INTRODUCTION

Abundant scientific and epidemiologic data over the past 20 years support significant harmful effects of endocrine disrupting chemicals, heavy metals, air pollution and climate change on human health and, specifically, reproductive health including fertility, pregnancy and neonatal outcomes, and risks of developing reproductive tract abnormalities.^{1,2,3,4,5,6,7,8,9,10,11,12,13,14,15,16} Unfortunately, patients, consumers, the public at large, healthcare providers in training and in practice, and governmental policy makers are largely unaware of these effects which carry high morbidity and may be preventable.^4,17 Moreover, healthcare professionals are mostly uncertain about how to take a history to screen for risk of exposures and how to advise about strategies to mitigate harms.^17,18 This chapter describes how individuals and populations are exposed to environmental toxicants and summarizes the evidence for harm to fertility potential and pregnancy outcomes, how to take an environmental history, and approaches for patient and provider education and mitigating strategies to minimize harm. Information conveyed herein is based on systematic reviews, meta-analyses, peer-reviewed scientific publications, commentaries, scoping reviews, narrative reviews, and professional society statements spanning mainly 2014–2024.

HOW PEOPLE ARE EXPOSED

There are four main ways to be exposed to environmental toxicants – inhalation, ingestion, transdermal, transplacental (and transgenerational).^3,10 Particularly vulnerable populations include the developing fetus, children, pregnant persons, the elderly, those with chronic diseases, those with disabilities, workers in hazardous jobs, and marginalized populations. Climate change, which involves global warming, extreme temperatures and weather, and increased air pollution, impacts water and food availability and quality¹⁹ (Figure 1). It derives mainly from burning fossil fuels (coal, oil, natural gas) to generate energy for industrial processes, electricity, and transportation. Air pollution contains particulate matter PM_2.5 and PM₁₀ (2.5 mm and 10 mm diameter, respectively), nitrogen oxides (NO_x), sulfur dioxide (SO₂), ozone (O₃), carbon monoxide (CO), and other components. It also includes endocrine disrupting chemicals (EDCs) (e.g., volatile hydrocarbons, heavy metals) that disrupt endocrine processes – highly relevant to reproductive health. Major sources of EDC exposures to people (Figure 2) are pesticides and industrial waste or accidents that contaminate nearby water and land (and thus human drinking water sources and food). Other exposure sources include personal care products, personal behaviors, lifestyle, hobbies, toys, home or work environments, digital receipts, and plastic waste end e-waste (Table 1).^4,10,20,21 As environmental toxicants are ubiquitous, awareness, education, and mitigation are key to optimize reproductive health.

METHODOLOGIES TO STUDY POSSIBLE REPRODUCTIVE HARM

Determining whether exposures cause harm is complicated, as studies often differ in study designs, primary outcomes, populations, controls, duration of exposure, age of exposure, genetic susceptibilities, and analytic approaches. That said, there is strong evidence for EDCs, air pollution and heat affecting reproductive health. Cause and effects for these exposures and mechanistic underpinnings for hormone signaling and disruption largely derive from laboratory animal and in vitro cell models.^3,21,22 Epidemiologic (mostly observational cohort) studies reveal data correlating environmental exposures and human health outcomes, and the Navigation Guide,²³ which bridges clinical and environmental health, integrates animal and human studies, predicts risk of harm, and strength of the evidence. Chemical mixtures are the rule in environmental exposures,^3,21 and exposures are routinely to multiple chemicals of different classes with similar or differing signaling mechanisms that can lead to synergistic, additive, or antagonistic or no effect on physiologic outcomes. Notably, mixture risk assessment bio-monitoring data and statistical modeling^24,25 are increasingly incorporating more real-life exposures on health outcomes. In addition, job exposure matrices^26,27provide the occupational health intersection, key in planning mitigation strategies in the workplace, and wild-life studies can be key as “canaries in the coal mine” for possible human health impacts. Notably, PM can cause systemic and local inflammation, and EDCs disrupt estrogen, androgen, signaling through epigenetic, gene expression and protein alterations, thereby altering cellular and organ functions in multiple systems.^3,21 Additionally, many in utero exposures can lead to effects in subsequent generations even without direct exposure due to transgenerational transmission of epigenetic marks in the genome inherited in future generations.²⁸ The following section summarizes evidence for effects of environmental toxicants, climate change, air pollution, and heat on fertility and pregnancy outcomes.

EVIDENCE OF REPRODUCTIVE HARM

Reproductive potential and competence

Endocrine-disrupting chemicals

Numerous studies demonstrate that EDCs can disrupt gamete, embryo, gonadal, and reproductive tract development and functions and increase risk of developing reproductive disorders in females and males associated with diminished reproductive capacity and poor pregnancy and neonatal outcomes^3,5,10,29 (Table 2). Assisted reproductive technologies (ART) and fertility cohorts give insights into EDCs affecting reproductive potential and outcomes (e.g., the Environment and Reproductive Health Study at Harvard University (https://www.hsph.harvard.edu/earth/) and the Longitudinal Investigation of Infertility and the Environment (LIFE) Study at the US National Institutes of Health (https://www.nichd.nih.gov/about/org/dir/dph/officebranch/eb/longitudinal). Studies on ART cohorts provide correlations of fertility parameters in blood, follicular fluid, urine, and seminal plasma, as well as oocyte, sperm and embryo quality, and fertilization, clinical pregnancy, and live birth rates.

Female reproductive potential and competence

Specific EDCs disrupt pre- and postnatal ovarian development and egg quality, and menopause timing, based on studies in multiple species and humans.³ These include bisphenol A (BPA), phthalate congeners, diethyl-stilbesterol (DES), polycyclic biphenyls (PCBs), perfluorooctanoic acid (PFOAs), dioxins, parabens, and fenvalerate^3,10 (Figure 3A). The well-known toxicants, first- and second-hand environmental tobacco smoke, reduce folliculogenesis, steroidogenesis, ovarian reserve, embryo transport, endometrial receptivity, endometrial angiogenesis, and uterine blood flow, increase the rate of spontaneous miscarriage and ectopic pregnant, result in poor IVF outcomes and promote early menopause by 1–4 years.^30,31 EDCs also disrupt normal reproductive tract development and function, e.g., in utero exposure to DES, leading to compromised fertility, increased risk of vaginal cancer in young, exposed adults, and abnormal gamete function.³ A recent systematic review of prospective ART cohort studies between 2000 and 2016 demonstrated greater EDC exposure levels correlating with diminished ovarian reserve and peak estradiol (E₂) levels during ovarian stimulation, poorer oocyte and embryo quality, and lower fertilization, implantation, clinical pregnancy, and live birth rates³² (Table 3).

Male reproductive potential and competence

Phthalates, estrogens, and dioxins (e.g., TCDD), are key disrupters of male external genitalia development prenatally, resulting in decreased Leydig and Sertoli cell function, INSL3, and steroidogenesis, and impaired germ cell differentiation^5,6,12,33,34 (Figure 3B). Downstream effects are cryptorchidism, hypospadias, short anogenital distance, and impaired testosterone and spermatogenesis, predisposing to reduced fecundity and impaired pregnancy rates later in life.³⁵ In adult men, EDCs, such as phthalate esters and organochlorines, are associated with abnormal sperm quality (count, morphology, motility),³⁶ leading to possible mitigation strategies for fertility goals. Notably, some persistent EDCs (long-lived in the environment) and non-persistent (those with short half-lives) correlate with couple fecundability with gender-specific impacts and stronger associations in males versus females.^37,38

Air pollution and heat

Female reproductive potential and competence

Several animal studies demonstrate that air pollutant components (e.g., diesel exhaust and PM_2.5) have adverse functional and structural impacts on oocytes and granulosa cells, and decreased primordial follicle numbers, blastocyst rates, litter sizes, implantation rates, and live born.^13,39,40 In humans, residential PM_2.5 exposure levels correlate inversely with antral follicle count (AFC)⁴¹ and anti-Mullerian hormone (AMH) levels,⁴² and high SO₂ levels during and up to 1 year prior to an ART cycle correlate with poor ovarian reserve and response to stimulation, especially in those ≤30 years old.⁴³ Interestingly, a 1°C residential location T_{average max} increases 90 days before ovarian reserve testing correlated with a 1.6% (95% CI, −2.8, −0.4) lower AFC.⁴⁴

Male reproductive potential and competence

Air pollutants can also affect testicular development and function. Animal models show air pollution constituents result in increased germline mutations, decreased sperm counts, motility, and germ cells, increased FSH, and altered seminiferous tubule morphology, especially in response to diesel exhaust.^13,16 In humans, adult exposures to vehicular traffic PAH, SO₂, NO_x, PM₁₀, and O₃ in diesel exhaust versus nonexposed individuals correlate with decreased sperm morphology and motility, increased DNA fragmentation and sex chromosome disomy.¹³

Spontaneous conception

Proximity to major roadways (<200 m) correlates with decreased spontaneous conception⁴⁵ and increased likelihood of pregnancy by 3% for every 200 m away from a major roadway.⁴⁶ Also, exposures to high PM_2.5 levels correlate with lower spontaneous fecundity, longer time-to-pregnancy, higher odds of infertility^47,48 and lower live birth rates.⁴⁹ However, a large web-based preconception cohort study of pregnancy planners (Pregnancy Study Online (PRESTO)) found that neither annual average, menstrual cycle-specific, nor preconception average exposure to ambient PM_2.5, NO₂, and O₃ were appreciably associated with reduced fecundability.⁵⁰ Why this study differs from most others is unclear, and comparison of study designs, patient populations, and biomonitoring approaches are warranted.

Assisted reproduction

Closer residential proximity to major roadways has been significantly associated with lower probability of implantation and live birth rates after ART.⁵¹ While most studies found that residential ambient air pollution levels (PM_{2.5 or 10}, NO₂, SO₂, CO, O₃) correlate with poor ART outcomes independent of when in the IVF cycle these were measured,^52,53,54 other studies found greater effect sizes at specific times during ART cycles – from 90 days before cycle start, during stimulation, at oocyte retrieval, and during and 35 days beyond embryo transfer (ultrasound visit), which were more prominent in patients <35 years old.^55,56 Interestingly, high PM exposures but not specific gaseous components of air pollution on cycle day 3 (before embryo transfer) had a negative impact on miscarriage rates and clinical pregnancy rates.⁵⁷ In contrast to these data overall, a large retrospective study of >250,000 fresh IVF cycles in the US reported no clear evidence of significant association between cycle outcomes (implantation, clinical pregnancy, and live birth rates) and daily PM_2.5 or O₃ levels.⁵⁸ Whether multiple air pollution components analyzed together or integrated over time would have a different outcome is yet to be determined.

Pregnancy outcomes

Endocrine-disrupting chemicals

There is a voluminous literature that supports EDC effects on pregnancy and neonatal outcomes.^7,10,18,59 EDCs and routes of maternal, fetal, and placental exposures are shown in Figure 4. Associations of EDC exposures and pregnancy and neonatal outcomes depend on the EDC chemical structure, solubility, whether persistent or non-persistent, dose and duration of exposure, timing of exposure during gestation, and what compartment is evaluated for exposure levels (maternal urine, plasma/serum, placenta, cord blood, amniotic fluid) and how these are measured.^7,59 Most studies evaluate data at a single gestational time point with limited attention to organ-specific differences in susceptibility windows across gestation in the fetus and that fetal sex can modulate EDC effects, and few stratify data for ethnicity, age, diet, pre-pregnancy weight, weight gain, and lifestyle factors. Important in mitigation strategies are these considerations and to follow the offspring longitudinally, as well as correlations of exposures with subsequent maternal morbidities.⁷ Overall, the data strongly support EDCs affecting gestational length (increased risk of preterm birth and some associated with delayed delivery), gestational fetal size (fetal intrauterine growth restriction, and small or large for gestational age), and congenital anomalies in the offspring. While maternal complications of pregnancy (spontaneous miscarriage, gestational hypertension, pre-eclampsia, and gestational diabetes) are on the rise globally, current evidence supports EDCs as contributors to the well-established demographic and lifestyle factors at play in these disorders.⁷ There is also substantial evidence of specific EDCs associated with poor neurodevelopmental and other adverse neonatal outcomes (Table 2). Mitigation strategies for minimizing harm to mothers and children are considered below.

Air pollution and heat

The majority of studies conclude that PM and gaseous components of air pollution, duration of exposures, and gestational windows of exposure correlate with adverse pregnancy outcomes, including spontaneous miscarriage, stillbirth, preterm birth (PTB), low birth weight (LBW), gestational hypertension (GH), very LBW, and pre-eclampsia.^{14,60,61,62,63} Some examples are presented below.

Spontaneous miscarriage

In a prospective cohort study of couples trying to conceive, exposure to air pollution throughout pregnancy was associated with loss, with O₃ and PM_<2.5mm associated with faster time to loss and sulfate compounds with increased risk of loss.⁶⁴ Spontaneous pregnancy loss rates were noted to correlate with air pollution in a study in Mongolia with seasonal PM_2.5, PM_10.0, SO₂, NO₂, and CO fluctuations tracking with miscarriage rates⁶⁵ (Figure 5A). Also, increased miscarriage and stillbirth rates correlate with satellite measures of PM_2.5 exposures during gestation in Africa⁶⁶ (Figure 5B), with similar findings in South Asia, especially among older women and in urban settings across India, Pakistan, and Bangladesh.⁶⁷

Low birth weight, preterm birth, and other

Maternal exposure to fine PM air pollution is associated with increased risk of PTB and LBW.^68,69 Exposure to high levels of air quality indicators (O₃, PM, CO, SO₂) in California was associated with increase risk of PTB at 20–27 gestational weeks,⁷⁰ attributed to epigenetic modifications, functional changes, and inflammation in the placenta.^71,72 A geospatial population-based cohort study using live birth records in Ohio (2007–2010) linked to average daily PM_2.5 measures, revealed that high levels of airborne PM especially during the 2nd trimester are associated with PTB.⁷³ In Florida PM_2.5 had consistent correlations with adverse outcomes (LBW PTD, very PTD); whereas O₃ had inconsistent effects.⁷⁴ In contrast, in Kansas, consistent associations between adverse pregnancy and birth outcomes with PM_2.5 exposure were not observed, although there was a positive link between increased O₃ exposure during pregnancy and a higher risk of PTB, GH, and LBW.⁷⁵ A large US study of 32,798,152 births revealed an association of air pollution and heat exposure with PTB, LBW, and stillbirth, across all US geographic regions, with highest risk sub-populations of patients with asthma and minority groups, especially Black mothers.⁷⁶ While most US studies concur regarding exposures and air pollution levels and poor pregnancy and neonatal outcomes, some observed differences likely reflect regional differences in air pollution exposures, heat, and patient sociodemographic and economic status and other features. Notably, across the globe the number of PM_2.5-associated preterm births in 2010 was estimated at 2.7 million, or 18% of total PTBs, with the highest burden in South/East Asia, North Africa, Middle East, and West sub-Saharan Africa.⁷⁷

A recent systematic review determined that global heat is associated with PTB, LBW, and stillbirth.⁷⁸ Direct effects of extreme heat on pregnant persons and in utero exposures⁷⁹ are shown in Table 4. Increased late PTB has been attributed to altered uterine blood flow in response to exposure to heat stress.⁸⁰ These effects are important to consider for maternal and neonatal health and impacts on healthcare systems⁷⁹ and offer opportunities for risk mitigation.

Climate change has increased wildfires across the globe that bring extreme heat, particulate matter air pollution, as well as ECDs volatilized from building materials and other sources. Studies have revealed associations with poor pregnancy outcomes, including increased risk of LBW⁸¹ and PTB⁸² rates. Underlying mechanisms are believed to derive from placental toxicity and inflammation.⁸³ Interestingly, in a study from the San Francisco Bay Area, exposure to wildfire specific PM_2.5 during the 2nd trimester of pregnancy between 2017 and 2020 was positively associated with increased risk of large for gestational age newborns and duration of exposure.⁸⁴ Notably, in California, 3.7% of preterm births between 2007 and 2012 were attributable to wildfire smoke.⁸⁵

EVIDENCE THAT INTERVENTION STRATEGIES DECREASE EDC BODY BURDENS

Several interventions have been evaluated for effectiveness in altering EDC and air pollution component levels in animals and humans and whether they impact phenotypes or health outcomes. For example, epigenetic modifiers (e.g., methyl donors) administered to pregnant agouti mice exposed to BPA throughout gestation resulted in decreased obesity and change in coat color of the offspring.⁸⁶ In humans, when children eating a conventional diet were changed to an organic diet, urinary metabolites of organophosphorus pesticides were non-detectable and then were elevated upon re-introduction of the conventional diet.⁸⁷ In the HERMOSA study of Latina girls in California, changing personal care products to those without triclosan, BP-3/oxybenzone, parabens, and phthalates for 3 days resulted in lowered urinary levels of these compounds.⁸⁸

Recently, the International federation of Gynecology and Obstetrics (FIGO) Committee on Impact of Pregnancy on Long-term Health and the Committee on Climate Change and Toxic Environmental Exposures published a semi-structured review, using PRISMA guidelines, to examine nutritional interventions on EDC levels in volunteers, ultimately to improve reproductive, perinatal, and obstetric outcomes.⁸⁹ Sixteen studies met criteria, ranging from 15 to 355 participants; three included pregnant participants, six included young healthy participants, two included families (parents, children), two examined interventions in only school-going children, four included mixed-gender populations with type 2 diabetes, cardiac atheromatous disease, and age over 60 years. Seven studies were randomized controlled trials (RCTs), three were RCT cross-over studies, and six were non-randomized experimental trials. The evidence overall supports organic food consumption and avoiding plastics and canned foods and beverages reduce dietary exposures to EDCs and body burdens. Moreover, avoidance of fast foods, dietary supplementation with iodine, a vegetarian diet, fatty fish diet, altering personal care products, and removing dust are all supported by evidence to lower EDCs and some multiple EDCs.⁸⁹ Using a similar approach, Park et al. conducted a scoping review⁹⁰ wherein ~ 50% of studies were single arm designs (no controls). They found most interventions resulted in lowered EDC levels in blood and/or urine and some studies overlapped with the Corbett.⁸⁹ Surprisingly, most volunteers did not want to change their diet even with EDC levels demonstrated to be lower with interventions – underscoring some challenges in mitigation strategies. In a 1-week study of Taiwanese girls at high risk of phthalate exposures, intervention strategies (frequent handwashing, using less shampoo and shower gel, not using plastic containers, or not eating food with plastic bag/plastic-wrap cover, microwaving food, or taking nutrition supplements, and reducing use of cosmetics/personal care products resulted in marked reduction in urinary phthalate congeners.⁹¹

Thus, while so far there is rare evidence that interventions to reduce EDCs in people lead directly to health improvements, the associations of EDCs with reproductive harm, described throughout this review, argue strongly in favor of implementing interventions that need to be acceptable, easy to do, with minimal side effects, and at low cost to practically mitigate risks. While disparities prevail in access to and affordability of some of these interventions (organic foods, glass and stainless-steel bottles and containers), empowering patients and citizens for safe environments is key. A large part of risk reduction includes governmental policies that go beyond what individuals can do for themselves, their families, and their communities. Examples include eliminating lead in gasoline that resulted in lowering blood levels of lead to <1 mg/dL in most countries,⁹² legislated public smoking bans in Scotland that coincided with reduced preterm birth rates,⁹³ and the PBDE ban in California in 2005, that reduced PBDE levels by 65% in pregnant women in the state between 2007 and 2012.⁹⁴ Thus, education, prevention, and advocacy, with patients as partners, are key to health and especially reproductive health.^{95,96,97,98,99,100}

CLINICAL MANAGEMENT

Environmental toxicants affect reproductive potential and fetal development during in sensitive periods, mainly during organogenesis, in the neonatal period, and in the reproductive years.¹ Thus, in utero and adult exposures to EDCs can compromise reproductive health (Table 5, summary). The question arises as to how much the public and healthcare providers know about adverse effects of environmental toxicants and reproductive health outcomes, what their personal, family, and community risks may be, and how to mitigate these risks.

Patient awareness

Several biomonitoring studies, surveys and focus group reports have provided information on what individuals know and want to know about environmental toxicants. Many pregnant persons queried were unaware of environmental toxicant impacts on reproductive health, and while some were concerned about toxicants, their healthcare providers were not addressing these issues and they did not trust publicly available resources.^101,102 A study on awareness and risk perceptions found that pregnant persons’ EDC risk perception was “modest”, and perceived exposure was higher than perceived susceptibility (i.e., they did not believe they were particularly susceptible to exposure but believed that exposure to EDCs was extremely dangerous.^103,104 Research on biomonitoring cohorts and pregnant persons underscored that patients want information on personal exposures to EDCs and believe they have the right to know.¹⁰⁵ Perceptions specifically about the link between exposure to EDCs and a decline in human male fertility was well received, contradicting assumptions that transparency about scientific uncertainty of EDCs elicits negative psychological effects.¹⁰⁶ Among a focus group of 19–65 year-olds of both genders, responses revealed generally little knowledge of and awareness about EDCs, their sources and associated health effects,¹⁰⁷ and while unaware of possible individual mitigation strategies, the majority expressed that it was the government’s responsibility to mitigate effects.¹⁰⁷ Thus, it is likely that patients before and during pregnancy want to know risks, and the challenge to healthcare teams is to be able to converse about these issues while caring for patients and being respectful of patient goals and values.

Healthcare provider awareness

The American Congress of Obstetricians and Gynecologists (ACOG) performed a mixed-methods study involving a national online survey of ACOG fellows and a focus group of obstetricians to determine their attitudes beliefs and practices regarding prenatal environmental exposures.¹⁷ Notably, 100% of respondents asked pregnant patients about alcohol consumption, diet, and smoking. However, <20% inquired about environmental exposures common in pregnant women in the US¹⁰⁸ The majority (78%) of obstetricians surveyed believed they could reduce patient exposures, but <20% reported taking an environmental health history because of competing clinical priorities, time limitations, not knowing what to say, and uncertainty about the state of the evidence, and mitigation strategies.¹⁷

Identifying risks, advising about mitigation strategies

Over the past 15 years, research organizations and professional organizations focused on reproductive health have issued statements/committee opinions/guidances to educate healthcare providers about EDC exposures and risks (and a few have focused also on climate change and heat (FIGO, Philippine Obstetrician and Gynecologist Society (POGS)) prior to and during pregnancy.^18,97,98,99 Links to these resources are in Box 1. The goal has been to empower healthcare providers to answer patient questions and provide resources for trainees, staff, themselves, and patients, and know referral mechanisms for challenging inquiries.

Clinicians do not need to be experts in environmental and occupational reproductive health to prevent adverse health outcomes.¹⁸ They can, e.g., provide information and discuss areas of uncertainty about environmental chemicals so patients can make informed choices based on their values and preferences. Complementary approaches requiring minimal time on the part of the busy clinician include ancillary staff putting information brochures in packets given to patients on entry to pre-conception and/or prenatal care and/or making brochures available in the waiting or exam rooms and on-line. In addition, staff can provide patients with information on nutritional counseling or other relevant health education regarding avoidance of toxic chemicals.^10,18,98

Taking an environmental exposure history

Key to capturing patient exposures in their home and work environments and resulting from lifestyle choices is taking an environmental exposure history.¹⁸ Examples of environmental toxicant exposure history forms are available at http://prhe.ucsf.edu/clinical-practice-resources. When counseling patients about exposures, important considerations include routes of exposures, toxicity, dose, frequency, duration, and timing (especially during developmental windows of vulnerability). Individual patient vulnerabilities warrant consideration including underlying health conditions and sociodemographic status.^10,109 It is also important to identify if patients have exposures to substances with reproductive toxicity, as they are at high risk for adverse reproductive outcomes,¹¹⁰ and legal workplace limits are not always designed to protect pregnant women.¹¹¹ Hobbies can also pose risk if they involve EDCs (e.g., solvents, heavy metals), and while exposures may be lower than those employed using similar products (e.g., jewelry making), those with hobbies likely have less training in safety, thus underscoring the importance of counseling.¹⁰

Risk mitigating strategies for patients and communities

Reducing or eliminating environmental toxic exposures prior to conception in males and females and throughout pregnancy are the most effective strategies to prevent adverse reproductive health consequences. An exposure history and advising patients on how to prevent exposures at home, work, and in the community, and with appropriate resources and referrals are critical to this process. Also, environmental injustice with disproportional exposures of socio-demographically disadvantaged communities that can exacerbate the impact of environmental exposures underscore the need for rigorous evaluations and thoughtful and supportive counseling of high-risk groups.¹⁰ Box 2 lists summary of practice points regarding mitigation strategies, most at low cost, recommended by several professional societies.^{4,9,10,89,98,99,100}

Also, some helpful resources for healthcare providers and patients include:

• https://www.hormone.org/your-health-and-hormones/endocrine-disrupting-chemicals-edcs
• https://www.who.int/en/news-room/fact-sheets/detail/household-air-pollution-and-health
• https://prhe.ucsf.edu/info
  • Toxic Matters: Protecting Our Families from Toxic Substances
  • Work Matters: When You Work with or Around Toxic Chemicals, What You Know Really Matters
  • Pesticides Matter: Steps to Reduce Exposure and Protect Your Health
  • What to Eat: A Guide to Your Daily Food Choices
• http://www.ewg.org/skindeep

CONCLUSIONS

Overall, the data to date strongly support a deleterious impact of EDCs and climate change (air pollution and heat) on female and male reproductive capacity and pregnancy and neonatal outcomes. It is key that health care professionals are educated about these issues and can converse with their patients, families, and communities, as well as policy makers about mitigation strategies. There is too much at risk for the current and future generations to do otherwise.

PRACTICE RECOMMENDATIONS