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To explore the fitting effect of the ARIMA, GM(1,1), and RANSAC model in the changes of white blood cells (WBC) in benzene-exposed workers, and select the optimal model to predict the WBC count of workers. Among 350 employees in an aerospace process manufacturing enterprise in Nanjing, workers with 10 years of benzene exposure were selected, and used Excel software to organize the WBC data, and the ARIMA model and RANSAC model were established by R software, and the GM(1, 1) model was established by DPS software, and the magnitude of the mean absolute percentage error (MAPE) of fitting three models to WBC counts was compared. The MAPE based on the ARIMA(2,1,2) model is 6.78%, the MAPE based on the GM(1,1) model is 5.19%, and the MAPE based on the RANSAC model is 6.37%, so the GM( 1,1) model was more suitable for fitting the trend of WBC counts in benzene exposed workers in this study. The GM(1,1) model is suitable for fitting WBC counts in a small sample size and can provide a short-term prediction of WBC counts in benzene-exposed workers and provide basic information for occupational health risk assessment of workers.

Benzene is one of the most common occupational hazards in the working environment which was in the list of group 1 carcinogens. This study applied four occupational health risk assessment models: EPA model; MOM model of Singapore; the International Council on Mining and Metals (ICMM) model, and the Technical guide WS/T 777-2021 of China. The models assessed both non-carcinogenic and carcinogenic effects of benzene for 1629 employees in 50 factories in Jiangsu Province (China) who were exposed to benzene in the working environment and analysis the risk between industries by principal component analysis (PCA) method. The highest occupational health hazard of benzene among the five industries is petroleum processing industry, then followed by chemical products manufacturing industry, special equipment manufacturing industry, wood processing and products industry, and at last the pharmaceutical manufacturing industry. The population of abnormal routine blood parameters in the subjects was mostly in the "wood products industry" group, and the concentration of benzene in "wood products industry" group is the lowest in 5 groups. The industries with low exposure concentration have higher blood abnormality rates; this may be caused by the fact that blood damage is more secretive under low occupational health risk.

Background The purpose of this study was to analyze nearly three decades of academic research on chronic low-level benzene exposure and hematotoxicity with qualitative and quantitative analysis. Methods Publications from 1992 to 2022 were extracted from the Science Citation Index Expanded (SCI-E) and the Social Sciences Citation Index (SSCI) of the Web of Science Core Collection (WoSCC) of Thomson Reuters. WoSCC, Microsoft Excel 2016, and Citespace were used to analyze the publication outcomes, journals, countries, institutions, authors, and research areas. Results As of July 13, 2022, there have been 521 papers published on chronic low-level benzene exposure and hematotoxicity. Environmental Health Perspectives has published the most articles, the United States is the leading country, Fudan University is the leading institution, Chen Y has published the most articles, Snyder R has co-cited the most articles, and Toxicology is ranked #1 in the research field. Conclusion Many high-quality articles have been published in the last three decades. Fudan University and the Chinese Center for Disease Control and Prevention are in the first echelon of research on long-term low-level benzene exposure and hematological toxicity. Chen Y, Ashley D, and Bertazzi P may be good candidates for collaboration in this research area. In the meantime, occupational disease researchers should pay close attention to the studies of hematological and carcinogenicity caused by occupational benzene exposure.

Benzene is an occupational and environmental toxicant, causing hematopoietic damage. Our study is aimed to extract the trend of benzene-induced leukemia (BIL) and qualitatively and quantitatively estimate research on it. Publications on BIL were identified from the Web of Science Core Collection (WoSCC). Microsoft Excel 2019 (Redmond, WA) and The CiteSpace 5.6.R5 software (Drexel University, Philadelphia, PA) were used to analyze the publication outcomes, countries, institutions, authors, keywords, and research frontiers. The overall 1152 publications were collected from 1990 to 2019 until November 6, 2020. Environ Health Persp had the highest number of articles published. The USA were the top country in terms of BIL. The Smith MT, Yin SN, Lan Q, and Hayes RB are both listed in the top 10 of co-cited authors, high contribution authors, and the authors of co-cited references. High IF articles account for a considerable proportion, among all the publications. Chinese institutions engaged in BIL and contributed a large part of articles. Exposure population, exposure dose, and exposure risk are the research hotspots in this field. The risk of benzene exposure on childhood leukemia is at issue, and the studies on attributable risk of benzene-induced leukemia are few. More early, sensitive, and specific epigenetic biomarkers of benzolism may be the leading research fields of benzene-induced leukemia in the next few years.

To establish a reasonable prediction model of pesticide poisoning and predict the future trend of pesticide poisoning in Jiangsu Province, so as to provide the basis for rational allocation of public health resources and formulation of prevention and control strategies, the number of pesticide poisoning in Jiangsu province from 2006 to 2020 was collected. Grey model (GM(1,1)) model, autoregressive integrated moving average model (ARIMA) model and exponential smoothing model were used for prediction and comparative analysis. Finally, the model with the best fitting effect was selected. The average relative errors of ARIMA(0,1,1)(0,1,0)12 model, Holt-Winters multiplicative model and GM(1,1) were 0.096, 0.058 and 0.274 separately. The fitting effect of GM model is the worst, while the fitting effect of ARIMA(0,1,1) (0,1,0)12 model and Holt-Winters multiplication model is relatively good, which can be basically used for prediction. Holt-Winters multiplicative model has the best fitting effect and the highest accuracy in predicting the number of pesticide poisoning. The numbers of pesticide poisonings in the next 3 years are 454, 410 and 368, with a total of 1232, according to the Holt-Winters multiplicative model. Through the prediction of the number of pesticide poisoning in the next 3 years, this paper also provides a basis for the formulation of pesticide-related policies in the future.

We report the Structure-based Pathogenicity Relationship Identifier (SPRI), a novel computational tool for accurate evaluation of pathological effects of missense single mutations and prediction of higher-order spatially organized units of mutation clusters. SPRI can effectively extract properties determining pathogenicity encoded in protein structures, and can identify deleterious missense mutations of germ line origin associated with Mendelian diseases, as well as mutations of somatic origin associated with cancer drivers. It compares favorably to other methods in predicting deleterious mutations. Furthermore, SPRI can discover spatially organized pathogenic higher-order spatial (patHOS) units of dele-terious mutations, including those of low recurrence, and can be used for discovery of candidate cancer driver genes and cancer driving mutations. We further demonstrate that SPRI can take advantage of AlphaFold2 predicted structures and can be deployed for saturation mutation analysis of the whole protein universe.

Noise-induced hearing loss (NIHL) remains a leading occupational related disease and is a serious public health problem. Hence, the identification of potential biomarkers for NIHL prevention and diagnosis has become an urgent work. To discover potential metabolic biomarkers of NIHL, plasma metabolomics analysis in 62 NIHL patients and 62 normal hearing controls was performed using ultrahigh-performance liquid chromatography coupled with quadrupole time-of-flight tandem mass spectrometry (UHPLC-Q-TOF MS). Orthogonal partial least square-discriminant analysis (OPLS-DA) model was applied to distinguish metabolite profile alterations in plasma samples between the two groups. The metabolites with a variable importance of projection (VIP) value1 and P value0.05 were considered to be potential metabolic biomarkers. KEGG database was performed to explore the involved pathways of potential biomarkers. Three autophagy-related genes (PI3K, AKT, and ATG5) were selected for further verification, and mRNA levels were detected using RT-qPCR analysis. Twenty plasma metabolites with VIP1 and P0.05 were significantly altered between the two groups. Totally, seven metabolic pathways involving the glycerophospholipid metabolism, glycosylphosphatidylinositol (GPI)-anchor biosynthesis, autophagy pathway, choline metabolism, the alpha-linolenic acid metabolism and linoleic acid metabolism, and retrograde endocannabinoid pathway were significantly related to NIHL. Furthermore, verification by RT-qPCR suggested that the mRNA expression levels of PI3K and AKT along with ATG5 were significantly lower in the NIHL patients compared with controls. In summary, the present study provides the first evidence that the identified aberrantly altered metabolites may be the potentially valuable biomarkers of NIHL for occupational noise-exposed workers. Autophagy signal pathway may be involved in the occurrence and development of NIHL. Moreover, this present study may be helpful to further better understand the metabolic changes in NIHL and be helpful for the understanding of pathogenic mechanism.

Our aim was to analyze the effects of benzene exposure on hematotoxicity in workers, with a focus on gender differences. The study was divided into three parts, and the survey included 218,061 workers. Since 2017, some workers are selected from the total workers each year to explore the possible influencing factors (age, duration of benzene exposure, TWA (8-h time-weighted average) of benzene, SPMA (S-phenylmercapturic acid), MDA (malondialdehyde), 8-OHdG (8-hydroxy-2'-deoxyguanosine) of different hematotoxicity of different genders). The abnormal rate of WBC (white blood cell), ANC (absolute neutrophil count), and platelets of female workers in the benzene exposure group was higher than that of males in the benzene exposure group and also higher than that of the female workers in the control group. Research results in 2019 showed increased SPMA as well as increases their DNA damage including 8-OHdG and MDA in benzene-exposed female workers compared to those in the control female group (all p < 0.05. SPMA, 8-OHdG, and MDA in benzene exposure female workers increased 555%, 183%, and 33.3%, respectively). Female workers are at significantly higher risk for blood system effects of benzene exposure. Therefore, more stringent standards and guidelines may be needed to protect the changing professional population, especially for females.

This study is to assess the correlation between blood concentration ranges of eight elements of tin smelting workers from Guangxi Liuzhou and their job type, working years, age, and sex.We collected blood samples of 218 tin smelting workers from a Chinese tin smelting factory and determined the levels of elements by inductively coupled plasma mass spectrometry.Within the blood concentrations of eight metal elements of the objects, the blood concentration of copper and zinc is affected by the job type of comprehensive work; that of arsenic and mercury is affected by refining; and that of chromium, cadmium, and lead is affected by primary smelting.We present the remarkable influence of four job types on the blood concentration of seven trace elements.

This study intended to explore the effect of C-Jun N-terminal kinases 1 (JNK1) polymorphisms on the sensitivity of individual hearing loss. A total of 1333 subjects, including 683 NIHL workers and 650 normal-hearing workers from east China, were included in this cross-sectional study. Genotyping of three JNK1 single nucleotide polymorphisms (rs9284, rs8428, and rs11598320) was performed. The relationship between different genotypes and noise-induced hearing loss was analyzed. Results show that rs11598320 TT genotype was associated with a higher risk of NIHL (OR 1.57, 95% CI 0.91–2.70). Stratified analysis indicated that the rs11598320 AT + AA genotype was associated with a decreased risk of hearing loss in subjects exposed to noise ≤ 16 years or a noise level > 92 dB (OR 0.68, 95% CI 0.50–0.93 and OR 0.64, 95% CI 0.42–0.96, respectively). The rs8428 TT genotype was associated with an increased risk of noise-induced hearing loss when the noise level was > 92 dB (OR 1.73, 95% CI 1.11–2.70). Haplotype TCT (rs9284–rs8424–rs11598320) was associated with an increased risk of noise-induced hearing loss (OR 1.30, 95% CI 1.00–1.68). Single nucleotide polymorphisms (rs11598320 and rs8424) in JNK1 can be used as new biomarkers of susceptibility for noise-induced hearing loss in Chinese workers.

This study investigated the relationship between genetic polymorphisms in the FAS gene and noise-induced hearing loss (NIHL) risk among Chinese workers exposed to occupational noise, and the molecular mechanism of NIHL caused by noise. In this case-control study, 692 NIHL workers and 650 controls were selected for genotyping of four single nucleotide polymorphisms (SNPs) of the FAS gene. Logistic regression was used to calculate the odds ratio (OR) and 95% confidence interval (CI) of the association of these genetic polymorphisms and NIHL. At the same time, a noise-exposed rat model was constructed to further clarify the effect of noise exposure on fas gene expression and the pathogenic mechanism of NIHL. Two polymorphisms, rs1468063 and rs2862833, were associated with NIHL in the case-control study. Individuals with the rs1468063-TT or rs2862833-AA genotypes had decreased NIHL risk (p < 0.01, p = 0.02, respectively). Compared with the control group, the hearing threshold of the case group of rats increased, while serum MDA, urine 8-OHdG, and fas gene expression increased, but let-7e expression decreased. Genetic polymorphisms in the FAS gene are related to the risk of NIHL in the Chinese population. Noise can cause a large amount of reactive oxygen species (ROS) in the cochlea tissue and blood, which lead to oxidative stress, lipid peroxidation, and DNA damage, further activating the FAS gene, and ultimately leading to hearing loss.

Inflammation is a complicated process and is considered to be responsible for the development of noise-induced hearing loss (NIHL). CARD8 is an important component of inflammasome that has been implicated in inflammation. To decide the relationship between the polymorphisms of CARD8 gene and NIHL risk and deduce the potential mechanism, three SNPs (rs2043211, rs1062808, and rs12459322) were genotyped in a Chinese population consisting of 610 NIHL cases and 612 normal hearing controls. The possible impacts of SNPs on CARD8 structure and function were assessed using a variety of bioinformatics tools. Plasmids expressing wild-type and/or mutated CARD8 were transfected into HEK293 cells to verify the effect of SNPs on CARD8 protein expression level by western blot. The results revealed that rs2043211 AA genotype and A allele were associated with decreased risk of NIHL. Stratified analysis found that the male, drinking and exposed to noise ≥ 92 dB, subjects harboring rs2043211 A allele had a low risk of NIHL. The haplotype AGG (rs2043211-rs1062808-rs12459322) was significantly associated with a decreased risk of NIHL. SNP rs2043211 was predicted to be deleterious and affects CARD8 protein structure and stability. Furthermore, the functional experiment showed the mutant CARD8 could significantly decrease the CARD8 protein expression level. This study confirms that rs2043211 A allele may reduce NIHL risk by causing the loss of PPI combined with the decreased CARD8 expression level leading to CARD8 functional changes, and it may be one valuable genetic biomarker of NIHL susceptibility for Chinese noise-exposed workers.

Occupational health and safety (OHS) is important for safeguarding workers during industrialization and pursuing economic benefits. We asked 123,943 junior college students from years 1–5 to complete an online questionnaire about their knowledge of occupational safety and health. A total of 101,577 students responded, with a response rate of 81.96%. The average score and pass rate for all valid respondents were 44.99 ± 12.53 and 75.2%, respectively. There were statistically significant differences in average scores and pass rates among students of different genders, levels, number of family members, and school locations. Government departments should increase investment in Occupational Safety and Health education for students in poverty-stricken areas, and should conduct regular assessments of students’ knowledge. Junior colleges should also strengthen learning in occupational health education.

Noise-induced hearing loss (NIHL) is a multifactorial disease caused by environmental, genetic and epigenetic variables. SUMOylation is a post-translational modification that regulates biological processes. The objective of this study was to determine the link between genetic variation in the chromobox 4 (CBX4) and the risk of NIHL. This study applied a case–control design with 588 cases and 582 controls, and the sample was predominantly male (93.76%). The T allele of CBX4 rs1285250 was found to be significantly linked with NIHL (P = 0.002) and showed strong associations in both the codominant and recessive models (TT versus CC, P = 0.005; TT/TC versus CC, P = 0.009). By constructing a mouse model of hearing loss because of noise exposure, changes in hearing thresholds were observed in noise-exposed mice, along with a decrease in the number of cochlear hair cells. Furthermore, noise promotes cochlear hair cell apoptosis by inducing SP1/CBX4 pathway activation. Further functional studies demonstrated that SP1 has an influence on the promoter activity of the CBX4 rs1285250 intron, with the promoter activity of the T allele being higher than that of the C allele. Knockdown of transcription factor SP1 reduced the expression of CBX4 expression and simultaneously reduced apoptosis in HEI-OC1 cells. Together, our findings have shown that CBX4 genetic polymorphism rs1285250 T-allele was associated with increased risk of NIHL and might be used as biomarkers for male workers exposed to noise. Furthermore, we speculate that the CBX4 of rs1285250 T-allele leads to a stronger potential enhancer activity from a predicted gain of stronger SP1 binding.

The purpose of this article was to investigate the association between the ubiquitin-associated domain-containing protein 2 (UBAC2) gene polymorphism and noise-induced hearing loss (NIHL) and to further explore the role of single-nucleotide polymorphism (SNP) in UBAC2 in NIHL. A case control study involving 660 NIHL cases and 581 controls was conducted in this research. After genotyping by multiplex polymerase chain reaction (PCR) with next-generation sequencing, the correlation between SNPs and NIHL was analyzed using logistic regression analysis. Haplotype analysis was performed by Haploview 4.1 software. Then luciferase reporter assays and siRNA were used to explore the mechanism of SNPs in UBAC2 affecting NIHL susceptibility. The correlation analysis showed that rs3825427 AA genotype, rs9517701 GG genotype, rs7999348 GG genotype, and rs2296860 AA genotype were all associated with increased risk of NIHL (P 0.05). The haplotype AGGA (rs3825427-rs9517701-rs7999348-rs2296860) also had a higher risk of NIHL (OR = 1.314; 95% CI, 1.098-1.572; P = 0.003). The results of the luciferase reporter assays showed that the fluorescence intensity of CTCF-OE + UBAC2 WT + TK was significantly higher than that of CTCF-NC + UBAC2 WT + TK and CTCF-OE + UBAC2 MT + TK (all P 0.01). In CTCF knockdown cells, the expression of UBAC2 was also significantly downregulated (P = 0.0038), indicating that the transcription factor CTCF positively regulated the expression of UBAC2 and the rs3825427 C allele acted as an enhancer, which can promote CTCF to bind to the promoter of UBAC2, thereby promoting transcription. UBAC2 gene polymorphism is related to NIHL susceptibility. The UBAC2 rs3825427 regulates the expression level of UBAC2 by affecting the combination of CTCF and DNA, thus affecting the susceptibility of NIHL.

This study was conducted to estimate the current prevalence of hypertension, cardiovascular condition and hearing difficulty of workers exposure to occupational noise, and to analyze any associations between these abnormal signs and occupational noise exposure. The subjects included 5205 noise-exposed workers. Workers with high noise exposure were more likely to have a higher threshold value than low exposure ones (P Adjusted OR = 1.59, 95% CI, 1.19–2.11) and hearing loss (Adjusted OR = 1.28, 95% CI, 1.03–1.60) when comparing to low-level noise exposure. In male workers, the prevalence of hearing difficulty in high exposure group was approximately 1.2 times worse than in low group (P = 0.006). In addition, exposure to high noise level demonstrated a significant association with hypertension and hearing loss when the duration time to occupational noise was longer than 10 years. Hypertension and hearing difficulty is more prevalent in the noise-exposed group (higher than 85 dB[A]). Steps to reduce workplace noise levels and to improve workplace-based health are thus urgently needed.

Benzene is widely employed in manufacturing and causes hematotoxic effects and leukemia in humans. A long intergenic noncoding RNA (lincRNA)-microRNA (miRNA)-mRNA coexpression and competing endogenous RNA (ceRNA) regulatory network was constructed by bioinformatics analysis based on a benzene-induced aplastic anemia (BIAA) mouse model. In this population-based study, we observed a trend consistent with that in the BIAA mice: lincRNA-p21 and p21 were upregulated, while miRNA-17-5p expression was downregulated in benzene-exposed workers. Moreover, multiple linear regressions indicated that lincRNA-p21 was negatively associated with white blood cell (WBC) counts. Predictive thresholds of hematotoxicity were identified by ROC curve analysis with S-phenylmercapturic acid (SPMA) and lincRNA-p21 showing a better predictive ability than the other parameters and the combination of SPMA and lincRNA-p21 exhibiting the highest predictive value for hematotoxicity. LincRNA-p21 was predominantly present in the cytoplasm of bone marrow cells (BMCs) and K562 cells as assessed by fluorescence in situ hybridization (FISH). Upon exploring the underlying mechanism by which lincRNA-p21 mediates benzene-induced hematotoxicity, we observed that the negative regulation of 1,4-benzoquinone (1,4-BQ) on cell cycle arrest and inhibition of K562 cell proliferation was partially relieved by lincRNA-p21 knockdown, which can inhibit the expression of P21 and thereby suppress the toxic effects of 1,4-BQ. Finally, dual-luciferase reporter gene and RIP assay showed that, by acting as a sponge, lincRNA-p21 reduced the activity of miRNA-17-5p and consequently increased the expression of p21. In conclusion, our research suggested that benzene induces hematotoxicity via the lincRNA-p21/miRNA-17-5p/p21 signaling which might contribute to the underlying mechanism of lincRNA-p21 in benzene-induced hematotoxicity. Therefore, lincRNA-p21 can serve as a potential biomarker for the early detection of hematopoiesis inhibition in individuals with long-term exposure to low-dose benzene.

Missense SNPs are key factors contributing towards many Mendelian disorders and complex diseases. Identifying whether a single amino acid substitution will lead to pathological effects is important for interpreting personal genome and for precision medicine. In this study, we describe a novel method for predicting whether a missense SNP likely brings about pathological effects. Our approach integrates sequence information, biophysical properties, and topological properties of protein structures. In our test dataset consisting of 500 deleterious variants and 500 neutral, our method achieves an accuracy of 0.823. The ROC curve of model has an AUC of 0.910. Our methods outperforms two well known methods, and is comparable with the widely used Polyphen-2 method, while requiring a much smaller amount (approximately 25%) of training data. Our method can be used to aid in distinguishing driver and passenger mutations in cancer and in assessing missense mutations assocaited with rare diseases. It can also be used to identifying mutations in rare disease where only limited patient exome data exsit.

Our aim was to analyze the effects of benzene exposure on hematotoxicity in workers, with a focus on gender differences. The study was divided into three parts, and the survey included 218,061 workers. Since 2017, some workers are selected from the total workers each year to explore the possible influencing factors (age, duration of benzene exposure, TWA (8-h time-weighted average) of benzene, SPMA (S-phenylmercapturic acid), MDA (malondialdehyde), 8-OHdG (8-hydroxy-2'-deoxyguanosine) of different hematotoxicity of different genders). The abnormal rate of WBC (white blood cell), ANC (absolute neutrophil count), and platelets of female workers in the benzene exposure group was higher than that of males in the benzene exposure group and also higher than that of the female workers in the control group. Research results in 2019 showed increased SPMA as well as increases their DNA damage including 8-OHdG and MDA in benzene-exposed female workers compared to those in the control female group (all p0.05. SPMA, 8-OHdG, and MDA in benzene exposure female workers increased 555%, 183%, and 33.3%, respectively). Female workers are at significantly higher risk for blood system effects of benzene exposure. Therefore, more stringent standards and guidelines may be needed to protect the changing professional population, especially for females.

Noise-induced-hearing-loss(NIHL) is a common occupational disease caused by various environmental and biological factors. To investigate the association between TAB2 and the susceptibility of NIHL of people exposed to occupational environments, a genetic association study was performed on selected companies with 588 cases and 537 healthy control subjects. Five selected single nucleotide polymorphisms (SNPs) in TAB2,incoluding rs2744434, rs521845, rs652921, rs7896, rs9485372, were genotyped after a collection of DNA samples. Evident differences in participants between the case group and the control group reveals the result that people with the TAB2 has a high probability of getting NIHL. The results show that rs521845 is deeply associated with the risk of NIHL and is available for the diagnosis in the future.

The purposes of the current study were to investigate the association of a few of single nucleotide polymorphisms (SNPs) within the AKT2 gene and noise-induced hearing loss (NIHL) susceptibility and explore the potential mechanism underlying NIHL. Three SNPs (rs2304186, rs41275750, and rs76524493) were genotyped in a Chinese population which consists of 690 NIHL patients and 650 normal hearing controls. Bioinformatic analysis was conducted to predict the potential miRNA-binding site of SNPs. Plasmid construction, cell transfection, and dual-luciferase reporter assay were performed to investigate the potential molecular mechanism of SNPs involving in NIHL. The results revealed that rs2304186 GT genotype (OR = 1.41; 95% CI = 1.09-1.83) and TT genotype (OR = 1.51; 95% CI = 1.08-2.10) imparted increased risk of NIHL, and the increased risk could also be found in a dominant model (OR = 1.44; 95% CI = 1.12-1.84). The stratification analysis showed that rs2304186 GT/TT conferred a higher risk for NIHL, especially in subgroups of male, age (35-45 and > 45 years), noise exposure time (> 16 years), and noise exposure level (≤ 85 and ≥ 92 dB), when GG genotype as a reference. Furthermore, the haplotype TCCTACT (rs2304186-rs41275750-rs76524493) was found to be significantly associated with a high risk of NIHL (OR = 1.19; 95% CI = 1.02-1.40). Functional experiments showed that rs2304186 G allele combined with hsa-miR-625-5p mimics could significantly decrease the luciferase activity compared with T allele, indicating that rs2304186 altered the binding affinity of hsa-miR-625-5p to SNP rs2304186 mutation region, thus directly targeting AKT2 gene. In conclusion, our study provides evidence for the first time that SNP rs2304186 of AKT2 3'UTR might affect NIHL susceptibility by altering the binding affinity of has-miR-625-5p to mutation region in an allele-specific manner and it may act as a potential biomarker of NIHL susceptibility.

Noise-induced hearing loss (NIHL) is one of these hazards which has been the second most common sensorineural hearing loss. Single-nucleotide polymorphisms (SNPs) mainly refer to the polymorphism of DNA sequence caused by the variation at the genomic nucleotide level. The influence of histone deacetylase 2 (HDAC2) variants on the risk of NIHL has not been studied. This research explored the association between HDAC2 and the development of NIHL. A total of 1146 industrial workers from one textile factory in east China were recruited to perform a case-control study. Basic clinical data such sex, age, smoking, and drinking was obtained by questionnaires; pure-toneaudiometry (PTA) tests were conducted by specialist physicians. Then, we performed genotyping of five selected SNPs (rs10499080, rs2475631, rs2499618, rs6568819, and rs3757016) in the HDAC2 gene in 600 NIHL patients and 546 controls. Finally, the main influences of the SNPs and their interactions with NIHL were assessed. Under the recessive model, there were statistically significant differences in the genotype frequencies of rs10499080 between two groups, and the results showed that individuals with rs10499080 CC+CT had a lower risk of NIHL (OR = 0.597, 95%CI = 0.357-0.998). Meanwhile, the significant difference in the genotype distributions between cases and controls was found in rs10499080 in the group with noise exposure of ≤ 16 years. But the following haplotype analysis showed that no association between all haplotypes in the HDAC2 gene and NIHL was been found. The genetic polymorphisms rs10499080 and rs6568819 within HDAC2 gene have an association with risk of NIHL. Workers exposed to noise with HDAC2 have a lower risk of NIHL.