Subscribe to RSS
DOI: 10.1055/s-0044-1800828
Environment and Reproduction
Human reproduction is a highly inefficient process. Infertility, the failure to conceive after 12 months of regular unprotected sexual intercourse, affects 15 to 25% of couples and may be caused by a range of abnormalities of the ovaries, uterus, fallopian tubes, endocrine system, and testes, among others.[1] [2] Impaired fecundity, which encompasses both infertility and difficulty carrying a pregnancy to birth, is estimated to affect twice as many couples, given the high rate of pregnancy loss.[3] [4] While it is unclear whether these estimates are increasing,[5] the use of infertility treatments has skyrocketed over the past two decades,[6] [7] suggesting that reproductive health may be on the decline. Corroborating this further is evidence of earlier puberty onset,[8] declining sperm counts,[9] increasing prevalence of congenital genital abnormalities,[10] and higher rates of pregnancy loss.[11] Due to the universal and rapid increase in these trends, new or increasing exposures to environmental pollutants are strongly suspected in the etiology.
This issue of Seminars in Reproductive Medicine provides a comprehensive update on how environmental exposures impact all aspects of reproduction in men and women including gynecological health, fertility, pregnancy outcomes, and reproductive aging. We start with two reviews that focus on the role of environmental exposures on gynecological conditions common among women. The first is a review authored by Drs. Peebles and Mahalingaiah on how environmental exposures, including air pollution, micro- and nanoplastics, heavy metals, and endocrine-disrupting chemicals, affect polycystic ovary syndrome (PCOS). PCOS, a hormonal condition characterized by irregular periods, excess androgen levels, and cysts in the ovaries, is the most common cause of anovulation and a leading cause of infertility.[12] It is also associated with a range of longer-term comorbidities.[12] Next, Drs. Fuzak and Pollack summarize the literature on nonpersistent endocrine-disrupting chemicals such as phthalates, bisphenols, and benzophenones, in relation to endometriosis. Endometriosis—a disease in which tissue similar to the lining of the uterus grows outside the uterus—is also a chronic, all-to-common gynecologic condition, associated with infertility and adverse pregnancy outcomes in women.[13] Since both of these gynecological conditions are characterized by hormonal disruptions, endocrine-disrupting chemicals are strongly hypothesized to play a role in their etiology.
We then have two reviews focused on the role of environmental exposures in male fertility and reproduction. The first one is a review by Dr. Pilsner and colleagues summarizing the epidemiologic and experimental literature on male exposure to per- and polyfluoroalkyl substances (PFAS) in relation to reproductive outcomes, with a focus on sperm epigenetics. Epigenetic changes in the sperm induced by environmental exposures is a biological pathway of growing interest to explain the relationships of exogenous chemicals, such as PFAS, with fertility outcomes as well as a couple's pregnancy outcomes. In the second review, Dr. Mitsunami and coauthors summarize their literature search aimed at identifying common study design characteristics of articles evaluating the relation between environmental hazards and male fertility (e.g., semen quality). They examine the ways in which each of these study design features limits progress on male fertility research and propose strategies to go beyond them and to advance the field.
The fifth review, by Dr. Hollenbach and others, then shifts the reader's focus to pregnancy and dives into the extensive literature on environmental exposures and a range of adverse pregnancy outcomes such as pregnancy loss and preterm birth while highlighting biological mechanisms that might explain the associations (e.g., inflammation, oxidative stress). Finally, our sixth and last review from Dr. Wu and colleagues summarizes the evidence on endocrine-disrupting chemicals such as heavy metals and PFAS and female reproductive aging. While ovarian follicle decline begins before birth, the depletion process becomes accelerated in women's mid-30s and cumulates at menopause. Studies seeking to quantify reproductive aging, therefore, tend to focus on proxies of ovarian reserve in reproductive-aged women, such as antral follicle count or anti-Mullerian hormone, and timing of menopause. As with many of the outcomes studied in the collection, accelerated ovarian aging not only impacts the length of a woman's childbearing years but also has far-reaching implications for many long-term outcomes such as cardiovascular and other chronic diseases.
Pollutants are in the food we eat, the water we drink, and the air we breathe. They are also found in the products we use throughout our daily lives. This makes exposure to potentially harmful chemicals an increasingly common health concern in the modern world, particularly for reproductive-aged men and women. As all of these reviews touch on, there is growing evidence that environmental exposures adversely impact human reproduction. As more couples delay parenthood,[14] more couples will encounter difficulties conceiving. Therefore, understanding the environmental drivers of human fertility is essential.
Publication History
Article published online:
10 March 2025
© 2025. Thieme. All rights reserved.
Thieme Medical Publishers, Inc.
333 Seventh Avenue, 18th Floor, New York, NY 10001, USA