Concurrent exposure to noise and smoking may be associated with more hearing loss than exposure to noise alone in the conventional and high frequencies. However, other differences between smokers and non-smokers may explain these differences as well.
Noise is one of the most pervasive hazardous factors in the workplace. Noise-induced hearing loss (NIHL) is the most common disorder related to noise exposure. Smoking is probably associated with hearing loss. The simultaneous effect of noise and smoking on hearing is a recent concern. In this study, we assessed the simultaneous effect of noise and smoking on standard pure tone audiometry (PTA) and distortion product otoacoustic emissions (DP-OAEs). This was an historical cohort study on 224 workers exposed to noise who were divided into two groups: Smokers and nonsmokers. DP-OAE response amplitudes were assessed. Data were analyzed by SPSS software (version 19) using Student's t-test and Mann-Whitney U test. One hundred and five subjects were smokers (case group) and 119 individuals were nonsmokers (control group). All the subjects were exposed to 91.08 ± 2.29 dBA [time-weighted average (TWA) for an 8 h work shift]. Mean DP-OAE response amplitude at frequencies higher than 1,000 Hz was significantly higher in the smokers than the nonsmokers. This study showed that smoking can aggravate the effect of noise on hearing in DP-OAEs.
Introduction: Previous study demonstrated that the baseline lung immune prognostic index (LIPI) was a potential biomarker which can identify advanced non-small cell lung cancer (NSCLC) patients who will benefit from treatment with immune checkpoint inhibitor (ICI). However, a recent study found that the LIPI might be an important prognostic biomarker irrespective of treatment modality for patients with metastatic NSCLC. It remains unclear whether LIPI is associated with long-term outcomes in unresected stage III NSCLC. Methods: Patients with LA-NSCLC treated with definitive radiotherapy (RT) between 2000 to 2017 were retrospectively reviewed. The pretreatment derived neutrophils/ (leukocytes minus neutrophils) ratio (dNLR) and lactate dehydrogenase (LDH) made up the LIPI and divided it into two groups (good, 0 score; poor, 1 to 2 scores). Overall survival (OS), progressionfree survival (PFS), locoregional relapse-free survival (LRRFS), and distant metastasis-free survival (DMFS) were calculated from the date of diagnosis. Kaplan-Meier method and Cox hazards regression analysis were used to explore associations between the LIPI and LA-NSCLC prognosis. Propensity score matching (PSM) was conducted to balance the confounding variables. Results: A total of 1079 patients were eligible for analysis. Patients with a poor pretreatment LIPI had significantly inferior OS, PFS, LRRFS, and DMFS than those with a good LIPI (median OS, 19.0 vs 25.0 months, Log-rank P < 0.001; median PFS, 10.0 vs 13.0 months, Log-rank P ¼ 0.001; median LRRFS, 13.0 vs 18.0 months, Log-rank P < 0.001; median DMFS, 15.0 vs 17.0 months, Logrank P ¼ 0.002). According to multivariate analysis, it was also found that the LIPI was an independent prognostic marker for OS (P ¼ 0.026,
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