Toxic Chemicals and Reproductive Health

Identifying the connections

Over the past few decades, the reproductive health of Americans appears to have declined. Diseases, disorders and conditions that affect the development and functioning of the male and female reproductive systems—including fertility problems, miscarriages, pre-term births, low birthweights and certain birth defects—have risen.  In addition, incidence rates of testicular cancer have increased, and breast and prostate cancers remain among the most common forms of cancer in the U.S. The exact role of environmental chemical exposures in reproductive health remains unclear, and a variety of factors likely contribute to these increases. A growing body of scientific evidence, however, has linked exposure to some toxic chemicals to a range of reproductive and childhood developmental problems.

For example, endocrine disruptors, some of which are found in everyday consumer products, can detrimentally mimic, block or change the levels of hormones that control fertility, reproduction and fetal development. Several endocrine-disrupting chemicals are common in the environment and have been found both in breast milk and umbilical cord blood. A brief overview of these chemicals and their effects observed in human and animal studies is presented in the chart on the next page.

Scientists have identified fetal development and the first few years of life as critical windows of vulnerability to endocrine-disrupting chemicals. Exposures to a variety of chemicals at conception, in pregnancy or during infancy can disrupt hormones and cause irreparable, lifelong damage or injury that may not become apparent until adulthood. Some studies suggest this harm, when it involves sperm or egg cells, may even extend into the next generation.

Although TSCA was enacted in 1976, most of the 80,000 chemicals in commerce have not been tested for reproductive health effects, nor have there been meaningful regulatory actions to manage exposure to most reproductive toxins. Eighty percent of the 3,000 high production volume chemicals in commerce have not been tested for developmental or pediatric toxicity. More than 700 of these chemicals are used in consumer products, resulting in widespread exposure to chemical mixtures. Surveys by the U.S. Centers for Disease Control and Prevention have identified measurable levels of more than 200 synthetic chemicals in the blood and urine of Americans, and virtually everyone in the United States has at least some of these substances in their bodies. The actual risk posed to people by these complex mixtures has yet to be determined, but even the limited data indicate that manufacturers, regulators, physicians and consumers should pay close attention to the emerging scientific evidence as new national policies are developed.


References:

1 Karen Perry Stillerman et al., “Environmental Exposures and Adverse Pregnancy Outcomes: A Review of the Science,” Reproductive Sciences 15, no. 7 (2008): 631-650. 
2 Anjani Chandra and Elizabeth Hervey Stephen, “Impaired Fecundity in the United States: 1982-1995,” Family Planning Perspectives 30, no. 1 (1998): 34-42. 
3 Anjani Chandra et al., “Fertility, Family Planning, and Reproductive Health of U.S. Women: Data from the 2002 National Survey of Family Growth,” National Center for Health Statistics, Vital and Health Statistics 23, no. 25 (2005). 
4 Stephanie J. Ventura et al., “Estimated Pregnancy Rates by Outcome for the United States, 1990-2004,” National Center for Health Statistics, National Vital Statistics Reports 56, no. 15 (2008). 
5 Stephanie J. Ventura et al., “Trends in Pregnancies and Pregnancy Rates by Outcome: Estimates for the United States, 1976-96,” National Center for Health Statistics, Vital and Health Statistics 21, no. 56 (2000). 
6 T.J. Mathews and Marian F. MacDorman, “Infant Mortality Statistics from the 2005 Period Linked Birth/Infant Death Data Set,” National Vital Statistics Reports 57, no. 2 (2008). 
7 Laurence S. Baskin, Katherine Himes and Theo Colborn, “Hypospadias and Endocrine Disruption: Is There a Connection?” Environmental Health Perspectives 109, no. 11 (2001): 1175-1183. 
8 Shanna H. Swan, Eric P. Elkin and Laura Fenster, “The Question of Declining Sperm Density Revisited: An Analysis of 101 Studies Published 1934-1996,” Environmental Health Perspectives 108, no. 10 (2000): 961-966.
9 Mona N. Shah et al., “Trends in Testicular Germ Cell Tumours by Ethnic Group in the United States,” International Journal of Andrology 30, no. 4 (2007): 206-213.
10 Jackie M. Schwartz and Tracey J. Woodruff, Shaping Our Legacy: Reproductive Health and the Environment, (San Francisco: University of California, San Francisco, and the Collaborative on Health and the Environment, 2008),
http://www.prhe.ucsf.edu/prhe/pubs/shapingourlegacy.pdf (accessed May 11, 2010). 
11 P.D. Darbre, “Environmental Oestrogens, Cosmetics and Breast Cancer,” Best Practices & Research. Clinical Endocrinology & Metabolism 20, no. 1 (2006): 121-143.
12 Lorenzo Richiardi, Andreas Pettersson and Olof Akre, “Genetic and Environmental Risk Factors for Testicular Cancer,” International Journal of Andrology 30, no. 4 (2007): 230-240.
13 Schwartz and Woodruff, Shaping Our Legacy: Reproductive Health and the Environment. 
14 Gina M. Solomon and Pilar M. Weiss, “Chemical Contaminants in Breast Milk: Time Trends and Regional Variability,” Environmental Health Perspectives 110, no. 6 (2002): A339-A347. 
15 Josef G. Thundiyil, Gina M. Solomon and Mark D. Miller, “Transgenerational Exposures: Persistent Chemical Pollutants in the Environment and Breast Milk,” Pediatric Clinics of North America 54, no. 1 (2007): 81-101.
16 Gilbert Schonfelder et al., “Parental Bisphenol A Accumulation in the Human Maternal-Fetal-Placental Unit,” Environmental Health Perspectives 110, no. 11 (2002): A703-A707.
17 Giuseppe Latini et al., “In Utero Exposure to Di-(2-ethylhexyl)phthalate and Duration of Human Pregnancy,” Environmental Health Perspectives 111, no. 14 (2003): 1783-1785.
18 Retha R. Newbold and Jerrold J. Heindel, “Developmental Exposures and Implications for Early and Latent Disease,” in Environmental Impacts on Reproductive Health and Fertility, ed. Tracey J. Woodruff et al., (Cambridge: Cambridge University Press, 2010). 
19 Sherry G. Selevan, Carole A. Kimmel and Pauline Mendola, “Identifying Critical Windows of Exposure for Children's Health,” Environmental Health Perspectives 108, Suppl. 3 (2000): 451-455. 
20 Andrew D. Crain et al., “Female Reproductive Disorders: The Roles of Endocrine-Disrupting Compounds and Developmental Timing,” Fertility and Sterility 90, no. 4 (2008): 911-940. 
21 Evanthia Diamanti-Kandarakis et al., “Endocrine-Disrupting Chemicals: An Endocrine Society Scientific Statement,” Endocrine Reviews 30, no. 4 (2009): 293-342.
22 Michael K. Skinner, Mohan Manikkam and Carlos Guerrero-Bosagna, “Epigenetic Transgenerational Actions of Environmental Factors in Disease Etiology,” Trends in Endocrinology and Metabolism 21, no. 4 (2010): 214-222.
23 Randy L. Jirtle and Michael K. Skinner, “Environmental Epigenomics and Disease Susceptibility,” Nature Reviews Genetics 8, no. 4 (2007): 253-262.
24 Association of Reproductive Health Professionals, Environmental Impacts on Reproductive Health, (Washington: ARHP Clinical Proceedings, 2010),
http://www.arhp.org/uploadDocs/CPRHE.pdf (accessed June 8, 2010).
25 Lynn R. Goldman and Sudha Koduru, “Chemicals in the Environment and Developmental Toxicity to Children: A Public Health and Policy Perspective,” Environmental Health Perspectives 108, no. 3 (2000): 443-448. 
26 Ibid. 
27 Centers for Disease Control and Prevention, Fourth National Report on Human Exposure to Environmental Chemicals, (Atlanta: Department of Health and Human Services, 2009),
http://www.cdc.gov/exposurereport/ (accessed March 27, 2010). 
28 National Research Council, Phthalates and Cumulative Risk Assessment: The Task Ahead, (Washington: National Academy Press, 2008).