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Published in final edited form as: Child Dev Perspect. 2022 Dec 12;17(1):32–38. doi: 10.1111/cdep.12472

Prenatal socioenvironmental exposures and autism spectrum disorder: A web of confusion

Aisha S Dickerson a, Asha S Dickerson b
PMCID: PMC10275509  NIHMSID: NIHMS1859339  PMID: 37334167

Abstract

Although evidence of heritability for autism spectrum disorder (ASD) is strong, studies of twin pairs suggest that at least some portion of the etiology is attributable to environmental factors, either directly or through interaction with genes. Given the multitude of environmental and psychosocial exposures that have been reported to increase atypical neurodevelopment in offspring, in this article, we summarize what prenatal air pollutant, chemical, and occupational exposures and psychosocial stressors have been reportedly associated with ASD and co-occurring neurodevelopmental disorders. We highlight consistencies in reported associations and recommend areas for research to close gaps in our understanding of environmental risk for ASD. Because this issue is of particular importance in historically marginalized communities and low- and middle-income countries, we also discuss the importance of environmental justice issues and exposure disparities in research, and we advocate for prioritizing policies to reduce disparities and improve service provision in vulnerable populations.

Keywords: neurodevelopment, environmental exposures, environmental justice

Introduction

Autism spectrum disorder (ASD) is a chronic disorder of the central nervous system that manifests in infancy or early childhood and is characterized by impairments or delay in communication and restricted or repetitive behaviors (Lord et al., 2018). Public attention to ASD has increased worldwide since the 1990s, which has influenced diagnostic and surveillance efforts to close gaps in epidemiologic knowledge (Zeidan et al., 2022). Although the prevalence of ASD has seemingly increased over the past few decades, this may be the result of changes in diagnostic criteria over time (Zeidan et al., 2022). Estimated median prevalence of ASD worldwide was reported as 100 per 10,000 with a range of 1 to 436 per 10,000 based on 99 reports from 34 countries with lower ascertainment in low- and middle-income countries (Zeidan et al., 2022). With an estimated lifetime financial burden of around $2 million for the care of an individual with ASD in the United States (Lyall et al., 2017), the significance of this disorder has garnered increased public health interest.

Although the etiology of ASD is not fully understood, evidence of heritability is strong, and studies of twin pairs suggest that at least some portion of the etiology is attributable to environmental factors (Lyall et al., 2017), either directly or through interaction with genes (Kalkbrenner et al., 2014; Thapar & Rutter, 2021). Additionally, exposures to certain toxicants can elicit epigenetic changes, which could affect the pathophysiology of ASD (Lyall et al., 2017; Williams & LaSalle, 2022). Hazardous toxicants can influence genetic changes in both parents and offspring, and several candidate environmental risk factors have been identified over the past few decades. However, many studies have used retrospectively collected data focusing on one time point of exposure, limiting the ability to assess causality.

Numerous environmental and psychosocial exposures have been reported to increase the likelihood of atypical neurodevelopment in offspring. Research on brain development must move away from a one-exposure model and into investigations of co-occurring socioenvironmental exposures, gene-environment interaction, and the impact of cumulative environmental and psychosocial stressors prior to pregnancy. This is particularly important in historically marginalized communities. With this in mind, in this article, we summarize what air pollutant, occupational, and chemical exposures, as well as psychosocial stressors, have been associated with ASD and commonly co-occurring conditions, focusing on prenatal socioenvironmental exposures in vulnerable populations. We also recommend areas for research to close gaps in our understanding of the relation between exposures and ASD.

Environmental Exposures and Prenatal Brain Development

Chemicals

Some industrial chemicals, such as lead, benzene, and toluene, are established neurotoxicants. Even exposure to low doses of industrial chemicals in utero can be detrimental to fetal brain development (Grandjean & Landrigan, 2014). Although the placenta offers some protection against chemical exposures, many toxicants like heavy metals easily cross the placenta and the blood-brain barrier, which is not fully developed until a few months after birth (Engelhardt & Liebner, 2014). Thus, certain toxicants can interfere with neurodevelopment during gestation through transport across the placenta after maternal exposures. Of particular interest is exposure to endocrine-disrupting chemicals, which can influence levels of hormones essential for brain development (Schug et al., 2015). These can include pesticides, which have reported associations with ASD through biomarkers of prenatal exposure as well as residential proximity to agricultural land (Kalkbrenner et al., 2014; Lyall et al., 2017). Furthermore, a considerable amount of research has investigated exposure to heavy metals, which can directly affect neurodevelopment through oxidative insult (Dickerson, Rotem et al., 2017; Grandjean & Landrigan, 2014). With some metals also acting as endocrine disruptors (Lyall et al., 2017), and established associations between prenatal exposure to lead and ASD (Kalkbrenner et al., 2014), heavy metal exposures are of great concern.

Occupational Exposures

Regarding occupational exposures, some studies have indicated associations between parents’ work-related exposures to disinfectants, solvents, and pesticides, and risk of ASD (Bemanalizadeh et al., 2022; Dickerson et al., 2014; Kalkbrenner et al., 2014). Volatile organic chemicals are common in occupations related to construction and supply production through persistent exposures to combustion byproducts, paints, and solvents, all of which have been established as neurotoxic (Grandjean & Landrigan, 2014; Kalkbrenner et al., 2014). A recent review and meta-analysis of prenatal parental occupational exposures and ASD concluded that there were not significant associations between parental exposures to pesticides, exhaust, or solvents and ASD, but that parents’ occupational exposure to metals may increase the risk of ASD in offspring (Bemanalizadeh et al., 2022). Although evidence of associations between parents’ occupational exposures and ASD is limited, many of these chemicals can bioaccumulate prior to pregnancy and later metabolize to expose the fetus during pregnancy.

However, many of these studies used self-reported occupational exposures, recorded parents’ occupations at or around the time of birth, had a small number of participants, had broad categories of exposure (e.g., ever/never, high/low), and used chemical classifications rather than assessing individual chemicals. Therefore, the potential for exposure misclassification and the absence of exposure time windows relevant to mutations of sperm and eggs may mitigate possible associations between estimated parental occupational exposures and risk of ASD in offspring.

Air Pollution

Air pollutants can be both directly transferred to the fetus through maternal circulation (depending on the chemical) and indirectly affect fetal growth by altering the in utero environment via inflammation and oxidative stress, so they are of particular concern to neurodevelopment (Grandjean & Landrigan, 2014; Kalkbrenner et al., 2014). Several studies have found associations between ASD and exposure to particulate matter and ambient air toxicant concentrations, as well as proximity to roadways and industrial facilities (Dickerson et al., 2016; Dickerson et al., 2015; Lam et al., 2016). Some studies have used the Environmental Protection Agency’s National Air Toxics Assessment data to evaluate associations between specific species of particulate matter during pregnancy and ASD symptomology and diagnosis to identify associations with ambient lead, manganese, mercury, nickel, ethylene thiourea, volatile organic chemicals, and 4-Nitrophenol (Dickerson et al., 2016; Kalkbrenner et al., 2018; Lam et al., 2016), but results have been conflicting.

Furthermore, male fetuses may be more vulnerable to exposure to toxicants, which may in part explain the higher prevalence of ASD in boys; however, sex-specific susceptibility can vary by toxicant and greater susceptibility in one group does not discount the hazards observed in the other. Overall, results from studies using data on air pollutant species have been conflicting and were often conducted in individual cohorts with smaller samples. Additionally, while some of these studies attempted to examine joint effects of environmental exposures (Dickerson et al., 2016; Kalkbrenner et al., 2018), few have also investigated the combined influence of air pollution exposures and psychosocial stressors (Lett et al., 2017).

A Vulnerability Framework for Neurodevelopmental Risk

Psychosocial Stressors

The importance of minimizing psychosocial stress in pregnant women has long been discussed in public and clinical health. Repeated chronic stressors, often resulting from systemic discrimination and segregation, can manifest within a household, workplace, school system, and community (DeFur et al., 2007). Although discrimination based on race/ethnicity is the most prolific and ubiquitous form of discrimination in the United States and worldwide, discrimination and inequalities can also be inflicted based on sex, gender identity, nationality, class, religion, age, physical ability, or other characteristics socially constructed as less than based on regional norms. Discrimination based on these identities alone and in combination leads to various inequities and hardships.

Furthermore, the economic difficulties experienced by people living in low- and middle-income countries can be compounded by extreme lack of necessary resources and frequent hardships. The adverse influence of psychosocial stressors on these groups during pregnancy is associated with neurodevelopment (Hyde et al., 2022; Sandman et al., 2012), and may interact with multiple environmental hazards to significantly magnify the adverse health impact of environmental exposures (Payne-Sturges et al., 2018). Additionally, exogenous psychosocial stressors can lead to individual-level impacts on cardiovascular load, sleep quality, and mental health, along with immune responses and inflammation (Burger et al., 2020), which have also been associated with adverse neurodevelopment. Removal of this stress and even the ability to sit and rest is often a privilege not afforded to women in poverty.

Additionally, unemployment or underemployment inhibits access to basic necessities, increasing the likelihood of experiencing additional environmental and psychosocial stressors. These include access to adequate housing, living in high-crime neighborhoods, struggling with food insecurity, and anxiety concerning current and future financial obligations. As researchers continue to study these issues, there is consensus that adverse outcomes, including ASD and co-occurring neurodevelopmental disorders, are more prevalent in children of distressed mothers, especially when considering maternal depression (Burger et al., 2020; Carlsson et al., 2021). A healthy prenatal environment is critical for optimal neurodevelopment, and the presence of psychosocial stressors and environmental hazards can disrupt this development (Demers et al., 2021; Payne-Sturges et al., 2018).

Community Disadvantage

Sources of both physical and social environmental factors—at the individual, community, and area levels—may synergistically interact with biological and psychosocial characteristics, potentially increasing cumulative risk for various adverse health outcomes (DeFur et al., 2007; Payne-Sturges et al., 2018). Under-resourced neighborhoods populated with residents with low incomes and members of historically underserved racial/ethnic communities often experience a greater exposure to multiple environmental hazards with links to adverse health outcomes (Mikati et al., 2018; Morello-Frosch et al., 2011; Payne-Sturges, Gee, & Cory-Slechta, 2021). These geographies of susceptibility and exposure contribute to the production of health disparities (Morello-Frosch et al., 2011; Payne-Sturges, Gee, & Cory-Slechta, 2021). Community-level disadvantage, such as neighborhood poverty, low-quality housing, and residential segregation, have also been associated with a range of hazardous environmental exposures, including industrial air pollution, compromised nutritional intake, and disproportionate other harmful toxicant exposures (see Figure 1). Finally, research on inequalities in low- and middle-income countries, where exposure to multiple environmental toxicants and social inequalities are pervasive, is lacking due to gaps in access to resources and assessments of exposure (Mustapha et al., 2022).

Figure 1.

Figure 1

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A Conceptual Illustration of Joint Environmental and Psychosocial Stressors Across Differing Time Points and Potential Modes of Action for Atypical Neurodevelopment

Directions for Research

Exposure Assessment Windows

Although researchers have examined windows of exposure through differences in timing during pregnancy, many toxicants can store for years. Therefore, we need a cumulative approach to assessing exposures. Lead, a notably hazardous neurotoxicant, can accumulate in bone over a lifetime and be released into the bloodstream as bone metabolizes during pregnancy and lactation (Kovacs, 2016). Additionally, several lipophilic compounds and chemical solvents can accumulate in adipose tissue, then be released into the blood and transferred to the fetus as fat is rapidly broken down during the third trimester of pregnancy, and to infants via breastmilk during lactation (Herrera & Ortega-Senovilla, 2010). However, many studies have used retrospectively collected data focusing on one time point of exposure, limiting the ability to assess causality. Researchers should aim to address more fully the issue of relevant windows of joint parental exposures through population-based studies with objectively and prospectively collected data in early life and at reproductive age, allowing for rigorous individual-level estimation of exposure over different time points.

Genetic Studies

Fetal development is a period of rapid neural growth, synapsis, and aggregation. These biological processes depend on gene expression, and any alteration of these genes can yield brain alterations with long-term developmental consequences (Castagna et al., 2022). Both environmental and psychosocial stressors could illicit epigenetic changes that could lead to differing expressions of neurobehaviors and symptomology, which may be a pathway to atypical neurodevelopment (Lyall et al., 2017; Williams & LaSalle, 2022). Specifically, as parents encounter hazardous exposures, molecular damage may alter gene expression; this alteration could occur along the germline prior to conception and pregnancy and directly affect fetal development, or it could alter a mother’s ability to metabolize and excrete toxicants, increasing potential in utero exposures.

Risk of epigenetic mutations in the germline can also increase with parental age, which may in part explain the increased risk of ASD with both maternal and paternal age (Lyall et al., 2017). Although studies of parental exposures have focused on transmission from the mother to the oocyte or fetus, male-mediated developmental impact may occur via paternal exposures (Payne-Sturges et al., 2022). This could include DNA damage that harms spermatogenesis, transfer of exposures to mothers through household contamination, and transmission of toxicants through seminal fluid. Sperm quality plays an important role in embryonic development and associations among ASD, assisted reproductive technology, and paternal age (Lyall et al., 2017): Previous associations between sperm quality and neurodevelopment in offspring could be mediated by fathers’ exposures.

As technology to determine epigenetic alterations becomes more available and as more studies collect these data and collaborate to achieve statistical power suitable for analysis, researchers should be able to study these factors. Efforts to investigate the exposome—all exposures experienced over the lifetime—in combination with epigenetics will contribute to a more thorough understanding of what part gene-environment interaction plays in the etiology of ASD.

Environmental Inequality in Under-Resourced Communities

Research has continuously demonstrated disparities in adverse health outcomes in children from historically marginalized populations, indicating that they have consistently worse fetal and developmental outcomes (Payne-Sturges, Gee, & Slechta, 2021), as well as impairments in behavior, mental health, and cognition (Shonkoff & Garner, 2012). These vulnerable populations also have been disproportionately burdened with more exposure to toxicants, including high-traffic road pollution, contaminated water sources, lead-based paint, and air pollution from nearby industrial facilities, along with less access to services and quality of care (Morello-Frosch et al., 2011; Payne-Sturges, Gee, et al., 2021). This burden is even more prominent in low- and middle-income countries where resources are limited, infrastructure is weak, and pollution is abundant (Mustapha et al., 2022).

Investigating these disparities in environmental health requires adequately assessing both environmental and social factors. Several epidemiologic investigations of environmental exposures and neurodevelopment treat socioeconomic factors as confounders when the occurrence of environmental disparities in marginalized, under-resourced communities, commonly inhabited by minoritized, immigrant residents with low incomes, suggests that they are effect modifiers. Additionally, many studies continue to evaluate these co-occurring exposures and stressors separately, ignoring the influence of environmental justice issues (Payne-Sturges et al., 2018). This is especially important in neurodevelopment, with previously mentioned observed physiological effects of in utero psychosocial stressors on the developing fetal brain (Burger et al., 2020; Demers et al., 2021).

Neurodevelopmental impairments subsequent to environmental and psychosocial exposures in families with low incomes are compounded by greater financial burden for care in families that are already ill-equipped to handle these expenses, and often results in a cyclic gap in educational achievements and income attainability (Attina et al., 2019). Furthermore, with the capacity for ASD research and clinical service provision still developing along with competing health priorities (e.g., nutrition, infection, mortality) in low- and middle-income communities (Hahler & Elsabbagh, 2015; Zeidan et al., 2022), the need to reduce morbidities from ASD and co-occurring conditions is of great concern. Researchers need to investigate modifiable risk factors for ASD, especially in historically marginalized populations that are often overburdened with exposures to known neurotoxicants but have more barriers to access to care for ASD and co-occurring neurodevelopmental disorders.

Co-Occurring Risk Factors

Individuals from historically marginalized populations, including racially/ethnically minoritized individuals, often experience multiple environmental exposures through residential segregation into sacrifice zones—communities of low-income and minoritized residents disproportionately burdened with environmental pollution (Bullard, 2011). They face a combination of ambient exposures to air pollutants, aging piping for drinking water, and proximity to pollution sources, as well as more hazardous occupational exposures as a result of limited employment opportunities due to discriminatory hiring practices and lower education levels. Such exposures are more frequent and widespread in low- and middle-income countries (Mustapha et al., 2022).

Considering that both hazardous exposures and psychosocial stressors harm immune function, nutrient metabolism, and neurodevelopment, together they could compound the risk of ASD when parents experience both (Payne-Sturges, Cory-Slechta et al., 2021). Sources of both physical and environmental factors—at individual, community, and area levels—may interact with biological and psychosocial characteristics, potentially increasing cumulative risk (DeFur et al., 2007; Payne-Sturges et al., 2018). Additionally, psychosocial stressors commonly associated with health disparities may amplify the effects of these environmental exposures in more vulnerable populations (Demers et al., 2021; Morello-Frosch et al., 2011; Payne-Sturges, Gee, & Slechta, 2021; Payne-Sturges et al., 2018). With further established knowledge that exposures to chemicals are often experienced as mixtures, researchers should use advanced statistical approaches to assess the impact of joint exposures—both environmental and psychosocial. Furthermore, with disproportionate exposures in marginalized and under-resourced communities, these analyses could identify the greatest risk to neurodevelopment and ascertain the most important areas of priority for policy change.

Conclusion

Although few studies have examined the possible relations among environmental exposures, psychosocial stressors, and disparities for adverse health outcomes, they have often attempted to do so with small samples or using a cross-sectional design. As research progresses into prospective evaluations of environmental exposure in relation to ASD and co-occurring neurodevelopmental disorders, vulnerable populations that experience a disproportionate burden of exposure, disease, and disparities must be prioritized. Epidemiologic studies of environmental effects on human disease should not just model the direct effects of individual environmental hazards independent of area-based stressors; they should examine these exposures using multilevel modeling that considers environmental, social, and psychosocial factors at the community level with more focus on the critical role of racial/ethnicity segregation and socioeconomic status. These studies should also assess socioenvironmental exposures both before and during pregnancy, with an emphasis on modeling time-varying mixtures of exposure in both parents.

In light of the undermeasured impact of these exposures on ASD in vulnerable populations and in low- and middle-income countries due to disparities in diagnosis, research results underscore the public health significance of reducing pollutants and remediating toxicants, especially in under-resourced communities. Scientific evidence supports efforts to reduce individual and widespread municipal exposures to improve children’s development and overall public health through policy changes. Considering that children from historically marginalized populations are diagnosed with ASD and other neurodevelopmental disorders less frequently and later due to gaps in access to care and culturally competent assessment (Dickerson & Dickerson, 2020; Dickerson, Rahbar et al., 2017; Hahler & Elsabbagh, 2015; Zeidan et al., 2022), the risk of these disorders must be reduced along with improved services. Scientists and clinicians must advocate for reductions in chronic hazardous exposures, fair distribution of existing pollutants and their sources, and equitable cognitive assessments to boost capacity and address more fully the racial/ethnic and socioeconomic disparities in ASD. Clinicians offering prenatal care should routinely identify hazardous exposures; they should also promote health through guidance on how to avoid exposures and education on remediation measures to avoid neurodevelopmental impairment. These efforts could then transition into long-term community recovery and away from resilience through avoiding continued stressors instead of expecting those afflicted to overcome them.

Acknowledgements:

This article was produced with support from the Bloomberg American Health Initiative, which is funded by a grant from the Bloomberg Philanthropies. Aisha Dickerson was supported in part by a career development award (K01-ES032046, AD) and Environmental influences on Child Health Outcomes (ECHO) Opportunities for Infrastructure funding (U2C OD023375) from the National Institutes of Health.

Footnotes

Competing financial interests: No authors have any competing financial interests to declare.

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