Mapping Cumulative Risk in Delaware: Approach and Implications for Health Equity.

BACKGROUND: Addressing health equity requires attention to upstream determinants of health, including environmental and social factors that act in tandem to increase communities' exposure to and vulnerability to toxicants. Cumulative risk assessment, which evaluates combined risks from environmental and social factors, is a useful approach for estimating potential drivers of health disparities. We developed a cumulative risk score of multiple indices of environmental and social conditions and assessed block group-level differences in New Castle County, Delaware. METHODS: This cross-sectional study used choropleth maps to visualize the distribution of environmental, social, and cumulative risks and Moran's I statistics to assess spatial clustering of cumulative risk across the county and among individual block groups. RESULTS: Findings indicate that environmental risk rarely occurs without social risk and that environmental and social risks co-occur in distinct areas, resulting in large-scale clustering of cumulative risk. Areas of higher cumulative risk had more Black residents and people of lower socioeconomic status. CONCLUSIONS: Replicable measures of cumulative risk can show how environmental and social risks are inequitably distributed by race and socioeconomic status, as seen here in New Castle County. Such measures can support upstream approaches to reduce health disparities resulting from histories of environmental racism.

Zika virus infection of pregnant rats and associated neurological consequences in the offspring.

Zika virus (ZIKV) is a mosquito-borne flavivirus associated with microcephaly and other neurological disorders in infants born to infected mothers. Despite being declared an international emergency by the World Health Organization, very little is known about the mechanisms of ZIKV pathogenesis or the long-term consequences of maternal ZIKV infection in the affected offspring, largely due to the lack of appropriate rodent models. To address this issue, our lab has developed a working model of prenatal ZIKV infection in rats. In this study, we infected immune competent pregnant female rats with 105-107 PFU of ZIKV (PRVABC59, Puerto Rico/Human/Dec 2015) in order to examine its pathogenesis in the dams and pups. We examined the febrile response and sickness behavior in the dams, in addition to neonatal mortality, microglia morphology, cortical organization, apoptosis, and brain region-specific volumes in the offspring. Here, we demonstrate that pregnant and non-pregnant female rats have a distinct febrile response to ZIKV infection. Moreover, prenatal ZIKV infection increased cell death and reduced tissue volume in the hippocampus and cortex in the neonatal offspring. For the first time, we demonstrate the efficacy and validity of an immunocompetent rat model for maternal ZIKV infection that results in significant brain malformations in the neonatal offspring.