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1.
Artigo em Inglês | MEDLINE | ID: mdl-34596687

RESUMO

CONTEXT: Organizational justice has been linked to lower risk of several chronic conditions among employees, but less is known about the long-term mechanisms underlying this risk reduction. OBJECTIVE: To assess whether self-reported organizational justice is associated with individual and composite metabolic trajectories. DESIGN: 25 years follow-up of the Whitehall II prospective cohort study. SETTING: Middle-aged public servants from the United Kingdom. PARTICIPANTS: Data on 8,182 participants were used. MAIN OUTCOME MEASURES: Levels of eleven anthropometric, glycaemic, lipid and blood pressure biomarkers were measured at five timepoints (1991-2013). We used generalized estimating equations and group-based trajectory modelling to investigate the relationship between organizational justice and biomarker trajectories. RESULTS: High vs. low organizational justice were associated with lower waist (-1.7 cm) and hip (-1 cm) circumference, BMI (-0.6 kg/m 2), triglycerides (-1.07 mmol/L) and fasting insulin (-1.08 µIU/mL) trajectories. Two latent metabolic trajectory clusters were identified: a high-risk and a low-risk cluster. High organizational justice (vs. low) were associated with belonging to the low-risk cluster (ORpooled=1.47). The low-risk cluster demonstrated lower baseline levels of most biomarkers and better glycaemic control, whereas the high-risk cluster showed higher baseline levels of most biomarkers, glycaemic deterioration, but also greater improvements in lipid levels over time. CONCLUSIONS: People with high organizational justice had more favourable long-term cardiometabolic biomarkers patterns than those with low organizational justice, a potential mechanism contributing to the lower risk of chronic diseases in the first group. Further intervention studies are warranted to determine whether improvement of organizational justice might improve long-term health.

2.
J Am Heart Assoc ; : e021436, 2021 Oct 06.
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.
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
4.
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.

5.
Alzheimers Dement ; 2021 Sep 27.
Artigo em Inglês | MEDLINE | ID: mdl-34569688

RESUMO

INTRODUCTION: The determinants of the secular decline in the incidence of dementia are not clear. The aim of this study was to investigate the influences of four factors-education, wealth, cerebrovascular health, and general health-on the secular decline. METHODS: A cohort study was conducted of all individuals aged ≥65 years in Denmark from 2005 through 2018 (N = 1,757,168). Annual incidence rates of dementia and population attributable risks of the four factors were calculated and birth cohort trends were examined. RESULTS: The incidence of dementia declined by 22.5% in men and 34.2% in women from 2005 through 2018. Population attributable risks of lower education, lower wealth, and stroke likewise declined. Independent of these improvements, the incidence of dementia fell across successive birth cohorts. DISCUSSION: Most of the observed plasticity in late-onset dementia is associated with a risk decline across successive birth cohorts that is independent of improvements in traditional risk factors.

6.
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.

7.
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.

8.
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
9.
Ann Am Thorac Soc ; 18(2): 238-246, 2021 02.
Artigo em Inglês | MEDLINE | ID: mdl-33090904

RESUMO

Rationale: Few longitudinal studies have assessed the relationship between occupational exposures and lung-function decline in the general population with a sufficiently long follow-up.Objectives: To examine the potential association in two large cohorts: the ECRHS (European Community Respiratory Health Survey) and the SAPALDIA (Swiss Cohort Study on Air Pollution and Lung and Heart Diseases in Adults).Methods: General-population samples of individuals aged 18 to 62 were randomly selected in 1991-1993 and followed up approximately 10 and 20 years later. Spirometry (without bronchodilation) was performed at each visit. Coded complete job histories during follow-up visits were linked to a job-exposure matrix, generating cumulative exposure estimates for 12 occupational exposures. Forced expiratory volume in 1 second (FEV1) and forced vital capacity (FVC) were jointly modeled in linear mixed-effects models, fitted in a Bayesian framework, taking into account age and smoking.Results: A total of 40,024 lung-function measurements from 17,833 study participants were analyzed. We found accelerated declines in FEV1 and the FEV1/FVC ratio for exposure to biological dust, mineral dust, and metals (FEV1 = -15.1 ml, -14.4 ml, and -18.7 ml, respectively; and FEV1/FVC ratio = -0.52%, -0.43%, and -0.36%, respectively; per 25 intensity-years of exposure). These declines were comparable in magnitude with those associated with long-term smoking. No effect modification by sex or smoking status was identified. Findings were similar between the ECRHS and the SAPALDIA cohorts.Conclusions: Our results greatly strengthen the evidence base implicating occupation, independent of smoking, as a risk factor for lung-function decline. This highlights the need to prevent or control these exposures in the workplace.

10.
Environ Int ; 143: 105983, 2020 10.
Artigo em Inglês | MEDLINE | ID: mdl-32736159

RESUMO

BACKGROUND: The association between air pollution and mortality is well established, yet some uncertainties remain: there are few studies that account for road traffic noise exposure or that consider in detail the shape of the exposure-response function for cause-specific mortality outcomes, especially at low-levels of exposure. OBJECTIVES: We examined the association between long-term exposure to particulate matter [(PM) with a diameter of <2.5 µm (PM2.5), <10 µm (PM10)], and nitrogen dioxide (NO2) and total and cause-specific mortality, accounting for road traffic noise. METHODS: We used data on 24,541 females (age > 44 years) from the Danish Nurse Cohort, who were recruited in 1993 or 1999, and linked to the Danish Causes of Death Register for follow-up on date of death and its cause, until the end of 2013. Annual mean concentrations of PM2.5, PM10, and NO2 at the participants' residences since 1990 were estimated using the Danish DEHM/UBM/AirGIS dispersion model, and annual mean road traffic noise levels (Lden) were estimated using the Nord2000 model. We examined associations between the three-year running mean of PM2.5, PM10, and NO2 with total and cause-specific mortality by using time-varying Cox Regression models, adjusting for individual characteristics and residential road traffic noise. RESULTS: During the study period, 3,708 nurses died: 843 from cardiovascular disease (CVD), 310 from respiratory disease (RD), and 64 from diabetes. In the fully adjusted models, including road traffic noise, we detected associations of three-year running mean of PM2.5 with total (hazard ratio; 95% confidence interval: 1.06; 1.01-1.11), CVD (1.14; 1.03-1.26), and diabetes mortality (1.41; 1.05-1.90), per interquartile range of 4.39 µg/m3. In a subset of the cohort exposed to PM2.5 < 20 µg/m3, we found even stronger association with total (1.19; 1.11-1.27), CVD (1.27; 1.01-1.46), RD (1.27; 1.00-1.60), and diabetes mortality (1.44; 0.83-2.48). We found similar associations with PM10 and none with NO2. All associations were robust to adjustment for road traffic noise. DISCUSSION: Long-term exposure to low-levels of PM2.5 and PM10 is associated with total mortality, and mortality from CVD, RD, and diabetes. Associations were even stronger at the PM2.5 levels below EU limit values and were independent of road traffic noise.


Assuntos
Poluentes Atmosféricos , Poluição do Ar , Ruído dos Transportes , Poluentes Atmosféricos/análise , Poluição do Ar/efeitos adversos , Poluição do Ar/análise , Estudos de Coortes , Dinamarca/epidemiologia , Exposição Ambiental/efeitos adversos , Exposição Ambiental/análise , Feminino , Humanos , Ruído dos Transportes/efeitos adversos , Material Particulado/efeitos adversos , Material Particulado/análise
11.
Occup Environ Med ; 76(4): 222-229, 2019 04.
Artigo em Inglês | MEDLINE | ID: mdl-30700596

RESUMO

OBJECTIVES: Chronic bronchitis (CB) is an important chronic obstructive pulmonary disease (COPD)-related phenotype, with distinct clinical features and prognostic implications. Occupational exposures have been previously associated with increased risk of CB but few studies have examined this association prospectively using objective exposure assessment. We examined the effect of occupational exposures on CB incidence in the European Community Respiratory Health Survey. METHODS: Population samples aged 20-44 were randomly selected in 1991-1993, and followed up twice over 20 years. Participants without chronic cough or phlegm at baseline were analysed. Coded job histories during follow-up were linked to the ALOHA Job Exposure Matrix, generating occupational exposure estimates to 12 categories of chemical agents. Their association with CB incidence over both follow-ups was examined with Poisson models using generalised estimating equations. RESULTS: 8794 participants fulfilled the inclusion criteria, contributing 13 185 observations. Only participants exposed to metals had a higher incidence of CB (relative risk (RR) 1.70, 95% CI 1.16 to 2.50) compared with non-exposed to metals. Mineral dust exposure increased the incidence of chronic phlegm (RR 1.72, 95% CI 1.43 to 2.06). Incidence of chronic phlegm was increased in men exposed to gases/fumes and to solvents and in women exposed to pesticides. CONCLUSIONS: Occupational exposures are associated with chronic phlegm and CB, and the evidence is strongest for metals and mineral dust exposure. The observed differences between men and women warrant further investigation.


Assuntos
Bronquite Crônica/etiologia , Incidência , Exposição Ocupacional/efeitos adversos , Adulto , Austrália/epidemiologia , Bronquite Crônica/complicações , Bronquite Crônica/epidemiologia , Tosse/epidemiologia , Tosse/etiologia , Poeira , Europa (Continente)/epidemiologia , Feminino , Gases/efeitos adversos , Inquéritos Epidemiológicos , Humanos , Estudos Longitudinais , Masculino , Pessoa de Meia-Idade , Exposição Ocupacional/estatística & dados numéricos , Praguicidas/efeitos adversos , Fatores de Risco , Fumar/efeitos adversos , Fumar/epidemiologia , Estados Unidos/epidemiologia
12.
Am J Public Health ; 108(8): 1059-1065, 2018 08.
Artigo em Inglês | MEDLINE | ID: mdl-29927657

RESUMO

OBJECTIVES: To examine whether subsidized housing, specifically public housing and rental assistance, is associated with asthma in the Boston, Massachusetts, adult population. METHODS: We analyzed a pooled cross-sectional sample of 9554 adults taking part in 3 Boston Behavioral Risk Factor Surveillance System surveys from 2010 to 2015. We estimated odds ratios for current asthma in association with housing status (public housing development [PHD] resident, rental assistance [RA] renter, non-RA renter, nonrenter nonowner, homeowner as reference) in logistic regression analyses adjusting for year, age, sex, race/ethnicity, education, and income. RESULTS: The odds of current asthma were 2.02 (95% confidence interval [CI] = 1.35, 3.03) and 2.34 (95% CI = 1.60, 3.44) times higher among PHD residents and RA renters, respectively, than among homeowners. We observed smoking-related effect modification (interaction P = .04); elevated associations for PHD residents and RA renters remained statistically significant (P < .05) only among ever smokers. Associations for PHD residents and RA renters remained consistent in magnitude in comparison with non-RA renters who were eligible for subsidized housing according to income. CONCLUSIONS: Public housing and rental assistance were strongly associated with asthma in this large cross-sectional sample of adult Boston residents.


Assuntos
Asma/epidemiologia , Habitação Popular/estatística & dados numéricos , Adolescente , Adulto , Boston/epidemiologia , Estudos Transversais , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Vigilância em Saúde Pública , Adulto Jovem
13.
Thorax ; 73(11): 1008-1015, 2018 11.
Artigo em Inglês | MEDLINE | ID: mdl-29574416

RESUMO

BACKGROUND: Occupational exposures have been associated with an increased risk of COPD. However, few studies have related objectively assessed occupational exposures to prospectively assessed incidence of COPD, using postbronchodilator lung function tests. Our objective was to examine the effect of occupational exposures on COPD incidence in the European Community Respiratory Health Survey. METHODS: General population samples aged 20-44 were randomly selected in 1991-1993 and followed up 20 years later (2010-2012). Spirometry was performed at baseline and at follow-up, with incident COPD defined using a lower limit of normal criterion for postbronchodilator FEV1/FVC. Only participants without COPD and without current asthma at baseline were included. Coded job histories during follow-up were linked to a Job-Exposure Matrix, generating occupational exposure estimates to 12 categories of agents. Their association with COPD incidence was examined in log-binomial models fitted in a Bayesian framework. FINDINGS: 3343 participants fulfilled the inclusion criteria; 89 of them had COPD at follow-up (1.4 cases/1000 person-years). Participants exposed to biological dust had a higher incidence of COPD compared with those unexposed (relative risk (RR) 1.6, 95% CI 1.1 to 2.3), as did those exposed to gases and fumes (RR 1.5, 95% CI 1.0 to 2.2) and pesticides (RR 2.2, 95% CI 1.1 to 3.8). The combined population attributable fraction for these exposures was 21.0%. INTERPRETATION: These results substantially strengthen the evidence base for occupational exposures as an important risk factor for COPD.


Assuntos
Previsões , Inquéritos Epidemiológicos/métodos , Doenças Profissionais/complicações , Exposição Ocupacional/efeitos adversos , Doença Pulmonar Obstrutiva Crônica/epidemiologia , Adulto , Austrália/epidemiologia , Europa (Continente)/epidemiologia , Feminino , Seguimentos , Humanos , Incidência , Masculino , Doenças Profissionais/epidemiologia , Doença Pulmonar Obstrutiva Crônica/etiologia , Testes de Função Respiratória , Estudos Retrospectivos , Fatores de Risco , Adulto Jovem
14.
Environ Int ; 103: 23-29, 2017 06.
Artigo em Inglês | MEDLINE | ID: mdl-28351767

RESUMO

BACKGROUND: Previous studies have linked both extreme and sub-optimal air temperature to cardiopulmonary morbidity and mortality, especially in older individuals. However, the underlying mechanisms are yet to be determined. OBJECTIVES: We hypothesized that short-term increases in air temperature may induce blood mitochondrial DNA (mtDNA) lesions in older individuals, which could contribute to temperature-related pathogenesis. METHODS: We repeatedly measured mtDNA lesions in blood samples from 654 participants in the Normative Aging Study from 1999 to 2013 (1142 observations) by quantitative long-amplicon polymerase chain reaction assay. Hourly temperature data were obtained from the Boston Logan Airport weather station (located approximately 12km from the clinical site). We calculated 2-, 7-, and 14-day moving averages of 24-hour mean and 24-hour variability of temperature. We fit covariate-adjusted linear-mixed models accounting for repeated measures to evaluate the association between short-term increases in mean and variability of temperature with mtDNA lesions within each season. RESULTS: Interquartile increases in 7- and 14-day moving averages of 24-hour mean temperature in summer were associated with a 0.17 (95% CI: 0.07, 0.27; p=0.0007) and 0.21 (95% CI: 0.10, 0.32; p=0.0001) increase in the number of mtDNA lesions per 10kb, respectively. Results were similar when we further adjusted for temperature variability. We also observed significant associations between increases in temperature variability and mtDNA lesions independent of mean air temperature. An interquartile range increase in the 7-day moving average of 24-hour standard deviation in summer was associated with a 0.19 (95% CI: 0.07, 0.31; p=0.0023) increase in the number of mtDNA lesions per 10kb. CONCLUSIONS: Short-term exposure to higher mean air temperature was associated with increased mtDNA lesions in older adults, supporting the hypothesis that sub-optimal meteorological conditions may induce pathophysiological responses among susceptible populations.


Assuntos
Dano ao DNA , DNA Mitocondrial , Temperatura , Idoso , Idoso de 80 Anos ou mais , Boston , Humanos , Modelos Lineares , Masculino , Estações do Ano
15.
Environ Health Perspect ; 125(2): 207-214, 2017 02.
Artigo em Inglês | MEDLINE | ID: mdl-27504716

RESUMO

BACKGROUND: The biological mechanisms by which cleaning products and disinfectants-an emerging risk factor-affect respiratory health remain incompletely evaluated. Studying genes by environment interactions (G × E) may help identify new genes related to adult-onset asthma. OBJECTIVES: We identified interactions between genetic polymorphisms of a large set of genes involved in the response to oxidative stress and occupational exposures to low molecular weight (LMW) agents or irritants on adult-onset asthma. METHODS: Our data came from three large European cohorts: Epidemiological Family-based Study of the Genetics and Environment of Asthma (EGEA), Swiss Cohort Study on Air Pollution and Lung and Heart Disease in Adults (SAPALDIA), and European Community Respiratory Health Survey in Adults (ECRHS). A candidate pathway-based strategy identified 163 genes involved in the response to oxidative stress and potentially related to exposures to LMW agents/irritants. Occupational exposures were evaluated using an asthma job-exposure matrix and job-specific questionnaires for cleaners and healthcare workers. Logistic regression models were used to detect G × E interactions, adjusted for age, sex, and population ancestry, in 2,599 adults (mean age, 47 years; 60% women, 36% exposed, 18% asthmatics). p-Values were corrected for multiple comparisons. RESULTS: Ever exposure to LMW agents/irritants was associated with current adult-onset asthma [OR = 1.28 (95% CI: 1.04, 1.58)]. Eight single nucleotide polymorphism (SNP) by exposure interactions at five loci were found at p < 0.005: PLA2G4A (rs932476, chromosome 1), near PLA2R1 (rs2667026, chromosome 2), near RELA (rs931127, rs7949980, chromosome 11), PRKD1 (rs1958980, rs11847351, rs1958987, chromosome 14), and PRKCA (rs6504453, chromosome 17). Results were consistent across the three studies and after accounting for smoking. CONCLUSIONS: Using a pathway-based selection process, we identified novel genes potentially involved in adult asthma by interaction with occupational exposure. These genes play a role in the NF-κB pathway, which is involved in inflammation. Citation: Rava M, Ahmed I, Kogevinas M, Le Moual N, Bouzigon E, Curjuric I, Dizier MH, Dumas O, Gonzalez JR, Imboden M, Mehta AJ, Tubert-Bitter P, Zock JP, Jarvis D, Probst-Hensch NM, Demenais F, Nadif R. 2017. Genes interacting with occupational exposures to low molecular weight agents and irritants on adult-onset asthma in three European studies. Environ Health Perspect 125:207-214; http://dx.doi.org/10.1289/EHP376.


Assuntos
Irritantes/análise , Doenças Profissionais/epidemiologia , Exposição Ocupacional/estatística & dados numéricos , Material Particulado/análise , Adulto , Asma/epidemiologia , Europa (Continente)/epidemiologia , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Peso Molecular , NF-kappa B/genética , Polimorfismo de Nucleotídeo Único
16.
Expert Rev Respir Med ; 10(8): 861-72, 2016 08.
Artigo em Inglês | MEDLINE | ID: mdl-27187563

RESUMO

INTRODUCTION: Due to contradictory literature we have performed a systematic review and meta-analyse of population-based studies that have used Job Exposure Matrices to assess occupational exposure and risk of Chronic Obstructive Pulmonary Disease (COPD). AREAS COVERED: Two researchers independently searched databases for published articles using predefined inclusion criteria. Study quality was assessed, and results pooled for COPD and chronic bronchitis for exposure to biological dust, mineral dust, and gases/fumes using a fixed and random effect model. Five studies met predetermined inclusion criteria. The meta-analysis showed low exposure to mineral dust, and high exposure to gases/fumes were associated with an increased risk of COPD. We also found significantly increased the risk of chronic bronchitis for low and high exposure to biological dust and mineral dust. Expert commentary: The relationship between occupational exposure assessed by the JEM and the risk of COPD and chronic bronchitis shows significant association with occupational exposure. However, the heterogeneity of the meta-analyses suggests more wide population-based studies with older age groups and longitudinal phenotype assessment of COPD to clarify the role of occupational exposure to COPD risk.


Assuntos
Doenças Profissionais/etiologia , Exposição Ocupacional/efeitos adversos , Doença Pulmonar Obstrutiva Crônica/etiologia , Poeira , Gases , Humanos , Doença Pulmonar Obstrutiva Crônica/fisiopatologia , Fatores de Risco
17.
Environ Health Perspect ; 124(9): 1353-60, 2016 09.
Artigo em Inglês | MEDLINE | ID: mdl-26955062

RESUMO

BACKGROUND: It is unknown if ambient fine particulate matter (PM2.5) is associated with lower renal function, a cardiovascular risk factor. OBJECTIVE: We investigated whether long-term PM2.5 exposure was associated with estimated glomerular filtration rate (eGFR) in a cohort of older men living in the Boston Metropolitan area. METHODS: This longitudinal analysis included 669 participants from the Veterans Administration Normative Aging Study with up to four visits between 2000 and 2011 (n = 1,715 visits). Serum creatinine was measured at each visit, and eGFR was calculated according to the Chronic Kidney Disease Epidemiology Collaboration equation. One-year exposure to PM2.5 prior to each visit was assessed using a validated spatiotemporal model that utilized satellite remote-sensing aerosol optical depth data. eGFR was modeled in a time-varying linear mixed-effects regression model as a continuous function of 1-year PM2.5, adjusting for important covariates. RESULTS: One-year PM2.5 exposure was associated with lower eGFRs; a 2.1-µg/m3 interquartile range higher 1-year PM2.5 was associated with a 1.87 mL/min/1.73 m2 lower eGFR [95% confidence interval (CI): -2.99, -0.76]. A 2.1 µg/m3-higher 1-year PM2.5 was also associated with an additional annual decrease in eGFR of 0.60 mL/min/1.73 m2 per year (95% CI: -0.79, -0.40). CONCLUSIONS: In this longitudinal sample of older men, the findings supported the hypothesis that long-term PM2.5 exposure negatively affects renal function and increases renal function decline. CITATION: Mehta AJ, Zanobetti A, Bind MC, Kloog I, Koutrakis P, Sparrow D, Vokonas PS, Schwartz JD. 2016. Long-term exposure to ambient fine particulate matter and renal function in older men: the VA Normative Aging Study. Environ Health Perspect 124:1353-1360; http://dx.doi.org/10.1289/ehp.1510269.


Assuntos
Poluentes Atmosféricos/toxicidade , Exposição Ambiental , Taxa de Filtração Glomerular/efeitos dos fármacos , Material Particulado/toxicidade , Adulto , Idoso , Idoso de 80 Anos ou mais , Pressão Sanguínea , Boston , Estudos de Coortes , Creatinina/sangue , Humanos , Testes de Função Renal , Modelos Lineares , Estudos Longitudinais , Masculino , Pessoa de Meia-Idade , Tamanho da Partícula , Veteranos/estatística & dados numéricos , Adulto Jovem
18.
Am J Clin Nutr ; 103(2): 542-50, 2016 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-26791184

RESUMO

BACKGROUND: It is unknown whether habitual intake of dietary flavonoids, known for their antioxidative and anti-inflammatory properties, affects longitudinal change in lung function. OBJECTIVE: We investigated whether different flavonoid subclasses present in the habitual diet were associated with beneficial changes in lung function over time in the elderly. DESIGN: This longitudinal analysis included 839 participants from the VA (Veterans Affairs) Normative Aging Study whose lung function [forced expiratory volume in 1 s (FEV1) and forced vital capacity (FVC)] was measured at 2 and up to 5 visits between 1992 and 2008 (n = 2623 measurements). Yearly average intake of major flavonoid subclasses (anthocyanins, flavanones, flavan-3-ols, flavonols, flavones, and polymers) was calculated from food-frequency questionnaires at each visit. We estimated adjusted differences in annual change in lung function associated with each flavonoid subclass, categorized into quartiles, in linear mixed-effects regression models after adjustment for lifestyle and dietary confounders. RESULTS: Strong inverse associations were found between anthocyanin intake and age-related decline in lung function. Independent of dietary and nondietary risk factors, slower rates of FEV1 and FVC decline by 23.6 (95% CI: 16.6, 30.7) and 37.3 (95% CI: 27.8, 46.8) mL/y, respectively, were observed in participants in the fourth quartile of intake compared with participants in the first quartile (P-trend < 0.0001). The protective associations observed for anthocyanin intake were present in both current/former and never smokers. Compared with no or very low intakes, an intake of ≥2 servings of anthocyanin-rich blueberries/wk was associated with slower decline in FEV1 and FVC by 22.5 (95% CI: 10.8, 34.2) and 37.9 (95% CI: 22.1, 53.7) mL/y, respectively. To a lesser extent, higher flavan-3-ol intake was also associated with slower lung function decline. CONCLUSIONS: An attenuation of age-related lung function decline was associated with higher dietary anthocyanin intake in this longitudinal sample of predominantly elderly men. Further prospective studies are needed to confirm these novel associations.


Assuntos
Envelhecimento , Antocianinas/uso terapêutico , Anti-Inflamatórios não Esteroides/uso terapêutico , Antioxidantes/uso terapêutico , Dieta , Pneumopatias/prevenção & controle , Pulmão/crescimento & desenvolvimento , Adulto , Idoso , Idoso de 80 Anos ou mais , Antocianinas/administração & dosagem , Anti-Inflamatórios não Esteroides/administração & dosagem , Antioxidantes/administração & dosagem , Boston/epidemiologia , Estudos de Coortes , Comportamento Alimentar , Volume Expiratório Forçado , Humanos , Estudos Longitudinais , Pulmão/fisiologia , Pulmão/fisiopatologia , Pneumopatias/epidemiologia , Pneumopatias/fisiopatologia , Masculino , Pessoa de Meia-Idade , Inquéritos Nutricionais , Fatores de Risco , Veteranos , Capacidade Vital
19.
Environ Health Perspect ; 124(7): 983-90, 2016 07.
Artigo em Inglês | MEDLINE | ID: mdl-26731791

RESUMO

BACKGROUND: Epidemiological studies have reported associations between particulate matter (PM) concentrations and cancer and respiratory and cardiovascular diseases. DNA methylation has been identified as a possible link but so far it has only been analyzed in candidate sites. OBJECTIVES: We studied the association between DNA methylation and short- and mid-term air pollution exposure using genome-wide data and identified potential biological pathways for additional investigation. METHODS: We collected whole blood samples from three independent studies-KORA F3 (2004-2005) and F4 (2006-2008) in Germany, and the Normative Aging Study (1999-2007) in the United States-and measured genome-wide DNA methylation proportions with the Illumina 450k BeadChip. PM concentration was measured daily at fixed monitoring stations and three different trailing averages were considered and regressed against DNA methylation: 2-day, 7-day and 28-day. Meta-analysis was performed to pool the study-specific results. RESULTS: Random-effect meta-analysis revealed 12 CpG (cytosine-guanine dinucleotide) sites as associated with PM concentration (1 for 2-day average, 1 for 7-day, and 10 for 28-day) at a genome-wide Bonferroni significance level (p ≤ 7.5E-8); 9 out of these 12 sites expressed increased methylation. Through estimation of I2 for homogeneity assessment across the studies, 4 of these sites (annotated in NSMAF, C1orf212, MSGN1, NXN) showed p > 0.05 and I2 < 0.5: the site from the 7-day average results and 3 for the 28-day average. Applying false discovery rate, p-value < 0.05 was observed in 8 and 1,819 additional CpGs at 7- and 28-day average PM2.5 exposure respectively. CONCLUSION: The PM-related CpG sites found in our study suggest novel plausible systemic pathways linking ambient PM exposure to adverse health effect through variations in DNA methylation. CITATION: Panni T, Mehta AJ, Schwartz JD, Baccarelli AA, Just AC, Wolf K, Wahl S, Cyrys J, Kunze S, Strauch K, Waldenberger M, Peters A. 2016. A genome-wide analysis of DNA methylation and fine particulate matter air pollution in three study populations: KORA F3, KORA F4, and the Normative Aging Study. Environ Health Perspect 124:983-990; http://dx.doi.org/10.1289/ehp.1509966.


Assuntos
Poluentes Atmosféricos/análise , Poluição do Ar/estatística & dados numéricos , Metilação de DNA , Exposição Ambiental/estatística & dados numéricos , Material Particulado/análise , Doenças Cardiovasculares/epidemiologia , Estudo de Associação Genômica Ampla , Alemanha/epidemiologia , Humanos , Doenças Respiratórias/epidemiologia , Estados Unidos/epidemiologia
20.
Occup Environ Med ; 72(8): 546-552, 2015 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-25666844

RESUMO

OBJECTIVES: The purpose of this study is to determine the trajectory of lung function change after exposure cessation to occupational organic dust exposure, and to identify factors that modify improvement. METHODS: The Shanghai Textile Worker Study is a longitudinal study of 447 cotton workers exposed to endotoxin-containing dust and 472 silk workers exposed to non-endotoxin-containing dust. Spirometry was performed at 5-year intervals. Air sampling was performed to estimate individual cumulative exposures. The effect of work cessation on forced expiratory volume in 1 s (FEV1) was modelled using generalised additive mixed effects models to identify the trajectory of FEV1 recovery. Linear mixed effects models incorporating interaction terms were used to identify modifiers of FEV1 recovery. Loss to follow-up was accounted for with inverse probability of censoring weights. RESULTS: 74.2% of the original cohort still alive participated in 2011. Generalised additive mixed models identified a non-linear improvement in FEV1 for all workers after exposure cessation, with no plateau noted 25 years after retirement. Linear mixed effects models incorporating interaction terms identified prior endotoxin exposure (p=0.01) and male gender (p=0.002) as risk factors for impaired FEV1 improvement after exposure cessation. After adjusting for gender, smoking delayed the onset of FEV1 gain but did not affect the overall magnitude of change. CONCLUSIONS: Lung function improvement after cessation of exposure to organic dust is sustained. Endotoxin exposure and male gender are risk factors for less FEV1 improvement.


Assuntos
Poluentes Ocupacionais do Ar/efeitos adversos , Poeira , Endotoxinas/efeitos adversos , Pulmão/efeitos dos fármacos , Exposição Ocupacional/efeitos adversos , Recuperação de Função Fisiológica , Indústria Têxtil , China , Emprego , Feminino , Seguimentos , Volume Expiratório Forçado , Humanos , Estudos Longitudinais , Pulmão/fisiopatologia , Pneumopatias/fisiopatologia , Pneumopatias/reabilitação , Masculino , Doenças Profissionais/fisiopatologia , Doenças Profissionais/reabilitação , Fatores de Risco , Fumar , Têxteis
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