Affiliations of authors: P. Brennan, J, Butler, P. Boffetta, International Agency for Research on Cancer, Lyon, France; A. Agudo, Institute for Epidemiological and Clinical Research, Mataró, Spain; S. Benhamou, National Institute of Health and Medical Research, Paris, France; S. Darby, Imperial Cancer Research Fund, Oxford, UK; C. Fortes, Epidemiology Unit, Latium Region, Rome, Italy; K.-H. Jöckel, Institute of Medical Informatics, Biometry and Epidemiology, Essen, Germany; M. Kreuzer, H.-E. Wichman, GSF Institute for Epidemiology, Munich, Germany; F. Nyberg, International Agency for Research on Cancer, Lyon, and Institute of Environmental Medicine, Karolinska Institute, Stockholm, Sweden; H. Pohlabeln, Bremen Institute for Prevention Research, Bremen, Germany; R. Saracci, International Agency for Research on Cancer, Lyon, and National Research Council, Pisa, Italy.
Correspondence to: Paul Brennan, Ph.D., ECE Unit, International Agency for Research on Cancer, 150 cours Albert-Thomas, 69372 Lyon, France (e-mail: brennan{at}iarc.fr).
A recent meta-analysis based on 4626 cases concluded that the relative risk of lung cancer in lifelong nonsmokers who lived with a smoker was 1.24 (95% confidence interval [CI] = 1.13-1.36) (1). Subsequently, we reported in the Journal (2) the results from a large case-control study of environmental tobacco smoke (ETS) and lung cancer based in 12 European centers. This study provided an odds ratio (OR) for lung cancer of 1.14 (95% CI = 0.88-1.47) for spousal and workplace exposure to ETS; the increase was most apparent among those in the top quartile of exposure (OR = 1.31; 95% CI = 0.88-1.94) and the top decile of exposure (OR = 1.46; 95% CI = 0.96-2.22) (P value for trend = .01). It could be argued that such increased risks associated with ETS might not represent a causal effect but may be due to confounding by dietary factors. To further elucidate this critical issue, we have analyzed the data of the European study by examining the joint relationship between dietary consumption, exposure to ETS, and lung cancer.
Eight of the 12 centers have collected detailed food-frequency information on both case
patients and control subjects, including information on intake of various fruits and vegetables,
allowing weighted estimates of intake of several carotenoids combined (-carotene,
ß-carotene, lutein, zeaxanthin, and lycopene), ß-carotene alone, and retinol to be
calculated (3). Dietary variables that showed a protective effect for lung
cancer in the overall analysis and that were available for a majority of the centers included fruit,
lettuce, tomato, carrot, and cheese consumption as well as intake of carotenoids, ß-carotene,
and retinol (3). To enable direct comparisons, the ORs for combined
spousal and workplace exposures to high levels of ETS (upper quartile versus lower three
quartiles) were calculated for the subset of centers with dietary information. The ORs for high
ETS exposure were 1.40 in all eight centers (95% CI = 1.05-1.88), 1.36 in seven
centers with information on fruit consumption (95% CI = 1.01-1.83), 1.32 in seven
centers with information on lettuce consumption (95% CI = 0.97-1.81), 1.58 in
seven centers with information on carotene consumption (95% CI = 1.20-2.08),
and 1.16 in the five centers with information on tomato consumption (95% CI =
0.77-1.75).
Table 1 reports the results of the analysis. Increased ORs for ETS were consistently observed both among subjects with high dietary consumption (OR in the fifth column versus those in the third column) and among subjects with low dietary consumption (OR in the sixth column versus OR in the fourth column), indicating no confounding by dietary items in the association between ETS and lung cancer. In addition, the highest ORs were observed when comparing the two extreme categories, i.e., subjects with low dietary consumption and high ETS exposure (sixth column) versus subjects with high dietary consumption and low ETS exposure (third column). These results add weight to the causal interpretation of the association between ETS and lung cancer, as one would not expect to find this mutual enhancement effect of ETS and dietary items if the ETS association with lung cancer were an artifact. At the same time, the results suggest that the combination of these two common risk factors can increase the risk of lung cancer among nonsmokers by as much as twofold.
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REFERENCES
1
Hackshaw AK, Law MR, Wald NJ. The accumulated evidence on
lung cancer and environmental tobacco smoke. BMJ 1997;315:980-8.
2
Boffetta P, Agudo A, Ahrens W, Benhamou E, Benhamou S,
Darby SC, et al. Multicenter case-control study of exposure to environmental tobacco smoke and
lung cancer in Europe. J Natl Cancer Inst 1998;90:1440-50.
3 Brennan P, Fortes C, Butler J, Agudo A, Benhamou S, Darby SC, et al. A multicenter case-control study of diet and lung cancer among nonsmokers. Cancer Causes Control 2000;11:49-58.[Medline]
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