work on them was declared secret. Some became the deadly nerve gases. Others, of closely
allied structure, became insecticides. The organic phos phorus ins ecticides act on the living
organism in a peculiar way. They have the ability to destroy e nzy mes—en zy mes that pe rfo rm
neces sary functions in the body. Their target is the nervous s ys tem, whethe r the victim is an
ins ect or a warm-blooded animal. Under normal conditions , an impuls e pas s es from nerve to
nerve with the aid of a ‘chemical transmitter’ called acetylcholine, a substance that performs an
essential function and the n dis appears. Indeed, its existence is so ephemeral that medical
res earchers are unable, without s pecial procedures , to s ample it before the body has des troyed
it. This transient nature of the transmitting chemical is necessary to the normal functioning of
the body. If the acetylcholine is not des troyed as s oon as a nerve impuls e has pass ed, impuls es
continue to flas h acros s the bridge from nerve to nerve, as the chemical exerts its effects in an
ever more intensified manner. The movements of the whole body become uncoordinated:
tre mors , mus cular s pas ms , convuls ions , and death quickly res ult. This contingency has been
provided for by the body. A protective e nzy me called cholines teras e is at hand to des troy the
transmitting chemical once it is no longer needed. By this means a precis e balance is s truck and
the body never builds up a dangerous amount of acetylcholine. But on contact with the organic
phos phorus ins ecticides , the protective enzyme is des troye d, and as the quantity of the enzyme
is reduced that of the trans mitting chemical builds up. In this effect, the organic phos phorus
compounds res emble the alkaloid pois on mus carine, found in a pois onous mus hroom, the fly
amanita.
Repeated exposures may lower the cholinesterase level until an individual reaches the brink of
acute pois oning, a brink over which he may be pus hed by a very s mall additional expos ure. For
this reas on it is cons idered important to make periodic examinations of the blood of s pray
operators and others regularly expos ed. Parathi on is one of the mos t widely us ed of the organic
phos phates. It is als o one of the mos t powerful and dangerous. Honeybees become ‘wildly
agitated and bellicose’ on contact with it, perform frantic cleaning movements, and are near
death within half an hour. A chemis t, thi nking to learn by the mos t direct pos s ible means the
dose acutely toxic to human beings, swallowed a minute amount, equivalent to about .00424
ounce. Paralysis followed so instantaneously that he could not reach the antidotes he had
prepa red at hand, and s o he died. Parathion is now s aid to be a favorite ins trument of suicide in
Finland. In recent years the State of California has reported an average of more than 200 cases
of accidental parathion pois oning annually. In many parts of the world the fatality rate from
parathion is startling: 100 fatal cases in India and 67 in Syria in 1958, and an average of 336
deaths per year in Japan. Yet s ome 7,000,000 pounds of parathion are now applied to fields and
orchards of the United States—by hand s prayers , motorized blowe rs and dus ters , and by
airplane. The amount used on California farms alone could, according to one medical authority,
‘provide a lethal dose for 5 to 10 times the whole world’s population.’
One of the few circ ums tances that s ave us from extinction by this means is the fact that
parathion and other che micals of this group are decompos ed rathe r rapidly. Their res idues on
the crops to which they are applied are therefore relatively s hort-lived compared wi th the
chlorinated hy drocarbons. However, the y las t long enough to create hazards and produce
consequences that range from the merely serious to the fatal. In Riverside, California, eleven
out of thirty men picking oranges became violently ill and all but one had to be hospitalized.
Their s ymptoms were ty pical of parathion pois oning.
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