Abstract
Uranium (U) is a heavy metal used in military and industrial settings, with a large portion being mined from the Southwest region of the United States. Uranium has uses in energy and military weaponry, but the mining process has released U into soil and surface waters that may pose threats to human and environmental health. The majority of literature regarding U’s human health concern focuses on outcomes based on unintentional ingestion or inhalation, and limited data are available about its influence via cutaneous contact. Utilizing skin dermis cells, we evaluated U’s topical chemotoxicity. Employing soluble depleted uranium (DU) in the form of uranyl nitrate (UN), we hypothesized that in vitro exposure of UN will have cytotoxic effects on primary dermal fibroblasts by affecting cell viability and metabolic activity and, further, may delay wound healing aspects via altering cell proliferation and migration. Using environmentally relevant levels of U found in water (0.1 M to 100 M [UN]; 23.8–23,800 ppb [U]), we quantified cellular mitosis and migration through growth curves and in vitro scratch assays. Cells were exposed from 24 h to 144 h for a time-course evaluation of UN chemical toxicity. The effects of UN were observed at concentrations above and below the Environmental Protection Agency threshold for safe exposure limits. UN exposure resulted in a dose-dependent decrease in the viable cell count; however, it produced an increase in metabolism when corrected for the viable cells present. Furthermore, cellular proliferation, population doubling, and percent closure was hindered at levels ≥10 M UN. Therefore, inadvertent exposure may exacerbate pre-existing skin diseases in at-risk demographics, and additionally, it may substantially interfere in cutaneous tissue repair processes.
Highlights
The cellular metabolism was diminished in dermal fibroblasts proportionally to increasing levels of uranyl nitrate (UN), as indicated by a significant decline in resazurin reduction (Figure 1)
After 24 h of exposure, a statistically significant decrease in metabolic activity was measured in cells exposed to 0.1–100 μM UN compared to control
This concentration is above the EPA MCL and is already deemed not safe for human exposure; this level is found in abundance in the United States Southwest
Summary
In the mid 1900s, large-scale U mining for military and industrial applications were conducted on the Colorado Plateau in the Southwestern United States [1,2]. During this time, an estimated 30 million tons of U ore was extracted and transported to mills for processing [3,4,5]. The isotope in the highest abundance 238 U, known as depleted uranium due to its relatively low radioactivity, is a waste product of the nitric acid enrichment process [6]. This isotope of uranium has been implemented in armor-piercing round ammunition during the Cold War; the reduction needed for 238 U has resulted in the accumulation of depleted uranium in mill tailings, and it
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