity neurokinin-1 receptor (NK-1R) for SP. Finally, treatment (10 mg/kg im) with SR-140333B, an NK-1R antagonist, significantly prevented 20-min FS-induced hypoxemia and pulmonary edema 24 h after insult. Further examination indicated that SR-140333B (1.0 or 10.0 mg/kg im) fully abolished early (1 h) plasma extravasation following FS. Collectively, these findings suggest that a combination of sustained SP and NEP inactivity induces an exaggerated neurogenic inflammation mediated by NK-1R, which may lead to an uncontrolled influx of protein-rich edema fluid and cells into the alveoli as a consequence of increased vascular permeability.

Early Diagnosis of Respiratory Abnormalities in Asbestos-Exposed Workers by the Forced Oscillation Technique.

PubMed

de Sá, Paula Morisco; Castro, Hermano Albuquerque; Lopes, Agnaldo José; Melo, Pedro Lopes de

2016-01-01

The current reference test for the detection of respiratory abnormalities in asbestos-exposed workers is spirometry. However, spirometry has several shortcomings that greatly affect the efficacy of current asbestos control programs. The forced oscillation technique (FOT) represents the current state-of-the-art technique in the assessment of lung function. This method provides a detailed analysis of respiratory resistance and reactance at different oscillatory frequencies during tidal breathing. Here, we evaluate the FOT as an alternative method to standard spirometry for the early detection and quantification of respiratory abnormalities in asbestos-exposed workers. Seventy-two subjects were analyzed. The control group was composed of 33 subjects with a normal spirometric exam who had no history of smoking or pulmonary disease. Thirty-nine subjects exposed to asbestos were also studied, including 32 volunteers in radiological category 0/0 and 7 volunteers with radiological categories of 0/1 or 1/1. FOT data were interpreted using classical parameters as well as integer (InOr) and fractional-order (FrOr) modeling. The diagnostic accuracy was evaluated by investigating the area under the receiver operating characteristic curve (AUC). Exposed workers presented increased obstruction (resistance p<0.001) and a reduced compliance (p<0.001), with a predominance of obstructive changes. The FOT parameter changes were correlated with the standard pulmonary function analysis methods (R = -0.52, p<0.001). Early respiratory abnormalities were identified with a high diagnostic accuracy (AUC = 0.987) using parameters obtained from the FrOr modeling. This accuracy was significantly better than those obtained with classical (p<0.001) and InOr (p<0.001) model parameters. The FOT improved our knowledge about the biomechanical abnormalities in workers exposed to asbestos. Additionally, a high diagnostic accuracy in the diagnosis of early respiratory abnormalities in asbestos

Reduction in emergency department visits for children's asthma, ear infections, and respiratory infections after the introduction of state smoke-free legislation.

PubMed

Hawkins, Summer Sherburne; Hristakeva, Sylvia; Gottlieb, Mark; Baum, Christopher F

2016-08-01

Despite the benefits of smoke-free legislation on adult health, little is known about its impact on children's health. We examined the effects of tobacco control policies on the rate of emergency department (ED) visits for childhood asthma (N=128,807), ear infections (N=288,697), and respiratory infections (N=410,686) using outpatient ED visit data in Massachusetts (2001-2010), New Hampshire (2001-2009), and Vermont (2002-2010). We used negative binomial regression models to analyze the effect of state and local smoke-free legislation on ED visits for each health condition, controlling for cigarette taxes and health care reform legislation. We found no changes in the overall rate of ED visits for asthma, ear infections, and upper respiratory infections after the implementation of state or local smoke-free legislation or cigarette tax increases. However, an interaction with children's age revealed that among 10-17-year-olds state smoke-free legislation was associated with a 12% reduction in ED visits for asthma (adjusted incidence rate ratios (aIRR) 0.88; 95% CI 0.83, 0.95), an 8% reduction for ear infections (0.92; 0.88, 0.97), and a 9% reduction for upper respiratory infections (0.91; 0.87, 0.95). We found an overall 8% reduction in ED visits for lower respiratory infections after the implementation of state smoke-free legislation (0.92; 0.87, 0.96). The implementation of health care reform in Massachusetts was also associated with a 6-9% reduction in all children's ED visits for ear and upper respiratory infections. Our results suggest that state smoke-free legislation and health care reform may be effective interventions to improve children's health by reducing ED visits for asthma, ear infections, and respiratory infections. Copyright © 2016 Elsevier Inc. All rights reserved.

Naloxone Antagonizes Soman-induced Central Respiratory Depression in Rats.

PubMed

Škrbić, Ranko; Stojiljković, Miloš P; Ćetković, Slavko S; Dobrić, Silva; Jeremić, Dejan; Vulović, Maja

2017-06-01

The influence of naloxone on respiration impaired by the highly toxic organophosphate nerve agent soman in anaesthetized rats was investigated. Soman, administered in a dose that was ineffective in blocking the electrically induced contractions of the phrenic nerve-diaphragm preparation in situ, induced a complete block of the spontaneous respiratory movements of the diaphragm, indicating the domination of central over the peripheral effects. Naloxone dose-dependently antagonized the soman-induced respiratory blockade. Atropine, at a dose that was per se ineffective in counteracting soman-induced respiratory depression, potentiated the protective effects of naloxone and completely restored respiration. Naloxone remained completely ineffective in antagonizing respiratory depression induced by the muscarinic receptor agonist the oxotremorine. It is assumed that naloxone antagonizes soman-induced respiratory inhibition by blocking endogenous opioidergic respiratory control pathways that are independent of the stimulation of muscarinic receptors. © 2016 Nordic Association for the Publication of BCPT (former Nordic Pharmacological Society).

Electronic cigarette, effective or harmful for quitting smoking and respiratory health: A quantitative review papers.

PubMed

Heydari, Gholamreza; Ahmady, Arezoo Ebn; Chamyani, Fahimeh; Masjedi, Mohammadreza; Fadaizadeh, Lida

2017-01-01

In recent years, electronic cigarettes (ECs) have been heavily advertised as an alternative smoking device as well as a possible cessation method. We aimed to review all published scientific literature pertaining to ECs and to present a simple conclusion about their effects for quitting smoking and respiratory health. This was a cross-sectional study with a search of PubMed, limited to English publications upto September 2014. The total number of papers which had ECs in its title and their conclusions positive or negative regarding ECs effects were computed. The number of negative papers was subtracted from the number of positive ones to make a score. Of the 149 articles, 137 (91.9%) were accessible, of which 68 did not have inclusion criteria. In the 69 remaining articles, 24 studies supported ECs and 45 considered these to be harmful. Finally, based on this evidence, the score of ECs (computed result with positive minus negative) was -21. Evidence to suggest that ECs may be effective and advisable for quitting smoking or a safe alternative for smoking is lacking and may instead harm the respiratory system. However, further studies are needed.

Protective effect of bacoside A on cigarette smoking-induced brain mitochondrial dysfunction in rats.

PubMed

Anbarasi, Kothandapani; Vani, Ganapathy; Devi, Chennam Srinivasulu Shyamala

2005-01-01

Chronic exposure to cigarette smoke affects the structure and function of mitochondria, which may account for the pathogenesis of smoking-related diseases. Bacopa monniera Linn., used in traditional Indian medicine for various neurological disorders, was shown to possess mitrochondrial membrane-stabilizing properties in the rat brain during exposure to morphine. We investigated the protective effect of bacoside A, the active principle of Bacopa monniera, against mitochondrial dysfunction in rat brain induced by cigarette smoke. Male Wistar albino rats were exposed to cigarette smoke and administered bacoside A for a period of 12 weeks. The mitochondrial damage in the brain was assessed by examining the levels of lipid peroxides, cholesterol, phospholipid, cholesterol/phospholipid (C/P) ratio, and the activities of isocitrate dehydrogenase, alpha-ketoglutarate dehydrogenase, succinate dehydrogenase, malate dehydrogenase, NADH dehydrogenase, and cytochrome C oxidase. The oxidative phosphorylation (rate of succinate oxidation, respiratory control ratio and ADP/O ratio, and the levels of ATP) was evaluated for the assessment of mitochondrial functional capacity. We found significantly elevated levels of lipid peroxides, cholesterol, and C/P ratio, and decreased levels of phospholipids and mitochondrial enzymes in the rats exposed to cigarette smoke. Measurement of oxidative phosphorylation revealed a marked depletion in all the variables studied. Administration of bacoside A prevented the structural and functional impairment of mitochondria upon exposure to cigarette smoke. From the results, we suggest that chronic cigarette smoke exposure induces damage to the mitochondria and that bacoside A protects the brain from this damage by maintaining the structural and functional integrity of the mitochondrial membrane.

The contribution of benzene to smoking-induced leukemia.

PubMed

Korte, J E; Hertz-Picciotto, I; Schulz, M R; Ball, L M; Duell, E J

2000-04-01

Cigarette smoking is associated with an increased risk of leukemia; benzene, an established leukemogen, is present in cigarette smoke. By combining epidemiologic data on the health effects of smoking with risk assessment techniques for low-dose extrapolation, we assessed the proportion of smoking-induced total leukemia and acute myeloid leukemia (AML) attributable to the benzene in cigarette smoke. We fit both linear and quadratic models to data from two benzene-exposed occupational cohorts to estimate the leukemogenic potency of benzene. Using multiple-decrement life tables, we calculated lifetime risks of total leukemia and AML deaths for never, light, and heavy smokers. We repeated these calculations, removing the effect of benzene in cigarettes based on the estimated potencies. From these life tables we determined smoking-attributable risks and benzene-attributable risks. The ratio of the latter to the former constitutes the proportion of smoking-induced cases attributable to benzene. Based on linear potency models, the benzene in cigarette smoke contributed from 8 to 48% of smoking-induced total leukemia deaths [95% upper confidence limit (UCL), 20-66%], and from 12 to 58% of smoking-induced AML deaths (95% UCL, 19-121%). The inclusion of a quadratic term yielded results that were comparable; however, potency models with only quadratic terms resulted in much lower attributable fractions--all < 1%. Thus, benzene is estimated to be responsible for approximately one-tenth to one-half of smoking-induced total leukemia mortality and up to three-fifths of smoking-related AML mortality. In contrast to theoretical arguments that linear models substantially overestimate low-dose risk, linear extrapolations from empirical data over a dose range of 10- to 100-fold resulted in plausible predictions.

Inhibition of IFN-γ-dependent antiviral airway epithelial defense by cigarette smoke

PubMed Central

2010-01-01

Background Although individuals exposed to cigarette smoke are more susceptible to respiratory infection, the effects of cigarette smoke on lung defense are incompletely understood. Because airway epithelial cell responses to type II interferon (IFN) are critical in regulation of defense against many respiratory viral infections, we hypothesized that cigarette smoke has inhibitory effects on IFN-γ-dependent antiviral mechanisms in epithelial cells in the airway. Methods Primary human tracheobronchial epithelial cells were first treated with cigarette smoke extract (CSE) followed by exposure to both CSE and IFN-γ. Epithelial cell cytotoxicity and IFN-γ-induced signaling, gene expression, and antiviral effects against respiratory syncytial virus (RSV) were tested without and with CSE exposure. Results CSE inhibited IFN-γ-dependent gene expression in airway epithelial cells, and these effects were not due to cell loss or cytotoxicity. CSE markedly inhibited IFN-γ-induced Stat1 phosphorylation, indicating that CSE altered type II interferon signal transduction and providing a mechanism for CSE effects. A period of CSE exposure combined with an interval of epithelial cell exposure to both CSE and IFN-γ was required to inhibit IFN-γ-induced cell signaling. CSE also decreased the inhibitory effect of IFN-γ on RSV mRNA and protein expression, confirming effects on viral infection. CSE effects on IFN-γ-induced Stat1 activation, antiviral protein expression, and inhibition of RSV infection were decreased by glutathione augmentation of epithelial cells using N-acetylcysteine or glutathione monoethyl ester, providing one strategy to alter cigarette smoke effects. Conclusions The results indicate that CSE inhibits the antiviral effects of IFN-γ, thereby presenting one explanation for increased susceptibility to respiratory viral infection in individuals exposed to cigarette smoke. PMID:20504369

Autonomic cardiovascular responses to smoke exposure in conscious rats

DOE Office of Scientific and Technical Information (OSTI.GOV)

Nakamura, T.; Hayashida, Y.

1992-05-01

Autonomic cardiovascular responses and the change in renal sympathetic nerve activity (RSNA) in response to smoke exposure were investigated in unrestrained conscious rats. Smoke exposure caused a prominent increase in RSNA (to 557.3 +/- 221.9% of the control level) and plasma norepinephrine (from 0.18 +/- 0.08 (control) to 0.66 +/- 0.22 ng/ml (at peak response of smoke exposure)), a slight increase in arterial blood pressure (from 89.6 +/- 3.3 to 103.6 +/- 3.8 mmHg), and marked bradycardia (from 386.6 +/- 12.8 to 231.3 +/- 20.6 beats/min). Respiratory rate in conscious rats was initially increased (from 1.6 +/- 0.1 to 6.1more » +/- 0.3 breaths/s) but was decreased (to 0.9 +/- 0.1 breaths/s) at the peak phase of the cardiovascular responses to smoke inhalation. Blood gases and pH reflected these changes in respiratory rate to some extent. Sinoaortic denervation did not attenuate the bradycardia (from 402 +/- 17.5 to 255.8 +/- 16.2 beats/min) or increase in RSNA (to 413.4 +/- 74.9%) that occurred during smoke inhalation. Atropine sulfate abolished the bradycardic response (from 440.4 +/- 13.8 to 485.4 +/- 8.6 beats/min). Initial tachypnea was also observed in both sinoaortic denervated rats and atropine-treated rats. Anesthesia, induced by pentobarbital sodium (30 mg/kg iv) or alpha-chloralose (65 mg/kg iv), abolished the bradycardia, the increase in RSNA, and the change in respiratory rate caused by smoke exposure. Ablation of the olfactory lobes also greatly attenuated the smoke-induced increase in RSNA (to 150.9 +/- 22.9%), bradycardia (from 372.9 +/- 19.6 to 376.3 +/- 24.1 beats/min), and the respiratory change.(ABSTRACT TRUNCATED AT 250 WORDS)« less

Enhanced pain perception prior to smoking cessation is associated with early relapse.

PubMed

Nakajima, Motohiro; al'Absi, Mustafa

2011-09-01

Accumulated evidence suggests that nicotine induces analgesia, and endogenous pain regulatory mechanisms may be altered by chronic smoking. The extent to which individual differences in pain perception are related to smokers' ability to abstain from smoking has not been directly examined. Seventy-one smokers who were interested in quitting completed a pre-cessation laboratory session which included the cold pressor test (CPT). Pain ratings were collected during and after CPT. Also, mood changes, cardiovascular measures, and salivary cortisol samples were evaluated prior to, during, and after CPT. Participants attended 4 weekly follow-up assessment sessions after their quit day. Cox regression analysis revealed that higher pain ratings during and after CPT predicted greater risk for smoking relapse. These results remained significant after affective and physiological responses to CPT were controlled, suggesting that pain ratings prior to smoking cessation are potentially useful in identifying smokers who are at greater risk of early smoking relapse and may reflect underlying putative risk for nicotine dependence and relapse. Copyright © 2011 Elsevier B.V. All rights reserved.

Cigarette smoke-induced Egr-1 upregulates proinflammatory cytokines in pulmonary epithelial cells.

PubMed

Reynolds, Paul R; Cosio, Manuel G; Hoidal, John R

2006-09-01

Chronic obstructive pulmonary disease (COPD) is the fourth leading cause of death worldwide and is a progressive and irreversible disorder. Cigarette smoking is associated with 80-90% of COPD cases; however, the genes involved in COPD-associated emphysema and chronic inflammation are poorly understood. It was recently demonstrated that early growth response gene 1 (Egr-1) is significantly upregulated in the lungs of smokers with COPD (Ning W and coworkers, Proc Natl Acad Sci 2004;101:14895-14900). We hypothesized that Egr-1 is activated in pulmonary epithelial cells during exposure to cigarette smoke extract (CSE). Using immunohistochemistry, we demonstrated that pulmonary adenocarcinoma cells (A-549) and primary epithelial cells lacking basal Egr-1 markedly induce Egr-1 expression after CSE exposure. To evaluate Egr-1-specific effects, we used antisense (alphaS) oligodeoxynucleotides (ODN) to knock down Egr-1 expression. Incorporation of Egr-1 alphaS ODN significantly decreased CSE-induced Egr-1 mRNA and protein, while sense ODN had no effect. Via Egr-1-mediated mechanisms, IL-1beta and TNF-alpha were significantly upregulated in pulmonary epithelial cells exposed to CSE or transfected with Egr-1. To investigate the relationship between Egr-1 induction by smoking and susceptibility to emphysema, we determined Egr-1 expression in strains of mice with different susceptibilities for the development of smoking-induced emphysema. Egr-1 was markedly increased in the lungs of emphysema-susceptible AKR/J mice chronically exposed to cigarette smoke, but only minimally increased in resistant NZWLac/J mice. In conclusion, Egr-1 is induced by cigarette smoke and functions in proinflammatory mechanisms that likely contribute to the development of COPD in the lungs of smokers.

Inactivity-induced respiratory plasticity: Protecting the drive to breathe in disorders that reduce respiratory neural activity☆

PubMed Central

Strey, K.A.; Baertsch, N.A.; Baker-Herman, T.L.

2013-01-01

Multiple forms of plasticity are activated following reduced respiratory neural activity. For example, in ventilated rats, a central neural apnea elicits a rebound increase in phrenic and hypoglossal burst amplitude upon resumption of respiratory neural activity, forms of plasticity called inactivity-induced phrenic and hypoglossal motor facilitation (iPMF and iHMF), respectively. Here, we provide a conceptual framework for plasticity following reduced respiratory neural activity to guide future investigations. We review mechanisms giving rise to iPMF and iHMF, present new data suggesting that inactivity-induced plasticity is observed in inspiratory intercostals (iIMF) and point out gaps in our knowledge. We then survey conditions relevant to human health characterized by reduced respiratory neural activity and discuss evidence that inactivity-induced plasticity is elicited during these conditions. Understanding the physiological impact and circumstances in which inactivity-induced respiratory plasticity is elicited may yield novel insights into the treatment of disorders characterized by reductions in respiratory neural activity. PMID:23816599

Cigarette Smoking Accelerated Brain Aging and Induced Pre-Alzheimer-Like Neuropathology in Rats

PubMed Central

Ho, Yuen-Shan; Yang, Xifei; Yeung, Sze-Chun; Chiu, Kin; Lau, Chi-Fai; Tsang, Andrea Wing-Ting; Mak, Judith Choi-Wo; Chang, Raymond Chuen-Chung

2012-01-01

Cigarette smoking has been proposed as a major risk factor for aging-related pathological changes and Alzheimer's disease (AD). To date, little is known for how smoking can predispose our brains to dementia or cognitive impairment. This study aimed to investigate the cigarette smoke-induced pathological changes in brains. Male Sprague-Dawley (SD) rats were exposed to either sham air or 4% cigarette smoke 1 hour per day for 8 weeks in a ventilated smoking chamber to mimic the situation of chronic passive smoking. We found that the levels of oxidative stress were significantly increased in the hippocampus of the smoking group. Smoking also affected the synapse through reducing the expression of pre-synaptic proteins including synaptophysin and synapsin-1, while there were no changes in the expression of postsynaptic protein PSD95. Decreased levels of acetylated-tubulin and increased levels of phosphorylated-tau at 231, 205 and 404 epitopes were also observed in the hippocampus of the smoking rats. These results suggested that axonal transport machinery might be impaired, and the stability of cytoskeleton might be affected by smoking. Moreover, smoking affected amyloid precursor protein (APP) processing by increasing the production of sAPPβ and accumulation of β–amyloid peptide in the CA3 and dentate gyrus region. In summary, our data suggested that chronic cigarette smoking could induce synaptic changes and other neuropathological alterations. These changes might serve as evidence of early phases of neurodegeneration and may explain why smoking can predispose brains to AD and dementia. PMID:22606286

Mechanisms of lung endothelial barrier disruption induced by cigarette smoke: role of oxidative stress and ceramides.

PubMed

Schweitzer, Kelly S; Hatoum, Hadi; Brown, Mary Beth; Gupta, Mehak; Justice, Matthew J; Beteck, Besem; Van Demark, Mary; Gu, Yuan; Presson, Robert G; Hubbard, Walter C; Petrache, Irina

2011-12-01

The epithelial and endothelial cells lining the alveolus form a barrier essential for the preservation of the lung respiratory function, which is, however, vulnerable to excessive oxidative, inflammatory, and apoptotic insults. Whereas profound breaches in this barrier function cause pulmonary edema, more subtle changes may contribute to inflammation. The mechanisms by which cigarette smoke (CS) exposure induce lung inflammation are not fully understood, but an early alteration in the epithelial barrier function has been documented. We sought to investigate the occurrence and mechanisms by which soluble components of mainstream CS disrupt the lung endothelial cell barrier function. Using cultured primary rat microvascular cell monolayers, we report that CS induces endothelial cell barrier disruption in a dose- and time-dependent manner of similar magnitude to that of the epithelial cell barrier. CS exposure triggered a mechanism of neutral sphingomyelinase-mediated ceramide upregulation and p38 MAPK and JNK activation that were oxidative stress dependent and that, along with Rho kinase activation, mediated the endothelial barrier dysfunction. The morphological changes in endothelial cell monolayers induced by CS included actin cytoskeletal rearrangement, junctional protein zonula occludens-1 loss, and intercellular gap formation, which were abolished by the glutathione modulator N-acetylcysteine and ameliorated by neutral sphingomyelinase inhibition. The direct application of ceramide recapitulated the effects of CS, by disrupting both endothelial and epithelial cells barrier, by a mechanism that was redox and apoptosis independent and required Rho kinase activation. Furthermore, ceramide induced dose-dependent alterations of alveolar microcirculatory barrier in vivo, measured by two-photon excitation microscopy in the intact rat. In conclusion, soluble components of CS have direct endothelial barrier-disruptive effects that could be ameliorated by glutathione

Respiratory effects of cigarette smoke, dust, and histamine in newborn rabbits

DOE Office of Scientific and Technical Information (OSTI.GOV)

Trippenbach, T.; Kelly, G.

1988-02-01

We studied the respiratory effects of cigarette smoke, 5% histamine aerosol, and dust in unanesthetized 1- to 7-day-old rabbits in a body plethysmograph. Cigarette smoke immediately provoked the animal's arousal and irregular breathing. Histamine and dust had no effect in some of the youngest animals. In others, 5-15 s from the onset of the exposure to either of the two stimuli, respiratory rate increased and the depth of breathing decreased. These changes were more pronounced with age. The fact that effects of dust and aerosol lessened with time of exposure showed adaptation to the stimuli. The age dependence of themore » reflex response was also observed after injection of 50 micrograms of histamine per kilogram into the external jugular vein in anesthetized (50 mg ketamine + 3 mg acepromazine per kg) and tracheostomized rabbits during the 1st wk of life. In 1-day-old animals, a short-lasting excitation was followed by apnea or a prolongation of expiratory phase. Peak amplitude of the diaphragmatic EMG (EMGdi) increased in all animals, but only in the youngest was the EMGdi increase paralleled by an increase in tidal volume. In vagotomized animals or animals pretreated with H1-blocker, histamine never affected timing parameters in animals greater than 1 day old. In the youngest animals, respiratory depression due to histamine was not abolished after vagotomy or promethazine. The results imply that inputs from the upper airways and the rapidly adapting pulmonary mechanoreceptors exert their effects on the pattern of breathing immediately after birth in rabbits. The importance of those inputs increases with maturation.« less

Perinatal exposure to environmental tobacco smoke is associated with changes in DNA methylation that precede the adult onset of lung disease in a mouse model.

PubMed

Cole, Elizabeth; Brown, Traci A; Pinkerton, Kent E; Postma, Britten; Malany, Keegan; Yang, Mihi; Kim, Yang Jee; Hamilton, Raymond F; Holian, Andrij; Cho, Yoon Hee

2017-08-01

Prenatal and early-life environmental tobacco smoke (ETS) exposure can induce epigenetic alterations associated with inflammation and respiratory disease. The objective of this study was to address the long-term epigenetic consequences of perinatal ETS exposure on latent respiratory disease risk, which are still largely unknown. C57BL/6 mice were exposed to prenatal and early-life ETS; offspring lung pathology, global DNA, and gene-specific methylation were measured at two adult ages. Significant alterations in global DNA methylation and promoter methylation of IFN-γ and Thy-1 were found in ETS-exposed offspring at 10-12 and 20 weeks of age. These sustained epigenetic alterations preceded the onset of significant pulmonary pathologies observed at 20 weeks of age. This study suggests that perinatal ETS exposure induces persistent epigenetic alterations in global DNA, as well as IFN-γ and Thy-1 promoter methylation that precede the adult onset of fibrotic lung pathology. These epigenetic findings could represent potential biomarkers of latent respiratory disease risk.

Naloxone reversal of buprenorphine-induced respiratory depression.

PubMed

van Dorp, Eveline; Yassen, Ashraf; Sarton, Elise; Romberg, Raymonda; Olofsen, Erik; Teppema, Luc; Danhof, Meindert; Dahan, Albert

2006-07-01

The objective of this investigation was to examine the ability of the opioid antagonist naloxone to reverse respiratory depression produced by the mu-opioid analgesic, buprenorphine, in healthy volunteers. The studies were designed in light of the claims that buprenorphine is relatively resistant to the effects of naloxone. In a first attempt, the effect of an intravenous bolus dose of 0.8 mg naloxone was assessed on 0.2 mg buprenorphine-induced respiratory depression. Next, the effect of increasing naloxone doses (0.5-7 mg, given over 30 min) on 0.2 mg buprenorphine-induced respiratory depression was tested. Subsequently, continuous naloxone infusions were applied to reverse respiratory depression from 0.2 and 0.4 mg buprenorphine. All doses are per 70 kg. Respiration was measured against a background of constant increased end-tidal carbon dioxide concentration. An intravenous naloxone dose of 0.8 mg had no effect on respiratory depression from buprenorphine. Increasing doses of naloxone given over 30 min produced full reversal of buprenorphine effect in the dose range of 2-4 mg naloxone. Further increasing the naloxone dose (doses of 5 mg or greater) caused a decline in reversal activity. Naloxone bolus doses of 2-3 mg, followed by a continuous infusion of 4 mg/h, caused full reversal within 40-60 min of both 0.2 and 0.4 mg buprenorphine-induced respiratory depression. Reversal of buprenorphine effect is possible but depends on the buprenorphine dose and the correct naloxone dose window. Because respiratory depression from buprenorphine may outlast the effects of naloxone boluses or short infusions, a continuous infusion of naloxone may be required to maintain reversal of respiratory depression.

Using Peer Injunctive Norms to Predict Early Adolescent Cigarette Smoking Intentions

PubMed Central

Zaleski, Adam C.; Aloise-Young, Patricia A.

2013-01-01

The present study investigated the importance of the perceived injunctive norm to predict early adolescent cigarette smoking intentions. A total of 271 6th graders completed a survey that included perceived prevalence of friend smoking (descriptive norm), perceptions of friends’ disapproval of smoking (injunctive norm), and future smoking intentions. Participants also listed their five best friends, in which the actual injunctive norm was calculated. Results showed that smoking intentions were significantly correlated with the perceived injunctive norm but not with the actual injunctive norm. Secondly, the perceived injunctive norm predicted an additional 3.4% of variance in smoking intentions above and beyond the perceived descriptive norm. These results demonstrate the importance of the perceived injunctive norm in predicting early adolescent smoking intentions. PMID:24078745

Pulmonary effects of active smoking and secondhand smoke exposure among adolescent students in Juárez, Mexico.

PubMed

Bird, Yelena; Staines-Orozco, Hugo

2016-01-01

increased respiratory symptoms and reduction of pulmonary function test values. Public health initiatives that aim to prevent smoking initiation, assist in cessation, and lessen SHS exposure of adolescents need to be school-based and employed as early as middle school.

“Pulmonary Effects of Maternal Smoking on the Fetus and Child: Effects on Lung Development, Respiratory Morbidities, and Life Long Lung Health”

PubMed Central

McEvoy, Cindy T.; Spindel, Eliot R.

2016-01-01

Summary Maternal smoking during pregnancy is the largest preventable cause of abnormal in-utero lung development. Despite well known risks, rates of smoking during pregnancy have only slightly decreased over the last ten years, with rates varying from 5-40% worldwide resulting in tens of millions of fetal exposures. Despite multiple approaches to smoking cessation about 50% of smokers will continue to smoke during pregnancy. Maternal genotype plays an important role in the likelihood of continued smoking during pregnancy and the degree to which maternal smoking will affect the fetus. The primary effects of maternal smoking on offspring lung function and health are decreases in forced expiratory flows, decreased passive respiratory compliance, increased hospitalization for respiratory infections, and an increased prevalence of childhood wheeze and asthma. Nicotine appears to be the responsible component of tobacco smoke that affects lung development, and some of the effects of maternal smoking on lung development can be prevented by supplemental vitamin C. Because nicotine is the key agent for affecting lung development, e-cigarette usage during pregnancy is likely to be as dangerous to fetal lung development as is maternal smoking. PMID:27639458

A novel swine model of ricin-induced acute respiratory distress syndrome.

PubMed

Katalan, Shahaf; Falach, Reut; Rosner, Amir; Goldvaser, Michael; Brosh-Nissimov, Tal; Dvir, Ayana; Mizrachi, Avi; Goren, Orr; Cohen, Barak; Gal, Yoav; Sapoznikov, Anita; Ehrlich, Sharon; Sabo, Tamar; Kronman, Chanoch

2017-02-01

Pulmonary exposure to the plant toxin ricin leads to respiratory insufficiency and death. To date, in-depth study of acute respiratory distress syndrome (ARDS) following pulmonary exposure to toxins is hampered by the lack of an appropriate animal model. To this end, we established the pig as a large animal model for the comprehensive study of the multifarious clinical manifestations of pulmonary ricinosis. Here, we report for the first time, the monitoring of barometric whole body plethysmography for pulmonary function tests in non-anesthetized ricin-treated pigs. Up to 30 h post-exposure, as a result of progressing hypoxemia and to prevent carbon dioxide retention, animals exhibited a compensatory response of elevation in minute volume, attributed mainly to a large elevation in respiratory rate with minimal response in tidal volume. This response was followed by decompensation, manifested by a decrease in minute volume and severe hypoxemia, refractory to oxygen treatment. Radiological evaluation revealed evidence of early diffuse bilateral pulmonary infiltrates while hemodynamic parameters remained unchanged, excluding cardiac failure as an explanation for respiratory insufficiency. Ricin-intoxicated pigs suffered from increased lung permeability accompanied by cytokine storming. Histological studies revealed lung tissue insults that accumulated over time and led to diffuse alveolar damage. Charting the decline in PaO2/FiO2 ratio in a mechanically ventilated pig confirmed that ricin-induced respiratory damage complies with the accepted diagnostic criteria for ARDS. The establishment of this animal model of pulmonary ricinosis should help in the pursuit of efficient medical countermeasures specifically tailored to deal with the respiratory deficiencies stemming from ricin-induced ARDS. © 2017. Published by The Company of Biologists Ltd.

A novel swine model of ricin-induced acute respiratory distress syndrome

PubMed Central

Katalan, Shahaf; Falach, Reut; Rosner, Amir; Goldvaser, Michael; Brosh-Nissimov, Tal; Dvir, Ayana; Mizrachi, Avi; Goren, Orr; Cohen, Barak; Gal, Yoav; Sapoznikov, Anita; Ehrlich, Sharon; Kronman, Chanoch

2017-01-01

ABSTRACT Pulmonary exposure to the plant toxin ricin leads to respiratory insufficiency and death. To date, in-depth study of acute respiratory distress syndrome (ARDS) following pulmonary exposure to toxins is hampered by the lack of an appropriate animal model. To this end, we established the pig as a large animal model for the comprehensive study of the multifarious clinical manifestations of pulmonary ricinosis. Here, we report for the first time, the monitoring of barometric whole body plethysmography for pulmonary function tests in non-anesthetized ricin-treated pigs. Up to 30 h post-exposure, as a result of progressing hypoxemia and to prevent carbon dioxide retention, animals exhibited a compensatory response of elevation in minute volume, attributed mainly to a large elevation in respiratory rate with minimal response in tidal volume. This response was followed by decompensation, manifested by a decrease in minute volume and severe hypoxemia, refractory to oxygen treatment. Radiological evaluation revealed evidence of early diffuse bilateral pulmonary infiltrates while hemodynamic parameters remained unchanged, excluding cardiac failure as an explanation for respiratory insufficiency. Ricin-intoxicated pigs suffered from increased lung permeability accompanied by cytokine storming. Histological studies revealed lung tissue insults that accumulated over time and led to diffuse alveolar damage. Charting the decline in PaO2/FiO2 ratio in a mechanically ventilated pig confirmed that ricin-induced respiratory damage complies with the accepted diagnostic criteria for ARDS. The establishment of this animal model of pulmonary ricinosis should help in the pursuit of efficient medical countermeasures specifically tailored to deal with the respiratory deficiencies stemming from ricin-induced ARDS. PMID:28067630

Immune-regulating effects of exercise on cigarette smoke-induced inflammation

PubMed Central

Madani, Ashkan; Alack, Katharina; Richter, Manuel Jonas; Krüger, Karsten

2018-01-01

Long-term cigarette smoking (LTCS) represents an important risk factor for cardiac infarction and stroke and the central risk factor for the development of a bronchial carcinoma, smoking-associated interstitial lung fibrosis, and chronic obstructive pulmonary disease. The pathophysiologic development of these diseases is suggested to be promoted by chronic and progressive inflammation. Cigarette smoking induces repetitive inflammatory insults followed by a chronic and progressive activation of the immune system. In the pulmonary system of cigarette smokers, oxidative stress, cellular damage, and a chronic activation of pattern recognition receptors are described which are followed by the translocation of the NF-kB, the release of pro-inflammatory cytokines, chemokines, matrix metalloproteases, and damage-associated molecular patterns. In parallel, smoke pollutants cross directly through the alveolus–capillary interface and spread through the systemic bloodstream targeting different organs. Consequently, LTCS induces a systemic low-grade inflammation and increased oxidative stress in the vascular system. In blood, these processes promote an increased coagulation and endothelial dysfunction. In muscle tissue, inflammatory processes activate catabolic signaling pathways followed by muscle wasting and sarcopenia. In brain, several characteristics of neuroinflammation were described. Regular exercise training has been shown to be an effective nonpharmacological treatment strategy in smoke-induced pulmonary diseases. It is well established that exercise training exerts immune-regulating effects by activating anti-inflammatory signaling pathways. In this regard, the release of myokines from contracting skeletal muscle, the elevations of cortisol and adrenalin, the reduced expression of Toll-like receptors, and the increased mobilization of immune-regulating leukocyte subtypes might be of vital importance. Exercise training also increases the local and systemic

Optimal control problem in correlation between smoking and epidemic of respiratory diseases

NASA Astrophysics Data System (ADS)

Aldila, D.; Apri, M.

2014-02-01

Smoking appears to be a risk factor that may increase the number of different pulmonary infections. This link is likely to be mediated by smoking adverse effects on the respiratory defenses. A mathematical model to describe correlation between the number of smokers and its effect on the number of infected people suffer from respiratory disease like influenza is constructed in this paper. Promotion of healthy life is accounted in the model as an optimal control problem to reduce the number of smokers. In this work, the transition rates from smokers to non-smokers and from non-smokers to smokers are regarded as the control variables. Assuming the control variables are constant, equilibrium points of the model can be obtained analytically. The basic reproductive ratio as the endemic threshold is taken from the spectral radius of the next-generation matrix. Using numerical simulation, we show that the healthy life promotion can reduce the number of infected person significantly by reducing the number of smokers. Furthermore, different initial conditions to show different situations in the field are also simulated. It is shown that a large effort to increase the transition rate from smokers to non-smokers and to reduce the transition from non-smokers to smokers should be applied in the endemic reduction scenario.

The Smoking Outcome Expectation Scale and Anti-Smoking Self-Efficacy Scale for Early Adolescents: Instrument Development and Validation

ERIC Educational Resources Information Center

Chen, Chen-Ju; Yeh, Ming-Chen; Tang, Fu-In; Yu, Shu

2015-01-01

Smoking-related outcome expectation and self-efficacy have been found to be associated with adolescent smoking initiation. There is, however, a lack of appropriate instruments to investigate early adolescents' smoking outcome expectations and antismoking self-efficacy. The purpose of this study was to develop and validate the Smoking Outcome…

Urinary cotinine and parent history (questionnaire) as indicators of passive smoking and predictors of lower respiratory illness in infants.

PubMed

Margolis, P A; Keyes, L L; Greenberg, R A; Bauman, K E; LaVange, L M

1997-06-01

Studies of the effects of passive smoking on lower respiratory illness (LRI) have relied on questionnaires to measure exposure. We studied the association between two measures of passive smoking and the incidence of acute LRI in infants. We analyzed data from a community-based cohort study of respiratory illness during the first year of life in North Carolina. The incidence of LRI was determined by telephone calls at 2-week intervals. Environmental, demographic, and psychosocial risk factors for LRI were measured during home interviews. Tobacco smoke exposure was measured as the mean number of cigarettes smoked per day in the infant's presence. Smoke absorption by the infants was measured by the urinary cotinine/ creatinine ratio. Of the 485 infants in the study, 325 (67%) had telephone follow-up and at least two home interviews. In bivariate analyses, reported tobacco smoke exposure and urinary cotinine were associated with LRI. Only the association between reported exposure and LRI remained significant after adjusting for confounders, [adjusted incidence of LRI (episodes/child-year) non-exposed: 0.6; < or = 10 cigarettes/day: 0.9 (RR 1.5, 95% CI: 1.1, 2.0); > 10 cigarettes/day: 1.3 (RR 2.2, 95% CI: 1.3, 3.8)]. We conclude that infants reportedly exposed to tobacco smoke have an increased incidence of LRI. There are differences between questionnaire and biochemical measures of passive smoking. Urinary cotinine will not necessarily improve the validity of studies of the relationship of passive smoking to LRI in infants.

A brain-targeted ampakine compound protects against opioid-induced respiratory depression.

PubMed

Dai, Wei; Xiao, Dian; Gao, Xiang; Zhou, Xin-Bo; Fang, Tong-Yu; Yong, Zheng; Su, Rui-Bin

2017-08-15

The use of opioid drugs for pain relief can induce life-threatening respiratory depression. Although naloxone effectively counteracts opioid-induced respiratory depression, it diminishes the efficacy of analgesia. Our studies indicate that ampakines, in particular, a brain-targeted compound XD-8-17C, are able to reverse respiratory depression without affecting analgesia at relatively low doses. Mice and rats were subcutaneously or intravenously injected with the opioid agonist TH-030418 to induce moderate or severe respiratory depression. XD-8-17C was intravenously administered before or after TH-030418. The effect of XD-8-17C on opioid-induced respiratory depression was evaluated in terms of the opioid-induced acute death rate, arterial blood gas analysis and pulmonary function tests. In addition, the hot-plate test was conducted to investigate whether XD-8-17C influenced opioid-induced analgesia. Pre-treatment with XD-8-17C significantly reduced opioid-induced acute death, and increased the median lethal dose of TH-030418 by 4.7-fold. Blood gas analysis and pulmonary function tests demonstrated that post-treatment with XD-8-17C alleviated respiratory depression, as indicated by restoration of arterial blood gas (pO 2 , sO 2 , cK + ) and lung function parameters (respiratory frequency, minute ventilation) to the normal range. The hot-plate test showed that XD-8-17C had no impact on the antinociceptive efficacy of morphine. The ability of XD-8-17C to reverse opioid-induced respiratory depression has the potential to increase the safety and convenience of opioid treatment. These findings contribute to the discovery of novel therapeutic agents that protect against opioid-induced respiratory depression without loss of analgesia. Copyright © 2017 Elsevier B.V. All rights reserved.

Longitudinal follow-up study of smoking-induced emphysema progression in low-dose CT screening of lung cancer

NASA Astrophysics Data System (ADS)

Suzuki, H.; Matsuhiro, M.; Kawata, Y.; Niki, N.; Nakano, Y.; Ohmatsu, H.; Kusumoto, M.; Tsuchida, T.; Eguchi, K.; Kaneko, Masahiro; Moriyama, N.

2014-03-01

Chronic obstructive pulmonary disease is a major public health problem that is predicted to be third leading cause of death in 2030. Although spirometry is traditionally used to quantify emphysema progression, it is difficult to detect the loss of pulmonary function by emphysema in early stage, and to assess the susceptibility to smoking. This study presents quantification method of smoking-induced emphysema progression based on annual changes of low attenuation volume (LAV) by each lung lobe acquired from low-dose CT images in lung cancer screening. The method consists of three steps. First, lung lobes are segmented using extracted interlobar fissures by enhancement filter based on fourdimensional curvature. Second, LAV of each lung lobe is segmented. Finally, smoking-induced emphysema progression is assessed by statistical analysis of the annual changes represented by linear regression of LAV percentage in each lung lobe. This method was applied to 140 participants in lung cancer CT screening for six years. The results showed that LAV progressions of nonsmokers, past smokers, and current smokers are different in terms of pack-year and smoking cessation duration. This study demonstrates effectiveness in diagnosis and prognosis of early emphysema in lung cancer CT screening.

Early Exposure to Movie Smoking Predicts Established Smoking by Older Teens and Young Adults

PubMed Central

Dalton, Madeline A.; Beach, Michael L.; Adachi-Mejia, Anna M.; Longacre, Meghan R.; Matzkin, Aurora L.; Sargent, James D.; Heatherton, Todd F.; Titus-Ernstoff, Linda

2009-01-01

OBJECTIVE Movie smoking exposure is a strong predictor of smoking initiation by adolescents; however, we do not know whether it is a long-term predictor of established smoking. We conducted a prospective study to determine whether movie smoking exposure during early adolescence predicts established smoking in older teens and young adults. DESIGN We assessed movie smoking exposure and smoking status through a written school-based survey in 1999, when participants were 10 to 14 years of age. We enrolled 73% (n = 2603) of those who had never tried smoking in a follow-up study. In 2006–2007, we conducted telephone interviews with 69% (n = 1791) of the cohort to ascertain current smoking status. The primary outcome was established smoking, defined as having smoked >100 cigarettes. Mean age at follow-up was 18.7 years. RESULTS Thirteen percent (n = 235) progressed from never smoking to established smoking during the follow-up period. Eighty-nine percent (n = 209) of established smokers smoked during the 30 days before the survey. Even after controlling for a wide range of baseline characteristics, the relative risk for established smoking increased by one third with each successive quartile of movie smoking exposure. Those in the highest quartile for baseline movie smoking exposure were twice as likely to be established smokers at follow-up compared with those in the lowest quartile. CONCLUSIONS Movie smoking exposure significantly predicted progression to established smoking in long-term follow-up. We estimate that 34.9% of established smoking in this cohort can be attributed to movie smoking exposure. PMID:19336346

Effects of the Irish smoking ban on respiratory health of bar workers and air quality in Dublin pubs.

PubMed

Goodman, Patrick; Agnew, Michelle; McCaffrey, Marie; Paul, Gillian; Clancy, Luke

2007-04-15

Environmental tobacco smoke (ETS) causes disease in nonsmokers. Workplace bans on smoking are interventions to reduce exposure to ETS to try to prevent harmful health effects. On March 29, 2004, the Irish government introduced the first national comprehensive legislation banning smoking in all workplaces, including bars and restaurants. This study examines the impact of this legislation on air quality in pubs and on respiratory health effects in bar workers in Dublin. Exposure study. Concentrations of particulate matter 2.5 microm or smaller (PM(2.5)) and particulate matter 10 microm or smaller (PM(10)) in 42 pubs were measured and compared before and after the ban. Benzene concentrations were also measured in 26 of the pubs. Health effects study. Eighty-one barmen volunteered to have full pulmonary function studies, exhaled breath carbon monoxide, and salivary cotinine levels performed before the ban and repeated 1 year after the ban. They also completed questionnaires on exposure to ETS and respiratory symptoms on both occasions. Exposure study. There was an 83% reduction in PM(2.5) and an 80.2% reduction in benzene concentration in the bars. Health effects study. There was a 79% reduction in exhaled breath carbon monoxide and an 81% reduction in salivary cotinine. There were statistically significant improvements in measured pulmonary function tests and significant reductions in self-reported symptoms and exposure levels in nonsmoking barmen volunteers after the ban. A total workplace smoking ban results in a significant reduction in air pollution in pubs and an improvement in respiratory health in barmen.

Three Measures of Forest Fire Smoke Exposure and Their Associations with Respiratory and Cardiovascular Health Outcomes in a Population-Based Cohort

PubMed Central

Brauer, Michael; MacNab, Ying C.; Kennedy, Susan M.

2011-01-01

Background: During the summer of 2003 numerous fires burned in British Columbia, Canada. Objectives: We examined the associations between respiratory and cardiovascular physician visits and hospital admissions, and three measures of smoke exposure over a 92-day study period (1 July to 30 September 2003). Methods: A population-based cohort of 281,711 residents was identified from administrative data. Spatially specific daily exposure estimates were assigned to each subject based on total measurements of particulate matter (PM) ≤ 10 μm in aerodynamic diameter (PM10) from six regulatory tapered element oscillating microbalance (TEOM) air quality monitors, smoke-related PM10 from a CALPUFF dispersion model run for the study, and a SMOKE exposure metric for plumes visible in satellite images. Logistic regression with repeated measures was used to estimate associations with each outcome. Results: The mean (± SD) exposure based on TEOM-measured PM10 was 29 ± 31 μg/m3, with an interquartile range of 14–31 μg/m3. Correlations between the TEOM, smoke, and CALPUFF metrics were moderate (0.37–0.76). Odds ratios (ORs) for a 30-μg/m3 increase in TEOM-based PM10 were 1.05 [95% confidence interval (CI), 1.03–1.06] for all respiratory physician visits, 1.16 (95% CI, 1.09–1.23) for asthma-specific visits, and 1.15 (95% CI, 1.00–1.29) for respiratory hospital admissions. Associations with cardiovascular outcomes were largely null. Conclusions: Overall we found that increases in TEOM-measured PM10 were associated with increased odds of respiratory physician visits and hospital admissions, but not with cardiovascular health outcomes. Results indicating effects of fire smoke on respiratory outcomes are consistent with previous studies, as are the null results for cardiovascular outcomes. Some agreement between TEOM and the other metrics suggests that exposure assessment tools that are independent of air quality monitoring may be useful with further refinement. PMID

Increased Burden of Respiratory Disease in the First Six Months of Life Due to Prenatal Environmental Tobacco Smoke: Krakow Birth Cohort Study

ERIC Educational Resources Information Center

Jedrychowski, Wieslaw; Galas, Alek Sander; Flak, Elzbieta; Jacek, Ryszard; Penar, Agnieszka; Spengler, John; Perera, Frederica P.

2007-01-01

The main purpose of our study was to assess the effects of prenatal tobacco smoke on respiratory symptoms and on doctor consultations in a birth cohort of 445 infants who had no smoking mothers and who had no postnatal exposure to environmental tobacco smoke (ETS). Before and after delivery, questionnaires and interviews with mothers were…

The Effect of a Smoking Ban on Hospitalization Rates for Cardiovascular and Respiratory Conditions in Prince Edward Island, Canada

PubMed Central

Gaudreau, Katherine; Sanford, Carolyn J.; Cheverie, Connie; McClure, Carol

2013-01-01

Background This is the first study to have examined the effect of smoking bans on hospitalizations in the Atlantic Canadian socio-economic, cultural and climatic context. On June 1, 2003 Prince Edward Island (PEI) enacted a province-wide smoking ban in public places and workplaces. Changes in hospital admission rates for cardiovascular (acute myocardial infarction, angina, and stroke) and respiratory (chronic obstructive pulmonary disease and asthma) conditions were examined before and after the smoking ban. Methods Crude annual and monthly admission rates for the above conditions were calculated from April 1, 1995 to December 31, 2008 in all PEI acute care hospitals. Autoregressive Integrated Moving Average time series models were used to test for changes in mean and trend of monthly admission rates for study conditions, control conditions and a control province after the comprehensive smoking ban. Age- and sex-based analyses were completed. Results The mean rate of acute myocardial infarctions was reduced by 5.92 cases per 100,000 person-months (P = 0.04) immediately after the smoking ban. The trend of monthly angina admissions in men was reduced by −0.44 cases per 100,000 person-months (P = 0.01) in the 67 months after the smoking ban. All other cardiovascular and respiratory admission changes were non-significant. Conclusions A comprehensive smoking ban in PEI reduced the overall mean number of acute myocardial infarction admissions and the trend of angina hospital admissions. PMID:23520450

The effect of a smoking ban on hospitalization rates for cardiovascular and respiratory conditions in Prince Edward Island, Canada.

PubMed

Gaudreau, Katherine; Sanford, Carolyn J; Cheverie, Connie; McClure, Carol

2013-01-01

This is the first study to have examined the effect of smoking bans on hospitalizations in the Atlantic Canadian socio-economic, cultural and climatic context. On June 1, 2003 Prince Edward Island (PEI) enacted a province-wide smoking ban in public places and workplaces. Changes in hospital admission rates for cardiovascular (acute myocardial infarction, angina, and stroke) and respiratory (chronic obstructive pulmonary disease and asthma) conditions were examined before and after the smoking ban. Crude annual and monthly admission rates for the above conditions were calculated from April 1, 1995 to December 31, 2008 in all PEI acute care hospitals. Autoregressive Integrated Moving Average time series models were used to test for changes in mean and trend of monthly admission rates for study conditions, control conditions and a control province after the comprehensive smoking ban. Age- and sex-based analyses were completed. The mean rate of acute myocardial infarctions was reduced by 5.92 cases per 100,000 person-months (P = 0.04) immediately after the smoking ban. The trend of monthly angina admissions in men was reduced by -0.44 cases per 100,000 person-months (P = 0.01) in the 67 months after the smoking ban. All other cardiovascular and respiratory admission changes were non-significant. A comprehensive smoking ban in PEI reduced the overall mean number of acute myocardial infarction admissions and the trend of angina hospital admissions.

Effects of intratracheal administration of nuclear factor-kappaB decoy oligodeoxynucleotides on long-term cigarette smoke-induced lung inflammation and pathology in mice

PubMed Central

2009-01-01

To determine if nuclear factor-κB (NF-κB) activation may be a key factor in lung inflammation and respiratory dysfunction, we investigated whether NF-κB can be blocked by intratracheal administration of NF-κB decoy oligodeoxynucleotides (ODNs), and whether decoy ODN-mediated NF-κB inhibition can prevent smoke-induced lung inflammation, respiratory dysfunction, and improve pathological alteration in the small airways and lung parenchyma in the long-term smoke-induced mouse model system. We also detected changes in transcriptional factors. In vivo, the transfection efficiency of NF-κB decoy ODNs to alveolar macrophages in BALF was measured by fluorescein isothiocyanate (FITC)-labeled NF-κB decoy ODNs and flow cytometry post intratracheal ODN administration. Pulmonary function was measured by pressure sensors, and pathological changes were assessed using histology and the pathological Mias software. NF-κB and activator protein 1(AP-1) activity was detected by the electrophoretic motility shift assay (EMSA). Mouse cytokine and chemokine pulmonary expression profiles were investigated by enzyme-linked immunosorbent assay (ELISA) in bronchoalveolar lavage fluid (BALF) and lung tissue homogenates, respectively, after repeated exposure to cigarette smoke. After 24 h, the percentage of transfected alveolar macrophages was 30.00 ± 3.30%. Analysis of respiratory function indicated that transfection of NF-κB decoy ODNs significantly impacted peak expiratory flow (PEF), and bronchoalveolar lavage cytology displayed evidence of decreased macrophage infiltration in airways compared to normal saline-treated or scramble NF-κB decoy ODNs smoke exposed mice. NF-κB decoy ODNs inhibited significantly level of macrophage inflammatory protein (MIP) 1α and monocyte chemoattractant protein 1(MCP-1) in lung homogenates compared to normal saline-treated smoke exposed mice. In contrast, these NF-κB decoy ODNs-treated mice showed significant increase in the level of tumor

Does acute tobacco smoking prevent cue-induced craving?

PubMed

Schlagintweit, Hera E; Barrett, Sean P

2016-05-01

Smoking cessation aids appear to be limited in their ability to prevent craving triggered by exposure to smoking-associated stimuli; however, the extent to which cue-induced cravings persist following denicotinized or nicotine-containing tobacco smoking is not known. Thirty (17 male) ⩾12-hour abstinent dependent smokers completed two sessions during which they smoked a nicotine-containing or denicotinized cigarette. Instructions regarding the nicotine content of the cigarette varied across sessions, and all participants were exposed to a neutral cue followed by a smoking cue after cigarette consumption. Craving was assessed before and after cigarette consumption and cue exposure. Reduced intentions to smoke were associated with both nicotine expectancy (p<0.05) and nicotine administration (p<0.01), while reduced withdrawal-related craving was uniquely associated with nicotine administration (p<0.05). Smoking-associated stimuli increased craving regardless of nicotine expectancy or administration (p-values<0.001). While both nicotine pharmacology and expectancy appear to contribute to craving reduction associated with acute tobacco smoking, neither smoking-related nicotine administration nor expectation prevents increases in craving following exposure to smoking-associated stimuli. These findings suggest that cue-induced craving may be resistant to various pharmacological and psychological interventions. © The Author(s) 2016.

Inhibition of protein kinase A and GIRK channel reverses fentanyl-induced respiratory depression.

PubMed

Liang, Xiaonan; Yong, Zheng; Su, Ruibin

2018-06-11

Opioid-induced respiratory depression is a major obstacle to improving the clinical management of moderate to severe chronic pain. Opioids inhibit neuronal activity via various pathways, including calcium channels, adenylyl cyclase, and potassium channels. Currently, the underlying molecular pathway of opioid-induced respiratory depression is only partially understood. This study aimed to investigate the mechanisms of opioid-induced respiratory depression in vivo by examining the effects of different pharmacological agents on fentanyl-induced respiratory depression. Respiratory parameters were detected using whole body plethysmography in conscious rats. We show that pre-treatment with the protein kinase A (PKA) inhibitor H89 reversed the fentanyl-related effects on respiratory rate, inspiratory time, and expiratory time. Pre-treatment with the G protein-gated inwardly rectifying potassium (GIRK) channel blocker Tertiapin-Q dose-dependently reversed the fentanyl-related effects on respiratory rate and inspiratory time. A phosphodiesterase 4 (PDE4) inhibitor and cyclic adenosine monophosphate (cAMP) analogs did not affect fentanyl-induced respiratory depression. These findings suggest that PKA and GIRK may be involved in fentanyl-induced respiratory depression and could represent useful therapeutic targets for the treatment of fentanyl-induced ventilatory depression. Copyright © 2018 Elsevier B.V. All rights reserved.

Exercise Training Reverses Extrapulmonary Impairments in Smoke-exposed Mice.

PubMed

Bowen, T Scott; Aakerøy, Lars; Eisenkolb, Sophia; Kunth, Patricia; Bakkerud, Fredrik; Wohlwend, Martin; Ormbostad, Anne Marie; Fischer, Tina; Wisloff, Ulrik; Schuler, Gerhard; Steinshamn, Sigurd; Adams, Volker; Bronstad, Eivind

2017-05-01

Cigarette smoking is the main risk factor for chronic obstructive pulmonary disease and emphysema. However, evidence on the extrapulmonary effects of smoke exposure that precede lung impairments remains unclear at present, as are data on nonpharmacological treatments such as exercise training. Three groups of mice, including control (n = 10), smoking (n = 10), and smoking with 6 wk of high-intensity interval treadmill running (n = 11), were exposed to 20 wk of fresh air or whole-body cigarette smoke. Exercise capacity (peak oxygen uptake) and lung destruction (histology) were subsequently measured, whereas the heart, peripheral endothelium (aorta), and respiratory (diaphragm) and limb (extensor digitorum longus and soleus) skeletal muscles were assessed for in vivo and in vitro function, in situ mitochondrial respiration, and molecular alterations. Smoking reduced body weight by 26% (P < 0.05) without overt airway destruction (P > 0.05). Smoking impaired exercise capacity by 15% while inducing right ventricular dysfunction by ~20%, endothelial dysfunction by ~20%, and diaphragm muscle weakness by ~15% (all P < 0.05), but these were either attenuated or reversed by exercise training (P < 0.05). Compared with controls, smoking mice had normal limb muscle and mitochondrial function (cardiac and skeletal muscle fibers); however, diaphragm measures of oxidative stress and protein degradation were increased by 111% and 65%, respectively (P < 0.05), but these were attenuated by exercise training (P < 0.05). Prolonged cigarette smoking reduced exercise capacity concomitant with functional impairments to the heart, peripheral endothelium, and respiratory muscle that preceded the development of overt emphysema. However, high-intensity exercise training was able to reverse these smoke-induced extrapulmonary impairments.

Early respiratory acidosis is a new risk factor for pneumonia after lung resection.

PubMed

Planquette, Benjamin; Le Pimpec-Barthes, Françoise; Trinquart, Ludovic; Meyer, Guy; Riquet, Marc; Sanchez, Olivier

2012-03-01

Postoperative pneumonia (POP) is a life-threatening complication of lung resection (LR). Its risk factors, bacteriological profile and outcome are not well known. The aims of this study were to describe the outcome and causal bacteria and to identify risk factors for POP. We reviewed all cases admitted to intensive care after LR. Clinical parameters, operative and postoperative data were recorded. POP was suspected on the basis of fever, radiographic infiltrate, and either leucocytosis or purulent sputum. The diagnosis was confirmed by culture of a respiratory sample. Risk factors for POP were identified by univariate and multivariate analysis. We included 159 patients in this study. POP was diagnosed in 23 patients (14.4%) and was associated with a higher hospital mortality rate (30% versus 5%, P = 0.0007) and a longer hospital stay. Members of the Enterobacteriaceae and Pseudomonas species were the most frequently identified pathogens. Early respiratory acidosis (ERA; OR, 2.94; 95% CI, 1.1-8.1), blood transfusion (OR, 3.8; 95% CI, 1.1-13.1), bilobectomy (OR, 7.26; 95% CI, 1.2-43.1) and smoking history (OR, 1.84; 95% CI, 1.1-3) were identified as independent risk factors. ERA may be a risk factor for POP and could serve as a target for therapeutic interventions.

Early emergence of Yersinia pestis as a severe respiratory pathogen.

PubMed

Zimbler, Daniel L; Schroeder, Jay A; Eddy, Justin L; Lathem, Wyndham W

2015-06-30

Yersinia pestis causes the fatal respiratory disease pneumonic plague. Y. pestis recently evolved from the gastrointestinal pathogen Y. pseudotuberculosis; however, it is not known at what point Y. pestis gained the ability to induce a fulminant pneumonia. Here we show that the acquisition of a single gene encoding the protease Pla was sufficient for the most ancestral, deeply rooted strains of Y. pestis to cause pneumonic plague, indicating that Y. pestis was primed to infect the lungs at a very early stage in its evolution. As Y. pestis further evolved, modern strains acquired a single amino-acid modification within Pla that optimizes protease activity. While this modification is unnecessary to cause pneumonic plague, the substitution is instead needed to efficiently induce the invasive infection associated with bubonic plague. These findings indicate that Y. pestis was capable of causing pneumonic plague before it evolved to optimally cause invasive infections in mammals.

Innate Immunity to Respiratory Infection in Early Life

PubMed Central

Lambert, Laura; Culley, Fiona J.

2017-01-01

Early life is a period of particular susceptibility to respiratory infections and symptoms are frequently more severe in infants than in adults. The neonatal immune system is generally held to be deficient in most compartments; responses to innate stimuli are weak, antigen-presenting cells have poor immunostimulatory activity and adaptive lymphocyte responses are limited, leading to poor immune memory and ineffective vaccine responses. For mucosal surfaces such as the lung, which is continuously exposed to airborne antigen and to potential pathogenic invasion, the ability to discriminate between harmless and potentially dangerous antigens is essential, to prevent inflammation that could lead to loss of gaseous exchange and damage to the developing lung tissue. We have only recently begun to define the differences in respiratory immunity in early life and its environmental and developmental influences. The innate immune system may be of relatively greater importance than the adaptive immune system in the neonatal and infant period than later in life, as it does not require specific antigenic experience. A better understanding of what constitutes protective innate immunity in the respiratory tract in this age group and the factors that influence its development should allow us to predict why certain infants are vulnerable to severe respiratory infections, design treatments to accelerate the development of protective immunity, and design age specific adjuvants to better boost immunity to infection in the lung. PMID:29184555

The impact of Michigan's Dr Ron Davis smoke-free air law on levels of cotinine, tobacco-specific lung carcinogen and severity of self-reported respiratory symptoms among non-smoking bar employees.

PubMed

Wilson, Teri; Shamo, Farid; Boynton, Katherine; Kiley, Janet

2012-11-01

To determine the impact on bar employee's health and exposure to secondhand smoke (SHS) before and after the implementation of Michigan's Dr Ron Davis smoke-free air law that went into effect on 1 May 2010, prohibiting smoking in places of work, including bars. This study used a pre/postintervention experimental design. The setting was bars in 12 Michigan counties. Subjects were bar employees, recruited through flyers and individual discussions with local health department staff. Participants completed a screening questionnaire to determine eligibility. A total of 40 eligible employees completed a demographic survey, provided urine samples for analysis of cotinine and 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL) and completed questionnaires on respiratory and general health status 6 weeks before and 6-10 weeks after the law went into effect. The main outcome measures were urine samples for total cotinine and total NNAL and data from a self-administered respiratory and general health status questionnaire collected during the pre-law and post-law study periods. There was a significant decrease in the mean cotinine levels from 35.9 ng/ml to a non-quantifiable value (p<0.001), and there was a significant reduction in the mean NNAL level from 0.086 pmol/ml to 0.034 pmol/ml (p<0.001) 2 months after implementation of the law. There was also a significant improvement in all six self-reported respiratory symptoms (p<0.001) and general health status (p<0.001). The reduction in the SHS biomarkers cotinine and NNAL and reported improvement in respiratory health demonstrates that the Michigan smoke-free workplace law is protecting bar employee health.

Early Life Wildfire Smoke Exposure Is Associated with Immune Dysregulation and Lung Function Decrements in Adolescence.

PubMed

Black, Carolyn; Gerriets, Joan E; Fontaine, Justin H; Harper, Richart W; Kenyon, Nicholas J; Tablin, Fern; Schelegle, Edward S; Miller, Lisa A

2017-05-01

The long-term health effects of wildfire smoke exposure in pediatric populations are not known. The objectives of this study were to determine if early life exposure to wildfire smoke can affect parameters of immunity and airway physiology that are detectable with maturity. We studied a mixed-sex cohort of rhesus macaque monkeys that were exposed as infants to ambient wood smoke from a series of Northern California wildfires in the summer of 2008. Peripheral blood mononuclear cells (PBMCs) and pulmonary function measures were obtained when animals were approximately 3 years of age. PBMCs were cultured with either LPS or flagellin, followed by measurement of secreted IL-8 and IL-6 protein. PBMCs from a subset of female animals were also evaluated by Toll-like receptor (TLR) pathway mRNA analysis. Induction of IL-8 protein synthesis with either LPS or flagellin was significantly reduced in PBMC cultures from wildfire smoke-exposed female monkeys. In contrast, LPS- or flagellin-induced IL-6 protein synthesis was significantly reduced in PBMC cultures from wildfire smoke-exposed male monkeys. Baseline and TLR ligand-induced expression of the transcription factor, RelB, was globally modulated in PBMCs from wildfire smoke-exposed monkeys, with additional TLR pathway genes affected in a ligand-dependent manner. Wildfire smoke-exposed monkeys displayed significantly reduced inspiratory capacity, residual volume, vital capacity, functional residual capacity, and total lung capacity per unit of body weight relative to control animals. Our findings suggest that ambient wildfire smoke exposure during infancy results in sex-dependent attenuation of systemic TLR responses and reduced lung volume in adolescence.

Firewood, smoke and respiratory diseases in developing countries—The neglected role of outdoor cooking

PubMed Central

2017-01-01

Smoke from cooking in the kitchen is one of the world’s leading causes of premature child death, claiming the lives of 500,000 children under five annually. This study analyses the role of outdoor cooking and the prevalence of respiratory diseases among children under five years by means of probit regressions using information from 41 surveys conducted in 30 developing countries from Asia, Africa and Latin America. I find that outdoor cooking reduces respiratory diseases among young children aged 0-4 by around 9 percent, an effect that reaches 13 percent among children aged 0-1. The results suggest that simple behavioral interventions, such as promoting outdoor cooking, can have a substantial impact on health hazards. PMID:28658290

Resolvin D1 prevents smoking-induced emphysema and promotes lung tissue regeneration.

PubMed

Kim, Kang-Hyun; Park, Tai Sun; Kim, You-Sun; Lee, Jae Seung; Oh, Yeon-Mok; Lee, Sang-Do; Lee, Sei Won

2016-01-01

Emphysema is an irreversible disease that is characterized by destruction of lung tissue as a result of inflammation caused by smoking. Resolvin D1 (RvD1), derived from docosahexaenoic acid, is a novel lipid that resolves inflammation. The present study tested whether RvD1 prevents smoking-induced emphysema and promotes lung tissue regeneration. C57BL/6 mice, 8 weeks of age, were randomly divided into four groups: control, RvD1 only, smoking only, and smoking with RvD1 administration. Four different protocols were used to induce emphysema and administer RvD1: mice were exposed to smoking for 4 weeks with poly(I:C) or to smoking only for 24 weeks, and RvD1 was injected within the smoking exposure period to prevent regeneration or after completion of smoking exposure to assess regeneration. The mean linear intercept and inflammation scores were measured in the lung tissue, and inflammatory cells and cytokines were measured in the bronchoalveolar lavage fluid. Measurements of mean linear intercept showed that RvD1 significantly attenuated smoking-induced lung destruction in all emphysema models. RvD1 also reduced smoking-induced inflammatory cell infiltration, which causes the structural derangements observed in emphysema. In the 4-week prevention model, RvD1 reduced the smoking-induced increase in eosinophils and interleukin-6 in the bronchoalveolar lavage fluid. In the 24-week prevention model, RvD1 also reduced the increased neutrophils and total cell counts induced by smoking. RvD1 attenuated smoking-induced emphysema in vivo by reducing inflammation and promoting tissue regeneration. This result suggests that RvD1 may be useful in the prevention and treatment of emphysema.

Smoking and subsequent risk of early retirement due to permanent disability.

PubMed

Husemoen, Lise Lotte N; Osler, Merete; Godtfredsen, Nina S; Prescott, Eva

2004-03-01

Smoking is the most important single preventable cause of a variety of common diseases, and a considerable share of premature death is attributable to smoking. Although the effects of smoking on morbidity and mortality are widely recognized, little is known about the impact of smoking on early retirement due to chronic disease. The objective of the study is to determine the effects of smoking behaviour on early retirement due to permanent disability in a large sample of the general population. Follow-up study based on data from three longitudinal population studies conducted in the Copenhagen area. The final study population comprised 9,053 persons, 5,623 men and 3,430 women. Endpoint was grant of disability pension in the period 1980-1985. Baseline information was obtained from a self-administered questionnaire. Information about disability pensions was obtained from Statistics Denmark. Data analysis was performed by univariate and multiple logistic regression analyses. Smoking was found to be strongly associated with the risk of being granted a disability pension after adjustment for various confounders. The risk increased with daily consumption reaching a maximum odds ratio of 5.66 (1.88-17.00) and 5.61 (2.11-14.92) in heavily smoking men and women, respectively, who were below age 60. Smokers are at considerably higher risk of early retirement due to chronic disease. In addition to the burden of disease, this leads to social and economic problems for the individual and has a significant economic impact on society.

Averting Opioid-induced Respiratory Depression without Affecting Analgesia.

PubMed

Dahan, Albert; van der Schrier, Rutger; Smith, Terry; Aarts, Leon; van Velzen, Monique; Niesters, Marieke

2018-05-01

The ventilatory control system is highly vulnerable to exogenous administered opioid analgesics. Particularly respiratory depression is a potentially lethal complication that may occur when opioids are overdosed or consumed in combination with other depressants such as sleep medication or alcohol. Fatalities occur in acute and chronic pain patients on opioid therapy and individuals that abuse prescription or illicit opioids for their hedonistic pleasure. One important strategy to mitigate opioid-induced respiratory depression is cotreatment with nonopioid respiratory stimulants. Effective stimulants prevent respiratory depression without affecting the analgesic opioid response. Several pharmaceutical classes of nonopioid respiratory stimulants are currently under investigation. The majority acts at sites within the brainstem respiratory network including drugs that act at α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors (ampakines), 5-hydroxytryptamine receptor agonists, phospodiesterase-4 inhibitors, D1-dopamine receptor agonists, the endogenous peptide glycyl-glutamine, and thyrotropin-releasing hormone. Others act peripherally at potassium channels expressed on oxygen-sensing cells of the carotid bodies, such as doxapram and GAL021 (Galleon Pharmaceuticals Corp., USA). In this review we critically appraise the efficacy of these agents. We conclude that none of the experimental drugs are adequate for therapeutic use in opioid-induced respiratory depression and all need further study of efficacy and toxicity. All discussed drugs, however, do highlight potential mechanisms of action and possible templates for further study and development.

Computerised respiratory sounds can differentiate smokers and non-smokers.

PubMed

Oliveira, Ana; Sen, Ipek; Kahya, Yasemin P; Afreixo, Vera; Marques, Alda

2017-06-01

Cigarette smoking is often associated with the development of several respiratory diseases however, if diagnosed early, the changes in the lung tissue caused by smoking may be reversible. Computerised respiratory sounds have shown to be sensitive to detect changes within the lung tissue before any other measure, however it is unknown if it is able to detect changes in the lungs of healthy smokers. This study investigated the differences between computerised respiratory sounds of healthy smokers and non-smokers. Healthy smokers and non-smokers were recruited from a university campus. Respiratory sounds were recorded simultaneously at 6 chest locations (right and left anterior, lateral and posterior) using air-coupled electret microphones. Airflow (1.0-1.5 l/s) was recorded with a pneumotachograph. Breathing phases were detected using airflow signals and respiratory sounds with validated algorithms. Forty-four participants were enrolled: 18 smokers (mean age 26.2, SD = 7 years; mean FEV 1 % predicted 104.7, SD = 9) and 26 non-smokers (mean age 25.9, SD = 3.7 years; mean FEV 1 % predicted 96.8, SD = 20.2). Smokers presented significantly higher frequency at maximum sound intensity during inspiration [(M = 117, SD = 16.2 Hz vs. M = 106.4, SD = 21.6 Hz; t(43) = -2.62, p = 0.0081, d z  = 0.55)], lower expiratory sound intensities (maximum intensity: [(M = 48.2, SD = 3.8 dB vs. M = 50.9, SD = 3.2 dB; t(43) = 2.68, p = 0.001, d z  = -0.78)]; mean intensity: [(M = 31.2, SD = 3.6 dB vs. M = 33.7,SD = 3 dB; t(43) = 2.42, p = 0.001, d z  = 0.75)] and higher number of inspiratory crackles (median [interquartile range] 2.2 [1.7-3.7] vs. 1.5 [1.2-2.2], p = 0.081, U = 110, r = -0.41) than non-smokers. Significant differences between computerised respiratory sounds of smokers and non-smokers have been found. Changes in respiratory sounds are often the earliest sign of disease. Thus, computerised respiratory sounds

Minocycline suppresses morphine-induced respiratory depression, suppresses morphine-induced reward, and enhances systemic morphine-induced analgesia

PubMed Central

Hutchinson, Mark R.; Northcutt, Alexis L.; Chao, Lindsey W.; Kearney, Jeffrey J.; Zhang, Yingning; Berkelhammer, Debra L.; Loram, Lisa C.; Rozeske, Robert R.; Bland, Sondra T.; Maier, Steven F.; Gleeson, Todd T.; Watkins, Linda R.

2008-01-01

Recent data suggest that opioids can activate immune-like cells of the central nervous system (glia). This opioid-induced glial activation is associated with decreased analgesia, owing to the release of proinflammatory mediators. Here we examine in rats whether the putative microglial inhibitor, minocycline, may affect morphine-induced respiratory depression and/or morphine-induced reward (conditioned place preference). Systemic co-administration of minocycline significantly attenuated morphine-induced reductions in tidal volume, minute volume, inspiratory force and expiratory force, but did not affect morphine-induced reductions in respiratory rate. Minocycline attenuation of respiratory depression was also paralleled with significant attenuation by minocycline of morphine-induced reductions in blood oxygen saturation. Minocycline also attenuated morphine conditioned place preference. Minocycline did not simply reduce all actions of morphine, as morphine analgesia was significantly potentiated by minocycline co-administration. Lastly, morphine dose-dependently increased cyclooxygenase-1 gene expression in a rat microglial cell line, an effect that was dose-dependently blocked by minocycline. Together, these data support that morphine can directly activate microglia in a minocycline-suppressible manner and suggest a pivotal role for minocycline-sensitive processes in the mechanisms of morphine-induced respiration depression, reward, and pain modulation. PMID:18706994

Early postnatal changes in respiratory activity in rat in vitro and modulatory effects of substance P.

PubMed

Shvarev, Y N; Lagercrantz, H

2006-10-01

Developmental changes in the respiratory activity and its modulation by substance P (SP) were studied in the neonatal rat brainstem-spinal cord preparation from the day of birth to day 3 (P0-P3). The respiratory network activity in the ventrolateral medulla was represented by two types of bursts: basic regular bursts with typical decrementing shape and biphasic bursts appearing after augmented biphasic discharges in inspiratory neurons. With advancing postnatal age the respiratory output was considerably modified; the basic rhythm became faster by 20%, whereas the biphasic burst rate, which was originally 15 times slower, declined further by 180% and the C4 burst duration significantly decreased by 20% due to reduced decay time without preceding changes in the central inspiratory drive. SP had an age-dependent excitatory effect on respiratory activity. In the basic rhythm, SP could induce transient rhythm cessations on P0-P2 but not on P3. For the biphasic burst frequency, the sensitivity to SP significantly decreased from P0 to P3, whereas the range of SP-induced changes increased. In both types of bursts, SP prolonged C4 burst duration due to increasing decay time. This effect was three times greater on P3 and did not depend on the central inspiratory drive. Our results suggest that the potency of SP to regulate the respiratory activity elevates during the early postnatal period. The developmental changes in the respiratory activity appear to represent the transient stage in the maturation of rhythm and pattern generation mechanisms facilitating adaptive behavior of a quickly growing organism.

Affective Motives for Smoking Among Early Stage Smokers

PubMed Central

Wahlquist, Amy E.; Garrett-Mayer, Elizabeth; Gray, Kevin M.; Saladin, Michael E.; Carpenter, Matthew J.

2014-01-01

Background: As most smokers initiate smoking during adolescence, assessment of smoking motives that underlie trajectories of dependence is critical for both prevention and cessation efforts. In the current study, we expected participants with higher nicotine dependence would smoke (a) less for positive reinforcement (PR) and (b) more for negative reinforcement (NR) motives. We secondarily assessed the relative contribution of PR to NR motives across levels of dependence. Methods: Data were drawn from a study on cue-elicited craving among occasional versus daily adolescent smokers aged 16–20 years (N = 111). Smoking motives were assessed in relation to 3 commonly used measures of nicotine dependence: (a) Fagerström Test for Nicotine Dependence (FTND), (b) Autonomy over Smoking Scale (AUTOS), and (c) Nicotine Dependence Syndrome Scale (NDSS). Results: Compared to occasional smokers, daily smokers had significantly higher scores on each dependence measure and endorsed more prominent NR smoking motives. Each measure of nicotine dependence was strongly associated with NR motives for smoking, although measures differed in their association with PR motives. As expected, the FTND, AUTOS, and NDSS each significantly predicted smoking motive difference score (PR − NR), such that higher dependence was associated with more prominent NR motives for smoking. Conclusions: Results are consistent with our understanding of dependence and provide further support for 3 common measures of nicotine dependence among early stage smokers. PMID:24924155

Early emergence of Yersinia pestis as a severe respiratory pathogen

PubMed Central

Zimbler, Daniel L.; Schroeder, Jay A.; Eddy, Justin L.; Lathem, Wyndham W.

2015-01-01

Yersinia pestis causes the fatal respiratory disease pneumonic plague. Y. pestis recently evolved from the gastrointestinal pathogen Y. pseudotuberculosis; however, it is not known at what point Y. pestis gained the ability to induce a fulminant pneumonia. Here we show that the acquisition of a single gene encoding the protease Pla was sufficient for the most ancestral, deeply rooted strains of Y. pestis to cause pneumonic plague, indicating that Y. pestis was primed to infect the lungs at a very early stage in its evolution. As Y. pestis further evolved, modern strains acquired a single amino-acid modification within Pla that optimizes protease activity. While this modification is unnecessary to cause pneumonic plague, the substitution is instead needed to efficiently induce the invasive infection associated with bubonic plague. These findings indicate that Y. pestis was capable of causing pneumonic plague before it evolved to optimally cause invasive infections in mammals. PMID:26123398

Social Stress, Smoking Behavior and Mortality from Cancer of the Respiratory System: A Macro-Social Analysis.

ERIC Educational Resources Information Center

Linsky, Arnold S.; And Others

This study investigated the relationship between the stressfulness of each state's social environment, smoking, and mortality rates for respiratory cancer. It was based on a health behavior model which assumed that under conditions of high stress some people fail to exercise normal prudence in either protecting their health or engage in practices…

Early Exercise Rehabilitation of Muscle Weakness in Acute Respiratory Failure Patients

PubMed Central

Berry, Michael J.; Morris, Peter E.

2013-01-01

Acute Respiratory Failure patients experience significant muscle weakness which contributes to prolonged hospitalization and functional impairments post-hospital discharge. Based on our previous work, we hypothesize that an exercise intervention initiated early in the intensive care unit aimed at improving skeletal muscle strength could decrease hospital stay and attenuate the deconditioning and skeletal muscle weakness experienced by these patients. Summary Early exercise has the potential to decrease hospital length of stay and improve function in Acute Respiratory Failure patients. PMID:23873130

Calls to Poison Centers for hookah smoking exposures.

PubMed

Retzky, Sandra S; Spiller, Henry A; Callahan-Lyon, Priscilla

2018-06-01

Over the past decade, smoking behaviors have changed in the US. Hookah or waterpipe smoking is increasing, especially among youth and young adults. Social media sites describe the "hookah high" or "buzz", which may be related to nicotine, carbon monoxide, or other inhalants in hookah smoke. Most important is the risk of carbon monoxide poisoning. Case reports include a high number of victims presenting with loss of consciousness from either syncope or seizures. Anaphylaxis and a very rare respiratory hypersensitivity reaction, acute eosinophilic pneumonia, have also been reported from hookah smoking in previously healthy young adults. This article provides background information on hookah smoking, describes hookah-induced acute injuries that could precipitate poison center calls, and offers suggestions for exposure characterization.

Do respiratory therapists receive training and education in smoking cessation? A national study of post-secondary training programs.

PubMed

Jordan, Timothy R; Khubchandani, Jagdish; Wiblishauser, Michael; Glassman, Tavis; Thompson, Amy

2011-10-01

To assess the tobacco-related education provided by post-secondary respiratory therapy training programs in the United States. A cross-sectional research design was used to survey the entire population of program directors of post-secondary, respiratory therapy training programs in the United States. A valid and reliable questionnaire was developed and mailed using a 2-wave mailing technique (73% return rate). Internal reliability coefficients (Cronbach alpha) for the various components of the questionnaire ranged from 0.78 to 0.91. More than half of programs (56%) offered no teaching on the 5R's. Nearly half (47%) offered no teaching on the 5A's. Of the 13 tobacco-related topics listed in the basic science and clinical science sections of the questionnaire, only one topic (i.e., diseases linked to tobacco use) received 3h or more of instruction by approximately a third of programs (35.8%). The majority of programs (>90%) spent no time teaching students about the socio-political aspects of tobacco use cessation. Moreover, 41% of programs did not formally evaluate students' competence in providing smoking cessation counseling to patients. Tobacco-related education is a very minor component of the education and training received by respiratory therapy students in the United States. Respiratory therapy training programs in the United States have great potential to strengthen the tobacco-related education that they provide to students. Practicing respiratory therapists would likely benefit from continuing medical education focused on how to use evidence-based smoking cessation counseling techniques with patients. Copyright © 2010 Elsevier Ireland Ltd. All rights reserved.

Survival of macrovascular disease, chronic kidney disease, chronic respiratory disease, cancer and smoking in patients with type 2 diabetes: BioBank Japan cohort.

PubMed

Yokomichi, Hiroshi; Nagai, Akiko; Hirata, Makoto; Kiyohara, Yutaka; Muto, Kaori; Ninomiya, Toshiharu; Matsuda, Koichi; Kamatani, Yoichiro; Tamakoshi, Akiko; Kubo, Michiaki; Nakamura, Yusuke; Yamagata, Zentaro

2017-03-01

The number of patients with diabetes is increasing worldwide. Macrovascular disease, chronic kidney disease, chronic respiratory disease, cancer and smoking frequently accompany type 2 diabetes. Few data are available related to mortality of Asians with diabetes associated with these serious comorbidities. The present study aimed to quantify the excess mortality risks of type 2 diabetic patients with comorbidities. We analysed the available records of 30,834 Japanese patients with type 2 diabetes from the BioBank Japan Project between 2003 and 2007. Men and women were followed up for median 8.03 and 8.30 years, respectively. We applied Cox proportional hazard model and Kaplan-Meier estimates for survival curves to evaluate mortality in diabetic patients with or without macrovascular disease, chronic respiratory disease, chronic kidney disease, cancer and smoking. Adjusted hazard ratios (HRs) for mortality were 1.39 (95% CI, 1.09-1.78) for male sex, 2.01 (95% CI, 1.78-2.26) per 10-year increment of age. Adjusted HRs of primary interest were 1.77 (95% CI, 1.42-2.22), macrovascular disease; 1.58 (95% CI, 1.08-2.31), chronic respiratory disease; 2.03 (95% CI, 1.67-2.47), chronic kidney disease; 1.16 (95% CI, 0.86-1.56), cancer; and 1.74 (95% CI, 1.30-2.31), current smoking. Diabetic patients with a past or current history of chronic kidney, macrovascular or respiratory diseases or smoking habit have exhibited the highest risk of mortality. Data were limited to those of survivors of comorbidities but we propose the need to improve comorbidities and terminate cigarette smoking for better prognosis in patients with diabetes. Copyright © 2017 The Authors. Production and hosting by Elsevier B.V. All rights reserved.

Effect of Smoking During Radiotherapy, Respiratory Insufficiency, and Hemoglobin Levels on Outcome in Patients Irradiated for Non-Small-Cell Lung Cancer

DOE Office of Scientific and Technical Information (OSTI.GOV)

Rades, Dirk; Setter, Cornelia M.S.; Schild, Steven E.

Purpose: To investigate the effect of smoking during radiotherapy (RT), respiratory insufficiency before RT, hemoglobin levels during RT, and additional factors on overall survival, locoregional control (LRC), and metastasis-free survival in non-small-cell lung cancer patients. Methods and Materials: The following factors were investigated in 181 patients who underwent RT for non-small-cell lung cancer: age, gender, Karnofsky performance score, histologic type, grade, T/N stage, American Joint Committee on Cancer stage, surgery, chemotherapy, respiratory insufficiency before RT, pack-years, smoking during RT, and hemoglobin levels during RT. Additionally, in the 129 patients who did not undergo surgery, the effect of the equivalent dosemore » in 2-Gy fractions (EQD2) (<60 Gy vs. 60 Gy vs. >60 Gy) on outcome was investigated. Results: On multivariate analysis, improved overall survival was associated with a lower T stage (p = 0.004), lower N stage (p 0.040), surgery (p = 0.010), and no respiratory insufficiency (p = 0.023). A Karnofsky performance score >70 achieved borderline significance (p = 0.056). Improved LRC was associated with a lower T stage (p = 0.007) and no smoking during RT (p = 0.029). Improved metastasis-free survival was associated with lower T stage (p < 0.001) and lower N stage (p < 0.001). In those patients who did not undergo surgery, an EQD2 of {>=}60 Gy was associated with a better outcome than an EQD2 of <60 Gy. Furthermore, an EQD2 >60 Gy resulted in better LRC than did an EQD2 of {<=}60 Gy. Conclusions: Smoking during RT had a significant effect on LRC, but we did not find that hemoglobin levels or respiratory insufficiency significantly affected LRC or metastasis-free survival in our patient population. Furthermore, our data suggest a dose-effect relationship in those patients who did not undergo surgery.« less

Cytologic analysis of alterations induced by Smoking and by alcohol consumption.

PubMed

Pavanello, Marcella Batista; Prado, Fernanda Almeida; Balducci, Ivan; Brandão, Adriana Aigotti Haberbeck; Almeida, Janete Dias

2006-01-01

To analyze cytologically the buccal mucosa of smoking and nonsmoking volunteers to determine what cellular changes are induced by cigarettes and alcohol consumption. In order to evaluate cellular changes induced by smoking and alcohol consumption, exfoliative cytology was used for the analysis of mucosal smears obtained from the buccal mucosa of 25 smokers and 25 nonsmokers. The number of cigarettes consumed, duration of smoking, presence or absence of alcohol ingestion, ingested alcohol dose and frequency of consumption, and most frequently used type of alcoholic beverage were determined using a questionnaire. Three smears from each individual stained by the Papanicolaou method were analyzed quantitatively and qualitatively under a light microscope by 2 experienced examiners in terms of inflammatory and dysplastic alterations and of the degree of epithelial maturation. Although numerous alterations were observed in smokers they corresponded up to only Papanicolaou class II and were not significantly different from nonsmokers (Mann-Whitney and chi2 tests, p < 0.05). A higher proportion of inflammatory cells (polymorphonuclear and mononuclear cells) were obtained from smokers as compared to nonsmokers, while the proportion of bacteria was similar in the 2 groups. The findings indicate that even after a short period of cigarette use and alcohol consumption, inflammatory alterations were detectable on exfoliative cytology of the buccal mucosa in a young group, demonstrating the usefulness of cytology for early detection in smokers.

Smoke regions extraction based on two steps segmentation and motion detection in early fire

NASA Astrophysics Data System (ADS)

Jian, Wenlin; Wu, Kaizhi; Yu, Zirong; Chen, Lijuan

2018-03-01

Aiming at the early problems of video-based smoke detection in fire video, this paper proposes a method to extract smoke suspected regions by combining two steps segmentation and motion characteristics. Early smoldering smoke can be seen as gray or gray-white regions. In the first stage, regions of interests (ROIs) with smoke are obtained by using two step segmentation methods. Then, suspected smoke regions are detected by combining the two step segmentation and motion detection. Finally, morphological processing is used for smoke regions extracting. The Otsu algorithm is used as segmentation method and the ViBe algorithm is used to detect the motion of smoke. The proposed method was tested on 6 test videos with smoke. The experimental results show the effectiveness of our proposed method over visual observation.

When you smoke your baby smokes: advancing maternal and child health through an academic alliance to improve health of mothers and their infants.

PubMed

Merritt, T Allen; Philips, Raylene; Armstrong, Stephanie; Mazela, Jan; Gadzinowski, Janusz

2010-01-01

The detrimental effect of tobacco exposure prior to conception and during pregnancy has been receiving much worldwide attention. Maternal smoking during pregnancy is associated with early-onset wheezing, increased respiratory illnesses, and a 2-fold increased risk for Sudden Infant Death Syndrome (SIDS). Adverse effects on the infant include altered infant behaviors such as an increased occurrence of infant colic or Attention Deficit Disorders (ADD). Studies have shown that a significant number of smoking woman "quit" smoking during pregnancy. However, a majority of women, 67% by 3 months and up to 90% by 6 month, resume smoking following delivery. An infant's birth related hospitalization is a "teachable moment" to address parental smoking, and to advocate for reducing fetal exposure to tobacco smoke. Academic alliance focused on well designed educative program can further increase rate of smoking free pregnant women and decrease smoking relapse rates significantly.

“Smoking Wet”

PubMed Central

Gilbert, Christopher R.; Baram, Michael; Cavarocchi, Nicholas C.

2013-01-01

Reports have suggested that the use of a dangerously tainted form of marijuana, referred to in the vernacular as “wet” or “fry,” has increased. Marijuana cigarettes are dipped into or laced with other substances, typically formaldehyde, phencyclidine, or both. Inhaling smoke from these cigarettes can cause lung injuries. We report the cases of 2 young adults who presented at our hospital with respiratory failure soon after they had smoked “wet” marijuana cigarettes. In both patients, progressive hypoxemic respiratory failure necessitated rescue therapy with extracorporeal membrane oxygenation. After lengthy hospitalizations, both patients recovered with only mild pulmonary function abnormalities. To our knowledge, this is the first 2-patient report of severe respiratory failure and rescue therapy with extracorporeal oxygenation after the smoking of marijuana cigarettes thus tainted. We believe that, in young adults with an unexplained presentation of severe respiratory failure, the possibility of exposure to tainted marijuana cigarettes should be considered. PMID:23466531

Foods and respiratory allergy.

PubMed

Novembre, E; de Martino, M; Vierucci, A

1988-05-01

Foods may induce respiratory symptoms by both reaginic and nonreaginic mechanisms. Asthma is one of the most common respiratory manifestations in children, and it is well known that many factors may provoke an attack. When considering the relationship between foods and asthma, we must keep in mind that food allergy may coexist with an inhalant allergy and that other nonallergens, such as pollutants, smoke, or additives, may modulate or modify bronchial reactivity and thus favor the food allergen action. In a study using clinical history, prick test, radioallergosorbent test, and double-blind food challenge, we demonstrated respiratory symptoms related to food allergy in 13 of 140 (9.2%) children with asthma. Asthma, in particular, was demonstrated in 8 of 140 (5.7%) patients. Food allergy respiratory symptoms are, in our experience, almost always associated with other clinical manifestations (e.g., cutaneous, gastrointestinal). The recognition of food-dependent IgE-mediated respiratory symptoms is essentially limited to those cases characterized by food allergy with asthmatic expression. It is possible, however, that in many cases foods may have a nonspecific role in the determination of asthma or in the preparation of bronchi for the possible consequent stimulus.

Efficacy of confrontational counselling for smoking cessation in smokers with previously undiagnosed mild to moderate airflow limitation: study protocol of a randomized controlled trial.

PubMed

Kotz, Daniel; Wesseling, Geertjan; Huibers, Marcus J H; van Schayck, Onno C P

2007-11-15

The use of spirometry for early detection of chronic obstructive pulmonary disease (COPD) is still an issue of debate, particularly because of a lack of convincing evidence that spirometry has an added positive effect on smoking cessation. We hypothesise that early detection of COPD and confrontation with spirometry for smoking cessation may be effective when applying an approach we have termed "confrontational counselling"; a patient-centred approach which involves specific communication skills and elements of cognitive therapy. An important aspect is to confront the smoker with his/her airflow limitation during the counselling sessions. The primary objective of this study is to test the efficacy of confrontational counselling in comparison to regular health education and promotion for smoking cessation delivered by specialized respiratory nurses in current smokers with previously undiagnosed mild to moderate airflow limitation. The study design is a randomized controlled trial comparing confrontational counselling delivered by a respiratory nurse combined with nortriptyline for smoking cessation (experimental group), health education and promotion delivered by a respiratory nurse combined with nortriptyline for smoking cessation (control group 1), and "care as usual" delivered by the GP (control group 2). Early detection of smokers with mild to moderate airflow limitation is achieved by means of a telephone interview in combination with spirometry. Due to a comparable baseline risk of airflow limitation and motivation to quit smoking, and because of the standardization of number, duration, and scheduling of counselling sessions between the experimental group and control group 1, the study enables to assess the "net" effect of confrontational counselling. The study has been ethically approved and registered. Ethical as well as methodological considerations of the study are discussed in this protocol. A significant and relevant effect of confrontational counselling

Affective motives for smoking among early stage smokers.

PubMed

Mathew, Amanda R; Wahlquist, Amy E; Garrett-Mayer, Elizabeth; Gray, Kevin M; Saladin, Michael E; Carpenter, Matthew J

2014-10-01

As most smokers initiate smoking during adolescence, assessment of smoking motives that underlie trajectories of dependence is critical for both prevention and cessation efforts. In the current study, we expected participants with higher nicotine dependence would smoke (a) less for positive reinforcement (PR) and (b) more for negative reinforcement (NR) motives. We secondarily assessed the relative contribution of PR to NR motives across levels of dependence. Data were drawn from a study on cue-elicited craving among occasional versus daily adolescent smokers aged 16-20 years (N = 111). Smoking motives were assessed in relation to 3 commonly used measures of nicotine dependence: (a) Fagerström Test for Nicotine Dependence (FTND), (b) Autonomy over Smoking Scale (AUTOS), and (c) Nicotine Dependence Syndrome Scale (NDSS). Compared to occasional smokers, daily smokers had significantly higher scores on each dependence measure and endorsed more prominent NR smoking motives. Each measure of nicotine dependence was strongly associated with NR motives for smoking, although measures differed in their association with PR motives. As expected, the FTND, AUTOS, and NDSS each significantly predicted smoking motive difference score (PR - NR), such that higher dependence was associated with more prominent NR motives for smoking. Results are consistent with our understanding of dependence and provide further support for 3 common measures of nicotine dependence among early stage smokers. © The Author 2014. Published by Oxford University Press on behalf of the Society for Research on Nicotine and Tobacco. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.

Cigarette smoke induces mitochondrial metabolic reprogramming in lung cells.

PubMed

Solanki, Hitendra S; Babu, Niraj; Jain, Ankit P; Bhat, Mohd Younis; Puttamallesh, Vinuth N; Advani, Jayshree; Raja, Remya; Mangalaparthi, Kiran K; Kumar, Mahesh M; Prasad, T S Keshava; Mathur, Premendu Prakash; Sidransky, David; Gowda, Harsha; Chatterjee, Aditi

2018-05-01

Cellular transformation owing to cigarette smoking is due to chronic exposure and not acute. However, systematic studies to understand the molecular alterations in lung cells due to cigarette smoke are lacking. To understand these molecular alterations induced by chronic cigarette smoke exposure, we carried out tandem mass tag (TMT) based temporal proteomic profiling of lung cells exposed to cigarette smoke for upto 12months. We identified 2620 proteins in total, of which 671 proteins were differentially expressed (1.5-fold) after 12months of exposure. Prolonged exposure of lung cells to smoke for 12months revealed dysregulation of oxidative phosphorylation and overexpression of enzymes involved in TCA cycle. In addition, we also observed overexpression of enzymes involved in glutamine metabolism, fatty acid degradation and lactate synthesis. This could possibly explain the availability of alternative source of carbon to TCA cycle apart from glycolytic pyruvate. Our data indicates that chronic exposure to cigarette smoke induces mitochondrial metabolic reprogramming in cells to support growth and survival. Copyright © 2017 Elsevier B.V. and Mitochondria Research Society. All rights reserved.

Early life adversity influences stress response association with smoking relapse.

PubMed

al'Absi, Mustafa; Lemieux, Andrine; Westra, Ruth; Allen, Sharon

2017-11-01

We examined the hypothesis that stress-related blunting of cortisol in smokers is particularly pronounced in those with a history of severe life adversity. The two aims of this study were first to examine hormonal, craving, and withdrawal symptoms during ad libitum smoking and after the first 24 h of abstinence in smokers who experienced high or low levels of adversity. Second, we sought to examine the relationship between adversity and hypothalamic-pituitary-adrenal (HPA) hormones to predict relapse during the first month of a smoking cessation attempt. Hormonal and self-report measures were collected from 103 smokers (49 women) during ad libitum smoking and after the first 24 h of abstinence. HPA hormones were measured during baseline rest and in response to acute stress in both conditions. All smokers were interested in smoking cessation, and we prospectively used stress response measures to predict relapse during the first 4 weeks of the smoking cessation attempt. The results showed that high adversity was associated with higher distress and smoking withdrawal symptoms. High level of early life adversity was associated with elevated HPA activity, which was found in both salivary and plasma cortisol. Enhanced adrenocorticotropic hormone (ACTH) stress response was evident in high-adversity but not in low-adversity relapsers. This study demonstrated that early life adversity is associated with stress-related HPA responses. The study also demonstrated that, among smokers who experienced a high level of life adversity, heightened ACTH and cortisol responses were linked with increased risk for smoking relapse.

Cigarette smoke induces β2-integrin-dependent neutrophil migration across human endothelium

PubMed Central

2011-01-01

Background Cigarette smoking induces peripheral inflammatory responses in all smokers and is the major risk factor for neutrophilic lung disease such as chronic obstructive pulmonary disease. The aim of this study was to investigate the effect of cigarette smoke on neutrophil migration and on β2-integrin activation and function in neutrophilic transmigration through endothelium. Methods and results Utilizing freshly isolated human PMNs, the effect of cigarette smoke on migration and β2-integrin activation and function in neutrophilic transmigration was studied. In this report, we demonstrated that cigarette smoke extract (CSE) dose dependently induced migration of neutrophils in vitro. Moreover, CSE promoted neutrophil adherence to fibrinogen. Using functional blocking antibodies against CD11b and CD18, it was demonstrated that Mac-1 (CD11b/CD18) is responsible for the cigarette smoke-induced firm adhesion of neutrophils to fibrinogen. Furthermore, neutrophils transmigrated through endothelium by cigarette smoke due to the activation of β2-integrins, since pre-incubation of neutrophils with functional blocking antibodies against CD11b and CD18 attenuated this transmigration. Conclusion This is the first study to describe that cigarette smoke extract induces a direct migratory effect on neutrophils and that CSE is an activator of β2-integrins on the cell surface. Blocking this activation of β2-integrins might be an important target in cigarette smoke induced neutrophilic diseases. PMID:21651795

Tobacco smoke exposure induces nicotine dependence in rats

PubMed Central

Small, Elysia; Shah, Hina P.; Davenport, Jake J.; Geier, Jacqueline E.; Yavarovich, Kate R.; Yamada, Hidetaka; Sabarinath, Sreedharan N.; Derendorf, Hartmut; Pauly, James R.; Gold, Mark S.; Bruijnzeel, Adrie W.

2013-01-01

RATIONALE Tobacco smoke contains nicotine and many other compounds that act in concert on the brain reward system. Therefore, animal models are needed that allow the investigation of chronic exposure to the full spectrum of tobacco smoke constituents. OBJECTIVES The aim of these studies was to investigate if exposure to tobacco smoke leads to nicotine dependence in rats. METHODS The intracranial self-stimulation procedure was used to assess the negative affective aspects of nicotine withdrawal. Somatic signs were recorded from a checklist of nicotine abstinence signs. Nicotine self-administration sessions were conducted to investigate if tobacco smoke exposure affects the motivation to self-administer nicotine. Nicotinic receptor autoradiography was used to investigate if exposure to tobacco smoke affects central α7 nicotinic acetylcholine receptor (nAChR) and non-α7 nAChR levels (primarily α4β2 nAChRs). RESULTS The nAChR antagonist mecamylamine dose-dependently elevated the brain reward thresholds of the rats exposed to tobacco smoke and did not affect the brain reward thresholds of the untreated control rats. Furthermore, mecamylamine induced more somatic withdrawal signs in the smoke exposed rats than in the control rats. Nicotine self-administration was decreased 1 day after the last tobacco smoke exposure sessions and was returned to control levels 5 days later. Tobacco smoke exposure increased the α7 nAChR density in the CA2/3 area and the stratum oriens and increased the non-α7 nAChR density in the dentate gyrus. CONCLUSION Tobacco smoke exposure leads to nicotine dependence as indicated by precipitated affective and somatic withdrawal signs and induces an upregulation of nAChRs in the hippocampus. PMID:19936715

Assessment of tobacco smoke effects on neonatal cardiorespiratory control using a semi-automated processing approach.

PubMed

Al-Omar, Sally; Le Rolle, Virginie; Beuchée, Alain; Samson, Nathalie; Praud, Jean-Paul; Carrault, Guy

2018-05-10

A semi-automated processing approach was developed to assess the effects of early postnatal environmental tobacco smoke (ETS) on the cardiorespiratory control of newborn lambs. The system consists of several steps beginning with artifact rejection, followed by the selection of stationary segments, and ending with feature extraction. This approach was used in six lambs exposed to 20 cigarettes/day for the first 15 days of life, while another six control lambs were exposed to room air. On postnatal day 16, electrocardiograph and respiratory signals were obtained from a 6-h polysomnographic recording. The effects of postnatal ETS exposure on heart rate variability, respiratory rate variability, and cardiorespiratory interrelations were explored. The unique results suggest that early postnatal ETS exposure increases respiratory rate variability and decreases the coupling between cardiac and respiratory systems. Potentially harmful consequences in early life include unstable breathing and decreased adaptability of cardiorespiratory function, particularly during early life challenges, such as prematurity or viral infection. Graphical abstract ᅟ.

[Interactive effects of environmental tobacco smoke and pets ownership on respiratory diseases and symptoms in children].

PubMed

Zhao, Yang; Liu, Yu-qin; Liu, Miao-miao; Wang, Da; Ren, Wan-hui; Gao, Feng; Dong, Guang-hui

2013-02-01

Over the past few decades, secondhand smoke exposure among children become more serious and with China's implementation of the national policy of family planning and the family structure change, domestic pet has gradually become popular. This survey aimed to investigate the interactive effects of pet ownership and environmental tobacco smoke (ETS) on children's respiratory diseases and symptoms. Using a cluster random sampling method, 5 elementary schools and 10 kindergartens were randomly selected from each district of Shenyang, and all children from the selected schools were recruited in this survey. The information about the children's respiratory diseases, conditions of pets ownership and ETS exposure were collected by an international standard questionnaire from American Thoracic Society. A total of 9679 questionnaires were distributed to all the students enrolled in the selected schools, and 8798 completed questionnaires were collected with a response rate of 90.9%. Finally, 8733 questionnaires were used for further analysis. The results showed that the number of the patients and the prevalence of persistent cough, persistent phlegm, doctor-diagnosed asthma, current asthma, wheeze, and allergic rhinitis in children were 835 (9.57%), 366 (4.42%), 559 (6.40%), 215 (2.46%), 229 (2.62%), 397 (4.55%), respectively. After controlling for the effects of age, gender and other confounding factors, the results from the multivariate unconditional logistic regression analysis showed that either pet ownership or the ETS exposure significantly increased the risk of prevalence of respiratory diseases and symptoms in children. Compared with control group children, only the prenatal exposure to passive smoking or domestic pets made the risk of children with allergic rhinitis increased respectively 34% (OR = 1.34, 95%CI = 0.99 - 1.80) and 106% (OR = 2.06, 95%CI = 1.28 - 3.31), while the exposure of these two factors made the risk of children with allergic rhinitis increased

[Treatment of patients with different degree of acute respiratory distress syndrome caused by inhalation of white smoke].

PubMed

Yang, F W; Xin, H M; Zhu, J H; Feng, X Y; Jiang, X C; Gong, Z Y; Tong, Y L

2017-12-20

Objective: To summarize the treatment experience of patients with different degree of acute respiratory distress syndrome (ARDS) caused by inhalation of white smoke from burning smoke bomb. Methods: A batch of 13 patients with different degree of ARDS caused by inhalation of white smoke from burning smoke bomb, including 2 patients complicated by pulmonary fibrosis at the late stage, were admitted to our unit in February 2016. Patients were divided into mild (9 cases), moderate (2 cases), and serious (2 cases) degree according to the ARDS Berlin diagnostic criteria. Patients with mild and moderate ARDS were conventionally treated with glucocorticoid. Patients with severe ARDS were sequentially treated with glucocorticoid and pirfenidone, and ventilator-assisted breathing, etc. were applied. The vital signs, arterial oxygenation index, changes of lung imaging, pulmonary ventilation function, general condition, and the other important organs/systems function were timely monitored according to the condition of patients. The above indexes were also monitored during the follow-up time of 10-15 months post injury. Data were processed with SPSS 18.0 statistical software. Results: (1) The symptoms of respiratory system of patients with mild and moderate ARDS almost disappeared after 3 days' treatment. Their arterial oxygenation index was decreased from post injury day 1 to 4, which almost recovered on post injury day 7 and completely recovered one month post injury. The symptoms of respiratory system of patients with severe ARDS almost disappeared at tranquillization condition 1-3 month (s) post injury. Their arterial oxygenation index was decreased from post injury day 3 to 21, which gradually recovered 1-3 month (s) post injury and was normal 15 months post injury. (2) Within 24 hours post injury, there was no obvious abnormality or only a little texture enlargement of lung in image of chest CT or X-rays of patients with mild and moderate ARDS. One patient with moderate

Cigarette smoke induced urocystic epithelial mesenchymal transition via MAPK pathways.

PubMed

Yu, Dexin; Geng, Hao; Liu, Zhiqi; Zhao, Li; Liang, Zhaofeng; Zhang, Zhiqiang; Xie, Dongdong; Wang, Yi; Zhang, Tao; Min, Jie; Zhong, Caiyun

2017-01-31

Cigarette smoke has been shown to be a major risk factor for bladder cancer. Epithelial-mesenchymal transition (EMT) is a crucial process in cancer development. The role of MAPK pathways in regulating cigarette smoke-triggered urocystic EMT remains to be elucidated. Human normal urothelial cells and BALB/c mice were used as in vitro and in vivo cigarette smoke exposure models. Exposure of human normal urothelial cells to cigarette smoke induced morphological change, enhanced migratory and invasive capacities, reduced epithelial marker expression and increased mesenchymal marker expression, along with the activation of MAPK pathways. Moreover, we revealed that ERK1/2 and p38 inhibitors, but rather JNK inhibitor, effectively attenuated cigarette smoke-induced urocystic EMT. Importantly, the regulatory function of ERK1/2 and p38 pathways in cigarette smoke-triggered urocystic EMT was further confirmed in mice exposed to CS for 12 weeks. These findings could provide new insight into the molecular mechanisms of cigarette smoke-associated bladder cancer development as well as its potential intervention.

Assessing the effects of the Spanish partial smoking ban on cardiovascular and respiratory diseases: methodological issues.

PubMed

Galán, Iñaki; Simón, Lorena; Flores, Víctor; Ortiz, Cristina; Fernández-Cuenca, Rafael; Linares, Cristina; Boldo, Elena; Medrano, María José; Pastor-Barriuso, Roberto

2015-12-01

Recent research has assessed the impact of tobacco laws on cardiovascular and respiratory morbidity. In this study, we also examined whether the association between the implementation of the 2005 Spanish smoking ban and hospital admissions for cardiovascular and respiratory diseases varies according to the adjustment for potential confounders. Ecological time series analysis. Residents of Madrid and Barcelona cities (Spain). Data on daily emergency room admissions for acute myocardial infarction, cerebrovascular disease, chronic obstructive pulmonary disease (COPD), and asthma derived from the 2003-2006 Spanish hospital admissions registry. Changes in admission rates between 2006 and the 2003-2005 period were estimated using additive Poisson models allowing for overdispersion adjusted for secular trend in admission, seasonality, day of the week, temperature, number of flu and acute respiratory infection cases, pollution levels, tobacco consumption prevalence and, for asthma cases, pollen count. In Madrid, fully adjusted models failed to detect significant changes in hospital admission rates for any disease during the study period. In Barcelona, however, hospital admissions decreased by 10.2% (95% CI 3.8% to 16.1%) for cerebrovascular diseases and by 16.0% (95% CI 7.0% to 24.1%) for COPD. Substantial changes in effect estimates were observed on adjustment for linear or quadratic trend. Effect estimates for asthma-related admissions varied substantially when adjusting for pollen count in Madrid, and for seasonality and tobacco consumption in Barcelona. Our results confirm that the potential impact of a smoking ban must be adjusted for the underlying secular trend. In asthma-related admissions, pollen count, seasonality and tobacco consumption must be specified in the model. The substantial variability in effects detected between the two cities of Madrid and Barcelona lends strong support for a nationwide study to assess the overall effect of a smoking ban in Spain

Maternal Smoking during Pregnancy, Prematurity and Recurrent Wheezing in Early Childhood

PubMed Central

Robison, Rachel G; Kumar, Rajesh; Arguelles, Lester M; Hong, Xiumei; Wang, Guoying; Apollon, Stephanie; Bonzagni, Anthony; Ortiz, Kathryn; Pearson, Colleen; Pongracic, Jacqueline A; Wang, Xiaobin

2013-01-01

Summary Background Prenatal maternal smoking and prematurity independently affect wheezing and asthma in childhood. Objective We sought to evaluate the interactive effects of maternal smoking and prematurity upon the development of early childhood wheezing. Methods We evaluated 1448 children with smoke exposure data from a prospective urban birth cohort in Boston. Maternal antenatal and postnatal exposure was determined from standardized questionnaires. Gestational age was assessed by the first day of the last menstrual period and early prenatal ultrasound (preterm<37 weeks gestation). Wheezing episodes were determined from medical record extraction of well and ill/unscheduled visits. The primary outcome was recurrent wheezing, defined as ≥ 4 episodes of physician documented wheezing. Logistic regression models and zero inflated negative binomial regression (for number of episodes of wheeze) assessed the independent and joint association of prematurity and maternal antenatal smoking on recurrent wheeze, controlling for relevant covariates. Results In the cohort, 90 (6%) children had recurrent wheezing, 147 (10%) were exposed to in utero maternal smoke and 419 (29%) were premature. Prematurity (odds ratio [OR] 2.0; 95% CI, 1.3-3.1) was associated with an increased risk of recurrent wheezing, but in utero maternal smoking was not (OR 1.1, 95% CI 0.5-2.4). Jointly, maternal smoke exposure and prematurity caused an increased risk of recurrent wheezing (OR 3.8, 95% CI 1.8-8.0). There was an interaction between prematurity and maternal smoking upon episodes of wheezing (p=0.049). Conclusions We demonstrated an interaction between maternal smoking during pregnancy and prematurity on childhood wheezing in this urban, multiethnic birth cohort. PMID:22290763

Lung Microbiota Is Related to Smoking Status and to Development of Acute Respiratory Distress Syndrome in Critically Ill Trauma Patients.

PubMed

Panzer, Ariane R; Lynch, Susan V; Langelier, Chaz; Christie, Jason D; McCauley, Kathryn; Nelson, Mary; Cheung, Christopher K; Benowitz, Neal L; Cohen, Mitchell J; Calfee, Carolyn S

2018-03-01

Cigarette smoking is associated with increased risk of acute respiratory distress syndrome (ARDS) in patients after severe trauma; however, the mechanisms underlying this association are unknown. To determine whether cigarette smoking contributes to ARDS development after trauma by altering community composition of the lung microbiota. We studied the lung microbiota of mechanically ventilated patients admitted to the ICU after severe blunt trauma. To do so, we used 16S ribosomal RNA gene amplicon sequencing of endotracheal aspirate samples obtained on ICU admission (n = 74) and at 48 hours after admission (n = 30). Cigarette smoke exposure (quantified using plasma cotinine), ARDS development, and other clinical parameters were correlated with lung microbiota composition. Smoking status was significantly associated with lung bacterial community composition at ICU admission (P = 0.007 by permutational multivariate ANOVA [PERMANOVA]) and at 48 hours (P = 0.03 by PERMANOVA), as well as with significant enrichment of potential pathogens, including Streptococcus, Fusobacterium, Prevotella, Haemophilus, and Treponema. ARDS development was associated with lung community composition at 48 hours (P = 0.04 by PERMANOVA) and was characterized by relative enrichment of Enterobacteriaceae and of specific taxa enriched at baseline in smokers, including Prevotella and Fusobacterium. After severe blunt trauma, a history of smoking is related to lung microbiota composition, both at the time of ICU admission and at 48 hours. ARDS development is also correlated with respiratory microbial community structure at 48 hours and with taxa that are relatively enriched in smokers at ICU admission. The data derived from this pilot study suggest that smoking-related changes in the lung microbiota could be related to ARDS development after severe trauma.

A longitudinal study of the reciprocal relationship between ever smoking and urgency in early adolescence.

PubMed

Burris, Jessica L; Riley, Elizabeth; Puleo, Gabriella E; Smith, Gregory T

2017-09-01

Among early adolescents in the United States (U.S.), the prevalence of cigarette smoking is at its lowest level in recent decades. Nonetheless, given the risks of smoking in early development, it remains critically important to study both risk factors for smoking and risks from smoking. This longitudinal study with U.S. early adolescents examines smoking initiation and tests a model of reciprocal prediction between ever smoking and the personality trait of urgency (i.e., mood-based impulsivity), a trait that increases risk for multiple forms of dysfunction. Participants (n=1906; 90% 10-11 years old, 50% female, 39% racial minorities at baseline) completed questionnaires 1-2 times per year starting in 5th grade and ending in 9th grade. Structural equation modeling allowed tests of bidirectional relationships between ever smoking and urgency controlling for pubertal status and negative affect at each wave. Incidence of ever smoking increased from 5% to 27% over time, with current smoking around 5% at the last wave. Urgency at each wave predicted ever smoking at the next wave above and beyond covariates and prior smoking (all p<0.01). Likewise, with one exception, ever smoking predicted an increase in urgency at the subsequent wave above and beyond covariates and prior urgency (all p<0.05). Results show that risk for smoking increases with higher levels of urgency and urgency increases secondary to engagement in smoking. Future work should therefore explore urgency as a point of prevention for smoking and smoking cessation as a means to mitigate mood-based impulsivity. Copyright © 2017 Elsevier B.V. All rights reserved.

The impact of exposure to biomass smoke versus cigarette smoke on inflammatory markers and pulmonary function parameters in patients with chronic respiratory failure.

PubMed

Ocakli, Birsen; Acarturk, Eylem; Aksoy, Emine; Gungor, Sinem; Ciyiltepe, Fulya; Oztas, Selahattin; Ozmen, Ipek; Agca, Meltem Coban; Salturk, Cuneyt; Adiguzel, Nalan; Karakurt, Zuhal

The aim of this study was to evaluate the impact of exposure to biomass smoke vs cigarette smoke on serum inflammatory markers and pulmonary function parameters in patients with chronic respiratory failure (CRF). A total of 106 patients with CRF divided into age and gender-matched groups of cigarette-smoke exposure (n=55, mean [SD] age: 71.0 [12.0] years, 92.7% were females) and biomass smoke exposure (n=51, mean [SD] age: 73.0 [11.0] years, 94.1% were females) were included in this retrospective study. Data on patient demographics (age and gender), inflammatory markers, including neutrophil-to-lymphocyte ratio, C-reactive protein, platelet/mean platelet volume ratio, arterial blood gas analysis, and pulmonary function test findings, including forced expiratory volume in 1 second (FEV 1 ), forced vital capacity (FVC), and FEV 1 /FVC were obtained from medical records. Carbon dioxide partial pressure levels were significantly higher in the biomass smoke exposure than in the cigarette smoke exposure group (mean [SD] 51.0 [8.0] vs 47.0 [8.0] mmHg, p =0.026, respectively). Spirometry revealed similarly low levels for FEV 1 (%) (38.0 [16.0] vs 40.0 [12.0]%) and FVC (%) (45.0 [19.0] vs 39.0 [19.0]%) in cigarette-smoke and biomass smoke exposure groups, whereas biomass smoke exposure was associated with significantly higher FEV 1 /FVC (75.0 [14.0] vs 58.0 [12.0]%, p =0.001), lower FVC (mL) (mean [SD] 744.0 [410.0] vs 1,063.0 [592.0] mL, p =0.035) and lower percentage of patients with FEV 1 /FVC <70% (36.8% vs 82.0%, p <0.001) than cigarette smoke exposure. Our findings indicate similarly increased inflammatory markers and abnormally low pulmonary function test findings in both biomass smoke exposure and cigarette smoke exposure groups, emphasizing the adverse effects of biomass smoke exposure on lungs to be as significant as cigarette smoke exposure. Association of biomass smoke exposure with higher likelihood of FEV 1 /FVC ratio of >70% and more prominent loss of vital

Smoking-related interstitial lung diseases.

PubMed

Caminati, A; Graziano, P; Sverzellati, N; Harari, S

2010-12-01

In pulmonary pathology, a wide spectrum of morphological changes is related to the consequences of smoking, and recognizing them on surgical specimens and on small transbronchial biopsies represents a challenge for the pathologist. Respiratory bronchiolitis, also referred to as smoker's bronchiolitis, is a common histologic feature found in the lung tissue of cigarette smokers. When identified as the sole histopathologic finding in the clinical setting of symptomatic interstitial lung disease, a diagnosis of respiratory bronchiolitis-interstitial lung disease is made. Since smoking is recognized to cause a variety of histologic patterns encompassing respiratory bronchiolitis, respiratory bronchiolitis-interstitial lung disease, desquamative interstitial pneumonia and pulmonary Langerhans cell hystiocytosis, smoking-related interstitial lung disease may be a useful concept to keep in mind for the pathologists. The relationship of smoking with each of these entities has been largely established on the basis of epidemiologic evidence. Although they have been retained as distinct and separate conditions in various classifications of interstitial lung diseases, these entities share a number of clinical, radiologic, and pathologic features suggesting that they represent a spectrum of patterns of interstitial lung disease occurring in predisposed individuals who smoke. Evaluation of histologic features, particularly in surgical lung biopsy samples, is important in making the distinction between these disorders. However, even after tissue biopsy, it may sometimes be difficult to clearly separate these entities. Recently, respiratory bronchiolitis-interstitial lung disease with fibrosis has been described and postulated that this is a smoking-related condition distinct from fibrotic non-specific interstitial pneumonia.

Developmental Trajectories of Cigarette Smoking from Adolescence to the Early Thirties: Personality and Behavioral Risk Factors

PubMed Central

Brook, David W.; Brook, Judith S.; Zhang, Chenshu; Whiteman, Martin; Cohen, Patricia; Finch, Stephen J.

2013-01-01

The purpose of this study was to identify distinct trajectories of cigarette smoking from ages 14 to 32, and to examine adolescent personality factors that distinguish trajectories of smoking behavior. Participants (N=975) were randomly selected and followed prospectively since 1975. Follow-up data on cigarette use and personality and behavioral attributes were collected at five points in time, using structured interviews given in private by trained interviewers. Of these subjects, 746 comprised the cohort used in this study. Growth mixture modeling identified five smoking trajectory groups: nonsmokers, occasional smokers, late starters, quitters, and heavy/continuous smokers. Adolescent personality and behavioral risk factors such as lower ego integration, more externalizing behavior, and lower educational aspirations distinguished the trajectory groups. No gender differences were noted. The findings supported the hypotheses indicating multiple distinct trajectory groups of smoking behavior. Smoking behavior appeared in early adolescence and most often continued into adulthood. Emotional difficulties (i.e., lower ego integration), externalizing behavior, and lower educational aspirations in early adolescence were associated both with smoking at an early age and with continuing to smoke into the thirties. To be more effective, smoking prevention programs should target personality and behavioral variations, before smoking becomes habitual, particularly focused on characteristics reflecting behavioral problems as manifested in emotional difficulties, externalizing behavior, and low educational aspirations in early adolescence. The implications for research, prevention, and treatment are discussed. PMID:18686175

Surviving With Smog and Smoke: Precision Interventions?

PubMed

Cai, Hua; Wang, Chen

2017-11-01

Despite continuous efforts of regional governmental agencies, air pollution remains a major threat to public health worldwide. In January 2017, a severe episode of smog similar to the Great Smog of 1952 occurred in London. The longest episode of Chinese haze also developed in Beijing, during which levels of particulate matter < 2.5 μm rose to 500 μg/m 3 . European smog and Chinese haze are associated with large numbers of premature deaths each year, at 400,000 and 1.2 million, respectively, primarily from respiratory diseases, cerebrovascular diseases, and ischemic heart diseases. In addition to air pollution, some are exposed to other harmful environmental factors, such as secondhand smoke. For countries with large populations of smokers, such as China, India, the United States, and Russia, surviving both smog and smoke is a serious problem. With novel genomic and epigenomic studies revealing air pollution- and smoking-induced mutational signatures and epigenetic editing in diseases such as lung cancer, it has become feasible to develop precision strategies for early intervention in the disease-causing pathways driven by the specific mutations or epigenetic regulations, or both. New therapies guided by gene-drug interactions and genomic biomarkers may also be developed. We discuss both perspectives regarding the urgent need to manage the toxic effects of smog and smoke for the benefit of global health and the novel concept of precision intervention to protect the exposed individuals when exposure to smog and secondhand smoke cannot be voluntarily avoided or easily modified. Copyright © 2017 American College of Chest Physicians. Published by Elsevier Inc. All rights reserved.

Philip Morris toxicological experiments with fresh sidestream smoke: more toxic than mainstream smoke

PubMed Central

Schick, S; Glantz, S

2005-01-01

Background: Exposure to secondhand smoke causes lung cancer; however, there are little data in the open literature on the in vivo toxicology of fresh sidestream cigarette smoke to guide the debate about smoke-free workplaces and public places. Objective: To investigate the unpublished in vivo research on sidestream cigarette smoke done by Philip Morris Tobacco Company during the 1980s at its Institut für Biologische Forschung (INBIFO). Methods: Analysis of internal tobacco industry documents now available at the University of California San Francisco Legacy Tobacco Documents Library and other websites. Results: Inhaled fresh sidestream cigarette smoke is approximately four times more toxic per gram total particulate matter (TPM) than mainstream cigarette smoke. Sidestream condensate is approximately three times more toxic per gram and two to six times more tumourigenic per gram than mainstream condensate by dermal application. The gas/vapour phase of sidestream smoke is responsible for most of the sensory irritation and respiratory tract epithelium damage. Fresh sidestream smoke inhibits normal weight gain in developing animals. In a 21day exposure, fresh sidestream smoke can cause damage to the respiratory epithelium at concentrations of 2 µg/l TPM. Damage to the respiratory epithelium increases with longer exposures. The toxicity of whole sidestream smoke is higher than the sum of the toxicities of its major constituents. Conclusion: Fresh sidestream smoke at concentrations commonly encountered indoors is well above a 2 µg/m3 reference concentration (the level at which acute effects are unlikely to occur), calculated from the results of the INBIFO studies, that defines acute toxicity to humans. Smoke-free public places and workplaces are the only practical way to protect the public health from the toxins in sidestream smoke. PMID:16319363

Plasma cytokine levels fall in preterm newborn infants on nasal CPAP with early respiratory distress.

PubMed

Carvalho, Clarissa Gutierrez; Silveira, Rita de Cassia; Neto, Eurico Camargo; Procianoy, Renato Soibelmann

2015-01-01

Early nCPAP seems to prevent ventilator-induced lung injury in humans, although the pathophysiological mechanisms underlying this beneficial effect have not been clarified yet. To evaluate plasma levels IL-1β, IL-6, IL-8, IL-10, and TNF-α immediately before the start of nCPAP and 2 hours later in preterm infants. Prospective cohort including preterm infants with 28 to 35 weeks gestational age with moderate respiratory distress requiring nCPAP. Extreme preemies, newborns with malformations, congenital infections, sepsis, surfactant treatment, and receiving ventilatory support in the delivery room were excluded. Blood samples were collected right before and 2 hours after the start of nCPAP. 23 preterm infants (birth weight 1851±403 grams; GA 32.3±1.7 weeks) were treated with nCPAP. IL-1β, IL-10, TNF-α levels were similar, IL-8 levels were reduced in 18/23 preterm infants and a significant decrease in IL-6 levels was observed after 2 hours of nCPAP. All newborns whose mothers received antenatal steroids had lower cytokine levels at the onset of nCPAP than those whose mothers didn't receive it; this effect was not sustained after 2 hours of nCPAP. Early use nCPAP is not associated with rising of plasma pro-inflammatory cytokines and it seems to be a less harmful respiratory strategy for preterm with moderate respiratory distress.

Parental Smoking Exposure and Adolescent Smoking Trajectories

PubMed Central

Gilman, Stephen E.; Rende, Richard; Luta, George; Tercyak, Kenneth P.; Niaura, Raymond S.

2014-01-01

OBJECTIVE: In a multigenerational study of smoking risk, the objective was to investigate the intergenerational transmission of smoking by examining if exposure to parental smoking and nicotine dependence predicts prospective smoking trajectories among adolescent offspring. METHODS: Adolescents (n = 406) ages 12 to 17 and a parent completed baseline interviews (2001–2004), and adolescents completed up to 2 follow-up interviews 1 and 5 years later. Baseline interviews gathered detailed information on parental smoking history, including timing and duration, current smoking, and nicotine dependence. Adolescent smoking and nicotine dependence were assessed at each time point. Latent Class Growth Analysis identified prospective smoking trajectory classes from adolescence into young adulthood. Logistic regression was used to examine relationships between parental smoking and adolescent smoking trajectories. RESULTS: Four adolescent smoking trajectory classes were identified: early regular smokers (6%), early experimenters (23%), late experimenters (41%), and nonsmokers (30%). Adolescents with parents who were nicotine-dependent smokers at baseline were more likely to be early regular smokers (odds ratio 1.18, 95% confidence interval 1.05–1.33) and early experimenters (odds ratio 1.04, 95% confidence interval 1.04–1.25) with each additional year of previous exposure to parental smoking. Parents’ current non-nicotine–dependent and former smoking were not associated with adolescent smoking trajectories. CONCLUSIONS: Exposure to parental nicotine dependence is a critical factor influencing intergenerational transmission of smoking. Adolescents with nicotine-dependent parents are susceptible to more intense smoking patterns and this risk increases with longer duration of exposure. Research is needed to optimize interventions to help nicotine-dependent parents quit smoking early in their children’s lifetime to reduce these risks. PMID:24819567

Smoking and Early Pregnancy Thyroid Hormone and Anti-Thyroid Antibody Levels in Euthyroid Mothers of the Northern Finland Birth Cohort 1986

PubMed Central

Männistö, Tuija; Hartikainen, Anna-Liisa; Vääräsmäki, Marja; Bloigu, Aini; Surcel, Heljä-Marja; Pouta, Anneli; Järvelin, Marjo-Riitta; Ruokonen, Aimo

2012-01-01

Background Smokers in the general population have lower thyrotropin (TSH) and higher free triiodothyronine (fT3) and free thyroxine (fT4) concentrations, but the results in pregnant population vary from no effect to a decrease in TSH and fT4 concentrations and an increase in fT3 levels. Our objective was to further evaluate the question of whether there is an association between smoking, before and during pregnancy, with maternal thyroid function during pregnancy and with the risk for subsequent hypothyroidism. Methods Our study population was a prospective population-based cohort (N=9362), the Northern Finland Birth Cohort 1986, with extensive data throughout gestation. The mothers underwent serum sampling in early pregnancy. The samples were assayed for TSH, fT3, fT4, thyroid-peroxidase antibodies (TPO-Ab), and thyroglobulin antibodies (TG-Abs) (n=5805). Mothers with thyroid dysfunction diagnosed before or during pregnancy were excluded, leaving 4837 euthyroid mothers. The smoking status of mothers and fathers were requested by questionnaires during pregnancy. Subsequent maternal morbidity relating to hypothyroidism 20 years after the index pregnancy was evaluated using national registers. Results Euthyroid mothers who smoked before, or continued smoking during first trimester of pregnancy, had higher serum fT3 (p<0.001) and lower fT4 (p=0.023) concentrations than nonsmokers. Smoking in the second trimester was associated with higher fT3 (p<0.001) concentrations, but no difference in fT4 concentrations compared with nonsmokers. TG-Abs were less common among smoking than nonsmoking mothers (2.5% vs. 4.7%, p<0.001), but the prevalence of TPO-Ab was similar. Paternal smoking had no independent effect on maternal early pregnancy thyroid hormone or antibody concentrations. The risk of subsequent maternal hypothyroidism after follow-up of 20 years was similar among prepregnancy smokers and nonsmokers. Conclusions In euthyroid women, smoking during pregnancy was

Maternal Smoking and the Risk of Cancer in Early Life - A Meta-Analysis.

PubMed

Rumrich, Isabell Katharina; Viluksela, Matti; Vähäkangas, Kirsi; Gissler, Mika; Surcel, Heljä-Marja; Hänninen, Otto

2016-01-01

In spite of the well-known harmful effects on the fetus, many women continue smoking during pregnancy. Smoking as an important source of toxic chemicals may contribute to the developmental origin of diseases. The aim of this work was to pursue the possible association between maternal smoking and cancer in early life. Specifically, we wanted to identify the associated early life cancer types, and to quantify the associations. In a systematic literature search 825 articles were identified in PubMed and Web of Science, and 55 more through the reference lists. Of these 62 fulfilled the criteria for inclusion in meta-analyses. Using Mantel-Haenszel or DerSimonian and Laird method, depending on heterogeneity of the studies, pooled estimates and 95% confidence intervals for eight cancer types were calculated. Smoking during pregnancy was associated with an increased risk for for brain and central nervous system tumors (OR = 1.09; 95% CI = 1.02-1.17). Although the risk for lymphoma was also associated (OR = 1.21; 95% CI = 1.05-1.34), it did not hold up in subgroup analyses. Leukemia was not found to be associated with maternal smoking. Five other cancer types (bone, soft tissue, renal, hepatic, and germ cell cancer) were also examined, but the number of studies was too limited to exclude the possibility of maternal smoking as a risk factor for cancer in offspring. According to our meta-analyses, maternal smoking is associated with nervous system cancers, but not with leukemia in early life. Confirming or rejecting associations of maternal smoking with lymphoma and the five other cancer types requires further studies.

Chronic air-flow limitation does not increase respiratory epithelial permeability assessed by aerosolized solute, but smoking does

DOE Office of Scientific and Technical Information (OSTI.GOV)

Huchon, G.J.; Russell, J.A.; Barritault, L.G.

1984-09-01

To determine the separate influences of smoking and severe air-flow limitation on aerosol deposition and respiratory epithelial permeability, we studied 26 normal nonsmokers, 12 smokers without airway obstruction, 12 nonsmokers with chronic obstructive pulmonary disease (COPD), and 11 smokers with COPD. We aerosolized 99mTc-labeled diethylene triamine pentaacetic acid to particles approximately 1 micron activity median aerodynamic diameter. Levels of radioactivity were plotted semilogarithmically against time to calculate clearance as percent per minute. The distribution of radioactivity was homogeneous in control subjects and in smokers, but patchy in both groups with COPD. No difference was found between clearances of the controlmore » group (1.18 +/- 0.31% min-1), and nonsmoker COPD group (1.37 +/- 0.82% min-1), whereas values in smokers without COPD (4.00 +/- 1.70% min-1) and smokers with COPD (3.62 +/- 2.88% min-1) were significantly greater than in both nonsmoking groups. We conclude that (1) small particles appear to deposit peripherally, even with severe COPD; (2) respiratory epithelial permeability is normal in nonsmokers with COPD; (3) smoking increases permeability by a mechanism unrelated to air-flow limitation.« less

Pre- and Postnatal Parental Smoking and Acute Otitis Media in Early Childhood

PubMed Central

Håberg, Siri E.; Bentdal, Yngvild E.; London, Stephanie J.; Kværner, Kari J.; Nystad, Wenche; Nafstad, Per

2010-01-01

Aim To explore associations between acute otitis media in early childhood and prenatal and postnatal tobacco smoke exposure. Methods Subjects were 32,077 children born 2000 – 2005 in the Norwegian Mother and Child Study with questionnaire data on tobacco smoke exposure and acute otitis media up to 18 months of age. Multivariate regression models were used to obtain adjusted relative risks for acute otitis media. Results Acute otitis media was slightly more common in children exposed to parental smoking. The incidence from 0–6 months was 4.7% in unexposed children, and 6.0% in children exposed both pre-and postnatally. After adjusting for postnatal exposure and covariates, the relative risk for acute otitis media 0–6 months when exposed to maternal smoking in pregnancy was 1.34, 95% confidence interval: 1.06–1.69. Maternal smoking in pregnancy was associated with acute otitis media up to 12 months of age. Compared to non-exposed children, there was a slightly increased risk of recurrent acute otitis media for children exposed both pre- and postnatally with a relative risk of 1.24, 95% confidence interval: 1.01–1.52,. Conclusion Even in a cohort with relatively low exposure levels of parental smoking, maternal smoking in pregnancy was associated with an increased risk of acute otitis media in early childhood. PMID:19764924

Bilirubin treatment suppresses pulmonary inflammation in a rat model of smoke-induced emphysema.

PubMed

Wei, Jingjing; Zhao, Hui; Fan, Guoquan; Li, Jianqiang

2015-09-18

Cigarette smoking is a significant risk factor for emphysema, which is characterized by airway inflammation and oxidative damage. To assess the capacity of bilirubin to protect against smoke-induced emphysema. Smoking status and bilirubin levels were recorded in 58 patients with chronic obstructive pulmonary diseases (COPD) and 71 non-COPD participants. The impact of smoking on serum bilirubin levels and exogenous bilirubin (20 mg/kg/day) on pulmonary injury was assessed in a rat model of smoking-induced emphysema. At sacrifice lung histology, airway leukocyte accumulation and cytokine and chemokine levels in serum, bronchoalveolar lavage fluid (BALF) and lung were analyzed. Oxidative lipid damage and anti-oxidative components was assessed by measuring malondialdehyde, superoxide dismutase (SOD) activity and glutathione. Total serum bilirubin levels were lower in smokers with or without COPD than non-smoking patients without COPD (P < 0.05). Indirect serum bilirubin levels were lower in COPD patients than patients without COPD (P < 0.05). In rats, cigarette smoke reduced serum total and indirect bilirubin levels. Administration of bilirubin reduced mean linear intercept and mean alveoli area, increased mean alveoli number, reduced macrophage, neutrophil and TNF-α content of BALF, and increased BALF and serum IL-10 level, but lowered local and systemic CCL2, CXCL2, CXCL8 and IL-17 levels. Bilirubin suppressed the smoke-induced systemic and regional oxidative lipid damage associated with increased SOD activity. Bilirubin attenuated smoking-induced pulmonary injury by suppressing inflammatory cell recruitment and pro-inflammatory cytokine secretion, increasing anti-inflammatory cytokine levels, and anti-oxidant SOD activity in a rat model of smoke-induced emphysema. Copyright © 2015. Published by Elsevier Inc.

Ambient biomass smoke and cardio-respiratory hospital admissions in Darwin, Australia

PubMed Central

Johnston, Fay H; Bailie, Ross S; Pilotto, Louis S; Hanigan, Ivan C

2007-01-01

Background Increasing severe vegetation fires worldwide has been attributed to both global environmental change and land management practices. However there is little evidence concerning the population health effects of outdoor air pollution derived from biomass fires. Frequent seasonal bushfires near Darwin, Australia provide an opportunity to examine this issue. We examined the relationship between atmospheric particle loadings <10 microns in diameter (PM10), and emergency hospital admissions for cardio-respiratory conditions over the three fire seasons of 2000, 2004 and 2005. In addition we examined the differential impacts on Indigenous Australians, a high risk population subgroup. Methods We conducted a case-crossover analysis of emergency hospital admissions with principal ICD10 diagnosis codes J00–J99 and I00–I99. Conditional logistic regression models were used to calculate odds ratios for admission with 10 μg/m3 rises in PM10. These were adjusted for weekly influenza rates, same day mean temperature and humidity, the mean temperature and humidity of the previous three days, days with rainfall > 5 mm, public holidays and holiday periods. Results PM10 ranged from 6.4 – 70.0 μg/m3 (mean 19.1). 2466 admissions were examined of which 23% were for Indigenous people. There was a positive relationship between PM10 and admissions for all respiratory conditions (OR 1.08 95%CI 0.98–1.18) with a larger magnitude in the Indigenous subpopulation (OR1.17 95% CI 0.98–1.40). While there was no relationship between PM10 and cardiovascular admissions overall, there was a positive association with ischaemic heart disease in Indigenous people, greatest at a lag of 3 days (OR 1.71 95%CI 1.14–2.55). Conclusion PM10 derived from vegetation fires was predominantly associated with respiratory rather than cardiovascular admissions. This outcome is consistent with the few available studies of ambient biomass smoke pollution. Indigenous people appear to be at higher risk

Assessing motivation to smoking cessation in hospitalized patients.

PubMed

Sepúlveda-Sánchez, Juana María; Canca-Sánchez, José Carlos; Rivas-Ruiz, Francisco; Martín-García, Mónica; Lorente Márquez, Celia; Timonet-Andreu, Eva María

To assess motivation to quit smoking in patients admitted to an acute care hospital, determine predictors of readiness to change, and identify a risk group that requires targeted motivational interviewing. A cross-sectional descriptive study. A retrospective study was performed on the medical records of 248 patients aged >18 years with smoking habits admitted to the medical and surgery units of a district hospital between May 2014 and April 2015. The data collected included sociodemographic data, data on respiratory function, number of cigarettes smoked per day, motivation to quit smoking, patient-reported readiness to quit, history of respiratory diseases and previous admissions. The Richmond test revealed that 54% of patients (n=134) were poorly motivated to quit smoking vs. 11.74% (n=29) who reported to be highly motivated. The group of patients who reported to be willing to receive support (n=77) was prevailingly composed of men (p=.009) admitted to a medical care unit (p=.026) -mainly the Unit of Cardiology (51%)- who smoked 11/29 cigarettes/day (p=.015). Dyspnoea at admission, a history of respiratory disease and previous admissions for respiratory problems were not predictors of readiness to quit. This study identifies a risk group of patients with respiratory disease, low motivation to quit smoking and poor readiness to receive smoke cessation support, that should be the target of motivational approaches to behavior change. Copyright © 2016 Elsevier España, S.L.U. All rights reserved.

Comparative analysis of the effects of hubble-bubble (Sheesha) and cigarette smoking on respiratory and metabolic parameters in hubble-bubble and cigarette smokers.

PubMed

Al Mutairi, Sana S; Shihab-Eldeen, Aida A; Mojiminiyi, Olusegun A; Anwar, Alia Aisha

2006-07-01

Hazard of smoking tobacco is believed to be minimized by smoking hubble-bubble (HB) instead of cigarettes. Our aims were to (i) develop an assay for estimating nicotine and cotinine; and (ii) evaluate the effect of smoking on respiratory and metabolic parameters in cigarette and HB smokers. Urine samples were collected from 152 volunteer smokers (75 cigarette and 77 HB) as well as from 16 healthy controls. We optimized an HPLC method for the determination of nicotine and cotinine. Subjects were asked to complete a chronic respiratory symptoms questionnaire and to undergo spirometry. Fasting blood samples were collected for the determination of their lipid profile. The intra-assay coefficients of variation for nicotine and cotinine were 16.6% and 6.6%, respectively. The mean of cotinine in cigarette smokers (1321.4 ng/mL) was significantly (P = 0.008) higher than the mean cotinine (677.6 ng/mL) in HB smokers. The mean nicotine level in cigarette smokers (1487.3 ng/mL) was significantly (P < 0.0001) higher than the mean nicotine (440.5 ng/mL) in HB smoker. The urinary cotinine and nicotine levels of the control subjects were lower than the detection levels of the assay. The mean high-density lipoprotein cholesterol was lower in cigarette smokers (0.99 mmol/L) compared with HB smoker smokers (1.02 mmol/L) but this was not significant (P = 0.28). Spirometric values were comparable among the three groups but the chronic respiratory symptoms in the smoking groups appeared at an earlier age in the HB smokers compared with the cigarettes smokers (P < 0.05). Smoking HB does not reduce the risk of tobacco exposure and it's potentially harmful metabolites on health.

Edaravone attenuates lipopolysaccharide-induced acute respiratory distress syndrome associated early pulmonary fibrosis via amelioration of oxidative stress and transforming growth factor-β1/Smad3 signaling.

PubMed

Wang, Xida; Lai, Rongde; Su, Xiangfen; Chen, Guibin; Liang, Zijing

2018-01-01

Pulmonary fibrosis is responsible for the both short-term and long-term outcomes in patients with acute respiratory distress syndrome (ARDS). There is still no effective cure to improve prognosis. The purpose of this study was to investigate whether edaravone, a free radical scavenger, have anti-fibrosis effects in the rat model of ARDS associated early pulmonary fibrosis by lipopolysaccharide (LPS) administration. Rats were subjected to intravenous injection of LPS, and edaravone was given intraperitoneally after LPS administration daily for 7 consecutive days. LPS treatment rapidly increased lung histopathology abnormalities, coefficient of lung, hydroxyproline and collagen I levels, stimulated myofibroblast differentiation and induced expression of TGF-β1 and activation of TGF-β1/Smad3 signaling as early as day 7 after LPS injection. Moreover, LPS intoxication significantly increased the contents of malondialdehyde (MDA), interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α), whereas it dramatically decreased superoxide dismutase (SOD) and glutathione peroxidase (GSH-PX) activities from day 1 after LPS treatment. On the contrary, edaravone treatment ameliorated LPS-induced myofibroblast differentiation and pulmonary fibrosis, simultaneously, and attenuated LPS-stimulated oxidative stress and activation of TGF-β1/Smad3 signaling. Collectively, edaravone may attenuate ARDS associated early pulmonary fibrosis through amelioration of oxidative stress and TGF-β1/Smad3 signaling pathway. Edaravone may be a promising drug candidate for the treatment of ARDS-related pulmonary fibrosis in early period. Copyright © 2017 Elsevier Inc. All rights reserved.

Respiratory effects in people exposed to arsenic via the drinking water and tobacco smoking in southern part of Pakistan.

PubMed

Arain, Muhammad Balal; Kazi, Tasneem Gul; Baig, Jameel Ahmed; Jamali, Muhammad Khan; Afridi, Hassan Imran; Jalbani, Nusrat; Sarfraz, Raja Adil; Shah, Abdul Qadir; Kandhro, Ghulam Abbas

2009-10-15

In this study, a survey has been conducted during 2005-2007 on surface and groundwater arsenic (As) contamination and its impact on the health of local population, of villages located on the banks of Manchar lake, southern part of Sindh, Pakistan. We have also assessed the relationship between arsenic exposure through respiratory disorders in male subjects with drinking water and smoking cigarettes made from tobacco grown in agricultural land irrigated with As contaminated lake water. The biological samples (blood and scalp hair) were collected from As exposed subjects (100% smokers) and age matched healthy male subjects (40.2% smoker and 59.8% non smokers) belong to unexposed areas for comparison purposes. The As concentration in drinking water (surface and underground water), agricultural soil, cigarette tobacco and biological samples were determined by electrothermal atomic absorption spectrometry. The range of As concentrations in lake water was 35.2-158 microg/L (average 97.5 microg/L), which is 3-15 folds higher than permissible limit of World Health Organization (WHO, 2004). While the As level in local cigarette tobacco was found to be 3-6 folds higher than branded cigarettes (0.37-0.79 microg/g). Arsenic exposed subjects (with and without RD) had significantly elevated levels of As in their biological samples as compared to referent male subject of unexposed area. These respiratory effects were more pronounced in individuals who had also As induced skin lesions. The linear regressions showed good correlations between As concentrations in water versus hair and blood samples of exposed subjects with and without respiratory problems.

Frequency-risk relationships between second-hand smoke exposure and respiratory symptoms among adolescents: a cross-sectional study in South China.

PubMed

Chen, Zhiyao; Liu, Guocong; Chen, Jianying; Li, Shunming; Jiang, Ting; Xu, Bin; Ye, Xiaohua

2018-04-03

Although previous studies have suggested an association between second-hand smoke (SHS) exposure and respiratory symptoms, current evidence is inconsistent. Additionally, it remains unclear whether there are frequency-risk relationships between SHS exposure and respiratory symptoms among adolescents. A cross-sectional survey was conducted using a stratified cluster sampling method to obtain a representative sample of high school students in Guangzhou, China. The respiratory symptoms were defined as persistent cough or sputum for three consecutive months during the past 12 months. Self-reported SHS exposure was defined as non-smokers' inhalation of the smoke exhaled from smokers on ≥1 day a week in the past 7 days. The univariable and multivariable logistic regression models were fitted to explore the potential frequency-risk relationships between SHS exposure and respiratory symptoms. Among 3575 students, the overall prevalence of SHS exposure was 69.2%, including 49.5% for SHS in public places, 34.5% in homes, 22.7% in indoor campuses and 29.2% in outdoor campuses. There were significantly increased risks of having respiratory symptoms corresponding to SHS exposure in public places (OR=1.60, 95% CI 1.30 to 1.95), in homes (OR=1.53, 95% CI 1.25 to 1.87), in indoor campuses (OR=1.43, 95% CI 1.14 to 1.79) and in outdoor campuses (OR=1.37, 95% CI 1.10 to 1.69) using no exposure as reference. Notably, we observed monotonic frequency-risk relationships between setting-specific(eg, homes, public places and campuses) SHS exposure and respiratory symptoms. Our findings suggest that setting-specific SHS exposure is associated with a significant, dose-dependent increase in risk of respiratory symptoms. © Article author(s) (or their employer(s) unless otherwise stated in the text of the article) 2018. All rights reserved. No commercial use is permitted unless otherwise expressly granted.

Respiratory involvements among women exposed to the smoke of traditional biomass fuel and gas fuel in a district of Bangladesh.

PubMed

Alim, Md Abdul; Sarker, Mohammad Abul Bashar; Selim, Shahjada; Karim, Md Rizwanul; Yoshida, Yoshitoku; Hamajima, Nobuyuki

2014-03-01

Burning of biomass fuel (cow-dung, crop residue, dried leaves, wood, etc.) in the kitchen releases smoke, which may impair the respiratory functions of women cooking there. This paper aimed to compare the respiratory symptoms between biomass fuel users and gas fuel users in Bangladesh. A cross-sectional survey was conducted through face-to-face interviews and chest examination of 224 adult women using biomass fuel in a rural village and 196 adult women using gas fuel in an urban area. The prevalence of respiratory involvement (at least one among nine symptoms and two diseases) was significantly higher among biomass users than among gas users (29.9 vs. 11.2 %). After adjustment for potential confounders by a logistic model, the odds ratio (OR) of the biomass users for the respiratory involvement was significantly higher (OR = 3.23, 95 % confidence interval 1.30-8.01). The biomass fuel use elevated symptoms/diseases significantly; the adjusted OR was 3.04 for morning cough, 7.41 for nasal allergy, and 5.94 for chronic bronchitis. The mean peak expiratory flow rate of biomass users (253.83 l/min) was significantly lower than that of gas users (282.37 l/min). The study shows significant association between biomass fuel use and respiratory involvement among rural women in Bangladesh, although the potential confounding of urban/rural residency could not be ruled out in the analysis. The use of smoke-free stoves and adequate ventilation along with health education to the rural population to increase awareness about the health effects of indoor biomass fuel use might have roles to prevent these involvements.

Baseline measurements of smoke exposure among wildland firefighters.

PubMed

Reinhardt, Timothy E; Ottmar, Roger D

2004-09-01

Extensive measurements of smoke exposure among wildland firefighters are summarized, showing that firefighters can be exposed to significant levels of carbon monoxide and respiratory irritants, including formaldehyde, acrolein, and respirable particulate matter. Benzene was also measured and found to be well below permissible exposure limits, with the highest concentrations occurring among firefighters working with engines and torches burning petroleum-based fuel. Exposures to all pollutants were higher among firefighters at prescribed burns than at wildfires, while shift-average smoke exposures were lowest among firefighters who performed initial attack of wildfires in the early stages of the fires. Smoke exposure reaches its highest levels among firefighters maintaining fire within designated firelines and performing direct attack of spot fires that cross firelines. These events and the associated smoke exposures were positively correlated with increasing ambient wind speeds, which hamper fire management and carry the convective plume of the fire into firefighters' breathing zone. The pollutants measured in smoke were reasonably well-correlated with each other, enabling estimation of exposure to multiple pollutants in smoke from measurements of a single pollutant such as carbon monoxide.

Effect of maternal smoking cessation before and during early pregnancy on fetal and childhood growth.

PubMed

Suzuki, Kohta; Sato, Miri; Zheng, Wei; Shinohara, Ryoji; Yokomichi, Hiroshi; Yamagata, Zentaro

2014-01-01

Maternal smoking during pregnancy is a major cause of intrauterine growth restriction and childhood obesity, but only a few studies have examined the association of smoking cessation before and during pregnancy with fetal and childhood growth. We examined this association in a prospective cohort study in Japan. Our study included children born between 1991 and 2006 and their mothers. Using a questionnaire, maternal smoking status was recorded at pregnancy. The anthropometric data of the children were collected during a medical check-up at age 3 years. Multiple linear and logistic regression models were used for data analysis stratified by sex. In total, 2663 mothers reported their smoking status during early pregnancy, and data were collected from 2230 (83.7%) children at age 3 years. Maternal smoking during pregnancy was associated with a significant reduction in birth weight (approximately 120-150 g). Body mass index at age 3 years was significantly higher among boys born to smoking mothers than among boys born to nonsmoking mothers. Maternal smoking during pregnancy was associated with overweight at age 3 years among boys (adjusted odds ratio, 2.4; 95% CI, 1.03-5.4). However, among women who stopped smoking in early pregnancy, there was no increase in the risks of a small for gestational age birth or childhood overweight at age 3 years. Children born to mothers who stopped smoking before or during early pregnancy had appropriate fetal and childhood growth.

Genotoxicity and fetal abnormality in streptozotocin-induced diabetic rats exposed to cigarette smoke prior to and during pregnancy.

PubMed

Damasceno, D C; Volpato, G T; Sinzato, Y K; Lima, P H O; Souza, M S S; Iessi, I L; Kiss, A C I; Takaku, M; Rudge, M V C; Calderon, I M P

2011-10-01

Maternal hyperglycemia during early pregnancy is associated with increased risk of abnormalities in the offspring. Malformation rates among the offspring of diabetic mothers are 2-5-fold higher than that of the normal population, and congenital malformations are the major cause of mortality and morbidity in the offspring of diabetic mothers. Metabolic changes, such as hyperglycemia and the metabolites obtained from cigarettes both increase the production of reactive oxygen species (ROS) in the embryo or fetus, causing DNA damage. To evaluate the maternal and fetal genotoxicity, and to assess the incidence of fetal anomaly in diabetic female rats exposed to cigarette smoke at different stages of pregnancy in rats. Diabetes was induced by streptozotocin administration and cigarette smoke exposure was produced by a mechanical smoking device that generated mainstream smoke that was delivered into a chamber. Female Wistar rats were randomly assigned to: non-diabetic (ND) and diabetic (D) groups exposed to filtered air; a diabetic group exposed to cigarette smoke prior to and during pregnancy (DS) and a diabetic group only exposed to cigarette smoke prior to pregnancy (DSPP). On pregnancy day 21, blood samples were obtained for DNA damage analysis and fetuses were collected for congenital anomaly assessment. Statistical significance was set at p<0.05 for all analysis. Exposure of diabetic rats to tobacco smoke prior to pregnancy increased fetal DNA damage, but failed to induce teratogenicity. Thus, these results reinforce the importance for women to avoid exposure to cigarette smoke long before they become pregnant. © J. A. Barth Verlag in Georg Thieme Verlag KG Stuttgart · New York.

Respiratory disease in pregnancy.

PubMed

Mehta, Niharika; Chen, Kenneth; Hardy, Erica; Powrie, Raumond

2015-07-01

Many physiological and anatomical changes of pregnancy affect the respiratory system. These changes often affect the presentation and management of the various respiratory illnesses in pregnancy. This article focuses on several important respiratory issues in pregnancy. The management of asthma, one of the most common chronic illnesses in pregnancy, remains largely unchanged compared to the nonpregnant state. Infectious respiratory illness, including pneumonia and tuberculosis, are similarly managed in pregnancy with antibiotics, although special attention may be needed for antibiotic choices with more pregnancy safety data. When mechanical ventilation is necessary, consideration should be given to the maternal hemodynamics of pregnancy and fetal oxygenation. Maintaining maternal oxygen saturation above 95% is recommended to sustain optimal fetal oxygenation. Cigarette smoking has known risks in pregnancy, and current practice guidelines recommend offering cognitive and pharmacologic interventions to pregnant women to assist in smoking cessation. Copyright © 2015 Elsevier Ltd. All rights reserved.

Reward Dependence Moderates Smoking-Cue- and Stress-Induced Cigarette Cravings

PubMed Central

Michalowski, Alexandra; Erblich, Joel

2014-01-01

Cigarette cravings following exposure to smoking cues in a smoker's environment are thought to play an important role in cessation failure. The possibility that dispositional factors may impact cue-induced cravings, though intriguing, has received little attention. According to Cloninger's tridimensional personality theory, factors such as reward dependence (RD), harm avoidance (HA), and novelty seeking (NS) may figure prominently in risk for addiction, as well as relapse, in individuals attempting to abstain from drug and alcohol use. Particularly interesting in this regard is the possibility that smokers with higher levels of RD, who are especially sensitive to reward signals, will have heightened craving reactions to smoking cues. To that end, non-treatment-seeking nicotine dependent smokers (n=96, Mean age=41.1, 47% African American, 17% Caucasian, 22% Hispanic, 19.3 cigs/day, FTND=7.5) underwent a classic experimental cue-induction, during which they were exposed to imagery of: (1) smoking, (2) neutral, and (3) stress cues, and reported their cigarette cravings (0-100) before and after each exposure. Participants also completed the Tridimensional Personality Questionnaire. Not surprisingly, smoking and stress cues (but not neutral cues) elicited significant elevations in craving (p's < 0.0001). Consistent with study hypothesis, smokers who scored higher on RD had stronger craving reactions to both smoking cues (p < .02) and stress cues (p < .03). Findings raise the possibility that dispositional characteristics, in particular, reward dependence, influence smoking by potentiating reactions to environmental smoking cues. Furthermore, the similar effects of RD on stress-induced craving suggest that both cue-and stress-induced cravings may be influenced by a common underlying disposition. PMID:25133977

Reward dependence moderates smoking-cue- and stress-induced cigarette cravings.

PubMed

Michalowski, Alexandra; Erblich, Joel

2014-12-01

Cigarette cravings following exposure to smoking cues in a smoker's environment are thought to play an important role in cessation failure. The possibility that dispositional factors may impact cue-induced cravings, though intriguing, has received little attention. According to Cloninger's Tridimensional Personality Theory, factors such as reward dependence (RD), harm avoidance (HA), and novelty seeking (NS) may figure prominently in risk for addiction, as well as relapse, in individuals attempting to abstain from drug and alcohol use. Particularly interesting in this regard is the possibility that smokers with higher levels of RD, who are especially sensitive to reward signals, will have heightened craving reactions to smoking cues. To that end, non-treatment-seeking nicotine dependent smokers (n=96, mean age=41.1, 47% African American, 17% Caucasian, 22% Hispanic, 19.3cigs/day, FTND=7.5) underwent a classic experimental cue-induction, during which they were exposed to imagery of: (1) smoking, (2) neutral, and (3) stress cues, and reported their cigarette cravings (0-100) before and after each exposure. Participants also completed the Tridimensional Personality Questionnaire. Not surprisingly, smoking and stress cues (but not neutral cues) elicited significant elevations in craving (p's<0.0001). Consistent with study hypothesis, smokers who scored higher on RD had stronger craving reactions to both smoking cues (p<.02) and stress cues (p<.03). Findings raise the possibility that dispositional characteristics, in particular, reward dependence, influence smoking by potentiating reactions to environmental smoking cues. Furthermore, the similar effects of RD on stress-induced craving suggest that both cue-and stress-induced cravings may be influenced by a common underlying disposition. Copyright © 2014 Elsevier Ltd. All rights reserved.

The AIMAR recommendations for early diagnosis of chronic obstructive respiratory disease based on the WHO/GARD model*

PubMed Central

2014-01-01

Respiratory diseases in Italy already now represent an emergency (they are the 3rd ranking cause of death in the world, and the 2nd if Lung cancer is included). In countries similar to our own, they result as the principal cause for a visit to the general practitioner (GP) and the second main cause after injury for recourse to Emergency Care. Their frequency is probably higher than estimated (given that respiratory diseases are currently underdiagnosed). The trend is towards a further increase due to epidemiologic and demographic factors (foremost amongst which are the widespread diffusion of cigarette smoking, the increasing mean age of the general population, immigration, and pollution). Within the more general problem of chronic disease care, chronic respiratory diseases (CRDs) constitute one of the four national priorities in that they represent an important burden for society in terms of mortality, invalidity, and direct healthcare costs. The strategy suggested by the World Health Organization (WHO) is an integrated approach consisting of three goals: inform about health, reduce risk exposure, improve patient care. The three goals are translated into practice in the three areas of prevention (1-primary, 2-secondary, 3-tertiary) as: 1) actions of primary (universal) prevention targeted at the general population with the aim to control the causes of disease, and actions of Predictive Medicine - again addressing the general population but aimed at measuring the individual’s risk for disease insurgence; 2) actions of early diagnosis targeted at groups or - more precisely - subgroups identified as at risk; 3) continuous improvement and integration of care and rehabilitation support - destined at the greatest possible number of patients, at all stages of disease severity. In Italy, COPD care is generally still inadequate. Existing guidelines, institutional and non-institutional, are inadequately implemented: the international guidelines are not always adaptable to

The AIMAR recommendations for early diagnosis of chronic obstructive respiratory disease based on the WHO/GARD model*.

PubMed

Nardini, Stefano; Annesi-Maesano, Isabella; Del Donno, Mario; Delucchi, Maurizio; Bettoncelli, Germano; Lamberti, Vincenzo; Patera, Carlo; Polverino, Mario; Russo, Antonio; Santoriello, Carlo; Soverina, Patrizio

2014-01-01

Respiratory diseases in Italy already now represent an emergency (they are the 3(rd) ranking cause of death in the world, and the 2(nd) if Lung cancer is included). In countries similar to our own, they result as the principal cause for a visit to the general practitioner (GP) and the second main cause after injury for recourse to Emergency Care. Their frequency is probably higher than estimated (given that respiratory diseases are currently underdiagnosed). The trend is towards a further increase due to epidemiologic and demographic factors (foremost amongst which are the widespread diffusion of cigarette smoking, the increasing mean age of the general population, immigration, and pollution). Within the more general problem of chronic disease care, chronic respiratory diseases (CRDs) constitute one of the four national priorities in that they represent an important burden for society in terms of mortality, invalidity, and direct healthcare costs. The strategy suggested by the World Health Organization (WHO) is an integrated approach consisting of three goals: inform about health, reduce risk exposure, improve patient care. The three goals are translated into practice in the three areas of prevention (1-primary, 2-secondary, 3-tertiary) as: 1) actions of primary (universal) prevention targeted at the general population with the aim to control the causes of disease, and actions of Predictive Medicine - again addressing the general population but aimed at measuring the individual's risk for disease insurgence; 2) actions of early diagnosis targeted at groups or - more precisely - subgroups identified as at risk; 3) continuous improvement and integration of care and rehabilitation support - destined at the greatest possible number of patients, at all stages of disease severity. In Italy, COPD care is generally still inadequate. Existing guidelines, institutional and non-institutional, are inadequately implemented: the international guidelines are not always adaptable

Acute respiratory failure secondary to mesalamine-induced interstitial pneumonitis

PubMed Central

Abraham, Albin; Karakurum, Ali

2013-01-01

Interstitial pneumonitis as an adverse effect of mesalamine therapy is a rare but potentially serious complication. Patients typically have a mild disease course with no documented cases of respiratory failure in published literature. Given its variable latent period and non-specific signs and symptoms, it may be difficult to diagnose. We present the case of a 65-year-old man who presented with symptoms of fever, shortness of breath and a non-productive cough, 2 weeks after initiation of therapy with mesalamine. His hospital course was complicated by acute respiratory failure requiring intubation and mechanical ventilation. Radiographic studies revealed bilateral lower lobe infiltrates and bronchosopy with bronchoalveolar lavage and transbronchial biopsy were consistent with a diagnosis of drug-induced interstitial pneumonitis. The aim of this paper is to highlight the importance of considering a diagnosis of mesalamine-induced lung injury in patients presenting with respiratory symptoms while on mesalamine therapy and to review relevant literature. PMID:23964037

Acute respiratory failure secondary to mesalamine-induced interstitial pneumonitis.

PubMed

Abraham, Albin; Karakurum, Ali

2013-08-20

Interstitial pneumonitis as an adverse effect of mesalamine therapy is a rare but potentially serious complication. Patients typically have a mild disease course with no documented cases of respiratory failure in published literature. Given its variable latent period and non-specific signs and symptoms, it may be difficult to diagnose. We present the case of a 65-year-old man who presented with symptoms of fever, shortness of breath and a non-productive cough, 2 weeks after initiation of therapy with mesalamine. His hospital course was complicated by acute respiratory failure requiring intubation and mechanical ventilation. Radiographic studies revealed bilateral lower lobe infiltrates and bronchosopy with bronchoalveolar lavage and transbronchial biopsy were consistent with a diagnosis of drug-induced interstitial pneumonitis. The aim of this paper is to highlight the importance of considering a diagnosis of mesalamine-induced lung injury in patients presenting with respiratory symptoms while on mesalamine therapy and to review relevant literature.

Non-smoking youths' "perceived" addiction to tobacco is associated with their susceptibility to future smoking.

PubMed

Okoli, Chizimuzo T C; Richardson, Chris G; Ratner, Pamela A; Johnson, Joy L

2009-12-01

Smoking initiation places adolescents at risk for adult onset diseases, including heart disease, respiratory illness, and cancer. Adolescents that smoke have levels of 'perceived' tobacco addiction that are associated with several measures of nicotine dependence. Nonsmoking adolescents also report feeling addicted to tobacco even with minimal or no prior tobacco use, suggesting some vulnerability to tobacco use. The purpose of this study was to examine the association between perceived tobacco addiction and smoking susceptibility among adolescents with very minimal tobacco use. A cross-sectional analysis was conducted of data obtained from 5155 nonsmokers who completed the British Columbia Youth Survey of Smoking and Health II, a school-based survey conducted during 2004. Measures included demographics, tobacco use (ever puffed a cigarette), substance use (marijuana and alcohol), exposure to family members' smoking in the home, peers' tobacco use, depressive symptoms, perceived physical and mental addiction to tobacco, and smoking susceptibility. The adolescents who were most susceptible to smoking were female, younger and in a lower school grade; had ever puffed a cigarette, had used alcohol or marijuana; had family members or peers who smoked; had higher depression scores, and higher perceived physical and mental addiction to tobacco. In multivariate logistic regression analysis, perceived mental addiction but not perceived physical addiction to tobacco was significantly associated with smoking susceptibility. Understanding factors associated with smoking initiation, and ways to identify "at- risk" adolescents can enhance early intervention and prevention programs. Perceived mental addiction to tobacco appears to be an important indicator of smoking susceptibility.

Smoking and Lung Cancer: A Geo-Regional Perspective.

PubMed

Rahal, Zahraa; El Nemr, Shaza; Sinjab, Ansam; Chami, Hassan; Tfayli, Arafat; Kadara, Humam

2017-01-01

Lung cancer is the leading cause of cancer-related deaths worldwide. Non-small cell lung cancer (NSCLC) represents the most frequently diagnosed subtype of this morbid malignancy. NSCLC is causally linked to tobacco consumption with more than 500 million smokers worldwide at high risk for this fatal malignancy. We are currently lagging in our knowledge of the early molecular (e.g., genomic) effects of smoking in NSCLC pathogenesis that would constitute ideal markers for early detection. This limitation is further amplified when considering the variable etiologic factors in NSCLC pathogenesis among different regions around the globe. In this review, we present our current knowledge of genomic alterations arising during early stages of smoking-induced lung cancer initiation and progression, including discussing the premalignant airway field of injury induced by smoking. The review also underscores the wider spectra and higher age-adjusted rates of tobacco (e.g., water-pipe smoke) consumption, along with elevated environmental carcinogenic exposures and relatively poorer socioeconomic status, in low-middle income countries (LMICs), with Lebanon as an exemplar. This "cocktail" of carcinogenic exposures warrants the pressing need to understand the complex etiology of lung malignancies developing in LMICs such as Lebanon.

The protective effect of parental expectations against early adolescent smoking initiation.

PubMed

Simons-Morton, Bruce G

2004-10-01

Substantial research and theory suggests that smoking initiation is socially mediated, with both peers and parents playing important roles. To learn more about how parenting behaviors influence smoking initiation, students (n=1002) from four middle schools were surveyed at the beginning of the sixth grade (T1), and the end of the sixth (T2) and seventh (T3) grades. T1 and T2-T1 predictors were regressed on smoking initiation at the end of seventh grade. In bivariate logistic regression analyses, association with friends who smoke, attitudes toward deviance, outcome expectations for smoking, perceived school climate, parental expectations, parental involvement at T1 and increases in these variables (T2-T1) were associated with smoking initiation at T3, but only the T1 measures of social competence, academic engagement, school adjustment, perceived prevalence, parental monitoring and parental involvement were associated with smoking initiation at T3. In multivariate logistic regression analyses, parental expectations were negatively associated, and increases in attitudes accepting of deviance and affiliation with friends who smoke were positively associated with smoking initiation. Analysis of interactions indicated that parental expectations and monitoring did not mediate the effect on smoking initiation of attitudes toward deviance or the number of friends who smoke. These findings provide evidence that parental expectations may protect early adolescents against smoking even in the context of increases in favorable attitudes and friends who smoking.

Smoke-free legislation and child health

PubMed Central

Faber, Timor; Been, Jasper V; Reiss, Irwin K; Mackenbach, Johan P; Sheikh, Aziz

2016-01-01

In this paper, we aim to present an overview of the scientific literature on the link between smoke-free legislation and early-life health outcomes. Exposure to second-hand smoke is responsible for an estimated 166 ,000 child deaths each year worldwide. To protect people from tobacco smoke, the World Health Organization recommends the implementation of comprehensive smoke-free legislation that prohibits smoking in all public indoor spaces, including workplaces, bars and restaurants. The implementation of such legislation has been found to reduce tobacco smoke exposure, encourage people to quit smoking and improve adult health outcomes. There is an increasing body of evidence that shows that children also experience health benefits after implementation of smoke-free legislation. In addition to protecting children from tobacco smoke in public, the link between smoke-free legislation and improved child health is likely to be mediated via a decline in smoking during pregnancy and reduced exposure in the home environment. Recent studies have found that the implementation of smoke-free legislation is associated with a substantial decrease in the number of perinatal deaths, preterm births and hospital attendance for respiratory tract infections and asthma in children, although such benefits are not found in each study. With over 80% of the world’s population currently unprotected by comprehensive smoke-free laws, protecting (unborn) children from the adverse impact of tobacco smoking and SHS exposure holds great potential to benefit public health and should therefore be a key priority for policymakers and health workers alike. PMID:27853176

Effects of Early Smoking Habits on Young Adult Female Voices in Greece.

PubMed

Tafiadis, Dionysios; Toki, Eugenia I; Miller, Kevin J; Ziavra, Nausica

2017-11-01

Cigarette use is a preventable cause of mortality and diseases. The World Health Organization states that Europe and especially Greece has the highest occurrence of smoking among adults. The prevalence of smoking among women in Greece was estimated to be over 30% in 2012. Smoking is a risk factor for many diseases. Studies have demonstrated the association between smoking and laryngeal pathologies as well as changes in voice characteristics. The purpose of this study was to estimate the effect of early smoking habit on young adult female voices and if they perceive any vocal changes using two assessment methods. The Voice Handicap Index and the acoustic analyses of voice measurements were used, with both serving as mini-assessment protocols. Two hundred and ten young females (110 smokers and 100 nonsmokers) attending the Technological Educational Institute of Epirus in the School of Health and Welfare were included. Statistically significant increases for physical and total scores of the Voice Handicap Index were found in the smokers group (P < 0.05). Significant changes were observed for the acoustic parameters between smoker and nonsmoker groups. The results of this study indicated observable signs of change in the voice acoustic characteristics of young adults with early smoking habits. Copyright © 2017 The Voice Foundation. Published by Elsevier Inc. All rights reserved.

Healthcare Cost of Smoking Induced Cardiovascular Disease in Tanzania.

PubMed

Kidane, Asmerom; Hepelwa, Aloyce; Ngeh, Ernest Tingum; Hu, Teh-Wei

2015-01-01

The study presented here estimates the total health care cost attributable to smoking induced cardiovascular disease in Tanzania. The study based on a survey conducted at a referral university hospital in Dar es Salaam in 2014. Assuming a 2% prevalence rate of cardiovascular disease and a population of 47.2 million, it was estimated that there are 943,800 cardiovascular patients in Tanzania. The proportion of ever smokers among the surveyed patients was found to be 25 percent yielding 240,400 patients who suffer from smoking induced cardiovascular diseases. Per capita annual expenditure per patient is estimated to be 566.6 US dollars and total annual expenditure for the country was estimated to be 136.1 million US dollars. On a per capita basis more direct and indirect cost is incurred on males compared to females; more is spent on the elderly (40 or more years) compared to the youth (less than 20 years). When compared with the mean annual household income of the surveyed population, the smoking induced per capita expenditure constitutes 35% of household income.

Predictors of Cigarette Smoking Initiation in Early, Middle, and Late Adolescence.

PubMed

O'Loughlin, Jennifer; O'Loughlin, Erin K; Wellman, Robert J; Sylvestre, Marie-Pierre; Dugas, Erika N; Chagnon, Miguel; Dutczak, Hartley; Laguë, Johanne; McGrath, Jennifer J

2017-09-01

Little is known about age-related differences in risk factors for cigarette smoking initiation. We identified predictors of initiation in early, middle, and late adolescence from among sociodemographic factors, indicators of smoking in the social environment, psychological characteristics, lifestyle indicators, and perceived need for cigarettes. Data were drawn from a longitudinal study of 1,801 children recruited at age 10-11 years from 29 elementary schools in Montreal, Canada. Multivariable logistic regression within a generalized estimating equations framework was used to identify predictors among never smokers across three 2-year windows: age 11-13 years (n = 1,221); age 13-15 years (n = 737); and age 15-17 years (n = 690). Among the 18 risk factors investigated, two differed across age. Friends' smoking, a strong risk factor in early adolescence (odds ratio [95% confidence interval] = 5.78 [3.90-8.58]), lost potency in late adolescence (1.83 [1.31-2.57]). Depressive symptoms, a risk factor in early and middle adolescence (1.60 [1.26-2.02] and 1.92 [1.45-2.54], respectively), were inversely associated in late adolescence (.76 [.58-1.00]). Sex, TV viewing, and weight-related goals were not associated with initiation at any age. All other factors were significant in two or three age groups. Most risk factors for smoking initiation were stable across age. Tobacco control interventions may be robust for risk factors across age groups and may not need adjustment. At all ages, interventions should focus on eliminating smoking in the social environment and on reducing the availability of tobacco products. Copyright © 2017 Society for Adolescent Health and Medicine. Published by Elsevier Inc. All rights reserved.

Neighborhood, Family, and Peer Factors Associated with Early Adolescent Smoking and Alcohol Use.

PubMed

Cambron, Christopher; Kosterman, Rick; Catalano, Richard F; Guttmannova, Katarina; Hawkins, J David

2018-02-01

There is broad agreement that neighborhood contexts are important for adolescent development, but there is less consensus about their association with adolescent smoking and alcohol use. Few studies have examined associations between neighborhood socioeconomic contexts and smoking and alcohol use while also accounting for differences in family and peer risk factors for substance use. Data drawn from the Seattle Social Development Project (N = 808), a gender-balanced (female = 49%), multiethnic, theory-driven longitudinal study originating in Seattle, WA, were used to estimate trajectories of smoking and alcohol use from 5th to 9th grade. Time-varying measures of neighborhood socioeconomic, family, and peer factors were associated with smoking and alcohol use at each wave after accounting for average growth in smoking and alcohol use over time and demographic differences. Results indicated that living in more socioeconomically disadvantaged neighborhoods, lower family income, lower family general functioning, more permissive family smoking environments, and affiliation with deviant peers were independently associated with increased smoking. Lower family functioning, more permissive family alcohol use environments, and deviant peers were independently associated with increased alcohol use. The effect of neighborhood disadvantage on smoking was mediated by family income and deviant peers while the effect of neighborhood disadvantage on alcohol use was mediated by deviant peers alone. Family functioning and family substance use did not mediate associations between neighborhood disadvantage and smoking or alcohol use. The results highlight the importance of neighborhood, family, and peer factors in early adolescent smoking and alcohol use. Future studies should examine the unique association of neighborhood disadvantage with adolescent smoking net of family socioeconomics, functioning, and substance use, as well as peer affiliations. Better understanding of the

Pulmonary function, respiratory symptoms, and dust exposures among workers engaged in early manufacturing processes of tea: a cohort study.

PubMed

Shieh, Tzong-Shiun; Chung, Jui-Jung; Wang, Chung-Jing; Tsai, Perng-Jy; Kuo, Yau-Chang; Guo, How-Ran

2012-02-13

To evaluate pulmonary function and respiratory symptoms in workers engaged in the early manufacturing processes of tea and to identify the associated factors, we conducted a study in a tea production area in Taiwan. We recruited tea workers who engaged in the early manufacturing process in the Mountain Ali area in Taiwan and a comparison group of local office workers who were matched for age, gender, and smoking habits. We performed questionnaire interviews, pulmonary function tests, skin prick tests, and measurement of specific IgE for tea on the participants and assessed tea dust exposures in the tea factories. The 91 participating tea workers had higher prevalence of respiratory symptoms than the comparison group (32 participants). Among tea workers, ball-rolling workers had the highest prevalence of symptoms and the highest exposures of inhalable dusts. At baseline, tea workers had similar pulmonary functions as the comparison group, but compared to the other tea workers ball-rolling workers had a lower ratio of the 1-second forced expiratory volume to forced vital capacity (FEV1/FVC) and a lower maximal mid-expiratory flow rate expressed as% of the predicted value--MMF (%pred). A total of 58 tea workers participated in the on-site investigation and the cross-shift lung function measurements. We found ball-rolling yielded the highest inhalable dust level, panning yielded the highest respirable dust level, and withering yielded the lowest levels of both dusts. Ball-rolling also yielded the highest coarse fraction (defined as inhalable dusts minus respirable dusts), which represented exposures from nose to tracheobronchial tract. During the shift, we observed significant declines in pulmonary function, especially in ball-rolling workers. Multiple regressions showed that age, height, work tasks, coarse fraction, and number of months working in tea manufacturing each year were independent predictors of certain pulmonary function parameters in tea workers. Tea

Nedocromil sodium reduces cigarette smoke-induced bronchoconstrictor hyperresponsiveness to substance P in the guinea-pig.

PubMed

Dusser, D J; Lacroix, H; Desmazes-Dufeu, N; Mordelet-Dambrine, M; Roisman, G L

1995-01-01

Acute exposure to cigarette smoke provokes airway hyperresponsiveness to substance P and inactivates neutral endopeptidase (NEP). To determine whether nedocromil sodium can prevent cigarette smoke-induced hyperresponsiveness to substance P, we studied two groups of anaesthetized guinea-pigs. One group of guinea-pigs was pretreated with aerosolized 0.9% NaCl solution (90 breaths), the other group was pretreated with aerosolized nedocromil sodium (10(-4) M, 90 breaths). In each animal, pretreatment was followed by either exposure to the smoke of one cigarette or exposure to air. After acute exposure to cigarette smoke or to air, we measured the change in total pulmonary resistance (RL) induced by increasing concentrations of aerosolized substance P. In the absence of nedocromil sodium, the bronchoconstrictor responses to substance P were greater in cigarette smoke-exposed guinea-pigs than in air-exposed animals. Aerosolized nedocromil sodium had no effect on the response to substance P in air-exposed animals, but it reduced cigarette smoke-induced hyperresponsiveness to substance P. The preventive effect on cigarette smoke-induced hyperresponsiveness to substance P was observed at concentrations of aerosolized nedocromil sodium of 3 x 10(-5), 10(-4), and 3 x 10(-4) M. In vitro, cigarette smoke solution inhibited NEP activity from lung membrane preparations, but this inhibitory effect was not modified by nedocromil sodium (10(-4) M). We conclude that aerosolized nedocromil sodium reduces cigarette smoke-induced airway hyperresponsiveness to substance P in vivo. This action of nedocromil sodium is not due to a protective effect on cigarette smoke-induced inactivation of NEP in vitro.

Smoke-induced microRNA and related proteome alterations. Modulation by chemopreventive agents.

PubMed

De Flora, Silvio; Balansky, Roumen; D'Agostini, Francesco; Cartiglia, Cristina; Longobardi, Mariagrazia; Steele, Vernon E; Izzotti, Alberto

2012-12-15

Dysregulation of microRNAs (miRNAs) has important consequences on gene and protein expression since a single miRNA targets a number of genes simultaneously. This article provides a review of published data and ongoing studies regarding the effects of cigarette smoke (CS), either mainstream (MCS) or environmental (ECS), on the expression of miRNAs and related proteins. The results generated in mice, rats, and humans provided evidence that exposure to CS results in an intense dysregulation of miRNA expression in the respiratory tract, which is mainly oriented in the sense of downregulation. In parallel, there was an upregulation of proteins targeted by the downregulated miRNAs. These trends reflect an attempt to defend the respiratory tract by means of antioxidant mechanisms, detoxification of carcinogens, DNA repair, anti-inflammatory pathways, apoptosis, etc. However, a long-lasting exposure to CS causes irreversible miRNA alterations that activate carcinogenic mechanisms, such as modulation of oncogenes and oncosuppressor genes, cell proliferation, recruitment of undifferentiated stem cells, inflammation, inhibition of intercellular communications, angiogenesis, invasion, and metastasis. The miRNA alterations induced by CS in the lung of mice and rats are similar to those observed in the human respiratory tract. Since a number of miRNAs that are modulated by CS and/or chemopreventive agents are subjected to single nucleotide polymorphisms in humans, they can be evaluated according to toxicogenomic/pharmacogenomics approaches. A variety of cancer chemopreventive agents tested in our laboratory modulated both baseline and CS-related miRNA and proteome alterations, thus contributing to evaluate both safety and efficacy of dietary and pharmacological agents. Copyright © 2012 UICC.

Increased genetic vulnerability to smoking at CHRNA5 in early-onset smokers.

PubMed

Hartz, Sarah M; Short, Susan E; Saccone, Nancy L; Culverhouse, Robert; Chen, LiShiun; Schwantes-An, Tae-Hwi; Coon, Hilary; Han, Younghun; Stephens, Sarah H; Sun, Juzhong; Chen, Xiangning; Ducci, Francesca; Dueker, Nicole; Franceschini, Nora; Frank, Josef; Geller, Frank; Gubjartsson, Daniel; Hansel, Nadia N; Jiang, Chenhui; Keskitalo-Vuokko, Kaisu; Liu, Zhen; Lyytikäinen, Leo-Pekka; Michel, Martha; Rawal, Rajesh; Rosenberger, Albert; Scheet, Paul; Shaffer, John R; Teumer, Alexander; Thompson, John R; Vink, Jacqueline M; Vogelzangs, Nicole; Wenzlaff, Angela S; Wheeler, William; Xiao, Xiangjun; Yang, Bao-Zhu; Aggen, Steven H; Balmforth, Anthony J; Baumeister, Sebastian E; Beaty, Terri; Bennett, Siiri; Bergen, Andrew W; Boyd, Heather A; Broms, Ulla; Campbell, Harry; Chatterjee, Nilanjan; Chen, Jingchun; Cheng, Yu-Ching; Cichon, Sven; Couper, David; Cucca, Francesco; Dick, Danielle M; Foroud, Tatiana; Furberg, Helena; Giegling, Ina; Gu, Fangyi; Hall, Alistair S; Hällfors, Jenni; Han, Shizhong; Hartmann, Annette M; Hayward, Caroline; Heikkilä, Kauko; Hewitt, John K; Hottenga, Jouke Jan; Jensen, Majken K; Jousilahti, Pekka; Kaakinen, Marika; Kittner, Steven J; Konte, Bettina; Korhonen, Tellervo; Landi, Maria-Teresa; Laatikainen, Tiina; Leppert, Mark; Levy, Steven M; Mathias, Rasika A; McNeil, Daniel W; Medland, Sarah E; Montgomery, Grant W; Muley, Thomas; Murray, Tanda; Nauck, Matthias; North, Kari; Pergadia, Michele; Polasek, Ozren; Ramos, Erin M; Ripatti, Samuli; Risch, Angela; Ruczinski, Ingo; Rudan, Igor; Salomaa, Veikko; Schlessinger, David; Styrkársdóttir, Unnur; Terracciano, Antonio; Uda, Manuela; Willemsen, Gonneke; Wu, Xifeng; Abecasis, Goncalo; Barnes, Kathleen; Bickeböller, Heike; Boerwinkle, Eric; Boomsma, Dorret I; Caporaso, Neil; Duan, Jubao; Edenberg, Howard J; Francks, Clyde; Gejman, Pablo V; Gelernter, Joel; Grabe, Hans Jörgen; Hops, Hyman; Jarvelin, Marjo-Riitta; Viikari, Jorma; Kähönen, Mika; Kendler, Kenneth S; Lehtimäki, Terho; Levinson, Douglas F; Marazita, Mary L; Marchini, Jonathan; Melbye, Mads; Mitchell, Braxton D; Murray, Jeffrey C; Nöthen, Markus M; Penninx, Brenda W; Raitakari, Olli; Rietschel, Marcella; Rujescu, Dan; Samani, Nilesh J; Sanders, Alan R; Schwartz, Ann G; Shete, Sanjay; Shi, Jianxin; Spitz, Margaret; Stefansson, Kari; Swan, Gary E; Thorgeirsson, Thorgeir; Völzke, Henry; Wei, Qingyi; Wichmann, H-Erich; Amos, Christopher I; Breslau, Naomi; Cannon, Dale S; Ehringer, Marissa; Grucza, Richard; Hatsukami, Dorothy; Heath, Andrew; Johnson, Eric O; Kaprio, Jaakko; Madden, Pamela; Martin, Nicholas G; Stevens, Victoria L; Stitzel, Jerry A; Weiss, Robert B; Kraft, Peter; Bierut, Laura J

2012-08-01

Recent studies have shown an association between cigarettes per day (CPD) and a nonsynonymous single-nucleotide polymorphism in CHRNA5, rs16969968. To determine whether the association between rs16969968 and smoking is modified by age at onset of regular smoking. Primary data. Available genetic studies containing measures of CPD and the genotype of rs16969968 or its proxy. Uniform statistical analysis scripts were run locally. Starting with 94,050 ever-smokers from 43 studies, we extracted the heavy smokers (CPD >20) and light smokers (CPD ≤10) with age-at-onset information, reducing the sample size to 33,348. Each study was stratified into early-onset smokers (age at onset ≤16 years) and late-onset smokers (age at onset >16 years), and a logistic regression of heavy vs light smoking with the rs16969968 genotype was computed for each stratum. Meta-analysis was performed within each age-at-onset stratum. Individuals with 1 risk allele at rs16969968 who were early-onset smokers were significantly more likely to be heavy smokers in adulthood (odds ratio [OR] = 1.45; 95% CI, 1.36-1.55; n = 13,843) than were carriers of the risk allele who were late-onset smokers (OR = 1.27; 95% CI, 1.21-1.33, n = 19,505) (P = .01). These results highlight an increased genetic vulnerability to smoking in early-onset smokers.

Respiratory symptoms, lung function decrement and chronic obstructive pulmonary disease in pre-menopausal Indian women exposed to biomass smoke.

PubMed

Mukherjee, Sayali; Roychoudhury, Sanghita; Siddique, Shabana; Banerjee, Madhuchanda; Bhattacharya, Purba; Lahiri, Twisha; Ray, Manas Ranjan

2014-12-01

The impact of chronic exposure to smoke from biomass burning on respiratory health has been examined. Six-hundred and eighty-one non-smoking women (median age 35 years) from eastern India who cook exclusively with biomass (wood, dung and crop residues) and 438 age-matched women from similar neighborhood who cook with liquefied petroleum gas (LPG) were examined. Pulmonary function test was done by spirometry. The concentrations of particulate matter having diameter of < 10 µm (PM10) and < 2.5 µm (PM2.5) in indoor air was measured by real-time aerosol monitor. Compared with LPG users, biomass users had greater prevalence of upper (50.9 versus 28.5%) and lower respiratory symptoms (71.8 versus 30.8%) and dyspnea (58.4 versus 19.9%). They showed reduction in all parameters measured by spirometer especially in mid-expiratory volume. PM10 and PM2.5 concentration in biomass using kitchen were 2-3-times more than LPG-using kitchen, and the decline in spirometry values was positively associated PM10 and PM2.5 levels in indoor air after controlling education, family income and kitchen location as potential confounders. Overall, 29.7% of biomass users and 16.4% of LPG users had deficient lung function, and restrictive type of deficiency was predominant. Chronic obstructive pulmonary disease (COPD) was diagnosed in 4.6% of biomass and 0.9% of LPG users. Women who predominantly used dung cake and did not possess separate kitchen had poorer lung function. Cumulative exposure to biomass smoke causes lung function decrement and facilitates COPD development even in non-smoking and relatively young pre-menopausal women.

[Smoking history worldwide--cigarette smoking, passive smoking and smoke free environment in Switzerland].

PubMed

Brändli, Otto

2010-08-01

After the invention of the cigarette 1881 the health consequences of active smoking were fully known only in 1964. Since 1986 research findings allow increasingly stronger conclusions about the impact of passive smoking on health, especially for lung cancer, cardiovascular and respiratory disease in adults and children and the sudden infant death syndrome. On the basis of current consumption patterns, approximately 450 million adults will be killed by smoking between 2000 and 2050. At least half of these adults will die between age 30 and 69. Cancer and total deaths due to smoking have fallen so far only in men in high-income countries but will rise globally unless current smokers stop smoking before or during middle age. Higher taxes, regulations on smoking, including 100 % smoke free indoor spaces, and information for consumers could avoid smoking-associated deaths. Irland was 2004 the first country worldwide introducing smoke free bars and restaurants with positive effects on compliance, health of employees and business. In the first year after the introduction these policies have resulted in a 10 - 20 % reduction of acute coronary events. In Switzerland smoke free regulations have been accepted by popular vote first in the canton of Ticino in 2006 and since then in 15 more cantons. The smoking rate dropped from 33 to 27 % since 2001.

EGR-1 regulates Ho-1 expression induced by cigarette smoke

DOE Office of Scientific and Technical Information (OSTI.GOV)

Chen, Huaqun, E-mail: chenhuaqun@njnu.edu.cn; Wang, Lijuan; Gong, Tao

2010-05-28

As an anti-oxidant molecule, heme oxygenase-1 (HO-1) has been implicated in the protection of lung injury by cigarette smoke (CS). The mechanisms regulating its expression have not been defined. In this report, the role of early growth response 1 (EGR-1) in the regulation of Ho-1 expression was investigated. In C57BL/6 mice with CS exposure, HO-1 was greatly increased in bronchial epithelial cells and alveolar inflammatory cells. In primary cultured mouse lung fibroblasts and RAW264.7 cells exposed to cigarette smoke water extract (CSE), an increase in HO-1 protein level was detected. In addition, CSE induced HO-1 expression was decreased in Egr-1more » deficient mouse embryo fibroblasts (Egr-1{sup -/-} MEFs). Nuclear localization of EGR-1 was examined in mouse lung fibroblasts after exposure to CSE. Luciferase reporter activity assays showed that the enhancer region of the Ho-1 gene containing a proposed EGR-1 binding site was responsible for the induction of HO-1. A higher increase of alveolar mean linear intercept (Lm) was observed in lung tissues, and a larger increase in the number of total cells and monocytes/macrophages from bronchial alveolar lavage fluid was found in CS-exposed mice by loss of function of EGR-1 treatment. In summary, the present data demonstrate that EGR-1 plays a critical role in HO-1 production induced by CS.« less

Effect of passive smoking on growth and infection rates of breast-fed and non-breast-fed infants.

PubMed

Yilmaz, Gonca; Hizli, Samil; Karacan, Candemir; Yurdakök, Kadriye; Coşkun, Turgay; Dilmen, Uğur

2009-06-01

The aim of the present study was to determine the effect of passive tobacco smoking on growth and infection rate of infants, and to evaluate whether breast-feeding might be protective against harmful effects of cigarette smoke. A cross-sectional study on 254 6-7-month-old infants was carried out. A questionnaire was given to mothers; and infants' head circumference, bodyweight, height, and urinary cotinine levels were measured. Multivariate analysis of factors influencing lower respiratory tract infections showed that smoking mothers increased the rate by 9.1-fold; breast-feeding decreased it by 3.3-fold; formula feeding at birth increased it by a factor of 15.2; another smoker at home increased it by a factor of 40.1. Multivariate analysis of factors influencing upper respiratory tract infections showed that smoking mothers increased the rate by a factor of 23; early formula feeding increased it by a factor of 62; breast-feeding decreased it by a factor of 5; smoking fathers increased it by a factor of 15. Multivariate analysis of factors influencing otitis media found that smoking mothers and fathers increased it by a factor of 9.4 and 6.15, respectively, and breast-feeding decreased it by a factor of 5.4. Tobacco smoke exposure of infants has negative consequences on growth, otitis media, and upper and lower respiratory tract infections. Breast-feeding promoted the growth of infants who were passively exposed to tobacco smoke and protected them against infections. Smoking should not be permitted in households with infants. When this is impossible, breast-feeding should be promoted to protect the infants against the health hazards of passive smoking.

The Impact of Smoking in Adolescence on Early Adult Anxiety Symptoms and the Relationship between Infant Vulnerability Factors for Anxiety and Early Adult Anxiety Symptoms: The TOPP Study

PubMed Central

Moylan, Steven; Gustavson, Kristin; Karevold, Evalill; Øverland, Simon; Jacka, Felice N.; Pasco, Julie A.; Berk, Michael

2013-01-01

Cigarette smoking is increased in people with trait anxiety and anxiety disorders, however no longitudinal data exist illuminating whether smoking in adolescence can influence the developmental trajectory of anxiety symptoms from early vulnerability in infancy to adult anxiety expression. Using The Tracing Opportunities and Problems in Childhood and Adolescence (TOPP) Study, a community-based cohort of children and adolescents from Norway who were observed from the age of 18months to age 18–19years, we explored the relationship between adolescent smoking, early vulnerability for anxiety in infancy (e.g. shyness, internalizing behaviors, emotional temperaments) and reported early adult anxiety. Structural equation modeling demonstrated that adolescent active smoking was positively associated with increased early adulthood anxiety (β = 0.17, p<0.05), after controlling for maternal education (proxy for socioeconomic status). Adolescent anxiety did not predict early adult smoking. Adolescent active smoking was a significant effect modifier in the relationship between some infant vulnerability factors and later anxiety; smoking during adolescence moderated the relationship between infant internalizing behaviors (total sample: active smokers: β = 0.85,p<0.01, non-active smokers: ns) and highly emotional temperament (total sample: active smokers: β = 0.55,p<0.01,non-active smokers: ns), but not shyness, and anxiety in early adulthood. The results support a model where smoking acts as an exogenous risk factor in the development of anxiety, and smoking may alter the developmental trajectory of anxiety from infant vulnerability to early adult anxiety symptom expression. Although alternative non-mutually exclusive models may explain these findings, the results suggest that adolescent smoking may be a risk factor for adult anxiety, potentially by influencing anxiety developmental trajectories. Given the known adverse health effects of cigarette smoking and

Early Childhood Lower Respiratory Illness and Air Pollution

PubMed Central

Hertz-Picciotto, Irva; Baker, Rebecca James; Yap, Poh-Sin; Dostál, Miroslav; Joad, Jesse P.; Lipsett, Michael; Greenfield, Teri; Herr, Caroline E.W.; Beneš, Ivan; Shumway, Robert H.; Pinkerton, Kent E.; Šrám, Radim

2007-01-01

Background Few studies of air pollutants address morbidity in preschool children. In this study we evaluated bronchitis in children from two Czech districts: Teplice, with high ambient air pollution, and Prachatice, characterized by lower exposures. Objectives Our goal was to examine rates of lower respiratory illnesses in preschool children in relation to ambient particles and hydrocarbons. Methods Air monitoring for particulate matter < 2.5 μm in diameter (PM2.5) and polycyclic aromatic hydrocarbons (PAHs) was conducted daily, every third day, or every sixth day. Children born May 1994 through December 1998 were followed to 3 or 4.5 years of age to ascertain illness diagnoses. Mothers completed questionnaires at birth and at follow-up regarding demographic, lifestyle, reproductive, and home environmental factors. Longitudinal multivariate repeated-measures analysis was used to quantify rate ratios for bronchitis and for total lower respiratory illnesses in 1,133 children. Results After adjustment for season, temperature, and other covariates, bronchitis rates increased with rising pollutant concentrations. Below 2 years of age, increments in 30-day averages of 100 ng/m3 PAHs and of 25 μg/m3 PM2.5 resulted in rate ratios (RRs) for bronchitis of 1.29 [95 % confidence interval (CI), 1.07–1.54] and 1.30 (95% CI, 1.08–1.58), respectively; from 2 to 4.5 years of age, these RRs were 1.56 (95% CI, 1.22–2.00) and 1.23 (95% CI, 0.94–1.62), respectively. Conclusion Ambient PAHs and fine particles were associated with early-life susceptibility to bronchitis. Associations were stronger for longer pollutant-averaging periods and, among children > 2 years of age, for PAHs compared with fine particles. Preschool-age children may be particularly vulnerable to air pollution–induced illnesses. PMID:17938744

Exposure to neonatal cigarette smoke causes durable lung changes but does not potentiate cigarette smoke–induced chronic obstructive pulmonary disease in adult mice

PubMed Central

McGrath-Morrow, Sharon; Malhotra, Deepti; Lauer, Thomas; Collaco, J. Michael; Mitzner, Wayne; Neptune, Enid; Wise, Robert; Biswal, Shyam

2016-01-01

The impact of early childhood cigarette smoke (CS) exposure on CS-induced chronic obstructive pulmonary disease (COPD) is unknown. This study was performed to evaluate the individual and combined effects of neonatal and adult CS exposure on lung structure, function, and gene expression in adult mice. To model a childhood CS exposure, neonatal C57/B6 mice were exposed to 14 days of CS (Neo CS). At 10 weeks of age, Neo CS and control mice were exposed to 4 months of CS. Pulmonary function tests, bronchoalveolar lavage, and lung morphometry were measured and gene expression profiling was performed on lung tissue. Mean chord lengths and lung volumes were increased in neonatal and/or adult CS-exposed mice. Differences in immune, cornified envelope protein, muscle, and erythrocyte genes were found in CS-exposed lung. Neonatal CS exposure caused durable structural and functional changes in the adult lung but did not potentiate CS-induced COPD changes. Cornified envelope protein gene expression was decreased in all CS-exposed mice, whereas myosin and erythrocyte gene expression was increased in mice exposed to both neonatal and adult CS, suggesting an adaptive response. Additional studies may be warranted to determine the utility of these genes as biomarkers of respiratory outcomes. PMID:21649527

Antinociception induced by chronic exposure of rats to cigarette smoke.

PubMed

Anderson, Kenton L; Pinkerton, Kent E; Uyeminami, Dale; Simons, Christopher T; Carstens, Mirela Iodi; Carstens, E

2004-08-05

To investigate if chronic exposure to cigarette smoke induces analgesia, rats were exposed to concentrated cigarette smoke in an environmental chamber over four successive 5-day blocks (6 h/day), with 2 smoke-free days between blocks. A control group was exposed to room air. Tail flick latencies increased significantly (analgesia) during each smoke exposure block, with a relative decline in analgesia across blocks (tolerance) and a return to control levels during the first three smoke-free interludes while remaining higher after the conclusion of the 4-week exposure period. Mechanical (von Frey) withdrawal thresholds declined over time in smoke-exposed and control groups, with the smoke-exposed group showing significantly lower thresholds. Plasma nicotine reached 95.4 +/- 32 (S.D.) ng/ml at the end of weekly smoke exposure and declined to 44.9 +/- 10.6 ng/ml 24 h after withdrawal. Rats lost weight during smoke exposure and quickly regained weight during smoke-free interludes and at the cessation of smoke exposure. Analgesia may contribute to the initiation of smoking, and rapid reversal of the analgesic effect following acute exposure may contribute to the difficulty in quitting smoking.

Changes in circulating peptide YY and ghrelin are associated with early smoking relapse.

PubMed

Lemieux, Andrine M; al'Absi, Mustafa

2018-01-01

Ghrelin and peptide YY (PYY) during ad libitum smoking have been associated with decreased reported craving (ghrelin) and increased positive affect (PYY), and higher baseline ghrelin levels predicted subsequent increased risk of smoking relapse. The current study assessed PYY and ghrelin during ad libitum smoking and again after the initial 48h of a smoking cessation attempt. The data compared smokers who abstained for 28days (n=37), smokers who relapsed (n=54), and nonsmokers (n=37). Plasma samples and subjective measures assessing craving and mood were collected at the beginning of each session. Results showed that relapsers experienced greater levels of distress (ps <0.01). While nonsmokers and abstainers showed no change in ghrelin across the initial 48h, relapsers declined (p <0.01). With PYY, relapsers increased (p <0.05) across the early abstinent phase. PYY and ghrelin may be useful predictors of relapse, specifically in reference to early withdrawal. Copyright © 2017. Published by Elsevier B.V.

Clinical significance of early smoking withdrawal effects and their relationships with nicotine metabolism: preliminary results from a pilot study.

PubMed

Hendricks, Peter S; Delucchi, Kevin L; Benowitz, Neal L; Hall, Sharon M

2014-05-01

Although the early time course of smoking withdrawal effects has been characterized, the clinical significance of early withdrawal symptoms and their predictors are unknown. This study evaluated the relationships of early smoking withdrawal effects with quit attempt outcomes and the rate of nicotine metabolism. Eleven treatment-seeking smokers abstained from smoking for 4 hr in the laboratory before a quit attempt. Withdrawal measures included heart rate, sustained attention, and self-report. Following baseline assessment, withdrawal measures were administered every 30 min. At the conclusion of the 4-hr early withdrawal session, participants received a brief smoking cessation intervention and then returned 1 week and 12 weeks later for outcome assessments that included biochemically confirmed smoking abstinence, cigarettes smoked in the past 24hr, and self-reported withdrawal symptoms. The rate of nicotine metabolism was estimated at intake with the nicotine metabolite ratio (trans-3'-hydroxycotinine/cotinine) measured in saliva. Greater self-reported negative affect and concentration difficulty during early withdrawal, most notably anxiety, were related with poorer quit attempt outcomes. There was some indication that although a faster increase in craving and greater hunger during early withdrawal were associated with more favorable outcomes, a greater decrease in heart rate during this time was associated with poorer outcomes. Faster nicotine metabolism was related to a faster increase in anxiety but a slower increase in craving during early withdrawal. These findings lend support to the clinical significance of early smoking withdrawal effects. The rate of nicotine metabolism may be a useful predictor of early withdrawal symptoms.

Nicotine dependence, "background" and cue-induced craving and smoking in the laboratory.

PubMed

Dunbar, Michael S; Shiffman, Saul; Kirchner, Thomas R; Tindle, Hilary A; Scholl, Sarah M

2014-09-01

Nicotine dependence has been associated with higher "background" craving and smoking, independent of situational cues. Due in part to conceptual and methodological differences across past studies, the relationship between dependence and cue-reactivity (CR; e.g., cue-induced craving and smoking) remains unclear. 207 daily smokers completed six pictorial CR sessions (smoking, negative affect, positive affect, alcohol, smoking prohibitions, and neutral). Individuals rated craving before (background craving) and after cues, and could smoke following cue exposure. Session videos were coded to assess smoking. Participants completed four nicotine dependence measures. Regression models assessed the relationship of dependence to cue-independent (i.e., pre-cue) and cue-specific (i.e., pre-post cue change for each cue, relative to neutral) craving and smoking (likelihood of smoking, latency to smoke, puff count). Dependence was associated with background craving and smoking, but did not predict change in craving across the entire sample for any cue. Among alcohol drinkers, dependence was associated with greater increases in craving following the alcohol cue. Only one dependence measure (Wisconsin Inventory of Smoking Dependence Motives) was consistently associated with smoking reactivity (higher likelihood of smoking, shorter latency to smoke, greater puff count) in response to cues. While related to cue-independent background craving and smoking, dependence is not strongly associated with laboratory cue-induced craving under conditions of minimal deprivation. Dependence measures that incorporate situational influences on smoking correlate with greater cue-provoked smoking. This may suggest independent roles for CR and traditional dependence as determinants of smoking, and highlights the importance of assessing behavioral CR outcomes. Copyright © 2014 Elsevier Ireland Ltd. All rights reserved.

A Longitudinal Examination of the Relation Between Internalizing Problem Behaviors and Early Adolescent Cigarette Smoking.

PubMed

Aloise-Young, Patricia A; Zaleski, Adam C; Swaim, Randall C

2017-01-01

The purpose of the present study was to investigate the longitudinal relation between internalizing problem behaviors (measured with the anxious/depressed and somatic complaints subscales of the Achenbach Teacher's Report Form) and self-reported cigarette smoking behavior and intentions during early adolescence. In addition, a possible mediating role of perceived harm was investigated. Sixth graders and their teachers were surveyed in the sixth grade and students were surveyed again in the seventh grade. Smoking behavior and intentions were assessed with five items including lifetime use, 30-day use, tobacco user status (nonsmoker to heavy smoker), and two intentions/behavioral expectations items. In addition to perceived harm from smoking, reasons for smoking and reasons for not smoking were included on the survey. As hypothesized, teacher reports of sixth-grade internalizing problem behaviors were negatively related to seventh-grade smoking behavior and intentions. Moreover, perceived harm from smoking was negatively related to smoking and intentions. The hypothesized mediating role of perceived harm in the internalizing to smoking relationship was not supported. Potential differences in the relation between internalizing and smoking across adolescence are discussed. Specifically, the results of the present study and an examination of prior literature suggest that in early adolescence internalizing problems are negatively related to cigarette smoking, whereas in middle and late adolescence the opposite is true.

Early pulmonary events of nose-only water pipe (shisha) smoking exposure in mice

PubMed Central

Nemmar, Abderrahim; Hemeiri, Ahmed Al; Hammadi, Naser Al; Yuvaraju, Priya; Beegam, Sumaya; Yasin, Javed; Elwasila, Mohamed; Ali, Badreldin H; Adeghate, Ernest

2015-01-01

Water pipe smoking (WPS) is increasing in popularity and prevalence worldwide. Convincing data suggest that the toxicants in WPS are similar to that of cigarette smoke. However, the underlying pathophysiologic mechanisms related to the early pulmonary events of WPS exposure are not understood. Here, we evaluated the early pulmonary events of nose-only exposure to mainstream WPS generated by commercially available honey flavored “moasel” tobacco. BALB/c mice were exposed to WPS 30 min/day for 5 days. Control mice were exposed using the same protocol to atmospheric air only. We measured airway resistance using forced oscillation technique, and pulmonary inflammation was evaluated histopathologically and by biochemical analysis of bronchoalveolar lavage (BAL) fluid and lung tissue. Lung oxidative stress was evaluated biochemically by measuring the level of reactive oxygen species (ROS), lipid peroxidation (LPO), reduced glutathione (GSH), catalase, and superoxide dismutase (SOD). Mice exposed to WPS showed a significant increase in the number of neutrophils (P < 0.05) and lymphocytes (P < 0.001). Moreover, total protein (P < 0.05), lactate dehydrogenase (P < 0.005), and endothelin (P < 0.05) levels were augmented in bronchoalveolar lavage fluid. Tumor necrosis factor α (P < 0.005) and interleukin 6 (P < 0.05) concentrations were significantly increased in lung following the exposure to WPS. Both ROS (P < 0.05) and LPO (P < 0.005) in lung tissue were significantly increased, whereas the level and activity of antioxidants including GSH (P < 0.0001), catalase (P < 0.005), and SOD (P < 0.0001) were significantly decreased after WPS exposure, indicating the occurrence of oxidative stress. In contrast, airway resistance was not increased in WPS exposure. We conclude that subacute, nose-only exposure to WPS causes lung inflammation and oxidative stress without affecting pulmonary function suggesting that inflammation and oxidative stress are

Early pulmonary events of nose-only water pipe (shisha) smoking exposure in mice.

PubMed

Nemmar, Abderrahim; Al Hemeiri, Ahmed; Al Hammadi, Naser; Yuvaraju, Priya; Beegam, Sumaya; Yasin, Javed; Elwasila, Mohamed; Ali, Badreldin H; Adeghate, Ernest

2015-03-01

Water pipe smoking (WPS) is increasing in popularity and prevalence worldwide. Convincing data suggest that the toxicants in WPS are similar to that of cigarette smoke. However, the underlying pathophysiologic mechanisms related to the early pulmonary events of WPS exposure are not understood. Here, we evaluated the early pulmonary events of nose-only exposure to mainstream WPS generated by commercially available honey flavored "moasel" tobacco. BALB/c mice were exposed to WPS 30 min/day for 5 days. Control mice were exposed using the same protocol to atmospheric air only. We measured airway resistance using forced oscillation technique, and pulmonary inflammation was evaluated histopathologically and by biochemical analysis of bronchoalveolar lavage (BAL) fluid and lung tissue. Lung oxidative stress was evaluated biochemically by measuring the level of reactive oxygen species (ROS), lipid peroxidation (LPO), reduced glutathione (GSH), catalase, and superoxide dismutase (SOD). Mice exposed to WPS showed a significant increase in the number of neutrophils (P < 0.05) and lymphocytes (P < 0.001). Moreover, total protein (P < 0.05), lactate dehydrogenase (P < 0.005), and endothelin (P < 0.05) levels were augmented in bronchoalveolar lavage fluid. Tumor necrosis factor α (P < 0.005) and interleukin 6 (P < 0.05) concentrations were significantly increased in lung following the exposure to WPS. Both ROS (P < 0.05) and LPO (P < 0.005) in lung tissue were significantly increased, whereas the level and activity of antioxidants including GSH (P < 0.0001), catalase (P < 0.005), and SOD (P < 0.0001) were significantly decreased after WPS exposure, indicating the occurrence of oxidative stress. In contrast, airway resistance was not increased in WPS exposure. We conclude that subacute, nose-only exposure to WPS causes lung inflammation and oxidative stress without affecting pulmonary function suggesting that inflammation and oxidative stress are early

[Respiratory symptoms and obstructive ventilatory disorder in Tunisian woman exposed to biomass].

PubMed

Kwas, H; Rahmouni, N; Zendah, I; Ghedira, H

2017-04-01

In some Tunisian cities, especially semi-urbanized, the exposure to the smoke produced during combustion of the biomass, main source of pollution of indoor air, remains prevalent among non-smoking women. To assess the relationship between exposure to biomass smoke and the presence of obstructive ventilatory disorder in the non-smoking women in semi-urban areas of Tunisia. Cross etiological study, using a questionnaire, including 140 non-smoking women responsible for cooking and/or exposed during heating by traditional means with objective measurement of their respiratory functions. We found 81 women exposed to biomass for a period of≥20 hours-years and 59 unexposed women. Exposed women reported more respiratory symptoms namely exertional dyspnea and/or chronic cough than unexposed. Of the 140 women, 14 women have an FEV/FEV6<70% of which 13 are exposed to biomass. We found a correlation between respiratory symptoms and obstructive ventilatory disorder in exposed women. The air pollution inside the home during the traditional activities of cooking and/or heating is a respiratory risk factor for non-smoking women over the age of 30 years. Exposure to biomass smoke can cause chronic respiratory symptoms and persistent obstructive ventilatory disorder that can consistent with COPD. Copyright © 2016 Elsevier Masson SAS. All rights reserved.

Indoor air and respiratory health in preadolescent children

NASA Astrophysics Data System (ADS)

Gomzi, M.

The effect of indoor exposure to nitrogen dioxide, ammonia, particulate matter and parental tobacco smoke on respiratory health was studied over a period of six months in all second graders born and living in two area of continental Croatia 8-10 yr of age. The study group was divided into two sections corresponding to area of residence (industrial/rural). Information on respiratory symptoms was collected from a self-administered questionnaire completed by the parents of the children. The mean values of concentrations of indoor air pollution that had been recorded in 24-h samples of air collected at schools were mostly below threshold limit for ambient pollution. In addition, information on parental smoking, the density of habitation and the type of fuel used for heating and/or cooking in the home was obtained by a questionnaire. In the investigated period the prevalence of respiratory illness was 22% in the children exposed to lower indoor air pollution and 25% in those exposed to higher indoor air pollution. Exposure to parental smoking was also associated with more respiratory symptoms (28 : 19%). The results indicate that the measured air pollutants only had a slight effect on the respiratory health of preadolescent children. However, the effect of exposure to parental smoking was more pronounced.

Smoking-Cue Induced Brain Activation In Adolescent Light Smokers

PubMed Central

Rubinstein, Mark L.; Luks, Tracy L.; Moscicki, Anna-Barbara; Dryden, Wendy; Rait, Michelle A.; Simpson, Gregory V.

2010-01-01

Purpose Using fMRI, we examined whether or not adolescents with low levels of nicotine exposure (light smokers) display neural activation in areas shown to be involved with addiction in response to smoking-related stimuli. Design/Setting/Participants Twelve adolescent light smokers (aged 13 to17, smoked 1 to 5 cigarettes per day) and 12 non-smokers (ages 13 to 17, never smoked a cigarette) from the San Francisco Bay Area underwent fMRI scanning. During scanning they viewed blocks of photographic smoking and control cues. Smoking cues consisted of pictures of people smoking cigarettes and smoking-related objects such as lighters and ashtrays. Neutral cues consisted of everyday objects and people engaged in everyday activities. Findings For smokers, smoking cues elicited greater activation than neutral cues in the mesolimbic reward circuit (left anterior cingulate (T=7.88, p<.001), right hippocampus (T=6.62, p<.001) and right parahippocampal gyrus (T=4.70, p<.001)). We found activation from smoking cues versus neutral cues within both the left and right frontal medial orbital regions (T=5.09, p<.001 and T=3.94, p=.001 respectively), which may be unique to adolescents. Non-smokers showed no significant difference in activation between smoking-related cues and neutral cues. Conclusions Our finding that smoking cues produced activation in adolescent light smokers in brain regions seen in adult and heavy teen smokers suggests that even at low levels of smoking, adolescents exhibit heightened reactivity to smoking cues. This paper adds to the existing literature suggesting that nicotine dependence may begin with exposure to low levels of nicotine, underscoring the need for early intervention among adolescent smokers. PMID:21185518

Trait hostility and hostile interpretation biases in daily smokers: associations with reasons for smoking, motivation to quit, and early smoking lapse.

PubMed

Cougle, Jesse R; Hawkins, Kirsten A; Macatee, Richard J; Zvolensky, Michael J; Sarawgi, Shivali

2014-09-01

Hostility has emerged as an important predictor of smoking cessation difficulties, though the mechanisms underlying the hostility and smoking relationship are poorly understood. Further, research has yet to explore relations between hostile interpretation biases and different aspects of smoking behavior. In the present study, current daily smokers (N = 106) were administered measures of smoking characteristics, smoking motivation, reasons for quitting, hostility, and hostile interpretation bias. Neither trait hostility nor hostile interpretation bias were uniquely associated with motivation to quit, reasons for quitting, nicotine dependence, or problematic symptoms following past cessation attempts. However, hostility and hostile interpretation biases were uniquely associated with different reasons for smoking. Additionally, greater hostile interpretation bias (but not hostility) was uniquely associated with early relapse following past cessation attempts. The current findings add uniquely to the growing, but still relatively small, literature on hostility and smoking and implicate hostile interpretation bias as a potential treatment target in smoking cessation interventions.

Acute exercise induces biphasic increase in respiratory mRNA in skeletal muscle

DOE Office of Scientific and Technical Information (OSTI.GOV)

Ikeda, Shin-ichi; Kizaki, Takako; Haga, Shukoh

2008-04-04

Peroxisome proliferator-activated receptor {gamma} coactivator-1{alpha} (PGC-1{alpha}) promotes the expression of oxidative enzymes in skeletal muscle. We hypothesized that activation of the p38 MAPK (mitogen-activated protein kinase) in response to exercise was associated with exercise-induced PGC-1{alpha} and respiratory enzymes expression and aimed to demonstrate this under the physiological level. We subjected mice to a single bout of treadmill running and found that the exercise induced a biphasic increase in the expression of respiratory enzymes mRNA. The second phase of the increase was accompanied by an increase in PGC-1{alpha} protein, but the other was not. Administration of SB203580 (SB), an inhibitor ofmore » p38 MAPK, suppressed the increase in PGC-1{alpha} expression and respiratory enzymes mRNA in both phases. These data suggest that p38 MAPK is associated with the exercise-induced expression of PGC-1{alpha} and biphasic increase in respiratory enzyme mRNAs in mouse skeletal muscle under physiological conditions.« less

Superiority of PC-SOD to other anti-COPD drugs for elastase-induced emphysema and alteration in lung mechanics and respiratory function in mice.

PubMed

Tanaka, Ken-Ichiro; Sato, Keizo; Aoshiba, Kazutetsu; Azuma, Arata; Mizushima, Tohru

2012-06-15

Bronchodilators (such as ipratropium bromide), steroids (such as fluticasone propionate), and newly developed anti-inflammatory drugs (such as roflumilast) are used for patients with chronic obstructive pulmonary disease (COPD). We recently reported that lecithinized superoxide dismutase (PC-SOD) confers a protective effect in mouse models of COPD. We here examined the therapeutic effect of the combined administration of PC-SOD with ipratropium bromide on pulmonary emphysema and compared the effect of PC-SOD to other types of drugs. The severity of emphysema in mice was assessed by various criteria. Lung mechanics (elastance) and respiratory function (ratio of forced expiratory volume in the first 0.05 s to forced vital capacity) were assessed. Administration of PC-SOD by inhalation suppressed elastase-induced pulmonary emphysema, alteration of lung mechanics, and respiratory dysfunction. The concomitant intratracheal administration of ipratropium bromide did not alter the ameliorating effects of PC-SOD. Administration of ipratropium bromide, fluticasone propionate, or roflumilast alone did not suppress the elastase-induced increase in the pulmonary level of superoxide anion, pulmonary inflammatory response, pulmonary emphysema, alteration of lung mechanics, or respiratory dysfunction as effectively as did PC-SOD. PC-SOD, but not the other drugs, showed a therapeutic effect even when the drug was administered after the development of emphysema. PC-SOD also suppressed the cigarette smoke-induced pulmonary inflammatory response and increase in airway resistance. Based on these results, we consider that the inhalation of PC-SOD would be therapeutically beneficial for COPD.

Respiratory disease in United States farmers

PubMed Central

Hoppin, Jane A; Umbach, David M; Long, Stuart; Rinsky, Jessica L; Henneberger, Paul K; Salo, Paivi M; Zeldin, Darryl C; London, Stephanie J; Alavanja, Michael C R; Blair, Aaron; Freeman, Laura E Beane; Sandler, Dale P

2015-01-01

Objectives Farmers may be at increased risk for adverse respiratory outcomes compared with the general population due to their regular exposures to dusts, animals and chemicals. However, early life farm exposures to microbial agents may result in reduced risk. Understanding respiratory disease risk among farmers and identifying differences between farmers and other populations may lead to better understanding of the contribution of environmental exposures to respiratory disease risk in the general population. Methods We compared the prevalence of self-reported respiratory outcomes in 43548 participants from the Agricultural Health Study (AHS), a prospective cohort of farmers and their spouses from Iowa and North Carolina, with data from adult participants in the National Health and Nutrition Examination Survey (NHANES) over the same period (2005–2010). Results AHS participants had lower prevalences of respiratory diseases (asthma, adult-onset asthma, chronic bronchitis and emphysema), but higher prevalences of current respiratory symptoms (wheeze, cough and phlegm) even after controlling for smoking, body mass index and population characteristics. The overall prevalence of asthma in the AHS (7.2%, 95% CI 6.9 to 7.4) was 52% of that in NHANES (13.8%, 95% CI 13.3 to 14.3), although the prevalence of adult-onset asthma among men did not differ (3.6% for AHS, 3.7% for NHANES). Conversely, many respiratory symptoms were more common in the AHS than NHANES, particularly among men. Conclusions These findings suggest that farmers and their spouses have lower risk for adult-onset respiratory diseases compared with the general population, and potentially higher respiratory irritation as evidenced by increased respiratory symptoms. PMID:24913223

Early Life Wildfire Smoke Exposure Is Associated with Immune Dysregulation and Lung Function Decrements in Adolescence

PubMed Central

Black, Carolyn; Gerriets, Joan E.; Fontaine, Justin H.; Harper, Richart W.; Kenyon, Nicholas J.; Tablin, Fern; Schelegle, Edward S.

2017-01-01

The long-term health effects of wildfire smoke exposure in pediatric populations are not known. The objectives of this study were to determine if early life exposure to wildfire smoke can affect parameters of immunity and airway physiology that are detectable with maturity. We studied a mixed-sex cohort of rhesus macaque monkeys that were exposed as infants to ambient wood smoke from a series of Northern California wildfires in the summer of 2008. Peripheral blood mononuclear cells (PBMCs) and pulmonary function measures were obtained when animals were approximately 3 years of age. PBMCs were cultured with either LPS or flagellin, followed by measurement of secreted IL-8 and IL-6 protein. PBMCs from a subset of female animals were also evaluated by Toll-like receptor (TLR) pathway mRNA analysis. Induction of IL-8 protein synthesis with either LPS or flagellin was significantly reduced in PBMC cultures from wildfire smoke–exposed female monkeys. In contrast, LPS- or flagellin-induced IL-6 protein synthesis was significantly reduced in PBMC cultures from wildfire smoke–exposed male monkeys. Baseline and TLR ligand–induced expression of the transcription factor, RelB, was globally modulated in PBMCs from wildfire smoke–exposed monkeys, with additional TLR pathway genes affected in a ligand-dependent manner. Wildfire smoke–exposed monkeys displayed significantly reduced inspiratory capacity, residual volume, vital capacity, functional residual capacity, and total lung capacity per unit of body weight relative to control animals. Our findings suggest that ambient wildfire smoke exposure during infancy results in sex-dependent attenuation of systemic TLR responses and reduced lung volume in adolescence. PMID:28208028

Life Course Exposure to Smoke and Early Menopause and Menopausal Transition

PubMed Central

Tawfik, Heba; Kline, Jennie; Jacobson, Judith; Tehranifar, Parisa; Protacio, Angeline; Flom, Julie D.; Cirillo, Piera; Cohn, Barbara A.; Terry, Mary Beth

2015-01-01

Objective Early age at menopause is associated with increased risk of cardiovascular disease, stroke, osteoporosis and all-cause mortality. Cigarette smoke exposure in adulthood is an established risk factor for earlier age at natural menopause and may be related to age at menopausal transition. Using data from two U.S. birth cohorts, we examined the association between smoke exposure at various stages of the life course (prenatal, childhood exposure to parental smoking and adult smoke exposure) with menopause status in 1,001 women aged 39 – 49 years at follow-up. Methods We used logistic regression analysis, adjusting for age at follow-up, to estimate odds ratios (ORs) and 95% confidence intervals (CI) relating smoke exposure to natural menopause and menopausal transition. Results The magnitudes of the associations for natural menopause were similar, but not statistically significant after adjustment for confounders for i) women with prenatal smoke exposure who did not smoke at adult follow-up (OR= 2.7 [95% CI 0.8, 9.4]) and ii) current adult smokers who were not exposed prenatally (OR= 2.8 [95% CI 0.9, 9.0]). Women who had been exposed to prenatal smoke and were current smokers had three times the risk of experiencing natural menopause (adjusted OR=3.4 [95% CI 1.1, 10.3]) compared to women without smoke exposure in either time period. Only current smoking of long duration (>26 years) was associated with the timing of the menopausal transition. Conclusion Our data suggest that exposure to smoke both prenatally and around the time of menopause accelerates ovarian aging. PMID:25803667

Life course exposure to smoke and early menopause and menopausal transition.

PubMed

Tawfik, Hebatullah; Kline, Jennie; Jacobson, Judith; Tehranifar, Parisa; Protacio, Angeline; Flom, Julie D; Cirillo, Piera; Cohn, Barbara A; Terry, Mary Beth

2015-10-01

Early age at menopause is associated with increased risk of cardiovascular disease, stroke, osteoporosis, and all-cause mortality. Cigarette smoke exposure in adulthood is an established risk factor for earlier age at natural menopause and may be related to age at the menopausal transition. Using data from two US birth cohorts, we examined the association between smoke exposure at various stages of the life course (prenatal exposure, childhood exposure to parental smoking, and adult smoke exposure) and menopause status in 1,001 women aged 39 to 49 years at follow-up. We used logistic regression analysis (adjusting for age at follow-up) to estimate odds ratios (ORs) and 95% confidence intervals (CI) relating smoke exposure to natural menopause and the menopausal transition. The magnitudes of the associations for natural menopause were similar but not statistically significant after adjustment for confounders among (i) women with prenatal smoke exposure who did not smoke on adult follow-up (OR, 2.7; 95% CI, 0.8-9.4) and (ii) current adult smokers who were not exposed prenatally (OR, 2.8; 95% CI, 0.9-9.0). Women who had been exposed to prenatal smoke and were current smokers had three times the risk of experiencing earlier natural menopause (adjusted OR, 3.4; 95% CI, 1.1-10.3) compared with women without smoke exposure in either period. Only current smoking of long duration (>26 y) was associated with the timing of the menopausal transition. Our data suggest that exposure to smoke both prenatally and around the time of menopause accelerates ovarian aging.

Cue-reactors: individual differences in cue-induced craving after food or smoking abstinence.

PubMed

Mahler, Stephen V; de Wit, Harriet

2010-11-10

Pavlovian conditioning plays a critical role in both drug addiction and binge eating. Recent animal research suggests that certain individuals are highly sensitive to conditioned cues, whether they signal food or drugs. Are certain humans also more reactive to both food and drug cues? We examined cue-induced craving for both cigarettes and food, in the same individuals (n = 15 adult smokers). Subjects viewed smoking-related or food-related images after abstaining from either smoking or eating. Certain individuals reported strong cue-induced craving after both smoking and food cues. That is, subjects who reported strong cue-induced craving for cigarettes also rated stronger cue-induced food craving. In humans, like in nonhumans, there may be a "cue-reactive" phenotype, consisting of individuals who are highly sensitive to conditioned stimuli. This finding extends recent reports from nonhuman studies. Further understanding this subgroup of smokers may allow clinicians to individually tailor therapies for smoking cessation.

Determinants of Chronic Respiratory Symptoms among Pharmaceutical Factory Workers

PubMed Central

Enquselassie, Fikre; Tefera, Yifokire; Gizaw, Muluken; Wakuma, Samson; Woldemariam, Messay

2018-01-01

Background Chronic respiratory symptoms including chronic cough, chronic phlegm, wheezing, shortness of breath, and chest pain are manifestations of respiratory problems which are mainly evolved as a result of occupational exposures. This study aims to assess determinants of chronic respiratory symptoms among pharmaceutical factory workers. Methods A case control study was carried out among 453 pharmaceutical factory workers with 151 cases and 302 controls. Data was collected using pretested and structured questionnaire. The data was analyzed using descriptive statistics and bivariate and multivariate analysis. Result Previous history of chronic respiratory diseases (AOR = 3.36, 95% CI = 1.85–6.12), family history of chronic respiratory diseases (AOR = 2.55, 95% CI = 1.51–4.32), previous dusty working environment (AOR = 2.26, 95% CI = 1.07–4.78), ever smoking (AOR = 3.66, 95% CI = 1.05–12.72), and service years (AOR = 1.86, 95% CI = 1.16–2.99) showed statistically significant association with chronic respiratory symptoms. Conclusion Previous history of respiratory diseases, family history of chronic respiratory diseases, previous dusty working environment, smoking, and service years were determinants of chronic respiratory symptoms. Public health endeavors to prevent the burden of chronic respiratory symptoms among pharmaceutical factory workers should target the reduction of adverse workplace exposures and discouragement of smoking. PMID:29666655

Smoking induces long-lasting effects through a monoamine-oxidase epigenetic regulation.

PubMed

Launay, Jean-Marie; Del Pino, Muriel; Chironi, Gilles; Callebert, Jacques; Peoc'h, Katell; Mégnien, Jean-Louis; Mallet, Jacques; Simon, Alain; Rendu, Francine

2009-11-23

Postulating that serotonin (5-HT), released from smoking-activated platelets could be involved in smoking-induced vascular modifications, we studied its catabolism in a series of 115 men distributed as current smokers (S), never smokers (NS) and former smokers (FS) who had stopped smoking for a mean of 13 years. 5-HT, monoamine oxidase (MAO-B) activities and amounts were measured in platelets, and 5-hydroxyindolacetic acid (5-HIAA)--the 5-HT/MAO catabolite--in plasma samples. Both platelet 5-HT and plasma 5-HIAA levels were correlated with the 10-year cardiovascular Framingham relative risk (P<0.01), but these correlations became non-significant after adjustment for smoking status, underlining that the determining risk factor among those taken into account in the Framingham risk calculation was smoking. Surprisingly, the platelet 5-HT content was similar in S and NS but lower in FS with a parallel higher plasma level of 5-HIAA in FS. This was unforeseen since MAO-B activity was inhibited during smoking (P<0.00001). It was, however, consistent with a higher enzyme protein concentration found in S and FS than in NS (P<0.001). It thus appears that MAO inhibition during smoking was compensated by a higher synthesis. To investigate the persistent increase in MAO-B protein concentration, a study of the methylation of its gene promoter was undertaken in a small supplementary cohort of similar subjects. We found that the methylation frequency of the MAOB gene promoter was markedly lower (P<0.0001) for S and FS vs. NS due to cigarette smoke-induced increase of nucleic acid demethylase activity. This is one of the first reports that smoking induces an epigenetic modification. A better understanding of the epigenome may help to further elucidate the physiopathology and the development of new therapeutic approaches to tobacco addiction. The results could have a larger impact than cardiovascular damage, considering that MAO-dependent 5-HT catabolism is also involved in

Development of a long-term ovine model of cutaneous burn and smoke inhalation injury and the effects of early excision and skin autografting

PubMed Central

Yamamoto, Yusuke; Enkhbaatar, Perenlei; Sakurai, Hiroyuki; Rehberg, Sebastian; Asmussen, Sven; Ito, Hiroshi; Sousse, Linda E.; Cox, Robert A.; Deyo, Donald J.; Traber, Lillian D.; Traber, Maret G.; Herndon, David N.; Traber, Daniel L.

2013-01-01

Smoke inhalation injury frequently increases the risk of pneumonia and mortality in burn patients. The pathophysiology of acute lung injury secondary to burn and smoke inhalation is well studied, but long-term pulmonary function, especially the process of lung tissue healing following burn and smoke inhalation, has not been fully investigated. By contrast, early burn excision has become the standard of care in the management of major burn injury. While many clinical studies and small-animal experiments support the concept of early burn wound excision, and show improved survival and infectious outcomes, we have developed a new chronic ovine model of burn and smoke inhalation injury with early excision and skin grafting that can be used to investigate lung pathophysiology over a period of 3 weeks. Materials and methods Eighteen female sheep were surgically prepared for this study under isoflurane anesthesia. The animals were divided into three groups: an Early Excision group (20% TBSA, third-degree cutaneous burn and 36 breaths of cotton smoke followed by early excision and skin autografting at 24 h after injury, n = 6), a Control group (20% TBSA, third-degree cutaneous burn and 36 breaths of cotton smoke without early excision, n = 6) and a Sham group (no injury, no early excision, n = 6). After induced injury, all sheep were placed on a ventilator and fluid-resuscitated with Lactated Ringers solution (4 mL/% TBS/kg). At 24 h post-injury, early excision was carried out to fascia, and skin grafting with meshed autografts (20/1000 in., 1:4 ratio) was performed under isoflurane anesthesia. At 48 h post-injury, weaning from ventilator was begun if PaO2/FiO2 was above 250 and sheep were monitored for 3 weeks. Results At 96 h post-injury, all animals were weaned from ventilator. There are no significant differences in PaO2/FiO2 between Early Excision and Control groups at any points. All animals were survived for 3 weeks without infectious complication in Early Excision

Cigarette smoke induced genotoxicity and respiratory tract pathology: evidence to support reduced exposure time and animal numbers in tobacco product testing

PubMed Central

Dalrymple, Annette; Ordoñez, Patricia; Thorne, David; Walker, David; Camacho, Oscar M.; Büttner, Ansgar; Dillon, Debbie; Meredith, Clive

2016-01-01

Abstract Many laboratories are working to develop in vitro models that will replace in vivo tests, but occasionally there remains a regulatory expectation of some in vivo testing. Historically, cigarettes have been tested in vivo for 90 days. Recently, methods to reduce and refine animal use have been explored. This study investigated the potential of reducing animal cigarette smoke (CS) exposure to 3 or 6 weeks, and the feasibility of separate lung lobes for histopathology or the Comet assay. Rats were exposed to sham air or CS (1 or 2 h) for 3 or 6 weeks. Respiratory tissues were processed for histopathological evaluation, and Alveolar type II cells (AEC II) isolated for the Comet assay. Blood was collected for Pig-a and micronucleus quantification. Histopathological analyses demonstrated exposure effects, which were generally dependent on CS dose (1 or 2 h, 5 days/week). Comet analysis identified that DNA damage increased in AEC II following 3 or 6 weeks CS exposure, and the level at 6 weeks was higher than 3 weeks. Pig-a mutation or micronucleus levels were not increased. In conclusion, this study showed that 3 weeks of CS exposure was sufficient to observe respiratory tract pathology and DNA damage in isolated AEC II. Differences between the 3 and 6 week data imply that DNA damage in the lung is cumulative. Reducing exposure time, plus analyzing separate lung lobes for DNA damage or histopathology, supports a strategy to reduce and refine animal use in tobacco product testing and is aligned to the 3Rs (replacement, reduction and refinement). PMID:27160659

Cigarette smoke induced genotoxicity and respiratory tract pathology: evidence to support reduced exposure time and animal numbers in tobacco product testing.

PubMed

Dalrymple, Annette; Ordoñez, Patricia; Thorne, David; Walker, David; Camacho, Oscar M; Büttner, Ansgar; Dillon, Debbie; Meredith, Clive

2016-06-01

Many laboratories are working to develop in vitro models that will replace in vivo tests, but occasionally there remains a regulatory expectation of some in vivo testing. Historically, cigarettes have been tested in vivo for 90 days. Recently, methods to reduce and refine animal use have been explored. This study investigated the potential of reducing animal cigarette smoke (CS) exposure to 3 or 6 weeks, and the feasibility of separate lung lobes for histopathology or the Comet assay. Rats were exposed to sham air or CS (1 or 2 h) for 3 or 6 weeks. Respiratory tissues were processed for histopathological evaluation, and Alveolar type II cells (AEC II) isolated for the Comet assay. Blood was collected for Pig-a and micronucleus quantification. Histopathological analyses demonstrated exposure effects, which were generally dependent on CS dose (1 or 2 h, 5 days/week). Comet analysis identified that DNA damage increased in AEC II following 3 or 6 weeks CS exposure, and the level at 6 weeks was higher than 3 weeks. Pig-a mutation or micronucleus levels were not increased. In conclusion, this study showed that 3 weeks of CS exposure was sufficient to observe respiratory tract pathology and DNA damage in isolated AEC II. Differences between the 3 and 6 week data imply that DNA damage in the lung is cumulative. Reducing exposure time, plus analyzing separate lung lobes for DNA damage or histopathology, supports a strategy to reduce and refine animal use in tobacco product testing and is aligned to the 3Rs (replacement, reduction and refinement).

Early History of Chronic Obstructive Pulmonary Disease 1808-1980.

PubMed

Watson, R Ann; Pride, Neil B

2016-01-01

COPD has become a more popular research area in the last 3 decades, yet the first clear descriptions of acute and chronic bronchitis were in 1808. This brief history, comprehensively referenced, leads us through the early developments in respiratory physiology and their applications. It emphasises the early history of chronic bronchitis and emphysema in the 19(th) and early 20(th) centuries, long before the dominant effects of cigarette smoking emerged. This remains relevant to developing countries today.

Coal home heating and environmental tobacco smoke in relation to lower respiratory illness in Czech children, from birth to 3 years of age

DOE Office of Scientific and Technical Information (OSTI.GOV)

Baker, R.J.; Hert-Picciotto, I.; Dostal, M.

2006-07-15

The objective of this study was to evaluate how indoor pollution from tobacco and home heating may adversely affect respiratory health in young children. A total of 452 children born 1994-1996 in two districts in the Czech Republic participated. Lower respiratory illness (LRI) diagnoses occurred more frequently in children from homes heated by coal (vs. other energy sources or distant furnaces; rate ratio (RR) = 1.45; 95% confidence interval (CI), 1.07-1.97). Maternal prenatal smoking and other adult smokers also increased LRI rates (respectively: RR = 1.48; 95% CI, 1.10-2.01; and RR = 1.29; 95% CI, 1.01-1.65). Cooking fuels (primarily electricity,more » natural gas, or propane) were not associated with LRI incidence. For children never breast-fed, coal home heating and mother's smoking conferred substantially greater risks: RR = 2.77 (95% CI, 1.45-5.27) and RR = 2.52 (95% CI, 1.31-4.85), respectively. This maternal smoking and coal home heating increased risk for LRI in the first 3 years of life, particularly in children not breast-fed.« less

Legislative smoking bans for reducing harms from secondhand smoke exposure, smoking prevalence and tobacco consumption.

PubMed

Frazer, Kate; Callinan, Joanne E; McHugh, Jack; van Baarsel, Susan; Clarke, Anna; Doherty, Kirsten; Kelleher, Cecily

2016-02-04

provided in this update, an increase of eight countries from the original review. The nature of the intervention precludes randomized controlled trials. Thirty-six studies used an interrupted time series study design, 23 studies use a controlled before-and-after design and 18 studies are before-and-after studies with no control group; six of these studies use a cohort design. Seventy-two studies reported health outcomes, including cardiovascular (44), respiratory (21), and perinatal outcomes (7). Eleven studies reported national mortality rates for smoking-related diseases. A number of the studies report multiple health outcomes. There is consistent evidence of a positive impact of national smoking bans on improving cardiovascular health outcomes, and reducing mortality for associated smoking-related illnesses. Effects on respiratory and perinatal health were less consistent. We found 24 studies evaluating the impact of national smoke-free legislation on smoking behaviour. Evidence of an impact of legislative bans on smoking prevalence and tobacco consumption is inconsistent, with some studies not detecting additional long-term change in existing trends in prevalence. Since the first version of this review was published, the current evidence provides more robust support for the previous conclusions that the introduction of a legislative smoking ban does lead to improved health outcomes through reduction in SHS for countries and their populations. The clearest evidence is observed in reduced admissions for acute coronary syndrome. There is evidence of reduced mortality from smoking-related illnesses at a national level. There is inconsistent evidence of an impact on respiratory and perinatal health outcomes, and on smoking prevalence and tobacco consumption.

DIFFERENTIAL GENE EXPRESSION INDUCED BY RESPIRATORY SYNCTIAL VIRUS IN HUMAN BRONCHIAL EPITHELIAL CELLS

EPA Science Inventory

Respiratory syncytial virus (RSV), a negative-stranded RNA virus, is a common viral pathogen for respiratory infection in both children and immunocompromised adults. Early host defense may play a critical role in determining the severity of the infection. To gain further insight ...

Maternal prenatal smoking, parental antisocial behavior, and early childhood physical aggression.

PubMed

Huijbregts, Stephan C J; Séguin, Jean R; Zoccolillo, Mark; Boivin, Michel; Tremblay, Richard E

2008-01-01

This study investigated joint effects of maternal prenatal smoking and parental history of antisocial behavior on physical aggression between ages 17 and 42 months in a population sample of children born in Québec (N = 1,745). An analysis of variance (ANOVA) showed significant main effects of maternal prenatal smoking and a significant interaction between maternal prenatal smoking and mother's history of antisocial behavior in the prediction of children's probability to display high and rising physical aggression. The interaction indicated that the effects of heavy smoking during pregnancy (> or =10 cigarettes/day) were greater when the mother also had a serious history of antisocial behavior. The effects remained significant after the introduction of control variables (e.g., hostile-reactive parenting, family functioning, parental separation/divorce, family income, and maternal education). Another significant interaction not accounted for by control variables was observed for maternal prenatal smoking and family income, indicating more serious effects of maternal prenatal smoking under relatively low-income, conditions. Both interactions indicate critical adversities that, in combination with maternal prenatal smoking, have supra-additive effects on (the development of) physical aggression during early childhood. These findings may have implications for the selection of intervention targets and strategies.

Early smoking initiation and associated factors among in-school male and female adolescents in seven African countries.

PubMed

Peltzer, K

2011-09-01

This report examines the prevalence and common correlates of early smoking initiation among male and female school children across seven African countries. The total sample included 17,725 school children aged 13 to 15 years from nationally representative samples in seven African countries. Univariate and multivariate analyses were conducted to assess the relationship between early smoking initiation, health compromising behaviours, mental distress, protective factors and socio-economic status variables. Overall 15.5% had experienced smoking initiation before age 14, with the percentages 20.1% among boys and 10.9% among girls. In multivariable analysis, early smoking initiation was among boys associated with ever drunk from alcohol use (OR = 4.73, p = 0.001), ever used drugs (OR = 2.36, p = 0.04) and ever had sex (OR = 1.63, p = 0.04). Among girls, it was associated with higher education (OR = 5.77, p = 0.001), ever drunk from alcohol use (OR = 4.76, p = 0.002), parental or guardian tobacco use (OR = 2.83, p = 0.001) and suicide ideation (OR = 2.05, p = 0.02). The study found a high prevalence of early smoking initiation among 13-15 year-olds in seven African countries. Various risk factors have been identified in boys and girls who initiate smoking before age 14, forming a distinct risk group in this setting. Specific interventions are needed for boys and girls in the preteen years, before smoking initiation.

Role of tachykinins in ozone-induced airway hyperresponsiveness to cigarette smoke in guinea pigs.

PubMed

Wu, Z X; Morton, R F; Lee, L Y

1997-09-01

Acute exposure to ozone (O3) induces airway hyperresponsiveness to various inhaled bronchoactive substances. Inhalation of cigarette smoke, a common inhaled irritant in humans, is known to evoke a transient bronchoconstrictive effect. To examine whether O3 increases airway responsiveness to cigarette smoke, effects of smoke inhalation challenge on total pulmonary resistance (RL) and dynamic lung compliance (Cdyn) were compared before and after exposure to O3 (1.5 ppm, 1 h) in anesthetized guinea pigs. Before O3 exposure, inhalation of two breaths of cigarette smoke (7 ml) at a low concentration (33%) induced a mild and reproducible bronchoconstriction that slowly developed and reached its peak (DeltaRL = 67 +/- 19%, DeltaCdyn = -29 +/- 6%) after a delay of >1 min. After exposure to O3 the same cigarette smoke inhalation challenge evoked an intense bronchoconstriction that occurred more rapidly, reaching its peak (DeltaRL = 620 +/- 224%, DeltaCdyn = -35 +/- 7%) within 20 s, and was sustained for >2 min. By contrast, sham exposure to room air did not alter the bronchomotor response to cigarette smoke challenge. Pretreatment with CP-99994 and SR-48968, the selective antagonists of neurokinin type 1 and 2 receptors, respectively, completely blocked the enhanced responses of RL and Cdyn to cigarette smoke challenge induced by O3. These results show that O3 exposure induces airway hyperresponsiveness to inhaled cigarette smoke and that the enhanced responses result primarily from the bronchoconstrictive effect of endogenous tachykinins.

[Respiratory symptoms and obstructive ventilatory disorder in Tunisian woman exposed to biomass].

PubMed

Kwas, H; Rahmouni, N; Zendah, I; Ghédira, H

2017-06-01

In some Tunisian cities, especially semi-urbanized, the exposure to the smoke produced during combustion of the biomass, main source of pollution of indoor air, remains prevalent among non-smoking women. To assess the relationship between exposure to biomass smoke and the presence of obstructive ventilatory disorder in the non-smoking women in semi-urban areas of Tunisia. Cross etiological study, using a questionnaire, including 140 non-smoking women responsible for cooking and/or exposed during heating by traditional means with objective measurement of their respiratory functions. We found 81 women exposed to biomass for a period > or equal to 20 hours-years and 59 unexposed women. Exposed women reported more respiratory symptoms namely exertional dyspnea and/or chronic cough than unexposed. Of the 140 women, 14 women have an FEV/FEV6 <70 % of which 13 are exposed to biomass. We found a correlation between respiratory symptoms and obstructive ventilatory disorder in exposed women. The air pollution inside the home during the traditional activities of cooking and/or heating is a respiratory risk factor for non-smoking women over the age of 30 years. Exposure to biomass smoke can cause chronic respiratory symptoms and persistent obstructive ventilatory disorder that can be consistent with COPD. Copyright © 2017 Elsevier Masson SAS. All rights reserved.

Nicotinic receptor involvement in antinociception induced by exposure to cigarette smoke.

PubMed

Simons, Christopher T; Cuellar, Jason M; Moore, Justin A; Pinkerton, Kent E; Uyeminami, Dale; Carstens, Mirela Iodi; Carstens, E

2005-12-02

Direct exposure of rats to tobacco smoke induces antinociception. We presently investigated if this antinociception is mediated via nicotinic and/or mu-opioid receptors. Adult male rats were surgically implanted with Alzet osmotic minipumps that delivered either saline (control), the nicotinic antagonist mecamylamine, or the opiate antagonist naltrexone (3 mg/kg/day i.v. for 21 days). Nocifensive responses were assessed on alternate days using tail-flick reflex latency (TFL) over a 3-week period. During the second week, the rats were exposed to concentrated cigarette smoke in an environmental chamber for 6 h/day for 5 consecutive days; a control group was similarly exposed to filtered cigarette smoke. Rats receiving mecamylamine and naltrexone exhibited a significant weight loss after the first day of infusion. All treatment groups additionally exhibited significant weight loss during exposure to unfiltered or filtered smoke. The saline group exhibited significant antinociception on the first day of smoke exposure with rapid development of tolerance. The mecamylamine and naltrexone groups did not exhibit significant antinociception. Controls exposed to filtered smoke (with approximately 50% lower nicotine concentration) also exhibited significant analgesia on the first exposure day with rapid development of tolerance. Exposure to high levels of cigarette smoke, or to filtered smoke with a lower nicotine concentration in the vapor phase, induces antinociception with rapid development of tolerance. The antinociceptive effect appears to be mediated via nicotinic and mu-opioid receptors.

A new experimental model of cigarette smoke-induced emphysema in Wistar rats*, **

PubMed Central

Kozma, Rodrigo de las Heras; Alves, Edson Marcelino; Barbosa-de-Oliveira, Valter Abraão; Lopes, Fernanda Degobbi Tenorio Quirino dos Santos; Guardia, Renan Cenize; Buzo, Henrique Vivi; de Faria, Carolina Arruda; Yamashita, Camila; Cavazzana, Manzelio; Frei, Fernando; Ribeiro-Paes, Maria José de Oliveira; Ribeiro-Paes, João Tadeu

2014-01-01

OBJECTIVE: To describe a new murine model of cigarette smoke-induced emphysema. METHODS: Twenty-four male Wistar rats were divided into two groups: the cigarette smoke group, comprising 12 rats exposed to smoke from 12 commercial filter cigarettes three times a day (a total of 36 cigarettes per day) every day for 30 weeks; and the control group, comprising 12 rats exposed to room air three times a day every day for 30 weeks. Lung function was assessed by mechanical ventilation, and emphysema was morphometrically assessed by measurement of the mean linear intercept (Lm). RESULTS: The mean weight gain was significantly (approximately ten times) lower in the cigarette smoke group than in the control group. The Lm was 25.0% higher in the cigarette smoke group. There was a trend toward worsening of lung function parameters in the cigarette smoke group. CONCLUSIONS: The new murine model of cigarette smoke-induced emphysema and the methodology employed in the present study are effective and reproducible, representing a promising and economically viable option for use in studies investigating the pathophysiology of and therapeutic approaches to COPD. PMID:24626269

Student seminar on smoking: A novel way to introduce different perspectives on smoking to medical students.

PubMed

Iqbal, Saima P; Rafi, Shahid; Rahman, Matiur

2013-03-01

The respiratory module at Shifa College of Medicine (SCM) is delivered in third year with emphasis on respiratory pathophysiology and respiratory medicine. Smoking as a topic was introduced to emphasize the preventive aspects of respiratory illnesses. An innovative approach to involve students in their learning was developed. To determine whether this innovation would be well received and effective for students' learning about smoking, we carried out this study. This is a one group post-test quasi-experiment. Two days were assigned for a smoking seminar. The class of 106 students was divided into 10 batches, and each batch was assigned a theme related to smoking. These themes were developed by the faculty, and each theme was related to a different perspective on smoking. A post-test questionnaire was distributed at the end of the seminar for feedback to see what aspects of students' learning were highlighted and what needed to be improved upon. Questions related to the usefulness of the activity were incorporated into the questionnaire and the students were asked to agree or disagree on a five-point Likert scale. Most (68.3%) students agreed that this activity improved their knowledge regarding smoking, and 54.8% agreed that it also helped in application of this knowledge. Improvement in presentation and counseling skills (59.8%), evidence-based medicine (47.6%), and softer skills, such as teamwork (72%) and creativity (63.4%), were also reported to be enhanced. Seminars led by the students have shown to be effective in breaking the monotony and generating an interest of the topic. Such an activity serves as a small step to make our graduates more empathic, humane, competent, and skilful.

Cigarette smoking: an epidemiological overview.

PubMed

Wald, N J; Hackshaw, A K

1996-01-01

The detailed mortality and morbidity statistics on smoking tend to conceal the overall impact of the habit on health. About 3 million people die each year from smoking in economically developed countries, half of them before the age of 70. Cancers of eight sites are recognized as being caused by smoking--lung cancer almost entirely and the others (upper respiratory, bladder, pancreas, oesophagus, stomach, kidney, leukaemia) to a substantial extent. Six other potentially fatal diseases are also judged to be caused by smoking: respiratory heart disease, chronic obstructive lung disease, stroke, pneumonia, aortic aneurysm and ischaemic heart disease, the most common cause of death in economically developed countries. Non-fatal diseases, such as peripheral vascular disease, cataracts, hip fracture, and periodontal disease, which cause appreciable disability, cost and inconvenience are also caused by smoking. In pregnancy, smoking increases the risk of limb reduction defects, spontaneous abortion, ectopic pregnancy, and low birth weight. While there are some diseases for which smoking shows a protective effect, the 'benefits' of these are negligible in relation to the illness and premature mortality caused by smoking. About 20% of all deaths in developed countries are caused by smoking; an enormous human cost which can be completely avoided.

Longitudinal study of parental smoking habits and development of asthma in early childhood.

PubMed

Kanoh, Miki; Kaneita, Yoshitaka; Hara, Megumi; Harada, Shohei; Gon, Yasuhiro; Kanamaru, Hiroshi; Ohida, Takashi

2012-01-01

This study examined the association between parental smoking habits and the development of asthma in early childhood by using representative samples. The survey subjects included all of the 53,575 babies born in Japan during the periods January 10-17 and July 10-17, 2001. The families of the subjects were asked to complete questionnaires that were delivered by post at 6 months, 1 year 6 months, 2 years 6 months, 3 years 6 months, and 4 years 6 months postpartum. The first survey contained questions regarding the smoking habits of the parents. The second to fifth surveys asked if the child had needed medical attention for the treatment of asthma. Data from 36,888 subjects (collection rate: 68.9%) were analyzed. The 4-year cumulative incidence of asthma was 12.0%. Maternal indoor smoking significantly increased the risk of asthma development in children, 4-year risk 14.4% vs. 11.7%, risk ratio=1.24, 95% CI: 1.11 to 1.38. No statistically significant association was found between paternal smoking and asthma development in children. In order to prevent the development of asthma in early childhood, it is necessary to formulate measures to stop or discourage maternal smoking. Copyright © 2011. Published by Elsevier Inc.

Early Childhood Household Smoke Exposure Predicts Less Task-Oriented Classroom Behavior at Age 10

ERIC Educational Resources Information Center

Pagani, Linda S.; Fitzpatrick, Caroline

2016-01-01

Secondhand tobacco smoke is considered a developmental neurotoxicant especially given underdeveloped vital systems in young children. An ecological test of its negative influence on brain development can be made by examining the prospective association between early childhood household smoke exposure and later classroom behavior. Using a…

Changes in hospitalizations for chronic respiratory diseases after two successive smoking bans in Spain

PubMed Central

Simón, Lorena; Boldo, Elena; Ortiz, Cristina; Fernández-Cuenca, Rafael; Linares, Cristina; Medrano, María José; Pastor-Barriuso, Roberto

2017-01-01

Background Existing evidence on the effects of smoke-free policies on respiratory diseases is scarce and inconclusive. Spain enacted two consecutive smoke-free regulations: a partial ban in 2006 and a comprehensive ban in 2011. We estimated their impact on hospital admissions via emergency departments for chronic obstructive pulmonary disease (COPD) and asthma. Methods Data for COPD (ICD-9 490–492, 494–496) came from 2003–2012 hospital admission records from the fourteen largest provinces of Spain and from five provinces for asthma (ICD-9 493). We estimated changes in hospital admission rates within provinces using Poisson additive models adjusted for long-term linear trends and seasonality, day of the week, temperature, influenza, acute respiratory infections, and pollen counts (asthma models). We estimated immediate and gradual effects through segmented-linear models. The coefficients within each province were combined through random-effects multivariate meta-analytic models. Results The partial ban was associated with a strong significant pooled immediate decline in COPD-related admission rates (14.7%, 95%CI: 5.0, 23.4), sustained over time with a one-year decrease of 13.6% (95%CI: 2.9, 23.1). The association was consistent across age and sex groups but stronger in less economically developed Spanish provinces. Asthma-related admission rates decreased by 7.4% (95%CI: 0.2, 14.2) immediately after the comprehensive ban was implemented, although the one-year decrease was sustained only among men (9.9%, 95%CI: 3.9, 15.6). Conclusions The partial ban was associated with an immediate and sustained strong decline in COPD-related admissions, especially in less economically developed provinces. The comprehensive ban was related to an immediate decrease in asthma, sustained for the medium-term only among men. PMID:28542337

Nicotine Dependence, “Background” and Cue-Induced Craving and Smoking in the Laboratory

PubMed Central

Dunbar, Michael S.; Shiffman, Saul; Kirchner, Thomas; Tindle, Hilary; Scholl, Sarah

2014-01-01

Background Nicotine dependence has been associated with higher “background” craving and smoking, independent of situational cues. Due in part to conceptual and methodological differences across past studies, the relationship between dependence and cue-reactivity (CR; e.g., cue-induced craving and smoking) remains unclear. Methods 207 daily smokers completed six pictorial CR sessions (smoking, negative affect, positive affect, alcohol, smoking prohibitions, and neutral). Individuals rated craving before (background craving) and after cues, and could smoke following cue exposure. Session videos were coded to assess smoking. Participants completed four nicotine dependence measures. Regression models assessed the relationship of dependence to cue-independent (i.e., pre-cue) and cue-specific (i.e., pre-post cue change for each cue, relative to neutral) craving and smoking (likelihood of smoking, latency to smoke, puff count). Results Dependence was associated with background craving and smoking, but did not predict change in craving across the entire sample for any cue. Among alcohol drinkers, dependence was associated with greater increases in craving following the alcohol cue. Only one dependence measure (Wisconsin Inventory of Smoking Dependence Motives) was consistently associated with smoking reactivity (higher likelihood of smoking, shorter latency to smoke, greater puff count) in response to cues. Conclusion While related to cue-independent background craving and smoking, dependence is not strongly associated with laboratory cue-induced craving under conditions of minimal deprivation. Dependence measures that incorporate situational influences on smoking correlate with greater cue-provoked smoking. This may suggest independent roles for CR and traditional dependence as determinants of smoking, and highlights the importance of assessing behavioral CR outcomes. PMID:25028339

Bacoside A: Role in Cigarette Smoking Induced Changes in Brain

PubMed Central

Vani, G.; Anbarasi, K.; Shyamaladevi, C. S.

2015-01-01

Cigarette smoking (CS) is a major health hazard that exerts diverse physiologic and biochemical effects mediated by the components present and generated during smoking. Recent experimental studies have shown predisposition to several biological consequences from both active and passive cigarette smoke exposure. In particular, passive smoking is linked to a number of adverse health effects which are equally harmful as active smoking. A pragmatic approach should be considered for designing a pharmacological intervention to combat the adverse effects of passive smoking. This review describes the results from a controlled experimental condition, testing the effect of bacoside A (BA) on the causal role of passive/secondhand smoke exposure that caused pathological and neurological changes in rat brain. Chronic exposure to cigarette smoke induced significant changes in rat brain histologically and at the neurotransmitter level, lipid peroxidation states, mitochondrial functions, membrane alterations, and apoptotic damage in rat brain. Bacoside A is a neuroactive agent isolated from Bacopa monnieri. As a neuroactive agent, BA was effective in combating these changes. Future research should examine the effects of BA at molecular level and assess its functional effects on neurobiological and behavioral processes associated with passive smoke. PMID:26413118

Bacoside A: Role in Cigarette Smoking Induced Changes in Brain.

PubMed

Vani, G; Anbarasi, K; Shyamaladevi, C S

2015-01-01

Cigarette smoking (CS) is a major health hazard that exerts diverse physiologic and biochemical effects mediated by the components present and generated during smoking. Recent experimental studies have shown predisposition to several biological consequences from both active and passive cigarette smoke exposure. In particular, passive smoking is linked to a number of adverse health effects which are equally harmful as active smoking. A pragmatic approach should be considered for designing a pharmacological intervention to combat the adverse effects of passive smoking. This review describes the results from a controlled experimental condition, testing the effect of bacoside A (BA) on the causal role of passive/secondhand smoke exposure that caused pathological and neurological changes in rat brain. Chronic exposure to cigarette smoke induced significant changes in rat brain histologically and at the neurotransmitter level, lipid peroxidation states, mitochondrial functions, membrane alterations, and apoptotic damage in rat brain. Bacoside A is a neuroactive agent isolated from Bacopa monnieri. As a neuroactive agent, BA was effective in combating these changes. Future research should examine the effects of BA at molecular level and assess its functional effects on neurobiological and behavioral processes associated with passive smoke.

Duox2-induced innate immune responses in the respiratory epithelium and intranasal delivery of Duox2 DNA using polymer that mediates immunization.

PubMed

Jeon, Yung Jin; Kim, Hyun Jik

2018-05-01

Respiratory mucosa especially nasal epithelium is well known as the first-line barrier of air-borne pathogens. High levels of reactive oxygen species (ROS) are detected in in vitro cultured human epithelial cells and in vivo lung. With identification of NADPH oxidase (Nox) system of respiratory epithelium, the antimicrobial role of ROS has been studied. Duox2 is the most abundant Nox isoform and produces the regulated amount of ROS in respiratory epithelium. Duox2-derived ROS are involved in antiviral innate immune responses but more studies are needed to verify the mechanism. In respiratory epithelium, Duox2-derived ROS is critical for recognition of virus through families retinoic acid-inducible gene-I (RIG-I) and melanoma differentiation-associated protein 5 (MDA5) at the early stage of antiviral innate immune responses. Various secreted interferons (IFNs) play essential roles for antiviral host defense by downstream cell signaling, and transcription of IFN-stimulated genes is started to suppress viral replication. Type I and type III IFNs are verified more responsible for influenza A virus (IAV) infection in respiratory epithelium and Duox2 is required to regulate IFN-related immune responses. Transient overexpression of Duox2 using cationic polymer polyethylenimine (PEI) induces secretion of type I and type III IFNs and significantly attenuated IAV replication in respiratory epithelium. Here, we discuss Duox2-mediated antiviral innate immune responses and the role of Duox2 as a mucosal vaccine to resist respiratory viral infection.

[Smoking at workplace - Legislation and health aspect of exposure to second-hand tobacco smoke].

PubMed

Lipińska-Ojrzanowska, Agnieszka; Polańska, Kinga; Wiszniewska, Marta; Kleniewska, Aneta; Dörre-Kolasa, Dominika; Walusiak-Skorupa, Jolanta

2015-01-01

Tobacco smoke contains thousands of xenobiotics harmful to human health. Their irritant, toxic and carcinogenic potential has been well documented. Passive smoking or exposure to second-hand smoke (SHS) in public places, including workplace, poses major medical problems. Owing to this fact there is a strong need to raise workers' awareness of smoking-related hazards through educational programs and to develop and implement legislation aimed at eliminating SHS exposure. This paper presents a review of reports on passive exposure to tobacco smoke and its impact on human health and also a review of binding legal regulations regarding smoking at workplace in Poland. It has been proved that exposure to tobacco smoke during pregnancy may lead to, e.g., preterm delivery and low birth weight, sudden infant death syndrome, lung function impairment, asthma and acute respiratory illnesses in the future. Exposure to tobacco smoke, only in the adult age, is also considered as an independent risk factor of cardiovascular diseases, acute and chronic respiratory diseases and cancer. Raising public awareness of tobacco smoke harmfulness should be a top priority in the field of workers' health prevention. Occupational medicine physicians have regular contacts with occupationally active people who smoke. Thus, occupational health services have a unique opportunity to increase employees and employers' awareness of adverse health effects of smoking and their prevention. This work is available in Open Access model and licensed under a CC BY-NC 3.0 PL license.

Equine respiratory pharmacology.

PubMed

Foreman, J H

1999-12-01

Differentiation of diseases of the equine respiratory tract is based on history, clinical signs, auscultation, endoscopy, imaging, and sampling of airway exudate. Upper respiratory therapies include surgical correction of airway obstructions; flushing of localized abscesses (strangles), guttural pouch disease, or sinusitis; and oral or parenteral antibiotic and anti-inflammatory therapy if deemed necessary. Pneumonia usually is treated with antimicrobials, anti-inflammatories, and bronchodilators. Pleural drainage is indicated if significant pleural effusion is present. The most commonly used therapies for early inflammatory and chronic allergic obstructive conditions include bronchodilators and anti-inflammatories. Acute respiratory distress, particularly acute pulmonary edema, is treated with diuretics (usually furosemide), intranasal oxygen, bronchodilators, corticosteroids, and alleviation of the underlying cause. Furosemide also had been used in North America as a race-day preventative for exercise-induced pulmonary hemorrhage (EIPH), but recent data have shown that furosemide may be a performance-enhancing agent itself.

Role of OSGIN1 in mediating smoking-induced autophagy in the human airway epithelium.

PubMed

Wang, Guoqing; Zhou, Haixia; Strulovici-Barel, Yael; Al-Hijji, Mohammed; Ou, Xuemei; Salit, Jacqueline; Walters, Matthew S; Staudt, Michelle R; Kaner, Robert J; Crystal, Ronald G

2017-07-03

Enhanced macroautophagy/autophagy is recognized as a component of the pathogenesis of smoking-induced airway disease. Based on the knowledge that enhanced autophagy is linked to oxidative stress and the DNA damage response, both of which are linked to smoking, we used microarray analysis of the airway epithelium to identify smoking upregulated genes known to respond to oxidative stress and the DNA damage response. This analysis identified OSGIN1 (oxidative stress induced growth inhibitor 1) as significantly upregulated by smoking, in both the large and small airway epithelium, an observation confirmed by an independent small airway microarray cohort, TaqMan PCR of large and small airway samples and RNA-Seq of small airway samples. High and low OSGIN1 expressors have different autophagy gene expression patterns in vivo. Genome-wide correlation of RNAseq analysis of airway basal/progenitor cells showed a direct correlation of OSGIN1 mRNA levels to multiple classic autophagy genes. In vitro cigarette smoke extract exposure of primary airway basal/progenitor cells was accompanied by a dose-dependent upregulation of OSGIN1 and autophagy induction. Lentivirus-mediated expression of OSGIN1 in human primary basal/progenitor cells induced puncta-like staining of MAP1LC3B and upregulation of MAP1LC3B mRNA and protein and SQSTM1 mRNA expression level in a dose and time-dependent manner. OSGIN1-induction of autophagosome, amphisome and autolysosome formation was confirmed by colocalization of MAP1LC3B with SQSTM1 or CD63 (endosome marker) and LAMP1 (lysosome marker). Both OSGIN1 overexpression and knockdown enhanced the smoking-evoked autophagic response. Together, these observations support the concept that smoking-induced upregulation of OSGIN1 is one link between smoking-induced stress and enhanced-autophagy in the human airway epithelium.

Do parents who smoke underutilize health care services for their children? A cross sectional study within the longitudinal PIAMA study.

PubMed

Jacobs-van der Bruggen, Monique A M; Wijga, Alet H; Brunekreef, Bert; de Jongste, Johan C; Baan, Caroline A; Kerkhof, Marjan; Smit, Henriette A

2007-06-12

A higher prevalence of respiratory symptoms and an associated increase in health care utilization among children with parents who smoke is to be expected. From previous studies however, it appears that parents who smoke may underutilize health services for their children, especially with respect to respiratory care. This study explores the validity and generalizability of the previous assumption. Data were obtained from a Dutch birth-cohort study; the Prevention and Incidence of Asthma and Mite Allergy (PIAMA) project. Information regarding parental smoking, the child's respiratory symptoms and health care use and potential confounders were obtained by postal questionnaires. Multivariate logistic models were used to relate parental smoking to the child's respiratory symptoms and health care use. The study comprised 3,564, 4-year old children. In the crude analysis, respiratory symptoms were more frequent among children with a parent who smoked, while health care utilization for respiratory symptoms was not significantly different between children with or without a parent who smoked. In the multivariate analyses, maternal smoking had a larger impact on the child's respiratory symptoms and health care use as compared to paternal smoking. Maternal smoking was positively associated with mild respiratory symptoms of the child, adjusted odds ratio [AOR] 1.50 (1.19-1.91), but not with severe respiratory symptoms AOR 1.03 (0.75-1.40). Among children with mild respiratory symptoms, children with a mother who smoked were less likely to be taken to the general practitioner (GP) for respiratory symptoms, than children with mothers who did not smoke, AOR 0.58 (0.33-1.01). This finding was less pronounced among children with severe respiratory symptoms AOR 0.86 (0.49-1.52). Neither GP visits for non-respiratory symptoms nor specialized care for respiratory disease were significantly associated with parental smoking. Mothers who smoke appear to underutilize health care for their

Role of chymase in cigarette smoke-induced pulmonary artery remodeling and pulmonary hypertension in hamsters.

PubMed

Wang, Tao; Han, Su-Xia; Zhang, Shang-Fu; Ning, Yun-Ye; Chen, Lei; Chen, Ya-Juan; He, Guang-Ming; Xu, Dan; An, Jin; Yang, Ting; Zhang, Xiao-Hong; Wen, Fu-Qiang

2010-03-31

Cigarette smoking is an important risk factor for pulmonary arterial hypertension (PAH) in chronic obstructive pulmonary disease (COPD). Chymase has been shown to function in the enzymatic production of angiotensin II (AngII) and the activation of transforming growth factor (TGF)-beta1 in the cardiovascular system. The aim of this study was to determine the potential role of chymase in cigarette smoke-induced pulmonary artery remodeling and PAH. Hamsters were exposed to cigarette smoke; after 4 months, lung morphology and tissue biochemical changes were examined using immunohistochemistry, Western blotting, radioimmunoassay and reverse-transcription polymerase chain reaction. Our results show that chronic cigarette smoke exposure significantly induced elevation of right ventricular systolic pressures (RVSP) and medial hypertrophy of pulmonary arterioles in hamsters, concurrent with an increase of chymase activity and synthesis in the lung. Elevated Ang II levels and enhanced TGF-beta1/Smad signaling activation were also observed in smoke-exposed lungs. Chymase inhibition with chymostatin reduced the cigarette smoke-induced increase in chymase activity and Ang II concentration in the lung, and attenuated the RVSP elevation and the remodeling of pulmonary arterioles. Chymostatin did not affect angiotensin converting enzyme (ACE) activity in hamster lungs. These results suggest that chronic cigarette smoke exposure can increase chymase activity and expression in hamster lungs. The capability of activated chymase to induce Ang II formation and TGF-beta1 signaling may be part of the mechanism for smoking-induced pulmonary vascular remodeling. Thus, our study implies that blockade of chymase might provide benefits to PAH smokers.

Evaluation of whole cigarette smoke induced oxidative stress in A549 and BEAS-2B cells.

PubMed

Zhang, Shimin; Li, Xiang; Xie, Fuwei; Liu, Kejian; Liu, Huimin; Xie, Jianping

2017-09-01

Cigarette smoke is a complex and oxidative aerosol. Previous researches on the hazards of cigarette smoke mainly focused on the adverse bioeffects induced by its condensates or gas vapor phase, which ignored the dynamic processes of smoking and the cigarette smoke aging. To overcome these disadvantages, we performed air-liquid interface exposure of whole smoke, which used native and unmodified smoke and ensured the exposure similar to physiological inhalation. Our results indicated that whole cigarette smoke induced lung epithelial cells (A549) and bronchial epithelial cells (BEAS-2B) damages in cytotoxicity assays (methyl thiazoly tetrazolium and neutral red uptake assays). In addition, A549 and BEAS-2B cells showed oxidative damages in whole smoke exposure, with concentration change of several biomarkers (reduced and oxidized glutathione, malondialdehyde, 4-hydroxyhydroxy-2-nonenal, extracellular superoxide dismutase, and 8-hydroxyl deoxyguanosine). These results indicate that whole smoke-induced oxidative stress occurs in two different kinds of cells at air-liquid interface. Copyright © 2017 Elsevier B.V. All rights reserved.

FORMALDEHYDE-INDUCED GENE EXPRESSION IN F344 RAT NASAL RESPIRATORY EPITHELIUM.

EPA Science Inventory

Formaldehyde-induced gene expression in F344 rat nasal respiratory epithelium

ABSTRACT

Formaldehyde, an occupational and environmental toxicant used extensively in the manufacturing of many household and personal use products, is known to induce squamous cell carci...

Early Childhood Household Smoke Exposure Predicts Less Task-Oriented Classroom Behavior at Age 10.

PubMed

Pagani, Linda S; Fitzpatrick, Caroline

2016-10-01

Secondhand tobacco smoke is considered a developmental neurotoxicant especially given underdeveloped vital systems in young children. An ecological test of its negative influence on brain development can be made by examining the prospective association between early childhood household smoke exposure and later classroom behavior. Using a longitudinal birth cohort, we examined the unique contribution of household tobacco smoke exposure to children's subsequent classroom engagement at age 10. From child ages 1.5 to 7 years, parents of 2,055 participants from the Quebec Longitudinal Study of Child Development reported on household smoking by themselves and other home occupants. At age 10, fourth-grade teachers reported on the child's classroom engagement. In terms of prevalence, 58% of parents reported that their children were never exposed to smoke in the home, while 34% and 8% of children were exposed to transient and continuous household smoke, respectively. Compared with never exposed children, those who were exposed to transient and continuous household smoke scored 13% and 9% of a standard deviation lower on classroom engagement in fourth grade, standardized B = -.128 (95% confidence interval = -.186, -.069) and standardized B = -.093 (95% confidence interval = -.144, -.043), respectively. Compared with their never exposed peers, children exposed to transient and continuous early childhood household smoke showed proportionately less classroom engagement, which reflects task-orientation, following directions, and working well autonomously and with others. This predisposition poses risks for high school dropout, which from a population health perspective is closely linked with at-risk lifestyle habits and unhealthy outcomes. © 2015 Society for Public Health Education.

Effect of smoking on gene expression profile - overall mechanism, impact on respiratory system function, and reference to electronic cigarettes.

PubMed

Kopa, Paulina Natalia; Pawliczak, Rafał

2018-07-01

Cigarette smoke has a crucial impact on transcriptome alteration by its effect on chromatin remodeling and DNA methylation status. The first mechanism is associated with the histone acetylation/deacetylation balance damage as a result of increased activity of NFĸB and lipid peroxidation products, which lead to an increased activity of HATs and DNMTs and reduced HDACs. The second mechanism is connected with direct damaging of DNA by smoke components, activation of downstream repair mechanism and recruitment of DNMTs into the breakage site, 'nicotine effect' and carbon monoxide (CO) activity on gene transcription and DNA methylation reduction. Cigarette smoking activates oxidative and inflammatory response and leads to uncontrolled structural changes in airways and alters gene expression. Such changes have a characteristic similar to that for COPD patients. Therefore, smoking is determined as a key risk factor for chronic respiratory disease development. Furthermore, electronic cigarettes, an alternative of tobacco cigarettes, also affect gene expression profile, which suggests some similarities in action mechanisms for both conventional and electronic cigarettes. However, there is only a limited number of trials discussing this issue and future investigations are needed.

Autophagy Has a Beneficial Role in Relieving Cigarette Smoke-Induced Apoptotic Death in Human Gingival Fibroblasts.

PubMed

Kim, Moon-Soo; Yun, Jeong-Won; Park, Jin-Ho; Park, Bong-Wook; Kang, Young-Hoon; Hah, Young-Sool; Hwang, Sun-Chul; Woo, Dong Kyun; Byun, June-Ho

2016-01-01

The deleterious role of cigarette smoke has long been documented in various human diseases including periodontal complications. In this report, we examined this adverse effect of cigarette smoke on human gingival fibroblasts (HGFs) which are critical not only in maintaining gingival tissue architecture but also in mediating immune responses. As well documented in other cell types, we also observed that cigarette smoke promoted cellular reactive oxygen species in HGFs. And we found that this cigarette smoke-induced oxidative stress reduced HGF viability through inducing apoptosis. Our results indicated that an increased Bax/Bcl-xL ratio and resulting caspase activation underlie the apoptotic death in HGFs exposed to cigarette smoke. Furthermore, we detected that cigarette smoke also triggered autophagy, an integrated cellular stress response. Interesting, a pharmacological suppression of the cigarette smoke-induced autophagy led to a further reduction in HGF viability while a pharmacological promotion of autophagy increased the viability of HGFs with cigarette smoke exposures. These findings suggest a protective role for autophagy in HGFs stressed with cigarette smoke, highlighting that modulation of autophagy can be a novel therapeutic target in periodontal complications with cigarette smoke.

Respiratory health effects of cannabis: position statement of the Thoracic Society of Australia and New Zealand.

PubMed

Taylor, D R; Hall, W

2003-07-01

Both the gaseous and the particulate phases of tobacco and cannabis smoke contain a similar range of harmful chemicals. However, differing patterns of inhalation mean that smoking a 'joint' of cannabis results in exposure to significantly greater amounts of combusted material than with a tobacco cigarette. The histopathological effects of cannabis smoke exposure include changes consistent with acute and chronic bronchitis. Cellular dysplasia has also been observed, suggesting that, like tobacco smoke, cannabis exposure has the potential to cause malignancy. These features are consistent with the clinical presentation. Symptoms of cough and early morning sputum production are common (20-25%) even in young individuals who smoke cannabis alone. Almost all studies indicate that the effects of cannabis and tobacco smoking are additive and independent. Public health education should dispel the myth that cannabis smoking is relatively safe by highlighting that the adverse respiratory effects of smoking cannabis are similar to those of smoking tobacco, even although it remains to be confirmed that smoking cannabis alone leads to the development of chronic lung disease.

A neuronal mechanism of propofol-induced central respiratory depression in newborn rats.

PubMed

Kashiwagi, Masanori; Okada, Yasumasa; Kuwana, Shun-Ichi; Sakuraba, Shigeki; Ochiai, Ryoichi; Takeda, Junzo

2004-07-01

The neural mechanisms of propofol-induced central respiratory depression remain poorly understood. In the present study, we studied these mechanisms and the involvement of gamma-aminobutyric acid (GABA)A receptors in propofol-induced central respiratory depression. The brainstem and the cervical spinal cord of 1- to 4-day-old rats were isolated, and preparations were maintained in vitro with oxygenated artificial cerebrospinal fluid. Rhythmic inspiratory burst activity was recorded from the C4 spinal ventral root. The activity of respiratory neurons in the ventrolateral medulla was recorded using a perforated patch-clamp technique. We found that bath-applied propofol decreased C4 inspiratory burst rate, which could be reversed by the administration of a GABAA antagonist, bicuculline. Propofol caused resting membrane potentials to hyperpolarize and suppressed the firing of action potentials in preinspiratory and expiratory neurons. In contrast, propofol had little effect on resting membrane potentials and action potential firing in inspiratory neurons. Our findings suggest that the depressive effects of propofol are, at least in part, mediated by the agonistic action of propofol on GABAA receptors. It is likely that the GABAA receptor-mediated hyperpolarization of preinspiratory neurons serves as the neuronal basis of propofol-induced respiratory depression in the newborn rat.

The NF-κB family member RelB regulates microRNA miR-146a to suppress cigarette smoke-induced COX-2 protein expression in lung fibroblasts.

PubMed

Zago, Michela; Rico de Souza, Angela; Hecht, Emelia; Rousseau, Simon; Hamid, Qutayba; Eidelman, David H; Baglole, Carolyn J

2014-04-21

Diseases due to cigarette smoke exposure, including chronic obstructive pulmonary disease (COPD) and lung cancer, are associated with chronic inflammation typified by the increased expression of cyclooxygenase-2 (COX-2) protein. RelB is an NF-κB family member that suppresses cigarette smoke induction of COX-2 through an unknown mechanism. The ability of RelB to regulate COX-2 expression may be via miR-146a, a miRNA that attenuates COX-2 in lung fibroblasts. In this study we tested whether RelB attenuation of cigarette smoke-induced COX-2 protein is due to miR-146a. Utilizing pulmonary fibroblasts deficient in RelB expression, together with siRNA knock-down of RelB, we show the essential role of RelB in diminishing smoke-induced COX-2 protein expression despite robust activation of the canonical NF-κB pathway and subsequent induction of Cox-2 mRNA. RelB did not regulate COX-2 protein expression at the level of mRNA stability. Basal levels of miR-146a were significantly lower in Relb-deficient cells and cigarette smoke increased miR-146a expression only in Relb-expressing cells. Inhibition of miR-146a had no effects on Relb expression or induction of Cox-2 mRNA by cigarette smoke but significantly increased COX-2 protein. These data highlight the potential of a RelB-miR-146a axis as a novel regulatory pathway that attenuates inflammation in response to respiratory toxicants. Copyright © 2014 Elsevier Ireland Ltd. All rights reserved.

Carbamylation of vimentin is inducible by smoking and represents an independent autoantigen in rheumatoid arthritis

PubMed Central

Ospelt, Caroline; Bang, Holger; Feist, Eugen; Camici, Giovanni; Keller, Stephan; Detert, Jacqueline; Krämer, Anette; Gay, Steffen; Ghannam, Khetam; Burmester, Gerd R

2017-01-01

Objectives Smoking has been connected to citrullination of antigens and formation of anti-citrullinated peptide antibodies (ACPAs) in rheumatoid arthritis (RA). Since smoking can modify proteins by carbamylation (formation of homocitrulline), this study was conducted to investigate these effects on vimentin in animal models and RA. Methods The efficiency of enzymatic carbamylation of vimentin was characterised. B-cell response was investigated after immunisation of rabbits with different vimentin isoforms. Effects of tobacco smoke exposure on carbamylation of vimentin and formation of autoantibodies were analysed in mice. The antibody responses against isoforms of vimentin were characterised with respect to disease duration and smoking status of patients with RA. Results Enzymatic carbamylation of vimentin was efficiently achieved. Subsequent citrullination of vimentin was not disturbed by homocitrullination. Sera from rabbits immunised with carbamylated vimentin (carbVim), in addition to carbVim also recognised human IgG-Fc showing rheumatoid factor-like reactivity. Smoke-exposed mice contained detectable amounts of carbVim and developed a broad immune response against carbamylated antigens. Although the prevalence of anti-carbamylated antibodies in smokers and non-smokers was similar, the titres of carbamylated antibodies were significantly increased in sera of smoking compared with non-smoking RA. CarbVim antibodies were observed independently of ACPAs in early phases of disease and double-positive patients for anti-mutated citrullinated vimentin (MCV) and anti-carbVim antibodies showed an extended epitope recognition pattern towards MCV. Conclusions Carbamylation of vimentin is inducible by cigarette smoke exposure. The polyclonal immune response against modified antigens in patients with RA is not exclusively citrulline-specific and carbamylation of antigens could be involved in the pathogenesis of disease. Trial registration number ISRCTN36745608; Eudra

Critical Review of Health Impacts of Wildfire Smoke Exposure.

PubMed

Reid, Colleen E; Brauer, Michael; Johnston, Fay H; Jerrett, Michael; Balmes, John R; Elliott, Catherine T

2016-09-01

Wildfire activity is predicted to increase in many parts of the world due to changes in temperature and precipitation patterns from global climate change. Wildfire smoke contains numerous hazardous air pollutants and many studies have documented population health effects from this exposure. We aimed to assess the evidence of health effects from exposure to wildfire smoke and to identify susceptible populations. We reviewed the scientific literature for studies of wildfire smoke exposure on mortality and on respiratory, cardiovascular, mental, and perinatal health. Within those reviewed papers deemed to have minimal risk of bias, we assessed the coherence and consistency of findings. Consistent evidence documents associations between wildfire smoke exposure and general respiratory health effects, specifically exacerbations of asthma and chronic obstructive pulmonary disease. Growing evidence suggests associations with increased risk of respiratory infections and all-cause mortality. Evidence for cardiovascular effects is mixed, but a few recent studies have reported associations for specific cardiovascular end points. Insufficient research exists to identify specific population subgroups that are more susceptible to wildfire smoke exposure. Consistent evidence from a large number of studies indicates that wildfire smoke exposure is associated with respiratory morbidity with growing evidence supporting an association with all-cause mortality. More research is needed to clarify which causes of mortality may be associated with wildfire smoke, whether cardiovascular outcomes are associated with wildfire smoke, and if certain populations are more susceptible. Reid CE, Brauer M, Johnston FH, Jerrett M, Balmes JR, Elliott CT. 2016. Critical review of health impacts of wildfire smoke exposure. Environ Health Perspect 124:1334-1343; http://dx.doi.org/10.1289/ehp.1409277.

Critical Review of Health Impacts of Wildfire Smoke Exposure

PubMed Central

Reid, Colleen E.; Brauer, Michael; Johnston, Fay H.; Jerrett, Michael; Balmes, John R.; Elliott, Catherine T.

2016-01-01

Background: Wildfire activity is predicted to increase in many parts of the world due to changes in temperature and precipitation patterns from global climate change. Wildfire smoke contains numerous hazardous air pollutants and many studies have documented population health effects from this exposure. Objectives: We aimed to assess the evidence of health effects from exposure to wildfire smoke and to identify susceptible populations. Methods: We reviewed the scientific literature for studies of wildfire smoke exposure on mortality and on respiratory, cardiovascular, mental, and perinatal health. Within those reviewed papers deemed to have minimal risk of bias, we assessed the coherence and consistency of findings. Discussion: Consistent evidence documents associations between wildfire smoke exposure and general respiratory health effects, specifically exacerbations of asthma and chronic obstructive pulmonary disease. Growing evidence suggests associations with increased risk of respiratory infections and all-cause mortality. Evidence for cardiovascular effects is mixed, but a few recent studies have reported associations for specific cardiovascular end points. Insufficient research exists to identify specific population subgroups that are more susceptible to wildfire smoke exposure. Conclusions: Consistent evidence from a large number of studies indicates that wildfire smoke exposure is associated with respiratory morbidity with growing evidence supporting an association with all-cause mortality. More research is needed to clarify which causes of mortality may be associated with wildfire smoke, whether cardiovascular outcomes are associated with wildfire smoke, and if certain populations are more susceptible. Citation: Reid CE, Brauer M, Johnston FH, Jerrett M, Balmes JR, Elliott CT. 2016. Critical review of health impacts of wildfire smoke exposure. Environ Health Perspect 124:1334–1343; http://dx.doi.org/10.1289/ehp.1409277 PMID:27082891

Association of established smoking among adolescents with timing of exposure to smoking depicted in movies.

PubMed

Primack, Brian A; Longacre, Meghan R; Beach, Michael L; Adachi-Mejia, Anna M; Titus, Linda J; Dalton, Madeline A

2012-04-04

It is not known whether exposure to smoking depicted in movies carries greater influence during early or late adolescence. We aimed to quantify the independent relative contribution to established smoking of exposure to smoking depicted in movies during both early and late adolescence. We prospectively assessed 2049 nonsmoking students recruited from 14 randomly selected public schools in New Hampshire and Vermont. At baseline enrollment, students aged 10-14 years completed a written survey to determine personal, family, and sociodemographic characteristics and exposure to depictions of smoking in the movies (early exposure). Seven years later, we conducted follow-up telephone interviews to ascertain follow-up exposure to movie smoking (late exposure) and smoking behavior. We used multiple regression models to assess associations between early and late exposure and development of established smoking. One-sixth (17.3%) of the sample progressed to established smoking. In analyses that controlled for covariates and included early and late exposure in the same model, we found that students in the highest quartile for early exposure had 73% greater risk of established smoking than those in the lowest quartile for early exposure (27.8% vs 8.6%; relative risk for Q4 vs Q1 = 1.73, 95% confidence interval = 1.14 to 2.62). However, late exposure to depictions of smoking in movies was not statistically significantly associated with established smoking (22.1% vs 14.0%; relative risk for Q4 vs Q1 = 1.13, 95% confidence interval = 0.89 to 1.44). Whereas 31.6% of established smoking was attributable to early exposure, only an additional 5.3% was attributable to late exposure. Early exposure to smoking depicted in movies is associated with established smoking among adolescents. Educational and policy-related interventions should focus on minimizing early exposure to smoking depicted in movies.

Association of Established Smoking Among Adolescents With Timing of Exposure to Smoking Depicted in Movies

PubMed Central

Longacre, Meghan R.; Beach, Michael L.; Adachi-Mejia, Anna M.; Titus, Linda J.; Dalton, Madeline A.

2012-01-01

Background It is not known whether exposure to smoking depicted in movies carries greater influence during early or late adolescence. We aimed to quantify the independent relative contribution to established smoking of exposure to smoking depicted in movies during both early and late adolescence. Methods We prospectively assessed 2049 nonsmoking students recruited from 14 randomly selected public schools in New Hampshire and Vermont. At baseline enrollment, students aged 10–14 years completed a written survey to determine personal, family, and sociodemographic characteristics and exposure to depictions of smoking in the movies (early exposure). Seven years later, we conducted follow-up telephone interviews to ascertain follow-up exposure to movie smoking (late exposure) and smoking behavior. We used multiple regression models to assess associations between early and late exposure and development of established smoking. Results One-sixth (17.3%) of the sample progressed to established smoking. In analyses that controlled for covariates and included early and late exposure in the same model, we found that students in the highest quartile for early exposure had 73% greater risk of established smoking than those in the lowest quartile for early exposure (27.8% vs 8.6%; relative risk for Q4 vs Q1 = 1.73, 95% confidence interval = 1.14 to 2.62). However, late exposure to depictions of smoking in movies was not statistically significantly associated with established smoking (22.1% vs 14.0%; relative risk for Q4 vs Q1 = 1.13, 95% confidence interval = 0.89 to 1.44). Whereas 31.6% of established smoking was attributable to early exposure, only an additional 5.3% was attributable to late exposure. Conclusions Early exposure to smoking depicted in movies is associated with established smoking among adolescents. Educational and policy-related interventions should focus on minimizing early exposure to smoking depicted in movies. PMID:22423010

Effect of smoking parameters on the particle size distribution and predicted airway deposition of mainstream cigarette smoke.

PubMed

Kane, David B; Asgharian, Bahman; Price, Owen T; Rostami, Ali; Oldham, Michael J

2010-02-01

It is known that puffing conditions such as puff volume, duration, and frequency vary substantially among individual smokers. This study investigates how these parameters affect the particle size distribution and concentration of fresh mainstream cigarette smoke (MCS) and how these changes affect the predicted deposition of MCS particles in a model human respiratory tract. Measurements of the particle size distribution made with an electrical low pressure impactor for a variety of puffing conditions are presented. The average flow rate of the puff is found to be the major factor effecting the measured particle size distribution of the MCS. The results of these measurements were then used as input to a deterministic dosimetry model (MPPD) to estimate the changes in the respiratory tract deposition fraction of smoke particles. The MPPD dosimetry model was modified by incorporating mechanisms involved in respiratory tract deposition of MCS: hygroscopic growth, coagulation, evaporation of semivolatiles, and mixing of the smoke with inhaled dilution air. The addition of these mechanisms to MPPD resulted in reasonable agreement between predicted airway deposition and human smoke retention measurements. The modified MPPD model predicts a modest 10% drop in the total deposition efficiency in a model human respiratory tract as the puff flow rate is increased from 1050 to 3100 ml/min, for a 2-s puff.

Respiratory health issues in the Asia-Pacific region: an overview.

PubMed

Jamrozik, Euzebiusz; Musk, Arthur William

2011-01-01

The Asia-Pacific region is home to a large heterogeneous population whose respiratory health is influenced by diverse social, economic and environmental factors. Despite this variability, the most prevalent causes of respiratory morbidity and mortality are tobacco smoking, infection, and air pollution. This review aims to summarize current respiratory health issues in the region including smoking-related diseases especially COPD, lung cancer and infectious problems such as pandemic influenza, the severe acute respiratory syndrome coronavirus, bacterial pneumonia and tuberculosis, as well as the contribution of air pollution to respiratory disease. Published data on trends in the epidemiology and management of respiratory diseases and are summarized; finally, the limitations of available data and projections for the future of respiratory health in the region are discussed. © 2010 Commonwealth of Australia. Respirology © 2010 Asian Pacific Society of Respirology.

Effects of passive inhalation of cigarette smoke on structural and functional parameters in the respiratory system of guinea pigs

PubMed Central

de Vasconcelos, Thiago Brasileiro; de Araújo, Fernanda Yvelize Ramos; de Pinho, João Paulo Melo; Soares, Pedro Marcos Gomes; Bastos, Vasco Pinheiro Diógenes

2016-01-01

ABSTRACT Objective: To evaluate the effects of passive inhalation of cigarette smoke on the respiratory system of guinea pigs. Methods: Male guinea pigs were divided into two groups: control and passive smoking, the latter being exposed to the smoke of ten cigarettes for 20 min in the morning, afternoon and evening (30 cigarettes/day) for five days. After that period, inflammatory parameters were studied by quantifying mesenteric mast cell degranulation, as well as oxidative stress, in BAL fluid. In addition, we determined MIP, MEP, and mucociliary transport (in vivo), as well as tracheal contractility response (in vitro). Results: In comparison with the control group, the passive smoking group showed a significant increase in mast cell degranulation (19.75 ± 3.77% vs. 42.53 ± 0.42%; p < 0.001) and in the levels of reduced glutathione (293.9 ± 19.21 vs. 723.7 ± 67.43 nM/g of tissue; p < 0.05); as well as a significant reduction in mucociliary clearance (p < 0.05), which caused significant changes in pulmonary function (in MIP and MEP; p < 0.05 for both) and airway hyperreactivity. Conclusions: Passive inhalation of cigarette smoke caused significant increases in mast cell degranulation and oxidative stress. This inflammatory process seems to influence the decrease in mucociliary transport and to cause changes in pulmonary function, leading to tracheal hyperreactivity. PMID:27812632

Environmental tobacco smoke aerosol in non-smoking households of patients with chronic respiratory diseases

NASA Astrophysics Data System (ADS)

Chalbot, Marie-Cecile; Vei, Ino-Christina; Lianou, Maria; Kotronarou, Anastasia; Karakatsani, Anna; Katsouyanni, Klea; Hoek, Gerard; Kavouras, Ilias G.

2012-12-01

Fine particulate matter samples were collected in an urban ambient fixed site and, outside and inside residencies in Athens greater area, Greece. n-Alkanes, iso/anteiso-alkanes and polycyclic aromatic hydrocarbons (PAHs) were identified by gas chromatography and mass spectrometry. The values of concentration diagnostic ratios indicated a mixture of vehicular emissions, fuel evaporation, oil residues and environmental tobacco smoke (ETS) in outdoor and indoor samples. Particulate iso/anteiso-alkanes, specific tracers of ETS, were detected in both non-smoking and smoking households. The indoor-to-outdoor ratios of particulate iso/anteiso-alkanes and unresolved complex mixture (a tracer of outdoor air pollution) in non-smoking households were comparable to the measured air exchange rate. This suggested that penetration of outdoor air was solely responsible for the detection of tobacco smoke particulate tracers in indoor non-smoking environments. Overall, residential outdoor concentrations accounted for a large fraction (from 25 up to 79%) of indoor aliphatic and polyaromatic hydrocarbons. Open windows/doors and the operation of an air condition unit yielded also in higher indoor concentrations than those measured outdoors.

Smoking Through a Topography Device Diminishes Some of the Acute Rewarding Effects of Smoking

PubMed Central

Juliano, Laura M.

2016-01-01

Abstract Background: Smoking topography (ST) devices are an important methodological tool for quantifying puffing behavior (eg, puff volume, puff velocity) as well as identifying puffing differences across individuals and situations. Available ST devices are designed such that the smoker’s mouth and hands have direct contact with the device rather than the cigarette itself. Given the importance of the sensorimotor aspects of cigarette smoking in smoking reward, it is possible that ST devices may interfere with the acute rewarding effects of smoking. Despite the methodological importance of this issue, few studies have directly compared subjective reactions to smoking through a topography device to naturalistic smoking. Methods: Smokers ( N = 58; 38% female) smoked their preferred brand of cigarettes one time through a portable topography device and one time naturalistically, in counterbalanced order across two laboratory sessions. Smoking behavior (eg, number of puffs) and subjective effects (eg, urge reduction, affect, smoking satisfaction) were assessed. Results: Negative affect reduction was greater in the natural smoking condition relative to the topography condition, but differences were not significant on measures of urge, withdrawal, or positive affect. Self-reported smoking satisfaction, enjoyment of respiratory tract sensations, psychological reward, craving reduction, and other rewarding effects of smoking were also significantly greater in the naturalistic smoking condition. Conclusions: The effects of using a ST device on the smoking experience should be considered when it is used in research as it may diminish some of the rewarding effects of smoking. Implications: When considering the inclusion of a smoking topography device in one’s research, it is important to know if use of that device will alter the smoker’s experience. This study assessed affective and subjective reactions to smoking through a topography device compared to naturalistic

Cotinine Concentration in Serum Correlates with Tobacco Smoke-Induced Emphysema in Mice

NASA Astrophysics Data System (ADS)

Xu, Xin; Su, Yunchao; Fan, Z. Hugh

2014-01-01

Secondhand smoke (SHS) has been associated with a variety of adverse health outcomes in nonsmokers, including emphysema (a chronic obstructive pulmonary disease). One way to detect SHS exposure is to measure the concentration of cotinine, the primary metabolite of nicotine, in bodily fluids. We have developed a method for cotinine analysis by combining micellar electrokinetic chromatography with enrichment techniques. We employed the method to measure cotinine concentrations in serum samples of mice exposed to tobacco smoke for 12 or 24 weeks and found that it was 3.1-fold or 4.8-fold higher than those exposed to room air for the same period. Further, we investigated the morphological changes in lungs of mice and observed tobacco smoke induced emphysema. Our results indicate that the method can be used to measure cotinine and there is an association between the serum cotinine concentration and tobacco smoke-induced emphysema in mice.

Glutathione-S-transferase P protects against endothelial dysfunction induced by exposure to tobacco smoke.

PubMed

Conklin, Daniel J; Haberzettl, Petra; Prough, Russell A; Bhatnagar, Aruni

2009-05-01

Exposure to tobacco smoke impairs endothelium-dependent arterial dilation. Reactive constituents of cigarette smoke are metabolized and detoxified by glutathione-S-transferases (GSTs). Although polymorphisms in GST genes are associated with the risk of cancer in smokers, the role of these enzymes in regulating the cardiovascular effects of smoking has not been studied. The P isoform of GST (GSTP), which catalyzes the conjugation of electrophilic molecules in cigarette smoke such as acrolein, was expressed in high abundance in the mouse lung and aorta. Exposure to tobacco smoke for 3 days (5 h/day) decreased total plasma protein. These changes were exaggerated in GSTP(-/-) mice. Aortic rings isolated from tobacco smoke-exposed GSTP(-/-) mice showed greater attenuation of ACh-evoked relaxation than those from GSTP(+/+) mice. The lung, plasma, and aorta of mice exposed to tobacco smoke or acrolein (for 5 h) accumulated more acrolein-adducted proteins than those tissues of mice exposed to air, indicating that exposure to tobacco smoke results in the systemic delivery of acrolein. Relative to GSTP(+/+) mice, modification of some proteins by acrolein was increased in the aorta of GSTP(-/-) mice. Aortic rings prepared from GSTP(-/-) mice that inhaled acrolein (1 ppm, 5 h/day for 3 days) or those exposed to acrolein in an organ bath showed diminished ACh-induced arterial relaxation more strongly than GSTP(+/+) mice. Acrolein-induced endothelial dysfunction was prevented by pretreatment of the aorta with N-acetylcysteine. These results indicate that GSTP protects against the endothelial dysfunction induced by tobacco smoke exposure and that this protection may be related to the detoxification of acrolein or other related cigarette smoke constituents.

Phrenic Nerve Conduction Study in the Early Stage of Guillain-Barre Syndrome as a Predictor of Respiratory Failure.

PubMed

Sen, Barun Kumar; Pandit, Alak

2018-01-01

Guillain-Barré syndrome (GBS) has unpredictable clinical course with severe complication of respiratory failure. To identify clinical profiles and electrophysiological study particularly non-invasive Phrenic nerve conduction study in patients of early GBS to predict respiratory failure. 64 adult (age≥18yrs) patients of early GBS (onset ≤ 14 days) during the study period from January 2014 to October 2015 were evaluated by clinical profiles of age, gender, antecedent infection, time to peak disability, single breath counts, cranial nerve involvement, autonomic dysfunction and non-invasive Phrenic nerve conduction study. Patients with predisposition factors of polyneuropathy like diabetes mellitus, hypothyroidism, vitamin deficiency, renal failure were excluded. Among 64 patients abnormal phrenic nerve conduction study was seen in 65.62% cases (42/64) and 45.23% (19/42) of them developed respiratory failure. Phrenic nerve sum latency, amplitude, duration and area were abnormal in those who developed respiratory failure and they had sum of phrenic nerve latency >28 msec, sum of CMAP amplitude <300 μV, sum of CMAP duration >50 msec and sum of area < 4 mVmS. None with normal phrenic nerve study developed respiratory failure. It was found that age, gender, preceding infection, autonomic involvement and types of GB syndrome had no influence on development of respiratory failure (p>0.05). Rapid disease progression to peak disability, more severe disease, shorter single breath counts and cranial nerve involvement were seen more often in patients with respiratory failure. Abnormal Phrenic nerve conduction study in the early Guillain-Barré syndrome might be of great value independently in predicting impending respiratory failure.

Mitochondrial Respiratory Function Induces Endogenous Hypoxia

PubMed Central

Prior, Sara; Kim, Ara; Yoshihara, Toshitada; Tobita, Seiji; Takeuchi, Toshiyuki; Higuchi, Masahiro

2014-01-01

Hypoxia influences many key biological functions. In cancer, it is generally believed that hypoxic condition is generated deep inside the tumor because of the lack of oxygen supply. However, consumption of oxygen by cancer should be one of the key means of regulating oxygen concentration to induce hypoxia but has not been well studied. Here, we provide direct evidence of the mitochondrial role in the induction of intracellular hypoxia. We used Acetylacetonatobis [2-(2′-benzothienyl) pyridinato-kN, kC3’] iridium (III) (BTP), a novel oxygen sensor, to detect intracellular hypoxia in living cells via microscopy. The well-differentiated cancer cell lines, LNCaP and MCF-7, showed intracellular hypoxia without exogenous hypoxia in an open environment. This may be caused by high oxygen consumption, low oxygen diffusion in water, and low oxygen incorporation to the cells. In contrast, the poorly-differentiated cancer cell lines: PC-3 and MDAMB231 exhibited intracellular normoxia by low oxygen consumption. The specific complex I inhibitor, rotenone, and the reduction of mitochondrial DNA (mtDNA) content reduced intracellular hypoxia, indicating that intracellular oxygen concentration is regulated by the consumption of oxygen by mitochondria. HIF-1α was activated in endogenously hypoxic LNCaP and the activation was dependent on mitochondrial respiratory function. Intracellular hypoxic status is regulated by glucose by parabolic dose response. The low concentration of glucose (0.045 mg/ml) induced strongest intracellular hypoxia possibly because of the Crabtree effect. Addition of FCS to the media induced intracellular hypoxia in LNCaP, and this effect was partially mimicked by an androgen analog, R1881, and inhibited by the anti-androgen, flutamide. These results indicate that mitochondrial respiratory function determines intracellular hypoxic status and may regulate oxygen-dependent biological functions. PMID:24586439

CHARACTERIZATION OF NORMAL HUMAN LUNG LYMPHOCYTES AND INTERLEUKIN-2-INDUCED LUNG T CELL LINES

EPA Science Inventory

Lymphocytes from the lower respiratory tract were obtained by bronchoalveolar lavage of healthy, non-smoking individuals. arious monoclonal antibodies characterizing activated T cells, helper-inducer and suppressor-inducer T cell subsets, and naive versus memory cells were used t...

[Cannabis use and impairment of respiratory function].

PubMed

Underner, M; Urban, T; Perriot, J; Peiffer, G; Meurice, J-C

2013-04-01

Cannabis is the most commonly smoked illicit substance in many countries including France. It can be smoked alone in plant form (marijuana) but in our country it is mainly smoked in the form of cannabis resin mixed with tobacco. The technique of inhaling cannabis differs from that of tobacco, increasing the time that the smoke spends in contact with the bronchial mucosal and its impact on respiratory function. One cigarette composed of cannabis and tobacco is much more harmful than a cigarette containing only tobacco. In cannabis smokers there is an increased incidence of respiratory symptoms and episodes of acute bronchitis. Cannabis produces a rapid bronchodilator effect; chronic use provokes a reduction in specific conductance and increase in airways resistance. Studies on the decline of Forced Expiratory Volume are discordant. Cannabis smoke and tetrahydrocannabinol irritate the bronchial tree. They bring about histological signs of airways inflammation and alter the fungicidal and antibacterial activity of alveolar macrophages. Inhalation of cannabis smoke is a risk factor for lung cancer. Stopping smoking cannabis will bring about important benefits for lung function. This should encourage clinicians to offer patients support in quitting smoking. Copyright © 2013 SPLF. Published by Elsevier Masson SAS. All rights reserved.

Determinants of early-life lung function in African infants

PubMed Central

Willemse, Lauren; Visagie, Ane; Czövek, Dorottya; Nduru, Polite; Vanker, Aneesa; Stein, Dan J; Koen, Nastassja; Sly, Peter D; Hantos, Zoltán; Hall, Graham L; Zar, Heather J

2017-01-01

Background Low lung function in early life is associated with later respiratory illness. There is limited data on lung function in African infants despite a high prevalence of respiratory disease. Aim To assess the determinants of early lung function in African infants. Method Infants enrolled in a South African birth cohort, the Drakenstein child health study, had lung function measured at 6–10 weeks of age. Measurements, made with the infant breathing via a facemask during natural sleep, included tidal breathing, sulfur hexafluoride multiple breath washout and the forced oscillation technique. Information on antenatal and early postnatal exposures was collected using questionnaires and urine cotinine. Household benzene exposure was measured antenatally. Results Successful tests were obtained in 645/675 (95%) infants, median (IQR) age of 51 (46–58) days. Infant size, age and male gender were associated with larger tidal volume. Infants whose mothers smoked had lower tidal volumes (−1.6 mL (95% CI −3.0 to −0.1), p=0.04) and higher lung clearance index (0.1 turnovers (95% CI 0.01 to 0.3), p=0.03) compared with infants unexposed to tobacco smoke. Infants exposed to alcohol in utero or household benzene had lower time to peak tidal expiratory flow over total expiratory time ratios, 10% (95% CI −15.4% to −3.7%), p=0.002) and 3.0% (95% CI −5.2% to −0.7%, p=0.01) lower respectively compared with unexposed infants. HIV-exposed infants had higher tidal volumes (1.7 mL (95% CI 0.06 to 3.3) p=0.04) compared with infants whose mothers were HIV negative. Conclusion We identified several factors including infant size, sex, maternal smoking, maternal alcohol, maternal HIV and household benzene associated with altered early lung function, many of which are factors amenable to public health interventions. Long-term study of lung function and respiratory disease in these children is a priority to develop strategies to strengthen child health. PMID:27856821

Respiratory-Induced Prostate Motion Using Wavelet Decomposition of the Real-Time Electromagnetic Tracking Signal

DOE Office of Scientific and Technical Information (OSTI.GOV)

Lin, Yuting; Liu, Tian; Yang, Xiaofeng

2013-10-01

Purpose: The objective of this work is to characterize and quantify the impact of respiratory-induced prostate motion. Methods and Materials: Real-time intrafraction motion is observed with the Calypso 4-dimensional nonradioactive electromagnetic tracking system (Calypso Medical Technologies, Inc. Seattle, Washington). We report the results from a total of 1024 fractions from 31 prostate cancer patients. Wavelet transform was used to decompose the signal to extract and isolate the respiratory-induced prostate motion from the total prostate displacement. Results: Our results show that the average respiratory motion larger than 0.5 mm can be observed in 68% of the fractions. Fewer than 1% ofmore » the patients showed average respiratory motion of less than 0.2 mm, whereas 99% of the patients showed average respiratory-induced motion ranging between 0.2 and 2 mm. The maximum respiratory range of motion of 3 mm or greater was seen in only 25% of the fractions. In addition, about 2% patients showed anxiety, indicated by a breathing frequency above 24 times per minute. Conclusions: Prostate motion is influenced by respiration in most fractions. Real-time intrafraction data are sensitive enough to measure the impact of respiration by use of wavelet decomposition methods. Although the average respiratory amplitude observed in this study is small, this technique provides a tool that can be useful if one moves to smaller treatment margins (≤5 mm). This also opens ups the possibility of being able to develop patient specific margins, knowing that prostate motion is not unpredictable.« less

Benefits of smoking bans on preterm and early-term births: a natural experimental design in Switzerland.

PubMed

Vicedo-Cabrera, Ana M; Schindler, Christian; Radovanovic, Dragana; Grize, Leticia; Witassek, Fabienne; Dratva, Julia; Röösli, Martin; Perez, Laura

2016-12-01

Birth outcomes are relevant for future children's heath. Capitalising on a natural experimental design in Switzerland, we evaluated how regional smoking bans introduced at different time points affected birth outcomes, including preterm and early-term births. We used birth registry data of all singleton neonates born in Switzerland (2007-2012). We developed canton-specific interrupted time-series followed by random meta-analysis to evaluate the benefits of smoking bans on preterm (<37 gestational weeks) and early-term (37-38 gestational weeks) births. Heterogeneity across type of ban and contextual characteristics was explored through metaregression. A time-to-event approach was used for evaluating duration of pregnancy under the smoking bans and effects, taking into account individual maternal factors. We observed a decrease in the risk of preterm birth of 3.6% (95% CI, -9.3% to 2.5%), and early-term birth of 5.0% (95% CI -7.5% to -2.5%). Results showed a clear dose-response relationship. Greater risk reductions were obtained for preterm births in areas with more comprehensive bans (-6.8%; 95% CI -12.1% to 0.1%), and for pregnancies with the longest gestational time under smoking bans (HR, 0.991; 95% CI 0.984 to 0.997 per 10% increase in duration). Benefits were unequal across outcomes and characteristics of cantons and mothers. Smoking bans resulted in improved birth outcomes in Switzerland with cantons that adopted more comprehensive smoking bans achieving greater benefits. Early-term births constitute a previously ignored though important group. Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://www.bmj.com/company/products-services/rights-and-licensing/.

An early-stage epidemic: a systematic review of correlates of smoking among Chinese women.

PubMed

Ding, Ding; Gebel, Klaus; Oldenburg, Brian F; Wan, Xia; Zhong, Xuefeng; Novotny, Thomas E

2014-08-01

Despite the historically low smoking prevalence among Chinese women, there is a trend of future increase. We systematically reviewed the correlates of smoking among Chinese girls and women. We conducted a systematic review of literature on correlates of smoking among Chinese women using Medline and China Academic Journals databases. Following the PRISMA statement, two investigators independently searched for literature, identified and reviewed papers, assessed the quality of the papers, and extracted information. The characteristics of studies and correlates of smoking were synthesized separately for youth and adults. A total of 15 articles (11 on adults, 4 on youth) met the inclusion criteria. Based on these studies, peer smoking was the most consistent correlate of smoking among Chinese girls. Among Chinese women, partner smoking, job-related stress, and exposure to cigarettes made for women were consistent correlates of smoking. Knowledge of harms and negative attitudes towards smoking were found to be negatively associated with smoking. Overall, the evidence base for smoking among Chinese women is limited. Although smoking among Chinese women is still at an early stage, it is becoming more prevalent among specific population subgroups, such as rural-to-urban migrant workers. Although further research is needed, findings from the current study provide a roadmap for research and policy on prevention of smoking among Chinese girls and women.

[Health consequences of passive smoking].

PubMed

Haustein, K O

2001-06-01

Environmental tobacco smoking (ETS) represents a main risk factor for the generation of diseases of the respiratory tract and of the cardiovascular system in spite of statements to the contrary. ETS enhances the risk of lung cancer by a factor of 2-3. Newborn and small children (< 2 years of life) are at high risk if they live within this period of time in a household exposed to maternal more than fraternal smoking. Endothelial cells of the blood vessels are damaged as early as during the first month of life of passive smoking children, and these defects can be detected during the first decade of life. ETS over a period of more than ten years changes the intima/media ratio by enhancing the thickness of the vessel wall. Additionally, poor health behaviour is seen in households of smokers because the behaviour of the parents is transferred to that of their children, and this behaviour is the starting point of further health risks and damages. The presented data should cause a call for primary smoking prevention preferably among children and young persons on the one hand, and the organisation of programs against ETS at the workplace and in public buildings, as well as in the private house on the other hand. Non-smokers must be informed about the risks and dangers of ETS more than it is the case up to now.

Phrenic Nerve Conduction Study in the Early Stage of Guillain–Barre Syndrome as a Predictor of Respiratory Failure

PubMed Central

Sen, Barun Kumar; Pandit, Alak

2018-01-01

Background: Guillain-Barré syndrome (GBS) has unpredictable clinical course with severe complication of respiratory failure. Objective: To identify clinical profiles and electrophysiological study particularly non-invasive Phrenic nerve conduction study in patients of early GBS to predict respiratory failure. Methods: 64 adult (age≥18yrs) patients of early GBS (onset ≤ 14 days) during the study period from January 2014 to October 2015 were evaluated by clinical profiles of age, gender, antecedent infection, time to peak disability, single breath counts, cranial nerve involvement, autonomic dysfunction and non-invasive Phrenic nerve conduction study. Patients with predisposition factors of polyneuropathy like diabetes mellitus, hypothyroidism, vitamin deficiency, renal failure were excluded. Results: Among 64 patients abnormal phrenic nerve conduction study was seen in 65.62% cases (42/64) and 45.23% (19/42) of them developed respiratory failure. Phrenic nerve sum latency, amplitude, duration and area were abnormal in those who developed respiratory failure and they had sum of phrenic nerve latency >28 msec, sum of CMAP amplitude <300 μV, sum of CMAP duration >50 msec and sum of area < 4 mVmS. None with normal phrenic nerve study developed respiratory failure. It was found that age, gender, preceding infection, autonomic involvement and types of GB syndrome had no influence on development of respiratory failure (p>0.05). Rapid disease progression to peak disability, more severe disease, shorter single breath counts and cranial nerve involvement were seen more often in patients with respiratory failure. Conclusion: Abnormal Phrenic nerve conduction study in the early Guillain-Barré syndrome might be of great value independently in predicting impending respiratory failure. PMID:29720799

Deployment-related Respiratory Issues.

PubMed

Morris, Michael J; Rawlins, Frederic A; Forbes, Damon A; Skabelund, Andrew J; Lucero, Pedro F

2016-01-01

Military deployment to Southwest Asia since 2003 in support of Operations Enduring Freedom/Iraqi Freedom/New Dawn has presented unique challenges from a pulmonary perspective. Various airborne hazards in the deployed environment include suspended geologic dusts, burn pit smoke, vehicle exhaust emissions, industrial air pollution, and isolated exposure incidents. These exposures may give rise to both acute respiratory symptoms and in some instances development of chronic lung disease. While increased respiratory symptoms during deployment are well documented, there is limited data on whether inhalation of airborne particulate matter is causally related to an increase in either common or unique pulmonary diseases. While disease processes such as acute eosinophilic pneumonia and exacerbation of preexisting asthma have been adequately documented, there is significant controversy surrounding the potential effects of deployment exposures and development of rare pulmonary disorders such as constrictive bronchiolitis. The role of smoking and related disorders has yet to be defined. This article presents the current evidence for deployment-related respiratory symptoms and ongoing Department of Defense studies. Further, it also provides general recommendations for evaluating pulmonary health in the deployed military population.

Adverse Health Effects of Thirdhand Smoke: From Cell to Animal Models

DOE Office of Scientific and Technical Information (OSTI.GOV)

Hang, Bo; Wang, Pin; Zhao, Yue

The newly identified smoke hazard, thirdhand smoke (THS), has gained public attention in recent years but its health impact and biological effects are largely unknown. THS may be defined by “the four Rs”: tobacco chemicals that remain, react, re-emit, and/or are resuspended long after active smoking has ceased. This review summarizes recent research progress in the effects of THS on genotoxicity, metabolism and early life development using cellular and animal models. We first reported that THS generated in laboratory systems caused significant DNA damage in human cell lines. Our finding that THS significantly induces oxidative base lesions has been confirmedmore » in skin wounds of mice models exposed to THS. THS also induced metabolomic changes in human reproductive cell lines. Furthermore, we demonstrated that early exposure to THS not only negatively impacts body weight in both male and female mice, but also induces persistent changes to immunological parameters in peripheral blood in these mice. These results indicate that THS is genotoxic at realistic experimental doses and that there may be a window of susceptibility for some forms of cellular damage induced by THS.« less

Adverse Health Effects of Thirdhand Smoke: From Cell to Animal Models

DOE PAGES

Hang, Bo; Wang, Pin; Zhao, Yue; ...

2017-04-28

The newly identified smoke hazard, thirdhand smoke (THS), has gained public attention in recent years but its health impact and biological effects are largely unknown. THS may be defined by “the four Rs”: tobacco chemicals that remain, react, re-emit, and/or are resuspended long after active smoking has ceased. This review summarizes recent research progress in the effects of THS on genotoxicity, metabolism and early life development using cellular and animal models. We first reported that THS generated in laboratory systems caused significant DNA damage in human cell lines. Our finding that THS significantly induces oxidative base lesions has been confirmedmore » in skin wounds of mice models exposed to THS. THS also induced metabolomic changes in human reproductive cell lines. Furthermore, we demonstrated that early exposure to THS not only negatively impacts body weight in both male and female mice, but also induces persistent changes to immunological parameters in peripheral blood in these mice. These results indicate that THS is genotoxic at realistic experimental doses and that there may be a window of susceptibility for some forms of cellular damage induced by THS.« less

Adverse Health Effects of Thirdhand Smoke: From Cell to Animal Models.

PubMed

Hang, Bo; Wang, Pin; Zhao, Yue; Sarker, Altaf; Chenna, Ahmed; Xia, Yankai; Snijders, Antoine M; Mao, Jian-Hua

2017-04-28

The newly identified smoke hazard, thirdhand smoke (THS), has gained public attention in recent years but its health impact and biological effects are largely unknown. THS may be defined by "the four Rs": tobacco chemicals that remain, react, re-emit, and/or are resuspended long after active smoking has ceased. This review summarizes recent research progress in the effects of THS on genotoxicity, metabolism and early life development using cellular and animal models. We first reported that THS generated in laboratory systems caused significant DNA damage in human cell lines. Our finding that THS significantly induces oxidative base lesions has been confirmed in skin wounds of mice models exposed to THS. THS also induced metabolomic changes in human reproductive cell lines. Furthermore, we demonstrated that early exposure to THS not only negatively impacts body weight in both male and female mice, but also induces persistent changes to immunological parameters in peripheral blood in these mice. These results indicate that THS is genotoxic at realistic experimental doses and that there may be a window of susceptibility for some forms of cellular damage induced by THS.

Early High-Frequency Oscillatory Ventilation in Pediatric Acute Respiratory Failure. A Propensity Score Analysis.

PubMed

Bateman, Scot T; Borasino, Santiago; Asaro, Lisa A; Cheifetz, Ira M; Diane, Shelley; Wypij, David; Curley, Martha A Q

2016-03-01

The use of high-frequency oscillatory ventilation (HFOV) for acute respiratory failure in children is prevalent despite the lack of efficacy data. To compare the outcomes of patients with acute respiratory failure managed with HFOV within 24-48 hours of endotracheal intubation with those receiving conventional mechanical ventilation (CMV) and/or late HFOV. This is a secondary analysis of data from the RESTORE (Randomized Evaluation of Sedation Titration for Respiratory Failure) study, a prospective cluster randomized clinical trial conducted between 2009 and 2013 in 31 U.S. pediatric intensive care units. Propensity score analysis, including degree of hypoxia in the model, compared the duration of mechanical ventilation and mortality of patients treated with early HFOV matched with those treated with CMV/late HFOV. Among 2,449 subjects enrolled in RESTORE, 353 patients (14%) were ever supported on HFOV, of which 210 (59%) had HFOV initiated within 24-48 hours of intubation. The propensity score model predicting the probability of receiving early HFOV included 1,064 patients (181 early HFOV vs. 883 CMV/late HFOV) with significant hypoxia (oxygenation index ≥ 8). The degree of hypoxia was the most significant contributor to the propensity score model. After adjusting for risk category, early HFOV use was associated with a longer duration of mechanical ventilation (hazard ratio, 0.75; 95% confidence interval, 0.64-0.89; P = 0.001) but not with mortality (odds ratio, 1.28; 95% confidence interval, 0.92-1.79; P = 0.15) compared with CMV/late HFOV. In adjusted models including important oxygenation variables, early HFOV was associated with a longer duration of mechanical ventilation. These analyses make supporting the current approach to HFOV less convincing.

Respiratory symptoms and airflow limitation in asphalt workers

PubMed Central

Randem, B; Ulvestad, B; Burstyn, I; Kongerud, J

2004-01-01

Aims: To assess the occurrence of respiratory symptoms and signs of airflow limitations in a group of asphalt workers. Methods: All 64 asphalt workers and a reference group of 195 outdoor construction workers from the same company participated in a cross-sectional study. Spirometric tests and a questionnaire on respiratory symptoms and smoking habits were administered. Respiratory symptoms and lung function were adjusted for age and smoking. Results: The FEV1/FVC% ratio was significantly lower in the asphalt workers than in the referents. Symptoms of eye irritation, chest tightness, shortness of breath on exertion, chest wheezing, physician diagnosed asthma, and chronic obstructive pulmonary disease (COPD) were all significantly more prevalent among the asphalt workers. Conclusion: In asphalt workers there is an increased risk of respiratory symptoms, lung function decline, and COPD compared to other construction workers. PMID:15031397

Immunoregulation of Bone Marrow-Derived Mesenchymal Stem Cells on the Chronic Cigarette Smoking-Induced Lung Inflammation in Rats

PubMed Central

Li, Xiaoyan; Wang, Junyan; Cao, Jing; Ma, Lijuan; Xu, Jianying

2015-01-01

Impact of bone mesenchymal stem cell (BMSC) transfusion on chronic smoking-induced lung inflammation is poorly understood. In this study, a rat model of smoking-related lung injury was induced and the rats were treated with vehicle or BMSCs for two weeks. Different subsets of CD4+ T cells, cytokines, and anti-elastin in the lungs as well as the lung injury were characterized. Serum and lung inducible nitric oxide synthase (iNOS) and STAT5 phosphorylation in lymphocytes from lung tissue were also analyzed. Results indicated that transfusion of BMSCs significantly reduced the chronic smoking-induced lung injury, inflammation, and levels of lung anti-elastin in rats. The frequency of Th1 and Th17 cells and the levels of IL-2, IL-6, IFN-γ, TNF-α, IL-17, IP-10, and MCP-1 increased, but the frequency of Tregs and IL-10 decreased. Transfusion of BMSCs significantly modulated the imbalance of immune responses by mitigating chronic smoking-increased Th1 and Th17 responses, but enhancing Treg responses in the lungs of rats. Transfusion of BMSCs limited chronic smoking-related reduction in the levels of serum and lung iNOS and mitigated smoking-induced STAT5 phosphorylation in lymphocytes from lung tissue. BMSCs negatively regulated smoking-induced autoimmune responses in the lungs of rats and may be promising for the intervention of chronic smoking-related lung injury. PMID:26665150

Smoking Through a Topography Device Diminishes Some of the Acute Rewarding Effects of Smoking.

PubMed

Ross, Kathryn C; Juliano, Laura M

2016-05-01

Smoking topography (ST) devices are an important methodological tool for quantifying puffing behavior (eg, puff volume, puff velocity) as well as identifying puffing differences across individuals and situations. Available ST devices are designed such that the smoker's mouth and hands have direct contact with the device rather than the cigarette itself. Given the importance of the sensorimotor aspects of cigarette smoking in smoking reward, it is possible that ST devices may interfere with the acute rewarding effects of smoking. Despite the methodological importance of this issue, few studies have directly compared subjective reactions to smoking through a topography device to naturalistic smoking. Smokers (N = 58; 38% female) smoked their preferred brand of cigarettes one time through a portable topography device and one time naturalistically, in counterbalanced order across two laboratory sessions. Smoking behavior (eg, number of puffs) and subjective effects (eg, urge reduction, affect, smoking satisfaction) were assessed. Negative affect reduction was greater in the natural smoking condition relative to the topography condition, but differences were not significant on measures of urge, withdrawal, or positive affect. Self-reported smoking satisfaction, enjoyment of respiratory tract sensations, psychological reward, craving reduction, and other rewarding effects of smoking were also significantly greater in the naturalistic smoking condition. The effects of using a ST device on the smoking experience should be considered when it is used in research as it may diminish some of the rewarding effects of smoking. When considering the inclusion of a smoking topography device in one's research, it is important to know if use of that device will alter the smoker's experience. This study assessed affective and subjective reactions to smoking through a topography device compared to naturalistic smoking. We found that smoking satisfaction, psychological reward, enjoyment

Genetic variants and early cigarette smoking and nicotine dependence phenotypes in adolescents.

PubMed

O'Loughlin, Jennifer; Sylvestre, Marie-Pierre; Labbe, Aurélie; Low, Nancy C; Roy-Gagnon, Marie-Hélène; Dugas, Erika N; Karp, Igor; Engert, James C

2014-01-01

While the heritability of cigarette smoking and nicotine dependence (ND) is well-documented, the contribution of specific genetic variants to specific phenotypes has not been closely examined. The objectives of this study were to test the associations between 321 tagging single-nucleotide polymorphisms (SNPs) that capture common genetic variation in 24 genes, and early smoking and ND phenotypes in novice adolescent smokers, and to assess if genetic predictors differ across these phenotypes. In a prospective study of 1294 adolescents aged 12-13 years recruited from ten Montreal-area secondary schools, 544 participants who had smoked at least once during the 7-8 year follow-up provided DNA. 321 single-nucleotide polymorphisms (SNPs) in 24 candidate genes were tested for an association with number of cigarettes smoked in the past 3 months, and with five ND phenotypes (a modified version of the Fagerstrom Tolerance Questionnaire, the ICD-10 and three clusters of ND symptoms representing withdrawal symptoms, use of nicotine for self-medication, and a general ND/craving symptom indicator). The pattern of SNP-gene associations differed across phenotypes. Sixteen SNPs in seven genes (ANKK1, CHRNA7, DDC, DRD2, COMT, OPRM1, SLC6A3 (also known as DAT1)) were associated with at least one phenotype with a p-value <0.01 using linear mixed models. After permutation and FDR adjustment, none of the associations remained statistically significant, although the p-values for the association between rs557748 in OPRM1 and the ND/craving and self-medication phenotypes were both 0.076. Because the genetic predictors differ, specific cigarette smoking and ND phenotypes should be distinguished in genetic studies in adolescents. Fifteen of the 16 top-ranked SNPs identified in this study were from loci involved in dopaminergic pathways (ANKK1/DRD2, DDC, COMT, OPRM1, and SLC6A3). Dopaminergic pathways may be salient during early smoking and the development of ND.

Maternal smoking during pregnancy increases the risk of recurrent wheezing during the first years of life (BAMSE).

PubMed

Lannerö, Eva; Wickman, Magnus; Pershagen, Goran; Nordvall, Lennart

2006-01-05

Exposure to cigarette smoking during foetal and early postnatal life may have implications for lung health. The aim of this study was to assess the possible effects of such exposure in utero on lower respiratory disease in children up to two years of age. A birth cohort of 4089 newborn infants was followed for two years using parental questionnaires. When the infant was two months old the parents completed a questionnaire on various lifestyle factors, including maternal smoking during pregnancy and after birth. At one and two years of age information was obtained by questionnaire on symptoms of allergic and respiratory diseases as well as on environmental exposures, particularly exposure to environmental tobacco smoke (ETS). Adjustments were made for potential confounders. When the mother had smoked during pregnancy but not after that, there was an increased risk of recurrent wheezing up to two years' age, ORadj = 2.2, (95% CI 1.3-3.6). The corresponding OR was 1.6, (95% CI 1.2-2.3) for reported exposure to ETS with or without maternal smoking in utero. Maternal smoking during pregnancy but no exposure to ETS also increased the risk of doctor's diagnosed asthma up to two years of age, ORadj = 2.1, (95% CI 1.2-3.7). Exposure to maternal cigarette smoking in utero is a risk factor for recurrent wheezing, as well as doctor's diagnosed asthma in children up to two years of age.

Maternal smoking during pregnancy increases the risk of recurrent wheezing during the first years of life (BAMSE)

PubMed Central

Lannerö, Eva; Wickman, Magnus; Pershagen, Goran; Nordvall, Lennart

2006-01-01

Background Exposure to cigarette smoking during foetal and early postnatal life may have implications for lung health. The aim of this study was to assess the possible effects of such exposure in utero on lower respiratory disease in children up to two years of age. Methods A birth cohort of 4089 newborn infants was followed for two years using parental questionnaires. When the infant was two months old the parents completed a questionnaire on various lifestyle factors, including maternal smoking during pregnancy and after birth. At one and two years of age information was obtained by questionnaire on symptoms of allergic and respiratory diseases as well as on environmental exposures, particularly exposure to environmental tobacco smoke (ETS). Adjustments were made for potential confounders. Results When the mother had smoked during pregnancy but not after that, there was an increased risk of recurrent wheezing up to two years' age, ORadj = 2.2, (95% CI 1.3 – 3.6). The corresponding OR was 1.6, (95% CI 1.2 – 2.3) for reported exposure to ETS with or without maternal smoking in utero. Maternal smoking during pregnancy but no exposure to ETS also increased the risk of doctor's diagnosed asthma up to two years of age, ORadj = 2.1, (95% CI 1.2 – 3.7). Conclusion Exposure to maternal cigarette smoking in utero is a risk factor for recurrent wheezing, as well as doctor's diagnosed asthma in children up to two yearsof age. PMID:16396689

Neural correlates of message tailoring and self-relatedness in smoking cessation programming.

PubMed

Chua, Hannah Faye; Liberzon, Israel; Welsh, Robert C; Strecher, Victor J

2009-01-15

Smoking leads to illnesses including addiction, cancer, and cardiovascular and respiratory diseases. Different intervention programs have become available. In the past decade, providing tailored smoking cessation messages has been shown to be more effective in inducing smoking cessation than one-size-fits-all interventions. However, little is known about the brain responses of smokers when they receive tailored smoking cessation messages. A neuroimaging study using blocked and event-related designs examined neural activity in 24 smokers exposed to high-tailored and low-tailored smoking cessation messages. In both blocked and event-related conditions, rostral medial prefrontal cortex and precuneus/posterior cingulate were engaged more during the processing of high-tailored smoking cessation messages than low-tailored smoking cessation messages. The activation patterns of smokers to tailored cessation messages show involvement of brain areas commonly implicated in self-related processing. Results seem to add support to the suggested role of self-relevance in tailored cessation programs, where previous studies have shown a potential mediating role of self-relevance on smoking abstinence. The findings are relevant to understanding the cognitive mechanisms underlying tailored message processing and might point to new directions for testing response to health communications programming.

Measurements of respiratory illness among construction painters.

PubMed

White, M C; Baker, E L

1988-08-01

The prevalence of different measurements of respiratory illness among construction painters was examined and the relation between respiratory illness and employment as a painter assessed in a cross sectional study of current male members of two local affiliates of a large international union of painters. Respiratory illness was measured by questionnaire and spirometry. Longer employment as a painter was associated with increased prevalence of chronic obstructive disease and an interactive effect was observed for smoking and duration of employment as a painter. Multiple regression analysis showed a significant association between years worked as a painter and a decrement in FEV1 equal to about 11 ml for each year worked. This association was larger among painters who had smoked. The prevalence of chronic bronchitis was significantly associated with increased use of spray application methods.

Evaluation of Nationwide Health Costs of Air Pollution and Cigarette Smoking

ERIC Educational Resources Information Center

Williams, J. R.; Justus, C. G.

1974-01-01

The findings of this study indicate cigarette smoking causes more respiratory diseases than does air pollution. The 1970 nationwide health cost of respiratory diseases is estimated at $6.22 billion. The effect of air pollution accounts for between 1 and 5 percent of this total cost while cigarette smoking represents 68 percent. (MLB)

Respiratory medicine in China: progress, challenges, and opportunities.

PubMed

Wang, Chen; Xiao, Fei; Qiao, Renli; Shen, Ying H

2013-06-01

The past century witnessed a rapid development of respiratory medicine in China. The major burden of respiratory disease has shifted from infectious diseases to chronic noninfectious diseases. Great achievements have been made in improving the national standard of clinical management of various respiratory diseases and in smoking control. The specialty of respiratory medicine is expanding into pulmonary and critical care medicine. Nevertheless, respiratory diseases remain a major public health problem, with new challenges such as air pollution and nosocomial infections. This review describes the history, accomplishments, new challenges, and opportunities in respiratory medicine in China.

Particles from wood smoke and traffic induce differential pro-inflammatory response patterns in co-cultures

DOE Office of Scientific and Technical Information (OSTI.GOV)

Kocbach, Anette; Herseth, Jan Inge; Lag, Marit

2008-10-15

The inflammatory potential of particles from wood smoke and traffic has not been well elucidated. In this study, a contact co-culture of monocytes and pneumocytes was exposed to 10-40 {mu}g/cm{sup 2} of particles from wood smoke and traffic for 12, 40 and 64 h to determine their influence on pro-inflammatory cytokine release (TNF-{alpha}, IL-1, IL-6, IL-8) and viability. To investigate the role of organic constituents in cytokine release the response to particles, their organic extracts and the washed particles were compared. Antagonists were used to investigate source-dependent differences in intercellular signalling (TNF-{alpha}, IL-1). The cytotoxicity was low after exposure tomore » particles from both sources. However, wood smoke, and to a lesser degree traffic-derived particles, induced a reduction in cell number, which was associated with the organic fraction. The release of pro-inflammatory cytokines was similar for both sources after 12 h, but traffic induced a greater release than wood smoke particles with increasing exposure time. The organic fraction accounted for the majority of the cytokine release induced by wood smoke, whereas the washed traffic particles induced a stronger response than the corresponding organic extract. TNF-{alpha} and IL-1 antagonists reduced the release of IL-8 induced by particles from both sources. In contrast, the IL-6 release was only reduced by the IL-1 antagonist during exposure to traffic-derived particles. In summary, particles from wood smoke and traffic induced differential pro-inflammatory response patterns with respect to cytokine release and cell number. Moreover, the influence of the organic particle fraction and intercellular signalling on the pro-inflammatory response seemed to be source-dependent.« less

Effects of expectancies and coping on pain-induced motivation to smoke.

PubMed

Ditre, Joseph W; Heckman, Bryan W; Butts, Emily A; Brandon, Thomas H

2010-08-01

The prevalence of tobacco smoking among persons with recurrent pain is approximately twice that observed in the general population. Smoking has been associated with the development and exacerbation of several chronically painful conditions. Conversely, there is both experimental and cross-sectional evidence that pain is a potent motivator of smoking. A recent study provided the first evidence that laboratory-induced pain could elicit increased craving and produce shorter latencies to smoke (Ditre & Brandon, 2008). To further elucidate interrelations between pain and smoking, and to identify potential targets for intervention, in the current study, we tested whether several constructs derived from social-cognitive theory influence the causal pathway between pain and increased motivation to smoke. Smokers (N = 132) were randomly assigned to 1 of 4 conditions in this 2 x 2 between-subjects experimental design. Results indicated that manipulations designed to (a) challenge smoking-related outcome expectancies for pain reduction and (b) enhance pain-related coping produced decreased urge ratings and increased latencies to smoke, relative to controls. An unexpected interaction effect revealed that although each manipulation was sufficient to reduce smoking urges, the combination was neither additive nor synergistic. These findings were integrated with those of the extant literature to conceptualize and depict a causal pathway between pain and motivation to smoke as moderated by smoking-related outcome expectancies and mediated by the use of pain coping behaviors. Copyright 2010 APA, all rights reserved

Smoked marijuana as a cause of lung injury.

PubMed

Tashkin, D P

2005-06-01

In many societies, marijuana is the second most commonly smoked substance after tobacco. While delta9-tetrahydrocannabinol (THC) is unique to marijuana and nicotine to tobacco, the smoke of marijuana, like that of tobacco, consists of a toxic mixture of gases and particulates, many of which are known to be harmful to the lung. Although far fewer marijuana than tobacco cigarettes are generally smoked on a daily basis, the pulmonary consequences of marijuana smoking may be magnified by the greater deposition of smoke particulates in the lung due to the differing manner in which marijuana is smoked. Whereas THC causes modest short-term bronchodilation, regular marijuana smoking produces a number of long-term pulmonary consequences, including chronic cough and sputum, histopathologic evidence of widespread airway inflammation and injury and immunohistochemical evidence of dysregulated growth of respiratory epithelial cells, that may be precursors to lung cancer. The THC in marijuana could contribute to some of these injurious changes through its ability to augment oxidative stress, cause mitochondrial dysfunction, and inhibit apoptosis. On the other hand, physiologic, clinical or epidemiologic evidence that marijuana smoking may lead to chronic obstructive pulmonary disease or respiratory cancer is limited and inconsistent. Habitual use of marijuana is also associated with abnormalities in the structure and function of alveolar macrophages, including impairment in microbial phagocytosis and killing that is associated with defective production of immunostimulatory cytokines and nitric oxide, thereby potentially predisposing to pulmonary infection. In view of the growing interest in medicinal marijuana, further epidemiologic studies are needed to clarify the true risks of regular marijuana smoking on respiratory health.

Longitudinal changes in prevalence of respiratory symptoms among Canadian grain elevator workers.

PubMed

Pahwa, Punam; McDuffie, Helen H; Dosman, James A

2006-06-01

To determine longitudinal changes in the prevalence of chronic respiratory symptoms among Canadian grain workers. Data on respiratory symptoms, smoking status, and pulmonary function were obtained approximately every 3 years (termed cycle) over 15 years beginning in 1978 from five regions of Canada. The number of grain workers participating in each cycle were as follows: cycle 1 (n = 5,702); cycle 2 (n = 5,491); cycle 3 (n = 3,713); cycle 4 (n = 2,847); and cycle 5 (n = 3,079). A procedure based on generalized estimating equations (PROC GENMOD; SAS Institute; Cary, NC) was used to fit marginal models to determine risk factors influencing the prevalence of chronic respiratory symptoms (wheeze, dyspnea, sputum, and cough). The prevalence (predicted probability based on the final model) of chronic respiratory symptoms had an increasing trend with increasing number of years in the grain industry from cycle 1 to cycle 3 (before dust control) for all three smoking categories (current smokers, ex-smokers, and nonsmokers). For cycle 4 and cycle 5 (after dust control), there was a reduction in the prevalence of these respiratory symptoms. For example, in cycle 1, the prevalence of chronic wheeze among current smoking grain workers increased from 12% (for those in the industry for < 5 years) to 44% (for those in the industry for > 35 years); in cycle 5, the prevalence of chronic wheeze among current smoking grain workers increased from 9% (for those in the industry for < 5 years) to 28% (for those in the industry for > 35 years). Similar trends were observed for ex-smokers and nonsmokers and for other chronic respiratory symptoms. Our results indicate that grain dust control was effective in reducing the prevalence of chronic respiratory symptoms among grain workers in all smoking and exposure categories.

Cigarette smoking induces heat shock protein 70 kDa expression and apoptosis in rat brain: Modulation by bacoside A.

PubMed

Anbarasi, K; Kathirvel, G; Vani, G; Jayaraman, G; Shyamala Devi, C S

2006-01-01

Cigarette smoking is associated with the development of several diseases and antioxidants play a major role in the prevention of smoking-related diseases. Apoptosis is suggested as a possible contributing factor in the pathogenesis of smoking-induced toxicity. Therefore the present study was designed to investigate the influence of chronic cigarette smoke exposure on apoptosis and the modulatory effect of bacoside A (triterpenoid saponin isolated from the plant Bacopa monniera) on smoking-induced apoptosis in rat brain. Adult male albino rats of Wistar strain were exposed to cigarette smoke and simultaneously administered with bacoside A (10 mg/kg b.w./day, orally) for a period of 12 weeks. Expression of brain hsp70 was analyzed by Western blotting. Apoptosis was identified by DNA fragmentation, terminal deoxynucleotidyl transferase-mediated deoxy uridine triphosphate nick end labeling (TUNEL) staining and transmission electron microscopy. The results showed that exposure to cigarette smoke induced hsp70 expression and apoptosis as characterized by DNA laddering, increased TUNEL-positive cells and ultrastructural apoptotic features in the brain. Administration of bacoside A prevented expression of hsp70 and neuronal apoptosis during cigarette smoking. We speculate that apoptosis may be responsible for the smoking-induced brain damage and bacoside A can protect the brain from the toxic effects of cigarette smoking.

Proteomic differences with and without ozone-exposure in a smoking-induced emphysema lung model

PubMed Central

Uh, Soo-Taek; Koo, So-My; Jang, An Soo; Park, Sung Woo; Choi, Jae Sung; Kim, Yong-Hoon

2015-01-01

Background/Aims Acute exacerbations in chronic obstructive pulmonary disease may be related to air pollution, of which ozone is an important constituent. In this study, we investigated the protein profiles associated with ozone-induced exacerbations in a smoking-induced emphysema model. Methods Mice were divided into the following groups: group I, no smoking and no ozone (NS + NO); group II, no smoking and ozone (NS + O); group III, smoking and no ozone (S + NO); and group IV, smoking and ozone (S + O). Bronchoalveolar lavage, the mean linear intercept (MLI) on hematoxylin and eosin staining, nano-liquid chromatography-tandem mass spectrometry (LC-MS/MS), and Western blotting analyses were performed. Results The MLIs of groups III (S + NO) and IV (S + O) (45 ± 2 and 44 ± 3 µm, respectively) were significantly higher than those of groups I (NS + NO) and II (NS + O) (26 ± 2 and 23 ± 2 µm, respectively; p < 0.05). Fourteen spots that showed significantly different intensities on image analyses of two-dimensional (2D) protein electrophoresis in group I (NS + NO) were identified by LC-MS/MS. The levels of six proteins were higher in group IV (S + O). The levels of vimentin, lactate dehydrogenase A, and triose phosphate isomerase were decreased by both smoking and ozone treatment in Western blotting and proteomic analyses. In contrast, TBC1 domain family 5 (TBC1D5) and lamin A were increased by both smoking and ozone treatment. Conclusions TBC1D5 could be a biomarker of ozone-induced lung injury in emphysema. PMID:25589837

Health risks of passive smoking.

PubMed

Papier, C M; Stellman, S D

1986-01-01

Passive or involuntary smoking is the inhalation of smoke which escapes directly into the air from the lit end of a burning cigarette. This unfiltered smoke contains the same toxic components of the mainstream smoke inhaled directly by the smoker, including numerous carcinogens, many in greater concentrations. It has long been known that exposure to this type of smoke leads to increased respiratory and other adverse health conditions in non-smokers, especially children. During the past five years, evidence has been accumulating that risk of lung cancer is also higher, particularly in non-smoking women whose husbands smoke. Despite uncertainties and differences in interpretation of various cancer studies, there is ample justification for public health measures now in place or proposed, such as restriction or elimination of smoking in the workplace and in public places.

[Passive smoking--health consequences and effects of exposure prevention].

PubMed

Raupach, T; Radon, K; Nowak, D; Andreas, S

2008-01-01

Passive smoking is the third leading but preventable cause of death worldwide. It is associated with an elevated risk of developing acute respiratory diseases, obstructive lung disorders, lung cancer, and cardiovascular disease. Whereas the dose-response relationship between second-hand smoke exposure and respiratory diseases is likely to be linear, a non-linear dose-response curve has been observed with respect to acute cardiovascular events. This explains the disproportionately high risk of myocardial infarction among passive smokers as compared to unexposed individuals. Over the last ten years, exposure to second-hand smoke has declined in Germany, but it is still substantial. With passive smoking in the home being a difficult target for preventive measures, public smoking bans have recently been shown to greatly reduce second-hand smoke-related morbidity and mortality. In addition, such measures are usually well tolerated and highly relevant regarding legal aspects related to workplace issues. This article summarises the current evidence on the health consequences of passive smoking and on the favourable effects of public smoking bans.

Cue-induced cigarette cravings and smoking cessation: the role of expectancies.

PubMed

Erblich, Joel; Montgomery, Guy H

2012-07-01

Cue-induced cigarette cravings have been oft studied as potentially important predictors of smoking cessation outcomes. The literature on the relationship between cue-induced cravings and cessation, however, remains mixed. One possible explanation for the discrepant results in the literature may be the as-yet untested variability in expectancies of craving. Indeed, as with many interoceptive responses, cravings and their downstream consequences may be influenced by expectancies. To date, no study has examined the influence of expected cravings following smoking cue exposures on actual craving experiences and cessation outcomes. The objective of this study, therefore, was to test the possibility that smokers' expected craving levels in response to smoking cues would be related to actual cravings following cue exposure and that expected cravings would be related to cessation outcomes. Nicotine-dependent adult smokers (n = 153) were exposed to sets of neutral and smoking cues and completed questionnaires assessing (a) prior to the exposures, the cigarette craving levels they expected to experience following the cue exposures and (b) following the exposures, their actual craving levels. Participants also reported the duration of their most recent quit attempt and their perceived future quit difficulty. Findings indicated that expected cravings assessed prior to the cue exposures were significantly related to actual cravings following the exposures. In addition, both expected cravings and actual cravings were related to shorter previous quit duration and higher perceived quit difficulty. Study results highlight the importance of considering both expected and actual cravings in cue-induced craving paradigms.

Cue-Induced Cigarette Cravings and Smoking Cessation: The Role of Expectancies

PubMed Central

Montgomery, Guy H.

2012-01-01

Introduction: Cue-induced cigarette cravings have been oft studied as potentially important predictors of smoking cessation outcomes. The literature on the relationship between cue-induced cravings and cessation, however, remains mixed. One possible explanation for the discrepant results in the literature may be the as-yet untested variability in expectancies of craving. Indeed, as with many interoceptive responses, cravings and their downstream consequences may be influenced by expectancies. To date, no study has examined the influence of expected cravings following smoking cue exposures on actual craving experiences and cessation outcomes. The objective of this study, therefore, was to test the possibility that smokers’ expected craving levels in response to smoking cues would be related to actual cravings following cue exposure and that expected cravings would be related to cessation outcomes. Methods: Nicotine-dependent adult smokers (n = 153) were exposed to sets of neutral and smoking cues and completed questionnaires assessing (a) prior to the exposures, the cigarette craving levels they expected to experience following the cue exposures and (b) following the exposures, their actual craving levels. Participants also reported the duration of their most recent quit attempt and their perceived future quit difficulty. Results: Findings indicated that expected cravings assessed prior to the cue exposures were significantly related to actual cravings following the exposures. In addition, both expected cravings and actual cravings were related to shorter previous quit duration and higher perceived quit difficulty. Conclusions: Study results highlight the importance of considering both expected and actual cravings in cue-induced craving paradigms. PMID:22218404

Protective effects of aerosolized scopolamine against soman-induced acute respiratory toxicity in guinea pigs.

PubMed

Perkins, Michael W; Pierre, Zdenka; Rezk, Peter; Song, Jian; Oguntayo, Samuel; Morthole, Venee; Sciuto, Alfred M; Doctor, Bhupendra P; Nambiar, Madhusoodana P

2011-12-01

The protective efficacy of the antimuscarinic agent scopolamine was evaluated against soman (o-pinacolyl methylphosphonofluoridate [GD])-induced respiratory toxicity in guinea pigs. Anesthetized animals were exposed to GD (841 mg/m(3)) by microinstillation inhalation exposure and treated 30 seconds later with endotracheally aerosolized scopolamine (0.25 mg/kg) and allowed to recover for 24 hours. Treatment with scopolamine significantly increased survival and reduced clinical signs of toxicity and body weight loss in GD-exposed animals. Analysis of bronchoalveolar lavage (BAL) fluid showed normalization of GD-induced increased cell death, total cell count, and protein following scopolamine treatment. The BAL fluid acetylcholinesterase and butyrylcholinesterase levels were also increased by scopolamine treatment. Respiratory dynamics parameters were normalized at 4 and 24 hours post-GD exposure in scopolamine-treated animals. Lung histology showed that scopolamine treatment reduced bronchial epithelial and subepithelial inflammation and multifocal alveolar septal edema. These results suggest that aerosolized scopolamine considerably protects against GD-induced respiratory toxicity.

[Respiratory diseases in black African carceral area].

PubMed

Toloba, Y; Soumaré, D; Ouattara, K; Kanouté, T; Boré, O; Dolo, O; Baya, B; Berthé, G; Diallo, S

2017-09-01

The measures for people in specific situations such as prisoners are part of the Millennium Development Goals (MDGs). The objective of this study was to assess respiratory pathologies in a black African carceral center. Retrospective study about the prevalence of respiratory pathologies in the arrest central house for men in Bamako (Mali), from May 2012 to April 2013. The admission records have served as data checking support on detainee's records. Statistical significance was investigated by the SAS 9.3 software with a threshold of 5%. Of 2740 admissions, 207 concerned respiratory pathologies (7.5%). All men, were of mean age 30±13 years (range 19-71). The respiratory diseases found were: pneumonia (33.8%), chronic bronchitis (26.6%), acute respiratory infection (14%), asthma (13.5%) and tuberculosis (5.3%). A definite diagnosis was made in 42% of cases. A tobacco intoxication was found in all age groups (CI 95%, R-square=0.01), without significant difference between the occurrence of cough in smoking and non-smoking men. According to their relative frequencies, the management of respiratory diseases requires collaboration between carceral health facilities and pneumological specialized services. Copyright © 2017 SPLF. Published by Elsevier Masson SAS. All rights reserved.

p-Benzoquinone-induced aggregation and perturbation of structure and chaperone function of α-crystallin is a causative factor of cigarette smoke-related cataractogenesis.

PubMed

Chowdhury, Aritra; Choudhury, Aparajita; Chakraborty, Shruti; Ghosh, Arunava; Banerjee, Victor; Ganguly, Shinjini; Bhaduri, Gautam; Banerjee, Rajat; Das, Kalipada; Chatterjee, Indu B

2018-02-01

Cigarette smoking is a significant risk factor for cataract. However, the mechanism by which cigarette smoke (CS) causes cataract remains poorly understood. We had earlier shown that in CS-exposed guinea pig, p-benzoquinone (p-BQ) derived from CS in the lungs is carried by the circulatory system to distant organs and induces various smoke-related pathogeneses. Here, we observed that CS exposure caused accumulation of the p-BQ-protein adduct in the eye lens of guinea pigs. We also observed accumulation of the p-BQ-protein adduct in resected lens from human smokers with cataract. No such accumulation was observed in the lens of never smokers. p-BQ is a strong arylating agent that forms Michael adducts with serum albumin and haemoglobin resulting in alterations of structure and function. A major protein in the mammalian eye lens is αA-crystallin, which is a potent molecular chaperone. αA-crystallin plays a key role in maintaining the integrity and transparency of the lens. SDS-PAGE indicated that p-BQ induced aggregation of αA-crystallin. Various biophysical techniques including UV-vis spectroscopy, fluorescence spectroscopy, FT-IR, bis-ANS titration suggested a perturbation of structure and chaperone function of αA-crystallin upon p-BQ modification. Our results indicate that p-BQ is a causative agent involved in the modification of αA-crystallin and pathogenesis of CS-induced cataract. Our findings would educate public about the impacts of smoking on eye health and help to discourage them from smoking. The study might also help scientists to develop new drugs for the intervention of CS-induced cataract at an early stage. Copyright © 2017 Elsevier B.V. All rights reserved.

The toxicology of zinc chloride smoke producing bombs and screens.

PubMed

El Idrissi, Ayman; van Berkel, Lisanne; Bonekamp, Nadia E; Dalemans, Diana J Z; van der Heyden, Marcel A G

2017-03-01

Zinc chloride (ZnCl 2 )-based smoke bombs and screens are in use since the Second World War (1939-1945). Many case descriptions on ZnCl 2 smoke inhalation incidents appeared since 1945. We provide a comprehensive overview of the clinical symptoms and underlying pathophysiology due to exposure to fumes from ZnCl 2 smoke producing bombs. In addition, we give a historical overview of treatment regimens and their outcomes. We performed a literature search on Medline, Scopus and Google Scholar databases using combinations of the following search terms "smoke bomb", "smoke screen", "ZnCl 2 ", "intoxication", "poisoning", "case report", "HE smoke", "hexachloroethane smoke", "smoke inhalation" and "white smoke". We retrieved additional reports based on the primary hits. We collected 30 case reports from the last seven decades encompassing 376 patients, 23 of whom died. Of all the patient descriptions, 31 were of sufficient detail for prudent analysis. Intoxication with clinical signs mainly took place in war situations and in military and fire emergency training sessions in enclosed spaces. Symptoms follow a biphasic course mainly characterised by dyspnoea, coughing and lacrimation, related to irritation of the airways in the first six hours, followed by reappearance of early signs complemented with inflammation related signs and tachycardia from 24 h onwards. Acute respiratory stress syndrome developed in severely affected individuals. Chest radiographs did not always correspond with clinical symptoms. Common therapy comprises corticosteroids, antibiotics and supplemental oxygen or positive pressure ventilation in 64% of the cases. Of the 31 patients included, eight died, three had permanent lung damage and 15 showed complete recovery, whereas in five patients outcome was not reported. Early signs likely relate to caustic reactions in the airway lining, whereas inhaled ZnCl 2 particles may trigger an inflammatory response and associated delayed fibrotic lung damage

Parental and household smoking and the increased risk of bronchitis, bronchiolitis and other lower respiratory infections in infancy: systematic review and meta-analysis.

PubMed

Jones, Laura L; Hashim, Ahmed; McKeever, Tricia; Cook, Derek G; Britton, John; Leonardi-Bee, Jo

2011-01-10

Passive smoke exposure increases the risk of lower respiratory infection (LRI) in infants, but the extensive literature on this association has not been systematically reviewed for nearly ten years. The aim of this paper is to provide an updated systematic review and meta-analysis of studies of the association between passive smoking and LRI, and with diagnostic subcategories including bronchiolitis, in infants aged two years and under. We searched MEDLINE and EMBASE (to November 2010), reference lists from publications and abstracts from major conference proceedings to identify all relevant publications. Random effect pooled odds ratios (OR) with 95% confidence intervals (CI) were estimated. We identified 60 studies suitable for inclusion in the meta-analysis. Smoking by either parent or other household members significantly increased the risk of LRI; odds ratios (OR) were 1.22 (95% CI 1.10 to 1.35) for paternal smoking, 1.62 (95% CI 1.38 to 1.89) if both parents smoked, and 1.54 (95% CI 1.40 to 1.69) for any household member smoking. Pre-natal maternal smoking (OR 1.24, 95% CI 1.11 to 1.38) had a weaker effect than post-natal smoking (OR 1.58, 95% CI 1.45 to 1.73). The strongest effect was on bronchiolitis, where the risk of any household smoking was increased by an OR of 2.51 (95% CI 1.96 to 3.21). Passive smoking in the family home is a major influence on the risk of LRI in infants, and especially on bronchiolitis. Risk is particularly strong in relation to post-natal maternal smoking. Strategies to prevent passive smoke exposure in young children are an urgent public and child health priority.

A Phosphatidylinositol 3-kinase-regulated Akt-independent signaling promotes cigarette smoke-induced FRA-1 expression.

PubMed

Zhang, Qin; Adiseshaiah, Pavan; Kalvakolanu, Dhananjaya V; Reddy, Sekhar P

2006-04-14

The FRA-1 proto-oncogene is overexpressed in a variety of human tumors and is known to up-regulate the expression of genes involved in tumor progression and invasion. The phosphatidylinositol 3-kinase (PI3K)-Akt pathway is also known to regulate these cellular processes. More importantly, respiratory toxicants and carcinogens activate both the PI3K-Akt pathway and FRA-1 expression in human bronchial epithelial (HBE) cells. In this study we investigated a potential link between the PI3K-Akt pathway and the cigarette smoke (CS)-stimulated epidermal growth factor receptor-mediated FRA-1 induction in non-oncogenic HBE cells. Treatment of cells with LY294002, an inhibitor of the PI3K-Akt pathway, completely blocked CS-induced FRA-1 expression. Surprisingly pharmacological inhibition of Akt had no significant effect on CS-induced FRA-1 expression. Likewise the inhibition of protein kinase C zeta, which is a known downstream effector of PI3K, did not alter FRA-1 expression. We found that the PI3K through p21-activated kinase 1 regulates FRA-1 proto-oncogene induction by CS and the subsequent activation of the Elk1 and cAMP-response element-binding protein transcription factors that are bound to the promoter in HBE cells.

[Early exercise training after exacerbation in patients with chronic respiratory failure].

PubMed

Takahashi, Hiromitsu; Molleyres, Sandrine; Dousse, Nicolas; Contal, Olivier; Janssens, Jean-Paul

2011-11-23

Patients who suffered from an exacerbation of a chronic respiratory disorder are often very limited in terms of their exercise capacity because of severe dyspnea and amyotrophy of peripheral muscles. Early implementation of pulmonary rehabilitation may help these patients to avoid the complications of a prolonged bedridden period, and increase more rapidly their mobility. Early rehabilitation has become more frequent, but requires special skills from the care givers (chest therapists). Techniques which enhance muscular performance and motility of patients who are recovering from an exacerbation such as electromoystimulation or mobilisation under non-invasive ventilation, give encouraging results; their impact on length of hospital stay requires further studies.

Exercise training attenuated chronic cigarette smoking-induced up-regulation of FIZZ1/RELMα in lung of rats.

PubMed

Ma, Wan-li; Cai, Peng-cheng; Xiong, Xian-zhi; Ye, Hong

2013-02-01

FIZZ/RELM is a new gene family named "found in inflammatory zone" (FIZZ) or "resistin-like molecule" (RELM). FIZZ1/RELMα is specifically expressed in lung tissue and associated with pulmonary inflammation. Chronic cigarette smoking up-regulates FIZZ1/RELMα expression in rat lung tissues, the mechanism of which is related to cigarette smoking-induced airway hyperresponsiveness. To investigate the effect of exercise training on chronic cigarette smoking-induced airway hyperresponsiveness and up-regulation of FIZZ1/RELMα, rat chronic cigarette smoking model was established. The rats were treated with regular exercise training and their airway responsiveness was measured. Hematoxylin and eosin (HE) staining, immunohistochemistry and in situ hybridization of lung tissues were performed to detect the expression of FIZZ1/RELMα. Results revealed that proper exercise training decreased airway hyperresponsiveness and pulmonary inflammation in rat chronic cigarette smoking model. Cigarette smoking increased the mRNA and protein levels of FIZZ1/RELMα, which were reversed by the proper exercise. It is concluded that proper exercise training prevents up-regulation of FIZZ1/RELMα induced by cigarette smoking, which may be involved in the mechanism of proper exercise training modulating airway hyperresponsiveness.

Comparative Risks of Aldehyde Constituents in Cigarette Smoke Using Transient Computational Fluid Dynamics/Physiologically Based Pharmacokinetic Models of the Rat and Human Respiratory Tracts

PubMed Central

Corley, Richard A.; Kabilan, Senthil; Kuprat, Andrew P.; Carson, James P.; Jacob, Richard E.; Minard, Kevin R.; Teeguarden, Justin G.; Timchalk, Charles; Pipavath, Sudhakar; Glenny, Robb; Einstein, Daniel R.

2015-01-01

Computational fluid dynamics (CFD) modeling is well suited for addressing species-specific anatomy and physiology in calculating respiratory tissue exposures to inhaled materials. In this study, we overcame prior CFD model limitations to demonstrate the importance of realistic, transient breathing patterns for predicting site-specific tissue dose. Specifically, extended airway CFD models of the rat and human were coupled with airway region-specific physiologically based pharmacokinetic (PBPK) tissue models to describe the kinetics of 3 reactive constituents of cigarette smoke: acrolein, acetaldehyde and formaldehyde. Simulations of aldehyde no-observed-adverse-effect levels for nasal toxicity in the rat were conducted until breath-by-breath tissue concentration profiles reached steady state. Human oral breathing simulations were conducted using representative aldehyde yields from cigarette smoke, measured puff ventilation profiles and numbers of cigarettes smoked per day. As with prior steady-state CFD/PBPK simulations, the anterior respiratory nasal epithelial tissues received the greatest initial uptake rates for each aldehyde in the rat. However, integrated time- and tissue depth-dependent area under the curve (AUC) concentrations were typically greater in the anterior dorsal olfactory epithelium using the more realistic transient breathing profiles. For human simulations, oral and laryngeal tissues received the highest local tissue dose with greater penetration to pulmonary tissues than predicted in the rat. Based upon lifetime average daily dose comparisons of tissue hot-spot AUCs (top 2.5% of surface area-normalized AUCs in each region) and numbers of cigarettes smoked/day, the order of concern for human exposures was acrolein > formaldehyde > acetaldehyde even though acetaldehyde yields were 10-fold greater than formaldehyde and acrolein. PMID:25858911

Vegetation fire smoke, indigenous status and cardio-respiratory hospital admissions in Darwin, Australia, 1996–2005: a time-series study

PubMed Central

Hanigan, Ivan C; Johnston, Fay H; Morgan, Geoffrey G

2008-01-01

Background Air pollution in Darwin, Northern Australia, is dominated by smoke from seasonal fires in the surrounding savanna that burn during the dry season from April to November. Our aim was to study the association between particulate matter less than or equal to 10 microns diameter (PM10) and daily emergency hospital admissions for cardio-respiratory diseases for each fire season from 1996 to 2005. We also investigated whether the relationship differed in indigenous Australians; a disadvantaged population sub-group. Methods Daily PM10 exposure levels were estimated for the population of the city from visibility data using a previously validated model. We used over-dispersed Poisson generalized linear models with parametric smoothing functions for time and meteorology to examine the association between admissions and PM10 up to three days prior. An interaction between indigenous status and PM10 was included to examine differences in the impact on indigenous people. Results We found both positive and negative associations and our estimates had wide confidence intervals. There were generally positive associations between respiratory disease and PM10 but not with cardiovascular disease. An increase of 10 μg/m3 in same-day estimated ambient PM10 was associated with a 4.81% (95%CI: -1.04%, 11.01%) increase in total respiratory admissions. When the interaction between indigenous status and PM10 was assessed a statistically different association was found between PM10 and admissions three days later for respiratory infections of indigenous people (15.02%; 95%CI: 3.73%, 27.54%) than for non-indigenous people (0.67%; 95%CI: -7.55%, 9.61%). There were generally negative estimates for cardiovascular conditions. For non-indigenous admissions the estimated association with total cardiovascular admissions for same day ambient PM10 and admissions was -3.43% (95%CI: -9.00%, 2.49%) and the estimate for indigenous admissions was -3.78% (95%CI: -13.4%, 6.91%), although ambient PM

A mouse model for MERS coronavirus-induced acute respiratory distress syndrome.

PubMed

Cockrell, Adam S; Yount, Boyd L; Scobey, Trevor; Jensen, Kara; Douglas, Madeline; Beall, Anne; Tang, Xian-Chun; Marasco, Wayne A; Heise, Mark T; Baric, Ralph S

2016-11-28

Middle East respiratory syndrome coronavirus (MERS-CoV) is a novel virus that emerged in 2012, causing acute respiratory distress syndrome (ARDS), severe pneumonia-like symptoms and multi-organ failure, with a case fatality rate of ∼36%. Limited clinical studies indicate that humans infected with MERS-CoV exhibit pathology consistent with the late stages of ARDS, which is reminiscent of the disease observed in patients infected with severe acute respiratory syndrome coronavirus. Models of MERS-CoV-induced severe respiratory disease have been difficult to achieve, and small-animal models traditionally used to investigate viral pathogenesis (mouse, hamster, guinea-pig and ferret) are naturally resistant to MERS-CoV. Therefore, we used CRISPR-Cas9 gene editing to modify the mouse genome to encode two amino acids (positions 288 and 330) that match the human sequence in the dipeptidyl peptidase 4 receptor, making mice susceptible to MERS-CoV infection and replication. Serial MERS-CoV passage in these engineered mice was then used to generate a mouse-adapted virus that replicated efficiently within the lungs and evoked symptoms indicative of severe ARDS, including decreased survival, extreme weight loss, decreased pulmonary function, pulmonary haemorrhage and pathological signs indicative of end-stage lung disease. Importantly, therapeutic countermeasures comprising MERS-CoV neutralizing antibody treatment or a MERS-CoV spike protein vaccine protected the engineered mice against MERS-CoV-induced ARDS.

Vasoprotective effects of resveratrol and SIRT1: attenuation of cigarette smoke-induced oxidative stress and proinflammatory phenotypic alterations

PubMed Central

Csiszar, Anna; Labinskyy, Nazar; Podlutsky, Andrej; Kaminski, Pawel M.; Wolin, Michael S.; Zhang, Cuihua; Mukhopadhyay, Partha; Pacher, Pal; Hu, Furong; de Cabo, Rafael; Ballabh, Praveen; Ungvari, Zoltan

2008-01-01

The dietary polyphenolic compound resveratrol, by activating the protein deacetylase enzyme silent information regulator 2/sirtuin 1 (SIRT1), prolongs life span in evolutionarily distant organisms and may mimic the cytoprotective effects of dietary restriction. The present study was designed to elucidate the effects of resveratrol on cigarette smoke-induced vascular oxidative stress and inflammation, which is a clinically highly relevant model of accelerated vascular aging. Cigarette smoke exposure of rats impaired the acetylcholine-induced relaxation of carotid arteries, which could be prevented by resveratrol treatment. Smoking and in vitro treatment with cigarette smoke extract (CSE) increased reactive oxygen species production in rat arteries and cultured coronary arterial endothelial cells (CAECs), respectively, which was attenuated by resveratrol treatment. The smoking-induced upregulation of inflammatory markers (ICAM-1, inducible nitric oxide synthase, IL-6, and TNF-α) in rat arteries was also abrogated by resveratrol treatment. Resveratrol also inhibited CSE-induced NF-κB activation and inflammatory gene expression in CAECs. In CAECs, the aforementioned protective effects of resveratrol were abolished by knockdown of SIRT1, whereas the overexpression of SIRT1 mimicked the effects of resveratrol. Resveratrol treatment of rats protected aortic endothelial cells against cigarette smoking-induced apoptotic cell death. Resveratrol also exerted antiapoptotic effects in CSE-treated CAECs, which could be abrogated by knockdown of SIRT1. Resveratrol treatment also attenuated CSE-induced DNA damage in CAECs (comet assay). Thus resveratrol and SIRT1 exert antioxidant, anti-inflammatory, and antiapoptotic effects, which protect the endothelial cells against the adverse effects of cigarette smoking-induced oxidative stress. The vasoprotective effects of resveratrol will likely contribute to its anti-aging action in mammals and may be especially beneficial in patho

Formaldehyde exposures from tobacco smoke: a review.

PubMed Central

Godish, T

1989-01-01

Reports of formaldehyde levels in mainstream, sidestream, and environmental tobacco smoke from nine studies are reviewed. Considerable disparity exists between formaldehyde production rates determined from mainstream-sidestream studies and those reporting levels in environmental tobacco smoke. Tobacco smoke does not appear to increase vapor-phase formaldehyde levels significantly in indoor environments, but formaldehyde exposure in mainstream smoke may pose a risk of upper respiratory system cancer and increase the risk of cancer in smokers. PMID:2665532

Think twice: misleading food-induced respiratory symptoms in children with food allergy.

PubMed

Ahrens, B; Mehl, A; Lau, S; Kroh, L; Magdorf, K; Wahn, U; Beyer, K; Niggemann, B

2014-03-01

Reported food-related symptoms of patients may sometimes be misleading. A correct delineation of food-induced symptoms is often difficult and various differential diagnoses have to be considered. We report on two cases of food-induced, predominantly respiratory symptoms (in one case life-threatening) in children with food allergy. First, a two-year-old boy with no history of allergies and suspected foreign body aspiration which was finally diagnosed as an anaphylactic reaction to fish, and secondly a six-year-old girl with multiple food allergies and allergic asthma who during an electively performed oral food challenge developed severe respiratory distress, drop in blood pressure, and asphyxia not due to an anaphylactic reaction but due to choking on an unnoticed sweet. These two cases represent challenging, life-threatening symptom constellations involving food-induced reactions in food allergic children, reminding us to question first impressions. © 2013 Wiley Periodicals, Inc.

Smoking and Early COPD as Independent Predictors of Body Composition, Exercise Capacity, and Health Status.

PubMed

Caram, Laura Miranda de Oliveira; Ferrari, Renata; Bertani, André Luís; Garcia, Thaís; Mesquita, Carolina Bonfanti; Knaut, Caroline; Tanni, Suzana Erico; Godoy, Irma

2016-01-01

The effects of tobacco smoke, mild/moderate COPD disease and their combined effect on health status (HS), body composition (BC), and exercise capacity (EC) impairment are still unclear. We hypothesized that smoking and early COPD have a joint negative influence on these outcomes. We evaluated 32 smokers (smoking history >10 pack/years), 32 mild/moderate COPD (current smokers or former smokers), and 32 never smokers. All individuals underwent medical and smoking status evaluations, pre and post-bronchodilator spirometry, BC [fat-free mass (FFM) and FFM index (FFMI)], EC [six-minute walk distance (6MWD)] and HS [Medical Outcomes Study 36-Item Short-Form Health Survey (SF-36)]. FFM (p = 0.02) and FFMI (p = 0.008) were lower in COPD than never smokers. 6MWT, as a percentage of reference values for the Brazilian population, was lower in COPD and smokers than never smokers (p = 0.01). Smokers showed worse SF-36 score for functional capacity than never smokers (p<0.001). SF-36 score for physical functioning (p<0.001) and role-emotional (p<0.001) were impaired in COPD patients than smokers. SF-36 scores for physical functioning (p<0.001), role-physical (p = 0.01), bodily pain (p = 0.01), vitality (p = 0.04) and role-emotional (p<0.001) were lower in COPD than never smokers. Multiple linear regression analysis showed that both COPD diagnosis and smoking were inversely associated with FFMI, 6MWD and HS. Smoking and early COPD have a joint negative influence on body composition, exercise capacity and health status.

A randomized controlled trial of two primary school intervention strategies to prevent early onset tobacco smoking.

PubMed

Storr, Carla L; Ialongo, Nicholas S; Kellam, Sheppard G; Anthony, James C

2002-03-01

In this article, we examine the impact of two universal, grade 1 preventive interventions on the onset of tobacco smoking as assessed in early adolescence. The classroom-centered (CC) intervention was designed to reduce the risk for tobacco smoking by enhancing teachers' behavior management skills in first grade and, thereby, reducing child attention problems and aggressive and shy behavior-known risk behaviors for later substance use. The family-school partnership (FSP) intervention targeted these early risk behaviors via improvements in parent-teacher communication and parents' child behavior management strategies. A cohort of 678 urban, predominately African-American, public school students were randomly assigned to one of three Grade 1 classrooms at entrance to primary school (age 6). One classroom featured the CC intervention, a second the FSP intervention, and the third served as a control classroom. Six years later, 81% of the students completed audio computer-assisted self-interviews. Relative to controls, a modest attenuation in the risk of smoking initiation was found for students who had been assigned to either the CC or FSP intervention classrooms (26% versus 33%) (adjusted relative risk for CC/control contrast=0.57, 95% confidence interval (CI), 0.34-0.96; adjusted relative risk for FSP/control contrast=0.69, 95% CI, 0.50-0.97). Results lend support to targeting the early antecedent risk behaviors for tobacco smoking.

Smoking and Pregnancy

MedlinePlus

Smoking and Pregnancy Smoking can cause problems for a woman trying to become pregnant or who is already pregnant, and for her baby ... too early • Pregnancy occurs outside of the womb Smoking causes these health effects. Smoking could cause these ...

Longitudinal study of respiratory function and symptoms in a non-smoking group of long-term officially-acknowledged victims of pollution-related illness.

PubMed

Tanaka, Takako; Asai, Masaharu; Yanagita, Yorihide; Nishinakagawa, Tsuyoshi; Miyamoto, Naomi; Kotaki, Kenji; Yano, Yudai; Kozu, Ryo; Honda, Sumihisa; Senjyu, Hideaki

2013-08-17

Air pollution is known to be a leading cause of respiratory symptoms. Many cross-sectional studies reported that air pollution caused respiratory disease in Japanese individuals in the 1960s. Japan has laws regulating air pollution levels and providing compensation for victims of pollution-related respiratory disease. However, long-term changes in respiratory function and symptoms in individuals who were exposed to air pollution in the 1960s have not been well studied. This study aimed to investigate longitudinal respiratory function and symptoms in older, non-smoking, long-term officially-acknowledged victims of pollution-related illness. The study included 563 officially-acknowledged victims of pollution-related illness living in Kurashiki, Okayama who were aged ≥ 65 years in 2009. Data were retrospectively collected from yearly respiratory symptom questionnaires and spirometry examinations conducted from 2000 to 2009. Respiratory function declined significantly from 2000 to 2009 (p < 0.01), but the mean annual changes were relatively small. The change in mean vital capacity was -40.5 ml/year in males and -32.7 ml/year in females, and the change in mean forced expiratory volume in 1 second was -27.6 ml/year in males and -23.9 ml/year in females. Dyspnea was the only symptom that worsened significantly from 2000 to 2009 in both sexes (males: p < 0.05, females: p < 0.01). Our results suggest that the high concentrations of air pollutants around 1970 resulted in a decrease in respiratory function and an increase in respiratory symptoms in the study population. From 2000 to 2009, the mean annual changes in respiratory function were within the normal range, even though the severity of dyspnea worsened. The changes in respiratory function and symptoms over the study period were probably due to aging. The laws governing air pollution levels and providing compensation for officially-acknowledged victims of pollution-related illness in Japan may be effective for

Longitudinal study of respiratory function and symptoms in a non-smoking group of long-term officially-acknowledged victims of pollution-related illness

PubMed Central

2013-01-01

Background Air pollution is known to be a leading cause of respiratory symptoms. Many cross-sectional studies reported that air pollution caused respiratory disease in Japanese individuals in the 1960s. Japan has laws regulating air pollution levels and providing compensation for victims of pollution-related respiratory disease. However, long-term changes in respiratory function and symptoms in individuals who were exposed to air pollution in the 1960s have not been well studied. This study aimed to investigate longitudinal respiratory function and symptoms in older, non-smoking, long-term officially-acknowledged victims of pollution-related illness. Methods The study included 563 officially-acknowledged victims of pollution-related illness living in Kurashiki, Okayama who were aged ≥ 65 years in 2009. Data were retrospectively collected from yearly respiratory symptom questionnaires and spirometry examinations conducted from 2000 to 2009. Results Respiratory function declined significantly from 2000 to 2009 (p < 0.01), but the mean annual changes were relatively small. The change in mean vital capacity was −40.5 ml/year in males and −32.7 ml/year in females, and the change in mean forced expiratory volume in 1 second was −27.6 ml/year in males and −23.9 ml/year in females. Dyspnea was the only symptom that worsened significantly from 2000 to 2009 in both sexes (males: p < 0.05, females: p < 0.01). Conclusions Our results suggest that the high concentrations of air pollutants around 1970 resulted in a decrease in respiratory function and an increase in respiratory symptoms in the study population. From 2000 to 2009, the mean annual changes in respiratory function were within the normal range, even though the severity of dyspnea worsened. The changes in respiratory function and symptoms over the study period were probably due to aging. The laws governing air pollution levels and providing compensation for officially-acknowledged victims of pollution

[Hospitality workers' exposure to environmental tobacco smoke before and after implementation of smoking ban in public places: a review of epidemiological studies].

PubMed

Polańska, Kinga; Hanke, Wojciech; Konieczko, Katarzyna

2011-01-01

Environmental tobacco smoke (ETS) exposure induces serious negative health consequences, of which the increased risk of cardiovascular diseases, cancer, respiratory symptoms and poor pregnancy outcomes appear to be most important. Taking into account those health consequences of ETS exposure most countries have introduced legislation to ban or restrict smoking in public places. In this paper the effectiveness of the introduced legislation was analyzed with regard to the protection of hospitality workers from ETS exposure in the workplace. The analysis of 12 papers published after 2000 covered the year of publication, type of legislation, study population, hospitality venue (pub, bar, restaurant, disco) and type of markers or self-reported perception of exposure to ETS. The analysis indicates that the legislation to ban smoking in hospitality venues protects workers from ETS exposure when the venues are 100% tobacco smoke free. The reduction of the cotinine level in biological samples after the implementation of smoke free law was 57-89%, comparing to the biomarker level in the samples taken before the new law was introduced. About 90% of reduction in nicotine and PM levels was also noted. In addition, the positive self perception reported by workers proved the effectiveness of new legislation protecting them from ETS exposure.

Respiratory Abnormalities among Occupationally Exposed, Non-Smoking Brick Kiln Workers from Punjab, India.

PubMed

Tandon, Supriya; Gupta, Sharat; Singh, Sharanjeet; Kumar, Avnish

2017-07-01

Brick manufacturing industry is one of the oldest and fast-growing industries in India that employs a large section of people. Brick kiln workers are occupationally exposed to air pollutants. Nonetheless, only a few studies have so far been conducted on their respiratory health. To investigate the extent of respiratory impairment in brick kiln workers and to correlate it with the duration of exposure. A cross-sectional study was conducted. Spirometric parameters of 110 non-smoking male brick kiln workers aged 18-35 years in Patiala district, Punjab, India, were compared with an age-matched comparison group of 90 unexposed individuals. Brick kiln workers showed a significant (p<0.05) decline in forced expiratory volume in 1 second (FEV 1 ), forced vital capacity (FVC), forced mid-expiratory flow rate (FEF 25-75% ) and peak expiratory flow rate (PEFR) compared with those of the comparison group. The extent of deterioration in lung function of brick kiln workers was associated with the duration of exposure. In workers with >8 years of exposure, the mean values of FEV 1 (1.92 L), FVC (2.01 L), FEF 25-75% (2.19 L/s) and PEFR (4.81 L/s) were significantly (p<0.05) lower than those recorded in workers with <8 years of exposure in whom the values were 2.01 L, 2.68 L, 2.71 L/s, and 5.76 L/s, respectively. There is a significant association between exposure to workplace pollutants and lung function deterioration among brick kiln workers.

Neural correlates of message tailoring and self-relatedness in smoking cessation programming

PubMed Central

Chua, Hannah Faye; Liberzon, Israel; Welsh, Robert C.; Strecher, Victor J.

2011-01-01

BACKGROUND Smoking leads to illnesses including addiction, cancer, and cardiovascular and respiratory diseases. Different intervention programs have become available. In the past decade, providing tailored smoking cessation messages has been shown to be more effective in inducing smoking cessation than one-size-fits-all interventions. However, little is known about the brain responses of smokers when they receive tailored smoking cessation messages. METHODS A neuroimaging study using blocked and event-related designs examined neural activity in 24 smokers exposed to high-tailored and low-tailored smoking cessation messages. RESULTS: In both blocked and event-related conditions, rostral medial prefrontal cortex and precuneus/posterior cingulate were engaged more during the processing of high-tailored smoking cessation messages than low-tailored smoking cessation messages. CONCLUSION The activation patterns of smokers to tailored cessation messages show involvement of brain areas commonly implicated in self-related processing. Results seem to add support to the suggested role of self-relevance in tailored cessation programs, where previous studies have shown a potential mediating role of self-relevance on smoking abstinence. The findings are relevant to understanding the cognitive mechanisms underlying tailored message processing and may point to new directions for testing response to health communications programming. PMID:18926523

Detrimental effects of secondhand smoke exposure on infants with cystic fibrosis.

PubMed

Kopp, Benjamin T; Sarzynski, Lisa; Khalfoun, Sabrina; Hayes, Don; Thompson, Rohan; Nicholson, Lisa; Long, Frederick; Castile, Robert; Groner, Judith

2015-01-01

Secondhand smoke (SHS) has deleterious respiratory, immune, and nutritional effects in children, but there is little data regarding the effects of SHS exposure in infants with cystic fibrosis (CF). A retrospective chart review was undertaken from 2008 to 2012 of 75 infants with CF. Growth, lung function, Chest CT imaging, and microbiologic characteristics were compared between 4 and 12 months for SHS and non-SHS exposed patients. SHS exposed infants with CF had decreased growth between 4 and 12 months compared to non-SHS exposed infants. SHS exposure was associated with increased bronchodilator responsiveness and air trapping, but no other lung function or radiologic differences. SHS exposure was also associated with increased methicillin resistant Staphylococcus aureus (MRSA) and anaerobic growth on respiratory culture. There was no difference in Pseudomonas aeruginosa between groups. There were no differences in antibiotic use or hospitalizations between the groups. SHS exposure in CF infants is associated with diminished growth, increased air trapping and bronchodilator responsiveness, and propensity to culture MRSA and facultative anaerobic bacteria, suggesting the need for early, aggressive parental smoking cessation interventions to prevent SHS exposure complications. © 2014 Wiley Periodicals, Inc.

The MAP kinase JNK2 mediates cigarette smoke-induced arterial thrombosis.

PubMed

Breitenstein, Alexander; Stämpfli, Simon F; Reiner, Martin F; Shi, Yi; Keller, Stephan; Akhmedov, Alexander; Schaub Clerigué, Ariane; Spescha, Remo D; Beer, Hans-Jürg; Lüscher, Thomas F; Tanner, Felix C; Camici, Giovanni G

2017-01-05

Despite public awareness of its deleterious effects, smoking remains a major cause of death. Indeed, it is a risk factor for atherothrombotic complications and in line with this, the introduction of smoking ban in public areas reduced smoking-associated cardiovascular complications. Nonetheless, smoking remains a major concern, and molecular mechanisms by which it causes cardiovascular disease are not known. Peripheral blood monocytes from healthy smokers displayed increased JNK2 and tissue factor (TF) gene expression compared to non-smokers (n=15, p<0.05). Similarly, human aortic endothelial cells exposed to cigarette smoke total particulate matter (CS-TPM) revealed increased TF expression mediated by JNK2 (n=4; p<0.05). Wild-type and JNK2 -/- mice were exposed to cigarette smoke for two weeks after which arterial thrombosis was investigated. Wild-type mice exposed to smoke displayed reduced time to thrombotic arterial occlusion (n=8; p<0.05) and increased tissue factor activity (n=7; p<0.05) as compared to wild-type controls (n=6), while JNK2 -/- mice exposed to smoke maintained an unaltered thrombotic potential (n=8; p=NS) and tissue factor activity (n=8) comparable to that of JNK2 -/- and wild-type controls (n=6; p=NS). Smoking caused an increased production of reactive oxygen species (ROS) in wild-type but not in JNK2 -/- mice (n=7; p<0.05 for wild-type mice and n=5-6; p=NS for JNK2 -/- mice). In conclusion, the MAP kinase JNK2 mediates cigarette smoke-induced TF activation, arterial thrombosis and ROS production. These results underscore a major role of JNK2 in smoke-mediated thrombus formation and may offer an attractive target to prevent smoke-related thrombosis in those subjects which do not manage quitting.

Chronic respiratory disease in the regional and remote population of the Northern Territory Top End: A perspective from the specialist respiratory outreach service.

PubMed

Kruavit, Anuk; Fox, Melissa; Pearson, Rebecca; Heraganahally, Subash

2017-10-01

To study the demographic, rates and types of chronic respiratory conditions in Indigenous and non-Indigenous patients in regional and remote communities of Northern Territory Top End, who were referred to the specialist respiratory outreach service. A retrospective, observational study over a 2 years period. Remote community health clinics within the Northern Territory Top End visited by the specialist respiratory outreach team. Only patients referred to respiratory specialist outreach team were included. There were 444 participants, with 210 males and 234 females. In total, 79.3% were Indigenous. The rates of chronic respiratory disease diagnoses and smoking status within the different communities and health district regions. Chronic obstructive pulmonary disease (COPD) was the most common primary respiratory condition in our cohort of patients (50.5%) followed by sleep apnoea in (14.2%), bronchiectasis in (11.6%), asthma (11%), interstitial lung disease (2.5%), nodule/cancer (1.8%) sarcoidosis (0.2%) and others (9.2%). COPD, smoking status and bronchiectasis was more frequently noted among the Indigenous patients compared to non-Indigenous patients (56.3% versus 28.3%, P < 0.001), (52.6% versus 25.0%, P < 0.001), and (12.5% versus 3.3%, P = 0.01) respectively. Obstructive sleep apnoea was more commonly diagnosed in non-Indigenous patients. Indigenous patients of the remote and rural communities of the Top End have significantly higher rates of smoking and COPD compared to non-Indigenous patients. Bronchiectasis is also more common among Indigenous patients. Further efforts are warranted to develop strategies to address the disparity and optimise the respiratory outreach service to this population. © 2017 National Rural Health Alliance Inc.

Cardiorespiratory hospitalisation and mortality reductions after smoking bans in Switzerland.

PubMed

Vicedo-Cabrera, Ana M; Röösli, Martin; Radovanovic, Dragana; Grize, Leticia; Witassek, Fabienne; Schindler, Christian; Perez, Laura

2017-01-19

Smoking bans are considered one of the most effective policies to reduce population exposure to tobacco smoke and prevent adverse health outcomes. However, evidence on the effect of contextual variables on the effectiveness of smoking bans is still lacking. The patchwork of cantonal smoke-free laws in Switzerland was used as a quasi-experimental setting to assess changes after their introduction in: hospitalisations and mortality due to cardiorespiratory diseases in adults; total hospitalisations and hospitalisations due to respiratory disorders in children; and the modifying effects of contextual factors and the effectiveness of the laws. Using hospital and mortality registry data for residents in Switzerland (2005-2012), we conducted canton-specific interrupted time-series analyses followed by random effects meta-analyses to obtain nationwide smoking ban estimates by subgroups of age, sex and causes of hospitalisation or death. Heterogeneity of the impact caused by strictness of the ban and other smoking-related characteristics of the cantons was explored through meta-regression. Total hospitalisation rates due to cardiovascular and respiratory diseases did not significantly change after the introduction of the ban. Post-ban changes were detected in ischaemic heart disease hospitalisations, with a 2.5% reduction (95% confidence interval [CI)] -6.2 to 1.3%) for all ages and 5.5% (95% CI -10.8 to -0.2%) in adults 35-64 years old. Total mortality due to respiratory diseases decreased by 8.2% (95% CI -15.2 to -0.6%) over all ages, and chronic obstructive pulmonary disease mortality decreased by 14.0% (95% CI -22.3 to -4.5%) in adults ≥65 years old. Cardiovascular mortality did not change after the introduction of the ban, but there was an indication of post-ban reductions in mortality due to hypertensive disorders (-5.4%, 95% CI -12.6 to 2.3%), and congestive heart failure (-6.0%, 95% CI -14.5 to 3.4%). No benefits were observed for hospitalisations due to

Locoregional Tumor Extension and Preoperative Smoking are Significant Risk Factors for Early Recurrence After Esophagectomy for Cancer.

PubMed

Mantziari, Styliani; Allemann, Pierre; Winiker, Michael; Demartines, Nicolas; Schäfer, Markus

2018-07-01

Tumor recurrence during the first year after oncological esophagectomy has been reported in up to 17-66% of patients. However, little is known as to the risk factors potentially associated with this adverse outcome. The aim of this retrospective observational study was to identify clinically relevant parameters associated with early recurrence. All patients with squamous cell cancer or adenocarcinoma of the esophagus or gastroesophageal junction, operated with curative intent in our center from 2000 to 2014, were screened for this study. Univariate analysis was conducted to identify variables potentially associated with early recurrence, and clinically relevant parameters with P < 0.1 were included in multiple logistic regression. Survival analyses were conducted with the Kaplan-Meier method. Significance threshold was set at P < 0.05. Among the 164 included patients, 46 (28%) presented early recurrence. Eight patients (17.4%) had locoregional and 38 patients (82.6%) metastatic recurrence. Advanced T and N stages, lymph node capsular effraction, a high positive-to-resected lymph node ratio, positive resection margins, poor response to neoadjuvant treatment, preoperative active smoking, malnutrition and dysphagia were associated with early recurrence on a univariate level. In multivariable analysis, preoperative smoking (OR 2.76, 95% CI 1.28-6.17), pT stage (OR 1.72, 95% CI 1.18-2.58) and an increased positive-to-resected lymph node ratio (OR 6.72, 95% CI 1.08-48.51) remained independently associated with ER. Our study identified both patient- and tumor-related parameters as risk factors for early recurrence after oncological esophagectomy. Of particular interest, active smoking was significantly associated with this adverse outcome, highlighting the importance of preoperative smoking cessation.

Enhanced Neutralizing Antibody Response Induced by Respiratory Syncytial Virus Prefusion F Protein Expressed by a Vaccine Candidate

PubMed Central

Liang, Bo; Surman, Sonja; Amaro-Carambot, Emerito; Kabatova, Barbora; Mackow, Natalie; Lingemann, Matthias; Yang, Lijuan; McLellan, Jason S.; Graham, Barney S.; Kwong, Peter D.; Schaap-Nutt, Anne; Collins, Peter L.

2015-01-01

ABSTRACT Respiratory syncytial virus (RSV) and human parainfluenza virus type 3 (HPIV3) are the first and second leading viral agents of severe respiratory tract disease in infants and young children worldwide. Vaccines are not available, and an RSV vaccine is particularly needed. A live attenuated chimeric recombinant bovine/human PIV3 (rB/HPIV3) vector expressing the RSV fusion (F) glycoprotein from an added gene has been under development as a bivalent vaccine against RSV and HPIV3. Previous clinical evaluation of this vaccine candidate suggested that increased genetic stability and immunogenicity of the RSV F insert were needed. This was investigated in the present study. RSV F expression was enhanced 5-fold by codon optimization and by modifying the amino acid sequence to be identical to that of an early passage of the original clinical isolate. This conferred a hypofusogenic phenotype that presumably reflects the original isolate. We then compared vectors expressing stabilized prefusion and postfusion versions of RSV F. In a hamster model, prefusion F induced increased quantity and quality of RSV-neutralizing serum antibodies and increased protection against wild-type (wt) RSV challenge. In contrast, a vector expressing the postfusion F was less immunogenic and protective. The genetic stability of the RSV F insert was high and was not affected by enhanced expression or the prefusion or postfusion conformation of RSV F. These studies provide an improved version of the previously well-tolerated rB/HPIV3-RSV F vaccine candidate that induces a superior RSV-neutralizing serum antibody response. IMPORTANCE Respiratory syncytial virus (RSV) and human parainfluenza virus type 3 (HPIV3) are two major causes of pediatric pneumonia and bronchiolitis. The rB/HPIV3 vector expressing RSV F protein is a candidate bivalent live vaccine against HPIV3 and RSV. Previous clinical evaluation indicated the need to increase the immunogenicity and genetic stability of the RSV F

Cooking fuel smoke and respiratory symptoms among women in low-income areas in Maputo.

PubMed

Ellegård, A

1996-09-01

The association between exposure to air pollution from cooking fuels and health aspects was studied in Maputo. Mozambique. Almost 1200 randomly selected women residing in the suburbs of Maputo were interviewed and 218 were monitored for air pollution. The fuels most commonly used were wood, charcoal, electricity, and liquified petroleum gas (LPG). Wood users were exposed to significantly higher levels of particulate pollution during cooking time (1200 micrograms/m3) than charcoal users (540 micrograms/m3) and users of modern fuels (LPG and electricity) (200-380 micrograms/m3). Wood users were found to have significantly more cough symptoms than other groups. This association remained significant when controlling for a large number of environmental variables. There was no difference in cough symptoms between charcoal users and users of modern fuels. Other respiratory symptoms such as dyspnea, wheezing, and inhalation and exhalation difficulties were not associated with wood use. Reducing wood use would likely improve acute respiratory health effects in wood users and possibly improve the ambient air pollution conditions in Maputo. To reduce the health impact of wood smoke exposure, it appears that the least costly and quickest method would be to encourage charcoal use to a greater extent, although high carbon monoxide levels would have to be addressed. Turning to modern fuels is beyond the means of most these households in the short term and could not be shown to be more effective.

Promoting smoking cessation among parents: effects on smoking-related cognitions and smoking initiation in children.

PubMed

Schuck, Kathrin; Otten, Roy; Kleinjan, Marloes; Bricker, Jonathan B; Engels, Rutger C M E

2015-01-01

Parental smoking is associated with an increased risk of smoking among youth. Epidemiological research has shown that parental smoking cessation can attenuate this risk. This study examined whether telephone counselling for parents and subsequent parental smoking cessation affect smoking-related cognitions and smoking initiation among children of smoking parents. Data of a two-arm randomized controlled trial were used in which 512 smoking parents were recruited into cessation support through their children's primary schools. After the baseline assessment, smoking parents were randomly assigned to tailored telephone counselling or a standard self-help brochure. Parental cessation was measured as 6-month prolonged abstinence at the 12-month follow-up. Children's smoking-related cognitions and smoking initiation were examined at 3-month, 12-month, and 30-month follow-up. No statistical evidence was found that children of parents who received telephone counselling tailored to smoking parents or children of parents who achieved prolonged abstinence differ in smoking-related cognitions (i.e., smoking outcome expectancies, perceived safety of smoking, self-efficacy to refrain from smoking, susceptibility to smoking) or smoking initiation rate on any follow-up assessment. This study is the first to examine the effects of an evidence-based smoking cessation treatment for parents and treatment-induced parental smoking cessation on cognitive and behavioural outcomes among children. Although descriptive statistics showed lower smoking initiation rates among children of parents who achieved prolonged abstinence, there was no statistical evidence that telephone counselling tailored to parents or treatment-induced parental smoking cessation affects precursors of smoking or smoking initiation among youth. Copyright © 2014 Elsevier Ltd. All rights reserved.

Combined smoking cues enhance reactivity and predict immediate subsequent smoking.

PubMed

Conklin, Cynthia A; McClernon, F Joseph; Vella, Elizabeth J; Joyce, Christopher J; Salkeld, Ronald P; Parzynski, Craig S; Bennett, Lee

2018-01-23

Cue reactivity (CR) research has reliably demonstrated robust cue-induced responding among smokers exposed to common proximal smoking cues (e.g., cigarettes, lighter). More recent work demonstrates that distal stimuli, most notably the actual environments in which smoking previously occurred, can also gain associative control over craving. In the real world proximal cues always occur within an environment; thus, a more informative test of how cues affect smokers might be to present these two cue types simultaneously. Using a combined-cue counterbalanced cue reactivity paradigm, the present study tested the impact of proximal (smoking and neutral) + personal environment (smoking and nonsmoking places) pictorial cues, on smokers' subjective and behavioral cue reactivity; as well as the extent to which cue-induced craving predicts immediate subsequent smoking in a within-subjects design. As anticipated, the dual smoking cue combination (ProxS+EnvS) led to the greatest cue-induced craving relative to the other three cue combinations (ProxS+EnvN, ProxN+EnvS, ProxN+-EnvN), p's < .004. Dual smoking cues also led to significantly shorter post-trial latencies to smoke, p's < .01. Overall cue reactivity difference score (post-trial craving minus baseline craving) was predictive of subsequent immediate smoking indexed by: Post-trial latency to smoke (B= -2.69, SE= 9.02; t(143) = -2.98, p = .003); total puff volume (B= 2.99, SE= 1.13; t(143)= 2.65, p = .009); and total number of puffs (B= .053, SE= .027; t(143)= 1.95, p = .05). The implications of these findings for better understanding the impact of cues on smoking behavior and cessation are discussed. This novel cue reactivity study examined smokers' reactivity to combined proximal and distal smoking cues. Exposure to a combination of two smoking cues (proximal and environment) led to the greatest increases in cue-induced craving and smoking behavior compared to all other cue combinations. Further, the overall magnitude of

Smoking Behavior, Attitudes of Second-Hand Smoke, and No-Smoking Policies on a University Campus

ERIC Educational Resources Information Center

Polacek, Georgia N. L. Johnston; Atkins, Janet L.

2008-01-01

Smoking, when condoned as socially acceptable, overtly establishes such behavior as normal and risk-free. Scientific evidence verifies that cigarette smoking pervasively damages the body, causes early death, costs billions of dollars annually in medical care for smokers, and poses serious health risks to nonsmokers exposed to secondhand smoke. Yet…

Cigarette smoke-induced alveolar epithelial-mesenchymal transition is mediated by Rac1 activation.

PubMed

Shen, Hui-juan; Sun, Yan-hong; Zhang, Shui-juan; Jiang, Jun-xia; Dong, Xin-wei; Jia, Yong-liang; Shen, Jian; Guan, Yan; Zhang, Lin-hui; Li, Fen-fen; Lin, Xi-xi; Wu, Xi-mei; Xie, Qiang-min; Yan, Xiao-feng

2014-06-01

Epithelial-mesenchymal transition (EMT) is the major pathophysiological process in lung fibrosis observed in chronic obstructive pulmonary disease (COPD) and lung cancer. Smoking is a risk factor for developing EMT, yet the mechanism remains largely unknown. In this study, we investigated the role of Rac1 in cigarette smoke (CS) induced EMT. EMT was induced in mice and pulmonary epithelial cells by exposure of CS and cigarette smoke extract (CSE) respectively. Treatment of pulmonary epithelial cells with CSE elevated Rac1 expression associated with increased TGF-β1 release. Blocking TGF-β pathway restrained CSE-induced changes in EMT-related markers. Pharmacological inhibition or knockdown of Rac1 decreased the CSE exposure induced TGF-β1 release and ameliorated CSE-induced EMT. In CS-exposed mice, pharmacological inhibition of Rac1 reduced TGF-β1 release and prevented aberrations in expression of EMT markers, suggesting that Rac1 is a critical signaling molecule for induction of CS-stimulated EMT. Furthermore, Rac1 inhibition or knockdown abrogated CSE-induced Smad2 and Akt (PKB, protein kinase B) activation in pulmonary epithelial cells. Inhibition of Smad2, PI3K (phosphatidylinositol 3-kinase) or Akt suppressed CSE-induced changes in epithelial and mesenchymal marker expression. Altogether, these data suggest that CS initiates EMT through Rac1/Smad2 and Rac1/PI3K/Akt signaling pathway. Our data provide new insights into the fundamental basis of EMT and suggest a possible new course of therapy for COPD and lung cancer. Copyright © 2014 Elsevier B.V. All rights reserved.

Sulfur mustard and respiratory diseases.

PubMed

Tang, Feng Ru; Loke, Weng Keong

2012-09-01

Victims exposed to sulfur mustard (HD) in World War I and Iran-Iraq war, and those suffered occupational or accidental exposure have endured discomfort in the respiratory system at early stages after exposure, and marked general physical deterioration at late stages due to pulmonary fibrosis, bronchiolitis obliterans or lung cancer. At molecule levels, significant changes of cytokines and chemokines in bronchoalveolar lavage and serum, and of selectins (in particular sE-selectin) and soluble Fas ligand in the serum have been reported in recent studies of patients exposed to HD in Iran-Iraq war, suggesting that these molecules may be associated with the pathophysiological development of pulmonary diseases. Experimental studies in rodents have revealed that reactive oxygen and nitrogen species, their product peroxynitrite (ONOO(-)), nitric oxide synthase, glutathione, poly (adenosine diphosphate-ribose) polymerase, activating protein-1 signaling pathway are promising drug targets for preventing HD-induced toxicity, whereas N-acetyl cysteine, tocopherols, melatonin, aprotinin and many other molecules have been proved to be effective in prevention of HD-induced damage to the respiratory system in different animal models. In this paper, we will systemically review clinical and pathophysiological changes of respiratory system in victims exposed to HD in the last century, update clinicians and researchers on the mechanism of HD-induced acute and chronic lung damages, and on the relevant drug targets for future development of antidotes for HD. Further research directions will also be proposed.

Impaired Transcriptional Response of the Murine Heart to Cigarette Smoke in the Setting of High Fat Diet and Obesity

DOE Office of Scientific and Technical Information (OSTI.GOV)

Tilton, Susan C.; Karin, Norman J.; Webb-Robertson, Bobbie-Jo M.

Smoking and obesity are each well-established risk factors for cardiovascular heart disease, which together impose earlier onset and greater severity of disease. To identify early signaling events in the response of the heart to cigarette smoke exposure within the setting of obesity, we exposed normal weight and high fat diet-induced obese (DIO) C57BL/6 mice to repeated inhaled doses of mainstream (MS) or sidestream (SS) cigarette smoke administered over a two week period, monitoring effects on both cardiac and pulmonary transcriptomes. MS smoke (250 μg wet total particulate matter (WTPM)/L, 5 h/day) exposures elicited robust cellular and molecular inflammatory responses inmore » the lung with 1466 differentially expressed pulmonary genes (p < 0.01) in normal weight animals and a much-attenuated response (463 genes) in the hearts of the same animals. In contrast, exposures to SS smoke (85 μg WTPM/L) with a CO concentration equivalent to that of MS smoke (250 CO ppm) induced a weak pulmonary response (328 genes) but an extensive cardiac response (1590 genes). SS smoke and to a lesser extent MS smoke preferentially elicited hypoxia- and stress-responsive genes as well as genes predicting early changes of vascular smooth muscle and endothelium, precursors of cardiovascular disease. The most sensitive smoke-induced cardiac transcriptional changes of normal weight mice were largely absent in DIO mice after smoke exposure, while genes involved in fatty acid utilization were unaffected. At the same time, smoke exposure suppressed multiple proteome maintenance genes induced in the hearts of DIO mice. Together, these results underscore the sensitivity of the heart to SS smoke and reveal adaptive responses in healthy individuals that are absent in the setting of high fat diet and obesity.« less

Impaired transcriptional response of the murine heart to cigarette smoke in the setting of high fat diet and obesity.

PubMed

Tilton, Susan C; Karin, Norman J; Webb-Robertson, Bobbie-Jo M; Waters, Katrina M; Mikheev, Vladimir; Lee, K Monica; Corley, Richard A; Pounds, Joel G; Bigelow, Diana J

2013-07-15

Smoking and obesity are each well-established risk factors for cardiovascular heart disease, which together impose earlier onset and greater severity of disease. To identify early signaling events in the response of the heart to cigarette smoke exposure within the setting of obesity, we exposed normal weight and high fat diet-induced obese (DIO) C57BL/6 mice to repeated inhaled doses of mainstream (MS) or sidestream (SS) cigarette smoke administered over a two week period, monitoring effects on both cardiac and pulmonary transcriptomes. MS smoke (250 μg wet total particulate matter (WTPM)/L, 5 h/day) exposures elicited robust cellular and molecular inflammatory responses in the lung with 1466 differentially expressed pulmonary genes (p < 0.01) in normal weight animals and a much-attenuated response (463 genes) in the hearts of the same animals. In contrast, exposures to SS smoke (85 μg WTPM/L) with a CO concentration equivalent to that of MS smoke (~250 CO ppm) induced a weak pulmonary response (328 genes) but an extensive cardiac response (1590 genes). SS smoke and to a lesser extent MS smoke preferentially elicited hypoxia- and stress-responsive genes as well as genes predicting early changes of vascular smooth muscle and endothelium, precursors of cardiovascular disease. The most sensitive smoke-induced cardiac transcriptional changes of normal weight mice were largely absent in DIO mice after smoke exposure, while genes involved in fatty acid utilization were unaffected. At the same time, smoke exposure suppressed multiple proteome maintenance genes induced in the hearts of DIO mice. Together, these results underscore the sensitivity of the heart to SS smoke and reveal adaptive responses in healthy individuals that are absent in the setting of high fat diet and obesity.

Modifications of the National Early Warning Score for patients with chronic respiratory disease.

PubMed

Pedersen, N E; Rasmussen, L S; Petersen, J A; Gerds, T A; Østergaard, D; Lippert, A

2018-02-01

The National Early Warning Score (NEWS) uses physiological variables to detect deterioration in hospitalized patients. However, patients with chronic respiratory disease may have abnormal variables not requiring interventions. We studied how the Capital Region of Denmark NEWS Override System (CROS), the Chronic Respiratory Early Warning Score (CREWS) and the Salford NEWS (S-NEWS) affected NEWS total scores and NEWS performance. In an observational study, we included patients with chronic respiratory disease. The frequency of use of CROS and the NEWS total score changes caused by CROS, CREWS and S-NEWS were described. NEWS, CROS, CREWS and S-NEWS were compared using 48-h mortality and intensive care unit (ICU) admission within 48 h as outcomes. We studied 11,266 patients during 25,978 admissions; the use of CROS lowered NEWS total scores in 40% of included patients. CROS, CREWS and S-NEWS had lower sensitivities than NEWS for 48-h mortality and ICU admission. Specificities and PPV were higher. CROS, CREWS and S-NEWS downgraded, respectively, 51.5%, 44.9% and 32.8% of the NEWS total scores from the 'mandatory doctor presence' and 'immediate doctor presence and specialist consultation' total score intervals to lower intervals. Capital Region of Denmark NEWS Override System was frequently used in patients with chronic respiratory disease. CROS, CREWS and S-NEWS reduced sensitivity for 48-h mortality and ICU admission. Using the methodology prevalent in the NEWS literature, we cannot conclude on the safety of these systems. Future prospective studies should investigate the balance between detection rate and alarm fatigue of different systems, or use controlled designs and patient-centred outcomes. © 2017 The Acta Anaesthesiologica Scandinavica Foundation. Published by John Wiley & Sons Ltd.

Vitamin E isoform γ-tocotrienol protects against emphysema in cigarette smoke-induced COPD.

PubMed

Peh, Hong Yong; Tan, W S Daniel; Chan, Tze Khee; Pow, Chen Wei; Foster, Paul S; Wong, W S Fred

2017-09-01

Inflammation and oxidative stress contribute to emphysema in COPD. Although corticosteroids are the standard of care for COPD, they do not reduce oxidative stress, and a subset of patients is steroid-resistant. Vitamin E isoform γ-tocotrienol possesses both anti-inflammatory and anti-oxidative properties that may protect against emphysema. We aimed to establish the therapeutic potential of γ-tocotrienol in cigarette smoke-induced COPD models in comparison with prednisolone. BALB/c mice were exposed to cigarette smoke for 2 weeks or 2 months. γ-Tocotrienol and prednisolone were given orally. Bronchoalveolar lavage (BAL) fluid and lung tissues were assessed for inflammation, oxidative damage, and regulation of transcription factor activities. Emphysema and lung function were also evaluated. γ-Tocotrienol dose-dependently reduced cigarette smoke-induced BAL fluid neutrophil counts and levels of cytokines, chemokines and oxidative damage biomarkers, and pulmonary pro-inflammatory and pro-oxidant gene expression, but restored lung endogenous antioxidant activities. γ-Tocotrienol acted by inhibiting nuclear translocation of STAT3 and NF-κB, and up-regulating Nrf2 activation in the lungs. In mice exposed to 2-month cigarette smoke, γ-tocotrienol ameliorated bronchial epithelium thickening and destruction of alveolar sacs in lungs, and improved lung functions. In comparison with prednisolone, γ-tocotrienol demonstrated better anti-oxidative efficacy, and protection against emphysema and lung function in COPD. We revealed for the first time the anti-inflammatory and antioxidant efficacies of γ-tocotrienol in cigarette smoke-induced COPD models. In addition, γ-tocotrienol was able to attenuate emphysematous lesions and improve lung function in COPD. γ-Tocotrienol may have therapeutic potential for the treatment of COPD. Copyright © 2017 Elsevier Inc. All rights reserved.

Is there a link between passive smoke exposure and early-onset myopia in preschool Asian children?

PubMed

Chua, Sharon Yu Lin; Ikram, Mohammad Kamran; Tan, Chuen Seng; Stone, Richard A; Cai, Shirong; Gluckman, Peter D; Yap, Seng Chong; Yap, Fabian; Wong, Tien-Yin; Ngo, Cheryl S; Saw, Seang-Mei

2016-07-01

To investigate the association of passive tobacco smoke exposure with early-onset myopia among three-year-old children in Singapore. Pregnant mothers who attended their first trimester clinic at two major maternity units were recruited into the GUSTO birth cohort. The current analysis comprised 572 three-year-old children, who underwent cycloplegic autorefraction and axial length (AL) measurements. Myopia was defined as spherical equivalent (SE) of ≤-0.50 dioptres (D). Either parent completed questionnaires describing their child's exposure to passive smoke at six months, one and two years of age. There were 197 children (36.2%) who were exposed to passive smoke from birth to before six months. Compared to non-exposed children, children exposed to any passive smoke from birth to before six months experienced greater myopia prevalence (adjusted OR = 2.79; 95% CI: 1.24-6.29; p = 0.01). The odds of myopia in a child was greater if a smoker smokes at home, in the family car, or in the presence of the child (adjusted OR = 3.95; 95% CI: 1.41-11.09; p < 0.01) compared to non-exposed child. In contrast to myopia, childhood exposure to passive smoke did not systematically shift mean values for SE or AL. In this prospective birth cohort study, we found that childhood exposure to passive smoke from birth to before six months slightly increased the risk of early-onset myopia. This may indicate a delayed response to passive smoke exposure before six months and the development of myopia at three years of age. Our study is limited by the small number of myopic children at this young age. Thus, larger prospective studies using more objective cotinine level measures are required to fully establish and understand the influence of tobacco smoke on refractive development in older children. © 2016 The Authors Ophthalmic & Physiological Optics © 2016 The College of Optometrists.

Smoke-Free Policies in the World's 50 Busiest Airports - August 2017.

PubMed

Tynan, Michael A; Reimels, Elizabeth; Tucker, Jennifer; King, Brian A

2017-11-24

Exposure to secondhand smoke from burning tobacco products causes premature death and disease, including coronary heart disease, stroke, and lung cancer among nonsmoking adults and sudden infant death syndrome, acute respiratory infections, middle ear disease, exacerbated asthma, respiratory symptoms, and decreased lung function in children (1,2). The U.S. Surgeon General has concluded that there is no risk-free level of exposure to secondhand smoke (1). Previous CDC reports on airport smoke-free policies found that most large-hub airports in the United States prohibit smoking (3); however, the extent of smoke-free policies at airports globally has not been assessed. CDC assessed smoke-free policies at the world's 50 busiest airports (airports with the highest number of passengers traveling through an airport in a year) as of August 2017; approximately 2.7 billion travelers pass through these 50 airports each year (4). Among these airports, 23 (46%) completely prohibit smoking indoors, including five of the 10 busiest airports. The remaining 27 airports continue to allow smoking in designated smoking areas. Designated or ventilated smoking areas can cause involuntary secondhand smoke exposure among nonsmoking travelers and airport employees. Smoke-free policies at the national, city, or airport authority levels can protect employees and travelers from secondhand smoke inside airports.

Teacher respiratory health symptoms in relation to school and home environment.

PubMed

Lin, Shao; Lawrence, Wayne R; Lin, Ziqiang; Francois, Melissa; Neamtiu, Iulia A; Lin, Qiaoxuan; Csobod, Eva; Gurzau, Eugen S

2017-11-01

Few studies have evaluated teachers' respiratory health, especially its relationship with school/home environment, and school policies. This study assessed asthma and smoking prevalence among teachers in Romania, teacher's perception and knowledge of the school environment, policies and asthma management, and how school and home environment affected asthma, allergy, and respiratory infection symptoms. This cross-sectional study obtained information from 104 Romanian teachers utilizing teacher questionnaire data for Romania only, as part of the Schools Indoor Pollution and Health: Observatory Network in Europe (SINPHONIE) study, a multicenter European research project conducted between 2010 and 2012. The SINPHONIE questionnaire collected comprehensive information on school and home environment, respiratory symptoms, smoking, and school policies. We used unconditional logistic regression analysis to examine environment-outcome relationships while controlling for socio-demographics and co-exposures. Our results showed the prevalence of asthma-like symptoms and smoking among teachers in Romania was higher than in other SINPHONIE schools and among US teachers. Factors statistically associated with asthma, allergy, and respiratory infection (all p < 0.05) include perception of health related to poor air quality in school, inappropriate cleaning of ventilation systems, dwelling proximity to busy traffic, and multiple school/home exposures. We also found lack of asthma management and environmental policies in the investigated Romanian schools. We concluded that multiple school and home environmental factors were related to respiratory and allergic symptoms. High asthma burden and smoking are important public health problems in Romania. Future studies including larger sample size and exposure measurements are needed to confirm our findings.

[Peri-operative management of smoking].

PubMed

Ruppert, A-M; Amrioui, F; Fallet, V; Cadranel, J

2018-05-22

Smoking is a public health issue, especially during the perioperative period. Tobacco increases the risk of hospital mortality by 20% and major postoperative complications by 40%. Active smoking is associated with respiratory complications particularly bronchospasm and pneumonia, but also all surgical complications as scar infections, local thrombosis, suture release and delayed bone healing. The perioperative period is an opportunity to stop smoking. Smoking cessation should always be recommended, regardless of the surgery and the date of intervention. All health professionals, doctors, surgeons, anesthetists, but also nurses and physiotherapists, must inform smokers of the benefits of stopping smoking, offer them a dedicated support and a personalized follow-up. Tobacco consultation and the prescription of nicotine replacement increase the rate of smoking cessation. Stopping smoking reduces perioperative complications and is associated with health benefits that increase with time. Copyright © 2018 Elsevier Masson SAS. All rights reserved.

Time-course effects of aerobic physical training in the prevention of cigarette smoke-induced COPD.

PubMed

Toledo-Arruda, Alessandra C; Vieira, Rodolfo P; Guarnier, Flávia A; Suehiro, Camila L; Caleman-Neto, Agostinho; Olivo, Clarice R; Arantes, Petra M M; Almeida, Francine M; Lopes, Fernanda D T Q S; Ramos, Ercy M C; Cecchini, Rubens; Lin, Chin Jia; Martins, Milton Arruda

2017-09-01

A previous study by our group showed that regular exercise training (ET) attenuated pulmonary injury in an experimental model of chronic exposure to cigarette smoke (CS) in mice, but the time-course effects of the mechanisms involved in this protection remain poorly understood. We evaluated the temporal effects of regular ET in an experimental model of chronic CS exposure. Male C57BL/6 mice were divided into four groups: Control (sedentary + air), Exercise (aerobic training + air), Smoke (sedentary + smoke), and Smoke + Exercise (aerobic training + smoke). Mice were exposed to CS and ET for 4, 8, or 12 wk. Exercise protected mice exposed to CS from emphysema and reductions in tissue damping and tissue elastance after 12 wk ( P < 0.01). The total number of inflammatory cells in the bronchoalveolar lavage increased in the Smoke group, mainly due to the recruitment of macrophages after 4 wk, neutrophils and lymphocytes after 8 wk, and lymphocytes and macrophages after 12 wk ( P < 0.01). Exercise attenuated this increase in mice exposed to CS. The protection conferred by exercise was mainly observed after exercise adaptation. Exercise increased IL-6 and IL-10 in the quadriceps and lungs ( P < 0.05) after 12 wk. Total antioxidant capacity and SOD was increased and TNF-α and oxidants decreased in lungs of mice exposed to CS after 12 wk ( P < 0.05). The protective effects of exercise against lung injury induced by cigarette smoke exposure suggests that anti-inflammatory mediators and antioxidant enzymes play important roles in chronic obstructive pulmonary disease development mainly after the exercise adaptation. NEW & NOTEWORTHY These experiments investigated for the first time the temporal effects of regular moderate exercise training in cigarette smoke-induced chronic obstructive pulmonary disease. We demonstrate that aerobic conditioning had a protective effect in emphysema development induced by cigarette smoke exposure. This effect was most likely secondary to an

NF-{kappa}B inhibition is involved in tobacco smoke-induced apoptosis in the lungs of rats

DOE Office of Scientific and Technical Information (OSTI.GOV)

Zhong Caiyun; Zhou Yamei; Pinkerton, Kent E.

2008-07-15

Apoptosis is a vital mechanism for the regulation of cell turnover and plays a critical role in tissue homeostasis and development of many disease processes. Previous studies have demonstrated the apoptotic effect of tobacco smoke; however, the molecular mechanisms by which tobacco smoke triggers apoptosis remain unclear. In the present study we investigated the effects of tobacco smoke on the induction of apoptosis in the lungs of rats and modulation of nuclear factor-kappa B (NF-{kappa}B) in this process. Exposure of rats to 80 mg/m{sup 3} tobacco smoke significantly induced apoptosis in the lungs. Tobacco smoke resulted in inhibition of NF-{kappa}Bmore » activity, noted by suppression of inhibitor of {kappa}B (I{kappa}B) kinase (IKK), accumulation of I{kappa}B{alpha}, decrease of NF-{kappa}B DNA binding activity, and downregulation of NF-{kappa}B-dependent anti-apoptotic proteins, including Bcl-2, Bcl-xl, and inhibitors of apoptosis. Initiator caspases for the death receptor pathway (caspase 8) and the mitochondrial pathway (caspase 9) as well as effector caspase 3 were activated following tobacco smoke exposure. Tobacco smoke exposure did not alter the levels of p53 and Bax proteins. These findings suggest the role of NF-{kappa}B pathway in tobacco smoke-induced apoptosis.« less