Table III.
p value2 |
|||||
---|---|---|---|---|---|
Genetic ancestry |
Smoking status |
Pack yr |
Gender | Age | |
GSTM1 | |||||
SAE3 | 0.48 | 0.61 | 0.73 | 0.99 | 0.65 |
AM | 0.61 | 0.61 | 0.034 | 0.50 | 0.89 |
GSTT1 | |||||
SAE | 0.26 | 0.68 | 0.23 | 0.46 | 0.25 |
AM | 0.53 | 0.75 | 0.88 | 0.39 | 0.28 |
GSTT2 | |||||
AM | 0.10 | 0.34 | 0.19 | 0.99 | 0.90 |
Significance by p value of potential confounding variables on observed associations of CNV genotypewith GST isoenzyme gene expression is shown. GSTT2 was not significantly expressed in smallairway epithelium by Affymetrix “P-call”.
p values represent chi-squared tests except for pack-year and age, each of which was tested for interaction with CNV genotype by two factor ANOVA.
SAE, small airway epithelium; AM = alveolar macrophage.
Pack-yr was significantly higher among heterozygotes (haploid) for GSTM1 CNV than amonghomozygous nulls and wild types (diploid). There was a trend towards lower alveolar macrophageGSTM1 gene expression levels in smokers with greater than the median pack-yr smoking history, p=0.07.