Epidemiological evidence relating environmental smoke to COPD in lifelong non-smokers: a systematic review

Abstract

Some evidence suggests environmental tobacco smoke (ETS) Background: might cause chronic obstructive pulmonary disease (COPD). We reviewed available epidemiological data in never smokers.We identified epidemiological studies providing estimates of relative Methods: risk (RR) with 95% confidence interval (CI) for various ETS exposure indices. Confounder-adjusted RRs for COPD were extracted, or derived using standard methods. Meta-analyses were conducted for each exposure index, with tests for heterogeneity and publication bias. For the main index (spouse ever smoked or nearest equivalent), analyses investigated variation in RR by location, publication period, study type, sex, diagnosis, study size, confounder adjustment, never smoker definition, and exposure index definition.: Twenty-eight relevant studies were identified; nine European or Results Middle Eastern, nine Asian, eight American and two from multiple countries. Five were prospective, seven case-control and 16 cross-sectional. The COPD definition involved death or hospitalisation in seven studies, GOLD stage 1+ criteria in twelve, and other definitions in nine. For the main index, random-effects meta-analysis of 33 heterogeneous (p<0.001) estimates gave a RR of 1.20 (95%CI 1.08-1.34). Higher estimates for females (1.59,1.16-2.19, n=11) than males (1.29,0.94-1.76, n=7) or sexes combined (1.10,0.99-1.22, n=15 where sex-specific not available), and lower estimates for studies of 150+ cases (1.08,0.97-1.20, n=13) partly explained the heterogeneity. Estimates were higher for Asian studies (1.34,1.08-1.67, n=10), case-control studies (1.55,1.04-2.32, n=8), and COPD mortality or hospitalisation (1.40,1.12-1.74, n=11). Some increase was seen for severer COPD (1.29,1.10-1.52, n=7). Dose-response evidence was heterogeneous. Evidence for childhood (0.88,0.72-1.07, n=2) and workplace (1.12,0.77-1.64, n=4) exposure was limited, but an increase was seen for overall adulthood exposure (1.20,1.03-1.39, n=17). We discuss study weaknesses that may bias estimation of the association of COPD with ETS.: Although the evidence suggests ETS increases COPD, study Conclusions

Second-Hand Smoke Exposure Associated with Risk of Respiratory Symptoms, Asthma, and COPD in 20,421 Adults from the General Population

“…Previous studies examining second-hand smoke exposure also reported susceptibility to COPD, 1,11,23,24 supporting the observations in the current study. A Chinese study of 6,497 adults found an increased odds ratio for spirometry-defined COPD of 1.48 in those individuals who had been exposed to second-hand smoking at home and work for 40 hours a week or more for more than 5 years, 1 and two meta-analyses have found elevated risk estimates for COPD of 1.20 and 1.66 among non-smokers who had been exposed to second-hand smoking.…”

“…A Chinese study of 6,497 adults found an increased odds ratio for spirometry-defined COPD of 1.48 in those individuals who had been exposed to second-hand smoking at home and work for 40 hours a week or more for more than 5 years, 1 and two meta-analyses have found elevated risk estimates for COPD of 1.20 and 1.66 among non-smokers who had been exposed to second-hand smoking. 23,24 We found an elevated odds ratio for COPD of 1.24 in individuals exposed to lifelong second-hand smoking in the general population, present irrespective of adjustments for age, sex, and smoking status. In addition, previous studies have also reported reduced lung function in individuals exposed to secondhand smoking.…”

Determinants of impaired lung function and lung cancer prediction among never-smokers in the UK Biobank cohort

“…The effect of ETS on pulmonary function and COPD has been well-described in the literature and several synthesizing studies have been conducted and evidence suggests SHS increases COPD. Although, weaknesses in existing studies, such as potential confounding by smoking need to be addressed to provide more definitive evidence [36,37].…”

The relationship of cigarette smoking in Japan to lung cancer, COPD, ischemic heart disease and stroke: A systematic review

“…This review is concerned with the effects of active smoking in Japan on the four diseases concerned. Recent reviews by ourselves 73– 76 and others 77 have found that evidence in Japan on passive smoking is very sparse, except for lung cancer. For IHD, our recent review 75 cites only the Hirayama study 78 as reporting a non-significant relative risk of 1.16 (95% CI 0.94–1.43), while our review of passive smoking and stroke 74 cites the Hirayama study as finding “no significant trend” and a study by Nishino et al 79 as giving a relative risk of 0.75 (0.80–1.12).…”

“…For IHD, our recent review 75 cites only the Hirayama study 78 as reporting a non-significant relative risk of 1.16 (95% CI 0.94–1.43), while our review of passive smoking and stroke 74 cites the Hirayama study as finding “no significant trend” and a study by Nishino et al 79 as giving a relative risk of 0.75 (0.80–1.12). Our review of passive smoking and COPD 76 again cited only the relative risk from the Hirayama study of 1.38 (0.86–2.21), though one very recently published study by Ukawa et al 80 did report significantly increased RRs of 2.40 (1.39–4.15) and 2.88 (1.68–4.93) for passive smoking at home for ≤4 days per week and almost every day, as compared to none.…”