AI Article Synopsis
- The study aimed to investigate how certain genetic variations in XRCC1, XPD, XRCC3, and CCND1 might affect the time it takes for workers exposed to benzene to develop chronic poisoning.
- Researchers analyzed 80 patients using a technique called PCR-RFLP to identify specific genetic polymorphisms and employed the Kaplan-Meier method to assess their relationship with the latency of benzene poisoning.
- Findings indicated that individuals with the XRCC1 G27466A variant had a longer latency period for developing chronic poisoning, while those with certain variants in the CCND1 gene also experienced a significant delay compared to others, suggesting that these genetic factors may influence the disease's onset.
Article Abstract
Objective: To explore the association between genetic polymorphisms of XRCC1, XPD, XRCC3 and CCND1 and latency of occupational chronic benzene poisoning.
Methods: 80 patients diagnosed with occupational chronic benzene poisoning were investigated. PCR-RFLP was applied to detect the single nucleotide polymorphisms of C26304T, G27466A, G28152A, G36189A of XRCC1, C22541A, C23591T, A35931C of XPD, C18067T of XRCC3 and G870A of CCND1. Their relationship with the latency of chronic benzene poisoning was analyzed by Kaplan-Meier method.
Results: The association of XRCC1 G27466A subgroup with the latency of chronic benzene poisoning was observed, as well as that of CCDN1G870A subgroup. The benzene-exposed workers with XRCC1 27466G/G homozygous wild genotype developed chronic benzene poisoning 6.9 years later than those had homozygous (27466A/A) or heterozygous (27466G/A) mutant alleles. On the other hand, the latency developing chronic benzene poisoning was longer in workers with homozygous (CCND1 870A/A) or heterozygous (CCND1 870G/A) mutant alleles than in those carrying 870G/G homozygous wild genotype (14.9 vs. 8.7 years).
Conclusion: The polymorphisms of XRCC1 and CCND1 potentially modify the latency of the chronic benzene poisoning among workers exposed to benzene.
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