Human bronchial epithelial cell injuries induced by fine particulate matter from sandstorm and non-sandstorm periods: Association with particle constituents.
Epidemiological studies have demonstrated the exacerbation of respiratory diseases following sandstorm-derived particulate matter (PM) exposure. The presence of anthropogenic and biological agents on the sandstorm PM and the escalation of PM<2.5μm (PM2.5) pollution in China have led to serious concerns regarding the health effects of PM2.5 during Asian sandstorms. We investigated how changes in PM2.5 composition, as the weather transitioned towards a sandstorm, affected human airway epithelial cells. Six PM2.5 samples covering two sandstorm events and their respective background and transition periods were collected in Baotou, an industrial city near the Gobi Desert in China. PM samples from all three periods had mild cytotoxicity in human bronchial epithelial cell line BEAS-2B, which was positively correlated with the contents of polycyclic aromatic hydrocarbons and several metals. All PM samples potently increased the release of interleukin-6 (IL-6) and interleukin-8 (IL-8). Endotoxin in all samples contributed significantly to the IL-6 response, with only a minor effect on IL-8. Cr was positively correlated with both IL-6 and IL-8 release, while Si was only associated with the increase of IL-6. Our study suggests that local agricultural and industrial surroundings in addition to the sandstorm play important roles in the respiratory effects of sandstorm-derived PM.
Institute of Reproductive & Child Health/Ministry of Health Key Laboratory of Reproductive Health, School of Public Health, Peking University, Beijing 100191, China. Electronic address: binwangpku@foxmail.com.
Bin
B
Wang
Department of Pathobiology & Diagnostic Investigation, College of Veterinary Medicine, Michigan State University, East Lansing 48824, USA. Electronic address: lining3@msu.edu.
Ning
N
Li
Department of Occupational & Environmental Health Sciences, School of Public Health, Peking University, Beijing 100191, China. Electronic address: lotus321321@126.com.
Furong
F
Deng
Department of Pathobiology & Diagnostic Investigation, College of Veterinary Medicine, Michigan State University, East Lansing 48824, USA.
Nicholas
N
Buglak
Department of Pathobiology & Diagnostic Investigation, College of Veterinary Medicine, Michigan State University, East Lansing 48824, USA.
George
G
Park
Laboratory for Earth Surface Processes, College of Urban & Environmental Sciences, Peking University, Beijing 100871, China.
Shu
S
Su
Institute of Reproductive & Child Health/Ministry of Health Key Laboratory of Reproductive Health, School of Public Health, Peking University, Beijing 100191, China.
Aiguo
A
Ren
Jiangsu Provincial Academy of Environmental Science, Nanjing 210036, China.
Guofeng
G
Shen
Laboratory for Earth Surface Processes, College of Urban & Environmental Sciences, Peking University, Beijing 100871, China.
Shu
S
Tao
Department of Occupational & Environmental Health Sciences, School of Public Health, Peking University, Beijing 100191, China.
Xinbiao
X
Guo
D000393:Air Pollutants / Q000032:analysis*; D002681:China / Q000453:epidemiology; D004781:Environmental Exposure / Q000032:analysis* / Q000706:statistics & numerical data*; D004847:Epithelial Cells; D006801:Humans; D015850:Interleukin-6; D016209:Interleukin-8; D008171:Lung Diseases / Q000453:epidemiology*; D008685:Meteorological Concepts; D052638:Particulate Matter / Q000032:analysis*
D000393:Air Pollutants; D015850:Interleukin-6; D016209:Interleukin-8; D052638:Particulate Matter
Human bronchial epithelial cells; Inflammation; Local environmental surroundings; Particle constituents; Sandstorm particles