Daily News Archive
November 3, 2006
Suspected in Decreasing Fertility Rates
(Beyond Pesticides, November 3, 2006)
As more researchers investigate the effects of environmental exposure
to pesticides and other toxic chemicals, evidence increasingly suggests
that these chemicals contribute to infertility, according to a new article
published in the November edition of Environmental Health Perspectives.
Studies point to affects on both male and female factors contributing
to impaired fecundity.
Recent studies have
indicated negative trends in fertility. Data from the December 2005
report of the Centers for Disease Control and Prevention's National
Survey on Family Growth (NSFG)
reveals the fastest-growing segment of U.S. women with impaired fecundity
(the capacity to conceive and carry a child to term) is those under
25. Based on this report, approximately 12% of American couples experienced
impaired fecundity in 2002. This is a 20% increase from the 6.1 million
couples that reported an inability to have children in 1995.
assessments, wildlife studies, and animal and human studies hint at
multiple factors including: exposure to low-level environmental contaminants
such as phthalates, polychlorinated biphenyls (PCBs), dioxins, pesticides,
and other chemicals may be subtly undermining our ability to reproduce.
Unfortunately, there is lack of definitive information available for
couples experiencing fertility problems due to difficulties in defining
measures of fecundity and research challenges involved when studying
to be more to it than can be explained from traditional understanding
about impacts," says Joseph Isaacs, president and CEO of RESOLVE:
The National Infertility Association. "As a patient advocacy group,
we believe more research into environmental impacts is needed. We fear
that future generations may be at risk because of exposures to toxic
substances as early as in utero."
The study of endocrine
disruption is revealing mechanisms that show how specific environmental
contaminants can alter fertility. A robust body of literature details
reproductive effects in fish,
amphibians, and reptiles
related to exposure to endocrine disruptors. Evidence of these effects
has also been seen in wild mammals such as polar
bears and seals. Laboratory animal experiments have confirmed these
A selection of findings
linking pesticides to impaired human fecundity:
- One key report
was a 12 September 1992 review in the British Medical Journal indicating
significant declines in sperm counts in many countries between 1938
and 1990. The findings were controversial because the reviewed studies
used inconsistent designs and methods. In November 1997, however,
confirmed the findings for males in the United States and indicated
an even sharper decline among European men.
- Researchers saw
significant reductions in sperm concentration, motility, and total
motile sperm in men from Columbia, Missouri, compared with men in
New York City, Minneapolis, and Los Angeles. In an in-depth follow-up
variables between the Columbia and Minneapolis men, the researcher
discovered that the Missouri group had had higher exposure to agricultural
pesticides. Further, men with low sperm counts were more likely to
have higher urine metabolite levels of the pesticides alachlor, atrazine,
metolachlor, and diazinon.
- Another geographically
based study, INUENDO,
investigates risks to human fertility from persistent environmental
organochlorines. The European Commission project centers on Arctic
populations including Swedish fishermen and the Inuit of North America
and Greenland, whose exposure to persistent organic pollutants such
as PCBs and DDT metabolites (including DDE) are among the highest
in the world. "There are many indications from animal studies
and from wildlife studies, but very few indications from human studies
telling us whether we have a problem or not," says Jens Peter
Bonde, M.D., Ph.D., who serves as coordinator of INUENDO.
idea [behind INUENDO] was to go to places in the world where we
know that people have high level of exposures to substances that
are suspected to cause these effects in fertility," says Dr.
Bonde. "That's the reason we went to Greenland and to Sweden,
where fishermen are known to have very high exposure levels; we
have other populations that have lower levels of exposures, so we
have contrasts of exposure." Results published in March 2006
in Human Reproduction suggested a longer time to pregnancy
related to serum concentrations of PCB and DDE in mothers and fathers.
suggested an altered sex ratio of offspring (fewer boys than would
otherwise be expected) related to PCB and DDE exposures.
themselves offer another platform for investigation. Hugh Taylor,
M.D., director of the Yale Center for Research in Reproductive Biology,
leads a team investigating the role of estrogen-regulated Hox genes
that direct uterine development. The researchers initially focused
on DES effects and discovered that the compound alters expression
of the Hoxa10 gene in mice, affecting the tissue type that grows in
the uterus, cervix, and vagina. Effects were triggered only with exposure
during development, but not during adulthood, and later experiments
revealed that the pesticide methoxychlor had similar effects.