FIGO committee opinion: Environmental drivers of gynecologic and reproductive health

This paper is an output of the FIGO Committee on Climate Change and Toxic Environmental Exposures, with significant contribution from the University of California, San Francisco Program on Reproductive Health and the Environment (UCSF PRHE). ND contributed significantly to oversight and management of all content, scientific writing, evidence review, and cognitive input. JZ, AH, KG, DD, FE, and DG contributed significantly to scientific writing, evidence review, and cognitive input. RS contributed significantly to scientific writing and evidence review. EM contributed significantly to scientific writing and cognitive input. BD contributed significantly to cognitive input.

Environmental exposures can influence hormonal regulation, ovarian function, and overall reproductive health. For patients seeking fertility treatment, managing menstrual disorders, or living with chronic gynecologic conditions such as endometriosis, PCOS, or fibroids, environmental risk reduction is an increasingly relevant aspect of care. While clinicians do not need to be toxicology experts, they can offer practical, evidence‐based advice to help patients reduce exposures that may impair reproductive health or interfere with treatment outcomes. Diet is a foundational pillar of reproductive health counseling. Patients should be encouraged to consume a nutrient‐rich, anti‐inflammatory diet that emphasizes whole grains, fresh fruits and vegetables, plant‐based fats, and lean proteins. Emphasizing organic produce—particularly for items known to carry high pesticide residues—can help reduce exposure to endocrine‐disrupting chemicals like organophosphates. 6 Reducing intake of ultra‐processed foods and foods packaged in plastics can also lower dietary exposure to phthalates and BPA. 2 , 61 , 77 Patients attempting conception may benefit from additional counseling on prenatal supplements that are certified for purity, free from heavy metals and industrial solvents. 78 For individuals with reproductive health conditions such as PCOS or fibroids, lifestyle interventions are often the first line of management. Moderate physical activity and weight regulation can improve hormonal balance and reduce systemic inflammation. In fact, recent large‐scale research also shows that accumulating around 7000 steps daily (about 3 miles or 5 km) can reduce overall cancer risk by approximately 11%, with 9000 steps linked to a 16% reduction. 79 Lifestyle counseling should also include awareness of environmental exposures that may offset these gains. Avoiding tobacco smoke, limiting alcohol, and staying hydrated with water stored in glass or stainless‐steel containers are all simple but impactful recommendations. Patients living in urban areas or regions with frequent air quality alerts should be advised to avoid outdoor exertion on high pollution days, especially during ovulation or assisted reproduction cycles. 1 , 80 Many personal care products contain chemicals known to disrupt endocrine function or mimic estrogen, including parabens, phthalates, and certain ultraviolet filters. Patients should be encouraged to choose “fragrance‐free” or “parabens‐free” rather than “unscented” products with transparent ingredient labeling. 78 This includes body lotions, hair sprays, cosmetics, and menstrual hygiene products. Repeated low‐dose exposures to these products over time have been linked to conditions such as endometriosis, uterine fibroids, and earlier menopause. 1 Toxic chemicals can also accumulate in the home. Patients should be advised to improve indoor air quality by ventilating living spaces and using high‐efficiency particulate air (HEPA) filters. Drycleaning should be limited given its use of toxic chemicals and dry‐cleaned garments should be aired out separately prior to wearing due to solvent residues. 3 Cleaning products should be evaluated for respiratory irritants or chemical fragrances, which can act as hormone disruptors. Whenever possible, patients can opt for homemade alternatives using vinegar, baking soda, and castile soap. For patients with unexplained infertility, clinicians may also consider screening for exposure to heavy metals or persistent organic pollutants, especially in older homes or near industrial sites. 2 , 78 Occupational exposures remain an underrecognized contributor to reproductive dysfunction. Patients working in cosmetology, agriculture, manufacturing, laboratories, or janitorial services can be exposed to higher levels of chemicals that affect ovarian function or menstrual regulation. Clinicians can normalize the conversation around workplace safety and encourage patients to report concerns. In some cases, consultation with an occupational health specialist may be warranted, particularly if fertility treatment is planned or ongoing. 6 Use of adequate personal protective equipment, proper ventilation, and material safety data sheets (MSDS) are practical tools to enhance workplace safety and reduce cumulative exposure. By incorporating these practical, accessible strategies into routine gynecologic and fertility care, clinicians can empower patients to take an active role in protecting their reproductive health. As scientific literature continues to evolve, early engagement with environmental health can support better outcomes and reduce disparities in reproductive care.

There was no funding received for this study.

Environmental exposures affecting gynecologic and reproductive health are not experienced equally. Structural inequalities—including racial segregation, occupational risk, environmental zoning, and limited access to clean water, safe housing, or healthy food—contribute to disproportionate rates of infertility, fibroids, hormone‐related cancers, and reproductive aging among marginalized populations. For instance, uterine fibroids disproportionately affect women of African descent in the USA, where black women are 2–3 times more likely to develop fibroids than white women, often experiencing earlier onset and more severe symptoms. 96 Similar disparities have been documented in Brazil, the Caribbean, and sub‐Saharan Africa, reflecting a global trend of higher fibroid prevalence and morbidity in women of African ancestry. 96 , 97 , 98 Addressing these inequities requires more than individual‐level counseling. OBGYNs must engage in policy and systems‐level interventions that shift the structural conditions driving disproportionate exposure and disease. This includes supporting regulations that restrict toxic chemicals, advocating for environmental justice policies at the local and national level, and partnering with public health agencies to improve environmental surveillance and community protections. Within healthcare systems, OBGYNs can lead initiatives to incorporate environmental screening into electronic health records, promote safer product procurement, and educate peers and trainees about environmental health literacy. Practical examples might include engagement of OBGYNs in policy and systems‐level interventions that shift the structural conditions driving disproportionate exposure and disease. Within healthcare systems, OBGYNs can help with the cascade of information to lead initiatives that incorporate environmental screening into electronic health records, promote safer product procurement, and educate peers and trainees about environmental health literacy. This includes informing and supporting regulations that restrict toxic chemicals, advocating for environmental justice policies at the local and national level, and partnering with public health agencies to improve environmental surveillance and community protections. National OBGYN colleges and societies are also responsible for the education and training of the future of healthcare workers and clinicians providing care in these areas and they all must urgently include environmental exposures as part of education and continued professional development curricula. Professional responsibility extends beyond clinical excellence—it includes the ethical imperative to act on upstream determinants of reproductive health. As trusted voices in the care of women and gender‐diverse individuals, OBGYNs are uniquely positioned to influence both public policy and clinical practice. By aligning environmental advocacy with reproductive health equity, the specialty can help ensure that all patients—regardless of race, income, or geography—have a fair opportunity to conceive, carry, and control their reproductive lives in safe and healthy environments.

Environmental exposures are increasingly recognized as important contributors to both female and male infertility, affecting core reproductive processes such as hormone regulation, oocyte maturation, spermatogenesis, and gamete viability. According to the evidence summarized in Table  2 , several key environmental agents—including EDCs, air pollution, heavy metals, and microplastics—demonstrate high‐level associations with impaired fertility outcomes in both sexes. Multiple high‐quality reviews have identified a range of environmental exposures that negatively affect female fertility (Table  2 ). Ambient air pollution—including particulate matter (PM 2.5 , PM 10 ) and nitrogen dioxide—has been associated with reduced ovarian reserve, as reflected by lower AMH levels and decreased antral follicle count. 28 Similarly, formaldehyde, an airborne chemical found in industrial and indoor environments, has been recognized as a reproductive toxicant by the US Environmental Protection Agency. 29 Among EDCs, BPA is one of the most well‐documented. BPA exposure can increase the risk of impaired ovarian function and has been linked to decreased fecundability. 30 , 31 Plastics, particularly microplastics, have emerged as a novel concern for reproductive health. Systematic review findings indicate potential effects on ovarian function and hormone balance, although human data remain limited and evolving. 32 A growing body of systematic reviews and toxicological assessments has identified several environmental exposures that negatively impact male reproductive health. Among the most consistently implicated are air pollutants, EDCs, heavy metals, pesticides, and microplastics (Table  2 ). Air pollution, including formaldehyde, PM 2.5 , and polycyclic aromatic hydrocarbons, can increase the risk of reduced sperm quality and increased oxidative stress in reproductive tissues. The US Environmental Protection Agency and systematic reviews and have identified formaldehyde as a reproductive toxicant. 29 , 33 , 34 Endocrine disruptors such as PFAS and phthalates can impair testosterone production, leading to reduced semen quality, and increased sperm DNA fragmentation. For example, phthalates are known to increase adverse male reproductive health effects. 3 These compounds act on the hypothalamic–pituitary–gonadal axis, disrupting hormonal balance essential for spermatogenesis. 7 , 35 Heavy metals such as lead and cadmium have been linked to oxidative damage, abnormal hormone profiles, and decreased fertility. 36 , 37 , 38 Pesticide exposure has been shown to significantly reduce sperm count, motility, and morphology, especially in occupationally exposed individuals. 39 Emerging evidence on microplastics suggests potential disruption of testicular function and endocrine balance, although human data remain limited. 32 Counseling opportunity: For couples pursuing assisted reproductive technologies, particular attention should be paid to environmental exposures that can affect ovarian reserve and sperm quality. Patients with diminished ovarian reserve may be more vulnerable to cumulative environmental insults, and male partners should be counseled on avoiding extreme heat exposure, tobacco smoke, and occupational or chemical exposures known to impair spermatogenesis. Counseling opportunity: For couples pursuing assisted reproductive technologies, particular attention should be paid to environmental exposures that can affect ovarian reserve and sperm quality. Patients with diminished ovarian reserve may be more vulnerable to cumulative environmental insults, and male partners should be counseled on avoiding extreme heat exposure, tobacco smoke, and occupational or chemical exposures known to impair spermatogenesis. While its etiology is multifactorial, emerging evidence suggests that environmental exposures—particularly EDCs—may play a significant role in the development and severity of PCOS. These exposures can interact with genetic, metabolic, and hormonal pathways, influencing the onset and progression of the syndrome. EDCs have emerged as potential contributors to the development and severity of PCOS. One of the most studied compounds in this category is BPA, a chemical widely used in plastics and food packaging. In a multicenter case–control study conducted among women of reproductive age, BPA exposure was significantly associated with increased odds of PCOS. 40 This association was observed alongside elevated levels of BPA analogs, suggesting that cumulative exposure to structurally similar compounds may further exacerbate endocrine disruption. Although classified as Level 2b evidence due to its observational design, the findings from this large, multisite study 40 reinforce growing concern about BPA's impact on hormonal balance and ovarian function. Mechanistically, animal models show that BPA disrupts ovarian glucose metabolism and insulin sensitivity by downregulating the glucose transporter GLUT4 in ovarian granulosa cells via activation of the aryl hydrocarbon receptor (AHR), which contributes to insulin resistance—a central feature of PCOS. 41 Additional human and animal studies have demonstrated that BPA can directly stimulate androgen production in ovarian theca cells and is positively correlated with circulating testosterone and androstenedione levels. 42 Counseling opportunity: Lifestyle modification remains a cornerstone of PCOS management and clinicians should counsel patients on practical changes that can significantly improve symptoms. A low carbohydrate, low glycemic diet can enhance insulin sensitivity and support weight management—both critical factors in reducing androgen excess and restoring ovulatory function. Even modest weight loss (5%–10% of body weight) has been shown to improve menstrual regularity and metabolic outcomes. Counseling opportunity: Lifestyle modification remains a cornerstone of PCOS management and clinicians should counsel patients on practical changes that can significantly improve symptoms. A low carbohydrate, low glycemic diet can enhance insulin sensitivity and support weight management—both critical factors in reducing androgen excess and restoring ovulatory function. Even modest weight loss (5%–10% of body weight) has been shown to improve menstrual regularity and metabolic outcomes. While the exact pathophysiology of endometriosis remains unclear, it is widely accepted as a multifactorial disease, influenced by genetic, environmental, and immune factors. 43 , 44 Environmental exposures, particularly to EDCs, have gained attention as potential contributors to the disease. Emerging evidence implicates several environmental toxicants, particularly organochlorine chemicals, in the development and progression of endometriosis. Systematic reviews have found that organochlorine exposures, such as organochlorine pesticides, polychlorinated biphenyls (PCBs), and dioxins, can increase the risk of endometriosis (Table  2 ). These are also persistent organic pollutants (POPs) known for their endocrine‐disrupting and immunomodulatory properties. 45 These agents may contribute to endometriosis pathogenesis by mimicking estrogen, promoting local inflammatory responses, and interfering with progesterone signaling, which is essential for normal endometrial differentiation and immune tolerance. 46 For example, dioxins can mimic estrogen, enhancing local estrogen production in ectopic endometrial cells through upregulated aromatase activity and steroidogenic factor‐1 (SF1) overexpression 47 on one hand, and progesterone resistance on the other, thus exacerbating lesion growth, as progesterone usually suppresses endometrial proliferation. 48 Counseling opportunity: Nutritional modifications that focus on avoiding harmful chemicals and promoting anti‐inflammatory and antioxidant‐rich foods may help alleviate symptoms and potentially slow disease progression. Being mindful of the use of daily products can also be crucial in minimizing EDC exposure, as several everyday items, particularly those in personal care and food storage, contain known endocrine disruptors. Counseling opportunity: Nutritional modifications that focus on avoiding harmful chemicals and promoting anti‐inflammatory and antioxidant‐rich foods may help alleviate symptoms and potentially slow disease progression. Being mindful of the use of daily products can also be crucial in minimizing EDC exposure, as several everyday items, particularly those in personal care and food storage, contain known endocrine disruptors. Uterine fibroids, or leiomyomata, are hormone‐responsive tumors increasingly linked to environmental exposures. Based on Table  2 , several classes of toxicants—including EDCs and heavy metals—have been associated with increased fibroid risk. Among EDCs, phthalates have been identified as a key concern. Analysis from the FORGE cohort showed altered microRNA expression in fibroid tissue with higher phthalate exposure, suggesting both hormonal and epigenetic disruption. 49 Additional endocrine‐active agents such as organophosphate esters and phenols, which are commonly found in flame retardants and consumer plastics, have also been associated with fibroid development. 50 , 51 Heavy metals, including mercury, cadmium, and lead, have been associated with fibroid prevalence in population studies. Data from NHANES revealed a dose‐dependent relationship between blood levels of these metals and fibroid risk. 52 , 53 Although the evidence is classified as Level 2b, the consistent findings and biologic plausibility—through oxidative stress, inflammation, and estrogenic mimicry—underscore a meaningful connection between toxicant exposure and fibroid pathogenesis. Counseling opportunity: Practical guidance includes avoiding personal care products with phthalates or synthetic fragrances, minimizing the use of plastic containers for food storage especially when heated, and opting for “fragrance‐free” household products. Counseling opportunity: Practical guidance includes avoiding personal care products with phthalates or synthetic fragrances, minimizing the use of plastic containers for food storage especially when heated, and opting for “fragrance‐free” household products. Emerging research suggests that environmental exposures may influence the timing and progression of menopause through mechanisms involving endocrine disruption, oxidative stress, and accelerated ovarian aging. Key contributors include PFAS, phthalates, persistent POPs, and heavy metals. Phthalates, commonly found in plastics and personal care products, have been associated with altered sex hormone profiles and earlier onset of menopause. These compounds act as endocrine disruptors, interfering with estrogen synthesis and signaling, which may contribute to premature ovarian insufficiency. 53 PFAS exposure has been linked to increased likelihood of natural menopause, independent of confounders. These chemicals persist in the body and may disrupt steroid hormone production and follicular survival. 54 Additionally, POPs—including pesticides, PCBs, and dioxins—have been associated with early menopause. These agents accumulate in adipose tissue and interfere with hormonal homeostasis, potentially disrupting the hypothalamic–pituitary–ovarian axis. 55 Heavy metals such as arsenic, cadmium, and mercury have been associated with reduced ovarian reserve and earlier menopausal transition. These metals are believed to exert toxicity through oxidative stress and direct follicular damage, leading to accelerated depletion of the oocyte pool. 56 Collectively, these findings suggest that long‐term, low‐dose exposure to environmental toxicants may alter the natural trajectory of reproductive aging, highlighting the importance of environmental history in midlife care. Counseling opportunity: For women approaching or undergoing the menopausal transition, clinicians should provide counseling on reducing environmental exposures that may accelerate ovarian aging or worsen menopausal symptoms. Framing these changes as part of preventive midlife care can empower women to take control of modifiable risk factors that may influence the timing and experience of menopause. Counseling opportunity: For women approaching or undergoing the menopausal transition, clinicians should provide counseling on reducing environmental exposures that may accelerate ovarian aging or worsen menopausal symptoms. Framing these changes as part of preventive midlife care can empower women to take control of modifiable risk factors that may influence the timing and experience of menopause. Environmental exposures—including EDCs, air pollutants, heavy metals, pesticides, and industrial particulates—are increasingly implicated in the pathogenesis of gynecologic cancers. These agents can disrupt hormonal signaling, promote chronic inflammation, impair immune surveillance, and induce DNA damage, all of which contribute to carcinogenesis in hormone‐sensitive tissues. Furthermore, EDCs can lead to proliferation of hormone‐sensitive tissue (e.g. breast, endometrium, ovaries), genomic instability, altered immune surveillance, and carcinogenesis via estrogen receptor activation and epigenetic changes. 57 , 58 , 59 , 60 , 61 Specifically, PFAS have been associated with ovarian cancer risk through mechanisms involving estrogen receptor modulation and interference with immune surveillance. 62 PFAS are persistent compounds that accumulate in the body and are known to disrupt steroid hormone signaling, potentially contributing to ovarian carcinogenesis. In addition, talc and asbestos, both mineral dusts, can increase the risk of ovarian cancer due to their inflammatory and possibly genotoxic effects when introduced into the pelvic cavity. 63 , 64 Chronic exposure may contribute to cellular transformation via mesothelial irritation and promotion of oxidative stress pathways. Uterine cancer has been associated with environmental exposures to PFAS, which can influence hormone‐sensitive endometrial tissues. These substances may act through estrogenic mechanisms and persistent endocrine disruption, increasing risk for endometrial hyperplasia and malignancy. 65 Although further mechanistic studies are needed, existing evidence supports a biologically plausible link between PFAS exposure and uterine carcinogenesis, particularly in hormonally sensitive individuals. Airborne carcinogens such as ethylene oxide, nitrogen dioxide (NO 2 ), polycyclic aromatic hydrocarbons, benzene, and secondhand smoke have been associated with elevated breast cancer risk, particularly through mechanisms involving DNA damage, oxidative stress, and endocrine interference. 62 , 64 , 66 , 67 , 68 Among EDCs, the PCBs, PFAS, and brominated flame retardants have been shown to accumulate in breast tissue and interfere with estrogen receptor activity, potentially initiating or promoting tumor growth. 69 , 70 , 71 , 72 Cadmium, a known xenoestrogen, has been identified as a contributor to breast cancer risk by mimicking estrogen at the cellular level and promoting proliferation of hormone‐sensitive tissue. 73 Additional nonchemical exposures such as light at night, which disrupts circadian regulation of melatonin, have also been implicated in breast cancer development due to altered hormonal signaling. 74 Pesticide exposure, particularly to dichlorodiphenyltrichloroethane (DDT) and related compounds, has also been associated with increased breast cancer risk. These compounds can persist in adipose tissue, where they may act as estrogen mimics and disrupt normal hormone signaling pathways. 75 Counseling opportunity: Physical activity and maintaining a healthy body mass index are essential to reduce estrogen dominance from adipose tissue. A pooled study by the American Cancer Society, NCI, and Harvard found that meeting the equivalent of 2.5–5 h per week of moderate activity—such as brisk walking—was linked to a 6%–10% lower risk of breast cancer. 76 Counseling opportunity: Physical activity and maintaining a healthy body mass index are essential to reduce estrogen dominance from adipose tissue. A pooled study by the American Cancer Society, NCI, and Harvard found that meeting the equivalent of 2.5–5 h per week of moderate activity—such as brisk walking—was linked to a 6%–10% lower risk of breast cancer. 76

To guide the development of this article, we used a structured committee consensus process to determine which gynecologic and reproductive health outcomes would be included. The selection was based on two primary criteria: (1) existence of a substantial, high‐quality body of evidence linking the outcome to environmental exposures; and (2) relevance and applicability of the outcome to clinical practice in diverse geographic, economic, and healthcare contexts. The committee included experts in gynecology, reproductive endocrinology, environmental epidemiology, and global women's health. Outcomes were selected through a series of iterative discussions, with the goal of prioritizing conditions that are common, clinically significant, and potentially modifiable through environmental risk reduction. The final set of outcomes includes infertility, diminished ovarian reserve, endometriosis, polycystic ovary syndrome (PCOS), uterine fibroids, menopause, and hormonally mediated cancers such as breast, endometrial, and ovarian cancer. These outcomes reflect a wide spectrum of reproductive life stages and conditions where environmental exposures are known or strongly suspected to contribute to pathophysiology, symptom burden, or disease progression. We scoped the literature for high‐quality evidence evaluating the association between prenatal environmental exposures and the outcomes of interest. We searched PubMed for recent, relevant systematic reviews published in the English language on April 1, 2025. The search yielded 674 articles, which were then screened for relevance. We supplemented this by searching the websites of authoritative bodies for applicable evidence. For outcomes with limited systematic reviews and consensus statements, we sought high‐quality primary literature. We tiered the evidence according to the following categorizations: Level 1 Evidence includes systematic reviews that evaluated the certainty in the body of evidence using the Grading of Recommendations Assessment, Development and Evaluation (GRADE) approach or other equivalent methods, which we can rely on to draw conclusions on whether there is an association between exposure and outcome. Level 2a Evidence includes systematic reviews that conducted a risk of bias assessment and meta‐analysis but did not evaluate certainty in the body of evidence, and therefore, we are less confident in our ability to draw conclusions from their findings. Level 2b Evidence includes well‐designed primary studies. Level 1 Evidence includes systematic reviews that evaluated the certainty in the body of evidence using the Grading of Recommendations Assessment, Development and Evaluation (GRADE) approach or other equivalent methods, which we can rely on to draw conclusions on whether there is an association between exposure and outcome. Level 2a Evidence includes systematic reviews that conducted a risk of bias assessment and meta‐analysis but did not evaluate certainty in the body of evidence, and therefore, we are less confident in our ability to draw conclusions from their findings. Level 2b Evidence includes well‐designed primary studies. Specifically, we prioritized systematic reviews that utilized methods endorsed by the United States National Academies of Sciences, Engineering, and Medicine, including the National Toxicology Program's approach and the Navigation Guide methodology. 7 , 23 , 24 , 25 , 26 , 27 Table  2 is organized by health outcomes (infertility, PCOS, endometriosis, uterine fibroids, menopause, and gynecologic cancer) and lists environmental exposures with supporting references. By grouping exposures alongside specific reproductive health outcomes, the table highlights recurring patterns—such as the role of air pollution and EDCs across multiple conditions—and underscores areas where high‐level evidence, including systematic reviews and meta‐analyses, has established causality or strong associations. This organization also makes it easier for clinicians and policymakers to translate scientific findings into targeted interventions and preventive strategies. Of note, all studies meet at least Level 2b Evidence: well‐designed primary studies. Systematic reviews and meta‐analyses are designated in bold. Toxic environmental exposures and reported associations with adverse reproductive health outcomes. Air pollution Ambient air pollution (PM 2.5 , PM 10 , nitrogen dioxide) 28* Formaldehyde 29 Ambient air pollution (PM 2.5 , PM 10 , nitrogen dioxide) 28* Formaldehyde 29 Endocrine‐disrupting chemicals Bisphenol A 30*, , 31 Bisphenol A 30*, , 31 Plastics Microplastics 32* Microplastics 32* Air pollution Formaldehyde 29 Ambient air pollution 33 Polycyclic aromatic hydrocarbons 34 Carbon disulfide 34 Formaldehyde 29 Ambient air pollution 33 Polycyclic aromatic hydrocarbons 34 Carbon disulfide 34 Endocrine‐disrupting chemicals Per‐ and polyfluoroalkyl substances 35* Phthalates 7 Per‐ and polyfluoroalkyl substances 35* Phthalates 7 Heavy metals Lead, cadmium 36 * , 37 * , 38 Lead, cadmium 36 * , 37 * , 38 Plastics Microplastics 32 * Microplastics 32 * Bisphenol A 40 Organochlorine pesticides, polychlorinated biphenyls, dioxin 45 * Phthalates 49 Plasticizers, organophosphate esters 50 Phenols 51 Mercury, cadmium, lead 52 , 53 PFAS 54 Phthalates 53 Pesticides, polychlorinated biphenyls, dioxin 55 Arsenic, cadmium, mercury 56 Endocrine‐disrupting chemicals PFAS 62 PFAS 62 Minerals Talc 63 Asbestos 64 Talc 63 Asbestos 64 Endocrine‐disrupting chemicals PFAS 65 Air pollution Ethylene oxide 66 Nitrogen dioxide 67 * Secondhand smoke 99 Polycyclic aromatic hydrocarbons 68 Benzene 62 Ethylene oxide 66 Nitrogen dioxide 67 * Secondhand smoke 99 Polycyclic aromatic hydrocarbons 68 Benzene 62 Endocrine‐disrupting chemicals Polychlorinated biphenyls 69 PFAS 71 Brominated flame retardants 72 Polychlorinated biphenyls 69 PFAS 71 Brominated flame retardants 72 Heavy metals Cadmium 73 Cadmium 73 Pesticides DDT 75 DDT 75 Abbreviations: DDT, dichlorodiphenyltrichloroethane; PCOS, polycystic ovary syndrome; PFAS, per‐ and polyfluoroalkyl substances; PM, particulate matter.

While laboratory testing for patients for many of the chemicals discussed in this article may not always be feasible or clinically applicable, there are options for directed testing when indicated. In countries such as the USA, Canada, UK, and across the Nordic region, the capacity for clinical environmental toxicity testing varies significantly. Lead remains the most consistently tested and actionable toxicant during pregnancy, particularly in high‐risk populations; for instance, Centers for Disease Control and Prevention guidelines recommend blood lead testing for pregnant and lactating women when exposure risk is identified. 81 Testing for other heavy metals like mercury, cadmium, and arsenic is less routine but may be available when specific risk factors are present. 82 In contrast, testing for pesticides and PFAS is generally confined to public health surveillance or specialized commercial laboratories. For example, while Canada has conducted biomonitoring for PFAS in maternal and cord blood, PFAS are not regularly tested in drinking water systems and access to broader testing remains limited. 83 A number of commercial laboratories offer testing for phthalates, BPA, and PFAS. 84 While these tests are increasingly available, they are not standardized and lack universal clinical thresholds. 84 Timing of sample collection is critical to understanding toxic exposures. 84 For research and clinical utility, sample handling, preservation, and storage must be rigorously standardized. 85 For country‐specific laboratory testing details, see Appendix  S1 in the online supporting information. Intrinsic factors, which include biological traits like age, genetic makeup, and pre‐existing health conditions, and extrinsic factors, which include psychosocial stress from experiencing income inequality, violence, racism, healthcare inequity, or food insecurity, can individually or collectively increase susceptibility to harm from chemical exposures. 86 , 87 , 88 , 89 , 90 , 91 , 92 Exposure to toxic environmental contaminants is inequitably distributed. Historically marginalized and underserved communities often face a disproportionate burden of exposure to both chemical and nonchemical stressors. 93 The impact of chronic and compounded stress can result in increased allostatic load, leading to elevated cortisol levels, altered immune and inflammatory function, and increased disease susceptibility. 94 , 95 Neglecting to consider the combined impact of these stressors underestimates the risk to human health among these communities and leaves them susceptible to increased harm. Understanding these mechanisms underscores the importance of integrating environmental health considerations into obstetric care. Clinicians can play a pivotal role in mitigating risks by staying informed about environmental exposures and counseling patients accordingly.

Clinicians do not need to be environmental health experts to effectively incorporate environmental considerations into reproductive care. Many of the clinical scenarios discussed throughout this document—such as infertility, endometriosis, or hormonally mediated cancers—are already familiar to practicing OBGYNs. What is new is the growing understanding that environmental exposures are contributing factors to these conditions and that clinicians can play a proactive role in addressing and preventing them through patient counseling, risk assessment, and preventive guidance. 1 , 6 This article provides evidence‐based frameworks for integrating environmental health into routine care without requiring specialized training. Practical strategies, such as taking brief environmental exposure histories, recognizing high‐risk settings, and advising patients on simple steps to reduce exposure—particularly during sensitive windows like preconception, pregnancy, puberty, and menopause—can be both impactful and feasible in everyday practice. 2 In addition, clinicians should remain aware of regional environmental health alerts, such as air quality advisories, contamination events, or extreme heat warnings, which may warrant temporary modifications in patient counseling or care plans. Collaborating with public health agencies and referring patients to trusted environmental health resources can further extend the reach of clinical guidance. Ultimately, incorporating environmental health into reproductive care enhances the clinician's ability to offer comprehensive, preventive, and equity‐focused care.

Environmental exposures are a modifiable contributor to a wide range of gynecologic and reproductive conditions, including infertility, PCOS, uterine fibroids, hormonally mediated cancers, and disorders of reproductive aging. These exposures—ranging from EDCs and heavy metals to air pollution and occupational hazards—interact with hormonal, metabolic, and inflammatory pathways that shape reproductive health across the lifespan. While further research is needed to identify the reproductive hazards of the many chemicals on the marketplace that do not currently have such data due to lack of regulatory requirements, the existing evidence is sufficient to inform clinical action today. Simple, evidence‐based counseling on diet, physical activity in a healthy environment, product use, occupational risk, and environmental health behaviors can empower patients to reduce harmful exposures and support their personal and reproductive well‐being, and the health of our planet. At the same time, addressing environmental threats to gynecologic health requires more than patient‐level intervention. Disparities in exposure and outcomes—driven by race, income, geography, and other synergies—demand that OBGYNs extend their leadership beyond the clinic. This includes advocating for stronger regulatory protections, collaborating with public health and community partners, and integrating environmental literacy into routine care. As guardians of women's health, OBGYNs are uniquely positioned to lead a movement that recognizes environmental safety as essential to gynecologic and reproductive health.

Environmental exposures are increasingly understood to play a critical role in gynecologic and fertility health. In recent decades, FIGO—along with its national society members—has built consensus around the emerging reality: that scientific evidence has established that exposure to toxic environmental agents can profoundly affect women's health. 1 , 2 Across the reproductive lifespan, women are exposed to a complex mixture of environmental agents—including industrial chemicals, heavy metals, air pollutants, and endocrine‐disrupting compounds—that can interfere with hormonal signaling, reproductive organ function, and systemic metabolic regulation. 1 Throughout this article these connections are referred to as environmental drivers of gynecologic and reproductive health. This scientific understanding comes against a backdrop of a proliferation of synthetic chemicals in everyday life. Over recent decades the scale of synthetic chemical production has grown immensely, with fossil fuel extraction and petrochemical expansion serving as major drivers. Over 350 000 chemicals and mixtures have been registered globally, yet fewer than 5% of these have undergone safety evaluations—a critical deficit highlighted in recent literature. 3 Many of these substances, including phthalates, per‐ and polyfluoroalkyl substances (PFAS), and flame retardants, are endocrine‐disrupting chemicals (EDCs) derived from fossil fuels and are now embedded in consumer items such as plastics, cosmetics, building materials, and children's products. These chemicals have pervaded modern life, pervasive not just in industrial settings but in everyday environments such as our air, water, food, and household products. 3 Plastic materials in particular have become woven into nearly every aspect of modern living, spanning packaging, household products, food containers, clothing, and more. These plastic items do not simply disappear; they fragment into microscopic particles known as microplastics, which are now virtually unavoidable in our environments and bodies. Studies confirm that microplastics are consistently found in human breast milk, placentas, infant formula, and meconium, indicating exposure beginning in utero and continuing through breastfeeding and early infancy. Alarmingly, one investigation detected microplastics in approximately 75% of human breast milk samples analyzed, while other research has shown microplastics present in every section of the human placenta examined. 4 , 5 Many of these exposures are difficult to detect, occurring through exposures via air, water, food, personal care products, and occupational environments. The underlying mechanisms that link exposures to adverse reproductive health outcomes are diverse, encompassing endocrine disruption, oxidative stress, epigenetic alterations, and immune dysregulation. Importantly, many reproductive disorders linked to environmental exposures manifest over years or decades, with potential intergenerational consequences for health and fertility. 1 As trusted health advisors, obstetricians and gynecologists (OBGYNs) have an essential role in integrating environmental health into routine gynecologic and fertility care. This includes taking environmental histories, counseling patients on risk reduction and healthy lifestyles, and advocating for healthier environments through institutional and policy change. Addressing these environmental drivers is not only a matter of clinical relevance, it is central to reproductive justice and equitable access to safe and healthy reproductive lives. 2 , 6 This article intends to link a wide range of environmental drivers of maternal and child health, which are presumed to be novel to most clinicians, with familiar and crucial health outcomes in women's health. To optimize clinical utility this information is presented in four distinct sections. This review focuses on those environmental chemicals and pollutants for which there is evidence of exposures and health effects, but it is important to note that there are no data on the effects or exposures to the vast majority of chemicals due to lack of sufficient government policies. 1 , 2 , 3 , 6 The section on Common Mechanisms details the underlying mechanisms and pathophysiology that link diverse exposures like EDCs, air pollution, and extreme weather through common pathways of disease in gynecologic and reproductive health. Evidence Review summarizes the latest literature relevant to these clinical encounters with a priority on high‐quality systematic reviews and authoritative consensus statements. Clinical Encounters synthesizes the evidence review with condition‐specific understanding of disease, risk, and focused clinical counseling. Finally, Common Advice presents strategies for avoidance and risk mitigation that apply broadly across these clinical encounters.

The authors have no conflicts of interest to declare.

Environmental exposures play a significant role in gynecologic and fertility health, disrupting hormonal balance, impairing ovarian function, and contributing to reproductive disorders. Key mechanisms include endocrine disruption, oxidative stress, inflammation, and epigenetic modifications. EDCs are substances in the environment that disrupt the normal function of the endocrine system by interfering with the activity of endogenous hormones by blocking, mimicking, or altering the levels of hormones in our blood. 7 EDCs can also affect how hormones are made, broken down, or stored in the body, or change our sensitivity to specific hormones. 7 Even small alterations to hormone levels can have significant and lasting impacts on health, especially during sensitive life stages like pregnancy. Because EDCs can have significant health impacts at very low levels of exposure, these chemicals are of particular concern. 3 There are over 1000 chemicals that are suspected to be EDCs based on their probable endocrine‐disrupting properties. EDCs can be identified through 10 key characteristics for how they interact with hormones and their receptors, and hormone‐responsive cells: (1) receptor ligand or agonist; (2) receptor antagonist; (3) receptor expression; (4) signal transduction; (5) epigenetic alterations; (6) hormone synthesis; (7) hormone transport; (8) hormone distribution or circulating hormone levels; (9) hormone breakdown or clearance; and (10) fate (proliferation, apoptosis, differentiation). 8 See Table  1 for common examples of EDCs. Common examples of endocrine‐disrupting chemicals (EDCs). Certain EDCs, such as phthalates and bisphenol A (BPA), have been shown to disrupt estrogen and androgen signaling pathways, altering levels of estradiol, testosterone, and anti‐Müllerian hormone (AMH), which are critical for ovarian follicle development and spermatogenesis. 9 Although endocrine disruption is one of the most common mechanisms by which chemicals can cause reproductive harm, there are several other common mechanisms by which chemicals may act to induce reproductive harm, including oxidative stress, mitochondrial dysfunction, epigenetic modifications, disruption of meiosis and mitosis, and apoptosis/necrosis. Many chemicals trigger the production of reactive oxygen species (ROS), including within reproductive cells, like oocytes or granulosa cells. ROS are highly unstable and can damage other vital cellular components such as DNA, lipids, and proteins. ROS‐related damage can result in chromosomal instability, atresia, and impaired adenosine triphosphate production, ultimately leading to mutation accumulation or cell death. 10 Air pollutants, especially PM 2.5 , can induce oxidative stress and inflammation, disrupting ovarian function and impairing fertility. 1 Exposure to air pollutants has been associated with decreased ovarian reserve, reduced antral follicle count, and lower AMH levels, especially among women aged over 35 years. 11 Furthermore, air pollution has been linked to reduced success rates in assisted reproductive technologies, such as in vitro fertilization (IVF), by affecting oocyte quality and embryo development. 12 Environmental chemicals, including air pollutants, heavy metals, phthalates, and certain pesticides, can disrupt the normal function of the mitochondria by disrupting membrane potential, inhibiting electron transport chain enzymes, and changing mitochondrial DNA (mtDNA) copy number, among other mechanisms. At the cellular level, these effects can reduce adenosine triphosphate production, impair cell growth and differentiation, trigger apoptosis, and increase ROS production, resulting in cellular oxidative damage. Biomarkers like mtDNA copy number, mtDNA mutations, oxidative damage markers, and mitochondrial membrane potential are increasingly used to capture these effects. 13 Chemical‐induced mitochondrial dysfunction during pregnancy can have adverse impacts on fetal development. For example, prenatal exposure to nitrogen dioxide (NO 2 ), an air pollutant, was linked to reduced placental mtDNA content and lower birth weight, with mediation analysis suggesting that mtDNA reduction explains part of this association. 14 Exposure to environmental chemicals like certain pesticides, BPA, heavy metals, and air pollution can induce changes in DNA methylation, histone modifications, and/or noncoding RNA expression, leading to long‐lasting alterations in gene regulation and chromatin architecture without altering the underlying DNA sequence. These epigenetic shifts can disrupt gametogenesis, alter hormone receptor signaling, and cause developmental abnormalities, with some effects persisting across generations. 15 , 16 Additionally, prenatal PM 2.5 exposure can lead to significant decrease in the levels of synapsin I protein, a key synaptic marker regulating neurotransmitter release. 17 Toxic chemicals may interrupt the process of cell division by interfering with DNA repair, the spindle apparatus, or gene expression, resulting in aneuploidy, breaks in DNA, or cell cycle arrest in gametes. The lasting effects include egg loss, miscarriage, infertility, and chromosomal abnormalities in offspring. 18 , 19 Pregnancy and fertility are especially vulnerable to the effects of rising ambient temperatures, which can disrupt endocrine function and compromise reproductive outcomes. Physiological stress from heat exposure can alter menstrual regularity, impede oocyte maturation, and increase the risk of pregnancy loss. 20 Experimental evidence indicates that heat stress impairs ovarian function—including follicular development, granulosa cell viability, and oocyte quality—across mammalian models, underscoring mechanisms relevant to human fertility. 21 Epidemiological studies reinforce these findings: women undergoing IVF cycles exposed to extreme ambient temperatures experienced significantly lower clinical pregnancy and live birth rates, with higher early pregnancy loss rates during hotter periods. 22 In addition, elevated ambient temperatures have been associated with lower antral follicle counts before treatment—an early indicator of reduced ovarian reserve. 22 Together, this evidence suggests that heat stress exerts its effects via endocrine disruption, oxidative damage, and placental dysfunction—mirroring mechanisms seen in obstetric heat‐related morbidity.

Appendix S1. FIGO Committee Opinion: Environmental drivers of gynecologic and reproductive health.