Pesticide Residues in Man - Pesticides: Evaluation of Environmental Pollution - page 497

Farm workers occupationally exposed to OP pesticides through their application to
cotton fields in Menoufiya Governorate, Egypt, were examined (Farahat et al. 2007).
Results indicated that exposed individuals exhibited significantly lower performance
than did nonexposed controls on six neurological tests (similarities, digital symbol,
trail making part A and B, letter cancellation, digital span, and Benton visual retention).
Serum AChE was significantly lower in exposed (87.34 U/mL) than control (108.25 U/
mL) participants, and longer duration of work with pesticides was associated with a
lower AChE level.
15.5.2 India
According to Gupta (2004), there have been a number of outbreaks of accidental poisoning
by pesticides, in India, that deserve special mention. The first report of poisoning due to
pesticides was from Kerala in 1958, where over 100 people died after consuming wheat
flour contaminated with parathion (Karunakaran 1958). In the same year, poisoning in
Kerala caused deaths of 102 people. This was mainly due to careless handling and stor-
age of wheat. Subsequently, several cases of human and animal poisonings, in addition to
deaths of birds and fishes, have been reported. Out of the 35 cases of malathion (diazole)
poisoning reported during 1967-1968, five died. Electrocardiography (ECG) changes were
recorded in all the cases. Autopsy and histopathological studies revealed damage to the
myocardium (Sethuraman 1977).
In another report from Madhya Pradesh, 12 humans who consumed wheat contami-
nated with aldrin dust and Gammexane for 6-12 months developed symptoms of poison-
ing, which consisted of myoclonic jerks, generalized colonic convulsions, and weakness in
the extremities (Gupta 1975). In another outbreak in 1977, eight cases of grand mal seizers
were reported from a village of Uttar Pradesh, following accidental ingestion of HCH-
contaminated wheat (Nag et al. 1977).
Epidemiological studies conducted on occupational pesticide workers have shown that
exposure to dibromochloropropane (DBCP), chlordecone, endosulfan, ethyldibromide,
DDT, carbaryl, and ethylmethiniphos causes abortion, still births, defects in offspring,
male infertility, neonatal deaths, congenital defects, testicular dysfunction, and abnormal-
ities (Kumar et al. 2000b).
In India, cotton field workers exposed to various pesticides had an increased risk of male
infertility and male-mediated adverse reproductive outcomes such as abortions, stillbirths,
neonatal deaths, and congenital defects (Rupa et al. 1991). DDT and its metabolites, HCH
and its isomers, and PCBs have been detected in the seminal fluid, cervical mucus, and
follicular fluid (Talamanca et al. 2001). In another study, an association between the serum
PCBs and p,p ′ -DDE and abnormal sperm motility, sperm count, and sperm morphology
was established in populations without specific exposure to these chemicals (Hauser et al.
2002). An in vitro study has shown that lindane depolarizes the human sperm membrane
and inhibits the sperm cytological responsiveness to progesterone, the physiological ago-
nist that stimulates the onset of acrosome reaction at the site of fertilization (Silvestroni
and Palleschi 1999).
Studies on 356 workers in four units manufacturing HCH in India revealed neurologi-
cal symptoms (21%) with significant increase in liver enzymes, which were related to the
intensity of exposure (Nigam et al. 1993). Observations confined to health surveillance
in male formulators engaged in the production of dust and liquid formulations of vari-
ous pesticides (malathion, methyl parathion, DDT, and lindane) revealed several types of
adverse effects and reproductive problems (Gupta et al. 1984).