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1.
Environ Res ; 180: 108841, 2019 Oct 19.
Artigo em Inglês | MEDLINE | ID: mdl-31655330

RESUMO

BACKGROUND: We hypothesized that particulate matter (PM) gamma activity (gamma radiation associated with PM) is associated with systemic effects. OBJECTIVE: Examine short-term relationships between ambient and indoor exposures to PM gamma activities with systemic inflammation and endothelial activation in chronic obstructive pulmonary disease (COPD) patients. METHODS: In 85 COPD patients from Eastern Massachusetts, USA from 2012 to 2014, plasma C-reactive protein (CRP), interleukin-6 (IL-6), and soluble vascular cell adhesion molecule-1 (sVCAM-1) were measured seasonally up to four times. We used US EPA RadNet data measuring ambient gamma radiation attached to PM adjusted for background radiation, and estimated in-home gamma radiation exposures using the ratio of in-home-to-ambient sulfur in PM2.5. Linear mixed-effects regression models were used to determine associations between moving averages of PM gamma activities through the week before phlebotomy with these biomarkers. We explored ambient and indoor PM2.5, black carbon (BC), and NO2 as confounders. RESULTS: Ambient and indoor PM gamma activities measured as energy spectra classes 3 through 9 were positively associated with CRP and IL-6. For example, averaged from phlebotomy day through previous 6 days, each IQR increase in indoor PM gamma activity for each spectra class, was associated with an CRP increase ranging from 7.45% (95%CI: 2.77, 12.4) to 13.4% (95%CI: 5.82, 21.4) and for ambient exposures were associated with an increase of 8.75% (95%CI: -0.57, 18.95) to 14.8% (95%CI: 4.5, 26.0). Indoor exposures were associated with IL-6 increase of 3.56% (95%CI: 0.31, 6.91) to 6.46% (95%CI:1.33, 11.85) and ambient exposures were associated with an increase of 0.03% (95%CI: -6.37, 6.87) to 3.50% (95%CI: -3.15, 10.61). There were no positive associations with sVCAM-1. Sensitivity analyses using two-pollutant models showed similar effects. CONCLUSIONS: Our results demonstrate that short-term exposures to environmental PM gamma radiation activities were associated with systemic inflammation in COPD patients.

2.
Artigo em Inglês | MEDLINE | ID: mdl-31636367

RESUMO

BACKGROUND: Lead is a ubiquitous toxicant following three compartment kinetics with the longest half-life found in bones. Patella and tibia lead levels-validated measures of cumulative exposure-require specialized X-ray-fluorescence-spectroscopy available only in a few centers worldwide. We developed minimally invasive biomarkers reflecting individual cumulative lead exposure using blood DNA methylation profiles-obtainable via Illumina 450K or IlluminaEPIC bead-chip assays. METHODS: We developed and tested two methylation-based biomarkers from 348 Normative Aging Study (NAS) elderly men. We selected methylation sites with strong associations with bone lead levels via robust regressions analysis and constructed the biomarkers using elastic nets. Results were validated in a NAS subset, reporting specificity, and sensitivity. FINDINGS: Participants were 73 years old on average (standard deviation, SD = 6), with moderate lead levels of (mean ± SD patella: 27 ± 18 µg/g; tibia:21 ± 13 µg/g). Methylation-based biomarkers for lead in patella and tibia included 59 and 138 DNA methylation sites, respectively. Estimated lead levels were significantly correlated with actual measured values, (r = 0.62 patella, r = 0.59 tibia) and had low mean square error (MSE) (MSE = 0.68 patella, MSE = 0.53 tibia). Means and distributions of the estimated and actual lead levels were not significantly different across patella and tibia bones (p > 0.05). Methylation-based biomarkers discriminated participants highly exposed (>median) to lead with a specificity of 74 and 73% for patella and tibia lead levels, respectively, with 70% sensitivity. INTERPRETATION: DNA methylation-based lead biomarkers are novel tools that can be used to reconstruct decades' worth of individual cumulative lead exposure using only blood DNA methylation profiles and may help identify the consequences of cumulative exposure.

3.
Epidemiology ; 30(5): 617-623, 2019 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-31386643

RESUMO

BACKGROUND: Maternal exposure to fine particulate air pollution (PM2.5) during pregnancy is associated with lower newborn birthweight, which is a risk factor for chronic disease. Existing studies typically report the average association related with PM2.5 increase, which does not offer information about potentially varying associations at different points of the birthweight distribution. METHODS: We retrieved all birth records in Massachusetts between 2001 and 2013 then restricted our analysis to full-term live singletons (n = 775,768). Using the birthdate, gestational age, and residential address reported at time of birth, we estimated the average maternal PM2.5 exposure during pregnancy of each birth. PM2.5 predictions came from a model that incorporates satellite, land use, and meteorologic data. We applied quantile regression to quantify the association between PM2.5 and birthweight at each decile of birthweight, adjusted for individual and neighborhood covariates. We considered effect modification by indicators of individual and neighborhood socioeconomic status (SES). RESULTS: PM2.5 was negatively associated with birthweight. An interquartile range increase in PM2.5 was associated with a 16 g [95% confidence interval (CI) = 13, 19] lower birthweight on average, 19 g (95% CI = 15, 23) lower birthweight at the lowest decile of birthweight, and 14 g (95% CI = 9, 19) lower birthweight at the highest decile. In general, the magnitudes of negative associations were larger at lower deciles. We did not find evidence of effect modification by individual or neighborhood SES. CONCLUSIONS: In full-term live births, PM2.5 and birthweight were negatively associated with more severe associations at lower quantiles of birthweight.

4.
Circulation ; 140(8): 645-657, 2019 Aug 20.
Artigo em Inglês | MEDLINE | ID: mdl-31424985

RESUMO

BACKGROUND: DNA methylation is implicated in coronary heart disease (CHD), but current evidence is based on small, cross-sectional studies. We examined blood DNA methylation in relation to incident CHD across multiple prospective cohorts. METHODS: Nine population-based cohorts from the United States and Europe profiled epigenome-wide blood leukocyte DNA methylation using the Illumina Infinium 450k microarray, and prospectively ascertained CHD events including coronary insufficiency/unstable angina, recognized myocardial infarction, coronary revascularization, and coronary death. Cohorts conducted race-specific analyses adjusted for age, sex, smoking, education, body mass index, blood cell type proportions, and technical variables. We conducted fixed-effect meta-analyses across cohorts. RESULTS: Among 11 461 individuals (mean age 64 years, 67% women, 35% African American) free of CHD at baseline, 1895 developed CHD during a mean follow-up of 11.2 years. Methylation levels at 52 CpG (cytosine-phosphate-guanine) sites were associated with incident CHD or myocardial infarction (false discovery rate<0.05). These CpGs map to genes with key roles in calcium regulation (ATP2B2, CASR, GUCA1B, HPCAL1), and genes identified in genome- and epigenome-wide studies of serum calcium (CASR), serum calcium-related risk of CHD (CASR), coronary artery calcified plaque (PTPRN2), and kidney function (CDH23, HPCAL1), among others. Mendelian randomization analyses supported a causal effect of DNA methylation on incident CHD; these CpGs map to active regulatory regions proximal to long non-coding RNA transcripts. CONCLUSION: Methylation of blood-derived DNA is associated with risk of future CHD across diverse populations and may serve as an informative tool for gaining further insight on the development of CHD.

5.
Environ Int ; 130: 104865, 2019 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-31200153

RESUMO

BACKGROUND: Radon is an inert gas formed from the decay of naturally-occurring materials in the earth's crust. It infiltrates into homes from soil, water, and construction materials. Its decay products are radionuclides, which attach to ambient particles. Residential radon is one of the leading risk factors for lung cancer. The scarce evidence for associations with other mortality causes originates mostly from occupational studies. METHODS: In a cohort study with 14 years of follow-up (2000-2013), we evaluated the association between chronic radon exposure and all-cause mortality, and explored whether there are subpopulations who are more vulnerable to radon effects. We included 87,296,195 person-years of follow-up from all Medicare beneficiaries in the Mid-Atlantic and Northeastern U.S. states. We examined the association between the logarithm of county-averaged radon (ln(Rn)) and mortality and assessed effect modification by chronic conditions. RESULTS: An interquartile range increase in the ln(Rn) was associated with a 2·62% increase (95% CI 2·52%; 2·73%) in mortality, independent of PM2.5 exposure. Larger mortality risks were observed among individuals with respiratory, cardiovascular and metabolic diseases, with the highest associations observed among those with diabetes (4·98% increase), heart failure (4·58% increase), and chronic obstructive pulmonary disease (4·49% increase). CONCLUSION: We found an increased risk for all-cause mortality associated with increased radon exposure. The risk was enhanced among susceptible individuals with chronic conditions. We believe this is the first cohort study to identify populations at higher risk for non-malignant health consequences of radon exposure. Due to the limitations in exposure assessment and availability of individual confounders, these findings should be interpreted with caution.

7.
Environ Int ; 126: 228-233, 2019 05.
Artigo em Inglês | MEDLINE | ID: mdl-30822651

RESUMO

Human-induced climate change has accelerated in recent decades, causing adverse health effects. However, the impact of the changing climate on neurological disorders in the older population is not well understood. We applied time-varying Cox proportional hazards models to estimate the associations between hospital admissions for dementia and the mean and variability of summer and winter temperatures in New England. We estimated seasonal temperatures for each New England zip code using a satellite-based prediction model. By characterizing spatial differences and temporal fluctuations in seasonal temperatures, we observed a lower risk of dementia-associated hospital admissions in years when local temperatures in either summer (hazard ration [HR] = 0.98; 95% confidence interval [CI]: 0.96, 1.00) or winter (HR = 0.97; 95% CI: 0.94, 0.99) were higher than average, and a greater risk of dementia-associated admissions for older adults living in zip codes with higher temperature variations. Effect modifications by sex, race, age, and dual eligibility were considered to examine vulnerability of population subgroups. Our results suggest that cooler-than-average temperatures and higher temperature variability increase the risk of dementia-associated hospital admissions. Thus, climate change may affect progression of dementia and associated hospitalization costs.


Assuntos
Mudança Climática , Demência/epidemiologia , Hospitalização/estatística & dados numéricos , Temperatura Ambiente , Idoso , Idoso de 80 Anos ou mais , Feminino , Humanos , Masculino , New England/epidemiologia , Estações do Ano
8.
Artigo em Inglês | MEDLINE | ID: mdl-30845676

RESUMO

Features of the environment may modify the effect of particulate matter ≤2.5 µm in aerodynamic diameter (PM2.5) on health. Therefore, we investigated how neighborhood sociodemographic and land-use characteristics may modify the association between PM2.5 and cardiovascular mortality. We obtained residence-level geocoded cardiovascular mortality cases from the Massachusetts Department of Public Health (n = 179,986), and PM2.5 predictions from a satellite-based model (2001⁻2011). We appended census block group-level information on sociodemographic factors and walkability, and calculated neighborhood greenness within a 250 m buffer surrounding each residence. We found a 2.54% (1.34%; 3.74%) increase in cardiovascular mortality associated with a 10 µg/m³ increase in two-day average PM2.5. Walkability or greenness did not modify the association. However, when stratifying by neighborhood sociodemographic characteristics, smaller PM2.5 effects were observed in greener areas only among cases who resided in neighborhoods with a higher population density and lower percentages of white residents or residents with a high school diploma. In conclusion, the PM2.5 effects on cardiovascular mortality were attenuated by higher greenness only in areas with sociodemographic features that are highly correlated with lower socioeconomic status. Previous evidence suggests health benefits linked to neighborhood greenness may be stronger among lower socioeconomic groups. Attenuation of the PM2.5⁻mortality relationship due to greenness may explain some of this evidence.


Assuntos
Doenças Cardiovasculares/induzido quimicamente , Doenças Cardiovasculares/mortalidade , Material Particulado/efeitos adversos , Características de Residência , Fatores Socioeconômicos , Efeitos Colaterais e Reações Adversas Relacionados a Medicamentos , Feminino , Humanos , Renda , Masculino , Massachusetts , Caminhada
9.
Environ Res ; 171: 36-43, 2019 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-30654247

RESUMO

BACKGROUND: Short-term exposure to air pollution has been associated with cardiovascular events, potentially by promoting endothelial cell activation and inflammation. A few large-scale studies have examined the associations and have had mixed results. METHODS: We included 3820 non-current smoking participants (mean age 56 years, 54% women) from the Framingham Offspring cohort examinations 7 (1998-2001) and 8 (2005-2008), and Third Generation cohort examination 1 (2002-2005), who lived within 50 km of a central monitoring station. We calculated the 1- to 7-day moving averages of fine particulate matter (PM2.5), black carbon (BC), sulfate (SO42-), nitrogen oxides (NOx), and ozone before examination visits. We used linear mixed effect models for P-selectin, monocyte chemoattractant protein 1 (MCP-1), intercellular adhesion molecule 1, lipoprotein-associated phospholipase A2 activity and mass, and osteoprotegerin that were measured up to twice, and linear regression models for CD40 ligand and interleukin-18 that were measured once, adjusting for demographics, life style and clinical factors, socioeconomic position, time, and meteorology. RESULTS: We found negative associations of PM2.5 and BC with P-selectin, of ozone with MCP-1, and of SO42- and NOx with osteoprotegerin. At the 5-day moving average, a 5 µg/m3 higher PM2.5 was associated with 1.6% (95% CI: - 2.8, - 0.3) lower levels of P-selectin; a 10 ppb higher ozone was associated with 1.7% (95% CI: - 3.2, - 0.1) lower levels of MCP-1; and a 20 ppb higher NOx was associated with 2.0% (95% CI: - 3.6, - 0.4) lower levels of osteoprotegerin. CONCLUSIONS: We did not find evidence of positive associations between short-term air pollution exposure and endothelial cell activation. On the contrary, short-term exposure to higher levels of ambient pollutants were associated with lower levels of P-selectin, MCP-1, and osteoprotegerin in the Framingham Heart Study.

10.
Environ Health Perspect ; 126(12): 127008, 2018 12.
Artigo em Inglês | MEDLINE | ID: mdl-30570336

RESUMO

BACKGROUND: Particulate matter (PM) air pollution has been associated with decreased pulmonary function, but the exposure­response relationship in chronic obstructive pulmonary disease (COPD) patients is uncertain, and most studies have only focused on exposures to ambient pollution. OBJECTIVES: We aimed to assess associations between pulmonary function and indoor and ambient PM [Formula: see text] ([Formula: see text]) and black carbon (BC). METHODS: Between November 2012 and December 2014, 125 patients with COPD (mean age, 73.4 y) who were not currently smoking and without known indoor BC sources were recruited. Indoor BC and [Formula: see text] were measured in each home for a week in each season, up to four times a year, followed by in-person spirometry pre- and post-bronchodilator. Ambient exposures were available from a central site monitor. Multivariable adjusted mixed effects regression models were used to assess associations scaled per interquartile range (IQR) of exposure. RESULTS: There were 367 study visits; the median (IQR) indoor BC and [Formula: see text] were 0.19 (0.22) [Formula: see text] and 6.67 (5.80) [Formula: see text], respectively. Increasing indoor exposures to BC were associated with decreases in pre-bronchodilator forced expiratory volume in 1 s [Formula: see text] and forced vital capacity (FVC), and [Formula: see text]. For example, in multivariable adjusted models, each IQR increase in indoor BC from the weekly integrated filter was associated with a [Formula: see text] [95% confidence interval (CI): [Formula: see text], [Formula: see text]] decrease in pre-bronchodilator [Formula: see text]. Increases in indoor [Formula: see text] were associated with decreases in [Formula: see text] and FVC of smaller magnitude than those for indoor BC; however, the results were less precise. Ambient BC was not associated with pre-bronchodilator pulmonary function, ambient [Formula: see text] was only associated with decreases in FVC and increases in [Formula: see text], and neither indoor nor ambient BC or [Formula: see text] were associated with post-bronchodilator pulmonary function. CONCLUSIONS: Low-level exposures to indoor BC and [Formula: see text], but not ambient exposures, were consistently associated with decreases in pre-bronchodilator pulmonary function. There was no association between exposures and post-bronchodilator pulmonary function. https://doi.org/10.1289/EHP3668.


Assuntos
Poluição do Ar em Ambientes Fechados/efeitos adversos , Material Particulado/efeitos adversos , Doença Pulmonar Obstrutiva Crônica/fisiopatologia , Fuligem/efeitos adversos , Idoso , Idoso de 80 Anos ou mais , Poluição do Ar , Broncodilatadores/uso terapêutico , Exposição Ambiental/efeitos adversos , Feminino , Volume Expiratório Forçado/fisiologia , Humanos , Masculino , Massachusetts/epidemiologia , Pessoa de Meia-Idade , Tamanho da Partícula , Capacidade Vital/fisiologia
11.
Environ Int ; 121(Pt 2): 1210-1216, 2018 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-30376999

RESUMO

BACKGROUND: Decay products of radioactive materials may attach to ambient fine particles and form radioactive aerosol. Internal ionizing radiation source from inhaled radioactive aerosol may contribute to the fine particulate matter (PM2.5)-inflammation pathway. However, few studies in humans have examined the associations. OBJECTIVES: To examine the associations between particle radioactivity and biomarkers of oxidative stress and inflammation among participants from the Framingham Offspring and Third Generation cohorts. METHODS: We included 3996 participants who were not current smokers and lived within 50 km from our central air pollution monitoring station. We estimated regional mean gross beta radioactivity from monitors in the northeastern U.S. as a surrogate for ambient radioactive particles, and calculated the 1- to 28-day moving averages. We used linear regression models for fibrinogen, tumor necrosis factor α, interleukin-6, and myeloperoxidase which were measured once, and linear mixed effect models for 8-epi-prostaglandin F2α, C-reactive protein, intercellular adhesion molecule-1 (ICAM-1), monocyte chemoattractant protein-1 (MCP-1), P-selectin, and tumor necrosis factor receptor-2 that were measured up to twice, adjusting for demographics, individual- and area-level socioeconomic positions, time, meteorology, and PM2.5. We also examined whether the associations differed by median age, sex, diabetes status, PM2.5 levels, and black carbon levels. RESULTS: The mean age was 54 years and 54% were women. An interquartile range (3 × 10-3 pCi/m3) higher beta radioactivity level at the 7-day moving average was associated with 5.09% (95% CI: 0.92, 9.43), 2.65% (1.10, 4.22), and 4.71% (95% CI: 3.01, 6.44) higher levels of interleukin-6, MCP-1, and P-selectin, but with 7.01% (95% CI: -11.64, -2.15) and 2.70% (95% CI: -3.97, -1.42) lower levels of 8-epi-prostaglandin F2α and ICAM-1, respectively. CONCLUSIONS: Regional mean particle radioactivity was positively associated with interleukin-6, MCP-1, and P-selectin, but negatively with ICAM-1 and 8-epi-prostaglandin F2α among our study participants.

12.
Sci Total Environ ; 645: 1057-1064, 2018 Dec 15.
Artigo em Inglês | MEDLINE | ID: mdl-30248831

RESUMO

BACKGROUND: Mounting evidence suggests that the natural and built environment can affect human health, but relatively few studies have considered links between features of the residential natural and built environment other than air pollution and complications of pregnancy. OBJECTIVES: To quantify the impact of features of the maternal residential natural and built environments on risk of gestational diabetes mellitus (GDM), gestational hypertension and preeclampsia among 61,640 women who delivered at a single hospital in Rhode Island between 2002 and 2012. METHODS: We estimated residential levels of ambient fine particulate matter (PM2.5) and black carbon (BC) using spatiotemporal models, neighborhood green space using remote sensing and proximity to recreational facilities, and neighborhood blue space using distance to coastal and fresh water. We used logistic regression to separately estimate the association between each feature and GDM, gestational hypertension, and preeclampsia, adjusting for individual and neighborhood markers of socioeconomic status. RESULTS: GDM, gestational hypertension, and preeclampsia were diagnosed in 8.0%, 5.0%, and 3.6% of women, respectively. We found 2nd trimester PM2.5 (OR = 1.08, 95% CI: 1.00, 1.15 per interquartile range increase in PM2.5) and living close to a major roadway (1.09, 95% CI: 1.00, 1.19) were associated with higher odds of GDM, while living <1 km from the coast was associated with lower odds of GDM (0.87, 95% CI: 0.78, 0.96). Living <500 m from a recreational facility was associated with lower odds of gestational hypertension (0.89, 95% CI: 0.80, 0.99). None of these features were associated with odds of preeclampsia. Results were qualitatively similar in mutually-adjusted models and sensitivity analyses. CONCLUSIONS: In this small coastal US state, risk of GDM was positively associated with PM2.5 and proximity to busy roadways, and negatively associated with proximity to blue space, highlighting the importance of the natural and built environment to maternal health.

13.
Sci Total Environ ; 639: 868-875, 2018 Oct 15.
Artigo em Inglês | MEDLINE | ID: mdl-29929325

RESUMO

BACKGROUND: Particulate matter < 2.5 µm in diameter (PM2.5) and heat are strong predictors of morbidity, yet few studies have examined the effects of long-term exposures on non-fatal events, or assessed the short and long-term effect on health simultaneously. OBJECTIVE: We jointly investigated the association of short and long-term exposures to PM2.5 and temperature with hospital admissions, and explored the modification of the associations with the short-term exposures by one another and by temperature variability. METHODS: Daily ZIP code counts of respiratory, cardiac and stroke admissions of adults ≥65 (N = 2,015,660) were constructed across New-England (2001-2011). Daily PM2.5 and temperature exposure estimates were obtained from satellite-based spatio-temporally resolved models. For each admission cause, a Poisson regression was fit on short and long-term exposures, with a random intercept for ZIP code. Modifications of the short-term effects were tested by adding interaction terms with temperature, PM2.5 and temperature variability. RESULTS: Associations between short and long-term exposures were observed for all of the outcomes, with stronger effects of long-term exposures to PM2.5. For respiratory admissions, the short-term PM2.5 effect (percent increase per IQR) was larger on warmer days (1.12% versus -0.53%) and in months of higher temperature variability (1.63% versus -0.45%). The short-term temperature effect was higher in months of higher temperature variability as well. For cardiac admissions, the PM2.5 effect was larger on colder days (0.56% versus -0.30%) and in months of higher temperature variability (0.99% versus -0.56%). CONCLUSIONS: We observed synergistic effects of short-term exposures to PM2.5, temperature and temperature variability. Long-term exposures to PM2.5 were associated with larger effects compared to short-term exposures.

14.
Artigo em Inglês | MEDLINE | ID: mdl-29895795

RESUMO

Natural vegetation, or greenness, may benefit maternal health and consequently, fetal growth, by providing opportunities for physical activity and psychological restoration, and decreasing detrimental environmental exposures. We retrieved Massachusetts Birth Registry data from 2001⁻2013 and investigated the association between residential greenness and birthweight in full-term births (≥37 weeks gestation). We calculated average residential greenness during pregnancy using 250 m normalized difference vegetation index (NDVI) from satellites. We estimated associations between greenness and continuous birthweight, term low birthweight (TLBW: <2500 g), and small for gestational age (SGA: <10th percentile of birthweight stratified by sex and gestational age) adjusted for individual and neighborhood covariates and considered nonlinearity and effect modification. Higher greenness exposure was associated with higher birthweight with stronger associations in the lower than higher range of greenness. Greenness was associated with lower odds of TLBW (OR 0.98; 95% CI 0.97, 0.99 per 0.1 increase in NDVI) and SGA (OR 0.98; 95% 0.97, 0.99) and associations varied by population density (TLBW) and socioeconomic status (TLBW, SGA). Our results suggest that greenness is beneficial to fetal growth exhibited by higher birthweight and lower odds of TLBW and SGA. Unlike prior studies, associations with TLBW and SGA appeared stronger among those with higher socioeconomic status.

15.
Environ Res ; 165: 358-364, 2018 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-29783085

RESUMO

RATIONALE: Evidence linking traffic-related particle exposure to systemic effects in chronic obstructive lung disease (COPD) patients is limited. OBJECTIVES: Assess relationships between indoor black carbon (BC), a tracer of traffic-related particles, and plasma biomarkers of systemic inflammation and endothelial activation. METHODS: BC was measured by reflectance in fine particle samples over a mean of 7.6 days in homes of 85 COPD patients up to 4 times seasonally over a year. After the completion of sampling, plasma C-reactive protein (CRP), interleukin-6 (IL-6), and soluble vascular adhesion molecule-1 (sVCAM-1) were measured. Current smokers and homes with major sources of BC were excluded; therefore, indoor BC was primarily a measure of infiltrated outdoor BC. Mixed effects regression models with a random intercept for each participant were used to assess BC effects at different times (1-9 days before phlebotomy) and in the multi-day sample. RESULTS: Measured median BC was 0.19 µg/m3 (interquartile range, IQR=0.22 µg/m3). Adjusting for season, race, age, BMI, heart disease, diabetes, ambient temperature, relative humidity, a recent cold or similar illness, and blood draw time, there was a positive relationship between BC and CRP. The largest effect size was for BC averaged over the previous seven days (11.8% increase in CRP per IQR; 95%CI = 1.8-22.9). Effects were greatest among non-statin users and persons with diabetes. There were positive effects of BC on IL-6 only in non-statin users. There were no associations with sVCAM-1. CONCLUSIONS: These results demonstrate exposure-response relationships between indoor BC with biomarkers of systemic inflammation in COPD patients, with stronger relationships in persons not using statins and with diabetes.

17.
JAMA Cardiol ; 3(6): 463-472, 2018 Jun 01.
Artigo em Inglês | MEDLINE | ID: mdl-29617535

RESUMO

Importance: Tumor necrosis factor α (TNF-α) is a proinflammatory cytokine with manifold consequences for mammalian pathophysiology, including cardiovascular disease. A deeper understanding of TNF-α biology may enhance treatment precision. Objective: To conduct an epigenome-wide analysis of blood-derived DNA methylation and TNF-α levels and to assess the clinical relevance of findings. Design, Setting, and Participants: This meta-analysis assessed epigenome-wide associations in circulating TNF-α concentrations from 5 cohort studies and 1 interventional trial, with replication in 3 additional cohort studies. Follow-up analyses investigated associations of identified methylation loci with gene expression and incident coronary heart disease; this meta-analysis included 11 461 participants who experienced 1895 coronary events. Exposures: Circulating TNF-α concentration. Main Outcomes and Measures: DNA methylation at approximately 450 000 loci, neighboring DNA sequence variation, gene expression, and incident coronary heart disease. Results: The discovery cohort included 4794 participants, and the replication study included 816 participants (overall mean [SD] age, 60.7 [8.5] years). In the discovery stage, circulating TNF-α levels were associated with methylation of 7 cytosine-phosphate-guanine (CpG) sites, 3 of which were located in or near DTX3L-PARP9 at cg00959259 (ß [SE] = -0.01 [0.003]; P = 7.36 × 10-8), cg08122652 (ß [SE] = -0.008 [0.002]; P = 2.24 × 10-7), and cg22930808(ß [SE] = -0.01 [0.002]; P = 6.92 × 10-8); NLRC5 at cg16411857 (ß [SE] = -0.01 [0.002]; P = 2.14 × 10-13) and cg07839457 (ß [SE] = -0.02 [0.003]; P = 6.31 × 10-10); or ABO, at cg13683939 (ß [SE] = 0.04 [0.008]; P = 1.42 × 10-7) and cg24267699 (ß [SE] = -0.009 [0.002]; P = 1.67 × 10-7), after accounting for multiple testing. Of these, negative associations between TNF-α concentration and methylation of 2 loci in NLRC5 and 1 in DTX3L-14 PARP9 were replicated. Replicated TNF-α-linked CpG sites were associated with 9% to 19% decreased risk of incident coronary heart disease per 10% higher methylation per CpG site (cg16411857: hazard ratio [HR], 0.86; 95% CI, 0.78-1.95; P = .003; cg07839457: HR, 0.89; 95% CI, 0.80-0.94; P = 3.1 × 10-5; cg00959259: HR, 0.91; 95% CI, 0.84-0.97; P = .002; cg08122652: HR, 0.81; 95% CI, 0.74-0.89; P = 2.0 × 10-5). Conclusions and Relevance: We identified and replicated novel epigenetic correlates of circulating TNF-α concentration in blood samples and linked these loci to coronary heart disease risk, opening opportunities for validation and therapeutic applications.

18.
Eur Respir J ; 51(1)2018 01.
Artigo em Inglês | MEDLINE | ID: mdl-29371377

RESUMO

Acute exacerbations and worsening of idiopathic pulmonary fibrosis (IPF) have been associated with exposure to ozone (O3), nitrogen dioxide (NO2) and particulate matter, but chronic exposure to air pollution might also affect the incidence of IPF. We investigated the association between chronic exposure to NO2, O3 and particulate matter with an aerodynamic diameter <10 µm (PM10) and IPF incidence in Northern Italy between 2005 and 2010.Daily predictions of PM10 concentrations were obtained from spatiotemporal models, and NO2 and O3 hourly concentrations from fixed monitoring stations. We identified areas with homogenous exposure to each pollutant. We built negative binomial models to assess the association between area-specific IPF incidence rate, estimated through administrative databases, and average overall and seasonal PM10, NO2, and 8-hour maximum O3 concentrations.Using unadjusted models, an increment of 10 µg·m-3 in NO2 concentration was associated with an increase between 7.93% (95% CI 0.36-16.08%) and 8.41% (95% CI -0.23-17.80%) in IPF incidence rate, depending on the season. After adjustment for potential confounders, estimated effects were similar in magnitude, but with larger confidence intervals.Although confirmatory studies are needed, our results trace a potential association between exposure to traffic pollution and the development of IPF.

19.
Environ Res ; 161: 464-471, 2018 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-29220799

RESUMO

BACKGROUND: How adaptation and intensity of heat waves affect heat wave-related mortality is unclear, making health projections difficult. METHODS: We estimated the effect of heat waves, the effect of the intensity of heat waves, and adaptation on mortality in 209 U.S. cities with 168 million people during 1962-2006. We improved the standard time-series models by incorporating the intensity of heat waves using excess heat factor (EHF) and estimating adaptation empirically using interactions with yearly mean summer temperature (MST). We combined the epidemiological estimates for heat wave, intensity, and adaptation with the Coupled Model Intercomparison Project Phase 5 (CMIP5) multi-model dataset to project heat wave-related mortality by 2050. RESULTS: The effect of heat waves increased with its intensity. Adaptation to heat waves occurred, which was shown by the decreasing effect of heat waves with MST. However, adaptation was lessened as MST increased. Ignoring adaptation in projections would result in a substantial overestimate of the projected heat wave-related mortality (by 277-747% in 2050). Incorporating the empirically estimated adaptation into projections would result in little change in the projected heat wave-related mortality between 2006 and 2050. This differs regionally, however, with increasing mortality over time for cities in the southern and western U.S. but decreasing mortality over time for the north. CONCLUSIONS: Accounting for adaptation is important to reduce bias in the projections of heat wave-related mortality. The finding that the southern and western U.S. are the areas that face increasing heat-related deaths is novel, and indicates that more regional adaptation strategies are needed.

20.
Environ Int ; 111: 14-22, 2018 02.
Artigo em Inglês | MEDLINE | ID: mdl-29161632

RESUMO

OBJECTIVE: To examine associations of proximity to major roadways, sustained exposure to fine particulate matter (PM2.5), and acute exposure to ambient air pollutants with adipokines and measures of glucose homeostasis among participants living in the northeastern United States. METHODS: We included 5958 participants from the Framingham Offspring cohort examination cycle 7 (1998-2001) and 8 (2005-2008) and Third Generation cohort examination cycle 1 (2002-2005) and 2 (2008-2011), who did not have type 2 diabetes at the time of examination visit. We calculated 2003 annual average PM2.5 at participants' home address, residential distance to the nearest major roadway, and daily PM2.5, black carbon (BC), sulfate, nitrogen oxides (NOx), and ozone concentrations. We used linear mixed effects models for fasting glucose, insulin, and homeostasis model assessment of insulin resistance (HOMA-IR) which were measured up to twice, and used linear regression models for adiponectin, resistin, leptin, and hemoglobin A1c (HbA1c) which were measured only once, adjusting for demographics, socioeconomic position, lifestyle, time, and seasonality. RESULTS: The mean age was 51years and 55% were women. Participants who lived 64m (25th percentile) from a major roadway had 0.28% (95% CI: 0.05%, 0.51%) higher fasting plasma glucose than participants who lived 413m (75th percentile) away, and the association appeared to be driven by participants who lived within 50m from a major roadway. Higher exposures to 3- to 7-day moving averages of BC and NOx were associated with higher glucose whereas the associations for ozone were negative. The associations otherwise were generally null and did not differ by median age, sex, educational attainment, obesity status, or prediabetes status. CONCLUSIONS: Living closer to a major roadway or acute exposure to traffic-related air pollutants were associated with dysregulated glucose homeostasis but not with adipokines among participants from the Framingham Offspring and Third Generation cohorts.


Assuntos
Adipocinas/sangue , Poluentes Atmosféricos/análise , Poluição do Ar/análise , Glucose/metabolismo , Adulto , Idoso , Estudos de Coortes , Monitoramento Ambiental , Feminino , Hemoglobina A Glicada/análise , Homeostase , Habitação , Humanos , Modelos Lineares , Masculino , Pessoa de Meia-Idade , Óxidos de Nitrogênio/análise , Ozônio/análise , Material Particulado/análise , Fuligem/análise , Sulfatos/análise , Emissões de Veículos
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