Systemic pretreatment of mice with the antioxidant dimethylthiourea abrogated ROFA-s-mediated AHR. The AHR caused by ROFA-s was reproduced by a mixture of its major metal components (Ni, V, Zn, Co, Mn, Cu) but not by any individual metal alone. BAL analysis showed a minor influx of neutrophils, which was maximal at 12 h after exposure and essentially resolved by the time point of maximal AHR (48 h after exposure). Physiologic testing of airway function (non invasive plethysmography) showed increased Penh, an index of airway hyperresponsiveness (AHR), in a time- and dose-dependent manner after exposure to ROFA-s. Mice were exposed to aerosols of the soluble leachate of residual oil fly ash (ROFA-s). This study sought to further characterize the pulmonary effects of residual oil fly ash (ROFA), an experimentally useful surrogate for combustion-derived particulates in ambient air. Particulate air pollution is associated with exacerbation of asthma and other respiratory disorders.
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