Objectives: To investigate 4 loci of 3 HSP70 genes in caustic soda production plant former workers, who have been exposed to metallic mercury vapors for a long time, and including numerous cases of chronic mercury intoxication (CMI). Material and Methods: Polymorphisms in HSP70 gene family members (HSP1A1 (+190G/C, rs1043618), HSPA1B (+1267A/G and +2074G/C, rs1061581) and HSP1AL (+2437T/C, rs2227956)) genes were studied among 120 male workers involved in caustic soda production by mercury electrolysis at 2 plants in Eastern Siberia. These subjects had been chronically exposed to metallic mercury vapors for > 5 years and divided into 3 groups based on the occurrence and time of the CMI diagnosis, or absence of this disease. The Group 1 consisted of individuals (N = 46), who had had contact with mercury but were not diagnosed with the CMI. The Group 2 included workers (N = 56), who were diagnosed with the CMI longer than 14 years ago. The Group 3 consisted of the subjects (N = 18), who had been diagnosed with the CMI 3-5 years ago. The logistic regression analysis was used for 3 genetic models with and without adjustment for age and duration of mercury vapor exposure. Results: We found that genotypes СС-HSPA1A (+190G/C) and GG-HSPA1B (+1267A/G) had a high predictive risk of the CMI development (adjusted odds ratio (OR adj ) = 5.58, p = 0.026 and OR adj = 14.7, p = 0.0015, respectively). Twelve individuals with the CMI had a specific combination of СС-HSPA1A (+190G/C) and GG-HSPA1B (+1267A/G) genotypes, which strongly associated with the diagnosis (OR adj = 12.3, p = 0.0285). Moreover, significant association with the CMI was also obtained for the haplotype G-C of 1267A/G and 190G/C polymorphisms (OR = 2.1, p = 0.018). Conclusions: The association of СС-HSPA1A (+190G/C) and GG-HSPA1B (+1267A/G) genotypes and their combination for the CMI individuals suggests the role for HSPA1 genes in mercury-dependent mechanisms of the CMI development and progression. Int J Occup Med Environ Health 2017;30(1):77-85

The distribution of two CYP1A2 gene polymorphisms, CYP1A2*F and CYP1A2*D, was studied in a group of 38 men. Antipyrine elimination test was carried out and urinary cotinine was measured. The contribution of these CYP1A2 gene polymorphisms, age, and tobacco smoking to accumulation of three main antipyrine metabolites in the urine was evaluated by regression analysis. The impact of both studied polymorphisms was essential for urinary levels of 3-hydroxymethylantipyrine (metabolite most dependent on cytochrome P-4501A2) and hence, for functional activity of this isoform of the enzyme.

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