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ObjectivesTo investigate the effects of smoking on hearing loss among workers exposed to occupational noise.MethodsFrom the results of a special workers health examination performed in 2011, we enrolled 8,543 subjects exposed to occupational noise and reviewed the findings. Using self-reported questionnaires and health examination results, we collected data on age, smoking status, disease status, height, weight, and biochemistry and pure tone audiometry findings. We divided the workers into 3 groups according to smoking status (non-smoker, ex-smoker, current smoker). Current smokers (n = 3,593) were divided into 4 groups according to smoking amount (0.05–9.9, 10–19.9, 20–29.9, ≥30 pack-years). We analyzed the data to compare hearing thresholds between smoking statuses using analysis of covariance (ANCOVA) after controlling for confounder effects.ResultsAccording to ANCOVA, the hearing thresholds of current smokers at 2 k, 3 k, and 4 kHz were significantly higher than that of the other groups. Multiple logistic regression for smoking status (reference: non-smokers) showed that the adjusted odds ratios of current smokers were 1.291 (95% confidence interval [CI]: 1.055–1.580), 1.180 (95% CI: 1.007–1.383), 1.295 (95% CI: 1.125–1.491), and 1.321 (95% CI: 1.157–1.507) at 1 k, 2 k, 3 k, and 4 kHz, respectively. Based on smoking amount, the adjusted odds ratios were 1.562 (95% CI: 1.013–2.408) and 1.643 (95% CI: 1.023–2.640) for the 10–19.9 and ≥30 pack-years group, respectively, at 1 kHz (reference: 0.05–9.9 pack-years). At 2 kHz, the adjusted odds ratios were increased statistically significantly with smoking amount for all groups. At all frequencies tested, the hearing thresholds of noise-exposed workers were significantly influenced by current smoking, in particular, the increase of hearing loss at low frequencies according to smoking amount was more prevalent.ConclusionsCurrent smoking significantly influenced hearing loss at all frequencies in workers exposed to occupational noise, and heavier smoking influenced low-frequency hearing loss more greatly. There was a dose–response relationship between smoking amount and low-frequency hearing thresholds; however, this was not observed for high-frequency hearing thresholds. Therefore, well-designed prospective studies are needed to clarify the effects of smoking on the degree of hearing loss.

Chronic exposure to arsenic is well known as the cause of cardiovascular diseases such as hypertension. To investigate the effect of arsenic on blood vessels, we examined whether arsenic affected the contraction of aortic rings in an isolated organ bath system. Treatment with arsenite, a trivalent inorganic species, increased vasoconstriction induced by phenylephrine or serotonin in a concentration-dependent manner. Among the arsenic species tested—arsenite, pentavalent inorganic species (arsenate), monomethylarsonic acid (MMAV), and dimethylarsinic acid (DMAV)—arsenite was the most potent. Similar effects were also observed in aortic rings without endothelium, suggesting that vascular smooth muscle plays a key role in enhancing vasoconstriction induced by arsenite. This hypercontraction by arsenite was well correlated with the extent of myosin light chain (MLC) phosphorylation stimulated by phenylephrine. Direct Ca2+ measurement using fura-2 dye in aortic strips revealed that arsenite enhanced vasoconstriction induced by high K+ without concomitant increase in intracellular Ca2+ elevation, suggesting that, rather than direct Ca2+ elevation, Ca2+ sensitization may be a major contributor to the enhanced vasoconstriction by arsenite. Consistent with these in vitro results, 2-hr pretreatment of 1.0 mg/kg intravenous arsenite augmented phenylephrine-induced blood pressure increase in conscious rats. All these results suggest that arsenite increases agonist-induced vasoconstriction mediated by MLC phosphorylation in smooth muscles and that calcium sensitization is one of the key mechanisms for the hypercontraction induced by arsenite in blood vessels.

This study is performed to detect changes of gene expression in substantia nigra (SN) and striatum in manganese (Mn)-exposed mice brain. The cDNA array is a recently developed molecular biological method that can detect the differential expression of several hundreds of genes simultaneously and is therefore advantageous in the study of trace metal intoxication effect at the genetic level. Using this technology, we discovered 5 genes in the mouse striatum and 9 genes in SN changed by more than 50% following Mn exposure. Depression were observed in two genes (neural cell adhesion protein BIG2, heavy neurofilament subunit genes) in striatum and three genes (light neurofilament subunit, brain acyl-CoA synthetase II, heavy neurofilament subunit genes) in the SN. However three genes (N-acetylglucosaminyltransferase I, S100β β β β β, and synaptonemal complex protein I genes) in striatum and six genes (noggin, striatin, Ost oncogene, S100β β β β β, calcium/calmodulindependent protein kinase kinase beta, and N-acetylglucosaminyltransferase I genes) in SN were elevated following Mn exposure. Immunohistochemical study revealed that protein levels of S100β β β β β also increased following Mn treatment. Activated astrocytes overexpressing S100β β β β β are invariably and intimately associated with decreased expression of heavy and light neurofilament subunits which is a distinguishing feature of neurodegeneration by Mn exposure. All our findings suggested that neuronal degenerations occur in SN as well as striatum of mice exposed to Mn.

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