Physicochemistry and cardiovascular toxicity of metal fume PM 2.5

A study of human coronary artery endothelial cells and welding workers

Chane Yu Lai, Ching Huang Lai, Hsiao Chi Chuang, Chih Hong Pan, Cheng Chieh Yen, Wen Yi Lin, Jen Kun Chen, Lian Yu Lin, Kai Jen Chuang

研究成果: 雜誌貢獻文章

9 引文 (Scopus)

摘要

Occupational exposure to welding fumes causes a higher incidence of cardiovascular disease; however, the association remains unclear. To clarify the possible association, exposure assessment of metal fumes with an aerodynamic diameter of <2.5 μm (PM 2.5) in welding and office areas was characterized in a shipyard in Taiwan. Cardiovascular toxicity caused by PM 2.5 was determined in workers (in both the welding and office areas). Significant amounts of bimodal metal fume particles with count median diameters (CMDs) of 14.1∼15.1 and 126.3∼135.8 nm were produced in the shipyard. Metal fume PM 2.5 resulted in decreased cell viability and increased levels of 8-hydroxy-2'-deoxyguanosine (8-OHdG), interleukin (IL)-6, and nitric oxide (NO) in human coronary artery epithelial cells (HCAECs). We recruited 118 welding workers and 45 office workers for a personal PM 2.5 exposure assessment and determination of urinary levels of 8-OHdG, 8-iso-prostaglandin F2α (8-iso-PGF2α), and various metals. We observed that a 10-μg/m 3 increase in the mean PM 2.5 concentration was associated with a 2.15% increase in 8-OHdG and an 8.43% increase in 8-iso-PGF2α in welding workers. Both 8-OHdG and 8-iso-PGF2α were associated with Fe and Zn in the urine. In conclusion, metal fume PM 2.5 could increase the risk of cardiovascular toxicity after inhalation.
原文英語
文章編號33515
期刊Scientific Reports
6
DOIs
出版狀態已發佈 - 九月 19 2016

指紋

Welding
Coronary Vessels
Endothelial Cells
Metals
Dinoprost
Occupational Exposure
Taiwan
Inhalation
Interleukin-6
Cell Survival
Nitric Oxide
Cardiovascular Diseases
Epithelial Cells
Urine
Incidence

ASJC Scopus subject areas

  • General

引用此文

Physicochemistry and cardiovascular toxicity of metal fume PM 2.5 : A study of human coronary artery endothelial cells and welding workers. / Lai, Chane Yu; Lai, Ching Huang; Chuang, Hsiao Chi; Pan, Chih Hong; Yen, Cheng Chieh; Lin, Wen Yi; Chen, Jen Kun; Lin, Lian Yu; Chuang, Kai Jen.

於: Scientific Reports, 卷 6, 33515, 19.09.2016.

研究成果: 雜誌貢獻文章

Lai, Chane Yu ; Lai, Ching Huang ; Chuang, Hsiao Chi ; Pan, Chih Hong ; Yen, Cheng Chieh ; Lin, Wen Yi ; Chen, Jen Kun ; Lin, Lian Yu ; Chuang, Kai Jen. / Physicochemistry and cardiovascular toxicity of metal fume PM 2.5 : A study of human coronary artery endothelial cells and welding workers. 於: Scientific Reports. 2016 ; 卷 6.
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abstract = "Occupational exposure to welding fumes causes a higher incidence of cardiovascular disease; however, the association remains unclear. To clarify the possible association, exposure assessment of metal fumes with an aerodynamic diameter of <2.5 μm (PM 2.5) in welding and office areas was characterized in a shipyard in Taiwan. Cardiovascular toxicity caused by PM 2.5 was determined in workers (in both the welding and office areas). Significant amounts of bimodal metal fume particles with count median diameters (CMDs) of 14.1∼15.1 and 126.3∼135.8 nm were produced in the shipyard. Metal fume PM 2.5 resulted in decreased cell viability and increased levels of 8-hydroxy-2'-deoxyguanosine (8-OHdG), interleukin (IL)-6, and nitric oxide (NO) in human coronary artery epithelial cells (HCAECs). We recruited 118 welding workers and 45 office workers for a personal PM 2.5 exposure assessment and determination of urinary levels of 8-OHdG, 8-iso-prostaglandin F2α (8-iso-PGF2α), and various metals. We observed that a 10-μg/m 3 increase in the mean PM 2.5 concentration was associated with a 2.15{\%} increase in 8-OHdG and an 8.43{\%} increase in 8-iso-PGF2α in welding workers. Both 8-OHdG and 8-iso-PGF2α were associated with Fe and Zn in the urine. In conclusion, metal fume PM 2.5 could increase the risk of cardiovascular toxicity after inhalation.",
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