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Humans, in general, have a limited capacity for metabolizing, for example,
chlorinated hydrocarbons (Roan and Morgan 1971). Pesticides cause mild
acute and subacute liver-cell damage and affect renal function and possibly
B cells in the pancreas (Amr et al. 1984a,b,c). Hepatic susceptibility to pesticides
is also related to low dietary protein as well as parasitic infestations and
other demographic factors.
The high degree of abnormal liver function in workers not suffering from
bilharzia may indicate a toxic effect of the pesticides; among those with
bilharzia, the bilharzial infestation and the chemical effects of pesticides may
have exerted effects in an additive or synergistic manner. However, the chronic
hepatocellular damage among those heavily exposed to pesticides cannot be
discounted. Our findings focus attention on the importance of initial and
periodic medical examinations to identify those with liver fibrosis or with
liver-function abnormalities.
There was some evidence of renal pathology in subjects exposed to pesticides.
Toxic compounds may damage the kidneys directly and release renal antigens,
eliciting the production of antiglomerular basement-membrane antibodies.
This may be followed by antigen--antibody or autoimmune reactions. Susceptibility
to this autoimmune reaction might be inherited (Kleinknecht et al.
1980).
The occurrence of hypertension among pesticide workers is thought to be
attributable to the possible arteriosclerotic effects of pesticides (Hill and
Carpenter 1982); their abnormal ECGs might be due to either normal aging
processes or myocardial pesticide effects. However, abnormal ECGs were
significantly more prevalent among younger workers in the rural group, but
in older workers in the urban group. A possible explanation is repeated
infestation by bilharzia in the former and the cumulative effect of pesticides
in the latter. The high prevalence of bilharzia and the extensive exposure to
pesticides in the rural plant may explain the higher number of cardiorespiratory
disorders (e.g., bilharzial corpulmonale and cardiomyopathy) in the rural
workers (Wegever et al. 1982). Young workers exposed to zinc phosphide are
also more frequently found to have abnormal ECGs (Amr et al. 1984a,b,c).
Zipf et al. (1976) reported evidence of cardiac muscle damage, with abnormal
ECG tracings associated with chest pain, palpitation, and dyspnea in pesticide-exposed
subjects. In spite of the larger number of abnormal ECGs among
exposed workers in our study, there were no significant differences between
the two exposed groups and the control subjects except for ill-defined pathological
effects.
Anemia among Egyptians is usually a result of parasitic infestation, but may
also be attributable to pesticide exposure (Klimmer 1969). McConnell et al.
(1980) noted a dose-related, progressive anemia due to exposure to pentachiorophenol;
pentachlorophenol is also associated with leukocytosis
(Clemmer et al. 1980). The most likely explanation for blood dyscrasia associated
with pesticide exposure appears to be idiosyncratic bone-marrow
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