Chlorinated hydrocarbon pesticides are used widely in agriculture, structural pest control, and malaria control programs around the world. Lindane is used medicinally for the treatment of lice and scabies. Chlorinated hydrocarbons are of major toxicologic concern, and many (eg, DDT [dichloro-diphenyl-trichloroethane] and chlordane) have been banned from commercial use because they persist in the environment and accumulate in biological systems. Despite being banned decades ago, these substances are still being measured in the environment and food chain in ongoing studies. In 2002, sale of lindane was banned in California.
Mechanism of toxicity
Chlorinated hydrocarbons are neurotoxins that interfere with transmission of nerve impulses, especially in the brain, resulting in behavioral changes, involuntary muscle activity, and depression of the respiratory center. They may also sensitize the myocardium to arrhythmogenic effects of catecholamines, and many can cause liver or renal injury, possibly owing to generation of toxic metabolites. In addition, some chlorinated hydrocarbons may be carcinogenic.
Pharmacokinetics. Chlorinated hydrocarbons are well absorbed from the GI tract, across the skin, and by inhalation. They are highly lipid-soluble and accumulate with repeated exposure. Elimination does not follow first-order kinetics; compounds are released slowly from body stores over days to several months or years.
Toxic dose. The acute toxic doses of these compounds are highly variable, and reports of acute human poisonings are limited. Table II–21 ranks the relative toxicity of several common compounds.
Table II-21 Chlorinated Hydrocarbons ||Download (.pdf)
Table II-21 Chlorinated Hydrocarbons
Low Toxicity (Animal Oral LD50 >1 g/kg)
Moderately Toxic (Animal Oral LD50 >50 mg/kg)
Highly Toxic (Animal Oral LD50 <50 mg/kg)
Ingestion of as little as 1 g of lindane can produce seizures in a child, and 10–30 g is considered lethal in an adult. The estimated adult lethal oral doses of aldrin and chlordane are 3–7 g each; that of dieldrin, 2–5 g. A 49-year-old man died after ingesting 12 g of endrin. A 20-year-old man survived a 60-g endosulfan ingestion but was left with a chronic seizure disorder.
Skin absorption is a significant route of exposure, especially with aldrin, dieldrin, and endrin. Extensive or repeated (as little as two applications on two successive days) whole-body application of lindane to infants has resulted in seizures and death.
Clinical presentation. Shortly after acute ingestion, nausea and vomiting occur, followed by paresthesias of the tongue, lips, and face; confusion; tremor; obtundation; coma; seizures; and respiratory depression. Because chlorinated hydrocarbons are highly lipid-soluble, the duration of toxicity may be prolonged.
Recurrent or delayed-onset seizures have been reported.
Arrhythmias may occur owing to myocardial sensitivity to catecholamines.
Metabolic acidosis may occur.
Signs of hepatitis or renal injury may develop.
Hematopoietic dyscrasias can develop late.
Diagnosis is based on the history of exposure and clinical presentation.
Specific levels. Chlorinated hydrocarbons can be measured in the serum, but levels are not routinely available.