Tropospheric ozone

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Petr75
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Re: Tropospheric ozone

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2018 Mar 28
Trends in onroad transportation energy and emissions. https://www.ncbi.nlm.nih.gov/pubmed/29589998

Abstract
Globally, 1.3 billion onroad vehicles consume 79 quadrillion BTU of energy, mostly gasoline and diesel fuels, emit 5.7 gigatonnes of CO2, and emit other pollutants to which approximately 200,000 annual premature deaths are attributed. Improved vehicle energy efficiency and emission controls have helped offset growth in vehicle activity. New technologies are diffusing into the vehicle fleet in response to fuel efficiency and emission standards. Empirical assessment of vehicle emissions is challenging because of myriad fuels and technologies, inter-vehicle variability, multiple emission processes, variability in operating conditions, and varying capabilities of measurement methods. Fuel economy and emissions regulations have been effective in reducing total emissions of key pollutants. Real-world fuel use and emissions are consistent with official values in the U.S. but not in Europe or countries that adopt European standards. Portable emission measurements systems, which uncovered a recent emissions cheating scandal, have a key role in regulatory programs to ensure conformity between "real driving emissions" and emission standards. The global vehicle fleet will experience tremendous growth, especially in Asia. Although existing data and modeling tools are useful, they are often based on convenience samples, small sample sizes, large variability and unquantified uncertainty. Vehicles emit precursors to several important secondary pollutants, including ozone and secondary organic aerosols, which requires a multipollutant emissions and air quality management strategy. Gasoline and diesel are likely to persist as key energy sources to mid-century. Adoption of electric vehicles is not a panacea with regard to greenhouse gas emissions unless coupled with policies to change the power generation mix. Depending on how they are actually implemented and used, autonomous vehicles could lead to very large reductions or increases in energy consumption. Numerous other trends are addressed with regard to technology, emissions controls, vehicle operations, emission measurements, impacts on exposure, and impacts on public health.
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Re: Tropospheric ozone

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is nature or man harder on the atmosphere?

The planet is constantly releasing pollution and toxins into the atmosphere both above and below the surface. And always has.

How much energy in a volcanic eruption?

Volcanoes also release mind-boggling quantities of energy, though usually not quite on the scale of hurricanes (thankfully for those who live near!). But if we look at a well-known major volcanic eruption, the eruption of Mount St. Helens in 1980, we find that: "In all, Mount St. Helens released 24 megatons of thermal energy, 7 of which was a direct result of the blast. This is equivalent to 1,600 times the size of the atomic bomb dropped on Hiroshima" (U.S. Geological Survey).

But Mount St. Helens wasn't even at the top of the scale of Volcanic Explosivity Index. It was a class 5, and the scale goes up all the way to 8, which are called "mega-colossal" eruptions. These class 8 super-volcanos erupt extremely rarely (otherwise we wouldn't be here), but when they do, more than 1,000 cubic kilometers of rock and ash are ejected, the climate of the whole planet is affected for extended periods of time, and mass-extinctions can be expected. Now that is powerful! To get anywhere close to that kind of energy release, the U.S. and Russia would have to use their entire nuclear arsenals simultaneously, and even that might not be enough to compare depending on how long the volcanic eruption lasts.


Here is an interesting article from Scientific American:

Are Volcanoes or Humans Harder on the Atmosphere?

https://www.scientificamerican.com/arti ... or-humans/



Underwater vents release tremendous amount of pollution and toxins as well.

Yet life goes on...




My point? Tropospheric ozone has probably always been with us. Are your points on the matter accurate? Perhaps!
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Re: Tropospheric ozone

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- Life goes on, I have no doubt about it. Petr

- Ozone enhances the airway inflammation initiated by diesel exhaust https://www.sciencedirect.com/science/a ... 110600597X#

- Evolution of multiple sclerosis prevalence and phenotype in Latin America. https://www.ncbi.nlm.nih.gov/pubmed/29649790
..Both, prevalence and incidence, are increasing.. (Why? I do not know. Volcals?)
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Re: Tropospheric ozone

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MS

2018 Apr 4
Stanford University School of Medicine, US
Hyaluronan in immune dysregulation and autoimmune diseases.
https://www.ncbi.nlm.nih.gov/pubmed/29625181

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O3

2010 Dec 1
Duke University, Durham, US
Hyaluronan fragments contribute to the ozone-primed immune response to lipopolysaccharide.
https://www.ncbi.nlm.nih.gov/pubmed/21037098
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Re: Tropospheric ozone

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MS

2018 Apr 20.
Department of Veterinary Sciences, LMU Munich, Munich, Germany
Bovine spastic syndrome: a review.
https://www.ncbi.nlm.nih.gov/pubmed/29678888

Bovine spastic syndrome (BSS) was described for the first time in 1941. The disease occurs in various-maybe even all-cattle breeds and is a chronic-progressive neuromuscular disorder that commonly affects cattle of at least three years of age. Typical clinical signs of the disease are clonic-tonic cramps of the hindlimbs that occur in attacks. Since BSS does not recover, affected animals can only be treated symptomatically by improving welfare conditions and management factors, or with physical therapy or drugs. Although still not irrevocably proven, BSS is assumed to be a hereditary disease. Therefore, affected animals should be excluded from breeding, which negatively affects economics and breeding. Besides epidemiology, clinical signs, aetiopathogenesis, diagnosis and treatment, this review discusses genetic aspects and differences to the similar disease bovine spastic paresis. Furthermore, this review also picks up the discussion on possible parallels between human multiple sclerosis and BSS as a further interesting aspect, which might be of great interest for future research.

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O3

September 2005
Lupi Chemical Research, Via Casilina, Řím, Itálie
On the action of ozone on whole bovine blood
https://www.sciencedirect.com/science/a ... 1005000947

Abstract

The reaction between whole bovine blood and ozone has been studied. The ozonization reaction was monitored spectrophotometrically by using the B-band and the Q-bands of hemoglobin contained in the red blood cells. Ozone causes the destruction of the hemin prosthetic groups present in the hemoglobin of the red cells and the toxicological and medical implications of this fact are briefly discussed.

Although hemoglobin of the red cells appears to be the preferred target of ozone attack, there are other substrates in blood which are susceptible to ozonolysis reactions: fatty acids and cholesterol. The reaction between cholesterol and ozone was explored both polarimetrically and spectrophotometrically and it has been shown that this molecule also can be degraded by ozone in blood.
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Re: Tropospheric ozone

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MS
The Impact of Hemoglobin Levels on Multiple Sclerosis
https://www.specialtypharmacytimes.com/ ... -sclerosis
Findings from a recent study suggest that brain shrinkage in patients with multiple sclerosis (MS) may be linked to leaked hemoglobin protein in the blood. Hemoglobin transports iron and oxygen throughout the body via red blood cells.
Investigators believe that treatments lowering hemoglobin levels could potentially slow the progression of the disease, according to a study published by Wellcome Open Research.
"These are exciting but early results,” said lead author of the study Charles Bangham, PhD. “If further studies confirm them, they may suggest new avenues of treatment, and hopefully more options to offer patients in the future." ..
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Re: Tropospheric ozone

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October 2018
Institute for Clinical Evaluative Sciences, Toronto, ON, Canada, ..
Long-term exposure to air pollution and the incidence of multiple sclerosis: A population-based cohort study
https://www.sciencedirect.com/science/a ... 5118303013

Highlights
•No associations of MS incidence with PM2.5 and NO2 were observed.
•There was a tendency for increasing MS incidence in relation to O3.
• Females exhibited a higher risk of developing MS in association with O3 than males.

..Conclusions
In this large population-based cohort, we did not observe significant associations between MS incidence and long-term exposures to PM2.5, NO2, and O3 in adults in Ontario, 2001–2013.
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Re: Tropospheric ozone

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MS

2018 Aug 22.
Center for Antibody Drug, Institute of Biomedicine and Biotechnology, Shenzhen Institutes of Advanced Technology, Chinese Academy of Sciences, Shenzhen, China
MicroRNA-mediated Regulation of Th17/Treg Balance in Autoimmune Disease.
https://www.ncbi.nlm.nih.gov/pubmed/30133700

Abstract
Th17 cells and regulatory T (Treg) cells are two distinct T cell subsets which have opposite effects on immune functions. While Th17 cells are a key effector in the immune response and play critical roles in the development of autoimmunity and inflammation, Treg cells orchestrate the overall immune response and maintain peripheral immune tolerance by regulating the activity of the effector T cells. However, the developmental pathways for Th17 and Treg cells are reciprocally interconnected and there is a significant amount of plasticity between them. Disturbed Th17/Treg balance contributes to the development of autoimmune diseases, like EAE and multiple sclerosis. MicroRNAs (miRNAs) are small non-coding RNA molecules that post-transcriptionally regulate gene expression. Recently, emerging evidence demonstrates that miRNAs play an important role in regulating the pathogenesis of autoimmune diseases through the modulation of Th17/Treg balance. This review will provide an overview of the dysregulated miRNAs and their functions in modulating the Th17/Treg balance in autoimmune diseases. This article is protected by copyright. All rights reserved.
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2018 Aug 9
Department of Biomedical and Specialty Surgical Sciences, University of Ferrara, via Fossato di Mortara, Italy.
Changes in expression profiles of internal jugular vein wall and plasma protein levels in multiple sclerosis.
https://www.ncbi.nlm.nih.gov/pubmed/30134823
CONCLUSIONS:
This study provides for the first time expression patterns of the IJV wall, suggesting signatures of altered vascular mRNA profiles in MS disease also independently from CCSVI. The combined transcriptome-protein analysis provides intriguing links between IJV wall transcript alteration and plasma protein expression, thus highlighting proteins of interest for MS pathophysiology.

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O3

2014 Jun 15
Gillings School of Global Public Health, University of North Carolina, Chapel Hill
Air toxics and epigenetic effects: ozone altered microRNAs in the sputum of human subjects
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4060009/

Abstract
Ozone (O3) is a criteria air pollutant that is associated with numerous adverse health effects, including altered respiratory immune responses. Despite its deleterious health effects, possible epigenetic mechanisms underlying O3-induced health effects remain understudied. MicroRNAs (miRNAs) are epigenetic regulators of genomic response to environmental insults and unstudied in relationship to O3 inhalation exposure. Our objective was to test whether O3 inhalation exposure significantly alters miRNA expression profiles within the human bronchial airways. Twenty healthy adult human volunteers were exposed to 0.4 ppm O3 for 2 h. Induced sputum samples were collected from each subject 48 h preexposure and 6 h postexposure for evaluation of miRNA expression and markers of inflammation in the airways. Genomewide miRNA expression profiles were evaluated by microarray analysis, and in silico predicted mRNA targets of the O3-responsive miRNAs were identified and validated against previously measured O3-induced changes in mRNA targets. Biological network analysis was performed on the O3-associated miRNAs and mRNA targets to reveal potential associated response signaling and functional enrichment. Expression analysis of the sputum samples revealed that O3 exposure significantly increased the expression levels of 10 miRNAs, namely miR-132, miR-143, miR-145, miR-199a*, miR-199b-5p, miR-222, miR-223, miR-25, miR-424, and miR-582-5p. The miRNAs and their predicted targets were associated with a diverse range of biological functions and disease signatures, noted among them inflammation and immune-related disease. The present study shows that O3 inhalation exposure disrupts select miRNA expression profiles that are associated with inflammatory and immune response signaling. These findings provide novel insight into epigenetic regulation of responses to O3 exposure.
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Re: Tropospheric ozone

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MS

November 2018
Genetic Engineering and Genome Editing Laboratory, Stem Cell Biology Research Center, Yazd Reproductive Sciences Institute, Shahid Sadoughi University of Medical Sciences, Yazd, Iran
The miR-223: An Inflammatory MicroRNA Involved in Pathogenesis of Multiple Sclerosis
http://ijml.ssu.ac.ir/browse.php?a_id=2 ... =en&html=1

.. Conclusion
According to current literature, it is now increasingly evidenced that miR-223 is involved in the pathogenesis of MS. As stated above, miR-223 is highly dysregulated in MS patients as well as EAE mouse models. It might have the potential to generate a further understanding of the mechanisms underlying MS. The miR-223 has been reported to be upregulated in T-reg cells, plasma, blood cells, PBMCs and brain white matter tissue from MS patients and EAE mice. Such reports provide evidence that miR-223 may be a suitable choice for further studies as a novel therapeutic goal. It can also be used as a biomarker for diagnosis and monitor disease status in MS and a prognostic marker of treatment responsiveness.

(Frodo, http://www.thisisms.com/forum/ms-etiolo ... 30610.html )

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O3
(and again)

2014 Jun 15
Department of Environmental Sciences and Engineering, Gillings School of Global Public Health, University of North Carolina
Air toxics and epigenetic effects: ozone altered microRNAs in the sputum of human subjects
https://www.ncbi.nlm.nih.gov/pubmed/24771714

Abstract

Ozone (O3) is a criteria air pollutant that is associated with numerous adverse health effects, including altered respiratory immune responses. Despite its deleterious health effects, possible epigenetic mechanisms underlying O3-induced health effects remain understudied. MicroRNAs (miRNAs) are epigenetic regulators of genomic response to environmental insults and unstudied in relationship to O3 inhalation exposure. Our objective was to test whether O3 inhalation exposure significantly alters miRNA expression profiles within the human bronchial airways. Twenty healthy adult human volunteers were exposed to 0.4 ppm O3 for 2 h. Induced sputum samples were collected from each subject 48 h preexposure and 6 h postexposure for evaluation of miRNA expression and markers of inflammation in the airways. Genomewide miRNA expression profiles were evaluated by microarray analysis, and in silico predicted mRNA targets of the O3-responsive miRNAs were identified and validated against previously measured O3-induced changes in mRNA targets. Biological network analysis was performed on the O3-associated miRNAs and mRNA targets to reveal potential associated response signaling and functional enrichment. Expression analysis of the sputum samples revealed that O3 exposure significantly increased the expression levels of 10 miRNAs, namely miR-132, miR-143, miR-145, miR-199a*, miR-199b-5p, miR-222, miR-223, miR-25, miR-424, and miR-582-5p. The miRNAs and their predicted targets were associated with a diverse range of biological functions and disease signatures, noted among them inflammation and immune-related disease. The present study shows that O3 inhalation exposure disrupts select miRNA expression profiles that are associated with inflammatory and immune response signaling. These findings provide novel insight into epigenetic regulation of responses to O3 exposure.

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Petr75
Until the primary problem with the intestines is confirmed, I will occasionally bother with O3.
Exclusion for RS - O3 or PM, air problem - would be enough to use for a year Biosphere 2
https://en.wikipedia.org/wiki/Biosphere_2
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Re: Tropospheric ozone

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MS

Oxidative Stress Related to Iron Metabolism in Relapsing Remitting Multiple Sclerosis Patients With Low Disability.
PMC https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6378854/

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O3

2014 Jun
National Health and Environmental Effects Research Laboratory, Office of Research and Development, United States Environmental Protection Agency, Research Triangle Park
Iron decreases biological effects of ozone exposure.
https://www.ncbi.nlm.nih.gov/pubmed/24862973

Abstract
CONTEXT:
Ozone (O₃) exposure is associated with a disruption of iron homeostasis and increased availability of this metal which potentially contributes to an oxidative stress and biological effects.
OBJECTIVE:
We tested the postulate that increased concentrations of iron in cells, an animal model and human subjects would significantly impact the biological effects of O₃ exposure.
RESULTS:
Exposure to 0.4 ppm O₃ for 5 h increased mRNA for both Superoxide Dismutase-1 (SOD1) and Cyclooxygenase-2 (COX2) in normal human bronchial epithelial (NHBE) cells. Pre-treatment of NHBE cells with 200 µM ferric ammonium citrate (FAC) for 4 h diminished changes in both SOD1 and COX2 following O₃ exposure. mRNA transcript levels and associated protein release of the pro-inflammatory mediators IL-6 and IL-8 were increased by O₃ exposure of NHBE cells; changes in these endpoints after O₃ exposure were significantly decreased by FAC pre-treatment of the cells. Exposure of CD-1 mice to 2 ppm O₃ for 3 h significantly increased lavage indices of inflammation and airflow limitation. Pre-treatment of the animals with pharyngeal aspiration of FAC diminished the same endpoints. Finally, the mean loss of pulmonary function in 19 healthy volunteers exposed to 0.3 ppm O₃ for 2 h demonstrated significant correlations with either their pre-exposure plasma ferritin or iron concentrations.
DISCUSSION AND CONCLUSION:
We conclude that greater availability of iron after O₃ exposure does not augment biological effects. On the contrary, increased available iron decreases the biological effects of O₃ exposure in cells, animals and humans.
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Re: Tropospheric ozone

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2018 / I
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Impact of ozone on claudins and tight junctions in the lungs.[/b] https://www.ncbi.nlm.nih.gov/pubmed/29673049

A Mixed-Methods Study to Examine the Role of Psychosocial Stress and Air Pollution .. https://www.ncbi.nlm.nih.gov/pubmed/29679333

Impacts of transportation sector emissions on future https://www.ncbi.nlm.nih.gov/pubmed/29684896

A review of epidemiological research on stroke and dementia and exposure to air pollution. https://www.ncbi.nlm.nih.gov/pubmed/29699457

Oxidation-induced modifications of the catalytic subunits of plasma fibrin-stabilizing factor https://www.ncbi.nlm.nih.gov/pubmed/29738861

Ambient air pollution and human performance .. https://www.ncbi.nlm.nih.gov/pubmed/29737586

Sex-specific microRNA expression networks in an acute mouse model of ozone-induced lung inflammation https://www.ncbi.nlm.nih.gov/pubmed/29739446

Neuroendocrine Regulation of Air Pollution Health Effects: Emerging Insights. https://www.ncbi.nlm.nih.gov/pubmed/29846720

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Asthma, Environment and Pollution: Where the Rubber Hits the Road. https://www.ncbi.nlm.nih.gov/pubmed/29845404
Short-Term Exposure to Ambient Air Pollution and Asthma Mortality https://pubmed.ncbi.nlm.nih.gov/3087133 ... mortality/
Sex Differences in the Impact of Dietary Fiber on Pulmonary Responses to Ozone https://www.ncbi.nlm.nih.gov/pubmed/31913653
MS and Asthma https://multiplesclerosis.net/living-wi ... nd-asthma/
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Interleukin-1α Mediates Ozone-Induced Myeloid Differentiation Factor-88-Dependent Epithelial Tissue Injury and Inflammation. https://www.ncbi.nlm.nih.gov/pubmed/29867931

Short-term exposure to air pollution: Associations with lung function and inflammatory markers in non-smoking, healthy adults. https://www.ncbi.nlm.nih.gov/pubmed/30312964

Ozone and cardiac arrest: The role of previous hospitalizations. https://www.ncbi.nlm.nih.gov/pubmed/30399483

Cancer risk from exposure to particulate matter and ozone according to obesity and health-related behaviors: A nationwide population-based cross-sectional study https://www.ncbi.nlm.nih.gov/pubmed/30420440

Changing places to study short-term effects of air pollution on cardiovascular health: a panel study.
https://www.ncbi.nlm.nih.gov/pubmed/30453974

Air pollution during pregnancy and neonatal outcome: a review. https://www.ncbi.nlm.nih.gov/pubmed/22856675

Air pollution exposures and blood pressure https://www.ncbi.nlm.nih.gov/pubmed/30605850

Particulate matters and gaseous pollutants in indoor environment and Association of ultra-fine particulate matters (PM1) with lung function. https://www.ncbi.nlm.nih.gov/pubmed/30610585

Ambient ozone pollution is associated with decreased semen quality https://www.ncbi.nlm.nih.gov/pubmed/30688213

Effect of short-term fluctuations in outdoor air pollution on the number of hospital admissions due to acute myocardial infarction among inhabitants of Krakow, Poland. PM10 https://www.ncbi.nlm.nih.gov/pubmed/30688288

Elucidating Mechanisms of Long-Term Gasoline Vehicle Exhaust Exposure-Induced Erectile Dysfunction in a Rat Model.
PM10 https://www.ncbi.nlm.nih.gov/pubmed/30692026

Association between particulate matter air pollution and risk of depression and suicide: systematic review and meta-analysis. PM2,5 https://www.ncbi.nlm.nih.gov/pubmed/30719959

Long-Term Exposure to Air Pollution and Survival After Ischemic Stroke. https://www.ncbi.nlm.nih.gov/pubmed/30741622

Impacts of air pollution on human and ecosystem health, and implications for the National Emission Ceilings Directive: Insights from Italy. https://www.ncbi.nlm.nih.gov/pubmed/30739052



The effects of particulate matters on allergic rhinitis in Nanjing, China. https://www.ncbi.nlm.nih.gov/pubmed/30805838

High-Level PM2.5/PM10 Exposure Is Associated With Alterations in the Human Pharyngeal Microbiota Composition. https://www.ncbi.nlm.nih.gov/pubmed/30804895

The association of sleep with neighborhood physical and social environment. https://www.ncbi.nlm.nih.gov/pubmed/30036811

Uptake of ozone and modification of lipids in Betula Pendula pollen. https://www.ncbi.nlm.nih.gov/pubmed/30041161

Interactions between oxidative stress, autophagy and apoptosis in A549 cells treated with aged black carbon. https://www.ncbi.nlm.nih.gov/pubmed/30240709

Sex Differences in Pulmonary Responses to Ozone in Mice. Role of the Microbiome. https://www.ncbi.nlm.nih.gov/pubmed/30240285

Stress axis variability is associated with differential ozone-induced lung inflammatory signaling and injury biomarker response. https://www.ncbi.nlm.nih.gov/pubmed/30236519

The effects of personal short-term exposure to ambient ozone on blood pressure and vascular endothelial function: a mechanistic study based on DNA methylation and metabolomics. https://www.ncbi.nlm.nih.gov/pubmed/30259740

Significant effects of exposure to relatively low level ozone on daily mortality in 17 cities from three Eastern Asian Countries. https://www.ncbi.nlm.nih.gov/pubmed/30278365
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Re: Tropospheric ozone

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MS

2019 Apr 2
From the Department of Internal Medicine (R.A.M., A.G., S.A.S.), Department of Community Health Sciences (R.A.M., A.G., R.F., S.L.), and Manitoba Centre for Health Policy (R.F., M.Y.), Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg; and Department of Medicine (Neurology) (E.K., H.T.), University of British Columbia and The Djavad Mowafaghian Centre for Brain Health, Vancouver, Canada
Traditional risk factors may not explain increased incidence of myocardial infarction in MS
https://www.ncbi.nlm.nih.gov/pubmed/30842298
Abstract
OBJECTIVE:
To compare the risk of incident acute myocardial infarction (AMI) in the multiple sclerosis (MS) population and a matched population without MS, controlling for traditional vascular risk factors.
METHODS:
We conducted a retrospective matched cohort study using population-based administrative (health claims) data in 2 Canadian provinces, British Columbia and Manitoba. We identified incident MS cases using a validated case definition. For each case, we identified up to 5 controls without MS matched on age, sex, and region. We compared the incidence of AMI between cohorts using incidence rate ratios (IRR). We used Cox proportional hazards regression to compare the hazard of AMI between cohorts adjusting for sociodemographic factors, diabetes, hypertension, and hyperlipidemia. We pooled the provincial findings using meta-analysis.
RESULTS:
We identified 14,565 persons with MS and 72,825 matched controls. The crude incidence of AMI per 100,000 population was 146.2 (95% confidence interval [CI] 129.0-163.5) in the MS population and 128,8 (95% CI 121,8-135,8) in the matched population. After age standardization, the incidence of AMI was higher in the MS population than in the matched population (IRR 1.18; 95% CI 1.03-1.36). After adjustment, the hazard of AMI was 60% higher in the MS population than in the matched population (hazard ratio 1.63; 95% CI 1.43-1.87).
CONCLUSION:
The risk of AMI is elevated in MS, and this risk may not be accounted for by traditional vascular risk factors.

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O3

2005 Feb 8
INSERM U558, Faculté de Médecine, 37 Allées Jules Guesde, 31073 Toulouse Cedex, France
Ozone air pollution is associated with acute myocardial infarction.
https://www.ncbi.nlm.nih.gov/pubmed/15699276
Abstract
BACKGROUND:
Despite the diversity of the studied health outcomes, types and levels of pollution, and various environmental settings, there is substantial evidence for a positive link between urban air pollution and cardiovascular diseases. The objective of this study was to test the associations between air pollutants and the occurrence of acute myocardial infarction (AMI).
METHODS AND RESULTS:
Pollutant concentrations (SO2, NO2, and O3) were measured hourly as part of the automated air quality network. Since 1985, an AMI registry (the Toulouse MONICA Project) has been collecting data in the southwest of France. All cases of AMI and sudden and probable cardiac deaths are recorded for subjects 35 to 64 years of age. We studied the short-term exposure effect of pollution on the risk of AMI (from January 1, 1997, to June 30, 1999) using a case-crossover design method. We performed a conditional logistic regression analysis to calculate relative risks (RRs) and their 95% CIs. After adjustment for temperature, relative humidity, and influenza epidemics, the RRs (for an increase of 5 microg/m3 of O3 concentration) for AMI occurrence were significant for the current-day and 1-day-lag measurements (RR, 1.05; 95% CI, 1.01 to 1.08; P=0.009; and RR, 1.05; 95% CI, 1.01 to 1.09; P=0.007, respectively). Subjects 55 to 64 years of age with no personal history of ischemic heart disease were the most susceptible to develop an AMI (RR, 1.14; 95% CI, 1.06 to 1.23). NO2 and SO2 exposures were not significantly associated with the occurrence of AMI.
CONCLUSIONS:
Observational data confirm that short-term O3 exposure within a period of 1 to 2 days is related to acute coronary events in middle-aged adults without heart disease, whereas NO2 and SO2 are not.
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Re: Tropospheric ozone

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2019 May
Research Center, University of Social Welfare and Rehabilitation Sciences, Tehran, Iran
A comprehensive evaluation of the association between ambient air pollution and adverse health outcomes of major organ systems: a systematic review with a worldwide approach
https://www.ncbi.nlm.nih.gov/pubmed/30903465

Abstract
Ambient air pollution is nowadays one of the most crucial contributors to deteriorating health status worldwide. The components of air pollution include PM2.5 and PM10, NO2, SO2, CO, O3, and organic compounds. They are attributed to several health outcomes, for instance, cardiovascular diseases (CVD), respiratory diseases, birth outcomes, neurologic diseases, and psychiatric diseases. The objective of this study is to evaluate the association between different ambient air pollutants and the above-mentioned health outcomes. In this systematic review, a total of 76 articles was ultimately selected from 2653 articles, through multiple screening steps by the aid of a set of exclusion criteria as non-English articles, indoor air pollution assessment, work-related, occupational and home-attributed pollution, animal studies, tobacco smoking effects, letters to editors, commentaries, animal experiments, reviews, case reports and case series, out of 19,862 published articles through a systematic search in PubMed, Web of Science, and Scopus. Then, the associations between air pollution and different health outcomes were measured as relative risks and odds ratios. The association between air pollutants, PM2.5 and PM10, NO2, SO2, CO, O3, and VOC with major organ systems health was investigated through the gathered studies. Relative risks and/or odds ratios attributed to each air pollutant/outcome were ultimately reported. In this study, a thorough and comprehensive discussion of all aspects of the contribution of ambient air pollutants in health outcomes was proposed. To our knowledge up to now, there is no such comprehensive outlook on this issue. Growing concerns in concert with air pollution-induced health risks impose a great danger on the life of billions of people worldwide. Should we propose ideas and schemes to reduce ambient air pollutant, there will be dramatic reductions in the prevalence and occurrence of health-threatening conditions.
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Re: Tropospheric ozone

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2019 Mar 21
Atmospheric Science Unit, Department of Environmental Science and Analytical Chemistry, Stockholm University, Sweden
Association between Mortality and Short-Term Exposure to Particles, Ozone and Nitrogen Dioxide in Stockholm, Sweden
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6466204/

Abstract
In this study, the effects on daily mortality in Stockholm associated with short-term exposure to ultrafine particles (measured as number of particles with a diameter larger than 4 nm, PNC₄), black carbon (BC) and coarse particles (PM2.5⁻10) have been compared with the effects from more common traffic-pollution indicators (PM10, PM2.5 and NO₂) and O₃ during the period 2000⁻2016. Air pollution exposure was estimated from measurements at a 20 m high building in central Stockholm. The associations between daily mortality lagged up to two days (lag 02) and the different air pollutants were modelled by using Poisson regression. The pollutants with the strongest indications of an independent effect on daily mortality were O₃, PM2.5⁻10 and PM10. In the single - pollutant model, an interquartile range (IQR) increase in O₃ was associated with an increase in daily mortality of 2.0% (95% CI: 1.1⁻3.0) for lag 01 and 1.9% (95% CI: 1.0⁻2.9) for lag 02. An IQR increase in PM2.5⁻10 was associated with an increase in daily mortality of 0.8% (95% CI: 0.1⁻1.5) for lag 01 and 1.1% (95% CI: 0.4 1.8 ) for lag 02. PM10 was associated with a significant increase only at lag 02, with 0.8% (95% CI: 0.08⁻1.4) increase in daily mortality associated with an IQR increase in the concentration. NO₂ exhibits negative associations with mortality. The significant excess risk associated with O₃ remained significant in two-pollutant models after adjustments for PM2.5⁻10, BC and NO₂. The significant excess risk associated with PM2.5⁻10 remained significant in a two-pollutant model after adjustment for NO₂. The significantly negative associations for NO₂ remained significant in two-pollutant models after adjustments for PM2.5⁻10, O₃ and BC. A potential reason for these findings, where statistically significant excess risks were found for O₃, PM2.5⁻10 and PM10, but not for NO₂, PM2.5, PNC₄ and BC, is behavioral factors that lead to misclassification in the exposure. The concentrations of O₃ and PM2.5⁻10 are in general highest during sunny and dry days during the spring, when exposure to outdoor air tend to increase, while the opposite applies to NO₂, PNC₄ and BC, with the highest concentrations during the short winter days with cold weather, when people are less exposed to outdoor air.



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Frequency of relapses of multiple sclerosis by month of the year (a)
Paolo Zamboni and Roberto Manfredini

https://bmcneurol.biomedcentral.com/art ... 377-10-105
https://www.eboro.cz
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Petr75
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Re: Tropospheric ozone

Post by Petr75 »

MS


2019 May 7
MAPK pathway and B cells overactivation in multiple sclerosis revealed by phosphoproteomics and genomic analysis.
https://www.ncbi.nlm.nih.gov/pubmed/31004050
viewtopic.php?f=1&t=30974

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O3


2000 May
Ozone treatment rapidly activates MAP kinase signalling in plants

Abstract
Brief exposure to ozone, a potent cross-inducer of plant stress responses, leads within minutes to activation of an ERK-type MAP kinase (approximately 46 kDa) in tobacco. This activation process is calcium-dependent and can be blocked both by free radical quenchers and by a specific inhibitor of MEK-1 (MAPKK). Hydrogen peroxide and superoxide anion radicals can substitute for ozone as the activation stimulus, which does not appear to require salicylate as an intermediary. The properties of the ozone-induced MAPK suggest that it may be SIPK (salicylate-induced protein kinase), a tobacco MAPK that is activated by a variety of stress treatments. The ability of ozone to activate SIPK indicates that this protein kinase acts as a very early transducer of redox stress signals in plant cells.
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