is a birth defect of the penis in which the position of the opening
is shifted from its normal place on the head of the penis to somewhere
along the shaft. The most extreme forms of hypospasias find the
opening at the base, or even in the scrotum. Modest cases of this
debilitating birth defect can be corrected through reconstructive
surgery, but the most extreme cases sometimes cannot. The cause
of hypospadias in humans has not been established, other than
to observe that it must result from a developmental error in the
womb that has prevented complete masculinization of the reproductive
with laboratory animals reveal that hypospadias can be repeatedly
and reliable produced by exposure to several endocrine disrupting
chemicals, including DDE and vinclozilin, a commonly used fungicide.
US Centers for Disease Control undertook a study
of the rate of hypospadias in the US because of these animal studies.
They had become concerned about endocrine disruption and decided
that if it were a real problem, then there should be evidence
in US health trends. They surveyed the animal studies looking
for a reliable effect produced by endocrine disruption that, were
it expressed in humans, would be readily and reliably detected.
They were particularly interested in finding a health endpoint
in which any changes in rate measured over time would not have
been a result of differences in diagnosis or detection. This is
a classic problem in longitudinal health studies. They selected
hypospadias to study because it met these criteria.
CDC's analysis of the changes in the frequency of hypospadias
in the United States revealed a striking pattern: the rate has
more than doubled since 1970. Indeed by 1993, hypospadias was
detected in one out of every 125 boys born in the United States
research has also revealed increases in hypospadias in several
other countries, particularly Japan and Scandinavia. Data
analyzed by Leonard Paulozzi of the US CDC indicates that
the increase in hypospadias in some industrialized countries may
have leveled off in the mid-1980s.
published in 2002 suggests but does not prove an ambiguous link
to exposure to DDE in the womb. The study involved an analysis
of umbilical cord blood kept frozen since it had been sampled
during the period 1959-1965. More...