Excessive exposure to high noise level environments has the potential to cause noise-induced hearing loss (NIHL), and cigarette smoking has also been shown to have a potential adverse effect on hearing. The aim of this study was to determine whether smoking interacts with noise in the development of hearing loss, and if so, the extent of the contribution from smoking on NIHL. A cross-sectional study was designed to assess the effect of smoking on NIHL in 517 male workers (non-smokers: N = 199; smokers: N = 318) exposed to a high-level industrial noise environment in China. Shift-long temporal waveforms of the noise that workers were exposed to for evaluation of noise exposures, and audiometric threshold measures were obtained on all selected subjects. The subjects used hearing protection devices only within the last 1-2 years. The results suggest that smoking has an adverse effect on NIHL in workers exposed to high level industrial noise, i.e., the median high frequency hearing thresholds were significantly greater in smokers than non-smokers exposed to noise for more than 10 years. This effect was observed at 4.0 and 6.0 kHz. Smoking did not have an adverse effect on NIHL in workers exposed to noise less than 10 years. Multivariate regression analysis revealed that the odds ratio (OR) for high frequency hearing loss (i.e., hearing threshold greater than 40 dB at 4.0 kHz) were 1.94 for smokers in comparison to non-smokers. The results suggest that: (1) smokers have a higher risk of developing high frequency hearing loss than non-smokers with a similar occupational noise exposure, and (2) the interaction between cigarette smoking and high-level noise exposure may be additive. There is a need to develop and analyze a larger database of workers with well-documented exposures and smoking histories for better understanding of the effect of smoking on NIHL incurred from high-level industrial noise exposures. A better understanding of the role of smoking may lead to its incorporation into hearing risk assessment for noise exposure.
This study examined: (1) the value of using the statistical metric, kurtosis [β(t)], along with an energy metric to determine the hazard to hearing from high level industrial noise environments, and (2) the accuracy of the International Standard Organization (ISO-1999:1990) model for median noise-induced permanent threshold shift (NIPTS) estimates with actual recent epidemiological data obtained on 240 highly screened workers exposed to high-level industrial noise in China. A cross-sectional approach was used in this study. Shift-long temporal waveforms of the noise that workers were exposed to for evaluation of noise exposures and audiometric threshold measures were obtained on all selected subjects. The subjects were exposed to only one occupational noise exposure without the use of hearing protection devices. The results suggest that: (1) the kurtosis metric is an important variable in determining the hazards to hearing posed by a high-level industrial noise environment for hearing conservation purposes, i.e., the kurtosis differentiated between the hazardous effects produced by Gaussian and non-Gaussian noise environments, (2) the ISO-1999 predictive model does not accurately estimate the degree of median NIPTS incurred to high level kurtosis industrial noise, and (3) the inherent large variability in NIPTS among subjects emphasize the need to develop and analyze a larger database of workers with well-documented exposures to better understand the effect of kurtosis on NIPTS incurred from high level industrial noise exposures. A better understanding of the role of the kurtosis metric may lead to its incorporation into a new generation of more predictive hearing risk assessment for occupational noise exposure.
BackgroundThe recent increase in bacterial resistance to antibiotics has promoted the exploration of novel antibacterial materials. As a result, many researchers are undertaking work to identify new lantibiotics because of their potent antimicrobial activities. The objective of this study was to provide details of a lantibiotic-like gene cluster in Paenibacillus elgii B69 and to produce the antibacterial substances coded by this gene cluster based on culture screening.ResultsAnalysis of the P. elgii B69 genome sequence revealed the presence of a lantibiotic-like gene cluster composed of five open reading frames (elgT1, elgC, elgT2, elgB, and elgA). Screening of culture extracts for active substances possessing the predicted properties of the encoded product led to the isolation of four novel peptides (elgicins AI, AII, B, and C) with a broad inhibitory spectrum. The molecular weights of these peptides were 4536, 4593, 4706, and 4820 Da, respectively. The N-terminal sequence of elgicin B was Leu-Gly-Asp-Tyr, which corresponded to the partial sequence of the peptide ElgA encoded by elgA. Edman degradation suggested that the product elgicin B is derived from ElgA. By correlating the results of electrospray ionization-mass spectrometry analyses of elgicins AI, AII, and C, these peptides are deduced to have originated from the same precursor, ElgA.ConclusionsA novel lantibiotic-like gene cluster was shown to be present in P. elgii B69. Four new lantibiotics with a broad inhibitory spectrum were isolated, and these appear to be promising antibacterial agents.
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