The origin of
coal worker's pneumoconiosis (CWP) has been long debated. A recent epidemiological study shows a correlation between what is essentially the concentration of
pyrite within
coal and the prevalence of CWP in miners.
Hydrogen peroxide and
hydroxyl radical, both
reactive oxygen species (ROS), form as byproducts of
pyrite oxidative dissolution in air-saturated water. Motivated by the possible importance of ROS in the pathogenesis of CWP, we conducted an experimental study to evaluate if ROS form as byproducts in the oxidative dissolution of
pyrite in simulated lung fluid (SLF) under biologically applicable conditions and to determine the persistence of
pyrite in SLF. While the rate of
pyrite oxidative dissolution in SLF is suppressed by 51% when compared to that in air-saturated water, the initial amount of
hydrogen peroxide formed as a byproduct in SLF is nearly doubled.
Hydroxyl radical is also formed in the experiments with SLF, but at lower concentrations than in the experiments with water. The formation of these ROS indicates that the reaction mechanism for
pyrite oxidative dissolution in SLF is no different from that in water. The elevated
hydrogen peroxide concentration in SLF suggests that the decomposition, via the Fenton mechanism to
hydroxyl radical or with Fe(III) to form water and molecular
oxygen, is initially inhibited by the presence of SLF components. On the basis of the oxidative dissolution rate of
pyrite measured in this paper, it is calculated that a respirable two micron
pyrite particle will take over 3 years to dissolve completely.