Daily News Archive
From November 3, 2006                                                                                                        

Pesticides 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.

Environmental exposure 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 environmental contaminants.

"There seems 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 wildlife findings.

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, a review 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 study comparing 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.

    "The basic 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. Additional results suggested an altered sex ratio of offspring (fewer boys than would otherwise be expected) related to PCB and DDE exposures.

  • Genes 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.

Source: Environmental Health Perspectives