Tropospheric ozone

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Petr75
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Re: Tropospheric ozone

Post by Petr75 » Wed Jul 03, 2019 8:33 am

2019 May 28
Department of Otolaryngology-Head and Neck Surgery, Capital Institute of Pediatrics, Beijing, China
Pediatric Epistaxis and Its Correlation Between Air Pollutants in Beijing From 2014 to 2017
https://www.ncbi.nlm.nih.gov/pubmed/31138029

Abstract
BACKGROUND:
Epistaxis is a common symptom in children. The effect of air pollution on epistaxis is not yet clear.
OBJECTIVES:
To explore the characteristics of pediatric epistaxis in Beijing and its correlation with air pollutants.
MATERIAL AND METHODS:
Data were collected from 2014 to 2017 in Otolaryngology Department of Capital Institute of Pediatrics. Children diagnosed with epistaxis with relevant information with the same period of municipal air pollutants' concentration were compared.
RESULTS:
The annual visits of epistaxis showed a bimodal trend. The incidence of epistaxis in infants was low, increased with age, reached the peak between the ages of 4 to 5, and then gradually decreased with age. In different age groups, male patients were more than females. From 2014 to 2017 in Beijing, particulate matter less than 2.5 μm in diameter (PM2.5), particulate matter less than 10 μm in diameter (PM10), sulfur dioxide (SO2), nitrogen dioxide (NO2), and carbon monoxide (CO) showed a downtrend, lower in summer than in the other 3 seasons. Ozone (O3) was significantly higher in 2016 and 2017, showed an increase trend in summer. The incidence of epistaxis was negatively correlated with PM2.5, PM10, SO2, NO2 and CO, which was positively correlated with O3 ( P < .05).
CONCLUSIONS:
Pediatric epistaxis in Beijing changes with age and has obvious seasonal variation. There are some correlations between air pollutants and the incidence of epistaxis in children.

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Petr75
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Posts: 418
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Re: Tropospheric ozone

Post by Petr75 » Thu Sep 12, 2019 10:49 am

MS

2019
Department of Neurology , Isfahan University of Medical Sciences , Isfahan , The Islamic Republic of Iran
Elevated CSF concentration of CCL3 and CCL4 in relapsing remitting multiple sclerosis patients
https://www.ncbi.nlm.nih.gov/pubmed/31268406

Abstract
CCL3 and CCL4 are considered as inflammatory cytokines and involved in progression of various neurologic disorders as multiple sclerosis (MS). The aim of this study was to evaluate the association between cerebrospinal fluid (CSF) levels of above mentioned inflammatory cytokines and relapsing remitting multiple sclerosis (RRMS. In this case-control study, 40 unrelated patients (without family relationship) with RRMS and 40 age and sex matched subjects as control group were enrolled. CSF samples obtained from all patients and control group and levels of CCL3 and CCL4 were determined in CSF. The mean CSF level of CCL3 was significantly higher in RRMS patients than healthy controls (29.71±18.56 vs. 10.62±6.85, p<0.01). The CSF levels of CCL4 was also higher in RRMS patients compared with healthy controls (33.62±21.50 vs. 13.74±4.90, p<0.01). We found a positive correlation between CSF levels of CCL3 and disease duration (r=+0.32 and p=0.04) and expanded disability status scale (EDSS) (r=+45, p=0.03). We also found a positive correlation between CSF level of CCL4 and disease duration (r=+0.76 and p<0.01) and EDSS (r=+0.73, p<0.01). Present study showed contribution of CCL3 and CCL4 in MS pathogenesis and suggested them as markers of severity of disease. Investigation of chemokines responsible for attract of pathogenic T lymphocyte and macrophage in to the central nerves system(CNS) is crucial for therapeutic targets in MS
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O3

2017 Jan
Department of Pharmacology and Toxicology, Rutgers University Ernest Mario School of Pharmacy, Piscataway, New Jersey
Editor's Highlight: Role of Spleen-Derived Macrophages in Ozone-Induced Lung Inflammation and Injury.
https://www.ncbi.nlm.nih.gov/pubmed/27708193

Abstract
Macrophages and inflammatory mediators have been implicated in ozone toxicity. In these studies, we used splenectomized (SPX) mice to assess the contribution of splenic monocytes to pulmonary inflammation and injury induced by ozone. Cells and tissue were collected 24-72 h after exposure of mice to air or ozone (0.8 ppm, 3 h). Following ozone exposure, increased numbers of pro-inflammatory CD11b + Ly6CHi and anti-inflammatory CD11b + Ly6CLo monocytes were observed in spleens of control (CTL) mice. CD11b + Ly6CHi and MMP-9+ pro-inflammatory macrophages were also observed in lungs of CTL mice after ozone, along with CD11b + Ly6CLo and mannose receptor (MR)+ anti-inflammatory macrophages. This was accompanied by increased lung expression of proteins involved in monocyte/macrophage trafficking including CCL3, CCL4, CCR1, and AT1R. Splenectomy resulted in decreases in pro-inflammatory macrophages in the lung and down regulation of CCR2, CCL2, and CCL4, but increases in CD11b + Ly6CLo anti-inflammatory macrophages. CD11b+Ly6G+Ly6C+ granulocytic (G)- and monocytic (M)-myeloid derived suppressor cells (MDSC)s were also detected in the lungs and spleens of CTL mice; these increased after ozone exposure. Splenectomy was associated with a decrease in G-MDSCs in the lung, with no effect on M-MDSCs. Changes in lung macrophage subpopulations and MDSCs in SPX mice were correlated with reduced ozone toxicity, as measured by decreases in bronchoalveolar lavage protein content and reduced 4-hydroxynonenal expression in the lung. These data suggest that the spleen is a source of pro-inflammatory/cytotoxic macrophages that contribute to ozone-induced lung injury, inflammation, and oxidative stress.

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wiki https://en.wikipedia.org/wiki/CCL3

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Petr75
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Posts: 418
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Re: Tropospheric ozone

Post by Petr75 » Sun Sep 15, 2019 10:50 am

MS

March 22, 2017
Department of Psychiatry, Sunnybrook Health Sciences Centre and University of Toronto
Multiple sclerosis and suicide
https://journals.sagepub.com/doi/full/1 ... 8517702553

Abstract
Mortality rates are elevated in people with multiple sclerosis (MS) relative to the general population. There is, however, some uncertainty whether suicide contributes to this. Epidemiological data suggest that the standardized mortality ratio (SMR) for suicide in MS is approximately twice that of the general population with younger males in the first few years following diagnosis most at risk. Rates of suicidal intent, a potential harbinger of more self-destructive behavior, are also elevated, but the frequency with which intent is followed by suicide is not known. Depression, severity of depression, social isolation, and alcohol abuse are associated with thoughts of suicide. The variables linked with suicide and suicidal intent are therefore well defined and should be readily available from routine clinical inquiry. While vigilance on the part of clinicians is required, particularly in the context of high-risk patients, it is also recognized that prevention is dependent on full disclosure of intent.

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O3

2019 Jul 12
Department of Public Health, College of Health Sciences, Kaohsiung Medical University , Kaohsiung , Taiwan
Does ambient ozone air pollution trigger suicide attempts? A case cross-over analysis in Taipei
https://www.ncbi.nlm.nih.gov/pubmed/31298077

Abstract
Epidemiologic studies indicated that exposure to ambient air pollutants was associated with increased mortality rates attributed to suicide. The objective of this study was to investigate the potential relationship between ambient ozone (O3) levels and daily number of hospital admissions for suicide attempts in Taipei for the period 2008-2012 using a time-stratified case-crossover analysis. In the single-pollutant model (without adjustment for other pollutants), the risk of committing a suicide attempt increased by 9% on warm days and 27% on cool days for each interquartile range (IQR) rise in O3 levels, respectively. The concentration of O3 was thus significantly associated with daily number of suicide attempts both on warm and cool days. In the two-pollutant models, O3 levels remained significant after the inclusion of other air pollutants (particulate matter (PM10), PM2.5, sulfur dioxide (SO2), nitrogen dioxide (NO2), and carbon monoxide (CO)) on cool days. However, on warm days, no significant correlation was found between O3 levels and reported daily number of suicide attempts. The relationship between O3 and suicide attempts appeared to be dependent upon temperature; however, the basis for these observations requires further investigation.

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Petr75
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Posts: 418
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Re: Tropospheric ozone

Post by Petr75 » Wed Oct 09, 2019 7:30 am

2019 Jan
Department of Epidemiology and Biostatistics, School of Public Health, Anhui Medical University, Hefei, China
Association between ambient air pollution and Parkinson's disease: Systematic review and meta-analysis.
https://www.ncbi.nlm.nih.gov/pubmed/30391837

Abstract
Air pollution has been evaluated as a possible risk factor for Parkinson's disease (PD), but, the present results are inconsistent and have not been combined. We performed a systematic review and meta-analysis to estimate the association between long-term exposure to ambient air pollution and PD, given the nature of disease etiology. A total of 10 studies were identified by searching Web of Science, Science Direct, and PubMed before October 2017. We found a significantly increased risk of PD with 10 parts per billion (ppb) increase in nitrogen oxides (NOx) exposure (relative risk (RR) = 1.06; 95% confidence interval (CI): 1.04, 1.09). The pooled RR for the association between carbon monoxide (CO) exposure, 1 parts per million (ppm) increment, and the risk of PD was 1.65 (95% CI: 1.10, 2.48). The pooled RRs for the association between nitrogen dioxide (NO2) and ozone (O3) exposure per 1 ppb increment, and the risk of PD were 1.01 (95% CI: 1.00, 1.03) and 1.01 (95% CI: 1.00, 1.02), respectively. There was a significant heterogeneity in the meta-analysis for fine particulate matter (PM2.5), NO2, sulfur dioxide (SO2), and CO. We concluded that NO2, NOx, CO and O3 exposure were associated with an increased risk of PD, although there is high risk of bias. The dose-response effects evaluated by high-quality studies are needed. Researches should be expanded to low- and/or middle- income countries where indoor and outdoor air pollution are high. CAPSULE: Long-term exposure to ambient NO2, NOx, CO and O3 can increase the risk of Parkinson's disease.

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Petr75
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Posts: 418
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Re: Tropospheric ozone

Post by Petr75 » Fri Oct 11, 2019 10:59 am

MS


15 July 2019
IL-17A is associated with the breakdown of the blood-brain barrier in relapsing-remitting multiple sclerosis
https://www.sciencedirect.com/science/a ... 2818305794

Abstract
IL-17 has been implicated in the pathogenesis of multiple sclerosis (MS). Here, we show that blockade of IL-17A, but not IL-17F, attenuated experimental autoimmune encephalomyelitis (EAE). We further show that IL-17A levels were elevated in the CSF of relapsing-remitting MS (RRMS) patients and that they correlated with the CSF/serum albumin quotient (Qalb), a measure of blood-brain barrier (BBB) dysfunction. We then demonstrated that the combination of IL-17A and IL-6 reduced the expression of tight junction (TJ)-associated genes and disrupted monolayer integrity in the BBB cell line hCMEC/D3. However, unlike IL-17A, IL-6 in the CSF from RRMS patients did not correlate with Qalb. These data highlight the potential importance of targeting IL-17A in preserving BBB integrity in RRMS.
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2019 Sep 30
Department of Experimental Pathology, Immunology and Microbiology, American University of Beirut, Lebanon
Endosomal Toll-Like Receptors Mediate Enhancement of Interleukin-17A Production Triggered by Epstein-Barr Virus DNA in Mice
https://www.ncbi.nlm.nih.gov/pubmed/31375581

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O3


2018 Nov 14
Departamento de Fisiología, Facultad de Medicina, Universidad Nacional Autónoma de México, Ciudad de México
Effect of exposure to low doses of ozone on interleukin 17A expression during progressive neurodegeneration in the rat hippocampus.
https://www.ncbi.nlm.nih.gov/pubmed/30447855

Abstract
INTRODUCTION:
Chronic exposure to low doses of ozone causes oxidative stress and loss of regulation of the inflammatory response, leading to progressive neurodegeneration.
OBJECTIVE:
We studied the effect of chronic exposure to low doses of ozone on IL-17A concentration and expression in neurons, microglia, astrocytes, and T cells in the rat hippocampus.
METHODS:
We used 72 Wistar rats, divided into 6 groups (n=12): a control group (no ozone exposure) and 5 groups exposed to ozone (0.25ppm, 4h daily) for 7, 15, 30, 60, and 90 days. We processed 6 rats from each group to quantify IL-17A by ELISA; the remaining 6 were processed for immunohistochemistry (against IL-17A and GFAP, Iba1, NeuN, and CD3).
RESULTS:
The ELISA study data showed a significant increase in IL-17A concentrations in the 7-, 15-, 30-, and 60-day exposure groups, with regard to the control group (P<.05). Furthermore, they indicate that hippocampal neurons were the cells showing greatest immunoreactivity against IL-17A between 60 and 90 days of exposure to ozone; we also observed an increase in activated astrocytes in the 30- and 60-day exposure groups.
CONCLUSION:
Exposure to ozone in rats induces an increase in IL-17A expression, mainly in hippocampal neurons, accompanied by hippocampal astrocyte activation during chronic neurodegeneration, similar to that observed in Alzheimer disease in humans.

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wiki https://en.wikipedia.org/wiki/Interleukin_17

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