- 1 School of Public Health, University of California, Los Angeles, CA 90095-1772, USA,
- 2 Department of Preventive Medicine, State University of New York, Stony Brook, NY 11794-8036, USA
- Correspondence to: J E Enstrom
- Accepted 7 March 2003
Objective To measure the relation between environmental tobacco smoke, as estimated by smoking in spouses, and long term mortality from tobacco related disease.
Design Prospective cohort study covering 39 years.
Setting Adult population of California, United States.
Participants 118 094 adults enrolled in late 1959 in the American Cancer Society cancer prevention study (CPS I), who were followed until 1998. Particular focus is on the 35 561 never smokers who had a spouse in the study with known smoking habits.
Main outcome measures Relative risks and 95% confidence intervals for deaths from coronary heart disease, lung cancer, and chronic obstructive pulmonary disease related to smoking in spouses and active cigarette smoking.
Results For participants followed from 1960 until 1998 the age adjusted relative risk (95% confidence interval) for never smokers married to ever smokers compared with never smokers married to never smokers was 0.94 (0.85 to 1.05) for coronary heart disease, 0.75 (0.42 to 1.35) for lung cancer, and 1.27 (0.78 to 2.08) for chronic obstructive pulmonary disease among 9619 men, and 1.01 (0.94 to 1.08), 0.99 (0.72 to 1.37), and 1.13 (0.80 to 1.58), respectively, among 25 942 women. No significant associations were found for current or former exposure to environmental tobacco smoke before or after adjusting for seven confounders and before or after excluding participants with pre-existing disease. No significant associations were found during the shorter follow up periods of 1960-5, 1966-72, 1973-85, and 1973-98.
Conclusions The results do not support a causal relation between environmental tobacco smoke and tobacco related mortality, although they do not rule out a small effect. The association between exposure to environmental tobacco smoke and coronary heart disease and lung cancer may be considerably weaker than generally believed.
Contributors JEE conceived the study and obtained funding, conducted the extended follow up, analysed the data, and drafted the manuscript; he will act as guarantor for the paper. GCK contributed to the follow up questionnaire, advised on the data analysis and interpretation, and contributed extensively to the manuscript.
Funding The American Cancer Society initiated CPS I in 1959, conducted follow up until 1972, and has maintained the original database. Extended follow up until 1997 was conducted at the University of California at Los Angeles with initial support from the Tobacco-Related Disease Research Program, a University of California research organisation funded by the Proposition 99 cigarette surtax (www.ucop.edu/srphome/trdrp). After continuing support from the Tobacco-Related Disease Research Program was denied, follow up through 1999 and data analysis were conducted at University of California at Los Angeles with support from the Center for Indoor Air Research, a 1988-99 research organisation that received funding primarily from US tobacco companies.24
Competing interests In recent years JEE has received funds originating from the tobacco industry for his tobacco related epidemiological research because it has been impossible for him to obtain equivalent funds from other sources. GCK never received funds originating from the tobacco industry until last year, when he conducted an epidemiological review for a law firm which has several tobacco companies as clients. He has served as a consultant to the University of California at Los Angeles for this paper. JEE and GCK have no other competing interests. They are both lifelong non-smokers whose primary interest is an accurate determination of the health effects of tobacco.