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Interaction Effects of Long-Term Air Pollution Exposure and Variants in the GSTP1, GSTT1 and GSTCD Genes on Risk of Acute Myocardial Infarction and Hypertension: A Case-Control Study

Artikel i vetenskaplig tidskrift
Författare Anna Levinsson
Anna-Carin Olin
L. Modig
Santosh Dahgam
Lena Björck
Annika Rosengren
Fredrik Nyberg
Publicerad i PLoS ONE
Volym 9
Nummer/häfte 6
Sidor e99043
ISSN 1932-6203
Publiceringsår 2014
Publicerad vid Institutionen för medicin, avdelningen för samhällsmedicin och folkhälsa, enheten för arbets-och miljömedicin
Institutionen för medicin, avdelningen för molekylär och klinisk medicin
Sidor e99043
Språk en
Länkar dx.doi.org/10.1371/journal.pone.009...
Ämneskategorier Klinisk medicin

Sammanfattning

INTRODUCTION: Experimental and epidemiological studies have reported associations between air pollution exposure, in particular related to vehicle exhaust, and cardiovascular disease. A potential pathophysiological pathway is pollution-induced pulmonary oxidative stress, with secondary systemic inflammation. Genetic polymorphisms in genes implicated in oxidative stress, such as GSTP1, GSTT1 and GSTCD, may contribute to determining individual susceptibility to air pollution as a promoter of coronary vulnerability. AIMS: We aimed to investigate effects of long-term traffic-related air pollution exposure, as well as variants in GSTP1, GSTT1 and GSTCD, on risk of acute myocardial infarction (AMI) and hypertension. In addition, we studied whether air pollution effects were modified by the investigated genetic variants. METHODS: Genotype data at 7 single nucleotide polymorphisms (SNPs) in the GSTP1 gene, and one in each of the GSTT1 and GSTCD genes, as well as air pollution exposure estimates, were available for 119 AMI cases and 1310 randomly selected population controls. Population control individuals with systolic blood pressure >/=140 mmHg, diastolic blood pressure >/=90 mmHg or on daily antihypertensive medication were defined as hypertensive (n = 468). Individual air pollution exposure levels were modeled as annual means of NO2 (marker of vehicle exhaust pollutants) using central monitoring data and dispersion models, linking to participants' home addresses. RESULTS: Air pollution was significantly associated with risk of AMI: OR 1.78 (95%CI 1.04-3.03) per 10 microg/m3 of long-term NO2 exposure. Three GSTP1 SNPs were significantly associated with hypertension. The effect of air pollution on risk of AMI varied by genotype strata, although the suggested interaction was not significant. We saw no obvious interaction between genetic variants in the GST genes and air pollution exposure for hypertension. CONCLUSION: Air pollution exposure entails an increased risk of AMI, and this risk differed over genotype strata for variants in the GSTP1, GSTT1 and GSTCD genes, albeit not statistically-significantly.

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