CORRESPONDENCE

Re: Passive Smoking Exposure and Female Breast Cancer Mortality

Kenneth C. Johnson

Correspondence to: Kenneth C. Johnson, Ph.D., Cancer Bureau, Centre for Chronic Disease Prevention and Control, Health Canada, LCDC Bldg, P.L. 0601C1, Tunney's Pasture, Ottawa, ON, Canada, K1S 2Z7 (e-mail: Ken_LCDC_Johnson{at}hc-sc.gc.ca).

The study by Wartenberg et al. (1) is a welcome addition to the literature investigating the relationship between exposure to environmental tobacco smoke (ETS) and breast cancer risk: Large prospective studies are important for understanding etiologic issues. Careful examination of the American Cancer Society's Cancer Prevention Study II (CPS-II) analyses is warranted, however, given that the negative findings are apparently at odds with the results of eight other published studies [cited in (1,2)].

I will focus on CPS-II's main analysis, in which ETS exposure is based exclusively on the husband's smoking history. (The secondary analysis, based on women's self-reported ETS exposure in 1982, ignores historical exposure, including exposure from the 32.6% of husbands who were former smokers.) Nonspousal ETS exposure has been common in the United States (3), and ETS misclassification may dilute risk (4). Fontham et al. (5) found that 64% of never-smoking women controls in a five-U.S.-city study reported childhood ETS exposure, 14% reported nonspousal adult household exposure, 24% reported social exposure, and 60% reported exposure from co-workers. These exposures were often long term—at least 16 years in 61% of childhood exposures and in 42% of social and workplace exposures.

In fact, Fontham et al. (5) found that 96% of women had had regular ETS exposure, 90% of them as adults. [Canadian and British studies, cited in (1), also found that women had extensive nonspousal ETS exposure.] Although the study populations of the CPS-II and of Fontham et al. are demographically different (95% versus 61% white and 43% versus 7% college graduates, respectively), a similar percentage of husbands smoked (58.5% and 61.1%, respectively). Thus, the findings of Fontham et al. may be useful for approximating potential CPS-II levels of nonspousal ETS exposure.

Table 1Go provides three examples of the potential impact of relying solely on spousal ETS exposure in CPS-II rather than on the more extensive exposure assessment reported by Fontham et al. (5). An underlying relative risk (RR) of 2.0 for breast cancer among ETS-exposed women could be diluted to 1.14, and an underlying RR of 2.50 among women exposed to high levels of ETS could also be diluted to 1.14. Expected random variation around the diluted point estimates could further obscure underlying risks.


View this table:
[in this window]
[in a new window]
 
Table 1. Potential impact of exposure misclassification on an underlying environmental tobacco smoke (ETS)–breast cancer relative risk of 2.0 among never smokers when ETS exposure status is based solely on spousal smoking
 
Wartenberg et al. (1) contend that their exposure measures are valid because other CPS-II analyses found weak, statistically nonsignificant RRs among wives of smokers of 1.16 for heart disease death and 1.2 for lung cancer death, comparable to risks in other spousal-exposure-based studies. However, lung cancer risk appears to have a linear dose–response gradient with passive smoking (5), and the ETS–heart disease risk is driven by acute (i.e., recent) ETS exposure. By contrast, the other breast cancer studies have found similar summary passive and active smoking RRs (both approaching 2.0), suggesting a nonlinear dose–response relationship, perhaps involving a genetically susceptible subgroup. If any considerable period of ETS exposure substantially increased risk of breast cancer (Table 1Go, example 3), misclassification of historic exposure might obscure underlying breast cancer risk more than it obscures lung cancer risk.

Wartenberg et al. (1) suggest that their study and the two other cohort studies are homogeneous in finding a low risk of breast cancer associated with ETS, in contrast to the case–control studies, which suggest an RR approaching 2. However, although the overall breast cancer risk associated with any spousal ETS exposure was 1.3 in both other cohort studies (conducted in countries where nonspousal ETS exposure was traditionally uncommon), Hirayama reported an RR of 1.86 (95% confidence interval [CI] = 1.02 to 3.38) among Japanese women aged 50–69 years with spouses who smoked 20 or more cigarettes daily (6), and Jee et al. (7) reported an RR of 1.7 (95% CI = 1.0 to 2.8) among Korean women whose husbands had smoked for 30 or more years.

Although the CPS-II analyses found little association between ETS exposure and breast cancer risk, given the positive findings in eight other studies and the likelihood of extensive nonspousal exposure, the CPS-II results are also consistent with a positive association obscured by a high level of exposure misclassification.

REFERENCES

1 Wartenberg D, Calle EE, Thun MJ, Heath CW Jr, Lally C, Woodruff T. Passive smoking exposure and female breast cancer mortality. J Natl Cancer Inst 2000;92:1666–73.[Abstract/Free Full Text]

2 Zhao Y, Shi Z, Liu L, et al. Matched case– control study for detecting risk factors of breast cancer in women living in Chengdu. Zhonghua Liu Xing Bing Xue Za Zhi [Chin J Epidemiol] 1999;20:91–4.

3 Hammond SK. Exposure of U.S. workers to environmental tobacco smoke. Environ Health Perspect 1999;107 Suppl 2:329–40.

4 Rothman KJ, Greenland S. Modern epidemiology. 2nd ed. Philadelphia (PA): Lippincott-Raven; 1998.

5 Fontham ET, Correa P, Reynolds P, Wu-Williams A, Buffler PA, Greenberg RS, et al. Environmental tobacco smoke and lung cancer in nonsmoking women. A multicenter study. JAMA 1994;271:1752–9.[Abstract]

6 Wells AJ. Breast cancer, cigarette smoking, and passive smoking [letter]. Am J Epidemiol 1991; 133:208–10.[Medline]

7 Jee SH, Ohrr H, Kim IS. Effects of husbands' smoking on the incidence of lung cancer in Korean women. Int J Epidemiol 1999;28:824–8.[Abstract]


This article has been cited by other articles in HighWire Press-hosted journals:


             
Copyright © 2001 Oxford University Press (unless otherwise stated)
Oxford University Press Privacy Policy and Legal Statement