Among these antioxidant genes, glutathione S-transferase Mu 1 (GSTM1) has been most extensively characterized because it has a null polymorphism that is highly prevalent in the population and associated with increased risk of inflammatory lung diseases.
The GSTM1 null genotype is associated with increased airways inflammation 24 hours after ozone exposure, which is consistent with the lag time observed between increased ambient air ozone exposure and exacerbations of lung disease.
Thus, individuals homozygous for the GSTM1 gene deletion, especially in the under-41 age group (SCB: P = 0.001; MSB: P = 0.04) with an average smoking history of 16-30 pack-years (SCB: P = 0.002; MSB: P = 0.01) are more prone to chronic lung diseases, such as SCB and MCB, than are GSTM1 +/+ or 0/+ subjects.
We assessed whether homozygous GSTM1-null or GSTT1-null genotypes or the NAT2 slow-acetylator genotype were associated with increased risks for the development of malignant and nonmalignant asbestos-related pulmonary disorders in a cohort of Finnish construction workers.