Traffic-related air pollution in marginalized neighborhoods: a community perspective.

OBJECTIVES: Marginalized communities are exposed to higher levels of traffic-related air pollution (TRAP) than the general population. TRAP exposure is linked to pulmonary toxicity, neurotoxicity, and cardiovascular toxicity often through mechanisms of inflammation and oxidative stress. Early life exposure to TRAP is also implicated in higher rates of asthma in these same communities. There is a critical need for additional epidemiological, in vivo, and in vitro studies to define the health risks of TRAP exposure affecting the most vulnerable groups to set strict, protective air pollution standards in these communities. MATERIALS AND METHODS: A literature review was conducted to summarize recent findings (2010-2024) concerning TRAP exposure and toxic mechanisms that are relevant to the most affected underserved communities. CONCLUSIONS: Guided by the perspectives of NYC community scientists, this contemporary review of toxicological and epidemiological studies considers how the exposome could lead to disproportionate exposures and health effects in underserved populations.

HIF-1 regulates pathogenic cytotoxic T cells in lupus skin disease.

Cutaneous lupus erythematosus (CLE) is a disfiguring autoimmune skin disease characterized by an inflammatory infiltrate rich in T cells, which are strongly implicated in tissue damage. How these cells adapt to the skin environment and promote tissue inflammation and damage is not known. In lupus nephritis, we previously identified an inflammatory gene program in kidney-infiltrating T cells that is dependent on HIF-1, a transcription factor critical for the cellular and developmental response to hypoxia as well as inflammation-associated signals. In our present studies using a mouse model of lupus skin disease, we find that skin-infiltrating CD4+ and CD8+ T cells also express high levels of HIF-1. Skin-infiltrating T cells demonstrated a strong cytotoxic signature at the transcript and protein levels, and HIF-1 inhibition abrogated skin and systemic diseases in association with decreased T cell cytotoxic activity. We also demonstrate in human CLE tissue that the T cell-rich inflammatory infiltrate exhibited increased amounts of HIF-1 and a cytotoxic signature. Granzyme B-expressing T cells were concentrated at sites of skin tissue damage in CLE, suggesting relevance of this pathway to human disease.