CHALCOPYRITE-DERIVED REACTIVE OXYGEN SPECIES: A COMBINED ACELLULAR AND CELLULAR STUDY

Mineral-driven ROS formation has been linked to the development of diseases such as silicosis, asbestosis, and coal workers pneumoconiosis. Earlier work has shown that pyrite (FeS₂) will form hydrogen peroxide and hydroxyl radicals (referred to as reactive oxygen species, ROS) when dispersed in water. Recent work has also shown that ROS are upregulated in human epithelial cells when exposed to pyrite. Chalcopyrite (CuFeS₂) is often found along with pyrite in ore deposits and it is also found in coal. Here we evaluated the ability of chalcopyrite, the most abundant copper sulfide on earth, to form ROS when dispersed in water using two separate probes. In addition, we determined the viability and ROS upregulation in human epithelial cells as a function of chalcopyrite dose and time.

The results of the acellular studies showed that chalcopyrite generates hydroxyl radicals but less so compared to pyrite. However, chalcopyrite does produce far more hydrogen peroxide than pyrite when dispersed in water. This result indicates that chalcopyrite, unlike pyrite, is less efficient in promoting the conversion of hydrogen peroxide to hydroxyl radical via the Fenton reaction. The cellular studies indicate that exposure to chalcopyrite is comparable to pyrite, in that it triggers rapid cell death and significant ROS upregulation in the remaining living cells.

Taken together the results of acellular and cellular experiments indicate that chalcopyrite generates ROS when placed in water and that the mineral also induces cell death and cellular ROS upregulation. Given that copper mining is ongoing and that there are a considerable number of communities living near chalcopyrite-containing mine tailings, these results suggest that dust originating from copper ore or tailing piles may be harmful to workers and the wider community.