Inhalation of high concentrations of zinc oxide particles (ZnO) may cause metal fume fever. In an earlier human inhalation study, no effects were observed after exposure to ZnO concentrations of 0.5 mg/m3. Further data from experimental studies with pure ZnO in the concentration range between 0.5 and 2.5 mg/m3 are not available. It was the aim of this experimental study to establish the concentration-response relationship of pure nano-sized ZnO particles. Sixteen healthy subjects were exposed to filtered air and ZnO particles (0.5, 1.0 and 2.0 mg/m3) for 4 h on 4 different days, including 2 h of cycling with a low workload. The effects were assessed before, immediately after, and about 24 h after each exposure. Effect parameters were symptoms, body temperature, inflammatory markers and clotting factors in blood, and lung function. Concentration-dependent increases in symptoms, body temperature, acute phase proteins and neutrophils in blood were detected after ZnO inhalation. Significant effects were detected with ZnO concentrations of 1.0 mg/m3 or higher, with the most sensitive parameters being inflammatory markers in blood. A concentration-response relationship with nano-sized ZnO particles in a low concentration range was demonstrated. Systemic inflammatory effects of inhaled nano-sized ZnO particles were observed at concentrations well below the occpational exposure limit for ZnO in many countries. It is recommended to reassess the exposure limit for ZnO at workplaces.

/pdf/concentration-dependent-systemic-response-after-inhalation-1mcehn8nji.pdf

Concentration-dependent systemic response after inhalation of nano-sized zinc oxide particles in human volunteers

(1) Background: Welding fumes (WFs) are composed of fine and ultrafine particles, which may reach the distal airways and represent a risk factor for respiratory diseases. (2) Methods: In vitro and in vivo studies to understand WFs pathogenesis were selected. Epidemiological studies, original articles, review, and meta-analysis to examine solely respiratory disease in welders were included. A systematic literature search, using PubMed, National Institute for Occupational Safety and Health Technical Information Center (NIOSHTIC), and Web of Science databases, was performed. (3) Results: Dose, time of exposure, and composition of WFs affect lung injury. Inflammation, lung defense suppression, oxidative stress, DNA damage, and genotoxic effects were observed after exposure both to mild and stainless steel WFs. (4) Conclusions: The detection of lung diseases associated with specific occupational exposure is crucial as complete avoidance or reduction of the exposure is difficult to achieve. Further studies in the area of particle research may aid the understanding of mechanisms involved in welding-related lung disease and to expand knowledge in welding-related cardiovascular diseases.

Welding Fumes, a Risk Factor for Lung Diseases.

Inhaled nanoparticles constitute a potential health hazard due to their size-dependent lung deposition and large surface to mass ratio. Exposure to high levels contributes to the risk of developing respiratory and cardiovascular diseases, as well as of lung cancer. Particle-induced acute phase response may be an important mechanism of action of particle-induced cardiovascular disease. Here, the authors review new important scientific evidence showing causal relationships between inhalation of particle and nanomaterials, induction of acute phase response, and risk of cardiovascular disease. Particle-induced acute phase response provides a means for risk assessment of particle-induced cardiovascular disease and underscores cardiovascular disease as an occupational disease.

https://onlinelibrary.wiley.com/doi/epdf/10.1002/smll.201907476

Acute Phase Response as a Biological Mechanism-of-Action of (Nano)particle-Induced Cardiovascular Disease.

Objective Recently, it has been shown that exposure to welding fumes containing both zinc and copper leads to asymptomatic systemic inflammation in humans as shown by an increase of blood C-reactive protein. In the present study, it was investigated which metal is responsible for this effect. Methods Fifteen healthy male subjects were exposed under controlled conditions to welding fumes containing either zinc, or copper, or copper and zinc. Results For each exposure blood C-reactive protein increased. Conclusions Copper- and zinc-containing welding fumes are able to induce systemic inflammation.

Single and Combined Exposure to Zinc- and Copper-Containing Welding Fumes Lead to Asymptomatic Systemic Inflammation.

Increasing evidence suggests that welding fume exposure is associated with systemic inflammation. Although celluar metabolites may be associated with inflammation, there is limited information on metabolomic changes during welding fume exposure. Such changes may play an important role in the occurrence, development, and prevention of metal-associated diseases. We aim to investigate human metabolomics changes pre- and post-welding fume exposure. This study included 52 boilermakers totally. We collected plasma samples pre- and post-shift welding fume exposure and prepared samples using the automated MicroLab STAR® system. Metabolite concentrations were measured using ultra performance liquid chromatography - tandem mass spectrometer (UPLC-MS/MS) methods. Two-way analysis of variance was used to test the significance of metabolite changes with false discovery rate correction. Analysis detected several metabolic changes after welding fume exposure, mainly involved in the lipid pathway [glucocorticoid class (cortisol, corticosterone, and cortisone), acylcarnitine class, and DiHOME species (9,10-DiHOME and 12,13-DiHOME)], amino acid utilization (isoleucine, proline and phenylalanine), and S-(3-hydroxypropyl) mercapturic acid (3-HPMA). These compounds are all associated with inflammation according to previous studies. Further, additive interaction effects linked smoking and 3-HPMA levels. In the metabolite set enrichment analysis for diseases, the top two disease-associated metabolite pathways were systemic inflammation-related diseases including rheumatoid arthritis and systemic lupus erythematosus. This global metabolomics study shows evidence that metabolite changes during welding fume exposure are closely associated with systemic inflammation. The altered metabolites detected may be potential health monitoring biomarkers for boilermakers, especially for inflammation-related disease prevention.

/pdf/welding-fume-exposure-is-associated-with-inflammation-a-3gni2zafy2.pdf

Welding fume exposure is associated with inflammation: a global metabolomics profiling study.

Systemic serum amyloid A as a biomarker for exposure to zinc and/or copper-containing metal fumes

Objective Emissions from a particular welding process, metal inert gas brazing of zinc-coated steel, induce an increase in C-reactive protein. In this study, it was investigated whether inflammatory effects could also be observed for other welding procedures. Methods Twelve male subjects were separately exposed to (1) manual metal arc welding fumes, (2) filtered air, and (3) metal active gas welding fumes for 6 hours. Inflammatory markers were measured in serum before, and directly, 1 and 7 days after exposure. Results Although C-reactive protein concentrations remained unchanged, neutrophil concentrations increased directly after exposure to manual metal arc welding fumes, and endothelin-1 concentrations increased directly and 24 hours after exposure. After exposure to metal active gas and filtered air, endothelin-1 concentrations decreased. Conclusions The increase in the concentrations of neutrophils and endothelin-1 may characterize a subclinical inflammatory reaction, whereas the decrease of endothelin-1 may indicate stress reduction.

Assessment of the Biological Effects of Welding Fumes Emitted From Metal Active Gas and Manual Metal Arc Welding in Humans.

Abstract Background Short-term inhalation of occupationally relevant ultrafine zinc/copper (Zn/Cu) containing welding fumes has been shown to induce subclinical systemic inflammation, associated with an elevated risk for cardiovascular diseases. The involvement of noncoding RNAs (lncRNAs) in this setting is currently unknown. However, lncRNAs have been reported to fulfill essential roles in, e.g., cardiovascular diseases, inflammation, infectious diseases, and pollution-related lung disorders. Methods In this study, the specific lncRNAs levels of the 4 lncRNAs CoroMarker, MALAT1, CDR1as and LINC00460 were determined by RT-qPCR in THP-1 macrophages exposed to Zn/Cu metal fume suspensions for 1, 2, and 4 hours in vitro. Furthermore, 14 subjects were exposed to Zn/Cu containing welding fumes (at 2.5 mg/m 3 ) for 6 hours. Before, 6, 10, and 29 hours after exposure start, whole blood cell lncRNAs levels were determined by RT-qPCR. Results In THP-1 macrophages, we observed a 2.3-fold increase of CDR1as at 1 h (Wilcoxon p = 0.03), a non-significant increase of CoroMarker at 1 h, and an increase of LINC00460 at 2 h ( p = 0.03) and at 4 h ( p = 0.06). In whole blood cells, we determined a non-significant upregulation of CDR1as at 6 h ( p = 0.2), a significant downregulation of CoroMarker at 6 h ( p = 0.04), and a significant upregulation of LINC00460 levels at 10 h ( p = 0.04) and 29 h ( p = 0.04). MALAT-1 remained unchanged in both settings. Conclusion The orientation of regulation of the lncRNAs is (except for CoroMarker) similar in the in vitro and in vivo experiments and in line with their described functions. Therefore, these results, e.g. the upregulation of the potential risk marker for cardiovascular diseases, CDR1as, contribute to understanding the underlying mechanisms of Zn/Cu-induced subclinical inflammation in metal workers. 

/pdf/the-human-long-noncoding-rnas-coromarker-malat1-cdr1as-and-14gp3dyz.pdf

The human long noncoding RNAs CoroMarker, MALAT1, CDR1as, and LINC00460 in whole blood of individuals after controlled short-term exposure with ultrafine metal fume particles at workplace conditions, and in human macrophages in vitro

Correction: The human long noncoding RNAs CoroMarker, MALAT1, CDR1as, and LINC00460 in whole blood of individuals after controlled short‑term exposure with ultrafine metal fume particles at workplace conditions, and in human macrophages in vitro

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