MedWire News: Exposure to tobacco smoke during childhood or as an adult does not increase the risk for developing breast cancer among women who have never smoked, a large prospective study has shown.
The researchers claim that previous positive findings from retrospective studies suggesting such a link have been distorted by the fact that women were more likely to report past exposures because they knew that they had breast cancer.
A recent collaborative analysis of 53 epidemiological studies found that cigarette smoking had little or no independent effect on the risk of women developing breast cancer, note Kirstin Pirie and colleagues from the University of Oxford in the UK.
Furthermore, in 2004, the International Agency for Research on Cancer endorsed the "lack of carcinogenicity of tobacco smoking in humans for cancers of the female breast."
It has been suggested, however, that passive smoke exposure might increase breast cancer among those who have never smoked - based largely on the findings reported from 14 epidemiologic studies.
Noting potential bias in the design of these studies, the researchers investigated passive smoking in 224,917 never smokers aged an average of 58 years who enrolled in The Million Women Study between 1996 and 2001.
Women were asked if their parents had smoked when they were born and when they were 10 years old, and also if they were currently living with a partner who smoked.
As reported in the International Journal of Epidemiology, women who were exposed to passive smoke as children were at no greater risk for developing breast cancer than those who were not exposed (adjusted relative risk [RR]=0.98), nor were women who were exposed as adults (RR=1.02).
Results did not vary with regard to parity, alcohol consumption, body mass index, age at menarche, age at first birth, whether or not the woman worked, use of oral contraceptives, or use of hormone replacement therapy.
The authors acknowledge that some previous studies have demonstrated a potential interaction between smoke exposure and N-acetyltransferase 2 genotype variants. However, they say larger studies such as the present one are needed to confirm any link.
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