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1.
Environ Health Perspect ; 127(8): 87001, 2019 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-31393792

RESUMO

BACKGROUND: Telomere length is a molecular marker of biological aging. OBJECTIVE: Here we investigated whether early-life exposure to residential air pollution was associated with leukocyte telomere length (LTL) at 8 y of age. METHODS: In a multicenter European birth cohort study, HELIX (Human Early Life Exposome) ([Formula: see text]), we estimated prenatal and 1-y childhood exposure to nitrogen dioxide ([Formula: see text]), particulate matter with aerodynamic diameter [Formula: see text] ([Formula: see text]), and proximity to major roads. Average relative LTL was measured using quantitative real-time polymerase chain reaction (qPCR). Effect estimates of the association between LTL and prenatal, 1-y childhood air pollution, and proximity to major roads were calculated using multiple linear mixed models with a random cohort effect and adjusted for relevant covariates. RESULTS: LTL was inversely associated with prenatal and 1-y childhood [Formula: see text] and [Formula: see text] exposures levels. Each standard deviation (SD) increase in prenatal [Formula: see text] was associated with a [Formula: see text] (95% CI: [Formula: see text], [Formula: see text]) change in LTL. Prenatal [Formula: see text] was nonsignificantly associated with LTL ([Formula: see text] per SD increase; 95% CI: [Formula: see text], 0.6). For each SD increment in 1-y childhood [Formula: see text] and [Formula: see text] exposure, LTL shortened by [Formula: see text] (95% CI: [Formula: see text], [Formula: see text]) and [Formula: see text] (95% CI: [Formula: see text], 0.1), respectively. Each doubling in residential distance to nearest major road during childhood was associated with a 1.6% (95% CI: 0.02, 3.1) lengthening in LTL. CONCLUSION: Lower exposures to air pollution during pregnancy and childhood were associated with longer telomeres in European children at 8 y of age. These results suggest that reductions in traffic-related air pollution may promote molecular longevity, as exemplified by telomere length, from early life onward. https://doi.org/10.1289/EHP4148.

2.
Environ Int ; 131: 104927, 2019 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-31326824

RESUMO

BACKGROUND: The association between air pollution exposure and emotional and behavioural problems in children is unclear. We aimed to assess prenatal and postnatal exposure to several air pollutants and child's depressive and anxiety symptoms, and aggressive symptoms in children of 7-11 years. METHODS: We analysed data of 13182 children from 8 European population-based birth cohorts. Concentrations of nitrogen dioxide (NO2), nitrogen oxides (NOx), particulate matter (PM) with diameters of ≤10 µm (PM10), ≤ 2.5 µm (PM2.5), and between 10 and 2.5 µm (PMcoarse), the absorbance of PM2.5 filters (PM2.5abs), and polycyclic aromatic hydrocarbons (PAHs) were estimated at residential addresses of each participant. Depressive and anxiety symptoms and aggressive symptoms were assessed at 7-11 years of age using parent reported tests. Children were classified in borderline/clinical range or clinical range using validated cut offs. Region specific models were adjusted for various socio-economic and lifestyle characteristics and then combined using random effect meta-analysis. Multiple imputation and inverse probability weighting methods were applied to correct for potential attrition bias. RESULTS: A total of 1896 (14.4%) children were classified as having depressive and anxiety symptoms in the borderline/clinical range, and 1778 (13.4%) as having aggressive symptoms in the borderline/clinical range. Overall, 1108 (8.4%) and 870 (6.6%) children were classified as having depressive and anxiety symptoms, and aggressive symptoms in the clinical range, respectively. Prenatal exposure to air pollution was not associated with depressive and anxiety symptoms in the borderline/clinical range (e.g. OR 1.02 [95%CI 0.95 to 1.10] per 10 µg/m3 higher NO2) nor with aggressive symptoms in the borderline/clinical range (e.g. OR 1.04 [95%CI 0.96 to 1.12] per 10 µg/m3 higher NO2). Similar results were observed for the symptoms in the clinical range, and for postnatal exposures to air pollution. CONCLUSIONS: Overall, our results suggest that prenatal and postnatal exposure to air pollution is not associated with depressive and anxiety symptoms or aggressive symptoms in children of 7 to 11 years old.

3.
Environ Health Perspect ; 127(5): 57012, 2019 May.
Artigo em Inglês | MEDLINE | ID: mdl-31148503

RESUMO

BACKGROUND: Prenatal exposure to air pollution has been associated with childhood respiratory disease and other adverse outcomes. Epigenetics is a suggested link between exposures and health outcomes. OBJECTIVES: We aimed to investigate associations between prenatal exposure to particulate matter (PM) with diameter [Formula: see text] ([Formula: see text]) or [Formula: see text] ([Formula: see text]) and DNA methylation in newborns and children. METHODS: We meta-analyzed associations between exposure to [Formula: see text] ([Formula: see text]) and [Formula: see text] ([Formula: see text]) at maternal home addresses during pregnancy and newborn DNA methylation assessed by Illumina Infinium HumanMethylation450K BeadChip in nine European and American studies, with replication in 688 independent newborns and look-up analyses in 2,118 older children. We used two approaches, one focusing on single cytosine-phosphate-guanine (CpG) sites and another on differentially methylated regions (DMRs). We also related PM exposures to blood mRNA expression. RESULTS: Six CpGs were significantly associated [false discovery rate (FDR) [Formula: see text]] with prenatal [Formula: see text] and 14 with [Formula: see text] exposure. Two of the [Formula: see text] CpGs mapped to FAM13A (cg00905156) and NOTCH4 (cg06849931) previously associated with lung function and asthma. Although these associations did not replicate in the smaller newborn sample, both CpGs were significant ([Formula: see text]) in 7- to 9-y-olds. For cg06849931, however, the direction of the association was inconsistent. Concurrent [Formula: see text] exposure was associated with a significantly higher NOTCH4 expression at age 16 y. We also identified several DMRs associated with either prenatal [Formula: see text] and or [Formula: see text] exposure, of which two [Formula: see text] DMRs, including H19 and MARCH11, replicated in newborns. CONCLUSIONS: Several differentially methylated CpGs and DMRs associated with prenatal PM exposure were identified in newborns, with annotation to genes previously implicated in lung-related outcomes. https://doi.org/10.1289/EHP4522.

4.
Mol Biol Evol ; 36(4): 852-860, 2019 04 01.
Artigo em Inglês | MEDLINE | ID: mdl-30657943

RESUMO

Gene-environment association (GEA) studies are essential to understand the past and ongoing adaptations of organisms to their environment, but those studies are complicated by confounding due to unobserved demographic factors. Although the confounding problem has recently received considerable attention, the proposed approaches do not scale with the high-dimensionality of genomic data. Here, we present a new estimation method for latent factor mixed models (LFMMs) implemented in an upgraded version of the corresponding computer program. We developed a least-squares estimation approach for confounder estimation that provides a unique framework for several categories of genomic data, not restricted to genotypes. The speed of the new algorithm is several order faster than existing GEA approaches and then our previous version of the LFMM program. In addition, the new method outperforms other fast approaches based on principal component or surrogate variable analysis. We illustrate the program use with analyses of the 1000 Genomes Project data set, leading to new findings on adaptation of humans to their environment, and with analyses of DNA methylation profiles providing insights on how tobacco consumption could affect DNA methylation in patients with rheumatoid arthritis. Software availability: Software is available in the R package lfmm at https://bcm-uga.github.io/lfmm/.


Assuntos
Adaptação Biológica/genética , Algoritmos , Estudo de Associação Genômica Ampla , Software , Artrite Reumatoide/genética , Clima , Metilação de DNA , Interação Gene-Ambiente , Humanos , Fumar/efeitos adversos
5.
Environ Int ; 121(Pt 2): 1079-1086, 2018 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-30389379

RESUMO

Outdoor air pollution is a leading environmental cause of death and cancer incidence in humans. We aimed to estimate the fraction of lung cancer incidence attributable to fine particulate matter (PM2.5) exposure in France, and secondarily to illustrate the influence of the input data and the spatial resolution of information on air pollution levels on this estimate. The population attributable fraction (PAF) was estimated using a nationwide spatially refined chemistry-transport model with a 2-km spatial resolution, neighbourhood-scale population density data, and a relative risk from a published meta-analysis. We used the WHO guideline value for PM2.5 exposure (10 µg/m3) as reference. Sensitivity analyses consisted in attributing the nation-wide median exposure to all areas and using alternative input data such as reference of PM2.5 exposure level and relative risk. Population-weighted median PM2.5 level in 2005 was 13.8 µg/m3; 87% of the population was exposed above the guideline value. The burden of lung cancer attributable to PM2.5 exposure corresponded to 1466 cases, or 3.6% of all cases diagnosed in 2015. Sensitivity analyses showed that the use of a national median of PM2.5 exposure would have led to an underestimation of the PAF by 11% (population-weighted median) and by 72% (median of raw concentration), suggesting that our estimates would have been higher with even more finely spatially-resolved models. When the PM2.5 reference level was replaced by the 5th percentile of country-scale exposure (4.9 µg/m3), PAF increased to 7.6%. Other sensitivity analyses resulted in even higher PAFs. Improvements in air pollution are crucial for quantitative health impacts assessment studies. Actions to reduce PM2.5 levels could substantially reduce the burden of lung cancer in France.

6.
Environ Health Perspect ; 126(7): 077005, 2018 07.
Artigo em Inglês | MEDLINE | ID: mdl-30024382

RESUMO

BACKGROUND: The urban exposome is the set of environmental factors that are experienced in the outdoor urban environment and that may influence child development. OBJECTIVE: The authors' goal was to describe the urban exposome among European pregnant women and understand its socioeconomic determinants. METHODS: Using geographic information systems, remote sensing and spatio-temporal modeling we estimated exposure during pregnancy to 28 environmental indicators in almost 30,000 women from six population-based birth cohorts, in nine urban areas from across Europe. Exposures included meteorological factors, air pollutants, traffic noise, traffic indicators, natural space, the built environment, public transport, facilities, and walkability. Socioeconomic position (SEP), assessed at both the area and individual level, was related to the exposome through an exposome-wide association study and principal component (PC) analysis. RESULTS: Mean±standard deviation (SD) NO2 levels ranged from 13.6±5.1 µg/m3 (in Heraklion, Crete) to 43.2±11 µg/m3 (in Sabadell, Spain), mean±SD walkability score ranged from 0.22±0.04 (Kaunas, Lithuania) to 0.32±0.07 (Valencia, Spain) and mean±SD Normalized Difference Vegetation Index ranged from 0.21±0.05 in Heraklion to 0.51±0.1 in Oslo, Norway. Four PCs explained more than half of variation in the urban exposome. There was considerable heterogeneity in social patterning of the urban exposome across cities. For example, high-SEP (based on family education) women lived in greener, less noisy, and less polluted areas in Bradford, UK (0.39 higher PC1 score, 95% confidence interval (CI): 0.31, 0.47), but the reverse was observed in Oslo (-0.57 PC1 score, 95% CI: -0.73, -0.41). For most cities, effects were stronger when SEP was assessed at the area level: In Bradford, women living in high SEP areas had a 1.34 higher average PC1 score (95% CI: 1.21, 1.48). CONCLUSIONS: The urban exposome showed considerable variability across Europe. Pregnant women of low SEP were exposed to higher levels of environmental hazards in some cities, but not others, which may contribute to inequities in child health and development. https://doi.org/10.1289/EHP2862.

7.
Environ Int ; 118: 334-347, 2018 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-29935799

RESUMO

BACKGROUND: Air pollution exposure represents a major health threat to the developing foetus. DNA methylation is one of the most well-known molecular determinants of the epigenetic status of cells. Blood DNA methylation has been proven sensitive to air pollutants, but the molecular impact of air pollution on new-borns has so far received little attention. OBJECTIVES: We investigated whether nitrogen dioxide (NO2), particulate matter (PM10), temperature and humidity during pregnancy are associated with differences in placental DNA methylation levels. METHODS: Whole-genome DNA-methylation was measured using the Illumina's Infinium HumanMethylation450 BeadChip in the placenta of 668 newborns from the EDEN cohort. We designed an original strategy using a priori biological information to focus on candidate genes with a specific expression pattern in placenta (active or silent) combined with an agnostic epigenome-wide association study (EWAS). We used robust linear regression to identify CpGs and differentially methylated regions (DMR) associated with each exposure during short- and long-term time-windows. RESULTS: The candidate genes approach identified nine CpGs mapping to 9 genes associated with prenatal NO2 and PM10 exposure [false discovery rate (FDR) p < 0.05]. Among these, the methylation level of 2 CpGs located in ADORA2B remained significantly associated with NO2 exposure during the 2nd trimester and whole pregnancy in the EWAS (FDR p < 0.05). EWAS further revealed associations between the environmental exposures under study and variations of DNA methylation of 4 other CpGs. We further identified 27 DMRs significantly (FDR p < 0.05) associated with air pollutants exposure and 13 DMRs with meteorological conditions. CONCLUSIONS: The methylation of ADORA2B, a gene whose expression was previously associated with hypoxia and pre-eclampsia, was consistently found here sensitive to atmospheric pollutants. In addition, air pollutants were associated to DMRs pointing towards genes previously implicated in preeclampsia, hypertensive and metabolic disorders. These findings demonstrate that air pollutants exposure at levels commonly experienced in the European population are associated with placental gene methylation and provide some mechanistic insight into some of the reported effects of air pollutants on preeclampsia.

8.
Environ Res ; 165: 110-117, 2018 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-29684737

RESUMO

While the effects of weather variability on cardio-respiratory mortality are well described, research examining the effects on morbidity, especially for vulnerable populations, is warranted. We investigated the associations between lung function and outdoor temperature (T in Celsius degrees (°C)) and relative humidity (RH), in a cohort of elderly men, the Normative Aging Study. Our study included 1103 participants whose forced vital capacity (FVC), forced expiratory volume in one second (FEV1), and weather exposures were assessed one to five times during the period 1995-2011 (i.e. 3162 observations). Temperature and relative humidity were measured at one location 4 h to 7 days before lung function tests. We used linear mixed-effects models to examine the associations with outdoor T and RH. A 5-degree increase in the 3-day moving average T was associated with a significant 0.7% decrease (95%CI: -1.24, -0.20) in FVC and a 5% increase in the 7-day moving average RH was associated with a significant 0.2% decrease (95%CI: -0.40, -0.02) in FVC and FEV1. The associations with T were greater when combined with higher exposures of black carbon with a 1.6% decrease (95%CI -2.2; -0.9) in FVC and a 1% decrease (95%CI -1.7; -0.4) in FEV1. The relationships between T and RH and lung function were linear. No synergistic effect of T and RH was found. Heat and lung function are two predictors of mortality. Our findings suggest that increases in temperature and relative humidity are related to decreases in lung function, and such observations might be amplified by high black carbon levels.

9.
Int J Cancer ; 142(5): 874-882, 2018 03 01.
Artigo em Inglês | MEDLINE | ID: mdl-28836271

RESUMO

The interaction between the (epi)genetic makeup of an individual and his/her environmental exposure record (exposome) is accepted as a determinant factor for a significant proportion of human malignancies. Recent evidence has highlighted the key role of epigenetic mechanisms in mediating gene-environment interactions and translating exposures into tumorigenesis. There is also growing evidence that epigenetic changes may be risk factor-specific ("fingerprints") that should prove instrumental in the discovery of new biomarkers in cancer. Here, we review the state of the science of epigenetics associated with environmental stimuli and cancer risk, highlighting key developments in the field. Critical knowledge gaps and research needs are discussed and advances in epigenomics that may help in understanding the functional relevance of epigenetic alterations. Key elements required for causality inferences linking epigenetic changes to exposure and cancer are discussed and how these alterations can be incorporated in carcinogen evaluation and in understanding mechanisms underlying epigenome deregulation by the environment.


Assuntos
Exposição Ambiental/efeitos adversos , Epigênese Genética , Epigenômica , Interação Gene-Ambiente , Neoplasias/etiologia , Animais , Metilação de DNA , Humanos , Neoplasias/patologia , Fatores de Risco
10.
J Epidemiol Community Health ; 71(10): 1026-1036, 2017 10.
Artigo em Inglês | MEDLINE | ID: mdl-28830952

RESUMO

BACKGROUND: Exposure to atmospheric pollutants is a danger for the health of pregnant mother and children. Our objective was to identify individual (socioeconomic and behavioural) and contextual factors associated with atmospheric pollution pregnancy exposure at the nationwide level. METHOD: Among 14 921 women from the French nationwide ELFE (French Longitudinal Study of Children) mother-child cohort recruited in 2011, outdoor exposure levels of PM2.5, PM10 (particulate matter <2.5 µm and <10 µm in diameter) and NO2 (nitrogen dioxide) were estimated at the pregnancy home address from a dispersion model with 1 km resolution. We used classification and regression trees (CART) and linear regression to characterise the association of atmospheric pollutants with individual (maternal age, body mass index, parity, education level, relationship status, smoking status) and contextual (European Deprivation Index, urbanisation level) factors. RESULTS: Patterns of associations were globally similar across pollutants. For the CART approach, the highest tertile of exposure included mainly women not in a relationship living in urban and socially deprived areas, with lower education level. Linear regression models identified different determinants of atmospheric pollutants exposure according to the residential urbanisation level. In urban areas, atmospheric pollutants exposure increased with social deprivation, while in rural areas a U-shaped relationship was observed. CONCLUSION: We highlighted social inequalities in atmospheric pollutants exposure according to contextual characteristics such as urbanisation level and social deprivation and also according to individual characteristics such as education, being in a relationship and smoking status. In French urban areas, pregnant women from the most deprived neighbourhoods were those most exposed to health-threatening atmospheric pollutants.


Assuntos
Poluentes Atmosféricos/efeitos adversos , Exposição Ambiental/efeitos adversos , Poluição Ambiental/efeitos adversos , Características de Residência , Fatores Socioeconômicos , Urbanização , Adulto , Criança , Estudos de Coortes , Feminino , França , Humanos , Masculino , Exposição Materna , Dióxido de Nitrogênio/efeitos adversos , Material Particulado/efeitos adversos , Gravidez , Gestantes , População Rural , População Urbana , Emissões de Veículos
11.
Eur Respir J ; 49(1)2017 01.
Artigo em Inglês | MEDLINE | ID: mdl-28100545

RESUMO

An irreversible loss in lung function limits the long-term success in lung transplantation. We evaluated the role of chronic exposure to ambient air pollution on lung function levels in lung transplant recipients (LTRs).The lung function of 520 LTRs from the Cohort in Lung Transplantation (COLT) study was measured every 6 months. The levels of air pollutants (nitrogen dioxide (NO2), particulate matter with an aerodynamic cut-off diameter of x µm (PMx) and ozone (O3)) at the patients' home address were averaged in the 12 months before each spirometry test. The effects of air pollutants on forced expiratory volume in 1 s (FEV1) and forced vital capacity (FVC) in % predicted were estimated using mixed linear regressions. We assessed the effect modification of macrolide antibiotics in this relationship.Increased 12-month levels of pollutants were associated with lower levels of FVC % pred (-2.56%, 95% CI -3.86--1.25 for 5 µg·m-3 of PM10; -0.75%, 95% CI -1.38--0.12 for 2 µg·m-3 of PM2.5 and -2.58%, 95% CI -4.63--0.53 for 10 µg·m-3 of NO2). In patients not taking macrolides, the deleterious association between PM and FVC tended to be stronger and PM10 was associated with lower FEV1Our study suggests a deleterious effect of chronic exposure to air pollutants on lung function levels in LTRs, which might be modified with macrolides.


Assuntos
Poluição do Ar/efeitos adversos , Transplante de Pulmão , Pulmão/fisiopatologia , Material Particulado/análise , Disfunção Primária do Enxerto/fisiopatologia , Adolescente , Adulto , Idoso , Aloenxertos , Bronquiolite Obliterante/etiologia , Bronquiolite Obliterante/fisiopatologia , Doença Crônica , Exposição Ambiental , Feminino , Volume Expiratório Forçado , França , Humanos , Modelos Lineares , Estudos Longitudinais , Masculino , Pessoa de Meia-Idade , Dióxido de Nitrogênio/análise , Ozônio/análise , Espirometria , Capacidade Vital , Adulto Jovem
12.
Am J Epidemiol ; 185(4): 247-258, 2017 02 15.
Artigo em Inglês | MEDLINE | ID: mdl-28087514

RESUMO

Atmospheric pollutants and meteorological conditions are suspected to be causes of preterm birth. We aimed to characterize their possible association with the risk of preterm birth (defined as birth occurring before 37 completed gestational weeks). We pooled individual data from 13 birth cohorts in 11 European countries (71,493 births from the period 1994-2011, European Study of Cohorts for Air Pollution Effects (ESCAPE)). City-specific meteorological data from routine monitors were averaged over time windows spanning from 1 week to the whole pregnancy. Atmospheric pollution measurements (nitrogen oxides and particulate matter) were combined with data from permanent monitors and land-use data into seasonally adjusted land-use regression models. Preterm birth risks associated with air pollution and meteorological factors were estimated using adjusted discrete-time Cox models. The frequency of preterm birth was 5.0%. Preterm birth risk tended to increase with first-trimester average atmospheric pressure (odds ratio per 5-mbar increase = 1.06, 95% confidence interval: 1.01, 1.11), which could not be distinguished from altitude. There was also some evidence of an increase in preterm birth risk with first-trimester average temperature in the -5°C to 15°C range, with a plateau afterwards (spline coding, P = 0.08). No evidence of adverse association with atmospheric pollutants was observed. Our study lends support for an increase in preterm birth risk with atmospheric pressure.


Assuntos
Poluentes Atmosféricos/efeitos adversos , Pressão Atmosférica , Conceitos Meteorológicos , Nascimento Prematuro/etiologia , Europa (Continente) , Humanos , Nascimento Prematuro/induzido quimicamente , Modelos de Riscos Proporcionais , Saúde da População Urbana
13.
Environ Health Perspect ; 125(1): 104-110, 2017 01.
Artigo em Inglês | MEDLINE | ID: mdl-27448387

RESUMO

BACKGROUND: Prenatal exposure to air pollution is considered to be associated with adverse effects on child health. This may partly be mediated by mechanisms related to DNA methylation. OBJECTIVES: We investigated associations between exposure to air pollution, using nitrogen dioxide (NO2) as marker, and epigenome-wide cord blood DNA methylation. METHODS: We meta-analyzed the associations between NO2 exposure at residential addresses during pregnancy and cord blood DNA methylation (Illumina 450K) in four European and North American studies (n = 1,508) with subsequent look-up analyses in children ages 4 (n = 733) and 8 (n = 786) years. Additionally, we applied a literature-based candidate approach for antioxidant and anti-inflammatory genes. To assess influence of exposure at the transcriptomics level, we related mRNA expression in blood cells to NO2 exposure in 4- (n = 111) and 16-year-olds (n = 239). RESULTS: We found epigenome-wide significant associations [false discovery rate (FDR) p < 0.05] between maternal NO2 exposure during pregnancy and DNA methylation in newborns for 3 CpG sites in mitochondria-related genes: cg12283362 (LONP1), cg24172570 (3.8 kbp upstream of HIBADH), and cg08973675 (SLC25A28). The associations with cg08973675 methylation were also significant in the older children. Further analysis of antioxidant and anti-inflammatory genes revealed differentially methylated CpGs in CAT and TPO in newborns (FDR p < 0.05). NO2 exposure at the time of biosampling in childhood had a significant impact on CAT and TPO expression. CONCLUSIONS: NO2 exposure during pregnancy was associated with differential offspring DNA methylation in mitochondria-related genes. Exposure to NO2 was also linked to differential methylation as well as expression of genes involved in antioxidant defense pathways. Citation: Gruzieva O, Xu CJ, Breton CV, Annesi-Maesano I, Antó JM, Auffray C, Ballereau S, Bellander T, Bousquet J, Bustamante M, Charles MA, de Kluizenaar Y, den Dekker HT, Duijts L, Felix JF, Gehring U, Guxens M, Jaddoe VV, Jankipersadsing SA, Merid SK, Kere J, Kumar A, Lemonnier N, Lepeule J, Nystad W, Page CM, Panasevich S, Postma D, Slama R, Sunyer J, Söderhäll C, Yao J, London SJ, Pershagen G, Koppelman GH, Melén E. 2017. Epigenome-wide meta-analysis of methylation in children related to prenatal NO2 air pollution exposure. Environ Health Perspect 125:104-110; http://dx.doi.org/10.1289/EHP36.


Assuntos
Poluentes Atmosféricos/análise , Poluição do Ar/estatística & dados numéricos , Metilação de DNA , Exposição Materna/estatística & dados numéricos , Dióxido de Nitrogênio/análise , Efeitos Tardios da Exposição Pré-Natal/epidemiologia , Criança , Feminino , Humanos , Recém-Nascido , Londres , Gravidez
14.
J Air Waste Manag Assoc ; 67(1): 27-38, 2017 01.
Artigo em Inglês | MEDLINE | ID: mdl-27589199

RESUMO

Airborne particulate matter (PM) is derived from diverse sources-natural and anthropogenic. Climate change processes and remote sensing measurements are affected by the PM properties, which are often lumped into homogeneous size fractions that show spatiotemporal variation. Since different sources are attributed to different geographic locations and show specific spatial and temporal PM patterns, we explored the spatiotemporal characteristics of the PM2.5/PM10 ratio in different areas. Furthermore, we examined the statistical relationships between AERONET aerosol optical depth (AOD) products, satellite-based AOD, and the PM ratio, as well as the specific PM size fractions. PM data from the northeastern United States, from San Joaquin Valley, CA, and from Italy, Israel, and France were analyzed, as well as the spatial and temporal co-measured AOD products obtained from the MultiAngle Implementation of Atmospheric Correction (MAIAC) algorithm. Our results suggest that when both the AERONET AOD and the AERONET fine-mode AOD are available, the AERONET AOD ratio can be a fair proxy for the ground PM ratio. Therefore, we recommend incorporating the fine-mode AERONET AOD in the calibration of MAIAC. Along with a relatively large variation in the observed PM ratio (especially in the northeastern United States), this shows the need to revisit MAIAC assumptions on aerosol microphysical properties, and perhaps their seasonal variability, which are used to generate the look-up tables and conduct aerosol retrievals. Our results call for further scrutiny of satellite-borne AOD, in particular its errors, limitations, and relation to the vertical aerosol profile and the particle size, shape, and composition distribution. This work is one step of the required analyses to gain better understanding of what the satellite-based AOD represents. IMPLICATIONS: The analysis results recommend incorporating the fine-mode AERONET AOD in MAIAC calibration. Specifically, they indicate the need to revisit MAIAC regional aerosol microphysical model assumptions used to generate look-up tables (LUTs) and conduct retrievals. Furthermore, relatively large variations in measured PM ratio shows that adding seasonality in aerosol microphysics used in LUTs, which is currently static, could also help improve accuracy of MAIAC retrievals. These results call for further scrutiny of satellite-borne AOD for better understanding of its limitations and relation to the vertical aerosol profile and particle size, shape, and composition.


Assuntos
Aerossóis/química , Poluentes Atmosféricos/química , Monitoramento Ambiental/métodos , Material Particulado/química , Poluição do Ar , Calibragem , California , França , Israel , Itália , Tamanho da Partícula
15.
Environ Res ; 151: 1-10, 2016 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-27447442

RESUMO

Satellite-derived (SAT) and chemical transport model (CTM) estimates of PM2.5 and NO2 are increasingly used in combination with Land Use Regression (LUR) models. We aimed to compare the contribution of SAT and CTM data to the performance of LUR PM2.5 and NO2 models for Europe. Four sets of models, all including local traffic and land use variables, were compared (LUR without SAT or CTM, with SAT only, with CTM only, and with both SAT and CTM). LUR models were developed using two monitoring data sets: PM2.5 and NO2 ground level measurements from the European Study of Cohorts for Air Pollution Effects (ESCAPE) and from the European AIRBASE network. LUR PM2.5 models including SAT and SAT+CTM explained ~60% of spatial variation in measured PM2.5 concentrations, substantially more than the LUR model without SAT and CTM (adjR2: 0.33-0.38). For NO2 CTM improved prediction modestly (adjR2: 0.58) compared to models without SAT and CTM (adjR2: 0.47-0.51). Both monitoring networks are capable of producing models explaining the spatial variance over a large study area. SAT and CTM estimates of PM2.5 and NO2 significantly improved the performance of high spatial resolution LUR models at the European scale for use in large epidemiological studies.


Assuntos
Poluentes Atmosféricos/análise , Modelos Teóricos , Dióxido de Nitrogênio/análise , Material Particulado/análise , Movimentos do Ar , Monitoramento Ambiental/estatística & dados numéricos , Europa (Continente) , Análise de Regressão , Comunicações Via Satélite
16.
Am J Hum Genet ; 98(4): 680-96, 2016 Apr 07.
Artigo em Inglês | MEDLINE | ID: mdl-27040690

RESUMO

Epigenetic modifications, including DNA methylation, represent a potential mechanism for environmental impacts on human disease. Maternal smoking in pregnancy remains an important public health problem that impacts child health in a myriad of ways and has potential lifelong consequences. The mechanisms are largely unknown, but epigenetics most likely plays a role. We formed the Pregnancy And Childhood Epigenetics (PACE) consortium and meta-analyzed, across 13 cohorts (n = 6,685), the association between maternal smoking in pregnancy and newborn blood DNA methylation at over 450,000 CpG sites (CpGs) by using the Illumina 450K BeadChip. Over 6,000 CpGs were differentially methylated in relation to maternal smoking at genome-wide statistical significance (false discovery rate, 5%), including 2,965 CpGs corresponding to 2,017 genes not previously related to smoking and methylation in either newborns or adults. Several genes are relevant to diseases that can be caused by maternal smoking (e.g., orofacial clefts and asthma) or adult smoking (e.g., certain cancers). A number of differentially methylated CpGs were associated with gene expression. We observed enrichment in pathways and processes critical to development. In older children (5 cohorts, n = 3,187), 100% of CpGs gave at least nominal levels of significance, far more than expected by chance (p value < 2.2 × 10(-16)). Results were robust to different normalization methods used across studies and cell type adjustment. In this large scale meta-analysis of methylation data, we identified numerous loci involved in response to maternal smoking in pregnancy with persistence into later childhood and provide insights into mechanisms underlying effects of this important exposure.


Assuntos
Metilação de DNA , Epigênese Genética , Fumar/efeitos adversos , Asma/etiologia , Asma/genética , Criança , Pré-Escolar , Mapeamento Cromossômico , Fenda Labial/etiologia , Fenda Labial/genética , Fissura Palatina/etiologia , Fissura Palatina/genética , Grupo com Ancestrais do Continente Europeu/genética , Feminino , Estudos de Associação Genética , Humanos , Lactente , Recém-Nascido , Gravidez
17.
Med Sci (Paris) ; 32(1): 21-6, 2016 Jan.
Artigo em Francês | MEDLINE | ID: mdl-26850603

RESUMO

Epidemiological researches in the field of DOHaD are in favor of a role of early environment, including chemical (pesticides), physical (air pollution), nutritional or psychosocial environment, on child and adult health. Disentangling the different factors of environment that may affect health, especially over time, and identifying critical periods of exposure remains a major challenge. The biological mechanisms involved remain elusive in human beings. Nevertheless, it seems that whatever the nature of the exposure, epigenetic mechanisms are currently discussed to explain how the environment may alter biological systems over time.


Assuntos
Doença/etiologia , Estudos Epidemiológicos , Saúde , Efeitos Tardios da Exposição Pré-Natal/epidemiologia , Adulto , Dieta , Meio Ambiente , Poluição Ambiental/efeitos adversos , Poluição Ambiental/estatística & dados numéricos , Epigênese Genética/fisiologia , Feminino , Interação Gene-Ambiente , Humanos , Gravidez , Efeitos Tardios da Exposição Pré-Natal/etiologia , Psicologia
18.
Environ Int ; 88: 86-93, 2016 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-26724585

RESUMO

INTRODUCTION: Air pollution exposure has been linked to impaired cognitive aging, but little is known about biomarkers modifying this association. MicroRNAs (miRNAs) control gene expression and neuronal programming. miRNA levels vary due to single nucleotide polymorphisms (SNPs) in genes processing miRNAs from precursor molecules. OBJECTIVES: To investigate whether SNPs in miRNA-processing genes are associated with cognition and modify the relationship between black carbon (BC), marker of traffic-related pollution, and cognitive functions. METHODS: 533 Normative Aging Study men (mean±SD 72±7years) were tested ≤4 times (mean=1.7 times) using seven cognitive tests between 1995 and 2007. We tested interactions of 16 miRNA-related SNPs with 1-year average BC from a validated land-use-regression model. We used covariate-adjusted logistic regression for low (≤25) Mini-Mental tate Examination (MMSE) and mixed-effect regression for a global cognitive score combining six other tests. RESULTS: Global cognition was negatively associated with the homozygous minor variant of rs595961 AGO1 (-0.42SD; 95%CI: (-0.71, -0.13)) relative to the major variant. BC-MMSE association was stronger in heterozygous carriers of rs11077 XPO5 (OR=1.99; 95%CI: (1.39, 2.85)) and minor variant carriers of GEMIN4 rs2740348 (OR=1.34; 95%CI: (1.05, 1.7)), compared to their major variant. The BC-global-cognition association was stronger in heterozygous carriers of GEMIN4 rs4968104 (-0.10SD; 95%CI: (-0.18, -0.02)), and GEMIN4 rs910924 (-0.09SD; 95%CI: (-0.17, -0.02)) relative to the major variant. Blood miRNA expression analyses showed associations only of XPO5 rs11077 with miR-9 and miR-96. CONCLUSIONS: Carriers of particular miRNA-processing SNPs had higher susceptibility to BC in BC-cognition associations, possibly due to influences on miRNA expression.


Assuntos
Poluentes Atmosféricos/toxicidade , Poluição do Ar/efeitos adversos , Carbono/toxicidade , Cognição/efeitos dos fármacos , Exposição Ambiental/efeitos adversos , MicroRNAs/metabolismo , Polimorfismo de Nucleotídeo Único , Idoso , Poluentes Atmosféricos/análise , Poluição do Ar/análise , Boston , Carbono/análise , Exposição Ambiental/análise , Humanos , Modelos Logísticos , Masculino , Fuligem/análise
19.
Environ Int ; 84: 161-73, 2015 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-26300245

RESUMO

Studies of air pollution effects during pregnancy generally only consider exposure in the outdoor air at the home address. We aimed to compare exposure models differing in their ability to account for the spatial resolution of pollutants, space-time activity and indoor air pollution levels. We recruited 40 pregnant women in the Grenoble urban area, France, who carried a Global Positioning System (GPS) during up to 3 weeks; in a subgroup, indoor measurements of fine particles (PM2.5) were conducted at home (n=9) and personal exposure to nitrogen dioxide (NO2) was assessed using passive air samplers (n=10). Outdoor concentrations of NO2, and PM2.5 were estimated from a dispersion model with a fine spatial resolution. Women spent on average 16 h per day at home. Considering only outdoor levels, for estimates at the home address, the correlation between the estimate using the nearest background air monitoring station and the estimate from the dispersion model was high (r=0.93) for PM2.5 and moderate (r=0.67) for NO2. The model incorporating clean GPS data was less correlated with the estimate relying on raw GPS data (r=0.77) than the model ignoring space-time activity (r=0.93). PM2.5 outdoor levels were not to moderately correlated with estimates from the model incorporating indoor measurements and space-time activity (r=-0.10 to 0.47), while NO2 personal levels were not correlated with outdoor levels (r=-0.42 to 0.03). In this urban area, accounting for space-time activity little influenced exposure estimates; in a subgroup of subjects (n=9), incorporating indoor pollution levels seemed to strongly modify them.


Assuntos
Poluição do Ar em Ambientes Fechados/análise , Dióxido de Nitrogênio/análise , Adulto , Algoritmos , Monitoramento Ambiental/métodos , Feminino , França , Sistemas de Informação Geográfica , Substâncias Perigosas , Humanos , Modelos Teóricos , Gravidez , Análise de Regressão , Análise Espaço-Temporal , População Urbana , Adulto Jovem
20.
Thorax ; 70(2): 133-7, 2015 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-25414198

RESUMO

BACKGROUND: Black carbon (BC) is a pro-oxidant, traffic-related pollutant linked with lung function decline. We evaluated the influence of genetic variation in the oxidative stress pathway on the association between long-term BC exposure and lung function decline. METHODS: Lung function parameters (FVC and FEV1) were measured during one or more study visits between 1995 and 2011 (n=651 participants) among an elderly cohort: the Normative Aging Study. Residential BC exposure levels were estimated using a spatiotemporal land use regression model. We evaluated whether oxidative stress variants, combined into a genetic score, modify the association between 1-year and 5-year moving averages of BC exposure and lung function levels and rates of decline, using linear mixed models. RESULTS: We report stronger associations between long-term BC exposure and increased rate of lung function decline, but not baseline lung function level, among participants with higher oxidative stress allelic risk profiles compared with participants with lower risk profiles. Associations were strongest when evaluating 5-year moving averages of BC exposure. A 0.5 µg/m(3) increase in 5-year BC exposure was associated with a 0.1% yearly increase in FVC (95% CI -0.5 to 0.7) among participants with low genetic risk scores and a 1.3% yearly decrease (95% CI -1.8 to -0.8) among those with high scores (p-interaction=0.0003). DISCUSSION: Our results suggest that elderly men with high oxidative stress genetic scores may be more susceptible to the effects of BC on lung function decline. The results, if confirmed, should inform air-quality recommendations in light of a potentially susceptible subgroup.


Assuntos
Volume Expiratório Forçado/genética , Pulmão/fisiopatologia , Exposição Ocupacional/efeitos adversos , Estresse Oxidativo/genética , Fuligem/toxicidade , Capacidade Vital/genética , Idoso , Catalase/genética , Glutamato-Cisteína Ligase/genética , Glutationa S-Transferase pi/genética , Glutationa Transferase/genética , Heme Oxigenase-1/genética , Humanos , Masculino , NAD(P)H Desidrogenase (Quinona)/genética , Polimorfismo Genético , Fatores de Tempo
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