Gilmour et al. in the presence of tobacco smoke exposure, hypersensitivity reactions to allergens are stronger. Indeed, based on the current knowl- edge, ETS is likely to be the most important indoor pollutant that is harmful for human health. The literature for this review on ETS and asthma is based on a Medline database (http://www.ncbi.nlm.nih.gov/entrez/query. fcgi?db=PubMed&itool=toolbar) search up to May 2004, but because of space constrictions, we reference previous reviews when possible and describe in detail only some recent longi- tudinal or incident case–control studies. ETS and induction of asthma in children. Since the 1980s, numerous large studies have identified significant relations between parental smoking and development of asthma in children (Cook and Strachan 1997, 1998; Jaakkola 2000; J.J.K. Jaakkola and Jaakkola 2002). Meta-analyses based on these studies have shown a dose-dependent increase in chil- dren’s rates of asthma related to increasing number of household smokers (Cook and Strachan 1997), with the strongest effect detected in the youngest children (California EPA 1997; Strachan and Cook 1997, 1998). Maternal smoking has been reported to have a stronger effect than other household mem- bers’ smoking, raising concern of the poten- tial role of prenatal tobacco smoke exposure. Recent studies have addressed the role of pre- natal versus postnatal exposure. A cohort study of 499 children of atopic parents from Boston found that maternal smoking during pregnancy was associated with an increased risk of asthma in the ﬁrst year of life, with an odds ratio (OR) of 1.83 [95% confidence interval (CI), 1.12–3.00; Gold et al. 1999]. In a study based on the Finnish birth cohort that included almost 60,000 children, the risk of developing asthma among children 7 years of age increased in a dose-dependent pattern with the mothers’ smoking rates in preg- nancy: OR 1.25 (95% CI, 1.09–1.44) for < 10 cigarettes/day and 1.36 (1.14–1.63) for > 10 cigarettes/day (Jaakkola and Gissler 2004). Signiﬁcant associations persisted even after adjustment was made for low birth weight and duration of pregnancy, suggesting that the effect of passive smoking on asthma was independent of these factors. ETS and induction of asthma in adults. Fewer studies have been published on ETS exposure and asthma in adults. To date one longitudinal, three case–control and at least six cross-sectional studies have reported associa- tions between ETS exposure and adult-onset asthma, with ORs between 1.15 and 3.30 [reviewed by Jaakkola (2000) and by M.S. Jaakkola and Jaakkola (2002)]. In many studies the risk of asthma was more strongly related to workplace ETS exposure than to home expo- sure, and several studies showed evidence of a dose–response relation. A problem with most studies was that they included existing (preva- lent) cases of asthma, making it impossible to distinguish development of asthma in adult- hood from exacerbation of established disease. Another methodologic issue was the reliance on questionnaire reports of asthmatic symptoms or diagnosed asthma, as it may be difﬁcult to dis- tinguish between asthma and chronic obstruc- tive pulmonary disease without clinical investigations. To address these challenges Jaakola et al. (2003) conducted a population- based case–control study with incident cases of asthma. The study assessed the effect of ETS exposure on adult-onset asthma and estimated the fraction of asthma attributable to ETS exposure in the past year. All new clinically diagnosed cases of asthma in individuals 21–63 years of age were recruited from 1997 to 2000 in a geographically deﬁned area in south- ern Finland through all health care facilities diagnosing asthma in this area. A random sam- ple of the source population (residents of the Pirkanmaa Hospital district, 21–63 years of age) was recruited as controls. A total of 521 asthma cases and 932 controls without asthma participated, including 239 persons with asthma and 487 controls who were never- smokers. These never-smokers formed the study population for the analysis on ETS expo- sure. Exposure to ETS was assessed on the basis of a self-administered questionnaire. Table 1 shows the results of ORs for asthma related to ETS exposure after adjusting for confounders including gender, age, education, parental atopy, and other occupational exposures in multivariate logistic regression. ETS exposure at work during the past 12 months was related to a significantly increased risk of adult-onset Table 1. Exposure to ETS among cases and controls and adjusted OR of adult-onset asthma in relation to ETS exposure at home and at work. ETS exposure Past 12 months At work At home Cumulative cigarette-years (home and work) 0 1–49 50–99 100–149 ≥ 150 Adapted from Jaakkola et al. (2003). 628 Cases [n (%)] Controls [n (%)] 34 (15.6) 7 (3.0) 104 (43.5) 26 (10.9) 22 (9.2) 19 (8.0) 68 (28.5) 41 (9.0) 8 (1.7) 231 (47.4) 91 (18.7) 44 (9.0) 25 (5.1) 96 (19.7) OR 2.16 4.77 1.00 0.80 1.30 2.01 1.84 95% CI 1.26–3.72 1.29–17.7 0.48–1.36 0.71–2.35 1.02–3.99 1.21–2.80 asthma, with an excess risk of 116% (95% CI, 26–272). Home exposure was associated with an even higher risk, but the CI range for this OR was wide because of a small number of study subjects being exposed at home (Table 1). Assessment of exposure quantitatively as cumu- lative exposure combining home and workplace exposures as cigarette-years suggested a dose–response relation with the risk of asthma. The fraction of exposed cases for which asthma was attributable to ETS exposure in the past year was 49% (95% CI, 16–69). The fraction of all asthma cases in the working age popula- tion (i.e., population-attributable fraction) attributable to ETS exposure in the last year was 8.0%. Conclusions on ETS and possibilities for prevention. Considering the number of stud- ies, their validity, evidence of dose–response relations, and biological plausibility, it can be concluded that a) there is some evidence for the effect of maternal smoking in pregnancy on the risk of asthma in childhood; b) post- natal exposure to ETS shows a causal link with the development of asthma in childhood; c) there is strong evidence that ETS is related to an increased risk of adult-onset asthma; and d) elimination or reduction of ETS exposure could prevent a considerable fraction of asthma in both children and adults. Banning of smoking in the workplaces has been shown to reduce employees’ exposure to ETS and consequently fetal exposure of chil- dren of working pregnant mothers. For exam- ple, in Finland reformation of the tobacco control law in 1995 to protect employees from workplace ETS exposure led to a dramatic decline in tobacco smoke exposure at work in a 4-year follow-up of nine large- or medium- sized workplaces in southern Finland (Table 2; Heloma and Jaakkola 2003). This study also showed a decline in active smoking during the follow-up, suggesting that the legislation was able to affect home ETS exposure as well. To reduce childhood exposure, parents should be educated and encouraged not to smoke, or if they already are smokers, to quit, through support in family planning and pre- natal health care and at schools. Based on stud- ies from Finland (Jaakkola et al. 1994, 2001) and elsewhere (Owen et al. 1998), intensive support should be provided for certain groups at high risk for smoking during pregnancy and Table 2. ETS exposure (%) in nine large- or medium- sized workplaces before and after 1995 reformation of the national tobacco control legislation in Finland. Daily ETS 1994–1995 exposure at work (n = 605) 1995–1996 (n = 681) Not at all < 1 hr 1–4 hr > 4 hr 20.7 28.8 17.7 32.9 54.2 28.6 9.0 8.2 Adapted from Heloma and Jaakkola (2003). 1998 (n = 474) 70.7 17.5 8.4 3.4 VOLUME 114 | NUMBER 4 | April 2006 • Environmental Health Perspectives