Ambient particulate matter (PM) is a worldwide health issue of concern. However, limited information is available regarding the toxic contributions of the nitro-derivatives of polycyclic aromatic hydrocarbons (nitro-PAHs). This study intend to examine whether 1-nitropyrene (1-NP) and 3-nitrofluoranthene (3-NF) could activate the nuclear factor-erythroid 2-related factor 2/antioxidant response element (Nrf2/ARE) antioxidant defense system, and whether the phosphatidylinositol 3-kinase/protein kinase B (PI3K/Akt) pathway participates in regulating pro-inflammatory responses in A549 cells. Firstly, 1-NP and 3-NF concentration-dependently induced cellular apoptosis, reactive oxygen species (ROS) generation, DNA damage, S phase cell cycle arrest and differential expression of related cytokine genes. Secondly, 1-NP and 3-NF activated the Nrf2/ARE defense system, as evidenced by increased protein expression levels and nuclear translocation of transcription factor Nrf2, elevated Nrf2/ARE binding activity, up-regulated expression of the target gene heme oxygenase-1 (HO-1). Significantly increased protein expression of DNA-dependent protein kinase catalytic subunit (DNA-PKcs) and phosphorylation level of Akt indicated that the PI3K/Akt pathway was activated during pro-inflammatory process. Further, both PI3K inhibitor (LY294002) and Akt inhibitor (MK-2206) reversed the elevated TNF-alpha expression to control level. Our results suggested that Nrf2/ARE pathway activation might cause an initiation step in cellular protection against oxidative stress caused by nitro-PAHs, and the PI3K/Akt pathway participated in regulating inflammatory responses.

Epidemiological studies have showed an association between black carbon (BC) exposure and adverse health effects. This study intends to investigate the influence of oxidation processes in atmosphere on the initial cellular responses of BC. The changes of gene expressions induced by fresh BC (FBC) and ozone oxidized BC (OBC) in human lung epithelial A549 cells were analyzed. And their toxic effects presented by viability, LDH release and DNA damage were compared. Totally 47, 000 genes in A549 cells were examined using Affymetrix Human U133 plus 2.0 chips. Some of the differentially expressed genes were verified by reverse transcription-quantitative polymerase chain reaction (RT-qPCR). The results showed that 1446 genes (including 756 up -regulated and 690 down -regulated) and 1594 genes (including 788 up-regulated" and 806 down -regulated genes) were significantly changed by FBC and OBC respectively. Only 4 of 14 (FBC)/15 (OBC) oxidative stress related genes,up-or down -regulated by FBC and OBC, were identical; 13 of 29 (FBC)/31 (OBC) inflammation related genes, and 6 of 20 (FBC)/18 (OBC) autophagy related genes were identical. No obvious differences were observed between the toxic effects of FBC and OBC. The cytotoxicity of OBC and FBC in A549 cells is at least partially induced by oxidative stress and consequent inflammation or autophagy process. Previous studies indicated that OBC may be more toxic than FBC. However, our results suggested that FBC and OBC might lead to diverse toxic endpoints through activating different molecular pathways. (C) 2017 Elsevier Ltd. All rights reserved.

Atmospheric particulate polycyclic aromatic hydrocarbons (PAHs) have been drawing sustained attention due to their health risk and effects on air pollution. It is essential to determine the main sources and reduce atmospheric levels of PAHs to protect human health. PAHs in PM2.5 have been detected at five sites located in five districts in Shanghai, a modern metropolitan city in China. Spatial and temporal variations of composition profiles and sources of PAHs at each site in each season were investigated. The results showed that atmospheric particulate PAHs level in Shanghai was the lowest in summer and the highest in winter, dominated by high molecular weight (HMW) PAHs. Analysis with a combination of coefficients of Pearson's correlation and coefficient of divergences indicated heterogeneous spatial and temporal distribution for LMW PAHs and homogenous distribution for HMW PAHs. Diagnostic ratios and positive matrix factorization (PMF) model both identified pyrogenic sources as the main contributor of PAHs in Shanghai, with vehicular source contribution of 32-43% to the total PAHs annually and around 20% from biomass burning emissions in urban and urban buildup areas. While in winter, coal combustion and biomass burning could act as two major sources of PAHs in suburban areas, which could contribute to >70% of total PAHs measured in PM2.5 in Shanghai. (C) 2016 Elsevier B.V. All rights reserved.

Polycyclic aromatic hydrocarbons (PAHs), formed through incomplete combustion process, have adverse health effects. To investigate spatial distribution and sources of PAHs in North China, PAHs with passive sampling in 90 gridded sites during June to September in 2011 were analyzed. The average concentration of the sum of fifteen PAHs in North China is 220 +/- 14 ng/m(3), with the highest in Shanxi, followed by Shandong and Hebei, and then the Beijing-Tianjin area. Major sources of PAHs are identified for each region of North China, coke process for Shanxi, biomass burning for Hebei and Shandong, and coal combustion for Beijing-Tianjin area, respectively. Emission inventory is combined with back trajectory analysis to study the influence of emissions from surrounding areas at receptor sites. Shanxi and Beijing-Tianjin areas are more influenced by sources nearby while regional sources have more impact on Hebei and Shandong areas. Results from this study suggest the areas where local emission should be the major target for control and areas where both local and regional sources should be considered for PAH abatement in North China. (C) 2016 Elsevier B.V. All rights reserved.

Fine particulate matter (PM2.5) pollution poses significant health risks worldwide, including metabolic syndrome-related diseases with the characteristic feature of insulin resistance. However, the mechanism and influencing factors of this effect are poorly understood. In this serial in vitro study, we aimed at testing the hypothesis that macrophage-mediated effects of PM2.5 on hepatic insulin resistance depend on its chemical composition. Mouse macrophages were exposed to PM2.5 that had been collected during summer or winter in Beijing, which represented different compositions of PM2.5. Thereafter, hepatocytes were treated with macrophage-conditioned medium (CM). PM2.5 induced interleukin-6, tumor necrosis factor-alpha, and monocyte chemoattractant protein-1 expression and secretion in macrophages, particularly after winter PM2.5 exposure. Correspondingly, winter CM weakened hepatocellular insulin-stimulated glucose consumption. Further investigation revealed that the normal insulin pathway was suppressed in winter CM-treated hepatocytes, with increased phosphorylation of insulin receptor substrate 1 at serine residue 307 (Ser307) and decreased phosphorylation of protein kinase B (PKB/AKT) and forkhead box transcription factor O1 (FoxO1). Moreover, c-Jun N-terminal kinase, a key moderator of the sensitivity response to insulin stimulation, was activated in hepatocytes treated with winter CM. Although further studies are warranted, this preliminary study suggested an association between PM composition and insulin resistance, thus contributing to our understanding of the systemic toxicity of PM2.5.

The relationship between polycyclic aromatic hydrocarbons (PAHs) and hypertension remains a subject of debate. The aims of this study were to determine an association of concentrations of PAHs in housewives' hair with hypertension risk and the modification effect of single nucleotide polymorphisms (SNPs) related to Phase I metabolism of PAHs. We recruited 405 women for a cross-sectional study in Shanxi Province, China, including 170 with hypertension (the case group) and 235 without hypertension (the control group). We analyzed 26 individual PAHs in hair samples and the SNPs of the genes including cytochrome P450, family 1, subfamily A, polypeptide 1 (CYP1A1), CYP1A2, CYP1B1 and CYP2E1. Our results showed that seven PAHs in hair samples were measured with detection rate >70%. Only acenaphthylene was found to be associated with an increased risk of hypertension with adjustment for the potential confounders following Bonferroni correction, whereas others not. No SNPs of the concerned genes were found to be associated with the risk of hypertension. A multiple interaction effect of PAHs in housewives' hair and SNPs on hypertension risk was not observed. It was concluded that PAHs tended to contribute to the formation of hypertension. (C) 2016 Published by Elsevier Ltd.

As part of the 12th Five-Year Plan, the Chinese government has developed air pollution prevention and control plans for key regions with a focus on the power, transport, and industrial sectors. Here, we investigate the contribution of residential emissions to regional air pollution in highly polluted eastern China during the heating season, and find that dramatic improvements in air quality would also result from reduction in residential emissions. We use the Weather Research and Forecasting model coupled with Chemistry to evaluate potential residential emission controls in Beijing and in the Beijing, Tianjin, and Hebei (BTH) region. In January and February 2010, relative to the base case, eliminating residential emissions in Beijing reduced daily average surface PM2.5 (particulate mater with aerodynamic diameter equal or smaller than 2.5 micrometer) concentrations by 14 +/- 7 mu g.m(-3) (22 +/- 6% of a baseline concentration of 67 +/- 41 mu g.m(-3); mean +/- SD). Eliminating residential emissions in the BTH region reduced concentrations by 28 +/- 19 mu g.m(-3) (40 +/- 9% of 67 +/- 41 mu g.m(-3)), 44 +/- 27 mu g.m(-3) (43 +/- 10% of 99 +/- 54 mu g.m(-3)), and 25 +/- 14 mu g.m(-3) (35 +/- 8% of 70 +/- 35 mu g.m(-3)) in Beijing, Tianjin, and Hebei provinces, respectively. Annually, elimination of residential sources in the BTH region reduced emissions of primary PM2.5 by 32%, compared with 5%, 6%, and 58% achieved by eliminating emissions from the transportation, power, and industry sectors, respectively. We also find air quality in Beijing would benefit substantially from reductions in residential emissions from regional controls in Tianjin and Hebei, indicating the value of policies at the regional level.

This study aims to simulate depositions of size-segregated particles in human airway in Beijing, China during seasons when fine particulate matter concentrations are high (December 2011 and April 2012). Particle size distributions (5.6-560 nm, electrical mobility diameter) near a major road in Beijing were measured by the TSI Fast Mobility Particle Sizer (FMPS). The information of size distributions provided by FMPS was applied in the Multiple-Path Particle Dosimetry model (MPPD) to quantify number and mass depositions of particles in human airway including extrathoracic (ET), tracheobronchial (TB), and pulmonary (PUL) regions of exposed Chinese in Beijing. Our results show that under ambient conditions, particle number concentration (NC) deposition in PUL is the highest in the three major regions of human airway. The total particle NC deposition in human airway in winter is higher than that in spring, especially for ultrafine particles (1.8 times higher) while particle mass concentration (MC) deposition is higher in spring. Although particle MC in clean days are much lower than that in heavily polluted days, total particle NC deposition in human airway in clean days is comparable to that in heavily polluted days. NC deposition for nucleation mode particles (10-20 nm, aerodynamic diameter) in clean days is higher than that in heavily polluted days. MC deposition for accumulation mode particles (100-641 nm, aerodynamic diameter) in heavily polluted days is much higher than that in clean days, while that of nucleation mode is negligible. The temporal variation shows that the arithmetic mean and the median values of particle NC and MC depositions in the evening are both the highest, followed by morning and noon, and it is most likely due to increased contribution from traffic emissions. (C) 2015 Elsevier Ltd. All rights reserved.

Atmospheric polycyclic aromatic hydrocarbons (PAHs) and their derivatives are of great concern due to their adverse health effects. However, source identification and apportionment of these compounds, particularly their nitrated and hydroxylated derivatives (i.e., NPAHs and OHPAHs), in fine particulate matter (PM2.5) in Hong Kong are still lacking. In this study, we conducted a 1-year observation at an urban site in Hong Kong. PM2.5-bound PAHs and their derivatives were measured, with median concentrations of 4590, 44.4 and 31.6 pg m(-3) for Sigma(21)PAHs, Sigma(13)NPAHs, and Sigma(12)OHPAHs, respectively. Higher levels were observed on regional pollution days than on long regional transport (LRT) or local emission days. Based on positive matrix factorization analysis, four sources were determined: marine vessels, vehicle emissions, biomass burning, and a mixed source of coal combustion and NPAHs secondary formation. Coal combustion and biomass burning were the major sources of PAHs, contributing over 85% of PAHs on regional and LRT days. Biomass burning was the predominant source of OHPAHs throughout the year, while NPAHs mainly originated from secondary formation and fuel combustion. For benzo[a]pyrene (BaP)-based PM2.5 toxicity, the mixed source of coal combustion and NPAHs secondary formation was the major contributor, followed by biomass burning and vehicle emissions. (C) 2016 Elsevier Ltd. All rights reserved.

Nitrated polycyclic aromatic hydrocarbons (NPAHs) are strong environmental mutagens and carcinogens originating from both primary emissions and secondary reactions in the atmosphere. The sources and the toxicity of different NPAH species could vary greatly; therefore a specie-specific source apportionment is essential to evaluate their health risks and to formulate controlling regulations. However, few studies have reported source apportionment of NPAHs species to date. In this study, we developed an easy-to-perform method for the apportionment of primary versus secondary sources of airborne NPAHs based on the relationship between NPAHs and NO2. After log-transformation of both NPAHs and NO2 concentrations, a slope of beta between these two variables was obtained by the linear regression. When (3 is significantly smaller than 1, it indicates primary emissions while 13 significantly greater than 1 suggests secondary formation. We have validated this method with data previously collected in Beijing. A good correlation, with R value of 0.57, was observed between results produced by this new method and by Positive Matrix Factorization (PMF). The correlation could be further improved (R = 0.71) if the gas/particle partition of NPAHs is taken into consideration. This developed method enables the source apportionment for individual NPAHs species and could be used to validate the results of other receptor models. (C) 2016 Elsevier Ltd. All rights reserved.

Air pollution is among the top threats to human health in China. As air toxicants, polycyclic aromatic hydrocarbons (PAHs) could bring significant risks to population; however, the exposure to PAHs in China and its health impact are not fully understood. In 2012, a summer exchange program allowed 10 students to travel from Los Angeles to Beijing and stay there for 10 weeks. Based on the program, this study investigated the difference in urinary concentration of 12 hydroxylated-PAHs (Sigma 12OH-PAHs) and malondialdehyde (MDA) between the two cities. The median concentration of Sigma 12OH-PAHs in Beijing (14.1 mu g g(-1) creatinine) was significantly higher than that in Los Angeles (5.78 mu g g(-1) creatinine), indicating a higher exposure in Beijing. The ratios of homogeneous OH-PAHs (e.g., 1-/2-OH-NAP) changed significantly between the two cities (p < 0.01), which might suggest a potential alteration in metabolism subsequent to exposure. A significant association between Sigma 12OH-PAHs and MDA (p < 0.01) was observed, with the association varying between the two cities. This study suggests that exposure to PAHs might be linked to metabolism alteration and calls for future studies to investigate the role this possible alteration played in the health effects of PAHs exposure.

China has become one of the major recycling sites for the electronic waste (e-waste) from worldwide. Pollutants emerged from the e-waste dismantling and the subsequent health effects to populations are of great concern. Typically, exposure to organic pollutants, such as bisphenol A (BPA) especially generated from primitive dismantling, is an important scientific issue for their adverse health effects to local residents. In this study, 29 e-waste dismantling workers and 24 local residents from a dismantling area in North China were recruited as the exposure group. Residents (N = 53) living 40 km away from this e-waste area were selected as the reference. The median concentration of urinary BPA of the exposure group was 10.7 mu g.g(-1) creatinine, which was significantly higher than that of the references (0.66 mu g.g(-1) creatinine; P < 0.01), indicating that working and/or living in the e-waste area caused the elevated body burden of BPA. Urinary 8-hydroxy-2'-deoxyguanosine (8-OHdG) of the exposure group (median: 236 mu g.g(-1) creatinine) was higher than that of the references (median: 142 mu g.g(-1) creatinine) with a marginal significance (P = 0.055). Meanwhile, serum levels of glutathione S-transferase (GSH-ST) and Cu/Zn-Superoxide dismutase (Cu/Zn-SOD) were significantly lower in the exposure group, while glutathione peroxidase (GSHPx) was higher when compared to the references (P < 0.01). Significantly positive association between urinary BPA and 8-OHdG was found (P < 0.05); however, significantly negative association was found between BPA and serum GSH-ST (P < 0.01). After controlling for confounders, 34.9% (95% CI: 19.4%-52.3%) increment of urinary 8-OHdG and 5.46% (95% CI: 1.17%-9.56%) decrement of serum GSH-ST per one-fold increase of BPA were estimated. Those results provided evidence on high exposure level of BPA among the populations from the e-waste dismantling area and a high risk of oxidative damage to DNA.

The mechanism of health effects caused by organohalogen pollutants, e.g., toxins from electronic waste (e-waste), is poorly understood. We supposed that microRNAs (miRNAs), an important post-transcriptional regulator, could play a role in this process. In this study, fasting peripheral blood samples were collected from residents living at an e-waste site in northern China and a nearby reference population. Concentrations of e-waste related organohalogen pollutants in plasma from the exposure group were higher than the corresponding measurement in the reference group. Correspondingly, sixty miRNAs in plasma showed > 2-fold change between the two groups in microarray analysis. Among them, miR-125a-5p was confirmed to be upregulated by qRT-PCR and its validated targets were enriched in responses to xenobiotics and cancer related pathways. Furthermore, significant positive conelations were found between levels of miR-125a-5p in plasma and reactive oxygen species (ROS) in polymorphonuclear neutrophil leukocytes (P < 0.05). These evidences suggested oxidative stress might be an intermediate between e-waste related POPs exposure and alteration of plasma miRNA.

Exposure to fine and ultrafine particles as well as particulate polycyclic aromatic hydrocarbons (PAHs) by commuters in three transportation modes (walking, subway and bus) were examined in December 2011 in Beijing, China. During the study period, real-time measured median PM2.5 mass concentration (PMC) for walking, riding buses and taking the subway were 26.7, 32.9 and 56.9 mu g m(-3), respectively, and particle number concentrations (PNC) were 1.1 x 10(4), 1.0 x 10(4) and 2.2 x 10(4) cm(-3). Commuters were exposed to higher PNC in air-conditioned buses and aboveground-railway, but higher PMC in underground-subway compared to aboveground-railway. PNC in roadway modes (bus and walking) peaked at noon, but was lower during traffic rush hours, negatively correlated with PMC. Toxic potential of particulate-PAHs estimated based on benzo(a)pyrene toxic equivalents (BaP TEQs) showed that walking pedestrians were subjected to higher BaP TEQs than bus (2.7-fold) and subway (3.6-fold) commuters, though the highest PMC and PNC were observed in subway. (C) 2015 Elsevier Ltd. All rights reserved.

Eighty-seven soil samples collected from North China were analyzed for decabromodiphenyl ethane (DBDPE). The concentrations of DBDPE ranged from undetectable to 1612 ng/g, with the highest concentration present in Shandong. Additionally, the mean concentration of DBDPE in Shandong was found to be onefold higher than those found in Hebei and Shanxi, likely due to DBDPE production in Shandong. Relatively high concentrations of DBDPE in soils were also present in the south of Tianjin, where e-waste recycling may provide a source in this region. The fractions of DBDPE [DBDPE/(DBDPE + BDE209)] were lower than 0.5 in most soil samples, in agreement with the fact that deca-BDE is currently the main additive in brominated flame retardants (BFR) used in China. An obvious decreasing trend in DBDPE concentrations from east to west in North China was noted, with relatively higher DBDPE concentrations present in Shandong. A soil ingestion exposure assessment showed that for most sites, soil ingestion EDI was slightly lower than inhalation EDI; exceptions were found in several polluted sites, where soil ingestion was a more significant exposure route.

Fine particulate matter (PM2.5) is a significant health issue in Chinese megacities. However, little information is available regarding the PM2.5-bound toxic organics, especially their sources, atmospheric transformations, and health implications. In this study, we assessed the levels of polycyclic aromatic hydrocarbons (PAHs) and their nitrated, hydroxylated, and oxygenated derivatives (i.e., NPAHs, OHPAHs, and OPAHs, respectively) in PM2.5 collected in Beijing over a 1year period. The median concentration of 23 PAHs, 15 NPAHs, 16 OHPAHs, and 7 OPAHs in PM2.5 was 53.8, 1.14, 1.40, and 3.62ngm(-3), respectively. Much higher concentrations and mass percentages for all species were observed in the heating season, indicating a higher toxicity of PM2.5 during this period of time. Positive matrix factorization was applied to apportion the sources of PAHs and their derivatives. It was found that traffic emissions in the nonheating season, and coal combustion and biomass burning in the heating season, were the major primary sources of PAHs and their derivatives. Secondary formation, however, contributed significantly to the derivatives of PAHs (especially NPAHs and OPAHs) in the nonheating season, suggesting significant impacts of atmospheric transformation on the toxicity of PM2.5.

The occurrence of polycyclic aromatic hydrocarbons (PAHs) and nitrated derivatives (NPAHs), as well as their transformation may have significant health impacts on humans. To investigate the level, spatial distribution and the transformation process of PAHs and NPAHs in North China, we performed a gridded field passive air sampling campaign in summer of 2011. The median concentration of 25 PAH congeners and 13 NPAHs was 294 ng m(-3) (or 26.7 mu g sample(-1)) and 203 ng sample(-1), respectively. Relative higher level of PAHs in Shanxi Province and NPAHs in megacities was observed. In North China, coal/biomass combustion and photochemical formation was the predominant source of PAHs and NPAHs, respectively. To investigate the relationship between these pollutants, a model incorporating NPAHs, PAHs and NO2 was established, and the result indicated that NO2 will promote the transformation processes from PAHs to NPAHs, which may increase the total toxicity of PAH-NPAH mixtures. (C) 2014 Elsevier Ltd. All rights reserved.

Polycyclic aromatic hydrocarbons (PAHs) belong to a class of ubiquitous pollutants and are possibly associated with adverse health effects. In this study, we aimed to assess PAH exposure by measuring the hydroxylated metabolites (hydroxy-PAHs) in urine samples of a rural population from the North China Plain and to explore the possible associations between PAH exposure and oxidative stress indicated by urinary malondialdehyde (MDA) and 8-hydroxy-2'-deoxyguanosine (8-OHdG). High levels of urinary hydroxy-PAHs were observed, with the geometric mean concentrations of 0.57, 2.2, 5.0, 7.0, and 16.6 mu g g(-1) creatinine for 1-hydroxypyrene, hydroxyphenanthrenes, hydroxyfluorenes, hydroxybiphenyls, and hydroxynaphthalenes, respectively. Particularly in the winter season, the exposures were 2.3-6.0-fold of those in the spring. Corresponding to PAH exposure, levels of urinary MDA were positively associated with hydroxy-PAHs after controlling for confounders in the linear regression models (p < 0.05). An estimation indicated 21.3-39.3 % increment of urinary MDA per one-fold increase of hydroxy-PAHs. In contrast, no significant correlation was found between urinary 8-OHdG and hydroxy-PAHs; alternatively, living at the e-waste recycling site was found a significant factor on this oxidative DNA damage. These results provide evidence on high PAH exposure and the induction of oxidative stress on lipid peroxidation for this rural population.

Electronic waste (e-waste) has created a worldwide environmental and health problem, by generating a diverse group of hazardous compounds such as persistent organic pollutants (POPs). Our previous studies demonstrated that populations from e-waste exposed region have a significantly higher level of chromosomal aberrancy and incidence of DNA damage. In this study, we further demonstrated that various POPs persisted at a significantly higher concentration in the exposed group than those in the unexposed group. The level of reactive oxygen species and micronucleus rate were also significantly elevated in the exposed group. RNA sequencing analysis revealed 31 genes in DNA damage responses and repair pathways that were differentially expressed between the two groups (Log 2 ratio > 1 or < -1). Our data demonstrated that both females and males of the exposed group have activated a series of DNA damage response genes; however many important DNA repair pathways have been dysregulated. Expressions of NEIL1/3 and RPA3, which are critical in initiating base pair and nucleotide excision repairs respectively, have been downregulated in both females and males of the exposed group. In contrast, expression of RNF8, an E3 ligase involved in an error prone non-homologous end joining repair for DNA double strand break, was upregulated in both genders of the exposed group. The other genes appeared to be differentially expressed only when the males or females of the two groups were compared respectively. Importantly, the expression of cell cycle regulatory gene CDC25A that has been implicated in multiple kinds of malignant transformation was significantly upregulated among the exposed males while downregulated among the exposed females. In conclusion, our studies have demonstrated significant correlations between e-waste disposing and POPs accumulation, DNA lesions and dysregulation of multiple DNA damage repair mechanisms in the residents of the e-waste exposed region. (C) 2014 Elsevier Inc. All rights reserved.