Introduction to Endocrine Disrupting Chemicals

in homes with indoor DDT spraying have decreased sperm quality (64) that may
lead to diminished fertility. There is also some evidence to suggest that exposure to
DDTs shorten the lactation period (67). A brief summary of these and other health
effects of DDT in humans is provided in Box 3.
Like most EDCs, the health consequences of DDT exposures are most pronounced
when exposure occurs in developing fetuses and children. When girls are exposed
to DDTs early in life before the breast is fully matured, this is associated with increased
risk of breast cancer later in life (78). Several human studies indicate that
DDT increases risk of urogenital birth defects such as cryptorchidism (failure of
the testes to descend), and a rat study also showed that fetal DDT exposure caused
male reproductive abnormalities (67). Evidence that early life exposure to DDTs
may contribute to an earlier onset of puberty (menarche) in girls, together with
adult studies showing that DDTs are associated with longer menstrual cycles and
earlier menopause, suggest that DDT may disrupt the menstrual cycle across life
(67). A recent study of rats showed that high doses of DDT to grandparent rats increased
obesity of their rat grandchildren (79); though the dose was much higher
than found in people, it certainly calls attention to the potential effect that high
DDT use worldwide in the middle of last century may be having on the current
worldwide obesity epidemic.
Negative Endocrine Health Outcome: Type 2 Diabetes (T2D)
Numerous epidemiological studies have demonstrated a strong positive association
between the DDT metabolite DDE and T2D risk (80). These studies came
from countries that have banned DDT use for decades, and also from areas contaminated
with higher levels of DDTs. The diabetes epidemic continues to grow
dramatically in countries where DDT is still in use, such as in South Africa and
India (81-83). These documented human associations are corroborated by studies
demonstrating that both low prenatal- and high adult- exposure to DDT caused
features of T2D in adult rodents (84-86). Indeed experimental studies have shown
that DDT increases circulating blood glucose, a hallmark of diabetes, in part by
increasing enzymes that make glucose (85). Under normal circumstances, increased
glucose levels cause the pancreas to produce insulin, which in turn reduces
glucose. Mice exposed to DDT become insulin resistant, a central feature of T2D,
because their DDT exposure reduces the normal ability of the pancreas to secrete
insulin in response to high glucose (84).
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