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Air pollution, obesity, genes and cellular adhesion molecules.

ABSTRACT: Particulate matter has been associated with acute cardiovascular outcomes, but our understanding of the mechanism is incomplete. We examined the association between particulate matter and cell adhesion molecules. We also investigated the modifying effect of genotype and phenotype variation to gain insight into the relevant biological pathways for this association.We used mixed regression models to examine the association of PM(2.5) (particulate matter < or = 2.5 microm in diameter) and black carbon with serum concentrations of soluble intercellular adhesion molecule (sICAM-1) and soluble vascular cell adhesion molecule (sVCAM-1), markers of endothelial function and inflammation, in a longitudinal study of 809 participants in the Normative Ageing Study (1819 total observations). We also examined whether this association was modified by genotype, obesity or diabetes status. Genes selected for analyses were either related to oxidative stress, endothelial function, lipid metabolism or metal processing.Black carbon during the 2 days prior to blood draw was significantly associated with increased sVCAM-1 (4.5% increase per 1 microg/m(3), 95% CI 1.1 to 8.0). Neither pollutant was associated with sICAM-1. Larger effects of black carbon on sVCAM were seen in subjects with obesity (p=0.007) and who were GSTM1 null (p=0.02).Black carbon is associated with markers of endothelial function and inflammation. Genes related to oxidative defence may modify this association.

SUBMITTER: Madrigano J

PROVIDER: S-EPMC3229824 | biostudies-literature | 2010 May

REPOSITORIES: biostudies-literature

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Air pollution, obesity, genes and cellular adhesion molecules.

Madrigano Jaime J Baccarelli Andrea A Wright Robert O RO Suh Helen H Sparrow David D Vokonas Pantel S PS Schwartz Joel J

Occupational and environmental medicine 20091102 5

<h4>Objectives</h4>Particulate matter has been associated with acute cardiovascular outcomes, but our understanding of the mechanism is incomplete. We examined the association between particulate matter and cell adhesion molecules. We also investigated the modifying effect of genotype and phenotype variation to gain insight into the relevant biological pathways for this association.<h4>Methods</h4>We used mixed regression models to examine the association of PM(2.5) (particulate matter < or = 2. ...[more]

PMID: 19884647

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Project description:OBJECTIVE: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. METHODS: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. RESULTS: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. CONCLUSION: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.

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Air pollution, obesity, genes and cellular adhesion molecules.

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Air pollution, obesity, genes and cellular adhesion molecules.

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