Chemicals and female reproductive health

What is female reproductive health?

In the context of chemicals and health, female reproductive health is a broad concept encompassing development of the female reproductive organs, sexual development, fertility, and the ability to give birth to healthy babies.

Issues include the age at which girls go through puberty, the age of menopause, the ease with which women can conceive, the chance of complications during pregnancy, the likelihood of giving birth prematurely or to an underweight baby, the healthy development of the foetus, and also diseases specific to the female reproductive system, such as endometriosis, polycystic ovary syndrome (PCOS) or ovarian, uterine, cervical and vaginal cancers.

How can chemicals affect female reproductive health?

Exposure to oestrogen-like chemicals is of particular interest to researchers, due to the hormone’s central role in a woman’s physiology. Clues as to the sorts of reproductive problems that might result from exposure to oestrogen-like chemicals before birth are coming from studying women who took the oestrogenic drug diethylstilbestrol (DES) while pregnant.

Between the 1940s and 1970s DES was prescribed to millions of women to prevent pregnancy complications, but was found to increase their daughters’ risk of developing breast cancer, precancerous lesions in the cervix, infertility and early menopause. Their daughters were also more likely to experience complications during pregnancy, with increased risk of preterm delivery, miscarriage, tubal pregnancy, stillbirth and preeclampsia (Swan 2000).

Subtle influences on reproductive health problems can also have broader health implications. For example, going through puberty early not only increases the risk of psychological problems, it also increases a woman’s lifetime exposure to oestrogen, which is a risk factor in breast cancer. Preterm birth and decreased birth weight increase the risk of a range of developmental and health problems for the newborn child, while early menopause increases a woman’s risk of osteoporosis, colon and ovarian cancer, heart attack and stroke.

To make things even more complicated, female reproductive health is not only determined by the function of oestrogen and other female hormones, but by many physiological processes in the body. For example, thyroid hormones play an important role in sexual maturation. The ways in which chemicals may affect reproductive health is therefore highly complex, particularly when healthy development of the foetus is considered.

How might chemicals be affecting female reproductive health?

The balance of sex hormones during development is critical so oestrogen-like chemicals are of obvious concern including phytoestrogens, some phthalates, BPA, parabens, phenols and UV filters in sunscreens, especially in light of recent research showing that a single exposure to estradiol or testosterone in newborn mice increases their risk of polycystic ovarian syndrome (PCOS) as adults (Sotomayor-Zárate et al. 2011).

Bisphenol A (BPA) is one of the chemicals most well-studied for reproductive health effects and has been found to change the development of the uterus in female primates exposed while in the womb. Possible links are also emerging between higher levels of BPA exposure and reduced numbers of viable eggs in women(Bloom et al. 2011).

The perfluorinated compounds PFOS and PFOA (also known as C8 compounds) have been linked to both delayed puberty in girls (Lopez-Espinosa et al. 2011) and premature menopause in women (Knox et al. 2011), while there is some evidence connecting phthalates, BPA and phenols with early puberty.

There is evidence that phthalates and pesticides have an effect on fertility and pregnancy outcomes, increasing the amount of time it takes a woman to conceive and increasing the risk of preterm birth and decreased birth weight (Burdorf et al. 2011).

PBDE flame retardants may also lower the chance of conception in a given time window (Harley et al. 2010), while phthalates may also increase the risk of endometriosis and uterine fibroids. Animal studies indicate that exposure to dioxin in the womb appears not only to make it more difficult for female offspring to become pregnant, but even the daughters and granddaughters of those offspring in turn (Bruner-Tran & Osteen 2011).

Further Reading

Environmental exposures and mammary gland development. This scientific review concludes that early life environmental exposures can alter breast development and increase susceptibility to breast cancer, and concludes by recommending that effects on breast development should be incorporated in chemical risk assessment.

Flame retardants reduce women’s fertility. Scientific epidemiological study finding that women with higher levels of a certain kind of flame retardant in their blood find it more difficult to conceive.

Little Women. TIME Magazine looks for explanations as to why girls seem to be going through puberty an average of one year earlier than they did 20 years ago.

Selection of references

Bloom MS, Kim D, Vom Saal FS, Taylor JA, Cheng G, Lamb JD, Fujimoto VY. Bisphenol A exposure reduces the estradiol response to gonadotropin stimulation during in vitro fertilization. Fertil Steril. 2011 Sep;96(3):672-677.e2. Epub 2011 Aug 3. PubMed PMID: 21813122; PubMed Central PMCID: PMC3168558.

Bruner-Tran KL, Osteen KG. Developmental exposure to TCDD reduces fertility and negatively affects pregnancy outcomes across multiple generations. Reprod Toxicol. 2011 Apr;31(3):344-50. Epub 2010 Oct 16. PubMed PMID: 20955784; PubMed Central PMCID: PMC3044210.

Burdorf A, Brand T, Jaddoe VW, Hofman A, Mackenbach JP, Steegers EA. The effects of work-related maternal risk factors on time to pregnancy, preterm birth and birth weight: the Generation R Study. Occup Environ Med. 2011 Mar;68(3):197-204. Epub 2010 Dec 20. PubMed PMID: 21172792.

Harley KG, Marks AR, Chevrier J, Bradman A, Sjödin A, Eskenazi B. PBDE concentrations in women’s serum and fecundability. Environ Health Perspect. 2010 May;118(5):699-704. Epub 2010 Jan 13. PubMed PMID: 20103495; PubMed Central PMCID: PMC2866688.

Knox SS, Jackson T, Javins B, Frisbee SJ, Shankar A, Ducatman AM. Implications of early menopause in women exposed to perfluorocarbons. J Clin Endocrinol Metab. 2011 Jun;96(6):1747-53. Epub 2011 Mar 16. PubMed PMID: 21411548; PubMed Central PMCID: PMC3206400.

Lopez-Espinosa MJ, Fletcher T, Armstrong B, Genser B, Dhatariya K, Mondal D, Ducatman A, Leonardi G. Association of Perfluorooctanoic Acid (PFOA) and Perfluorooctane Sulfonate (PFOS) with age of puberty among children living near a chemical plant. Environ Sci Technol. 2011 Oct 1;45(19):8160-6. Epub 2011 May 2. PubMed PMID: 21534542.

Sotomayor-Zárate R, Tiszavari M, Cruz G, Lara HE. Neonatal exposure to single doses of estradiol or testosterone programs ovarian follicular development-modified hypothalamic neurotransmitters and causes polycystic ovary during adulthood in the rat. Fertil Steril. 2011 Dec;96(6):1490-6. Epub 2011 Oct 6. PubMed PMID: 21982285.

Swan SH. Intrauterine exposure to diethylstilbestrol: long-term effects in humans. APMIS. 2000 Dec;108(12):793-804. Review. PubMed PMID: 11252812.