ACPM Position Statement: Air Pollution and Environmental Justice.

The American Lung Association's "State of the Air" 2023 report reveals almost 36% of Americans live with unhealthy levels of air pollution. Studies link air pollution with acute respiratory symptoms and exacerbation of respiratory and cardiovascular diseases. Differential air pollution exposures between white and nonwhite communities are significant components of environmental injustices. Even during the coronavirus disease 2019 (COVID-19) lockdown, when the United States experienced significant decreases in polluting activities, these differences persisted. The American College of Preventive Medicine's Science and Translation Committee conducted a nonsystematic literature review to explore initiatives addressing air pollution as a key component of environmental justice, the state of the science regarding health impacts, and evidence supporting mitigations to reduce those impacts. We recommend advocacy for cleaner energy sources and increasing green space; and increasing research, surveillance, and education and training on linkages between air pollutants and health. We recommend preventive medicine physicians raise awareness about increased risks of cardiovascular disease, cancer, asthma, and reduced lung function with air pollution exposure. Preventive medicine physicians may also educate patients and other practitioners about exposures, and how "conventional" disease prevention strategies may have unintended consequences; and influence healthcare leaders to improve efficiency and reduce emissions. We also recommend physicians utilize social determinants of health Z-Codes to capture environmental factors. Private payers should incorporate pollution exposure data into social determinants of health risk adjustments for Medicare Advantage programs. Medicaid agencies should develop provider recommendations for pediatric populations, and states should finance in-home interventions for asthma.

Report of the Pathogenesis and Pathophysiology of Lyme Disease Subcommittee of the HHS Tick Borne Disease Working Group.

An understanding of the pathogenesis and pathophysiology of Lyme disease is key to the ultimate care of patients with Lyme disease. To better understand the various mechanisms underlying the infection caused by Borrelia burgdorferi, the Pathogenesis and Pathophysiology of Lyme Disease Subcommittee was formed to review what is currently known about the pathogenesis and pathophysiology of Lyme disease, from its inception, but also especially about its ability to persist in the host. To that end, the authors of this report were assembled to update our knowledge about the infectious process, identify the gaps that exist in our understanding of the process, and provide recommendations as to how to best approach solutions that could lead to a better means to manage patients with persistent Lyme disease.

GLI1 is a central mediator of EWS/FLI1 signaling in Ewing tumors.

The Ewing Sarcoma Family Tumors (ESFT) consist of the classical pathologic entities of Ewing Sarcoma and peripheral Primitive Neuroectodermal Tumor. Occurring largely in the childhood through young adult years, these tumors have an unsurpassed propensity for metastasis and have no defined cell of origin. The biology of these aggressive malignancies centers around EWS/FLI1 and related EWS/ETS chimeric transcription factors, which are largely limited to this tumor class. Much progress has been made in the identification of a network of loci whose expression is modulated by EWS/FLI1 and its congeners. To date, little progress has been made in reconstructing the sequence of direct and indirect events that produce this network of modulated loci. The recent identification of GLI1 as an upregulated target of EWS/ETS transcription factors suggests a target which may be a more central mediator in the ESFT signaling network. In this paper, we further define the relationship of EWS/FLI1 expression and GLI1 upregulation in ESFT. This relationship is supported with data from primary tumor specimens. It is consistently observed across multiple ESFT cell lines and with multiple means of EWS/FLI1 inhibition. GLI1 inhibition affects tumor cell line phenotype whether shRNA or endogenous or pharmacologic inhibitors are employed. As is seen in model transformation systems, GLI1 upregulation by EWS/FLI1 appears to be independent of Hedgehog stimulation. Consistent with a more central role in ESFT pathogenesis, several known EWS/FLI1 targets appear to be targeted through GLI1. These findings further establish a central role for GLI1 in the pathogenesis of Ewing Tumors.