Could Dirty Air Cause Diabetes?

IIt has been assumed that damage from exposure to tobacco smoke and other particulate air pollutants is imposed primarily on the lungs and is associated with increased morbidity and mortality rates in patients with preexisting lung disease. This is supported by a considerable amount of previous data, such as the mortality data from the December 1952 London smog disaster, which may have caused as many as 12 000 deaths, almost all in patients with preexisting lung disease.1 Total suspended particulate matter (PM) was as high as 3000 μg/m3. Similar patterns of elevated morbidity and mortality rates, primarily in patients with preexisting lung disease, have been documented in other acute episodes of air pollution in the past.2 However, evidence from the past 10 years shows that sudden increases in ambient air pollution can also rapidly raise morbidity and mortality rates in patients with existing cardiovascular disease, as much or more than the rise associated with lung disease. In the present issue of Circulation , Pope and associates3 report interesting new data on the effects on mortality rate of long-term differences, as opposed to sudden transient increases, in levels of air pollution. Data were derived from a large, comprehensive study initiated by the American Cancer Society and linked to cancer prevention. The study involved a large population of subjects enrolled in 1982 from metropolitan centers in all 50 states and Puerto Rico. Vital status of participants was collected every 2 years for the subsequent 16 years, and a cause of death was identified for 98% of the known fatalities. Metropolitan area of residence was known for each participant, and particle counts of fine particulates were averaged over quarterly intervals throughout the year for each included metropolitan area. A questionnaire provided additional data, allowing for differences in mortality …

Hypertension Editors' Picks: Air Pollution.

Addressing the Burden of Disease Attributable to Air Pollution in India: The Need to Integrate across Household and Ambient Air Pollution Exposures

Ambient particulate matter has been associated consistently with an increased risk for mortality largely due to cardiovascular diseases.1 Although the relative risk estimates from epidemiological studies are small, they apply to almost the entire population of the United States. Consequently, exposure to ambient particles produces considerable burden of disease, and its mitigation offers the benefit of improving life expectancy.2 Articles see pp 941 and 949 Over the past decade, research has substantiated the understanding of the pathophysiological mechanisms linking ambient particles to the cardiovascular system3,4 once it was noted that ambient air pollution elicits systemic inflammatory responses in the general population.5 An update of the American Heart Association statement on air pollution and cardiovascular disease3 is under way. Mechanisms considered for active and secondhand smoke as well as ambient air pollution are strikingly similar.4,6,7 They include progression of atherosclerotic plaques to vulnerable forms, prothrombotic states, endothelial dysfunction, and altered autonomic nervous system control (Figure). Increased systemic oxidative stress is considered the key mechanism responsible for most of these pathophysiological changes. Increased risks for cardiovascular disease in general and coronary artery disease in particular have been documented for active and secondhand smoke as well as ambient particulate matter. Deep venous thrombosis has been added to this list recently.8 Figure. Overview on pathomechanism linking ambient air pollution,4 secondhand smoke,7 and active smoking to acute coronary syndromes. Nevertheless, the public health relevance of particulate matter in the light of the smoking literature remains hotly debated. Smokers are exposed to considerably higher cumulative doses of particulate matter than the general nonsmoking population. Mortality due to low doses of ambient particles may be considered counterintuitive compared with doses of particles tolerated by smoking individuals. A systematic assessment of the exposure-response function ranging from low doses of inhaled particles …

Air Pollution and Coronary Risk in Kidney Transplant Recipients

Adverse respiratory effects and allergic susceptibility in relation to particulate air pollution: flirting with disaster.

Fine particulate: it matters.

Obesity, and more specifically accumulation of adipose tissue in the visceral and subcutaneous abdominal locations, is a major risk factor for the development of cardiovascular pathologies including hypertension and atherosclerosis, as well as metabolic disorders such as type 2 diabetes. During recent years, “metaflammation” or metabolically-triggered inflammation1 has emerged as a key process involved in the clustering of those conditions. Although several metabolically active organs such as the liver, muscle, and, recently, the intestine2 certainly play major roles, the white adipose tissue appears as a central and primary player as both a source and site of inflammation. Accumulation of adipose tissue macrophages (ATMs) has been well-described in obese conditions in mice and humans.3–5 Moreover, the ATM proinflammatory phenotype has been linked to the development of insulin resistance in mice,4 although the exact nature of the proinflammatory myeloid cells, ie, macrophages or dentritic cells, remains to be determined.6 Nevertheless, the causal link between inflammation and insulin resistance was further strengthened by the specific knock-out of the inflammation coordinator IkappaB kinase beta of myeloid cells, which gave protection against insulin resistance.7 The study of Kintscher and al in this issue8 extends those original observations to cells of adaptative immunity. The authors suggest that the accumulation of T-lymphocytes, assessed mainly through gene expression analyses and immunohistochemistry, occurs in the perigonadal adipose tissue of mice on …

Inflammatory polarisation of adipose tissue macrophages (ATMs) plays a critical role in the development of obesity-associated metabolic diseases such as insulin resistance and diabetes. Our previous study indicated that dietary luteolin (LU) could prevent the establishment of insulin resistance in mice fed a high-fat diet (HFD). Here, we further investigated the effects of LU, which is a natural flavonoid, on pre-established insulin resistance and obesity-associated ATM polarisation in mice. Five-week-old C57/BL6 mice were fed on a low-fat diet or HFD for 20weeks, with some mice receiving supplementation with 0.01% LU from weeks 1 or 10 of the HFD to assess the actions of LU on insulin resistance and ATM polarisation. Furthermore, the role of LU in metabolic-dysfunction-associated macrophage phenotypes was investigated in vitro. Dietary LU supplementation, either for 20weeks or from weeks 10 to 20 of an HFD, significantly improved insulin resistance in HFD-fed mice. In addition, inflammatory macrophage infiltration and polarisation were suppressed in mouse epididymal adipose tissues. Furthermore, LU treatment directly reversed lipopolysaccharide-stimulated and metabolism-regulated molecules, and induced inflammatory polarisation in mouse RAW264.7 cells and peritoneal cavity resident macrophages. Finally, using the selective AMP-activated protein kinase (AMPK) inhibitor compound C and Ampkα1 (also known as Prkaa1) silencing with siRNA, we found that LU activated AMPKα1 in macrophages to inhibit their inflammatory polarisation and enhanced insulin signals in adipocytes that were stimulated with macrophage-conditioned media. Dietary LU ameliorated insulin resistance in diet-induced obese mice by promoting AMPKα1 signalling in ATMs.

Vol. 127, No. 9 ErratumOpen AccessErratum: “Mortality Risk and Fine Particulate Air Pollution in a Large, Representative Cohort of U.S. Adults”is correction ofMortality Risk and Fine Particulate Air Pollution in a Large, Representative Cohort of U.S. Adults C. Arden Pope III, Jacob S. Lefler, Majid Ezzati, Joshua D. Higbee, Julian D. Marshall, Sun-Young Kim, Matthew Bechle, Kurtis S. Gilliat, Spencer E. Vernon, Allen L. Robinson, and Richard T. Burnett C. Arden Pope III Search for more papers by this author , Jacob S. Lefler Search for more papers by this author , Majid Ezzati Search for more papers by this author , Joshua D. Higbee Search for more papers by this author , Julian D. Marshall Search for more papers by this author , Sun-Young Kim Search for more papers by this author , Matthew Bechle Search for more papers by this author , Kurtis S. Gilliat Search for more papers by this author , Spencer E. Vernon Search for more papers by this author , Allen L. Robinson Search for more papers by this author , and Richard T. Burnett Search for more papers by this author Published:27 September 2019CID: 099002https://doi.org/10.1289/EHP6182Cited by:7AboutSectionsPDF ToolsDownload CitationsTrack Citations ShareShare onFacebookTwitterLinked InReddit In the final sentence of the Acknowledgments section, the sentence “Findings and conclusions of this research are those of the authors and do not necessarily represent the views of the National Center for Health Statistics (NCHS) Research Data Center (RDC), the NCHS, the U.S. EPA, or the Centers for Disease Control and Prevention” should be “Findings and conclusions of this research are those of the authors and do not necessarily represent the views of the National Center for Health Statistics (NCHS) Research Data Center (RDC), the NCHS, the U.S. EPA, the Centers for Disease Control and Prevention, or Cornerstone Research.”The authors apologize for the error.FiguresReferencesRelatedDetailsCited by Thind M, Tessum C and Marshall J (2022) Environmental Health, Racial/Ethnic Health Disparity, and Climate Impacts of Inter-Regional Freight Transport in the United States, Environmental Science & Technology, 10.1021/acs.est.2c03646, 57:2, (884-895), Online publication date: 17-Jan-2023. Wu Y, Xu Z, Liu S, Tang M and Lu S (2022) Emission Characteristics of Particulate Matter from Coal-Fired Power Units with Different Load Conditions, Water, Air, & Soil Pollution, 10.1007/s11270-022-05919-9, 233:11, Online publication date: 1-Nov-2022. Jun Y, Song I, Kim O and Kim S (2022) Impact of limited residential address on health effect analysis of predicted air pollution in a simulation study, Journal of Exposure Science & Environmental Epidemiology, 10.1038/s41370-022-00412-1, 32:4, (637-643), Online publication date: 1-Jul-2022. Cano M, Reina T, Portillo E, Gallego Fernández L and Navarrete B (2021) Characterization of emissions of condensable particulate matter under real operation conditions in cement clinker kilns using complementary experimental techniques, Science of The Total Environment, 10.1016/j.scitotenv.2021.147472, 786, (147472), Online publication date: 1-Sep-2021. Kataoka H, Tanaka K, Tazuya-Murayama K, Yamashita T and Nishikawa J (2021) Cytotoxic Effects of Water-Soluble Extracts of Coarse and Fine Atmospheric Particulate Matter on Mast Cell Lines, Biological and Pharmaceutical Bulletin, 10.1248/bpb.b20-00576, 44:1, (57-62), Online publication date: 1-Jan-2021. Ou J, Hanson H, Ramsay J, Kaddas H, Pope C, Leiser C, VanDerslice J and Kirchhoff A (2020) Fine Particulate Matter Air Pollution and Mortality among Pediatric, Adolescent, and Young Adult Cancer Patients, Cancer Epidemiology, Biomarkers & Prevention, 10.1158/1055-9965.EPI-19-1363, 29:10, (1929-1939), Online publication date: 1-Oct-2020. Coffman E, Burnett R and Sacks J (2020) Quantitative Characterization of Uncertainty in the Concentration–Response Relationship between Long-Term PM 2.5 Exposure and Mortality at Low Concentrations , Environmental Science & Technology, 10.1021/acs.est.0c02770 Related articlesMortality Risk and Fine Particulate Air Pollution in a Large, Representative Cohort of U.S. Adults24 July 2019Environmental Health Perspectives Vol. 127, No. 9 September 2019Metrics About Article Metrics Publication History Manuscript received5 September 2019Manuscript accepted17 September 2019Originally published27 September 2019 Financial disclosuresPDF download License information EHP is an open-access journal published with support from the National Institute of Environmental Health Sciences, National Institutes of Health. All content is public domain unless otherwise noted. Note to readers with disabilities EHP strives to ensure that all journal content is accessible to all readers. However, some figures and Supplemental Material published in EHP articles may not conform to 508 standards due to the complexity of the information being presented. If you need assistance accessing journal content, please contact [email protected]. Our staff will work with you to assess and meet your accessibility needs within 3 working days.

ObjectivePrevious studies proved the effect of long-term exposure to air pollution or physical activity (PA) on the risk of systemic inflammation-induced multimorbidity (SIIM), while the evidence regarding their joint effects was rare, especially in low- and middle-income countries. Therefore, we aimed to examine the extent of interaction or joint relations of PA and air pollution with SIIM.MethodsThis study included 72,172 participants from China Multi-Ethnic Cohort.The average concentrations of ambient particulate matter pollutants (PM1, PM2.5, and PM10) were estimated using satellite-based random forest models. Self-reported information on a range of physical activities related to occupation, housework, commuting, and leisure activities was collected by an interviewer-administered questionnaire. A total of 11 chronic inflammatory systemic diseases were assessed based on self-reported lifetime diagnosis or medical examinations. SIIM was defined as having ≥ 2 chronic diseases related to systemic inflammation. Logistic regression models were used to assess the complex associations of air pollution particulate matter and PA with SIIM.ResultsWe found positive associations between long-term air pollution particulates exposure and SIIM, with odds ratios (95%CI) of 1.07 (1.03 to 1.11), 1.18 (1.13 to 1.24), and 1.08 (1.05 to 1.12) per 10 µg/m3 increase in PM1, PM2.5, and PM10. No significant multiplicative interaction was found between ambient air pollutant exposure and PA on SIIM, whereas negative additive interaction was observed between long-term exposure to PM2.5 and PA on SIIM. The positive associations between low volume PA and SIIM were stronger among those exposed to high-level air pollution particulates. Compared with individuals engaged in high volume PA and exposed to low-level ambient air pollutants, those engaged in low volume PA and exposed to high-level ambient air pollutants had a higher risk of SIIM (OR = 1.49 in PM1 exposure, OR = 1.84 in PM2.5 exposure, OR = 1.19 in PM10 exposure).ConclusionsLong-term (3 years average) exposure to PM1, PM2.5, and PM10 was associated with an increased risk of SIIM. The associations were modified by PA, highlighting PA’s importance in reducing SIIM for all people, especially those living in high-level air pollution regions.

Epidemiologic studies report associations between particulate air pollution and increased mortality from pulmonary diseases. This study was performed to examine whether the exposure to ambient gaseous and particulate air pollution leads to an alteration of the differential white blood cell count in patients with chronic pulmonary diseases like chronic bronchitis, chronic obstructive pulmonary disease, and asthma. A prospective panel study was conducted in Erfurt, Eastern Germany, with 12 repeated differential white blood cell counts in 38 males with chronic pulmonary diseases. Hourly particulate and gaseous air pollutants and meteorological data were acquired. Mixed models with a random intercept adjusting for trend, meteorology, weekday, and other risk variables were used.In this explorative analysis, we found an immediate decrease of polymorphonuclear leukocytes in response to an increase of most gaseous and particulate pollutants. Lymphocytes increased within 24 h in association with all gaseous pollutants but showed only minor effects in regard to particulate air pollution. Monocytes showed an increase associated with ultrafine particles, and nitrogen monoxide. The effect had two peaks in time, one 0–23 h before blood withdrawal and a second one with a time lag of 48–71 h. The increase of particulate and gaseous air pollution was associated with multiple changes in the differential white blood cell count in patients with chronic pulmonary diseases.

Air pollution in Pakistan, and the region at large, has become one of the greatest environmental risks to health. Three major cities of Pakistan, Lahore, Karachi, and Peshawar, have been declared the worst in the world for their Air Quality Index and PM air pollution. The population residing in these cities is facing adverse health 2.5 effects. Children, with developing lungs and geriatric patients with chronic diseases are the worst affected. The impact of short-term and long-term exposure to air pollution includes premature mortality, exacerbated chronic heart and lung disease, lung cancer, decreased lung function in children as well as school absenteeism 1

Air Quality Modelling Application to Evaluate Effects of PM Air Concentrations on Urban Population Exposure.

Diesel Exhaust Particulates Exacerbate Asthma-Like Inflammation by Increasing CXC Chemokines