PMID: 

Hypertension. 2019 Dec ;74(6):1349-1356. Epub 2019 Oct 21. PMID: 31630576

Abstract Title: 

Acute Effects of High-Level PMExposure on Central Blood Pressure.

Abstract: 

Central aortic blood pressure (BP) has been increasingly recognized as having a closer relationship with cardiovascular risks than peripheral BP. However, the effects of particulate matter pollution on central aortic BP have not been clearly demonstrated. In this study, we assessed the association between short-term ambient fine particulate matter (with an aerodynamic diameter≤2.5 μm; PM) exposure and central aortic BP in a Chinese community-based population. A total of 4715 visits were in our final analysis, including 2151 visits at the baseline and 2564 visits at the follow-up. Central aortic systolic BP (cSBP) was measured noninvasively using the method of radial artery tonometry with Omron HEM-9000AI machine. Data from air pollution monitoring stations were used to estimate daily PMexposure. Generalized additive mixed models with clinical and meteorologic covariates adjusted were used to examine the association between PMexposure and cSBP. The relationships between PMexposure and cSBP were nonlinear, and significant increments of cSBP were observed when the PMexposure concentration was above 100μg/cm. An interquartile range increase (80.25μg/m) in daily PMon the day of cSBP measurement (lag 0 day) was associated with 2.54 mm Hg (95% CI, 0.92-4.16) elevation in cSBP. The associations of PMwith cSBP were not modified by age, sex, body mass index, medications, and comorbid diseases except for cardiovascular disease. Our findings demonstrated that short-term exposure to high concentration of ambient PMabove 100μg/cmwas associated with significant increases in central aortic BP in a Chinese community-based population.

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PMID: 

BMJ. 2012 Oct 9 ;345:e6743. Epub 2012 Oct 9. PMID: 23047970

Abstract Title: 

The absence of an independent inquiry into the Wakefield case is a lost opportunity.

Abstract: 

[n/a]

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PMID: 

Environ Int. 2019 12 ;133(Pt B):105205. Epub 2019 Oct 19. PMID: 31639600

Abstract Title: 

Is long-term exposure to air pollution associated with poor sleep quality in rural China?

Abstract: 

BACKGROUND: Poor sleep quality is associated with poor quality of life and may even lead to mental illnesses. Several studies have indicated the association between exposure to air pollution and sleep quality. However, the evidence is very limited in China, especially in rural areas.METHODS: Participants in this study were obtained from the Henan Rural Cohort established during 2015-2017. Sleep quality was evaluated using the Pittsburgh Sleep Quality Index (PSQI) in the baseline survey. Poor sleep quality was defined by the global score of PSQI > 5. Participants' exposures to PM, PM(particulate matter with aerodynamic diameters≤2.5 μm and 10 μm, respectively) and NO(nitrogen dioxide) during the three years before the baseline survey were estimated using a satellite-based prediction. The associations between long-term exposure to air pollutants and sleep quality were examined using both the linear regression and logistic regression models.RESULTS: The IQRs (interquartile range) of mean levels of participants' exposures to PM, PMand NOwere 3.3 µg/m, 8.8 µg/m, and 4.8 µg/m, respectively. After adjusted for potential confounders, the global score of PSQI (and 95%CI, 95% confidence intervals) increased by 0.16 (0.04, 0.27), 0.09 (-0.01, 0.19) and 0.14 (0.03, 0.24), associated with per IQR increase in PM, PMand NO, respectively. The odds ratios (and 95%CI) of poor sleep quality associated with per IQR increase in PM, PMand NOwere 1.15 (1.03, 1.29), 1.11 (1.02, 1.21) and 1.14 (1.03, 1.25), respectively.CONCLUSIONS: Long-term exposures to PM, PMand NOwere associated with poor sleep quality in rural China. Improvement of air quality may help to improve sleep quality among rural population of China.

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PMID: 

BMJ. 2012 Sep 14 ;345:e6220. Epub 2012 Sep 14. PMID: 22983630

Abstract Title: 

University College London issues new research standards but says it won't investigate Wakefield.

Abstract: 

University College London has updated its mechanisms for safeguarding research participants and ensuring the quality and ethical standards of its research. In doing so it has taken account of lessons learnt from the case of Andrew Wakefield, whose research into a possible link between the measles, mumps, and rubella (MMR) vaccine and autism led to him being struck off the UK medical register. But it says it will not investigate the Wakefield case further, despite calls from the BMJ to do so.

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PMID: 

J Allergy Clin Immunol. 2019 Oct 21. Epub 2019 Oct 21. PMID: 31647966

Abstract Title: 

Particulate matter of 2.5μm or less in diameter disturbs the balance of T17/regulatory T cells by targeting glutamate oxaloacetate transaminase 1 and hypoxia-inducible factor 1α in an asthma model.

Abstract: 

BACKGROUND: Epidemiologic evidence suggests that exposure to particulate matter of 2.5μm or less in diameter (PM2.5) aggravates asthma.OBJECTIVE: We sought to investigate the underlying mechanisms between PM2.5 exposure and asthma severity.METHODS: The relationship between PM2.5 exposure and asthma severity was investigated in an asthma model with CD4T cell-specific aryl hydrocarbon receptor (AhR)-null mice. Effects of PM2.5 and polycyclic aromatic hydrocarbons (PAHs) on differentiation of T17/regulatory T (Treg) cells were investigated by using flow cytometry and quantitative RT-PCR. Mechanisms were investigated by using mRNA sequencing, chromatin immunoprecipitation, bisulfite sequencing, and glycolysis rates.RESULTS: PM2.5 impaired differentiation of Treg cells, promoted differentiation of T17 cells, and aggravated asthma in an AhR-dependent manner. PM2.5 and one of its prominent PAHs, indeno[1,2,3-cd]pyrene (IP), promoted differentiation of T17 cells by upregulating hypoxia-inducible factor 1α expression and enhancing glycolysis through AhRs. Exposure to PM2.5 and IP enhanced glutamate oxaloacetate transaminase 1 (Got1) expression through AhRs and accumulation of 2-hydroxyglutarate, which inhibited ten-eleven translocation methylcytosine dioxygenase 2 activity, resulting in hypermethylation in the forkhead box P3 locus and impaired differentiation of Treg cells. A GOT1 inhibitor, (aminooxy)acetic acid, ameliorated asthma by shifting differentiation of T17 cells to Treg cells. Similar regulatory effects of exposure to PM2.5 or IP on T17/Treg cell imbalance were noted in human T cells, and in a case-control design PAH exposure appeared to be a potential risk factor for asthma.CONCLUSIONS: The AhR-hypoxia-inducible factor 1α and AhR-GOT1 molecular pathways mediate pulmonary responses on exposure to PM2.5 through their ability to disturb the balance of T17/Treg cells.

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PMID: 

Haematologica. 2019 Dec ;104(12):2349-2357. Epub 2019 Oct 31. PMID: 31672903

Abstract Title: 

Novel evidence for a greater burden of ambient air pollution on cardiovascular disease.

Abstract: 

Ambient and household air pollution is a major health problem worldwide, contributing annually to approximately seven million of all-cause avoidable deaths, shorter life expectancy, and significant direct and indirect costs for the community. Air pollution is a complex mixture of gaseous and particulate materials that vary depending on their source and physicochemical features. Each material has detrimental effects on human health, but a number of experimental and clinical studies have shown a strong impact for fine particulate matter (PM). In particular, there is more and more evidence that PMexerts adverse effects particularly on the cardiovascular system, contributing substantially (mainly through mechanisms of atherosclerosis, thrombosis and inflammation) to coronary artery and cerebrovascular disease, but also to heart failure, hypertension, diabetes and cardiac arrhythmias. In this review, we summarize knowledge on the mechanisms and magnitude of the cardiovascular adverse effects of short-and long-term exposure to ambient air pollution, particularly for the PMsize fraction. We also emphasize that very recent data indicate that the global mortality and morbidity burden of cardiovascular disease associated with this air pollutant is dramatically greater than what has been thought up to now.

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PMID: 

Clin Sci (Lond). 2019 Nov 15 ;133(21):2171-2187. PMID: 31696218

Abstract Title: 

Particulate matter exposure aggravates osteoarthritis severity.

Abstract: 

Several diseases have been linked to particulate matter (PM) exposure. Outdoor activities, such as road running or jogging, are popular aerobic exercises due to few participatory limitations. Osteoarthritis (OA) is a progressive degenerative joint disease, usually observed at age 40, and not noticed before pain or diagnosis. Although exercise has health benefits, it is unclear whether outdoor jogging in higher PM (standard reference material 1649b, SRM 1649b) concentration environments could affect OA development or severity. Hence, a PM exposure monosodium iodoacetate (MIA)-induced OA animal jogged model was established for investigation. Results showed that high doses of PM (5 mg) significantly increased pro-inflammatory factors such as tumor necrosis factorα (TNF-α), interleukin (IL)-1β, and IL-6, and M1 macrophages in the lung region, also obtained in systemic IL-6 and TNF-α expressions in this MIA-OA rat model. Moreover, levels of osteocalcin, cartilage oligomeric matrix protein (COMP), and N-telopeptides of type I collagen were especially influenced in MIA+PM groups. Morphological and structural changes of the knee joint were detected by micro-computed tomography images (micro-CT) and immunohistochemistry. MIA + PM rats exhibited severe bone density decrease, cartilage wear, and structure damages, accompanied by lower levels of physical activity, than the sham group and groups receiving MIA or PM alone. The findings suggest that the severity of OA could be promoted by PM exposure with a PM concentration effect via systemic inflammatory mechanisms. To the best of our knowledge, this is the first study to provide direct effects of PMexposure on OA severity.

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PMID: 

Zhongguo Ying Yong Sheng Li Xue Za Zhi. 2019 Jul 28 ;35(4):293-296. PMID: 31701708

Abstract Title: 

[The protective effects of vitamin E on lung injury caused by high temperature and PMin COPD rats].

Abstract: 

OBJECTIVE: To investigate the effects of vitamin E on the respiratory function impairment in rats with chronic obstructive pulmonary disease (COPD) after exposed to high temperature and PM.METHODS: Fifty-four 7-week-old SPF male Wistar rats were randomly divided into 9 experimental groups (n=6). The rat COPD model was established by lipopolysaccharide (LPS) and smoke exposure. After modeled, the rats were tracheal instilled with PM(0 mg/ml, 3.2 mg/ml) and intraperitoneally injected with vitamin E at the dose of 40 mg/kg (20 mg/ml). Part of rats (high temperature groups) were then exposed to high temperature (40℃), once (8 h) a day for three consecutive days. After the last exposure, the lung function of rats was detected. The expression levels of inducible nitric oxide synthase (iNOS), tumor necrosis factor-α (TNF-α) and monocyte chemotactic protein-1 (MCP-1) were detected by corresponding ELISA kits.RESULTS: Compared with the control group, exposure of high temperature and PMcould inhibit the lung function of COPD rats significantly (P＜0.05); the level of MCP-1 was increased significantly in PM-exposure groups (P＜0.05); iNOS was increased significantly in the groups of high temperature (P＜0.05). Compared with the single-PMexposure groups, TNF-α in lung was decreased in the normal temperature health group and high temperature COPD group (P＜0.05) after treated with vitamin E; MCP-1 was decreased in all vitamin E-treated groups (P＜0.05); the decreased iNOS only appeared in the group of high temperature with vitamin E treatment.CONCLUSION: High temperature and PMcould aggravate the inflammation of COPD rats. As an antioxidant, vitamin E may protect the lung from the damage effects.

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PMID: 

BMC Public Health. 2019 Nov 9 ;19(1):1496. Epub 2019 Nov 9. PMID: 31706295

Abstract Title: 

Associations between ambient air pollution and cancer incidence in Taiwan: an ecological study of geographical variations.

Abstract: 

BACKGROUND: Air pollution is a global public health concern. The World Health Organization has recently set up a goal of saving 7 million people globally by 2030 from air pollution related death. We conducted an ecological study of geographical variation to explore the association between air pollution (specifically, particulate matter

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PMID: 

Brain Behav. 2019 Dec ;9(12):e01453. Epub 2019 Nov 11. PMID: 31709780

Abstract Title: 

Effects of early postnatal exposure to fine particulate matter on emotional and cognitive development and structural synaptic plasticity in immature and mature rats.

Abstract: 

INTRODUCTION: Fine particulate matter (PM2.5) is closely associated with many neurological disorders including neurodegenerative disease, stroke, and brain tumors. However, the toxic effects of PM2.5 on neurodevelopment remain unclear. In this study, we aimed to determine the neurotoxic effects of early postnatal exposure to PM2.5 in immature and mature rats.METHODS: We exposed neonatal rats to PM2.5 (2 or 10 mg/kg body weight) through intranasal instillation from postnatal day (PND) 3-15, once a day. Emotional and cognitive development were evaluated using the elevated plus maze, forced swimming, and Morris water maze tests. Hippocampal tissue was collected and subjected to transmission electron microscopy observation and western blot analysis.RESULTS: Rats had lower body weight after exposure to high dose of PM2.5. The behavioral test results indicated that high-dose PM2.5 exposure led to increased anxiety-like symptoms in immature and mature rats, apparent depressive-like behaviors in mature rats, and impaired spatial learning and memory abilities in immature rats, and low-dose PM2.5 exposure increased anxiety-like behaviors in immature rats. Further, high-dose PM2.5 exposure contributed to fewer synapses, thinner postsynaptic density, and shorter active zone in immature and mature rats, and also decreased expressions of synaptophysin (SYP), growth associated protein-43 (GAP43), and postsynaptic density-95 (PSD95) in immature rats, SYP and PSD95 in mature rats. Moreover, low-dose PM2.5 exposure diminished the expression of PSD95 in immature rats. In addition, high-dose PM2.5 exposure reduced brain-derived neurotrophic factor (BDNF) expression and cAMP response element binding protein (CREB) phosphorylation in both immature and mature rats, and low-dose PM2.5 exposure lessened BDNF expression and CREB phosphorylation in immature rats.CONCLUSIONS: Our findings indicate that PM2.5 impairs emotional and cognitive development by disrupting structural synaptic plasticity, possibly via the CREB/BDNF signaling pathway.

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