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Synergistic Effects of Genetic Polymorphism and Air Pollution on Markers of Endothelial Dysfunction in Children



Poursafa P1 ; Kelishadi R2, 3 ; Haghjooyjavanmard S4 ; Rafiei L4 ; Keramatian K3
Authors
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Authors Affiliations
  1. 1. Department of Environment Protection, Environment Research Center, Isfahan University of Medical Sciences (IUMS), Isfahan, Iran
  2. 2. Department of Pediatrics, School of Medicine, IUMS, Isfahan, Iran
  3. 3. Child Growth and Development Research Center, IUMS, Isfahan, Iran
  4. 4. Department of Physiology, Applied Physiology Research Center, IUMS, Isfahan, Iran

Source: Journal of Research in Medical Sciences Published:2012

Abstract

Background: This study aims to determine the association of some genetic polymorphisms in the relationship of air pollutants on the serum levels of thrombomodulin (TM) and tissue factor (TF) in a population-based sample of children and adolescents. Materials and Methods: This cross-sectional study was conducted among 110 participants (52.8% girls) with a mean age of 12.7 + 2.3 years, in Isfahan, Iran. Genotypes of TM G33-A and + 5466A > G polymorphisms were determined by the polymerase chain reaction - restriction length fragment polymorphism method (PCR-RFLP). The enzyme-linked immunosorbent assay (ELISA) was used for measurement of serum TM and TF. Results: The following genotypes were identified for TM: GG in 69.2%, GA in27.2%, and AA in 3.6% of the participants. Considering TF, 108 participants were homozygous for the + 5466A allele, and two subjects had + 5466AG genotype. The mean pollution standards index (PSI) value was at a moderate level; the mean particulate matter measured up to 10 μm (PM 10); and ozone (O 3), nitrogen dioxide, and sulfur dioxide were considerably high. The mean serum TF and TM levels were not significantly different among the participants with the aforementioned genotypes. Among participants exposed to high quartiles of O 3, PM 10, and PSI, the TM-33G / A polymorphism (GA + AA genotype) increased the Odds ratio (OR) of the low serum TM level. There was no statistically significant association in the areas of low pollution. Conclusion: The findings of our study support the synergistic effect of the TM-33G / A polymorphism and air pollutants on factors associated with the onset of the atherosclerosis. This might be confirmatory evidence for gene-environment interaction, and related effects on atherogenesis from early life.
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