TOXAPHENE

Toxaphene is an organochlorine insecticide that is similar to other compounds such as endrin, dieldrin, aldrin, dichlorodiphenyltrichloroethane (DDT), lindane, and chlordecone. Manufacturing of toxaphene was started in the 1940s and was highly effective on cotton and certain food crops. In addition to its use as an insecticide, toxaphene was also used to eliminate certain species of fish in aquatic environments. Toxaphene itself consists of a mixture of hundreds of different chemicals with a major identified toxic component being heptachlorobornane. The use of toxaphene peaked in 1974 after DDT was banned in 1972 with nearly 400 000 metric tons being distributed into the environment (both land and aquatic uses). This use began to subside, yet nearly 100 000 metric tons was still used in 1980 shortly before the complete ban on toxaphene usage. Large quantities of toxaphene were released into the environment. The overall chlorine content of toxaphene is nearly 70% by weight with most of the organic compounds comprising toxaphene being chlorinated. The molecular weight of the various components of toxaphene can range from 308 to 551 g mol^-1. The mean formula weight is approximately 414 g mol^-1. Toxaphene can be found as an yellowish-waxy substance that is relatively volatile and can be transported in the atmosphere. If inhaled, especially in larger quantities, toxaphene has been shown to cause significant damage to the lungs/respiratory tract, central nervous system, and kidneys. The use of toxaphene as an insecticide was banned in the early 1980s and completely banned in the United States in 1990. In addition to its ban in North America, toxaphene has been also banned in Europe, yet its use in developing countries still persists. Toxaphene is not readily soluble in water and tends to deposit in the soil and sediment, as well as the atmosphere. Microorganisms in the soil tend to degrade toxaphene very slowly. Toxaphene does not degrade as slowly as DDT but has been demonstrated to persist in the environment for extended and significant periods of time.

yellow waxy solid

Yellow, waxy, nonflammable solid with a chlorine or terpene-like odor. Odor threshold concentration from water is 140 μg/L (quoted, Keith and Walters, 1992).

Formerly used as an insecticide

Pesticide used primarily on cotton, lettuce, tomatoes, corn, peanuts, wheat and soybean.

Toxaphene is an insecticide that contains over 200–700 chemicals and can exist as an yellow to amber solid or gas. Heavily used in the United States until 1982, its use was completely banned in 1990. Toxaphene was used primarily to control insects on cotton crops in the southern United States; it has also been used to control pests on livestock and to control unwanted fish in aquatic environments. Reports have indicated that fish are low metabolizers of toxaphene, whereas other aquatic life such as snails can be extensive metabolizers, thus reducing the toxicity of toxaphene to aquatic life other than fish (Isensee et al., 1979).

Insecticide. Not recommended for use in dairy barns or on milking animals (Penumarthy).

Following release of technical toxaphene into the environment, the congeners are expected to undergo differential transformation, and degradation via abiotic and biotic processes, resulting in different mixtures of persistent toxaphene congeners, commonly termed weathered. Transformation and degradation processes are expected to include dechlorination and dehydrochlorination.

Yellow, waxy solid with a pleasant piney odor. Used as an insecticide, primarily for cotton and early growth stages of vegetables. Also peas, soybeans, peanut, corn, and wheat. Not produced commercially in the U.S. since 1982. Only registered for scabies control on cattle in the U.S.

Insoluble in water.

TOXAPHENE is decomposed by sunlight and heat. TOXAPHENE is decomposed in the presence of alkali. TOXAPHENE is corrosive to iron. TOXAPHENE is incompatible with strong oxidizers. TOXAPHENE is non corrosive in the absence of moisture.

Carcinogen.

Camphechlor is extremely toxic: the probable oral lethal dose (human) is 5-50 mg/kg or between 7 drops and 1 teaspoonful for 70 kg (150 lb.) person.

Highly toxic by ingestion; moderately toxicby skin contact and inhalation; may causeskin irritation and allergic dermatitis; causedadverse reproductive effects in experimentalanimals; ingestion of about 1.5–3 g may befatal to adult human; toxic effects in animals include central nervous system stimulation, tremors, convulsions, and liver injury;oral LD50 value (rats): ～100 mg/kg: sufficient evidence of carcinogenicity in animals,causing liver cancer; RCRA Waste Number P123.
LD50 oral (rat): 50 mg/kg
LD50 skin (rat): 600 mg/kg
Studies on the cancer risk assessment oftoxaphene in rodents have shown that itincreased incidence of neoplasms of endocrine organs, thyroid, pituitary, adrenal andmammary glands and reproductive systems(Buranatrevedth 2004).

Container may explode in heat of fire. Toxic vapors are generated when heated. Releases hydrochloric acid in the presence of alkali, on prolonged exposure to sunlight, and at temperatures above 311F. Avoid strong oxidizers, corrosive to iron.

Confirmed carcinogen with experimental carcinogenic and tumorigenic data. Human poison by ingestion and possibly other routes. Experimental poison by ingestion, intraperitoneal, and possibly other routes. Moderately toxic experimentally by inhalation and skin contact. Human systemic effects by ingestion and skin contact: somnolence, convulsions or effect on seizure threshold, coma, and allergic skin dermatitis. A skin irritant; absorbed through the skin. Experimental teratogenic and reproductive effects. Human mutation data reported. Liver injury has been reported. Lethal amounts of toxaphene can enter the body through the mouth, lungs, and skin. Systemic absorption of the insecticide is increased by the presence of lgestible oils, and liquid preparations of the insecticide, which penetrate the skin more readily than do dusts and wettable powders.A toxic mixture of organochlorine pesticides stored to some extent in body fat. It resembles chlordane and, to some extent, camphor in its physiological action. It causes diffuse stimulation of the brain and spinal cord resulting in generahzed convulsions of a tonic or clonic character. Death usually results from respiratory failure. Detoxification appears to occur in the liver. The lethal ingestion dose for humans is estimated to be 2-7 g, a toxicity of about four times that of DDT. At least seven human deaths have been reported due to toxaphene, all in chddren. Two families have been made ill by eating vegetables containing a large residue of toxaphene. When heated to decomposition it emits toxic fumes of Cl-.

Toxaphene is reasonably anticipated to be a human carcinogen based on sufficient evidence of carcinogenicity from studies in experimental animals.

Soil. Under reduced soil conditions, about 50% of the C-Cl bonds were cleaved (dechlorinated) by Fe2+ porphyrins forming two major toxicants having molecular formulas C10H10Cl8 (Toxicant A) and C10H11Cl7 (Toxicant B). Toxicant A reacted with reduced hematin yielding two reductive dechlorination products (C10H11Cl7), two dehydrodechlo- rination products (C10H9Cl7) and two other products (C10H10Cl6). Similarly, products formed from the reaction of Toxicant B with reduced hematin included two reductive dechlorination products (C10H12Cl6), one dehydrochlorination product (C10H10Cl6) and two products having the molecular formula C10H11Cl5 (Khalifa et al., 1976). The reported dissipation rate of toxaphene from soil is 0.010/day (Seiber et al., 1979).
Photolytic. Dehydrochlorination will occur after prolonged exposure to sunlight releas- ing hydrochloric acid (U.S. Department of Health and Human Services, 1989). Two compounds isolated from toxaphene, 2-exo,3-exo,5,5,6-endo,8,9,10,10-nonachlor
Chemical/Physical. Saleh and Casida (1978) demonstrated that Toxicant B (2,2,5- endo,6-exo,8,9,10-heptachlorobornane), the most active component of toxaphene, under- went reductive dechlorination at the geminal dichloro position yielding 2-endo,
Toxaphene will slowly undergo hydrolysis resulting in the loss of chlorine atoms and the formation of hydrochloric acid (Kollig, 1993). The hydrolysis rate constant for tox- aphene at pH 7 and 25°C was determined to be 8 × 10–6/hour, resulting in a half-life of 9.9 years (Ellington et al., 1987).
Emits toxic chloride fumes when heated to decomposition (Lewis, 1990).

The neuroexcitatory properties of toxaphene are due to its ability to reduce chloride uptake into neurons, leading to depolarization of the cells and hyperactivity. It is believed that toxaphene acts on the picrotoxin-binding site on the gammaaminobutyric acid (GABA)A receptor. Toxaphene may also impair calcium transport which will interfere with numerous neuronal pathways and function.