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DDT And Other Chlorinated Hydrocarbon Pesticides
The use of DDT and other chlorinated hydrocarbon insecticides increased following World War II due to their effectiveness against a wide range of insect pests, residual activity, and relatively low mammalian toxicity. More recently the use of many of these insecticides has become limited due to their persistence in biological systems.
Included in the chlorinated hydrocarbon insecticide group are DDT (dichlorodiphenyl trichloroethane), methoxychlor, aldrin, dieldrin, chlordane, toxaphene, endrin, heptachlor, and lindane (gamma isomer of benzene hexachloride (BHC)). These are trade names for closely related hydrocarbon compounds to which several chlorine atoms have been joined. Chlordane, lindane, and toxaphene were commonly used pesticides applied to animal skin for control of external parasites. Endrin was the only insecticide registered for control of the Pale Western Cutworm and was used to control this parasite by Western wheat and barley growers. Also included in the organochlorine chemical group were polychlorinated biphenyls (PCB's) which were not insecticides but were present in the environment as industrial pollutants.
When used according to the manufacturer's specifications, the organochlorine compounds were considered to be relatively safe, but the objection to their use stemmed from the fact that they are not degraded by natural biological processes and become a permanent part of the environment.
DDT is fat soluble and is disseminated by air and water to terrestrial and aquatic ecosystems. When DDT enters a water environment, it is taken up by aquatic animals and becomes part of the food chain, accumulating and concentrating in the fat of predatory species. DDT also remains residual in upper soil layers and accumulates in many terrestrial animal species.
Transmission and Development
Since absorption from the gut is poor, the major portion of ingested DDT is excreted unchanged in the feces, with the remaining DDT excreted in the bile or stored in adipose tissue from which it is removed and gradually eliminated in the urine. DDT is metabolized by the liver, is fat soluble and therefore, its absorption through the skin is enhanced when present in an oil base solution or emulsion form. Absorption by the lung is rapid when DDT is present as an aerosol. Dieldrin may be absorbed from the skin in a dry powder.
Acute toxicity can occur due to either acute exposure or as a result of the utilization of fat containing high concentrations of accumulated DDT during periods of starvation. The DDT which was stored in the fat is suddenly released into the bloodstream and results in signs of acute organochlorine poisoning.
One of the major effects of organochlorine toxicity in wildlife (avian species) was the decline in eggshell thickness with a resultant decrease in reproductive success. There was a direct correlation between high DDE (metabolite of DDT) levels in the eggs and thinning of the eggshells. Contaminated eggs also had a greater incidence of embryonic mortality and there often was decreased survivability of hatchlings partly due to abnormal parenting behavior.
Clinical signs of acute chlorinated hydrocarbon poisoning can occur minutes to hours after exposure and include nervous hyperirritability in response to stimulation. Spasmodic twitching and muscle quivering (including the muscles of the eyelids) increase in frequency and intensity until the entire body is trembling. The animal may exhibit an apprehensiveness progressing to frenzy and incoordination which may lead to convulsions and/or blind staggers.
Signs of DDT toxicity in birds include ataxia, wing droop, jerkiness in gait, tremors, and convulsions. When symptoms are prolonged for a few days, acute toxic tubular nephrosis may result. If the insecticide is eaten, an enteritis will be present and result in dehydration. Aldrin and dieldrin produce signs of toxicity similar to those of organophosphates due to an inhibition of acetylcholinesterase.
Signs of PCB toxicity vary with the species affected, from no clinical signs to signs comparable to DDT toxicity.
At the time of necropsy, petechial and ecchymotic hemorrhages will be seen on the heart (which usually stops during systole) and the myocardium will appear whitish in color. The lungs appear congested and darkened in color and in some cases, there may be blood-tinged exudate in the bronchioles. The liver may be affected with fatty degeneration, focal necrosis, or cirrhosis.
Diagnosis is based on clinical signs and necropsy examination. The differential diagnosis for organochlorine toxicity is tetanus and strychnine poisoning. Definitive diagnosis can be made by laboratory analysis of organochlorine residues in brain or fat tissue. The brain is the best tissue for organochlorine determination as the brain is the lethal site of action, but an approximate level can be obtained from fat analysis.
Treatment for organochlorine toxicity in wildlife species is generally not practical. Where applicable, a gastric lavage with sodium sulfate or charcoal can be performed for acute ingestion but only if the animal is not convulsing. Phenobarbital or diazepam (Valium) can be given to prevent and control tremors and convulsions and fluids given to prevent dehydration.
DDT was banned by the Environmental Protection Agency in 1972, but due to its residual activity and accumulation in biological systems, it could still cause mortalities but is not likely a factor in limiting certain bird populations. In heavily organochlorine-polluted areas, pesticide burdens are rapidly eliminated when uncontaminated feeds are made available. Levels of chlorinated hydrocarbons are occasionally found in avian species that have died, but this is a rare occurrence.
Control of organochlorine poisoning is aimed at prevention of environmental contamination and monitoring of organochlorine levels. The species used to monitor organochlorine levels in the environment were the woodcock (terrestrial ecosystems) and herring gull (aquatic ecosystems).
Mortality in wildlife due to chlorinated hydrocarbon poisoning is seldom observed in Michigan anymore. Due to the banning of many of the highly toxic chlorinated hydrocarbon compounds in the 1970's, the possibility of exposure today is rare. The importance of these compounds to humans is comparable.
For questions about wildlife diseases, please contact the Michigan DNR Wildlife Disease Laboratory.