2000 journal article
Residual Oil Fly Ash induces cytotoxicity and mucin hypersecretion by guinea pig tracheal epithelial cells in vitro via an oxidant-mediated mechanism.
Toxicology and Applied Pharmacology, 163, 221–230.
1999 journal article
Cytotoxicity and cytokine gene expression in airway epithelial cells exposed to residual oil fly ash-particles: role of soluble metals.
American Journal of Physiology. Lung Cellular and Molecular Physiology, 277, 498–510.
Exposure of differentiated rodent airway epithelial cells in vitro to particles of residual fly ash (ROFA) induces cytotoxicity and generation of reactive oxygen species.
Proceedings of the 10th International Colloquium on Lung Fibrosis, Vol. 10, p. 26.
Particles of Residual Oil Fly Ash (ROFA) induce toxicity and mucin hypersecretion in rodent airway epithelial cells in vitro via an oxidant-mediated mechanism.
Toxicology Letters, Vol. 95, p. 224.
Vanadium content and related oxidative stress appear to determine airway epithelial cell responses to emission source particulate matter.
FASEB Journal, Vol. 12, p. A337.
Airway epithelial cell responses to fly ash (ROFA) particles: contribution of soluble transition metals.
American Journal of Respiratory and Critical Care Medicine, Vol. 155, p. A197.
Injury of rat tracheal epithelial cultures by exposure to residual oil fly ash (ROFA) involves generation of the hydroxyl radical.
American Journal of Respiratory and Critical Care Medicine, Vol. 153, p. A542.
Role or reactive oxygen and nitrogen species in the response of airway epithelium to particulates.
Proceedings of the 6th International Meeting of the Toxicology of Natural and Man-Made Fibrous and Non-Fibrous Particles., Vol. 6, p. 139.