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Lung inflammation and injury were significantly elevated compared to the reference welding fume samples (GMA-MS and GMA-SS) at early time points after treatment with 0.5 mg of the Ni�CCu WF sample. Importantly, and unlike the response to the GMA-MS and GMA-SS fume samples, the significant increase in inflammation and injury was observed to persist over a 2 month period when the dose of the Ni�CCu WF sample was increased to 2.0 mg. In regards to the reference welding fume samples, the results from the current study DNA Methyltransferase inhibitor ic50 confirm previous observations; in that the GMA-MS fume at the higher dose had only a slight transient effect on lung injury and inflammation and no effect at the lower dose. This finding correlated well with earlier studies that examined the pulmonary effects of GMA-MS fume after a single intratracheal instillation1,4 or after exposure to a relatively high concentration of 40 mg/m3 of fume by inhalation for 10 days.35 These results and findings from the current study suggest that the pneumotoxic potential of GMA-MS fume is quite low. As was observed previously, intratracheal instillation of the GMA-SS fume induced significant lung this website injury and inflammation early after treatment with the response returning to control values for most parameters by four to five weeks.1 Previous studies have shown stainless steel welding fume to be highly reactive and to enhance leukocyte production of ROS and inflammatory cytokines in comparison to the GMA-MS fume.31,36,37 However, unlike what was observed in the persistence of the adverse lung effect caused by the Ni�CCu WF sample, it has been demonstrated in animal studies that the potential for chronic pulmonary toxicity of the GMA-SS fume is low if exposure is ceased.1 Because of the observed differences in pulmonary response among the three welding fumes, an in vitro study was performed to examine a potential mechanism and determine if the different particle samples had an effect on lung macrophage viability and production of ROS. All three welding fumes were capable of inducing free radical production in the presence of primary lung macrophages (Fig. 5), as significant hydroxyl radical (?OH) peaks were measured Bumetanide for each (PBS, 10.33 �� 2.25, GMA-MS, 48.58 �� 8.63, GMA-SS, 61.60 �� 9.79, and Ni�CCu WF, 82.92 �� 12.19 mm peak height). Moreover, GMA-MS and GMA-SS significantly induced (P
