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eactions to the pesticides in occupationally exposed individuals. Among
workers exposed to zinc phosphide, number of red blood cells and percentage
of hemoglobin were significantly higher (Amr et al. 1984a,b,c), probably due
to the irritative stimulant effects on the homeopathic system of small doses of
zinc phosphide.
Impairment of ventilatory function observed in both exposed and control
groups was probably related to pesticide exposure in the former and hazards
in the textile-industry environment in the latter. Although respiratory problems
have been linked to pesticide exposure (Lehnigk et al. 1985; Mechkow et
al. 1987), the significantly more prevalent symptoms observed among young
workers in the rural plant compared with urban workers may also be linked
with smoking habits and parasitic infestations.
Cases of asthma have been linked with exposure to organophosphate pesticides
(Hayes 1982), but it is uncertain whether the active ingredient or other
components in the formulation produce the effects. Carbarnates may cause
fibrotic changes noticed among survivors of suicide attempts (WHO 1984). A
high rate of impairment of ventilatory function (70%) was observed among
workers exposed to zinc phosphide (Amy et al. 1984a,b,c); Koilpakov (1987)
reported significant deviation from standard functional parameters among
workers exposed to pesticides. Asthma and impaired ventilatory function
among those exposed to organophosphates may have a biochemical basis:
accumulation of endogenous acetyicholine with consequent cholinergic stimulation
after AChE inhibition. However, among those exposed to DDT, the
effects might be due to either the interaction of DDT with beta-receptor
adenylate cyclase complex (Dudeja et al. 1980) or interaction with adrenal
cytochrome P450 and inhibition of endogenous steroid formation.
Reduction in AChE activity is an indicator of exposure to organophosphate
and carbamate pesticides. It is a measure of the biochemical effect of the
pesticide rather than of the pesticide itself. Cholinesterase inhibitors (organophosphates
and carbamates) prevent the breakdown of AChE, which consequently
builds up in the brain and in the peripheral synapses (Risch and
Janowsky 1984). Significant depressive (Bowers et al. 1964), neurologic, and
cardiorespiratory symptoms are often displayed as a result. These clinical
manifestations may be due to the direct effect of the pesticides on the nervous
system, myocardium, and bone marrow, or indirectly due to the metabolic
changes that coincide with the high pesticide level in blood, e.g., effects of
hormones, trace elements, and enzymes. The degree to which blood AChE
activity was reduced in both exposed groups seems to reflect insufficient
awareness of acute pesticide poisoning by attending physicians as well as a
lack of appropriate safety measures and ventilation systems in the working
environment.
The long retention time of pyrethroids, organophosphates, and carbamate
compounds in the blood of the exposed urban workers might be due to heavy
exposure, liver damage, or both. Blood contamination with chlorinated hydro-
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