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While animal studies
have shown that exposure to chemicals in the early development
stages of life can cause or increase vulnerability to cancer
later in life, few human studies have approached this topic,
according to a recent review.
Most human research
in cancer risk from contaminant exposure begins at the time
of diagnosis or afterward. However, if a baby is exposed to
several endocrine-disrupting compounds in utero, changes may
occur that lengthen the period of sensitivity to carcinogens.
Therefore, even if the compounds don't cause cancer directly,
they may contribute to cancer risk by increasing susceptibility.
An embryo and fetus
develop at much faster rate than adults. While this development
occurs, cell division and growth is rapid. These rapid changes
provide many opportunities for mistakes, whether mutagenic
or caused by outside changes, to occur. Since cell division
and growth do not occur at this rapid rate in adulthood, the
chances of mistakes being made are much more common in an
embryo or fetus than in an adult. Additionally, barriers such
as the blood-brain barrier are not yet complete in the womb,
and mechanisms that help detoxify contaminants do not fully
develop until after birth, both of which leave the embryo
and fetus more vulnerable still.
The report reviews
several human studies that suggest a causal relationship between
developmental exposure to contaminants and cancer in children
and young adults. Studies reviewed include occupational exposures
of parents and brain cancers in children, pesticides, paints,
paint thinners and solvents and leukemia, and cigarette smoke
and childhood cancer. The authors note that since childhood
cancers are so uncommon, prospective studies rarely have a
large enough sample to yield conclusive results, and animal
studies for developmental exposures and early age or adult
cancer are more convincing and extensive than the available
epidemiological data.
Animal studies
have shown that prenatal and early postnatal exposure to radiation
and chemicals causes cancers in the exposed animals later
in life.
Researchers have
found, however, that developmental exposure to carcinogens
can increase sensitivity to carcinogens later in life. For
example, one study showed that adults who had been exposed
to ethylene thiourea (ETU), an industrial chemical, perinatally
developed more cancers when exposed to the chemical in adulthood
than those exposed only in adulthood.
The effects of
developmental exposure to several specific endocrine-disrupting
compounds are also discussed in the report. Diethystilbestrol,
a synthetic estrogen, has been linked to vaginal cancer in
young adult women and possibly to testicular cancer in young
adult men; genistein, a phytoestrogen in soy, has been linked
to the development of uterine cancer in mice; polyhalogenated
aromatic hydrocarbons, which include polychlorinated biphenyls
(PCBs), polybrominated biphenyls (PBBs) and dioxins, have
been linked to a variety of cancers; and Atrazine, a weed
killer, has been found to prolong the period of sensitivity
to carcinogens and alter mammary gland development during
puberty.
The authors question
why epidemiological studies often measure contaminant exposure
in adults after adverse effects have occurred, when it appears
that developmental exposure could be critical to disease vulnerability.
OurStolenFuture.org
November, 2002
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