Assessment of Particulate Matter Toxicity and Physicochemistry at the Claim 28 Uranium Mine Site in Blue Gap, AZ

Particulate matter (PM) inhalation is known to have adverse effects on the respiratory and cardiovascular systems. Community concerns in the southwestern US have been expressed in regions of extensive open-pit hard-rock (especially uranium) mining that windblown dusts may pose an excess health risk. To address these concerns, we have undertaken a campaign to detail: (1) the amount and composition of the PM2.5 in the region, (2) meteorological characteristics, such as wind speed and direction, and (3) and immunological and physiological responses of mice after PM2.5 exposures. For toxicity studies, C57BL/6 and apolipoprotein E-null (ApoE-/-, a vascular inflammation model) mice were exposed to concentrated ambient PM2.5 in a mobile laboratory located approximately 1 km from the Claim 28 uranium mine site, for 1 or 28 days for 4 hours/day to approximately 80 µg/m3 PM2.5. Lungs and aortas were collected for mRNA markers of inflammatory disease, followed by qPCR to gauge the possible inflammatory responses by using inflammatory-specific probes. Cell counts from bronchoalveolar lavage was conducted to examine influx of macrophages and neutrophils into the lungs. Overall, exposure to PM2.5 in the region of the Blue Gap Tachee Claim 28 uranium mine showed only modest evidence of overt pulmonary injury or inflammation. Notably, there was also little evidence of ambient air contamination from uranium or vanadium from the site, which also aligned with meteorological factors that were generally protective of potential community exposures. Effects were consistent with previous demonstrated work with pulmonary inflammation related to PM2.5 exposures