Autism spectrum disorders (ASDs) are a major public health concern in the United States affecting more than 1% of the nation's children in all racial, ethnic, and socioeconomic groups. The male-to-female prevalence ratio of roughly 4:1 in ASD is a well-recognized, but poorly-understood, phenomenon. An explicit focus on potential etiologic pathways consistent with this gender difference should be a priority in attempts to elucidate ASD causal mechanisms, including those amenable to environmental influence. Androgens, in particular testosterone, produced during pregnancy act on the brain to produce permanent gender differences in structure and function. Some researchers have hypothesized that ASD is an extreme presentation of "male brain," with fetal testosterone as the possible determining factor. Few endocrine disrupting chemicals are known to act on androgens; however, triclosans and triclocarbans (TCS/TCC) have been shown to have androgenic potential and are now widely used in liquid soap, toothpaste, mouth rinse, and other personal care products. Capitalizing on the availability of stored biosamples from a prospective cohort study of 213 mothers of children with ASD at the start of a subsequent pregnancy, we propose to assess prenatal TCS/TCC exposure in maternal prenatal urine samples and fetal testosterone levels in both cord blood and meconium and then and correlate these measures with ASD-related outcomes evaluated at 12 mos and 36 mos of age in the children born into the cohort. Fetal testosterone level will be explored as a potential mediating and/or moderating factor in associations between TCS/TCC and early ASD-related outcomes. The study will investigate a potentially avoidable environmental ASD risk factor, provide evidence related to an etiologic mechanism that comports with the observed ASD gender ratio, and generate i data on a fetal testosterone levels as assessed in meconium. ExpandCollapse Abstract