Long-term Noise Exposure Research Articles

Noise Exposure in the Workplace, Genetic Susceptibility, and Incidence of Atrial Fibrillation: A Prospective Cohort Study.

No study explored the association of noise exposure in the workplace and genetic susceptibility with incidence of atrial fibrillation (AF). We aimed to assess the separate and joint relationship of noise exposure in the workplace and genetic susceptibility with the risk of AF. We included 167 577 participants without AF at baseline in UK Biobank. Cox proportional hazards models were used to assess the separate and joint association of noise exposure in the workplace and genetic susceptibility with the risk of AF. During a median follow-up of 11.83 years, we observed 9355 AF cases. Compared with no noise exposure in the workplace, the hazard ratios (HRs) and were 1.08 (95% CI, 0.99-1.18) for noise exposure in the workplace of <1 year, 1.03 (95% CI, 0.95-1.12) for noise exposure in the workplace of around 1 to 5 years, and 1.08 (95% CI, 1.02-1.14) for noise exposure in the workplace of >5 years, respectively, after adjusting for potential confounders. Genetic risk was positively associated with AF, compared with low genetic risk (tertile 1), the HRs were 1.50 (95% CI, 1.41-1.59) for medium genetic risk (tertile 2) and 2.51 (95% CI, 2.38-2.65) for high genetic risk (tertile 3). However, no interaction between noise exposure in the workplace and genetic susceptibility was observed (P>0.05). Long-term noise exposure in the workplace is positively associated with a higher incidence of AF regardless of genetic background.

Road-traffic noise exposure and coronary atherosclerosis in the Swedish CArdioPulmonary bioImage Study (SCAPIS).

Road-traffic noise may influence the development of cardiovascular events such as stroke and myocardial infarction, but etiological mechanisms remain unclear. This study aimed to assess the relationship between long-term road-traffic noise exposure and coronary atherosclerosis in Sweden. In the Swedish CArdioPulmonary bioImage Study (SCAPIS) cohort, including 30,154 subjects aged 50-65 years, recruited between 2013 and 2018, coronary atherosclerosis was measured based on computer tomography (CT) scans as coronary artery calcium score, segment involvement score (SIS), and non-calcified plaques (NCP) at enrollment. Based on modified Nordic model, road-traffic noise exposure was modeled for 2000, 2013, and 2018 with interpolation for intermediate years. We investigated the association between time-weighted long-term exposure to road-traffic noise (Lden) and the prevalence of atherosclerosis using ordinal logistic regression models adjusting for potential socioeconomic, behavioral, and environmental confounders, including air pollution. No clear associations were found between road-traffic noise and coronary atherosclerosis. The odds ratio for coronary artery calcium score was 1.00 (95% confidence interval [CI] = 0.96, 1.04), SIS 0.99 (0.96, 1.03), and NCP 0.98 (0.90, 1.03) per interquartile range (9.4 dB Lden) for road-traffic noise exposure during 10 years before enrollment. No consistent associations were observed in site-specific analyses or using shorter exposure periods. Furthermore, exposure-response analyses revealed no clear trends, and there were no strong interactions between road-traffic noise and cardiovascular risk factors in relation to the atherosclerosis markers. Long-term exposure to road-traffic noise was not linked to coronary atherosclerosis or calcification in relatively healthy, middle-aged populations in Sweden.

Environmental noise monitoring using distributed hierarchical wireless acoustic sensor network

Acoustic noise pollution is one of many problems people face as cities grow. Long-term noise exposure can result in a series of physical and mental health diseases that are highly harmful to foetuses and newborns. Hence, many IoT-based wireless sensor network systems have been proposed for automated monitoring for long-term operation. However, these systems suffer from weaknesses in functionality, power consumption, costs, and scalability, which hinder large-scale deployment. In this study, we propose a distributed hierarchical wireless acoustic sensor network for environmental noise monitoring to do sound classification and A-weighted sound-pressure-level measurement to address the shortcomings of existing systems. A series of tests and comparisons are performed in diagnosing the performance with respect to recording continuity, packet loss, recording quality, accuracy on A-weighted sound pressure level calculations, and costs. Results show that this proposed network structure is feasible as a part of hardware implementation in a large-scale, low-cost, and high-scalable environmental noise monitoring system to classify sound.

Long-term nighttime aircraft noise exposure and risk of hypertension in a prospective cohort of female nurses

There is growing interest in cardiometabolic outcomes associated with nighttime noise, given that noise can disturb sleep and sleep disturbance can increase cardiometabolic risk such as hypertension. However, there is little empirical research evaluating the association between nighttime aircraft noise and hypertension risk. In this study, we expand on previous work to evaluate associations between nighttime aircraft noise exposure and self-reported hypertension incidence in the Nurses' Health Studies (NHS/NHSII), two US-wide cohorts of female nurses. Annual nighttime average aircraft sound levels (Lnight) surrounding 90 airports for 1995–2015 (in 5-year intervals) were modeled using the Aviation Environmental Design Tool and assigned to participants’ geocoded addresses over time. Hypertension risk was estimated for each cohort using time-varying Cox proportional-hazards models for Lnight dichotomized at 45 dB (dB), adjusting for individual-level hypertension risk factors, area-level socioeconomic status, region, and air pollution. Random effects meta-analysis was used to combine cohort results. Among 63,229 NHS and 98,880 NHSII participants free of hypertension at study baseline (1994/1995), we observed 33,190 and 28,255 new hypertension cases by 2014/2013, respectively. Although ∼1% of participants were exposed to Lnight ≥45 dB, we observed an adjusted hazard ratio (HR) of 1.10 (95% CI: 0.96, 1.27) in NHS and adjusted HR of 1.12 (95% CI: 0.98, 1.28) in NHSII, comparing exposure to Lnight ≥45 versus <45 dB(A). In meta-analysis, we observed an adjusted HR of 1.11 (95% CI: 1.01, 1.23). These results were attenuated with adjustment for additional variables such as body mass index. Our findings support a modest positive association between nighttime aircraft noise and hypertension risk across NHS/NHSII, which may reinforce the concept that sleep disturbance contributes to noise-related disease burden.

Effects of acoustic environment on sleep and mental health in residential regions near railways

Noise is an important environmental risk factor for physical and mental health. Furthermore, long-term noise exposure is burdensome for the mind and body and has become a serious problem. Rail transportation is one of the main methods used to transport goods in China; however, the noise and vibrations generated by freight trains have serious impacts on residents in nearby regions. To further investigate the relationship between railway noise and road noise exposure and changes in sleep duration and mental health scores, a field study in Harbin, China, was conducted and a health risk prediction model was constructed. The results showed that for every 1 dB increase in the Equivalent continuous A-weighted sound pressure level (LAeq), the percentage of deep sleep among residents living near the railway decreased by 0.2 %. Although residents near the railway reported similar sleep evaluations compared to those living farther away, they exhibited poorer mental health. Cox risk modeling indicates that the risk of mental health problems is approximately three times higher for those living near the railway. These findings potentially provide benefits in developing strategies to reduce the risk of mental illness for people residing near railways.

Gastrodin Ameliorates Learning and Memory Impairments Caused by Long-Term Noise Exposure.

The developing brain is significantly affected by long-term exposure to noise at an early age, leading to functional disorders such as learning and memory impairments. Gastrodin (GAS), a natural organic compound, is an extraction of phenolic glycoside from the rhizome of Gastrodia elata. Clinically, GAS is extensively utilised for the treatment of neurological disorders. This study aimed to explore the effect and mechanism of GAS on noise exposure-induced learning and memory impairments. Rats aged 21 days were exposed to a 90 dB noise environment for 4 weeks and divided into the noise group, the noise + GAS group, and the control group to establish a noise exposure model. After noise exposure treatment, the improvement effect of GAS on the memory of rats was evaluated by Y-maze and Morris water maze. Enzyme-linked immunosorbent assay was utilised to determine the effect of GAS on neurotransmitter levels in the hippocampal tissue of noise-exposed rats. Western blot was applied for the detection of the protein levels of neurotrophic factors. The GAS treatment significantly improved spatial memory and increased the levels of key neurotransmitters (norepinephrine, dopamine and serotonin) and neurotrophic factors (neurotrophin-3 and brain-derived neurotrophic factor) in the hippocampal tissues of noise-exposed rats. These alterations correlate with enhanced cognitive functions, suggesting a neuroprotective effect of GAS against noise-induced cognitive impairments. This study supports the potential of GAS to treat noise-induced learning and memory impairments by modulating neurotransmitter secretion and enhancing the expression levels of neurotrophic factors. These findings offer potential therapeutic avenues for cognitive impairments induced by noise exposure.

Associations of long-term exposure to air pollution and noise with body composition in children and adults: Results from the LEAD general population study

BackgroundWhile long-term air pollution and noise exposure has been linked to increasing cardiometabolic disease risk, potential effects on body composition remains unclear. This study aimed to investigate the associations of long-term air pollution, noise and body composition. MethodsWe used repeated data from the LEAD (Lung, hEart, sociAl, boDy) study conducted in Vienna, Austria. Body mass index (BMI; kg/m2), fat mass index (FMI; z-score), and lean mass index (LMI; z-score) were measured using dual-energy x-ray absorptiometry at the first (t0; 2011-ongoing) and second (t1; 2017-ongoing) examinations. Annual particulate matter (PM10) and nitrogen dioxide (NO2) concentrations were estimated with the GRAMM/GRAL model (2015–2021). Day-evening-night (Lden) and night-time (Lnight) noise levels from transportation were modeled for 2017 following the European Union Directive 2002/49/EC. Exposures were assigned to residential addresses. We performed analyses separately in children/adolescents and adults, using linear mixed-effects models with random participant intercepts and linear regression models for cross-sectional and longitudinal associations, respectively. Models were adjusted for co-exposure, lifestyle and sociodemographics. ResultsA total of 19,202 observations (nt0 = 12,717, nt1 = 6,485) from participants aged 6–86 years (mean age at t0 = 41.0 years; 52.9 % female; mean PM10 = 21 µg/m3; mean follow-up time = 4.1 years) were analyzed. Among children and adolescents (age ≤ 18 years at first visit), higher PM10exposure was cross-sectionally associated with higher FMI z-scores (0.09 [95 % Confidence Interval (CI): 0.03, 0.16]) and lower LMI z-scores (−0.05 [95 % CI: −0.10, −0.002]) per 1.8 µg/m3. Adults showed similar trends in cross-sectional associations as children, though not reaching statistical significance. We observed no associations for noise exposures. Longitudinal analyses on body composition changes over time yielded positive associations for PM10, but not for other exposures. ConclusionAir pollution exposure, mainly PM10, was cross-sectionally and longitudinally associated with body composition in children/adolescents and adults. Railway/road-traffic noise exposures showed no associations in both cross-sectional and longitudinal analyses.

Relationship Between Work-Related Noise Exposure and Cognitive Impairment: A Cross-Sectional Study in China

Background: Noise exposure and the risk of cognitive impairment are currently major public health issues. Objective: This study aimed to analyze the relationship between noise exposure and early impairment of cognitive function from the perspective of occupational epidemiology and to provide evidence for the long-term prevention and treatment of dementia in the context of aging. Methods: This study was conducted in China between May and August 2021. The independent variables were the type of hazardous factors, duration of noise exposure, perceived noise intensity, and cumulative noise exposure (CNE). The dependent variable was cognitive function, which was measured using the Mini-Mental State Examination (MMSE) and Montreal Cognitive Assessment (MoCA). Multiple linear and logistic regression were used to analyze the relationship between noise exposure and cognitive function and to establish an effect curve. Results: The detection rates of cognitive dysfunction using the MMSE and MoCA were 1.1% and 36.2%, respectively. The predicted MMSE and MoCA scores showed a downward trend within the CNE value ranging from 90–140 dB.time. Each unit increase in CNE decreased cognitive function scores by 0.025 (0.037, 0.013) and 0.020 (0.037, 0.003) points,respectively. Conclusions: From the perspective of occupational epidemiology, these findings reveal a potential link between long-term noise exposure and early cognitive impairment.

Research progress in genetics of noise-induced hearing loss

Noise-induced hearing loss（NIHL） is an acquired sensorineural hearing loss induced by long-term noise exposure. The susceptibility of exposed people may vary even in the same noise environment. With the development of sequencing techniques, genes related to oxidative stress, immunoinflammatory, ion homeostasis, energy metabolism, DNA damage repair and other mechanisms in NIHL have been reported continuously. And some genes may interact with noise exposure indexes. In this article, population studies on NIHL-related gene polymorphisms and gene-environment interactions in the past 20 years are reviewed, aimed to providing evidence for the construction of NIHL-related risk prediction models and the formulation of individualized interventions.

Long-term exposure to transportation noise in relation to global cognitive decline and cognitive impairment: Results from a Swedish longitudinal cohort

Background and aimsTransportation noise is an environmental exposure with mounting evidence of adverse health effects. Besides the increased risk of cardiovascular and metabolic diseases, recent studies suggest that long-term noise exposure might accelerate cognitive decline in older age. We examined the association between transportation noise and cognitive function in a cohort of older adults. MethodsThe present study is based on 2594 dementia-free participants aged 60 + years from the Swedish National study on Aging and Care in Kungsholmen (SNAC-K). Global cognition score and CIND (cognitive impairment, no dementia) were assessed with a comprehensive neuropsychological battery at baseline and up to 16 years. Residential transportation noise resulting from road traffic, railway, and aircraft were estimated at the most exposed façade and the time-weighted average exposure was assessed. Linear mixed-effect models were used to assess the effect of long-term traffic noise exposure on the rate of change in global cognition score. Hazard ratios (HRs) and 95 % confidence intervals (CIs) of CIND by transportation noise exposure were obtained with Cox proportional hazard models. ResultsGlobal cognition score decreased at an average rate of −0.041 (95 %CI −0.043, −0.039) per year. Aircraft noise was associated with a 0.007 (per 10 dB Lden; 95 %CI −0.012, −0.001) faster annual rate of decline. Global cognition score seems to be not affected by road traffic and railway noise. During the follow-up, 422 (21 %) participants developed CIND. A 10-dB Lden difference in exposure to aircraft and railway noise was associated with a 16 % (HR 1.16, 95 %CI 0.91, 1.49) and 26 % (HR 1.26, 95 %CI 1.01, 1.56) increased hazard of CIND in the multi-pollutant model, respectively. No association was found for road traffic (HR 1.00, 95 %CI 0.83, 1.21). ConclusionsTransportation noise was linked to cognitive impairment and faster cognitive decline among older adults. Future studies are warranted to confirm our results.

Microglial activation in the lateral amygdala promotes anxiety-like behaviors in mice with chronic moderate noise exposure.

Long-term non-traumatic noise exposure, such as heavy traffic noise, can elicit emotional disorders in humans. However, the underlying neural substrate is still poorly understood. We exposed mice to moderate white noise for 28 days to induce anxiety-like behaviors, measured by open-field, elevated plus maze, and light-dark box tests. Invivo multi-electrode recordings in awake mice were used to examine neuronal activity. Chemogenetics were used to silence specific brain regions. Viral tracing, immunofluorescence, and confocal imaging were applied to define the neural circuit and characterize the morphology of microglia. Exposure to moderate noise for 28 days at an 85-dB sound pressure level resulted in anxiety-like behaviors in open-field, elevated plus maze, and light-dark box tests. Viral tracing revealed that fibers projecting from the auditory cortex and auditory thalamus terminate in the lateral amygdala (LA). A noise-induced increase in spontaneous firing rates of the LA and blockade of noise-evoked anxiety-like behaviors by chemogenetic inhibition of LA glutamatergic neurons together confirmed that the LA plays a critical role in noise-induced anxiety. Noise-exposed animals were more vulnerable to anxiety induced by acute noise stressors than control mice. In addition to these behavioral abnormalities, ionized calcium-binding adaptor molecule 1 (Iba-1)-positive microglia in the LA underwent corresponding morphological modifications, including reduced process length and branching and increased soma size following noise exposure. Treatment with minocycline to suppress microglia inhibited noise-associated changes in microglial morphology, neuronal electrophysiological activity, and behavioral changes. Furthermore, microglia-mediated synaptic phagocytosis favored inhibitory synapses, which can cause an imbalance between excitation and inhibition, leading to anxiety-like behaviors. Our study identifies LA microglial activation as a critical mediator of noise-induced anxiety-like behaviors, leading to neuronal and behavioral changes through selective synapse phagocytosis. Our results highlight the pivotal but previously unrecognized roles of LA microglia in chronic moderate noise-induced behavioral changes.

Utilizing Artificial Neural Networks for Establishing Hearing-Loss Predicting Models Based on a Longitudinal Dataset and Their Implications for Managing the Hearing Conservation Program

BackgroundThough the artificial neural network (ANN) technique has been used to predict noise-induced hearing loss (NIHL), the established prediction models have primarily relied on cross-sectional datasets, and hence, they may not comprehensively capture the chronic nature of NIHL as a disease linked to long-term noise exposure among workers. MethodsA comprehensive dataset was utilized, encompassing eight-year longitudinal personal hearing threshold levels (HTLs) as well as information on seven personal variables and two environmental variables to establish NIHL predicting models through the ANN technique. Three subdatasets were extracted from the afirementioned comprehensive dataset to assess the advantages of the present study in NIHL predictions. ResultsThe dataset was gathered from 170 workers employed in a steel-making industry, with a median cumulative noise exposure and HTL of 88.40 dBA-year and 19.58 dB, respectively. Utilizing the longitudinal dataset demonstrated superior prediction capabilities compared to cross-sectional datasets. Incorporating the more comprehensive dataset led to improved NIHL predictions, particularly when considering variables such as noise pattern and use of personal protective equipment. Despite fluctuations observed in the measured HTLs, the ANN predicting models consistently revealed a discernible trend. ConclusionsA consistent correlation was observed between the measured HTLs and the results obtained from the predicting models. However, it is essential to exercise caution when utilizing the model-predicted NIHLs for individual workers due to inherent personal fluctuations in HTLs. Nonetheless, these ANN models can serve as a valuable reference for the industry in effectively managing its hearing conservation program.

Long-term noise exposures and cardiovascular diseases mortality: A study in 5 U.S. states

BackgroundPrevious studies have linked noise exposure with adverse cardiovascular events. However, evidence remains inconsistent, and most previous studies only focused on traffic noise, excluding other anthropogenic sources like constructions, industrial process and commercial activities. Additionally, few studies have been conducted in the U.S. or evaluated the non-linear exposure-response relationships. MethodsWe conducted a relative incidence analysis study using all cardiovascular diseases mortality as cases (n = 936,019) and external causes mortality (n = 232,491) as contrast outcomes. Mortality records geocoded at residential addresses were obtained from five U.S. states (Indiana, 2007; Kansas, 2007–2009, Missouri, 2010–2019, Ohio, 2007–2013, Texas, 2007–2016). Time-invariant long-term noise exposure was obtained from a validated model developed based on acoustical measurements across 2000–2014. Noises from both natural sources (natural activities, including animals, insects, winds, water flows, thunder, etc.) and anthropogenic sources (human activities, including transportation, industrial activities, community facilities & infrastructures, commercial activities, entertainments, etc.) were included. We used daytime and nighttime total anthropogenic noise & day-night average sound pressure level combining natural and anthropogenic sources as exposures. Logistic regression models were fit controlling for Census tract-level & individual-level characteristics. We examined potential modification by sex by interaction terms and potential non-linear associations by thin plate spline terms. ResultsWe observed positive associations for daytime anthropogenic L50 (sound level exceeded 50% of time) noise (10-dBA OR = 1.047, 95%CI 1.025–1.069), nighttime anthropogenic L50 noise (10-dBA OR = 1.061, 95%CI 1.033–1.091) in a two-exposure-term model, and overall Ldn (day-night average) sound pressure level (10-dBA OR = 1.064, 95%CI 1.040–1.089) in single-exposure-term model. Females were more susceptible to all three exposures. All exposures showed monotonic positive associations with cardiovascular mortality up to certain thresholds around 45–55 dBA, with a generally flattened or decreasing trend beyond those thresholds. ConclusionsBoth daytime anthropogenic and nighttime anthropogenic noises were associated with cardiovascular disease mortality, and associations were stronger in females.

Association between Noise and Cardiovascular Disease in a Nationwide U.S. Prospective Cohort Study of Women Followed from 1988 to 2018.

Long-term noise exposure is associated with cardiovascular disease (CVD), including acute cardiovascular events such as myocardial infarction and stroke. However, longitudinal cohort studies in the U.S. of long-term noise and CVD are almost exclusively from Europe and few modeled nighttime noise, when an individual is likely at home or asleep, separately from daytime noise. We aimed to examine the prospective association of outdoor long-term nighttime and daytime noise from anthropogenic sources with incident CVD using a U.S.-based, nationwide cohort of women. We linked nighttime and daytime anthropogenic modeled noise estimates from a U.S. National Parks Service model (: sound pressure levels exceeded 50 percent of the time) to geocoded residential addresses of 114,116 participants in the Nurses' Health Study. We used time-varying Cox proportional hazards models to estimate risk of incident CVD, coronary heart disease (CHD), and stroke associated with long-term average (14-y measurement period) noise exposure, adjusted for potential individual- and area-level confounders and CVD risk factors (1988-2018; biennial residential address updates; monthly CVD updates). We assessed effect modification by population density, region, air pollution, vegetation cover, and neighborhood socioeconomic status, and explored mediation by self-reported average nightly sleep duration. Over 2,548,927 person-years, there were 10,331 incident CVD events. In fully adjusted models, the hazard ratios for each interquartile range increase in nighttime noise (3.67 dBA) and daytime noise (4.35 dBA), respectively, were 1.04 (95% CI: 1.02, 1.06) and 1.04 (95% CI: 1.02, 1.07). Associations for total energy-equivalent noise level () measures were stronger than for the anthropogenic statistical noise measures. Similar associations were observed for CHD and stroke. Interaction analyses suggested that associations of nighttime and daytime noise with CVD did not differ by prespecified effect modifiers. We found no evidence that inadequate sleep ( h/night) mediated associations of nighttime noise and CVD. Outdoor anthropogenic nighttime and daytime noise at the residential address was associated with a small increase in CVD risk in a cohort of adult female nurses. https://doi.org/10.1289/EHP12906.

A study examining the long-term effects of aircraft noise on the surrounding residents before the opening of Long Thanh Airport

Long Thanh Airport (LT) is a new airport scheduled to open in 2025 and serve as the largest aviation hub in Vietnam. The residents are expected to experience adverse health effects from long-term noise exposure once LT begins operation. This study aims to serve as a basis for comparing the impact of environmental changes before and after the opening of LT. This study assesses the health of the residents in ten residential areas under the planned flight paths of LT. Currently, before the new airport operates, environmental noise around LT is primarily caused by traffic noise from nearby roads near the selected houses. The 24-hour A-weighted equivalent continuous sound level (LAeq) at a representative house in each area ranged from 51 to 72 dB. In August 2022, 641 residents were surveyed to assess their health conditions. It was found that traffic noise was the most frequently cited environmental nuisance among the surveyed participants. However, the regression model considers contextual factors, noise exposure, and other factors impacting health and indicates that the health of the residents is associated with factors beyond noise exposure, such as noise sensitivity, mobility, and attitude towards transport modes.

Effects of Aircraft Noise on Sleep: Federal Aviation Administration National Sleep Study Protocol.

Aircraft noise can disrupt sleep and impair recuperation. The last U.S. investigation into the effects of aircraft noise on sleep dates back more than 20 years. Since then, traffic patterns and the noise levels produced by single aircraft have changed substantially. It is therefore important to acquire current data on sleep disturbance relative to varying degrees of aircraft noise exposure in the U.S. that can be used to check and potentially update the existing noise policy. This manuscript describes the design, procedures, and analytical approaches of the FAA's National Sleep Study. Seventy-seven U.S. airports with relevant nighttime air traffic from 39 states are included in the sampling frame. Based on simulation-based power calculations, the field study aims to recruit 400 participants from four noise strata and record an electrocardiogram (ECG), body movement, and sound pressure levels in the bedroom for five consecutive nights. The primary outcome of the study is an exposure-response function between the instantaneous, maximum A-weighted sound pressure levels (dBA) of individual aircraft measured in the bedroom and awakening probability inferred from changes in heart rate and body movement. Self-reported sleep disturbance due to aircraft noise is the secondary outcome that will be associated with long-term average noise exposure metrics such as the Day-Night Average Sound Level (DNL) and the Nighttime Equivalent Sound Level (Lnight). The effect of aircraft noise on several other physiological and self-report outcomes will also be investigated. This study will provide key insights into the effects of aircraft noise on objectively and subjectively assessed sleep disturbance.

Association between Long-term Noise Exposure and Bipolar Disorder: a Community-based Cohort Study in Taiwan

Association between Long-term Noise Exposure and Bipolar Disorder: a Community-based Cohort Study in Taiwan

Development of a real-time noise estimation model for construction sites

As construction noise negatively affects the health and quality of life of stakeholders, field managers need to properly monitor and manage noise. Thus, the authors developed a model that estimates real-time noise levels at a construction site and the surroundings to enable preemptive responses to noise-related issues. To accurately estimate noise, necessary field data were collected using an unmanned aerial vehicle (UAV) and noise sensors. The noise estimation model was composed of two sub-models: the noise-customized spatial interpolation model and the noise propagation model. The noise-customized spatial interpolation model was developed to estimate the internal noise of the construction site using a few sensor noise levels. Meanwhile, the noise propagation model was developed to estimate the noise level outside the construction site using internal noise estimation results, obstacles, weather information, and noise sources information. The model was evaluated through field tests at a construction technology demonstration center, environments identical to real construction sites in South Korea. The model showed satisfactory performance, with an accuracy of 96.71% and a root mean square error (RMSE) of 2.62 for the internal construction site noise and an accuracy of 96.03% and an RMSE of 2.70 for outside the construction site. To facilitate the usage of the noise estimation results for field managers, the research team visualized the results using the Unity 3D Engine. The results will enable field managers to assess workers’ long-term noise exposure and respond to potential civil complaints, gearing up to realize environmental, social, and governance (ESG) goals in the construction industry.

Predictive value of serum proteomic biomarkers for noise-induced hearing loss.

Early detection of noise-induced hearing loss (NIHL) in patients with long-term noise exposure is vital for improving public health and reducing social burden. However, at present, the diagnosis of NIHL mainly depends on audiometric testing, and the primary test is pure-tone audiometry. Moreover, testing requires professional operators and complex equipment; thus, NIHL is often diagnosed at a later disease stage. Using a liquid chromatography-tandem mass spectrometry (LC-MS/MS)-based proteomic approach, we identified 9 differentially expressed proteins (DEPs), namely, 6 upregulated serum proteins and 3 downregulated serum proteins, in samples from 50 ground crew personnel working at an air force station. Then, according to the results, we predicted that caldesmon (CALD1), myocilin (MYOC), zyxin (ZYX), creatine kinase M-type (CKM), insulin-like growth factor-binding protein 2 (IGFBP2), complement factor H-related protein 4 (CFHR4), prenylcysteine oxidase 1 (PCYOX1), heat shock cognate 71 kDa protein (HSPA8), and immunoglobulin lambda variable 3-21 (IGLV3-21) were associated with NIHL. We selected these DEPs as variables to perform logistic regression. Finally, a logistic regression model was constructed based on IGFBP2, ZYX, CKM, and CFHR4. The area under the curve was 0.894 (95% CI = 0.812 to 0.977). These findings suggested that IGFBP2, ZYX, CKM, and CFHR4 in serum are differentially expressed in NIHL patients and have the potential to be biomarkers for predicting the risk for NIHL. Further experiments in mice showed that ZYX and IGFBP2 in the cochlear were increased after noise exposure. ZYX and IGFBP2 may be involved in the occurrence and development of NIHL.

Effect of Noise and Music on Neurotransmitters in the Amygdala: The Role Auditory Stimuli Play in Emotion Regulation.

Stress caused by noise is becoming widespread globally. Noise may lead to deafness, endocrine disorders, neurological diseases, and a decline in mental health. The mechanism behind noise-induced neurodevelopmental abnormalities is unclear, but apoptosis and pro-inflammatory signals may play an important role. In this study, weaned piglets were used as a model to explore noise-induced neurodevelopmental abnormalities. We hypothesized that long-term noise exposure would induce anxiety and cause acute stress, exhibited by alterations in neurotransmission in the amygdala. A total of 72 hybrid piglets (Large White × Duroc × Min Pig) were randomly divided into three groups, including noise (exposed to mechanical noise, 80-85 dB), control (blank, exposed to natural background sound, <40 dB), and music (positive control, exposed to Mozart K.448, 60-70 dB) groups. The piglets were exposed to 6 h of auditory noise daily (10:00-16:00) for 28 days. Compared with the control group, piglets exposed to noise showed more aggressive behavior. The expression of Caspase3, Caspase9, Bax, NF-κB (p56), TLR4, MYD88, I κ B α, IL-1 β, TNF-α, and IL-12RB2 was significantly upregulated in the amygdala, while the expression of Nrf2, HO-1, CAT, and SOD was downregulated in piglets in the noise group. Cell death occurred, and numerous inflammatory cells accumulated in the amygdala of piglets in the noise group. Targeted metabolomics showed that the content of inhibitory neurotransmitter GABA was higher in the amygdala of piglets in the noise group. Compared with the noise group, piglets in the music group displayed more positive emotion-related behaviors. Compared with the noise group, the expression of genes related to apoptosis, inflammation, and oxidative damage was lower in the music group. Cells of the amygdala in the music group were also of normal morphology. Our results show that noise-induced stress causes apoptosis and neuroinflammation in the amygdala and induces anxiety during the early neonatal neural development of piglets. In contrast, to some extent, music alleviates noise-induced anxiety.