Skyrocketing pollution: assessing the environmental fate of July 4th fireworks in New York City.

BACKGROUND: Pyrotechnic displays often lead to significant increases in poor air quality. The widespread environmental fate-involving air, water, and spatial-temporal analyses-of fireworks-produced pollutants has seldom been investigated. OBJECTIVE: This study examined the environmental fate of pollutants from the largest fireworks event in the U.S.: Macy's Fourth of July Fireworks show in New York City (NYC). METHODS: Real-time PM2.5 and gravimetric PM2.5 and PM10 were collected at locations along the East River of NYC. Airborne particles were assayed for trace elements (X-ray fluorescence) and organic and elemental carbon (OC/EC). River water samples were evaluated by ICP-MS for heavy-metal water contamination. Spatial-temporal analyses were created using PM2.5 concentrations reported by both EPA and PurpleAir monitoring networks for NYC and 5 other major metropolitan areas. RESULTS: The fireworks event resulted in large increases in PM2.5 mass concentrations at the river-adjacent sampling locations. While background control PM2.5 was 10-15 µg/m3, peak real-time PM2.5 levels exceeded 3000 µg/m3 at one site and 1000 µg/m3 at two other locations. The integrated gravimetric PM2.5 and PM10 concentrations during the fireworks event ranged from 162 to 240 µg/m3 and 252 to 589 µg/m3, respectively. Zn, Pb, Sb, and Cu more than doubled in river water samples taken after the event, while S, K, Ba, Cu, Mg, Fe, Sr, Ti, and Zn increased in airborne PM2.5 from the fireworks. Data from hyperlocal monitoring networks for NYC and other metropolitan areas yielded similar, but generally smaller, increases in PM2.5 levels. IMPACT: Fireworks shows have been associated with environmental contamination. This comprehensive analysis considers the fate of pollutants from the largest annual U.S. pyrotechnic show through air, water, and hyperlocal temporal characterization.

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.

E-Cigarette Exposure Alters Neuroinflammation Gene and Protein Expression in a Murine Model: Insights from Perinatally Exposed Offspring and Post-Birth Mothers.

The use of E-cigarettes, often considered a safer alternative to traditional smoking, has been associated with high rates of cellular toxicity, genetic alterations, and inflammation. Neuroinflammatory impacts of cigarette smoking during pregnancy have been associated with increased risks of adverse childhood health outcomes; however, it is still relatively unknown if the same propensity is conferred on offspring by maternal vaping during gestation. Results from our previous mouse inhalation studies suggest such a connection. In this earlier study, pregnant C57BL/6 mice were exposed daily to inhaled E-cig aerosols (i.e., propylene glycol and vegetable glycerin, [PG/VG]), with or without nicotine (16 mg/mL) by whole-body inhalation throughout gestation (3 h/d; 5 d/week; total ~3-week) and continuing postnatally from post-natal day (PND) 4-21. As neuroinflammation is involved in the dysregulation of glucose homeostasis and weight gain, this study aimed to explore genes associated with these pathways in 1-mo.-old offspring (equivalent in humans to 12-18 years of age). Results in the offspring demonstrated a significant increase in glucose metabolism protein levels in both treatment groups compared to filtered air controls. Gene expression analysis in the hypothalamus of 1 mo. old offspring exposed perinatally to E-cig aerosols, with and without nicotine, revealed significantly increased gene expression changes in multiple genes associated with neuroinflammation. In a second proof-of-principal parallel study employing the same experimental design, we shifted our focus to the hippocampus of the postpartum mothers. We targeted the mRNA levels of several neurotrophic factors (NTFs) indicative of neuroinflammation. While there were suggestive changes in mRNA expression in this study, levels failed to reach statistical significance. These studies highlight the need for ongoing research on E-cig-induced alterations in neuroinflammatory pathways.