Abstract
BackgroundNoise-induced hearing loss (NIHL) is a complex disease caused by environmental and genetic risk factors. This study was to explore the association of noise kurtosis, triphosphopyridine nucleotide oxidase 3 (NOX3) and lifestyles with NIHL.MethodsThis case-control study included 307 patients with NIHL and 307 matched control individuals from Zhejiang province of China. General characteristics, noise exposure data, the exfoliated cells of the oral mucosa, and lifestyle details of individuals were collected. The kompetitive allele specific polymerase chain reaction (KASP) method was used to analyze the genotypes of three single nucleotide polymorphisms (SNPs) of NOX3.ResultsPeople who exposed to complex noise had a higher risk of NIHL than those exposed to steady noise (adjusted: OR = 1.806, P = 0.002). The GT genotype of additive model and TT + GT genotype of dominant model in NOX3 rs12195525 decreased the risk of NIHL (adjusted: OR = 0.618, P = 0.043; OR = 0.622, P = 0.036). Smoking and exposure to high video volume increased the risk of NIHL (adjusted: OR = 1.486, P = 0.038; OR = 1.611, P = 0.014). Oppositely, regular physical exercise decreased the risk of NIHL (adjusted: OR = 0.598, P = 0.004). A positive interaction was found between complex noise and lifestyles including high video volume exposure and no physical exercise in the additive models (RERI = 1.088, P < 0.001; RERI = 1.054, P = 0.024). A positive interaction was also found between NOX3 rs12195525 GG genotype and lifestyles including smoking and high video volume exposure in the additive models (RERI = 1.042, P = 0.005; RERI = 0.774, P = 0.044).ConclusionsNoise temporal structure, NOX3 rs12195525 polymorphism, and the three lifestyles of smoking, video volume, and physical exercise were related to the NIHL. There were the interactions between noise temporal structure and the lifestyle of video volume or physical exercise, as well as between NOX3 and the lifestyle of smoking or video volume. These results provide a theoretical basis for the prevention and genetic testing of NIHL.
Highlights
Noise-induced hearing loss (NIHL) is irreversible hearing loss caused by cochlear hair cell death combined with synaptic damage resulting from accumulated noise exposure [1, 2]
Within the strata of smoking, high video volume exposure or no physical exercise, people exposed to complex noise had a higher risk of NIHL than those exposed to steady noise (OR = 2.175, 95% Confidence interval (CI) = 1.244– 3.805, P = 0.006; Odds ratio (OR) = 2.243, 95% confidence intervals (95% CI) = 1.441–3.492, P < 0.001; OR = 2.242, 95% CI = 1.417–3.546, P = 0.001)
Within the strata of TT + GT genotype, people who were exposed to complex noise had a higher tendency of NIHL than those exposed to steady noise (OR = 3.429, 95% CI = 1.051–11.187, P = 0.041)
Summary
Noise-induced hearing loss (NIHL) is irreversible hearing loss caused by cochlear hair cell death combined with synaptic damage resulting from accumulated noise exposure [1, 2]. Noise research was mainly focused on the equivalent continuous sound levels (Leq) and cumulative noise exposure (CNE) These values are formulated using the equal energy hypothesis (EEH), which assumes that the cochlear impact of noise exposure is proportional to the duration of exposure multiplied by the noise intensity. This method is suitable for continuous or steady-state noise, but not for unstable and complex noise. The advantage of kurtosis would be that all peaks would be accounted for as well as the relative difference between peak and background levels They proposed that kurtosis statistics could be used to classify the temporal structure of complex noise. Noise-induced hearing loss (NIHL) is a complex disease caused by environmental and genetic risk factors. This study was to explore the association of noise kurtosis, triphosphopyridine nucleotide oxidase 3 (NOX3) and lifestyles with NIHL
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