Abstract
Exposure to low-dose ionizing radiation in occupational settings raises concerns about chromosomal aberrations (CAs) and their potential impact on genomic stability. Copy number variations (CNVs), structural genomic changes, influence susceptibility to environmental stressors and radiation-induced damage. This study analyzed CAs in 180 nuclear power plant workers exposed to occupational radiation and 45 controls, stratified by GSTM1 and GSTT1 CNVs. Workers exhibited significantly higher frequencies of chromatid-type and chromosome-type aberrations, of 5.47 and 3.01 per 500 cells, respectively, compared to 3.57 and 0.64 in controls (p < 0.001 for both). In the relatively high-exposure group, chromatid-type aberrations decreased with increasing GSTM1 and GSTT1 copy numbers. For GSTM1, individuals with zero copies showed 6.37 ± 3.47 aberrations per 500 cells, compared to 5.02 ± 3.05 for one copy and 4.67 ± 2.40 for two or more copies (p = 0.06). A similar trend was observed for GSTT1, with 6.00 ± 3.29 aberrations per 500 cells for zero copies, 5.38 ± 2.79 for one copy, and 4.11 ± 4.26 for two or more copies (p = 0.05). Poisson regression analysis further supported these findings after adjusting for potential confounders such as age, smoking status, and alcohol intake. Workers with null genotypes exhibited a 1.36-fold increase in chromatid-type aberrations compared to those with higher copy numbers under relatively high-exposure conditions, suggesting a synergy effect between GSTM1 and GSTT1 null genotypes in modulating radiation-induced aberrations. These findings underscore the role of genetic susceptibility, particularly involving GSTM1 and GSTT1 CNVs, in modulating radiation-induced chromosomal damage. The observed gene-environment interaction in the relatively high-exposure group suggests that pre-existing CNVs contribute to chromosomal instability under radiation exposure.