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      Longitudinal Associations Between Ambient Air Pollution With Insulin Sensitivity, β-Cell Function, and Adiposity in Los Angeles Latino Children

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          Abstract

          Evidence suggests that ambient air pollution (AAP) exposure may contribute to the development of obesity and type 2 diabetes. The objective of this study was to determine whether exposure to elevated concentrations of nitrogen dioxide (NO 2) and particulate matter with aerodynamic diameter <2.5 (PM 2.5) had adverse effects on longitudinal measures of insulin sensitivity (S I), β-cell function, and obesity in children at high risk for developing diabetes. Overweight and obese Latino children (8–15 years; n = 314) were enrolled between 2001 and 2012 from Los Angeles, CA, and followed for an average of 3.4 years (SD 3.1 years). Linear mixed-effects models were fitted to assess relationships between AAP exposure and outcomes after adjusting for covariates including body fat percent. Higher NO 2 and PM 2.5 were associated with a faster decline in S I and a lower S I at age 18 years, independent of adiposity. NO 2 exposure negatively affected β-cell function, evidenced by a faster decline in disposition index (DI) and a lower DI at age 18 years. Higher NO 2 and PM 2.5 exposures over follow-up were also associated with a higher BMI at age 18 years. AAP exposure may contribute to development of type 2 diabetes through direct effects on S I and β-cell function.

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          Insulin resistance and insulin secretory dysfunction as precursors of non-insulin-dependent diabetes mellitus. Prospective studies of Pima Indians.

          The relative roles of obesity, insulin resistance, insulin secretory dysfunction, and excess hepatic glucose production in the development of non-insulin-dependent diabetes mellitus (NIDDM) are controversial. We conducted a prospective study to determine which of these factors predicted the development of the disease in a group of Pima Indians. A body-composition assessment, oral and intravenous glucose-tolerance tests, and a hyperinsulinemic--euglycemic clamp study were performed in 200 non-diabetic Pima Indians (87 women and 113 men; mean [+/- SD] age, 26 +/- 6 years). The subjects were followed yearly thereafter for an average of 5.3 years. Diabetes developed in 38 subjects during follow-up. Obesity, insulin resistance (independent of obesity), and low acute plasma insulin response to intravenous glucose (with the degree of obesity and insulin resistance taken into account) were predictors of NIDDM: The six-year cumulative incidence of NIDDM was 39 percent in persons with values below the median for both insulin action and acute insulin response, 27 percent in those with values below the median for insulin action but above that for acute insulin response, 13 percent in those with values above the median for insulin action and below that for acute insulin response, and 0 in those with values originally above the median for both characteristics. Insulin resistance is a major risk factor for the development of NIDDM: A low acute insulin response to glucose is an additional but weaker risk factor.
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            Environmental Inequality in Exposures to Airborne Particulate Matter Components in the United States

            Background: Growing evidence indicates that toxicity of fine particulate matter ≤ 2.5 μm in diameter (PM2.5) differs by chemical component. Exposure to components may differ by population. Objectives: We investigated whether exposures to PM2.5 components differ by race/ethnicity, age, and socioeconomic status (SES). Methods: Long-term exposures (2000 through 2006) were estimated for 215 U.S. census tracts for PM2.5 and for 14 PM2.5 components. Population-weighted exposures were combined to generate overall estimated exposures by race/ethnicity, education, poverty status, employment, age, and earnings. We compared population characteristics for tracts with and without PM2.5 component monitors. Results: Larger disparities in estimated exposures were observed for components than for PM2.5 total mass. For race/ethnicity, whites generally had the lowest exposures. Non-Hispanic blacks had higher exposures than did whites for 13 of the 14 components. Hispanics generally had the highest exposures (e.g., 152% higher than whites for chlorine, 94% higher for aluminum). Young persons (0–19 years of age) had levels as high as or higher than other ages for all exposures except sulfate. Persons with lower SES had higher estimated exposures, with some exceptions. For example, a 10% increase in the proportion unemployed was associated with a 20.0% increase in vanadium and an 18.3% increase in elemental carbon. Census tracts with monitors had more non-Hispanic blacks, lower education and earnings, and higher unemployment and poverty than did tracts without monitors. Conclusions: Exposures to PM2.5 components differed by race/ethnicity, age, and SES. If some components are more toxic than others, certain populations are likely to suffer higher health burdens. Demographics differed between populations covered and not covered by monitors.
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              Air pollution and incidence of hypertension and diabetes mellitus in black women living in Los Angeles.

              Evidence suggests that longer-term exposure to air pollutants over years confers higher risks of cardiovascular morbidity and mortality than shorter-term exposure. One explanation is that the cumulative adverse effects that develop over longer durations lead to the genesis of chronic disease. Preliminary epidemiological and clinical evidence suggests that air pollution may contribute to the development of hypertension and type 2 diabetes mellitus. We used Cox proportional hazards models to assess incidence rate ratios (IRRs) and 95% confidence intervals (CIs) for incident hypertension and diabetes mellitus associated with exposure to fine particulate matter (PM(2.5)) and nitrogen oxides in a cohort of black women living in Los Angeles. Pollutant levels were estimated at participants' residential addresses with land use regression models (nitrogen oxides) and interpolation from monitoring station measurements (PM(2.5)). Over follow-up from 1995 to 2005, 531 incident cases of hypertension and 183 incident cases of diabetes mellitus occurred. When pollutants were analyzed separately, the IRR for hypertension for a 10-μg/m(3) increase in PM(2.5) was 1.48 (95% CI, 0.95-2.31), and the IRR for the interquartile range (12.4 parts per billion) of nitrogen oxides was 1.14 (95% CI, 1.03-1.25). The corresponding IRRs for diabetes mellitus were 1.63 (95% CI, 0.78-3.44) and 1.25 (95% CI, 1.07-1.46). When both pollutants were included in the same model, the IRRs for PM(2.5) were attenuated and the IRRs for nitrogen oxides were essentially unchanged for both outcomes. Our results suggest that exposure to air pollutants, especially traffic-related pollutants, may increase the risk of type 2 diabetes mellitus and possibly of hypertension.
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                Author and article information

                Journal
                Diabetes
                Diabetes
                diabetes
                diabetes
                Diabetes
                Diabetes
                American Diabetes Association
                0012-1797
                1939-327X
                July 2017
                30 January 2017
                : 66
                : 7
                : 1789-1796
                Affiliations
                [1] 1Department of Preventive Medicine, Division of Environmental Health, University of Southern California, Los Angeles, CA
                [2] 2Department of Public Health, California State University, Los Angeles, CA
                [3] 3Sonoma Technology, Inc., Petaluma, CA
                [4] 4Department of Pediatrics, University of Southern California, Los Angeles, CA
                [5] 5Department of Preventive Medicine, Diabetes and Obesity Research Institute, University of Southern California, Los Angeles, CA
                [6] 6Department of Physiology and Biophysics, University of Southern California, Los Angeles, CA
                Author notes
                Corresponding author: Michael I. Goran, goran@ 123456usc.edu .
                Author information
                http://orcid.org/0000-0002-1228-9070
                Article
                1416
                10.2337/db16-1416
                5482082
                28137791
                dd72480e-d23d-4d25-9c7e-d52a91b67175
                © 2017 by the American Diabetes Association.

                Readers may use this article as long as the work is properly cited, the use is educational and not for profit, and the work is not altered. More information is available at http://www.diabetesjournals.org/content/license.

                History
                : 17 November 2016
                : 24 January 2017
                Page count
                Figures: 3, Tables: 3, Equations: 0, References: 42, Pages: 8
                Funding
                Funded by: National Institute of Environmental Health Sciences, DOI http://dx.doi.org/10.13039/100000066;
                Award ID: T32ES013678
                Award ID: P01ES022845
                Award ID: 5P30ES007048
                Award ID: P50ES026086
                Award ID: 83615801-0
                Funded by: National Center on Minority Health and Health Disparities, DOI http://dx.doi.org/10.13039/100000096;
                Award ID: P60MD002254
                Funded by: National Institute of Diabetes and Digestive and Kidney Diseases, DOI http://dx.doi.org/10.13039/100000062;
                Award ID: R01DK59211
                Funded by: Environmental Protection Agency, DOI http://dx.doi.org/10.13039/501100001589;
                Award ID: RD83544101
                Award ID: 83615801
                Categories
                Metabolism

                Endocrinology & Diabetes
                Endocrinology & Diabetes

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