Application of Biodegradable Pesticides in India
291
feeding of zineb (1.0 glkg per day) has produced marked hyperplasia of thyroid
in male rats, suggesting the blockade of iodide-iodine conversion. It also produced testicular damage in rats (Raizada et ai., 1979).
Repeated administration of organophosphorus insecticides such as quinalphos, methyl demeton, and phosphamidon in low doses inhibited acetylcholinesterase activity and induced no ill effects in animals. Rest and immediate
cessation from further exposure to insecticides normalized the level of acetylcholinesterase activity. The behavior of different species of test animals, like
rats, rabbits, guinea pigs, and domestic goats, toward low levels of organophosphorus compounds was comparable (Dikshith et ai., 1980a-c, unpublished
data).
10.9.4. Toxicity to Man
Pesticides have exerted highly neurotoxic effects in animals and humans.
Studies have hitherto stressed the convulsive properties of several pesticidal
compounds that are used in pest and vector control operations (Joy, 1976). These
potentially toxic chemicals are also known to mimic neurologic syndromes such
as headaches, peripheral neuropathy, ataxia, seizures, status epilepticus, and
clinical entities resembling pulmonary edema, myocardial infarction, diabetic
comas, encephalitis, and asthma (Holmes, 1965). While assessing the health
hazards of pesticide residues, two types of injury have to be considered: first,
the possibility of an acute illness resulting from ingesting residues for a short
period of time, and second, the long-term effects that may accrue after ingesting
small quantities of residues daily for many years. Exposure to residues appears
to cause only a mild disease manifested as gastrointestinal symptoms. Epidemiologically, the symptoms noticed due to residues are quite distinguishable
from the acute effects produced by direct exposure. The majority of individuals
with high amounts of body residues frequently become sick. In contrast, in
poisoning episodes due to direct exposure to technical grade or formulations of
pesticides, it is unusual to have more than one or two cases among any group
of workers. Accidental poisoning in Kerala due to parathion-contaminated flour
and in Karnataka and the involvement of members of the food chain like fish
and crabs in the Handigodu syndrome have focused attention on exercising greater
caution and control in the spread of pesticides to villages. With regard to organophosphorus pesticides, cases of acute poisoning were reported in individuals
exposed to these in their occupations. Over 100 deaths in India during the spring
of 1958 resulted from eating food accidently contaminated with parathion during
shipment (Mutalik et ai., 1966; Karunakaran, 1958; Report of the National
Institute of Nutrition, 1977).
Periodic surveys have indicated that humans in India show significantly
higher storage levels than their counterparts in the USA. Signs of intoxication
due to aldrin and dieldrin involve the central nervous system and may include
291
feeding of zineb (1.0 glkg per day) has produced marked hyperplasia of thyroid
in male rats, suggesting the blockade of iodide-iodine conversion. It also produced testicular damage in rats (Raizada et ai., 1979).
Repeated administration of organophosphorus insecticides such as quinalphos, methyl demeton, and phosphamidon in low doses inhibited acetylcholinesterase activity and induced no ill effects in animals. Rest and immediate
cessation from further exposure to insecticides normalized the level of acetylcholinesterase activity. The behavior of different species of test animals, like
rats, rabbits, guinea pigs, and domestic goats, toward low levels of organophosphorus compounds was comparable (Dikshith et ai., 1980a-c, unpublished
data).
10.9.4. Toxicity to Man
Pesticides have exerted highly neurotoxic effects in animals and humans.
Studies have hitherto stressed the convulsive properties of several pesticidal
compounds that are used in pest and vector control operations (Joy, 1976). These
potentially toxic chemicals are also known to mimic neurologic syndromes such
as headaches, peripheral neuropathy, ataxia, seizures, status epilepticus, and
clinical entities resembling pulmonary edema, myocardial infarction, diabetic
comas, encephalitis, and asthma (Holmes, 1965). While assessing the health
hazards of pesticide residues, two types of injury have to be considered: first,
the possibility of an acute illness resulting from ingesting residues for a short
period of time, and second, the long-term effects that may accrue after ingesting
small quantities of residues daily for many years. Exposure to residues appears
to cause only a mild disease manifested as gastrointestinal symptoms. Epidemiologically, the symptoms noticed due to residues are quite distinguishable
from the acute effects produced by direct exposure. The majority of individuals
with high amounts of body residues frequently become sick. In contrast, in
poisoning episodes due to direct exposure to technical grade or formulations of
pesticides, it is unusual to have more than one or two cases among any group
of workers. Accidental poisoning in Kerala due to parathion-contaminated flour
and in Karnataka and the involvement of members of the food chain like fish
and crabs in the Handigodu syndrome have focused attention on exercising greater
caution and control in the spread of pesticides to villages. With regard to organophosphorus pesticides, cases of acute poisoning were reported in individuals
exposed to these in their occupations. Over 100 deaths in India during the spring
of 1958 resulted from eating food accidently contaminated with parathion during
shipment (Mutalik et ai., 1966; Karunakaran, 1958; Report of the National
Institute of Nutrition, 1977).
Periodic surveys have indicated that humans in India show significantly
higher storage levels than their counterparts in the USA. Signs of intoxication
due to aldrin and dieldrin involve the central nervous system and may include