FIGO committee opinion: Environmental drivers of obstetric health and early childhood development

Abstract

Environmental exposures are increasingly recognized as critical, yet underappreciated, determinants of reproductive, perinatal, and early childhood health. Developed through a structured consensus process and grounded in systematic evidence review, this FIGO committee opinion provides a comprehensive synthesis of the current evidence linking environmental toxicants—including air pollution, endocrine‐disrupting chemicals, heavy metals, and climate‐related stressors—to common obstetric outcomes such as preterm birth, hypertensive disorders of pregnancy, gestational diabetes, and impaired fetal growth, as well as to early childhood outcomes including neurodevelopmental delay, metabolic disease, and atopic conditions. This article also outlines common biological mechanisms, such as endocrine disruption, oxidative stress, epigenetic modification, and placental dysfunction, and provides clinicians with actionable guidance for integrating environmental health into reproductive care through screening, counseling, and advocacy. Special attention is paid to the role of social and structural inequities in amplifying exposure risks and health disparities. By linking environmental drivers to familiar clinical outcomes, this guidance empowers obstetricians and allied professionals to engage in preventive care that safeguards maternal and child health across the life course. FIGO calls on reproductive health professionals to embrace this leadership role—not only in clinical practice, but in shaping policies that protect current and future generations.

1. INTRODUCTION

Environmental factors are increasingly demonstrated as critical, yet underaddressed, determinants of obstetric health and early childhood development. In recent decades, FIGO—along with its national member societies—has built consensus around the emerging reality: that scientific evidence has established that exposure to toxic environmental agents—ranging from industrial chemicals and air pollutants to endocrine‐disrupting compounds and climate‐related stressors—can profoundly affect maternal, fetal, and child health across the life course. ¹ , ² Throughout this article, these connections are referred to as environmental drivers of maternal and child health.

Pregnancy represents a uniquely vulnerable window in human development. During this period, even low‐level exposures to environmental hazards can disrupt placental function, alter fetal epigenetic programming, and contribute to adverse birth outcomes such as preterm birth, fetal growth restriction, and neurodevelopmental impairment. ³ , ⁴ , ⁵ Data also suggest that the preconception period plays a pivotal role, with environmental exposures to both women and men of reproductive age influencing gamete quality and early embryonic development. ¹

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. ⁴ 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. ⁴

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. ⁶ , ⁷

Disparities in exposure are shaped by structural inequities, including poverty, occupational risk, and systemic factors. These social determinants intersect with environmental risks to amplify adverse outcomes among historically marginalized populations, underscoring the need for a systems approach to perinatal environmental health. ¹ , ²

Obstetricians and gynecologists are well‐positioned to lead clinical and public health efforts to identify and mitigate environmental risks. Integrating environmental health into routine reproductive care—through screening, counseling, advocacy, and policy engagement—is essential to safeguarding maternal and child health globally. ² , ³

This article intends to identify the links between 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 obstetrics and early childhood development. To optimize clinical utility, this information is presented in four distinct sections.

The section on Common Mechanisms details the underlying mechanisms and pathophysiology that link diverse exposures like endocrine disrupting chemicals, air pollution, and extreme weather through common pathways of disease in obstetric health and early childhood development. Evidence Review summarizes the latest literature relevant to common 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.

2. CLINICIANS' ROLE IN ENVIRONMENTAL HEALTH

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 article, such as preterm birth, gestational diabetes, or prenatal risk for developmental delay, are already familiar to practicing obstetrician/gynecologists (OBGYNs). International guidance has affirmed the important role that OBGYNs can play in addressing the health impacts of climate change, both through patient counseling and broader advocacy efforts. ² , ⁴

In using this article, clinicians should find 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, and puberty—can be both impactful and feasible in everyday practice.

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 a clinician's ability to offer comprehensive, preventive, and evidence‐based care.

3. COMMON MECHANISMS: PATHOPHYSIOLOGY

Environmental exposures during pregnancy and early childhood can disrupt critical biological processes, leading to adverse obstetric outcomes and long‐term developmental challenges. Key mechanisms include endocrine disruption, oxidative stress, inflammation, and epigenetic modifications.

3.1. Endocrine disruption

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. ⁸ EDCs can also affect how hormones are made, broken down, or stored in the body, or change our sensitivity to specific hormones. ⁸ Even small alterations to hormone levels can have significant and lasting impacts on health, especially during sensitive life stages like pregnancy. ⁴ Because EDCs can have significant health impacts at very low levels of exposure, these chemicals are of particular concern.

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). ⁹

Certain EDCs, such as phthalates and bisphenol A (BPA), have been shown to disrupt androgen and estrogen signaling pathways, respectively, altering levels of estradiol, testosterone, and anti‐Müllerian hormone (AMH), which are critical for ovarian follicle development and spermatogenesis. ¹⁰

These chemicals can also interfere with fetal development; for example, they can cross the placenta, affecting the developing endocrine system and leading to outcomes such as fetal growth restriction, neurodevelopmental disorders, and reproductive anomalies. ¹ , ¹¹ Studies have suggested that prenatal exposure to EDCs may increase the risk of cognitive and behavioral impairments, including lower IQ scores and increased risk of autism spectrum disorder. ¹ , ¹² , ¹³ Additionally, EDCs can disrupt the maternal immune system, contributing to poor pregnancy outcomes. ⁵ , ¹⁴ , ¹⁵

3.2. Other common mechanisms

Endocrine disruption is one of the most common mechanisms by which chemicals can cause reproductive harm. However, 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.

Oxidative stress

Exposure to environmental chemicals, including certain pesticides, can trigger the production of reactive oxygen species (ROS), which are highly reactive molecules that can damage vital cellular components, such as DNA, lipids, and protein, leading to oxidative stress. ¹⁶ Oxidative stress can result in chromosomal instability, impaired mitochondrial adenosine triphosphate production, mutation accumulation, and cell death. During pregnancy, chemical‐induced oxidative stress can have adverse effects on the developing fetus; for example, air pollutants, particularly PM_2.5, can induce oxidative stress and inflammation, disrupting placental function and fetal development. ¹⁷

Mitochondrial dysfunction

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. ¹⁸ Chemical‐induced mitochondrial dysfunction during pregnancy can have adverse impacts on fetal development. For example, prenatal exposure to nitrogen dioxide (NO₂), 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. ¹⁹

Epigenetic modifications

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. ²⁰ , ²¹ Additionally, prenatal PM_2.5 exposure can lead to a significant decrease in the levels of synapsin I protein, a key synaptic marker regulating neurotransmitter release. ²²

Disruption of meiosis and mitosis

Environmental chemicals like BPA and pesticides can interrupt the process of cell division by interfering with DNA repair, the spindle apparatus, or gene expression, resulting in aneuploidy, DNA breaks, or cell cycle arrest in gametes. For example, exposure to certain pesticides, including the organophosphate pesticide diazinon, impaired gamete differentiation, resulting in embryonic lethality and reduced reproduction. ²³ Similarly, EDCs, BPA, and quaternary ammonium disinfectants have been shown to alter meiotic progression and gamete formation, indicating risks for egg loss, infertility, pregnancy loss, and potential chromosomal abnormalities or aneuploidy in offspring. ²⁴

3.3. Thermoregulation

Pregnancy profoundly alters maternal thermoregulation through physiological adaptations such as increased blood volume, elevated basal metabolic rate, and enhanced cutaneous blood flow, all of which are designed to support fetal development. ²⁵ However, these adaptations simultaneously reduce a pregnant individual's capacity to dissipate heat. When ambient temperatures exceed thermoregulatory limits, this can result in core body temperature elevations that precipitate deleterious effects on both the mother and fetus. ²⁶ These include maternal dehydration leading to hypovolemia, reduced uterine and placental perfusion, systemic inflammation, and oxidative stress, which may contribute to hypertensive disorders of pregnancy, preterm labor, low birthweight, and stillbirth [26]. Understanding these mechanisms supports current clinical guidance that emphasizes adequate hydration, cooling strategies, and avoidance of high outdoor heat exposure in pregnancy.

4. EVIDENCE REVIEW

4.1. Methods

Selection of outcomes

The selection of clinical outcomes for this article was determined through a structured consensus process involving multidisciplinary input from obstetricians, pediatricians, environmental health scientists, and public health experts. The goal was to identify reproductive, perinatal, and early childhood outcomes that are strongly supported by the scientific literature on environmental exposures and broadly relevant to clinical practice across diverse global contexts.

Through iterative discussion and evidence review, the committee prioritized outcomes that included preterm birth, low birthweight, hypertensive disorders of pregnancy (including pre‐eclampsia), impaired neurodevelopment (including developmental delay, attention‐deficit/hyperactivity disorder (ADHD), and autism), early metabolic disorders (such as childhood obesity and gestational diabetes), and atopic conditions (including eczema, allergic rhinitis, and food allergy). This outcome selection process ensured the guidance reflects both scientific rigor and clinical practicality for implementation by OBGYNs and allied providers worldwide.

Identification of evidence

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 excluded evidence exclusively evaluating early childhood exposure to environmental contaminants.

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.

Of note, in our reporting we prioritized systematic reviews that utilized methods endorsed by the US National Academies of Sciences, Engineering, and Medicine, including the National Toxicology Program's approach and the Navigation Guide methodology. ⁸ , ²⁷ , ²⁸ , ²⁹ , ³⁰ , ³¹

4.2. Summary of evidence

Table 1 is organized by health outcomes (birth outcomes, pregnancy complications, neurodevelopmental harm, metabolic conditions, allergic conditions) 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.

TABLE 1.

Toxic environmental exposures and adverse reproductive health outcomes.

Health outcome	Environmental exposure and level of evidence. All references meet at least Level 2b standard (systematic reviews and meta‐analyses are designated in bold and using *)
Birth outcomes
Preterm birth	Air pollution Ambient air pollution (PM 2.5 , PM 10 , nitrogen dioxide, sulfur dioxide, ozone, carbon monoxide) 32 * , 33 * Wildfires 34 * Ethylene oxide 92 Secondhand smoke 93 Household pollution (polluting fuels) 35
	Ambient temperature Extreme heat and cold 32 * , 36 *
	Endocrine‐disrupting chemicals PFAS 40 * Phthalates 41 , 42 , 43 * BPA 44 * Polybrominated biphenyl ethers 94
	Heavy metals Lead 37 Cadmium, chromium, copper, manganese 43 *
Low birthweight	Air pollution Wildfires 34 * Ambient air pollution (e.g. PM2.5) 32 , 95 , 96 Household pollution (polluting fuels) 35 , 97
	Endocrine‐disrupting chemicals PFAS 49 , 98 Polychlorinated biphenyls 99
	Heavy metals Lead 37 , 100 Mercury 39 Cadmium 38 , 101
Pregnancy complications
Pre‐eclampsia	Air pollution Ambient air pollution (PM 2.5 , nitrogen dioxide, nitrogen oxides) 45 * Ambient air pollution (ozone) 102
	Ambient temperature Extreme heat in early pregnancy 46 * , 47 *
	Endocrine‐disrupting chemicals PFAS 48 * , 49
Neurodevelopmental harm
Neurodevelopmental harm	Air pollution Combustion‐related air pollution (e.g. PAHs, nitrogen dioxide, PM2.5) 12 , 50
	Endocrine‐disrupting chemicals Polybrominated diphenyl ethers, 12 , 51 * Phthalates 52 PFAS 52 Polychlorinated biphenyls 12
	Heavy metals Lead, mercury, cadmium 12
	Pesticides Organophosphate pesticides 12 , 56
Metabolic conditions
Gestational diabetes	Air pollution Ambient air pollution 57 *
	Ambient temperature Extreme heat 25
	Endocrine‐disrupting chemicals 61 , 103 Polychlorinated biphenyls PFAS Phthalates Polybrominated diphenyl ethers
	Heavy metals Arsenic, antimony, copper 64
	Ultra‐processed foods 66 *
Childhood obesity	Air pollution PM 2.5 50 *
	Endocrine‐disrupting chemicals BPA 60 * Pesticides 62
	Persistent organic pollutants Dichlorodiphenyldichloroethylene, hexachlorobenzene 63
	Food preparation Acrylamide 65
Allergic conditions
Allergic rhinitis	Air pollution PM 2.5 , nitrogen dioxide 68 * , 69 * Secondhand smoke 104
	Endocrine‐disrupting chemicals Phthalates 71
Eczema	Air pollution Nitrogen dioxide 70 Secondhand smoke 105

Abbreviations: BPA, bisphenol A; PFAS, per‐ and polyfluoroalkyl substances; PM, particulate matter.

5. CLINICAL ENCOUNTERS

5.1. Preterm birth and low birthweight

While clinical risk factors for preterm birth and low birthweight—such as maternal infection, hypertension, and multiple gestation—are well known, environmental exposures are increasingly recognized as significant, modifiable contributors to these outcomes. Established and emerging evidence demonstrates that toxic chemicals in the air, home, and broader climate can disrupt placental function, trigger systemic inflammation, and alter fetal development (Table 1). Understanding these associations is essential for obstetricians seeking to mitigate preventable environmental risks during pregnancy.

Air pollution

Among the most strongly supported exposures is air pollution. Fine particulate matter (PM_2.5 and PM₁₀), nitrogen dioxide, ozone, sulfur dioxide, and carbon monoxide can increase the risk of preterm birth and low birthweight. Exposure to wildfire smoke and household air pollution from the use of polluting fuels further compounds these risks. This is supported by systematic reviews ³² and other meta‐analyses. ³³ , ³⁴ Additional Level 2a evidence comes from studies focused on low‐ and middle‐income countries, highlighting the global relevance of this exposure. ³⁵ The common mechanisms section provides examples of how oxidative stress, which can be triggered by air pollution, negatively impacts placental function.

Extreme ambient temperature

Extreme ambient temperatures—both heat and cold—can influence the risk of preterm birth, particularly when exposures occur during early gestation or the third trimester. ³² Pregnancies exposed to heatwaves are more likely to deliver prematurely, and this association holds across geographic regions. The evidence supporting this link includes an umbrella review with meta‐analyses and systematic review. ³² , ³⁶

Heavy metals

Heavy metal exposure, particularly to lead, cadmium, and mercury, can increase the risk of adverse birth outcomes. Lead exposure, in particular, can increase the risk of low birthweight and preterm delivery, as documented in the US Environmental Protection Agency's 2024 Integrated Science Assessment. ³⁷ Cadmium and mercury, often found in contaminated food or industrial runoff, are similarly linked to low birthweight. These conclusions are based on evidence including systematic reviews and meta‐analyses. ³⁸ , ³⁹

Endocrine‐disrupting chemicals

EDCs represent another major category of concern. Compounds such as PFAS, phthalates, BPA, and polybrominated diphenyl ethers can interfere with placental function, hormone regulation, and fetal development. High‐quality evidence, including reviews using the Navigation Guide systematic review methodology conclude they can increase the risk of preterm birth and low birthweight. ⁴⁰ , ⁴¹ , ⁴² , ⁴³ , ⁴⁴ Additional Level 2a studies have examined disparities in exposure and outcomes. For example, recent pooled cohort analyses indicate that racially marginalized populations may face disproportionately high levels of phthalate exposures, compounding their baseline risk of adverse birth outcomes. ⁴² Table 2 provides common examples of EDCs.

Counseling opportunity: Specific to the risks of extreme heat during pregnancy, counsel toward increased oral hydration to stay well ahead of thirst using a nonplastic container; advise patients about regional heat alerts by tracking local apps; monitor additional weather information such as humidity and wet bulb temperature to account for experienced heat rather than isolation temperature readings

TABLE 2.

Common examples of endocrine‐disrupting chemicals (EDCs) ^a .

Common EDCs	What are they used in?
Phthalates, parabens, ultraviolet filters	Cosmetics (hair spray, nail polish, shampoo, lotion), fragrances, children's toys, medical tubing, sunscreen
Per‐ and poly‐fluorochemicals (PFAS)	Textiles, clothing, nonstick pans and food wrappers, microwave popcorn bags, old Teflon cookware
Bisphenol A (BPA), phthalates, phenol	Plastics and food storage materials, lining of food and beverage cans
Lead, phthalates, cadmium	Children's products
Dichlorodiphenyltrichloroethane (DDT), chlorpyrifos, atrazine, 2,4‐D, glyphosate	Pesticides
Polychlorinated biphenyls (PCBs) and dioxins	Industrial solvents or lubricants and their byproducts
Brominated flame retardants, PCBs	Electronics and building materials
Triclosan	Anti‐bacterial soaps, personal care products
Polybrominated diphenyl ethers (PBDEs)	Flame retardants, carpet, mattresses, furniture, electronics, textiles

^a Adapted from Ruiz and Patisaul. Endocrine‐disrupting chemicals (EDCs). January 24, 2022. https://www.endocrine.org/patient‐engagement/endocrine‐library/edcs.

5.2. Pre‐eclampsia

Pre‐eclampsia is a complex hypertensive disorder of pregnancy that arises after 20 weeks of gestation and involves both maternal and placental dysfunction. While its precise etiology remains multifactorial, environmental exposures are increasingly recognized as significant contributors to risk (Table 1). At a mechanistic level, these environmental exposures often converge on common biological pathways, including oxidative stress, systemic inflammation, and endothelial dysfunction—all central to the pathophysiology of pre‐eclampsia.

Air pollution

Among the most well‐documented exposures are air pollutants such as fine particulate matter (PM_2.5), nitrogen dioxide, and ozone, which can increase the risk of pre‐eclampsia. These are supported by a systematic review and meta‐analysis conducted by the National Toxicology Program. ⁴⁵ The mechanism is thought to involve impaired placental perfusion due to systemic inflammation and endothelial injury. ⁴⁵

Extreme ambient temperature

Beyond chemical factors, climate‐related exposures are emerging as important contributors. Exposure to extreme heat, particularly during early pregnancy, can increase the risk of pre‐eclampsia; recent meta‐analyses identified this risk factor. ⁴⁶ , ⁴⁷ Mechanistically, heat stress may contribute to dehydration, increased maternal cardiovascular load, and altered placental development.

Endocrine‐disrupting chemicals

EDCs, including phthalates, BPA, and PFAS, can interfere with hormonal regulation and placental development. In particular, PFAS exposure can increase the risk of hypertensive disorders of pregnancy across multiple studies. ⁴⁸ , ⁴⁹

Counseling opportunity: Addressing workplace accommodations can further support maternal vascular health during pregnancy, with recommendations such as limited hours, remote work where possible, no strenuous activity, and allowance for more frequent breaks

5.3. Childhood developmental delay and neurodevelopmental harm

Several categories of environmental exposures are associated with significant risks to early childhood development, beginning in utero (Table 1). While the underlying causes of neurodevelopmental harm are not yet fully resolved, the role of environmental drivers, particularly during pregnancy, is increasingly understood to play a prominent role.

Air pollution

Among the most rigorously studied exposures are air pollutants, particularly PM_2.5, nitrogen dioxide, and polycyclic aromatic hydrocarbons. These pollutants have been linked to an increased risk of autism spectrum disorder and cognitive impairment, with Level 2a evidence from systematic reviews and meta‐analyses. ¹² , ⁵⁰ Mechanistically, studies have shown that prenatal PM_2.5 exposure can lead to a significant decrease in the levels of synapsin I protein, a key synaptic marker regulating neurotransmitter release. ²²

Endocrine‐disrupting chemicals

EDCs are another major category of concern. Phthalates, polybrominated diphenyl ethers, polychlorinated biphenyls, and PFAS are associated with ADHD, reduced IQ scores, and other executive functioning deficits. These exposures can interfere with thyroid hormone regulation and neurodevelopmental gene expression during critical fetal windows. Notably, systematic reviews and Level 2a evidence support this finding for several of these chemicals and increased risk of neurodevelopmental harm. ⁵¹ , ⁵²

Heavy metals

Heavy metals, including lead, mercury, and cadmium, are historically recognized as potent neurotoxins, prominently described in the experience of Minamata disease where methylmercury poisoning led to grave neurological impairment in exposed fetuses. ⁵³ Prenatal and early postnatal exposure to these metals increase the risk of reduced IQ, attention deficits, and neurodevelopmental harm. This evidence is consistent and longstanding, supported by assessments from the US Environmental Protection Agency and consensus statements. ¹² , ³⁷

Pesticides

Pesticide exposure, especially to organophosphate compounds like chlorpyrifos and diazinon, has also been linked to ADHD and impaired motor development and cognition. These pesticides disrupt cholinergic signaling, induce oxidative stress, and lead to neuronal damage during critical brain development periods. ⁵⁴ , ⁵⁵ Consensus statements report moderate to strong associations, particularly in populations with higher exposure levels through diet or occupation. ¹² , ⁵⁶

Counseling opportunity: Avoid sources of heavy metals, particularly lead, by using water filters on faucets where feasible. Also be mindful of exposure to old paint as a source of lead, such as in cracked window frames and doors

5.4. Gestational diabetes and childhood obesity

The intrauterine environment plays a pivotal role in shaping long‐term metabolic outcomes for both mother and child. Endocrine signaling pathways that govern glucose metabolism, lipid storage, and energy balance can be disrupted by environmental exposures during pregnancy, with lasting consequences for fetal programming and postnatal health. Among the most concerning outcomes are gestational diabetes mellitus (GDM) and childhood obesity (Table 1).

Air pollution

Ambient air pollution, particularly fine particulate matter (PM_2.5), is associated with systemic inflammation and oxidative stress that may impair maternal insulin sensitivity and alter placental metabolic function. PM_2.5 can increase the risk of GDM, supported by a systematic review and meta‐analysis. ⁵⁷ Similarly, prenatal exposure to PM_2.5 has been linked to higher rates of childhood obesity, with global studies showing consistent effects across regions. ⁵⁰

Endocrine‐disrupting chemicals

EDCs such as BPA, phthalates, and PFAS are mechanistically known to interfere with hormonal regulation during fetal development. Prenatal exposure to BPA and phthalates has been associated with variable trajectory in childhood adiposity, higher body mass index, and early‐life metabolic syndrome. ⁵⁸ , ⁵⁹ BPA has been strongly associated with increased adiposity in childhood. ⁶⁰ Meta‐analyses also support the association of maternal exposure to phthalates and PFAS with increased risk for GDM and childhood obesity. ⁶¹ , ⁶² Persistent organic pollutants such as dichlorodiphenyldichloroethylene (DDE) and hexachlorobenzene (HCB) have been implicated in prenatal metabolic disruption and greater risk of obesity in offspring. ⁶³

Extreme ambient temperature

Extreme heat exposure during pregnancy has also emerged as an independent risk factor for GDM, likely through mechanisms involving dehydration, inflammation, and cardiovascular strain. ²⁶ A 2025 meta‐analysis found consistent associations between heat exposure and adverse maternal metabolic outcomes, supporting Level 2a evidence. ²⁵

Heavy metals

Heavy metals, including arsenic, antimony, and copper, are classified as metalloestrogens for their ability to mimic or interfere with estrogenic signaling. These agents can impair pancreatic beta‐cell function and disrupt insulin homeostasis, contributing to the development of GDM. Systematic review data support Level 2a evidence for this link. ⁶⁴

Nutrition and dietary contaminants

Additionally, dietary contaminants—such as acrylamide, formed during high‐temperature cooking—are associated with intrauterine growth restriction followed by accelerated postnatal growth—a known trajectory for later‐life obesity. ⁶⁵ Similarly, ultra‐processed foods consumed during pregnancy have been associated with increased risk of GDM and pre‐eclampsia. ⁶⁶

Counseling opportunity: Avoid exposure to EDCs by choosing paraben‐ and phthalate‐free products, avoiding nonstick cookware and plastic food containers, and selecting fresh or organic foods when possible

5.5. Atopic disorders: Allergic rhinitis, eczema, food allergy

Atopic disorders—including allergic rhinitis, eczema, and food allergy—are increasingly prevalent in early childhood, with evidence pointing to in utero and early‐life environmental exposures as key contributors. During fetal and neonatal immune system development, even low‐level exposure to air pollutants, tobacco smoke, and EDCs can disrupt immune regulation, heighten inflammatory responses, and increase the risk of allergic sensitization. These exposures interact with genetic and microbiome‐related factors, suggesting that the origins of atopic disease are rooted not only in heredity, but also in the prenatal environment. ⁶⁷ , ⁶⁸

Air pollution

Air pollution is one of the most consistent environmental contributors to allergic conditions. Prenatal exposure to PM_2.5, nitrogen dioxide, and other combustion‐related pollutants can increase the risk of allergic rhinitis and eczema in children. These exposures can alter immune system regulation and increase systemic inflammation, predisposing infants to hypersensitivity reactions. The evidence includes multiple Level 2a systematic reviews. ⁶⁸ , ⁶⁹ , ⁷⁰

Endocrine‐disrupting chemicals

Prenatal and early‐life exposure to phthalates may also increase the risk of allergic rhinitis and other atopic outcomes through immune dysregulation and epigenetic modification. This relationship is supported by Level 2a evidence. ⁷¹

Although direct evidence for food allergy is less robust, the same inflammatory and immune‐disrupting pathways triggered by air pollutants, phthalates, and secondhand smoke are likely relevant. Additionally, disruption of the maternal or infant microbiome by these exposures may contribute to food sensitization, although further research is needed.

Counseling opportunity: Minimize exposure to air pollution by avoiding outdoor activity on high smog days, which can be tracked by regional apps; using air purifiers indoors; and avoiding secondhand smoke entirely

6. COMMON ADVICE: AVOIDANCE AND MITIGATION

Clinicians have an essential role in helping patients minimize their exposure to toxic environmental agents during preconception, pregnancy, and early childhood. While complete avoidance of all environmental risks is not realistic, as many sources of exposure are outside a patient's control (e.g. air pollution), there are several practical strategies that obstetric care providers can share to support healthier outcomes for mothers and infants. ³ , ⁴ , ⁷²

6.1. Diet and nutrition

Nutrition is a critical area where counseling can be both accessible and effective. Patients should be encouraged to consume a varied and balanced diet rich in fruits, vegetables, whole grains, and lean proteins and avoid ultra‐processed foods. When available and affordable, organic produce has been shown to reduce dietary pesticide exposure—a concern particularly relevant during pregnancy. ³ , ¹⁴ Patients should also be encouraged to thoroughly wash produce before preparing and eating it.

It is also important to advise pregnant individuals to avoid fish known to have high levels of mercury—such as shark, swordfish, tuna, and king mackerel—and to choose safer, low mercury alternatives like salmon, sardines, and trout, which are also rich in omega‐3 fatty acids that support healthy neurodevelopment. ³ In daily food preparation, storing meals in glass or stainless‐steel containers and avoiding microwaving in plastic containers can help limit harmful chemicals like PFAS and phthalates from leaching into food. ⁴ , ⁷² Cooking with cast iron or stainless steel can also help reduce exposures to PFAS—chemicals that are present in nonstick cookware.

6.2. Lifestyle and physical activity

Physical activity is another important area of lifestyle counseling. Moderate, regular exercise such as walking, swimming, or prenatal yoga not only benefits maternal cardiovascular health but also reduces oxidative stress, which may exacerbate the impact of environmental exposures. ³ Many regional apps can provide specific alerts about outdoor air quality and extreme heat advisories. In tandem, clinicians should reinforce the importance of avoiding tobacco smoke and alcohol—both of which contain harmful chemicals linked to adverse pregnancy and developmental outcomes. ³

6.3. Personal care products

Personal care products are a common source of exposure to EDCs such as phthalates and parabens. Patients should be encouraged to use products labeled “phthalate‐free” or “fragrance‐free”, as these are less likely to contain harmful additives. ³ , ⁷² Caution is also warranted with cosmetics such as nail polish and hair dye, which may contain formaldehyde, toluene, and dibutyl phthalate—compounds linked to reproductive toxicity and developmental harm. ⁷²

6.4. Home environment

The home environment can be optimized with a few proactive steps. Improving indoor air quality by ventilating rooms regularly and using HEPA‐filter air purifiers can reduce exposure to pollutants such as volatile organic compounds and household dust, which acts as reservoir for toxic chemicals like heavy metals, phthalates, and PFAS. Patients should be advised to avoid scented air fresheners and candles, which can emit potentially hazardous chemicals like formaldehyde. ⁷³ For cleaning, natural alternatives such as vinegar and baking soda are safer options compared to many commercial products that may contain respiratory irritants or endocrine disruptors. ⁷²

Additionally, regular wet mopping and wet dusting—preferably with microfiber tools—are important to limit exposure to household dust by minimizing dust resuspension. ⁴ , ⁷⁴ Patients living in older homes should also test for lead‐based paint and radon gas, given their well‐established links to pregnancy complications and neurodevelopmental delays. ⁷⁵

Furthermore, shoe removal indoors is a simple yet effective strategy to reduce tracking in outdoor contaminants, such as pesticides and chemicals. ⁴ , ⁷⁶ During cooking, using a stove ventilation fan helps remove combustion byproducts and ultrafine particles, improving indoor air quality. Lastly, avoiding pesticide sprays by employing alternative pest control (such as traps or sealed food storage) and hiring licensed professionals is recommended to reduce exposure to harmful chemicals. ⁷⁶

6.5. Work environment

Environmental risk in the workplace should also be considered. Clinicians can ask about occupational exposures to solvents, pesticides, or heavy metals, especially for patients in agriculture, manufacturing, cosmetology, or laboratory settings. Where needed, consultation with occupational health specialists can ensure appropriate accommodations and access to protective equipment during pregnancy. ³ Encouraging patients to use personal protective equipment and follow safety protocols can mitigate the risks associated with chemical exposures at work.

7. REGULATED AND CLINICALLY ENDORSED TESTING

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. ⁷⁷ Testing for other heavy metals like mercury, cadmium, and arsenic is less routine but may be available when specific risk factors are present. ⁷⁸

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. ⁷⁹ A number of commercial laboratories offer testing for phthalates, BPA, and PFAS. ⁸⁰ While these tests are increasingly available, they are not standardized and lack universal clinical thresholds. ⁸⁰

Timing of sample collection is critical to understanding toxic exposures. ⁸⁰ For research and clinical utility, sample handling, preservation, and storage must be rigorously standardized. ⁸¹ Country‐specific laboratory testing details are given in Appendix S1.

7.1. Combined impact of chemical and nonchemical stressors

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. ⁴ , ³¹ , ⁸² , ⁸³ , ⁸⁴ , ⁸⁵ , ⁸⁶ , ⁸⁷

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. ⁸⁸ 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. ³ , ⁸⁹ , ⁹⁰ 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.

8. ADVOCACY AND THE LEADERSHIP ROLE OF OBSTETRICIANS/GYNECOLOGISTS

Environmental exposures are not evenly distributed. Communities of color, low‐income populations, migrants, and those living in areas of industrial activity or environmental degradation face a disproportionate burden of toxic chemical exposure and adverse reproductive outcomes. Structural inequities—such as housing segregation, limited access to clean air and water, and exposure to occupational hazards—amplify the risks of preterm birth, low birthweight, and developmental disorders. ¹ , ³² Addressing these disparities is not only a matter of public health, but an opportunity for physician leadership through advocacy. We have thus demonstrated a compelling need for action. While many governments and health systems may be aware of these links, there are many that are not and so it falls to OBGYNs to advocate for the women we care for.

OBGYNs are uniquely positioned to champion this work. Prior FIGO calls to action have identified the central position OBGYNs can play in mitigating the harmful effects of environmental hazards, while optimizing maternal and child health through sustainable interventions. ² While clinical counseling is critical, it must be paired with engagement in systems‐level change. This includes partnering with public health departments to respond to air quality alerts, advocating for regulatory reform of toxic chemicals, and supporting community efforts to remediate environmental hazards. ⁹¹

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 future determinants of reproductive health. 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.

To advance these goals, OBGYNs must embrace a broader vision of professional leadership—one that extends beyond the clinic and into the policymaking spaces where upstream determinants of health are decided. This is not ancillary to our mission; it is at the heart of it. When we advocate for clean air, safe housing, and toxic‐free consumer products, we are not stepping outside the scope of our practice—we are practicing medicine at its most preventive and its most powerful.

9. CONCLUSION

Environmental exposures represent a critical, yet often overlooked, determinant of obstetric outcomes and early childhood development. High‐quality evidence, which continues to grow, finds that air pollution, EDCs, heavy metals, extreme heat, and other environmental stressors can increase the risk of adverse outcomes, including preterm birth, low birthweight, pre‐eclampsia, neurodevelopmental harm, metabolic disorders, and atopic conditions. These risks are not uniformly distributed, as disparities based on geography, occupation, socioeconomic status, and structural inequality mean that the burden of exposure disproportionately affects the most vulnerable.

OBGYNs are uniquely positioned to intervene. By incorporating environmental risk assessment into routine prenatal care, offering targeted counseling on exposure avoidance, and advocating for healthier environments, clinicians can help prevent harm before it occurs. Importantly, this work does not require expertise in environmental science; it requires awareness, practical tools, and a willingness to engage. Protecting reproductive health begins not just in the clinic, but in the air we breathe, the products we use, and the policies we shape. In safeguarding our environment, we are safeguarding the health of the next generation.

AUTHOR CONTRIBUTIONS

This is a product 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 and TW contributed significantly to oversight and management of all content, scientific writing, evidence review, and cognitive input. EL, AB, and RJ contributed significantly to scientific writing, summary of evidence, evidence review, and cognitive input. JZ, AH, KG, DD, FE, and DG contributed significantly to scientific writing, evidence review, and cognitive input. EM contributed significantly to scientific writing and cognitive input. BD contributed significantly to cognitive input.

CONFLICT OF INTEREST STATEMENT

The authors have no conflict of interest to declare.

FUNDING

There was no funding received for this study.

Supporting information

Appendix S1.

DeNicola N, Lasher E, BakenRa A, et al. FIGO committee opinion: Environmental drivers of obstetric health and early childhood development. Int J Gynecol Obstet. 2025;171:951‐964. doi: 10.1002/ijgo.70549

DATA AVAILABILITY STATEMENT

Data sharing not applicable – no new data generated, or the article describes entirely theoretical research.