Research on the effects of adversity has led to mounting interest in examining the differential impact of adversity as a function of its timing and type. The current study examines whether the effects of different types (i.e., physical, sexual, and emotional abuse) and timing (i.e., early, middle childhood, adolescence, or adulthood) of adversity on maternal mental and physical health outcomes in pregnancy, are best accounted for by a cumulative model or independent effects model. Women from a prospective pregnancy cohort (N =3,362) reported retrospectively on their experiences of adversity (i.e., physical, sexual, and emotional abuse) in early childhood (0–5 years], middle childhood (6–12 years], adolescence (13–18 years], and adulthood (19+ years]. Measures of overall health, stress, anxiety, and depression were gathered in pregnancy. Results showed that a cumulative formative latent model was selected as more parsimonious than a direct effects model. Results also supported a model where the strength of the effect of adversity did not vary across abuse timing or type. Thus, cumulative adversity resulted in greater physical and mental health difficulties. In conclusion, cumulative adversity is a more parsimonious predictor of maternal physical and mental health outcomes than adversity at any one specific adversity timing or subtype.

The current study assessed whether the proportion of childhood (age 0–9 years) in poverty altered the developmental trajectories (ages 9–24) of multimethodological indicators of psychological well-being. In addition, we tested whether exposure to cumulative risk over time mediated the association between poverty exposure and psychological well-being. Measures of psychological well-being included internalizing and externalizing symptoms, a behavioral index of learned helplessness (task persistence), and chronic physiological stress (allostatic load). Exposure to poverty during childhood predicted the trajectory of each development outcome: individuals with more poverty exposure during childhood showed (a) relatively high levels of internalizing symptoms that diminished more slowly with maturation, (b) relatively high levels of externalizing symptoms that increased faster over time, (c) less task persistence indicative of greater learned helplessness, and (d) higher levels of chronic physiological stress which increased faster over time relative to persons with less childhood poverty exposure. Trajectories of cumulative risk exposure from physical and psychosocial surroundings from 9–24 years accounted for the association between childhood poverty and the growth curves of internalizing and externalizing symptoms but not for learned helplessness or chronic physiological stress. Additional sensitivity analyses indicate that early childhood disadvantage is particularly problematic for each outcome, except for internalizing symptoms which seem sensitive to the combination of early and lifetime poverty exposure. We also explored whether domains of cumulative risk as well as two alternatives, maternal sensitivity or family cohesion, functioned as mediators. Little evidence emerged for any of these alternative mediating constructs.

We examined associations between preschool children's cumulative risk exposure, dyadic interaction patterns, and self-control abilities in 238 mother–child dyads. Positive interactive synchrony, relationship ruptures, and latency to repair were micro-coded during a 3–5 minute joint challenge task. Children's self-control was assessed via two laboratory tasks and by parent report. Structural equation modeling and mediation analyses were utilized to examine the direct and indirect effects of cumulative risk on children's observed and parent-reported self-control abilities. Parent–child interactive processes of dyadic synchrony and latency to repair ruptures in synchrony were examined as mediators. Dyadic synchrony and latency to repair ruptures were found to mediate associations between cumulative risk exposure and children's behavioral and parent-reported self-control. Children exposed to more cumulative risk engaged in less dyadic synchrony and experienced longer latencies to repair ruptures with their caregiver, which in turn was associated with lower child self-control. Though cross-sectional, findings suggest dyadic synchrony and repair processes may represent viable mechanistic pathways linking cumulative risk exposure and deficits in child self-control. However, independent replications using longitudinal and experimental intervention designs are needed to determine causal pathways and inform new approaches for targeting the effects of early risk exposure through a focus on two-generational interventions.

Additive and bidirectional effects of executive control and hypothalamic–pituitary–adrenal (HPA) axis regulation on children's adjustment were examined, along with the effects of low income and cumulative risk on executive control and the HPA axis. The study utilized longitudinal data from a community sample of preschool age children (N = 306, 36–39 months at Time 1) whose families were recruited to overrepresent low-income contexts. We tested the effects of low income and cumulative risk on levels and growth of executive control and HPA axis regulation (diurnal cortisol level), the bidirectional effects of executive control and the HPA axis on each other, and their additive effects on children's adjustment problems, social competence and academic readiness. Low income predicted lower Time 4 executive control, and cumulative risk predicted lower Time 4 diurnal cortisol level. There was little evidence of bidirectional effects of executive control and diurnal cortisol. However, both executive control and diurnal cortisol predicted Time 4 adjustment, suggesting additive effects. There were indirect effects of income on all three adjustment outcomes through executive control, and of cumulative risk on adjustment problems and social competence through diurnal cortisol. The results provide evidence that executive control and diurnal cortisol additively predict children's adjustment and partially account for the effects of income and cumulative risk on adjustment.

Since W. E. B. Du Bois documented the physical and social environments of Philadelphia’s predominantly African American Seventh Ward over a century ago, there has been continued interest in understanding the distribution of social and physical environments by racial make-up of communities. Characterization of these environments allows for documentation of inequities, identifies communities which encounter heightened risk, and can inform action to promote health equity. In this paper, we apply and extend Du Bois’s approach to examine the contemporary distribution of physical environmental exposures, health risks, and social vulnerabilities in the Detroit metropolitan area, one of the most racially-segregated areas in the United States. We begin by mapping the proximity of sensitive populations to hazardous land uses, their exposure to air pollutants and associated health risks, and social vulnerabilities, as well as cumulative risk (combined proximity, exposure, and vulnerability), across Census tracts. Next, we assess, quantitatively, the extent to which communities of color experience excess burdens of environmental exposures and associated health risks, economic and age-related vulnerabilities, and cumulative risk. The results, depicted in maps presented in the paper, suggest that Census tracts with greater proportions of people of color disproportionately encounter physical environmental exposures, socioeconomic vulnerabilities, and combined risk. Quantitative tests of inequality confirm these distributions, with statistically greater exposures, vulnerabilities, and cumulative risk in Census tracts with larger proportions of people of color. Together, these findings identify communities that experience disproportionate cumulative risk in the Detroit metropolitan area and quantify the inequitable distribution of risk by Census tract relative to the proportion of people of color. They identify clear opportunities for prioritizing communities for legislative, regulatory, policy, and local actions to promote environmental justice and health equity.