Atrazine and Breast Cancer: A Framework Assessment of the Toxicological and Epidemiological Evidence

The causal relationship between atrazine exposure and the occurrence of breast cancer in women was evaluated using the framework developed by Adami et al. (2011) wherein biological plausibility and epidemiological evidence were combined to conclude that a causal relationship between atrazine exposure and breast cancer is “unlikely”. Carcinogenicity studies in female Sprague-Dawley (SD) but not Fischer-344 rats indicate that high doses of atrazine caused a decreased latency and an increased incidence of combined adenocarcinoma and fibroadenoma mammary tumors. There were no effects of atrazine on any other tumor type in male or female SD or Fischer-344 rats or in three strains of mice. Seven key events that precede tumor expression in female SD rats were identified. Atrazine induces mammary tumors in aging female SD rats by suppressing the luteinizing hormone surge, thereby supporting a state of persistent estrus and prolonged exposure to endogenous estrogen and prolactin. This endocrine mode of action has low biological plausibility for women because women who undergo reproductive senescence have low rather than elevated levels of estrogen and prolactin. Four alternative modes of action (genotoxicity, estrogenicity, upregulation of aromatase gene expression or delayed mammary gland development) were considered and none could account for the tumor response in SD rats. Epidemiological studies provide no support for a causal relationship between atrazine exposure and breast cancer. This conclusion is consistent with International Agency for Research on Cancer’s classification of atrazine as “unclassifiable as to carcinogenicity” and the United States Environmental Protection Agency's classification of atrazine as “not likely to be carcinogenic.

Noticing Pesticide Spray Drift From Agricultural Pesticide Application Areas and Breast Cancer: a Case-Control Study

Objectives: To examine the relationship between self-reported noticing of pesticide spray drift from agricultural areas and breast cancer.Methods: A case-control study of breast cancer was conducted in Western Australia from 2009 to 2011. Awareness of pesticide spray drift from agricultural areas was assessed by a self-report of whether the participant had noticed spray drift. To evaluate recall bias, we stratified the analysis by participants’ belief about whether pesticides increase the risk of breast cancer. Unconditional logistic regression was used to calculate odds ratios (ORs) and 95% confidence intervals (CIs). This analysis included 1,743 controls and 1,169 cases. Sensitivity analysis for potential selection and isclassificationbias was also conducted.Results: Among women who reported ‘ever noticed’ pesticide spray drift from agricultural areas, an increased risk of breast cancer was also observed (OR=1.43; 95% CI 1.15, 1.78). A dose response relationship between lifetime exposure to noticing pesticide spray drift and risk of breast cancer was observed (p<0.001). An increased risk of breast cancer was observed among women who noticed pesticide spray drift: initially at the age of 20 or younger (OR=1.61; 95% CI 1.19, 2.16); at least 20 years before diagnosis (OR=1.51; 95% CI 1.19, 1.92); and for 10 years or more (OR=1.51; 95% CI 1.18, 1.94).Conclusion: These findings support the hypothesis that women who ever noticed spray drift or who first noticed spray drift at a younger age had increased risk of breast cancer