Je. Atkinson et al., ASSESSMENT OF OCULAR TOXICITY IN DOGS DURING 6 MONTHS EXPOSURE TO A POTENT ORGANOPHOSPHATE, Journal of applied toxicology, 14(2), 1994, pp. 145-152
Exposure to anticholinesterase pesticides has been associated with the
development of ocular toxicity in humans and animals, ranging from bl
urred vision to degeneration of the optic nerve. Based on the concern
for human safety, the US Environmental Protection Agency has recently
required additional studies for this class of compounds, focusing on b
iochemical, functional and histopathological evaluation of the ocular
system. This study was designed to determine the effects on the eye of
ethyl parathion, a highly toxic organophosphate, when administered or
ally to 30 beagle dogs (five of each sex per group) at doses of 2.4, 7
.9 or 794 mu g kg(-1)day(-1) for 6 months. Control animals received co
rn oh. Routine ophthalmoscopic and slit lamp examinations, refraction
and intraocular pressure determinations and electroretinograms were pe
rformed as functional assessments at various intervals over the study.
Plasma and erythrocyte cholinesterase were determined at weeks 1, 6,
14, 20 and 26, while brain, retinal and ocular muscle cholinesterase w
ere measured at week 26 only. Histopathological examination of the ret
ina, optic nerve, ocular muscle and ciliary body was conducted at term
ination. Plasma and erythrocyte cholinesterase was markedly depressed
at 7.9 and 794 mu g kg(-1)day(-1) as early as week 1. Retinal cholines
terase was decreased (37-55%) from control values in the 794 mu g kg(-
1)day(-1) group only. Ocular muscle cholinesterase was comparable in t
reated and control groups at termination. No functional impairment of
the eye was noted over the 6-month study. Based on refractive indices,
intraocular pressure and evaluation of electroretinograms, it was con
cluded that administration of ethyl parathion at doses up to 794 mu g
kg(-1)day(-1) for 6 months does not produce functional or histopatholo
gical changes indicative of ocular toxicity. Cholinesterase inhibition
, observed early in the study, does not appear to be related to the de
velopment of ocular toxicity.