Info

676-24,000 2000

Source: Connell and Miller (1984).

TCDD is absorbed in the liver by first-order kinetics and stored. It is slowly converted to polar metabolites and excreted. Elimination in rats is also first order and can be described by a one-compartment model. Half-lives of 17 and 31 days have been measured. However, biomagnification has not been proven for dioxin.

The toxic effects of chlorinated dioxins are similar to PCBs. They are strong inducers of microsomal enzymes. They are toxic to the liver, immune system, and to fetuses. Teratogenic effects have been observed at dosages as low as 1/400 of the LD50 for the maternal rat. Dioxins cause cancer in laboratory animals, including rats at 2 ppb. Tumors appear in the liver, respiratory tract, and oral cavity, among other places. In humans, chlorinated dioxins are known to produce chloracne, but no evidence of carcinogenicity has been found. The extrapolation to humans is complicated by the extreme variability in toxicity between different animals. The oral LD50 for guinea pigs is 0.6 to 2 mg per kilogram of body weight in a single oral dose, for mouse it is 114 to 284 mg/kg, and in hamsters it is

Dioxin has been responsible for a number of notorious pollution episodes. It is an ingredient of Agent Orange, the military defoliant used in Vietnam to deprive the enemy of cover. In that application it was blamed for numerous toxic effects to exposed American soldiers. Catfish and carp taken from the Dong Nai River in South Vietnam were found to have from 0.320 to 1.02 mg/kg body burdens. Agent Orange manufacturing plants in the United States, including in Cleveland, Ohio and Newark, New Jersey, were found to be heavily contaminated as well.

In 1971, a company that manufactured 2,4,5-trichlorophenol hired a used oil dealer to dispose of manufacturing wastes. The oil dealer mixed the material with waste oil and was subsequently hired to spray oil for dust control at several riding stables in Times Beach, Missouri. Shortly after the spraying, it was noticed that birds and insects nearby had begun to die. The horses also became ill, and many died, including 65 of 125 at one stable. The incident came to the attention of authorities when a 6-year-old girl became ill with hemorrhagic cystitis. Others affected included a 10-year-old girl with nosebleeds and headaches and two 3-year-old boys with chloracne. It took three years before the problem was traced to dioxin and the oil dealer. Up to 37 sites had been sprayed. Many had soil contamination levels higher than 100 mg/kg, and some more than 1.0 mg/kg. A flood subsequently spread the contamination over a large area, which was evacuated by the U.S. EPA and subsequently remediated.

Near Seveso, Italy (near Milan), in 1976, a trichlorophenol reaction vessel at a 2,4,5-T manufacturing plant released an unknown amount of dioxin over an area of 2000 ha (about 5000 acres). Soil TCDD dosages ranged from <0.75 to 5000 mg/m2, resulting in concentrations averaging 3.5 mg/kg in the top 7 cm of the soil. Extensive plant and animal mortality occurred, including hundreds of small pets. Body burden measured in small wild animals include 4.5 mg/kg in field mice and 12.0 mg/kg in earthworms. In humans 135 cases of chloracne were confirmed, mostly in children, but no deaths; 14 required hospi-talization within 8 days and some required treatment for some years. An area of 108 ha (267 acres) was evacuated of all residents and remains so today.

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