OBJECTIVE: Recent studies suggest that air pollution plays a role in type 2 diabetes (T2D) incidence and mortality. The underlying physiological mechanisms have yet to be established. We hypothesized that air pollution adversely affects insulin sensitivity and secretion and serum lipid levels. RESEARCH DESIGN AND METHODS: Participants were selected from BetaGene (n = 1,023), a study of insulin resistance and pancreatic β-cell function in Mexican Americans. All participants underwent DXA and oral and intravenous glucose tolerance tests and completed dietary and physical activity questionnaires. Ambient air pollutant concentrations (NO2, O3, and PM2.5) for short- and long-term periods were assigned by spatial interpolation (maximum interpolation radius of 50 km) of data from air quality monitors. Traffic-related air pollution from freeways (TRAP) was estimated using the dispersion model as NOx. Variance component models were used to analyze individual and multiple air pollutant associations with metabolic traits. RESULTS: Short-term (up to 58 days cumulative lagged averages) exposure to PM2.5 was associated with lower insulin sensitivity and HDL-to-LDL cholesterol ratio and higher fasting glucose and insulin, HOMA-IR, total cholesterol, and LDL cholesterol (LDL-C) (all P ≤ 0.036). Annual average PM2.5 was associated with higher fasting glucose, HOMA-IR, and LDL-C (P ≤ 0.043). The effects of short-term PM2.5 exposure on insulin sensitivity were largest among obese participants. No statistically significant associations were found between TRAP and metabolic outcomes. CONCLUSIONS: Exposure to ambient air pollutants adversely affects glucose tolerance, insulin sensitivity, and blood lipid concentrations. Our findings suggest that ambient air pollutants may contribute to the pathophysiology in the development of T2D and related sequelae.

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 (NO2) and particulate matter with aerodynamic diameter <2.5 (PM2.5) had adverse effects on longitudinal measures of insulin sensitivity (SI), 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 NO2 and PM2.5 were associated with a faster decline in SI and a lower SI at age 18 years, independent of adiposity. NO2 exposure negatively affected β-cell function, evidenced by a faster decline in disposition index (DI) and a lower DI at age 18 years. Higher NO2 and PM2.5 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 SI and β-cell function.

Growing evidence indicates exposure to air pollution contributes to obesity and cardiometabolic disease risk in children and adults, however studies are lacking in young adulthood, an important transitional period in the life course. The aim of this study was to examine the associations of short- and long-term regional ambient and near-roadway air pollution (NRAP) exposures on adiposity and cardiometabolic health in young adults aged 17-22 years. From 2014 to 2018, a subset of participants (n = 158) were recruited from the Children's Health Study to participate in the Meta-AIR (Metabolic and Asthma Incidence Research) study to assess obesity (body composition and abdominal adiposity) and cardiometabolic health (fasting glucose, fasting insulin and lipid profiles) measures. Prior 1-month and 1-year average air pollution exposures were calculated from residential addresses. This included nitrogen dioxide (NO2), ozone (O3), particulate matter with aerodynamic diameter < 10 μm (PM10), particulate matter with aerodynamic diameter < 2.5 μm (PM2.5) and NRAP (freeway, non-freeway, and total nitrogen oxides (NOx)) exposures. Linear regression models examined associations of prior 1-month (short-term) and 1-year (long-term) air pollution exposures on obesity and cardiometabolic factors adjusting for covariates and past childhood air pollution exposures. In the Meta-AIR study, we conducted a comprehensive analysis with short- and long-term regional ambient and NRAP exposures (in both single- and multi-pollutant models) and obesity- and cardiometabolic-related outcomes and found associations with a few outcomes. A 1 standard deviation (SD) change in long-term NO2 exposure was associated with a 11.3 mg/dL higher level of total cholesterol (p = 0.04) and 9.4 mg/dL higher level of low-density lipoproteins (LDL)-cholesterol (p = 0.04). Amongst obese participants, associations between long-term NO2 and total cholesterol and LDL-cholesterol were 4.5 and 9 times larger than the associations in non-obese participants (pinteraction = 0.008 and 0.03, respectively). Additionally, we observed a statistically significant association with increased short-term O3 exposure and higher triglyceride and very-low-density lipoprotein (VLDL) cholesterol levels (p = 0.04), lower high-density lipoprotein (HDL) cholesterol levels (p = 0.03), and higher hepatic fat levels (p = 0.02). Amongst glucose-related factors, long-term PM2.5 exposure was associated with higher levels of insulin area under the curve (p = 0.03). There were no other statistically significant associations with short- or long-term air pollutants and BMI, other measures of adiposity, and cardiometabolic outcomes. Higher exposure to regional air pollutants, namely prior 1-year average NO2, was associated with higher fasting serum lipid measures. These associations were more pronounced in obese participants, suggesting obesity may exacerbate the effects of air pollution exposure on lipid levels in young adults. This study did not find any other associations between short- and long-term ambient and NRAP exposures across a range of other obesity and cardiometabolic indicators. Further studies in young adults are warranted as our study suggests potential deleterious associations of both short- and long-term air pollution exposures and lipid metabolism.

Background: To date, no studies have assessed the longitudinal changes of dietary intake on metabolic risk factors in Latino youth.Objective: We asse

Objective: The purpose of this report is to investigate the associations between metabolic syndrome (MS) and levels of morning serum cortisol in a cohort of overweight Latino youth. Design: Subjects were 205 overweight, Latino youth (age 8–13 yr, body mass index percentile > 85, family history positive for type 2 diabetes). Measures included body composition by dual-energy x-ray absorptiometry, intraabdominal adipose tissue (IAAT) by magnetic resonance imaging, insulin sensitivity by frequently sampled iv glucose tolerance test/minimal model, fasting lipids, and serum cortisol. Results: Children with MS had higher body mass index percentile, total body fat mass, and IAAT and lower insulin sensitivity than those without MS. Children with MS had higher morning serum cortisol levels, whether unadjusted (10.1 ± 3.7 vs. 9.0 ± 2.8 μg/dl, P < 0.05) or after adjusting for age, gender, total body fat and lean tissue mass, and insulin sensitivity (10.4 ± 0.4 vs. 8.9 ± 0.3 μg/dl, P < 0.01). Increasing number of features of MS was associated with higher cortisol levels, after adjusting for covariates (P = 0.001). Among individual features of MS, systolic blood pressure had the strongest relationship with adjusted cortisol level (r = 0.34; P < 0.001), followed by diastolic blood pressure and fasting plasma glucose (both r = 0.23; P < 0.01). IAAT was associated with cortisol (r = 0.16; P < 0.05), whereas high-density lipoprotein, triglycerides, and waist circumference were not. Conclusions: In overweight, Latino youth, MS is associated with higher morning serum cortisol levels, independent of body fat and insulin sensitivity. More studies are needed to investigate the role of relative hypercortisolism and chronic stress in obesity-related metabolic disorders in children.

Context and Objective: The purpose of the present study was to investigate the cross-sectional and longitudinal associations of serum morning cortisol and aspects of insulin action in Latino children and adolescents (8–13 yr) at risk for type 2 diabetes. Design and Participants: The present study includes a cross-sectional analysis in 211 participants and a longitudinal analysis in a subset of 143 participants. Results: At baseline, cortisol was negatively associated with fasting glucose (r = 0.23; P < 0.01), β-cell function (disposition index, r = −0.24; P < 0.05), and acute insulin response to glucose (r = −0.27; P < 0.05). Baseline cortisol was also significantly related to the change in insulin sensitivity over 1 yr (r = −0.23; P < 0.05). These results did not differ by Tanner stage or sex. Conclusions: Cortisol contributes to the reduction in insulin sensitivity at an early age in Latino children and adolescents. Specifically, cortisol is negatively associated with potential compensatory mechanisms for insulin resistance, such as increased β-cell function and increased insulin release to a glucose challenge, by exacerbating the progression toward insulin resistance in this population. The results underline the relevance of glucocorticoid reduction for the prevention of metabolic disease in Latino children and adolescents.