A Multigenerational Model of Environmental Risk for Black, Indigenous, and People of Color (BIPOC) Children and Families

Abstract

Background:

In recent years, public discourse has increasingly brought institutional and structural racism to the foreground of discussion on the well-being of BIPOC (Black, Indigenous, and People of Color) communities. Environmental toxicity in combination with the social triggers of institutional and structural racism are among the factors that shape the short- and long-term health of BIPOC Americans across multiple lifespans.

Objectives:

We outline a $2+$ Generation Model for examining the mechanisms through which institutional and structural racism promotes the intergenerational transmission of environmental health risk and family and interpersonal relationships across the life course and across multiple generations. We present the model’s theoretical underpinnings and rationale, discuss model limitations and needed sources of data, and implications for research, policy, and intervention.

Discussion:

Parents and children are not only biologically linked in terms of transmission of environmental toxicities, but they are also linked socially and intergenerationally. The $2+$ Generation Model foregrounds family and interpersonal relationships occurring within developmental contexts that are influenced by environmental toxicity as well as institutional and structural racism. In sum, the $2+$ Generation Model highlights the need for an equity-first interdisciplinary approach to environmental health and redirects the burden of risk reduction away from the individual and onto the institutions and structures that perpetuate the racial disparities in exposure. Doing so requires institutional investment in expanded, multigenerational, and multimethod datasets. https://doi.org/10.1289/EHP13110

Introduction

The onset of racial and socioeconomic unrest of 2020 have brought institutional and structural racism to the forefront of the social consciousness.^1,2 Although the attention may be new, the impact of racism in all its forms on the wellbeing of BIPOC (Black, Indigenous, and People of Color) communities is not.³ We contend that it is critically important that researchers accurately specify the impacts of racism on human health and well-being to give the important scientific background to policymakers so they can take action to reduce those impacts. We further encourage researchers, practitioners, and policymakers to move beyond examining individual-level racial discrimination to examining racism that is intentionally or unintentionally woven into the fabric of everyday life. In this commentary, we introduce for the first time a conceptual model for examining how institutional and structural racism promote the intergenerational transmission of environmental health risks for BIPOC children and families in the United States. We synthesize two foundational theories in the human development and family sciences with developmental, family, and environmental health research into a proposed $2+$ Generation Model to describe how institutional and structural racism contributes to intergenerational transmission of environmental health risk.

Krieger defines institutional racism as race-based “… discriminatory policies or practices carried out by state or nonstate institutions…”⁴ (p. 650), e.g., race correction algorithms in medicine.^5,6 Structural racism reflects the web of, “… interconnected institutions, whose linkages are historically rooted and culturally reinforced. It refers to the totality of ways in which societies foster racial discrimination, through mutually reinforcing inequitable systems,”³ (p. 1,454), e.g., the “War on Drugs.”^7,8 Understanding that discriminatory practices, laws, and policies exist within individual institutions and that people interact with multiple institutions at once (health care, education, environmental) is critical to advancing research, creating effective intervention, and implementing effective policy change.

We prioritize institutional and structural racism for this model, rather than individual racism and discrimination, because of the growing body of literature across multiple disciplines pointing to endemic racism as a factor in BIPOC health and well-being.⁹ However, our intent is not to argue for an ultimate subset of variables that represent institutional and structural racism, nor is it to assume that racism is the only factor driving environmental health risk in BIPOC communities and families. Instead, we propose a conceptual framework and needed resources for translating institutional and structural racism from the amorphous “water we swim in”¹⁰ (p. 118) to clearly identifiable and measurable factors to determine the conditions under which it influences intergenerational environmental exposures at the individual, family, and/or community levels.

We propose the $2+$ Generation Model as a heuristic framework for examining the intergenerational impacts of environmental toxicants and toxicant mixtures such that the model could be used to formulate research questions across different historically marginalized racial/ethnic groups. We first present the rationale and theoretical underpinnings of the model. As developmental scientists, we emphasize the developmental processes and family and interpersonal relationships that take place prior to and alongside environmental toxicant exposures. We use lead exposure in a parent–child dyad as a case example because lead is a legacy pollutant that continues to impact multiple generations of primarily lower income and Black children and families.¹¹ Second, we discuss the limitations of the model and needed data sources for its use to begin to address the inequities in multigenerational environmental toxicant exposures. In our discussion we emphasize that implementation of the model is dependent on specific research questions through interdisciplinary and community-engaged collaboration. Third, we conclude by discussing implications of the model for research, policy, and intervention at the individual, family, and community levels.

Discussion

Our commentary is based on the premise that parents and children are most often socially, biologically, and intergenerationally linked but that researchers in the respective developmental and environmental health fields often examine social and biological risk factors in isolation. We argue that missing from biological explanations of how environmental toxicants can have intergenerational effects is consideration of how variables such as intergenerational trauma, parent–child relations, home and neighborhood context, schooling, and health care exacerbate or attenuate both risk for exposure and impacts of exposure once they occur. For example, the same parent with chronic lead exposure may have cognitive and behavioral sequelae that make it more difficult to engage in high-quality parenting practices and to benefit from participation in otherwise high-quality, family-based intervention. Similarly, the child, parent, and grandparent who have been exposed to environmental toxicants are likely to be the same individuals who are at risk for exposure to individual- and community-level violence, intergenerational trauma, and household chaos^12–14 and have suboptimal or maladaptive parent–child interactions.

Research about how institutions individually and synergistically impact development is currently limited in that it has not yet addressed how initial events in Generation 1 can be linked to subsequent exposure to chemical, nonchemical, and psychosocial stressors in Generation 2 and later. Arah¹⁵ stated the issue succinctly: “Health is not entirely individual; it is relative to the individual’s context, which in turn is fashioned out of the interactions that exist between members of any defined collective whose health (read: population health) is defined by the health and context of its members” (p. 238). Life-course epidemiology¹⁶ is increasingly used to address intergenerational transmission of disease and to emphasize the sociocultural and sociohistorical contexts leading up to disease. Yet, we contend that this emphasis on sociocultural and sociohistorical contexts still pays insufficient attention to the family and interpersonal relationships that both influence and are influenced by exposure to environmental toxicants. Thus, we present the $2+$ Generation Model with the intention of specifically raising the importance of these family and interpersonal connections on environmental health in later generations.

Central tenets of the developmental and family sciences include that human development occurs in a variety of settings broadly referred to as “developmental contexts.” For the present purposes these contexts are considered to be embedded in multiple systems.¹⁷ For example, a child’s language skills develop, in part, due to interactions with a variety of peers and caregivers in settings that are embedded in physical and social spaces and shaped by norms, mores, and laws established over time.^17,18 Similarly, developmental and family scientists are concerned with a wide array of “developmental outcomes.” These outcomes can range from fetal development to family social mobility, depending on researcher focus. Researchers may also focus on shorter-term indicators of lifespan outcomes such as academic achievement and graduation, and other commonly used metrics of child outcome such as self-regulation and social competence.

Features of the $2+$ Generation Model

We rely on two theories within the developmental and family sciences to frame the $2+$ Generation Model. Glen Elder’s Life Course Theory (LCT^18–20) provides necessary underpinnings to probe the contextual and interpersonal mechanisms driving transmission of exposure risk across multiple generations (Table 1). According to LCT, human development occurs within sociohistorical contexts, family members impact each other’s experiences (linked lives), salient life events alter individual and/or life course trajectories (turning points), and humans make choices and take actions that are constrained by their sociohistorical contexts (human agency). LCT also emphasizes how the timing at which events occur can influence what the outcomes are (timing in lives). Thus, exposure to chemical, nonchemical, and psychosocial stressors as well as exposures to high-quality interventions and protective factors can occur at any point in the lifespan, resulting in possibly different short- and long-term effects. As we describe later in this commentary, we propose that the tasks of specifying developmental time points, stressors, intervention, protective factors, and effects require multidisciplinary scientific teams working collaboratively and equitably with key community and policy stakeholders.

Table 1.

Core concepts of Life Course Theory.^18–20

Concept	Description
Historical time and place	“…the life course of individuals is embedded in and shaped by the historical times and places they experience over their lifetime.”20 (p. 3)
Timing in lives	“…the developmental impact of a succession of life transitions or events is contingent on when they occur in a person’s life.”20 (p. 3)
Linked lives	“…lives are lived interdependently, and social and historical influences are expressed through this network of shared relationships.”20 (p. 4).
Human agency	“…individuals construct their own life course through the choices and actions they take within the opportunities and constraints of history and social circumstances.”20 (p. 4)

The mechanisms through which institutional and structural racism work to impact environmental health risk and family and interpersonal relationships across the life course are observable through the culmination of Urie Bronfenbrenner’s theorizing about how human development takes place, the Person-Process-Context-Time (PPCT) model (Table 2).^21,22 PPCT is a systems framework most recognized for its description of human development occurring through proximal processes, the “primary engines of development.” Proximal processes are “progressively more complex reciprocal interaction between an active, evolving biopsychological human organism and the persons, objects, and symbols in its immediate external environment” (p. 620²¹) that occur regularly over time. Further, “The form, power, content, and direction of the proximal processes affecting development vary systematically as a joint function of the characteristics of the developing person; of the environment—both immediate and more remote—in which the processes are taking place; the nature of the developmental outcomes under consideration; and the social continuities and changes occurring over time through the life course and the historical period during which the person has lived” (p. 620–621²¹).

Table 2.

Person-Process-Context-Time model.^21,22

Concept	Description	Example
Person	Individual characteristics	Biological sex, age, developmental status, existing environmental toxin burden
Process	Psychological or behavior acts that take place in real time and are associated with maintenance, alteration, or transformation of mental or physical states	Parent–child relationships, self-regulation development, gross or fine motor development
Context	Physical, socioemotional, and/or mental “settings”	Housing quality, school quality, community economic status, parental and family influence, home environment
Time	Lifespan of an organism, cohort effects, historical time	Prenatal, infancy through early childhood, pre- vs. post-COVID, Civil Rights Era

By incorporating PPCT and LCT, the $2+$ generation model allows for theory-building and new empirical research around both the social and biological mechanisms underlying intergenerational transmission of environmental health risk via institutional and structural racism. The model shares characteristics with the Environmental Exposures and Early Child Development (E3CD) proof-of-concept model.^23,24 E3CD illustrates how institutional and structural racism sets the stage for poor neurodevelopmental outcomes for Black children by increasing their exposure to environmental toxicants.^23,24 Payne-Sturges et al. point to the iterative nature of institutional and structural racism, contending that exposure and lack of intervention in one generation increases community vulnerability for poor outcomes across generations through subsequent exposures.²⁵ We seek to push thinking further by adding that not only is persistent toxicant exposure a vital issue but so are community and family relationships within the contexts of these exposures. Thus, we expand on previous work with our emphasis on relational dynamics that are embedded in sociohistorical and physical contexts that are in part shaped by institutional and structural racism. We focus on how the $2+$ Generation Model can be especially useful when considering potential interventions designed to ameliorate negative effects of toxicant exposures within and across generations. Such practices, policies, and interventions can potentially reduce environmental burden and positively impact child and family well-being. Later in this commentary we describe possible research and interventions using lead as a case example and integrating the prevention approaches from harm reduction engineering literature.

The $2+$ Generation Model incorporates developmental scientist Velma McBride Murry’s assessment that individual generations develop within contexts shaped by the “toxic oppressive upstream waters”(p. 2,113²⁶) of institutional and structural racism (Figure 1). We expand on Murry’s assertion that institutional and structural racism are upstream oppression and her critical evaluation of resilience and resistance processes in African-American families to propose that concurrent ISR occurring within generations can exacerbate negative impacts of developmental context on exposure to chemical, nonchemical, and psychosocial stress (${\text{cISR}}_{\mathrm{a}}$) and exposure to chemical, nonchemical, and psychosocial stress to developmental outcomes (${\text{cISR}}_{\mathrm{b}}$). Simultaneously, high-quality intervention and effective policy can mitigate negative impacts of developmental context on exposure to chemical, nonchemical, and psychosocial stress (${\text{cM}}_{\mathrm{a}}$), as well as from chemical, nonchemical, and psychosocial stress to developmental outcomes such as educational attainment, physical and psychological health (${\text{cM}}_{\mathrm{b}}$).

Figure 1.

Within-generation environmental health risk. In keeping with Iruka et al.’s premise that Institutional and Structural Racism (ISR) are “the water we swim in” (p. 118),¹⁰ the outer box represents the wider context of unspecified institutional and structural racism. The contextual embeddedness of Black, Indigenous, or People of Color within a generation are depicted as three concentric circles. ISR establishes suboptimal Developmental Contexts, which in turn, lead to exposure to Chemical, Non-Chemical, and Psychosocial Stress. These stresses then elevate risks for poor Developmental Outcomes. Based on the shared premises of Bronfenbrenner’s Person-Process-Context-Time^21,22 model and Elder’s Life Course Theory,^18–20 human development occurs, in part, through relationships that are embedded in sociohistorical and physical contexts. These relational dynamics take place in a broader social context that includes factors that exacerbate or mitigate the impacts across the concentric circles. Concurrent ISR (cISR) occurs within a generation and can exacerbate negative impacts of Developmental Context on exposure to chemical, nonchemical, and psychosocial stress (${\text{cISR}}_{\mathrm{a}}$, indicated by a single-lined arrow) and to Developmental Outcomes (${\text{cISR}}_{\mathrm{b}}$, indicated by a single-lined arrow). Simultaneously, high-quality intervention and effective policy can mitigate negative impacts of Developmental Context on exposure to chemical, nonchemical, and psychosocial stress (${\text{cM}}_{\mathrm{a}}$, indicated by a double-lined arrow) and chemical, nonchemical, and psychosocial stress to Developmental Outcomes (${\text{cM}}_{\mathrm{b}}$, indicated by a double-lined arrow). Currently unknown or unspecified epigenetic effects (EPI) (indicated by dashed-line arrow) are not the focus of this relational model, but growing literature indicates the importance of epigenetic impacts of racism. This depiction of within-generation environmental health risk is then embedded in the multigenerational model (Figure 2).

Specific events, policies, and practices or regulations and laws shape developmental contexts that can be perpetuated across multiple generations (Figure 2). Historic institutionally or structurally racist policies, practices, or events can be both recent occurrences (hISR), e.g., the decision-making leading to the Flint, Michigan, water contamination crisis,²⁷ or more distant practices, e.g., redlining.²⁸ The model foregrounds family and interpersonal relationships occurring within broader developmental contexts and does not negate other pathways for influence. The model similarly recognizes the potential for ongoing influences of historic institutional and structural racism that affect developmental context and social mobility but is unrelated to the theorized developmental paths. Finally, recent innovations in the study of epigenetic x environment interactions suggest multiple points across generations at which there could be transgenerational environmental effects (see, for examples, Bollati and Bacarelli²⁹ for proposed models of the interplay between the environment and human epigenome and Aroke et al., Brody et al., Kaufman et al., and Miller-Kleinhenz et al.^30–33 for discussions of the transgenerational epigenetic impacts of racism).

Figure 2.

$2+$ Generation Model of environmental health risk. This framework is a heuristic for examining the intergenerational impacts of environmental toxicants and toxicant mixtures based on the premise that human development is embedded in sociohistorical and physical contexts.^18–22 Application of the model to specific situations or populations requires not only multi-disciplinary collaborations, but also obtaining the perspectives and experiences of members of historically marginalized racial/ethnic groups that have been impacted by policies, practices, and events. The model is depicted in three generations, but it can extend further with the availability of more extensive multigenerational data. The outer box represents the wider context of unspecified institutional and structural racism (ISR), i.e., “the water we swim in” (p. 118),¹⁰ and corresponds to Bronfenbrenner’s macrosystem concept.¹⁷ The transmission of environmental health risk from a historical event is depicted across three generations. A historic institutionally or structurally racist policy, practice, or event (hISR) is identified that creates a Developmental Context of chemical, nonchemical, and psychosocial risk that leads to poor Developmental Outcomes in Generation 1 (path ${\mathrm{A}}_1$, indicated by a solid-lined arrow). The ${\mathrm{A}}_1$ path is moderated both by contemporary policies, laws, or practices that can mitigate (${\text{cM}}_1$, indicated by a solid-lined arrow) and contemporary ISR (${\text{cISR}}_1$, indicated by a solid-lined arrow) that can exacerbate its effects. People from Generation 1 are now parents and caregivers to Generation 2 (${\mathrm{A}}_2$, indicated by a solid-lined arrow), carrying forward their experiences to Generation 2 both biologically and through parent–child interactions. The ${\mathrm{A}}_2$ path is also moderated by contemporary policies, laws, or practices that can mitigate (${\text{cM}}_2$, indicated by solid-lined arrow) and contemporary ISR (${\text{cISR}}_2$_, indicated by solid-lined arrow) that can exacerbate Generation 1 effects on Generation 2. Generation 2 concurrently experiences unique contextual exposures to chemical, nonchemical, and psychosocial risk, as well as contemporary moderators like institutional and structural racism (${\text{cISR}}_{\mathrm{a},\mathrm{b}}$, indicated by a solid-line arrow) and high-quality intervention (${\text{cM}}_{\mathrm{a},\mathrm{b}}$, as depicted in Figure 1). The model continues with the ${\mathrm{A}}_3$ path from Generation 2 to Generation 3, which is similarly moderated by contemporary institutional and structural racism (${\text{cISR}}_3$, indicated by a solid-lined arrow) and mitigating policies, laws, or practices (${\mathrm{M}}_3$, indicated by a solid-lined arrow). Given the contemporary literature about the pervasiveness of ISR, we also recognize the potential for ongoing influences of hISR (oISR, indicated by dash-lined arrows leading to Generations 1, 2, and 3) that can affect developmental context and social mobility. Similarly, currently unknown or unspecified epigenetic effects (EPI, depicted by a dashed-line arrow leading to Generations 1, 2, and 3), are not the focus of this relational model, but the growing literature indicates the importance of epigenetic impacts of racism.

Relational moderators within and across generations.

LCT and the PPCT model guide our premise that parents’ and children’s lives are most often biologically, socially, and intergenerationally linked.^18,21,22 Thus, the developmental timing of interest, i.e., timing in lives, can range from in utero to old age, and person characteristics can include factors such as temperament or health comorbidities that potentially interact with physical and social contexts to influence developmental processes. Importantly, these moderators can also include the continued effects of previous toxicant exposures as well as new toxicant exposures.

Research and interventions directed toward two or more generations are increasingly common in the prevention and developmental sciences, with the simplest example of a $2+$ generation intervention being family therapy. There are multiple high-quality interventions that positively impact parent and child responses to psychosocial stress^34,35 and attenuate negative developmental outcomes through direct intervention with children or by engaging parents and children in family-based intervention.^35–37 Longitudinal studies demonstrate that high-quality interventions can have positive impacts across individual lifespans.^38–40 For example, recent focus on the impact of interventions such as unconditional cash transfers on child and family well-being^41,42 may be a promising means to impact the path connecting generations, thereby promoting social mobility and reducing the risk for psychosocial stressors for subsequent generations. There is also evidence that both environmental justice efforts and environmental intervention can have positive impacts on risk for exposure.^43,44

Yet, despite the growing evidence of positive effects of individual- and family-based intervention on children’s developmental outcomes in context of psychosocial stressors,^45–47 to our knowledge there is little information about whether these interventions can attenuate the impact of chemical or nonchemical stressors in the physical environment on well-being in one or more generations. If empirically validated and widely implemented for this purpose, these interventions could have potential population-level effects. Nevertheless, they would still operate by “fixing” families rather than by mitigating or eliminating environmental toxins. We suggest that person, process, and context interventions, combined with intentional antiracist policies and practices that shape the larger system,¹⁰ may be a means of reducing institutional and structural racism’s impact on the quality and safety of the developmental context.

Concurrent and historic institutional and structural racism in the $2\mathbf{+}$ generation model.

Institutional and structural racism are not relics of the past.³ The $2+$ Generation Model provides a means of conceptualizing how the impacts of historic institutional and structural racism (hISR) can be compounded by concurrent institutional and structural racism. Ongoing impacts of hISR, like redlining, and newer impacts of concurrent institutional and structural racism (cISR), can have lasting effects on the structures and neighborhoods of US cities within and across generations that also yield increased exposure to a multitude of chemical, nonchemical, and psychosocial stressors.⁴⁸

Institutionally racist policies and practices combine to perpetuate a structurally racist system that persists, with or without racist intent.^3,4 Examples include judicial weakening of the Voter Rights Act⁴⁹ and partisan gerrymandering⁵⁰ that impact voting access and behavior, as well as racial bias in medical training and health care^51,52 impacting health outcomes and in law enforcement, criminal charging, and sentencing.⁵³ Similarly, institutional policies and practices have been applied in ways that differentially route Black Americans into the judicial system,^54,55 which, along with housing and job discrimination for adults with criminal convictions,⁵⁶ can have devastating financial and emotional impacts.^57,58 These financial and emotional impacts⁵⁸ can negatively shape the developmental contexts of successive generations⁵⁹ and can perpetuate environmental and social risk exposures to children who are forced to remain in substandard housing, move frequently, experience poor housing, or experience homelessness.^60,61 Similarly, practices and policies that prevent formerly incarcerated or court-involved adults in one generation from obtaining jobs or social resources potentially condemn future generations to developmental contexts that increase their environmental risk.^62,63

Relatedly, policies and practices aimed at promoting healthy development, reducing environmental health risk, and promoting social mobility exist in concert with policies and practices that may be de facto institutionally or structurally racist. Yet, little is known about whether potentially positive impacts of intervention or policy change may be diminished by concurrent institutional and structural racism. Understanding the impact of institutional and structural racism on individuals and families is crucial to discerning why and for whom otherwise high-quality interventions do or do not work. To date, much of the child and family development intervention literature focuses on the characteristics of the intervention itself with less consideration of the sociohistorical contexts in which the interventions occur.^64–66 There is, moreover, little information about whether the context of intergenerational environmental toxicant exposure could counteract, or even render harmful, some family-based intervention. Each of these paths need further study at both the person and population levels.

Case Example: Intergenerational Transmission of Lead Risk and Lead Effects

Writing in The Annual Review of Sociology, Muller et al. said that “Who is exposed to lead and why are fundamentally social questions” (p. 264). Further, those authors point out that not only is lead exposure socially determined but that lead exposure has social consequences “… that themselves depend in part on children’s social environments” (p. 265⁴⁸). They point to National Health and Nutrition Examination Survey (NHANES) data between 1976 and 2010 (34 y) showing that Black children have more than double the rate of elevated blood lead in comparison with White children, even while the standards for “elevated blood lead” have decreased over time. It only takes a moment’s thought to realize that people who were children from 1976 to 1980 are now middle-aged adults who have raised a second—perhaps third⁶⁷—generation of children.

Lead exposure is a prime example of the potential utility of the $2+$ Generation Model. Consider the development of a hypothetical parent–child dyad living in a historically redlined ZIP code in a city with known lead contamination, hISR.^68–70 The parent’s early lifespan lead exposure in Generation 1 could have occurred through contact with a variety of environmental sources, including dust, soil, and water. The subsequent accumulation of lead in their body has numerous negative health effects, including deficits in attention, impulse control, and emotion regulation,^71–75 which are associated with poor lifetime physical and psychological health, socioeconomic status (SES), and social mobility.^76–78

The effects of lead can also be transmitted to Generation 2 not just through socioemotional effects on parents, but also biologically. The biological mechanisms for transmission of lead and its effect from women to their children are well-known. Bone is the primary storage organ from which lead mobilizes during physiological stress such as pregnancy and lactation.⁷⁹ Lead in the bloodstream crosses the placenta, putting the fetus at risk of suffering from prematurity, low birth weight (LBW), and later childhood cognitive and behavioral deficits.⁷⁴ In utero, lead can block neurotransmitter connections and inhibit synaptic structures, especially during the last trimester of pregnancy, a critical period for the fetus’ brain growth.⁸⁰ As lead accumulates in the body throughout development, exposure can cause permanent adverse changes in brain function, imposing intellectual disadvantages on children before they are even born.⁸¹ Furthermore, animal studies indicate potential for lead in males to be associated with lowered fertility,⁸² and limited studies of humans indicate potential associations between males’ chronic exposure to occupational lead and risk for LBW birth.⁸³ Research using rodent models also suggests the potential for synergistic maternal lead and maternal stress effects leading to poor health outcomes in offspring.⁸⁴

The $2+$ Generation Model’s foundations in LCT and PPCT also emphasize that these biological connections influence and are influenced by the social connections between parents and children and the broader contexts in which these connections occur. Extending this example, the hypothetical child in Generation 1 who was exposed to lead as a result of an initial hISR is now an adult who is less likely to have moved into safer housing for reasons that include their lead burden.⁷⁸ Their child, born in Generation 2, has an increased likelihood of exposure to environmental lead, along with exposure in utero and/or through breast milk.^79,85 Moreover, the cognitive, emotional, and social conditions associated with the parents’ lead burden likely impacts their child through less effective and warm parenting,⁸⁶ potentially exacerbating the negative impacts of lead exposure (Figure 2).

This parent–child dynamic takes place in a broader social context that includes both intervention and concurrent institutional and structural racism (Figure 1). For example, the child in this hypothetical dyad may be condemned to being born into a developmental context that increases their environmental risk if their parent was among the Black Americans differentially routed into the justice system and subsequently denied access to safe housing and social resources.^62,63 Simultaneously, efforts to improve the developmental outcomes in Generation 2 could be rendered ineffective or harmful due to previous generations’ exposures to environmental toxins and ongoing institutional and structural racism. Breastfeeding interventions are a prime example. The benefits of breastfeeding to infant development are well-established.^87–89 Yet, to our knowledge there are no investigations in the environmental health literature of the potential iatrogenic effects of breastfeeding intervention—or potential protective effects—among mother–infant dyads exposed to environmental toxicants. The lack of research into breastfeeding within the context of environmental toxicant exposure, along with factors such as racial bias in access and quality of perinatal care^90,91 and disparities in access to needed educational resources⁹² that impact child well-being, sets the stage for subsequent exposures in Generation 3 and beyond. Thus, there is a critical need for researchers to examine intervention and policy implementations in the contexts in which they occur.

Model Limitations, Constraints, and Needs

The $2+$ Generation Model prioritizes institutional and structural racism and requires that users identify an observable starting point in the form of laws, policy implementation(s), or historical event(s) that have differentially adverse impacts on individuals due to race/ethnicity, regardless of intent. This assumption is a strength, in that it can bolster attempts to identify causal chains between historic institutional or structural racism and current developmental outcomes using cross-sectional and cohort data. However, a limitation of specifying Generation 1 in this way is that salient factors that precede or co-occur with the identified historic institutional or structural racism (hISR) can remain unrecognized. This approach also requires the availability and reliability of historic developmental data, meaning that hISR that is more distant or that affect communities with historically less power and agency to define the problem^93,94 may have less-comprehensive data. The model is also agnostic about which sociohistorical systems and structures are most influential in any given path. Policies, practices, or events that seem race-neutral when enacted may not be when examined in historical and contemporary contexts. Conversely, poor individual and intergenerational outcomes may be explainable by simpler causal chains.

We propose the $2+$ Generation Model as a means of operationalizing institutional and structural racism and establishing when and how it is important in multigenerational environmental health outcomes. We offer that obtaining the perspectives and experiences of those impacted by policies and events, across sociodemographic groups, is critical to identifying where changes in systems need to occur. Similarly, identifying developmentally salient indicators requires targeting the developmental outcomes whose importance has already been established, such as predictors of life events like high school graduation, college intentions and matriculation, substance use initiation, and school suspension. Given these constraints, the model highlights the need for continued institutional support for expanded data and restructured datasets and equity-first interdisciplinarity.

Institutional support for expanded data and restructured datasets.

There are several existing databases examining how racial discrimination impacts long-term emotional, psychology, educational, and economic well-being,^95,96 with some structured for multigenerational analyses by linking parent and child data.^97,98 We suggest that incorporating multiple sources of data at different levels of granularity and at multiple scales into large, multigenerational studies of environmental risk and institutional and structural racism is essential to knowing how ostensibly race-neutral practices and policies, when viewed in the sociohistorical context, may differentially impact BIPOC individuals and communities.

The National Institutes of Health’s new data-sharing policy⁹⁹ presents an opportunity for wider collaboration and answering of complex intergenerational person–context–time questions. Linking multigeneration, multilevel, and multivariable interdisciplinarity data for the future of such research requires major institutional sponsorship.¹⁰⁰ Although projects have been initiated, such as the All of Us,¹⁰¹ NHANES,¹⁰² National Longitudinal Survey of Youth,¹⁰³ or The Future of Families and Child Wellbeing Study,¹⁰⁴ there is yet to be comprehensive data collection that recognizes the complexity of institutional and structural racism in the socioeconomic, educational, physical, mental and relational health, and geographical and environmental safety milieu. Further, in many longitudinal datasets, families and children who change residence frequently, change school districts, or change communities are simply “lost to follow-up.”¹⁰⁵

Equity-first interdisciplinarity.

There is a particular need for expanding methodological and theoretical frameworks away from approaches that prioritize individual responsibility and “grit,” decontexualize human experiences, pathologize communities of color, and devalue diverse ways of knowing.¹⁰⁶ We suggest this means incorporating community-engaged, qualitative, and historical methodologies into the environmental health sciences in ways that inform decision-making about what constitutes data, how the data are analyzed, and how the analyses are interpreted.²⁵

Even with institutional support, the $2+$ Generation Model, as with all models, is only as valuable as the assumptions and data that are used to inform it.²⁵ The proposed approach for thinking about intergenerational transmission of environmental health risk is informed by what Robert Bullard, the founder of the environmental justice movement called, “…an ethical analysis of strategies to eliminate unfair, unjust, and inequitable conditions and decisions …”.¹⁰⁷ The assumption of an identifiable hISR can bolster attempts to identify causal chains between historic institutional racism and current developmental outcomes using cross-sectional and cohort data. However, inherent to this “ethical analysis” is equitably including the voices of community members and longstanding leaders in the environmental justice movement so as not to perpetuate or create new inequalities in setting research and policy agendas.¹⁰⁸ Recent research in Native American communities on health disparities and community-based approaches to ameliorating them exemplifies an “equity first” approach.¹⁰⁹

Using the $2+$ Generation Model can challenge researchers to reexamine notions of what information constitutes “data” and to embrace a wide range of methodologies that allow for theory building and empirical examination of multigeneration pathways. Within the developmental and family sciences, there is a growth of conceptual frameworks that center individual and family development in race, racism, community, and social position.^110–112 Future research in both environmental and developmental sciences can question how institutional and structural racism work to impact lifelong well-being, both historically and contemporaneously at the community, family, and individual levels. Asking these questions has the potential to raise the importance of exploring creative new equitable potential pathways for intervention and policy change.

Developmental and family science researchers already have a long history of collecting indicators of the physical environment, such as household crowding and chaos, neighborhood quality, and perceived neighborhood safety.^113–116 Recent advances in wearable technology and interdisciplinary scholarship also provide opportunities to investigate how relational and environmental health are situated within the greater sociocultural context. As one example, with multidisciplinary colleagues in Human Development and Family Studies, Population Health Sciences, and Civil and Environmental Engineering, Dilworth-Bart and Malecki developed a protocol to assess chemical [particulate matter (PM) with aerodynamic diameter $\le 2.5\mathrm{\mu }\mathrm{m}$ (${\mathrm{PM}}_{2.5}$)], nonchemical (noise), and psychosocial (SES, maternal psychological well-being, language context) stress and their relation to self-regulation among preschool-age children that included wearable technology to measure air quality, language environment, and noise.^117,118 Future longitudinal interdisciplinary studies could include measures such as ecological momentary assessment¹¹⁹ that can provide insight into the daily social (including experiences and perceptions of ISR and discrimination) and environmental lives of children and families.

Payne-Sturges et al. further argue that the technical and epistemological challenges of studying environmental health and child development within the confines of structural racism require additional theory-building and analytic tools.²⁵ They point to the potential for system dynamics (SD) modeling as a means of moving “between ecological levels of analysis and to integrate network effects, account for time dimensions, and to integrate the role of context in understanding human and community health” (p. 2). In particular, the emphasis on examining “the mechanisms, processes, and pattern of systems behavior” (p. 2²⁵) make it a promising means of extending our understanding of historic ISR effects on development across multiple generations using data that are informed both by affected communities, researchers, and policymakers.

$2+$ Generation Model: Redirecting Risk Mitigation to Systems

There are still many important questions to be asked about the intergenerational impacts of exposures to environmental toxicants. Yet, extant research provides enough data to support immediate action to begin to dismantle aspects of institutional and structural racism. We assert that critical examinations of the contextual and intergenerational processes that drive development are among the first steps. Intervention efforts must also consider multiple factors that contribute to well-being across generations, e.g., income, health, education, environmental and public health policy, especially in the presence of institutional and structural racism.

In their recent Cochrane systematic review of household lead reduction intervention, for example, Nussbaumer-Streit et al. concluded that individual- and family-based education, the first-line lead reduction intervention at present, showed little to no effectiveness in reducing blood lead levels.¹²⁰ In addition to their ineffectiveness, communicating these interventions as a way for families to keep their children safe from lead hazards can reflect institutional gaslighting and perpetuates the notion that physical, psychological, and economic well-being result from simple grit and that lack of well-being results from moral failing. For example, shortly before the Flint lead contamination of drinking water was discovered, a mother’s 2-y-old child was discovered to have elevated blood lead. Reflecting on that time, the mother related that she felt blamed, “They told me I was not keeping my house clean enough, that I should have washed her hands more and dusted more. No one asked about the water” (p. 71¹²¹).

We argue that the inherent injustice of placing the burden of ineffective intervention on individual families and the pervasive sentiment that they are not trying hard enough limits both scientific understanding as well as motivation to implement meaningful change. The $2+$ Generation Model provides a means of identifying key points for changes to the system that are essential to prevent and reduce the effects of environmental toxicant exposure across generations, especially in communities of color. The model can be used as a lever to open new lines of inquiry and identify areas needing systemic change.

A similar systems approach to injury prevention was proposed in the 1970s by William Haddon et al. Rather than centering on only the accident victim and their actions, Haddon proposed centering on the system in which “accidents” occur. Haddon et al. proposed a three-part matrix of injury prevention: pre-event phase, event phase, and postevent phase, a deceptively simple framework for thinking about and acting toward prevention.^122,123 As Baker and Haddon comment, “… [Accidents] are commonly regarded as someone’s fault, rather than as a failure that could have been prevented by some change to the system” (p. 381; emphasis in original¹²²).

The pre-event phase concentrates on societal primary prevention by, if possible, eliminating exposure to the hazard.¹²² Examples pertinent to child development include childproof matches, covered electrical outlets, fences around swimming pools, and childproof medicine containers. In the event phase, Baker and Haddon suggested flame-retardant clothes, circuit breakers, life jackets, and water safety training. In the postevent phase, the Haddon matrix emphasizes reducing current harm and preventing further harm. Child-relevant examples include burn centers and rehabilitation, cardiopulmonary resuscitation (CPR) equipment, CPR training for the general population, and poison information and detoxification centers. We maintain that all these measures are instantiated at the societal level and currently taken for granted. Yet, they are powerful lifesavers.

Using the Haddon matrix in conjunction with the $2+$ Generation Model, the “injury” to be prevented consists of the negative effects of environmental toxicants on developmental outcomes. The pre-event phase includes the societal structures—in this case, institutional and structural racism, that allow toxicants to persist intergenerationally in housing, schools, day care facilities, soil, water, and other sources with potential to be contacted by children, as well as social structures such redlining, job discrimination, poor quality schools, etc., that constrain the agency of BIPOC individuals and communities. The event phase at the individual level could be operationalized using a biological marker such as blood lead level or diagnosis of a health condition such as attention deficit/hyperactivity disorder. But the “event” also includes the system in which it occurs, including the historic institutional and structural racism that set the stage for exposure in the first generation as well as concurrent institutional and structural racism. In the case of lead, the postevent phase would include societal structures such as availability of health care, continuity of health care, the attention of health care providers to blood lead testing, and follow-ups such as enforcement of abatement of lead sources, assessments of child psychoeducational functioning, treatment to improve educational and social outcomes for the child, along with family-based interventions and policy. Viewing environmental health as the outcome of an entire system with a repeated cycle across generations leads to the important idea of risk abatement as a primary prevention measure. In addition, the post-event phase takes on importance for ameliorating negative effects of toxicant exposure on the current generation and thereby reducing some of the effects on the next generation. Although family measures during the exposure event, such as regular home cleaning, improving nutrition, and washing children’s hands frequently, may reduce the severity of some exposure, we suggest such measures can be seen to be of lesser importance in the long run of intergenerational exposure than changing the societal structures that allow environmental toxicants to persist in the environments of BIPOC children in the first place.

Further, part of the harm prevention approach of the Haddon matrix^122,123 emphasizes postinjury care by professionals trained to deal with the condition. This emphasis implies care by professionals trained in child behavior and family systems such as school psychologists, health care providers, and behavior therapists, including continuity of care for those with frequent changes of residence. The Haddon matrix in the context of the $2+$ Generation Model, emphasizes maintaining individual and community agency while equitably providing for postinjury needs. In addition, the Haddon matrix draws attention to the next step of prevention: altering the societal structures and systems to disrupt the cycle.

Conclusion

Failures of society due to structural and institutional racism have resulted in significant disparities in environmental toxicant exposures due to race and SES. To identify points in the system that can and should be changed, the $2+$ Generation Model focuses on the sociohistorical systems and structures that set the stage for and perpetuate disparities in environmental health. We contend that doing so redirects the burden of risk mediation from the individual family to the government institutions and structures that are most appropriate for addressing them effectively.

We propose that the $2+$ Generation Model can be a powerful means of conceptualizing and then operationalizing how institutional and structural racism impacts intergenerational well-being through environmental toxicant exposures. Rather than a universal theory of how institutional and structural racism historically and concurrently contributes to intergenerational lead exposure and other disparities in environmental health, this model is applicable as a tool for creating new knowledge and informing novel interventions aimed at institutional and structural racism and environmental toxicants impacting multiple BIPOC communities.

The central point of this commentary is that adding this model to the range of tools used in the environmental health sciences (exposure analysis, epidemiology, toxicology, biostatistics, and surveillance) can function to foreground important questions of how current and historical social-environments influence both environmental toxicant exposures and the outcomes of such exposures on preexisting, structurally induced, racial disparities. Because the racial disparities in exposure persist, the steps to prevent future exposures include determining the historic and concurrent contexts in which the disparities began and are perpetuated. Emphasizing policies that support healthy lifespan development is an essential societal investment, one that can yield a multigenerational return.

Conclusions and opinions are those of the individual authors and do not necessarily reflect the policies or views of EHP Publishing or the National Institute of Environmental Health Sciences.