Vanadium is an inorganic Suprfund target chemical and is found at Superfund sites. Vanadium compounds have been shown to cause adverse effects on the respiratory tract of humans. Although it is described to cause bronchitis, wheezing and chest tightness in exposed individuals, it is not clear whether it causes asthma and asthmatic bronchitis. Our hypothesis is that exposure to airborne vanadium compounds causes bronchial hyperreactivity and stomatic bronchitis via an inflammatory mechanism. Further, we hypothesize that the upper airway (nasal) responses due to vanadium are well-correlated with the lower airway (bronchial) responses. We propose short-term and long-term prospective studies of vanadium-exposed workers which combine an assessment of lung function, bronchial responsiveness, nasal and bronchial fluid analyses with detailed personal and area environmental samples in addressing the main hypotheses. In addition, and in conjunction with Project 6, data on vanadium content of nasal and bronchial specimens will be used to develop dose-response models for this important environmental toxin. Vanadium compounds have also been shown in animal models to cause non- respiratory effects, e.g., kidney injury and insulinogenic effects. Since we have found vanadium compounds in ash to be very water-soluble, it is likely that vanadates exhibit non-respiratory health effects in humans. We therefore will also explore potential effects of vanadate exposure on human glucose concentrations. The epidemiologic and clinical investigation will be integrated with Project 6, which focuses on pathogenesis in order to simultaneously assets ambient exposures, biological markers of exposure, early effect, an physiologic changes in target organs. This integrated approach will provide new knowledge about the human toxicity of vanadium and related compounds.
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