The organochlorines or chlorinated hydrocarbons are a diverse group of agents belonging to three distinct chemical classes:
- dichlorodiphenylethanes (represented by DDT)
- chlorinated cyclodienes (represented by chlordane)
- chlorinated benzxenes and cyclohexanes(represented by lindane)
All are soluble in lipids and organic solvents but are insoluble in water. They are all poorly absorbed unless dissolved in organic solvents such as kerosene or other petroleum distillates.
Acute poisoning symptoms:
Initial symptoms include nausea, vomiting, headache, muscle tremors, and weakness. Symptoms may progress to delirium, convulsions, and death due to respiratory muscle paralysis.
Chronic poisoning symptoms:
Brain (cerebellum) and liver damage. These compounds also accumulate in body fat.
The dangerous doses of DDT in man show varied figures. A single ingestion of 10 mg/kg produced illness in some people but not all. Some people experience convulsions with 10 mg/kg whereas others do not show this symptom until 16 mg/kg. Dosages as high as 285 mg/kg show no fatalities. Part of the problem lies in the fact that DDT poisoning also involves some organic solvent used to make the DDT soluble for application.
The Pesticide Manual (8th edition, 1987) states on page 3880: "Though stored in body fat and excreted in milk, 17 humans who ate 35 mg/man daily (c.0.5 mg/kg) for 1.75 years suffered no ill effects."
Chlordane (Octachlor) is more dangerous to man with a fatality reported at a dose of 104 mg/kg (no solvent involved).
Chlordecone (Kepone) another organochlorine compound came to the forefront in 1975, when 76 of 148 workers in a factory in Hopewell, Virginia, developed a severe neurological syndrome. This condition now known as the "Kepone shakes" was characterized by tremors, behavioral changes, altered gait, liver and spleen damage and lowered sperm counts.
Similar findings were confirmed in animal studies.
CARBAMATE INSECTICIDES
Cholinesterase inhibitors.
The enzyme cholinesterase normally functions to destroy the neurotransmitter - acetylcholine - at
- parasympathetic nerve endings,
- motor nerve endings,
- autonomic ganglia,
- and the brain (central nervous system)
Acetylcholine levels, at these sites, build up when the enzyme cholinesterase is inhibited by the organophosphates and carbamate insecticides.
Skeletal muscle tremors and cramps are followed by flaccid paralysis.
A buildup of acetylcholine at parasympathetic nerve endings results in pupjillary constriction (miosis), blurring of vision (cycloplegia), diarrhea and cramping, salivation, sweating, bronchoconstriction (which may become asthma), depression of heart rate and blood pressure.
Formulations containing 1 - 95 percent of the active ingredients are currently available. A dosage of 120 mg of parathion led rapidly to death in one man. Children have died following accidental ingestion of 2 mg/person of parathion (0.1 mg/kg). Ingestion of 5 grams led to the death of a 75-year-old man about 1.5 hours after the accidental consumption. One woman survived a dose of 14 grams and one child survived a dose of 4 grams of malathion.
The primary difference between the organophosphates and carbamate insecticides lies in the type of treatment.
The carbamate insecticide (reversible anticholinesterases) symptoms can be controlled by atropine. The same atropine treatment can be used for poisoning by the organophosphates but in addition, pralidoximine (2-PAM) must also be administered. The organophosphates are irreversible cholinesterase inhibitors and 2-PAM is a cholinesterase reactivator.
The organophosphates and carbamates do not accumulate in body fat or the environment. However, the compounds are more toxic to rats and humans than the chlorinated hydrocarbons - as shown in Table 2 (end of article).
An interesting sidelight should be noted at this time. In 1984, 2,000 people died from poisoning in Bhopal, India by an accidental release of the gas methyl isocyanate.
Methyl isocyanate is used as an intermediate in the manufacture of Aldicarb (Temik). Aldicarb inhibits cholinesterase but was specificaslly designed to resemble acetylcholine structurally.
An accidental release of Aldicarb in West Virginia in 1985 resulted in an area alert and did result in at least 125 people being sent to the hospital - all showing symptoms of excessive parasympathetic nervous system stimulation (as noted above).