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Polycyclic Aromatic Hydrocarbons
Polycyclic aromatic hydrocarbons (PAHs) are a very stable group of chemicals with two or more adjacent aromatic rings. The compound is prominent in the environment, and the major sources are from combustion products of fuels, cigarette smoking, and smoked and grilled foods.[1] Inhalation is the major source of exposure, due to the precipitation of residues in the environment. PAHs are lipophilic and are stored in the fat tissues of the breast. The harmful effects caused by the compound occur in two different ways. Most PAHs interact with the estrogen receptor, causing it to have slight estrogen mimicking properties.[2] PAHs also associate with the aryl hydrocarbon receptor, which leads to alterations in cell signaling. These changes ultimately cause DNA mutations.[3] When these compounds are further broken down, they may interact with genes causing further DNA damage.[4]
Due to the polycyclic aromatic hydrocarbons ability to bind DNA, mammary cancers have been determined in laboratory testing on animals. This has led to numerous studies on the effects on humans. Cancer risk associated with PAH exposures in humans may vary due to the person’s ability of removing the contaminant from the body. During the detoxification process, PAH-DNA adduct lesions are formed. The existence of such adducts could suggest a high level of exposure to the contaminant, the person’s inability to eliminate the contaminant, or both. The Long Island Breast Cancer Study found that women in the highest quartile of exposure to PAHs showed a 50% increase in breast cancer risk.[5] Another study observed a twofold increase in the risk of breast cancer for those ever exposed to PAHs, with the highest risk found in those exposed for four or more years.[6] Occupational exposure also plays a critical role. In a study observing workers readily exposed to PAHs, an increased risk for breast cancer was found for pre-menopausal women.
Polychlorinated Biphenyls
Polychlorinated biphenyls (PCBs) are man-made organochlorine compounds that are currently banned. However, most products produced before the ban are still in use today, including plastics, paper, paints, and dyes. PCBs negatively affect cells in three different ways. Some act similar to estrogen, while others behave like anti-estrogen. Others are not hormonally active, but are able to stimulate enzyme systems in a similar fashion to toxic chemicals. Due to the lipophilic nature of organchlorine compounds, polychlorinated biphenyls can be detected in the adipose breast tissue of humans. Metabolites of PCBs in the breast tissue can produce reactive products that cause oxidative damage and negatively affect DNA. The reactions with DNA can alter the expression of genes and act as endocrine disruptors.
Laboratory animals exposed to the chemical exhibited an increased risk in mammary cancer.[7] Although PCBs play multiple roles in causing harmful effects in the cells, multiple studies do not show a correlation between high concentrations of PCBs and an increased risk in breast cancer. However, studies performed on those exposed to PCBs before the ban generally show an association with an increased risk for breast cancer. In a study with participants who exhibited such exposures, the concentrations of PCBs were significantly greater in the case studies than the control groups.
DDT
Dichlorodiphenyltrichloroethane (DDT) is a manmade organic compound that is primarily used as an insecticide. In the 1970’s, the chemical was banned in the United States due to its potential harmful effects on humans. However, DDT is still prevalent in third world countries, because of its use for malaria control. Due to its continued use in certain areas and persistence in the environment, every person contains some level of DDT in fat tissues of their body during their lifetime. The main exposure by humans is through ingestion of contaminated food, in which the chemical and its main metabolite, DDE, are retained.
Significant amounts of DDT are detected in body fat and human breast milk. Once in the body, DDT is broken down into its component compounds, which take on roles similar to estrogen. DDT is a probable carcinogen, because cancer induced cells in the breast tissue are promoted by estrogen. The chemical is also hormonally active, because after exposure DDT cannot be eliminated from the body. Because most women, who were heavily exposed to DDT during childhood, have not reached fifty years of age, the major effects of DDT exposure at a young age are yet to be determined.
Benzene
Benzene is a colorless liquid that is highly flammable. The compound is one of the most widely used solvents and continues to expand its use in the chemical industry. Exposures come from car exhaust, resins, nylon, synthetic fibers, rubbers, detergents, drugs, and pesticides. Its environmental detection is due to cigarette smoke, both primary and secondary, and the burning of crude oil. Due to its extensive use, those working as bus and truck operators, traffic and shipping managers, laboratory technologists, and painters have an increased risk of exposure. Benzene can also seep into groundwater from leaking storage tanks and hazard waste areas or by attaching itself to rain or snow. It is also one of the few chemicals to be listed by the National Toxicology Program as a known human carcinogen.
Laboratory animals exposed to levels of benzene produced mammary tumors. The animals showed to have numerous gene mutations as well. The effects of benzene on breast cancer risk in humans are difficult to determine, because benzene is generally accompanied with other chemicals during exposure due to combustion and other processes.
References
1. Gammon, M. Environmental Toxins and Breast Cancer on Long Island I. Polycyclic Aromatic Hydrocarbon DNA Adducts. Cancer Epidemiology, Biomarkers & Prevention. 2002:11; 677.
2. Pliskova M, Vondracek J, Vojtesek B, et al. Deregulation of cell proliferation by polycyclic aromatic hydrocarbons in human breast carcinoma MCF-7 cells reflects both genotoxic and nongenotoxic events. Toxicology Science. 2005:83:246-246.
3. Winn DM. Science and society: The Long Island Breast Cancer Study Project. Nature Reviews Cancer. 2005;5(12):986-994.
4. Brody JG, Rudel RA. Environmental Pollutants and Breast Cancer. Environmental Health Perspectives. 2003;111(8):1007.