Epidermis ; Humans ; Hyperpigmentation ; Keratinocytes ; Particulate Matter/toxicity*

Air Pollutants ; toxicity ; China ; epidemiology ; Cities ; Humans ; Mortality ; Particulate Matter ; toxicity

Ambient fine particulate matters (PM_2.5) refer to particulate matters with an aerodynamic diameter less than or equal to 2.5 μm. PM_2.5 enter the body through the target organ-lung, and can induce a variety of adverse health effects (such as cardiovascular diseases, diabetes, respiratory diseases, neurodegenerative diseases and adverse birth outcomes). PM_2.5 are known to have complex compositions (including water-soluble/-insoluble components and biological components), diverse sources and capacity of secondary transformation. Numerous epidemiological and toxicological studies indicated that different components of PM_2.5 may induce adverse health effects through different biological mechanisms. In adddition, co-exposure of different components and their interaction should also be considered. Thus here we have systematically reviewed studies in recent years about the toxicological effects and underlying mechanisms of different components of ambient fine particulate matters, including inflammatory response, oxidative stress, endoplasmic reticulum stress, activation of the NF-κB signaling pathway and so on. The information may give some insights into the prevention and treatment of adverse health effects caused by exposure to different components of PM_2.5.
Air Pollutants/toxicity* ; Cardiovascular Diseases/chemically induced* ; Humans ; Lung ; Oxidative Stress ; Particulate Matter/toxicity*

Recently, the International Agency for Research on Cancer (IARC) has classified outdoor air pollution and the particulate matter component of outdoor air pollution as class I carcinogen. Air pollution is consistently associated with lung cancer in epidemiologic and experimental studies. The IARC assessment is specifically designed as hazard identification, and it does not quantify the magnitude of the cancer risk. This article addresses the magnitude of the lung cancer risk in the population due to ambient air pollution exposure.
Air Pollutants ; toxicity ; Air Pollution ; adverse effects ; Carcinogens, Environmental ; toxicity ; Humans ; Lung Neoplasms ; etiology ; Particulate Matter ; toxicity ; Risk Factors

Objective: To reveal the crucial toxic components of ambient fine particles (PM_2.5) that affect the maturation and differentiation of megakaryocytes. Methods: Human megakaryocytes were exposed to the organic fractions, metallic fractions and water-soluble fractions of PM_2.5 at two exposure doses (i.e. actual air proportion concentration or the same concentration), respectively. The cell viability was performed to screen the non-cytotoxic levels of toxic components of PM_2.5 using the CCK-8 assay. CellTiter-Blue assay, morphological observation, flow cytometry analysis and WGA staining assay were used to evaluate the cell morphological changes, occurrence of DNA ploidy, alteration in the expressions of biomarkers and platelet formation, which were key indicators of the maturation and differentiation of megakaryocytes. Results: Compared to the control group, both metallic and organic components of PM_2.5 resulted in a lag in megakaryocytes with an increase in cell volume and the onset of DNA ploidy. Flow cytometry analysis showed that CD33 (the marker of myeloid-specific) decreased and CD41a (a megakaryocyte maturation-associated antigen) increased in metallic and organic components of PM_2.5 treatment groups. Moreover, compared to the control group, budding protrusions increased in metallic and organic components of PM_2.5 treatment groups. The water-soluble components had no effect on the maturation and differentiation of macrophages. Conclusion: Metallic and organic components of PM_2.5 are the crucial toxic components that promote the maturation and differentiation of megakaryocytes.
Biomarkers ; DNA/pharmacology* ; Humans ; Megakaryocytes/chemistry* ; Particulate Matter/toxicity* ; Sincalide/pharmacology* ; Water/pharmacology*

OBJECTIVE: To investigate the toxic damage and possible mechanism of chronic exposure of ambient particulate matter (PM METHODS: Mice were treated with different doses (150, 300, 600 mg/kg) of chitosan after exposure to PM RESULTS: Compared with the mice in control group, IL-2 secretion and CXCL12 expression were decreased in the bone marrow of PM CONCLUSION Chronic exposure of PM
Animals ; Bone Marrow ; Chitosan ; Hematopoietic Stem Cell Transplantation ; Hematopoietic System ; Mice ; Particulate Matter/toxicity*

Air pollution in China comes from multiple sources, including coal consumption, construction and industrial dust, and vehicle exhaust. Coal consumption in particular directly determines the emissions of three major air pollutants: dust, sulfur dioxide (SO(2)), and nitrogen oxide (NOx). The rapidly increasing number of civilian vehicles is expected to bring NOx emission to a very high level. Contrary to expectations, however, existing data show that the concentrations of major pollutants [particulate matter-10 (PM10), SO(2), and nitrogen dioxide (NO(2))] in several large Chinese cities have declined during the past decades, though they still exceed the national standards of ambient air quality. Archived data from China does not fully support that the concentrations of pollutants directly depend on local emissions, but this is likely due to inaccurate measurement of pollutants. Analyses on the cancer registry data show that cancer burden related to air pollution is on the rise in China and will likely increase further, but there is a lack of data to accurately predict the cancer burden. Past experience from other countries has sounded alarm of the link between air pollution and cancer. The quantitative association requires dedicated research as well as establishment of needed monitoring infrastructures and cancer registries. The air pollution-cancer link is a serious public health issue that needs urgent investigation.
Air Pollutants ; toxicity ; Air Pollution ; adverse effects ; Carcinogens, Environmental ; toxicity ; China ; Coal ; Humans ; Neoplasms ; etiology ; Nitrogen Dioxide ; toxicity ; Particulate Matter ; toxicity ; Sulfur Dioxide ; toxicity ; Vehicle Emissions ; toxicity

Objective: To screen the differential methylation sites, genes and pathways of air pollution fine particles (PM(2.5)) on human bronchial epithelial (HBE) cells by methylation chip and bioinformation technology, so as to provide scientific basis for further study of the toxicological mechanism of PM(2.5) on HBE cells. Methods: In August 2020, HBE cells were infected with 10 μg/ml and 50 μg/ml PM(2.5) aqueous solution for 24 h, namely PM(2.5) 10 μg/ml exposure group (low dose group) and PM(2.5) 50 μg/ml exposure group (high dose group) ; uninfected HBE cells were used as control group. The DNA fragments were hybridized with the chip, the chip scanned and read the data, analyzed the data, screened the differential methylation sites, carried out GO analysis and KEGG analysis of the differential methylation sites, and analyzed the interaction relationship of the overall differential methylation sites by functional epigenetic modules (FEMs). Results: Compared with the control group, 127 differential methylation sites were screened in the low-dose group, including 89 genes, including 55 sites with increased methylation level and 72 sites with decreased methylation level. The differential methylation sites were mainly concentrated in the Body region and UTR region. Compared with the control group, 238 differential methylation sites were screened in the high-dose group, including 168 genes, of which 127 sites had increased methylation level and 111 sites had decreased methylation level. The differential heterotopic sites were mainly concentrated in the Body region and UTR region. Through FEMs analysis, 8 genes with the most interaction were screened, of which 6 genes had significant changes in methylation level. MALT1 gene related to apoptosis was found in the heterotopic site of methylation difference in low-dose group; PIK3CA and ARID1A genes related to carcinogenesis were found in the heterotopic sites of methylation difference in high-dose group; TNF genes related to tumor inhibition were found in the results of FEMs analysis. Conclusion: After PM(2.5) exposure to HBE cells, the DNA methylation level is significantly changed, and genes related to apoptosis and carcinogenesis are screened out, suggesting that the carcinogenic mutagenic effect of PM(2.5) may be related to DNA methylation.
Air Pollutants/toxicity* ; Basic Helix-Loop-Helix Transcription Factors/analysis* ; Carcinogenesis ; DNA Methylation ; Humans ; Particulate Matter/toxicity* ; Technology

OBJECTIVETo study the genotoxicity of components of diesel engine exhausts with ethanol-diesel blending fuel. To provide scientific arguments to find more economical and less polluted fuels.

METHODSAmes test, comet assay and GC-MS technique were used to test the genotoxicity and 16 kinds of PAHs on diesel engine exhausts with different proportions of ethanol (E0, E5, E10, E20).

RESULTSBoth Ames test and comet assay were positive. It shows that diesel engine exhausts can lead to mutation and DNA damage, especially in pure diesel oil. But the content of 16 kinds of PAHs and DNA damage level decreased in exhausts of E5. With the increase of ethanol proportion in diesel oil, the content of 16 kinds of PAHs and DNA damage level increased.

CONCLUSIONCompared with pure diesel oil and high proportion of ethanol fuel, E5 can reduce the genotoxicity and the brake specific exhausts of PAHs.

Air Pollutants ; toxicity ; Air Pollution ; Carbon Monoxide ; Comet Assay ; DNA Damage ; Ethanol ; toxicity ; Gasoline ; toxicity ; Mutagenicity Tests ; Particulate Matter ; Vehicle Emissions ; toxicity

Objective: Fine particulate matter (PM _2.5) is an air pollutant that has become of great concern in recent years. Numerous studies have found that PM _2.5 may contribute to lung cancer, but the pathogenesis has not yet been fully elucidated. In this study, we explored the roles of exosomes from bronchial epithelial cells in PM _2.5-promoted lung cancer metastasis. Methods: Exosomes were isolated from cell supernatants. An animal model of lung metastasis (established by tail vein injection of A549-luc) and in vitro studies with lung cancer cell lines were used to investigate the effects of exosomes derived from PM _2.5-treated human bronchial epithelial cells (PHBE-exo). Results: The animal experiments revealed that PHBE-exo-treated mice showed stronger luciferase activity and a larger relative metastatic region in the lungs, thus indicating that PHBE-exo promoted the metastatic potential of lung cancer. Additionally, PHBE-exo promoted the migration, invasion and epithelial-to-mesenchymal transition of lung cancer cells, in a manner mediated by activation of c-Jun N-terminal kinase. Conclusion These results implied that PM _2.5 may promote the development of lung cancer through exosomes derived from bronchial epithelial cells, thus providing a potential interventional target for lung cancer. These findings broadened our understanding of cancer-promoting mechanisms of environmental pollutants.
Animals ; Epithelial Cells/metabolism* ; Epithelial-Mesenchymal Transition ; Exosomes/metabolism* ; Humans ; Lung Neoplasms/metabolism* ; Mice ; Particulate Matter/toxicity*