Volume 23
Number 1
2002

[Table of Contents]

Environmental tobacco smoke and deaths from coronary heart disease in Canada

Abstract

A series of recent meta-analyses have concluded that non-smokers who live with smokers face an elevated risk of coronary heart disease (CHD). In this study, we estimated the number of CHD deaths among non-smokers attributable to environmental tobacco smoke (ETS) exposure in their homes. Population-attributable risk estimates suggest that in 1997 over 800 Canadians died of CHD caused by passive exposure to ETS. This figure is likely an underestimation of the total number of CHD deaths attributable to ETS, since our study did not estimate the number of deaths among non-smokers caused by ETS exposure in the workplace. However, this partial picture can still help to highlight the burden of disease resulting from this pervasive involuntary environmental exposure.

Key words: coronary heart disease; environmental tobacco smoke; mortality; population attributable risk; smoking

Introduction

There is increasingly compelling evidence that exposure to environmental tobacco smoke (ETS) is associated with an increased risk of coronary heart disease (CHD) in non-smokers. ^{3,7,9,13,14,20} Three recent meta-analyses ^5,10,17 have reported significantly increased risks of similar magnitude for coronary heart disease among non-smokers exposed to ETS in their homes. Studies examining the exposure of non-smokers to ETS in the workplace have also reported significantly elevated risks of CHD compared to unexposed non-smokers.⁵

Much of the experimental work exploring the relationship between CHD and ETS has focused on acute effects.^2,4,20 Experimental studies demonstrate that acute exposure to ETS enhances platelet aggregation.^7,10 ETS exposure can injure the endothelial layer of blood vessels, which could contribute to the initiation or progression of atherogenesis; ⁷ ETS exposure may also increase the risk of developing atherosclerosis through the promotion of plaque development.³ A focus on the acute effects of ETS exposure seems appropriate, given the fall in CHD risk that occurs when active smoking stops. The US Surgeon General's report on the health benefits of smoking cessation concluded that the risk of CHD among former smokers is cut in half after just one year of cessation.¹⁶ Former smokers show some residual long-term elevated risk that declines over time.^4,16 It seems reasonable to assume that similar risk declines in non-smokers would occur when exposure to ETS ceases. There is support for this interpretation from prospective cohort studies, which have found a higher elevated risk of CHD among non-smokers living with current smokers than among non-smokers living with former smokers.^5,14

Coronary Heart Disease and ETS Exposure in Canada

Although the number of CHD deaths resulting from active smoking have been estimated for Canada, ^8,11 similar estimates for ETS are lacking. Estimating the number of deaths associated with passive exposure to ETS is more complex, since there are multiple settings of potential exposure, including the home, workplace and other public places. However, generating estimates based on what we do know about the exposure level in specific environments can highlight the burden of disease resulting from this type of involuntary exposure.

Methods

The number of CHD (ICD-9 rubrics 410-414) deaths among those aged 25 years or older by Canadian province in 1997 were obtained from Statistics Canada. Estimates of the prevalence of household exposure to passive cigarette smoking by province in 1999 were obtained from the Canadian Tobacco Use Monitoring Survey (CTUMS).⁶ This is an ongoing, cross-sectional survey that collects information from a representative sample of provincial residents on a range of tobacco control issues, including individual smoking status and ETS exposure in the home. Individuals were considered to be exposed to ETS if they were non-smokers (never smokers or those who had quit at least three years previously) and lived in a household in which smoking occurred every day or almost every day inside the home.

The incidence density ratio (relative risk) associated with exposure to environmental tobacco smoke was estimated from two recent meta-analyses. Thun and colleagues¹⁷ noted relative risks of 1.24 for males and 1.23 for females exposed to passive smoking, while He and colleagues⁵ estimated a relative risk of 1.25. Both of these meta-analyses examined more than 18 prospective cohort and case control studies. These individual studies, which included US, European and Asian studies using slightly different operational definitions of ETS home exposure, nevertheless reported very similar elevated CHD risk estimates for nonsmoking men and women. For this study, we used an estimate of 1.24, which is at the lower end of the range of risk estimates produced by these studies. Because relative risks in the study by Thun et al¹⁷ were almost identical for males and females, and to increase the precision of our estimates, we calculated passive smoking attributable deaths for both sexes combined.

Population-attributable risk (also known as attributable fraction)¹⁸ was estimated for each province using the following formula:

PAR = p(IDR - 1)/p(IDR - 1) + 1

where p is the proportion of the total population with the exposure (i.e., non-smokers regularly exposed to ETS in their homes) and IDR is the incidence density ratio estimated from the two cohort studies summarized above (IDR = 1.24). Passive smoking-attributable CHD mortality was calculated as the product of the passive smoking-attributable fraction and the number of CHD deaths.

Results

Prevalence of ETS Exposure

Table 1 summarizes the prevalence of active smoking and passive ETS exposure of non-smokers in the home in the 1999 Canadian population, age 25+. The table also includes a group of recent quitters (i.e., within the past three years). In 1999, an estimated 8% (approximate CI: ± 1%) of the Canadian population aged 25+ were non-smokers regularly exposed to ETS in their homes. The percentage within each province who were both non-smokers and were exposed to ETS in their homes ranges from a low of 3% in British Columbia to a high of 12% in Newfoundland and Quebec. On average, the degree of variability around these provincial estimates of ETS exposure was about ± 1.9%.

The national and provincial estimates of ETS exposure in the home combine the results for men and women. Preliminary analysis indicated that, although the prevalence of active smoking among men aged 25+ was somewhat higher than for women in 1999 (26% and 22%, respectively), the percentages of non-smoking men and women exposed to ETS in their homes were quite similar. Seven percent of all men and 8% of all women in Canada aged 25+ were non-smokers regularly exposed to ETS in their homes.

Estimated CHD Deaths Attributable to ETS

Population-attributable risk estimates suggest that in 1997 over 800 Canadians died from CHD as a result of involuntary tobacco smoke exposure in their homes (Table 2). A disproportionate number of men and women in Quebec and Newfoundland were estimated to have died from CHD resulting from passive smoking, reflecting the high prevalence of active and passive smoking in these provinces. The number of estimated deaths per 100,000 population was significantly lower in British Columbia, reflecting the very low prevalence of household exposure to second-hand cigarette smoke in the province. If the prevalence of exposure to environmental tobacco smoke across Canada could be lowered to the levels observed in British Columbia, there would be an estimated 480 fewer CHD deaths each year.

Discussion

In 1997, over 800 Canadian non-smokers were estimated to have died of coronary heart disease as a result of exposure to second-hand smoke in their homes. Our estimation is a good example of how the application of population attributable risk estimates can contribute to understanding the impact of an exposure in the population. In the current case, we are dealing with a modest increase in risk with exposure (e.g., RR of about 1.24), but an environmental exposure within the population that is quite large (e.g., 8% of the adult population aged 25+).

It is likely that we have underestimated the overall number of ETS-related deaths because only exposure in the home was considered; deaths attributable to workplace exposure were not included. Such workplace exposure may be substantial, given that a single smoker may expose multiple individuals within the workplace. In 1996-1997, 32% of men and 19% of women (aged 25+) who smoked every day worked in workplaces with no restrictions on smoking.

Our analysis is also likely to underestimate attributable deaths because we used ETS exposure data derived from a 1999 survey, rather than for 1997. Active smoking among older adults (age 25+) declined from 1996-1997 to 1999 (from 28% to 24%), and it is reasonable to assume that passive smoking prevalence also declined.^6,12 Since risks associated with CHD can fall quite dramatically after just one year in former active smokers,¹⁶ we also chose a relatively conservative definition of non-smoker, which included never smokers plus former smokers who had to have quit for at least three years. Our estimate also does not include any increased risk to current smokers that may result from their exposure to environmental tobacco smoke.

Our estimate of the number of CHD deaths attributable to ETS were derived from a single estimated relative risk. A more accurate estimate would have resulted from the use of age-specific relative risks; unfortunately, no satisfactory age-specific relative risks for CHD and ETS exposure among non-smokers are available. The limited evidence that does exist, however, suggests that this would result in only modest changes in the estimated number of CHD deaths attributable to ETS.¹⁹

Finally, although there is general acceptance that ETS exposure increases the risk of CHD in non-smokers, the magnitude of the effect is greater than might be anticipated based on the risk observed with active smoking. This has led a few to suggest that existing studies overestimate the relative risk associated with passive smoking and CHD,^1,15 which would, in turn, overestimate the number of deaths among non-smokers attributable to residential passive smoking. However, review of a range of experimental and clinical studies suggests that the impact of tobacco smoke on the heart is primarily acute and that the biological mechanisms involved in platelet aggregation, for example, are similar for both active and passive smoking. There is also evidence of a nonlinear dose-response relationship across passive and active smoking. Passive smoking produces elevated risks for CHD that are similar to low-level active smoking (e.g., about one cigarette per day). Glantz and Parmley³ have suggested that the reason active smoking does not produce higher (i.e., linear) dose-response results is because the effects of cigarette smoke on the heart may reach a saturation point, making a monotonic dose-response effect unlikely. Therefore, concerns about an overestimation of a passive smoking risk estimate is less tenable in light of the highly consistent relative risks across cohort studies, evidence for a plausible dose-response relationship, and evidence in support of biological plausibility.^3,7,13,19,20

In Canada, the rates of home exposure to ETS among non-smokers varies dramatically by province. The high proportion of non-smokers in Quebec exposed to ETS as compared to the low proportion in British Columbia reflects both the active smoking prevalence differences in these two provinces and provincial differences as to whether smokers face household smoking restrictions. Eighty-eight percent of smokers in Quebec lived in a household where someone smoked every day or almost every day inside the home, compared to 59% of smokers in British Columbia.⁶ If the prevalence of exposure to environmental tobacco smoke in Canada could be lowered to the levels observed in British Columbia, there would be an estimated 480 fewer coronary heart disease deaths each year in Canada.

Highlighting the number of CHD deaths caused by passive smoking in homes can have important implications for the development of public health programs and awareness campaigns. In particular, such information clearly underscores the importance of promoting smoke-free homes across Canada. Often, these programs and awareness campaigns focus on reducing ETS exposure in homes with children. These results indicate that promoting smoke-free homes can have a positive health impact on both children and adults.

Tobacco smoke is a potentially deadly environmental exposure. To provide some perspective on the degree of complacency with which ETS is often treated, Steenland¹³ pointed out that, within workplaces, environmental exposure limits for specific toxins are often set to contain the number of excess deaths resulting from exposure to the toxin. These environmental limits are usually in the range of one death in 10⁵ or one in 10⁶. As reported in Table 2, excess CHD deaths attributed to passive smoking are about 4 in 10⁵ for Canada as a whole, a rate that far exceeds what is acceptable for other toxic exposures.

The endpoint of this analysis was mortality, the most extreme adverse outcome associated with exposure to ETS. Glantz and Parmley³ have estimated that the occurrence of nonfatal myocardial infarction due to passive exposure to ETS is likely to be three times as high as deaths from CHD. These less extreme outcomes also contribute to the disease burden and health care costs associated with passive smoking and CHD.

References

1. Bailar JC, III. Passive smoking, coronary heart disease, and meta-analysis [editorial; comment]. N Engl J Med, 340: 958-959, 1999.

2. Glantz SA, Parmley WW. Passive smoking and heart disease. Epidemiology, physiology, and biochemistry. Circulation, 83:1-12, 1991.

3. Glantz SA, Parmley WW. Passive smoking and heart disease. Mechanisms and risk. JAMA, 273:1047-1053, 1995.

4. Glantz SA, Parmley WW. Passive and active smoking. A problem for adults. [editorial; comment] Circulation, 94:596-598, 1996.

5. He J, Vupputuri S, Allen K, Prerost MR, Hughes J, Whelton PK. Passive smoking and the risk of coronary heart disease - a meta-analysis of epidemiologic studies. N Engl J Med, 340:920-926, 1999.

6. Health Canada. Canadian Tobacco Use Monitoring Survey (Full Year, 1999), Microdata file. Released Oct 31, 2000. Ottawa, Ontario.

7. Howard G, Thun MJ. Why is environmental tobacco smoke more strongly associated with coronary heart disease than expected? A review of potential biases and experimental data. Environ Health Perspect, 107 Suppl 6:853-858, 1999.

8. Illing EM, Kaiserman MJ. Mortality attributable to tobacco use in Canada and its regions, 1991. Can J Public Health, 86:257-265, 1995.

9. Jamrozik K, Colditz GA. Passive smoking and coronary heart disease [letter; comment]. N Engl J Med, 341:698-700, 1999.

10. Law MR, Morris JK, Wald NJ. Environmental tobacco smoke exposure and ischaemic heart disease: an evaluation of the evidence. BMJ, 315: 973-980, 1997.

11. Single E, Robson L, Rehm J, Xie X, Xi X. Morbidity and mortality attributable to alcohol, tobacco, and illicit drug use in Canada [published erratum appears in Am J Public Health 1999 May;89(5):785]. Am J Public Health, 89: 385-390, 1999.

12. Statistics Canada. National Population Health Survey, 1996/97. Microdata file. 1998. Ottawa, Ontario.

13. Steenland K. Passive smoking and the risk of heart disease. JAMA, 267:94-99, 1992.

14. Steenland K, Thun M, Lally C, Heath C, Jr. Environmental tobacco smoke and coronary heart disease in the American Cancer Society CPS-II cohort. Circulation, 94: 622-628, 1996.

15. Sterling TD, Rosenbaum WL, Weinkam JJ. Risk attribution and tobacco-related deaths. Am J Epidemiol, 138:128-139, 1993.

16. Surgeon General. The health benefits of smoking cessation: A report of the Surgeon General. 1990. Rockville, Md: US Public Health Service, Dept of Health and Human Services.

17. Thun M, Henley J, Apicella L. Epidemiologic studies of fatal and nonfatal cardiovascular disease and ETS exposure from spousal smoking. Environ Health Perspect, 107 Suppl 6:841-846, 1999.

18. Last JM. (Ed.) A Dictionary of Epidemiology, Third Edition. Oxford University Press, 1995.

19. Wells AJ. An estimate of adult mortality in the United States from Passive Smoking. Environment Int, 14: 249-265, 1988.

20. Wells AJ. Passive smoking as a cause of heart disease. J Am Coll Cardiol, 24:546-554, 1994.

Author References

Margaret de Groh and Howard I Morrison, Centre for Disease Prevention and Control, Health Canada

Correspondence: Dr Margaret de Groh, Disease Intervention, Health Canada, AL: 1910, Tunney's Pasture, Ottawa, Ontario K1A 1B4; Fax: (613) 941-2633;
E-mail: margaret_de_groh@hc-sc.gc.ca

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