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
Epistaxis is a common symptom in children. The effect of air pollution on epistaxis is not yet clear.
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.
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).
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.
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
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
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.
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.
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
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.
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
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.
Relationship Between Ozone Air Pollution and Daily Suicide Mortality: A Time-Stratified Case-Crossover Study in Taipei https://pubmed.ncbi.nlm.nih.gov/3087011 ... in-taipei/
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.
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.
2019 Nov 22
National Clinical Research Center for Geriatric Disorders, Xuanwu Hospital of Capital Medical University, 45 Changchun Road, Xicheng District, Beijing, China
The impact of long-term exposure to ambient air pollution and second-hand smoke on the onset of Parkinson disease: a review and meta-analysis.
2014 Apr 3
Parkinsonism associated with multiple sclerosis: A report of eight new cases and a review on the literature
Although concomitancy of MS and PD were suggested because of casual relationship or as an accident, limited studies on this issue do not support the accidental occurrence of MS and PD. Cases which were reported until now represent both casual and accidental aspect. Moreover, the exact etiology of MS and PD still remains unclear and put more weight for difficulty of explanation and results in controversial hypothesizes. Further pathophysiological studies are needed to clarify different aspects.
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
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.
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
2020 Jan 27
Immune Regulation Research Group, School of Biochemistry and Immunology, Trinity Biomedical Sciences Institute, Trinity College Dublin
https://pubmed.ncbi.nlm.nih.gov/3202349 ... c-t-cells/
..Interleukin-17A (IL-17A) is a major mediator of tissue inflammation in many autoimmune diseases.
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.
Chronic exposure to low doses of ozone causes oxidative stress and loss of regulation of the inflammatory response, leading to progressive neurodegeneration.
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.
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).
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.
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.
Environmental Health Science and Research Bureau, Health Canada, Ottawa, Ontario, Canada
Ambient PM2.5, O₃, and NO₂ Exposures and Associations with Mortality over 16 Years of Follow-Up in the Canadian Census Health and Environment Cohort (CanCHEC).
Few studies examining the associations between long-term exposure to ambient air pollution and mortality have considered multiple pollutants when assessing changes in exposure due to residential mobility during follow-up.
We investigated associations between cause-specific mortality and ambient concentrations of fine particulate matter (≤ 2.5 μm; PM2.5), ozone (O3), and nitrogen dioxide (NO2) in a national cohort of about 2.5 million Canadians.
We assigned estimates of annual concentrations of these pollutants to the residential postal codes of subjects for each year during 16 years of follow-up. Historical tax data allowed us to track subjects' residential postal code annually. We estimated hazard ratios (HRs) for each pollutant separately and adjusted for the other pollutants. We also estimated the product of the three HRs as a measure of the cumulative association with mortality for several causes of death for an increment of the mean minus the 5th percentile of each pollutant: 5.0 μg/m3 for PM2.5, 9.5 ppb for O3, and 8.1 ppb for NO2.
PM2.5, O3, and NO2 were associated with nonaccidental and cause-specific mortality in single-pollutant models. Exposure to PM2.5 alone was not sufficient to fully characterize the toxicity of the atmospheric mix or to fully explain the risk of mortality associated with exposure to ambient pollution. Assuming additive associations, the estimated HR for nonaccidental mortality corresponding to a change in exposure from the mean to the 5th percentile for all three pollutants together was 1.075 (95% CI: 1.067, 1.084). Accounting for residential mobility had only a limited impact on the association between mortality and PM2.5 and O3, but increased associations with NO2.
In this large, national-level cohort, we found positive associations between several common causes of death and exposure to PM2.5, O3, and NO2.
2019 Apr 1
Associations between Ozone and Fine Particulate Matter and Respiratory Illness Found to Vary between Children and Adults. Implications for U.S. Air Quality Policy https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6444659/
Department of Family Medicine, Konkuk University School of Medicine, Konkuk University Medical Centre, Seoul, South Korea
Association between long-term exposure of ambient air pollutants and cardiometabolic diseases: A 2012 Korean Community Health Survey
BACKGROUND AND AIM:
The associations of long-term exposure to particulate matter <10 μm in size (PM10), nitrogen dioxide (NO2), carbon monoxide (CO), sulfur dioxide (SO2), and ozone (O3) with cardiometabolic diseases (CMD) remain uncertain in the Korean population. Therefore, we sought to examine the associations between PM10, NO2, CO, SO2, and O3 and CMD using data collected from the Korean Community Health Survey.
METHODS AND RESULTS:
We selected 100,867 adults aged 19 years or older who had lived in the same domicile for ≥10 years and surveyed them to collect data on socioeconomic characteristics; health-related behaviors; obesity; and physician-diagnosed CMD history, including hypertension, diabetes mellitus, dyslipidemia, stroke, myocardial infarction, and ischemic heart disease. We calculated interquartile ranges for PM10, NO2, CO, SO2, and O3 from the 10 year average concentrations (2003-2012). Hypertension, diabetes mellitus, and dyslipidemia were positively associated with PM10, NO2, CO, SO2, and O3 after adjusting for confounding factors. Obesity was positively associated with PM10, NO2, SO2, and O3. On the other hand, we found no associations between stroke, myocardial infarction, and ischemic heart disease and exposure to PM10, NO2, CO, SO2, and O3 in these subjects. In subjects aged ≥65 years, the risk of dyslipidemia was markedly increased under exposure to NO2 and CO compared to subjects aged <65 years. The risk of obesity was also significantly increased under exposure to PM10 and NO2. However, sex differences in these associations were not found.
Long-term exposure to PM10, NO2, CO, SO2, and O3 may be a risk factor of CMD in Korean adults.
2019 Apr 30
Ascorbic acid and thiols as potential biomarkers of ozone tolerance in tropical wheat cultivars.
Preventive and therapeutic potential of ascorbic acid in neurodegenerative diseases
Vitamin C promotes oligodendrocytes generation and remyelination
Should we rebrand multiple sclerosis a dementia? https://www.msard-journal.com/article/S ... 3/fulltext
2019 Aug 9
Department of Epidemiology- Lazio Regional Health Service, Rome, Italy
Long-term exposure to air pollution and hospitalization for dementia in the Rome longitudinal study.
Few studies have explored the role of air pollution in neurodegenerative processes, especially various types of dementia. Our aim was to evaluate the association between long-term exposure to air pollution and first hospitalization for dementia subtypes in a large administrative cohort.
We selected 350,844 subjects (free of dementia) aged 65-100 years at inclusion (21/10/2001) and followed them until 31/12/2013. We selected all subjects hospitalized for the first time with primary or secondary diagnoses of various forms of dementia. We estimated the exposure at residence using land use regression models for nitrogen oxides (NOx, NO2) and particulate matter (PM) and a chemical transport model for ozone (O3). We used Cox models to estimate the association between exposure and first hospitalization for dementia and its subtypes: vascular dementia (Vd), Alzheimer's disease (Ad) and senile dementia (Sd).
We selected 21,548 first hospitalizations for dementia (7497 for Vd, 7669 for Ad and 7833 for Sd). Overall, we observed a negative association between exposure to NO2 (10 μg/m3) and dementia hospitalizations (HR = 0.97; 95% CI: 0.96-0.99) and a positive association between exposure to O3, NOx and dementia hospitalizations, (O3: HR = 1.06; 95% CI: 1.04-1.09 per 10 μg/m3; NOx: HR = 1.01; 95% CI: 1.00-1.02 per 20 μg/m3).H. Exposure to NOx, NO2, PM2.5, and PM10 was positively associated with Vd and negatively associated with Ad. Hospitalization for Sd was positively associated with exposure to O3 (HR = 1.20; 95% CI: 1.15-1.24 per 10 μg/m3).
Our results showed a positive association between exposure to NOx and O3 and hospitalization for dementia and a negative association between NO2 exposure and hospitalization for dementia. In the analysis by subtype, exposure to each pollutants (except O3) demonstrated a positive association with vascular dementia, while O3 exposure was associated with senile dementia. The results regarding vascular dementia are a clear indication that the brain effects of air pollution are linked with vascular damage.
Journal of Neurochemistry
Ozone inhalation activates stress-responsive regions of the CNS
https://www.researchgate.net/publicatio ... of_the_CNS
Ozone (O3), a major component of air pollution, has considerable impact on public health. Besides the well-described respiratory tract inflammation and dysfunctions, there is accumulating evidence indicating that O3 exposure affects brain functions. However, the mechanisms through which O3 exerts toxic effects on the brain remain poorly understood. This work aimed at precisely characterizing CNS neuronal activation after O3 inhalation using Fos staining in adult rat. We showed that, together with lung inflammation, O3 exposure caused a sustained time- and dose-dependent neuronal activation in the dorsolateral regions of the nucleus tractus solitarius overlapping terminal fields of lung afferents running in vagus nerves. Furthermore, we highlighted neuronal activation in interconnected central structures such as the caudal ventrolateral medulla, the parabrachial nucleus, the central nucleus of the amygdala, the bed nucleus of the stria terminalis and the paraventricular hypothalamic nucleus. In contrast, we did not detect any neuronal activation in the thoracic spinal cord where lung afferents running in spinal nerves terminate. Overall, our results demonstrate that O3 challenge evokes a lung inflammation that induces the activation of nucleus tractus solitarius neurons through the vagus nerves and promotes neuronal activation in stress-responsive regions of the CNS...
Nutritional Neuroscience · July 2019
Maqui berry ( Aristotelia chilensis ) extract improves memory and decreases oxidative stress in male rat brain exposed to ozone
https://www.researchgate.net/publicatio ... d_to_ozone
2019 Aug 20
Unit of Neurology and Neurorehabilitation, IRCCS Neuromed, Pozzilli (IS), Italy
Interleukin-6 Disrupts Synaptic Plasticity and Impairs Tissue Damage Compensation in Multiple Sclerosis.
Background: Synaptic plasticity helps in reducing the clinical expression of brain damage and represents a useful mechanism to compensate the negative impact of new brain lesions in multiple sclerosis (MS). Inflammation, altering synaptic plasticity, could negatively influence the disease course in relapsing-remitting MS (RR-MS). Objective: In the present study, we explored whether interleukin (IL)-6, a major proinflammatory cytokine involved in MS pathogenesis, alters synaptic plasticity and affects the ability to compensate for ongoing brain damage. Methods: The effect of IL-6 incubation on long-term potentiation (LTP) induction was explored in vitro, in mice hippocampal slices. We also explored the correlation between the cerebrospinal fluid (CSF) levels of this cytokine and the LTP-like effect induced by the paired associative stimulation (PAS) in a group of RR-MS patients. Finally, we examined the correlation between the CSF levels of IL-6 at the time of diagnosis and the prospective disease activity in a cohort of 150 RR-MS patients. Results: In vitro LTP induction was abolished by IL-6. Consistently, in patients with MS, a negative correlation emerged between IL-6 CSF concentrations and the effect of PAS. In MS patients, longer disease duration before diagnosis was associated with higher IL-6 CSF concentrations. In addition, elevated CSF levels of IL-6 were associated with greater clinical expression of new inflammatory brain lesions, unlike in patients with low or absent IL-6 concentrations, who had a better disease course. Conclusions: IL-6 interfering with synaptic plasticity mechanisms may impair the ability to compensate the clinical manifestation of new brain lesions in RR-MS patients.
2016 Mar 5
Department of Pediatrics, The Pennsylvania State University College of Medicine, 500 University Drive
Sex-specific IL-6-associated signaling activation in ozone-induced lung inflammation.
Acute ozone (O3) exposure has known deleterious effects on the respiratory system and has been linked with respiratory disease and infection. Inflammatory lung disease induced by air pollution has demonstrated greater severity and poorer prognosis in women vs. men. Both severe damage to the bronchial-alveolar epithelium and malfunctioning of bronchial-blood barrier have been largely attributed to the pathobiology of O3-induced inflammatory response, but the associated mechanisms in the male and female lung remain unknown.
Here, we investigated sex-based differential regulation of lung interleukin-6 (IL-6) and its downstream signaling pathways JAK2/STAT3 and AKT1/NF-κB in response to O3 exposure in a mouse model. We exposed male and female mice (in different stages of the estrous cycle) to 2 ppm of O3 or filtered air (FA) for 3 h, and we harvested lung tissue for protein expression analysis by Western blot.
We found significant up-regulation of IL-6 and IL-6R in females and IL-6 in males in response to O3 vs. FA. Ozone exposure induced a significant increase in STAT3-Y705 phosphorylation in both females and males. Males exposed to O3 had decreased levels of JAK2, but increased JAK2 (Y1007+Y1008) phosphorylation, while females exposed to O3 showed significant up-regulation of both proteins. Both NF-κB (p105/p50) and AKT1 protein levels were significantly increased only in females exposed to O3. In addition, females exposed to O3 during proestrus displayed increased expression of selected genes when compared to females exposed to O3 in other estrous cycle stages.
Together, our observations indicate a sex-based and estrous cycle-dependent differential lung inflammatory response to O3 and involvement of two converging JAK2/STAT3 and AKT1/NF-κB pathways. To our knowledge, this is the first study specifically addressing the impact of the estrous cycle in O3-associated lung inflammatory pathways.
School of Public Health, National Defense Medical Center, Neihu Dist., Taipei City, Taiwan
Air Pollution Exposure and Cognitive Function in Taiwanese Older Adults: A Repeated Measurement Study.
Studies related to air pollution exposure and neurocognitive disorders, specifically cognitive impairment, among older adults are limited. We investigated the association between short-term and long-term exposure to ambient air pollution (i.e., particulate matter with an aerodynamic diameter of <10 μm and ozone) and the effects of their interaction on cognitive function in a community-dwelling, free-living elderly population. Study participants were in a multiple-wave representative sample, namely the Taiwan Longitudinal Study on Aging (n = 2241). In four surveys between 1996 and 2007, their cognitive function was assessed using the Short Portable Mental Status Questionnaire (SPMSQ). We estimated air pollution from 1993 to 2007, including daily concentrations of PM10 and O3 from air quality monitoring stations, based on the administrative zone of each participant's residence. Generalized linear mixed models were used to examine these associations after adjusting for covariates. We found that long-term exposure to PM10 and O3 was significantly associated with cognitive impairment (OR = 1.094, 95% CI: 1.020, 1.174 for PM10; OR = 1.878, 95% CI: 1.363, 2.560 for O3). The joint effect of exposure to PM10 and O3 was associated with cognitive impairment (p < 0.001). Co-exposure to ambient PM10 and O3 may deteriorate cognitive function in older adults.
Association between ambient air pollution and daily hospital admissions for ischemic stroke: A nationwide time-series analysis.
In vitro study evaluating the instantaneous treatment of ozonised olive oil on human sperm.
Short-term exposure to air pollution: Associations with lung function and inflammatory markers in non-smoking, healthy adults.
An Iron-Containing Metal-Organic Framework as a Highly Efficient Catalyst for Ozone Decomposition.
Pediatric Epistaxis and Its Correlation Between Air Pollutants in Beijing From 2014 to 2017.
Short-term exposure to ambient ozone and inflammatory biomarkers in cross-sectional studies of children and adolescents: Results of the GINIplus and LISA birth cohorts. https://www.ncbi.nlm.nih.gov/pubmed/31563778
Spatio-temporal evolution of ozone pollution and its influencing factors in the Beijing-Tianjin-Hebei Urban Agglomeration
2019 Nov 1
Department of Clinical Pharmacy, Faculty of Pharmacy, University of Medicine and Pharmacy, Craiova, Romania
Targeted Metabolomic Analysis of Serum Fatty Acids for the Prediction of Autoimmune Diseases
Autoimmune diseases (ADs) are rapidly increasing worldwide and accumulating data support a key role of disrupted metabolism in ADs. This study aimed to identify an improved combination of Total Fatty Acids (TFAs) biomarkers as a predictive factor for the presence of autoimmune diseases. A retrospective nested case-control study was conducted in 403 individuals. In the case group, 240 patients diagnosed with rheumatoid arthritis, thyroid disease, multiple sclerosis, vitiligo, psoriasis, inflammatory bowel disease, and other AD were included and compared to 163 healthy individuals. Targeted metabolomic analysis of serum TFAs was performed using GC-MS, and 28 variables were used as input for the predictive models. The primary analysis identified 12 variables that were statistically significantly different between the two groups, and metabolite-metabolite correlation analysis revealed 653 significant correlation coefficients with 90% level of significance (p < 0.05)...
Jun 15, 2016
1Division of Cardiovascular Medicine, University of Maryland School of Medicine
Ozone-induced Metabolic Effects in Humans
https://www.atsjournals.org/doi/full/10 ... 601-0142ED
A common feature of the fasting and feasting states, polar opposites in the metabolic spectrum, is mobilization of free fatty acid (FFAs) into the circulation for vastly different reasons. With fasting, insulin levels are normally low, and counterregulatory hormones (e.g., catecholamines and glucagon) rise, to increase lipolysis and provide FFAs for β-oxidation to produce energy. In the healthy post-prandial state, FFAs are reduced due to the opposite hormonal responses. However, in obese, overfed, or insulin-resistant individuals, the coordination of intermediary metabolism breaks down. An increase in FFA flux to the liver occurs owing to persistent adipocyte lipolysis in the face of selective insulin resistance, which thereafter serves to further promote development of the metabolic syndrome.
In this issue of the Journal, Miller and colleagues (pp. 1382–1391) describe the acute effects (2-h exposure) of ozone inhalation (0.3 ppm) among healthy humans, undergoing intermittent exercise, on a previously unaddressed aspect of changes in intermediate pathways of metabolism (1). The investigators performed a post hoc exploration of the circulating steroid and lipid metabolome from stored plasma samples, obtained 1 hour after exposure from a previous study (2). Ozone is a common gaseous pollutant that exerts negative cardiopulmonary effects and is of considerable global public health importance...
School of Bioresources and Technology, King Mongkut's University of Technology Thonburi, Bangkok, Thailand
Contribution of Bacillus cereus ERBP in ozone detoxification by Zamioculcas zamiifolia plants: Effect of ascorbate peroxidase, catalase and total flavonoid contents for ozone detoxification.
Eighteen plant species were screened for ozone (O3) removal in a continuous system. Zamioculcas zamiifolia had the highest O3 removal efficiency. To enhance O3 removal by Z. zamiifolia, adding a compatible endophytic bacteria, Bacillus cereus ERBP into Z. zamiifolia was studied. After operating under an O3 continuous system (150-250 ppb) at a flow rate of 0.3 L min-1 for 80 h, inoculated plants (74%) exhibited higher O3 removal efficiency than non-inoculated ones (53%). In addition, after O3 exposure (80 h), the population of B. cereus ERBP in inoculated plants was significantly increased in both shoots approximately 35 folds and leaves 13 folds compared to inoculated plants without O3 exposure. The results also showed that B. cereus ERBP had the ability to protect Z. zamiifolia against O3 stress conditions. The increase in B. cereus ERBP populations was attributed to the significant increase in ascorbate peroxidase (APX) and catalase (CAT) activity. In addition, increasing B. cereus ERBP populations led to raise total flavonoid contents which is one of antioxidant compounds. Increasing APX, CAT activities, and total flavonoid contents can enhance O3 detoxification in plant tissues. The mechanism of B. cereus ERBP for enhancing O3 phytoremediation was proposed in this study. The results suggested that B. cereus ERBP was a potential tool for alleviating O3 stress on Z. zamiifolia and enhancing O3 phytoremediation efficiency.