New Directions in Understanding the Role of Environmental Contaminants in Child Development: Four Themes

Abstract

Environmental contaminants, which include several heavy metals, persistent organic pollutants, and other harmful chemicals, impair several domains of child development. This article describes four themes from recent research on the impact of environmental contaminants on child development. The first theme, disparities in exposure, focuses on how marginalized communities are disproportionately exposed to harmful environmental contaminants. The second theme, complexity of exposures, encapsulates recent emphases on timing of exposures and mixtures of multiple exposures. The third theme, mechanisms that link exposures to outcomes, focuses on processes that elucidate how contaminants impact outcomes. The fourth theme, mitigating risks associated with exposures, sheds light on potential protective factors that could ameliorate many of the harmful effects of contaminant exposures. Developmental scientists are well-positioned to contribute to interdisciplinary research that addresses these themes, which could foster additional conceptual and empirical innovations and inform policies and practices to mitigate risks and improve children’s well-being.

The physical environment plays a critical role in human health and well-being across the lifespan. Unfortunately, exposure to harmful contaminants in the physical environment is nearly ubiquitous. Based on a recent estimate from the World Health Organization, approximately 92% of the world population is exposed to harmful levels of ambient air pollution (World Health Organization, 2016). Environmental contaminants include heavy metals like lead, mercury, cadmium, and arsenic. Other environmental contaminants include persistent organic pollutants (e.g., polyfluoroalkyl substances [PFAS]) and bisphenol A [BPA]). Recent crises related to environmental contaminants include lead in water in Flint, Michigan (Hanna-Attisha et al., 2016), PFAS exposures near a chemical plant in West Virginia (Barry et al., 2013), and the ubiquity of BPA in numerous consumer products (Vandenberg et al., 2007). These crises underscore the importance of studying the extent to which environmental contaminants impact children.

Evidence suggests that exposure to environmental contaminants influences several domains of child development. For example, lead exposure is associated with lower IQ among children, even at low levels of exposure (Schwartz, 1994). Lead exposure as well as exposure to other heavy metals is also linked to behavior problems, including symptoms of attention deficit hyperactivity disorder (e.g., Boucher et al., 2012; Rodriguez-Barranco et al., 2013). Evidence that links contaminant exposures to physical health outcomes is also emerging, including a potential association between exposure to BPA and risk for obesity (Wang et al., 2013). Unfortunately, with few exceptions (see, for example, Manczak, Miller, & Gotlib, 2020), research on contaminant exposures and negative childhood outcomes in the environmental psychology, environmental health, and toxicology literatures has not translated into increased attention to these exposures in the developmental science literature (Trentacosta et al., 2016). For example, even though contaminant exposures are linked to executive function difficulties (e.g., Nigg et al., 2008), developmental scientists focus almost exclusively on parenting and other aspects of the psychosocial environment (e.g., schooling) when examining contextual contributors to childhood executive function (Trentacosta & Riggs, 2020). The current article provides an overview of recent directions in research on environmental contaminants that can deepen understanding of child development. These recent directions are organized into four themes. Because it is beyond the scope of the current article to provide a comprehensive review of the empirical literature for each theme, we provide multiple illustrative examples for each theme. Table 1 presents an overview of the themes, examples of research on each theme, and examples of how developmental scientists can contribute to future research on each theme, which are expanded upon in the subsequent sections. The overarching goal of this article is to underscore the idea that increasing developmental scientists’ involvement in research on environmental contaminants could strengthen and enrich developmental theories and empirical research on child development, which could inform practices and policies to mitigate risks and improve childhood well-being.

Table 1.

Overview of Four Research Themes

Theme	An Example of Existing Research on the Theme	An Example of How Developmental Scientists Can Contribute to Future Research on the Theme
Disparities in Exposures	Studies have found that children in marginalized communities are disproportionately exposed to neurotoxic chemicals that predict neuropsychological impairments and developmental delays (e.g., Leech et al., 2016).	Apply systems theories to develop hypotheses pertaining to how children’s complex ecological context contributes to their exposure to toxicants and subsequent health disparities.
Complexities of Exposures	Longitudinal studies have used weighted quantile sum regression to identify the relative contributions of mixtures of chemical exposures to subsequent developmental outcomes (e.g., Tanner, Hallerback, et al., 2020).	Use cutting-edge statistical models to study mixtures and pinpoint specific windows of increased susceptibility.
Mechanisms Linking Contaminant Exposures to Childhood Outcomes	Investigations informed by the Developmental Origins of Health and Disease hypothesis have demonstrated that early life contaminant exposures result in epigenetic changes, which may lead to later life health problems (Tran & Miyake, 2017).	Apply longitudinal mediation models to investigate the role that environmental contaminants may play in initiating developmental cascades involving epigenetic and brain-based pathways.
Protective Factors that Mitigate Risks Associated with Exposures	Aspects of the caregiving context have been examined as factors that may attenuate associations between contaminant exposures and poor developmental outcomes (e.g., Manczak et al., 2020).	Use moderation models to study conceptually-relevant features of the caregiving context in order to identify which features function as compensatory or protective processes.

Disparities in Exposures

Environmental contaminant exposures are a threat to environmental and social justice for children because they disproportionately expose children in marginalized communities to a variety of contaminants that increase their risk for a wide range of negative outcomes (National Research Council, 2012). The urgent need to address racial and socioeconomic health disparities was made evident by two recent high-profile public health crises, the Flint Water Crisis (Bellinger, 2016) in the United States, and the worldwide COVID-19 pandemic (Garg, 2020), which has disproportionately harmed racial minority and low-income communities due to underlying geographic, economic, and health inequities (Wu et al., 2020).

Recent research on contaminant exposures is shedding light on which children and families are disproportionately exposed and where exposures are concentrated. For example, chronic childhood lead exposure occurs primarily in urban centers, particularly in neighborhoods with low-income, substandard housing, high-traffic roads, aging infrastructure, and/or industrial sites (Leech et al., 2016). Despite newer policies enforcing tighter regulations on pollutants, the soil, water, and dust in these living centers are still contaminated via legacy effects. Due to the history of structural racism in the United States (Bailey et al., 2017)—e.g., the Great Migration, residential segregation, racist zoning laws, redlining, housing and job discrimination—racial and ethnic minorities, especially African Americans, are more likely to be born and develop in these environments. Consequently, Black children are three times more likely than White children to have elevated lead exposure levels (Leech et al., 2016). Pregnant Black mothers, who are more likely to live and have developed in these environments, often have lead in their bodies that transfers to the developing fetus through the placenta. Postnatally, children are exposed through re-suspended dust and drinking water in their homes (including contaminant transfer from parents’ place of work) and schools. Formula-feeding, which is more common among non-Hispanic Blacks and low-income groups, is a primary medium of exposure (Leech et al., 2016). However, breast-feeding also transfers lead when the mothers were lead-exposed, another form of intergenerational transfer that perpetuates exposure disparities. Since lead exposure has been linked to a long list of acute and chronic health conditions, neuropsychological impairments, and developmental delays, the exposure disparities help explain other disparities such as the achievement gap (Miranda et al., 2009). More research is needed to understand the developmental pathways by which exposure disparities perpetuate the achievement gap, which likely perpetuates the wealth gap (Shapiro et al., 2013), which in turn perpetuates exposure disparities and thus, a cycle of injustice.

Exposure disparities also take other forms and affect other vulnerable populations around the world. For example, air pollution inequalities (traced by nitrogen dioxide) in four French metropolitan areas have been associated with the spatial and socioeconomic composition of the cities and their historical evolutions (Padilla et al., 2014). In Tijuana, Mexico, female-headed households were found to be disproportionately exposed to carcinogenic hazardous air pollutants (HAPS) (Grineski et al., 2015), and in Houston, Texas, neighborhoods with relatively high same-sex partner households, especially male-partnered households, were more exposed to HAPS even after controlling for race, ethnicity, SES, and other risk factors (Collins et al., 2017). A recent study of exposure to 143 chemicals in 38,080 U.S. women found the highest disparities in non-Hispanic Black, Mexican American, Other Hispanic, and Multi-Racial women with respect to pesticides, metabolites, parabens, monoethyl phthalate, mercury, and arsenic (Nguyen et al., 2020). Latinos, African Americans, and low-income individuals are significantly more exposed to endocrine-disrupting chemicals (EDCs) such as PCDs, organochlorine pesticides, bisphenol A, and phthalates, which are linked to metabolic diseases, especially diabetes, that disproportionately affect these populations (Ruiz et al., 2018). Finally, epigenetic research is revealing how the long history of higher nutritional stress, psychosocial stress, and toxicant exposures in marginalized social groups leads to harmful epigenetic changes that endure across the lifespan and can be transmitted to offspring and grandoffspring, which helps explain current health disparities (Thayer & Kuzawa, 2011). These findings highlight the importance of research on the interaction of psychosocial urban stress, urban food deserts, and contaminant exposures, as these same epigenetic mechanisms will pass on disparities to future generations until environments are made more equitable.

The full scope and intensity of the long-term adverse effects of exposure disparities will be elucidated by studies designed to measure the interaction of developmental domains, developmental cascades, and/or intergenerational impacts (Bellinger et al., 2016). Developmental scientists can use an array of systems theories to inform new hypotheses about the ways the child’s ecological context creates and maintains exposure and health disparities. For example, Bronfenbrenner’s Bioecological Model of Human Development (Bronfenbrenner & Morris, 2006) has been used to integrate contaminant exposure disparities into a larger framework that relates group identity, material allocation, and inter-group conflict to the reproduction of social class and its attendant child health disparities (Kramer et al., 2017). The “riskscape” is another research framework that explains how stressors and buffers at the individual and community level affect a child’s allostatic load, which plays a role in the adverse effects of environmental contaminants and partially accounts for related health disparities (Morello-Frosch & Shenassa, 2006). New research on interventions designed to lighten allostatic load may lower the rates of low birth weight, preterm birth, and infant and mother mortality caused by the “triple jeopardy” of socioeconomic stress, racial disparities, and environmental contaminants.

Finally, the public health exposome is a transdisciplinary model designed to identify mechanisms by which exogenous and endogenous exposures impact biopsychosocial systems across space, time, and place, resulting in poor individual health outcomes and population-level disparities (Juarez et al., 2014). This model can help guide developmental scientists through the application of multi-level and “Big Data” analytic techniques to investigate contaminant exposure disparities while also considering other disparities that are known to play a role in child development. For example, mixtures of several contaminant exposures, which will be described in the next section, could be studied in tandem with multiple features of the psychosocial environment (e.g., disparities within the home, school, and neighborhood contexts) that also contribute to enduring childhood disparities.

Complexities of Exposures

In response to the single exposure paradigm that has been dominant in empirical research on environmental contaminants (Tanner et al., 2020a), research has begun to examine how variability in contaminant mixtures and exposure timing relates to key developmental outcomes. The developmental effects of environmental mixtures are not best construed as the summation of the intrinsic and fixed toxicity of individual chemicals. Rather, they are best construed as interactions between the kinds and quantities of chemicals in the mixture and the developmental processes taking place when the child is sequentially or simultaneously exposed to these chemicals. Impacts of the level and timing of exposure are well demonstrated by a growing number of studies using deciduous (baby) teeth to identify critical periods when prenatal and postnatal metal exposure most strongly alters neurodevelopment. Tooth-matrix biomarkers allow researchers to trace exposures back to the second and third trimesters on an almost weekly level of specificity (Arora & Austin, 2013). As a result, some time and dose dependent effects of chemical exposures have been revealed, exemplified by the case of manganese (Mn).

Both a dearth and surplus of Mn exposure predict adverse neurodevelopmental outcomes, and although greater prenatal Mn exposure has been associated with improved childhood visual spatial ability (when lead exposure levels are not high), greater postnatal exposure has been associated with lower visual spatial ability (in boys only) (Claus Henn et al., 2018). Moreover, whereas higher prenatal and early postnatal Mn exposure protected against hyperactivity and attention problems (ages 8 – 11), higher Mn levels at 6 postnatal months increased the risk for anxious behaviors (Horton et al., 2018). Thus, the relationship between environmental chemicals and later neurodevelopmental outcomes may be impacted by processes in the developmental period in which the exposure occurred. Studies measuring exposure at a single time point are likely to miss these developmental effects entirely or capture only the neurotoxic or neuroprotective effects. Similarly, studies following the single exposure paradigm will miss the complexities of contaminant mixtures that are rapidly gaining attention.

Mixtures, or exposure to multiple chemical stressors, are imperative to study, as fetuses, infants, and children encounter unique combinations of chemical stressors in the exposome that can produce additive effects, potentiation, antagonism, and unique interactions with nonchemical stressors such as maternal depression (Tanner et al., 2020a). For example, the adverse effect of arsenic (As) on general cognitive functioning was increased when lead (Pb) was a co-exposure even though Pb had no independent effect, while the antagonistic interaction of Mn and mercury (Hg) mitigated the adverse effect of Hg on general cognitive functioning (Freire et al., 2018). Traditional multiple regression approaches are often not suitable for mixture analysis because datasets typically contain large sets of correlated exposure variables with interactive and time-dependent relations; however, a variety of advanced statistical and machine learning approaches have recently gained ascendency because they can handle such datasets and support interpretation. As one example, weighted quantile sum (WQS) regression (Carrico et al., 2015) is often preferable to standard multiple regression approaches, as it handles multicollinearity while also estimating the cumulative effect of a mixture on an outcome (i.e., the “body burden index”) and the relative contribution of each exposure. It does so by constructing a weighted additive index for a set of exposures through bootstrap sampling of a training data set. Tanner et al. (2020b) used WQS to estimate the cumulative and individual impact of 26 prenatal EDC exposures and found that higher mixture levels were associated with lower IQ in boys at age 7 and that BPF, a BPA replacement compound, was the largest contributor.

Though approaches have shed light on the temporal and interactive complexities of exposure, continued innovation is still needed, as mixtures are just beginning to be understood in relation to modifying variables. Recent comprehensive reviews of low level lead (Pb) and mercury (Hg) exposure in developing countries found that a variety Pb mixtures and Hg mixtures have been associated with increased risk for many adverse neurodevelopmental outcomes, but due to variability in mixture composition, exposure route and timing, and predisposing environmental and genetic factors, there are currently no clear links between specific mixtures and specific outcomes (Dorea, 2019a, 2019b). Furthermore, a review of 74 reviews of exposures and child neurodevelopment found that none met four criteria for methodological soundness, which led the authors to conclude that the methodological and analytical incommensurability of reviewed studies made the literature of limited use to public health decision-making (LaKind et al., 2017). In addition to using one or more of the advanced analytic approaches like WQS regression, studies would benefit from avoiding correlated measurement error of uniformly assessed biomarkers, implementing causal inference frameworks (Bind, 2019), using psychometrically strong outcome measures, investigating critical time windows, and accounting for relevant confounds. Developmental scientists’ quantitative and methodological expertise would strengthen these studies, as would their extensive consideration of time windows of susceptibility and sensitive periods in the developmental literature.

Mechanisms Linking Contaminant Exposures to Child Outcomes

A growing body of literature has focused on mechanisms that link contaminant exposures to child developmental outcomes. More specifically, research within this thematic area addresses how exposure relates to outcomes. From a developmental cascade perspective (Masten & Cicchetti, 2010), contaminant exposures may impact functioning at multiple levels across child and adolescent development. For example, among Inuit children in northern Quebec, Canada, childhood lead exposure was not directly associated with adolescent outcomes, but lead exposure was indirectly associated with adolescent externalizing behaviors, cannabis use, and binge drinking via externalizing behaviors during childhood (Desrochers-Couture et al., 2019). Studying biologically plausible mechanisms is an especially important avenue for research in order to elucidate how contaminant exposures impact child development. Here we provide a brief overview of two relevant mechanistic processes with select empirical examples.

Epigenetic changes likely play a key mechanistic role in accounting for the behavioral, cognitive, and health-related changes brought about by contaminant exposures. Epigenetic changes, which are also increasingly emphasized in research on the role of psychosocial factors in child development (van Ijzendoorn et al., 2011), refer to modifications that impact gene expression without altering the DNA sequence. Within environmental science, epigentic changes that result from contaminant exposures and influence later outcomes have been posited as a key manifestation of the Developmental Origin of Health and Disease (DOHaD) hypothesis (Tran & Miyake, 2017). The DOHaD hypothesis stems from the observation that later life health problems and mortality originate with early life experiences and exposures, beginning in the intra-uterine environment (Barker, 2007). The DOHaD hypothesis has spurred a more extensive search for plausible mechanisms that may account for the longer-term outcomes associated with early experiences. For example, DNA methylation, which is one key epigenetic change that can result in silencing of gene expression, has been studied as a consequence of prenatal development during a time of famine, which is one of the main in utero experiences that contributed to the original formulation of the DOHaD hypothesis. Individuals who were prenatally exposed to famine during war time have unique patterns of DNA methylation within gene loci that are linked to cardiovascular and metabolic diseases (Tobi et al., 2009). Tran and Miyake (2017) recently summarized research on epigenetic changes that stem from contaminant exposures and have implications for child development. For example, in a relatively large birth cohort study in Mexico, maternal bone lead burden impacted the developing fetus’s epigenome, as indexed by cord blood genomic DNA methylation (Pilsner et al., 2009). The epigenome could also play a central role in trasgenerational inheritence, meaning that contaminant exposures in one generation could influence subsequent generations via epigenetic inheritence. However, as Tran and Miyake (2017) noted, most existing epigenetic research on environmental contaminant exposures has been conducted with non-human animals and/or has not included child developmental outcomes.

Changes in brain structure and function are also purported to play a key mechanistic role in the link between contaminant exposures and later behavioral, cognitive, and health outcomes. For example, adult farm workers who had past lead exposure had smaller brain volumes across several regions of interest (ROIs) and more white matter lesions (Stewart et al., 2006). Moreover, in the same cohort, larger brain volumes in ROIs were associated with better cognitive functioning across several domains (Schwartz et al., 2007). Like the study of epigenetic processes, investigations of exposure effects on brain structure and function have increasingly focused on the effects of prenatal exposure, including impacts on fetal brain development. In a recent study that examined lead exposure and brain connectivity during the fetal period, there were age-related increases in connectivity between bilateral insula cortices among fetuses that did not have measurable lead exposure (Thomason et al., 2019). Increased cross-hemispheric connectivity is a normative fetal brain maturational process, which suggests a possible developmental delay in this process among the lead exposed fetuses. Of course, changes in brain structure and connectivity follow a cascade that includes several molecular mechanisms. For example, DMT1, which is a transporter protein, may play a role in the link between manganese exposure and function in the basal ganglia, which is a brain region that has been associated with manganese exposure (Chen et al., 2016). More research is needed that directly examines molecular and brain-related pathways from contaminant exposures to child behavioral, cognitive, and health-related outcomes.

Developmental science can enrich future research on epigenetic and brain-based mechanistic pathways linking contaminant exposures to child behavioral, cognitive, and health outcomes. Because epigenetics and neuroscience are both incorporated into models of the roles of non-chemical exposures in child development, developmental scientists are well-positioned to participate in transdisciplinary teams that study these pathways. Furthermore, statistical tests of longitudinal mediation and indirect effects are needed to systematically evaluate the hypothesized mechanistic pathways that link contaminant exposures to child developmental outcomes. Developmental scientists often possess considerable conceptual and quantitative expertise on mediation and indirect effects that further undescores the importance of their involvement in transdisciplinary teams studying contaminant exposures. Specifically, developmental scientists could help advance the conceptualization and analysis of the ways in which specific epigentic changes (e.g., DNA methylation) and brain-related processes (e.g., basal ganglia circuitry) link contaminant exposures to key developmental outcomes. In addition, the science of development will be enriched by a greater appreciation for the central role that environmental contaminants may play in the cascade of epigenetic and brain-based pathways that are increasingly the focus of longitudinal research on the role of parents, caregivers, and other psychosocial factors in children’s early development (e.g., Schwartz et al., 2017).

Protective Factors that Mitigate Risks Associated with Exposures

Contaminant exposures do not uniformly lead to adverse developmental outcomes, and there are several psychological, biological, and nutritional factors that could mitigate risk (Bellinger et al., 2016). Broadly speaking, the search for protective factors reflects consideration of individual differences that could either partially or fully ameliorate vulnerability to the behavioral, cognitive, and health-related risk factors associated with exposure to contaminants. For example, research using animal models has provided compelling evidence that an “enriched environment” can mitigate risks associated with contaminant exposures. Lead exposed rats that experienced environmental enrichment, which included additional space and toys in their cages, had fewer spatial learning deficits (Guilarte et al., 2003). Unfortunately, there is relatively little human research that has rigorously and comprehensively tested protective or ameliorating processes following contaminant exposures. In this section, we provide an overview of research on two types of factors that could ameliorate risks associated with contaminant exposures: nutritional factors and aspects of the caregiving context.

Nutritional factors may play an important role in reducing the likelihood that children who have been exposed to contaminants will experience negative outcomes. For example, based on animal models that suggested that lycopene, an antioxidant found in tomatoes and other foods, may protect against the toxic effects of mercury exposure, a research study examined consumption of tomato products among Inuit children who often have high levels of mercury exposure (Gagne et al., 2013). This study found lower levels of mercury among children who ate more tomato products. Other nutrients that may play a protective role include essential elements like iron and zinc. For example, research suggests that iron intake and supplementation may reduce the risk of lead poisoning and lower blood lead concentrations (Kordas, 2017; Kwong et al., 2004). However, there are important caveats to keep in mind when considering this area of research, including the frequency with which deficiencies in key micronutrients co-occur with contaminant exposures. As one example, children who are exposed to high levels of contaminants due to air pollution may also have low levels of Vitamin D because they reside in low-income communities where outdoor activities are avoided due to safety concerns (Miller & Rayalam, 2017). In addition, randomized trials of essential element supplementation do not always support hypothesized reductions in contaminant levels following supplementation. For example, a randomized trial did not support a reduction in blood lead levels following iron supplementation (Rosado et al., 2006), although other trials have provided support for blood lead reductions following supplementation (Kordas, 2017). Therefore, while nutritional factors are promising sources of protection from risks associated with contaminant exposures, research is also needed on other potential protective factors, including features of children’s psychosocial environment.

A small body of research has examined psychosocial factors that may mitigate risks associated with contaminant exposures, including aspects of the caregiving context that are quite often the central focus of developmental science research. For example, in a study of lead exposure in Mexico City, maternal self-esteem predicted higher scores on the Bayley Scales of Infant Development (BSID) at 24 months of age, and there was some evidence that maternal self-esteem reduced the strength of the negative association between blood levels and BSID scores (Surkan et al., 2008). In a study of water contaminants including lead, nitrate, and arsenic, higher levels of overall contaminant exposure were associated with depressive symptoms among adolescents who reported that their parents engaged in higher levels of psychological control (Manczak et al., 2020). Notably, contaminant exposures were not associated with depressive symptoms among adolescents who reported lower levels of psychological control. It is important to also take into account that contaminant exposures may impair parents’ functioning within the caregiving context. In a study of mothers and preschoolers in Uruguay, elevated blood lead levels among either mothers or their children were associated with mothers’ perceptions that they were less skilled at discipline (Kordas et al., 2011). Thus, positive caregiver-child relationships have the potential to serve a protective function within families facing risks due to contaminant exposures, but the same families who would most benefit from protective processes might face more challenges within the caregiver-child dyad as a consequence of exposures.

There are several reasons why developmental scientists are uniquely positioned to expand, enrich, and strengthen research on factors that might protect children from the adverse consequences associated with contaminant exposures. First, several psychosocial factors, particularly aspects of the caregiving context, have received extensive theoretical and empirical attention within the developmental science literature, which could guide the selection of the constructs that are most likely to confer protection. Second, many developmental scientists have a wealth of expertise on important conceptual nuances such as the distinction between a compensatory process (a factor with a main effect that is independent of the role of the risk factor) and a protective process (a factor that statistically interacts with a risk factor to dampen the association between the risk factor and the negative outcome; Fergus & Zimmerman, 2005). Third, methodological critiques and tutorials have strengthened how moderators are analyzed and interpreted within developmental science (e.g., Widaman et al., 2012), and these recommendations could be applied to strengthen the rigor of research on protective factors within the literature on childhood contaminant exposures. These approaches could help developmental scientists pinpoint whether and how specific nutritional and caregiving factors interact synergistically to minimize negative outcomes associated with contaminant exposures. The approaches could also be applied to explore whether other aspects of nutrition (e.g., contaminants in food) and caregiving (e.g., harsh parenting) function as risk factors that exacerbate the likelihood of negative outcomes. Moreover, increasing developmental scientists’ understanding of which nutritional and caregiving factors interact with contaminant exposures in a risk or protective manner would further strengthen theories of childhood resilience.

Conclusion

As illustrated by the preceding overview, considerable progress has been made toward understanding the role of environmental contaminants in multiple domains of child development. Developmental scientists are well-equipped to contribute to further progress on research related to these themes, but there is relatively little integration between developmental science and relevant fields, including environmental psychology, environmental health, and toxicology. Individual developmental scientists have contributed to research programs that study contaminants and child development, but sustained efforts are needed to train developmental scientists on relevant methods and promote interdisciplinary collaboration, as has been described in more detail elsewhere (Trentacosta et al., 2016). One positive outcome of such efforts would be increased attention to environmental contaminants in cutting-edge journals that publish developmental scientists’ research, including in New Directions in Child and Adolescent Development, which would foster conceptual and theoretical innovations in our field.

Expanding the scope of developmental science theory and research to systematically incorporate the role of environmental contaminants in child development also has the potential to influence policies and practices. For example, increased understanding of the developmental mechanisms that link contaminant exposures to negative outcomes during childhood and adolescence could help determine where to direct resources for interventions and which kinds of policy changes would be most helpful. As another example, devoting further attention to specific features of the caregiving context that mitigate risks associated with contaminant exposures could help to pinpoint which psychosocial interventions would be most helpful and how to direct policy-related efforts to stem the tide of contaminants’ harmful impacts on children and adolescents. In summary, enhancing developmentally-informed research, policy, and practice related to environmental contaminants could mitigate risk and enhance well-being for millions of children who are especially vulnerable to contaminant exposures.