Autism spectrum disorders (ASDs) are complex, lifelong, neurodevelopmental conditions of largely unknown cause. They are much more common than previously believed, second in frequency only to mental retardation among the serious developmental disorders. Although a heritable component has been demonstrated in ASD etiology, putative risk genes have yet to be identified. Environmental risk factors may also play a role, perhaps via complex gene-environment interactions, but no specific exposures with significant population effects are known. A number of endogenous biomarkers associated with autism risk have been investigated, and these may help identify significant biologic pathways that, in turn, will aid in the discovery of specific genes and exposures. Future epidemiologic research should focus on expanding population-based descriptive data on ASDs, exploring candidate risk factors in large well-designed studies incorporating both genetic and environmental exposure data and addressing possible etiologic heterogeneity in studies that can stratify case groups and consider alternate endophenotypes.

Objectives We sought to examine racial and ethnic disparities in the recognition of autism spectrum disorders (ASDs). Methods Within a multisite network, 2568 children aged 8 years were identified as meeting surveillance criteria for ASD through abstraction of evaluation records from multiple sources. Through logistic regression with random effects for site, we estimated the association between race/ethnicity and documented ASD, adjusting for gender, IQ, birthweight, and maternal education. Results Fifty-eight percent of children had a documented autism spectrum disorder. In adjusted analyses, children who were Black (odds ratio [OR] = 0.79; 95% confidence interval [CI] = 0.64, 0.96), Hispanic (OR = 0.76; CI = 0.56, 0.99), or of other race/ethnicity (OR = 0.65; CI = 0.43, 0.97) were less likely than were White children to have a documented ASD. This disparity persisted for Black children, regardless of IQ, and was concentrated for children of other ethnicities when IQ was lower than 70. Conclusions Significant racial/ethnic dispatrities exist in the recognition of ASD. For some children in some racial/ethnic groups, the presence of intellectual disability may affect professionals’ further assessment of developmental delay. Our findings suggest the need for continued professional education related to the heterogeneity of the presentation of ASD.

No abstract

Objective At what age are children with an autism spectrum disorder (ASD) identified by community providers? What factors influence the timing of when children are identified with ASDs? This study examined the timing of when children with ASDs are identified. Method Data came from 13 sites participating in the Centers for Disease Control and Prevention’s 2002 multisite, ongoing autism surveillance program, the Autism and Developmental Disabilities Monitoring Network. Survival analysis was used to examine factors that influence the timing of community-based identification and diagnosis. Result Data from health and education records reveal that the median age of identification was 5.7 years (SE 0.08). Parametric survival models revealed that several factors were associated with a younger age of identification: being male, having IQ ≤ 70, and having experienced developmental regression. Significant differences in the age of identification among the 13 sites were also discovered. Conclusions The large gap between the age at which children can be identified and when they actually are identified suggests a critical need for further research, innovation, and improvement in this area of clinical practice.

The prevalence estimate of 45% for mild sleep disturbances in the TD cohort highlights pediatric sleep debt as a public health problem of concern. The prevalence estimate of 66% for moderate sleep disturbances in the ASD cohort underscores the significant sleep problems that the families of these children face. The predominant sleep disorders in the ASD cohort were behavioral insomnia sleep-onset type and insomnia due to PDD.