Overview

The term dioxin is commonly used to refer to a family of toxic chemicals that all share a similar chemical structure and a common mechanism of toxic action. This family includes eight of the chlorinated dibenzo dioxins (CDDs), ten of the polychlorinated dibenzo furans (PCDFs) and twelve of the polychlorinated biphenyls (PCBs)(#EPA). These are all organochlorine compounds. Dioxins are unintentionally produced by industrial, municipal, and domestic incineration and combustion processes, and there also are natural sources like brush and forest fires. As a consequence of industrialization, dioxin levels began increasing in the global environment. Declines in environmental levels began in the 1970s when dioxins were recognized as highly toxic chemicals and governments and industry took actions to prevent environmental pollution (#EPA). However, current exposure levels and dioxins' accumulation in the food chain, particularly in animal fat, still remain a concern.

As mentioned before, the CDD (chlorinated dibenzo dioxins) family is divided into eight groups of chemicals - their distribution is based on the number of chlorine atoms in the compound. The group with one chlorine atom is called the mono-chlorinated dioxin(s). The groups with two through eight chlorine atoms are called dichlorinated dioxin (DCDD), tri-chlorinated dioxin (TrCDD), tetra-chlorinated dioxin (TCDD), pentachlorinated dioxin (PeCDD), hexa-chlorinated dioxin (HxCDD), hepta-chlorinated dioxin (HpCDD), and octa-chlorinated dioxin (OCDD)(#ATSDR-Toxicological Profile for Dioxins).

2,3,7,8-TCDD is one of the most toxic and extensively studied of the CDDs and serves as a prototype for the toxicologically relevant or "dioxin-like" CDDs (#ATSDR-Toxicological Profile for Dioxins).

Chemical Description

2,3,7,8-TCDD (Tetrachlorinated Dibenzo-p-dioxin)(#PANNA)

In the pure form, CDDs are colorless solids or crystals. CDDs enter the environment as mixtures containing a variety of individual components and impurities (#ATSDR-Toxicological Profile for Dioxins).
2,3,7,8-TCDD is a by-product formed during the manufacture of 2,4,5-trichlorophenol (2,4,5-TCP). 2,4,5-TCP was used to produce hexachlorophene (used to kill bacteria) and the herbicide, 2,4,5-trichlorophenoxyacetic acid (2,4,5-T). Various formulations of 2,4,5-T have been used extensively for weed control on crops and range lands, and along roadways throughout the world. 2,4,5-T was a component of Agent Orange, which was used extensively by the U.S. military in the Vietnam War(#ATSDR-Toxic ological Profile for Dioxins).

Sources

CDDs are known to occur naturally, and are also produced by human activities. They are naturally produced from the incomplete combustion of organic material by forest fires or volcanic activity. CDDs are not intentionally manufactured by industry, except in small amounts for research purposes. They are unintentionally produced by industrial, municipal, and domestic incineration and combustion processes.
Currently, it is believed that CDD emissions associated with human incineration and combustion activities are the predominant environmental source (#ATSDR Toxicological Profile for Dioxins).

CDDs also have been detected at low concentrations in cigarette smoke, home-heating systems, and exhaust from cars running on leaded gasoline or unleaded gasoline, and diesel fuel. Dioxins had been also detected during chlorine bleaching of pulp and paper. Burning of many materials that may contain chlorine, such as plastics, wood treated with pentachlorophenol (PCP), pesticide-treated wastes, other polychlorinated chemicals (polychlorinated biphenyls or PCBs), and even bleached paper can produce CDDs (#ATSDR Toxicological Profile for Dioxins).

Routes of Exposure and Metabolism

The substance can be absorbed into the body by inhalation of dust, through the skin and by ingestion (#ICSC).
Being highly lipophilic, dioxins dissolve in fat. They need to be transformed in the liver to become water soluble before they can be excreted. However, dioxins are metabolized slowly and therefore tend to bioaccumulate, especially in fat and in the liver.
The speed of elimination of dioxins can vary with dose, quantity of body fat, age and sex. The process of elimination of dioxins and PCBs is similar in animals and man, but it is faster in most other mammals (#GreenFacts).

The developing fetus is most sensitive to dioxin exposure. The newborn, with rapidly developing organ systems, may also be more vulnerable to certain effects. Some individuals or groups of individuals may be exposed to higher levels of dioxins because of their diets (e.g., high consumers of fish in certain parts of the world) or their occupations (e.g., workers in the pulp and paper industry, in incineration plants and at hazardous waste sites, to name just a few)(#WHO).

Human Health Effects

Acute Health Effects
According to PANNA, short time exposure to dioxin (2,3,7,8 TCDD) can cause chloracne, redness and pain (#PANNA).

Chronic Health Effects
2,3,7,8 TCDD is listed as "known carcinogen" by IARC (International Agency for Research on Cancer) and also by U.S. National Toxicology Program Carcinogen List. According to the EU list (European Union Prioritization List) dioxin (2,3,7,8 TCDD) is an endocrine disrupting chemical (#PANNA).

In laboratory animals they have been linked to endometriosis (severe effects on the uterus), developmental and neurobehavorial effects (learning disabilities), developmental reproductive effects (low sperm count, genital malformations) and immunotoxic effects (#European commission).

Environmental Health Effects

In the environment dioxins can be commonly detected in air, soil, sediments and food. Dioxins are transported primarily through the air and are deposited on the surfaces of soil, buildings and pavement, water bodies, and the leaves of plants. Most dioxins are introduced to the environment through the air as trace products of combustion. The principal route by which dioxins are introduced to most rivers, streams and lakes is soil erosion and storm water runoff from urban areas (#EPA).

When released into the air, some dioxins may be transported long distances. Because of this, dioxins are found in most places in the world. When dioxins are released into water, they tend to settle into sediments where they can be further transported or ingested by fish and other aquatic organisms. Dioxins decompose very slowly in the environment and can be deposited on plants and taken up by animals and aquatic organisms. Dioxins may be concentrated in the food chain so that animals have higher concentrations than plants, water, soil, or sediments. Within animals, dioxins tend to accumulate in fat (#FDA).

Due to its very low water solubility, most of the 2,3,7,8-TCDD occurring in water is expected to be associated with sediments or suspended material. Aquatic sediments may be an important, and ultimate, environmental sink for all global releases of TCDD. Two processes which may be able to remove TCDD from water are photolysis and volatilization.
The photolysis half-life at the water's surface has been estimated to range from 21 hr in summer to 118 hr in winter; however, these rates will increase significantly as water depth increases. Many bottom sediments may therefore not be susceptible to significant photodegradation.
The volatilization half-life from the water column of an environmental pond has been estimated to be 46 days; however, when the effects of adsorption to sediment are considered, the volatilization model predicts an overall volatilization removal half-life of over 50 years.
Various biological screening studies have demonstrated that TCDD is generally resistant to biodegradation. The persistence half-life of TCDD in lakes has been estimated to be in excess of 1.5 yr(#Technical Factsheet on Dioxin, EPA).

If released to soil, TCDD is not expected to leach. As a rule, the amount of TCDD detected more than 8 cm below the surface has been approximately 1/10 or less than that detected down to 8 cm. Being only slightly soluble in water, its migration in soil may have occurred along with soil colloids and particles to which it may have been bound. Soil cores collected from roadsides in Times Beach, MO in 1985 which had been sprayed with waste oils containing TCDD in the early 1970s indicated that most of the TCDD had remained in the upper 15 cm.. Tests conducted by the USDA determined that vertical movement of 2,3,7,8-TCDD did not occur in a wide range of soil types.
Being only slightly soluble in water, its migration in soil may have occurred along with soil colloids and particles to which it may have been bound. Photodegradation on terrestrial surfaces may be an important transformation process. Volatilization from soil surfaces during warm conditions may be a major removal mechanism. The persistence half-life of TCDD on soil surfaces may vary from less than 1 yr to 3 yrs, but half-lives in soil interiors may be as long as 12 years. Screening studies have shown that TCDD is generally resistant to biodegradation (#Technical Factsheet on Dioxin, EPA).

If released to the atmosphere, vapor-phase TCDD may be degraded by reaction with hydroxyl radicals and direct photolysis. Particulate-phase TCDD may be physically removed from air by wet and dry deposition (#Technical Factsheet on Dioxin, EPA).

Bioconcentration in aquatic organisms has been demonstrated. Mean bioconcentration factors (BCF) of 29,200 (dry wt) and 5,840 (wet wt) were measured for fathead minnows over a 28 day exposure; the elimination half-life after exposure was found to be 14.5 days. Log BCFs of approximately 3.2 to 3.9 were determined for rainbow trout and fathead minnow in laboratory flow-through studies during 4-5 exposures. The following log BCFs have been reported for various aquatic organisms: snails, fish (Gambusia), daphnia 4.3-4.4; duckweed, algae, catfish, 3.6-3.95 (#Technical Factsheet on Dioxin, EPA).

Effects on wildlife
There is substantial evidence to indicate that populations of wildlife species high on the food chain are suffering health damage due to reproductive and developmental impairment due to background exposures to dioxins and related compounds. In the Great Lakes, exposure to dioxin-like compounds has been linked to large-scale hormonal, reproductive, and developmental impairment among numerous species of predator birds, fish and wildlife; these impacts are primarily transgenerational, affecting the offspring of the exposed organisms (#WFPHA, 2000).

• Lake trout embryos and sac fry are very sensitive to toxicity associated with maternal exposures to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and structurally related chemicals that act through a common aryl hydrocarbon receptor (AHR)-mediated mechanism of action. The loading of large amounts of these chemicals into Lake Ontario during the middle of the 20th century coincided with a population decline that culminated in extirpation of this species around 1960 (#Cook _et al._, 2003).

• Dioxin is responsible for inability of mink to reproduce around Lake Michigan (#Hochstein _et al._, 1998)

Regulation

EPA advises that children should not have more than 1 nanogram 2,3,7,8-TCDD per liter of water (ng/L) (ppt) in 1 day, or more than 0.01 ng/L per day for long-term exposure. For long-term exposure in adults, EPA recommends that there should not be more than 0.04 ng/L (ppt) in drinking water (#ATSDR-Toxicological Profile for Dioxins).

Recently the Environmental Working Group (EWG) has announced some alarming news regarding actual exposure to dioxins among Americans. EWG research found that the amount of dioxin a nursing infant ingests daily is up to 77 times higher than the level the agency has defined as harmless to the endocrine and immune systems. For cancer risk, the situation is even more dire: the general public is exposed (mostly through eating meat, dairy and shellfish ) to up to 1,200 times more dioxin than regulatory agencies typically consider safe. EPA is now working on "Reanalysis of Key Issues Related to Dioxin Toxicity" in order to establish a safe daily dose for human exposure to this hazardous chemical (#EWG, 2010).

Ways to Reduce Exposure

• Trimming fat from meat
• Consuming low fat dairy products
• Balanced diet (including adequate amounts of fruits, vegetables and cereals);it will help to avoid excessive exposure from a single source (#WHO).

External Links

* INTAKE OF DIOXINS AND RELATED COMPOUNDS FROM FOOD IN THE U.S. POPULATION
* DioxinFacts.org
* U.S. Department of Agriculture. Food Safety and Inspection service
* Medical News

Dioxin contamination incidents

* Tetrachlorodibenzo-p-dioxin in baby food made from chicken produced before and after the termination of ball clay use in chicken feed in the United States
* Seveso disaster
*Irish pork products recalled after dioxin is found
*Contamination of Guar Gum from India with Pentachlorophenol (PCP) and Dioxins

Breaking News

Dioxin News from Environmental Health News

Breaking stories

Scientific stories

References

Evironmental Protection Agency (EPA). Dioxin. Accessed 11.10.2010.

Agency for Toxic Substances and Disease Registry . ATSDR. December 1998. Accessed 11.10.2010.

International Chemical Safety Card (ICSC). 2,3,7,8-TETRACHLORODIBENZO-p-DIOXIN

GreenFacts. Accessed 11.09.2010.

Pesticide Action Network North America (PANNA). Pesticides Database-Chemicals. Accessed 10.25.2010.

European commission. Food Contaminants - Dioxins and PCBs. Accessed 11.10.2010.

U.S. Food and Drug Administration (FDA). Questions and Answers about Dioxins. May 2010. Accessed 11.09.2010.

Agency for Toxic Substances and Disease Registry (ATSDR). Public Health Statement Dioxins. December 1998.

World Health Organization (WHO).Dioxins and their effects on human health. May 2010. Accessed 11.11.2010.

DioxinFacts.org. Trends in Dioxin Emissions and Exposure in the United States. Accessed 11.11.2010.

Environmental Working Group (EWG). EPA Must Finish the Job of Protecting People from Dioxin. July 2010. Accessed 11.18.2010.

World Federation of Public Health Associations (WFPHA). Persistent Organic Pollutants and Human Health.

Technical Factsheet on Dioxin. Evironmental Protection Agency (EPA). National Primary Drinking Water Regulations.

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Cook, P, JA Robbins, DD Endicott, KB Lodge, PD Guiney, MK Walker, EW Zabelo and RE Peterson. Effects of Aryl Hydrocarbon Receptor-Mediated Early Life Stage Toxicity on Lake Trout Populations in Lake Ontario during the 20th Century.nEnviron. Sci. Technol., 2003, 37 (17), pp 3864-3877.

Hochstein, J., Bursian, S., and Aulerich, R. Effects ofdietary exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin in adult female mink (Mustela vison). Arch. Environ. Contam. Toxicol. 1998, 35, pp 348-353.