GSTM1, GSTT1, and GSTP1 polymorphisms and associations between air pollutants and markers of insulin resistance in elderly Koreans.
BACKGROUND
Previous studies have suggested that diabetes mellitus (DM) is an outcome of exposure to air pollution, and metabolic detoxification genes affect air pollution-related outcomes.


OBJECTIVE
We evaluated associations between air pollutants and markers of insulin resistance (IR), an underlying mechanism of type 2 DM, and effect modification by GSTM1, GSTT1, and GSTP1 genotypes among elderly participants in the Korean Elderly Environmental Panel (KEEP) study.


METHODS
We recruited 560 people ≥ 60 years of age and obtained blood samples from them up to three times between 2008 and 2010. For air pollution exposure, we used ambient air pollutant [i.e., particulate matter ≤ 10 µm in diameter (PM10), sulfur dioxide (SO2), ozone (O3), and nitrogen dioxide (NO2)] monitoring data. We measured levels of fasting glucose and insulin and derived the homeostatic model assessment (HOMA) index to assess IR. Mixed-effect models were used to estimate associations between air pollutants and IR indices on the same day or lagged up to 10 days prior, and effect modification by GSTM1, GSTT1, and GSTP1 genotypes.


RESULTS
Interquartile range increases in PM10, O3, and NO2 were significantly associated with IR indices, depending on the lag period. Associations were stronger among participants with a history of DM and among those with GSTM1-null, GSTT1-null, and GSTP1 AG or GG genotypes.


CONCLUSIONS
Our results suggest that PM10, O3, and NO2 may increase IR in the elderly, and that GSTM1-null, GSTT1-null, and GSTP1 AG or GG genotypes may increase susceptibility to potential effects of ambient air pollutants on IR.
Institute of Environmental Medicine, Seoul National University Medical Research Center, Seoul, Republic of Korea.
Jin Hee
JH
Kim
Yun-Chul
YC
Hong
D000368:Aged; D000369:Aged, 80 and over; D000393:Air Pollutants / Q000633:toxicity*; D015415:Biomarkers; D001786:Blood Glucose / Q000032:analysis*; D003920:Diabetes Mellitus / Q000139:chemically induced / Q000453:epidemiology* / Q000235:genetics; D004781:Environmental Exposure; D004784:Environmental Monitoring; D005215:Fasting; D005260:Female; D051549:Glutathione S-Transferase pi / Q000235:genetics / Q000378:metabolism; D005982:Glutathione Transferase / Q000235:genetics* / Q000378:metabolism; D006801:Humans; D007328:Insulin / Q000097:blood*; D007333:Insulin Resistance; D008297:Male; D008875:Middle Aged; D060885:Multiplex Polymerase Chain Reaction; D009585:Nitrogen Dioxide / Q000633:toxicity; D010126:Ozone / Q000633:toxicity; D052638:Particulate Matter / Q000633:toxicity; D011110:Polymorphism, Genetic; D011863:Radioimmunoassay; D056910:Republic of Korea / Q000453:epidemiology; D013458:Sulfur Dioxide / Q000633:toxicity
D000393:Air Pollutants; D015415:Biomarkers; D001786:Blood Glucose; D051549:Glutathione S-Transferase pi; D005982:Glutathione Transferase; D007328:Insulin; D009585:Nitrogen Dioxide; D010126:Ozone; D052638:Particulate Matter; D013458:Sulfur Dioxide; C413545:glutathione S-transferase T1; C496556:GSTP1 protein, human