PM<inf>10</inf>-related DNA damage, cytokinetic defects, and cell death in COPD patients from Chiang Dao district, Chiang Mai, Thailand

• Main Authors: Klintean Wunnapuk, Chaicharn Pothirat, Siriphorn Manokeaw, Nittaya Phetsuk, Warawut Chaiwong, Rochana Phuackchantuck, Tippawan Prapamontol
• Format: Journal
• Published: 2019
• Subjects: Environmental Science
• Online Access: https://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=85068309504&origin=inward; http://cmuir.cmu.ac.th/jspui/handle/6653943832/65626
• Institution: Chiang Mai University

© 2019, Springer-Verlag GmbH Germany, part of Springer Nature. Exposure to PM10 generated by biomass burning may reduce lung function and induce cytogenetic effects, especially in chronic obstructive pulmonary disease patients. This study investigated the frequency of DNA-damaged cells, cells with cytokinetic defect, and different types of cell death using a buccal micronucleus cytome assay. The correlations between each biomarker and lung function were investigated. The changes in these biomarkers associated with high pollutant levels (PM10 > 50 μg/m3) and low pollutant levels (PM10 < 50 μg/m3) were evaluated to explore whether PM10 exposure induced genotoxic damages and cytokinetic defects in COPD patients when the daily average PM10 concentration reached above 50 μg/m3. Fifty-eight COPD patients and 26 healthy subjects living in Chiang Dao district, Chiang Mai, Thailand, were recruited in this study. The results revealed that buccal cells with micronuclei (high vs low 1.09 ± 1.95 vs 0.29 ± 0.64 in COPD patients) and binucleated cells (high vs low 11.43 ± 18.68 vs 1.60 ± 1.31 and 7.77 ± 12.76 vs 1.00 ± 1.17 in COPD and healthy subjects, respectively) observed during the high pollutant period were more frequent than in the low pollutant period. Moreover, exposure to PM10 increased the risk of micronucleus induction in COPD patients 295.23-fold.