RESUMEN
The urban heat island effect exacerbates independent climate change-induced shifts toward longer, stronger, and more frequent heat extremes. Environmental inequity, driven by a history of racially motivated urban planning policies, has led particular demographics to bear the worst impacts of urban heat exposure and thus also climate change. These impacts cause adverse health outcomes in the form of heat emergencies. Through a novel demographic and spatial analysis of heat-related illness Emergency Medical Services data from Richmond, Virginia, this study investigates the relationships between heat health emergencies and intra-urban heat islands quantified through three heat exposure metrics. We also evaluate the accessibility of built refuge from urban heat in the form of public transit infrastructure, libraries, and government cooling centers in relation to these emergencies. We found that heat emergencies are inequitably distributed among racial, age, and socioeconomic groups in Richmond, particularly among residents identified as Male, Black or African American, 50+ years old, and experiencing mental health, intoxication, and/or homelessness. We found significant associations between the location of these heat emergencies and urban heat islands as estimated from remotely-sensed surface and community science-derived air temperature metrics, but not a co-estimated heat index. We also found that available refuge facilities are insufficiently located to protect individuals with reduced mobility across areas with the highest number of heat-related health emergencies. Community involvement in the mitigation and management of extreme heat threats, especially for those disproportionately impacted, is necessary to decrease the number of summertime heat illnesses.
RESUMEN
BACKGROUND: In 2016, a multijurisdictional team investigated an outbreak of Shiga toxin-producing Escherichia coli (STEC) serogroup O121 and O26 infections linked to contaminated flour from a large domestic producer. METHODS: A case was defined as infection with an outbreak strain in which illness onset was between December 21, 2015, and September 5, 2016. To identify exposures associated with the outbreak, outbreak cases were compared with non-STEC enteric illness cases, matched according to age group, sex, and state of residence. Products suspected to be related to the outbreak were collected for STEC testing, and a common point of contamination was sought. Whole-genome sequencing was performed on isolates from clinical and food samples. RESULTS: A total of 56 cases were identified in 24 states. Univariable exact conditional logistic-regression models of 22 matched sets showed that infection was significantly associated with the use of one brand of flour (odds ratio, 21.04; 95% confidence interval [CI], 4.69 to 94.37) and with tasting unbaked homemade dough or batter (odds ratio, 36.02; 95% CI, 4.63 to 280.17). Laboratory testing isolated the outbreak strains from flour samples, and whole-genome sequencing revealed that the isolates from clinical and food samples were closely related to one another genetically. Trace-back investigation identified a common flour-production facility. CONCLUSIONS: This investigation implicated raw flour as the source of an outbreak of STEC infections. Although it is a low-moisture food, raw flour can be a vehicle for foodborne pathogens.
