Abstract
In 2019, PM2.5 and PM1.0 samples were collected in Harbin City, Heilongjiang Province, China, to research their mass concentration, number concentration, metal composition analysis, impact on lung injury of mice, and metal source analysis. The results showed that the mass concentration of PM2.5 and PM1.0 in the whole year of 2019 showed a trend of high in winter and low in summer. The mass concentration of PM1.0 was 62~85% of the total mass concentration of PM2.5, and the changing trend of PM1.0 number concentration was lower than that of the two sides. Its size was negatively correlated with the temperature and no significant correlation with the relative humidity. The analysis of metal composition found that the emission of coal and motor vehicle exhaust increased the concentration of Zn, Pb, As, and Cu in PM1.0. And setting off fireworks and firecrackers during the Spring Festival caused the concentration of Ti, Al, and Mg to increase. The burning of biomass also made the K concentration higher in autumn and winter than the other two-quarters. PMF analysis showed that coal combustion, soil dust and vehicle exhaust were the main factors of PM1.0 pollution in winter. Electron microscope scanning showed that PM1.0 particle morphology in winter was mainly flocculent aggregated particles generated by coal combustion. In the study of the effects of atmospheric particulate matter on lung injury in mice, it was found that lactate dehydrogenase (LDH), acid phosphatase (ACP),alkaline phosphatase (AKP), and albumin (ALB) in lung tissue cells of mice exposed to air particulates increased, indicating that PM2.5 and PM1.0 had toxic effects on lung tissue cells of mice. The level of serum malondialdehyde (MDA), nitric oxide (NO), and nitric oxide synthase (NOS) in lung lavage fluid increased, and the activity of superoxide dismutase (SOD) decreased, which indicated that both PM2.5 and PM1.0 could cause oxidative damage in the body, and with the increase of the concentration of PM2.5 and PM1.0 in the air particles, the cytotoxic effect on the lung tissue of mice was enhanced and the degree of oxidative damage was increased.
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