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To distinguish the influences of fuel type and truck speed on chemical composition and sub-toxic effects of particulates (PM2.5) from engine emissions, biomarkers—interleukin-6 (IL-6), cytochrome P450 (CYP) 1A1, heme oxygenase (HO)-1, and NADPH-quinone oxidoreductase (NQO)-1—were studied in A549 human lung cells. Fuel type and truck speed preferentially affected the quantity and ion/polycyclic aromatic hydrocarbon (PAH) composition of PM2.5, respectively. Under idling operation, phenanthrene was the most abundant PAH. At high speed, more than 50% of the PAHs had high molecular weight (HMW), of which benzo[a]pyrene (B[a]P), benzo[ghi]perylene (B[ghi]P), and indeno[1,2,3-cd]pyrene (I[cd]P) were the main PAHs. B[a]P, B[ghi]P, and I[cd]P caused potent induction of IL-6, CYP1A1, and NQO-1, whereas phenanthrene mildly induced CYP1A1. Based on the PAH-mediated induction, the predicted increases in biomarkers were positively correlated with the measured increases. HMW-PAHs contribute to the biomarker induction by PM2.5, at high speed, which was reduced by co-exposure to epigallocatechin-3-gallate.

The significance of this work is that ambient PM

Vehicle emissions are an important source of particulate matter (PM) in urban areas and have well-known adverse health effects on human health. Oxidative potential (OP) is used as a quantification metric for indexing PM toxicity. In this study, by using a liquid spot sampler (LSS) and the dithiothreitol (DTT) assay, the diurnal OP variation was assessed at a ground-level urban monitoring station. Besides, since the monitoring station was adjacent to the main road, the correlation between OP and traffic volume was also evaluated. PM components, including metals, water-soluble inorganic aerosols (WSIAs), black carbon (BC), and polycyclic aromatic hydrocarbons (PAHs), were also simultaneously monitored. The daytime and evening mean ± std volume-normalized OP (OPv) were 0.46 ± 0.27 and 0.48 ± 0.26 nmol/min/m3, and exhibited good correlations with PM1.0 and BC; however, these concentrations were only weakly correlated with mass-normalized OP (OPm). The mean ± std OPm was higher in the daytime (41.3 ± 13.8 pmol/min/μg) than in the evening (36.1 ± 11.5 pmol/min/μg). According to the PMF analysis, traffic emissions dominated the diurnal OP contribution. Organic matter and individual metals associated with non-exhaust traffic emissions, such as Mn, Fe, and Cu, contributed substantially to OP. Diurnal variations of PAH concentrations suggest that photochemical reactions could enhance OP, highlighting the importance of atmospheric aging on PM toxicity.

This study aimed to find the characteristics of polychlorinated dibenzo-p-dioxins and dibenzofurans (PCDD/Fs) in fine particulate matter from different stationary emission sources (coal-fired boiler, CFB; municipal waste incinerator, MWI; electric arc furnace, EAF) in Taiwan and the relationship between PM2.5 and PM2.5-bound PCDD/Fs with Taiwanese mortality risk. PM2.5 was quantified using gravimetry and corresponding chemical analyses were done for PM2.5-bound chemicals. Mortality risks of PM2.5 exposure and PCDD/Fs exposure were calculated using Poisson regression. The highest concentration of PM2.5 (0.53 ± 0.39 mg/Nm3) and PCDD/Fs (0.206 ± 0.107 ng I-TEQ/Nm3) was found in CFB and EAF, respectively. Higher proportions of PCDDs over PCDFs were observed in the flue gases of CFB and MWI whereas it was reversed in EAF. For ambient air, PCDD/F congeners around the stationary sources were dominated by PCDFs in vapor phase. Positive matrix factorization (PMF) analysis found that the sources of atmosphere PCDD/Fs were 14.6% from EAF (r = 0.81), 52.6% from CFB (r = 0.74), 18.0% from traffic (r = 0.85) and 14.8% from MWI (r = 0.76). For the dioxin congener distribution, PCDDs were dominant in flue gases of CFB and MWI, PCDFs were dominant in EAF. It may be attributed to the different formation mechanisms among wastes incineration, steel-making, and coal-burning processes.

This study aimed to find the characteristics of polychlorinated dibenzo-p-dioxins and dibenzofurans (PCDD/Fs) in fine particulate matter from different stationary emission sources (coal-fired boiler, CFB; municipal waste incinerator, MWI; electric arc furnace, EAF) in Taiwan and the relationship between PM2.5 and PM2.5-bound PCDD/Fs with Taiwanese mortality risk. PM2.5 was quantified using gravimetry and corresponding chemical analyses were done for PM2.5-bound chemicals. Mortality risks of PM2.5 exposure and PCDD/Fs exposure were calculated using Poisson regression. The highest concentration of PM2.5 (0.53 ± 0.39 mg/Nm3) and PCDD/Fs (0.206 ± 0.107 ng I-TEQ/Nm3) was found in CFB and EAF, respectively. Higher proportions of PCDDs over PCDFs were observed in the flue gases of CFB and MWI whereas it was reversed in EAF. For ambient air, PCDD/F congeners around the stationary sources were dominated by PCDFs in vapor phase. Positive matrix factorization (PMF) analysis found that the sources of atmosphere PCDD/Fs were 14.6% from EAF (r = 0.81), 52.6% from CFB (r = 0.74), 18.0% from traffic (r = 0.85) and 14.8% from MWI (r = 0.76). For the dioxin congener distribution, PCDDs were dominant in flue gases of CFB and MWI, PCDFs were dominant in EAF. It may be attributed to the different formation mechanisms among wastes incineration, steel-making, and coal-burning processes.

The significance of this work is that ambient PM2.5 is a direct transmission mode for influenza virus infection to the human alveolar epithelium. The concentration of PM2.5 was 11.7 ± 5.5 μg/m3 in Taipei during 24 December 2019–13 January 2020. Approximately 79% of inhaled PM2.5 is able to reach the upper-to-lower airway, and 47% of PM2.5 is able to reach the alveolar epithelium for influenza virus infection. Influenza A and B viruses were detected in PM2.5 on 9 days, and the influenza A/H5 virus was detected on 15 days during the study period. FL and Pyr were negatively correlated with the influenza A virus. D(ah)P and Acp were positively correlated with the influenza B and A/H5 viruses, respectively. Cd, V, and Zn were positively correlated with the influenza A, B, and A/H5 viruses, respectively. Next, influenza A, B, and A/H5 viral plasmids interacted with carbon black, H2O2, DEPs, and UD. We observed that H2O2 significantly decreased levels of complementary DNA of the three influenza viruses. DEPs and UD significantly decreased influenza A and A/H5 viral levels. In conclusion, chemicals in PM2.5 may play vital roles in terms of viable influenza virus in the atmosphere.

In this research, we simultaneously studied the characteristics of particulate matter-bound PAHs from two industrial coal fire boilers, one highway tunnel, and PAHs from the ambient air of each source. In the stack gas, condensable particulate matter (CPM) was 10–30 times higher than filterable particulate matter (FPM2.5). The content of PAHs in each mg of PM2.5 at emission stack (479 ± 284 ng BaPeq/mg) was reduced by 1.7 times at the industrial vicinity (282 ± 264 ng BaPeq/mg). Inside the tunnel, the PAH content was (138 ± 23.8 ng BaPeq/mg). Such value was reduced with the reduction of human activities from urban (40.8 ± 22.3 ng BaPeq/mg) to rural (34.4 ± 23.9 ng BaPeq/mg) and background areas (3.03 ± 1.94 ng BaPeq/mg). Indeno[1,2,3-cd]pyrene and Benzo[g,h,i]perylene were found to be the major contributor of PAHs from the industrial emission (25–30%) and traffic source (60%). Source apportionment in ambient PAHs found fossil fuel burning (for both industry and traffic purposes), incineration, and biomass burning was major contributors of PAHs in the ambient air in Taiwan. Excessive cancer risk in the vicinity of industrial areas and central regions of Taiwan was higher than the EPA standard threshold of 10−4.