Abstract
Ototoxic effect of exposure to lead has been reported by many researchers. This study was undertaken with a view to investigate the relationship between blood lead level (BLL) and hearing loss in workers in a lead-acid battery manufacturing plant in Tehran, Iran. In a cross-sectional study, 609 male workers were recruited from different locations in the factory. Association between BLL and hearing loss in different frequencies were measured. Relationships were analyzed by logistic regressions. Statistical significance was defined as p-value <0.05. Six hundred nine male workers with mean age 40 ± 7 years and mean noise exposure level of 80 (75-85) dB were evaluated. BLLs were categorized into four quartiles, and hearing loss in each quartile was compared to the first one. In our regression models, BLL was associated significantly with high frequency hearing loss, adjusted odds ratios for the comparison of the fourth, third, and second quartiles to the first one are respectively: 3.98 (95% CI: 1.63-9.71, p < 0.00), 3.05 (95% CI: 1.28-7.26, p < 0.01), and 2.89 (95% CI: 1.11-7.51, p < 0.03). This study showed a dose-response relationship between BLL and hearing loss, after adjusting for potential confounders (age, body mass index, work duration, smoking, and occupational noise exposure) in logistic regressions. It is concluded that periodic hearing assessment by pure tone audiometry in workers exposed to lead should be recommended. However, additional studies are required to clarify the mechanisms of lead ototoxicity.
Highlights
Work-related ototoxic compounds include heavy metals, noise, solvents, and certain drugs, used in industry
Additional studies are required to clarify the mechanisms of lead ototoxicity
No significant differences were observed in hearing low frequencies between the 4 groups of blood lead level (BLL) exposure
Summary
Work-related ototoxic compounds include heavy metals, noise, solvents, and certain drugs, used in industry. They are known for their neurotoxic effects both on central and peripheral nervous systems. Mechanisms of ototoxicity include injury to the sensory cells, peripheral nerve endings of the cochlea and direct cochlear toxicity [1]. Recent findings indicate that inorganic Pb2+ can substitute for Ca2+ with certain intracellular Ca2+-binding proteins. Such observations suggest a variety of hypotheses for understanding the molecular basis of its toxic action, especially in reference to both the acute and chronic low level exposure models of neurotoxicity. Pb2+ interacts with calmodulin with an affinity at least equal to that for Ca2+ [3]
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