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Semi-diurnal distribution of polycyclic aromatic hydrocarbons bound to PM2.5 and PM0.1 during pollution episode in the urban area of Hanoi
Semi-diurnal distribution of polycyclic aromatic hydrocarbons bound to PM2.5 and PM0.1 during pollution episode in the urban area of Hanoi
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Semi-diurnal distribution of polycyclic aromatic hydrocarbons bound to PM2.5 and PM0.1 during pollution episode in the urban area of Hanoi
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Semi-diurnal distribution of polycyclic aromatic hydrocarbons bound to PM2.5 and PM0.1 during pollution episode in the urban area of Hanoi
Semi-diurnal distribution of polycyclic aromatic hydrocarbons bound to PM2.5 and PM0.1 during pollution episode in the urban area of Hanoi

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Semi-diurnal distribution of polycyclic aromatic hydrocarbons bound to PM2.5 and PM0.1 during pollution episode in the urban area of Hanoi
Semi-diurnal distribution of polycyclic aromatic hydrocarbons bound to PM2.5 and PM0.1 during pollution episode in the urban area of Hanoi
Journal Article

Semi-diurnal distribution of polycyclic aromatic hydrocarbons bound to PM2.5 and PM0.1 during pollution episode in the urban area of Hanoi

2024
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Overview
Every year, Hanoi suffers from several episodes (periods with daily concentration of PM 2.5 higher than 50 µg m −3 during at least two consecutive days). These episodes are of health concern because of the high concentration of PM 2.5 and/or PM 0.1 and the presence of PM-bound toxic components, such as, PAHs. In this study, the concentrations of PAHs bound to PM 2.5 and PM 0.1 in night-time and day-time samples during episode and non-episode periods in December 2021 were determined. The concentrations of PAHs bound to PM 2.5 were found to increase significantly from day-time samples of 3.24 ± 0.83 ng m −3 to night-time samples of 10.8 ± 4.45 ng m −3 in episode periods. However, PAHs bound to PM 0.1 increased slightly from day-time samples of 0.58 ± 0.12 ng m −3 to night-time samples of 0.89 ± 0.30 ng m −3 in episode periods. Diagnostic ratios of PAHs indicate that biomass/coal combustion and vehicular emission are the primary sources of PAHs. The incremental lifetime cancer risk was estimated to vary from 8.7E-09 to 2.5E-08 for children and 6.7E-08 to 2.2E-07 for adults, respectively. Accordingly, loss of life expectancy was estimated at 0.11 min and 0.82 min for children and adults, respectively. These findings imply that the carcinogenic impact induced by PAHs via inhalation is negligible during the episode period.