Dioxins and cancer
Dioxins, specifically 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), are highly toxic synthetic chemicals known for their severe health impacts, including their classification as a known human carcinogen since 2001. These substances are not manufactured for commercial use but are produced as by-products during various industrial processes, such as waste combustion and the manufacturing of organochlorine compounds. The primary route of human exposure is dietary, particularly through the consumption of meat, dairy, and fish, which can accumulate TCDD in their fat. Dioxins have been linked to a broad spectrum of health issues, with significant concerns regarding their role in the development of cancers, including lung cancer and non-Hodgkin lymphoma.
Individuals most at risk include those living near contaminated sites or working in related industries, such as waste incineration and chemical production. The carcinogenic effects of TCDD arise through its interaction with cellular receptors that can disrupt normal gene function, leading to malignancies over prolonged exposure. Historically, TCDD was associated with herbicides like Agent Orange used during the Vietnam War, and despite its phased-out use, it continues to be a concern due to its persistence in the environment and accumulation in living organisms. Understanding the implications of dioxin exposure is crucial for public health, especially in vulnerable populations.
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Dioxins and cancer
ROC STATUS: Under the heading “2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD),” known human carcinogen since 2001
ALSO KNOWN AS: 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD); polychlorinated dibenzo-p-dioxin (PCDD); persistent organic pollutants (POPs)
RELATED CANCERS: All cancers, including lung cancer and non-Hodgkin lymphoma
DEFINITION: Dioxins are polychlorinated dibenzo-p-dioxins (two benzene rings bridged with two oxygen atoms). The one in which carbons 2, 3, 7, and 8 are chlorinated is called 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). TCDD is the deadliest synthetic chemical—its toxicity is used as a benchmark to rate the toxicity of other chemicals through a value called a toxic equivalency factor (TEF). They cause various types of cancer and disrupt reproduction, development, immunity, and hormonal processes.
Exposure routes: All species are exposed to dioxins through inhalation or ingestion via air, water, and food. In humans, over 90 percent of exposure is due to diet. Meat fat, dairy, and fish and shellfish products are the largest sources of TCDD. They are found in the air, soil, and plants in small doses.
Where found: TCDD and other dioxins are not commercial products but formed as by-products during organochlorine manufacturing, waste combustion, and incineration operations. Dioxins contaminate the atmosphere through incineration and waste disposal; the land through manufacturing, agricultural herbicides, and incineration; and the water through effluent discharges, especially from pulp and paper plants. Residues of TCDD, because of its thermo- and bio-stability, are widely distributed in the air, soil, water, sediments, biota (flora and fauna of a region), and human food. Because it has very low solubility in water and a very high partition coefficient, it accumulates in fat, becomes concentrated in aquatic biota, and is ecomagnified through the food chain. Freshwater biota holds the highest amount of TCDD, which may also be bound to organics in sediments.
At risk: People at greatest risk for exposure to TCDD and other dioxins are those living near contaminated sites or eating contaminated foods, such as waste-incineration workers, firefighters, workers in chemical research facilities, those working in the production and use of pentachlorophenol and other chlorinated compounds, and those associated with chlorophenoxy herbicide (MCPA, 2,4-D, 2,4,5-T and mecoprop) production, use, and disposal.
Etiology and symptoms of associated cancers: TCDD has extreme potency for chronic biological effects. Some of its effects are common among animal species, while others are species-specific. For example, congenital disabilities and lowering of male sex hormones (testicular atrophy) have been reported in several bird and mammalian species. Chronic toxicity of TCDD increases with the duration of exposure.
TCDD is a teratogen (an agent of developmental malformations) and a carcinogen (an agent of malignancy). It affects the reproductive system (causing low sperm counts, lowering of testosterone, and testicular atrophy, among other effects) and developmental stages (leading to malformations in newborns). In humans, congenital disabilities, termination of pregnancy, decreased fertility (lower sperm count and testosterone and testicular atrophy), endometriosis, diabetes, learning disorders, skin and lung effects, and cancer are commonly recognized.
The half-life of TCDD in humans varies from seven to eleven years. Men cannot degrade TCDD, while women can transfer it to a fetus via the placenta and to a newborn via breast milk. TCDD causes neurobehavioral deficits and lowering of testosterone in neonates due to their exposure in utero. The US federal government, for example, has had to issue warnings about the consumption of TCDD-tainted Lake Michigan fish by women who are pregnant or want to become pregnant and by children and young adults.
The carcinogenic effects of TCDD are evident in the increased rate of both benign tumors and malignant tumors seen in those who experience significant exposures to the chemical. By binding to the “Ah receptor,” a protein ubiquitous in human and other vertebrate animal tissues that plays a major role in gene transcription, TCDD activates biological responses that can lead to carcinogenic activity. Because the chemical accumulates in fat over long periods of exposure, this carcinogenic activity increases with time, even with low chronic exposures.
History: First listed as a reasonably anticipated carcinogen in the National Toxicology Program’s Second Annual Report on Carcinogens (1981) from the US Department of Health and Human Services, TCDD underwent several subsequent studies. Some considered cancers in human populations occupationally exposed to TCDD, while others examined what occurred at the molecular and cellular levels in human and animal tissue exposed to TCDD. The data from studies conducted through 1996 were evaluated by the International Agency for Research on Cancer (IARC), whose results were published in 1997. The IARC concluded that exposure to TCDD was linked to an overall increased risk for all cancers combined, an increased risk for lung cancer, and an increased risk for non-Hodgkin lymphoma. The US government has, therefore, classified TCDD as a known human carcinogen since 2001.
TCDD was present in herbicides widely used in the 1960s and 1970s, including Agent Orange, used during the Vietnam War. Although TCDD is no longer used in these agents, it continues to occur as a by-product of paper and pulp bleaching (which is why some people, for example, prefer to use unbleached coffee filters and paper towels); in the incineration of solid municipal and hospital waste; in the production of metals; and the combustion of both wood and fossil fuels. Scientists have identified around 420 dioxin-related compounds, but only around thirty are toxic, with TCC being the most harmful.
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