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Cancer Action NY inc. |
| Breast Cancer Prevention | ||
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Fat Soluble Pollutant Carcinogens and Breast Cancer Risk Donald L. Hassig, Director, Cancer Action It has been recognized for a considerable number of years that an association exists between the consumption of animal fat foods and breast cancer (American Institute for Cancer Research, 1997; and Canadian Breast Cancer Initiative, 2001). In 2003, the Journal of the National Cancer Institute published, “Premenopausal Fat Intake and Risk of Breast Cancer”. The conclusion of the authors of this study was that consumption of animal fat during premenopausal years is associated with increased risk of breast cancer (Cho, 2003). When the contamination of animal fats with dioxins, furans, dioxin-like PCBs, hexachlorobenzene, and polycyclic aromatic hydrocarbons (PAHs), which have been designated as probable or known human carcinogens, is taken into account, it becomes clear that part of the cancer risk imposed by fat consumption can be attributed to these contaminants. Carcinogenic, fat-soluble pollutants reach elevated concentrations in breast tissue, thus completing the pathway whereby initiation and promotion of carcinogenesis can take place in the cells of the breast. An article titled, “Serum Dioxin Concentrations and Breast Cancer Risk in the Seveso Women’s Health Study”, has been published in Environmental Health Perspectives, the research journal of the National Institute of Environmental Health Sciences (Warner, 2002). Residents of the Seveso region of Italy were exposed to high levels of dioxins as the result of an explosion at a chemical factory. A statistically significant association between dioxin levels in blood serum and breast cancer incidence was reported in this study. According to the United States Environmental Protection Agency (US EPA), over 90 percent of the American public’s exposure to dioxins comes from the consumption of foods containing milk fat, fish fat, tallow and other animal fats (US EPA, 2003). Particulates, upon which are adsorbed dioxins and dioxin-like compounds, deposit from the polluted atmosphere onto animal feed crops such as pasture grass and corn. Entry into the aquatic food chains occurs via contamination of surface waters. Dioxins and other POPs accumulate in the animals’ fat tissue. The average American’s dioxin exposure thus takes place at lower levels of food contamination than that which existed in the Seveso Women’s Health Study. Nevertheless, the association demonstrated by this research should be taken into account for the purpose of determining a precautionary approach in so far as breast cancer prevention is concerned. Women need to significantly lower their intake of animal fat foods as a breast cancer preventive measure. Dioxins, furans, PCBs and hexachlorobenzene accumulate to ever increasing levels in the fat tissue of those who are regularly exposed. The level, which these chemicals attain in the body, is a very significant health determinant. Cancer risk is higher when elevated levels of cancer promoting dioxins and dioxin-like compounds are present. The International Agency for Research on Cancer lists dioxins, dioxin-like furans and PCBs, and hexachlorobenzene as human carcinogens. Based upon an extensive body of scientific research, the US EPA has upgraded the cancer risk of dioxin exposure (US EPA, 2003). Epidemiologic studies of several exposed groups: workers who manufactured or applied dioxin contaminated pesticides, including pentachlorophenol, and 2,4,5-T; victims of an industrial accident in Seveso, Italy, which released kilogram amounts of dioxin; and US Air Force personnel engaged in Project Ranch Hand, the spraying of Agent Orange during the Vietnam War, demonstrate a linear relationship between dioxin exposure and increased cancer risk. An oral dose slope factor of 1.0 x 10E-3 per pg dioxin TEQ/kg body weight/day has been derived from the US EPA risk model. The average American consumes a quantity of animal fat sufficient to impose a dioxin exposure of 1 pg dioxin TEQ/kg bw/day (see attached Table from US EPA dioxin reassessment). This level of exposure is associated with a 1 in 1000 excess risk of developing cancer. Doubling one’s intake of animal fat food results in a doubled cancer risk. During the 1970s and 1980s, dioxin levels in animal fat foods were considerably higher than current levels. Those who consumed animal fat produced over that time period have a significantly higher lifetime cancer risk. Cancers associated with dioxin exposure include soft tissue sarcoma, lung cancer, non-Hodgkins lymphoma, breast cancer, and prostate cancer. Lipophilic pollutants, such as dioxins, reach elevated concentrations in the fat tissue of the breast. The exposures these cells receive from fat-soluble carcinogens are many orders of magnitude higher than those received by cell types other than fat cells. Dioxins act to promote the development of tumors. Promotion involves the selective acceleration of cellular growth and division for initiated cell lines. The outcome of exposure to a promoting carcinogen is the more rapid development of a clinically detectable tumor, yielding earlier onset of the cancer. In utero and lactational exposure to 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) has been associated with developmental abnormalities in the rat mammary gland (Fenton, 2002). The permanent structural changes in mammary epithelium observed in this study may predispose rat offspring to breast cancer. The Long Island Breast Cancer Study reported an association between polycyclic aromatic hydrocarbon (PAH) exposure and increased incidence of breast cancer (Gammon, 2002). Stationary sources, motor vehicles and open waste burning are major sources of PAH releases to air. We are exposed to PAHs via two main routes, inhalation of polluted air, and consumption of foods that are contaminated with these fat-soluble pollutants. Food consumption is the dominant exposure pathway. An exposure rate of 3 milligrams/day has been estimated for the United States population. PAHs have been demonstrated to be genotoxic, forming DNA adducts in animal studies. Oral doses are reported to result in elevated incidence of mammary tumors in animals. The cancer potency of PAHs varies. Dibenz[a,h]anthracene is the most potent PAH carcinogen. Benzo[a]pyrene (BaP) ranks number two. A quantitative cancer risk estimate has been developed for BaP. This cancer potency factor is 7.3 per mg/kg bw/day. Based upon average diet, Americans are estimated to receive a dose of carcinogenic PAHs ranging from 1 to 5 micrograms/day. Utilizing this dose and the BaP cancer potency factor, upper-bound estimates of the cancer risk of PAH exposure are between 1 in 10,000 and 5 in 10,000. References: American Institute for Cancer Research. “Food Nutrition and the Prevention of Cancer: a global perspective”, 1997; www.aicr.org/reportsummaicr.html Canadian Breast Cancer Initiative. “Review of Lifestyle and Environmental Risk Factors for Breast Cancer”, The Canadian Breast Cancer Initiative Workshop on the Primary Prevention of Breast Cancer, Quebec City, Quebec, May, 2001 Cho, E, et al. “Premenopausal Fat Intake and Risk of Breast Cancer”; Journal of the National Cancer Institute, V 95: pp 1079-1085, July 2003 Fenton, S, et al. “Persistent Abnormalities in the Rat Mammary Gland following Gestational and Lactational Exposure to 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD)”; Toxicological Sciences, 67, pp 63-74, 2002 Gammon, M, et al. “Environmental Toxins and Breast Cancer on Long Island. I. Polycyclic Aromatic Hydrocarbon DNA Adducts”; Cancer Epidemiology, Biomarkers and Prevention, V 11: pp 677-685, August 2002
US EPA. “Exposure and Human Health Reassessment of 2,3,7,8-Tetrachlorodibenzo-p-Dioxin (TCDD) and Related Compounds”, 2003; http://www.epa.gov/ncea/pdfs/dioxin/nas-review/ Warner, M, et al. “Serum Dioxin Concentrations and Breast Cancer Risk in the Seveso Women’s Health Study”; Environmental Health Perspectives, V 110: No 7, pp 625-628, July 2002 For further information: Donald L. Hassig, Director, Cancer Action NY; 531 CR 28, Ogdensburg, NY 13669; canceraction@bluefrog.com; www.canceractionny.org; 315 393-1975
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OPEN WASTE BURNING AS A MAJOR SOURCE OF DIOXIN RELEASES Donald L. Hassig, Director, Cancer Action The 1997 US Environmental Protection Agency (US EPA) report, "Evaluation of Emissions from the Open Burning of Household Waste in Barrels", provides a quantification of pollutants released by open waste fires. (Lemieux, 1997) The author indicates that burning the residential waste (paper, plastics, rubber, foam rubber and metal foils) of 1.5 families in barrels can release an amount of dioxins into the environment equal to that released by a municipal solid waste incinerator burning 200 tons per day. In follow-up test burns, the Agency has determined that open waste burning creates and releases dioxins over a considerable range of values due to the highly complex nature of combustion. (Gullett, 2000) Open waste fires are highly productive of dioxins due to the low temperature at which combustion occurs and limited oxygen availability. Sooty, smoldering fires are the fires that create dioxins most prodigiously. When polyvinyl chloride (PVC) is burned, dioxin emissions are increased. Particulates, upon which are adsorbed dioxins and dioxin-like compounds, deposit from the polluted atmosphere onto animal feed crops such as pasture grass and corn. Entry into the aquatic food chains occurs via contamination of surface waters. Due to the highly persistent nature of these chemical pollutants, they bioaccumulate in the food chain. As set forth in the EPA’s most recent dioxin inventory, open waste burning is considered to be the largest source of dioxin releases to the environment. (US EPA, 2005) It is estimated that approximately 20 million burning barrels are utilized for waste disposal in the United States. A form of open burning that has been found to emit dioxins at greater rates than barrel burning is the burning of waste in open refuse heaps. Such fires are used for disposal of plastics and other waste materials on farms. These fires occur in close proximity to feed crops of cattle and other animals, and are thus likely to be particularly important in the contamination of the food supply. Many states have banned open waste burning. Enforcement of these bans will be a necessary factor in the elimination of this polluting waste disposal practice. Public education on the adverse health effects of exposure to the emissions of open waste fires can also significantly contribute to open burning elimination. References: Gullett, B. K., P. Lemieux, C. Winterrowd, D. Winters. 2000. PCDD/F Emissions from Uncontrolled Domestic Waste Burning. Presented at Dioxin ’00, 20th International Symposium on Halogenated and Environmental Organic Pollutants & POPs, held Aug 13-17 at Monterey, CA. Corrected revision of short paper in Organohalogen Compounds 46: 193-196. Lemieux, P. 1997. Evaluation of Emissions from the Open Burning of Household Waste in Barrels, Vol. 1. Technical Report, U.S. Environmental Protection Agency, National Risk Management Research Laboratory, Research Triangle Park, NC. EPA/600/R-97-134a (NTIS PB98-127343). US EPA. 2005. The Inventory of Sources and Environmental Releases of Dioxin-Like Compounds in the U.S.: the Year 2000 Update, March 2005 (EPA/600/p-03/002A), http://cfpub.epa.gov/ncea/cfm/recordisplay.cfm?deid=132080
Cancer Action is now working to increase public awareness of the dioxin cancer risk factor by providing high school health instructors with the most recent science on this subject. Health instructors are required by New York State Education Law to educate students on breast cancer prevention (see section 804(3)(a) below) .
§ 804. Health education regarding alcohol, drugs, tobacco abuse and
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