RÉSUMÉ
BACKGROUND: Evidence suggested that abiotic airborne exposures may be associated with changes in body composition. However, more evidence is needed to identify key pollutants linked to adverse health effects and their underlying biomolecular mechanisms, particularly in sensitive older adults. OBJECTIVES: Our research aimed to systematically assess the relationship between abiotic airborne exposures and changes in body composition among healthy older adults, as well as the potential mediating mechanisms through the serum lipidome. METHODS: From September 2018 to January 2019, we conducted a monthly survey among 76 healthy adults (60-69 years old) in the China Biomarkers of Air Pollutant Exposure (BAPE) study, measuring their personal exposures to 632 abiotic airborne pollutions using MicroPEM and the Fresh Air wristband, 18 body composition indicators from the InBody 770 device, and lipidomics from venous blood samples. We used an exposome-wide association study (ExWAS) and deletion/substitution/addition (DSA) model to unravel complex associations between exposure to contaminant mixtures and body composition, a Bayesian kernel machine regression (BKMR) model to assess the overall effect of key exposures on body composition, and mediation analysis to identify lipid intermediators. RESULTS: The ExWAS and DSA model identified that 2,4,5-T methyl ester (2,4,5-TME), 9,10-Anthracenedione (ATQ), 4b,8-dimethyl-2-isopropylphenanthrene, and 4b,5,6,7,8,8a,9,10-octahydro-(DMIP) were associated with increased body fat mass (BFM), fat mass indicators (FMI), percent body fat (PBF), and visceral fat area (VFA) in healthy older adults [Bonferroni-Hochberg false discovery rate (FDRBH)<0.05]. The BKMR model demonstrated a positive correlation between contaminants (anthracene, ATQ, copaene, di-epi-α-cedrene, and DMIP) with VFA. Mediation analysis revealed that phosphatidylcholine [PC, PC(16:1e/18:1), PC(16:2e/18:0)] and sphingolipid [SM, SM(d18:2/24:1)] mediated a significant portion, ranging from 12.27% to 26.03% (p-value <0.05), of the observed increase in VFA. DISCUSSION: Based on the evidence from multiple model results, ATQ and DMIP were statistically significantly associated with the increased VFA levels of healthy older adults, potentially regulated through lipid intermediators. These findings may have important implications for identifying potentially harmful environmental chemicals and developing targeted strategies for the control and prevention of chronic diseases in the future, particularly as the global population is rapidly aging. https://doi.org/10.1289/EHP13865.
Sujet(s)
Polluants atmosphériques , Composition corporelle , Exposition environnementale , Exposome , Lipidomique , Humains , Sujet âgé , Adulte d'âge moyen , Chine , Femelle , Polluants atmosphériques/analyse , Mâle , Exposition environnementale/statistiques et données numériques , Marqueurs biologiques/sang , Pollution de l'air/statistiques et données numériquesRÉSUMÉ
Epidemiological evidence on the impact of airborne organic pollutants on lung function among the elderly is limited, and their underlying biological mechanisms remain largely unexplored. Herein, a longitudinal panel study was conducted in Jinan, Shandong Province, China, involving 76 healthy older adults monitored over a span of five months repetitively. We systematically evaluated personal exposure to a diverse range of airborne organic pollutants using a wearable passive sampler and their effects on lung function. Participants' pulmonary function indicators were assessed, complemented by comprehensive multi-omics analyses of blood and urine samples. Leveraging the power of interaction analysis, causal inference test (CIT), and integrative pathway analysis (IPA), we explored intricate relationships between specific organic pollutants, biomolecules, and lung function deterioration, elucidating the biological mechanisms underpinning the adverse impacts of these pollutants. We observed that bis (2-chloro-1-methylethyl) ether (BCIE) was significantly associated with negative changes in the forced vital capacity (FVC), with glycerolipids mitigating this adverse effect. Additionally, 31 canonical pathways [e.g., high mobility group box 1 (HMGB1) signaling, phosphatidylinositol 3-kinase (PI3K)/AKT pathway, epithelial mesenchymal transition, and heme and nicotinamide adenine dinucleotide (NAD) biosynthesis] were identified as potential mechanisms. These findings may hold significant implications for developing effective strategies to prevent and mitigate respiratory health risks arising from exposure to such airborne pollutants. However, due to certain limitations of the study, our results should be interpreted with caution.
Sujet(s)
Polluants atmosphériques , Humains , Sujet âgé , Polluants atmosphériques/analyse , Polluants atmosphériques/toxicité , Mâle , Femelle , Chine , Études longitudinales , Adulte d'âge moyen , Poumon/effets des médicaments et des substances chimiques , Exposition environnementale/effets indésirables , Tests de la fonction respiratoire , Capacité vitale/effets des médicaments et des substances chimiquesRÉSUMÉ
What is already known on this topic?: Exposure to fine particulate matter (PM2.5) was linked to endocrine hormone disruption in the reproductive system. Nonetheless, it was unclear which specific components of PM2.5 were primarily responsible for these associations. What is added by this report?: The study presented the initial epidemiological evidence that brief exposure to PM2.5 can elevate estradiol levels in postmenopausal women. Various particle components had unique effects, with water-soluble ions and specific inorganic elements like Ag, As, Cd, Hg, Ni, Sb, Se, Sn, and Tl potentially playing significant roles in increasing estradiol levels. What are the implications for public health practice?: The study established that the prevalence of air pollution, along with its specific components, has been recognized as a novel risk factor affecting the balance of sex hormones.
RÉSUMÉ
BACKGROUND: Organophosphate esters (OPEs) are common endocrine-disrupting chemicals, and OPE exposure may be associated with type 2 diabetes (T2D). However, greater knowledge regarding the biomolecular intermediators underlying the impact of OPEs on T2D in humans are needed to understand biological etiology. OBJECTIVES: We explored the associations between OPE exposure and glycometabolic markers among older Chinese adults 60-69 years of age to elucidate the underlying mechanisms using a multi-omics approach. METHODS: This was a longitudinal panel study comprising 76 healthy participants 60-69 years of age who lived in Jinan city of northern China. The study was conducted once every month for 5 months, from September 2018 to January 2019. We measured a total of 17 OPEs in the blood, 11 OPE metabolites in urine, and 4 glycometabolic markers (fasting plasma glucose, glycated serum protein, fasting insulin, and homeostatic model assessment for insulin resistance). The blood transcriptome and serum/urine metabolome were also evaluated. The associations between individual OPEs and glycometabolic markers were explored. An adverse outcome pathway (AOP) was established to determine the biomolecules mediating the associations. RESULTS: Exposure to five OPEs and OPE metabolites (trimethylolpropane phosphate, triphenyl phosphate, tri-iso-butyl phosphate, dibutyl phosphate, and diphenyl phosphate) was associated with increased levels of glycometabolic markers. The mixture effect analysis further indicated the adverse effect of OPE mixtures. Multi-omics analyses revealed that the endogenous changes in the transcriptional and metabolic levels were associated with OPE exposure. The putative AOPs model suggested that triggers of molecular initiation events (e.g., insulin receptor and glucose transporter type 4) with subsequent key events, including disruptions in signal transduction pathways (e.g., phosphatidylinositol 3-kinase/protein kinase B and insulin secretion signaling) and biological functions (glucose uptake and insulin secretion), may constitute the diabetogenic effects of OPEs. DISCUSSION: OPEs are associated with the elevated risk of T2D among older Chinese adults 60-69 years of age. Implementing OPE exposure reduction strategies may help reduce the T2D burden among these individuals, if the relationship is causal. https://doi.org/10.1289/EHP11896.
Sujet(s)
Diabète de type 2 , Ignifuges , Insulinorésistance , Sujet âgé , Humains , Adulte d'âge moyen , Chine/épidémiologie , Diabète de type 2/épidémiologie , Peuples d'Asie de l'Est , Esters , Ignifuges/analyse , Organophosphates/urine , PhosphatesRÉSUMÉ
Age-related diseases account for almost half of all diseases among adults worldwide, and their incidence is substantially affected by the exposome, which is the sum of all exogenous and endogenous environmental exposures and the human body's response to these exposures throughout the entire lifespan. Herein, we perform a comprehensive review of the epidemiological literature to determine the key elements of the exposome that affect the development of age-related diseases and the roles of aging hallmarks in this process. We find that most exposure assessments in previous aging studies have used a reductionist approach, whereby the effect of only a single environmental factor or a specific class of environmental factors on the development of age-related diseases has been examined. As such, there is a lack of a holistic and unbiased understanding of the effect of multiple environmental factors on the development of age-related diseases. To address this, we propose several research strategies based on an exposomic framework that could advance our understanding-in particular, from a mechanistic perspective-of how environmental factors affect the development of age-related diseases. We discuss the statistical methods and other methods that have been used in exposome-wide association studies, with a particular focus on multiomics technologies. We also address future challenges and opportunities in the realm of multidisciplinary approaches and genome-exposome epidemiology. Furthermore, we provide perspectives on precise public health services for vulnerable populations, public communications, the integration of risk exposure information, and the bench-to-bedside translation of research on age-related diseases.
Sujet(s)
Exposome , États-Unis , Humains , Exposition environnementale/effets indésirables , Vieillissement/génétiqueRÉSUMÉ
BACKGROUND: circRNAs have been recognized as biomarkers of numerous diseases. We would like to explore the expression pattern and molecular mechanisms of circRNAs in the Chinese occupational mercury-exposed population. METHODS: The workers from a thermometer manufacturing plant and lamp factory in Jiangsu province of China were recruited in 2016. Blood samples were collected from the subjects with chronic mercury poisoning group, mercury absorption group, and the healthy controls. The differentially expressed circRNAs (DECRs) between the three groups were screened from serum samples using a circRNA microarray. The significant DECRs were validated by qRT-PCR, and their respective diagnostic values for mercury poisoning and mercury absorption were analyzed by receiver operating characteristic (ROC) curves. For in vitro experiments, 293T cells were treated with different doses of HgCl2 to determine the half-lethal concentration. The cells were transfected with the siRNA construct or expression plasmid of circRNA. The expression levels of JNK, p38, and caspase family proteins were analyzed by Western blotting. RESULTS: hsa_circ_0025244 was up-regulated in the mercury poisoning and absorption groups compared to the control group (P < 0.05), and positively correlated with the urine mercury levels (P < 0.05). The area under the ROC curve (AUC) of hsa_circ_0025244 for diagnosing occupational mercury poisoning was 0.748, indicating moderate accuracy (P < 0.001). Moreover, the diagnostic accuracy of occupational mercury absorption was high (P < 0.001) with an AUC of 0.918. Knockdown of hsa_circ_0025244 in 293T cells significantly reduced the expression levels of JNK/p38, and caspase family proteins compared to that in the control cells (P < 0.01), and its overexpression led to opposite effects (P < 0.05). CONCLUSIONS: hsa_circ_0025244 is a potential biomarker for mercury exposure and mediates mercury-induced apoptosis in 293T cells by activating the JNK/p38 MAPK signaling pathway.
Sujet(s)
Intoxication au mercure , Mercure , Apoptose , Marqueurs biologiques , Caspases/métabolisme , Humains , ARN circulaire/génétique , Petit ARN interférent , Courbe ROC , Transduction du signal , p38 Mitogen-Activated Protein Kinases/métabolismeRÉSUMÉ
Ambient PM2.5 (fine particulate matter with aerodynamic diameters ≤ 2.5 µm) is thought to be associated with the development of diabetes, but few studies traced the effects of PM2.5 components and pollution sources on the change in the fasting blood glucose (FBG). In the present study, we assessed the associations of PM2.5 constituents and their sources with the FBG in a general Chinese population aged over 40 years. Exposure to PM2.5 was positively associated with the FBG level, and each interquartile range (IQR) increase in a lag period of 30 days (18.4 µg/m3) showed the strongest association with an elevated FBG of 0.16 mmol/L (95% confidence interval: 0.04, 0.28). Among various constituents, increases in exposed elemental carbon, organic matter, arsenic, and heavy metals such as silver, cadmium, lead, and zinc were associated with higher FBG, whereas barium and chromium were associated with lower FBG levels. The elevated FBG level was closely associated with the PM2.5 from coal combustion, industrial sources, and vehicle emissions, while the association with secondary sources was statistically insignificant. Improving air quality by tracing back to the pollution sources would help to develop well-directed policies to protect human health.
Sujet(s)
Polluants atmosphériques , Pollution de l'air , Sujet âgé , Polluants atmosphériques/analyse , Pollution de l'air/analyse , Glycémie , Chine , Charbon , Études transversales , Poussière , Exposition environnementale/analyse , Jeûne , Humains , Minéraux , Matière particulaire/analyseRÉSUMÉ
OBJECTIVE: To investigate the potential association of cochlear clock genes (CRY1, CRY2, PER1, and PER2), the DNF gene (brain-derived neurotrophic factor), and the NTF3 gene (neurotrophin3) with susceptivity to noise-induced hearing loss (NIHL) among Chinese noise-exposed workers. METHODS: A nested case-control study was performed with 2056 noise-exposed workers from a chemical fiber factory and an energy company who underwent occupational health examinations in 2019 as study subjects. Propensity score matching was conducted to screen cases and controls by matching sex, age, and the consumption of tobacco and alcohol. A total of 1269 participants were enrolled. Then, general information and noise exposure of the study subjects were obtained through a questionnaire survey and on-site noise detection. According to the results of audiological evaluations, the participants were divided into the case group (n = 432, high-frequency threshold shift > 25 dB) and the matched control group (n = 837, high-frequency threshold shift ≤ 25 dB) by propensity score matching. Genotyping for PER1 rs2253820 and rs2585405; PER2 rs56386336 and rs934945; CRY1 rs1056560 and rs3809236; CRY2 rs2292910 and rs6798; BDNF rs11030099, rs7124442 and rs6265; and NTF3 rs1805149 was conducted using the TaqMan-PCR technique. RESULTS: In the dominant model and the co-dominant model, the distribution of PER1 rs2585405 genotypes between the case group and the control group was significantly different (P = 0.03, P = 0.01). The NIHL risk of the subjects with the GC genotype was 1.41 times the risk of those carrying the GG genotype (95% confidence interval (CI) of odds ratio (OR): 1.01-1.96), and the NIHL risk of the subjects with the CC genotype was 0.93 times the risk of those carrying the GG genotype (95%CI of OR: 0.71-1.21). After the noise exposure period and noise exposure intensities were stratified, in the co-dominant model, the adjusted OR values for noise intensities of ≤ 85 was 1.23 (95%CI: 0.99-1.53). In the dominant model, the adjusted OR values for noise exposure periods of ≤ 16 years and noise intensities of ≤ 85 were 1.88 (95%CI: 1.03-3.42) and 1.64 (95%CI: 1.12-2.38), respectively. CONCLUSION: The CC/CG genotype of rs2585405 in the PER1 gene was identified as a potential risk factor for NIHL in Chinese noise-exposed workers, and interaction between rs2585405 and high temperature was found to be associated with NIHL risk.
Sujet(s)
Surdité due au bruitRÉSUMÉ
BACKGROUND: The purpose of this study was twofold: (1) to measure the personal attenuation ratings (PARs) in Chinese workers wearing hearing protection devices (HPDs), to evaluate the effectiveness of the single number rating (SNR), the noise reduction rating (NRR), and the associated derated values of earplugs; and (2) to evaluate the effectiveness of one-on-one training along with earplug fit testing on PAR improvement. METHODS: Noise exposure measurements, one-on-one training, and fit tests to measure earplug attenuation were conducted at nine manufacturing facilities located in eastern China from 2016 to 2017. 503 workers participated in the study. Ninety-three percent were male. 199 workers were provided one-on-one training. RESULTS: Before training, 14% and 15% of the workers achieved the attenuation predicted by the manufacturer's SNR and NRR, 56% and 65% exceeded the derated SNR and NRR, respectively. Following one-on-one training, mean PAR improved significantly by 15 dB (p < 0.01); 26% of the workers achieved SNR and NRR, 79% and 91% met the associated derated values, respectively. CONCLUSIONS: Labeled noise attenuation ratings and their derated values overestimated the actual level of attenuation among workers wearing HPDs. One-on-one training along with earplug fit testing contributed to improved PARs.
Sujet(s)
Surdité due au bruit , Bruit au travail , Chine , Dispositifs de protection des oreilles , Surdité due au bruit/prévention et contrôle , Humains , Mâle , Installations industrielles et de fabricationRÉSUMÉ
The health impact of airborne contaminants has been challenging to assess due to current limitations in measurement technologies. The emergence of wearable passive samplers coupled with high resolution mass spectrometry (HR-MS) chemical analysis has enabled comprehensive characterization of personal exposures. We conducted a repeated-measure study among 84 older adults in Jinan, China, as part of the Biomarkers for Air Pollutants Exposure (China BAPE) study. Study objectives were: 1) to characterize the occurrence, magnitude, and distribution of personal exposure to airborne contaminants; 2) to evaluate the temporal variation of chemical exposures across the study population; and 3) to identify behavioral and environmental factors that influence the observed variance in chemical exposures. The FreshAir wristband was worn by participants for three consecutive days each month from September 2018 to January 2019 and collected with paired time-activity logs. Passive air samplers were also deployed in parallel at a local outdoor air monitoring station. Spearman's Rho trend test and trajectory cluster analysis were used to identify exposure trends and variation patterns, respectively. Out of the 70 airborne compounds of potential concern screened, 26 compounds from 10 chemical classes were found to be above detection thresholds across >70% of the study population. Personal exposures were predominantly characterized by nine polycyclic aromatic hydrocarbons (PAHs), four phthalates, three nitroaromatics, and two volatile organic compounds (VOCs). Phthalate personal exposures were positively correlated with outdoor temperatures while the inverse relationship was observed for certain PAHs (p < 0.05). Specifically, dimethyl phthalate (rs = 0.31) decreased as temperatures declined, while nitrobenzene (rs = -0.35) and naphthalene (rs = -0.40) increased as temperatures decreased. Compared to levels measured at the outdoor air monitoring site, personal exposure of phthalates was elevated (p < 0.05) and hexachlorobutadiene was lower across participants (p < 0.01). Personal exposure of these chemicals was further found to be weakly associated with daily duration participants spent outdoors. Individuals formed distinct clusters based on trajectories of chemical exposures across the sampling period (September to January), potentially suggestive of distinct emission sources. In conclusion, we demonstrate the feasibility of characterizing the occurrence and magnitude of personal exposure to airborne chemical contaminants using passive wristband samplers. The temporal variability of these personal exposure profiles was highlighted and with distinct trends identified across different groups of individuals. Future studies will integrate this data with other omics datasets collected from this population of Chinese older adults to investigate associations between exposure profiles and health relevant biomarkers, to provide evidence in feasibility of disease prevention through environmental improvements.
Sujet(s)
Polluants atmosphériques , Dispositifs électroniques portables , Sujet âgé , Polluants atmosphériques/analyse , Chine , Surveillance de l'environnement , Chromatographie gazeuse-spectrométrie de masse , HumainsRÉSUMÉ
Arctic warming associated with global climate change poses a significant threat to populations of wildlife in the Arctic. Since lipids play a vital role in adaptation of organisms to variations in temperature, high-resolution mass-spectrometry-based lipidomics can provide insights into adaptive responses of organisms to a warmer environment in the Arctic and help to illustrate potential novel roles of lipids in the process of thermal adaption. In this study, we studied an ecologically and economically important species-Arctic char (Salvelinus alpinus)-with a detailed multi-tissue analysis of the lipidome in response to chronic shifts in temperature using a validated lipidomics workflow. In addition, dynamic alterations in the hepatic lipidome during the time course of shifts in temperature were also characterized. Our results showed that early life stages of Arctic char were more susceptible to variations in temperature. One-year-old Arctic char responded to chronic increases in temperature with coordinated regulation of lipids, including headgroup-specific remodeling of acyl chains in glycerophospholipids (GP) and extensive alterations in composition of lipids in membranes, such as less lyso-GPs, and more ether-GPs and sphingomyelin. Glycerolipids (e.g., triacylglycerol, TG) also participated in adaptive responses of the lipidome of Arctic char. Eight-week-old Arctic char exhibited rapid adaptive alterations of the hepatic lipidome to stepwise decreases in temperature while showing blunted responses to gradual increases in temperature, implying an inability to adapt rapidly to warmer environments. Three common phosphatidylethanolamines (PEs) (PE 36:6|PE 16:1_20:5, PE 38:7|PE 16:1_22:6, and PE 40:7|PE 18:1_22:6) were finally identified as candidate lipid biomarkers for temperature shifts via machine learning approach. Overall, this work provides additional information to a better understanding of underlying regulatory mechanisms of the lipidome of Arctic organisms in the face of near-future warming.
Sujet(s)
Lipidomique , Truite , Animaux , Régions arctiques , Changement climatique , TempératureRÉSUMÉ
Background: There are few published studies concerning occupational exposure to glyphosate (GLY), and these are limited to spraying, horticulture and other agricultural aspects. Therefore, the concentration of glyphosate and its metabolite aminomethylphosphonic acid (AMPA), in the urine of workers exposed to glyphosate during glyphosate production was determined, and the relationship between internal (urinary glyphosate and AMPA concentration) and external exposure dose (time weighted average (TWA) value of glyphosate in the air of workplace) was analyzed. Methods: To avoid the influence of preparations, we selected people who were only involved in GLY production (without exposure to its preparations) as our research subjects. We collected 134 urine samples of workers exposed to GLY (prototype, not preparation). The urinary concentrations of GLY and AMPA (internal exposure dose) were detected by gas chromatography-mass spectrometry. The subjects' exposure to the amount of GLY in the air (external dose) was determined using ion chromatography. Conventional statistical methods, including quartiles, t-tests and regression analysis, were applied for data processing. Results: An on-site investigation revealed that the workers involved in centrifugation, crystallization, drying, and packaging and feeding were exposed to GLY. The TWA value of GLY in the workshop air was <0.02 mg/m3-34.58 mg/m3. The detection rates of GLY and AMPA in the urine samples were 86.6% and 81.3%, respectively. The concentration of urinary GLY was <0.020-17.202 mg/L (median, 0.292 mg/L). The urinary AMPA concentration was <0.010 mg/L-2.730 mg/L (median, 0.068 mg/L). The geometric means were 0.262 mg/L and 0.072 mg/L for GLY and AMPA, respectively. There was a correlation between the urinary concentration of GLY and AMPA and the TWA value of exposed workers (correlation coefficient [r] = 0.914 and 0.683, respectively; p < 0.01). Furthermore, there was a correlation between the urinary concentration of GLY and AMPA in the exposure group (r = 0.736, p < 0.01). Conclusions: The urinary concentration of GLY and AMPA of workers was correlated with the TWA value of workers' exposure, which could reflect the actual exposure of the workers.
Sujet(s)
Agriculture , Glycine/analogues et dérivés , Herbicides , Exposition professionnelle , Adulte , Chine , Femelle , Glycine/urine , Herbicides/urine , Humains , Mâle , Adulte d'âge moyen , Lieu de travail ,RÉSUMÉ
Noise-induced hearing loss (NIHL) is one of the most common occupational health risks in industrialized countries. It has been recognized to result from interactions between genetic and environmental factors. This study investigated the influence of genetic mutations in the potassium voltage-gated channel subfamily E regulatory subunit 1 (KCNE1) gene on susceptibility to NIHL. A total of 2689 industrial workers in eastern China were recruited to participate. Three single-nucleotide polymorphisms (SNPs) of KCNE1 were genotyped in noise-exposed workers who were classified into 589 cases and 639 control individuals. Then, main effects of the genotypes and their interactions with environmental factors were evaluated. Results showed that the rs3453 C allele located in KCNE1 3'-UTR region and the rs1805127 G allele in the encoding region were associated with increased risk of NIHL in the Chinese population. There is an association between TAA, TAG, and other (CAA/CGA) haplotypes (rs3453-rs11702354-rs1805127) and increased risk of NIHL with OR = 1.33, 1.43, and 2.93 (P = 0.022, 0.017, and 0.001 respectively) compared with CGG group. Results also showed a significant interaction between rs3453, rs1805127, and high-temperature exposure (P = 0.0002, adjusted OR = 1.85). The cellular evidence indicated that polymorphisms rs3453 and rs1805127 may play key roles in hearing loss through affecting KCNE1 expressions by the way of microRNA and protein respectively. The further animal study is still needed to confirm these mechanisms. KCNE1 rs3453 and rs1805127 may have a potential as biomarkers for screening the susceptibility to NIHL.
Sujet(s)
Surdité due au bruit , Animaux , Études cas-témoins , Chine , Prédisposition génétique à une maladie , Génotype , Humains , PotassiumRÉSUMÉ
INTRODUCTION: Noise-induced hearing loss (NIHL) is a common occupational disease that represents an irreversible hearing damage to the auditory system. It has been identified as a complicated disease involving both environmental and genetic factors. More efforts need to be made to explore the genes associated with susceptibility to NIHL. The main aim of this research is to detect the associations between SIK3 polymorphisms and NIHL susceptibility in Han people in China. METHODS: A case-control study was performed in 586 cases and 639 controls in a textile factory matched for sex, age, smoking, drinking, work time with noise, and intensity of noise exposure. Three single nucleotide polymorphisms (SNPs) (rs493134, rs6589574, and rs7121898) of SIK3 were genotyped in the participants. Then, the main influences of the SNPs on and their interactions with NIHL were assessed. RESULTS: Under the allelic model, distributions of rs493134 T, rs6589574 G, and rs7121898 A in the NIHL group are statistically different from those of the normal group (p = 0.001, p < 0.001, and p = 0.019, respectively). The following haplotype analysis shows that TAA (rs493134-rs6589574-rs7121898) may have a protective effect, while TGA (rs493134-rs6589574-rs7121898) (OR = 1.49, 95% CI = 1.25-1.79) may be a risk factor for NIHL. Multifactor dimensionality reduction analysis shows that the interaction of the 3 selected SNPs is associated with NIHL susceptibility (OR = 1.88, 95% CI = 1.50-2.36). CONCLUSION: The results suggest that 3 SNPs (rs493134, rs6589574, and rs7121898) of SIK3 may be an important part of NIHL susceptibility and can be applied in the prevention, early diagnosis, and treatment of NIHL in noise-exposed Chinese workers.
Sujet(s)
Surdité due au bruit/génétique , Bruit au travail/statistiques et données numériques , Protein kinases/génétique , Industrie textile , Adulte , Facteurs âges , Consommation d'alcool/épidémiologie , Asiatiques/génétique , Études cas-témoins , Chine/épidémiologie , Femelle , Prédisposition génétique à une maladie , Génotype , Haplotypes , Surdité due au bruit/épidémiologie , Humains , Mâle , Adulte d'âge moyen , Bruit au travail/effets indésirables , Polymorphisme de nucléotide simple , Facteurs de risque , Facteurs sexuels , Fumer/épidémiologieRÉSUMÉ
WHAT IS ALREADY KNOWN ABOUT THIS TOPIC?: Mercury is still used in the manufacture of some thermometers in China. This may pose health risks if exposure is not properly prevented and controlled. WHAT IS ADDED BY THIS REPORT?: An onsite investigation of a workplace at a thermometer facility in Jiangsu Province in 2019 found heavily elevated airborne and urinary mercury levels among a massive number of workers exposed to mercury. Traditional and obsolete technology as well as inadequate protection measures for occupational hazards caused this high level of exposure. WHAT ARE THE IMPLICATIONS FOR PUBLIC HEALTH PRACTICE?: Employers at thermometer producing facilities need to adopt effective protection measures and implement strict management. Monitoring exposure, adopting better engineering controls, diligent cleaning, and providing recommended personal protective equipment (PPE) along with training to their workers properly can alleviate mercury exposure at their facilities. In addition, transitioning to mercury-free thermometers would eliminate the risk of mercury exposure.
RÉSUMÉ
BACKGROUND: Extracellular long non-coding RNA (lncRNA) has attracted increasing attention as a potential biomarker to indicate disease status and physiological process. It plays a unique role in pathogenesis, and may be a new potential biomarker, especially for chronic hearing loss. Early screening of NIHL susceptible population is of great significance in reducing the incidence of NIHL. METHODS: The expression profiles of lncRNAs and mRNAs in serum of noise-induced hearing loss (NIHL) and exposure groups were detected by microarray technique in serum. The differentially expressed mRNAs was analyzed by GO and KEGG to identify related biological functions and signaling pathways. The top up-regulated and down regulated lncRNAs were identified by qRT-PCR. RESULTS: A total of 2,072 differentially expressed lncRNAs (889 up-regulated and 1,183 down-regulated) were included in NIHL subjects compared to exposed group by using microarrays. GO enrichment and KEGG pathway analysis showed that the expression pattern of mRNAs in serum of NIHL was associated with noise exposure. LncRNAs were verified by qRT-PCR, namely, LOC101928211, LOC101928804, and BANCR. The expression of LOC101928211 and LOC101928804 in the NIHL group was significantly higher than that in the exposed group, while the expression of BANCR was obviously decreased (P<0.001). CONCLUSIONS: In this study, lncRNAs and mRNAs expression profile in NIHL was preliminarily investigated in silico. The newly discovered lncRNAs might be involved in the pathological process of hearing loss and may serve as potential biomarkers to indicate long-term noise exposure-induced hearing loss.
RÉSUMÉ
Long-term and continuous noise exposure can result in noise-induced hearing loss (NIHL), which is a worldwide problem resulting from the interaction of environmental and genetic factors. The ATP2B2 gene polymorphism can destroy cochlear hair cells and increase the risk of NIHL. A case-control study of 760 Chinese textile workers was conducted to investigate the relationship between ATP2B2 polymorphisms and NIHL susceptibility. Venous blood was collected and questionnaires were conducted by professional physicians. A case group and a control group which were typed by individuals' pure-tone audiometry test results were set. Three polymorphism sites of ATP2B2 were genotyped by using the PCR technique. Analysis results revealed that the C allele of rs3209637 (95%CI = 1.08-2.58, odds ratio (OR) = 1.67, P = 0.027) was a dangerous factor and could add to risks of NIHL in the Chinese employees. The data of stratified analysis revealed that individuals who are exposed to noise > 95 dB with the rs3209637 C genotype have a higher susceptibility to NIHL (OR = 1.34, 95%CI = 1.07-1.68). Multifactor dimensionality reduction analysis revealed that the interaction between rs14154 and rs3209637 is linked to increased NIHL risk, and for the interaction among rs14154, smoking and drinking had the same function (OR = 1.54 and 1.77, 95%CI = 1.15-2.07, 1.33-2.37, and P = 0.0037 and P < 0.0001, respectively). Our results suggest that genetic polymorphism rs3209637 C within ATP2B2 is a risk factor for NIHL among Chinese employees and rs3209637 C could be a potential biomarker for NIHL patients.
RÉSUMÉ
OBJECTIVE: Noise-induced hearing loss (NIHL) is one of the most common occupational health risks in both developed and industrialized countries. It occurs as a result of interactions between genetic and environmental factors. Nevertheless, inherited genetic factors contributing to NIHL are not well understood. Therefore, we aim to investigate whether genetic mutations in three important base excision repair genes (OGG1, APEX1, and XRCC1) may influence susceptibility to NIHL. METHODS: Three SNPs in OGG1, APEX1, and XRCC1 were genotyped from 1170 noise-exposed workers and were classified into 117 most susceptible and 117 most resistant individuals. RESULTS: Results showed that the rs1799782 TT genotype located in the XRCC1 coding region and rs1130409 GG/GT in the APEX1 coding region were associated with increased risk for NIHL in a Chinese population. Compared to the rs1799782 C allele frequency, the T allele frequency was increased in the sensitive group (adjusted OR = 1.51, 95%CI = 1.01 to 2.26, P = 0.043). The rs1130409 G allele frequency was also increased in the sensitive group compared to the resistant group (adjusted OR = 1.59, 95%CI = 1.10 to 2.31, P = 0.015). Moreover, rs1130409 and drinking had a statistically significant interaction (P = 0.0002), while rs1799782, rs1130409, and smoking also had a statistically significant interaction (P < 0.0001). CONCLUSIONS: XRCC1 rs1799782 and APEX1 rs1130409 may have potential as biomarkers for the screening of susceptibility to NIHL in workers exposed severe noise.
Sujet(s)
Asiatiques/génétique , DNA-(apurinic or apyrimidinic site) lyase/génétique , Prédisposition génétique à une maladie , Surdité due au bruit/génétique , Polymorphisme de nucléotide simple , Protéine-1 de complémentation croisée de la réparation des lésions induites par les rayons X/génétique , Adulte , Études cas-témoins , DNA Glycosylases/génétique , Femelle , Études de suivi , Génotype , Surdité due au bruit/étiologie , Surdité due au bruit/anatomopathologie , Humains , Mâle , Exposition professionnelle/effets indésirables , PronosticRÉSUMÉ
BACKGROUND: Noise induced hearing loss (NIHL) is a polygenic disease involving both genetic and environmental factors, and is one of the most important occupational health hazards worldwide. To date, the influence of Notch1 variants on the risk to develop NIHL has not been illuminated. This study was conducted to explore the effects of Notch1 polymorphisms on individual susceptibility to NIHL. METHODS: A total of 2689 industrial workers from one textile factory in east China were recruited to participate in the current study. Venous blood was collected, basic clinical data was obtained by questionnaires and pure-tone audiometry (PTA) tests were conducted by specialist physicians. Next we performed genotyping of three selected SNPs (rs3124594, rs3124599 and rs3124603) in the Notch1 gene in 535 NIHL patients and 535 controls. Subsequently, the main effects of the genotypes and their interactions were evaluated. RESULTS: Our results revealed that individuals with a GG of rs3124594, TT of rs3124603 (OR = 4.70 and 1.59 respectively) and the haplotype AAC (rs3124594-rs3124599-rs3124603) (OR = 14.95) were associated with an increased risk of NIHL in our study cohort. Stratified analysis showed that an increased NIHL risk was found in individuals exposed to work related noise for ≤16 years that also had the rs3124594 GG or rs3124603 CT/TT genotype with an OR of 4.20 and 1.73 respectively. Multifactor dimensionality reduction analysis indicated that rs3124594, rs3124599 and rs3124603 interacted with each other and were related to an increased risk to develop NIHL (OR = 3.60). CONCLUSIONS: The genetic polymorphisms rs3124594 and rs3124603 within the Notch1 gene are associated with an increased risk of NIHL in a Chinese population and could potentially be used as biomarkers for NIHL in noise exposed workers.
Sujet(s)
Prédisposition génétique à une maladie , Surdité due au bruit/génétique , Maladies professionnelles/génétique , Polymorphisme de nucléotide simple , Récepteur Notch1/génétique , Industrie textile , Adulte , Asiatiques , Audiométrie tonale , Études cas-témoins , Femelle , Expression des gènes , Haplotypes , Surdité due au bruit/diagnostic , Surdité due au bruit/ethnologie , Surdité due au bruit/physiopathologie , Humains , Mâle , Adulte d'âge moyen , Réduction de dimensionnalité multifactorielle , Maladies professionnelles/diagnostic , Maladies professionnelles/ethnologie , Maladies professionnelles/physiopathologie , Enquêtes et questionnairesRÉSUMÉ
This study was conducted to explore the effects of DNMT1 and DNMT3A polymorphisms on susceptibility to noise-induced hearing loss (NIHL) in Chinese workers. A total of 2689 industrial workers from a single textile factory were recruited. Venous blood was collected, as were questionnaire and pure-tone audiometry (PTA) data by specialist physicians. Four selected SNPs (rs7578575, rs749131, rs1550117, and rs2228611) in DNMT1 and DNMT3A were genotyped in 527 NIHL patients and 527 controls. Then, main effects of the genotypes and their interactions were evaluated. Results revealed that the GG genotype at rs749131 and the AG/GG genotypes at rs1550117 and rs2228611 [odds ratio (OR) = 1.87, 2.57, and 1.98 respectively], as well as the haplotypes AGGG and TGGA (rs7578578-rs749131-rs1550117-rs2228611) (OR = 1.35 and 1.56, respectively) were associated with an increased risk of NIHL in the Chinese population. Multifactor dimensionality reduction analysis indicated that rs7578575, rs749131, and rs2228611 interact and are related to increased NIHL risk (OR = 1.63). The genetic polymorphisms rs749131 G, rs1550117 G, and rs2228611 G within the DNMT1 and DNMT3A genes are associated with an increased risk of NIHL in the Chinese population and have the potential to act as biomarkers for noise-exposed workers.