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1.
Eur J Oral Sci ; 128(6): 508-517, 2020 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-33073429

RESUMO

In this cross-sectional study, the prevalences of tooth loss, prosthetic dental restorations, and probing pocket depths (PPD) ≥4 mm, and their relationship to sociodemographic factors, were investigated in older Swiss adults. There were up to 1,673 participants aged ≥55 yr in the fourth survey of the Swiss Cohort Study on Air Pollution And Lung And Heart Disease In Adults (SAPALDIA4). Missing teeth, prosthetic dental restorations, and PPD ≥4 mm were recorded in clinical examinations conducted by field workers and compared with self-reported information from questionnaires. Examination data showed that participants were missing five teeth on average, 74.8% had a prosthetic dental restoration, and 21.1% had PPD of ≥4 mm. The mean number of missing teeth and the prevalences of tooth loss, fixed dental prostheses, and removable dental prostheses were associated with age, education level, smoking status, and time since last visit to a dentist. Comparison of data obtained by field workers and that from self-reports show a high level of agreement for the number of missing teeth and the prevalence of removable dental prostheses, but a lower level of agreement for self-reports of fixed dental prostheses and periodontitis.

2.
Environ Int ; 144: 106014, 2020 11.
Artigo em Inglês | MEDLINE | ID: mdl-32763645

RESUMO

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 [(ß: 0.02 (0.01, 0.03)] and aircraft Lden [ß: 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.

3.
Environ Int ; 143: 105960, 2020 10.
Artigo em Inglês | MEDLINE | ID: mdl-32682053

RESUMO

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.

4.
Am J Epidemiol ; 189(12): 1521-1528, 2020 12 01.
Artigo em Inglês | MEDLINE | ID: mdl-32510134

RESUMO

We estimated the association between regular physical activity and the incidence of restrictive spirometry pattern. Forced expiratory volume in 1 second (FEV1), forced vital capacity (FVC), and physical activity were assessed in 2 population-based European cohorts (European Community Respiratory Health Survey: n = 2,757, aged 39-67 years; and Swiss Study on Air Pollution and Lung and Heart Diseases in Adults: n = 2,610, aged 36-82 years) first in 2000-2002 and again approximately 10 years later (2010-2013). Subjects with restrictive or obstructive spirometry pattern at baseline were excluded. We assessed the association of being active at baseline (defined as being physically active at least 2-3 times/week for ≥1 hour) with restrictive spirometry pattern at follow-up (defined as a postbronchodilation FEV1/FVC ratio of at least the lower limit of normal and FVC of <80% predicted) using modified Poisson regression, adjusting for relevant confounders. After 10 years of follow-up, 3.3% of participants had developed restrictive spirometry pattern. Being physically active was associated with a lower risk of developing this phenotype (relative risk = 0.76, 95% confidence interval: 0.59, 0.98). This association was stronger among those who were overweight and obese than among those of normal weight (P for interaction = 0.06). In 2 large European studies, adults practicing regular physical activity were at lower risk of developing restrictive spirometry pattern over 10 years.


Assuntos
Exercício Físico/fisiologia , Volume Expiratório Forçado , Transtornos Respiratórios/epidemiologia , Capacidade Vital , Adulto , Idoso , Idoso de 80 Anos ou mais , Europa (Continente)/epidemiologia , Feminino , Humanos , Incidência , Estudos Longitudinais , Masculino , Pessoa de Meia-Idade , Espirometria
5.
BMC Pulm Med ; 20(1): 171, 2020 Jun 16.
Artigo em Inglês | MEDLINE | ID: mdl-32546146

RESUMO

BACKGROUND: Low lung function has been associated with increased body mass index (BMI). The aim of this study was to investigate whether the effect of BMI on lung function is mediated by DNA methylation. METHODS: We used individual data from 285,495 participants in four population-based cohorts: the European Community Respiratory Health Survey, the Northern Finland Birth Cohort 1966, the Swiss Study on Air Pollution and Lung Disease in Adults, and the UK Biobank. We carried out Mendelian randomisation (MR) analyses in two steps using a two-sample approach with SNPs as instrumental variables (IVs) in each step. In step 1 MR, we estimated the causal effect of BMI on peripheral blood DNA methylation (measured at genome-wide level) using 95 BMI-associated SNPs as IVs. In step 2 MR, we estimated the causal effect of DNA methylation on FEV1, FVC, and FEV1/FVC using two SNPs acting as methQTLs occurring close (in cis) to CpGs identified in the first step. These analyses were conducted after exclusion of weak IVs (F statistic < 10) and MR estimates were derived using the Wald ratio, with standard error from the delta method. Individuals whose data were used in step 1 were not included in step 2. RESULTS: In step 1, we found that BMI might have a small causal effect on DNA methylation levels (less than 1% change in methylation per 1 kg/m2 increase in BMI) at two CpGs (cg09046979 and cg12580248). In step 2, we found no evidence of a causal effect of DNA methylation at cg09046979 on lung function. We could not estimate the causal effect of DNA methylation at cg12580248 on lung function as we could not find publicly available data on the association of this CpG with SNPs. CONCLUSIONS: To our knowledge, this is the first paper to report the use of a two-step MR approach to assess the role of DNA methylation in mediating the effect of a non-genetic factor on lung function. Our findings do not support a mediating effect of DNA methylation in the association of lung function with BMI.

6.
Environ Health Perspect ; 128(6): 67003, 2020 06.
Artigo em Inglês | MEDLINE | ID: mdl-32484729

RESUMO

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.


Assuntos
Poluição do Ar/estatística & dados numéricos , Exposição Ambiental/estatística & dados numéricos , Ruído dos Transportes/estatística & dados numéricos , Adulto , Poluentes Atmosféricos , Aeronaves , Estudos de Coortes , DNA , Metilação de DNA/fisiologia , Feminino , Humanos , Modelos Lineares , Masculino , Pessoa de Meia-Idade , Dióxido de Nitrogênio , Material Particulado
7.
Swiss Med Wkly ; 150: w20266, 2020 Jun 15.
Artigo em Inglês | MEDLINE | ID: mdl-32579698

RESUMO

BACKGROUND: Non-communicable diseases (NCDs) account for the vast majority of deaths in Switzerland. Insufficient physical activity (PA) is an established NCD risk factor and PA is known to be beneficial for physical and mental wellbeing. Sedentary behaviour (SB) is an additional, independent risk factor and associated with frailty in older adults. This study aimed at describing cross-sectional PA patterns in a general population sample of subjects aged 52 years and older (52+) from eight areas across different language regions of Switzerland. Additionally, the predictive association of self-reported PA for objectively measured PA was tested. METHODS: Participants 52+ of the Swiss Cohort Study on Air Pollution And Lung and Heart Disease In Adults (SAPALDIA) who completed accelerometer data collection at the most recent follow-up (SAPALDIA4 in 2017/18) and provided information on determinants of interest (sex, age, body mass index [BMI], language region, education, employment status, civil status, smoking) were included in the analysis (n = 1314). The accelerometer-derived average time spent in different PA intensities (SB, light PA [LPA], moderate-to-vigorous PA [MVPA]) was estimated according to participant characteristics with control for season and wear time using multiple linear regressions. In further analyses, the predictive effect of changes in self-reported PA over roughly ten years between SAPALDIA2 (2001/02) and SAPALDIA3 (2010/11) (remaining inactive [RI]; becoming inactive [BI]; becoming active [BA]; remaining active [RA]) on the objectively measured SB, LPA and MVPA obtained seven years later by accelerometry (SAPALDIA4), was assessed using multiple linear regression models. RESULTS: Overall, 21.7% of 52+ participants met the Swiss recommendations for subjectively assessed PA. Obese participants, 75+ year-olds, smokers and subjects living alone spent more time in SB and less time in LPA and MVPA compared with participants with a BMI below 25 kg/m2, between 52 and 64 years old, not smoking and being married, respectively. Residents living in the French-speaking part of Switzerland were less likely to engage in MVPA compared with residents from the German-speaking part and thus were less likely to meet the PA recommendations. A trend for increasing PA and decreasing SB was observed consistently across the four groups (RI, BI, BA, RA) of predictive self-reported PA patterns with participants remaining active over the course of roughly ten years showing highest levels of PA and lowest levels of SB measured objectively at SAPALDIA4. CONCLUSION: The high proportion of SB points to the need of physical activity promotion for the older part of the population in Switzerland. According to our data, behavioural changes in PA are possible and sustainable as we can see in the group of participants becoming active and this is essential for health promotion recommendations.

8.
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.

9.
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.


Assuntos
Poluentes Atmosféricos/toxicidade , Frequência Cardíaca/efeitos dos fármacos , Material Particulado/toxicidade , Idoso , Poluentes Atmosféricos/análise , Doenças Cardiovasculares/induzido quimicamente , Estudos de Coortes , Feminino , Seguimentos , Glutationa Transferase/genética , Voluntários Saudáveis , Humanos , Modelos Lineares , Masculino , Pessoa de Meia-Idade , Obesidade/induzido quimicamente , Material Particulado/análise , Fumar
10.
Respir Med ; 146: 116-123, 2019 01.
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.


Assuntos
Exercício Físico/fisiologia , Pneumopatias Obstrutivas/fisiopatologia , Pulmão/fisiopatologia , Espirometria/efeitos adversos , Índice de Massa Corporal , Estudos Transversais , Europa (Continente)/epidemiologia , Feminino , Volume Expiratório Forçado/efeitos dos fármacos , Humanos , Pneumopatias Obstrutivas/epidemiologia , Masculino , Pessoa de Meia-Idade , Obesidade/epidemiologia , Prevalência , Estudos Prospectivos , Testes de Função Respiratória/métodos , Espirometria/métodos , Capacidade Vital/efeitos dos fármacos
11.
Environ Int ; 123: 399-406, 2019 02.
Artigo em Inglês | MEDLINE | ID: mdl-30622064

RESUMO

BACKGROUND: Epidemiological research on transportation noise uses different exposure assessment strategies based on façade point estimates or regulatory noise maps. The degree of exposure measurement error and subsequent potentially biased risk estimates related to exposure definition is unclear. We aimed to evaluate associations between transportation noise exposure and myocardial infarction (MI) mortality considering: assumptions about residential floor, façade point selection (loudest, quietest, nearest), façade point vs. noise map estimates, and influence of averaging exposure at coarser spatial scales (e.g. in ecological health studies). METHODS: Lden from the façade points were assigned to >4 million eligible adults in the Swiss National Cohort for the best match residential floor (reference), middle floor, and first floor. For selected floors, the loudest and quietest exposed façades per dwelling, plus the nearest façade point to the residential geocode, were extracted. Exposure was also assigned from 10 × 10 m noise maps, using "buffers" from 50 to 500 m derived from the maps, and by aggregating the maps to larger areas. Associations between road traffic and railway noise and MI mortality were evaluated by multi-pollutant Cox regression models, adjusted for aircraft noise, NO2 and socio-demographic confounders, following individuals from 2000 to 2008. Bias was calculated to express differences compared to the reference. RESULTS: Hazard ratios (HRs) for the best match residential floor were 1.05 (1.02-1.07) and 1.03 (1.01-1.05) per IQR (11.3 and 15.0 dB) for road traffic and railway noise, respectively. In most situations, comparing the alternative exposure definitions to this reference resulted in attenuated HRs. For example, assuming everyone resided on the middle or everyone on first floor introduced little bias (%Bias in excess risk: -1.9 to 4.4 road traffic and -4.4 to 10.7 railway noise). Using the noise grids generated a bias of approximately -26% for both sources. Averaging the maps at a coarser spatial scale led to bias from -19.4 to -105.1% for road traffic and 17.6 to -34.3% for railway noise and inflated the confidence intervals such that some HRs were no longer statistically significant. CONCLUSION: Changes in spatial scale introduced more bias than changes in residential floor. Use of noise maps to represent residential exposure may underestimate noise-induced health effects, in particular for small-scale heterogeneously distributed road traffic noise in urban settings.


Assuntos
Exposição Ambiental/análise , Infarto do Miocárdio/mortalidade , Ruído dos Transportes/efeitos adversos , Adulto , Aeronaves , Estudos de Coortes , Feminino , Habitação , Humanos , Masculino , Pessoa de Meia-Idade , Infarto do Miocárdio/etiologia , Modelos de Riscos Proporcionais , Medição de Risco , Suíça/epidemiologia , Transportes
12.
Eur Heart J ; 40(7): 598-603, 2019 02 14.
Artigo em Inglês | MEDLINE | ID: mdl-30357335

RESUMO

AIMS: The present study aimed to disentangle the risk of the three major transportation noise sources-road, railway, and aircraft traffic-and the air pollutants NO2 and PM2.5 on myocardial infarction (MI) mortality in Switzerland based on high quality/fine resolution exposure modelling. METHODS AND RESULTS: We modelled long-term exposure to outdoor road traffic, railway, and aircraft noise levels, as well as NO2 and PM2.5 concentration for each address of the 4.40 million adults (>30 years) in the Swiss National Cohort (SNC). We investigated the association between transportation noise/air pollution exposure and death due to MI during the follow-up period 2000-08, by adjusting noise [Lden(Road), Lden(Railway), and Lden(Air)] estimates for NO2 and/or PM2.5 and vice versa by multipollutant Cox regression models considering potential confounders. Adjusting noise risk estimates of MI for NO2 and/or PM2.5 did not change the hazard ratios (HRs) per 10 dB increase in road traffic (without air pollution: 1.032, 95% CI: 1.014-1.051, adjusted for NO2 and PM2.5: 1.034, 95% CI: 1.014-1.055), railway traffic (1.020, 95% CI: 1.007-1.033 vs. 1.020, 95% CI: 1.007-1.033), and aircraft traffic noise (1.025, 95% CI: 1.006-1.045 vs. 1.025, 95% CI: 1.005-1.046). Conversely, noise adjusted HRs for air pollutants were lower than corresponding estimates without noise adjustment. Hazard ratio per 10 µg/m³ increase with and without noise adjustment were 1.024 (1.005-1.043) vs. 0.990 (0.965-1.016) for NO2 and 1.054 (1.013-1.093) vs. 1.019 (0.971-1.071) for PM2.5. CONCLUSION: Our study suggests that transportation noise is associated with MI mortality, independent from air pollution. Air pollution studies not adequately adjusting for transportation noise exposure may overestimate the cardiovascular disease burden of air pollution.

13.
Environ Int ; 121(Pt 1): 879-889, 2018 12.
Artigo em Inglês | MEDLINE | ID: mdl-30347370

RESUMO

The contribution of different transportation noise sources to metabolic disorders such as obesity remains understudied. We evaluated the associations of long-term exposure to road, railway and aircraft noise with measures of obesity and its subphenotypes using cross-sectional and longitudinal designs. We assessed 3796 participants from the population-based Swiss Cohort Study on Air Pollution and Lung and Heart Diseases (SAPALDIA), who attended the visits in 2001 (SAP2) and 2010/2011 (SAP3) and who were aged 29-72 at SAP2. At SAP2 we measured body mass index (BMI, kg/m2). At SAP3 we measured BMI, waist circumference (centimetres) and Kyle body Fat Index (%) and derived overweight, central and general obesity. Longitudinally for BMI, we derived change in BMI, incidence of overweight and obesity and a 3-category outcome combining the latter two. We assigned source-specific 5-year mean noise levels before visits and during follow-up at the most exposed dwelling façade (Lden, dB), using Swiss noise models for 2001 and 2011 and participants' residential history. Models were adjusted for relevant confounders, including traffic-related air pollution. Exposure to road traffic noise was significantly associated with all adiposity subphenotypes, cross-sectionally (at SAP3) [e.g. beta (95% CI) per 10 dB, BMI: 0.39 (0.18; 0.59); waist circumference: 0.93 (0.37; 1.50)], and with increased risk of obesity, longitudinally (e.g. RR = 1.25, 95% CI: 1.04; 1.51, per 10 dB in 5-year mean). Railway noise was significantly related to increased risk of overweight. In cross-sectional analyses, we further identified a stronger association between road traffic noise and BMI among participants with cardiovascular disease and an association between railway noise and BMI among participants reporting bad sleep. Associations were independent of the other noise sources, air pollution and robust to all adjustment sets. No associations were observed for aircraft noise. Long-term exposure to transportation noise, particularly road traffic noise, may increase the risk of obesity and could constitute a pathway towards cardiometabolic and other diseases.


Assuntos
Tecido Adiposo/metabolismo , Exposição Ambiental/efeitos adversos , Ruído dos Transportes/efeitos adversos , Obesidade/epidemiologia , Adiposidade , Adulto , Biomarcadores/metabolismo , Índice de Massa Corporal , Estudos Transversais , Feminino , Humanos , Incidência , Estudos Longitudinais , Masculino , Pessoa de Meia-Idade , Obesidade/etiologia , Obesidade Abdominal/epidemiologia , Obesidade Abdominal/etiologia , Sobrepeso/epidemiologia , Sobrepeso/etiologia , Estudos Prospectivos , Suíça/epidemiologia , Adulto Jovem
14.
Environ Int ; 121(Pt 1): 741-750, 2018 12.
Artigo em Inglês | MEDLINE | ID: mdl-30321849

RESUMO

Transportation noise leads to sleep disturbance and to psychological and physiological sustained stress reactions, which could impact respiratory health. However, epidemiologic evidence on associations of objective transportation noise exposure and also perceived noise annoyance with respiratory morbidity is limited. We investigated independent associations of transportation noise exposure and noise annoyance with prevalent respiratory symptoms and incident asthma in adults. Using 17,138 observations (from 7049 participants) from three SAPALDIA (Swiss Cohort Study on Lung and Heart Diseases in Adults) surveys, we assessed associations of transportation noise exposure and noise annoyance with prevalent respiratory symptoms, and with incident asthma (in 10,657 nested observations from 6377 participants). Annual day-evening-night transportation noise comprising road, railway and aircraft Lden (Transportation Lden) was calculated for the most exposed façade of participants' residence using Swiss noise models. Transportation noise annoyance was assessed using an 11-point scale, and participants reported respiratory symptoms and doctor-diagnosed asthma at each survey. We estimated associations with transportation Lden (as well as source-specific Lden) and noise annoyance, independent of air pollution and other potential confounders, using mutually-adjusted mixed logistic and Poisson models and applying random intercepts at the level of the participants. Prevalent respiratory symptoms ranged from 5% (nocturnal dyspnoea) to 23% (regular cough/phlegm). Transportation noise annoyance, but not Lden, was independently associated with respiratory symptoms and current asthma in all participants, with odds ratios (OR) and 95% confidence intervals (CI) ranging between 1.03 (95%CI: 1.01, 1.06) and 1.07 (95% CI: 1.04, 1.11) per 1-point difference in noise annoyance. Both noise annoyance and Lden showed independent associations with asthma symptoms among asthmatics, especially in those reporting adult-onset asthma [ORLden: 1.90 (95% CI: 1.25, 2.89) per 10 dB; p-value of interaction (adult-onset vs. childhood-onset): 0.03; ORnoise annoyance: 1.06 (95%CI: 0.97, 1.16) per 1-point difference; p-value of interaction: 0.06]. No associations were found with incident asthma. Transportation noise level and annoyance contributed to symptom exacerbation in adult asthma. This suggests both psychological and physiological noise reactions on the respiratory system, and could be relevant for asthma care. More studies are needed to better understand the effects of objective and perceived noise in asthma aetiology and overall respiratory health.


Assuntos
Asma/epidemiologia , Exposição Ambiental , Humor Irritável , Ruído dos Transportes/estatística & dados numéricos , Adulto , Idoso , Asma/etiologia , Estudos de Coortes , Feminino , Humanos , Incidência , Masculino , Pessoa de Meia-Idade , Suíça/epidemiologia
15.
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.


Assuntos
Metilação de DNA/fisiologia , Pulmão/fisiologia , Vigilância da População , Poluição por Fumaça de Tabaco/efeitos adversos , Tabaco/efeitos adversos , alfa 1-Antitripsina/metabolismo , Adolescente , Adulto , Idoso , Criança , Pré-Escolar , Estudos de Coortes , Estudos Transversais , Europa (Continente)/epidemiologia , Feminino , Humanos , Lactente , Recém-Nascido , Estudos Longitudinais , Pulmão/efeitos dos fármacos , Masculino , Pessoa de Meia-Idade , Vigilância da População/métodos , Adulto Jovem , alfa 1-Antitripsina/genética
16.
Thorax ; 73(9): 825-832, 2018 09.
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.


Assuntos
Doença Pulmonar Obstrutiva Crônica/diagnóstico , Doença Pulmonar Obstrutiva Crônica/epidemiologia , Adulto , Testes de Provocação Brônquica , Feminino , Volume Expiratório Forçado , Humanos , Incidência , Masculino , Cloreto de Metacolina , Pessoa de Meia-Idade , Estudos Prospectivos , Adulto Jovem
17.
Int J Hyg Environ Health ; 221(3): 556-563, 2018 04.
Artigo em Inglês | MEDLINE | ID: mdl-29482991

RESUMO

BACKGROUND: Most epidemiological noise studies consider 24 h average noise exposure levels. Our aim was to exploratively analyze the impact of noise exposure at different time windows during day and night on cardiovascular mortality. METHODS: We generated Switzerland-wide exposure models for road traffic, railway and aircraft noise for different time windows for the year 2001. Combined noise source equivalent continuous sound levels (Leq) for different time windows at the most exposed façade were assigned to each of the 4.41 million Swiss National Cohort adult participants. Follow-up period was from 2000 to 2008. Hazard ratios (HR) of noise effects on various cardiovascular primary causes of death were computed by Cox regression models adjusted for potential confounders and NO2 levels. RESULTS: For most cardiovascular causes of death we obtained indications for a diurnal pattern. For ischemic heart disease the highest HR was observed for the core night hours from 01 h to 05 h (HR per standard deviation of Leq: 1.025, 95% CI: 1.016-1.034) and lower HR for the daytime 07 h to 19 h (1.018 [1.009-1.028]). Heart failure and daytime Leq yielded the highest HR (1.047 [1.027-1.068]). CONCLUSION: For acute cardiovascular diseases, nocturnal intermittent noise exposure tended to be more relevant than daytime exposure, whereas it was the opposite for chronic conditions such as heart failure most strongly associated with continuous daytime noise. This suggests that for acute diseases sleep is an important mediator for health consequences of transportation noise.


Assuntos
Aeronaves , Doenças Cardiovasculares/mortalidade , Exposição Ambiental/efeitos adversos , Veículos Automotores , Ruído dos Transportes/efeitos adversos , Ferrovias , Adulto , Idoso , Causas de Morte , Estudos de Coortes , Feminino , Insuficiência Cardíaca/mortalidade , Humanos , Estudos Longitudinais , Masculino , Pessoa de Meia-Idade , Ruído , Modelos de Riscos Proporcionais , Fatores de Risco , Suíça , Transportes
18.
Eur J Pediatr ; 177(5): 699-707, 2018 May.
Artigo em Inglês | MEDLINE | ID: mdl-29411143

RESUMO

Respiratory diseases are associated with increased cardiovascular risk in adults, but little is known on the early impact on the vasculature in youth. The SAPALDIA Youth study, the offspring study of the Swiss Study on Air Pollution and Lung and Heart Disease In Adults (SAPALDIA), investigated the association between physician-diagnosed asthma status and common carotid artery intima media thickness (CIMT). Offspring underwent standardized clinical protocols and provided information on early life factors, health, and lifestyle. The association between per subject averages of CIMT and asthma was estimated using mixed linear regression analyses adjusting for main confounders, testing for interaction with gender and age. Of 257 offspring (mean age 15 years, 53% female), 11.5% reported doctor-diagnosed asthma (male 17%, female 7%). Mean CIMT was significantly different by gender (male 0.53 mm (± 0.045), female 0.50 mm (± 0.048); p < 0.001). Interaction was highly significant by gender (p = 0.001) with significantly increased CIMT in asthmatic vs. non-asthmatics boys (difference 0.023 mm, 95% CI 0.003; 0.043), as compared to girls. CONCLUSION: Our study suggests an increased risk for early vascular change in adolescent asthmatic boys. Whereas the small number of girls limits the interpretation, the result necessitates further research into sex-specific atherosclerotic burden related to respiratory health in adolescence. What is Known: • Evidence points to a significant impact of adult respiratory disease on cardiovascular health indicators as well as on endpoints. • Inflammation is a key pathway in vascular change across the life course. What is New: • We observe an adverse association between physician-diagnosed asthma and carotid intima media thickness in adolescent boys. • Albeit a limited number of asthmatic girls, we hypothesize the gender typical timing of asthma or a higher male cardiovascular vulnerability as possible explanations for the gender-specific results.


Assuntos
Asma/complicações , Aterosclerose/etiologia , Espessura Intima-Media Carotídea , Fatores Sexuais , Adolescente , Artérias Carótidas/diagnóstico por imagem , Criança , Estudos Transversais , Feminino , Humanos , Masculino , Fatores de Risco , Suíça
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.
Environ Health Perspect ; 125(9): 097004, 2017 09 07.
Artigo em Inglês | MEDLINE | ID: mdl-28934719

RESUMO

BACKGROUND: The impact of different transportation noise sources and noise environments on arterial stiffness remains unknown. OBJECTIVES: We evaluated the association between residential outdoor exposure to annual average road, railway, and aircraft noise levels, total noise intermittency (IR), and total number of noise events (NE) and brachial-ankle pulse wave velocity (baPWV) following a cross-sectional design. METHODS: We measured baPWV (meters/second) in 2,775 participants (49-81 y old) at the second follow-up (2010-2011) of the Swiss Cohort Study on Air Pollution and Lung and Heart Diseases in Adults (SAPALDIA). We assigned annual average road, railway, and aircraft noise levels (Ldensource), total day- and nighttime NEtime and IRtime (percent fluctuation=0%, none or constant noise; percent fluctuation=100%, high fluctuation) at the most exposed façade using 2011 Swiss noise models. We applied multivariable linear mixed regression models to analyze associations. RESULTS: Medians [interquartile ranges (IQRs)] were baPWV=13.4 (3.1) m/s; Ldenair (57.6% exposed)=32.8 (8.0) dB; Ldenrail (44.6% exposed)=30.0 (8.1) dB; Ldenroad (99.7% exposed): 54.2 (10.6) dB; NEnight=123 (179); NEday=433 (870); IRnight=73% (27); and IRday=63.8% (40.3). We observed a 0.87% (95% CI: 0.31, 1.43%) increase in baPWV per IQR of Ldenrail, which was greater with IRnight>80% or with daytime sleepiness. We observed a nonsignificant positive association between Ldenroad and baPWV in urban areas and a negative tendency in rural areas. NEnight, but not NEday, was associated with baPWV. Associations were independent of the other noise sources and air pollution. CONCLUSIONS: Long-term exposure to railway noise, particularly in an intermittent nighttime noise environment, and to nighttime noise events, mainly related to road noise, may affect arterial stiffness, a major determinant of cardiovascular disease. Ascertaining noise exposure characteristics beyond average noise levels may be relevant to better understand noise-related health effects. https://doi.org/10.1289/EHP1136.


Assuntos
Doenças Cardiovasculares/epidemiologia , Exposição Ambiental/estatística & dados numéricos , Ruído dos Transportes/estatística & dados numéricos , Rigidez Vascular/fisiologia , Idoso , Idoso de 80 Anos ou mais , Poluição do Ar/estatística & dados numéricos , Índice Tornozelo-Braço , Estudos Transversais , Feminino , Humanos , Estilo de Vida , Modelos Lineares , Masculino , Pessoa de Meia-Idade , Análise de Onda de Pulso , Fatores de Risco , Suíça
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