Exposure to airborne iron oxide nanoparticles induces oxidative DNA damage and inflammatory responses: a pilot study in welders and in human lung epithelial cell line.

Autor: Thanachoksawang, Chatchai, Navasumrit, Panida, Hunsonti, Potchanee, Chompoobut, Chalida, Chaisatra, Krittinee, Autrup, Herman, Ruchirawat, Mathuros
Zdroj: Toxicology & Environmental Health Sciences; Dec2022, Vol. 14 Issue 4, p339-349, 11p
Abstrakt: Objective: Exposure to airborne metal nanoparticles causes detrimental health consequences and increases the risk of lung cancer in exposed humans. This study aimed to investigate the effects of metal nanoparticles on oxidative stress-mediated DNA damage and inflammation, both in humans exposed to metal nanoparticles and in human bronchial epithelial cells (BEAS-2B). Method: Effects of exposure to metal nanoparticles were studied in welders using a cross-over design. Concentrations of metals bound to nanoparticles were measured by a personal nanoparticle sampler and analyzed by ICP-MS. Blood and urine samples were collected to determine oxidative DNA damage and transcript expression of DNA damage-related genes. The mechanisms by which iron oxide nanoparticle (FeNP)-induced oxidative DNA damage, apoptosis, and induction of inflammatory genes were investigated in BEAS-2B cells. Results: FeNP is a major form of airborne metal nanoparticles, contributing to 79% of all toxic metals in welding fumes. Exposure to airborne FeNP in welders was positively associated with blood Fe concentrations. Welders exposed to metal nanoparticles without a protective mask had increased oxidative DNA damage, observed as reduced urinary 8-OHdG, which suggest a decrease in DNA repair capacity. This was in line with significantly decreased transcript expression of the DNA repair gene (OGG1) and anti-oxidative response gene (Nrf2), as well as increased expression of the inflammatory response gene (IL-6), compared with those observed in the same welders wearing protective masks. In the in vitro study, BEAS-2B cells treated with FeNP had a decrease in cell viability and an increase in ROS generation, 8-OHdG, and apoptosis activity (caspase3-7) in a dose-dependent manner. FeNP treatment downregulated the expressions of OGG1 and Nrf2 and upregulated the expressions of IL-6 and IL-8. Conclusion: Exposure to FeNP induces oxidative DNA damage and inflammation, and this may contribute to an increased risk of respiratory diseases and cancer development. [ABSTRACT FROM AUTHOR]
Databáze: Complementary Index
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