Pulmonary Functions, Oxidative Stress and DNA Damage in Workers of a Copper Processing Industry

Kumar, Sandeep; Khaliq, Farah; Singh, Savita; Ahmed, RS; Kumar, Rakesh; Deshmukh, P. S.; Banerjee, B. D.

doi:10.15171/ijoem.2016.612

Cited by 11 publications

(7 citation statements)

References 27 publications

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“…Similar findings were obtained by De Olivera et al (2011). A recent study on copper processing workers revealed DNA damage quantified by comet assay along with decreased antioxidant power of plasma and increased propensity for oxidative stress (Kumar et al, 2016). Several other studies also found significant positive associations between exposure to metals, oxidative stress parameters and primary DNA damage detected in comet assay (Kobal et al, 2004, Rohrdanz and Kahl, 2005and Pease et al, 2016.…”

Section: Discussionmentioning

confidence: 92%

Oxidative Stress and Genotoxicity Among Workers Exposed to Copper in a Factory for Non-Ferrous Industry in Egypt

Da¹,

Rashed

2019

Egypt. J. Occup. Med.

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Introduction: Exposure to high levels of copper at the workplace results in many adverse health effects with possible genotoxicity and carcinogenicity. Aim of work: To evaluate oxidative stress and detect the extent of DNA damage among workers at a copper processing factory. Materials and methods: The studied group is composed of 36 male workers from a copper processing factory and 34 male as a control group nonexposed to copper matched for age and socioeconomic status. Total antioxidant capacity was measured for all participants as an oxidative stress parameter, and urinary 8-OHdG was assayed by ELISA. Extent of DNA damage in leucocytes was also evaluated by comet assay as a biomarker of genotoxicity. Results: In the exposed workers, mean serum copper and urinary 8-OHdG were higher when compared to controls (155.1 ± 23 versus 77.9 ± 8.5 ug/dL and 9.7 ± 5 versus 4.1 ± 1.2 ng/mg creatinine, respectively; p<0.001 in each). T-AOC measured in exposed workers was significantly lower than that of the comparison group. There was significant DNA damage in leucocytes of exposed workers compared to the control group with mean comet tail length (9.5 ± 3.7 versus 5.7 ±1.4 mm; p < 0.001). T-AOC was negatively correlated with comet tail length; r=-0.64 and 8-OHdG showed positive correlation; r=0.71 (p < 0.001 for each). Linear regression models revealed that 8-OHdG is the significant predictor of DNA damage assayed by comet test whereas smoking, work duration and age had no significant effect on DNA damage. Conclusion: copper-exposed workers are at risk of oxidative stress with consequent DNA damage and potential genotoxic effect.

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Section: Discussionmentioning

confidence: 92%

Oxidative Stress and Genotoxicity Among Workers Exposed to Copper in a Factory for Non-Ferrous Industry in Egypt

Da¹,

Rashed

2019

Egypt. J. Occup. Med.

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“…Earlier studies showed that exposure to pollutants containing Cu, a major component exclusively detected in ABS emissions ( Figure 1 ), can cause oxidative stress and perturb major amino acids metabolisms including tryptophan [ 45 ], lysine [ 46 ], asparagine, glutamine, methionine, and cysteine [ 47 ], and arginine and proline metabolism [ 46 ]. Additionally, exposure to Cu can induce cytotoxicity [ 48 , 49 , 50 , 51 ], and cause mitochondrial dysfunction [ 48 ], which has shown to be associated with compromised lung function [ 52 ] and many other health issues [ 53 , 54 ]. Amino acid metabolism has a central regulatory function in regulating mitochondrial homeostasis, nucleotides biosynthesis, and antioxidant responses [ 41 , 42 , 43 , 44 ].…”

Section: Resultsmentioning

confidence: 99%

“…Prior studies also demonstrated that in vivo exposure to the thermo-oxidative degradation of ABS caused a decrease in tissue GSH level [ 87 , 88 ]. Furthermore, exposure to pollution containing Cu can also lead to GSH oxidation and depletion [ 51 , 89 ] and elevation of pro-inflammatory cytokines [ 48 , 50 , 90 ], and cause pulmonary inflammation and hypertension [ 91 ], resulting in serious respiratory diseases including COPD and pneumonia mortality [ 92 ]. Dysregulated cellular redox homeostasis is often associated with increased levels of cytokines.…”

Section: Resultsmentioning

confidence: 99%

“…Earlier studies showed that exposure to pollutants containing Cu, a major component exclusively detected in ABS emissions (Figure 1), can cause oxidative stress and perturb major amino acids metabolisms including tryptophan [45], lysine [46], asparagine, glutamine, methionine, and cysteine [47], and arginine and proline metabolism [46]. Additionally, exposure to Cu can induce cytotoxicity [48][49][50][51], and cause mitochondrial dysfunction [48], which has shown to be associated with compromised lung function [52] and many other health issues [53,54]. Amino acid metabolism has a central regulatory While both emissions had effects on nucleotides, vitamins, and cofactors, ABS emissions primarily altered amino acids and energy metabolisms that are known to regulate DNA damage and DNA repair (see Figures 4 and 6) [41][42][43][44], whereas exposure to PLA emissions led to fatty acid and carnitine dysregulation (see Figures 5 and 6).…”

Section: Impact Of Filament Selection On Metabolic Functionsmentioning

confidence: 99%

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Real-Time Exposure to 3D-Printing Emissions Elicits Metabolic and Pro-Inflammatory Responses in Human Airway Epithelial Cells

He,

Barnett,

Jeon

et al. 2024

Toxics

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Three-dimensional (3D) printer usage in household and school settings has raised health concerns regarding chemical and particle emission exposures during operation. Although the composition of 3D printer emissions varies depending on printer settings and materials, little is known about the impact that emissions from different filament types may have on respiratory health and underlying cellular mechanisms. In this study, we used an in vitro exposure chamber system to deliver emissions from two popular 3D-printing filament types, acrylonitrile butadiene styrene (ABS) and polylactic acid (PLA), directly to human small airway epithelial cells (SAEC) cultured in an air–liquid interface during 3D printer operation. Using a scanning mobility particle sizer (SMPS) and an optical particle sizer (OPS), we monitored 3D printer particulate matter (PM) emissions in terms of their particle size distribution, concentrations, and calculated deposited doses. Elemental composition of ABS and PLA emissions was assessed using scanning electron microscopy coupled with energy dispersive X-ray spectroscopy (SEM-EDX). Finally, we compared the effects of emission exposure on cell viability, inflammation, and metabolism in SAEC. Our results reveal that, although ABS filaments emitted a higher total concentration of particles and PLA filaments emitted a higher concentration of smaller particles, SAEC were exposed to similar deposited doses of particles for each filament type. Conversely, ABS and PLA emissions had distinct elemental compositions, which were likely responsible for differential effects on SAEC viability, oxidative stress, release of inflammatory mediators, and changes in cellular metabolism. Specifically, while ABS- and PLA-emitted particles both reduced cellular viability and total glutathione levels in SAEC, ABS emissions had a significantly greater effect on glutathione relative to PLA emissions. Additionally, pro-inflammatory cytokines including IL-1β, MMP-9, and RANTES were significantly increased due to ABS emissions exposure. While IL-6 and IL-8 were stimulated in both exposure scenarios, VEGF was exclusively increased due to PLA emissions exposures. Notably, ABS emissions induced metabolic perturbation on amino acids and energy metabolism, as well as redox-regulated pathways including arginine, methionine, cysteine, and vitamin B3 metabolism, whereas PLA emissions exposures caused fatty acid and carnitine dysregulation. Taken together, these results advance our mechanistic understanding of 3D-printer-emissions-induced respiratory toxicity and highlight the role that filament emission properties may play in mediating different respiratory outcomes.

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“…Although methylation was still not related to human Cu occupational exposure, in addition to its genomic toxicity, Cu can alter histone acetylation and histone deacetylase activity [ 73 ]. Excessive exposure to Cu in a processing industry leads to increased DNA damage and several parameters of oxidative stress, along with alterations in pulmonary function parameters [ 74 ]. In fact, oxidative stress may facilitate tumorigenesis by dysregulating cellular antioxidants, disrupting cell growth and proliferation [ 75 ], which are enabled by telomere balance in length, structure, and proper function [ 76 ].…”

Section: Discussionmentioning

confidence: 99%

Occupational Exposure to Pesticides in Tobacco Fields: The Integrated Evaluation of Nutritional Intake and Susceptibility on Genomic and Epigenetic Instability

Kahl

Dhillon

Fenech

et al. 2018

Oxidative Medicine and Cellular Longevity

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Pesticides used at tobacco fields are associated with genomic instability, which is proposed to be sensitive to nutritional intake and may also induce epigenetic changes. We evaluated the effect of dietary intake and genetic susceptibility polymorphisms in MTHFR (rs1801133) and TERT (rs2736100) genes on genomic and epigenetic instability in tobacco farmers. Farmers, when compared to a nonexposed group, showed increased levels of different parameters of DNA damage (micronuclei, nucleoplasmic bridges, and nuclear buds), evaluated by cytokinesis-block micronucleus cytome assay. Telomere length (TL) measured by quantitative PCR was shorter in exposed individuals. Global DNA methylation was significantly decreased in tobacco farmers. The exposed group had lower dietary intake of fiber, but an increase in cholesterol; vitamins such as B6, B12, and C; β-carotene; and α-retinol. Several trace and ultratrace elements were found higher in farmers than in nonfarmers. The MTHFR CT/TT genotype influenced nucleoplasmic bridges, nuclear buds, and TL in the exposed group, whereas TERT GT/TT only affected micronucleus frequency. We observed a positive correlation of TL and lipids and an inverse correlation of TL and fibers. The present data suggest an important role of dietary intake and subjects' genetic susceptibility to xenobiotics-induced damages and epigenetic alterations in tobacco farmers occupationally exposed to mixtures of pesticides.

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Pulmonary Functions, Oxidative Stress and DNA Damage in Workers of a Copper Processing Industry

Abstract: The observed DNA damage would be due to increased oxidative stress resulting from excessive exposure to copper.

Cited by 11 publications

References 27 publications

Oxidative Stress and Genotoxicity Among Workers Exposed to Copper in a Factory for Non-Ferrous Industry in Egypt

Oxidative Stress and Genotoxicity Among Workers Exposed to Copper in a Factory for Non-Ferrous Industry in Egypt

Real-Time Exposure to 3D-Printing Emissions Elicits Metabolic and Pro-Inflammatory Responses in Human Airway Epithelial Cells

Occupational Exposure to Pesticides in Tobacco Fields: The Integrated Evaluation of Nutritional Intake and Susceptibility on Genomic and Epigenetic Instability

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