Reproductive Health and Fertility Problems

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In the U.S. today, there is increasing concern that environmental contaminants may be harming the reproductive health and fertility of women and men. Reproductive and fertility problems appear to be on the rise.

In women:

  • At least 12% of women reported difficulty in conceiving and maintaining pregnancy in 2002, an increase of 40% from 1982.[1][2] From 1982 to 1995, the prevalence of infertility almost doubled in younger women, ages 18–25.[3][4] A recent update concludes that the trend may have leveled off, although there is disagreement on this.[5][6]
  • infertilityFibroids and other fertility-related diseases, like endometriosis and polycystic ovarian syndrome, are diagnosed more frequently now, which may be the result of a true increase, better detection, or both.[7]

In men:

  • According to a large study of men from the Boston area, testosterone levels in adult men are declining. This decline is not explained by an increase in age or other health or lifestyle factors such as obesity or smoking.[8]
  • Testicular cancer increased by 60% between 1973 and 2003 in the U.S.[9]
  • Sperm counts have declined in men in some areas of the U.S., Europe, and Australia.[10]

In children:

  • In U.S. girls, puberty is beginning earlier than in the past.[11] A weight-of-the-evidence evaluation of human and animal studies suggests that endocrine-disrupting chemicals, particularly estrogen mimics and anti-androgens, as well as increased body fat and certain social circumstances, can advance the onset of puberty.[12][13]
  • Reproductive tract abnormalities are increasing in certain populations. In one analysis of two U.S. surveillance systems, cryptorchidism (undescended testicle(s)) increased 200% between 1970 and 1993.[14] In some surveillance systems, the incidence of hypospadias (deformity of the penis) has increased, whereas in others, increases have leveled off.[15][16]

Testicular dysgenesis syndrome (described below), resulting from in utero exposure to endocrine-disrupting chemicals, has been proposed as an integrating explanation for the observed increases in testicular cancer, congenital abnormalities of the male reproductive tract, and decreases in sperm count.[17] Indeed, a growing and compelling body of evidence suggests that chemical exposures are likely to be influencing many of these trends in females and males.[18][19][20]

The financial consequences of these conditions are highly significant. In 2002, U.S. patients and their insurers spent an estimated $2.9 billion on infertility treatments alone.[21]

The link to chemical exposure

The CDC has published data showing that exposures to endocrine-disrupting chemicals like phthalates, bisphenol A (BPA), perfluorinated compounds, and cadmium are common. The CDC reports that almost everyone has these chemicals in their bodies, some at levels near or above those shown in scientific studies to cause adverse effects on reproductive health.[22][23][24]

Recent investigations show that higher levels of exposure to endocrine-disrupting chemicals are associated with adverse effects on reproductive measures and birth outcomes in the general population, including reduced sperm quality in men, premature birth, low birth weight, and behavioral changes in children.[25][26][27][28][29][30] These findings are consistent with a large body of experimental laboratory data.

The examples below illustrate the reason for concern about exposure to some chemicals and the potential impacts on reproductive health. Unfortunately, there are far more chemicals about which we have little or no data on the potential for negative impacts.

Bisphenol A

baby-bottleOver the past decade, a wealth of new studies has shown that some chemicals can act as endocrine disruptors—chemicals that interfere with normal hormone function and regulation. Among these are animal studies that link prenatal and early-life exposures to BPA, which is found in polycarbonate plastic and some food and beverage can linings, to permanent reproductive changes and increased risks of later reproductive health problems, such as infertility and early puberty.[31][32]

Animal studies also show that prenatal exposures to BPA at levels similar to those experienced by people in the general population alter the development of the prostate and mammary glands, increasing the susceptibility for developing cancer later in life.[33][34] In laboratory animals, including non-human primates, BPA previously was shown to affect the development of the brain, causing changes in gender specific behaviors.[35] Recently, a human study reported that the higher a pregnant woman’s BPA levels were during her first 16 weeks of pregnancy, the more likely her child was to later show behavior somewhat atypical of its gender at age two. Girls engaged in more masculinized behaviors, while boys were more feminized.[36]

Phthalates

A wide range of wildlife populations has been adversely affected by exposure to endocrine-disrupting contaminants. Impacts among birds, fish, shellfish, mammals, and reptiles include decreased fertility and increased reproductive tract abnormalities, feminization and demasculinization in the males, and masculinization and defeminization in the females.[37]

Prenatal exposure to phthalates commonly found in personal care products, as a food contaminant, and in items made from PVC plastic, or vinyl, has been linked to altered development of the male reproductive system and feminized behaviors in boys. Some researchers now group the male birth defects—undescended testicle(s) and deformity of the penis—with two other conditions of the male reproductive tract—low sperm counts and testicular cancer. These four medical conditions are collectively called testicular dysgenesis syndrome (TDS). Animal studies suggest that a TDS-like condition can be observed after fetal exposure to phthalates.[38]

In November 2009, a study of mothers and their children found that boys born to mothers with higher levels of phthalates in their urine during pregnancy were more likely to exhibit feminized behaviors than boys whose mothers had lower levels of exposure.[39]

Perfluorinated chemicals

Studies of perfluorinated chemicals, commonly used in stain-proof and non-stick products, also may negatively affect reproductive health. Some studies have found that higher levels of maternal exposure to these compounds are tied to lower birth weight in newborns.[40][41][42][43] Another study found that Danish men with higher levels of perfluorinated compounds had fewer normal sperm and lower sperm concentrations.[44] A recent study of children living near a perfluorinated chemical production plant found both boys and girls had delayed puberty.[45] These findings are particularly concerning, since exposure to perfluorinated chemicals is nearly ubiquitous in the general population, including in women who are pregnant.[46][47]

Cadmium

Cadmium, a metal used in batteries, pigments, metal coatings, and plastics, is a known testicular toxicant and is linked to gynecological disorders such as endometriosis.[48] It also has been found to have hormonal properties.[49]

How chemical policy reform can help

Playing pattycakeIn June 2009, The Endocrine Society, a professional association devoted to research on hormones and the clinical practice of endocrinology, issued a scientific statement on endocrine-disrupting chemicals, which stated:[50]

The evidence for adverse reproductive outcomes (infertility, cancers, malformations) from exposure to endocrine disrupting chemicals is strong, and there is mounting evidence for effects on other endocrine systems, including thyroid, neuroendocrine, obesity and metabolism, and insulin and glucose homeostasis.

Among the statement’s recommendations for the future is this suggestion:

As endocrinologists, we suggest that The Endocrine Society actively engages in lobbying for regulation seeking to decrease human exposure to the many endocrine-disrupting agents.

In November 2009, the American Medical Association (AMA) passed a resolution introduced by The Endocrine Society that calls for the AMA to work with the federal government to enact new federal policies to decrease the public’s exposure to endocrine-disrupting chemicals.[51]

These “new federal policies” would come through effective reform of TSCA. Authoritative bodies have listed more than 50 industrial chemicals as causing reproductive toxicity.[52] TSCA reform should prioritize action on these and other chemicals—including bisphenol A, phthalates, and perfluorinated chemicals—which have been identified as harmful to reproduction and development. TSCA reform also should require evaluation of the effect of chemicals on reproduction and child development before they are introduced into the market and as a condition for remaining on the market.

Citations:

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  2. Chandra A, 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 2005;23(25).
  3. Chandra A, et al. Impaired fecundity in the United States: 1982–1995. Family Planning Perspectives 1998;30(1):34-42.
  4. Chandra A, 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 2005;23(25).
  5. Stephen E, et al. Declining estimates of infertility in the United States: 1982-2002. Fertility and Sterility 2006;86(3):516-523
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  8. Travison TG, et al. A population-level decline in serum testosterone levels in American men. The Journal of Clinical Endocrinology & Metabolism 2007:92(1):199-201.
  9. Shah M, et al. Trends in testicular germ cell tumours by ethnic group in the United States. International Journal of Andrology 2007;30:206-13.
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  11. Biro F, et al. Pubertal assessment method and baseline characteristics in a mixed longitudinal study of girls. Pediatrics 2010;126(3):3583-3590.
  12. Euling S, et al. Role of environmental factors in the timing of puberty. Pediatrics 2008;121(S3)S167-71.
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  15. Paulozzi L, et al. Hypospadias trends in two U.S. surveillance systems. Pediatrics 1997;100(5):831–34.
  16. Lund L, et al. Prevalence of hypospadias in Danish boys: a longitudinal study. European Urology 2009;55(5):1022-1026.
  17. Main K, et al. Genital anomalies in boys and the environment. Best Practices & Research, Clinical Endocrinology and Metabolism 2010;24(2):279-289.
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  24. Vandenberg LN, et al. Hormones and endocrine-disrupting chemicals: Low-dose effects and nonmonotonic dose responses. Endocrine Review [Internet]. 2012 [cited 2012 March 14]; 33(3) doi:10.1210/er.2011-1050. Available from: http://edrv.endojournals.org/content/early/2012/03/14/er.2011-1050.full.pdf.
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  26. Miao M, et al. In utero exposure to bisphenol-A and its effect on birth weight of offspring. Reproductive Toxicology 2011;32(1):64-8.
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  33. Prins GS, et al. Serum bisphenol A pharmacokinetics and prostate neoplastic responses following oral and subcutaneous exposures in neonatal Sprague-Dawley rats. Reproductive Toxicology 2011;31(1):1-9.
  34. Tharp A, et al. Bisphenol A alters the development of the rhesus monkey mammary gland. Proceedings of the National Academy of Sciences 2012;109(21):8190-8195.
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  40. Apelberg B, et al. Cord serum concentrations of perfluorooctane sulfonate (PFOS) and perfluorooctanoate (PFOA) in relation to weight and size at birth. Environmental Health Perspectives 2007;115(11):1670-1676.
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  49. Byrne C, et al. Cadmium—a metallohormone? Toxicology and Applied Pharmacology 2009:238(3):266-271.
  50. Diamanti-Kandarakis E, et al. Endocrine-disrupting chemicals: an Endocrine Society scientific statement. Endocrine Reviews 2009;30(4):293-342.
  51. American Medical Association Adopts Society’s Endocrine Disrupter Policy [Internet]. Chevy Chase: Endocrine Society; [2009 November 12]. Available from: http://www.endo-society.org/advocacy/insider/AMAAdoptsSocietyEDCPolicy.cfm.
  52. Chemicals Known to the State to Cause Cancer or Reproductive Toxicity List as of June 22, 2012 [Internet]. Sacramento: Proposition 65: The Safe Drinking Water and Toxic Enforcement Act of 1986, California Environmental Protection Agency; [2012 June 22]. Available from: http://oehha.ca.gov/prop65/prop65_list/files/P65single062212.pdf.

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