According to a review, the main mechanisms by which environmental compounds increase breast cancer risk are acting like hormones, especially estrogen, or affecting susceptibility to carcinogenesis. The evidence to date generally supports an association between breast cancer and polycyclic aromatic hydrocarbons (PAHs) and polychlorinated biphenyls (PCBs). dioxins and organic solvents, on the other hand, have only shown an association in sparse and methodologically limited studies, but are suggestive of an association. Overall, however, evidence is still based on a relatively small number of studies.

Xenoestrogens

Many xenoestrogens (industrially made estrogenic compounds) are endocrine disruptors, and potential risk factors of breast cancer. Endocrine disruption is the hypothesis that some chemicals in the body, such as Bisphenol A, are capable of interfering with the production, processing, and transmission of hormones.

A substantial and growing body of evidence indicates that exposures to certain toxic chemicals and hormone-mimicking compounds including chemicals used in pesticides, cosmetics and cleaning products contribute to the development of breast cancer.

The increasing prevalence of these substances in the environment may explain the increasing incidence of breast cancer, though direct evidence is sparse.

Rats exposed prenatally to environmentally relevant doses of BPA show an increased number of intraductal hyperplasias (precancerious lesions) in mammary glands that appear during adulthood, while high doses induce the development of carcinomas in breast tissue. Animals exposed to BPA during fetal life develop palpable tumors, and all studies show an increased susceptibility to mammary gland neoplasia that manifests during adulthood. Exposure of mouse dams to environmentally relevant levels of BPA during organogenesis results in considerable alterations in the mammary gland. It was concluded that perinatal exposure to low doses of BPA results in altered mammary gland morphogenesis, induction of precancerous lesions, and carcinoma in situ.

A study sought to determine whether early exposure to BPA could accelerate mammary carcinogenesis in a dimethylbenzanthracene (DMBA) model of rodent mammary cancer. In the study, scientists exposed neonatal/prebubertal rats to BPA via lactation from nursing dams treated orally with 0, 25, and 250 µg BPA/kg body weight/day. For tumorigenesis studies, female offspring were exposed to 30 mg dimethylbenzanthracene (DMBA)/kg body weight at 50 days of age. DMBA induces mammary tumors and allows chemicals that predispose for mammary cancer to increase the number of mammary adenocarcinomas. The results of the study showed that female rats in the control, BPA 25, and BPA 250 groups administered DMBA exhibited a BPA dose-dependent increase in mammary tumors. The groups had 2.84, 3.82, and 5.00 mammary tumors per rat respectively. Treatment with BPA also reduced tumor latency, with the median tumor latency of 65, 53, and 56.5 days for 0, BPA 25, and BPA 250 groups respectively. Maternal exposure to BPA during lactation decreased time to first tumor latency and increased the number of DMBA-induced mammary tumors in female offspring. If these effects found in rodents carry over to humans, even minimal exposure to BPA could cause an increased risk for breast cancer.

The elevated incidence of breast cancer in women has been associated with prolonged exposure to high levels of estrogens. Xenoestrogens, such as BPA have the capacity to perturb normal hormonal actions. This study provides evidence of the estrogenic effects of BPA. In this study the human breast epithelial cells MCF-10F were treated with 10-3 M, 10-4 M, 10-5 M and 10-6 M BPA continuously for two weeks. The cells treated with 10-3 M BPA died on the second day of treatment. The concentration of 10-4 M BPA was also toxic for the breast epithelial cells, and they died on the fourth day of treatment. This data indicated that these concentrations of BPA are toxic for MCF-10F cells. After the two-week observation period it was seen that the cells formed a high percentage of duct like structures in collagen. MCF-10F cells treated with 10-5 M and 10-6 M BPA formed a high percentage of solid masses, 27% and 20% respectively. This data indicates that BPA is able to induce neoplastic transformation of human breast epithelial cells. Epigenetic changes are involved in the early stages of cancer initiation by altering ductulogenesis. BPA was able to induce transformation of human breast MCF-10F epithelial cells. After treatment with BPA, the cells produced fewer collagen tubules and more solid masses.

Consumer groups recommend that people wishing to lower their exposure to bisphenol A avoid canned food and polycarbonate plastic containers (which shares resin identification code 7 with many other plastics) unless the packaging indicates the plastic is bisphenol A-free. The National Toxicology Panel recommends avoiding microwaving food in plastic containers, putting plastics in the dishwasher, or using harsh detergents on plastics, to avoid leaching.

Aromatic Amines

Aromatic amines are chemicals that are produced when products such as dyes, polyurethane products, and certain pesticides are made. They are also found in cigarette smoke, fuel exhaust, and in over cooked, burned meat. The three types of aromatic amines monocyclic, polycyclic, and heterocyclic have all been found in recent studies of breast health. Monocyclic amines have been found to cause mammary cancer in rats. Studies have shown that women who eat higher amounts of overcooked meat, meaning more exposure to heterocyclic amines, have also been diagnosed with more post-menopausal breast cancer. Heterocyclic amines also have the ability to copy estrogen and in laboratory studies have been found to encourage the growth of cancerous tumors on human tissue.

Benzene

Benzene is a petrochemical solvent. Benzene exposure mostly originates from air pollution resulting from industrial burning, exhaust and gas fumes, as well as cigarette smoke. The International Agency for Research on Cancer and the National Toxicology Program have labeled benzene as a definite human carcinogen. Multiple studies point to a correlation between benzene exposure and breast cancer risk. Laboratory studies on mice have shown that a high level of benzene exposure can lead to mammary cancer.