Alix S. Winter

Six Developmental Trajectories Characterize Children With Autism

OBJECTIVE: The goal of this study was to describe the typical longitudinal developmental trajectories of social and communication functioning in children with autism and to determine the correlates of these trajectories. METHODS: Children with autism who were born in California from 1992 through 2001 and enrolled with the California Department of Developmental Services were identified. Subjects with <4 evaluations present in the database were excluded, resulting in a sample of 6975 children aged 2 to 14 years. Score sequences were constructed based on 9 evaluative items for social, communication, and repetitive behavior functioning. Typical trajectories were identified by using group-based latent trajectory modeling, and multinomial logistic regression models were used to determine the odds of classification within each trajectory varied by individual and family-level factors. RESULTS: Six typical patterns of social, communication, and repetitive behavior functioning were identified. These trajectories displayed significant heterogeneity in developmental pathways, and children whose symptoms were least severe at first diagnosis tended to improve more rapidly than those severely affected. One group of ∼10% of children experienced rapid gains, moving from severely affected to high functioning. Socioeconomic factors were correlated with trajectory outcomes; children with non-Hispanic, white, well-educated mothers were more likely to be high functioning, and minority children with less-educated mothers or intellectual disabilities were very unlikely to experience rapid gains. CONCLUSIONS: Children with autism have heterogeneous developmental pathways. One group of children evidenced remarkable developmental change over time. Understanding what drives these outcomes is thus critical.

Spatial clusters of autism births and diagnoses point to contextual drivers of increased prevalence

Autism prevalence has risen dramatically over the past two decades in California. Although often suggested to have been crucial to the rise of autism, environmental and social contextual drivers of diagnosis have not been extensively examined. Identifying the spatial patterning of autism cases at birth and at diagnosis can help clarify which contextual drivers are affecting autisms rising prevalence. Children with autism not co-morbid with mental retardation served by the California Department of Developmental Services during the period 1992-2005 were matched to Californias Birth Master Files. We search for spatial clusters of autism at time of birth and at time of diagnosis using a spatial scan approach that controls for key individual-level risk factors. We then test whether indicators of neighborhood-level diagnostic resources are associated with the diagnostic clusters and assess the extent of clustering by autism symptom severity through a multivariate scan. Finally, we test whether children who move into neighborhoods with higher levels of resources are more likely to receive an autism diagnosis relative to those who do not move with regard to resources. Significant birth and diagnostic clusters of autism are observed independent of key individual-level risk factors. While the clusters overlap, there is a strong positive association between the diagnostic clusters and neighborhood-level diagnostic resources. In addition, children with autism who are higher functioning are more likely to be diagnosed within a cluster than children with autism who are lower functioning. Most importantly, children who move into a neighborhood with more diagnostic resources than their previous residence are more likely to subsequently receive an autism diagnosis than children whose neighborhood resources do not change. We identify birth and diagnostic clusters of autism in California that are independent of individual-level autism risk factors. Our findings implicate a causal relationship between neighborhood-level diagnostic resources and spatial patterns of autism incidence but do not rule out the possibility that environmental toxicants have also contributed to autism risk.

HOW JUDGES THINK ABOUT RACIAL DISPARITIES: SITUATIONAL DECISION-MAKING IN THE CRIMINAL JUSTICE SYSTEM†

Researchers have theorized how judges’ decision-making may result in the disproportionate presence of Blacks and Latinos in the criminal justice system. Yet, we have little evidence about how judges make sense of these disparities and what, if anything, they do to address them. By drawing on 59 interviews with state judges in a Northeastern state, we describe, and trace the implications of, judges’ understandings of racial disparities at arraignment, plea hearings, jury selection, and sentencing. Most judges in our sample attribute disparities, in part, to differential treatment by themselves and/or other criminal justice officials, whereas some judges attribute disparities only to the disparate impact of poverty and differences in offending rates. To address disparities, judges report employing two categories of strategies: noninterventionist and interventionist. Noninterventionist strategies concern only a judges own differential treatment, whereas interventionist strategies concern other actors’ possible differential treatment, as well as the disparate impact of poverty and facially neutral laws. We reveal how the use of noninterventionist strategies by most judges unintentionally reproduces disparities. Through our examination of judges’ understandings of racial disparities throughout the court process, we enhance understandings of American racial inequality and theorize a situational approach to decision-making in organizational contexts.

THE RACIAL ECOLOGY OF LEAD POISONING: Toxic Inequality in Chicago Neighborhoods, 1995-2013

This paper examines the racial ecology of lead exposure as a form of environmental inequity, one with both historical and contemporary significance. Drawing on comprehensive data from over one million blood tests administered to Chicago children from 1995-2013 and matched to over 2300 geographic block groups, we address two major questions: (1) What is the nature of the relationship between neighborhood-level racial composition and variability in children’s elevated lead prevalence levels? And (2) what is the nature of the relationship between neighborhood-level racial composition and rates of change in children’s prevalence levels over time within neighborhoods? We further assess an array of structural explanations for observed racial disparities, including socioeconomic status, type and age of housing, proximity to freeways and smelting plants, and systematic observations of housing decay and neighborhood disorder. Overall, our theoretical framework posits lead toxicity as a major environmental pathway through which racial segregation has contributed to the legacy of Black disadvantage in the United States. Our findings support this hypothesis and show alarming racial disparities in toxic exposure, even after accounting for possible structural explanations. At the same time, however, our longitudinal results show the power of public health policies to reduce racial inequities.

Short and Long Interpregnancy Intervals: Correlates And Variations by Pregnancy Timing Among U.S. Women

CONTEXT Short and long interpregnancy intervals are associated with adverse health outcomes. Little is known about the correlates of short and long interpregnancy intervals in the general population, and whether correlates vary by pregnancy intention. METHODS Data on 10,236 pregnancies following a live birth were drawn from the 1995, 2002 and 2006-2010 waves of the National Survey of Family Growth. Logistic regression was used to assess characteristics associated with womens reporting short interpregnancy intervals (less than 12 months) and long intervals (greater than 60 months). Analyses were stratified by whether women considered their pregnancies well timed or mistimed. RESULTS Thirty-one percent of pregnancies following short intervals and 47% following long intervals were well timed. Among well-timed pregnancies only, the odds of short intervals were elevated if women had been 35 or older, rather than aged 20-29, at last pregnancy (odds ratio, 2.3); if their prior infant had died (10.6); or if they had wanted their prior pregnancy sooner than it had occurred (2.2). Overall, the odds of long intervals were higher among minority groups than among whites (1.4-1.6) and were lower among women who had been 30 or older at prior pregnancy than among those who had been in their 20s (0.1-0.5); they increased with level of family income. Correlates of long intervals generally varied little by intention. CONCLUSIONS Although the majority of pregnancies at short intervals are unintended, specific subsets of women have elevated odds of intending short interpregnancy intervals.

From Lead Exposure in Early Childhood to Adolescent Health: A Chicago Birth Cohort

Objectives To assess the relationships between childhood lead exposure and 3 domains of later adolescent health: mental, physical, and behavioral. Methods We followed a random sample of birth cohort members from the Project on Human Development in Chicago Neighborhoods, recruited in 1995 to 1997, to age 17 years and matched to childhood blood test results from the Department of Public Health. We used ordinary least squares regression, coarsened exact matching, and instrumental variables to assess the relationship between average blood lead levels in childhood and impulsivity, anxiety or depression, and body mass index in adolescence. All models adjusted for relevant individual, household, and neighborhood characteristics. Results After adjustment, a 1 microgram per deciliter increase in average childhood blood lead level significantly predicts 0.06 (95% confidence interval [CI] = 0.01, 0.12) and 0.09 (95% CI = 0.03, 0.16) SD increases and a 0.37 (95% CI = 0.11, 0.64) point increase in adolescent impulsivity, anxiety or depression, and body mass index, respectively, following ordinary least squares regression. Results following matching and instrumental variable strategies are very similar. Conclusions Childhood lead exposure undermines adolescent well-being, with implications for the persistence of racial and class inequalities, considering structural patterns of initial exposure.

POISONED DEVELOPMENT: ASSESSING CHILDHOOD LEAD EXPOSURE AS A CAUSE OF CRIME IN A BIRTH COHORT FOLLOWED THROUGH ADOLESCENCE†

The consequences of lead exposure for later crime are theoretically compelling, but direct evidence from representative, longitudinal samples is sparse. By capitalizing on an original follow-up of more than 200 infants from the birth cohort of the Project on Human Development in Chicago Neighborhoods matched to their blood lead levels from around age 3 years, we provide several tests. Through the use of four waves of longitudinal data that include measures of individual development, family background, and structural inequalities in how lead becomes embodied, we assess the hypothesized link between early childhood lead poisoning and both parent-reported delinquent behavior and official arrest in late adolescence. We also test for mediating developmental processes of impulsivity and anxiety or depression. The results from multiple analytic strategies that make different assumptions reveal a plausibly causal effect of childhood lead exposure on adolescent delinquent behavior but no direct link to arrests. The results underscore lead exposure as a trigger for poisoned development in the early life course and call for greater integration of the environment into theories of individual differences in criminal behavior.