ABSTRACT
Objectives@#. Voice abuse in noisy environments can result in voice disorders. However, insufficient studies have sought to differentiate vocal cord lesions through laryngoscopic examinations among workers in noisy environments. This study investigated the relationship between a history of noise exposure in the workplace and benign vocal fold lesions (BVFLs). @*Methods@#. We used Korea National Health and Nutrition Examination Survey data from 2010 to 2012. The chi-square test was used to compare characteristics between two groups according to the presence or absence of BVFLs. To investigate the association between BVFLs and noise exposure in the workplace, we calculated adjusted odds ratios and 95% confidence intervals (CIs) using multiple logistic regression analysis. @*Results@#. In total, 10,170 participants with available laryngoscopy results were enrolled. Smoking history, hypertension, diabetes, and exposure to noise for more than 3 months at the workplace were significantly more common in participants with BVFLs. After adjusting for age, sex, smoking, drinking, obesity, hypertension, diabetes, income, education, and occupation as confounders, we confirmed that BVFLs were 1.52 times more likely (95% CI, 1.157–1.990) to occur in individuals with occupational noise exposure. @*Conclusion@#. Working in a noisy environment could induce BVFLs in workers through voice abuse. Social recognition that a noisy environment is a risk factor for BVFLs needs to be improved, and preventive measures should be implemented.
ABSTRACT
Peroxiredoxin (Prx), a family of ubiquitous thiol peroxidases, functions as a redox signaling regulator that controls cellular Hâ‚‚Oâ‚‚ in mammalian cells and has recently received attention for being overexpressed in various cancer types. In this study, we show that Prx type II (PrxII) is rather silenced in gastric cancer cells. PrxII expression is severely downregulated in 9 out of the 28 gastric cancer cell lines. Strikingly, PrxII expression is completely lost in three cell lines, MKN28, MKN74 and SNU484. Loss of PrxII expression is due to DNA methyltransferase 1-dependent methylation at the promoter region of the PrxII gene. Restoration of PrxII expression using a retroviral system markedly reduces the colony-forming ability and migratory activity of both MKN28 and SNU484 cells by inhibiting Src kinase. Mechanistically, PrxII peroxidase activity is essential for regulating gastric cancer cell migration. Bioinformatics analysis from The Cancer Genome Atlas stomach cancer data (STAD) revealed significantly low PrxII expression in gastric cancer patients and a negative correlation between PrxII expression and methylation levels. More importantly, low PrxII expression also strongly correlates with poor survival in cancer patients. Thus our study suggests that PrxII may be the first thiol peroxidase that simultaneously regulates both survival and metastasis in gastric cancer cells with high clinical relevance.