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Fine particulate matter (PM2.5) has been linked to cardiopulmonary disease and systemic effects in humans. However, few studies have investigated the particle bioreactivity in Chinese megacities during haze episodes. The objective of this study was to determine the contributions of chemical components in PM2.5 to particle bioreactivity in Chinese megacities during haze episodes. PM2.5 samples were collected in 14 megacities across China from 23 December 2013 to 16 January 2014. Average PM2.5 concentrations ranged 88.92~199.67 μg/m3. Organic carbon (OC), elemental carbon (EC), anions, and cations per unit of PM2.5 were linked to cellular bioreactivity (i.e., reactive oxygen species (ROS) as assessed by dichlorodihydrofluorescein diacetate (DCFH) and inflammation as assessed by interleukin (IL)-6 in A549 cells). The contributions of chemicals in PM2.5 to ROS and inflammation were examined by the Pearson correlation coefficient and random forests. These results indicated that OC, Ca2+, SO42−, Cl−, F−, K+, and NO3− contributed to ROS production, whereas OC, Cl−, EC, K+, F−, Na+, and Ca2+ contributed to inflammation. In conclusion, PM2.5-contained OC and acidic ions are important in regulation of oxidative stress and inflammation during haze episodes. Our findings suggest that severe haze PM2.5 events cause deterioration in air quality and may adversely affect human health. [ABSTRACT FROM AUTHOR]

Research on individual level polycyclic aromatic hydrocarbons (PAHs) exposure is scarce. Moreover, the independent contribution of ambient‐ and indoor‐origin PAHs to personal exposure remains poorly studied. We performed simultaneous ambient, residential indoor, and personal exposure measurements in a panel of healthy adults to investigate particle‐bound PAHs, focusing on their carcinogenic congeners (cPAHs). Average PAH concentrations were much higher in ambient and residential indoor than personal exposure, with distinct seasonal variations. We employed chrysene as a tracer to investigate residential indoor and personal PAHs exposure by origin. Personal cPAH exposure was largely attributable to ambient‐origin exposures (95.8%), whereas a considerable proportion of residential indoor PAHs was likely attributable to indoor emissions (33.8%). Benzo[a]pyrene equivalent (BaPeq) concentrations of cPAH accounted for 95.2%‒95.6% of total carcinogenic potential. Uncertainties in estimated PAHs (and BaPeq) exposure and cancer risks for adults were calculated using the Monte Carlo simulation. Cancer risks attributable to ambient, residential indoor, and personal cPAH inhalation exposures ranged from 4.0 × 10−6 to 1.0 × 10−5. A time‐activity weighted model was employed for personal PAH exposure estimations. Estimated cPAH exposures demonstrate high cancer risks for adults in Hong Kong, suggesting that exposure to indoor‐generated PAHs should be of great concern to the general population. [ABSTRACT FROM AUTHOR]

PM2.5 is a major component of air pollution in China and has a serious threat to public health. It is very important to quantify spatial characteristics of the health effects caused by outdoor PM2.5 exposure. This study analyzed the spatial distribution of PM2.5 concentration (45.9 μg/m3 national average in 2016) and premature mortality attributed to PM2.5 in cities at the prefectural level and above in China in 2016. Using the Global Exposure Mortality Model (GEMM), the total premature mortality in China was estimated to be 1.55 million persons, and the per capita mortality was 11.2 per 10,000 persons in the year 2016, resulting in higher estimates compared to the integrated exposure‐response model. We assessed the premature mortality attributed to PM2.5 through common diseases, including ischemic heart disease (IHD), cerebrovascular disease (CEV), chronic obstructive pulmonary disease (COPD), lung cancer (LC), and lower respiratory infections (LRI). The premature mortality due to IHD and CEV accounted for 68.5% of the total mortality, and the per capita mortality (per 10,000 persons) for all ages due to IHD was 3.86, the highest among diseases. For the spatial distribution of disease‐specific premature mortality, the top two highest absolute numbers of premature mortality associated with IHD, CEV, LC, and LRI, respectively, were found in Chongqing and Beijing. In 338 cities of China, we have found a significant positive spatial autocorrelation of per capita premature mortality, indicating the necessity of coordinated regional governance for an efficient control of PM2.5. Plain Language Summary: Fine particulate matter (PM2.5) concentrations have increased in general, in most developing countries in recent decades. In China, PM2.5 pollution has become a major component of air pollution and has serious health impacts. To obtain a comprehensive understanding of the national health impacts of PM2.5 in China, we have used the Global Exposure Mortality Model (GEMM) to estimate the premature mortality associated with PM2.5 exposure in 338 cities in China at the prefectural level and above. In addition, we analyzed the spatial distribution of premature mortality attributed to PM2.5 for five diseases, including ischemic heart disease (IHD), cerebrovascular disease (CEV), chronic obstructive pulmonary disease (COPD), lung cancer (LC), and lower respiratory infections (LRI). Our study finds that the total premature mortality associated with PM2.5 exposure in China for 2016 was 1.55 million persons. The top two highest absolute numbers of premature mortality associated with IHD, CEV, LC, and LRI, respectively were found in Chongqing and Beijing. Furthermore, cities with high per capita premature mortality tended to be spatially connected with other cities with high per capita premature mortality, indicating the coordinated regional governance should be adopted to reduce the impact of PM2.5 on human health. Key Points: Based on an extended observational network in China, 1.55 million premature deaths attributed to PM2.5 is estimated in 2016Higher premature mortality using the Global Exposure Mortality Model compared to the Integrated Exposure‐Response modelA positive spatial autocorrelation of the per capita premature mortality is found at the city levels [ABSTRACT FROM AUTHOR]

Exposure to road dust particulate matter (PM) causes adverse health impacts on the human airway. However, the effects of road dust on the upper airway epithelium in humans remain unclear. We investigated the involvement of the epidermal growth factor receptor (EGFR) after PM with an aerodynamic diameter of < 2.5 μm (PM2.5)-induced E-cadherin disruption of human pharyngeal epithelial cells. First, we collected road dust PM2.5 from 10 Chinese cities, including Wuhan, Nanjing, Shanghai, Guangzhou, Chengdu, Beijing, Lanzhou, Tianjin, Harbin, and Xi'an. Human pharyngeal FaDu cells were exposed to road dust PM2.5 at 50 μg/mL for 24 h, cytotoxicity (cell viability and lactate dehydrogenase (LDH)) was assessed, and expressions of the proinflammatory interleukin (IL)-6 and high-mobility group box 1 (HMGB1) protein, receptor for advanced glycation end products (RAGE), occludin, E-cadherin, EGFR, and phosphorylated (p)-EGFR were determined. The E-cadherin gene was then knocked down to investigate EGFR activation in FaDu cells. Exposure to road dust PM2.5 resulted in a decrease in cell viability and increases in LDH and IL-6. Our data suggested that PM2.5 could decrease expressions of occludin and E-cadherin and increase expressions of EGFR and p-EGFR, which was confirmed by E-cadherin-knockdown. Our results showed a negative association between the alterations in E-cadherin and total elemental components in correlation analysis, especially S, Cl, K, Ti, Mn, Fe, Cu, Zn, and Pb. Exposure to metals in PM2.5 from road dust may lead to loss of the barrier function of the upper airway epithelium and activation of the EGFR. Our study showed the adverse effects of road dust PM2.5 on pharyngeal epithelial cells of the human upper airway. [ABSTRACT FROM AUTHOR]

BACKGROUND: Ischemic heart disease (IHD) is a major public health concern. Although many epidemiologic studies have reported evidence of adverse effects of particulate matter (PM) mass on IHD, significant knowledge gaps remain regarding the potential impacts of different PM sources. Much the same as PM size, PM sources may influence toxicological characteristics. OBJECTIVES: We identified contributing sources to [PM.sub.10] mass and estimated the acute effects of [PM.sub.10] sources on daily emergency IHD hospitalizations in Hong Kong. METHODS: We analyzed the concentration data of 19 [PM.sub.10] chemical components measured between 2001 and 2007 by positive matrix factorization to apportion [PM.sub.10] mass, and used generalized additive models to estimate associations of interquartile range (IQR) increases in [PM.sub.10] exposures with IHD hospitalization for different lag periods (up to 5 days), adjusted for potential confounders. RESULTS: We identified 8 [PM.sub.10] sources: vehicle exhaust, soil/road dust, regional combustion, residual oil, fresh sea salt, aged sea salt, secondary nitrate, and secondary sulfate. Vehicle exhaust, secondary nitrate, and secondary sulfate contributed more than half of the [PM.sub.10] mass. Although associations with IQR increases in 2-day moving averages ([lag.sub.01]) were statistically significant for most sources based on single-source models, only [PM.sub.10] from vehicle exhaust [1.87% (95% CI: 0.66, 3.10); IQR = 4.9 µg/[m.sup.3]], secondary nitrate [2.28% (95% CI: 1.15, 3.42); IQR = 8.6 µg/[m.sup.3]], and aged sea salt [1.19% (95% CI: 0.04, 2.36); IQR = 5.9 µg/[m.sup.3]] were significantly associated with IHD hospitalizations in the multisource model. Analysis using chemical components provided similar findings. CONCLUSION: Emergency IHD hospitalization was significantly linked with [PM.sub.10] from vehicle exhaust, nitrate-rich secondary PM, and sea salt--related PM. Findings may help prioritize toxicological research and guide future monitoring and emission-control polices. CITATION: Pun VC, Yu IT, Ho KF, Qiu H, Sun Z, Tian L. 2014. Differential effects of source-specific particulate matter on emergency hospitalizations for ischemic heart disease in Hong Kong. Environ Health Perspect 122:391-396; http://dx.doi.org/10.1289/ehp.1307213, Introduction Over the past decades, epidemiologic evidence has linked ambient particulate matter (PM) pollution to increased cardiovascular morbidity and mortality (Dominici et al. 2006; Peng et al. 2009). Of the [...]

To provide long-term air pollutant exposure estimates for epidemiological studies, it is essential to test the feasibility of developing land-use regression (LUR) models using only routine air quality measurement data and to evaluate the transferability of LUR models between nearby cities. In this study, we develop and evaluate the intercity transferability of annual average LUR models for ambient respirable suspended particulates (PM10), fine suspended particulates (PM2.5), nitrogen dioxide (NO2), and ozone (O3) in the Taipei–Keelung metropolitan area of northern Taiwan in 2019. Ambient PM10, PM2.5, NO2, and O3 measurements at 30 fixed-site stations were used as the dependent variables, and a total of 156 potential predictor variables in six categories (i.e., population density, road network, land-use type, normalized difference vegetation index, meteorology, and elevation) were extracted using buffer spatial analysis. The LUR models were developed using the supervised forward linear regression approach. The LUR models for ambient PM10, PM2.5, NO2, and O3 achieved relatively high prediction performance, with R2 and leave-one-out cross-validation (LOOCV) R2 values of > 0.72 and > 0.53, respectively. The intercity transferability of LUR models varied among the air pollutants, with transfer-predictive R2 values of > 0.62 for NO2 and < 0.56 for the other three pollutants. The LUR-model-based 500 m×500 m spatial distribution maps of these air pollutants illustrated pollution hotspots and the heterogeneity of population exposure, which provide valuable information for policymakers in designing effective air pollution control strategies. The LUR-model-based air pollution exposure estimates captured the spatial variability of exposure for participants in a cohort study. This study highlights that LUR models can be reasonably established upon a routine monitoring network but there exist uncertainties when transferring LUR models between nearby cities. To the best of our knowledge, our study is the first to evaluate the intercity transferability of LUR models in Asia. [ABSTRACT FROM AUTHOR]