We investigated historical redlining, a government-sanctioned discriminatory policy, in relation to cardiovascular health (CVH) and whether associations were modified by present-day neighborhood physical and social environments. Data included 4,779 participants (mean age 62 y; SD = 10) from the baseline sample of the Multi-Ethnic Study of Atherosclerosis (MESA; 2000 to 2002). Ideal CVH was a summary measure of ideal levels of seven CVH risk factors based on established criteria (blood pressure, fasting glucose, cholesterol, body mass index, diet, physical activity, and smoking). We assigned MESA participants' neighborhoods to one of four grades (A: best, B: still desirable, C: declining, and D: hazardous) using the 1930s federal Home Owners' Loan Corporation (HOLC) maps, which guided decisions regarding mortgage financing. Two-level hierarchical linear and logistic models, with a random intercept to account for participants nested within neighborhoods (i.e., census tracts) were used to assess associations within racial/ethnic subgroups (non-Hispanic White, non-Hispanic Black, Hispanic, and non-Hispanic Chinese). We found that Black adults who lived in historically redlined areas had a 0.82 (95% CI -1.54, -0.10) lower CVH score compared to those residing in grade A (best) neighborhoods, in a given neighborhood and adjusting for confounders. We also found that as the current neighborhood social environment improved the association between HOLC score and ideal CVH weakened (P < 0.10). There were no associations between HOLC grade and CVH measures or effect modification by current neighborhood conditions for any other racial/ethnic group. Results suggest that historical redlining has an enduring impact on cardiovascular risk among Black adults in the United States.

Background

Autism spectrum disorder (ASD) affects more than 1% of children in the USA. 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 sex difference, such as those involving prenatal androgen exposure, may help elucidate causes of ASD. Furthermore, the multi-threshold liability model suggests that the genetic mechanisms in females with ASD may be distinct and may modulate ASD risk in families with female ASD in the pedigree.

Methods

We examined umbilical cord blood from 137 children in the Early Autism Risk Longitudinal Investigation (EARLI) cohort. EARLI is an ASD-enriched risk cohort with all children having an older sibling already diagnosed with ASD. Fetal testosterone (T), androstenedione (A4), and dehyroepiandrosterone (DHEA) levels were measured in cord blood using liquid chromatography-tandem mass spectrometry (LC-MS/MS). Robust linear regression models were used to determine associations between cord blood androgen levels and 12-month Autism Observation Scales for Infants (AOSI) scores and 36-month Social Responsiveness Scale (SRS) scores adjusting for potential confounders.

Results

Increasing androgens were not associated with increasing 12-month AOSI score or 36-month total SRS score in either boys or girls. However, the association between T and autistic traits among subjects with a female older affected sibling was greater at 12 months (test of interaction, P = 0.008) and deficits in reciprocal social behavior at 36 months were also greater (test of interaction, P = 0.006) than in subjects whose older affected sibling was male.

Conclusions

While increased prenatal testosterone levels were not associated with autistic traits at 12 or 36 months, our findings of a positive association in infants whose older ASD-affected siblings were female suggests an androgen-related mechanism that may be dependent on, or related to, genetic liability factors present more often in families containing female ASD cases. However, this initial finding, based on a small subgroup of our sample, should be interpreted with considerable caution.