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

Abstract

BackgroundTungsten inert gas (TIG) welding represents one of the most widely used metal joining processes in industry. It has been shown to generate a large majority of particles at the nanoscale and to have low mass emission rates when compared to other types of welding. Despite evidence that TIG fume particles may produce reactive oxygen species (ROS), limited data is available for the time course changes of particle-associated oxidative stress in exposed TIG welders.MethodsTwenty non-smoking male welding apprentices were exposed to TIG welding fumes for 60 min under controlled, well-ventilated settings. Exhaled breathe condensate (EBC), blood and urine were collected before exposure, immediately after exposure, 1 h and 3 h post exposure. Volunteers participated in a control day to account for oxidative stress fluctuations due to circadian rhythm. Biological liquids were assessed for total reducing capacity, hydrogen peroxide (H2O2), malondialdehyde (MDA), and 8-hydroxy-2′-deoxyguanosine (8-OHdG) concentrations at each time point. A linear mixed model was used to assess within day and between day differences.ResultsSignificant increases in the measured biomarkers were found at 3 h post exposure. At 3 h post exposure, we found a 24 % increase in plasma-H2O2 concentrations ([95%CI: 4 % to 46 %], p = 0.01); a 91 % increase in urinary-H2O2 ([2 % to 258 %], p = 0.04); a 14 % increase in plasma-8-OHdG ([0 % to 31 %], p = 0.049); and a 45 % increase in urinary-8-OHdG ([3 % to 105 %], p = 0.03). Doubling particle number concentration (PNC) exposure was associated with a 22 % increase of plasma-8-OHdG at 3 h post exposure (p = 0.01).ConclusionA 60-min exposure to TIG welding fume in a controlled, well-ventilated setting induced acute oxidative stress at 3 h post exposure in healthy, non-smoking apprentice welders not chronically exposed to welding fumes. As mass concentration of TIG welding fume particles is very low when compared to other types of welding, it is recommended that additional exposure metrics such as PNC are considered for occupational risk assessments. Our findings highlight the importance of increasing awareness of TIG welding fume toxicity, especially given the realities of welding workplaces that may lack ventilation; and beliefs among interviewed welders that TIG represents a cleaner and safer welding process.Electronic supplementary materialThe online version of this article (doi:10.1186/s12989-016-0143-7) contains supplementary material, which is available to authorized users.

Physicochemistry and cardiovascular toxicity of metal fume PM2.5: a study of human coronary artery endothelial cells and welding workers

“…However, we still observed significant increases in levels of urinary 8-OHdG and 8-iso-PGF2α in welding and office workers post-exposure. Our observations are consistent with previous findings in a control human exposure study 23 . Furthermore, we found that a 10-μg/m 3 increase in the mean PM 2.5 resulted in a 2.15% increase in 8-OHdG/uCr and a 8.43% increase in 8-iso-PGF2α/uCr in welding workers.…”

Environmental Metals and Cardiovascular Disease in Adults: A Systematic Review Beyond Lead and Cadmium

“…Although toxicological evidence regarding cardiovascular disease is sparse, in vivo studies suggest tungsten causes histological lesions in the heart [115] and can inactivate molybdenum-enzymes by replacing molybdenum binding sites [116]. Tungsten likely causes oxidative stress [7, 11, 112, 117] and can modify cobalt toxicity [118]. There is little epidemiological evidence of tungsten exposure and cardiovascular disease in the general population, although tungsten exposure has been associated with elevated blood pressure [119], excretion of reactive oxygen species [117], and DNA methylation and hydroxymethylation [120].…”

Welding Fumes, a Risk Factor for Lung Diseases

“…Welders who were exposed to aluminum TIG WFs for 60 minutes showed a 45% increase in urinary 8-OHdG and a 14% increase in plasma 8-OHdG after 3 h, which is a pre-mutagenic DNA adduct implicated in carcinogenesis. An exposure-response relationship was found between particle number concentration in WFs and plasma 8-OHdG concentration [67,68]. Acute and chronic exposures to particulate matter 2.5 (PM 2.5 ) generated from welding activities was associated with a modest change in DNA methylation of the inducible nitric oxide synthases (iNOS) gene.…”