CATEGORY*: IARC known carcinogen, NTP known carcinogen, Endocrine disruptor
USED IN: Incineration of products that contain polyvinyl chloride (PVC), polychlorinated biphenyls (PCBs), and other chemicals containing chlorine
THE GIST: Dioxins are known carcinogens and endocrine disruptors, and people are primarily exposed through consumption of animal and other food products. Babies can be exposed through breast milk.Though dioxin levels have been declining over the last few decades as a result of federal regulatory actions, most people still have significant levels of the chemical in their bodies.
State of the Evidence on Dioxins
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 polyvinyl chloride (PVC), polychlorinated biphenyls (PCBs) and other chlorinated compounds, by industrial processes that use chlorine, and by the combustion of diesel and gasoline.
TIPS FOR PREVENTION
Dioxin is a fat-seeking molecule so limit your consumption of protein sources that are high in animal fat such as meats and high-fat dairy products.More tips to eat and live better >
Dioxins break down very slowly, with half-lives between seven and 11 years in people (Schecter, 2006). They accumulate in the fat of wildlife and bioaccumulate up 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 the International Agency for Research on Cancer as a known human carcinogen (IARC, 1997). In 2000, the U.S. Environmental Protection Agency 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). Dioxins enter 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 (EPA 2010) have been declining over the past three decades. Yet, because the chemicals are persistent and bioaccumulate, most people in the United States still have substantial 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 statistically 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 lesser cumulative lifetime exposure (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, 2008); unfortunately, this is 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).
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 in the extensive area surrounding the explosion site were not higher 20 years after the explosion in people living in dioxin-contaminated areas during and after the accident. In the zone closest to the accident, however, researchers found that the tenfold increase in TCDD levels was associated with a statistically significant increase in incidence of breast cancer.
Follow-up 12 years later (in 2008-09), showed similar trends, although the results were not statistically significant (Warner, 2011). 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 all cancers (grouped together) for female workers, although there was a statistically 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).
In other studies, TDCC has been shown to inhibit estradiol-induced cell growth and proliferation as well as other pathways regulated by estrogens in a variety of human breast cancer cell culture lines (Yoshioka, 2012). Like the polycyclic aromatic hydrocarbons, dioxins exert their effects by activating both the aryl hydrocarbon receptor (AhR), an important mediator of cell growth and proliferation (Marlowe, 2005), as well other AhR-independent pathways including progesterone-receptor-mediated pathways (Chen, 2012; Labrecque, 2012; Yoshioka, 2012).
*For chemicals that have been shown to be carcinogens, we provide classifications from two authoritative bodies: the International Agency for Research on Cancer (IARC, an international body) and the National Toxicology Program (NTP, a division of the U.S. Department of Health and Human Services). We have categorized endocrine-disrupting compounds where the body of peer-reviewed research indicates a strong foundation for doing so.