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Evaluating health risks of environmental contaminants can be better achieved by considering toxic impacts across species. Hexavalent chromium [Cr(VI)] is a marine pollutant and global environmental contaminant. While Cr(VI) has been identified as a human lung carcinogen, health effects in marine species are poorly understood. Little is known about how Cr(VI) might impact humans and marine species differently. This study used a One Environmental Health Approach to compare the cytotoxicity and genotoxicity of particulate Cr(VI) in human and leatherback sea turtle (Dermochelys coriacea) lung fibroblasts. Leatherbacks may experience prolonged exposures to environmental contaminants and provide insight to how environmental exposures affect health across species. Since humans and leatherbacks may experience prolonged exposure to Cr(VI), and prolonged Cr(VI) exposure leads to carcinogenesis in humans, in this study we considered both acute and prolonged exposures. We found particulate Cr(VI) induced cytotoxicity in leatherback cells comparable to human cell data supporting current research that shows Cr(VI) impacts health across species. To better understand mechanisms of Cr(VI) toxicity we assessed the genotoxic effects of particulate Cr(VI) in human and leatherback cells. Particulate Cr(VI) induced similar genotoxicity in both cell lines, however, human cells arrested at lower concentrations than leatherback cells. We also measured intracellular Cr ion concentrations and found after prolonged exposure human cells accumulated more Cr than leatherback cells. These data indicate Cr(VI) is a health concern for humans and leatherbacks. The data also suggest humans and leatherbacks respond to chemical exposure differently, possibly leading to the discovery of species-specific protective mechanisms. Unlabelled Image • Cr(VI) is cytotoxic and genotoxic to leatherback sea turtle lung cells. • Leatherback and human cells respond differently to Cr(VI). • Cr(VI) exposure is a health concern for humans and leatherback sea turtles. [ABSTRACT FROM AUTHOR]

Hexavalent chromium [Cr(VI)] is a human lung carcinogen with widespread exposure risks. Cr(VI) causes DNA double strand breaks that if unrepaired, progress into chromosomal instability (CIN), a key driving outcome in Cr(VI)-induced tumors. The ability of Cr(VI) to cause DNA breaks and inhibit repair is poorly understood in human lung epithelial cells, which are extremely relevant since pathology data show Cr(VI)-induced tumors originate from bronchial epithelial cells. In the present study, we considered immortalized and primary human bronchial epithelial cells. Cells were treated with zinc chromate at concentrations ranging 0.05 to 0.4μg/cm2 for acute (24 h) and prolonged (120 h) exposures. DNA double strand breaks (DSBs) were measured by neutral comet assay and the status of homologous recombination repair, the main pathway to fix Cr(VI)-induced DSBs, was measured by RAD51 foci formation with immunofluorescence, RAD51 localization with confocal microscopy and sister chromatid exchanges. We found acute and prolonged Cr(VI) exposure induced DSBs. Acute exposure induced homologous recombination repair, but prolonged exposure inhibited it resulting in chromosome instability in immortalized and primary human bronchial epithelial cells. [Display omitted] • Cr(VI) is genotoxic to primary and immortalized human bronchial epithelial cells. • Acute Cr(VI) induces DNA breaks and their repair in human lung epithelial cells. • Prolonged Cr(VI) exposure induces DNA breaks in human bronchial epithelial cells. • Prolonged Cr(VI) exposure inhibits repair in human bronchial epithelial cells. • Particulate Cr(VI) induces chromosome instability in human bronchial epithelial cells. [ABSTRACT FROM AUTHOR]

Hexavalent chromium [Cr(VI)] is a well-known and widespread environmental contaminant associated with a variety of adverse health effects, in particular lung cancer. The primary route of exposure in humans is through inhalation. Particulate forms of Cr(VI) are the most potent but in vivo studies are difficult. Intratracheal instillation requires highly trained surgical procedures which also limits the number of repeated exposures possible and thus requires high doses. Inhalation studies can deliver lower more chronic doses but are expensive and generate dangerous aerosols. We evaluated an oropharyngeal aspiration exposure route for zinc chromate particles in Wistar rats. Animals were treated once per week for 90 days. We found chromium accumulated in the lungs, blood, and reproductive tissues of all treated animals. Additionally, we found inflammatory indicators in the lung were elevated and circulating lymphocytes had increased chromosomal damage. These results show oropharyngeal aspiration provides a practicable exposure route for chronic and sub-chronic exposures of Cr(VI) particles. • Oropharyngeal aspiration of zinc chromate particles leads to increased chromium levels in multiple tissues. • Sub-chronic exposure of zinc chromate particles in rats increased macrophage infiltration in the lungs. • Sub-chronic exposure of zinc chromate particles in rats increased chromosome instability in lymphocytes. [ABSTRACT FROM AUTHOR]