scholarly journals Insulin sensitizers prevent fine particulate matter-induced vascular insulin resistance and changes in endothelial progenitor cell homeostasis

2016 ◽  
Vol 310 (11) ◽  
pp. H1423-H1438 ◽  
Author(s):  
Petra Haberzettl ◽  
James P. McCracken ◽  
Aruni Bhatnagar ◽  
Daniel J. Conklin
Keyword(s):  
Insulin Resistance ◽  
Bone Marrow ◽  
Particulate Matter ◽  
Insulin Sensitivity ◽  
Ambient Air ◽  
Air Pollutant ◽  
Ambient Air Pollution ◽  
Endothelial Progenitor ◽  
Insulin Sensitizer ◽  
Circulating Levels

Exposure to fine particular matter (PM2.5) increases the risk of developing cardiovascular disease and Type 2 diabetes. Because blood vessels are sensitive targets of air pollutant exposure, we examined the effects of concentrated ambient PM2.5 (CAP) on vascular insulin sensitivity and circulating levels of endothelial progenitor cells (EPCs), which reflect cardiovascular health. We found that CAP exposure for 9 days decreased insulin-stimulated Akt phosphorylation in the aorta of mice maintained on control diet. This change was accompanied by the induction of IL-1β and increases in the abundance of cleaved IL-18 and p10 subunit of Casp-1, consistent with the activation of the inflammasome pathway. CAP exposure also suppressed circulating levels of EPCs (Flk-1+/Sca-1+ cells), while enhancing the bone marrow abundance of these cells. Although similar changes in vascular insulin signaling and EPC levels were observed in mice fed high-fat diet, CAP exposure did not exacerbate diet-induced changes in vascular insulin resistance or EPC homeostasis. Treatment with an insulin sensitizer, metformin or rosiglitazone, prevented CAP-induced vascular insulin resistance and NF-κB and inflammasome activation and restored peripheral blood and bone marrow EPC levels. These findings suggest that PM2.5 exposure induces diet-independent vascular insulin resistance and inflammation and prevents EPC mobilization, and that this EPC mobilization defect could be mediated by vascular insulin resistance. Impaired vascular insulin sensitivity may be an important mechanism underlying PM2.5-induced vascular injury, and pharmacological sensitization to insulin action could potentially prevent deficits in vascular repair and mitigate vascular inflammation due to exposure to elevated levels of ambient air pollution. Listen to this article's corresponding podcast at http://ajpheart.podbean.com/e/particulate-matter-induced-vascular-insulin-resistance/ .

Ambient Air Pollution: Respiratory Hazards to Children

PEDIATRICS ◽  
1993 ◽  
Vol 91 (6) ◽  
pp. 1210-1213
Author(s):  
Keyword(s):  
Air Pollution ◽  
Carbon Monoxide ◽  
Particulate Matter ◽  
Stratospheric Ozone ◽  
Ambient Air ◽  
Clean Air Act ◽  
Air Pollutant ◽  
Ambient Air Pollution ◽  
Motor Vehicles ◽  
Clean Air

Levels of many outdoor air pollutants decreased substantially after the passage of the Clean Air Act of 1970; however, levels of ozone, carbon monoxide, and particulate matter are still high enough to present hazards to children. Failure to meet the federal standards for these pollutants was a major force driving the adoption of the revised Clean Air Act of 1990. In addition, recent research indicates that acidic aerosols, for which there are no health-based standards, may be associated with adverse respiratory effects. As an ambient air pollutant, ozone is formed by the action of sunlight on nitrogen oxides and reactive hydrocarbons (both of which are emitted by motor vehicles and industrial sources). Ozone levels therefore tend to be highest on warm, sunny days, which are conducive to outdoor activities. In many areas ozone concentrations peak in the midafternoon, when children are likely to be playing outside. It is important to distinguish ground-level ozone air pollution from stratospheric ozone depletion by chlorofluorocarbons. These issues are unrelated. Carbon monoxide, a product of incomplete combustion, is emitted mainly from cars and other mobile sources. Airborne particulate matter is a variable and complex mixture of natural materials and substances released from numerous industries, motor vehicles, residential wood burning, construction and demolition, and other sources. Acidic aerosols are traceable mainly to combustion of sulfur-containing fossil fuels and to reactions of photochemical free radicals with nitrogen dioxide. Exposure to ambient air pollution in North America has been clearly associated with acute and subacute effects in epidemiologic investigations and in controlled exposure studies in environmental chambers.

scholarly journals Relationship between Air Pollutant Exposure and Gynecologic Cancer Risk

2021 ◽  
Vol 18 (10) ◽  
pp. 5353
Author(s):  
Qiwei Yu ◽  
Liqiang Zhang ◽  
Kun Hou ◽  
Jingwen Li ◽  
Suhong Liu ◽  
...  
Keyword(s):  
Air Pollution ◽  
Cancer Risk ◽  
Air Pollutants ◽  
Gynecological Cancer ◽  
Gynecologic Cancer ◽  
Ambient Air ◽  
Air Pollutant ◽  
Ambient Air Pollution ◽  
Short Term Exposure ◽  
Increased Risk

Exposure to air pollution has been suggested to be associated with an increased risk of women’s health disorders. However, it remains unknown to what extent changes in ambient air pollution affect gynecological cancer. In our case–control study, the logistic regression model was combined with the restricted cubic spline to examine the association of short-term exposure to air pollution with gynecological cancer events using the clinical data of 35,989 women in Beijing from December 2008 to December 2017. We assessed the women’s exposure to air pollutants using the monitor located nearest to each woman’s residence and working places, adjusting for age, occupation, ambient temperature, and ambient humidity. The adjusted odds ratios (ORs) were examined to evaluate gynecologic cancer risk in six time windows (Phase 1–Phase 6) of women’s exposure to air pollutants (PM2.5, CO, O3, and SO2) and the highest ORs were found in Phase 4 (240 days). Then, the higher adjusted ORs were found associated with the increased concentrations of each pollutant (PM2.5, CO, O3, and SO2) in Phase 4. For instance, the adjusted OR of gynecological cancer risk for a 1.0-mg m−3 increase in CO exposures was 1.010 (95% CI: 0.881–1.139) below 0.8 mg m−3, 1.032 (95% CI: 0.871–1.194) at 0.8–1.0 mg m−3, 1.059 (95% CI: 0.973–1.145) at 1.0–1.4 mg m−3, and 1.120 (95% CI: 0.993–1.246) above 1.4 mg m−3. The ORs calculated in different air pollution levels accessed us to identify the nonlinear association between women’s exposure to air pollutants (PM2.5, CO, O3, and SO2) and the gynecological cancer risk. This study supports that the gynecologic risks associated with air pollution should be considered in improved public health preventive measures and policymaking to minimize the dangerous effects of air pollution.

scholarly journals Personal exposure to particulate matter and heart rate variability among informal electronic waste workers at Agbogbloshie: a longitudinal study

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Afua A. Amoabeng Nti ◽  
Thomas G. Robins ◽  
John Arko Mensah ◽  
Duah Dwomoh ◽  
Lawrencia Kwarteng ◽  
...  
Keyword(s):  
Heart Rate ◽  
Heart Rate Variability ◽  
Particulate Matter ◽  
Electronic Waste ◽  
Ambient Air ◽  
Repeated Measurements ◽  
Ambient Air Pollution ◽  
Continuous Exposure ◽  
Cardiac Autonomic Dysfunction ◽  
Increased Risk

Abstract Background Informal electronic waste recycling activities are major contributors to ambient air pollution, yet studies assessing the effects or relationship between direct/continuous exposure of informal e-waste workers to particulate matter and cardiovascular function are rare. Methods Repeated measurements of fractions of PM2.5, PM10–2.5, and PM10 in personal air of informal e-waste workers, (n = 142) and a comparable group (n = 65) were taken over a period of 20 months (March 2017 to November, 2018). Concurrently, 5-min resting electrocardiogram was performed on each participant to assess resting heart rate variability indices. Linear mixed-effects models were used to assess the association between PM fractions and cardiac function. Results SDNN, RMSSD, LF, HF and LH/HF ratio were all associated with PM. Significant associations were observed for PM2.5 and Mean NN (p = 0.039), PM10 and SDNN (p = 0.035) and PM 10–2.5 and LH/HF (p = 0.039). A 10 μg/m3 increase in the concentrations of PM 2.5, PM10–2.5, and PM10 in personal air was associated with reduced HRV indices and increased resting HR. A 10 μg/m3 per interquartile (IQR) increase in PM10–2.5 and PM10, decreased SDNN by 11% [(95% CI: − 0.002- 0.000); (p = 0.187)] and 34% [(95% CI: − 0.002-0.001); (p = 0.035)] respectively. However, PM2.5 increased SDNN by 34% (95% CI: − 1.32-0.64); (p = 0.493). Also, 10 μg/m3 increase in PM2.5, PM10–2.5 and PM10 decreased RMSSD by 27% [(− 1.34–0.79); (p = 0.620)], 11% [(− 1.73, 0.95); (p = 0.846)] and 0.57% [(− 1.56–0.46); (p = 0.255%)]. Conclusion Informal e-waste workers are at increased risk of developing cardiovascular disease from cardiac autonomic dysfunction as seen in reduced HRV and increased heart rate.

scholarly journals Vasodilator-stimulated phosphoprotein protects against vascular inflammation and insulin resistance

2014 ◽  
Vol 307 (7) ◽  
pp. E571-E579 ◽  
Author(s):  
Andrew M. Cheng ◽  
Norma Rizzo-DeLeon ◽  
Carole L. Wilson ◽  
Woo Je Lee ◽  
Sanshiro Tateya ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Bone Marrow ◽  
Insulin Sensitivity ◽  
Vascular Tissue ◽  
Vascular Inflammation ◽  
Physiological Role ◽  
Whole Body ◽  
Aortic Tissue ◽  
Protective Effects ◽  
Downstream Mediator

Among the pleotropic effects of endothelial nitric oxide (NO) is protection against vascular inflammation during high-fat diet (HFD) feeding. The current work investigated the role of the enzyme vasodilatory-stimulated phosphoprotein (VASP) as a downstream mediator of the anti-inflammatory effect of NO signaling in vascular tissue. Relative to mice fed a low-fat diet (LFD), levels of VASP Ser239 phosphorylation, a marker of VASP activation, were dramatically reduced in aortic tissue of mice with obesity induced by consuming a HFD. As reported previously, the effect of the HFD was associated with increased aortic inflammation, as measured by increased NF-κB-dependent gene expression, and reduced vascular insulin sensitivity (including insulin-stimulated phosphorylation of eNOS and Akt). These effects of the HFD were recapitulated by VASP knockout, implying a physiological role for VASP to constrain inflammatory signaling and thereby maintain vascular insulin sensitivity. Conversely, overexpression of VASP in endothelial cells blocked inflammation and insulin resistance induced by palmitate. The finding that transplantation of bone marrow from VASP-deficient donors into normal recipients does not recapitulate the vascular effects of whole body VASP deficiency suggests that the protective effects of this enzyme are not mediated in immune or other bone marrow-derived cells. These studies implicate VASP as a downstream mediator of the NO/cGMP pathway that is both necessary and sufficient to protect against vascular inflammation and insulin resistance. As such, this work identifies VASP as a potential therapeutic target in the treatment of obesity-related vascular dysfunction.

scholarly journals The tumor suppressor TMEM127 regulates insulin sensitivity in a tissue-specific manner

2019 ◽  
Vol 10 (1) ◽  
Author(s):  
Subramanya Srikantan ◽  
Yilun Deng ◽  
Zi-Ming Cheng ◽  
Anqi Luo ◽  
Yuejuan Qin ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Insulin Sensitivity ◽  
Tumor Suppressor ◽  
Hepatic Glucose Production ◽  
Glucose Production ◽  
Suppressor Gene ◽  
Nutrient Sensing ◽  
Whole Body ◽  
Insulin Sensitizer

Abstract Understanding the molecular components of insulin signaling is relevant to effectively manage insulin resistance. We investigated the phenotype of the TMEM127 tumor suppressor gene deficiency in vivo. Whole-body Tmem127 knockout mice have decreased adiposity and maintain insulin sensitivity, low hepatic fat deposition and peripheral glucose clearance after a high-fat diet. Liver-specific and adipose-specific Tmem127 deletion partially overlap global Tmem127 loss: liver Tmem127 promotes hepatic gluconeogenesis and inhibits peripheral glucose uptake, while adipose Tmem127 downregulates adipogenesis and hepatic glucose production. mTORC2 is activated in TMEM127-deficient hepatocytes suggesting that it interacts with TMEM127 to control insulin sensitivity. Murine hepatic Tmem127 expression is increased in insulin-resistant states and is reversed by diet or the insulin sensitizer pioglitazone. Importantly, human liver TMEM127 expression correlates with steatohepatitis and insulin resistance. Our results suggest that besides tumor suppression activities, TMEM127 is a nutrient-sensing component of glucose/lipid homeostasis and may be a target in insulin resistance.

scholarly journals Gaseous Pollutants and Particulate Matter (PM) in Ambient Air and the Number of New Cases of Type 1 Diabetes in Children and Adolescents in the Pomeranian Voivodeship, Poland

2020 ◽  
Vol 2020 ◽  
pp. 1-7 ◽  
Author(s):  
Małgorzata Michalska ◽  
Katarzyna Zorena ◽  
Piotr Wąż ◽  
Maria Bartoszewicz ◽  
Agnieszka Brandt-Varma ◽  
...  
Keyword(s):  
Type 1 Diabetes ◽  
Particulate Matter ◽  
New Technologies ◽  
Renewable Energy Sources ◽  
Ambient Air ◽  
Air Pollutant ◽  
Pollutant Emissions ◽  
Gaseous Pollutants ◽  
High Exposure

The increase in type 1 diabetes mellitus (T1DM) incidence in children is worrying and not yet fully explored. It is suggested that probably air pollution exposure could contribute to the development of T1DM. The aim of the study was to investigate the relationship between the concentration of gaseous pollutants including, nitrogen dioxide (NO2), nitric oxides (NOx), sulphur dioxide (SO2), carbon monoxide (CO), and particulate matter (PM) in the air, and the number of new cases of T1DM in children. The number of new cases of T1DM was obtained from the Clinic of Paediatrics, Diabetology, and Endocrinology, Medical University of Gdańsk. The number of children of 0–18 years old in Pomeranian Voivodeship was acquired from the Statistical Yearbook. The concentrations of PM10 absorbance, NO2, NOx, SO2, and CO were measured at 41 measuring posts, between 1 January 2015 and 31 December 2016. It was detected that the average annual concentration of PM10 was higher than the value acceptable to the WHO. Furthermore, the average 24-hour concentration of PM10 was 92 μg/m3 and was higher compared to the acceptable value of 50 μg/m3 (acc. to EU and WHO). Moreover, the number of new cases of T1DM showed a correlation with the annual average concentration of PM10 (β = 2.396, p<0.001), SO2 (β = 2.294, p<0.001), and CO (β = 2.452, p<0.001). High exposure to gaseous pollutants and particulate matter in ambient air may be one of the factors contributing to the risk of developing T1DM in children. Therefore, it is important to take action to decrease air pollutant emissions in Poland. It is crucial to gradually but consistently eliminate the use of solid fuels, such as coal and wood in households, in favour of natural gas and electricity. The development of new technologies to improve air quality, such as “best available techniques” (BAT) or renewable energy sources (water, wind, and solar generation) is of critical importance as well.

scholarly journals Ambient Air Pollution and Hospital Admissions for Peptic Ulcers in Taipei: A Time-Stratified Case-Crossover Study

2019 ◽  
Vol 16 (11) ◽  
pp. 1916 ◽  
Author(s):  
Shang-Shyue Tsai ◽  
Hui-Fen Chiu ◽  
Chun-Yuh Yang
Keyword(s):  
Air Pollution ◽  
Peptic Ulcer ◽  
Crossover Study ◽  
Air Pollutants ◽  
Hospital Admissions ◽  
Ambient Air ◽  
Air Pollutant ◽  
Ambient Air Pollution ◽  
Research Database ◽  
Case Crossover

Very few studies have been performed to determine whether there is a relationship between air pollution and increases in hospitalizations for peptic ulcer, and for those that have occurred, their results may not be completely relevant to Taiwan, where the mixture of ambient air pollutants differ. We performed a time-stratified case-crossover study to investigate the possible association between air pollutant levels and hospital admissions for peptic ulcer in Taipei, Taiwan. To do this, we collected air pollution data from Taiwan's Environmental Protection Agency and hospital admissions for peptic ulcer data for the years 2009–2013 from Taiwan's National Health Insurance's research database. We used conditional logistic regression to analyze the possible association between the two, taking temperature and relative humidity into account. Risk was expressed as odds ratios and significance was expressed with 95% confidence intervals. In our single pollutant model, peptic ulcer admissions were significantly associated with all pollutants (PM10, PM2.5, SO2, NO2, CO, and O3) on warm days (>23 °C). On cool days (<23 °C), peptic ulcer admissions were significantly associated with PM10, NO2, and O3. In our two-pollutant models, peptic ulcer admissions were significantly associated NO2 and O3 when combined with each of the other pollutants on warm days, and with PM10, NO2, and O3 on cool days. It was concluded that the likelihood of peptic ulcer hospitalizations in Taipei rose significantly with increases in air pollutants during the study period.

scholarly journals Air pollution interventions and respiratory health: a systematic review

2020 ◽  
Vol 24 (2) ◽  
pp. 150-164 ◽  
Author(s):  
S. Saleh ◽  
W. Shepherd ◽  
C. Jewell ◽  
N. L. Lam ◽  
J. Balmes ◽  
...  
Keyword(s):  
Air Pollution ◽  
Particulate Matter ◽  
Respiratory Health ◽  
Grey Literature ◽  
Ambient Air ◽  
Ambient Air Pollution ◽  
Potential Health ◽  
Exposure Reduction ◽  
Air Pollution Exposure ◽  
Pollution Exposure

BACKGROUND: Indoor and ambient air pollution exposure is a major risk to respiratory health worldwide, particularly in low- and middle-income countries (LMICs). Interventional trials have mainly focused on alternatives to cooking stoves, with mixed results. Beyond cooking, additional sources of particulate matter also contribute to the burden of air pollution exposure. This review explores evidence from current randomised controlled trials (RCTs) on the clinical effectiveness of interventions to reduce particulate matter in LMICs.METHODS: Twelve databases and the grey literature (e.g., Government reports and policy papers) were searched. Eligible studies were RCTs conducted in LMICs aiming to reduce particulate exposure from any source and reporting on at least one clinical respiratory outcome (respiratory symptoms, lung function or clinical diagnoses). Data from relevant studies were systematically extracted, the risk of bias assessed and narrative synthesis provided.RESULTS: Of the 14 included studies, 12 tested ‘improved' cookstoves, most using biomass, but solar and bioethanol cookers were also included. One trial used solar lamps and another was an integrated intervention incorporating behavioural and environmental components for the treatment and prevention of chronic obstructive pulmonary disease. Of the six studies reporting child pneumonia outcomes, none demonstrated significant benefit in intention-to-treat analysis. Ten studies reported respiratory symptom outcomes with some improvements seen, but self-reporting made these outcomes highly vulnerable to bias. Substantial inter-study clinical and methodological heterogeneity precluded calculation of pooled effect estimates.CONCLUSION: Evidence from the RCTs performed to date suggests that individual household-level interventions for air pollution exposure reduction have limited benefits for respiratory health. More comprehensive approaches to air pollution exposure reduction must be developed so their potential health benefits can be assessed.

Air pollution and public health: the challenges for Delhi, India

2018 ◽  
Vol 33 (1) ◽  
pp. 77-86 ◽  
Author(s):  
Arun Kumar Sharma ◽  
Palak Baliyan ◽  
Prashant Kumar
Keyword(s):  
Air Pollution ◽  
Particulate Matter ◽  
Data Collection ◽  
Human Health ◽  
Bronchial Asthma ◽  
Suspended Particulate Matter ◽  
Ambient Air ◽  
Ambient Air Pollution ◽  
Aerodynamic Diameter ◽  
Suspended Particulate

AbstractMitigating the impact of pollution on human health worldwide is important to limit the morbidity and mortality arising from exposure to its effect. The level and type of pollutants vary in different urban and rural settings. Here, we explored the extent of air pollution and its impacts on human health in the megacity of Delhi (India) through a review of the published literature. The study aims at describing the extent of air pollution in Delhi, the magnitude of health problems due to air pollution and the risk relationship between air pollution and associated health effects. We found 234 published articles in the PubMed search. The search showed that the extent of air pollution in Delhi has been described by various researchers from about 1986 onwards. We synthesized the findings and discuss them at length with respect to reported values, their possible interpretations and any limitations of the methodology. The chemical composition of ambient air pollution is also discussed. Further, we discuss the magnitude of health problem with respect to chronic obstructive pulmonary diseases (COPD), bronchial asthma and other illnesses. The results of the literature search showed that data has been collected in last 28 years on ambient air quality in Delhi, though it lacks a scientific continuity, consistency of locations and variations in parameters chosen for reporting. As a result, it is difficult to construct a spatiotemporal picture of the air pollution status in Delhi over time. The number of sites from where data have been collected varied widely across studies and methods used for data collection is also non-uniform. Even the parameters studied are varied, as some studies focused on particulate matter ≤10 μm in aerodynamic diameter (PM10) and those ≤2.5 μm in aerodynamic diameter (PM2.5), and others on suspended particulate matter (SPM) and respirable suspended particulate matter (RSPM). Similarly, the locations of data collection have varied widely. Some of the sites were at busy traffic intersections, some on the terraces of offices and residential houses and others in university campuses or airports. As a result, the key question of the extent of pollution and its distribution across various parts of the city could be inferred. None of the studies or a combination of them could present a complete picture of the burden of diseases like COPD, bronchial asthma and other allergic conditions attributable to pollution in Delhi. Neither could it be established what fraction of the burden of the above diseases is attributable to ambient air pollution, given that other factors like tobacco smoke and indoor air pollution are also contributors to the causation of such diseases. In our discussion, we highlight the knowledge gaps and in the conclusion, we suggested what research can be undertaken to fill the these research gaps.

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