The architecture of functional brain network modulated by driving under train running noise exposure.

A noisy environment can considerably impact drivers' attention and fatigue, endangering driving safety. Consequently, this study designed a simulated driving experimental scenario to analyse the effects of noise generated during urban rail transit train operation on drivers' functional brain networks. The experiment recruited 16 participants, and the simulated driving scenario was conducted at noise levels of 50, 60, 70, and 80 dB. Functional connectivity between all electrode pairs across various frequency bands was evaluated using the weighted phase lag index (WPLI), and a brain network based on this was constructed. Graph theoretic analysis employed network global efficiency, degree, and clustering coefficient as metrics. Significant increases in the WPLI values of theta and alpha frequency bands were observed in high noise environments (70 dB, 80 dB), as well as enhanced brain synchronisation. Furthermore, concerning the topological metrics of brain networks, it was observed that the global efficiency of brain networks in theta and alpha frequency ranges, as well as the node degree and clustering coefficients, experienced substantial growth in high noise environments (70 dB, 80 dB) as opposed to 50 dB and 60 dB. This finding indicates that high-noise environments impact the reorganisation of functional brain networks, leading to a preference for network structures with improved global efficiency. Such findings may improve our understanding of the neural mechanisms of driving under noise exposure, and thus potentially reduce road accidents to some extent.

Road traffic noise exposure and its impact on health: evidence from animal and human studies-chronic stress, inflammation, and oxidative stress as key components of the complex downstream pathway underlying noise-induced non-auditory health effects.

In heavily urbanized world saturated with environmental pollutants, road traffic noise stands out as a significant factor contributing to widespread public health issues. It contributes in the development of a diverse range of non-communicable diseases, such as cardiovascular diseases, metabolic dysregulation, cognitive impairment, and neurodegenerative disorders. Although the exact mechanisms behind these non-auditory health effects remain unclear, the noise reaction model centres on the stress response to noise. When exposed to noise, the body activates the hypothalamic-pituitary-adrenal axis and the sympathetic nervous system, leading to the secretion of stress hormones like catecholamines and cortisol. Prolonged exposure to noise-induced stress results in chronic inflammation and oxidative stress. This review underscores the role of inflammation and oxidative stress in the progression of noise-induced vascular dysfunction, disruption of the circadian rhythm, accelerated aging, neuroinflammation, and changes in microbiome. Additionally, our focus is on understanding the interconnected nature of these health outcomes: These interconnected factors create a cascade effect, contributing to the accumulation of multiple risk factors that ultimately lead to severe adverse health effects.

Long-term exposure to road traffic noise and acute lower respiratory infections in the Danish Nurse Cohort.

BACKGROUND: Long-term exposure to road traffic noise is associated with cardiovascular disease, but the evidence on respiratory diseases is just emerging. We aimed to examine the association between long-term exposure to road traffic noise and the incidence of acute lower respiratory infections (ALRIs) in adults. METHODS: We followed 23,141 female nurses (age ≥ 44 years) from the Danish Nurse Cohort from baseline (1993 or 1999) to their first hospital contact (inpatient, outpatient, or emergency room) for ALRI, death, emigration or the end of 2015. The residential annual mean levels of road traffic noise (Lden) during the follow-up were estimated using the Nord2000 model. We applied time-varying Cox models to estimate the association of 3-year mean exposure to Lden with ALRIs incidence and piecewise analysis to estimate the threshold of Lden. We examined the robustness of the results by adjusting for residential exposure to air pollution, and the effect modification by attained age, socioeconomic status (SES), comorbidity, and lifestyle. RESULTS: During 18.5 years of follow-up, 2,004 nurses developed ALRIs. In a linear model, we detected a statistically significant positive association between Lden and ALRI, with a hazard ratio (HR) of 1.11 (95 % confidence interval (CI): 1.04, 1.17) per 9.2 dB (interquartile range, IQR). We observed non-linear association with a threshold at 57 dB, above which the HR was 1.25 (95 % CI: 1.09, 1.43) per IQR. Further adjustment for PM2.5 reduced the HRs slightly to 1.21 (95 % CI: 1.04, 1.40). The associations were stronger for nurses with asthma, and in those with lowest SES. CONCLUSION: We present novel findings in support of the association between long-term exposure to road traffic noise and ALRIs, independent of air pollution, suggesting noise as a risk factor for infectious respiratory diseases.

Long-term exposure to air pollution, road traffic noise and greenness, and incidence of myocardial infarction in women.

BACKGROUND: Emerging evidence shows that long-term exposure to air pollution, road traffic noise, and greenness can each be associated with cardiovascular disease, but only few studies combined these exposures. In this study, we assessed associations of multiple environmental exposures and incidence of myocardial infarction using annual time-varying predictors. MATERIALS AND METHODS: In a population-based cohort of 20,407 women in Sweden, we estimated a five-year moving average of residential exposure to air pollution (PM2.5, PM10 and NO2), road traffic noise (Lden), and greenness (normalized difference vegetation index, NDVI in 500 m buffers), from 1998 to 2017 based on annually varying exposures and address history. We used adjusted time-varying Cox proportional hazards regressions to estimate hazard ratios (HR) and 95 % confidence intervals (95 % CI) of myocardial infarction per interquartile range (IQR). Furthermore, we investigated interactions between the exposures and explored potential vulnerable subgroups. RESULTS: In multi-exposure models, long-term exposure to greenness was inversely associated with incidence of myocardial infarction (HR 0.89; 95 % CI 0.80, 0.99 per IQR NDVI increase). Stronger associations were observed in some subgroups, e.g. among women with low attained education and in overweight (BMI ≥ 25 kg/m2) compared to their counterparts. For air pollution, we observed a tendency of an increased risk of myocardial infarction in relation to PM2.5 (HR 1.07; 95 % CI 0.93, 1.23) and the association appeared stronger in women with low attained education (HR 1.30; 95 % CI 1.06, 1.58). No associations were observed for PM10, NO2 or road traffic noise. Furthermore, there were no clear interaction patterns between the exposures. CONCLUSION: Over a 20-year follow-up period, in multi-exposure models, we found an inverse association between residential greenness and risk of myocardial infarction among women. Furthermore, we observed an increased risk of myocardial infarction in relation to PM2.5 among women with low attained education. Road traffic noise was not associated with myocardial infarction.

Correlation between Long-Term Exposure to Traffic Noise and Risk of Type 2 Diabetes Mellitus.

OBJECTIVE: This study aimed to probe the correlation of long-term exposure to traffic noise with the risk of type 2 diabetes mellitus (T2DM). METHODS: The data of 480 community residents collected from April 2017 to April 2018 were retrospectively analyzed. Exposure levels for traffic noise were defined using 24-h mean traffic noise. Logistic regression calculated the association between long-term exposure to traffic noise and the risk of T2DM. RESULTS: Overall, 480 enrolled participants were divided into T2DM (n = 45) and non-T2DM (n = 435) groups. Participants with T2DM were older and more likely to be male, had higher BMI, and were frequent drinkers (P < 0.001). The T2DM group displayed higher exposure to traffic noise than the non-T2DM group (P < 0.001). According to quartiles of traffic noise, all participants were categorized into four groups: Q1 (<51.5 dB), Q2 (51.5-<53.9 dB), Q3 (53.9-<58.0 dB), and Q4 (≥58.0 dB). Prevalence of T2DM was 5.4% in Q1, 7.7% in Q2, 10.3% in Q3, and 14.1% in Q4 groups. Multifactor regression analysis showed that age, BMI, drinking history, and traffic noise exposure are risk factors for T2DM (P < 0.05), whereas sex does not seem to have a significant impact on T2DM (P > 0.05). CONCLUSION: Long-term exposure to traffic noise may elevate the risk of T2DM. This suggests that long-term exposure to high levels of traffic noise can increase the incidence of diabetes mellitus, which deserves further consideration.

Sleep Disturbance Caused by Step Changes in Railway Noise Exposure and Earthquakes.

Kyushu Shinkansen and conventional railway lines run parallel in the areas 5 km north of Kumamoto Station (northern area) and 12 km south of the station (southern area). Following the operation of the Kyushu Shinkansen Line in 2011, the adjacent conventional railway line in the north was elevated, a new station was operated in the south, and large earthquakes struck the Kumamoto area from March to April 2016. Sleep disturbances were compared before and after the interventions and earthquakes based on noise source (Shinkansen and conventional railways), area (northern and southern), and house type (detached and apartment) through socio-acoustic surveys from 2011 to 2017. The Shinkansen railway caused significantly less sleep disturbances in detached houses in the north after compared to before the earthquakes, presumably due to more frequent closures of bedroom windows in northern detached houses following the earthquakes. The Shinkansen railway caused significantly more sleep disturbances in apartments in the south after compared to before the earthquakes, presumably because the Shinkansen slowed down immediately after the earthquakes and returned to normal speed during the survey, suddenly increasing the noise exposure. There was no significant difference in the other six cases investigated. Overall, the interventions may not have caused significant differences in sleep disturbances. This article expands on the congress paper by Morihara et al. presented in the "Community Response to Noise" session at the 52nd International Congress and Exhibition on Noise Control Engineering in Makuhari, Japan, organized by the International Institute of Noise Control Engineering.

Traffic Noise Impacts Glucocorticoid Response, Activity, and Growth in Two Species of Tadpoles.

There is a large body of evidence linking increased noise to negative health effects for animals. Anthropogenic noise induces behavioral and physiological reactions across a range of taxa and increased traffic noise affects glucocorticoid (GC) hormones associated with the stress response in amphibians. GCs help to maintain homeostasis while balancing energetic trade-offs between reproduction, growth, and activity. Stressors during early development can impact fitness at later life stages. We measured growth, activity, and GCs in response to high levels of traffic noise in two tadpole species that differ in life history: Acris crepitans and Rana berlandieri. We predicted that earlier exposures to traffic noise will slow down the development and alter the behavior and GC concentrations differently than later exposures. Subjects were initially either exposed to natural levels of traffic noise for 8 days (early exposure) or a white noise control (later exposure), then the treatment was switched. Activity was measured via focal sampling and tadpoles were categorized as active if movement was detected. Tadpoles exposed to white noise initially maintained mass and activity throughout the experiment and early exposure to traffic noise had a greater impact on mass, activity, and GCs. Tadpoles exposed to traffic noise initially lost mass, with A. crepitans regaining mass but not R. berlandieri. When exposed earlier to traffic noise, R. berlandieri increased movement when shifted to the white noise treatment while A. crepitans did not significantly change activity. Acris creptians had higher corticosterone release rates compared to R. berlandieri, and in both species, release rates were higher for tadpoles exposed to noise earlier. The longer-lived R. berlandieri allocated more of their energetic resources into activity, while the shorter-lived A. crepitans allocated energy toward growth. Rana berlandieri and A. crepitans utilized different coping strategies to contend with early exposure to traffic noise, potentially due to differences in life histories. Our findings suggest that these tadpoles employ different coping mechanisms to modulate stress responses in noise-polluted environments, and these mechanisms could influence their fitness later in life. Further study is needed to understand the impact in more sensitive tadpole species.

Long-term exposure to air pollution and road traffic noise and incidence of dementia in the Danish Nurse Cohort.

INTRODUCTION: We examined the association of long-term exposure to air pollution and road traffic noise with dementia incidence in the Danish Nurse Cohort. METHODS: Female nurses were followed for dementia incidence (hospital contact or medication prescription) from 1993/1999 to 2020. Air pollution and road traffic noise levels were estimated at nurses' residences, and their associations with dementia were examined using Cox regression models. RESULTS: Of 25,233 nurses 1409 developed dementia. Particulate matter with a diameter of ≤2.5 µm (PM2.5) was associated with dementia incidence, after adjusting for lifestyle, socioeconomic status, and road traffic noise (hazard ratio [95% confidence interval] 1.35 [1.15-1.59] per interquartile range of 2.6 µg/m3). There was no association of PM2.5 with dementia in physically active nurses. Association with road traffic noise diminished after adjusting for PM2.5 (1.02 [0.93-1.11] per 7.6 dB). DISCUSSION: Long-term exposure to air pollution increases risk of dementia, and physical activity may moderate this risk. HIGHLIGHTS: Long-term exposure to air pollution was associated with increased risk of dementia among female nurses from the Danish Nurse Cohort. Association of air pollution with dementia was independent of road traffic noise. Association of road traffic noise with dementia diminished after adjusting for air pollution. Physical activity moderated adverse effects of air pollution on dementia.

Psychophysiological effects of walking in forests and urban built environments with disparate road traffic noise exposure: study protocol of a randomized controlled trial.

BACKGROUND: Stress is a widespread phenomenon and reality of everyday life, entailing negative consequences for physical and psychological wellbeing. Previous studies have indicated that exposure to greenspaces and nature-based interventions are promising approaches to reducing stress and promoting restoration. However, an increasing percentage of the population lives in urban regions with limited opportunities to spend time in greenspaces. In addition, urban settings typically feature increased levels of noise, which represents a major environmental stressor. Although various studies have compared the effects of exposure to greenspaces versus urban built environments, evidence of the effects of noise in this context is very limited. Psychophysiological benefits of exposure to greenspaces compared to urban built environments reported in earlier studies might be less (or at least not only) due to features of the greenspaces than to additional stressors, such as road traffic noise in the urban built environment. Hence, differences in the effects attributed to greenness in previous studies may also be due to potentially detrimental noise effects in comparison settings. This paper reports the study protocol for a randomized, controlled intervention study comparing the effects of walking in forest versus urban built environments, taking road traffic noise exposure during walks in the respective settings into account. METHODS: The protocol envisages a field study employing a pretest-posttest design to compare the effects of 30-min walks in urban built environments and forests with different road traffic noise levels. Assessments will consist of self-reported measures, physiological data (salivary cortisol and skin conductance), an attention test, and noise, as well as greenness measurements. The outcomes will be restoration, stress, positive and negative affect, attention, rumination, and nature connectedness. DISCUSSION: The results will inform about the restorative effect of walking in general, of exposure to different types of environments, and to different noise levels in these sites. The study will provide insights into the benefits of walking and nature-based interventions, taking into account the potential detrimental effects of noise exposure. It will thus facilitate a better understanding of low-threshold interventions to prevent stress and foster wellbeing. TRIAL REGISTRATION: ISRCTN48943261 ; Registered 23.11.2023.

Vessels and aircraft are chronic sources of anthropogenic noise in coastal marine and terrestrial soundscapes on Long Island, New York.

Passive acoustic data collected during 2020 and 2021 were used to monitor changes in both terrestrial and underwater soundscapes, as well as human activity from aircraft and vessels. Passive acoustic data were collected at two artificial reefs south of Long Island, as well as along ocean beaches in Southampton, NY. At the artificial reefs, vessel noise was recorded more frequently during 2020 than in 2021. Commercial vessels and multi-user charter fishing vessels were more abundant during 2020. Peaks in power spectral density occurred at 60, 90 and 120 Hz in 2020 and 2021, which are frequencies consistent with noise generated by commercial vessels, suggesting that vessels are a significant contributor to the soundscape of the artificial reefs. In the terrestrial environment, noise generated by aircraft was more common during 2021. Peaks in power spectral density were measured around 160 and 290 Hz at one of the ocean beach sites. These frequencies are consistent with noise generated by aircraft. This study documents the chronic extent of anthropogenic noise in both the underwater and terrestrial environments of Long Island, NY, as well as quantifies the occurrence of various noise sources in these habitats.

Long-term exposure to transportation noise and diabetes mellitus mortality: a national cohort study and updated meta-analysis.

BACKGROUND: Long-term exposure to transportation noise is related to cardio-metabolic diseases, with more recent evidence also showing associations with diabetes mellitus (DM) incidence. This study aimed to evaluate the association between transportation noise and DM mortality within the Swiss National Cohort. METHODS: During 15 years of follow-up (2001-2015; 4.14 million adults), over 72,000 DM deaths were accrued. Source-specific noise was calculated at residential locations, considering moving history. Multi-exposure, time-varying Cox regression was used to derive hazard ratios (HR, and 95%-confidence intervals). Models included road traffic, railway and aircraft noise, air pollution, and individual and area-level covariates including socio-economic position. Analyses included exposure-response modelling, effect modification, and a subset analysis around airports. The main findings were integrated into meta-analyses with published studies on mortality and incidence (separately and combined). RESULTS: HRs were 1.06 (1.05, 1.07), 1.02 (1.01, 1.03) and 1.01 (0.99, 1.02) per 10 dB day evening-night level (Lden) road traffic, railway and aircraft noise, respectively (adjusted model, including NO2). Splines suggested a threshold for road traffic noise (~ 46 dB Lden, well below the 53 dB Lden WHO guideline level), but not railway noise. Substituting for PM2.5, or including deaths with type 1 DM hardly changed the associations. HRs were higher for males compared to females, and in younger compared to older adults. Focusing only on type 1 DM showed an independent association with road traffic noise. Meta-analysis was only possible for road traffic noise in relation to mortality (1.08 [0.99, 1.18] per 10 dB, n = 4), with the point estimate broadly similar to that for incidence (1.07 [1.05, 1.09] per 10 dB, n = 10). Combining incidence and mortality studies indicated positive associations for each source, strongest for road traffic noise (1.07 [1.05, 1.08], 1.02 [1.01, 1.03], and 1.02 [1.00, 1.03] per 10 dB road traffic [n = 14], railway [n = 5] and aircraft noise [n = 5], respectively). CONCLUSIONS: This study provides new evidence that transportation noise is associated with diabetes mortality. With the growing evidence and large disease burden, DM should be viewed as an important outcome in the noise and health discussion.

Association of transportation noise with cardiovascular diseases.

This comprehensive article delves into the intricate and multifaceted issue of noise pollution, shedding light on its diverse sources, profound health implications, and the economic burden it imposes on societies. Noise pollution is an increasingly prevalent environmental challenge, impacting millions of people worldwide, often without their full awareness of its adverse effects. Drawing from a wealth of scientific research, the article underscores the well-established links between noise pollution and a spectrum of health issues, including cardiovascular diseases, sleep disturbances, and psychological stress. While exploring the sources and consequences of noise pollution, the article highlights the urgent need for a holistic and collaborative approach to mitigate its impact. This entails a combination of regulatory measures, technological innovations, urban planning strategies, and public education campaigns. It is increasingly evident that the detrimental effects of noise pollution extend beyond physical health, encompassing mental and social well-being. The article also addresses the synergistic relationship between noise pollution and other environmental stressors, emphasizing the importance of considering noise in conjunction with factors like air pollution and access to green spaces. It examines the potential of green spaces to mitigate the effects of noise pollution and enhance overall health.

Pre- and postnatal noise directly impairs avian development, with fitness consequences.

Noise pollution is expanding at an unprecedented rate and is increasingly associated with impaired reproduction and development across taxa. However, whether noise sound waves are intrinsically harmful for developing young-or merely disturb parents-and the fitness consequences of early exposure remain unknown. Here, by only manipulating the offspring, we show that sole exposure to noise in early life in zebra finches has fitness consequences and causes embryonic death during exposure. Exposure to pre- and postnatal traffic noise cumulatively impaired nestling growth and physiology and aggravated telomere shortening across life stages until adulthood. Consistent with a long-term somatic impact, early life noise exposure, especially prenatally, decreased individual offspring production throughout adulthood. Our findings suggest that the effects of noise pollution are more pervasive than previously realized.

A sound beginning of life starts before birth.

Long-term impact from prenatal noise exposure in birds should raise general concern.

Aircraft noise exposure and body mass index among female participants in two Nurses' Health Study prospective cohorts living around 90 airports in the United States.

OBJECTIVE: Aircraft noise exposure is linked to cardiovascular disease risk. One understudied candidate pathway is obesity. This study investigates the association between aircraft noise and obesity among female participants in two prospective Nurses' Health Study (NHS and NHSII) cohorts. METHODS: Aircraft day-night average sound levels (DNL) were estimated at participant residential addresses from modeled 1 dB (dB) noise contours above 44 dB for 90 United States (U.S.) airports in 5-year intervals 1995-2010. Biennial surveys (1994-2017) provided information on body mass index (BMI; dichotomized, categorical) and other individual characteristics. Change in BMI from age 18 (BMI18; tertiles) was also calculated. Aircraft noise exposures were dichotomized (45, 55 dB), categorized (<45, 45-54, ≥55 dB) or continuous for exposure ≥45 dB. Multivariable multinomial logistic regression using generalized estimating equations were adjusted for individual characteristics and neighborhood socioeconomic status, greenness, population density, and environmental noise. Effect modification was assessed by U.S. Census region, climate boundary, airline hub type, hearing loss, and smoking status. RESULTS: At baseline, the 74,848 female participants averaged 50.1 years old, with 83.0%, 14.8%, and 2.2% exposed to <45, 45-54, and ≥55 dB of aircraft noise, respectively. In fully adjusted models, exposure ≥55 dB was associated with 11% higher odds (95% confidence interval [95%CI]: -1%, 24%) of BMIs ≥30.0, and 15% higher odds (95%CI: 3%, 29%) of membership in the highest tertile of BMI18 (ΔBMI 6.7 to 71.6). Less-pronounced associations were observed for the 2nd tertile of BMI18 (ΔBMI 2.9 to 6.6) and BMI 25.0-29.9 as well as exposures ≥45 versus <45 dB. There was evidence of DNL-BMI trends (ptrends ≤ 0.02). Stronger associations were observed among participants living in the West, arid climate areas, and among former smokers. DISCUSSION: In two nationwide cohorts of female nurses, higher aircraft noise exposure was associated with higher BMI, adding evidence to an aircraft noise-obesity-disease pathway.

Transportation Noise Pollution and Cardiovascular Health.

Epidemiological studies have found that transportation noise increases the risk for cardiovascular morbidity and mortality, with solid evidence for ischemic heart disease, heart failure, and stroke. According to the World Health Organization, at least 1.6 million healthy life years are lost annually from traffic-related noise in Western Europe. Traffic noise at night causes fragmentation and shortening of sleep, elevation of stress hormone levels, and increased oxidative stress in the vasculature and the brain. These factors can promote vascular (endothelial) dysfunction, inflammation, and arterial hypertension, thus elevating cardiovascular risk. The present review focusses on the indirect, nonauditory cardiovascular health effects of noise. We provide an updated overview of epidemiological research on the effects of transportation noise on cardiovascular risk factors and disease, and mechanistic insights based on the latest clinical and experimental studies and propose new risk markers to address noise-induced cardiovascular effects in the general population. We will discuss the potential effects of noise on vascular dysfunction, oxidative stress, and inflammation in humans and animals. We will elaborately explain the underlying pathomechanisms by alterations of gene networks, epigenetic pathways, circadian rhythm, signal transduction along the neuronal-cardiovascular axis, and metabolism. We will describe current and future noise mitigation strategies. Finally, we will conduct an overall evaluation of the status of the current evidence of noise as a significant cardiovascular risk factor.

Noise and Vibration Generation and Response of Mice (Mus musculus) to Routine Intrafacility Transportation Methods.

Intrafacility transport of mice is an essential function for both laboratory and husbandry personnel. However, transport may induce a stress response that can alter research findings and negatively impact animal welfare. To determine minimally adverse intrafacility transport methods, in-cage noise and vibration exposure during transport on a variety of transport vehicles (hand carrying, stainless steel rack, flatbed cart, metal teacart, plastic teacart, and a cart with pneumatic wheels) were measured. Under-cage and in-cage padding was tested for its ability to decrease noise and vibration on each vehicle. Behavioral (open field test and elevated plus maze) and corticosterone responses of mice were then measured following transport on the most adverse (metal teacart) and least adverse (pneumatic cart) methods of multicage transport. Behavioral measures showed no difference between transported mice and untransported mice in both single- and group-housed settings. Plasma corticosterone was significantly elevated in mice transported on the metal teacart immediately following transport and continued to have elevated trends in circadian peaks during the 48h of sampling. The cart with pneumatic wheels was most effective at reducing noise and vibration, reflected in posttransport corticosterone readings that remained equivalent to those in untransported mice. This study demonstrates that mitigation of noise and vibration during cart transport may decrease the impact of transport on certain stress parameters in mice.

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

BACKGROUND AND AIMS: Transportation 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. METHODS: The 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. RESULTS: Global 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). CONCLUSIONS: Transportation noise was linked to cognitive impairment and faster cognitive decline among older adults. Future studies are warranted to confirm our results.

The Health-Related and Learning Performance Effects of Air Pollution and Other Urban-Related Environmental Factors on School-Age Children and Adolescents-A Scoping Review of Systematic Reviews.

PURPOSE OF REVIEW: This scoping review aims to assess the impact of air pollution, traffic noise, heat, and green and blue space exposures on the physical and cognitive development of school-age children and adolescents. While existing evidence indicates adverse effects of transport-related exposures on their health, a comprehensive scoping review is necessary to consolidate findings on various urban environmental exposures' effects on children's development. RECENT FINDINGS: There is consistent evidence on how air pollution negatively affects children's cognitive and respiratory health and learning performance, increasing their susceptibility to diseases in their adult life. Scientific evidence on heat and traffic noise, while less researched, indicates that they negatively affect children's health. On the contrary, green space exposure seems to benefit or mitigate these adverse effects, suggesting a potential strategy to promote children's cognitive and physical development in urban settings. This review underscores the substantial impact of urban exposures on the physical and mental development of children and adolescents. It highlights adverse health effects that can extend into adulthood, affecting academic opportunities and well-being beyond health. While acknowledging the necessity for more research on the mechanisms of air pollution effects and associations with heat and noise exposure, the review advocates prioritizing policy changes and urban planning interventions. This includes minimizing air pollution and traffic noise while enhancing urban vegetation, particularly in school environments, to ensure the healthy development of children and promote lifelong health.

Random effect generalized linear model-based predictive modelling of traffic noise.

Noise pollution is one of the negative consequences of growth and development in cities. Traffic noise pollution due to traffic growth is the main aspect that worsens city quality of life. Therefore, research around the world is being conducted to manage and reduce traffic noise. A number of traffic noise prediction models have been proposed employing fixed effect modelling approach considering each observation as independent; however, observations may have spatial and temporal correlations and unobserved heterogeneity. Random effect models overcome these problems. This study attempts to develop a random effect generalized linear model (REGLM) along with a machine learning random forest (RF) model to validate the results, concerning the parameters related to road, traffic and environmental conditions. Models were developed based on the experimental quantities in Delhi in year 2022-2023. Both the models performed comparably well in terms of coefficient of determination. Random forest models with R2= 0.75, whereas random effect generalized linear model had an R2= 0.70. REGLM model has the ability to quantify the effects of explanatory variables over traffic noise pollution and will be more helpful in prioritizing of resources and chalking out control strategies.