Organochlorine pesticide residues associated with mortality: additivity of chlordane and endrin.

Abstract

Mortality may be correlated with residue levels of organochlorine pesticides in the brains of exposed animals. Experimental studies have compared brain residues of animals that died with those of survivors of id› or similar exposure. Based on the results of such studies, lethal residue levels that may be used for diagnostic purposes have been established for some compounds. DALE et al. (1962) correlated the concentration of DDT with signs of poisoning in rats that were fed 200 parts per million (ppm) in the diet for 90 d and then partially starved for 10"d. DALE et al. (1963) further correlated the severity of signs of poisoning with brain residues of DDT resulting from a single oral dose (150 mg/kg) in rats. The validity of using brain residues of DDT and DDD for diagnosing cause-of-death in birds was demonstrated by STICKEL et al. (1966). Brain residues of DDT and DDD from dead or dying birds exposed to DDT were similar and were higher than brain residues of birds surviving exposure (STICKEL et al. 1966; STICKEL and STICKEL 1969). Rarely did cowbirds (Molothrus ater) fed 500 ppm DDT in the diet die with less than 30 ppm DDT + DDD in the brain. Though the relative contribution of DDT and DDD toward lethality was not determined, the investigators attributed mortality to the presence of residues of both of these chemicals in the brain. STICKEL et al. (1966) also presented supporting evidence from other reports which included residue levels of DDT and DDD in brains of birds collected from die-offs in the field. HILL et al. (1971) determined lethal ranges of DDT + DDD residues in brains of experimentally-treated songbirds. Brains of house sparrows (Passer domesticus) contained 18.0-37.9 ppm; bobwhite quail (Colinus virginianus), 16.5-37.9 ppm; cardinals (Cardinalis cardinalis), 16.6-24.0 ppm; and blue jays (Cyanocitta cristata), 12.0-19.6 ppm. STICKEL et al. (1969) concluded from results of experimental studies with Japanese quail (Coturnix coturnix) and from reports of others that brain residues of dieldrin exceeding 4-5 ppm were indicative of dieldrin-caused mortality in birds and mammals. Based on such experimental studies and residues of dieldrin detected in birds apparently dying from exposure in the environment, dieldrin has been implicated as the causative factor in some