Dioxins
CATEGORY: IARC known, NTP known, Endocrine disruptor
USED IN: Incineration of products that contain polyvinyl chloride (PVC), polychlorinated biphenyls (PCBs), and other chemicals containing chlorine
Dioxins are a group of chemicals that are similar in their chemical structure and their toxic effects on biological tissues (EPA, 2010). They are formed by the incineration of products containing PVC, PCBs and other chlorinated compounds as well as from industrial processes that use chlorine and from the combustion of diesel and gasoline. Dioxins break down very slowly, with half-lives between 7 and 11 years in people (Schecter, 2006). They accumulate in fat of wildlife and bioaccumulate across the food chain. Dioxins are known human carcinogens and endocrine disruptors. One of the dioxins (2,3,7,8-tetra chlorodibenzo-para-dioxin—TCDD) has been classified by IARC as a known human carcinogen (IARC, 1997). In 2000, the U.S. EPA officially declared TCDD to be a known carcinogen (ATSDR, 1999b).
People are exposed to dioxins primarily through consumption of animal and other food products (Kulkarni, 2008) and breast milk (WHO, 1996). Dioxin enters the food chain when vehicle exhaust or soot from incinerated chlorinated compounds falls on field crops later eaten by farm animals or enters waters from which seafood is caught (Kulkarni, 2008).
As a result of numerous regulatory actions taken by the federal government, dioxin levels in our food supplies (Lorber, 2009) and in the environment have been declining over the past three decades. Yet, because the chemicals are persistent and bioaccumulate, most Americans still have significant levels of dioxins in their bodies (Schecter, 2006). The most recent data in studies of a cross-section of Americans indicate that over 95 percent have measurable levels of dioxins in their bodies, and that older people have significantly higher body burdens of the chemicals than do younger people (Patterson, 2009). The lower concentrations in children and younger adults probably reflect both lower levels of dioxins in the environment and shorter durations of cumulative lifetime exposures (Collins, 2007).
Concentrations of dioxins in breast tissue may change dramatically over the span of a woman’s reproductive life. Data indicate that there is a substantial decrease in the amount of dioxin remaining in a woman’s breast fat tissue after she has breast-fed (Massart, 2005; cf Lakind, 2009), unfortunately because the chemicals have been passed on to her newborn via breast milk. Although the presence of toxic chemicals in breast milk is potentially dangerous, the beneficial nutrients and immune system boosters that are transferred from mother to infant far outweigh the potential toxic transfers (Nickerson, 2006). But in addition to potential transfer of dioxins to breast-feeding infants, the release of the chemicals from storage in breast fat cells, initiated by the process of milk synthesis, may actually trigger genotoxic (cancer-causing) effects in the breast tissue (Dip, 2008).
Compelling evidence of links between dioxin exposures and risk for breast cancer has emerged from a recent follow-up study on women exposed to dioxins during a chemical plant explosion in 1976 in Seveso, Italy (Pesatori, 2009). Scientists analyzed blood samples taken and stored at the time of the explosion and correlated the results with subsequent cases of cancer incidence, including that of breast cancer. Overall levels of cancer incidence were not higher 20 years after the accident in people in areas contaminated by dioxins during and after the accident. Researchers found that a tenfold increase in TCDD levels in the zone closest to the accident was associated with a significantly increased incidence of breast cancer. Women who were children at the time of the accident are just beginning to reach the age when breast cancer is most likely to develop, and researchers will continue to follow the Seveso women.
A retrospective mortality study in Germany examined deaths from cancer among people who had worked in a chemical factory in which they were exposed to high levels of TCDD. There was no increase in overall mortality from cancer for female workers, although there was a significant increase in deaths from breast cancer among those who worked in high-exposure regions of the factory (Manz, 1991).
A number of laboratory studies have demonstrated that when looking at later changes in mammary cancer rates, the timing of exposures to dioxins matters. Although exposing animals to dioxins in adulthood may not affect cancer rates, earlier exposures may have profound effects. Several studies have shown that administration of dioxin (especially TCDD) to pregnant rats leads to structural abnormalities in the development of their pups' mammary tissues and higher incidence of tumors when the pups grow to adulthood (Brown, 1998; Fenton, 2002; Lewis, 2001; Jenkins, 2007; La Merrill, 2009). TCDD may exert its cancer-causing effects both by decreasing the efficacy of tumor-suppressor mechanisms and by enhancing the estrogenic signaling within the mammary cells (Seifert, 2009).
