ASSESSMENT OF OCULAR TOXICITY IN DOGS DURING 6 MONTHS EXPOSURE TO A POTENT ORGANOPHOSPHATE

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.