Original Article Household Environmental Tobacco Smoke Exposure, Respiratory Symptoms and Asthma in Non-Smoker Adults: A Multicentric Population Study from India D. Gupta 1, A.N. Aggarwal 1, K. Chaudhry 2, S.K. Chhabra 3, G.A. D'Souza 4, S.K. Jindal 1, S.K. Katiyar 5, R. Kumar 1, B. Shah 2 and V.K. Vijayan 3 for Asthma Epidemiology Study Group Postgraduate Institute of Medical Education and Research 1, Chandigarh; Indian Council of Medical Research 2, New Delhi; Vallabhbhai Patel Chest Institute 3, Delhi; St. John's Medical College Hospital 4, Bangalore; and G.S.V.M. Medical College 5, Kanpur, India ABSTRACT Background. Exposure to environmental tobacco smoke (ETS ) is a risk factor for childhood asthma. Its association with asthma in adults is less clear. Methods. In a multicentric population study on asthma prevalence in adults, specific enquiries were made into childhood and adulthood exposure to household ETS, and its relationship with asthma diagnosis were analysed. Results. From a total of 73605 respondents, 62109 were studied after excluding current or past smokers. Overall observed prevalence of asthma was 2.0% (men 1.5%,women 2.5%, p<0.001). Of all asthma patients, history of ETS exposure was available in 48.6 percent. Prevalence of asthma in the ETS exposed subjects was higher compared to non-exposed individuals (2.2% vs 1.9%, p<0.05). Multiple logistic regression analysis showed a higher risk of having asthma in persons who were exposed to ETS compared to those not exposed (odds ratio [OR] 1.22, 95% CI 1.08-1.38) after adjusting for age, gender, usual residence, exposure to biomass fuels and atopy. Stratification of ETS exposure revealed that exposure during childhood and both during childhood and adulthood were significantly associated with asthma prevalence. Exposure only in adulthood was not a significant risk factor (OR 1.13, 95% CI 0.95-1.33). Persons reporting combined environmental tobacco smoke exposure from parents during childhood and spouse during adulthood had highest risk of having asthma (OR 1.69, 95% CI 1.38-2.07). Environmental tobacco smoke exposure was also significantly associated with prevalence of respiratory symptoms such as wheezing, cough and breathlessness. Conclusions. Environmental tobacco smoke exposure during childhood is an important risk factor for asthma and respiratory symptoms in non- smoking adults. [Indian J Chest Dis Allied Sci 2006; 48: 31-36] Key words: Asthma, Epidemiology, Prevalence, Risk factors, Environmental tobacco smoke, Passive smoking. INTRODUCTION Passive smoking or environmental tobacco smoke (ETS) exposure has been variously described as second-hand smoke or involuntary smoking. In the past, little attention, beyond its nuisance effect, was paid to the health consequences of passive smoking. An exhaustive report on health consequences of involuntary smoking by the United States Surgeon General, and reports by the United States Environmental Protection Agency, recently highlighted the increased risks of several diseases similar to those seen among smokers, in persons exposed to ETS at home or at work place 1,2. Asthma is a common respiratory disease resulting from an interaction between genetic susceptibility for this disease and exposure to various environmental factors. Tobacco smoking and exposure to ETS are some of the several important variables which are likely to affect the incidence, recognition and clinical presentation of asthma. Environmental tobacco smoke exposure as a risk factor for asthma and respiratory symptoms is now well accepted in children. There are several studies on the effects of parental smoking on childhood asthma. These include longitudinal as well as case control studies on incidence of asthma 3. Metaanalysis have also confirmed the association of ETS with asthma in children 4. In a large survey for prevalence of asthma among adolescent school children in Chandigarh, we had shown an increased risk for being an asthmatic if exposed to ETS 5. In adults, however, the effects of passive smoke exposure on respiratory health are still being debated. [Received: September 29, 2005; accepted: October 28, 2005] Correspondence and reprint requests: Dr S.K. Jindal, Professor and Head, Department of Pulmonary Medicine, Postgraduate Institute of Medical Education and Research, Chandigarh-160012, India; Tele.: 91-0172-2756821; Telefax: 91-0172-2745959; E-mail: skjindal@indiachest.org.
32 Passive Smoking and Asthma D. Gupta et al We have earlier shown that ETS can cause increased morbidity in adult asthmatics and can precipitate acute attacks 6,7. Environmental tobacco smoke has also been shown to be associated with development of bronchial hyper-responsiveness (BHR) in asymptomatic individuals and worsening of BHR in asthmatics 8,9. Here we describe the effects of ETS exposure on prevalence of asthma and respiratory symptoms in nonsmoking adults. MATERIAL AND METHODS We recently conducted a large multicentric population based epidemiological study for the prevalence of asthma in adults at Chandigarh (coordinating centre), Delhi, Kanpur and Bangalore 10. A salient feature of the methodology was that a single epidemiological definition of asthma as applicable to this study for field prevalence was used. A standardised and validated study-questionnaire based on the International Union Against Tuberculosis and Lung Diseases (IUATLD) respiratory symptom questionnaire was developed. This questionnaire was translated to local languages (Hindi and Kannada) and minor modifications done depending upon local needs. The method of data collection from the field in each region was uniform 10. All data were analysed centrally at the coordinating centre. The questionnaire had a special section on tobacco smoking (both active and passive). In case of nonsmokers, details of household exposure to ETS during childhood and adulthood were collected. After excluding smokers (defined as people with life time exposure equal to or more than 400 cigarettes or bidis), the prevalence of asthma and respiratory symptoms were studied in relation to ETS exposure. Multiple logistic regression modelling was done to assess influence of household ETS exposure on occurrence of bronchial asthma in adult nonsmokers, and odds ratio (OR) and corresponding 95% confidence intervals (95% CI) were calculated after adjusting for age, gender, usual residence, atopy and cooking fuel used at home. Logistic regression models were also constructed for timing and source of ETS exposure. All data were analysed using SPSS 10.0 software (SPSS Inc., Chicago, IL). RESULTS Information was collected from 73605 adult respondents. After excluding smokers, data from 62109 respondents (26926 men and 35183 women) were analyzed. Forty-five percent (28273) of these individuals reported exposure to ETS at home. ETS exposure was more common among women as compared to men (52% vs 37%). Prevalence of ETS exposure was less in urban areas and among the higher socio-economic strata (Table 1.) While a majority of respondents Table 1. Demographic profile of study population Number of Respondents Exposure to Household ETS Gender Men 26926 9965 (37.0%) Women 35183 18307 (52.0%) Age 15-24 years 19811 9771 (49.3%) 25-34 years 15670 7730 (49.3%) 35-44 years 10998 4904 (44.6%) 45-54 years 7558 2934 (38.8%) 55-64 years 4437 1663 (37.5%) 65-74 years 2572 919 (35.7%) >=75 years 1063 351 (33.0%) Usual residence Rural 27032 16140 (59.7%) Urban 33806 11408 (33.7%) Mixed 1271 724 (57.0%) Socio-economic status Low 21124 9456 (44.8%) Medium 36134 17380 (48.1%) High 4851 1436 (29.6%) Total 62109 28272 (45.5%) Table 2. Details of household environmental tobacco smoke exposure Men Women Total (N=26926) (N=35183) (N=62109) No environmental tobacco 63.1% 48.1% 54.6% smoke exposure Exposure in childhood 7.2% 7.3% 7.2% Exposure in adulthood 3.3% 20.5% 13.1% Exposure in both childhood 26.4% 24.1% 25.1% and adulthood Exposure from both 0.3% 11.2% 6.5% parents and spouse Exposure from parents only 30.4% 18.0% 23.4% Exposure from spouse only 0.4% 14.6% 8.5% Exposure from others in 5.9% 8.2% 7.2% the house exposed to ETS had exposure during both childhood and adulthood, more women had exposure only during adulthood as compared to men (20.5% vs 3.3%). Similarly ETS exposure from spouse was almost exclusively seen in women, while more men had exposure from parents alone during childhood (30.4% vs 18.0%; Table 2). The prevalence of respiratory symptoms was generally higher among ETS exposed individuals (Table 3). These differences were statistically significant for symptoms of wheezing, breathlessness and cough at night. Prevalence of other symptoms such as the early morning cough, phlegm in morning was similar in both the groups. The number of individuals reporting at least one respiratory symptom was also similar in two groups. The overall observed prevalence of asthma among non-smoker subjects was 2.0% (men 1.5%, women 2.5%, p<0.001). Of all asthmatics 48.6% (45.5% in non-
2006; Vol. 48 The Indian Journal of Chest Diseases & Allied Sciences 33 Table 3. Prevalence of respiratory symptoms in relation to household environmental tobacco smoke exposure Not Exposed Exposed Total p Value (N=33837) (N=28272) (N=62109) Wheezing 829 (2.5%) 781 (2.8%) 1610 (2.6%) 0.01 Morning tightnesss/breathlessness 733 (2.2%) 698 (2.5%) 1431 (2.3%) 0.01 Dyspnea on exertion 1704 (5.0%) 1441 (5.1%) 3145 (5.1%) 0.76 Dyspnea without exertion 610 (1.8%) 549 (1.9%) 1159 (1.9%) 0.21 Breathlessness at night 631 (1.9%) 590 (2.1%) 1221 (2.0%) 0.04 Cough at night 751 (2.2%) 729 (2.6%) 1480 (2.4%) 0.00 Cough in morning 751 (2.2%) 677 (2.4%) 1428 (2.3%) 0.16 Phlegm in morning 688 (2.0%) 613 (2.2%) 13.01 (2.1%) 0.24 Breathlessness 0.07 Usually breathless 858 (2.5%) 726 (2.6%) 1584 (2.6%) Breathing never satisfactory 256 (0.8%) 171 (0.6%) 427 (0.7%) Any respiratory symptom 2144 (6.3%) 1801 (6.4%) 3945 (6.4%) 0.86 asthmatics) were exposed to ETS. Prevalence of asthma was higher in persons ever exposed to ETS compared to not exposed individuals (2.19% vs 1.93%) [Table 4]. The differences in asthma prevalence were more marked for women in each category of exposure as compared to men (Table 4). The multiple logistic regression analysis confirmed the higher odds of having asthma in respondents ever exposed to ETS (OR 1.22; 95% CI 1.08-1.39) after adjusting for age, gender, usual residence, history of atopy and exposure to biomass fuels (Table 5). Table 4. Prevalence of asthma among non-smoker adults based on exposure to household environmental tobacco smoke (ETS) Men Women Total No ETS exposure 273 (1.61%) 381 (2.26%) 654 (1.93%) Ever exposed to ETS 122 (1.22%) 497 (2.71%) 619 (2.19%) ETS exposure in childhood only 32 (1.66%) 57 (2.21%) 89 (1.98%) ETS exposure in adulthood only 20 (2.23%) 226 (3.13%) 246 (3.03%) ETS exposure in both childhood and adulthood 69 (0.97%) 212 (2.50%) 281 (1.80%) ETS exposure from parents only 89 (1.09%) 101 (1.59%) 190 (1.31%) ETS exposure from spouse only 2 (1.96%) 170 (3.30%) 172 (3.28%) ETS exposure from both parents and spouse 3 (3.53%) 153 (3.90%) 156 (3.89%) ETS exposure from others in the house 28 (1.75%) 71 (2.47%) 99 (2.22%) Table 5. Multiple logistic regression modelling to assess influence of household environmental tobacco smoke (ETS) exposure on occurrence of bronchial asthma in adult nonsmokers, after adjusting for age, gender, residence, atopy and cooking fuel used at home OR (95% CI) OR (95% CI) OR (95% CI) No exposure to household ETS* 1.000 Exposure to household ETS 1.224 (1.080-1.387) No exposure to household ETS* 1.000 Household ETS exposure in childhood only 1.378 (1.085-1.751) Household ETS exposure in adulthood only 1.165 (0.985-1.378) Household ETS exposure in both childhood and adulthood 1.221 (1.044-1.427) No exposure to household ETS* 1.000 Household ETS exposure from parents only 1.075 (0.902-1.283) Household ETS Exposure from spouse only 1.205 (0.993-1.463) Household ETS exposure from both parents and spouse 1.691 (1.379-2.074) Household ETS exposure from others in the house 1.145 (0.909-1.443) Age 1.040 (1.036-1.043) 1.040 (1.036-1.044) 1.039 (1.035-1.043) Men* 1.000 1.000 1.000 Women 1.457 (1.234-1.720) 1.476 (1.248-1.745) 1.400 (1.180-1.659) Usual residence rural* 1.000 1.000 1.000 Usual residence urban 1.361 (1.188-1.560) 1.361 (1.187-1.560) 1.382 (1.205-1.585) Usual residence mixed 1.649 (1.145-2.374) 1.624 (1.126-2.342) 1.653 (1.148-2.380) No history suggestive of atopy* 1.000 1.000 1.000 History suggestive of atopy 14.782 (13.135-16.635) 14.774 (13.128-16.627) 14.776 (13.130-16.629) Not regularly cooking at home* 1.000 1.000 1.000 Cooking with biomass fuel 1.067 (0.863-1.319) 1.071 (0.866-1.325) 1.034 (0.835-1.280) Cooking with non-biomass fuel 0.794 (0.671-0.941) 0.789 (0.666-0.936) 0.784 (0.661-0.929) *: References category; Results are presented as odds ratio (OR), with 95% confidence intervals (95% CI) in parentheses.
34 Passive Smoking and Asthma D. Gupta et al Odds of having asthma were also significantly higher for exposure during childhood only and exposure both during childhood and adulthood. In terms of the person from whom the ETS exposure occurred, combined exposure from parents during childhood, as well as spouse during adulthood, had the highest odds (OR 1.69; 95% CI 1.38-2.07) for having asthma (Table 5). DISCUSSION ETS essentially comprises of a blend of side-stream smoke released from the burning end of a cigarette and the main-stream smoke exhaled by a smoker 11. It is a mixture of over 4000 gaseous and particulate chemical compounds. Although the concentrations of these pollutants get diluted to practically nil in the outdoor air, they attain significant levels in the indoor air. On an average, a smoker of one pack of cigarette was estimated to contribute about 20 µg/m 3 of indoor air particles in 24 hours 12. Concentrations of several toxic substances in the side-stream smoke are actually higher than in the main stream smoke, although the dilution by room air markedly reduces the inhaled concentration 13. In spite of the several curbs on public smoking imposed by different countries around the world, ETS exposure continues to remain a serious health issue. ETS exposure in adults ranges from 37% to 63% in the general population of USA 14. It is as high as 90% when biomarkers of ETS exposure are used for assessment 15. The prevalence of ETS exposure in 45.5% of our nonsmoking population was in tune with these findings. It is interesting to note that even though the health risks associated with ETS exposure are generally lower than those with active smoking, its public health impact is likely to be more pronounced in view of the much higher prevalence of ETS exposure as compared to active smokers (nearly three times in our study population). Despite the complexities involved in proving an association, information on passive smoking as a cause of asthma has been growing since the 1980 s. Two comprehensive reviews were published in 1986, i.e. the Report of the US Surgeon General on Health Consequences of Involuntary Smoking and the review by the National Research Council 1,8. Both these reports had a rather limited discussion on effects of ETS on asthma in adults. Even in a 1992 review by the US Environmental Protection Agency, no literature on passive smoking and risk of asthma in adults was cited 2. Since then, several investigators have described the association of ETS exposure with prevalence/incidence of asthma in adults 16. This is the first population based study from India that has studied the impact of ETS exposure on prevalence of asthma in adults. We found that ETS exposure was a significant risk factor for having asthma in adults (OR 1.22). One of the earliest study on the issue was the Swiss Study on Air Pollution and Lung Diseases in Adults (SAPALDIA) 17. In this crosssectional study, physician-diagnosed, incident asthma was found to be associated with self-reported ETS exposure in the previous 12 months (OR 1.39; 95% CI 1.04-1.86). In the same year, a significant association of self reported ETS-exposure (>1 pack/day) and obstructive lung diseases, which included asthma, chronic bronchitis or emphysema, was reported (OR 1.86; 95% CI 1.20-2.86) in a study from Philadelphia 18. More recent reports include a study involving over 47,000 adult non-smoking individuals attending a health care facility with multiple check-ups between 1979 and 1985 19. For both men and women, any exposure to ETS, as well as a heavy exposure to ETS (> 40 hours/week), was significantly associated with development of asthma or hay fever (ORs 1.14-1.22) 18. However, a dose response was not conclusively shown. A recent population based case-control study from Finland showed that nearly half of the incident asthma cases were attributable to ETS exposure 20. Some case-control studies have failed to demonstrate a convincing association of ETS exposure with asthma in adults. In a study on Swedish farmers, conducted through a postal survey to assess the current and the past ETS exposure, no association of asthma was found with any type of ETS exposure 21. The respiratory health impact of passive smoking was studied among 7892 adults (20-48 yrs) who had never smoked in the European Community Respiratory Health Survey 22. Compared to no ETS exposure, any ETS exposure was not associated with a greater risk of self-reported asthma (OR 1.15; 95% CI 0.84-1.58). Another population based study from Singapore also supported the risk of asthma among non smoking adult women residing with heavy smokers (OR 1.6; 95% CI 0.69-3.79) 23. One of the factors responsible for conflicting results observed in various studies is the lack of an agreement on, or of a gold standard for, epidemiological definition of asthma. Self reported asthma, the commonly employed tool in most surveys, might underestimate true prevalence 24. Several studies therefore report on new onset wheezing which is a more sensitive indicator of asthma in adults 25. We also studied the respiratory symptoms in relation to ETS exposure and found significantly higher prevalence of common respiratory symptoms like wheeze, breathlessness and cough among the ETS exposed individuals. Increased prevalence of respiratory symptoms has been reported in several recent studies among nonsmoking adults 26-28. Association of childhood exposure to ETS and asthma in adults has been examined in a population based Swedish study 29. The prevalence of asthma was more in adults who were exposed to ETS during childhood, compared to those who were not similarly exposed (7.6% vs 5.8%; p 0.035). Our findings also suggest that childhood exposure is important for
2006; Vol. 48 The Indian Journal of Chest Diseases & Allied Sciences 35 development of asthma, since exposures only during adulthood were not significantly associated with risk of having asthma in multivariate logistic regression analysis. Exposures from parents or spouse were more deleterious than ETS exposures from other family members, which is logical since the proximity of smoker to the non-smoker individual is an important factor to determine the magnitude of exposure, besides the environmental factors like ventilation, etc. Despite the association of asthma with ETS exposure in both adults and children, the pathogenesis is far less clear. Most of the studies on passive smoking and causation of asthma fulfil only a few of the Hill s nine criteria for causal association 30. Unlike COPD, active smoking is not causally related to asthma. Therefore, the criteria of plausibility, coherence and analogy are not directly applicable. Similarly, the criteria of specificity and experimental evidence also have little relevance. Most studies rely only on the strength of association, consistency, temporality and dose-response relationships. The dose-response relationships have been demonstrated with total daily duration of ETS exposure, number of smokers in the environment, duration of working with a smoker, a cumulative exposure index, or a biomarker of exsposure (nicotine level) 18,25. The observation that childhood exposure had higher odds ratios for asthma in adults provides some supporting evidence that ETS exposure (in children) may in fact be causally related the development of bronchial asthma later in life rather than acting as merely a trigger responsible for precipitation of an attack in an established patient. Bronchial hyperresponsiveness (BHR) is central to asthma pathophysiology. The current evidence on effect of ETS on BHR may suggest only a small but real increase in risk and this may be only one of the possible mechanisms involved in causation of asthma due to ETS exposure 8,9. Earlier investigators had believed that ETS exposure could lead to allergic sensitization in nonatopic individuals; however the balance of evidence did not support a positive association of atopy with parental smoking either before or after birth 31. We have also demonstrated positive association of ETS exposure with asthma after adjusting for atopy in multivariated analysis. To conclude, household ETS exposure during childhood is a significant risk factor for the development of asthma in adults. Combined ETS exposure from parents during childhood and spouse during adulthood is associated with maximum risk. It is therefore important that the public health campaigns focus at reducing ETS exposures at home as one of the important step towards primary prevention of asthma. 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