2019
TL, Alderete; R, Jin; DI, Walker; D, Valvi; Z, Chen; DP, Jones; C, Peng; FD, Gilliland; K, Berhane; DV, Conti; MI, Goran; L, Chatzi
Perfluoroalkyl substances, metabolomic profiling, and alterations in glucose homeostasis among overweight and obese Hispanic children: A proof-of-concept analysis Journal Article
In: Environ Int, vol. 126, pp. 445–453, 2019.
Abstract | BibTeX | Tags: environmental pollution
@article{pmid30844580,
title = {Perfluoroalkyl substances, metabolomic profiling, and alterations in glucose homeostasis among overweight and obese Hispanic children: A proof-of-concept analysis},
author = {Alderete TL and Jin R and Walker DI and Valvi D and Chen Z and Jones DP and Peng C and Gilliland FD and Berhane K and Conti DV and Goran MI and Chatzi L
},
year = {2019},
date = {2019-01-01},
journal = {Environ Int},
volume = {126},
pages = {445--453},
abstract = {To examine the prospective associations between exposure to perfluoroalkyl substances (PFASs) and longitudinal measurements of glucose metabolism in high-risk overweight and obese Hispanic children. Forty overweight and obese Hispanic children (8-14 years) from urban Los Angeles underwent clinical measures and 2-hour oral glucose tolerance tests (OGTT) at baseline and a follow-up visit (range: 1-3 years after enrollment). Baseline plasma perfluorooctanoic acid (PFOA), perfluorooctane sulfonate (PFOS), perfluorohexane sulfonic acid (PFHxS), and the plasma metabolome were measured by liquid-chromatography with high-resolution mass spectrometry. Multiple linear regression models were used to assess the association between baseline PFASs and changes in glucose homeostasis over follow-up. A metabolome-wide association study coupled with pathway enrichment analysis was performed to evaluate metabolic dysregulation associated with plasma PFASs concentrations. We performed a structural integrated analysis aiming to characterize the joint impact of all factors and to identify latent clusters of children with alterations in glucose homeostasis, based on their exposure and metabolomics profile. Each ln (ng/ml) increase in PFOA and PFHxS concentrations was associated with a 30.6 mg/dL (95% CI: 8.8-52.4) and 10.2 mg/dL (95% CI: 2.7-17.7) increase in 2-hour glucose levels, respectively. A ln (ng/ml) increase in PFHxS concentrations was also associated with 17.8 mg/dL increase in the glucose area under the curve (95% CI: 1.5-34.1). Pathway enrichment analysis showed significant alterations of lipids (e.g., glycosphingolipids, linoleic acid, and de novo lipogenesis), and amino acids (e.g., aspartate and asparagine, tyrosine, arginine and proline) in association to PFASs exposure. The integrated analysis identified a cluster of children with increased 2-h glucose levels over follow up, characterized by increased PFAS levels and altered metabolite patterns. This proof-of-concept analysis shows that higher PFAS exposure was associated with dysregulation of several lipid and amino acid pathways and longitudinal alterations in glucose homeostasis in Hispanic youth. Larger studies are needed to confirm these findings and fully elucidate the underlying biological mechanisms.},
keywords = {environmental pollution},
pubstate = {published},
tppubtype = {article}
}
2018
Alderete, TL; Jones, RB; Chen, Z; Kim, JS; Habre, R; Lurmann, F; Gilliland, FD; Goran, MI
Exposure to traffic-related air pollution and the composition of the gut microbiota in overweight and obese adolescents Journal Article
In: Environ. Res., vol. 161, pp. 472–478, 2018.
Abstract | BibTeX | Tags: environmental pollution, microbiota, traffic-related pollution
@article{pmid29220800,
title = {Exposure to traffic-related air pollution and the composition of the gut microbiota in overweight and obese adolescents},
author = {TL Alderete and RB Jones and Z Chen and JS Kim and R Habre and F Lurmann and FD Gilliland and MI Goran},
year = {2018},
date = {2018-01-01},
journal = {Environ. Res.},
volume = {161},
pages = {472--478},
abstract = {Traffic-related air pollution (TRAP) exposure has been linked to type 2 diabetes and metabolic dysfunction in humans. Animal studies suggest that air pollutants may alter the composition of the gut microbiota, which may negatively impact metabolic health through changes in the composition and/or function of the gut microbiome. The primary aim of this study was to determine whether elevated TRAP exposure was correlated with gut bacterial taxa in overweight and obese adolescents from the Meta-AIR (Metabolic and Asthma Incidence Research) study. The secondary aim was to examine whether gut microbial taxa correlated with TRAP were also correlated with risk factors for type 2 diabetes (e.g., fasting glucose levels). We additionally explored whether correlations between TRAP and these metabolic risk factors could be explained by the relative abundance of these taxa. Participants (17-19 years; n=43) were enrolled between 2014 and 2016 from Southern California. The CALINE4 line dispersion model was used to model prior year residential concentrations of nitrogen oxides (NOx) as a marker of traffic emissions. The relative abundance of fecal microbiota was characterized by 16S rRNA sequencing and spearman partial correlations were examined after adjusting for body fat percent. Freeway TRAP was correlated with decreased Bacteroidaceae (r=-0.48; p=0.001) and increased Coriobacteriaceae (r=0.48; p<0.001). These same taxa were correlated with fasting glucose levels, including Bacteroidaceae (r=-0.34; p=0.04) and Coriobacteriaceae (r=0.41; p<0.01). Further, freeway TRAP was positively correlated fasting glucose (r=0.45; p=0.004) and Bacteroidaceae and Coriobacteriaceae explained 24% and 29% of the correlation between TRAP and fasting glucose levels. Increased TRAP exposure was correlated with gut microbial taxa and fasting glucose levels. Gut microbial taxa that were correlated with TRAP partially explained the correlation between TRAP and fasting glucose levels. These results suggest that exposure to air pollutants may negatively impact metabolic health via alterations in the gut microbiota.},
keywords = {environmental pollution, microbiota, traffic-related pollution},
pubstate = {published},
tppubtype = {article}
}
Toledo-Corral, C M; Alderete, T L; Habre, R; Berhane, K; Lurmann, F W; Weigensberg, M J; Goran, M I; Gilliland, F D
Effects of air pollution exposure on glucose metabolism in Los Angeles minority children Journal Article
In: Pediatr Obes, vol. 13, no. 1, pp. 54–62, 2018.
Abstract | BibTeX | Tags: environmental pollution
@article{pmid27923100,
title = {Effects of air pollution exposure on glucose metabolism in Los Angeles minority children},
author = {C M Toledo-Corral and T L Alderete and R Habre and K Berhane and F W Lurmann and M J Weigensberg and M I Goran and F D Gilliland},
year = {2018},
date = {2018-01-01},
journal = {Pediatr Obes},
volume = {13},
number = {1},
pages = {54--62},
abstract = {Growing evidence indicates that ambient (AAP: NO2 , PM2.5 and O3 ) and traffic-related air pollutants (TRAP) contribute to metabolic disease risk in adults; however, few studies have examined these relationships in children. Metabolic profiling was performed in 429 overweight and obese African-American and Latino youth living in urban Los Angeles, California. This cross-sectional study estimated individual residential air pollution exposure and used linear regression to examine relationships between air pollution and metabolic outcomes. AAP and TRAP exposure were associated with adverse effects on glucose metabolism independent of body fat percent. PM2.5 was associated with 25.0% higher fasting insulin (p < 0.001), 8.3% lower insulin sensitivity (p < 0.001), 14.7% higher acute insulin response to glucose (p = 0.001) and 1.7% higher fasting glucose (p < 0.001). Similar associations were observed for increased NO2 exposure. TRAP from non-freeway roads was associated with 12.1% higher insulin (p < 0.001), 6.9% lower insulin sensitivity (p = 0.02), 10.8% higher acute insulin response to glucose (p = 0.003) and 0.7% higher fasting glucose (p = 0.047). Elevated air pollution exposure was associated with a metabolic profile that is characteristic of increased risk for type 2 diabetes. These results indicate that increased prior year exposure to air pollution may adversely affect type 2 diabetes-related pathophysiology in overweight and obese minority children.},
keywords = {environmental pollution},
pubstate = {published},
tppubtype = {article}
}
2017
Longitudinal Associations Between Ambient Air Pollution With Insulin Sensitivity, β-Cell Function, and Adiposity in Los Angeles Latino Children Journal Article
In: Diabetes, vol. 66, no. 7, pp. 1789–1796, 2017.
Abstract | BibTeX | Tags: environmental pollution
@article{pmid28137791,
title = {Longitudinal Associations Between Ambient Air Pollution With Insulin Sensitivity, β-Cell Function, and Adiposity in Los Angeles Latino Children},
year = {2017},
date = {2017-01-01},
journal = {Diabetes},
volume = {66},
number = {7},
pages = {1789--1796},
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 (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.},
keywords = {environmental pollution},
pubstate = {published},
tppubtype = {article}
}