The dependence between urinary mercury concentration and carotid arterial intima-media thickness in workers occupationally exposed to mercury vapour.

OBJECTIVES Mechanisms of the mercury effect on arterial vessel walls include increased free radicals generation, decreased nitric oxide synthesis and increased reactivity to vasoconstrictors, leading to accelerated development of atherosclerosis and arterial hypertension. The aim of this study was to evaluate the correlation between urinary mercury (Hg-U) concentration and carotid intima-media thickness (IMT) or intraventricular septum diastolic diameter (IVSDD) to find the best markers of mercury cardiovascular toxicity. MATERIALS AND METHODS The study included 154 workers of a chemical factory using mercury in chlorine production. Urinary mercury concentration was determined by atomic absorption spectrophotometry. Serum lipids were assessed by routine methods using enzymatic assay. Serum total antioxidant status (TAS) was determined by colorimetry. Measurements of IMT and IVSDD were made by ultrasound imaging using MEDISON SA 9900 PRIME system. RESULTS The mean Hg-U concentration was 1.9+/-2.7 microg/g creatinine in women (n = 29) and 5.6+/-12.2 microg/g creatinine in men (n = 125). In the group of non-smokers (n = 102) there was a positive linear correlation between Hg-U concentration and IMT (r = 0.1728; p < 0.05) and a negative dependence between high density cholesterol (HDL-C) and IMT (r = -0.2109; p < 0.01). The negative linear correlation between serum total antioxidant status (TAS) and carotid IMT (r = -0.2142; p < 0.05), and the positive correlation between HDL-C and TAS (r = 0.1953; p < 0.05) were shown to be valid for the total studied group. Serum lipids in women were normal, but in men the mean triglyceride level was higher than normal. CONCLUSIONS The occupational exposure to mercury vapour remains in a relationship with early, asymptomatic carotid atherosclerosis. The dependence between urinary mercury elimination and carotid intima-media thickness is evidenced in non-smoking workers. Defensive anti-atherosclerotic mechanisms in these workers are strongly related with HDL. In smokers, these protective mechanisms are disturbed.