There is an association between noise exposure and cognitive impairment, and noise may have a more severe impact on patients with Alzheimer\'s disease (AD) and mild cognitive impairment; however, the mechanisms need further investigation. This study used the classic AD animal model APP/PS1 mice to simulate the AD population, and C57BL/6J mice to simulate the normal population. We compared their cognitive abilities after noise exposure, analyzed changes in Cluster of Differentiation (CD) between the two types of mice using transcriptomics, identified the differential CD molecule: CD36 in APP/PS1 after noise exposure, and used its pharmacological inhibitor to intervene to explore the mechanism by which CD36 affects APP/PS1 cognitive abilities. Our study shows that noise exposure has a more severe impact on the cognitive abilities of APP/PS1 mice, and that the expression trends of differentiation cluster molecules differ significantly between C57BL/6J and APP/PS1 mice. Transcriptomic analysis showed that the expression of CD36 in the hippocampus of APP/PS1 mice increased by 2.45-fold after noise exposure (p < 0.001). Meanwhile, Western Blot results from the hippocampus and entorhinal cortex indicated that CD36 protein levels increased by approximately 1.5-fold (p < 0.001) and 1.3-fold (p < 0.05) respectively, after noise exposure in APP/PS1 mice. The changes in CD36 expression elevated oxidative stress levels in the hippocampus and entorhinal cortex, leading to a decrease in PI3K/AKT phosphorylation, which in turn increased M1-type microglia and A1-type astrocytes while reducing the numbers of M2-type microglia and A2-type astrocytes. This increased neuroinflammation in the hippocampus and entorhinal cortex, causing synaptic and neuronal damage in APP/PS1 mice, ultimately exacerbating cognitive impairment. These findings may provide new insights into the relationship between noise exposure and cognitive impairment, especially given the different expression trends of CD molecules in the two types of mice, which warrants further research.

OBJECTIVE: Noise exposure in the workplace has been linked to a number of health consequences. Our objectives were to explore the relationship between occupational noise and lipid metabolism and evaluate the possible mediating effect of obesity indices in those relationships with a cross-sectional study design.
METHODS: Cumulative noise exposure (CNE) was used to measure the level of noise exposure. Logistic regression models or generalized linear models were employed to evaluate the association of occupational noise and obesity with lipid metabolism markers. Cross-lagged analysis was conducted to explore temporal associations of obesity with lipid metabolism.
RESULTS: A total of 854 participants were included, with each one-unit increase in CNE, the values of total cholesterol/high-density lipoprotein cholesterol and low-density lipoprotein cholesterol/high-density lipoprotein cholesterol increased by 0.013 (95% confidence interval: 0.006, 0.020) and 0.009 (0.004, 0.014), as well as the prevalence of dyslipidemia increased by 1.030 (1.013, 1.048). Occupational noise and lipid metabolism markers were all positively associated with body mass index (BMI), waist circumference (WC), a Body Shape Index (ABSI) and a Body Shape Index and Body Roundness Index (BRI) (all P < 0.05). Moreover, BMI, WC, ABSI and BRI could mediate the associations of occupational noise with lipid metabolism; the proportions ranged from 21.51 to 24.45%, 23.84 to 30.14%, 4.86 to 5.94% and 25.59 to 28.23%, respectively (all P < 0.05).
CONCLUSIONS: Our study demonstrates a positive association between occupational noise and abnormal lipid metabolism, and obesity may partly mediate the association. Our findings reinforce the need to take practical steps to reduce or even eliminate the health risks associated with occupational noise.

OBJECTIVE: We aimed to evaluate the association of occupational noise with metabolic syndrome (MetS) and its components, and to assess the potential role of miRNAs in occupational noise-associated MetS.
METHODS: A total of 854 participants were enrolled in our study. Cumulative noise exposure (CNE) was estimated in conjunction with workplace noise test records and research participants\' employment histories. Logistic regression models adjusted for potential confounders were used to assess the association of CNE and miRNAs with MetS and its components.
RESULTS: We observed linear positive dose-response associations between occupational noise exposure and the prevalence of MetS (OR: 1.031; 95 % CI: 1.008, 1.055). And linear and nonlinear relationship were also found for the association of occupational noise exposure with high blood pressure (OR: 1.024; 95 % CI: 1.007, 1.041) and reduced high-density lipoprotein (OR: 1.051; 95 % CI: 1.031, 1.072), respectively. MiR-200a-3p, miR-92a-3p and miR-21-5p were inversely associated with CNE, or the prevalence of MetS and its components (all P < 0.05). However, we did not find any statistically significant mediation effect of miRNAs in the associations of CNE with MetS. Furthermore, the prevalence of bilateral hearing loss in high-frequency increased (OR: 1.036; 95 % CI: 1.008, 1.067) with CNE level rising, and participants with bilateral hearing loss in high-frequency had a significantly higher risk of MetS (OR: 1.727; 95 % CI: 1.048, 2.819).
CONCLUSIONS: Our study suggests that occupational noise exposure is associated with MetS and its components, and the role of miRNAs in noise-induced increasing MetS risk needs to be confirmed in future studies.

Excessive noise exposure presents significant health risks to humans, affecting not just the auditory system but also the cardiovascular and central nervous systems. This study focused on three male macaque monkeys as subjects. 90 dB sound pressure level (SPL) pure tone exposure (frequency: 500Hz, repetition rate: 40Hz, 1 min per day, continuously exposed for 5 days) was administered. Assessments were performed before exposure, during exposure, immediately after exposure, and at 7-, 14-, and 28-days post-exposure, employing auditory brainstem response (ABR) tests, electrocardiograms (ECG), and electroencephalograms (EEG). The study found that the average threshold for the Ⅴ wave in the right ear increased by around 30 dB SPL right after exposure (P < 0.01) compared to pre-exposure. This elevation returned to normal within 7 days. The ECG results indicated that one of the macaque monkeys exhibited an RS-type QRS wave, and inverted T waves from immediately after exposure to 14 days, which normalized at 28 days. The other two monkeys showed no significant changes in their ECG parameters. Changes in EEG parameters demonstrated that main brain regions exhibited significant activation at 40Hz during noise exposure. After noise exposure, the power spectral density (PSD) in main brain regions, particularly those represented by the temporal lobe, exhibited a decreasing trend across all frequency bands, with no clear recovery over time. In summary, exposure to 90 dB SPL noise results in impaired auditory systems, aberrant brain functionality, and abnormal electrocardiographic indicators, albeit with individual variations. It has implications for establishing noise protection standards, although the precise mechanisms require further exploration by integrating pathological and behavioral indicators.

Acoustic stimuli such as music or ambient noise can significantly affect physiological and psychological health in humans. We here summarize positive effects of music therapy in premature infant distress regulation, performance enhancement, sleep quality control, and treatment of mental disorders. Specifically, music therapy exhibits promising effects on treatment of neurological disorders such as Alzheimer\'s disease (AD) and Parkinson\'s disease (PD). We also highlight regulatory mechanisms by which auditory intervention affects an organism, encompassing modulation of immune responses, gene expression, neurotransmitter regulation and neural circuitry. As a safe, cost-effective and non-invasive intervention, music therapy offers substantial potential in treating a variety of neurological conditions.

Chronic noise exposure is correlated with gut microbiota dysbiosis and glucose and lipid metabolism disorders. However, evidence on the mechanisms underlying of gut microbiota alterations in chronic noise induced glucose and lipid metabolism disorders is limited, and the potential aftereffects of chronic noise exposure on metabolic disorders remain unclear. In present study, we established chronic daytime and nighttime noise exposure mice models to explore the effects and underlying mechanism of gut microbiota on chronic noise-induced glucose and lipid metabolism disorders. The results showed that exposure to chronic daytime or nighttime noise significantly increased the fasting blood glucose, serum and liver TG levels, impaired glucose tolerance, and decreased serum HDL-C levels and liver TC levels in mice. However, after 4 weeks of recovery, only serum TG of mice in nighttime noise recovery group remained elevated. Besides, exposure to chronic noise reduced the intestinal tight junction protein levels and increased intestinal permeability, while this effect did not completely dissipate even after the recovery period. Moreover, chronic noise exposure changed the gut microbiota and significantly regulated metabolites and metabolic pathways, and further activate hepatic gluconeogenesis CRTC2/CREB-PCK1 signaling pathway and lipid synthesis SREBP1/SCD signaling pathway through intestinal hepatic axis. Together, our findings demonstrated that chronic daytime and nighttime noise exposure could cause the glucose and lipid metabolism disorder by modulating the gut microbiota and serum metabolites, and activating hepatic gluconeogenic CREB/CRTC2-PCK1 signaling and lipid synthesis SREBP1/SCD signaling pathway. The potential aftereffects of noise exposure during wakefulness on metabolic disorders are more significant than that of noise exposure during sleep.

Noise pollution is increasingly prevalent in aquatic ecosystems, causing detrimental effects on growth and behavior of marine fishes. The physiological responses of fish to underwater noise are poorly understood. In this study, we used RNA-sequencing (RNA-seq) to study the transcriptome of the sonic muscle in small yellow croaker (Larimichthys polyactis) after exposure to a 120 dB noise for 30 min. The behavioral experiment revealed that noise exposure resulted in accelerated tail swimming behavior at the beginning of the exposure period, followed by loss of balance at the end of experiment. Transcriptomic analysis found that most highly expressed genes in the sonic muscle, including parvalbumin, slc25a4, and troponin C were related with energy metabolism and locomotor function. Further, a total of 1261 differentially expressed genes (DEGs) were identified, including 284 up-regulated and 977 down-regulated genes in the noise exposure group compared with the control group. Gene ontology (GO) analysis indicated that the most enriched categories of DEGs included protein folding and response to unfolding protein. Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis found over-represented pathways including protein processing in the endoplasmic reticulum, chaperones and folding catalysts, as well as arginine and proline metabolism. Specifically, many genes related to fatty acid and collagen metabolism were up-regulated in the noise exposure group. Taken together, our results indicate that exposure to noise stressors alters the swimming behavior of croaker, inducing endoplasmic reticulum stress, disrupting lipid metabolism, and causing collagen degradation in the sonic muscle of L. polyactis.

Epidemiological investigations show that noise exposure in early life is associated with health and cognitive impairment. The gut microbiome established in early life plays a crucial role in modulating developmental processes that subsequently affect brain function and behavior. Here, we examined the impact of early-life exposure to noise on cognitive function in adolescent rats by analyzing the gut microbiome and metabolome to elucidate the underlying mechanisms. Chronic noise exposure during early life led to cognitive deficits, hippocampal injury, and neuroinflammation. Early-life noise exposure showed significant difference on the composition and function of the gut microbiome throughout adolescence, subsequently causing axis-series changes in fecal short-chain fatty acid (SCFA) metabolism and serum metabolome profiles, as well as dysregulation of endothelial tight junction proteins, in both intestine and brain. We also observed sex-dependent effects of microbiota depletion on SCFA-related beneficial bacteria in adolescence. Experiments on microbiota transplantation and SCFA supplementation further confirmed the role of intestinal bacteria and related SCFAs in early-life noise-exposure-induced impairments in cognition, epithelial integrity, and neuroinflammation. Overall, these results highlight the homeostatic imbalance of microbiota-gut-brain axis as an important physiological response toward environmental noise during early life and reveals subtle differences in molecular signaling processes between male and female rats.

UNASSIGNED: The study aimed to evaluate the clinical characteristics and prognostic factors associated with unilateral sudden sensorineural hearing loss (SSNHL) related to environmental noise exposure before its onset.
UNASSIGNED: A total of 50 unilateral SSNHL patients exposed to environmental noise before onset (case group) and 924 unilateral SSNHL patients without any exposure to obvious inducing factors before onset (control group) were enrolled between January 2018 and October 2022. We retrospectively analyzed differences between both groups using the chi-square test, Fisher\'s exact tests, independent t-tests, and Mann-Whitney U-tests as appropriate before and after propensity score matching (PSM) based on sex, age, and initial pure-tone average (PTA). Prognostic factors for the case group were analyzed using univariate and multivariate logistic analyses between the effective and ineffective groups.
UNASSIGNED: Before PSM, significant differences were noted in age, sex, time to treatment, the proportion of combined diabetes mellitus, initial PTA, hearing gain, the incidence of vertigo or aural fulness, the rate of vestibular dysfunction or inner ear MRI abnormalities, the effective rate, the glucose and homocysteine levels, and the proportion of audiogram curve types (P < 0.05) between both groups. After PSM, compared to the control group, a longer time to treatment (Z= -3.02, P < 0.05), higher final PTA (Z= -2.39, P < 0.05), lower hearing gain (Z= -3.46, P < 0.05), lower rate of vestibular dysfunction (χ2 = 55.1, P < 0.001), and lower effective rate (χ2 = 4.87, P < 0.05) were observed in the case group. There was a significant difference between the audiogram curve types in both groups (χ2 = 14.9, P < 0.05). Time to treatment (95% confidence interval: 0.692-0.965, P < 0.05) and final PTA (95% confidence interval: 0.921-0.998, P < 0.05) were associated with the clinical outcomes for the case group.
UNASSIGNED: Unilateral SSNHL patients exposed to environmental noise triggers before onset showed a poorer effective rate and a lower rate of vestibular dysfunction than those who were not. The time to treatment and final PTA were associated with the prognosis of these patients.

Annoyance is a major health burden induced by environmental noise. However, our understanding of the health impacts of noise is seriously undermined by the fixed contextual unit and limited sound characteristics (e.g., the sound level only) used in noise exposure assessments as well as the stationarity assumption made for exposure-response relationships. To address these limitations, we analyze the complex and dynamic relationships between personal momentary noise annoyance and real-time noise exposure in various activity microenvironments and times of day, taking into account individual mobility, multiple sound characteristics and nonstationary relationships. Using real-time mobile sensing, we collected individual data of momentary noise annoyance, real-time noise exposure as well as daily activities and travels in Hong Kong. A new sound characteristic, namely sound increment, is defined to capture the sudden increase in sound level over time and is used along with the sound level to achieve a multi-faceted assessment of personal real-time noise exposure at the moment of annoyance responses. Further, the complex noise exposure-annoyance relationships are learned using logistic regression and random forest models while controlling the effects of daily activity microenvironments, individual sociodemographic attributes and temporal contexts. The results indicate that the effects of the real-time sound level and sound increment on personal momentary noise annoyance are nonlinear, despite the overall significant and positive impacts, and different sound characteristics can produce a joint effect on annoyance. We also find that the daily activity microenvironments and individual sociodemographic attributes can affect noise annoyance and its relationship with different sound characteristics to varying degrees. Due to the temporal changes in daily activities and travels, the noise exposure-annoyance relationships can also vary over different times of the day. These findings can inform both local governments and residents with scientific evidence to promote the creation of acoustically comfortable living environments.