PMID: 

Sci Total Environ. 2019 Nov 16 ;706:135522. Epub 2019 Nov 16. PMID: 31864998

Abstract Title: 

Association between air pollutants and development of chronic kidney disease: A systematic review and meta-analysis.

Abstract: 

BACKGROUND: The association between incident chronic kidney disease (CKD) or end-stage renal disease (ESRD) and exposure to outdoor air pollution is under debate. We aimed to examine this relationship based on a systematic review with random-effects meta-analysis.METHODS: We screened the literature on long-term air pollution exposure assessment in the general population using an electronic search of PubMed, Medline, Embase, and Cochrane Library from inception to 20 October 2019. Observational studies investigating the association between long-term exposure to gaseous (CO, SO, NO, O) or particulate (PMor PM) outdoor air pollutants and CKD, ESRD, or renal dysfunction were included, and summary risks were estimated.RESULTS: Of 4419 identified articles, 23 met our inclusion criteria after screening and 14 were included in the meta-analysis. Pooled effect estimates had the following summary risk ratios (RRs) for CKD: 1.10 (95% confidence intervals [CI] 1.00, 1.21; derived from four studies) per 10 μg/mincrease in PMand 1.16 (95% CI 1.05, 1.29; derived from four studies) for PM; 1.31 (95% CI 0.86, 2.00; derived from two studies) per 10 ppm increase in CO; and 1.11 (95% CI 1.09, 1.14; derived from three studies) per 10 ppb increase in NO. For the pooled effect on eGFR, increases in PMand PM(of 10 μg/m) were associated with eGFR decline by -0.83 (95% CI -1.54, -0.12; derived from two studies) and -4.11 (95% CI -12.64, 4.42; derived from two studies) mL/min/1.73 m, respectively.CONCLUSIONS: Air pollution was observed to be associated with CKD and renal function decline. Although more longitudinal studies are required, we argue that air pollution is pernicious to kidney health.

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PMID: 

J Immunol Res. 2019 ;2019:3486841. Epub 2019 Dec 1. PMID: 31871955

Abstract Title: 

PM2.5 Exposure in the Respiratory System Induces Distinct Inflammatory Signaling in the Lung and the Liver of Mice.

Abstract: 

Fine particulate matter 2.5 (PM2.5) is a harmful air pollutant currently threatening public health. Although many studies have been performed on the general negative effects of PM2.5 in mice and humans, the migration patterns of various immune cells in response to PM2.5 exposure remain unclear. In this study, we aimed to investigate the immune cell migratory response in the lung and the liver of intratracheally PM2.5-inoculated mice. To investigate the migration trajectory of immune cells in the lung and the liver tissues of mice, we employed microscopic tools including two-photon intravital imaging, histological analysis, and transmission electron microscopy. Our data from two-photon intravital imaging showed that there was no significant difference in the number of infiltrated neutrophils in the lung and the liver of PM2.5-treated mice, compared to the nontreated condition. However, from the histological analysis and the transmission electron microscopy after vascular perfusion to remove intravascular leukocytes, we observed that some leukocytes were frequently observed in the lung and the liver of PM2.5-treated mice. Interestingly, quantification of leukocyte population using flow cytometry showed significant increase of neutrophils and macrophages in the lung, but not much in the liver, 24 h post-PM2.5 treatment. These data imply that two-photon intravital imaging of the lung and the liver actually visualized neutrophils, which were adherent to the luminal side of the vasculature. We then conducted mRNA microarray analysis to further observe how PM2.5 affects gene expression patterns in the lung and the liver. PM2.5 treatment changed the mRNA expression associated with the IL-17 signaling pathway in the lung and changed the mRNA expression associated with metabolic pathways in the liver. In summary, these results suggest that the immune response in the lung is distinctly regulated from that in the liver under acute PM2.5-induced inflammation and that these organs consequently are regulated via distinct signaling pathways.

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PMID: 

Environ Health Perspect. 2019 Dec ;127(12):127008. Epub 2019 Dec 24. PMID: 31873044

Abstract Title: 

Long-Term Exposure to Ambient Fine Particulate Matter () and Lung Function in Children, Adolescents, and Young Adults: A Longitudinal Cohort Study.

Abstract: 

BACKGROUND: The association between long-term exposure to ambient fine particulate matter with aerodynamic diameter() and lung function in young people remains uncertain, particularly in Asia, where air pollution is generally a serious problem.OBJECTIVES: This study investigated the association between long-term exposure to ambientand lung function in Taiwanese children, adolescents, and young adults.METHODS: This study comprised 24,544 participants 6-24 years of age, with 33,506 medical observations made between 2000 and 2014. We used a spatiotemporal model to estimateconcentrations at participants' addresses. Spirometry parameters, i.e., forced vital capacity (FVC), forced expiratory volume in 1 s (), and maximum midexpiratory flow (MMEF), were determined. A generalized linear mixed model was used to examine the associations between long-term exposure to ambientand lung function. The odds ratios (ORs) of poor lung function were also calculated after adjusting for a range of covariates.RESULTS: Everyincrease in the 2-y averageconcentration was associated with decreases of 2.22% [95% confidence interval (CI):,], 2.94 (95% CI:,), and 2.79% (95% CI:,) in the FVC,, and MMEF, respectively. Furthermore, it was associated with a 20% increase in the prevalence of poor lung function (OR: 1.20; 95% CI: 1.12, 1.29).CONCLUSIONS: Two-year ambientconcentrations were inversely associated with lung function and positively associated with the prevalence of poor lung function in children, adolescents, and young adults in Taiwan. https://ift.tt/2Q6R650.

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PMID: 

Life Sci. 2019 Dec 21:117210. Epub 2019 Dec 21. PMID: 31874166

Abstract Title: 

Exposure to ambient dusty particulate matter impairs spatial memory and hippocampal LTP by increasing brain inflammation and oxidative stress in rats.

Abstract: 

OBJECTIVES: Exposure of healthy subjects to ambient airborne dusty particulate matter (PM) causes brain dysfunction. This study aimed to investigate the effect of sub-chronic inhalation of ambient PM in a designed special chamber to create factual dust storm (DS) conditions on spatial cognition, hippocampal long-term potentiation (LTP), inflammatory cytokines, and oxidative stress in the brain tissue.METHODS: Adult male Wistar rats (250-300 g) were randomly divided into four groups: Sham (clean air, the concentration of dusty PM was

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PMID: 

Sci Total Environ. 2019 Dec 14 ;707:135989. Epub 2019 Dec 14. PMID: 31874395

Abstract Title: 

The acute effects of fine particulate matter constituents on circulating inflammatory biomarkers in healthy adults.

Abstract: 

BACKGROUND: Systemic inflammation is considered one of the key mechanisms in the development of cardiovascular diseases induced by fine particulate matter (PM) air pollution. However, evidence concerning the effects of various PMconstituents on circulating inflammatory biomarkers were limited and inconsistent.OBJECTIVES: To evaluate the associations of short-term exposure to a variety of PMconstituents with circulating inflammatory biomarkers.METHODS: We conducted a panel study from May to October 2016 among 40 healthy adults in Shanghai, China. We monitored the concentrations of 27 constituents of PM. We applied linear mixed-effect models to analyze the associations of PMand its constituents with 7 inflammatory biomarkers, and further assessed the robustness of the associations by fitting models adjusting for PMmass and/or their collinearity. Benjamini-Hochberg false discovery rate was used to correct for multiple comparisons.RESULTS: The associations of PMwere strongest at lag 0 d with tumor necrosis factor-α (TNF-α), at lag 1 d with interleukin-6, interleukin-8, and interleukin-17A, at lag 02 d with monocyte chemoattractant protein-1 (MCP-1) and intercellular adhesion molecule-1 (ICAM-1). After correcting for multiple comparisons in all models, Cl, K, Si, K, As, and Pb were significantly associated with interleukin-8; SOand Se were marginally significantly associated with interleukin-8; SO, As, and Se were marginally significantly associated with TNF-α; and Si, K, Zn, As, Se, and Pb were marginally significantly associated with MCP-1.CONCLUSIONS: Our results suggested that some constituents (SO, Cl, K, and some elements) might be mainly responsible for systemic inflammation triggered by short-term PMexposure.

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PMID: 

Int J Mol Sci. 2019 Dec 24 ;21(1). Epub 2019 Dec 24. PMID: 31878205

Abstract Title: 

Deciphering the Code between Air Pollution and Disease: The Effect of Particulate Matter on Cancer Hallmarks.

Abstract: 

Air pollution has been recognized as a global health problem, causing around 7 million deaths worldwide and representing one of the highest environmental crises that we are now facing. Close to 30% of new lung cancer cases are associated with air pollution, and the impact is more evident in major cities. In this review, we summarize and discuss the evidence regarding the effect of particulate matter (PM) and its impact in carcinogenesis, considering the"hallmarks of cancer"described by Hanahan and Weinberg in 2000 and 2011 as a guide to describing the findings that support the impact of particulate matter during the cancer continuum.

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PMID: 

Am J Cardiol. 2019 Nov 19. Epub 2019 Nov 19. PMID: 31848029

Abstract Title: 

Statin Therapy and Risk of Incident Diabetes Mellitus in Adults With Cardiovascular Risk Factors.

Abstract: 

The association between statins and diabetes mellitus (DM) remains controversial. The Kaiser Permanente CHAMP Study identified adults without DM who had cardiovascular (CV) risk factors and no previous lipid lowering therapy (LLT) between 2008 and 2010. The CV risk factors included known atherosclerotic CV disease (ASCVD), elevated low-density lipoprotein cholesterol≥190 mg/dl, or a low-density lipoprotein cholesterol between 70 and 189 mg/dl and an estimated 10-year ASCVD risk ≥7.5%. Incident DM was defined as ≥2 abnormal tests (i.e., A1C ≥6.5% or a fasting blood glucose ≥126 mg/dl) or ≥1 abnormal test result plus a new diagnostic code or medication for DM. Among 213,289 eligible adults, 28,149 patients initiating statins were carefully matched to an equal number of patients who remained off LLT during follow-up. Compared with matched patients not receiving statins, those initiating statin therapy had the same mean age (67.9 ± 9.4 years) andgender (42.8% women). The crude rate (per 100 person-years) of incident DM was low (0.55, 95% confidence interval [CI] 0.52 to 0.59) but was marginally higher in patients who were treated with a statin (0.69, 95% CI 0.64 to 0.74) versus no LLT (0.42, 95% CI 0.38 to 0.46). After additional adjustment, statin therapy was associated with a modestly increased risk of incident DM (adjusted hazard ratio 1.17, 95% CI 1.02 to 1.34). In conclusion, in adults without DM at increased ASCVD risk, initiation of statin therapy was independently associated with a modestly higher risk of incident DM.

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PMID: 

BMC Gastroenterol. 2019 Dec 18 ;19(1):219. Epub 2019 Dec 18. PMID: 31852444

Abstract Title: 

Effects of alternate-day fasting on body weight and dyslipidaemia in patients with non-alcoholic fatty liver disease: a randomised controlled trial.

Abstract: 

BACKGROUND: Alternate-day fasting (ADF) is a novel diet therapy that may achieve reduction in body weight and improvement of dyslipidaemia, but the impact of this diet on patients with non-alcoholic fatty liver disease (NAFLD) remains unknown. The aim of this study was to evaluate the effects of ADF on the body weight and lipid profile of individuals with NAFLD.METHODS: NAFLD patients (n = 271) were randomised to the ADF group, time-restricted feeding (TRF) group, or the control group and subjected to the respective diet for 12 weeks. Anthropometric measurements (body weight, fat mass/fat-free mass) were performed, and plasma lipids were analysed enzymatically.RESULTS: Within 4 weeks, the body weight decreased significantly (P 

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PMID: 

Environ Int. 2019 Dec 24 ;135:105196. Epub 2019 Dec 24. PMID: 31881430

Abstract Title: 

Exposure to fine particulate matter and temporal dynamics of episodic memory and depressive symptoms in older women.

Abstract: 

BACKGROUND: Emerging data suggests PM(particulate matter with aerodynamic diameter

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PMID: 

Environ Pollut. 2019 Nov 9 ;258:113589. Epub 2019 Nov 9. PMID: 31841764

Abstract Title: 

Effects of ambient particulate matter on fasting blood glucose: A systematic review and meta-analysis.

Abstract: 

Studies have found that ambient particulate matter (PM) affects fasting blood glucose. However, the results are not consistent. We conducted a systematic review and meta-analysis to determine the relationship between PM with an aerodynamic diameter of 10 μm or less (PM) and PM with an aerodynamic diameter of 2.5 μm or less (PM) and fasting blood glucose. We searched PubMed, Web of Science, the Wanfang Database and the China National Knowledge Infrastructure up to April 1, 2019. A total of 24 papers were included in the review, and 17 studies with complete or convertible quantitative information were included in the meta-analysis. The studies were divided into groups by PM size fractions (PMand PM) and length of exposure. Long-term exposures were based on annual average concentrations, and short-term exposures were those lasting less than 28 days. In the long-term exposure group, fasting blood glucose increased 0.10 mmol/L (95% CI: 0.02, 0.17) per 10 μg/mof increased PMand 0.23 mmol/L (95% CI: 0.01, 0.45) per 10 μg/mof increased PM. In the short-term exposure group, fasting blood glucose increased 0.02 mmol/L (95% CI: -0.01, 0.04) per 10 μg/mof increased PMand 0.08 mmol/L (95% CI: 0.04, 0.11) per 10 μg/mof increased PM. Further prospective studies are needed to explore the relationship between ambient PM exposure and fasting blood glucose.

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