Oral contraceptives have been associated with a small increased risk of breast cancer in current users that diminishes over time. A well-conducted case-control study did not observe an association between breast cancer risk and oral contraceptive use for every use, duration of use, or recency of use.
Another case-control study found no increased risk of breast cancer associated with the use of injectable or implantable progestin-only contraceptives in women aged 35 to 64 years.
Whether occupational, environmental, or chemical exposures have an effect on breast cancer risk is controversial. Although some findings suggest that organochlorine exposures, such as those associated with insecticides, might be associated with an increase in breast cancer risk,[121,122] other case-control and nested case-control studies do not.[123,124,125,126,127,128] Studies reporting positive associations have been inconsistent in the identification of responsible organochlorines. Some of these substances have weak estrogenic effects, but their effect on breast cancer risk remains unproven. The use of dichloro-diphenyl-trichloroethane was banned in the United States in 1972, and the production of polychlorinated biphenyls was stopped in 1977.
Diet and vitamins
A low-fat diet might influence breast cancer risk through hormonal mechanisms. Ecologic studies show a positive correlation between international age-adjusted breast cancer mortality rates and the estimated per capita consumption of dietary fat. Results of case-control studies have been mixed. A pooled analysis of results from seven cohort studies found no evidence for an association between total dietary fat intake and breast cancer risk. A randomized controlled dietary modification study was undertaken among 48,835 postmenopausal women aged 50 to 79 years who were also enrolled in the WHI. The intervention promoted a goal of reducing total fat intake by 20%, using five servings per day of vegetables and fruit and six servings per day of grains. The intervention group was successful in reducing fat intake by approximately 10% for more than 8.1 years of follow-up, and the group was found to have lower estradiol and lower gamma-tocopherol levels, but no weight loss was shown. The incidence of invasive breast cancer was slightly lower in the intervention group, with an HR of 0.91 (95% CI, 0.83-1.01). Because the intervention group also initially lost weight relative to the control group, it is not clear whether any potential effect in reducing breast cancer results from lower dietary fat or lower weight. Likewise, there was no benefit derived from the low-fat diet for all cancer mortality, overall mortality, or cardiovascular disease.
Fruit and vegetable consumption has been examined for any protective effect against breast cancer. A pooled analysis of adult dietary data from eight cohort studies, which included 351,823 women in whom 7,377 incident cases of breast cancer occurred, provides little support for an association. When examining the dietary data treated as a continuous variable (based on grams of intake per day), there was no association with breast cancer. Comparing highest to lowest quartiles of intake, the pooled multivariate RRs of breast cancer were 0.93 (95% CI, 0.86-1.00) for total fruits, 0.96 (95% CI, 0.89-1.04) for total vegetables, and 0.93 (95% CI, 0.86-1.00) for total fruits and vegetables combined. Additionally, no statistically significant association was observed between any of the specific fruits and vegetables examined and breast cancer risk.