toxicological profile for malathion - Agency for Toxic Substances and ...

MALATHION 142
3. HEALTH EFFECTS
organs. Townsend and Carlson (1981) examined the influence of a series of chlorinated and brominated
benzenes on the toxicity of malathion (92% pure) in mice. Pretreatment of the mice orally for 7 days with
the halogenated benzenes increased the LD50 for malathion (decreased toxicity), the greatest increase was
seen with 1,2,4-tribromobenzene (from 1,370 to 2,053 mg/kg). In general, there was a good correlation
between the effects on lethality and increases in in vitro carboxylesterase activity with malathion or
malaoxon as substrate. Trisubstituted compounds were more protective than disubstituted, and
brominated benzenes were more active than chlorinated ones. A study of combined application of
hexachlorocyclohexane and malathion to the skin of guinea pigs for 30 days showed no significant
influence of either chemical on morbidity or mortality induced by the other (Dikshith et al. 1987).
The influence of the pesticide carbaryl on the developmental toxicity of malathion in rats was examined
by Lechner and Abdel-Rahman (1984). Doses of 50 mg/kg/day of malathion (unspecified purity)
administered for 3 months prior to mating and during gestation caused no significant teratogenicity or
embrytoxicity upon examination of Gd 20. The only significant effects of the combination were increases
in the number of litters with resorptions and in the percentage of resorptions which were greater than
expected from the simple addition of individual contributions. The same group of investigators also
examined the effects of an equimolar malathion/carbaryl combination on liver microsomal enzyme
activities (aminopyrine demethylase, aniline hydroxylase, nitrobenzoate reductase, and uridine
diphosphate-glucuronyl transferase) in a 7-day study in rats (Lechner and Abddel-Rahman 1985).
Treatment with malathion had no significant effect on the activities of any of the enzymes. Carbaryl
significantly increased the activity of uridine diphosphate-glucuronyl transferase and the same extent of
increase was seen in the group treated with the combination of pesticides. A further study by the same
group on the effect on serum enzymes and glutathione in rats showed that treatment with malathion
(50 mg/kg once or for 21 days) had no effect on serum transaminases, glutamic dehydrogenase, leucine
aminopeptidase, or β-glucuronidase activities. Malathion did not significantly affect blood glutathione
levels. Groups treated with the combination of malathion and carbaryl showed responses not significantly
different than those seen with the individual pesticides.
Moeller and Rider (1962) conducted a controlled oral study with volunteers to examine the influence of
EPN on malathion-induced cholinesterase activity inhibition. The pesticides were administered alone or
in various combinations for up to 56 days. Administration of 0.11 mg malathion/kg/day for 32 days or
0.23 mg/kg/day for 47 days did not produce any significant depression of plasma or RBC cholinesterase
activity or induce clinical signs. Malathion at 0.34 mg/kg/day for 56 days caused a maximum depression
of 25% in plasma cholinesterase approximately 3 weeks after cessation of treatment. A similar