Pulmonary Toxicity and Recovery from Inhalation of Manual Metal Arc Stainless Steel Welding Fumes in Rats

Yang, Mi-Jin; Kim, Jin-Sung; Yang, Young-Su; Cho, Jae-Woo; Choi, Sunghee; Chung, Yong-Hyun; Kim, Yong-Bum; Cho, Kyu-Hyuk; Lim, Chae-Woong; Kim, Choong-Yong; Song, Chang-Woo

doi:10.5487/tr.2008.24.2.119

Cited by 3 publications

(8 citation statements)

References 17 publications

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“…In the size distributions of the welding-fume particles, more than 90% of the fume particles had diameters equal to or less than 1.1 µm (Table 1 of Yang et al, 2008). The concentrations and …”

Section: Characterization Of Mma-ss Welding Fumesmentioning

confidence: 97%

“…The criteria used to grade the pulmonary lesions were as follows: grade -= normal; grade + = minimal; grade ++ = mild; grade + + + = moderate; grade + + ++ = marked; grade + + + + + = severe. elemental components of the MMA-SS welding fumes mainly consisted of metal particulate, including Fe, Cr, Mn, and Ni, and various gases, including O 3 , NO 2 , and nitrous fumes ( Table 2 of Yang et al, 2008).…”

Section: Characterization Of Mma-ss Welding Fumesmentioning

confidence: 99%

“…The measurement of the total cell numbers and differential counts of BAL cells were also performed as described previously (Yu et al, 2004;Yang et al, 2008). Several parameters were measured as indicators of pulmonary damage within the first acellular supernatant fraction of the BALF, as described by Yang et al, (2008). Albumin, β − N -acetyl glucosaminidase (β-NAG), lactate dehydrogenase (LDH), and alkaline phosphatase (ALP) were all assayed in the BALF.…”

Section: Evaluation Of Bronchoalveolar Lavage Fluid (Balf)mentioning

confidence: 99%

“…Bronchoalveolar lavage (BAL) was performed on d 31 for rats from each group, as described previously (Yu et al, 2004;Antonini et al, 2004;Yang et al, 2008). The rats were deeply euthanized with an overdose of isoflurane and exsanguinated by severing the abdominal aorta.…”

Section: Evaluation Of Bronchoalveolar Lavage Fluid (Balf)mentioning

confidence: 99%

“…The left lung was clamped off and the right lung was first washed out with 2 separate 3-ml aliquots of warm, calcium-and magnesium-free phosphate buffer solution (PBS), pH 7.4. The measurement of the total cell numbers and differential counts of BAL cells were also performed as described previously (Yu et al, 2004;Yang et al, 2008). Several parameters were measured as indicators of pulmonary damage within the first acellular supernatant fraction of the BALF, as described by Yang et al, (2008).…”

Section: Evaluation Of Bronchoalveolar Lavage Fluid (Balf)mentioning

confidence: 99%

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Recurrent Exposure to Welding Fumes Induces Insufficient Recovery from Inflammation

Yang

Sung³

et al. 2009

Inhalation Toxicology

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Previous studies on welding-fume-induced lung fibrosis have indicated that recovery is possible when the degree of exposure is short-term and moderate. However, this study investigated the recovery after recurrent exposure to welding fumes, as welders are invariably re-exposed to welding fumes after recovering from radiographic pneumoconiosis. Thus, to investigate the disease and recovery processes of welding-fume-induced pneumoconiosis in the case of recurrent welding-fume exposure, rats were exposed to manual metal arc-stainless steel (MMA-SS) welding fumes with a total suspended particulate (TSP) concentration of 51.4 ± 2.8 mg/m 3 (low dose) or 84.6 ± 2.9 mg/m 3 (high dose) for 2 h/day in an inhalation chamber for 1 mo and then allowed to recover from the inflammation for 1 mo. Thereafter, the rats were exposed again to MMA-SS with a TSP concentration of 44.1 ± 8.8 mg/m 3 (low dose) or 80.1 ± 9.8 mg/m 3 (high dose) for another 30 d and then allowed to recover from the inflammation for 1 mo. The recovery from the first exposure was then compared with that from the second exposure. The first and second exposures to MMA-SS welding fumes were found to produce significant increases in the lung weights and inflammatory parameters, including total cell numbers, alveolar macrophages (AMs), polymorphonuclear cells (PMNs), lymphocytes, and lactate dehydrogenase (LDH) in the bronchoalveolar lavage fluid (BALF) when compared with the unexposed controls.Following the first and second recovery, a significant reduction in inflammatory parameters of BALF was observed between the exposure and recovery groups. Histopathological observations showed foamy or pigmented macrophage accumulation, cellular debris, or pigment from burst macrophages after the first or second exposure. Following the first or second recovery, cellular debris or pigment from burst macrophages was cleared away from the lungs and accumulation of foamy or pigmented macrophages was decreased when compared to previous exposure.

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Section: Characterization Of Mma-ss Welding Fumesmentioning

confidence: 97%

Section: Characterization Of Mma-ss Welding Fumesmentioning

confidence: 99%

Section: Evaluation Of Bronchoalveolar Lavage Fluid (Balf)mentioning

confidence: 99%

Section: Evaluation Of Bronchoalveolar Lavage Fluid (Balf)mentioning

confidence: 99%

Section: Evaluation Of Bronchoalveolar Lavage Fluid (Balf)mentioning

confidence: 99%

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Recurrent Exposure to Welding Fumes Induces Insufficient Recovery from Inflammation

Yang

Sung³

et al. 2009

Inhalation Toxicology

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Activation of Autophagy Rescues Amiodarone-Induced Apoptosis of Lung Epithelial Cells and Pulmonary Toxicity in Rats

Lee

Choi

et al. 2013

Toxicological Sciences

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Amiodarone, bi-iodinated benzofuran derivative, is one of the most frequently prescribed and efficacious antiarrhythmic drugs. Despite its low incidence, amiodarone-induced pulmonary toxicity is of great concern and the leading cause of discontinuation. Autophagy is an essential homeostatic process that mediates continuous recycling of intracellular materials when nutrients are scarce. It either leads to a survival advantage or initiates death processes in cells under stress. In the present study, we investigated the role of autophagy in amiodarone-induced pulmonary toxicity. Amiodarone treatment-induced autophagy in H460 human lung epithelial cells and BEAS-2B normal human bronchial epithelial cells was demonstrated by increased LC3-II conversion, Atg7 upregulation, and autophagosome formation. Autophagic flux, as determined by the lysosomal inhibitor bafilomycin A1, was also increased following amiodarone treatment. To determine the role of autophagy in amiodarone toxicity, amiodarone-induced cell death was evaluated in the presence of 3-methyladenine or by knocking down the autophagy-related genes Atg7. Inhibition of autophagy decreased cellular viability and significantly increased apoptosis. Intratracheal instillation of amiodarone in rats increased the number of inflammatory cells recovered from bronchoalveolar lavage fluid, and periodic acid-Schiff-positive staining in bronchiolar epithelial cells. However, induction of autophagy by rapamycin treatment inhibited amiodarone-induced pulmonary toxicity. In conclusion, amiodarone treatment induced autophagy, which is involved in protection against cell death and pulmonary toxicity.

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Detection of Toxic Heavy Metal, Co(II) Trace via Voltammetry with Semiconductor Microelectrodes

Lee

Koo³

2017

ToxicolRes

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The cobalt (Co(II)) ion is a main component of alloys and considered to be carcinogenic, especially due to the carcinogenic and toxicological effects in the aquatic environment. The toxic trace of the Co(II) detection was conducted using the infrared photodiode electrode (IPDE) using a working electrode, via the cyclic and square-wave anodic stripping voltammetry. The results indicated a sensitive oxidation peak current of Co(II) on the IPDE. Under the optimal conditions, the common-type glassy carbon, the metal platinum, the carbon paste, and the carbon fiber microelectrode were compared with the IPDE in the electrolyte using the standard Co(II). The IPDE was found to be far superior to the others.

show abstract

Pulmonary Toxicity and Recovery from Inhalation of Manual Metal Arc Stainless Steel Welding Fumes in Rats

Cited by 3 publications

References 17 publications

Recurrent Exposure to Welding Fumes Induces Insufficient Recovery from Inflammation

Recurrent Exposure to Welding Fumes Induces Insufficient Recovery from Inflammation

Activation of Autophagy Rescues Amiodarone-Induced Apoptosis of Lung Epithelial Cells and Pulmonary Toxicity in Rats

Detection of Toxic Heavy Metal, Co(II) Trace via Voltammetry with Semiconductor Microelectrodes

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