Approximately 75% of farmworkers in the United States are Latino migrants, and about 50% of hired farmworkers do not have authorization to work in the United States. Farmworkers face numerous chemical, physical, and biological threats to their health. The adverse effects of these hazards may be amplified among Latino migrant farmworkers, who are concurrently exposed to various psychosocial stressors. Factors such as documentation status, potential lack of authorization to work in the United States, and language and cultural barriers may also prevent Latino migrants from accessing federal aid, legal assistance, and health programs. These environmental, occupational, and social hazards may further exacerbate existing health disparities among US Latinos. This population is also likely to be disproportionately impacted by emerging threats, including climate change and severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Latino migrant farmworkers are essential to agriculture in the United States, and actions are needed to protect this vulnerable population. Expected final online publication date for the Annual Review of Public Health, Volume 42 is April 2021. Please see http://www.annualreviews.org/page/journal/pubdates for revised estimates.

Background Venous thromboembolism (VTE) in trauma patients carries significant morbidity and mortality. We previously described how titrating enoxaparin dosing by anti‐Xa trough levels was associated with a lower VTE rate. We combined this strategy with a higher initial enoxaparin dose for a majority of patients and modified the electronic medical record (EMR) to encourage immediate dosing. We sought to determine if this systems‐based approach was associated with a decrease in VTE rate. Study Design A retrospective review was conducted of all trauma patients on prophylactic enoxaparin at an academic, Level I Trauma Center from 01/2013 to 05/2014 (PRE) and 06/2015 to 02/2018 (POST). The patients in PRE were prescribed enoxaparin 30 mg twice daily without dose adjustments. The patients in POST received 40 mg twice daily unless exclusion criteria applied, with doses titrated to maintain anti‐Xa trough levels between 0.1 and 0.2 IU/mL. Results There were 478 patients in the PRE and 1306 in the POST. Compared to PRE, POST patients were of similar age and were as likely to present after blunt trauma, although POST patients had lower injury severity scores (10 vs. 9, p < 0.01). The overall VTE rate was lower in POST (6.9% vs. 3.6%, p < 0.01). The adjusted risk of VTE (AOR 0.61, adjusted p = 0.04) was lower in POST and POST was independently protective for VTE (AOR 0.54; p = 0.01). Conclusion By implementing system changes to improve enoxaparin dosing after trauma, a significant reduction in VTE rate was observed. Wider application of this strategy should be considered.

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BACKGROUND How recurrent traumatic brain injury (rTBI) alters brain function years after insult is largely unknown. This study aims to characterize the mechanistic cause for long-term brain deterioration following rTBI using a rat model. METHODS Eighteen Sprague-Dawley wild-type rats underwent bilateral rTBI using a direct skull impact device or sham treatment, once per week for 5 weeks, and were euthanized 56 weeks after the first injury. Weekly rotarod performance measured motor deficits. Beam walk and grip strength were also assessed. Brain tissue were stained and volume was computed using Stereo Investigator's Cavalieri Estimator. The L5 cortical layer proximal to the injury site was microdissected and submitted for sequencing with count analyzed using R “DESeq2” and “GOStats.” Brain-derived neurotrophic factor (BDNF) levels were determined using enzyme-linked immunosorbent assay. RESULTS Rotarod data demonstrated permanent deficits 1 year after rTBI. Decreased beam walk performance and grip strength was noted among rTBI rodents. Recurrent traumatic brain injury led to thinner cortex and thinner corpus callosum, enlarged ventricles, and differential expression of 72 genes (25 upregulated, 47 downregulated) including dysregulation of those associated with TBI (BDNF, NR4A1/2/3, Arc, and Egr) and downregulation in pathways associated with neuroprotection and neuroplasticity. Over the course of the study, BDNF levels decreased in both rTBI and sham rodents, and at each time point, the decrease in BDNF was more pronounced after rTBI. CONCLUSION Recurrent traumatic brain injury causes significant long-term alteration in brain health leading to permanent motor deficits, cortical and corpus callosum thinning, and expansion of the lateral ventricles. Gene expression and BDNF analysis suggest a significant drop in pathways associated with neuroplasticity and neuroprotection. Although rTBI may not cause immediate neurological abnormalities, continued brain deterioration occurs after the initial trauma in part due to a decline in genes associated with neuroplasticity and neuroprotection.