Laboratory verification

Laboratory analysis is needed for verification of suspected pesticide poisoning. Analytical methods for an extensive number of pesticides and their metabolities have been developed (AU)

Lindane poisonings.

One percent lindane, widely used to treat scabies and pediculosis, presents toxicologic problems when used excessively. A 16-year-old mentally retarded boy accidentally ingested approximately 392 g of 1% lindane shampoo and recovered. A 2-month-old, 4.5-kg, male infant was found dead in his crib after excessive application of a 1% lindane lotion. In the former patient, initial serum levels of lindane were 206 parts per billion (ppb) declining to 1.0 ppb after 25 days. In the latter, lindane was identified in the brain at a concentration of 110 ppb. Brain levels of lindane were three times greater than the levels found in the blood. Although the relationship of this pesticide exposure to the fatal outcome in the second case was conjectural, it was illustrative of the problem of interpreting CNS events that occur shortly after excessive exposure to this insecticide.

Body distribution of malathion and its metabolites in a fatal poisoning by ingestion.

Eight autopsy samples from an individual who had ingested a large amount of malathion were analyzed fo four components: intact pesticide, malaoxon, malathion monocarboxylic acid (MCA), and malathion dicarboxylic acid (DCA). Malathion was present in all samples except liver. Highest concentrations were found in the gastric contents (8621 ppm) and adipose tissue (76.4 ppm). Malaoxon was identified in some tissues at very low levels; a significant amount was found only in fat (8.2 ppm). The MCA and DCA were detected in all tissue. The former was found in greater abundance: 221 ppm in bile, 106 ppm in kidney, and 103 ppm in the gastric contents.

Reduction of pesticide exposure with protective clothing for applicators and mixers.

Systemic pesticide illness in agricultural workers may result from excessive dermal exposure to pesticides. Workers who apply and mix pesticides (applicators and mixers) are not at special risk. Both acute and chronic exposures can occur from spillage or by environmental contamination of clothing. Two exposure assessment studies were conducted of Central Florida citrus grove workers who applied ethion daily. Measuring the percentage of penetration of ethion through clothing and measuring the daily urinary excretion of diethyl phosphate (DEP) were the techniques used to assess the protection afforded by changing daily to freshly laundered 100% cotton coveralls. Coveralls provided significantly greater protection than did regular clothing and the use of respirators.

Determination of organochlorine pesticides and metabolites in drinking water, human blood serum, and adipose tissue.

Previously published analytical procedures by which drinking water, human blood serum, and adipose tissue may be analyzed for trace amounts of organochlorine pesticides have been modified to permit use of smaller samples. Data on percent recovery, detector sensitivity, and limit of detectability have been collected for each of the three reported procedures. The methodology has been applied to 59 blood samples, 20 drinking water samples, and 10 necropsy adipose tissue samples. Only hexachlorobenzene and dieldrin were detected in water. Hexachlorobenzene, beta-hexachlorocyclohexane, dieldrin, p,p'DDE, and p,p'DDT were present in blood. No heptachlor, heptachlor epoxide, oxychlordane, trans-nonachlor, or o,p'-DDT was found. In.fat, the compounds present in blood plus oxychlordane, heptachlor epoxide, and trans-nonachlor were detected. No heptachlor, aldrin, o,p'-DDT, or alpha- or gamma-chlordane was present. The reported values are representative of the levels of persistent organochlorine pesticides and pesticide metabolites found in 1978 in white female residents of Dade County, Florida.

Human pesticide poisonings by a fat-soluble organophosphate insecticide.

In five cases of dichlofenthion poisoning due to suicidal ingestions, unusual toxicologic features were encountered. Initial symptoms were mild or delayed and severe cholinergic crises did not appear until 40 to 48 hours after ingestion. Two patients died, and in the three survivors, cholinesterase symptoms persisted for five to 48 days. An almost total inhibiton of both cholinesterase enzymes continued in one patient for 66 days, and prolonged antidotal therapy was required. Residues of the intact pesticide were detected in fat after 54 days in one patient, and in the blood for 75 days in another patient. The partition coefficient of dichlofenthion in fat was 20 times greater than parathion, and exceeded only by leptophos. Considering the chemical and toxicologic properties of this compound, we postulated that the mechanism of protracted intoxication is a slow release from adipose reservoirs.