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

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TLDR
A 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.
Abstract
Tungsten 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. Twenty 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. Significant 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). A 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.

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References
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IARC Monographs on the Evaluation of Carcinogenic Risks to Humans

TL;DR: This timely monograph is a distillation of knowledge of hepatitis B, C and D, based on a review of 1000 studies by a small group of scientists, and it is concluded that hepatitis D virus cannot be classified as a human carcinogen.
Journal ArticleDOI

Oxidative mechanisms in the toxicity of metal ions

TL;DR: Some mechanisms associated with the toxicities of metal ions are very similar to the effects produced by many organic xenobiotics, related to differences in solubilities, absorbability, transport, chemical reactions, and the complexes that are formed within the body.
Journal ArticleDOI

Advances in metal-induced oxidative stress and human disease

Klaudia Jomová, +1 more
- 10 May 2011 - 
TL;DR: An overview of redox and non-redox metal-induced formation of free radicals and the role of oxidative stress in toxic action of metals is provided.
Journal ArticleDOI

Measuring reactive species and oxidative damage in vivo and in cell culture: how should you do it and what do the results mean?

TL;DR: Methods used to trap RS, including spin trapping and aromatic hydroxylation, are critically examined, with a particular emphasis on those methods applicable to human studies and methods used to detect RS in cell culture.
Journal ArticleDOI

A review of recent studies on malondialdehyde as toxic molecule and biological marker of oxidative stress

TL;DR: The physiological origin of MDA is described, its toxicity is highlighted, and the most common methods of detection are insufficiently sensitive and disturbed by interference coming from related species or overestimation derived from stressing analysis conditions.
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