Welding Fumes, a Risk Factor for Lung Diseases.
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ABSTRACT:
SUBMITTER: Riccelli MG
PROVIDER: S-EPMC7177922 | biostudies-literature | 2020 Apr
REPOSITORIES: biostudies-literature
Publications
Welding Fumes, a Risk Factor for Lung Diseases.
Riccelli Maria Grazia MG Goldoni Matteo M Poli Diana D Mozzoni Paola P Cavallo Delia D Corradi Massimo M
International journal of environmental research and public health 20200408 7
(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 Technic ...[more]
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Project description:Many in the welding industry suffer from bronchitis, lung function changes, metal fume fever, and diseases related to respiratory damage. These phenomena are associated with welding fumes; however, the mechanism behind these findings remains to be elucidated. In this study, the lungs of cynomolgus monkeys were exposed to MMA-SS welding fumes for 229 days and allowed to recover for 153 days. After the exposure and recovery period, gene expression profiles were investigated using the Affymetrix GeneChip Human U133 plus 2.0. In total, it was confirmed that 1,116 genes were up-or downregulated (over 2-fold changes, P\0.01) for the T1 (31.4 ± 2.8 mg/m3) and T2 (62.5 ± 2.7 mg/m3) dose groups. Differentially expressed genes in the exposure and recovery groups were analyzed, based on hierarchical clustering, and were imported into Ingenuity Pathways Analysis to analyze the biological and toxicological functions. Functional analysis identified genes involved in immunological disease in both groups. Additionally, differentially expressed genes in common between monkeys and rats following welding fume exposure were compared using microarray data, and the gene expression of selected genes was verified by real-time PCR. Genes such as CHI3L1, RARRES1, and CTSB were up-regulated and genes such as CYP26B1, ID4, and NRGN were down-regulated in both monkeys and rats following welding fume exposure. This is the first comprehensive gene expression profiling conducted for welding fume exposure in monkeys, and these expressed genes are expected to be useful in helping to understand transcriptional changes in monkey lungs after welding fume exposure.
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| S-EPMC3979282 | biostudies-literature
Project description:Objective This study investigated whether low-to-moderate exposure to welding fumes is associated with adverse effects on the cardiovascular system. Methods To test this, we performed a longitudinal analysis of 78 mild steel welders and 96 controls; these subjects were examined twice, six years apart (ie, timepoints 1 and 2). All subjects (male and non-smoking at recruitment) completed questionnaires describing their health, work history, and lifestyle. We measured their blood pressure, endothelial function (by EndoPAT), and risk markers for cardiovascular disease [low-density lioprotein (LDL), homocysteine, C-reactive protein]. Exposure to welding fumes was assessed from the responses to questionnaires and measurements of respirable dust in their breathing zones adjusted for use of respiratory protection equipment. Linear mixed-effect regression models were used for the longitudinal analysis. Results Median respirable dust concentrations, adjusted for respirable protection, of the welders were 0.7 (5-95 percentile range 0.2-4.2) and 0.5 (0.1-1.9) mg/m 3at timepoints 1 and 2, respectively. Over the six-year period, welders showed a statistically significant increase in systolic [5.11 mm Hg, 95% confidence interval (CI) 1.92-8.31] and diastolic (3.12 mm Hg, 95% CI 0.74-5.5) blood pressure compared with controls (multi-variable adjusted mixed effect models). Diastolic blood pressure increased non-significantly by 0.22 mm Hg (95% CI -0.02-0.45) with every additional year of welding work. No consistent significant associations were found between exposure and endothelial function, LDL, homocysteine, or C-reactive protein. Conclusion Exposure to welding fumes at low-to-moderate levels is associated with increased blood pressure, suggesting that reducing the occupational exposure limit (2.5 mg/m 3for inorganic respirable dust in Sweden) is needed to protect cardiovascular health of workers.
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Project description:Background & aimsInhalation of welding fume may cause pulmonary disease known as welder's lung. At our centre we came across a number of welders with systemic iron overload and prolonged occupational history and we aimed at characterizing this novel clinical form of iron overload.MethodsAfter exclusion of other known causes of iron overload, 20 welders were fully evaluated for working history, hepatic, metabolic and iron status. MRI iron assessment was performed in 19 patients and liver biopsy in 12. We included 40 HFE-HH patients and 24 healthy controls for comparison.Results75% of patients showed lung HRCT alterations; 90% had s-FERR > 1000 ng/mL and 60% had TSAT > 45%. Liver iron overload was mild in 8 and moderate-severe in 12. The median iron removed was 7.8 g. Welders showed significantly lower TSAT and higher SIS and SIS/TIS ratio than HFE-HH patients. Serum hepcidin was significantly higher in welders than in HFE-HH patients and healthy controls. At liver biopsy, 50% showed liver fibrosis that was mild in four, and moderate-severe in two. Liver staging correlated with liver iron overload.ConclusionsWelders with prolonged fume exposure can develop severe liver iron overload. The mechanism of liver iron accumulation is quite different to that of HFE-HH suggesting that reticuloendothelial cells may be the initial site of deposition. We recommend routine measurement of serum iron indices in welders to provide adequate diagnosis and therapy, and the inclusion of prolonged welding fume exposure in the list of acquired causes of hyperferritinemia and iron overload.
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Project description:Exposures to high doses of manganese (Mn) via inhalation, dermal contact or direct consumption can cause adverse health effects. Welding fumes are a major source of manganese containing nanoparticles in occupational settings. Understanding the physicochemical properties of manganese-containing nanoparticles can be a first step in understanding their toxic potential following exposure. In particular, here we compare the size, morphology and Mn oxidation states of Mn oxide nanoparticles generated in the laboratory by arc discharge to those from welding collected in heavy vehicle manufacturing. Fresh nanoparticles collected at the exit of the spark discharge generation chamber consisted of individual or small aggregates of primary particles. These nanoparticles were allowed to age in a chamber to form chain-like aggregates of primary particles with morphologies very similar to welding fumes. The primary particles were a mixture of hausmannite (Mn3O4), bixbyite (Mn2O3) and manganosite (MnO) phases, whereas aged samples revealed a more amorphous structure. Both Mn2+ and Mn3+, as in double valence stoichiometry present in Mn3O4, and Mn3+, as in Mn2O3 and MnOOH, were detected by X-ray photoelectron spectroscopy on the surface of the nanoparticles in the laboratory nanoparticles and welding fumes. Dissolution studies conducted for these two Mn samples (aged and fresh fume) reveal different release kinetics of Mn ions in artificial lysosomal fluid (pH 4.5) and very limited dissolution in Gamble's solution (pH 7.4). Taken together, these data suggest several important considerations for understanding the health effects of welding fumes. First, the method of particle generation affects the crystallinity and phase of the oxide. Second, welding fumes consist of multiple oxidation states whether they are amorphous or crystalline or occur as isolated nanoparticles or agglomerates. Third, although the dissolution behavior depends on conditions used for nanoparticle generation, the dissolution of Mn oxide nanoparticles in the lysosome may promote Mn ions translocation into various organs causing toxic effects.
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Project description:ObjectiveThis study tested for an association between early cancer-related biomarkers and low-to-moderate exposure to fumes from welding mild steel.MethodsMale, non-smoking participants from southern Sweden were recruited and examined (N=338, 171 welders and 167 controls); of these, 78 welders and 96 controls were examined on two occasions six years apart. Exposure to welding fumes was evaluated by measuring respirable dust, welding years, and cumulative exposure. DNA methylation of CpG sites within the cancer-related genes AHRR, F2RL3, and B3GNTL1 was measured by pyrosequencing and relative mitochondrial DNA copy number and telomere length were measured by qPCR in whole-blood samples. Multivariate models were used for longitudinal analysis.ResultsMedian exposure to respirable dust was 0.7 mg/m3 at both timepoints, adjusted for use of personal protective equipment. Compared with controls, welders showed a significant decrease over time in DNA methylation of B3GNTL1 CpG1 and CpG4 [adjusted for age, body mass index, and smoking: β=-0.66, standard error (SE)=0.28; β=-0.48, SE=0.24, respectively]. In addition, exposure to respirable dust and cumulative exposure was associated with a decrease in methylation of F2RL3 CpG2 among all welders (adjusted β=-0.67, SE=0.23 and β=-0.03, SE=0.02, respectively). No significant associations were found for AHRR, mitochondrial DNA copy number, or telomere length.ConclusionLow-to-moderate exposure to welding fumes was associated with a small effect on selected early epigenetic biomarkers of cancer. The direction of the methylation pattern (lower methylation of specific CpG sites) indicates early lung cancer-related changes associated with mild steel welding.
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Project description:Welders or metal workers not being an exception are exposed to metals ions or oxides (fumes) at trace concentrations either through direct contact supplementation at occupational sites or indirectly through uptake from contaminated food, water or contaminated soil, dust, or air. The study aims to determine the effects of welding fumes exposure on haematological parameters in blood of experimental animals. The fumes were collected from welding sites during the activity by a skilled welder. 130 male experimental animals were utilized and made into 13 groups. 12 groups were given dosages calculated to correspond to real life workers exposure regimes and 1 group served as control. The dosages were administered intratracheally after been anaesthetized weekly for 12 weeks. The animals were sacrificed and whole blood samples were taken which was then subjected to haematological analysis. The parameters have revealed changes in values whereby RBC, WBC, % lymphocytes, HGB, HCT, MCV, MCH, PLT, PCT and P-LCC have exceeds the control groups values. There was an increase across the treatment groups. However, lymphocytes, MID, granulocytes, % granulocytes, MCHC and MPV have values which were less than the control and no different from one another statistically. This indicates that exposure to welding fumes could cause alterations to most RBC, WBC and PLT indices majorly by effecting an increase. Further studies should be carried out on the response of other markers of toxicity so as to have a broad perception of the effects.
| S-EPMC6593231 | biostudies-literature
Project description:Occupational exposure to particulate air pollution has been associated with an increased risk of cardiovascular disease. However, the risk to welders working today remains unclear. We aimed to elucidate the cardiovascular effects of exposure to welding fumes.In a cross-sectional study, structured interviews and biological sampling were conducted for 101 welders and 127 controls (all non-smoking males) from southern Sweden. Personal breathing zone sampling of respirable dust was performed. Blood pressure (BP) and endothelial function (using peripheral arterial tonometry) were measured. Plasma and serum samples were collected from peripheral blood for measurement of C-reactive protein, low-density lipoprotein, homocysteine, serum amyloid A, and cytokines.Welders were exposed to 10-fold higher levels of particles than controls. Welders had significantly higher BP compared to controls, an average of 5 mm Hg higher systolic and diastolic BP (P ≤ 0.001). IL-8 was 3.4 ng/L higher in welders (P=0.010). Years working as a welder were significantly associated with increased BP (β=0.35, 95%CI 0.13 - 0.58, P=0.0024 for systolic BP; β=0.32, 95%CI 0.16 - 0.48, P<0.001 for diastolic BP, adjusted for BMI) but exposure to respirable dust was not associated with BP. No clear associations occurred between welding and endothelial function, or other effect markers.A modest increase in BP was found among welders compared to controls suggesting that low-to-moderate exposure to welding fumes remains a risk factor for cardiovascular disease.
| S-EPMC4492943 | biostudies-other