Increase in oxidative stress levels following welding fume inhalation: a controlled human exposure study.

Occupational scenarios provide a unique setting to assess nanoparticle (NP) exposure and dose response related to the generation of oxidative stress in humans. Welding fume particles, in particular metallic NPs, have gained increased attention due to their potential for triggering oxidative stress reactions, and preliminary evidence that welding fumes may induce free radical activity has been demonstrated [1, 43]. It has been shown that certain metals in welding fumes can produce ROS such as hydroxyl radicals (·OH), superoxide anion (O2 –), singlet oxygen (1O2), and H2O2 [60, 63]. The ROS activity of welding fume particles has also been shown to be size dependent, with particles of the fine and ultrafine range (PM0.1—2.5 and PM0.1) generating higher ROS concentrations when compared with coarse PM10 (PM2.5-10) [9]. In the alveoli, ROS can react quickly with surrounding tissue, damage cell components and launch a cascade of local and systemic responses, which may lead to disease [56].Of various welding processes, Tungsten Inert Gas (TIG) welding is of particular interest for occupational health due to its propensity to generate metallic welding fume particles almost exclusively at the nanoscale [5, 42]. Due to its exceptionally strong and high quality welds, TIG welding has become one of the most popular welding methods in various industrial sectors [20, 36]. A recent characterization study of TIG welding fume particles found that mean ROS production potential at the breathing zone of welders in controlled, ventilated conditions exceeded average concentrations previously found in traffic polluted air [23]. However, despite the increase in TIG welding and evidence that it may generate acellular ROS, there is limited data available for oxidative stress biomarker concentrations in welders exposed to TIG welding fume.While the International Agency for Research on Cancer (IARC) categorizes welding fumes in Group 2B (possibly carcinogenic to humans), it has also noted that an unexplained reason for lung cancer risks still exists, which in turn demands more research on the generation of radical ROS and oxidative DNA damage in humans, for each of the numerous welding processes [30, 31]. However, existing studies on oxidative stress in welders face methodological drawbacks which hamper comprehensive assessments of exposure to ROS response. Epidemiological studies in industrial settings often lack complete exposure assessments, or are often unable to control for numerous welding parameters, making it difficult to disambiguate between heterogeneous aerosols. On the other hand, laboratory based studies often involve robotic welders and acknowledge that welding fume characteristics may substantially differ from occupational environments where fumes are generated by human welders [7].To address this gap, the aim of this study was to assess, under controlled conditions, the effect of TIG welding fume exposure on the time course changes of multiple oxidative stress biomarkers in the EBC, blood, and urine of apprentice welders before and at several time points post-exposure. We hypothesized that inhaled TIG welding fume NPs would initiate oxidative stress in the alveoli, which would be first manifest in the EBC, followed by an increase in oxidative stress markers in the circulation and urine. To test this hypothesis, we assessed the EBC, blood and urine of 20 apprentice welders exposed to TIG welding fume for total reducing capacity, MDA, H2O2, and 8-OHdG before and at several time points after exposure.