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Particulate matter (PM) can damage respiratory system, cardiovascular system, nervous system and immune system, but there are few researches on reproductive damage of particulate matter. The objectives of this study were to investigate the effect of short-term particulate matter 2.5 (PM
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ObjectiveTo explore the effect of Qingfei Jiangmai decoction （QJD） on the content of mercapturic acids in urine in healthy people amid PM2.5 （particles 2.5 microns or less in size） pollution. MethodA total of 84 healthy students of 18-30 years old in Beijing were recruited and they were randomized into the test group （42 in total， with 1 dropout） and control group （42 in total， with 3 dropouts）. During the pollution， the test group and the control group respectively took QJD granules and placebo for 7 days （1 bag/time， 2 times/day）， and another 7-day intervention with the same drugs was performed at an interval of 4 weeks. The time-activity patterns were recorded during the intervention. On-line solid phase extraction-liquid chromatography/tandem mass spectrometry （SPE-LC-MS/MS） was performed to detect the content of PM2.5-related metabolites S-phenylmercapturic acid （SPMA）， 3-hydroxypropylmercapturic acid （3-HPMA）， 3-hydroxy-1-methylpropylmercapturic acid （HMPMA）， N-acetyl-S-（2-nitrile ethyl）-L-cysteine （CEMA）， and N-acetyl-S-（2-hydroxy ethyl）-L-cysteine （HEMA） in urine before and after intervention. Statistical analysis was followed. ResultThe content of CEMA， HEMA， 3-HPMA， and HMPMA in the test group was all higher after the intervention than before the intervention， with the significant difference in HEMA （P<0.05）. After intervention， content of HEMA and SPMA was significantly higher in the test group than in the control group （P<0.05）， and the difference in HEMA （Z=-3.614， P<0.01） and HMPMA （Z=-1.988， P<0.05） before and after invention in the test group was significantly larger than that in the control group. After the intervention， HEMA in the test group was significantly higher than that in the control group （F=7.597， P<0.01）. ConclusionDuring PM2.5 pollution， QJD can increase the excretion of HEMA， a metabolite of ethylene oxide， in the urine of healthy people in Beijing， and enhance the detoxification process of toxic components in PM2.5， which is of great value in preventing and treating haze-related illnesses.
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Exposure to particulate matter 2.5 (PM2.5) potentially triggers airway inflammation by activating nuclear factor-κB (NF-κB). Sirtuin 2 (SIRT2) is a key modulator in inflammation. However, the function and specific mechanisms of SIRT2 in PM2.5-induced airway inflammation are largely understudied. Therefore, this work investigated the mechanisms of SIRT2 in regulating the phosphorylation and acetylation of p65 influenced by PM2.5-induced airway inflammation and bronchial hyperresponsiveness. Results revealed that PM2.5 exposure lowered the expression and activity of SIRT2 in bronchial tissues. Subsequently, SIRT2 impairment promoted the phosphorylation and acetylation of p65 and activated the NF-κB signaling pathway. The activation of p65 triggered airway inflammation, increment of mucus secretion by goblet cells, and acceleration of tracheal stenosis. Meanwhile, p65 phosphorylation and acetylation, airway inflammation, and bronchial hyperresponsiveness were deteriorated in SIRT2 knockout mice exposed to PM2.5. Triptolide (a specific p65 inhibitor) reversed p65 activation and ameliorated PM2.5-induced airway inflammation and bronchial hyperresponsiveness. Our findings provide novel insights into the molecular mechanisms underlying the toxicity of PM2.5 exposure. Triptolide inhibition of p65 phosphorylation and acetylation could be an effective therapeutic approach in averting PM2.5-induced airway inflammation and bronchial hyperresponsiveness.
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Animals , Mice , Inflammation , NF-kappa B/metabolism , Particulate Matter/toxicity , Signal Transduction , Sirtuin 2/metabolism , Transcription Factor RelA/metabolismABSTRACT
Background: Tuberculosis remains a major global health problem with 10.4 million incident cases in 2016. Although Mycobacterium tuberculosis is the causative agent, many environmental factors play a role in disease progression. Several respiratory hazards including smoking and indoor air pollution were suggested to increase the risk of tuberculosis, but only fewer studies has been conducted on the association between ambient air pollution and tuberculosis.Methods: Data on ambient air quality levels (annual mean concentration of particulate matter 2.5 µg/m3) for the year 2016 was collected from the World Health Organization (WHO) data base for 190 countries which comprises of 6 WHO regions. Similarly data on incidence and mortality rate of tuberculosis for the year 2016 was collected for the above countries from the WHO data base. The data were tabulated and statistical analysis was performed using Pearson’s correlation coefficient model to examine the association of annul mean concentration of particulate matter 2.5 with incidence and mortality rates of tuberculosis.Results: Incidence and mortality rates of tuberculosis were found to be increasing with increasing levels of air pollution. It was correlated using scatter plot. Pearson’s correlation coefficient for air pollution level and incidence of tuberculosis was 0.331 (95% CI: 0.435-0.883), (p<0.001), and for tuberculosis mortality was 0.39 (95% CI: 0.525-0.906) (p<0.001).Conclusions: The study suggests there is a significant positive relationship between ambient air pollution level and tuberculosis incidence and mortality rates.
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Objective@#To assess the pollution characteristics and risk assessment of carcinogenicity or non-carcinogenicity on heavy metals in PM2.5 in Shenzhen.@*Methods@#PM2.5 samples were collected monthly from the year of 2014 to 2015, and analyzed by seasons. 12 heavy metal elements (Pb, Hg, Mn, Sb, Al, As, Be, Cd, Cr, Ni, Se, Tl) in PM2.5 were detected by ICP-MS spectrometry. Health risk assessment was conducted using the recommended United States Environmental Protection Agency (USA EPA) model.@*Results@#The median of PM2.5 concentration was 45.10 μg/m3 in Longgang district of Shenzhen. The non-carcinogenecity risks of the metals in PM2.5 existed in spring, autumn and winter (HQ>1). Three metal elements including As, Mn and Cd have higher HQ levels. The carcinogenecity risk levels in four seasons were winter, autumn, spring and summer, respectively. The carcinogenecity risks in four seasons were between 10-6 to 10-4. As, Cr and Cd have higher carcinogenicityrisks.@*Conclusion@#The heavy metals in PM2.5 have both carcinogenecity risk and non-carcinogenecity risk to residents in Longgang district of Shenzhen, the occupational health management must be continuously strengthened, the further research and the measures for prevention and control should be considered.
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Niacinamide (NIA) is a water-soluble vitamin that is widely used in the treatment of skin diseases. Moreover, NIA displays antioxidant effects and helps repair damaged DNA. Recent studies showed that particulate matter 2.5 (PM(2.5)) induced reactive oxygen species (ROS), causing disruption of DNA, lipids, and protein, mitochondrial depolarization, and apoptosis of skin keratinocytes. Here, we investigated the protective effects of NIA on PM(2.5)-induced oxidative stress in human HaCaT keratinocytes. We found that NIA could inhibit the ROS generation induced by PM(2.5), as well block the PM(2.5)-induced oxidation of molecules, such as lipids, proteins, and DNA. Furthermore, NIA alleviated PM(2.5)-induced accumulation of cellular Ca²⁺, which caused cell membrane depolarization and apoptosis, and reduced the number of apoptotic cells. Collectively, the findings show that NIA can protect keratinocytes from PM(2.5)-induced oxidative stress and cell damage.
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Humans , Antioxidants , Apoptosis , Cell Membrane , DNA , Keratinocytes , Mitochondrial Proteins , Niacinamide , Oxidative Stress , Particulate Matter , Reactive Oxygen Species , Skin Diseases , Skin , VitaminsABSTRACT
Purpurogallin, a natural phenol obtained from oak nutgalls, has been shown to possess antioxidant, anticancer, and anti-inflammatory effects. Recently, in addition to ultraviolet B (UVB) radiation that induces cell apoptosis via oxidative stress, particulate matter 2.5 (PM(2.5)) was shown to trigger excessive production of reactive oxygen species. In this study, we observed that UVB radiation and PM(2.5) severely damaged human HaCaT keratinocytes, disrupting cellular DNA, lipids, and proteins and causing mitochondrial depolarization. Purpurogallin protected HaCaT cells from apoptosis induced by UVB radiation and/or PM(2.5). Furthermore, purpurogallin effectively modulates the pro-apoptotic and anti-apoptotic proteins under UVB irradiation via caspase signaling pathways. Additionally, purpurogallin reduced apoptosis via MAPK signaling pathways, as demonstrated using MAPK-p38, ERK, and JNK inhibitors. These results indicate that purpurogallin possesses antioxidant effects and protects cells from damage and apoptosis induced by UVB radiation and PM(2.5).
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Humans , Antioxidants , Apoptosis Regulatory Proteins , Apoptosis , DNA , Keratinocytes , Oxidative Stress , Particulate Matter , Phenol , Reactive Oxygen SpeciesABSTRACT
Particulate matter (PM) researches have long been focused on cardiovascular and puhnonary systems,however,several increasing evidences have showed that PM may be deleterious to human brain development as well.Recently,some studies showed that PM had strongly associated with autism spectrum disorder (ASD) especially PM2.5.Now,the epidemiological and clinical studies on the relationship between ASD and exposure to PM were conducted,expect to be helpful for future ASD etiology research,furthermore to formulate appropriate public policy.
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Objective To explore the role of the transcriptional factor activator protein (AP)-1 in mediating vascular endothelial growth factor ( VEGF) expression in human bronchial epithelial cells exposed to PM 2.5.Methods Beas-2B cells was treated with PM2.5.Luciferase assay was used to detect the activation status of AP-1 and transcription of VEGF in the Beas-2B cells.The induced activation of c-Jun, ATF2 and VEGF expression was tested by Western blotting assay.Results PM2.5 induced transactivation of the transcriptional factor AP-1, accompanied by phosphorylation of the AP-1 components, c-Jun and ATF2 in Beas-2B cells.Moreover, when AP-1 activation was inhibited by knocking down c-Jun or ATF2 expressions, induction of VEGF expression was partially attenuated in Beas-2B cells.Conclusion AP-1 is a critical transcriptional factor in mediating PM2.5-induced VEGF expression and inflammatory responses in human bronchial epithelial cells.
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A thermal desorption ( TD) device was developed and coupled to gas chromatography ( GC) or gas chromatography-mass spectrometry ( GC-MS ) for the qualitative and quantitative analysis of semi-volatile organic compounds on atmospheric particulate matters ( PM ) . The TD was operated by direct heating and placed on the GC injector, leading to high heating rate and easy transfer of analytes to GC without focusing of analytes by cold trap. For establishing the TD-GC method, the materials used for supporting PM samples, temperature and time of thermal desorption, and types of sample injection were investigated for detection of sixteen polycyclic aromatic hydrocarbons ( PAHs) and nine n-alkanes. The limits of detection of the proposed TD-GC method were in the range of 0. 014-0. 093 ng for PAHs, and 0. 016-0. 026 ng for n-alkanes, respectively, with the correlation coefficients of correlation above 0. 9975. The TD-GC method was applied to the determination of trace PAHs and n-alkanes on PM10 samples from three cities. The recoveries were in the range of 95%-135% ( PAHs) and 95%-115% ( n-alkanes) , respectively. Finally, the TD was coupled to GC-MS for comparison of the contents of PAHs and n-alkanes on PMx with different particulate size ( x=10 , 5, 2, 1, 0. 5, 0. 25, 0. 1).
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INTRODUÇÃO: A poluição em centros urbanos é produzida, principalmente, pela queima de combustíveis fósseis. Constitui problema que afeta a saúde da população, provocando doenças tanto no sistema respiratório, como sistemicamente em vários órgãos. Dentre as funções afetadas, realça o impacto da poluição sobre o sistema endócrino, podendo acometer as adrenais, tanto, no ser humano, como em roedores. Todavia, pouco se conhece sobre a ação nesta glândula. Assim, propusemo-nos a analisar os efeitos do ar poluído sobre as adrenais em duas gerações consecutivas de camundongas. OBJETIVOS: Analisar os efeitos do ar concentrado com material particulado (MP) 2,5um sobre as adrenais, avaliando as alterações histomorfométricas; a angiogênese pelo fator de crescimento vascular endotelial (VEGF-A); a pela proliferação celular por meio da proteína Ki-67 e o índice de apoptose pela caspase 3-clivada nas três zonas do córtex da adrenal. MATERIAL E MÉTODOS: Utilizaram-se 20 camundongas alocadas em biotério livre de poluentes, as quais foram acasalados na proporção de um macho para duas fêmeas. Após confirmação da cópula, foram divididas em 2 grupos de 10 animais cada. Acondicionou-se um grupo diariamente em uma câmara, onde as camundongas foram expostas a MP 2,5um à concentração de 600ug/m³ (G0P). O outro grupo, com 10 animais, foi alocado em outra câmara com ar filtrado (G0NP). A exposição ocorreu diariamente durante toda a prenhez das camundongas. Ao nascimento os conceptos, foram amamentados por 30 dias em amamentação, período onde não houve exposição aos poluentes. Após este período, as mães foram eutanasiadas para coleta das adrenais e as filhas sofreram o mesmo protocolo de exposição (G1P e G1NP - submetidas e não submetidas à poluição), não foram acasaladas, sendo eutanasiadas para coleta das adrenais ao fim do protocolo. As adrenais passaram por processamento histológico para coloração de H.E. e imunoistoquímico. RESULTADOS: As adrenais do grupo...
INTRODUCTION: The pollution in urban centers is produced mainly by the burning of fossil fuels. It's a concern of public health, causing diseases in both the respiratory system and the other organs. Among the affected functions, it is important to highlight the impact of pollution on the endocrine system and this effect on the adrenal glands, both in humans and in rodents. However, little is known on the action of pollutants on this gland. Therefore, the aim of this study was to analyze the effects of polluted air on the adrenal in two consecutive generations of female mice. OBJECTIVES: To assess the effects of concentrate air with particulate matter (PM) 2.5um on the adrenal cortex evaluating histomorphometric changes; angiogenesis by vascular endothelial growth factor (VEGF-A); the cell proliferation by Ki-67 index and apoptosis by cleaved caspase-3 in the three zones of the adrenal cortex. MATERIAL AND METHODS: We used 20 female mice in their cages free of pollutants. Those animals were mated at a ratio of one male to two females. After mating confirmation, animals were divided into 2 groups of 10 animals each. A group was daily allocated in a chamber where the female mice were exposed to PM 2.5um at a concentration of 600ug/m³ (G0P). The other group of 10 animals was allocated in another chamber with filtered air (G0NP). The exposure occurred daily throughout pregnancy period. At birth, the fetuses were breastfed for 30 days. During breastfeeding period there was no pollutants exposure. After this period, mothers were euthanized for adrenal collection and daughters suffered the same exposure protocol (G1P and G1NP - exposed and not exposed to pollution), but those were not mated, being euthanized for adrenal collection at the end of the protocol. The adrenal underwent histological processing for H.E. staining and immunohistochemistry. RESULTS: The adrenal of the G0P group had increased thickness of the zona glomerulosa and the G1P presented...
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Animals , Female , Mice , Adrenal Glands , Air Pollution , Apoptosis , Histology , Mice , Particulate Matter , Cell ProliferationABSTRACT
Accurate estimation of the exposure-response relationship between ambient urban particulate matters (PM) and public health is important for regulatory perspective of ambient urban particulate matters (PM). Ambient PM contains various transition metals and organic compounds. PM10 (aerodynamic diameter less than 10 microgram) is known to induce diverse diseases such as chronic cough, bronchitis, chest illness, etc. However, recent evaluation of PM2.5 (aerodynamic diameter less than 2.5 microgram) against health outcomes has suggested that the fine particles may be more closely associated with adverse respiratory health effects than particles of larger size. This study was performed to evaluate PM2.5-induced oxidative stress in rat lung epithelial cell in order to provide basic data for the risk assessment of PM2.5. PM2.5 showed higher cytotoxicity than PM10. Also, PM 2.5 induced more malondialdehyde (MDA) formation than PM10. In Hoechst 33258 dye staining and DNA fragmentation assay, apopotic changes were clearly detected in PM2.5 treated cells in compared to PM10. Expression of catalase mRNA was increased by PM2.5 rather than PM10. PM2.5 induced higher Mth1 mRNA than PM10. In pBR322 DNA treated with PM2.5, production of single strand breakage of DNA was higher than that of PM10. In Western blot analysis, PM2.5 induced more Nrf-2 protein, associated with diverse transcriptional and anti-oxidative stress enzymes, compared to PM10. Our data suggest that PM2.5 rather than PM10 may be responsible for PM-induced toxicity. Additional efforts are needed to establish the environmental standard of PM2.5.