Environmental exposure to tobacco smoke and lung function in young adults

The relationship between lung function and environmental exposure to tobacco smoke (passive smoking) was studied in 293 nonsmoking young men and women, 15 to 35 yr of age. A self-administered mailed questionnaire was used to assess the lifetime environmental exposure to cigarette smoke at home and at work for each subject. Lung function information used here had been gathered in the course of a previous study of the determinants of lung function in early adulthood. In men, maximal midexpiratory flow rate (FEF25-75) decreased in relation to an index of cumulative lifetime environmental exposure to tobacco smoke at home, after taking into account the effects of cumulative exposure at work as well as age, height, body size, respiratory pressures, and cooking fuels used at home. The components of this exposure index most closely related to the reduction in FEF25-75 were maternal smoking habits and exposure to second-hand smoke during childhood. In women, the diffusing capacity of the lung (DLCO) decreased in relation to cumulative exposure to tobacco smoke at work, after accounting for the effects of cumulative lifetime exposure at home and the other factors mentioned above. These findings contribute to the gathering evidence that environmental exposure to tobacco smoke is harmful to respiratory health, and suggest that the effects are not insignificant. For instance, the FEF25-75 of a young man 20 yr of age who had never smoked and always lived at home would be 800 ml less if both his parents smoked than if they did not.(ABSTRACT TRUNCATED AT 250 WORDS)     

Environmental tobacco smoke and health in the elderly.

The aims of this article are to synthesize the evidence on health effects of environmental tobacco smoke (ETS) in the elderly and to discuss questions for future research. Health effects are divided into aetiological and prognostic studies. There is convincing evidence that ETS causes lung cancer and coronary heart disease, both of which are diseases of the elderly. Several cross-sectional studies show increased occurrence of chronic respiratory symptoms and deficits in ventilatory lung function in relation to ETS exposure at home and/or at work. A limited number of studies have found significant relations between ETS exposure and asthma, chronic obstructive pulmonary disease (COPD), pneumococcal infections and stroke in the elderly. Longitudinal studies are needed before any definite conclusions can be made concerning ETS and noncarcinogenic respiratory diseases in the elderly. The potential role of environmental tobacco smoke exposure as a prognostic factor determining development of a pre-existing respiratory or heart disease is an important new area for research.     

Smoking and pediatric respiratory health

Many children are exposed to smoking both prenatally and postnatally. Prenatal exposure to mainstream smoke from the mother and even to environmental tobacco smoke (ETS) from the mother in utero has been shown to change fetal lung development and cause airflow obstruction and airway hyperresponsiveness. Children exposed to ETS postnatally have more symptoms of cough, wheeze, respiratory illnesses, decreases in lung function, and increases in airway responsiveness. Smoke exposure is associated with the early development of asthma, increased severity of asthma, and the development of allergy. Finally smoke exposure is associated with sudden infant death and airway obstruction. This article reviews the spectrum of effects of cigarette smoke exposure on the respiratory health of infants and children and highlights basic science research exploring the mechanisms of these effects.     

Respiratory health effects of the indoor environment in a population of Dutch children

The effect of indoor exposure to nitrogen dioxide on respiratory health was studied over a period of 2 yr in a population of nonsmoking Dutch children 6 to 12 yr of age. Lung function was measured at the schools, and information on respiratory symptoms was collected from a self-administered questionnaire completed by the parents of the children. Nitrogen dioxide was measured in the homes of all children with Palmes' diffusion tubes. In addition, information on smoking and dampness in the home was collected by questionnaire. There was no relationship between exposure to nitrogen dioxide in the home and respiratory symptoms. Respiratory symptoms were found to be associated with exposure to tobacco smoke and home dampness. There was a weak, negative association between maximal midexpiratory flow (MMEF) and exposure to nitrogen dioxide. FEV1, peak expiratory flow, and MMEF were all negatively associated with exposure to tobacco smoke. Home dampness was not associated with pulmonary function. Lung function growth, measured over a period of 2 yr, was not consistently associated with any of the indoor exposure variables. The development of respiratory symptoms over time was not associated with indoor exposure to nitrogen dioxide. There was a significant association between exposure to environmental tobacco smoke in the home and the development of wheeze. There was also a significant association between home dampness and the development of cough.     

Environmental factors and atmospheric pollutants.

Respiratory infections result from complex interactions between the infectious organism and the host, and exposure to environmental pollutants may alter host resistance. The atmospheric pollutants implicated in respiratory infections include acidic aerosols, particles, nitrogen dioxide, ozone, sulfur dioxide, and household allergens. An extensive epidemiological literature has been established linking environmental tobacco smoke to increased occurrence of lower respiratory tract infections in children; exposure to smoke from cooking and heating fires may also increase the risk of serious infections. Experimental evidence suggests that exposure to nitrogen dioxide and acidic aerosols may impair specific host defense mechanisms. Individuals with underlying lung or heart disease, as well as infants and the elderly, are among those most susceptible to the effects of environmental pollutants. Efforts should be directed toward reducing the exposure of children to environmental tobacco smoke and products of unvented combustion while investigations continue.     

The effect of passive smoking on respiratory health in children and adults.

Passive smoking, or environmental tobacco smoke (ETS), has been found to be causally associated with a large number of diseases in various organs although the evidence is sometimes conflicting. This review summarises the effects of passive smoking on respiratory symptoms, lung function and asthma in children and adults. In children, prenatal exposure to ETS is associated with impaired lung function and increased risk of developing asthma, while postnatal exposure mainly acts as a trigger factor for respiratory symptoms and asthma attacks. In adults, ETS exposure is associated with respiratory symptoms, asthma, a small but significant impairment of lung function and increased bronchial responsiveness. The consequence of workplace exposure seems to be more serious than domestic exposure. Legislative measures banning smoking at work have positive health effects in non-smokers and increase the quitting rate in smokers. Measures aimed at reducing childhood exposure to ETS should have high priority. Smoke cessation programmes for pregnant women attending antenatal clinics and for parents at the time of child hospitalisation for respiratory illness seem to have a fairly high success rate. Passive smoking is a widespread, important and avoidable risk factor for respiratory symptoms in both children and adults. Reducing passive smoking in the community will have a large positive effect on respiratory health.     

The role of environmental tobacco smoke in the origins and progression of asthma

Exposure to environmental tobacco smoke (ETS) is a major source of indoor air pollution and causes adverse effects on the respiratory health of individuals with asthma. At least one third of children and adults with asthma are exposed to ETS on a regular basis. There is convincing evidence for a causal relationship between exposure to ETS and development of asthma in children and in nonsmoking adults. Exposure to ETS also worsens asthma control in children and nonsmoking adults who have established asthma. The mechanism by which ETS causes these harmful effects is not established but may involve genetic predisposition, impairment of lung development, and altered lung inflammatory responses. Workplace smoking restrictions and reduced smoking in the home may lower the prevalence of asthma, improve asthma control, and reduce the use of medical services in both children and adults who are exposed to ETS.     

Relationship of pulmonary function among women and children to indoor air pollution from biomass use in rural Ecuador

Approximately half the world uses biomass fuel for domestic energy, resulting in widespread exposure to indoor air pollution (IAP) from biomass smoke. IAP has been associated with many respiratory diseases, though it is not clear what relationship exists between biomass use and pulmonary function. Four groups containing 20 households each were selected in Santa Ana, Ecuador based on the relative amount of liquid petroleum gas and biomass fuel that they used for cooking. Pulmonary function tests were conducted on each available member of the households 7 years of age. The pulmonary functions of both children (7-15 years) and women (16 years) were then compared between cooking fuel categories using multivariate linear regression, controlling for the effects of age, gender, height, and exposure to tobacco smoke. Among the 80 households, 77 children and 91 women performed acceptable and reproducible spirometry. In multivariate analysis, children living in homes that use biomass fuel and children exposed to environmental tobacco smoke had lower forced vital capacity and lower forced expiratory volume in 1s (P<0.05). However, no significant difference in pulmonary function was observed among women in different cooking categories. Results of this study demonstrate the harmful effects of IAP from biomass smoke on the lung function of children and emphasize the need for public health efforts to decrease exposure to biomass smoke.     

Respiratory health effects of exposure to environmental tobacco smoke

Tobacco smoke is a major component of indoor air pollution. Exposure to environmental tobacco smoke (ETS) is prevalent worldwide despite growing awareness of its adverse health effects on non-smokers. ETS contains the same toxic substances as identified in mainstream tobacco smoke. Cotinine (a metabolite of nicotine) can be measured in urine and serum of non-smokers exposed to ETS and reflects the degree of exposure. In children, exposure to ETS leads to reduced lung function, increased risk of lower respiratory tract illnesses, acute exacerbation of asthma resulting in hospitalization, increased prevalence of non-allergic bronchial hyperresponsiveness, increased risk for sudden infant death syndrome (SIDS) and possibly increased risk for asthma. Exposure to ETS is responsible for excess cost to the family's financial resources and demands on health services. In adults, exposure to ETS is associated with increased risk of lung cancer, particularly in those with high exposure and acute and chronic respiratory symptoms that improve after the cessation of exposure. Healthcare providers should advocate for non-smokers' rights in the community and support legislation to limit tobacco exposure.     

Air quality and particulate matter

Clean air is considered to be a key factor influencing human health. It is not only important for respiratory health but influences the homeostasis of the whole human organism. In this respect, all major national and international respiratory societies point to the extremely important role of national and international clean air acts that address both inner (i. e. tobacco smoke) and outer (i. e. environmental pollutants) air pollution. Due to research at the levels of pulmonary medicine and environmental medicine, the European Union has implemented new limit values. Clinical and experimental evidence points out that it is crucial to comply with these regulations since recent studies have shown that not only patients with lung diseases but also children and their lung development are endangered by high concentrations of air pollutants. With regard to the complexity of detrimental effects new national and international research programs should be established for the assessment of health effects of air pollutants.     

Indoor air pollution and the lung in low- and medium-income countries

Over half the world's population, mostly from developing countries, use solid fuel for domestic purposes and are exposed to very high concentrations of harmful air pollutants with potential health effects such as respiratory problems, cardiovascular problems, infant mortality and ocular problems. The evidence also suggests that, although the total percentage of people using solid fuel is decreasing, the absolute number is currently increasing. Exposure to smoke from solid fuel burning increases the risk of chronic obstructive pulmonary disease (COPD) and lung cancer in adults, and acute lower respiratory tract infection/pneumonia in children. Despite the heterogeneity among studies, the association between COPD and exposure to smoke produced by burning different types of solid fuel is consistent. However, there is strong evidence that while coal burning is a risk factor for lung cancer, exposure to other biomass fuel smoke is less so. There is some evidence that reduction of smoke exposure using improved cooking stoves reduces the risk of COPD and, possibly, acute lower respiratory infection in children, so approaches to reduce biomass smoke exposure are likely to result in reductions in the global burden of respiratory disease.     

The effect of parental smoking on lung function and development during infancy

While the adverse effects of parental smoking on respiratory health during childhood are well recognized, its potential impact on early lung development is less clear. This review summarizes current evidence on the effect of parental smoking on lung function during infancy. It is difficult to separate the effects of pre- and postnatal exposure, since the majority of mothers who smoke in pregnancy (currently around 30% worldwide) continue to do so thereafter. Nevertheless, measurements undertaken prior to any postnatal exposure have consistently demonstrated significant changes in tidal flow patterns in infants whose mothers smoked in pregnancy. While there is, as yet, no convincing evidence from studies in human infants that smoking during pregnancy is associated with increased airway responsiveness at birth, many studies have demonstrated a reduction in forced expiratory flows (on average by 20%) in infants exposed to parental smoking. While maternal smoking during pregnancy remains the most significant source of such exposure and is likely to be responsible for diminished airway function in early life, continuing postnatal tobacco smoke exposure will increase the risk of respiratory infections, the combination of both being responsible for the two- to fourfold increased risk of wheezing illnesses observed during the first year of life in infants whose parents smoke. These findings emphasize the need to keep infants in a smoke-free environment both before and after birth, not least because of growing awareness that airway function in later life is largely determined by that during foetal development and early infancy.     

Impact of smoke-free workplace legislation on exposures and health: possibilities for prevention.

The aims of this study were to review experiences with national or statewide smoke-free workplace legislation and data on the occurrence of environmental tobacco smoke (ETS) exposure at work, to present the best estimates for health effects related to workplace ETS exposure, and to calculate corresponding population attributable fractions (PAFs) for respiratory and cardiovascular diseases for 14 European countries and the USA. Systematic searches of the Medline database were carried out, with a cut-off date of November 2005. PAFs for the main outcomes were calculated from the best disease-specific effect estimates and country-specific prevalences of work ETS exposure. Significant numbers of workers are exposed to ETS at work, i.e. approximately 7.5 million workers in 15 European Union countries and 24.6 million in the USA. Workplace ETS exposure is causally linked to lung cancer and coronary heart disease, and is related to an increased risk of asthma in adults and reduced birthweight in newborns. Relatively strong evidence links ETS exposure to chronic obstructive pulmonary disease and stroke. PAFs in Europe and the USA showed that, at current workplace ETS exposure prevalences, the public health impact is substantial. Experience of national and statewide smoke-free workplace legislation from different countries shows that such legislation leads to significant reductions in employees' environmental tobacco smoke exposure at work, as well as improvements in respiratory and cardiac health.     

Exposición prenatal y posnatal al tabaco y síntomas respiratorios y alérgicos en los primeros años de vida

Background and objectives

To analyse the relationship between prenatal and postnatal tobacco exposure and the development of respiratory and allergy symptoms during the first 4 years of life.

Patients and methods

Prospective and multicentred cohort study that included the subjects belonging to AMICS (Asthma Multicentred Infant Cohort Study) located in Ashford (England), Barcelona and Minorca (Spain). We recruited 1611 children, followed from the pregnancy to the 4th year of life, whose parents annually answered a questionnaire on their tobacco consumption and their children's respiratory and allergy health. In the Barcelona cohort (n=487) a tobacco exposure biomarker (cotinine) was analysed on several matrices.

Results

Prenatal tobacco exposure is associated with a greater risk of hospitalisation due to respiratory infection, particularly in the second year of life, whereas postnatal tobacco exposure is associated more strongly with the presence of late wheezing presence and increases in the chance of being diagnosed with asthma at 4 years of age. The children prenatally and postnatally exposed had more persistent wheezing, persistent rhoncus, early cough, a higher number of upper respiratory infections per year and a greater number were diagnosed with asthma. The higher the levels of cotinine measured, the higher was the risk for wheezing. No relationship was seen between tobacco exposure and atopic symptoms.

Conclusions

Passive smoke exposure during pregnancy and childhood has very distinct clinical respiratory effects in children. Therefore, smoking cessation of childbearing age women must be a priority of preventive medicine.     

Lung function abnormalities in HIV‐infected adults and children

Despite the advent of antiretroviral therapy (ART), the human immunodeficiency virus (HIV) epidemic remains a global health crisis with a high burden of respiratory disease among infected persons. While the early complications of the epidemic were dominated by opportunistic infections, improved survival has led to the emergence of non‐infectious conditions that are associated with chronic respiratory symptoms and pulmonary disability. Obstructive ventilatory defects and reduced diffusing capacity are common findings in adults, and the association between HIV and chronic obstructive pulmonary disease is increasingly recognized. There is synergism between viral factors, opportunistic infections, conventional influences like tobacco smoke and biomass fuel exposure, and potentially, the immunological effects of ART on the development of HIV‐associated chronic obstructive lung disease. Pulmonary function data for HIV‐infected infants and children are scarce, but shows that bronchiectasis and obliterative bronchiolitis with severe airflow limitation are major problems, particularly in the developing world. However, studies from these regions are sorely lacking. There is thus a major unmet need to understand the influences of chronic HIV infection on the lung in both adults and children, and to devise strategies to manage and prevent these diseases in HIV‐infected individuals. It is important for clinicians working with HIV‐infected individuals to have an appreciation of their effects on measurements of lung function. This review therefore summarizes the lung function abnormalities described in HIV‐positive adults and children, with an emphasis on obstructive lung disease, and examines potential pathogenic links between HIV and the development of chronic pulmonary disability.     

The relationship of salivary cotinine to respiratory symptoms, spirometry, and exercise-induced bronchospasm in seven-year-old children

The effects of passive tobacco smoke exposure upon respiratory symptoms and lung function were assessed in a cross-sectional survey of 770 children 7 yr of age, using cotinine as a quantitative biochemical marker of exposure. Salivary cotinine levels were strongly related to the number of smokers in the home, but three-quarters of children from nonsmoking households had detectable salivary cotinine, and 10% of this group were in the upper two-fifths of the distribution of measured tobacco smoke exposure. Smoking by persons other than members of the household may deserve greater attention in future studies of young children. After adjustment for housing tenure, most respiratory symptoms were unrelated to salivary cotinine, but a "tendency for colds to go to the chest" was twice as prevalent in the upper two-fifths as in the lower two-fifths of the cotinine distribution. No association was found between salivary cotinine and reports of wheeze or measured reduction in FEV1 after 6 min of free running. After adjustment for sex, height, test conditions, and housing tenure, all baseline spirometric indices except FVC were inversely associated with salivary cotinine. Only FEF75-85 and FEF75 were significantly reduced, the difference for each index between the top and bottom quintiles of the cotinine distribution being about 7%, equivalent to a reduction of 1.1% (95% CL, 0.1 to 2.1%) per doubling of cotinine concentration. These changes may be evidence of small airways damage, which could later progress to more severe respiratory impairment.     

Lung function of school children with low levels of alpha1-antitrypsin and tobacco smoke exposure.

Exposure to environmental tobacco smoke (ETS) and other air pollutants has been associated with small decrements in lung function. The susceptibility to pollution exposure may, however, vary substantially between individuals. Children with an impaired protease-antiprotease balance may be particularly vulnerable. Therefore this study aimed to investigate the effects of ETS exposure on children with reduced levels of alpha1-antitrypsin (alpha1-AT). Random samples of school children (aged 9-11 yrs) (n=3,526) were studied according to the International Study of Asthma and Allergies in Childhood (ISAAC) phase II protocol, including parental questionnaires, pulmonary function and allergy testing. Blood samples were obtained to measure plasma levels of alpha1-AT and to genotype for pleomorphic protein inhibitor (Pi)Z and PiS alleles. Children with low levels of alpha1-AT (< or = 116 mg x dL(-1)) showed significant, albeit small decrements in baseline lung function. When exposed to ETS, pronounced decrements of pulmonary function, particularly in measures of mid- to end-expiratory flow rates, were seen in these children as compared to exposed children with normal levels of alpha1-AT. The mean levels of % predicted+/-SE in both groups were: maximum expiratory flow at 50% of vital capacity 79.4+/-7.2 versus 99.0+/-1.5, maximum expiratory flow at 25% of vital capacity 67.4+/-10.0 versus 100.3+/-2.1, maximal midexpiratory flow 73.7+/-8.6 versus 99.9+/-1.7. These findings suggest that school children with low levels of alpha1-antitrypsin are at risk of developing pronounced decrements in pulmonary function, particularly if they are exposed to environmental tobacco smoke. Parents of children with heterozygous alpha1-antitrypsin deficiency resulting in significantly reduced blood concentrations should be advised to prevent their children from being exposed to environmental tobacco smoke and dissuade them from taking up smoking.     

Involuntary smoking and asthma severity in children: data from the Third National Health and Nutrition Examination Survey

STUDY OBJECTIVES: We sought to determine the indicators of asthma severity among children in the United States with high and low levels of tobacco smoke exposure. DESIGN: Cross-sectional study. SETTING: Nationally representative survey of participants in the Third National Health and Nutrition Examination Survey (from 1988 to 1994). PARTICIPANTS: Five hundred twenty-three children with physician-diagnosed asthma. MEASUREMENTS AND RESULTS: We stratified the study participants into tertiles on the basis of serum levels of cotinine (a metabolite of nicotine that indicates tobacco smoke exposure). We used logistic and linear regression modeling, adjusting for known covariates, to determine the effect of high environmental tobacco smoke exposure on the following outcomes: asthma severity (determined using reported symptom and respiratory illness frequency); lung function; physician visits; and school absence. Among our study sample, 78.6% of children had mild asthma, 6.8% of children had moderate asthma, and 14.6% of children had severe asthma. Asthmatic children with high levels of smoke exposure, compared with those with low levels of exposure, were more likely to have moderate or severe asthma (odds ratio, 2.7 95% confidence interval [CI], 1.1 to 6.8) and decreased lung function, with a mean FEV(1) decrement of 213 mL or 8.1% (95% CI, -14.7 to -3.5). CONCLUSIONS: Involuntary smoke exposure is associated with increased asthma severity and worsened lung function in a nationally representative group of US children with asthma.     

Effects of in utero and environmental tobacco smoke exposure on lung function in boys and girls with and without asthma

To investigate whether the effects of in utero exposure to maternal smoking and environmental tobacco smoke (ETS) exposure on lung function vary by sex or asthma status, we examined medical history and tobacco smoke exposure data for 5,263 participants in the Children's Health Study. At study enrollment, parents or guardians of each subject completed a questionnaire, and lung function was measured spirometrically with maximum forced expiratory flow-volume maneuvers. To assess the in utero effects of maternal smoking and ETS exposure on lung function, we used regression splines that accounted for the nonlinear relationship between pulmonary function, height, and age. In utero exposure to maternal smoking was independently associated with deficits in lung function that were larger for children with asthma. Boys and girls with a history of in utero exposure to maternal smoking showed deficits in maximum midexpiratory flow (MMEF) and a decrease in the FEV(1)/FVC ratio. As compared with children without asthma, boys with asthma had significantly larger deficits from in utero exposure in FVC, MMEF, and FEV(1)/FVC, and girls with asthma had larger decreases in FEV(1)/FVC. The effect of ETS exposure varied by children's gender and asthma status. Deficits in flows associated with current ETS exposure were present in children with and without asthma but were significant only among children without asthma. Past ETS exposure was associated with reduced FEV(1), MMEF, and FEV(1)/FVC among boys with asthma. In contrast, past ETS exposure was associated with decreased flow rates in girls without asthma. In summary, both in utero exposure to maternal smoking and ETS exposure were associated with persistent deficits in lung function. The effects of in utero exposure were greatest among children with asthma.