Royal Victoria Hospital at McGill University found two thirds of 150 cases of uterine cancer
s tudied by them gave evidence of abnormally high es trogen levels. In 90 per cent of a later
series of 20 cases there was similar high estrogen activity.
It is possible to have liver damage sufficient to interfere with estrogen elimination without
detection of the damage by any tests now available to the medical profession. This can easily be
caus ed by the chlorinate d hydrocarbons , which, as we have s een, s et up changes in liver cells at
very low levels of intake. They also cause loss of the B vitamins. This, too, is extremely
important, for othe r chains of evidence s how the protective role of thes e vitamins agains t
cancer. The late C. P. Rhoads , onetime director of the Sl oan-Kettering Ins titute for Cancer
Res earch, found that tes t animals expos ed to a very potent chemical carcinogen developed no
cancer if they had been fed yeas t, a rich s ource of the natural B vitamins. A deficiency of thes e
vitamins has been found to accompa ny mouth cancer and perhaps cancer of other s ites in the
diges tive tract. This has been obs erved not only in the United States but in the far northe rn
parts of Sweden and Finland, whe re the diet is ordinarily deficient in vita mins. Groups prone to
primary liver cancer, as for example the Bantu tribes of Africa, are typically subject to
malnutrition. Cancer of the male breast is also prevalent in parts of Africa, associated with liver
disease and malnutrition. In postwar Greece enlargement of the male breas t was a common
accompanime nt of periods of starvation.
In brief, the argument for the indirect role of pes ticides in cancer is bas ed on their proven
ability to damage the liver and to reduce the s upply of B vitamins , thus leading to an increas e in
the ‘endogenous ’ es trogens , or thos e produced by the body its elf. Adde d to thes e are the wide
variety of synthetic estrogens to which we are increasingly exposed—thos e in cosmetics, drugs,
foods , and occupational expos ures. The combined effect is a matter that wa rrants the mos t
s erious concern....
Human expos ures to cancer-producing chemicals (including pes ticides ) are uncontrolled and
they are multi ple. An individual may have many different exposures to the same chemical.
Arsenic is an example. It exists in the environment of every individual in many different guis es :
as an air pollutant, a contaminant of water, a pesticide residue on food, in me dicines ,
cosmetics, wood preservatives, or as a coloring agent in paints and inks. It is quite possible that
no one of thes e expos ures alone would be s ufficient to precipitate malignancy—yet any single
s uppos edly ‘s afe dos e’ may be enough to tip the scales that are already loaded with other ‘safe
doses’. Or again the harm may be done by two or more different carcinogens acting together,
so that there is a summation of their effects. The individual expos ed to DDT, for example, is
almost certain to be exposed to other liver- damaging hydrocarbons , which are s o widely us ed
as solvents, paint removers, degreasing agents, dry -cleaning fluids, and anes thetics. What then
can be a ‘safe dos e’ of DDT? The situation is made even more complicated by the fact that one
chemical may act on another to alter its effect. Cancer may sometimes require the
comple mentary action of two che micals, one of which sensitizes the cell or tissue so that it may
later, unde r the action of anothe r or promoting agent, develop true malignancy. Thus , the
herbicides IPC and CIPC may act as initiators in the production of skin tumors, sowing the seeds
of malignancy that may be brought into actual being by s omething els e—perhaps a common
detergent.
There may be interaction, too, between a physical and a chemical agent. Leukemia may occur
as a two-step process, the malignant change being initiated by X-radiation, the promoting
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