Air Pollution and Insulin Resistance: Do All Roads Lead to Rome?

Kodavanti, Urmila P.

doi:10.2337/db14-1682

Cited by 28 publications

(11 citation statements)

References 18 publications

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“…Several reviews and a meta-analysis combined the epidemiological findings and quantified the risk increases for type 2 diabetes per 10 mg/m 3 increase in exposure between 5% and 27% for particulate matter (PM) #2.5mm in diameter (PM 2.5 ), 1-15% for PM #10mm in diameter (PM 10 ), and 1-11% for nitrogen dioxide (NO 2 ) (14,(16)(17)(18)(19)(20), depending on the studies included. Still, the underlying mechanisms are not fully understood, although a number of plausible pathways have been suggested, including systemic inflammation, oxidative stress, and neuronal mechanisms (12,14,15,21). Recent studies (10,(22)(23)(24)(25)(26)(27) investigating air pollution and IR as a precursor state of type 2 diabetes showed positive associations.…”

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confidence: 99%

Association Between Long-term Exposure to Air Pollution and Biomarkers Related to Insulin Resistance, Subclinical Inflammation, and Adipokines

et al. 2016

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Insulin resistance (IR) is present long before the onset of type 2 diabetes and results not only from inherited and lifestyle factors but also likely from environmental conditions. We investigated the association between modeled long-term exposure to air pollution at residence and biomarkers related to IR, subclinical inflammation, and adipokines. Data were based on 2,944 participants of the KORA (Cooperative Health Research in the Region Augsburg) F4 study conducted in southern Germany (2006-2008). We analyzed associations between individual air pollution concentration estimated by land use regression and HOMA-IR, glucose, insulin, HbA, leptin, and high-sensitivity C-reactive protein levels from fasting samples using multivariable linear regression models. Effect estimates were calculated for the whole study population and subgroups of individuals who did not have diabetes, had prediabetes, or had diabetes. Among all participants, a 7.9 μg/m increment in particulate matter of <10 μm was associated with higher HOMA-IR (15.6% [95% CI 4.0; 28.6]) and insulin (14.5% [3.6; 26.5]). Nitrogen dioxide was associated with HOMA-IR, glucose, insulin, and leptin. Effect estimates for individuals with prediabetes were much larger and highly statistically significant, whereas individuals who did not have diabetes or had diabetes showed rather weak associations. No association was seen for HbA level. Our results suggested an association between long-term exposure to air pollution and IR in the general population that was attributable mainly to individuals with prediabetes.

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confidence: 99%

Association Between Long-term Exposure to Air Pollution and Biomarkers Related to Insulin Resistance, Subclinical Inflammation, and Adipokines

et al. 2016

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“…Other lines of evidence suggest that non-inflammatory pathways might also link PM to insulin resistance (Brook et al, 2013), with experimental animal models providing evidence for insulin resistance in muscle tissues resulting from lipid and protein oxidation by-products upon acute exposure to ozone (Kodavanti, 2015;Vella et al, 2015). Hence, despite the strong evidence for a central role of pre-existing inflammation, e.g., due to asthma or being at genetic risk of obesity, other non-inflammation based mechanisms cannot be ruled out to underlie or contribute to the air pollution-diabetes association.…”

Section: Discussionmentioning

confidence: 98%

Air pollution and diabetes association: Modification by type 2 diabetes genetic risk score

Eze

Imboden

Kumar

et al. 2016

Environment International

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Exposure to ambient air pollution (AP) exposure has been linked to type 2 diabetes (T2D) risk. Evidence on the impact of T2D genetic variants on AP susceptibility is lacking. Compared to single variants, joint genetic variants contribute substantially to disease risk. We investigated the modification of AP and diabetes association by a genetic risk score (GRS) covering 63 T2D genes in 1524 first follow-up participants of the Swiss cohort study on air pollution and lung and heart diseases in adults. Genome-wide data and covariates were available from a nested asthma case-control study design. AP was estimated as 10-year mean residential particulate matter <10μm (PM10). We computed count-GRS and weighted-GRS, and applied PM10 interaction terms in mixed logistic regressions, on odds of diabetes. Analyses were stratified by pathways of diabetes pathology and by asthma status. Diabetes prevalence was 4.6% and mean exposure to PM10 was 22μg/m(3). Odds of diabetes increased by 8% (95% confidence interval: 2, 14%) per T2D risk allele and by 35% (-8, 97%) per 10μg/m(3) exposure to PM10. We observed a positive interaction between PM10 and count-GRS on diabetes [ORinteraction=1.10 (1.01, 1.20)], associations being strongest among participants at the highest quartile of count-GRS [OR: 1.97 (1.00, 3.87)]. Stronger interactions were observed with variants of the GRS involved in insulin resistance [(ORinteraction=1.22 (1.00, 1.50)] than with variants related to beta-cell function. Interactions with count-GRS were stronger among asthma cases. We observed similar results with weighted-GRS. Five single variants near GRB14, UBE2E2, PTPRD, VPS26A and KCNQ1 showed nominally significant interactions with PM10 (P<0.05). Our results suggest that genetic risk for T2D may modify susceptibility to air pollution through alterations in insulin sensitivity. These results need confirmation in diabetes cohort consortia.

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“…(28)(29)(30)(31). Although the biological mechanisms underlying this association are still unclear, animal studies have shown that high levels of air pollution may be equivalent to a high-fat diet in terms of its effects, involving immune activation, endoplasmic reticulum (ER) stress, oxidative stress and CNS inflammation (32,33). Some studies have investigated the association between GDM and air pollutant including nitric oxides (NOx), sulfur dioxide (SO2), ozone (O3), particulate matter with diameter ≤ 10µm (PM10) and particulate matter with diameter ≤ 2.5 (PM2.5).…”

Section: Introductionmentioning

confidence: 99%

Outdoor Air Pollution and Gestational Diabetes Mellitus: A Systematic Review and Meta-Analysis

Elshahidi

2019

ijph

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Background: During the past 20 years, the prevalence of gestational diabetes mellitus (GDM) has increased by ∼10%-100% in several race/ethnicity groups. There is an association between ambient air pollution (AAP) and GDM. This study aimed to summarize the evidence about the association between AAP and GDM. Methods: PubMed, Embase, Scopus, Web of Science and Cochrane Library were searched from inception till Oct 2017. Studies about the association between ambient air pollutants levels and GDM were included. Pooled effect estimates and their 95% confidence interval (CI) were calculated using R. Results: Eight studies met the inclusion criteria. The odds of developing GDM upon exposure to CO (per 1 ppm), NO (per 1 ppb), NO2 (per 10 µg/m3), NOx (per 1 ppb), O3 (per 10 ppb), SO2 (per 10 ppb), PM10 (per 10 µg/m3) and PM2.5 (per 10 µg/m3) were 1.47 (95% CI 0.88-2.06), 1.04 (95% CI 1.03-1.06), 1 (95% CI 0.93-1.08), 1.02 (95% CI 1-1.04), 1.05 (95% CI 0.94-1.16), 1.39 (95% CI 1.04-1.73), 0.97 (95% CI 0.94-0.99) and 1.12 (95% CI 0.93-1.31), respectively. Conclusion: The current literature showed evidence for an association between AAP and GDM. However, further well-designed studies are needed.

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Air Pollution and Insulin Resistance: Do All Roads Lead to Rome?

Cited by 28 publications

References 18 publications

Association Between Long-term Exposure to Air Pollution and Biomarkers Related to Insulin Resistance, Subclinical Inflammation, and Adipokines

Association Between Long-term Exposure to Air Pollution and Biomarkers Related to Insulin Resistance, Subclinical Inflammation, and Adipokines

Air pollution and diabetes association: Modification by type 2 diabetes genetic risk score

Outdoor Air Pollution and Gestational Diabetes Mellitus: A Systematic Review and Meta-Analysis

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