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1.
Environ Health Perspect ; 129(10): 107002, 2021 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-34605674

RESUMO

BACKGROUND: Transportation noise is increasingly acknowledged as a cardiovascular risk factor, but the evidence base for an association with stroke is sparse. OBJECTIVE: We aimed to investigate the association between transportation noise and stroke incidence in a large Scandinavian population. METHODS: We harmonized and pooled data from nine Scandinavian cohorts (seven Swedish, two Danish), totaling 135,951 participants. We identified residential address history and estimated road, railway, and aircraft noise for all addresses. Information on stroke incidence was acquired through linkage to national patient and mortality registries. We analyzed data using Cox proportional hazards models, including socioeconomic and lifestyle confounders, and air pollution. RESULTS: During follow-up (median=19.5y), 11,056 stroke cases were identified. Road traffic noise (Lden) was associated with risk of stroke, with a hazard ratio (HR) of 1.06 [95% confidence interval (CI): 1.03, 1.08] per 10-dB higher 5-y mean time-weighted exposure in analyses adjusted for individual- and area-level socioeconomic covariates. The association was approximately linear and persisted after adjustment for air pollution [particulate matter (PM) with an aerodynamic diameter of ≤2.5µm (PM2.5) and NO2]. Stroke was associated with moderate levels of 5-y aircraft noise exposure (40-50 vs. ≤40 dB) (HR=1.12; 95% CI: 0.99, 1.27), but not with higher exposure (≥50 dB, HR=0.94; 95% CI: 0.79, 1.11). Railway noise was not associated with stroke. DISCUSSION: In this pooled study, road traffic noise was associated with a higher risk of stroke. This finding supports road traffic noise as an important cardiovascular risk factor that should be included when estimating the burden of disease due to traffic noise. https://doi.org/10.1289/EHP8949.

2.
J Am Heart Assoc ; 10(20): e021436, 2021 Oct 19.
Artigo em Inglês | MEDLINE | ID: mdl-34612059

RESUMO

Background We examined the association of long-term exposure to air pollution and road traffic noise with incident heart failure (HF). Methods And Results Using data on female nurses from the Danish Nurse Cohort (aged >44 years), we investigated associations between 3-year mean exposures to air pollution and road traffic noise and incident HF using Cox regression models, adjusting for relevant confounders. Incidence of HF was defined as the first hospital contact (inpatient, outpatient, or emergency) between cohort baseline (1993 or 1999) and December 31, 2014, based on the Danish National Patient Register. Annual mean levels of particulate matter with a diameter <2.5 µm since 1990 and NO2 and road traffic noise since 1970 were estimated at participants' residences. Of the 22 189 nurses, 484 developed HF. We detected associations with all 3 pollutants, with hazard ratios (HRs) of 1.17 (95% CI, 1.01-1.36), 1.10 (95% CI, 0.99-1.22), and 1.12 (95% CI, 0.99-1.26) per increase of 5.1 µg/m3 in particulate matter with a diameter <2.5 µm, 8.6 µg/m3 in NO2, and 9.3 dB in road traffic noise, respectively. We observed an enhanced risk of HF incidence for those exposed to high levels of the 3 pollutants; however, the effect modification of coexposure was not statistically significant. Former smokers and nurses with hypertension showed the strongest associations with particulate matter with a diameter <2.5 µm (Peffect modification<0.05). Conclusions We found that long-term exposures to air pollution and road traffic noise were independently associated with HF.

3.
Environ Res ; : 112167, 2021 Oct 04.
Artigo em Inglês | MEDLINE | ID: mdl-34619123

RESUMO

BACKGROUND: Epidemiological studies have linked transportation noise and cardiovascular diseases, however, atrial fibrillation (AF) has received limited attention. We aimed to investigate the association between transportation noise and AF risk. METHODS: Over the period 1990-2017 we estimated road and railway noise (Lden) at the most and least exposed façades for all residential addresses across Denmark. We estimated time-weighted mean noise exposure for 3.6 million individuals age ≥35 years. Of these, 269,756 incident cases of AF were identified with a mean follow-up of 13.0 years. Analyses were conducted using Cox proportional hazards models with adjustment for individual and area-level sociodemographic covariates and long-term residential air pollution. RESULTS: A 10 dB higher 10-year mean road traffic noise at the most and least exposed façades were associated with incidence rate ratios (IRR) and 95% confidence intervals (CI) for AF of 1.006 (1.001-1.011) and 1.013 (1.007-1.019), respectively. After further adjustment for PM2.5, the IRRs (CIs) were 1.000 (0.995-1.005) and 1.007 (1.000-1.013), respectively. For railway noise, the IRRs per 10 dB increase in 10-year mean exposure were 1.017 (1.007-1.026) and 1.035 (1.021-1.050) for the most and least exposed façades, respectively, and were slightly attenuated when adjusted for PM2.5. Aircraft noise between 55 and 60 dB and ≥60 dB were associated with IRRs of 1.055 (0.996-1.116) and 1.036 (0.931-1.154), respectively, when compared to <45 dB. CONCLUSION: Transportation noise seems to be associated with a small increase in AF risk, especially for exposure at the least exposed façade.

4.
BMJ ; 374: n1904, 2021 09 01.
Artigo em Inglês | MEDLINE | ID: mdl-34470785

RESUMO

OBJECTIVE: To investigate the associations between air pollution and mortality, focusing on associations below current European Union, United States, and World Health Organization standards and guidelines. DESIGN: Pooled analysis of eight cohorts. SETTING: Multicentre project Effects of Low-Level Air Pollution: A Study in Europe (ELAPSE) in six European countries. PARTICIPANTS: 325 367 adults from the general population recruited mostly in the 1990s or 2000s with detailed lifestyle data. Stratified Cox proportional hazard models were used to analyse the associations between air pollution and mortality. Western Europe-wide land use regression models were used to characterise residential air pollution concentrations of ambient fine particulate matter (PM2.5), nitrogen dioxide, ozone, and black carbon. MAIN OUTCOME MEASURES: Deaths due to natural causes and cause specific mortality. RESULTS: Of 325 367 adults followed-up for an average of 19.5 years, 47 131 deaths were observed. Higher exposure to PM2.5, nitrogen dioxide, and black carbon was associated with significantly increased risk of almost all outcomes. An increase of 5 µg/m3 in PM2.5 was associated with 13% (95% confidence interval 10.6% to 15.5%) increase in natural deaths; the corresponding figure for a 10 µg/m3 increase in nitrogen dioxide was 8.6% (7% to 10.2%). Associations with PM2.5, nitrogen dioxide, and black carbon remained significant at low concentrations. For participants with exposures below the US standard of 12 µg/m3 an increase of 5 µg/m3 in PM2.5 was associated with 29.6% (14% to 47.4%) increase in natural deaths. CONCLUSIONS: Our study contributes to the evidence that outdoor air pollution is associated with mortality even at low pollution levels below the current European and North American standards and WHO guideline values. These findings are therefore an important contribution to the debate about revision of air quality limits, guidelines, and standards, and future assessments by the Global Burden of Disease.


Assuntos
Poluentes Atmosféricos/efeitos adversos , Poluição do Ar/efeitos adversos , Doenças Cardiovasculares/mortalidade , Exposição Ambiental/efeitos adversos , Doenças não Transmissíveis/mortalidade , Europa (Continente) , Humanos
5.
Lancet Planet Health ; 5(9): e620-e632, 2021 09.
Artigo em Inglês | MEDLINE | ID: mdl-34508683

RESUMO

BACKGROUND: Long-term exposure to outdoor air pollution increases the risk of cardiovascular disease, but evidence is unclear on the health effects of exposure to pollutant concentrations lower than current EU and US standards and WHO guideline limits. Within the multicentre study Effects of Low-Level Air Pollution: A Study in Europe (ELAPSE), we investigated the associations of long-term exposures to fine particulate matter (PM2·5), nitrogen dioxide (NO2), black carbon, and warm-season ozone (O3) with the incidence of stroke and acute coronary heart disease. METHODS: We did a pooled analysis of individual data from six population-based cohort studies within ELAPSE, from Sweden, Denmark, the Netherlands, and Germany (recruited 1992-2004), and harmonised individual and area-level variables between cohorts. Participants (all adults) were followed up until migration from the study area, death, or incident stroke or coronary heart disease, or end of follow-up (2011-15). Mean 2010 air pollution concentrations from centrally developed European-wide land use regression models were assigned to participants' baseline residential addresses. We used Cox proportional hazards models with increasing levels of covariate adjustment to investigate the association of air pollution exposure with incidence of stroke and coronary heart disease. We assessed the shape of the concentration-response function and did subset analyses of participants living at pollutant concentrations lower than predefined values. FINDINGS: From the pooled ELAPSE cohorts, data on 137 148 participants were analysed in our fully adjusted model. During a median follow-up of 17·2 years (IQR 13·8-19·5), we observed 6950 incident events of stroke and 10 071 incident events of coronary heart disease. Incidence of stroke was associated with PM2·5 (hazard ratio 1·10 [95% CI 1·01-1·21] per 5 µg/m3 increase), NO2 (1·08 [1·04-1·12] per 10 µg/m3 increase), and black carbon (1·06 [1·02-1·10] per 0·5 10-5/m increase), whereas coronary heart disease incidence was only associated with NO2 (1·04 [1·01-1·07]). Warm-season O3 was not associated with an increase in either outcome. Concentration-response curves indicated no evidence of a threshold below which air pollutant concentrations are not harmful for cardiovascular health. Effect estimates for PM2·5 and NO2 remained elevated even when restricting analyses to participants exposed to pollutant concentrations lower than the EU limit values of 25 µg/m3 for PM2·5 and 40 µg/m3 for NO2. INTERPRETATION: Long-term air pollution exposure was associated with incidence of stroke and coronary heart disease, even at pollutant concentrations lower than current limit values. FUNDING: Health Effects Institute.

6.
Environ Pollut ; 290: 118105, 2021 Dec 01.
Artigo em Inglês | MEDLINE | ID: mdl-34523530

RESUMO

Road transport is the main anthropogenic source of NOx in Europe, affecting human health and ecosystems. Thus, mitigation policies have been implemented to reduce on-road vehicle emissions, particularly through the Euro standard limits. To evaluate the effectiveness of these policies, we calculated NO2 and NOx concentration trends using air quality and meteorological measurements conducted in three European cities over 26 years. These data were also employed to estimate the trends in NOx emission factors (EFNOx, based on inverse dispersion modeling) and NO2:NOx emission ratios for the vehicle fleets under real-world driving conditions. In the period 1998-2017, Copenhagen and Stockholm showed large reductions in both the urban background NOx concentrations (-2.1 and -2.6% yr-1, respectively) and EFNOx at curbside sites (68 and 43%, respectively), proving the success of the Euro standards in diminishing NOx emissions. London presented a modest decrease in urban background NOx concentrations (-1.3% yr-1), while EFNOx remained rather constant at the curbside site (Marylebone Road) due to the increase in public bus traffic. NO2 primary emissions -that are not regulated- increased until 2008-2010, which also reflected in the ambient concentrations. This increase was associated with a strong dieselization process and the introduction of new after-treatment technologies that targeted the emission reduction of other species (e.g., greenhouse gases or particulate matter). Thus, while regulations on ambient concentrations of specific species have positive effects on human health, the overall outcomes should be considered before widely adopting them. Emission inventories for the on-road transportation sector should include EFNOx derived from real-world measurements, particularly in urban settings.

7.
BMJ ; 374: n1954, 2021 09 08.
Artigo em Inglês | MEDLINE | ID: mdl-34497091

RESUMO

OBJECTIVE: To investigate the association between long term residential exposure to road traffic and railway noise and risk of incident dementia. DESIGN: Nationwide prospective register based cohort study. SETTING: Denmark. PARTICIPANTS: 1 938 994 adults aged ≥60 years living in Denmark between 1 January 2004 and 31 December 2017. MAIN OUTCOME MEASURES: Incident cases of all cause dementia and dementia subtypes (Alzheimer's disease, vascular dementia, and Parkinson's disease related dementia), identified from national hospital and prescription registries. RESULTS: The study population included 103 500 participants with incident dementia, and of those, 31 219 received a diagnosis of Alzheimer's disease, 8664 of vascular dementia, and 2192 of Parkinson's disease related dementia. Using Cox regression models, 10 year mean exposure to road traffic and railway noise at the most (Ldenmax) and least (Ldenmin) exposed façades of buildings were associated with a higher risk of all cause dementia. These associations showed a general pattern of higher hazard ratios with higher noise exposure, but with a levelling off or even small declines in risk at higher noise levels. In subtype analyses, both road traffic noise and railway noise were associated with a higher risk of Alzheimer's disease, with hazard ratios of 1.16 (95% confidence interval 1.11 to 1.22) for road Ldenmax ≥65 dB compared with <45 dB, 1.27 (1.22 to 1.34) for road Ldenmin ≥55 dB compared with <40 dB, 1.16 (1.10 to 1.23) for railway Ldenmax ≥60 dB compared with <40 dB, and 1.24 (1.17 to 1.30) for railway Ldenmin ≥50 dB compared with <40 dB. Road traffic, but not railway, noise was associated with an increased risk of vascular dementia. Results indicated associations between road traffic Ldenmin and Parkinson's disease related dementia. CONCLUSIONS: This nationwide cohort study found transportation noise to be associated with a higher risk of all cause dementia and dementia subtypes, especially Alzheimer's disease.


Assuntos
Demência/epidemiologia , Ruído dos Transportes/estatística & dados numéricos , Idoso , Causalidade , Dinamarca/epidemiologia , Feminino , Humanos , Incidência , Masculino , Pessoa de Meia-Idade , Ruído dos Transportes/efeitos adversos , Modelos de Riscos Proporcionais , Estudos Prospectivos , Sistema de Registros
8.
Cancer Causes Control ; 32(12): 1447-1455, 2021 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-34467460

RESUMO

PURPOSE: Few studies have suggested that traffic noise is a risk factor for cancer, but evidence is inconclusive. We aimed to investigate whether road traffic and railway noise are associated with risk of colorectal cancer. METHODS: We obtained address history for all 3.5 million people above 40 years of age and living in Denmark for the period 1990-2017 and estimated road traffic and railway noise (Lden) at the most and least exposed facades of all addresses as well as air pollution (PM2.5). During follow-up (2000-2017), 35,881 persons developed colon cancer and 19,755 developed rectal cancer. Information on individual and area-level demographic and socioeconomic variables was collected from Danish registries. We analyzed data using Cox proportional hazards models, including traffic noise as time-varying 10-year average exposure. RESULTS: Exposure to road traffic noise at the most exposed façade was associated with an incidence rate ratio and 95% confidence interval for proximal colon cancer of 1.018 (0.999-1.038) per 10 dB higher noise. We observed no associations for road traffic noise at the least exposed façade or for railway noise in relation to proximal colon cancer. Also, we found no association between road traffic or railway noise and risk for distal colon cancer or rectal cancer. CONCLUSION: Traffic noise did not seem associated with higher risk for colorectal cancer, although the suggestion of a slightly higher risk of proximal colon cancer following exposure to road traffic noise warrants further research.

9.
Environ Res ; 203: 111886, 2021 Aug 16.
Artigo em Inglês | MEDLINE | ID: mdl-34411546

RESUMO

OBJECTIVE: Recent studies on air pollution and disease have been based on millions of participants within a region or country, relying entirely on register-based confounder adjustment. We aimed to investigate the effects of increasing adjustment for register- and questionnaire-based covariates on the association between air pollution and cardiometabolic diseases. METHODS: In a population-based cohort of 246,766 eligible participants randomly selected across Denmark in 2010 and 2013 and followed up until December 31, 2017, we identified 3,247 myocardial infarction (MI) cases, 4,166 stroke cases and 6,366 type 2 diabetes cases. Based on historical address-information, we calculated 5-year time-weighted exposure to PM2.5 and NO2 modelled using a validated air pollution model. We used Cox proportional hazards models to calculate hazard ratios (HR) with increasing adjustment for a number of individual- and area-level register-based covariates as well as lifestyle covariates assessed through questionnaires. RESULTS: We found that a 5 µg/m3 higher PM2.5 was associated with HRs (95% CI) for MI, stroke and diabetes, of respectively, 1.18 (0.91-1.52), 1.11 (0.88-1.40) and 1.24 (1.03-1.50) in the fully adjusted models. For all three diseases, adjustment for either individual-level, area-level or lifestyle covariates, or combinations of these resulted in higher HRs compared to HRs adjusted only for age, sex and calendar-year, most marked for MI and diabetes. Further adjustment for lifestyle in models with full register-based individual- and area-level adjustment resulted in only minor changes in HRs for all three diseases. CONCLUSIONS: Our findings suggest that in studies of air pollution and cardiometabolic disease, which use an adjustment strategy with a broad range of register-based socioeconomic variables, there is no effect on risk estimates from subsequent lifestyle adjustment.

10.
Environ Health Perspect ; 129(8): 87002, 2021 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-34338552

RESUMO

BACKGROUND: Associations between long-term exposure to air pollution and road traffic noise have been established for ischemic heart disease, but findings have been mixed for atrial fibrillation (AF). OBJECTIVES: The goal of the study was to examine associations of long-term exposure to road traffic noise and air pollution with AF. METHODS: Time-varying Cox regression models were used to estimate associations of 1-, 3-, and 23-y mean road traffic noise and air pollution exposures with AF incidence in 23,528 women enrolled in the Danish Nurse Cohort (age >44y at baseline in 1993 or 1999). AF diagnoses were ascertained via the Danish National Patient Register. Annual mean weighted 24-h average road traffic noise levels (Lden) at the nurses' residences, since 1970, were estimated using the Nord2000 model, and annual mean levels of particulate matter with a diameter <2.5µm (PM2.5) and nitrogen dioxide (NO2) were estimated using the DEHM/UBM/AirGIS model. RESULTS: Of 23,528 nurses with no prior AF diagnosis at the cohort baseline, 1,522 developed AF during follow-up. In a fully adjusted model (including PM2.5), the estimated risk of AF was 18% higher [hazard ratio (HR); 95% confidence interval (CI): 1.18; 1.02, 1.36] in nurses with residential 3-y mean Lden levels >58 dB vs. <48 dB, with similar findings for 1-y mean exposures. A 3.9-µg/m3 increase in 3-y mean PM2.5 was associated with incident AF before and after adjustment for concurrent exposure to road traffic noise (HR 1.09; 95% CI: 1.00, 1.20 and 1.08; 95% CI: 0.97, 1.19, respectively). Associations with 1-y mean PM2.5 exposures were positive but closer to the null and not significant. Associations with NO2 were null for all time periods before and after adjustment for road traffic noise and inverse when adjusted for concurrent PM2.5. CONCLUSION: Our analysis of prospective data from a cohort of Danish female nurses followed for up to 14 y provided suggestive evidence of independent associations between incident AF and 1- and 3-y exposures to road traffic noise and PM2.5. https://doi.org/10.1289/EHP8090.

11.
Int J Cancer ; 149(11): 1887-1897, 2021 Dec 01.
Artigo em Inglês | MEDLINE | ID: mdl-34278567

RESUMO

Particulate matter air pollution and diesel engine exhaust have been classified as carcinogenic for lung cancer, yet few studies have explored associations with liver cancer. We used six European adult cohorts which were recruited between 1985 and 2005, pooled within the "Effects of low-level air pollution: A study in Europe" (ELAPSE) project, and followed for the incidence of liver cancer until 2011 to 2015. The annual average exposure to nitrogen dioxide (NO2 ), particulate matter with diameter <2.5 µm (PM2.5 ), black carbon (BC), warm-season ozone (O3 ), and eight elemental components of PM2.5 (copper, iron, zinc, sulfur, nickel, vanadium, silicon, and potassium) were estimated by European-wide hybrid land-use regression models at participants' residential addresses. We analyzed the association between air pollution and liver cancer incidence by Cox proportional hazards models adjusting for potential confounders. Of 330 064 cancer-free adults at baseline, 512 developed liver cancer during a mean follow-up of 18.1 years. We observed positive linear associations between NO2 (hazard ratio, 95% confidence interval: 1.17, 1.02-1.35 per 10 µg/m3 ), PM2.5 (1.12, 0.92-1.36 per 5 µg/m3 ), and BC (1.15, 1.00-1.33 per 0.5 10-5 /m) and liver cancer incidence. Associations with NO2 and BC persisted in two-pollutant models with PM2.5 . Most components of PM2.5 were associated with the risk of liver cancer, with the strongest associations for sulfur and vanadium, which were robust to adjustment for PM2.5 or NO2 . Our study suggests that ambient air pollution may increase the risk of liver cancer, even at concentrations below current EU standards.

12.
Eur Respir J ; 57(6)2021 06.
Artigo em Inglês | MEDLINE | ID: mdl-34088754

RESUMO

BACKGROUND: Long-term exposure to ambient air pollution has been linked to childhood-onset asthma, although evidence is still insufficient. Within the multicentre project Effects of Low-Level Air Pollution: A Study in Europe (ELAPSE), we examined the associations of long-term exposures to particulate matter with a diameter <2.5 µm (PM2.5), nitrogen dioxide (NO2) and black carbon (BC) with asthma incidence in adults. METHODS: We pooled data from three cohorts in Denmark and Sweden with information on asthma hospital diagnoses. The average concentrations of air pollutants in 2010 were modelled by hybrid land-use regression models at participants' baseline residential addresses. Associations of air pollution exposures with asthma incidence were explored with Cox proportional hazard models, adjusting for potential confounders. RESULTS: Of 98 326 participants, 1965 developed asthma during a mean follow-up of 16.6 years. We observed associations in fully adjusted models with hazard ratios of 1.22 (95% CI 1.04-1.43) per 5 µg·m-3 for PM2.5, 1.17 (95% CI 1.10-1.25) per 10 µg·m-3 for NO2 and 1.15 (95% CI 1.08-1.23) per 0.5×10-5 m-1 for BC. Hazard ratios were larger in cohort subsets with exposure levels below the European Union and US limit values and possibly World Health Organization guidelines for PM2.5 and NO2. NO2 and BC estimates remained unchanged in two-pollutant models with PM2.5, whereas PM2.5 estimates were attenuated to unity. The concentration-response curves showed no evidence of a threshold. CONCLUSIONS: Long-term exposure to air pollution, especially from fossil fuel combustion sources such as motorised traffic, was associated with adult-onset asthma, even at levels below the current limit values.


Assuntos
Poluentes Atmosféricos , Poluição do Ar , Asma , Adulto , Poluentes Atmosféricos/análise , Poluição do Ar/análise , Criança , Exposição Ambiental/análise , Europa (Continente) , Humanos , Incidência , Material Particulado/análise , Suécia
13.
Cancer Causes Control ; 32(9): 935-942, 2021 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-34050843

RESUMO

PURPOSE: The etiology of Hodgkin lymphoma (HL) is obscure. Research on air pollution and risk of HL provides inconsistent results. We aimed to investigate the association between long-term residential exposure to air pollution and risk of adult Hodgkin lymphoma in Denmark. METHODS: We performed a nationwide register-based case-control study, including all (n = 2,681) Hodgkin lymphoma cases registered in the nationwide Danish Cancer Registry between 1989 and 2014. We randomly selected 8,853 age- and sex-matched controls from the entire Danish population using the Civil Registration System, and identified 20-year residential address history for all cases and controls. We modeled outdoor air pollution concentrations at all these addresses using the high-resolution multiscale air pollution model system DEHM/UBM/AirGIS. We used conditional logistic regression to estimate odds ratios adjusted for individual and neighborhood level sociodemographic variables. RESULTS: There was no association between 1, 5, 10, and 20 years' time-weighted average exposure to fine particles (PM2.5), O3, SO2, NO2, or the PM2.5 constituents OC, NH4, NO3, and SO4 and risk of Hodgkin lymphoma. CONCLUSION: Residential exposure to ambient air pollution does not seem to increase the risk of developing Hodgkin lymphoma.


Assuntos
Poluição do Ar , Doença de Hodgkin , Adulto , Poluentes Atmosféricos/efeitos adversos , Poluição do Ar/efeitos adversos , Estudos de Casos e Controles , Dinamarca/epidemiologia , Exposição Ambiental/efeitos adversos , Doença de Hodgkin/epidemiologia , Doença de Hodgkin/etiologia , Humanos , Material Particulado
14.
Eur Respir J ; 2021 May 13.
Artigo em Inglês | MEDLINE | ID: mdl-33986028

RESUMO

BACKGROUND: While air pollution has been linked to the development of chronic obstructive pulmonary disease (COPD), evidence on the role of environmental noise is just emerging. We examined the associations of long-term exposure to air pollution and road traffic noise with COPD incidence. METHODS: We defined COPD incidence for 24 538 female nurses from the Danish Nurse Cohort (age>44 years) as the first hospital contact between baseline (1993 or 1999) and 2015. We estimated residential annual mean concentrations of particulate matter with diameter<2.5 µm (PM2.5) since 1990 and nitrogen dioxide (NO2) since 1970 by the Danish DEHM/UBM/AirGIS modeling system, and road traffic noise (Lden) since 1970 by the Nord2000 model. Time-varying Cox regression models were applied to assess the associations of air pollution and road traffic noise with COPD incidence. RESULTS: 977 nurses developed COPD during 18.6 years' mean follow-up. We observed associations with COPD for all three exposures with hazard ratios (HRs) and 95% confidence intervals (CIs) of 1.19 (1.01, 1.41) per 6.26 µg·m-3 for PM2.5, 1.13 (1.05, 1.20) per 8.19 µg·m-3 for NO2, and 1.15 (1.06, 1.25) per 10 dB for Lden. Associations with NO2 and Lden attenuated slightly after mutual adjustment, but were robust to adjustment for PM2.5. Associations with PM2.5 were attenuated to null after adjustment for either NO2 or Lden. No potential interaction effect was observed between air pollutants and noise. CONCLUSIONS: Long-term exposure to air pollution, especially traffic-related NO2, and road traffic noise were independently associated with COPD.

15.
Environ Health Perspect ; 129(4): 47009, 2021 04.
Artigo em Inglês | MEDLINE | ID: mdl-33844598

RESUMO

BACKGROUND: Inconsistent associations between long-term exposure to particles with an aerodynamic diameter ≤2.5 µm [fine particulate matter (PM2.5)] components and mortality have been reported, partly related to challenges in exposure assessment. OBJECTIVES: We investigated the associations between long-term exposure to PM2.5 elemental components and mortality in a large pooled European cohort; to compare health effects of PM2.5 components estimated with two exposure modeling approaches, namely, supervised linear regression (SLR) and random forest (RF) algorithms. METHODS: We pooled data from eight European cohorts with 323,782 participants, average age 49 y at baseline (1985-2005). Residential exposure to 2010 annual average concentration of eight PM2.5 components [copper (Cu), iron (Fe), potassium (K), nickel (Ni), sulfur (S), silicon (Si), vanadium (V), and zinc (Zn)] was estimated with Europe-wide SLR and RF models at a 100×100 m scale. We applied Cox proportional hazards models to investigate the associations between components and natural and cause-specific mortality. In addition, two-pollutant analyses were conducted by adjusting each component for PM2.5 mass and nitrogen dioxide (NO2) separately. RESULTS: We observed 46,640 natural-cause deaths with 6,317,235 person-years and an average follow-up of 19.5 y. All SLR-modeled components were statistically significantly associated with natural-cause mortality in single-pollutant models with hazard ratios (HRs) from 1.05 to 1.27. Similar HRs were observed for RF-modeled Cu, Fe, K, S, V, and Zn with wider confidence intervals (CIs). HRs for SLR-modeled Ni, S, Si, V, and Zn remained above unity and (almost) significant after adjustment for both PM2.5 and NO2. HRs only remained (almost) significant for RF-modeled K and V in two-pollutant models. The HRs for V were 1.03 (95% CI: 1.02, 1.05) and 1.06 (95% CI: 1.02, 1.10) for SLR- and RF-modeled exposures, respectively, per 2 ng/m3, adjusting for PM2.5 mass. Associations with cause-specific mortality were less consistent in two-pollutant models. CONCLUSION: Long-term exposure to V in PM2.5 was most consistently associated with increased mortality. Associations for the other components were weaker for exposure modeled with RF than SLR in two-pollutant models. https://doi.org/10.1289/EHP8368.

16.
Environ Epidemiol ; 5(3): e148, 2021 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-33912785

RESUMO

Background: Evidence of nonauditory health effects of road traffic noise exposure is growing. This prospective cohort study aimed to estimate the association between long-term exposure to road traffic noise above a threshold and incident myocardial infarction (MI) in Denmark. Methods: In the Danish Nurse Cohort study, we used data of 22,378 women, at recruitment in 1993 and 1999, who reported information on MI risk factors. The participants' first hospital contact or out-of-hospital death due to MI were followed-up until 2014. We investigated a relationship between residential exposures to road traffic noise levels (Lden) up to 23 years and incident MI (overall, nonfatal, and fatal) using time-varying Cox regression models adjusting for potential confounders and air pollutants. We estimated thresholds of road traffic noise (53, 56, and 58 dB) associated with incident MI in a piece-wise linear regression model. Results: Of the 22,378 participants, 633 developed MI, 502 of which were nonfatal. We observed a non-linear relationship between the 23-year running mean of Lden and incident MI with a threshold level of 56 dB, above which hazard ratios (95% confidence intervals) were 1.30 (0.97, 1.75) for overall and 1.46 (1.05, 2.03) for nonfatal MI per 10 dB. The association with nonfatal MI attenuated slightly to 1.34 (0.95, 1.90) after adjustment for fine particles. Conclusions: We found that long-term exposure to road traffic noise above 56 dB may increase the risk of MI. The study findings suggest that road traffic noise above 56 dB may need regulation in addition to the regulation of ambient pollutants.

17.
Int J Epidemiol ; 50(4): 1147-1156, 2021 08 30.
Artigo em Inglês | MEDLINE | ID: mdl-33755127

RESUMO

BACKGROUND: Studies on transportation noise and incident stroke are few and inconclusive. We aimed to investigate associations between road-traffic and railway noise and the risk of incident stroke in the entire Danish population. METHODS: We estimated road-traffic and railway noise (Lden) at the most and least exposed façades for all residential addresses across Denmark (2.8 million) for the period 1990-2017. Based on this, we estimated the 10-year time-weighted mean noise exposure for 3.6 million Danes aged >35 years, of whom 184 523 developed incident stroke during follow-up from 2000 to 2017. Analyses were conducted using Cox proportional-hazards models, with adjustment for various individual- and area-level demographic and socio-economic covariates collected from registries and air pollution [fine particulate matter with particles with a diameter of ≤2.5 µm (PM2.5) and nitrogen dioxide (NO2)]. RESULTS: A 10-dB increase in the 10-year mean road-traffic noise at the most exposed façade was associated with an incidence rate ratio (IRR) of 1.04 [95% confidence interval (CI): 1.03-1.05] for all strokes. For road-traffic noise at the least exposed façade, the IRR per 10 dB was 1.03 (95% CI: 1.02-1.04) for all strokes. Railway noise was not associated with a higher risk of stroke. CONCLUSION: Road-traffic noise increased the risk of stroke. These findings add to the evidence of road-traffic noise as a cardiovascular risk factor.


Assuntos
Poluição do Ar , Ruído dos Transportes , Acidente Vascular Cerebral , Poluição do Ar/efeitos adversos , Dinamarca/epidemiologia , Exposição Ambiental/efeitos adversos , Exposição Ambiental/análise , Humanos , Ruído dos Transportes/efeitos adversos , Estudos Prospectivos , Acidente Vascular Cerebral/epidemiologia
18.
Environ Int ; 152: 106464, 2021 07.
Artigo em Inglês | MEDLINE | ID: mdl-33684733

RESUMO

BACKGROUND: Ambient air pollution is likely a risk factor for asthma, and recent evidence suggests the possible relevance of road traffic noise. OBJECTIVES: We examined the associations of long-term exposure to air pollution and road traffic noise with adult-asthma incidence. METHODS: We followed 28,731 female nurses (age > 44 years) from the Danish Nurse Cohort, recruited in 1993 and 1999, for first hospital contact for asthma from 1977 until 2015. We estimated residential annual mean concentrations of particulate matter with diameter < 2.5 µm (PM2.5) since 1990 and nitrogen dioxide (NO2) since 1970 with the Danish DEHM/UBM/AirGIS modeling system, and road traffic noise (Lden) since 1970 with the Nord2000 model. Time-varying Cox regression models were used to associate air pollution and road traffic noise exposure with asthma incidence. RESULTS: During 18.6 years' mean follow-up, 528 out of 23,093 participants had hospital contact for asthma. The hazard ratios (HR) and 95% confidence intervals for asthma incidence associated with 3-year moving average exposures were 1.29 (1.03, 1.61) per 6.3 µg/m3 for PM2.5, 1.16 (1.07, 1.27) per 8.2 µg/m3 for NO2, and 1.12 (1.00, 1.25) per 10 dB for Lden. The HR for NO2 remained unchanged after adjustment for either PM2.5 or Lden, while the HRs for PM2.5 and Lden attenuated to unity after adjustment for NO2. CONCLUSIONS: Long-term exposure to air pollution was associated with adult-asthma incidence independently of road traffic noise, with NO2 most relevant. Road traffic noise was not independently associated with adult-asthma incidence.


Assuntos
Poluentes Atmosféricos , Poluição do Ar , Asma , Ruído dos Transportes , Adulto , Poluentes Atmosféricos/análise , Poluição do Ar/efeitos adversos , Poluição do Ar/análise , Asma/epidemiologia , Asma/etiologia , Dinamarca/epidemiologia , Exposição Ambiental/análise , Feminino , Humanos , Incidência , Ruído dos Transportes/efeitos adversos , Material Particulado/análise
19.
Environ Int ; 147: 106371, 2021 02.
Artigo em Inglês | MEDLINE | ID: mdl-33422970

RESUMO

BACKGROUND: We evaluated methods for the analysis of multi-level survival data using a pooled dataset of 14 cohorts participating in the ELAPSE project investigating associations between residential exposure to low levels of air pollution (PM2.5 and NO2) and health (natural-cause mortality and cerebrovascular, coronary and lung cancer incidence). METHODS: We applied five approaches in a multivariable Cox model to account for the first level of clustering corresponding to cohort specification: (1) not accounting for the cohort or using (2) indicator variables, (3) strata, (4) a frailty term in frailty Cox models, (5) a random intercept under a mixed Cox, for cohort identification. We accounted for the second level of clustering due to common characteristics in the residential area by (1) a random intercept per small area or (2) applying variance correction. We assessed the stratified, frailty and mixed Cox approach through simulations under different scenarios for heterogeneity in the underlying hazards and the air pollution effects. RESULTS: Effect estimates were stable under approaches used to adjust for cohort but substantially differed when no adjustment was applied. Further adjustment for the small area grouping increased the effect estimates' standard errors. Simulations confirmed identical results between the stratified and frailty models. In ELAPSE we selected a stratified multivariable Cox model to account for between-cohort heterogeneity without adjustment for small area level, due to the small number of subjects and events in the latter. CONCLUSIONS: Our study supports the need to account for between-cohort heterogeneity in multi-center collaborations using pooled individual level data.


Assuntos
Poluentes Atmosféricos , Poluição do Ar , Poluentes Atmosféricos/análise , Poluição do Ar/análise , Estudos de Coortes , Exposição Ambiental/análise , Humanos , Material Particulado/análise
20.
Cardiology ; 146(1): 19-26, 2021.
Artigo em Inglês | MEDLINE | ID: mdl-33238279

RESUMO

Cardiovascular disease is one of the main causes of death and disability in the Western world, and there is increasing evidence that air pollution is a risk factor for developing sub-clinical cardiovascular diseases. Previous studies have shown a correlation between cardiovascular disease and short-term exposure to elevated air pollution levels. However, the literature on the impact of long-term effect of air pollution is limited. We have a unique opportunity to evaluate this correlation. The DEHM/UBM/AirGIS model system calculates air pollution in a high temporal and spatial resolution and traces air pollution retrospectively to year 1979. The model calculates accumulated exposure using annual exposure from PM2.5 in relation to home and work addresses and takes into account working hours and holidays. We link the results from this model system to a population-based cardiovascular screening cohort of 33,723 individuals in the age of 60-74 to assess the contribution of the specific accumulated air pollution to the presence of sub-clinical arteriosclerosis in the coronary vessels, abdominal aortic aneurysms, and peripheral arterial disease. This correlation will be further analyzed in relation to specific air pollutants. This study will introduce more precise data for a longer period of time and incorporate participant's home and work addresses.

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