Abstract
BACKGROUND: Participation in epidemiologic studies has declined, raising concerns about selection bias. While estimates derived from epidemiologic studies have been shown to be robust under a wide range of scenarios, additional empiric study is needed. The Georgia Study to Explore Early Development (GA SEED), a population-based case-control study of risk factors for autism spectrum disorder (ASD), provided an opportunity to explore factors associated with non-participation and potential impacts of non-participation on association studies. METHODS: GA SEED recruited preschool-aged children residing in metropolitan-Atlanta during 2007-2012. Children with ASD were identified from multiple schools and healthcare providers serving children with disabilities; children from the general population (POP) were randomly sampled from birth records. Recruitment was via mailed invitation letter with follow-up phone calls. Eligibility criteria included birth and current residence in study area and an English-speaking caregiver. Many children identified for potential inclusion could not be contacted. We used data from birth certificates to examine demographic and perinatal factors associated with participation in GA SEED and completion of the data collection protocol. We also compared ASD-risk factor associations for the final sample of children who completed the study with the initial sample of all likely ASD and POP children invited to potentially participate in the study, had they been eligible. Finally, we derived post-stratification sampling weights for participants who completed the study and compared weighted and unweighted associations between ASD and two factors collected via post-enrollment maternal interview: infertility and reproductive stoppage. RESULTS: Maternal age and education were independently associated with participation in the POP group. Maternal education was independently associated with participation in the ASD group. Numerous other demographic and perinatal factors were not associated with participation. Moreover, unadjusted and adjusted odds ratios for associations between ASD and several demographic and perinatal factors were similar between the final sample of study completers and the total invited sample. Odds ratios for associations between ASD and infertility and reproductive stoppage were also similar in unweighted and weighted analyses of the study completion sample. CONCLUSIONS: These findings suggest that effect estimates from SEED risk factor analyses, particularly those of non-demographic factors, are likely robust.