//static.cambridge.org/content/id/urn%3Acambridge.org%3Aid%3Aarticle%3AS2059866124005181/resource/name/firstPage-pdf-S2059866124005181a.jpg

The link between childhood adversity and adulthood depression is well-established; however, the underlying mechanisms are still being explored. Recent research suggests biological age may mediate the relationship between childhood adversity and depression in later life. This study examines if biological age mediates the relationship between childhood adversity and depression symptoms using an expanded set of biological age measures in an urban population-based cohort. Data from waves 1–3 of the Detroit Neighborhood Health Study (DNHS) were used in this analysis. Questions about abuse during childhood were coded to form a childhood adversity score similar to the Adverse Childhood Experience measure. Multiple dimensions of biological age, defined as latent variables, were considered, including systemic biological age (GrimAge, PhenoAge), epigenetic age (Horvath, SkinBlood), and immune age (cytomegalovirus, herpes simplex virus type 1, C-reactive protein, interleukin-6). Depression symptoms, modeled as a latent variable, were captured through the Patient Health Questionnaire-9 (PHQ-9). Models were adjusted for age, gender, race, parent education, and past depressive symptoms. Total and direct effects of childhood adversity on depression symptoms and indirect effects mediated by biological age were estimated. For total and direct effects, we observed a dose-dependent relationship between cumulative childhood adversity and depression symptoms, with emotional abuse being particularly influential. However, contrary to prior studies, in this sample, we found few direct effects of childhood adversity on biological age or biological age on depression symptoms and no evidence of mediation through the measures of biological age considered in this study. Further research is needed to understand how childhood maltreatment experiences are embodied to influence health and wellness.

<p>Progress toward racial health equity cannot be made if we cannot measure its fundamental driver – structural racism. As in other epidemiological studies, the first step is to measure the exposure. But how to measure structural racism is an ongoing debate. To characterize the approaches epidemiologists and other health researchers use to quantitatively measure structural racism, highlight methodological innovations, and identify gaps in the literature, we conducted a scoping review of the peer-reviewed and grey literature published during 2019-2021 to accompany the work of Groos et al. (J Health Dispar Res Pract. 2018;11(2):Article 13), which surveys the scope of structural racism measurement up to 2017. We identified several themes from the recent literature: the current predominant focus on measuring anti-Black racism, using residential segregation as well as other segregation-driven measures as proxies of structural racism, measuring structural racism as spatial exposures, an increasing call by epidemiologists and other health researchers to measure structural racism as a multidimensional, multi-level determinant of health and related innovations, the development of policy databases, the utility of simulated counterfactual approaches in the understanding of how structural racism drive racial health inequities, and the lack of measures of antiracism and limited work on later life effects. Our findings sketch out several future steps to improve the science around structural racism measurements, which is the key to advancing antiracism policies.</p>

Background: Urban racial arrest disparities are well known. Emerging evidence suggests that rural policing shares similar patterns as urban policing in the USA, but without receiving the same public scrutiny, raising the risk of biased rural policing going unnoticed. Methods: We estimated adult and adolescent arrest rates and rate ratios (RR) by race, rural-urban status, and US region based on 2016 Uniform Crime Reporting Program arrest and US Census population counts using general estimating equation Poisson regression models with a 4-way interaction between race, region, age group, and urbanicity. Results: With few exceptions, arrest rates were highest in small towns and rural areas, especially among Black and American Indian populations. Arrest rates differed between US regions with highest rates and racial disparities in the Midwest. For example, arrest rates among Black adults in the rural Midwest were 148.6 arrests [per 1000 population], 95% CI 131.4–168.0, versus 94.4 arrests, 95% CI 77.2–115.4 in the urban Midwest; and versus corresponding rural Midwest arrests among white adults, 32.7 arrests, 95% CI 30.8–34.8, Black versus white rural RR 4.54, 95% CI 4.09–5.04. Racial arrest disparities in the South were lower but still high, e.g., rural South, Black versus White adults, RR 1.86, 95% CI 1.71–2.03. Conclusions: Rural areas and small towns are potential hotspots of racial arrest disparities across the USA, especially in the Midwest. Approaches to overcoming structural racism in policing must include strategies targeted at rural/small town communities. Our findings underscore the importance of dismantling racist policing in all US communities.

Lead poisoning remains a persistent health issue for both humans and wildlife, despite strides to reduce lead contamination in the environment. Using Geographic Information Systems (GIS), this study explores the associations between blood lead levels (BLLs) in wildlife sentinels and possible built environment lead exposure risk factors in the Minneapolis-Saint Paul, Minnesota urban area. Results show a high-level of heterogeneity in animal BLLs (n = 472) across our urban environment and suggest that each kilometer increase in road density is associated with a 17.07% (95% CI: 1.48%, 35.05%) increase in BLL in our study species of Virginia opossums and Eastern gray squirrels, and a 14.28% (95% CI: 1.16%, 29.09%) increase in BLL of rock pigeons. For squirrels and opossums, we see an additional 5.72% (95% CI: 0.59%, 10.85%) increased risk of BLL for every 1000 people per square-mile. The relationship between animal sentinels and environmental hazards can give us an insight into the potential lead exposure risks for humans. The use of wildlife sentinel data to explore environmental risk factors supports a One Health approach to better address public health questions and aid in wildlife rehabilitation related to residual lead poisoning from ambient environmental exposures.

A number of recent papers have investigated the impact of hurricanes on economic growth. However, there is limited understanding of the investment component of local growth after hurricanes. Using hand collected and web-scraped statutory property tax rate data in the U.S., I find that local governments respond to hurricane impact by raising tax rates. I find the hike in tax rates is persistent for 3-4 years after hurricane impact. The response is four times larger for major hurricanes compared to minor hurricanes. However, the increase in tax rates is not expected to be large enough to cause significant out-migration after the average hurricane. I supplement these findings with a novel data set of firm facility-level hurricane impact. I find that firms initially decrease investment in the quarter following hurricane impact and increase it in the final quarters of the second year after impact. Taken together, my paper presents a novel set of stylized facts on government and firm mitigation investment response that can be interpreted in light of recent general equilibrium models with disaster risk.

Despite routine law enforcement use of chemical agents for crowd control, the reproductive health safety profiles of these products are unknown. Moreover, limited evidence has documented a link between such exposures and adverse reproductive health outcomes including abnormal uterine bleeding and potential pregnancy disruption. This cross-sectional study examined reproductive outcomes in adults with uteri exposed to chemical agents used by law enforcement, more commonly known as "tear gas". Participants were recruited through social media in the wake of police violence protests. Of the 1,276 participants included in analysis, 83% reported experiencing at least one of the outcomes of interest, included uterine cramping (69%), early menstrual bleeding (55%), breast tenderness (30%), and delayed menstrual bleeding (21%). Chemical agent exposure was significantly associated with higher odds of an adverse reproductive health outcome, those with 5 days or more of exposure have 2.6 times the odds (CI 1.61, 4.22) of adverse outcomes. and having a perception that one's menstruation may fluctuate according to psychosocial stressors was associated (OR=1.94, CI: 1.36, 2.79) with a higher odds of an adverse reproductive health experience. These findings suggest a potential relationship between exposure to chemical agents and adverse reproductive health outcomes. Given the pervasive use of these chemical agents and their potential for reproductive health harm, further investigation into the safety of these products and their impacts on individual and community health is warranted urgently.