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.
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.