Abstract
Chronic exposure to noise is a detrimental environmental factor that can contribute to occupational noise-induced deafness (ONID) in industrial workers. ONID is caused by both environmental and genetic factors, and negatively impacts workers and manufacturing industries in China. Polymorphisms in the paraoxonase 2 gene (PON2) is associated with noise-induced hearing loss, and PON3 expression may modulate oxidative stress in cells and tissues by reducing the levels of reactive oxygen species, which are prominent in ONID. We conducted a matched case-control study to investigate whether PON3 polymorphisms and activity were associated with susceptibility to ONID. We genotyped PON3 single nucleotide polymorphisms (SNPs) using Sanger sequencing and measured the plasma PON3 activity using enzyme-linked immunosorbent assay. Conditional logistic regression models were fitted to evaluate the potential risk factors of ONID. A total of 300 subjects were included (n = 150 ONID and n = 150 control cases) from October 2017 to October 2019. We identified two types of genotypes for the PON3 SNPs. The independent risk factors for ONID were genotype CT and allele C with Odd’s ratio (OR) = 2.12 (95% confidence interval [CI]: 1.18–3.84) and OR = 1.68 (95% CI: 1.06–2.66) for SNP rs11767787; AG and allele A with OR = 2.09 (95% CI: 1.25–3.47) and OR = 1.87 (95% CI: 1.19–2.93) for SNP rs13226149; and CT and allele T with OR = 2.59 (95% CI: 1.44–4.67) and OR = 1.95 (95% CI: 1.22–3.14) for SNP rs17882539, respectively. Furthermore, the plasma PON3 level (> 1504 U/L) was observed to be a protective factor associated with the lowest level of ONID (less than 991 U/L) after adjusting for confounding factors (OR = 0.27, 95% CI: 0.13–0.54). In conclusion, the PON3 polymorphisms rs11767787, rs13226149, and rs17882539 and plasma PON3 activity are associated with susceptibility to ONID in the Chinese population.
Highlights
Noise is the most important environmental factor that may be detrimental to health [1, 2], especially for hearing loss [3]
Noise-induced hearing loss (NIHL) is a sensorineural hearing deficit that begins with chronic exposure to the higher frequencies (3 to 6 kHz) and is the primary occupational disease predominantly found among industrial workers [1]
ONID cases were newly diagnosed at the Shenzhen Prevention and Treatment Center for Occupational Diseases according to the diagnosis of occupational noise-induced deafness (GBZ 49–2014) [27]
Summary
Noise is the most important environmental factor that may be detrimental to health [1, 2], especially for hearing loss [3]. Noise-induced hearing loss (NIHL) is a sensorineural hearing deficit that begins with chronic exposure to the higher frequencies (3 to 6 kHz) and is the primary occupational disease predominantly found among industrial workers [1]. The development of NIHL is mainly due to the duration of exposure, and the intensity and frequency of the noise, which results in cochlear epithelium damage. When industrial workers are exposed to excessive noise [8h 85 dB(A)] in the workplace, the cochlea consumes a lot of energy and releases a large number of free radicals (reactive oxygen species and reactive nitrogen) locally [6]. As the antioxidant system is unable to neutralize these free radicals, the cochlear sensorial epithelium becomes damaged [7]. Genes involved in the regulation of reactive oxygen species, such as superoxide dismutase, glutathione S-transferase, and catalase, may affect the vulnerability of the cochlea to NIHL [8, 9]
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