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.

Germline Elongator mutations in Sonic Hedgehog medulloblastoma.

Cancer genomics has revealed many genes and core molecular processes that contribute to human malignancies, but the genetic and molecular bases of many rare cancers remains unclear. Genetic predisposition accounts for 5 to 10% of cancer diagnoses in children1,2, and genetic events that cooperate with known somatic driver events are poorly understood. Pathogenic germline variants in established cancer predisposition genes have been recently identified in 5% of patients with the malignant brain tumour medulloblastoma3. Here, by analysing all protein-coding genes, we identify and replicate rare germline loss-of-function variants across ELP1 in 14% of paediatric patients with the medulloblastoma subgroup Sonic Hedgehog (MBSHH). ELP1 was the most common medulloblastoma predisposition gene and increased the prevalence of genetic predisposition to 40% among paediatric patients with MBSHH. Parent-offspring and pedigree analyses identified two families with a history of paediatric medulloblastoma. ELP1-associated medulloblastomas were restricted to the molecular SHHα subtype4 and characterized by universal biallelic inactivation of ELP1 owing to somatic loss of chromosome arm 9q. Most ELP1-associated medulloblastomas also exhibited somatic alterations in PTCH1, which suggests that germline ELP1 loss-of-function variants predispose individuals to tumour development in combination with constitutive activation of SHH signalling. ELP1 is the largest subunit of the evolutionarily conserved Elongator complex, which catalyses translational elongation through tRNA modifications at the wobble (U34) position5,6. Tumours from patients with ELP1-associated MBSHH were characterized by a destabilized Elongator complex, loss of Elongator-dependent tRNA modifications, codon-dependent translational reprogramming, and induction of the unfolded protein response, consistent with loss of protein homeostasis due to Elongator deficiency in model systems7-9. Thus, genetic predisposition to proteome instability may be a determinant in the pathogenesis of paediatric brain cancers. These results support investigation of the role of protein homeostasis in other cancer types and potential for therapeutic interference.

Differences in autophagy marker levels at birth in preterm vs. term infants.

BACKGROUND: Preterm infants are susceptible to oxidative stress and prone to respiratory diseases. Autophagy is an important defense mechanism against oxidative-stress-induced cell damage and involved in lung development and respiratory morbidity. We hypothesized that autophagy marker levels differ between preterm and term infants. METHODS: In the prospective Basel-Bern Infant Lung Development (BILD) birth cohort we compared cord blood levels of macroautophagy (Beclin-1, LC3B), selective autophagy (p62) and regulation of autophagy (SIRT1) in 64 preterm and 453 term infants. RESULTS: Beclin-1 and LC3B did not differ between preterm and term infants. However, p62 was higher (0.37, 95% confidence interval (CI) 0.05;0.69 in log2-transformed level, p = 0.025, padj = 0.050) and SIRT1 lower in preterm infants (-0.55, 95% CI -0.78;-0.31 in log2-transformed level, padj < 0.001). Furthermore, p62 decreased (padj-value for smoothing function was 0.018) and SIRT1 increased (0.10, 95% CI 0.07;0.13 in log2-transformed level, padj < 0.001) with increasing gestational age. CONCLUSION: Our findings suggest differential levels of key autophagy markers between preterm and term infants. This adds to the knowledge of the sparsely studied field of autophagy mechanisms in preterm infants and might be linked to impaired oxidative stress response, preterm birth, impaired lung development and higher susceptibility to respiratory morbidity in preterm infants. IMPACT: To the best of our knowledge, this is the first study to investigate autophagy marker levels between human preterm and term infants in a large population-based sample in cord blood plasma This study demonstrates differential levels of key autophagy markers in preterm compared to term infants and an association with gestational age This may be linked to impaired oxidative stress response or developmental aspects and provide bases for future studies investigating the association with respiratory morbidity.

Socio-environmental modifiers of heat-related mortality in eight Swiss cities: A case time series analysis.

In the light of growing urbanization and projected temperature increases due to climate change, heat-related mortality in urban areas is a pressing public health concern. Heat exposure and vulnerability to heat may vary within cities depending on structural features and socioeconomic factors. This study examined the effect modification of the temperature-mortality association of three socio-environmental factors in eight Swiss cities and population subgroups (<75 and ≥ 75 years, males, females): urban heat islands (UHI) based on within-city temperature contrasts, residential greenness measured as normalized difference vegetation index (NDVI) and neighborhood socioeconomic position (SEP). We used individual death records from the Swiss National Cohort occurring during the warm season (May to September) in the years 2003-2016. We performed a case time series analysis using conditional quasi-Poisson and distributed lag non-linear models with a lag of 0-3 days. As exposure variables, we used daily maximum temperatures (Tmax) and a binary indicator for warm nights (Tmin ≥20 °C). In total, 53,593 deaths occurred during the study period. Overall across the eight cities, the mortality risk increased by 31% (1.31 relative risk (95% confidence interval: 1.20-1.42)) between 22.5 °C (the minimum mortality temperature) and 35 °C (the 99th percentile) for warm-season Tmax. Stratified analysis suggested that the heat-related risk at 35 °C is 26% (95%CI: -4%, 67%) higher in UHI compared to non-UHI areas. Indications of smaller risk differences were observed between the low vs. high greenness strata (Relative risk difference = 13% (95%CI: -11%; 44%)). Living in low SEP neighborhoods was associated with an increased heat related risk in the non-elderly population (<75 years). Our results indicate that UHI are associated with increased heat-related mortality risk within Swiss cities, and that features beyond greenness are responsible for such spatial risk differences.

A cohort analysis of residential radon exposure and melanoma incidence in Switzerland.

Radon is a radioactive noble gas found in Earth's crust. It accumulates in buildings, and accounts for approximately half the ionizing radiation dose received by humans. The skin is considerably exposed to ionizing radiation from radon. We aimed to evaluate the association between residential radon exposure and melanoma and squamous cell carcinoma incidence. The study included 1.3 million adults (20 years and older) from the Swiss National Cohort who were residents of the cantons of Vaud, Neuchâtel, Valais, Geneva, Fribourg, and Ticino at the study baseline (December 04, 2000). Cases of primary tumours of skin (melanoma and squamous cell carcinoma) were identified using data from cantonal cancer registries. Long-term residential radon and ambient solar ultraviolet radiation exposures were assigned to each individual's address at baseline. Cox proportional hazard models with age as time scale, adjusted for canton, socioeconomic position, demographic data available in the census, and outdoor occupation were applied. Total and age specific effects were calculated, in the full population and in non-movers, and potential effect modifiers were tested. In total 4937 incident cases of melanoma occurred during an average 8.9 years of follow-up. Across all ages, no increased risk of malignant melanoma or squamous cell carcinoma incidence in relation to residential radon was found. An association was only observed for melanoma incidence in the youngest age group of 20-29 year olds (1.68 [95% CI: 1.29, 2.19] 100 Bq/m3 radon). This association was mainly in women, and in those with low socio-economic position. Residential radon exposure might be a relevant risk factor for melanoma, especially for young adults. However, the results must be interpreted with caution as this finding is based on a relatively small number of melanoma cases. Accumulation of radon is preventable, and measures to reduce exposure and communicate the risks remain important to convey to the public.

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.

Burden of disease in Germany attributed to ambient particulate matter pollution : Findings from the Global Burden of Disease Study 2019.

INTRODUCTION: Ambient fine particulate matter pollution with a diameter less than 2.5 micrometers (PM2.5) is a significant risk factor for chronic noncommunicable diseases (NCDs), leading to a substantial disease burden, decreased quality of life, and deaths globally. This study aimed to investigate the disease and mortality burdens attributed to PM2.5 in Germany in 2019. METHODS: Data from the Global Burden of Disease (GBD) Study 2019 were used to investigate disability-adjusted life-years (DALYs), years of life lost (YLLs), years lived with disability (YLDs), and deaths attributed to ambient PM2.5 pollution in Germany. RESULTS: In 2019, ambient PM2.5 pollution in Germany was associated with significant health impacts, contributing to 27,040 deaths (2.82% of total deaths), 568,784 DALYs (2.09% of total DALYs), 135,725 YLDs (1.09% of total YLDs), and 433,058 YLLs (2.92% of total YLLs). The analysis further revealed that cardiometabolic and respiratory conditions, such as ischemic heart disease, stroke, chronic obstructive pulmonary disease, lung cancer, and diabetes mellitus, were the leading causes of mortality and disease burden associated with ambient PM2.5 pollution in Germany from 1990-2019. Comparative assessments between 1990 and 2019 underscored ambient PM2.5 as a consistent prominent risk factor, ranking closely with traditional factors like smoking, arterial hypertension, and alcohol use contributing to deaths, DALYs, YLDs, and YLLs. CONCLUSION: Ambient PM2.5 pollution is one of the major health risk factors contributing significantly to the burden of disease and mortality in Germany, emphasizing the urgent need for targeted interventions to address its substantial contribution to chronic NCDs.

The association of road traffic noise with cognition in adolescents: A cohort study in Switzerland.

Environmental noise exposure has been shown to affect children's cognition, but the concept of cognition is multifaceted, and studies on associations with noise are still inconclusive and fragmented. We studied cognitive change within one year in 882 adolescents aged 10-17 years in response to road traffic noise exposure. Participants filled in a comprehensive questionnaire and underwent cognitive testing twice at an interval of one year. Figural and verbal memory was measured with the Intelligenz-Struktur-Test (IST), and concentration accuracy and constancy were measured with FAKT-II and d2 test. Exposure to noise and other environmental stressors were modelled for school and home location at baseline. Missing data was addressed with multiple imputation. Cross-sectional multilevel analyses and longitudinal change score analyses were performed. In cross-sectional analyses, figural memory was significantly reduced by -0.27 (95%CI -0.49,-0.04) units per 10 dB road traffic noise increase at home (Lden). Longitudinal analyses showed a significant reduction of concentration constancy Z-scores between baseline and follow-up by -0.13 (95%CI -0.25, 0.00) per 10 dB road traffic noise at home (Lden). Our study indicates that road traffic noise at home reduces cognitive performance in adolescents. Larger cohorts with longer follow-up time are needed to confirm these results.

Comparison of ambient radiofrequency electromagnetic field (RF-EMF) levels in outdoor areas and public transport in Switzerland in 2014 and 2021.

Mobile communication technology has evolved rapidly over the last ten years with a drastic increase in wireless data traffic and the deployment of new telecommunication technologies. The aim of this study was to evaluate the ambient radiofrequency electromagnetic field (RF-EMF) levels and temporal changes in various microenvironments in Switzerland in 2014 and 2021. We measured the ambient RF-EMF levels in V/m in the same 49 outdoor areas and in public transport in 2014 and 2021 using portable RF-EMF exposure meters carried in a backpack. The areas were selected to represent some typical types of microenvironments (e.g. urban city centres, suburban and rural areas). We calculated the summary statistics (mean, percentiles) in mW/m2 and converted back to V/m for each microenvironment. We evaluated the distribution and the variability of the ambient RF-EMF levels per microenvironment types in 2021. Finally, we compared the ambient RF-EMF mean levels in 2014 and 2021 using multilevel regression modelling. In outdoor areas, the average ambient RF-EMF mean levels per microenvironment in 2021 ranged from 0.19 V/m in rural areas to 0.43 V/m in industrial areas (overall mean: 0.27 V/m). In public transports, the mean levels were 0.27 V/m in buses, 0.33 V/m in trains and 0.36 V/m in trams. In 2021, mean levels across all outdoor areas were -0.022 V/m lower (95% confidence interval: -0.072, 0.030) than in 2014. Results from our comprehensive measurement study across Switzerland suggest that RF-EMF levels in public places have not significantly changed between 2014 and 2021 despite an 18-fold increase in mobile data transmission during that period. The absence of temporal changes may be owed to the shift to newer mobile communication technologies, which are more efficient.

Mortality attributable to ambient fine particulate matter and nitrogen dioxide in Switzerland in 2019: Use of two-pollutant effect estimates.

INTRODUCTION: Air pollution health risk assessments have traditionally used single-pollutant effect estimates for one proxy ambient air pollutant such as PM2.5. Two-pollutant effect estimates, i.e. adjusted for another correlated pollutant, theoretically enable the aggregation of pollutant-specific health effects minimizing double-counting. Our study aimed at estimating the adult mortality in Switzerland in 2019 attributable to PM2.5 from a single-pollutant effect estimate and to the sum of PM2.5 and NO2 from two-pollutant estimates; comparing the results with those from alternative global, European and Swiss effect estimates. METHODS: For the single-pollutant approach, we used a PM2.5 summary estimate of European cohorts from the project ELAPSE, recommended by the European Respiratory Society and International Society for Environmental Epidemiology (ERS-ISEE). To derive the two-pollutant effect estimates, we applied ELAPSE-based conversion factors to ERS-ISEE PM2.5 and NO2 single-pollutant effect estimates. Additionally, we used World Health Organization 2021 Air Quality Guidelines as counterfactual scenario, exposure model data from 2019 and Swiss lifetables. RESULTS: The single-pollutant effect estimate for PM2.5 (1.118 [1.060; 1.179] per 10 µg/m3) resulted in 2240 deaths (21,593 years of life lost). Using our derived two-pollutant effect estimates (1.023 [1.012; 1.035] per 10 µg/m3 PM2.5 adjusted for NO2 and 1.040 [1.023; 1.058] per 10 µg/m3 NO2 adjusted for PM2.5), we found 1977 deaths (19,071 years of life lost) attributable to PM2.5 and NO2 together (23% from PM2.5). Deaths using alternative effect estimates ranged from 1042 to 5059. DISCUSSION: Estimated premature mortality attributable to PM2.5 alone was higher than to both PM2.5 and NO2 combined. Furthermore, the proportion of deaths from PM2.5 was lower than from NO2 in the two-pollutant approach. These seemingly paradoxical results, also found in some alternative estimates, are due to statistical imprecisions of underlying correction methods. Therefore, using two-pollutant effect estimates can lead to interpretation challenges in terms of causality.

Aircraft noise exposure and risk for recurrent cardiovascular events after acute coronary syndrome: A prospective patient cohort study.

In several population based cohort studies associations between aircraft noise and various diagnoses of cardiovascular disease were observed. However, no study has yet addressed the risk of recurrences in relation to transportation noise in patients with acute coronary heart disease. We conducted a prospective patient cohort study of 737 individuals recruited from eleven cardiac centers in the Rhine-Main region in the vicinity of Frankfurt Airport. All patients had an angiographically confirmed acute coronary syndrome diagnosed between July 2013 and November 2018. Individual aircraft noise exposure at the place of residence was calculated using Soundplan software, and exposure to road traffic and railway noise was obtained from noise maps provided by the Hessian State Agency. Data was analyzed by means of Cox regression adjusted for relevant confounders. Recurrent event as non-fatal endpoint was defined as myocardial infarction, stroke, bypass surgery or percutaneous coronary intervention with stent implantation. In addition, all-cause mortality was evaluated. Follow-up data including socioeconomic and confounder information was obtained from 663 (90%) patients covering a mean follow-up period of 42 (range: 1-80) months. Mean Lden aircraft noise exposure was 48.1 dB. Adjusted hazard ratio (HR) for recurrence was 1.24 (95%-CI: 0.97-1.58) per 10 dB increase in Lden aircraft noise exposure. A combined analysis of recurrence and all-cause mortality yielded a HR of 1.31 (95%-CI: 1.03-1.66). Similar HRs were found for Lday and Lnight aircraft noise exposure. HRs for road traffic and railway noise were above unity but less pronounced and not significant. Observed exposure-response associations for aircraft noise were more pronounced than previously observed in population-based cohort studies suggesting that acute coronary heart disease patients are particularly vulnerable to effects from transportation noise. Measures to reduce environmental noise exposure may thus be helpful in improving clinical outcome of patients with coronary heart disease.

The association between real-life markers of phone use and cognitive performance, health-related quality of life and sleep.

INTRODUCTION: The real-life short-term implications of electromagnetic fields (RF-EMF) on cognitive performance and health-related quality of life have not been well studied. The SPUTNIC study (Study Panel on Upcoming Technologies to study Non-Ionizing radiation and Cognition) aimed to investigate possible correlations between mobile phone radiation and human health, including cognition, health-related quality of life and sleep. METHODS: Adult participants tracked various daily markers of RF-EMF exposures (cordless calls, mobile calls, and mobile screen time 4 h prior to each assessment) as well as three health outcomes over ten study days: 1) cognitive performance, 2) health-related quality of life (HRQoL), and 3) sleep duration and quality. Cognitive performance was measured through six "game-like" tests, assessing verbal and visuo-spatial performance repeatedly. HRQoL was assessed as fatigue, mood and stress on a Likert-scale (1-10). Sleep duration and efficiency was measured using activity trackers. We fitted mixed models with random intercepts per participant on cognitive, HRQoL and sleep scores. Possible time-varying confounders were assessed at daily intervals by questionnaire and used for model adjustment. RESULTS: A total of 121 participants ultimately took part in the SPUTNIC study, including 63 from Besancon and 58 from Basel. Self-reported wireless phone use and screen time were sporadically associated with visuo-spatial and verbal cognitive performance, compatible with chance findings. We found a small but robust significant increase in stress 0.03 (0.00-0.06; on a 1-10 Likert-scale) in relation to a 10-min increase in mobile phone screen time. Sleep duration and quality were not associated with either cordless or mobile phone calls, or with screen time. DISCUSSION: The study did not find associations between short-term RF-EMF markers and cognitive performance, HRQoL, or sleep duration and quality. The most consistent finding was increased stress in relation to more screen time, but no association with cordless or mobile phone call time.

Association between exposure to multiple air pollutants, transportation noise and cause-specific mortality in adults in Switzerland.

BACKGROUND: Long-term exposure to air pollution and noise is detrimental to health; but studies that evaluated both remain limited. This study explores associations with natural and cause-specific mortality for a range of air pollutants and transportation noise. METHODS: Over 4 million adults in Switzerland were followed from 2000 to 2014. Exposure to PM2.5, PM2.5 components (Cu, Fe, S and Zn), NO2, black carbon (BC) and ozone (O3) from European models, and transportation noise from source-specific Swiss models, were assigned at baseline home addresses. Cox proportional hazards models, adjusted for individual and area-level covariates, were used to evaluate associations with each exposure and death from natural, cardiovascular (CVD) or non-malignant respiratory disease. Analyses included single and two exposure models, and subset analysis to study lower exposure ranges. RESULTS: During follow-up, 661,534 individuals died of natural causes (36.6% CVD, 6.6% respiratory). All exposures including the PM2.5 components were associated with natural mortality, with hazard ratios (95% confidence intervals) of 1.026 (1.015, 1.038) per 5 µg/m3 PM2.5, 1.050 (1.041, 1.059) per 10 µg/m3 NO2, 1.057 (1.048, 1.067) per 0.5 × 10-5/m BC and 1.045 (1.040, 1.049) per 10 dB Lden total transportation noise. NO2, BC, Cu, Fe and noise were consistently associated with CVD and respiratory mortality, whereas PM2.5 was only associated with CVD mortality. Natural mortality associations persisted < 20 µg/m3 for PM2.5 and NO2, < 1.5 10-5/m BC and < 53 dB Lden total transportation noise. The O3 association was inverse for all outcomes. Including noise attenuated all outcome associations, though many remained significant. Across outcomes, noise was robust to adjustment to air pollutants (e.g. natural mortality 1.037 (1.033, 1.042) per 10 dB Lden total transportation noise, after including BC). CONCLUSION: Long-term exposure to air pollution and transportation noise in Switzerland contribute to premature mortality. Considering co-exposures revealed the importance of local traffic-related pollutants such as NO2, BC and transportation noise.

Increased Impact of Air Pollution on Lung Function in Preterm versus Term Infants: The BILD Study.

Rationale: Infants born prematurely have impaired capacity to deal with oxidative stress shortly after birth. Objectives: We hypothesize that the relative impact of exposure to air pollution on lung function is higher in preterm than in term infants. Methods: In the prospective BILD (Basel-Bern Infant Lung Development) birth cohort of 254 preterm and 517 term infants, we investigated associations of particulate matter ⩽10 µm in aerodynamic diameter (PM10) and nitrogen dioxide with lung function at 44 weeks' postconceptional age and exhaled markers of inflammation and oxidative stress response (fractional exhaled nitric oxide [FeNO]) in an explorative hypothesis-driven study design. Multilevel mixed-effects models were used and adjusted for known confounders. Measurements and Main Results: Significant associations of PM10 during the second trimester of pregnancy with lung function and FeNO were found in term and preterm infants. Importantly, we observed stronger positive associations in preterm infants (born 32-36 wk), with an increase of 184.9 (95% confidence interval [CI], 79.1-290.7) ml/min [Formula: see text]e per 10-µg/m3 increase in PM10, than in term infants (75.3; 95% CI, 19.7-130.8 ml/min) (pprematurity × PM10 interaction = 0.04, after multiple comparison adjustment padj = 0.09). Associations of PM10 and FeNO differed between moderate to late preterm (3.4; 95% CI, -0.1 to 6.8 ppb) and term (-0.3; 95% CI, -1.5 to 0.9 ppb) infants, and the interaction with prematurity was significant (pprematurity × PM10 interaction = 0.006, padj = 0.036). Conclusions: Preterm infants showed significantly higher susceptibility even to low to moderate prenatal air pollution exposure than term infants, leading to increased impairment of postnatal lung function. FeNO results further elucidate differences in inflammatory/oxidative stress response when comparing preterm infants with term infants.

Non-optimal apparent temperature and cardiovascular mortality: the association in Puducherry, India between 2011 and 2020.

BACKGROUND: Cardiovascular diseases (CVDs), the leading cause of death worldwide, are sensitive to temperature. In light of the reported climate change trends, it is important to understand the burden of CVDs attributable to temperature, both hot and cold. The association between CVDs and temperature is region-specific, with relatively few studies focusing on low-and middle-income countries. This study investigates this association in Puducherry, a district in southern India lying on the Bay of Bengal, for the first time. METHODS: Using in-hospital CVD mortality data and climate data from the Indian Meteorological Department, we analyzed the association between apparent temperature (Tapp) and in-hospital CVD mortalities in Puducherry between 2011 and 2020. We used a case-crossover model with a binomial likelihood distribution combined with a distributed lag non-linear model to capture the delayed and non-linear trends over a 21-day lag period to identify the optimal temperature range for Puducherry. The results are expressed as the fraction of CVD mortalities attributable to heat and cold, defined relative to the optimal temperature. We also performed stratified analyses to explore the associations between Tapp and age-and-sex, grouped and considered together, and different types of CVDs. Sensitivity analyses were performed, including using a quasi-Poisson time-series approach. RESULTS: We found that the optimal temperature range for Puducherry is between 30°C and 36°C with respect to CVDs. Both cold and hot non-optimal Tapp were associated with an increased risk of overall in-hospital CVD mortalities, resulting in a U-shaped association curve. Cumulatively, up to 17% of the CVD deaths could be attributable to non-optimal temperatures, with a slightly higher burden attributable to heat (9.1%) than cold (8.3%). We also found that males were more vulnerable to colder temperature; females above 60 years were more vulnerable to heat while females below 60 years were affected by both heat and cold. Mortality with cerebrovascular accidents was associated more with heat compared to cold, while ischemic heart diseases did not seem to be affected by temperature. CONCLUSION: Both heat and cold contribute to the burden of CVDs attributable to non-optimal temperatures in the tropical Puducherry. Our study also identified the age-and-sex and CVD type differences in temperature attributable CVD mortalities. Further studies from India could identify regional associations, inform our understanding of the health implications of climate change in India and enhance the development of regional and contextual climate-health action-plans.

The association of road traffic noise with problem behaviour in adolescents: A cohort study.

The findings of environmental noise exposure and behavioural disorders in children and adolescents are inconclusive, and longitudinal studies are scarce. We studied the response of behaviour and behavioural change within one year in a cohort of 886 adolescents in Switzerland aged 10-17 years in response to road traffic noise exposure. Participants filled in a comprehensive questionnaire at baseline and follow-up. It included the Strengths and Difficulties Questionnaire (SDQ), which measures self-rated positive and negative behaviours in five scales. We modelled road traffic noise for participants' most exposed facade at home and school addresses in various metrics (Lden, Lnight, Lday, Intermittency Ratio and Number of events). We addressed missing data with multiple imputation and performed mixed linear cross-sectional analyses and longitudinal change score analyses. In cross-sectional analyses, peer relationship problems increased by 0.15 units (95%CI: 0.02, 0.27; scale range: 0-10) per 10 dB road traffic noise increase. In longitudinal analyses, increases in SDQ scales between baseline and follow-up were not related to noise exposure. This study suggests subtle associations between road traffic noise exposure and behaviour problems in adolescents, but longer follow-up times may be needed to observe longitudinal changes.

Association of transportation noise with sleep during the first year of life: A longitudinal study.

STUDY OBJECTIVES: During infancy, adequate sleep is crucial for physical and neurocognitive development. In adults and children, night-time noise exposure is associated with sleep disturbances. However, whether and to what extent infants' sleep is affected, is unknown. Thus, this study investigated the relationship between nocturnal transportation noise and actimetry-derived habitual sleep behavior across the first year of life. METHODS: In 144 healthy infants (63 girls), nocturnal (23:00-7:00) transportation noise (i.e., road, railway, and aircraft) was modelled at the infants' individual places of residence. Using actimetry, we recorded movement patterns for 11 days in a longitudinal design at 3, 6, and 12 months of age and derived the recently proposed core sleep composites of night-time sleep duration, activity, and variability. Using linear mixed-effects models, we determined associations between noise exposure and sleep composites. Sex, gestational age, parents' highest educational level, infants' age, and the existence of siblings served as control variables. RESULTS: In models without interactions, night-time transportation noise was unrelated to sleep composites across the first year of life (p > .16). Exploratory analyses of an interaction between noise and the existence of siblings yielded an association between night-time transportation noise and sleep duration in infants without siblings only (p = .004). CONCLUSION: In our study, sleep in infants during the first year of life was relatively robust against external perturbation by night-time transportation noise. However, particularly in children without siblings increasing night-time transportation noise reduced sleep duration. This suggests that the habitual noise environment may modulate individual susceptibility to adverse effects of noise on sleep.

Personal radiofrequency electromagnetic field exposure of adolescents in the Greater London area in the SCAMP cohort and the association with restrictions on permitted use of mobile communication technologies at school and at home.

Personal measurements of radiofrequency electromagnetic fields (RF-EMF) have been used in several studies to characterise personal exposure in daily life, but such data are limitedly available for adolescents, and not yet for the United Kingdom (UK). In this study, we aimed to characterise personal exposure to RF-EMF in adolescents and to study the association between exposure and rules applied at school and at home to restrict wireless communication use, likely implemented to reduce other effects of mobile technology (e.g. distraction). We measured exposure to RF-EMF for 16 common frequency bands (87.5 MHz-3.5 GHz), using portable measurement devices (ExpoM-RF), in a subsample of adolescents participating in the cohort Study of Cognition, Adolescents and Mobile Phones (SCAMP) from Greater London (UK) (n = 188). School and home rules were assessed by questionnaire and concerned the school's availability of WiFi and mobile phone policy, and parental restrictions on permitted mobile phone use. Adolescents recorded their activities in real time using a diary app on a study smartphone, while characterizing their personal RF-EMF exposure in daily life, during different activities and times of the day. Data analysis was done for 148 adolescents from 29 schools who recorded RF-EMF data for a median duration of 47 h. The majority (74%) of adolescents spent part of their time at school during the measurement period. Median total RF-EMF exposure was 40 µW/m2 at home, 94 µW/m2 at school, and 100 µW/m2 overall. In general, restrictions at school or at home made little difference for adolescents' measured exposure to RF-EMF, except for uplink exposure from mobile phones while at school, which was found to be significantly lower for adolescents attending schools not permitting phone use at all, compared to adolescents attending schools allowing mobile phone use during breaks. This difference was not statistically significant for total personal exposure. Total exposure to RF-EMF in adolescents living in Greater London tended to be higher compared to exposure levels reported in other European countries. This study suggests that school policies and parental restrictions are not associated with a lower RF-EMF exposure in adolescents.

Estimated all-day and evening whole-brain radiofrequency electromagnetic fields doses, and sleep in preadolescents.

OBJECTIVE: To investigate the association of estimated all-day and evening whole-brain radiofrequency electromagnetic field (RF-EMF) doses with sleep disturbances and objective sleep measures in preadolescents. METHODS: We included preadolescents aged 9-12 years from two population-based birth cohorts, the Dutch Generation R Study (n = 974) and the Spanish INfancia y Medio Ambiente Project (n = 868). All-day and evening overall whole-brain RF-EMF doses (mJ/kg/day) were estimated for several RF-EMF sources including mobile and Digital Enhanced Cordless Telecommunications (DECT) phone calls (named phone calls), other mobile phone uses, tablet use, laptop use (named screen activities), and far-field sources. We also estimated all-day and evening whole-brain RF-EMF doses in these three groups separately (i.e. phone calls, screen activities, and far-field). The Sleep Disturbance Scale for Children was completed by mothers to assess sleep disturbances. Wrist accelerometers together with sleep diaries were used to measure sleep characteristics objectively for 7 consecutive days. RESULTS: All-day whole-brain RF-EMF doses were not associated with self-reported sleep disturbances and objective sleep measures. Regarding evening doses, preadolescents with high evening whole-brain RF-EMF dose from phone calls had a shorter total sleep time compared to preadolescents with zero evening whole-brain RF-EMF dose from phone calls [-11.9 min (95%CI -21.2; -2.5)]. CONCLUSIONS: Our findings suggest the evening as a potentially relevant window of RF-EMF exposure for sleep. However, we cannot exclude that observed associations are due to the activities or reasons motivating the phone calls rather than the RF-EMF exposure itself or due to chance finding.

Does night-time aircraft noise trigger mortality? A case-crossover study on 24 886 cardiovascular deaths.

AIMS: It is unclear whether night-time noise events, including from aeroplanes, could trigger a cardiovascular death. In this study, we investigate the potential acute effects of aircraft noise on mortality and the specific role of different night-time exposure windows by means of a case-crossover study design. METHODS AND RESULTS: We selected 24 886 cases of death from cardiovascular disease (CVD) from the Swiss National Cohort around Zürich Airport between 2000 and 2015. For night-time deaths, exposure levels 2 h preceding death were significantly associated with mortality for all causes of CVD [OR = 1.44 (1.03-2.04) for the highest exposure group (LAeq > 50 dB vs. <20 dB)]. Most consistent associations were observed for ischaemic heart diseases, myocardial infarction, heart failure, and arrhythmia. Association were more pronounced for females (P = 0.02) and for people living in areas with low road and railway background noise (P = 0.01) and in buildings constructed before 1970 (P = 0.36). We calculated a population attributable fraction of 3% in our study population. CONCLUSION: Our findings suggest that night-time aircraft noise can trigger acute cardiovascular mortality. The association was similar to that previously observed for long-term aircraft noise exposure.