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1.
Diabetes Res Clin Pract ; 156: 107845, 2019 Sep 11.
Artigo em Inglês | MEDLINE | ID: mdl-31520711

RESUMO

AIMS: We investigated the cross-sectional associations of Plasmodium infection (PI) with fasting glucose (FG) and glycated hemoglobin (HbA1c) in malaria-endemic south-central Côte d'Ivoire. METHODS: We studied 979 participants (non-pregnant; no treated diabetes; 51% males; 18-87 years) of the Côte 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 (ß) 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 (ß 0.34, 95% CI 0.06-0.63, pheterogeneity = 0.028), or family history of diabetes (ß 0.88, 95% CI 0.28-1.47, pheterogeneity = 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.

2.
Sci Rep ; 9(1): 8818, 2019 Jun 19.
Artigo em Inglês | MEDLINE | ID: mdl-31217483

RESUMO

We aim to investigate to what extent a set of immune markers mediate the association between air pollution and adult-onset asthma. We considered long-term exposure to multiple air pollution markers and a panel of 13 immune markers in peripheral blood samples collected from 140 adult cases and 199 controls using a nested-case control design. We tested associations between air pollutants and immune markers and adult-onset asthma using mixed-effects (logistic) regression models, adjusted for confounding variables. In order to evaluate a possible mediating effect of the full set of immune markers, we modelled the relationship between asthma and air pollution with a partial least square path model. We observed a strong positive association of IL-1RA [OR 1.37; 95% CI (1.09, 1.73)] with adult-onset asthma. Univariate models did not yield any association between air pollution and immune markers. However, mediation analyses indicated that 15% of the effect of air pollution on risk of adult-onset asthma was mediated through the immune system when considering all immune markers as a latent variable (path coefficient (ß) = 0.09; 95% CI: (-0.02, 0.20)). This effect appeared to be stronger for allergic asthma (22%; ß = 0.12; 95% CI: (-0.03, 0.27)) and overweight subjects (27%; ß = 0.19; 95% CI: (-0.004, 0.38)). Our results provides supportive evidence for a mediating effect of the immune system in the association between air pollution and adult-onset asthma.

4.
Eur Respir J ; 54(1)2019 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-31073081

RESUMO

Previous reports link differential DNA methylation (DNAme) to environmental exposures that are associated with lung function. Direct evidence on lung function DNAme is, however, limited. We undertook an agnostic epigenome-wide association study (EWAS) on pre-bronchodilation lung function and its change in adults.In a discovery-replication EWAS design, DNAme in blood and spirometry were measured twice, 6-15 years apart, in the same participants of three adult population-based discovery cohorts (n=2043). Associated DNAme markers (p<5×10-7) were tested in seven replication cohorts (adult: n=3327; childhood: n=420). Technical bias-adjusted residuals of a regression of the normalised absolute ß-values on control probe-derived principle components were regressed on level and change of forced expiratory volume in 1 s (FEV1), forced vital capacity (FVC) and their ratio (FEV1/FVC) in the covariate-adjusted discovery EWAS. Inverse-variance-weighted meta-analyses were performed on results from discovery and replication samples in all participants and never-smokers.EWAS signals were enriched for smoking-related DNAme. We replicated 57 lung function DNAme markers in adult, but not childhood samples, all previously associated with smoking. Markers not previously associated with smoking failed replication. cg05575921 (AHRR (aryl hydrocarbon receptor repressor)) showed the statistically most significant association with cross-sectional lung function (FEV1/FVC: pdiscovery=3.96×10-21 and pcombined=7.22×10-50). A score combining 10 DNAme markers previously reported to mediate the effect of smoking on lung function was associated with lung function (FEV1/FVC: p=2.65×10-20).Our results reveal that lung function-associated methylation signals in adults are predominantly smoking related, and possibly of clinical utility in identifying poor lung function and accelerated decline. Larger studies with more repeat time-points are needed to identify lung function DNAme in never-smokers and in children.

5.
Artigo em Inglês | MEDLINE | ID: mdl-30791383

RESUMO

A high body mass (BMI) index has repeatedly been associated with non-atopic asthma, but the biological mechanism linking obesity to asthma is still poorly understood. We aimed to test the hypothesis that inflammation and/or innate immunity plays a role in the obesity-asthma link. DNA methylome was measured in blood samples of 61 non-atopic participants with asthma and 146 non-atopic participants without asthma (non-smokers for at least 10 years) taking part in the Swiss Cohort Study on Air Pollution and Lung and Heart Diseases in Adults (SAPALDIA) study. Modification by DNA methylation of the association of BMI or BMI change over 10 years with adult-onset asthma was examined at each CpG site and differentially methylated region. Pathway enrichment tests were conducted for genes in a priori curated inflammatory pathways and the NLRP3-IL1B-IL17 axis. The latter was chosen on the basis of previous work in mice. Inflammatory pathways including glucocorticoid/PPAR signaling (p = 0.0023), MAPK signaling (p = 0.013), NF-κB signaling (p = 0.031), and PI3K/AKT signaling (p = 0.031) were enriched for the effect modification of BMI, while NLRP3-IL1B-IL17 axis was enriched for the effect modification of BMI change over 10 years (p = 0.046). DNA methylation measured in peripheral blood is consistent with inflammation as a link between BMI and adult-onset asthma and with the NLRP3-IL1B-IL17 axis as a link between BMI change over 10 years and adult-onset asthma in non-atopic participants.


Assuntos
Asma/genética , Índice de Massa Corporal , Metilação de DNA , Inflamação/metabolismo , Adulto , Animais , Estudos de Coortes , Feminino , Humanos , Sistema de Sinalização das MAP Quinases , Masculino , Camundongos , NF-kappa B/metabolismo , Obesidade/complicações , PPAR gama/metabolismo
6.
Nat Genet ; 51(3): 481-493, 2019 03.
Artigo em Inglês | MEDLINE | ID: mdl-30804560

RESUMO

Reduced lung function predicts mortality and is key to the diagnosis of chronic obstructive pulmonary disease (COPD). In a genome-wide association study in 400,102 individuals of European ancestry, we define 279 lung function signals, 139 of which are new. In combination, these variants strongly predict COPD in independent populations. Furthermore, the combined effect of these variants showed generalizability across smokers and never smokers, and across ancestral groups. We highlight biological pathways, known and potential drug targets for COPD and, in phenome-wide association studies, autoimmune-related and other pleiotropic effects of lung function-associated variants. This new genetic evidence has potential to improve future preventive and therapeutic strategies for COPD.


Assuntos
Predisposição Genética para Doença/genética , Pulmão/fisiopatologia , Doença Pulmonar Obstrutiva Crônica/genética , Idoso , Idoso de 80 Anos ou mais , Estudos de Casos e Controles , Feminino , Estudo de Associação Genômica Ampla/métodos , Humanos , Masculino , Pessoa de Meia-Idade , Polimorfismo de Nucleotídeo Único/genética , Fatores de Risco , Fumar/genética
7.
Environ Int ; 125: 107-116, 2019 04.
Artigo em Inglês | MEDLINE | ID: mdl-30716571

RESUMO

BACKGROUND: Epidemiological evidence on the influence of long-term exposure to traffic-related particulate matter (TPM10) on heart rate variability (HRV) is weak. OBJECTIVE: To evaluate the association of long-term exposure (10 years) with TPM10 on the regulation of the autonomic cardiovascular system and heart rate dynamics (HRD) in an aging general population, as well as potential modifying effects by the a priori selected factors sex, smoking status, obesity, and gene variation in selected glutathione S-transferases (GSTs). METHODS: We analyzed data from 1593 SAPALDIA cohort participants aged ≥ 50 years. For each participant, various HRV and HRD parameters were derived from 24-hour electrocardiogram recordings. Each parameter obtained was then used as the outcome variable in multivariable mixed linear regression models in order to evaluate the association with TPM10. Potential modifying effects were assessed using interaction terms. RESULTS: No association between long-term exposure to TPM10 and HRV/HRD was observed in the entire study population. However, HRD changes were found in subjects without cardiovascular morbidity and both HRD and HRV changes in non-obese subjects without cardiovascular morbidity. Subjects without cardiovascular morbidity with homozygous GSTM1 gene deletion appeared to be more susceptible to the effects of TPM10. CONCLUSION: This study suggests that long-term exposure to TPM10 triggers adverse changes in the regulation of the cardiovascular system. These adverse effects were more visible in the subjects without cardiovascular disease, in whom the overall relationship between TPM10 and HRV/HRD could not be masked by underlying morbidities and the potential counteracting effects of related drug treatments.

8.
Respir Med ; 146: 116-123, 2019 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-30665509

RESUMO

INTRODUCTION: Restrictive spirometry pattern is an under-recognised disorder with a poor morbidity and mortality prognosis. We compared physical activity levels between adults with a restrictive spirometry pattern and with normal spirometry. METHODS: Restrictive spirometry pattern was defined as a having post-bronchodilator FEV1/FVC ≥ Lower Limit of Normal and a FVC<80% predicted in two population-based studies (ECRHS-III and SAPALDIA3). Physical activity was measured using the International Physical Activity Questionnaire. The odds of having low physical activity (<1st study-specific tertile) was evaluated using adjusted logistic regression models. RESULTS: Subjects with a restrictive spirometry pattern (n = 280/4721 in ECRHS, n = 143/3570 in SAPALDIA) reported lower levels of physical activity than those with normal spirometry (median of 1770 vs 2253 MET·min/week in ECRHS, and 3519 vs 3945 MET·min/week in SAPALDIA). Subjects with a restrictive spirometry pattern were more likely to report low physical activity (meta-analysis odds ratio: 1.41 [95%CI 1.07-1.86]) than those with a normal spirometry. Obesity, respiratory symptoms, co-morbidities and previous physical activity levels did not fully explain this finding. CONCLUSION: Adults with a restrictive spirometry pattern were more likely to report low levels of physical activity than those with normal spirometry. These results highlight the need to identify and act on this understudied but prevalent condition.

9.
Infect Dis Poverty ; 7(1): 105, 2018 Nov 06.
Artigo em Inglês | MEDLINE | ID: mdl-30396368

RESUMO

BACKGROUND: As a result of epidemiological transition, the health systems of low- and middle-income countries are increasingly faced with a dual disease burden of infectious diseases and emerging non-communicable diseases. Little is known about the mutual influence of these two disease groups. The aim of this study was to investigate the co-occurrence of helminth infections and diabetes mellitus in adults in Lao People's Democratic Republic (Lao PDR). METHODS: We conducted a cross-sectional study among 1600 randomly selected adults aged 35 and older from four different socio-economical and ecological provinces. Information on socio-demographics, risk factors and health conditions was obtained from personal interviews. Clinical assessments including anthropometry (height, weight, waist and hip circumference) and blood pressure measurements were also conducted. Diabetes was classified based on self-reported diagnoses and a point-of-care glycated haemoglobin (HbA1c) test from finger prick blood samples. Stool samples for helminth diagnosis were examined with formalin-ether concentration technique for intestinal parasitic infections. The independent associations of helminth infections with diabetic status and HbA1c were assessed using multiple regression analyses. RESULTS: The prevalence of pre-diabetes and diabetes was 37.3% and 22.8%, respectively. Fifty-six percent of diabetic cases were undiagnosed and 85% of diagnosed diabetic cases had poor glycemic control. Participants from rural areas and from southern parts of the country had higher infection rates, with Opisthorchis viverrini, being the most common helminth infection (30.5%). We found a positive association between Taenia spp. infections and HbA1c (ß = 0.117; 95% CI: 0.042-0.200) and diabetes mellitus risk (OR = 2.98; 95% CI: 1.10-8.05). No other helminth species was associated with glycated hemoglobin. CONCLUSIONS: Hyperglycaemia and diabetic rates in Lao PDR are alarmingly high, but consistent with other high rates in the region. Given the high rates of under-diagnosis and poorly-controlled glycaemia in diabetes mellitus patients, routine diabetes screening and treatment is essential for the local healthcare system. Large longitudinal cohorts integrating biomarkers are warranted in the search of causal diabetes mellitus risk factors in the region. Common intestinal helminth infections, including O. viverrini, are unlikely to explain the high diabetes mellitus rates observed.

10.
Wellcome Open Res ; 3: 4, 2018.
Artigo em Inglês | MEDLINE | ID: mdl-30175238

RESUMO

Background: Over 90 regions of the genome have been associated with lung function to date, many of which have also been implicated in chronic obstructive pulmonary disease. Methods: We carried out meta-analyses of exome array data and three lung function measures: forced expiratory volume in one second (FEV 1), forced vital capacity (FVC) and the ratio of FEV 1 to FVC (FEV 1/FVC). These analyses by the SpiroMeta and CHARGE consortia included 60,749 individuals of European ancestry from 23 studies, and 7,721 individuals of African Ancestry from 5 studies in the discovery stage, with follow-up in up to 111,556 independent individuals. Results: We identified significant (P<2·8x10 -7) associations with six SNPs: a nonsynonymous variant in RPAP1, which is predicted to be damaging, three intronic SNPs ( SEC24C, CASC17 and UQCC1) and two intergenic SNPs near to LY86 and FGF10. Expression quantitative trait loci analyses found evidence for regulation of gene expression at three signals and implicated several genes, including TYRO3 and PLAU. Conclusions: Further interrogation of these loci could provide greater understanding of the determinants of lung function and pulmonary disease.

11.
Respir Res ; 19(1): 156, 2018 Aug 22.
Artigo em Inglês | MEDLINE | ID: mdl-30134983

RESUMO

BACKGROUND: The pathophysiological role of SERPINA1 in respiratory health may be more strongly determined by the regulation of its expression than by common genetic variants. A family based study of predominantly smoking adults found methylation at two Cytosine-phosphate-Guanine sites (CpGs) in SERPINA1 gene to be associated with chronic obstructive pulmonary disease risk. The objective of this study was to confirm the association of lung function with SERPINA1 methylation in general population samples by testing a comprehensive set of CpGs in the SERPINA gene cluster. We considered lung function level and decline in adult smokers from three European population-based cohorts and lung function level and growth in tobacco-smoke exposed children from a birth cohort. METHODS: DNA methylation using Illumina Infinium Human Methylation 450 k and EPIC beadchips and lung function were measured at two time points in 1076 SAPALDIA, ECRHS and NFBC adult cohort participants and 259 ALSPAC children. Associations of methylation at 119 CpG sites in the SERPINA gene cluster (PP4R4-SERPINA13P) with lung functions and circulating alpha-1-antitripsin (AAT) were assessed using multivariable cross-sectional and longitudinal regression models. RESULTS: Methylation at cg08257009 in the SERPINA gene cluster, located 32 kb downstream of SERPINA1, not annotated to a gene, was associated with FEV1/FVC at the Bonferroni corrected level in adults, but not in children. None of the methylation signals in the SERPINA1 gene showed associations with lung function after correcting for multiple testing. CONCLUSIONS: The results do not support a role of SERPINA1 gene methylation as determinant of lung function across the life course in the tobacco smoke exposed general population exposed.

13.
Nat Genet ; 50(8): 1072-1080, 2018 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-30013184

RESUMO

Allergic rhinitis is the most common clinical presentation of allergy, affecting 400 million people worldwide, with increasing incidence in westernized countries1,2. To elucidate the genetic architecture and understand the underlying disease mechanisms, we carried out a meta-analysis of allergic rhinitis in 59,762 cases and 152,358 controls of European ancestry and identified a total of 41 risk loci for allergic rhinitis, including 20 loci not previously associated with allergic rhinitis, which were confirmed in a replication phase of 60,720 cases and 618,527 controls. Functional annotation implicated genes involved in various immune pathways, and fine mapping of the HLA region suggested amino acid variants important for antigen binding. We further performed genome-wide association study (GWAS) analyses of allergic sensitization against inhalant allergens and nonallergic rhinitis, which suggested shared genetic mechanisms across rhinitis-related traits. Future studies of the identified loci and genes might identify novel targets for treatment and prevention of allergic rhinitis.

14.
Environ Int ; 120: 11-21, 2018 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-30055357

RESUMO

BACKGROUND: One of the potential mechanisms linking air pollution to health effects is through changes in DNA-methylation, which so far has mainly been analyzed globally or at candidate sites. OBJECTIVE: We investigated the association of personal and ambient air pollution exposure measures with genome-wide DNA-methylation changes. METHODS: We collected repeated 24-hour personal and ambient exposure measurements of particulate matter (PM2.5), PM2.5 absorbance, and ultrafine particles (UFP) and peripheral blood samples from a panel of 157 healthy non-smoking adults living in four European countries. We applied univariate mixed-effects models to investigate the association between air pollution and genome-wide DNA-methylation perturbations at single CpG (cytosine-guanine dinucleotide) sites and in Differentially Methylated Regions (DMRs). Subsequently, we explored the association of air pollution-induced methylation alterations with gene expression and serum immune marker levels measured in the same subjects. RESULTS: Personal exposure to PM2.5 was associated with methylation changes at 13 CpG sites and 69 DMRs. Two of the 13 identified CpG sites (mapped to genes KNDC1 and FAM50B) were located within these DMRs. In addition, 42 DMRs were associated with personal PM2.5 absorbance exposure, 16 DMRs with personal exposure to UFP, 4 DMRs with ambient exposure to PM2.5, 16 DMRs with ambient PM2.5 absorbance exposure, and 15 DMRs with ambient UFP exposure. Correlation between methylation levels at identified CpG sites and gene expression and immune markers was generally moderate. CONCLUSION: This study provides evidence for an association between 24-hour exposure to air pollution and DNA-methylation at single sites and regional clusters of CpGs. Analysis of differentially methylated regions provides a promising avenue to further explore the subtle impact of environmental exposures on DNA-methylation.

15.
Environ Int ; 119: 334-345, 2018 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-29990954

RESUMO

BACKGROUND: Epidemiologic evidence indicates common risk factors, including air pollution exposure, for respiratory and cardiovascular diseases, suggesting the involvement of common altered molecular pathways. OBJECTIVES: The goal was to find intermediate metabolites or metabolic pathways that could be associated with both air pollutants and health outcomes ("meeting-in-the-middle"), thus shedding light on mechanisms and reinforcing causality. METHODS: We applied a statistical approach named 'meet-in-the-middle' to untargeted metabolomics in two independent case-control studies nested in cohorts on adult-onset asthma (AOA) and cardio-cerebrovascular diseases (CCVD). We compared the results to identify both common and disease-specific altered metabolic pathways. RESULTS: A novel finding was a strong association of AOA with ultrafine particles (UFP; odds ratio 1.80 [1.26, 2.55] per increase by 5000 particles/cm3). Further, we have identified several metabolic pathways that potentially mediate the effect of air pollution on health outcomes. Among those, perturbation of Linoleate metabolism pathway was associated with air pollution exposure, AOA and CCVD. CONCLUSIONS: Our results suggest common pathway perturbations may occur as a consequence of chronic exposure to air pollution leading to increased risk for both AOA and CCVD.

16.
Thorax ; 73(9): 825-832, 2018 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-29720562

RESUMO

BACKGROUND: It has been debated, but not yet established, whether increased airway responsiveness can predict COPD. Recognising this link may help in identifying subjects at risk. OBJECTIVE: We studied prospectively whether airway responsiveness is associated with the risk of developing COPD. METHODS: We pooled data from two multicentre cohort studies that collected data from three time points using similar methods (European Community Respiratory Health Survey and Swiss Cohort Study on Air Pollution and Lung and Heart Diseases in Adults). We classified subjects (median age 37 years, 1st-3rd quartiles: 29-44) by their level of airway responsiveness using quintiles of methacholine dose-response slope at the first examination (1991-1994). Then, we excluded subjects with airflow obstruction at the second examination (1999-2003) and analysed incidence of COPD (postbronchodilator FEV1/FVC below the lower limit of normal) at the third examination (2010-2014) as a function of responsiveness, adjusting for sex, age, education, body mass index, history of asthma, smoking, occupational exposures and indicators of airway calibre. RESULTS: We observed 108 new cases of COPD among 4205 subjects during a median time of 9 years. Compared with the least responsive group (incidence rate 0.6 per 1000/year), adjusted incidence rate ratios for COPD ranged from 1.79 (95% CI 0.52 to 6.13) to 8.91 (95% CI 3.67 to 21.66) for increasing airway responsiveness. Similar dose-response associations were observed between smokers and non-smokers, and stronger associations were found among subjects without a history of asthma or asthma-like symptoms. CONCLUSIONS: Our study suggests that increased airway responsiveness is an independent risk factor for COPD. Further research should clarify whether early treatment in patients with high responsiveness can slow down disease progression.

17.
Atherosclerosis ; 270: 166-172, 2018 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-29432934

RESUMO

BACKGROUND AND AIMS: Alpha-1 antitrypsin (A1AT) is the most abundant serine protease inhibitor in human blood and exerts important anti-inflammatory and immune-modulatory effects. In combination with smoking or other long-term noxious exposures such as occupational dust and fumes, genetic A1AT deficiency can cause chronic obstructive pulmonary disease, a condition with elevated cardiovascular risk. The effects of A1AT deficiency on cardiovascular risk have hardly been studied today. METHODS: Using data from 2614 adults from the population-based SAPALDIA cohort, we tested associations of serum A1AT and SERPINA1 mutations with carotid intima-media thickness (CIMT, measured by B-mode ultrasonography) or self-reported arterial hypertension or cardiovascular disease in multiple regression models using a Mendelian Randomization like analysis design. Mutations Pi-S and Pi-Z were coded as ordinal genotype score (MM, MS, MZ/SS, SZ and ZZ), according to their progressive biological impact. RESULTS: Serum A1AT concentration presented a u-shaped association with CIMT. At the lower end of the A1AT distribution, an analogous, linear association between SERPINA1 score and higher CIMT was observed, resulting in an estimated 1.2% (95%-confidence interval -0.1-2.5) increase in CIMT per unit (p = 0.060). Genotype score was significantly associated with arterial hypertension with an odds ratio (OR) of 1.2 (1.0-1.5) per unit (p = 0.028). The association with cardiovascular disease was not significant (OR 1.3 (0.9-1.9)). CONCLUSIONS: Our results support a possible causal relationship between genetic A1AT deficiency and increased cardiovascular risk, which needs to be better taken into account for the management of affected patients and first-degree relatives.

18.
Environ Res ; 160: 247-255, 2018 01.
Artigo em Inglês | MEDLINE | ID: mdl-29031214

RESUMO

Oxidative potential (OP) of particulate matter (PM) is proposed as a biologically-relevant exposure metric for studies of air pollution and health. We aimed to evaluate the spatial variability of the OP of measured PM2.5 using ascorbate (AA) and (reduced) glutathione (GSH), and develop land use regression (LUR) models to explain this spatial variability. We estimated annual average values (m-3) of OPAA and OPGSH for five areas (Basel, CH; Catalonia, ES; London-Oxford, UK (no OPGSH); the Netherlands; and Turin, IT) using PM2.5 filters. OPAA and OPGSH LUR models were developed using all monitoring sites, separately for each area and combined-areas. The same variables were then used in repeated sub-sampling of monitoring sites to test sensitivity of variable selection; new variables were offered where variables were excluded (p > .1). On average, measurements of OPAA and OPGSH were moderately correlated (maximum Pearson's maximum Pearson's R = = .7) with PM2.5 and other metrics (PM2.5absorbance, NO2, Cu, Fe). HOV (hold-out validation) R2 for OPAA models was .21, .58, .45, .53, and .13 for Basel, Catalonia, London-Oxford, the Netherlands and Turin respectively. For OPGSH, the only model achieving at least moderate performance was for the Netherlands (R2 = .31). Combined models for OPAA and OPGSH were largely explained by study area with weak local predictors of intra-area contrasts; we therefore do not endorse them for use in epidemiologic studies. Given the moderate correlation of OPAA with other pollutants, the three reasonably performing LUR models for OPAA could be used independently of other pollutant metrics in epidemiological studies.


Assuntos
Monitoramento Ambiental , Modelos Teóricos , Material Particulado/análise , Meio Ambiente , Europa (Continente) , Oxirredução , Análise de Regressão
19.
Artigo em Inglês | MEDLINE | ID: mdl-29194408

RESUMO

Traffic noise has been linked to diabetes, with limited understanding of its mechanisms. We hypothesize that night-time road traffic noise (RTN) may impair glucose homeostasis through circadian rhythm disturbances. We prospectively investigated the relationship between residential night-time RTN and subsequent eight-year change in glycosylated hemoglobin (ΔHbA1c) in 3350 participants of the Swiss Cohort Study on Air Pollution and Lung and Heart Diseases in Adults (SAPALDIA), adjusting for diabetes risk factors and air pollution levels. Annual average RTN (Lnight) was assigned to participants in 2001 using validated Swiss noise models. HbA1c was measured in 2002 and 2011 using liquid chromatography. We applied mixed linear models to explore RTN-ΔHbA1c association and its modification by a genetic risk score of six common circadian-related MTNR1B variants (MGRS). A 10 dB difference in RTN was associated with a 0.02% (0.003-0.04%) increase in mean ΔHbA1c in 2142 non-movers. RTN-ΔHbA1c association was modified by MGRS among diabetic participants (Pinteraction = 0.001). A similar trend in non-diabetic participants was non-significant. Among the single variants, we observed strongest interactions with rs10830963, an acknowledged diabetes risk variant also implicated in melatonin profile dysregulation. Night-time RTN may impair glycemic control, especially in diabetic individuals, through circadian rhythm disturbances. Experimental sleep studies are needed to test whether noise control may help individuals to attain optimal glycemic levels.


Assuntos
Glicemia , Exposição Ambiental/efeitos adversos , Hemoglobina A Glicada/análise , Ruído dos Transportes/efeitos adversos , Adulto , Idoso , Idoso de 80 Anos ou mais , Estudos de Coortes , Feminino , Variação Genética , Habitação , Humanos , Modelos Lineares , Masculino , Melatonina/metabolismo , Pessoa de Meia-Idade , Receptor MT1 de Melatonina/genética , Fatores de Risco , Sono , Suíça
20.
JMIR Res Protoc ; 6(10): e210, 2017 Oct 27.
Artigo em Inglês | MEDLINE | ID: mdl-29079553

RESUMO

BACKGROUND: Individual-level concomitance of infectious diseases and noncommunicable diseases (NCDs) is poorly studied, despite the reality of this dual disease burden for many low- and middle-income countries (LMICs). OBJECTIVE: This study protocol describes the implementation of a cohort and biobank aiming for a better understanding of interrelation of helminth and Plasmodium infections with NCD phenotypes like metabolic syndrome, hypertension, and diabetes. METHODS: A baseline cross-sectional population-based survey was conducted over one year, in the Taabo health and demographic surveillance system (HDSS) in south-central Côte d'Ivoire. We randomly identified 1020 consenting participants aged ≥18 years in three communities (Taabo-Cité, Amani-Ménou, and Tokohiri) reflecting varying stages of epidemiological transition. Participants underwent health examinations consisting of NCD phenotyping (anthropometry, blood pressure, renal function, glycemia, and lipids) and infectious disease testing (infections with soil-transmitted helminths, schistosomes, and Plasmodium). Individuals identified to have elevated blood pressure, glucose, lipids, or with infections were referred to the central/national health center for diagnostic confirmation and treatment. Aliquots of urine, stool, and venous blood were stored in a biobank for future exposome/phenome research. In-person interviews on sociodemographic attributes, risk factors for infectious diseases and NCDs, medication, vaccinations, and health care were also conducted. Appropriate statistical techniques will be applied in exploring the concomitance of infectious diseases and NCDs and their determinants. Participants' consent for follow-up contact was obtained. RESULTS: Key results from this baseline study, which will be published in peer-reviewed literature, will provide information on the prevalence and co-occurrence of infectious diseases, NCDs, and their risk factors. The Taabo HDSS consists of rural and somewhat more urbanized areas, allowing for comparative studies at different levels of epidemiological transition. An HDSS setting is ideal as a basis for longitudinal studies since their sustainable field work teams hold close contact with the local population. CONCLUSIONS: The collaboration between research institutions, public health organizations, health care providers, and staff from the Taabo HDSS in this study assures that the synthesized evidence will feed into health policy towards integrated infectious disease-NCD management. The preparation of health systems for the dual burden of disease is pressing in low- and middle-income countries. The established biobank will strengthen the local research capacity and offer opportunities for biomarker studies to deepen the understanding of the cross-talk between infectious diseases and NCDs. TRIAL REGISTRATION: International Standard Randomized Controlled Trials Number (ISRCTN): 87099939; http://www.isrctn.com/ISRCTN87099939 (Archived by WebCite at http://www.webcitation.org/6uLEs1EsX).

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