Exposure to prenatal infection has been suggested to cause deficiencies in fetal neurodevelopment. In this study we included all children born in Denmark from 1980, through 2005. Diagnoses of autism spectrum disorders (ASDs) and maternal infection were obtained through nationwide registers. Data was analyzed using Cox proportional hazards regression. No association was found between any maternal infection and diagnosis of ASDs in the child when looking at the total period of pregnancy: adjusted hazard ratio = 1.14 (CI: 0.96-1.34). However, admission to hospital due to maternal viral infection in the first trimester and maternal bacterial infection in the second trimester were found to be associated with diagnosis of ASDs in the offspring, adjusted hazard ratio = 2.98 (CI: 1.29-7.15) and adjusted hazard ratio = 1.42 (CI: 1.08-1.87), respectively. Our results support prior hypotheses concerning early prenatal viral infection increasing the risk of ASDs.

Autism spectrum disorder (ASD) is a complex neurodevelopmental condition with lifelong impacts. Genetic and environmental factors contribute to ASD etiology, which remains incompletely understood. Significant advances in ASD epidemiology have been seen in the past decade. Current prevalence is estimated to be at least 1.5% in developed countries, with recent increases primarily among those without comorbid intellectual disability. Genetic studies have identified a number of rare de novo mutations, and gained footing in the areas of polygenic risk, epigenetics, polygenic risk, and gene x environment (GxE) interaction. Epidemiologic investigations focused on non-genetic factors have established advanced parental age and preterm birth as ASD risk factors, indicated that prenatal exposure to air pollution and short inter-pregnancy interval are potential risk factors, and suggest that further exploration of certain prenatal nutrients, metabolic conditions, and exposure to endocrine-disrupting chemicals is warranted. Future challenges and goals for ASD epidemiology are discussed.

Research suggests that heredity and early fetal development play a causal role in autism. This case-control study explored the association between perinatal factors, parental psychiatric history, socioeconomic status, and risk of autism. The study was nested within a cohort of all children born in Denmark after 1972 and at risk of being diagnosed with autism until December 1999. Prospectively recorded data were obtained from nationwide registries in Denmark. Cases totaled 698 children with a diagnosis of autism; each case was individually matched by gender, birth year, and age to 25 controls. Analyses by conditional logistic regression produced risk ratios and 95% confidence intervals. Adjusted analyses showed that the risk of autism was associated with breech presentation (risk ratio (RR) = 1.63, 95% confidence interval (CI): 1.18, 2.26), low Apgar score at 5 minutes (RR = 1.89, 95% CI: 1.10, 3.27), gestational age at birth <35 weeks (RR = 2.45, 95% CI: 1.55, 3.86), and parental psychiatric history (schizophrenia-like psychosis: RR = 3.44, 95% CI: 1.48, 7.95; affective disorder: RR = 2.91, 95% CI: 1.65, 5.14). Analyses showed no statistically significant association between risk of autism and weight for gestational age, parity, number of antenatal visits, parental age, or socioeconomic status. Results suggest that prenatal environmental factors and parental psychopathology are associated with the risk of autism. These factors seem to act independently.