Abstract

The taconite (iron ore) worker population of northeastern Minnesota, USA, is at higher risk of mesothelioma, lung cancer, and heart disease than the rest of the state population. Occupational exposures to the components of dust from taconite operations, which includes nonasbestiform amphibole elongate mineral paraticles, silica and cleavage fragments, may play an important role in the observed morbidity and mortality rates in this cohort. We hypothesised that oxidative stress and inflammation, induced by the dust from taconite operations and mediated by iron exposure, are important contributors to the development of cancer and cardiovascular disease in taconite workers. In support of this hypothesis, our preliminary analyses in a group of workers (N = 25) demonstrated that the levels of 3-(2-deoxy-β-D-erythro-pentafuranosyl)pyrimido[1,2-α]purin-10 (3 H)-one deoxyguanosine (M₁dG), a DNA adduct formed through the oxidative stress-induced lipid peroxidation, are higher in the blood of taconite workers with high estimated occupational exposures as compared to workers with low estimated exposures. We further expanded this research by analysing a wide panel of circulating cytokines and chemokines, M₁dG in blood DNA, as well as plasma iron levels, in 129 workers with variable estimated levels of occupational exposure to taconite dust and iron. The results of these analyses will be presented, and the relationship of biomarker levels with the available measures of occupational exposures will be discussed. The overall goal of this research is to identify inflammatory biomarker signatures that are associated with unique occupational exposures and are predictive of lung cancer and cardiovascular disease risk in taconite workers.