Introduction Diabetes mellitus (DM) and its severe complications contribute significantly to disability and, hence, burden of disease. Poor mental health, a frequent DM consequence, may hinder successful diabetes control in low-income and middle-income countries (LMICs). Evidence suggests social support as a cost-effective tool to improve diabetes self-management, behaviour and mental health. However, its real-world application in LMICs has rarely been tested. We aim to investigate the effect of a social support intervention on disease control, mental health and health-related quality of life in people with diabetes from Côte d’Ivoire (SoDDiCo) through a randomised controlled trial.Methods and analysis The trial will take place in the Centre Antidiabétique d’Abidjan, Institut National de Santé Publique, Abidjan, Côte d’Ivoire. We will prospectively randomise up to 1500 people with newly diagnosed diabetes into two parallel arms: intervention (routine care+family supporter accompanying clinical management) and control (routine care), using gender-stratified blocked randomisation with random block sizes of 10, 16, 20 and 24. Participants will undergo baseline, 3-month and 12-month postrandomisation assessments. The primary study outcome will be glycated haemoglobin (HbA1c). Secondary outcomes will include glycaemic control (HbA1c<7.0%), presence at follow-up visits, mental health and quality of life scores. Using intention-to-treat framework, we will assess the impact of the family support intervention on these endpoints over the course of the 1-year follow-up. Effect modification by baseline social capital will be assessed.Ethics and dissemination The SoDDiCo trial was approved by the Ethikkommission Nordwest- und Zentralschweiz (ref: AO_2021-00041; approved: 12 July 2021) and by Comité National d'Éthique des Sciences de la Vie et de la Santé (ref: 049-22/MSHPCMU/CNESVS-kp; approved: 20 April 2022). The randomised intervention trial will follow good clinical practice guidelines. All results will be made available to the public through abstracts at conferences as well as through peer-reviewed articles. International guidelines for authorship will be respected.Trial registration number ISRCTN10901121, ISRCTN registry.

BackgroundAlthough several randomized controlled trials (RCTs) published over the past 5 years show that prenatal or postnatal probiotics may prevent or optimize the treatment of childhood asthma and atopic disorders, findings from the systematic reviews and meta-analyses of these studies appear inconsistent. More recent RCTs have focused on postnatal probiotics, and linked specific probiotic strains to better disease outcomes.ObjectiveThis systematic review aimed to determine if postnatal probiotics are as effective as prenatal probiotics in preventing or treating childhood asthma and atopic disorders.MethodsWe searched the PubMed, Medline, Google Scholar, and EMBASE databases for RCTs published within the past 5 years (from 2017 to 2022). We included only full-text RCTs on human subjects published in or translated into the English language. We retrieved relevant data items with a preconceived data-extraction form and assessed the methodological quality of the selected RCTs using the Cochrane Collaboration's tool for assessing the risk of bias in randomized trials. We qualitatively synthesized the retrieved data to determine any significant differences in study endpoints of the probiotic and placebo groups.ResultsA total of 1,320 participants (688 and 632 in the probiotic and placebo groups) from six RCTs were investigated. One RCT showed that early Lactobacillus rhamnosus GG (LGG) led to a reduction in the cumulative incidence rate of asthma. Another study demonstrated that mixed strains of Lactobacillus paracasei and Lactobacillus fermentum could support clinical improvement in children with asthma while one trial reported a significant reduction in the frequency of asthma exacerbations using a mixture of Ligilactobacillus salivarius and Bifidobacterium breve. Three trials showed that a combination of LGG and Bifidobacterium animalis subsp lactis, Lactobacillus rhamnosus alone, and a probiotic mixture of Lactobacillus ŁOCK strains improved clinical outcomes in children with atopic dermatitis and cow-milk protein allergy.ConclusionsPostnatal strain-specific probiotics (in single or mixed forms) are beneficial in preventing and treating atopic dermatitis and other allergies. Similarly, specific strains are more effective in preventing asthma or improving asthma outcomes. We recommend more interventional studies to establish the most useful probiotic strain in these allergic diseases.

Abstract Background Schistosomiasis remains an important public health problem, also among adults, and infected individuals not treated serve as a reservoir for continued transmission. Despite this fact, evidence on the epidemiology of schistosomiasis in adults in Côte d’Ivoire is scanty. This study aimed to determine the prevalence and risk factors of Schistosoma infection and co-infection with other helminth species and Plasmodium among adults in the Taabo region in the south-central part of Côte d’Ivoire. Methods A cross-sectional survey was carried out in April and May 2017 in the frame of the “Côte d’Ivoire Dual Burden of Disease Study” (CoDuBu). A total of 901 randomly selected individuals, aged 18–90 years, provided blood, stool and urine samples for the diagnosis of malaria and helminth infections. Stool samples were subjected to the Kato-Katz technique for detection of Schistosoma mansoni and soil-transmitted helminth eggs, while urine samples were examined for eggs of Schistosoma haematobium and circulating cathodic antigen of S. mansoni. Risk factors and morbidity profiles were assessed using health examination and questionnaires. Multinomial logistic regressions were employed to identify risk factors and morbidity patterns associated with S. mansoni mono- and co-infections. Results The prevalence of S. mansoni and S. haematobium was 23.2% and 1.0%, respectively. Most S. mansoni were mono-infections (81.3%). Independent determinants of S. mansoni infection were young age, low socioeconomic status (mono- and co-infection) and poor hygiene practices (co-infection) (P < 0.05). S. mansoni infection was independently associated with higher pain and symptom scores (mono-infection), poor self-rated health and low healthcare use (co-infection) (P < 0.05). Conclusions This study showed that adults represent a substantial reservoir of S. mansoni. To sustain schistosomiasis control and improve people’s wellbeing, it is important to expand preventive chemotherapy from school-aged children to adults, coupled with hygiene and health education.

Background: Residential greenness has been associated with health benefits, but its biological mechanism is largely unknown. Investigation of greenness-related DNA methylation profiles can contribute to mechanistic understanding of the health benefits of residential greenness. Objective: To identify DNA methylation profiles associated with greenness in the immediate surroundings of the residence. Methods: We analyzed genome-wide DNA methylation in 1938 blood samples (982 participants) from the Swiss Cohort Study on Air Pollution and Lung and Heart Diseases in Adults (SAPALDIA). We estimated residential greenness based on normalized difference vegetation index at 30 x 30 m cell (green30) and 500 m buffer (green500) around the residential address. We conducted epigenome-wide association study (EWAS) to identify differentially methylated CpGs and regions, and enrichment tests by comparing to the CpGs that previous EWAS identified as associated with allergy, physical activity, and allostatic load-relevant biomarkers. Results: We identified no genome-wide significant CpGs, but 163 and 56 differentially methylated regions for green30 and green500, respectively. Green30-related DNA methylation profiles showed enrichments in allergy, physical activity, and allostatic load, while green500-related methylation was enriched in allergy and allostatic load. Conclusions: Residential greenness may have health impacts through allergic sensitization, stress coping, or behavioral changes. Exposure to more proximal greenness may be more health-relevant.

Background and Aim. Previous studies have explored relationships of air pollution and metabolic profiles with lung function. However, the metabolites linking air pollution and lung function and associated mechanisms have not been reviewed from a life-course perspective. Accordingly, causal inference regarding health effects of single exposures or mixtures remains limited. Methods. We conducted a narrative review summarizing recent evidence on the associations of metabolic profiles with both air pollution exposure and lung function taking different stages of life into consideration (linking metabolites to exposure and outcome). Results. Thirty-two studies were included with 10 studies analyzing air pollution-related metabolic profiles, and 22 analyzing lung function-related metabolic profiles. A wide range of metabolites were identified being associated with short- and long-term exposure, partly overlapping with those linked to lung function in the general population and respiratory diseases such as asthma and COPD, including compounds of amino acid and lipid metabolism. The existing studies show that metabolomics offers potential to identify biomarkers linked to both environmental exposures and respiratory outcomes, which can improve exposure assessment, causal understanding, and identification of individuals at risk. However, many studies suffer from small sample size, cross-sectional designs, preponderance on adult lung function, heterogeneity in exposure assessment, lack of confounding control and omics integration. Conclusions: Studies with prospectively and repeatedly collected biological samples and harmonized exposure assessment are needed to get insights into mechanisms and causality of life-long respiratory effects of air pollution. The ongoing EXposome Powered tools for healthy living in urbAN Settings (EXPANSE) project aims at addressing some of the shortcomings of earlier studies by combining biospecimens from large European cohorts covering different age groups, along with harmonized air pollution exposure and exposome data. Keywords: metabolomics, lung function, spirometry, Chronic obstructive pulmonary disease (COPD), air pollution

This narrative review aims to appraise the current evidence on using biomarkers of obstructive nephropathy to predict the onset and progression of chronic kidney disease (CKD) in infants with posterior urethral valves (PUV). PUV is the most frequently reported congenital anomaly of the kidney and urinary tract (CAKUT) associated with bladder outlet obstruction in male children. It contributes significantly to the CKD burden in childhood. Despite different approaches for its postnatal repair, evidence-based data still suggest a high risk of CKD and end-stage kidney disease (ESKD) later in childhood. In obstructive nephropathy, glomerular and tubulointerstitial lesions contribute to renal impairment. Although it may be difficult to predict these adverse renal outcomes in repaired PUV, detecting and monitoring future CKD appears enhanced using the combination of serum creatinine- or cystatin C-based estimated glomerular filtration rate (eGFR) and albuminuria. Given the drawbacks of these conventional biomarkers, there is a paradigm shift to novel biomarkers as tools for the early identification of glomerular and tubulointerstitial lesions seen in obstructive nephropathy. Most novel biomarkers are yet to be fully applied to routine clinical practice globally. Nevertheless, there is substantial evidence showing that they form part of the emerging diagnostics for obstructive nephropathy. From the reviewed studies, urine transforming growth factor-beta 1 (TGF-β1) is the most prominent biomarker among the novel biomarkers of obstructive nephropathy. However, other novel approaches like the machine learning (ML) model (a form of health-related artificial intelligence) and urodynamic parameters like bladder contractility index hold promise for PUV outcomes prediction (PUVOP). Because of the association of urine TGF-β1 with urine angiotensin level (a biomarker of the renin-angiotensin-aldosterone system [RAAS]), early angiotensin-converting enzyme inhibitor (ACEI) therapy in patients with PUV may potentially retard the progression of CKD and improve renal outcomes. Thus, future research directions will be to explore the role of ACEI as a pre-emptive treatment for poor renal outcomes in post valve-ablation patients and to conduct longitudinal studies that would properly demonstrate these biomarkers as predictors of these outcomes.

Previous studies have explored the relationships of air pollution and metabolic profiles with lung function. However, the metabolites linking air pollution and lung function and the associated mechanisms have not been reviewed from a life-course perspective. Here, we provide a narrative review summarising recent evidence on the associations of metabolic profiles with air pollution exposure and lung function in children and adults. Twenty-six studies identified through a systematic PubMed search were included with 10 studies analysing air pollution-related metabolic profiles and 16 studies analysing lung function-related metabolic profiles. A wide range of metabolites were associated with short- and long-term exposure, partly overlapping with those linked to lung function in the general population and with respiratory diseases such as asthma and COPD. The existing studies show that metabolomics offers the potential to identify biomarkers linked to both environmental exposures and respiratory outcomes, but many studies suffer from small sample sizes, cross-sectional designs, a preponderance on adult lung function, heterogeneity in exposure assessment, lack of confounding control and omics integration. The ongoing EXposome Powered tools for healthy living in urbAN Settings (EXPANSE) project aims to address some of these shortcomings by combining biospecimens from large European cohorts and harmonised air pollution exposure and exposome data.

Aging populations in Africa face a growing burden of non-communicable diseases (NCDs), contextualized in broad external exposome and weak health systems. These could accelerate aging and shorten lifespan. DNA methylation (DNAm) epigenetic clocks allow investigation of biological aging, and perform well in high-income countries. However, their validity has rarely been tested in low- and middle-income countries. We investigated the performance of epigenetic clocks (as aging biomarkers), and their cardio-metabolic risk profiles among adults in south-central Côte d’Ivoire. We derived four measures of epigenetic clocks (i.e., HorvathAge, HannumAge, PhenoAge and GrimAge) and their corresponding epigenetic age acceleration (EAA; Intrinsic, Extrinsic, PhenoAA and GrimAA) using genome-wide DNAm data from 393 participants of the Côte d’Ivoire dual burden of disease study, aged 18–79 years. Epigenetic age exhibited strong correlations (0.83 ≤ Pearson’s r ≤ 0.93) but weaker concordance (0.73 ≤ Lin’s rC ≤ 0.85) with chronological age. Epigenetic clocks optimally predicted chronological age at 32 (HannumAge), 62 (HorvathAge) and 78 (GrimAge) years. Multivariable linear EAA models identified male sex (IEAA, EEAA and GrimAA), lower household wealth (EEAA and PhenoAA), high-risk alcohol intake (PhenoAA and GrimAA), smoking (GrimAA), physical activity (IEAA and GrimAA) and body mass index [BMI] (GrimAA) as independent determinants. Physical activity and BMI exhibited quadratic associations with GrimAA. Illustratively, GrimAge was accelerated in underweight and obese participants. Risk associations of GrimAA were largely driven by age-adjusted DNAm surrogate plasminogen activator inhibitor-1 (DNAmPAI-1) and pack years. Multivariable logistic models of cardio-metabolic phenotypes identified EEAA, PhenoAA and DNAmPAI-1 as determinants of high blood pressure, fasting glucose, triglycerides and metabolic syndrome severity. We provide evidence validating the applicability of epigenetic clocks as aging biomarkers and potential link between sociodemographic and lifestyle-related factors, and cardio-metabolic health in the underrepresented African population. Future longitudinal studies incorporating broad environmental aspects and age-related clinical outcomes should allow to pinpoint the clinical and public health utility of DNAm clocks as mediators in NCD trajectory, in low- and middle-income countries.

Urinary tract infection (UTI) in children is one of the most common bacterial infections that propels inappropriate antibiotic use. Long-term, potentially fatal complications can occur if not properly treated. Prompt investigation and appropriate treatment would prevent these complications. Although urine culture remains the gold standard investigation for UTI, its process is cumbersome and requires time (24–72 hours). Hence, there has been growing interest in the use of urinary biomarkers. However, some conventional urinary biomarkers detected on urinalysis have poor sensitivity values when used singly as a screening tool. Thus, the searchlight has shifted to the role of novel biomarkers in UTI diagnosis. This narrative review aimed to determine if elevated levels of these biomarkers directly correlate with positive urine cultures. A positive correlation may imply that these biomarkers could serve as novel UTI diagnostics and thus augment urine culture requests. Established and recent serum and urinary biomarkers show disparate predictive abilities for UTI and its related complications. Some have elevated differential levels in upper and lower UTI or febrile and non-febrile UTI. All studies that investigated these biomarkers established culture-positive UTI, highlighting a direct correlation between positive urine cultures and increased concentrations of the biomarkers in body fluids. Because certain uropathogens were less likely to be associated with pyuria, the sensitivities of some neutrophil-related novel biomarkers (such as urine neutrophil gelatinase-associated lipocalin and human neutrophil peptides 1–3) were reduced in cases of UTI caused by these bacteria. While levels of these novel biomarkers directly correlate with positive urine cultures, it appears that there is yet no standalone biomarker with the optimal sensitivity and specificity for UTI. Although these novel biomarkers are promising, translating their measurements into clinical practice with specific clinical utilities will take time. Novel methods interrogating high-throughput serum (and urine) metabolome data with positive urine cultures in a platform-agnostic manner (metabolome-wide approach) will help confirm and identify novel biomarkers that might capture specific aetiologic agents or shared pathways of related agents. The authors recommend that future research on UTI diagnostics should specifically focus on identifying highly sensitive and specific standalone novel biomarkers that can be easily applied as a point-of-care investigation.

Depression and cardiovascular disease (CVD) are main contributors to the global disease burden and are linked. Pathophysiological pathways through increased blood pressure (BP) are a common focus in studies aiming to explain the relationship. However, studies to date have not differentiated between the predictive effect of depression on the course of BP versus hypertension diagnosis. Hence, we aimed to elucidate this relationship by incorporating these novel aspects in the context of a cohort study. We included initially normotensive participants (n = 3214) from the second (2001–2003), third (2009–2011), and fourth (2016–2018) waves of the Swiss Cohort Study on Air Pollution and Lung and Heart Diseases in Adults (SAPALDIA). We defined depression based on physician diagnosis, depression treatment and/or SF-36 Mental Health score < 50. The prospective association between depression and BP change was quantified using multivariable censored regression models, and logistic regression for the association between depression and incident hypertension diagnosis. All models used clustered robust standard errors to account for repeat measurements. The age-related increase in systolic BP was slightly lower among people with depression at baseline (β = − 2.08 mmHg/10 years, 95% CI − 4.09 to − 0.07) compared to non-depressed. A similar trend was observed with diastolic BP (β = − 0.88 mmHg/10 years, 95% CI − 2.15 to 0.39), albeit weaker and not statistically significant. Depression predicted the incidence of hypertension diagnosis (OR 1.86, 95% CI 1.33 to 2.60). Our findings do not support the hypothesis that depression leads to CVD by increasing BP. Future research on the role of depression in the pathway to hypertension and CVD is warranted in larger cohorts, taking into account healthcare utilization as well as medication for depression and hypertension.

Previous research has shown that the built environment plays a crucial role for health-related quality of life (HRQoL) and health care utilization. But, there is limited evidence on the independence of this association from lifestyle and social environment. The objective of this cross-sectional study was to investigate these associations, independent of the social environment, physical activity and body mass index (BMI). We used data from the third follow-up of the Swiss study on Air Pollution and Lung and Heart diseases In Adults (SAPALDIA), a population based cohort with associated biobank. Covariate adjusted multiple quantile and polytomous logistic regressions were performed to test associations of variables describing the perceived built environment with HRQoL and health care utilization. Higher HRQoL and less health care utilization were associated with less reported transportation noise annoyance. Higher HRQoL was also associated with greater satisfaction with the living environment and more perceived access to greenspaces. These results were independent of the social environment (living alone and social engagement) and lifestyle (physical activity level and BMI). This study provides further evidence that the built environment should be designed to integrate living and green spaces but separate living and traffic spaces in order to improve health and wellbeing and potentially save health care costs.

Fidèle K. Bassa (  delebassa@ymail.com ) Université Félix Houphouët-Boigny: Universite Felix Houphouet-Boigny https://orcid.org/0000-0001-7127-8745 Ikenna C. Eze Swiss Tropical and Public Health Institute: Schweizerisches Tropenund Public Health-Institut Ru n K. Assaré Université Félix Houphouët-Boigny: Universite Felix Houphouet-Boigny Clémence Essé Université Félix Houphouët-Boigny: Universite Felix Houphouet-Boigny Siaka Koné Centre Suisse de Recherches Scienti ques en Cote d'Ivoire Félix Acka Institut National de Santé Publique: Institut National de Sante Publique Véronique Laubhouet-Ko Ligue ivoirienne contre l'hypertension artérielle et les maladies cardiovasculaires Dinard Kouassi Institut National de Santé Publique: Institut National de Sante Publique Bassirou Bonfoh Centre Suisse de Recherches Scienti ques en Cote d'Ivoire Jürg Utzinger Swiss Tropical and Public Health Institute: Schweizerisches Tropenund Public Health-Institut Eliezer K. N'Goran Université Félix Houphouët-Boigny: Universite Felix Houphouet-Boigny

Background and Aims: Evidence linking short-term traffic noise exposure to endothelial dysfunction and oxidative stress is growing. We aimed at characterizing the chronic inflammatory role of population-level noise exposures and thus investigated the relationship between long-term exposure to source-specific traffic noise and biomarkers of chronic inflammation.

STUDY OBJECTIVES The present study aimed at assessing the temporal non-rapid eye movement (NREM) EEG arousal distribution within and across sleep cycles and its modifications with aging and nighttime transportation noise exposure, factors that typically increase the incidence of EEG arousals. METHODS Twenty-six young (19-33 years, 12 women) and 16 older (52-70 years, 8 women) healthy volunteers underwent a 6-day polysomnographic laboratory study. Participants spent two noise-free nights and four transportation noise exposure nights, two with continuous and two characterized by eventful noise (average sound levels of 45 dB, maximum sound levels between 50 and 62 dB for eventful noise). Generalized mixed models were used to model the time course of EEG arousal rates during NREM sleep and included cycle, age, and noise as independent variables. RESULTS Arousal rate variation within NREM sleep cycles was best described by a u-shaped course with variations across cycles. Older participants had higher overall arousal rates than the younger individuals with differences for the first and the fourth cycle depending on the age group. During eventful noise nights, overall arousal rates were increased compared to noise-free nights. Additional analyses suggested that the arousal rate time course was partially mediated by slow wave sleep (SWS). CONCLUSIONS The characteristic u-shaped arousal rate time course indicates phases of reduced physiological sleep stability both at the beginning and end of NREM cycles. Small effects on the overall arousal rate by eventful noise exposure suggest a preserved physiological within- and across-cycle arousal evolution with noise exposure, while aging affected the shape depending on the cycle.

Prospective evidence on the risk of depression in relation to transportation noise exposure and noise annoyance is limited and mixed. We aimed to investigate the associations of long-term exposure to source-specific transportation noise and noise annoyance with incidence of depression in the SAPALDIA (Swiss cohort study on air pollution and lung and heart diseases in adults) cohort.We investigated 4,581 SAPALDIA participants without depression in the year 2001/2002. Corresponding one-year mean road, railway and aircraft day-evening-night noise (Lden) was calculated at the most exposed façade of the participants’ residential floors, and transportation noise annoyance was assessed on an 11-point scale. Incident cases of depression were identified in 2010/2011, and comprised participants reporting physician diagnosis, intake of antidepressant medication or having a short form-36 mental health score < 50. We used robust Poisson regressions to estimate the mutually adjusted relative risks (RR) and 95% confidence intervals (CI) of depression, independent of traffic-related air pollution and other potential confounders.Incidence of depression was 11 cases per 1,000 person-years. In single exposure models, we observed positive but in part, statistically non-significant associations (per 10 dB) of road traffic Lden [RR: 1.06 (0.93, 1.22)] and aircraft Lden [RR: 1.19 (0.93, 1.53)], and (per 1-point difference) of noise annoyance [RR: 1.05 (1.02, 1.08)] with depression risk. In multi-exposure model, noise annoyance effect remained unchanged, with weaker effects of road traffic Lden [(RR: 1.02 (0.89, 1.17)] and aircraft Lden [(RR: 1.17 (0.90, 1.50)]. However, there were statistically significant indirect effects of road traffic Lden [(β: 0.02 (0.01, 0.03)] and aircraft Lden [β: 0.01 (0.002, 0.02)] via noise annoyance. There were no associations with railway Lden in the single and multi-exposure models [(RRboth models: 0.88 (0.75, 1.03)]. We made similar findings among 2,885 non-movers, where the effect modification and cumulative risks were more distinct. Noise annoyance effect in non-movers was stronger among the insufficiently active (RR: 1.09; 95%CI: 1.02, 1.17; pinteraction = 0.07) and those with daytime sleepiness [RR: 1.07 (1.02, 1.12); pinteraction = 0.008]. Cumulative risks of Lden in non-movers showed additive tendencies for the linear cumulative risk [(RRper 10dB of combined sources: 1.31 (0.90, 1.91)] and the categorical cumulative risk [(RRtriple- vs. zero-source ≥45 dB: 2.29 (1.02, 5.14)], and remained stable to noise annoyance.Transportation noise level and noise annoyance may jointly and independently influence the risk of depression. Combined long-term exposures to noise level seems to be most detrimental, largely acting via annoyance. The moderation of noise annoyance effect by daytime sleepiness and physical activity further contribute to clarifying the involved mechanisms. More evidence is needed to confirm these findings for effective public health control of depression and noise exposure burden.

Noise exposure is affecting health-related quality of life (HRQoL). There are many modelling approaches linking specific noise sources with single health-related outcomes. However, an integrated approach is missing taking into account measured levels as well as noise annoyance and sensitivity and assessing their independent association with HRQoL domains. Therefore, we investigated the predictive association of most common transportation noise sources (aircraft, railway and road traffic) as well as transportation noise annoyance and noise sensitivity with HRQoL using data from SAPALDIA (Swiss Cohort Study on Air Pollution and Lung and Heart Diseases in Adults). We assessed 2035 subjects, who participated in the second and third wave of SAPALDIA (3&4) and had complete information on exposure, outcome and covariates. At SAPALDIA3, we calculated annual means (Lden) of source-specific transportation noise exposure at the most exposed facade of participant's dwelling floor height. Participants reported noise annoyance on the widely used 11-point ICBEN scale and answered to 10 questions assessing individual noise sensitivity. To assess the potentially predictive effect of these noise exposures, HRQoL was assessed about 8 years later (SAPALDIA4) using the SF-36. We performed predictive multiple quantile regression models to elucidate associations of noise parameters measured at SAPALDIA3 with median SF-36 scores at SAPALDIA4. Source-specific transportation noise exposures showed few yet not consistent associations with HRQoL scores. We observed statistically significant negative associations of transportation noise annoyance with HRQoL scores covering mental health components (adjusted difference in SF-36 mental health score between highest vs. lowest annoyance tertile: −2.54 (95%CI: −3.89; −1.20). Noise sensitivity showed strongest and most consistent associations with HRQoL scores covering both general and mental health components (adjusted difference in SF-36 scores between highest vs. lowest sensitivity tertile: Mental health −5.96 (−7.57; −4.36); general health −5.16 (−7.08; −3.24)). Within all noise parameters, we predominantly observed negative associations of noise sensitivity with HRQoL attaining a magnitude of potential clinical relevance. This implies that factors other than transportation noise exposure may be relevant for this exposure-outcome relation. Nonetheless, transportation noise annoyance showed relevant associations with mental health components, indicating a negative association of transportation noise with HRQoL.

Aims: Chronic exposure to nocturnal transportation noise has been linked to cardiovascular disorders with sleep impairment as the main mediator. Here we examined whether nocturnal transportation noise affects the main stress pathways, and whether it relates to changes in the macro and micro structure of sleep. Methods and results: Twenty-six young healthy participants (12 women, 24.6 +/- 0.7 years, mean +/- SE) spent five consecutive 24-h days and one last morning in the laboratory. The first (baseline) and last (recovery) nights comprised a quiet ambient scenario. In-between, four different noise scenarios (low/medium/high intermittent road or rail scenarios with an identical equivalent continuous sound level of 45 dB) were randomly presented during the 8-h nights. Participants felt more annoyed from the transportation noise scenarios compared to the quiet ambient scenario played back during the baseline and recovery nights (F-5(,1)17 = 10.2, p < 0.001). Nocturnal transportation noise did not significantly impact polysomnographically assessed sleep macrostructure, blood pressure, nocturnal catecholamine levels and morning cytokine levels. Evening cortisol levels increased after sleeping with highly intermittent road noise compared to baseline (p = 0.002, noise effect: F-4(,)83 = 4.0, p = 0.005), a result related to increased cumulative duration of autonomic arousals during the noise nights (F-5,(106) = 3.4, p < 0.001; correlation: r(pearson) = 0.64, p = 0.006). Conclusion: Under controlled laboratory conditions, highly intermittent nocturnal road noise exposure at 45 dB increased the cumulative duration of autonomic arousals during sleep and next-day evening cortisol levels. Our results indicate that, without impairing sleep macrostructure, nocturnal transportation noise of 45 dB is a physiological stressor that affects the hypothalamic-pituitary-adrenal axis during the following day in healthy young good sleepers.

BACKGROUND:Few epigenome-wide association studies (EWAS) on air pollutants exist, and none have been done on transportation noise exposures, which also contribute to environmental burden of disease. OBJECTIVE:We performed mutually independent EWAS on transportation noise and air pollution exposures. METHODS:We used data from two time points of the Swiss Cohort Study on Air Pollution and Lung and Heart Diseases in Adults (SAPALDIA) from 1,389 participants contributing 2,542 observations. We applied multiexposure linear mixed-effects regressions with participant-level random intercept to identify significant Cytosine-phosphate-Guanine (CpG) sites and differentially methylated regions (DMRs) in relation to 1-y average aircraft, railway, and road traffic day-evening-night noise (Lden); nitrogen dioxide (NO2); and particulate matter (PM) with aerodynamic diameter <2.5μm (PM2.5). We performed candidate (CpG-based; cross-systemic phenotypes, combined into "allostatic load") and agnostic (DMR-based) pathway enrichment tests, and replicated previously reported air pollution EWAS signals. RESULTS:We found no statistically significant CpGs at false discovery rate <0.05. However, 14, 48, 183, 8, and 71 DMRs independently associated with aircraft, railway, and road traffic Lden; NO2; and PM2.5, respectively, with minimally overlapping signals. Transportation Lden and air pollutants tendentially associated with decreased and increased methylation, respectively. We observed significant enrichment of candidate DNA methylation related to C-reactive protein and body mass index (aircraft, road traffic Lden, and PM2.5), renal function and "allostatic load" (all exposures). Agnostic functional networks related to cellular immunity, gene expression, cell growth/proliferation, cardiovascular, auditory, embryonic, and neurological systems development were enriched. We replicated increased methylation in cg08500171 (NO2) and decreased methylation in cg17629796 (PM2.5). CONCLUSIONS:Mutually independent DNA methylation was associated with source-specific transportation noise and air pollution exposures, with distinct and shared enrichments for pathways related to inflammation, cellular development, and immune responses. These findings contribute in clarifying the pathways linking these exposures and age-related diseases but need further confirmation in the context of mediation analyses. https://doi.org/10.1289/EHP6174.

AIMS: We investigated the cross-sectional associations of Plasmodium infection (PI) with fasting glucose (FG) and glycated hemoglobin (HbA1c) in malaria-endemic south-central Cote d'Ivoire. Methods: We studied 979 participants (non-pregnant; no treated diabetes; 51% males; 18-87 years) of the Cote d'Ivoire Dual Burden of Disease study. Fasting venous blood was obtained for PI, FG, and HbA1c assessment. We defined PI as a positive malaria rapid diagnostic test (RDT) or microscopic identification of Plasmodium species. We applied multivariable linear regressions to assess beta coefficients (beta) and 95% confidence intervals (CIs) of PI positivity for FG and HbA1c independent of diabetes risk factors. Results: Prevalence of PI was 10.1% (5.5% microscopy; 9.7% RDT) without clinical fever. Prevalence of FG-based prediabetes (45.8%) and diabetes (3.6%) were considerably higher than HbA1c-based values (2.7% and 0.7%, respectively). PI was independently associated with FG among participants with higher body temperature (beta 0.34, 95% CI 0.06-0.63, p(heterogeneity) = 0.028), or family history of diabetes (beta 0.88, 95% CI 0.28-1.47, p(heterogeneity) = 0.009). Similar patterns observed with HbA1c were obliterated on accounting for FG. We also observed consistent associations with parasite density. Conclusions: FG-based diabetes diagnosis in the presence of asymptomatic PI may misclassify or overestimate diabetes burden in malaria-endemic settings. Longitudinal studies are needed to confirm these findings and determine the risk for diabetes. (C) 2019 The Authors. Published by Elsevier B.V. This is an open access article under the CC BYNC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).