title: Metal-sulfide mineral ores, Fenton chemistry and disease--particle induced inflammatory stress response in lung cells.
abstract: The inhalation of mineral particulates and other earth materials, such as coal, can initiate or enhance disease in humans. Workers in occupations with high particulate exposure, such as mining, are particularly at risk. The ability of a material to generate an inflammatory stress response (ISR), a measure of particle toxicity, is a useful tool in evaluating said exposure risk. ISR is defined as the upregulation of cellular reactive oxygen species (ROS) normalized to cell viability. This study compares the ISR of A549 human lung epithelial cells after exposure to well-characterized common metal-sulfide ore mineral separates. The evaluation of the deleterious nature of ore minerals is based on a range of particle loadings (serial dilutions of 0.002m(2)/mL stock) and exposure periods (beginning at 30min and measured systematically for up to 24h). There is a wide range in ISR values generated by the ore minerals. The ISR values produced by the sphalerite samples are within the range of inert materials. Arsenopyrite generated a small ISR that was largely driven by cell death. Galena showed a similar, but more pronounced response. Copper-bearing ore minerals generated the greatest ISR, both by upregulating cellular ROS and generating substantial and sustained cell death. Chalcopyrite and bornite, both containing ferrous iron, generated the greatest ISR overall. Particles containing Fenton metals as major constituents produce the highest ISR, while other heavy metals mainly generate cell death. This study highlights the importance of evaluating the chemistry, oxidation states and structure of a material when assessing risk management.
authors.affiliation: Department of Geosciences, Earth and Space Sciences Building, Stony Brook University, Stony Brook, NY 11784-2100, USA; Institute of Environmental Medicine, New York University, 57 Old Forge Road, Tuxedo, NY 10987, USA. Electronic address: Andrea.Harrington@nyumc.org.
authors.forename: Andrea D
authors.initials: AD
authors.lastname: Harrington
authors.affiliation: Department of Earth and Marine Sciences, Dowling College, 150 Idle Hour Boulevard, Oakdale, NY 11769, USA. Electronic address: asmirnov@dowling.edu.
authors.forename: Alexander
authors.initials: A
authors.lastname: Smirnov
authors.affiliation: Pharmacological Sciences - Stony Brook University Medical School, BST 8-192, Stony Brook University, Stony Brook, NY 11794-8651, USA. Electronic address: stella@pharm.stonybrook.edu.
authors.forename: Stella E
authors.initials: SE
authors.lastname: Tsirka
authors.affiliation: Department of Geosciences, Earth and Space Sciences Building, Stony Brook University, Stony Brook, NY 11784-2100, USA; Environmental Sciences Department, Brookhaven National Laboratory, Building 815E, Upton, NY 11973, USA. Electronic address: martin.schoonen@stonybrook.edu.
authors.forename: Martin A A
authors.initials: MA
authors.lastname: Schoonen
mesh_terms: D006861:Hydrogen Peroxide; D007501:Iron; D008168:Lung / Q000187:drug effects* / Q000473:pathology; D008903:Minerals / Q000633:toxicity*; D016273:Occupational Exposure; D052638:Particulate Matter / Q000633:toxicity*; D017382:Reactive Oxygen Species; D012307:Risk Factors; D013312:Stress, Physiological / Q000187:drug effects*; D013440:Sulfides / Q000633:toxicity*
chemical_list: C045076:Fenton's reagent; D008903:Minerals; D052638:Particulate Matter; D017382:Reactive Oxygen Species; D013440:Sulfides; D006861:Hydrogen Peroxide; D007501:Iron
keywords: Fenton chemistry; Inflammatory stress response; Occupational disease; Ore minerals; Oxidative stress
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