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1.
Sci Total Environ ; 804: 150091, 2022 Jan 15.
Artigo em Inglês | MEDLINE | ID: mdl-34517316

RESUMO

BACKGROUND: Ambient air pollution exposure has been associated with higher mortality risk in numerous studies. We assessed potential variability in the magnitude of this association for non-accidental, cardiovascular disease, respiratory disease, and lung cancer mortality in a country-wide administrative cohort by exposure assessment method and by adjustment for geographic subdivisions. METHODS: We used the Belgian 2001 census linked to population and mortality register including nearly 5.5 million adults aged ≥30 (mean follow-up: 9.97 years). Annual mean concentrations for fine particulate matter (PM2.5), nitrogen dioxide (NO2), black carbon (BC) and ozone (O3) were assessed at baseline residential address using two exposure methods; Europe-wide hybrid land use regression (LUR) models [100x100m], and Belgium-wide interpolation-dispersion (RIO-IFDM) models [25x25m]. We used Cox proportional hazards models with age as the underlying time scale and adjusted for various individual and area-level covariates. We further adjusted main models for two different area-levels following the European Nomenclature of Territorial Units for Statistics (NUTS); NUTS-1 (n = 3), or NUTS-3 (n = 43). RESULTS: We found no consistent differences between both exposure methods. We observed most robust associations with lung cancer mortality. Hazard Ratios (HRs) per 10 µg/m3 increase for NO2 were 1.060 (95%CI 1.042-1.078) [hybrid LUR] and 1.040 (95%CI 1.022-1.058) [RIO-IFDM]. Associations with non-accidental, respiratory disease and cardiovascular disease mortality were generally null in main models but were enhanced after further adjustment for NUTS-1 or NUTS-3. HRs for non-accidental mortality per 5 µg/m3 increase for PM2.5 for the main model using hybrid LUR exposure were 1.023 (95%CI 1.011-1.035). After including random effects HRs were 1.044 (95%CI 1.033-1.057) [NUTS-1] and 1.076 (95%CI 1.060-1.092) [NUTS-3]. CONCLUSION: Long-term air pollution exposure was associated with higher lung cancer mortality risk but not consistently with the other studied causes. Magnitude of associations varied by adjustment for geographic subdivisions, area-level socio-economic covariates and less by exposure assessment method.


Assuntos
Poluentes Atmosféricos , Poluição do Ar , Adulto , Poluentes Atmosféricos/análise , Poluentes Atmosféricos/toxicidade , Poluição do Ar/análise , Poluição do Ar/estatística & dados numéricos , Censos , Estudos de Coortes , Exposição Ambiental/análise , Exposição Ambiental/estatística & dados numéricos , Humanos , Material Particulado/análise , Material Particulado/toxicidade
2.
Environ Int ; 157: 106799, 2021 12.
Artigo em Inglês | MEDLINE | ID: mdl-34358916

RESUMO

BACKGROUND: A growing body of evidence indicates that cardiovascular health in adulthood, particularly that of the microcirculation, could find its roots during prenatal development. In this study, we investigated the association between pre- and postnatal air pollution exposure on heat-induced skin hyperemia as a dynamic marker of the microvasculature. METHODS: In 139 children between the ages of 4 and 6 who are followed longitudinally within the ENVIRONAGE birth cohort, we measured skin perfusion by Laser Doppler probes using the Periflux6000. Residential black carbon (BC), particulate (PM10 and PM2.5) air pollution, and nitrogen dioxide (NO2) levels were modelled for each participant's home address using a high-resolution spatiotemporal model for multiple time windows. We assessed the association between skin hyperemia and pre- and postnatal air pollution using multiple regression models while adjusting for relevant covariates. RESULTS: Residential BC exposure during the whole pregnancy averaged (IQR) 1.42 (1.22-1.58) µg/m3, PM10 18.88 (16.64 - 21.13) µg/m3, PM2.5 13.67 (11.5 - 15.56) µg/m3 and NO2 18.39 (15.52 - 20.31) µg/m3. An IQR increment in BC exposure during the third trimester of pregnancy was associated with an 11.5 % (95% CI: -20.1 to -1.9; p = 0.020) lower skin hyperemia. Similar effect estimates were retrieved for PM10, PM2.5 and NO2 (respectively 13.9 % [95% CI: -21.9 to -3.0; p = 0.003], 17.0 % [95% CI: -26.7 to -6.1; p = 0.004] and 12.7% [95 % CI: -22.2 to -1.9; p = 0.023] lower skin hyperemia). In multipollutant models, PM2.5 showed the strongest inverse association with skin hyperemia. Postnatal exposure to BC, PM10, PM2.5 or NO2, was not associated with skin hyperemia at the age of 4 to 6, and did not alter the previous reported prenatal associations when taken into account. CONCLUSION: Our findings support that BC, particulate air pollution, and NO2 exposure, even at low concentrations, during prenatal life, can have long-lasting consequences for the microvasculature. This proposes a role of prenatal air pollution exposures over and beyond postnatal exposure in the microvascular alterations which were persistent into childhood.


Assuntos
Poluentes Atmosféricos , Poluição do Ar , Adulto , Poluentes Atmosféricos/análise , Poluentes Atmosféricos/toxicidade , Poluição do Ar/análise , Poluição do Ar/estatística & dados numéricos , Carbono , Criança , Pré-Escolar , Exposição Ambiental/estatística & dados numéricos , Feminino , Humanos , Microcirculação , Dióxido de Nitrogênio , Material Particulado/análise , Material Particulado/toxicidade , Gravidez
3.
Health Place ; 70: 102603, 2021 07.
Artigo em Inglês | MEDLINE | ID: mdl-34166885

RESUMO

This study examines the associations between residential urban green spaces (UGS) and self-perceived health and natural cause mortality, applying an intersectional approach across gender, education and migrant background. We used data from the 2001 Belgian census linked to register data on emigration and mortality for the period 2001-2014, including 571,558 individuals aged 16-80 residing in Brussels (80% response rate). Residential UGS were assessed with the Normalized Difference Vegetation Index (NDVI) within a 300 m buffer from the residential address and perceived neighbourhood greenness. Multilevel logistic and Cox proportional hazards regression models were conducted to estimate associations between UGS and poor self-perceived health at baseline and natural cause mortality during follow-up. Residential UGS were inversely associated with both outcomes, but there were differences between groups. The strongest beneficial associations among women were found in the lower educated, regardless of their migrant background. For men the strongest association was found in those with tertiary education and Belgian origin. No significant beneficial associations were found in men originating from low and middle-income countries. Applying an intersectionality approach is crucial to understand health inequalities related to UGS exposure. Further research in different geographical contexts is needed to contrast our findings.


Assuntos
Censos , Parques Recreativos , Estudos de Coortes , Feminino , Nível de Saúde , Humanos , Masculino , Características de Residência , Fatores Socioeconômicos
4.
Environ Health ; 20(1): 11, 2021 02 11.
Artigo em Inglês | MEDLINE | ID: mdl-33573648

RESUMO

BACKGROUND: Exposure to air pollution during pregnancy has been associated with adverse pregnancy outcomes in studies worldwide, other studies have described beneficial effects of residential greenspace on pregnancy outcomes. The biological mechanisms that underlie these associations are incompletely understood. A biological stress response, which implies release of cortisol, may underlie associations of air pollution exposure and access to neighborhood greenspaces with health. METHODS: We explored residential exposure to air pollution and residential access to neighborhood greenspaces in relation to hair cortisol concentrations of participants in a prospective pregnancy cohort study in Flanders, Belgium. Hair samples were collected at the end of the second pregnancy trimester (n = 133) and shortly after delivery (n = 81). Cortisol concentrations were measured in 3-cm scalp-near hair sections, to reflect second and third pregnancy trimester cortisol secretion. We estimated long-term (3 months before sampling) residential exposure to fine particulate matter (PM2.5), nitrogen dioxide (NO2) and black carbon (BC), assessed residential distance to major roads and residential access to neighborhood greenspaces (NHGS). Associations between residential exposures and hair cortisol concentrations were studied using linear regression models while adjusting for season of sampling. RESULTS: Three-month mean residential NO2 and BC concentrations were positively associated with third pregnancy trimester hair cortisol concentrations (p = 0.008 and p = 0.017). Access to a large NHGS (10 ha or more within 800 m from residence) was negatively associated with third trimester hair cortisol concentrations (p = 0.019). Access to a large NHGS significantly moderated the association between residential proximity to major roads and second trimester hair cortisol concentrations (p = 0.021). Residential distance to major roads was negatively associated with second trimester hair cortisol concentrations of participants without access to a large NHGS (p = 0.003). The association was not significant for participants with access to a large NHGS. The moderation tended towards significance in the third pregnancy trimester (p < 0.10). CONCLUSIONS: Our findings suggest a positive association between long-term residential exposure to air pollution and biological stress during pregnancy, residential access to neighborhood greenspaces may moderate the association. Further research is needed to confirm our results. TRIAL REGISTRATION: The IPANEMA study is registered under number  NCT02592005 at clinicaltrials.gov .


Assuntos
Poluição do Ar/análise , Cabelo/química , Hidrocortisona/metabolismo , Parques Recreativos , Segundo Trimestre da Gravidez/metabolismo , Terceiro Trimestre da Gravidez/metabolismo , Adulto , Poluentes Atmosféricos/análise , Bélgica , Exposição Ambiental/análise , Feminino , Humanos , Gravidez , Estudos Prospectivos , Características de Residência , Estresse Psicológico/metabolismo , Emissões de Veículos/análise
5.
Environ Int ; 148: 106365, 2021 03.
Artigo em Inglês | MEDLINE | ID: mdl-33444880

RESUMO

BACKGROUND: Epidemiological studies suggest that residing close to green space reduce mortality rates. We investigated the relationship between long-term exposure to residential green space and non-accidental and cardio-respiratory mortality. METHODS: We linked the Belgian 2001 census to population and mortality register follow-up data (2001-2011) among adults aged 30 years and older residing in the five largest urban areas in Belgium (n = 2,185,170 and mean follow-up time 9.4 years). Residential addresses were available at baseline. Exposure to green space was defined as 1) surrounding greenness (2006) [normalized difference vegetation index (NDVI) and modified soil-adjusted vegetation index (MSAVI2)] within buffers of 300 m, 500 m, and 1000 m; 2) surrounding green space (2006) [Urban Atlas (UA) and CORINE Land Cover (CLC)] within buffers of 300 m, 500 m, and 1000 m; and 3) perceived neighborhood green space (2001). Cox proportional hazards models with age as the underlying time scale were used to probe into cause-specific mortality (non-accidental, respiratory, COPD, cardiovascular, ischemic heart disease (IHD), and cerebrovascular). Models were adjusted for several sociodemographic variables (age, sex, marital status, country of birth, education level, employment status, and area mean income). We further adjusted our main models for annual mean (2010) values of ambient air pollution (PM2.5, PM10, NO2 and BC, one at a time), and we additionally explored potential mediation with the aforementioned pollutants. RESULTS: Higher degrees of residential green space were associated with lower rates of non-accidental and respiratory mortality. In fully adjusted models, hazard ratios (HR) per interquartile range (IQR) increase in NDVI 500 m buffer (IQR: 0.24) and UA 500 m buffer (IQR: 0.31) were 0.97 (95%CI 0.96-0.98) and 0.99 (95%CI 0.98-0.99) for non-accidental mortality, and 0.95 (95%CI 0.93-0.98) and 0.97 (95%CI 0.96-0.99) for respiratory mortality. For perceived neighborhood green space, HRs were 0.93 (95%CI 0.92-0.94) and 0.94 (95%CI 0.91-0.98) for non-accidental and respiratory mortality, respectively. The observed lower mortality risks associated with residential exposure to green space were largely independent from exposure to ambient air pollutants. CONCLUSION: We observed evidence for lower mortality risk in associations with long-term residential exposure to green space in most but not all studied causes of death in a large representative cohort for the five largest urban areas in Belgium. These findings support the importance of the availability of residential green space in urban areas.


Assuntos
Poluentes Atmosféricos , Poluição do Ar , Adulto , Bélgica/epidemiologia , Censos , Estudos de Coortes , Exposição Ambiental/análise , Seguimentos , Humanos , Parques Recreativos , Material Particulado
6.
Environ Int ; 147: 106334, 2021 02.
Artigo em Inglês | MEDLINE | ID: mdl-33360673

RESUMO

BACKGROUND: Adequate intake of iodine is required for the production of thyroid hormones and contributes in pregnant women to a healthy brain development and growth in their offspring. To date, some evidence exists that fine particulate air pollution is linked with the fetal thyroid hormone homeostasis. However, possible effects of air pollutants on the placental iodine storage have not been investigated so far. OBJECTIVES: We investigated the association between air pollution exposure to particulate matter with a diameter less than 2.5 µm (PM2.5), NO2, and black carbon and the placental iodine load. METHODS: The current study is part of the ENVIRONAGE birth cohort and included 470 mother-newborn pairs. Iodine concentrations were measured in placental tissue. A high-resolution air pollution model was used to estimate the daily exposure to PM2.5, NO2, and black carbon over the entire pregnancy based on the maternal residential addresses. Distributed lag nonlinear models (DLNMs) were used to estimate gestational week-specific associations between placental iodine concentrations and the air pollutants to understand the impact of specific exposure windows. RESULTS: PM2.5 showed a positive association with placental iodine concentration between the 16th and 22nd week of gestation. In contrast, a significant inverse association between PM2.5 and placental iodine concentration was observed in gestational weeks 29-35. The effect estimate, for a 5 µg/m3 increment in PM2.5 concentration, was the strongest at week 32 (ß -0.11 µg/kg; 95%CI: -0.18 to -0.03). No associations were observed between placental iodine concentrations and NO2 or black carbon. Assuming causality, we estimated that placental iodine mediated 26% (-0.33 pmol/L; 95%CI: -0.70 to 0.04 pmol/L) of the estimated effect of a 5 µg/m3 increment in PM2.5 exposure on cord blood free thyroxine (FT4) concentrations. CONCLUSION: In utero exposure to particulate matter during the third trimester of pregnancy is linked with a lower placental iodine load. Furthermore, the effect of air pollution on cord blood FT4 levels was partially mediated by the placental iodine load.


Assuntos
Poluentes Atmosféricos , Poluição do Ar , Iodo , Poluentes Atmosféricos/efeitos adversos , Poluentes Atmosféricos/análise , Poluição do Ar/efeitos adversos , Poluição do Ar/análise , Bélgica , Feminino , Humanos , Recém-Nascido , Exposição Materna/efeitos adversos , Material Particulado/efeitos adversos , Material Particulado/análise , Gravidez
7.
Environ Res ; 191: 110032, 2020 12.
Artigo em Inglês | MEDLINE | ID: mdl-32814106

RESUMO

BACKGROUND: Living in green areas has been associated with several health benefits; however, the available evidence on such benefits for hypertension is still limited. This study aimed to investigate and compare the association between residential exposure to greenspace and hypertension in Barcelona, Spain and Brussels, Belgium. METHODS: This cross-sectional study was based on data from the 2016 Barcelona Health Interview Survey (HIS) (n = 3400) and the 2013 Belgian HIS (n = 2335). Both surveys were harmonized in terms of outcomes, confounders and exposure assessment. Residential exposure to greenspace was characterized as 1) surrounding greenspace (normalized difference vegetation index (NDVI) and modified soil-adjusted vegetation index 2 (MSAVI2)) across buffers of 100 m, 300 m, and 500 m; 2) surrounding green space across 300 m and 500 m buffers; and 3) Euclidean distance to the nearest green space. Our outcome was self-reported hypertension. We developed logistic regression models to evaluate the city-specific association between each greenspace measure and hypertension, adjusting for relevant covariates. RESULTS: One interquartile range (IQR) increase in residential distance to the nearest green space was associated with higher risk of hypertension in Barcelona [odds ratio (OR): 1.15; 95%CI 1.03-1.29 (IQR: 262.2)], but not in Brussels [OR: 0.95; 95%CI 0.77-1.17 (IQR: 215.2)]. Stratified analyses suggested stronger associations in older participants (≥65 years) for both cities. Findings for residential surrounding green space and greenspace were not conclusive. However, in Brussels, we found protective associations in older participants for both residential surrounding greenspace metrics [NDVI 300 m buffer OR: 0.51; 95%CI 0.32-0.81 (IQR: 0.21) and MSAVI2 300 m buffer OR: 0.51; 95%CI 0.32-0.83 (IQR: 0.18)]. We did not find any indication for the modification of our evaluated associations by sex and education level. CONCLUSION: Our study suggests that living closer to greenspace could be associated with lower risk of hypertension, particularly in older age. Future research is needed to replicate our findings in other settings and shed light on potential underlying mechanism(s).


Assuntos
Hipertensão , Parques Recreativos , Idoso , Bélgica/epidemiologia , Cidades , Estudos Transversais , Humanos , Hipertensão/epidemiologia , Espanha/epidemiologia
8.
Environ Int ; 142: 105860, 2020 09.
Artigo em Inglês | MEDLINE | ID: mdl-32599355

RESUMO

BACKGROUND: Air pollution exposure during pregnancy is an important environmental health issue. Epigenetics mediate the effects of prenatal exposure and could increase disease predisposition in later life. The oncogenic miR-17/92 cluster is involved in normal development and disease. OBJECTIVES: Here, for the first time the potential prenatal effects of particulate matter with a diameter<2.5 µm (PM2.5) exposure on expression of the miR-17/92 cluster in cord blood are explored. METHODS: In 370 mother-newborn pairs from the ENVIRONAGE birth cohort, expression of three members of the miR-17/92 cluster was measured in cord blood by qRT-PCR. Expression of C-MYC and CDKN1A, a cluster activator and a target gene, respectively, was also analyzed. Multivariable linear regression models were used to associate the relative m(i)RNA expression with prenatal PM2.5 exposure. RESULTS: PM2.5 exposure averaged (10th-90th percentile) 11.7 (9.0-14.4) µg/m3 over the entire pregnancy. In cord blood, miR-17 and miR-20a showed a -45.0% (95%CI: -55.9 to -31.4, p < 0.0001) and a -33.7% (95%CI: -46.9 to -17.2, p = 0.0003), decrease in expression in association with first trimester PM2.5 exposure, and a -32.5% (95%CI: -45.6 to -16.3, p = 0.0004) and -23.3% (95%CI: -38.1 to -4.8, p = 0.02), respectively, decrease in expression in association with PM2.5 exposure during the entire pregnancy. In association with third trimester PM2.5 exposure, a reduction of -25.8% (95%CI: -40.2 to -8.0, p = 0.007) and -14.2% (95%CI: -27.7 to 1.9, p = 0.08), for miR-20a and miR-92a expression, respectively, was identified. Only miR-92a expression (-15.7%, 95%CI: -27.3 to -2.4, p = 0.02) was associated with PM2.5 exposure during the last month of pregnancy. C-MYC expression was downregulated in cord blood in association with prenatal PM2.5 exposure during the first trimester and the entire pregnancy, in the adjusted model. DISCUSSION: Lower expression levels of the miR-17/92 cluster in cord blood in association with increased prenatal PM2.5 exposure were observed. Whether this oncogenic microRNA cluster plays a role in trans-placental carcinogenesis remains to be elucidated.


Assuntos
Poluentes Atmosféricos , Poluição do Ar , MicroRNAs , Poluentes Atmosféricos/toxicidade , Poluição do Ar/análise , Feminino , Sangue Fetal/química , Humanos , Recém-Nascido , Exposição Materna/efeitos adversos , MicroRNAs/genética , Material Particulado/análise , Material Particulado/toxicidade , Gravidez
9.
JAMA Netw Open ; 3(5): e205156, 2020 05 01.
Artigo em Inglês | MEDLINE | ID: mdl-32421184

RESUMO

Importance: Exposure to ambient air pollution has been associated with the risk of carcinogenesis in later life. Changes in histone modifications might have long-term adverse health effects. Objective: To investigate the association of prenatal exposure to ambient air pollution with levels of circulating total histone H3 and specific trimethylation marks (ie, H3 lysine 4, H3 lysine 36) in maternal cord blood. Design, Setting, and Participants: The Environmental Influence on Aging (ENVIRONAGE) birth cohort study included 609 mothers and their newborns. Participants were recruited when mothers entered the Hospital East Limburg (Genk, Belgium) for delivery between February 2010 and January 2017. The inclusion criteria were singleton pregnancies and the ability to fill out questionnaires in Dutch. Data analysis was conducted from March to August 2019. Exposures: Exposure to particulate matter with a diameter less than 2.5 µm (PM2.5), black carbon, and nitrogen dioxide during pregnancy was modeled with a high-resolution air pollution model on the basis of maternal address for each trimester of pregnancy as well as for the entire pregnancy. Main Outcomes and Measures: Circulating total histone H3 levels and specific trimethylation marks (ie, trimethylated H3 lysine 4 and trimethylated H3 lysine 36) in cord blood. Results: A total of 609 mother-newborn pairs were included in the study. Mean (SD) maternal age was 29.3 (4.6) years, 391 mothers (64.2%) never smoked, and 314 (51.3%) had a high education level. Overall, 322 newborns (52.4%) were boys, and mean (SD) birth weight was 3414 (485) g. Participants experienced mean (SD) exposure to PM2.5, black carbon, and nitrogen dioxide of 13.4 (2.6) µg/m3, 1.29 (0.31) µg/m3, and 17.98 (4.57) µg/m3, respectively, during their entire pregnancies. Trimethylated H3 lysine 4 and total histone H3 were positively associated with gestational PM2.5 exposure, with a 74.4% increment (95% CI, 26.7% to 140.2%, P < .001) and a 40.2% increment (95% CI, 24.1% to 58.3%, P < .001), respectively, observed for each 5-µg/m3 increase in PM2.5 exposure during the entire pregnancy. For the same exposure window, trimethylated H3 lysine 36 levels were inversely associated with PM2.5 exposure (-34.4%; 95% CI, -50.1% to -13.7%; P = .003). Exposure to black carbon during the entire pregnancy was positively associated with trimethylated H3 lysine 4 (38.4%; 95% CI, 6.2% to 80.3%; P = .003). Conclusions and Relevance: Associations of ambient air pollution with cord plasma histone H3 modifications during early life might indicate that circulating histones are a risk factor in the development of air pollution-associated disease later in life. Additional study is required to correctly estimate the long-term consequences of our findings.


Assuntos
Poluição do Ar/efeitos adversos , Sangue Fetal/química , Histonas/sangue , Exposição Materna , Adulto , Bélgica , Feminino , Humanos , Gravidez , Efeitos Tardios da Exposição Pré-Natal , Fatores de Risco
10.
BMC Med ; 18(1): 128, 2020 05 26.
Artigo em Inglês | MEDLINE | ID: mdl-32450864

RESUMO

BACKGROUND: Particulate matter exposure during in utero life may entail adverse health outcomes later in life. The microvasculature undergoes extensive, organ-specific prenatal maturation. A growing body of evidence shows that cardiovascular disease in adulthood is rooted in a dysfunctional fetal and perinatal development, in particular that of the microcirculation. We investigate whether prenatal or postnatal exposure to PM2.5 (particulate matter with a diameter ≤ 2.5 µm) or NO2 is related to microvascular traits in children between the age of four and six. METHODS: We measured the retinal microvascular diameters, the central retinal arteriolar equivalent (CRAE) and central retinal venular equivalent (CRVE), and the vessel curvature by means of the tortuosity index (TI) in young children (mean [SD] age 4.6 [0.4] years), followed longitudinally within the ENVIRONAGE birth cohort. We modeled daily prenatal and postnatal PM2.5 and NO2 exposure levels for each participant's home address using a high-resolution spatiotemporal model. RESULTS: An interquartile range (IQR) increase in PM2.5 exposure during the entire pregnancy was associated with a 3.85-µm (95% CI, 0.10 to 7.60; p = 0.04) widening of the CRVE and a 2.87-µm (95% CI, 0.12 to 5.62; p = 0.04) widening of the CRAE. For prenatal NO2 exposure, an IQR increase was found to widen the CRVE with 4.03 µm (95% CI, 0.44 to 7.63; p = 0.03) and the CRAE with 2.92 µm (95% CI, 0.29 to 5.56; p = 0.03). Furthermore, a higher TI score was associated with higher prenatal NO2 exposure. We observed a postnatal effect of short-term PM2.5 exposure on the CRAE and a childhood NO2 exposure effect on both the CRVE and CRAE. CONCLUSIONS: Our results link prenatal and postnatal air pollution exposure with changes in a child's microvascular traits as a fundamental novel mechanism to explain the developmental origin of cardiovascular disease.


Assuntos
Poluição do Ar/efeitos adversos , Microvasos/fisiopatologia , Material Particulado/efeitos adversos , Adulto , Pré-Escolar , Feminino , Humanos , Masculino , Gravidez , Estudos Prospectivos
11.
Intensive Care Med ; 46(6): 1204-1212, 2020 06.
Artigo em Inglês | MEDLINE | ID: mdl-32185459

RESUMO

PURPOSE: Air pollutant exposure constitutes a serious risk factor for the emergence or aggravation of (existing) pulmonary disease. The impact of pre-intensive care ambient air pollutant exposure on the duration of artificial ventilation was, however, not yet established. METHODS: The medical records of 2003 patients, admitted to the intensive care unit (ICU) of the Antwerp University Hospital (Flanders, Belgium), who were artificially ventilated on ICU admission or within 48 h after admission, for the duration of at least 48 h, were analyzed. For each patient's home address, daily air pollutant exposure [particulate matter with an aerodynamic diameter ≤ 2.5 µm (PM2.5) and ≤ 10 µm (PM10), nitrogen dioxide (NO2) and black carbon (BC)] up to 10 days prior to hospital admission was modeled using a high-resolution spatial-temporal model. The association between duration of artificial ventilation and air pollution exposure during the last 10 days before ICU admission was assessed using distributed lag models with a negative binomial regression fit. RESULTS: Controlling for pre-specified confounders, an IQR increment in BC (1.2 µg/m3) up to 10 days before admission was associated with an estimated cumulative increase of 12.4% in ventilation duration (95% CI 4.7-20.7). Significant associations were also observed for PM2.5, PM10 and NO2, with cumulative estimates ranging from 7.8 to 8.0%. CONCLUSION: Short-term ambient air pollution exposure prior to ICU admission represents an unrecognized environmental risk factor for the duration of artificial ventilation in the ICU.


Assuntos
Poluentes Atmosféricos , Poluição do Ar , Poluentes Atmosféricos/análise , Poluição do Ar/efeitos adversos , Poluição do Ar/análise , Bélgica , Cuidados Críticos , Humanos , Material Particulado/efeitos adversos , Material Particulado/análise
12.
Environ Int ; 130: 104853, 2019 09.
Artigo em Inglês | MEDLINE | ID: mdl-31226559

RESUMO

Elevated blood pressure (BP) in early life may lead to cardiovascular morbidity and mortality in later life. Air pollution exposure has been associated with increased BP in adults and children, but the contribution of prenatal air pollution exposure has rarely been assessed. In addition, we are not aware of any study on neonatal BP and maternal residential traffic and land use indicators during pregnancy. We investigated the association between newborn BP and prenatal air pollution, traffic and land use indicators, using data from 427 term (gestational age > 36 weeks) births from the ENVIRONAGE birth cohort. Newborn BP was measured using an automated device within 4 days after birth. Daily maternal residential air pollutants during pregnancy, including particulate matter with an aerodynamic diameter ≤ 2.5 µm (PM2.5) and ≤10 µm (PM10), black carbon (BC), and nitrogen dioxide (NO2), were modelled using a high-resolution spatial-temporal model. The association between newborn BP and air pollution during the last 15 weeks of pregnancy was assessed using distributed lag models. Each 5 µg/m3 increment in prenatal PM2.5 exposure was associated with a 2.4 mm Hg (95% CI, 0.5 to 4.2) higher systolic and a 1.8 mm Hg (95% CI, 0.2 to 3.5) higher diastolic BP at birth. Overall estimates for PM10 were similar but those for NO2 and BC did not reach significance. Associations between newborn BP and exposures during the last 4 to 5 weeks of pregnancy were significant for all pollutants. An IQR (20.3%) increment in percentage residential greenness in a 5 km radius was associated with a 1.2 mm Hg (95% CI, -2.5 to 0.1; p = 0.07) lower systolic and a 1.2 mm Hg (95% CI, -2.4 to -0.0; p = 0.05) lower diastolic BP. An IQR (4.1%) increment in percentage industrial area in a 5 km radius was associated with a 1.0 mm Hg (95% CI, 0.1 to 1.9; p = 0.03) higher diastolic BP. Residential traffic indicators did not significantly associate with newborn BP. Prenatal air pollution exposure, greenness, and industrial area at maternal residence may affect offspring BP from birth onwards.


Assuntos
Poluentes Atmosféricos/toxicidade , Pressão Sanguínea/efeitos dos fármacos , Dióxido de Nitrogênio/toxicidade , Material Particulado/toxicidade , Fuligem/toxicidade , Poluição do Ar/análise , Estudos de Coortes , Feminino , Idade Gestacional , Humanos , Recém-Nascido , Masculino , Gravidez
13.
Environ Res ; 168: 507-513, 2019 01.
Artigo em Inglês | MEDLINE | ID: mdl-30477822

RESUMO

INTRODUCTION: Particulate air pollution is probably causally related to increased risk of cardiovascular disease. Plasma homocysteine is an established cardiovascular disease risk factor. Recent studies show that exposure to particulate air pollution is associated with plasma homocysteine levels in adults but no studies on the association between prenatal air pollution and neonatal homocysteine levels exist. METHODS: In 609 newborns of the ENVIRONAGE (ENVIRonmental influence ON early AGEing) birth cohort, we investigated the association between prenatal particulate matter exposure with a diameter ≤ 2.5 µm (PM2.5) and cord plasma homocysteine levels, and in a subset (n = 490) we studied the interaction with 11 single nucleotide polymorphism (SNPs) in oxidative stress-related genes (CAT, COMT, GSTP1, SOD2, NQO1 and HFE), through multiple linear regression. PM2.5 levels were obtained using a high resolution spatial temporal interpolation method. Homocysteine levels were measured by the homocysteine enzymatic assay on a Roche/Hitachi cobas c system. SNPs were assessed on the Biotrove OpenArray SNP genotyping platform. RESULTS: In multivariable-adjusted models, cord plasma homocysteine levels were 8.1% higher (95% CI: 1.9 to 14.3%; p = 0.01) for each 5 µg/m³ increment in average PM2.5 exposure during the entire pregnancy. With regard to pregnancy trimesters, there was only an association in the 2nd trimester: 3.6% (95% CI: 0.9% to 6.4%; p = 0.01). The positive association between PM2.5 in and homocysteine was (borderline) statistically significantly modified by genetic variants in MnSOD (p interaction = 0.02), GSTP1 (p interaction = 0.07) and the sum score of the 3 studied SNPs in the CAT gene (p interaction=0.09), suggesting oxidative stress as an underlying mechanism of action. CONCLUSIONS: Exposure to particulate air pollution in utero is associated with higher cord blood homocysteine levels, possibly through generating oxidative stress. Increased air pollution-induced homocysteine levels in early life might predispose for cardiovascular and other diseases later in life.


Assuntos
Poluentes Atmosféricos , Poluição do Ar/estatística & dados numéricos , Homocisteína/sangue , Exposição Materna/estatística & dados numéricos , Adulto , Feminino , Sangue Fetal , Humanos , Recém-Nascido , Material Particulado , Gravidez
14.
Lancet Planet Health ; 2(4): e174-e183, 2018 04.
Artigo em Inglês | MEDLINE | ID: mdl-29615218

RESUMO

BACKGROUND: Exposure to particulate air pollution has been linked with risk of carcinogenesis. Damage to repair pathways might have long-term adverse health effects. We aimed to investigate the association of prenatal exposure to air pollution with placental mutation rate and the DNA methylation of key placental DNA repair genes. METHODS: This cohort study used data from the ongoing ENVironmental Influence ON early AGEing (ENVIRONAGE) birth cohort, which enrols pairs of mothers and neonates (singleton births only) at the East-Limburg Hospital (Genk, Belgium). Placental DNA samples were collected after birth. We used bisulfite-PCR-pyrosequencing to investigate the mutation rate of Alu (a marker for overall DNA mutation) and DNA methylation in the promoter genes of key DNA repair and tumour suppressor genes (APEX1, OGG1, PARP1, ERCC1, ERCC4, p53, and DAPK1). We used a high-resolution air pollution model to estimate exposure to particulate matter with a diameter less than 2·5 µm (PM2·5), black carbon, and NO2 over the entire pregnancy on the basis of maternal address. Alu mutation was analysed with a linear regression model, and methylation values of the selected genes were analysed in mixed-effects models. Effect estimates are presented as the relative percentage change in methylation for an ambient air pollution increment of one IQR (ie, the difference between the first and third quartiles of exposure in the entire cohort). FINDINGS: 500 biobanked placental DNA samples were randomly selected from 814 pairs of mothers and neonates who were recruited to the cohort between Feb 1, 2010, and Dec 31, 2014, of which 463 samples met the pyrosequencing quality control criteria. IQR exposure increments were 3·84 µg/m3 for PM2·5, 0·36 µg/m3 for black carbon, and 5·34 µg/m3 for NO2. Among these samples, increased Alu mutation rate was associated with greater exposure to PM2·5 (r=0·26, p<0·0001) and black carbon (r=0·33, p<0·0001), but not NO2. Promoter methylation was positively associated with PM2·5 in APEX1 (7·34%, 95% CI 0·52 to 14·16, p=0·009), OGG1 (13·06, 3·88 to 22·24, p=0·005), ERCC4 (16·31%, 5·43 to 27·18, p=0·01), and p53 (10·60%, 4·46 to 16·74, p=0·01), whereas promoter methylation of DAPK1 (-12·92%, -22·35 to -3·49, p=0·007) was inversely associated with PM2·5 exposure. Black carbon exposure was associated with elevated promoter methylation in APEX1 (9·16%, 4·06 to 14·25, p=0·01) and ERCC4 (27·56%, 17·58 to 37·55, p<0·0001). Promoter methylation was not associated with pollutant exposure in PARP1 and ERCC1, and NO2 exposure was not associated with methylation in any of the genes studied. INTERPRETATION: Transplacental in-utero exposure to particulate matter is associated with an increased overall placental mutation rate (as measured with Alu), which occurred in concert with epigenetic alterations in key DNA repair and tumour suppressor genes. Our results suggest that exposure to air pollution can induce changes to fetal and neonatal DNA repair capacity. Future studies will be essential to elucidate whether these changes persist and have a role in carcinogenic insults later in life. FUNDING: European Research Council and the Flemish Scientific Fund.


Assuntos
Poluentes Atmosféricos/efeitos adversos , Exposição Materna/efeitos adversos , Óxido Nítrico/efeitos adversos , Material Particulado/efeitos adversos , Fuligem/efeitos adversos , Adulto , Bélgica , Estudos de Coortes , Metilação de DNA/efeitos dos fármacos , Reparo do DNA/efeitos dos fármacos , Feminino , Genes Supressores de Tumor/efeitos dos fármacos , Humanos , Taxa de Mutação , Placenta/efeitos dos fármacos , Placenta/fisiologia , Gravidez , Adulto Jovem
15.
Environ Int ; 114: 231-241, 2018 05.
Artigo em Inglês | MEDLINE | ID: mdl-29524919

RESUMO

In mammals, a central clock maintains the daily rhythm in accordance with the external environment. At the molecular level, the circadian rhythm is maintained by epigenetic regulation of the Circadian pathway. Here, we tested the role of particulate matter with an aerodynamic diameter ≤ 2.5 µm (PM2.5) exposure during gestational life on human placental Circadian pathway methylation, as an important molecular target for healthy development. In 407 newborns, we quantified placental methylation of CpG sites within the promoter regions of the following genes: CLOCK, BMAL1, NPAS2, CRY1-2 and PER1-3 using bisulfite-PCR-pyrosequencing. Daily PM2.5 exposure levels were estimated for each mother's residence, using a spatiotemporal interpolation model. We applied mixed-effects models to study the methylation status of the Circadian pathway genes and in utero PM2.5 exposure, while adjusting for a priori chosen covariates. In a multi-gene model, placental Circadian pathway methylation was positively and significantly (p < 0.0001) associated with 3rd trimester PM2.5 exposure. Consequently, the single-gene models showed relative methylation differences [Log(fold change)] in placental NPAS2 (+0.16; p = 0.001), CRY1 (+0.59; p = 0.0023), PER2 (+0.36; p = 0.0005), and PER3 (+0.42; p = 0.0008) for an IQR increase (8.9 µg/m3) in 3rd trimester PM2.5 exposure. PM2.5 air pollution, an environmental risk factor leading to a pro-inflammatory state of the mother and foetus, is associated with the methylation pattern of genes in the Circadian pathway. The observed alterations in the placental CLOCK epigenetic signature might form a relevant molecular mechanism through which fine particle air pollution exposure might affect placental processes and foetal development.


Assuntos
Poluentes Atmosféricos/toxicidade , Ritmo Circadiano/efeitos dos fármacos , Metilação de DNA/efeitos dos fármacos , Exposição Materna , Material Particulado/toxicidade , Placenta/efeitos dos fármacos , Ritmo Circadiano/genética , Epigênese Genética/efeitos dos fármacos , Feminino , Humanos , Recém-Nascido , Placenta/química , Gravidez
16.
Epigenetics ; 13(2): 135-146, 2018.
Artigo em Inglês | MEDLINE | ID: mdl-27104955

RESUMO

Particulate matter (PM) exposure during in utero life may entail adverse health outcomes in later-life. Air pollution's adverse effects are known to alter gene expression profiles, which can be regulated by microRNAs (miRNAs). We investigate the potential influence of air pollution exposure in prenatal life on placental miRNA expression. Within the framework of the ENVIRONAGE birth cohort, we measured the expression of six candidate miRNAs in placental tissue from 210 mother-newborn pairs by qRT-PCR. Trimester-specific PM2.5 exposure levels were estimated for each mother's home address using a spatiotemporal model. Multiple regression models were used to study miRNA expression and in utero exposure to PM2.5 over various time windows during pregnancy. The placental expression of miR-21 (-33.7%, 95% CI: -53.2 to -6.2, P = 0.022), miR-146a (-30.9%, 95% CI: -48.0 to -8.1, P = 0.012) and miR-222 (-25.4%, 95% CI: -43.0 to -2.4, P = 0.034) was inversely associated with PM2.5 exposure during the 2nd trimester of pregnancy, while placental expression of miR-20a and miR-21 was positively associated with 1st trimester exposure. Tumor suppressor phosphatase and tensin homolog (PTEN) was identified as a common target of the miRNAs significantly associated with PM exposure. Placental PTEN expression was strongly and positively associated (+59.6% per 5 µg/m³ increment, 95% CI: 26.9 to 100.7, P < 0.0001) with 3rd trimester PM2.5 exposure. Further research is required to establish the role these early miRNA and mRNA expression changes might play in PM-induced health effects. We provide molecular evidence showing that in utero PM2.5 exposure affects miRNAs expression as well as its downstream target PTEN.


Assuntos
Poluentes Atmosféricos/efeitos adversos , Epigênese Genética , Exposição Materna , MicroRNAs/genética , Material Particulado/efeitos adversos , Placenta/metabolismo , Adulto , Poluentes Atmosféricos/farmacologia , Feminino , Humanos , Recém-Nascido , Masculino , PTEN Fosfo-Hidrolase/genética , PTEN Fosfo-Hidrolase/metabolismo , Material Particulado/farmacologia , Placenta/efeitos dos fármacos , Gravidez
17.
JAMA Pediatr ; 171(12): 1160-1167, 2017 12 01.
Artigo em Inglês | MEDLINE | ID: mdl-29049509

RESUMO

Importance: Telomere length is a marker of biological aging that may provide a cellular memory of exposures to oxidative stress and inflammation. Telomere length at birth has been related to life expectancy. An association between prenatal air pollution exposure and telomere length at birth could provide new insights in the environmental influence on molecular longevity. Objective: To assess the association of prenatal exposure to particulate matter (PM) with newborn telomere length as reflected by cord blood and placental telomere length. Design, Setting, and Participants: In a prospective birth cohort (ENVIRONAGE [Environmental Influence on Ageing in Early Life]), a total of 730 mother-newborn pairs were recruited in Flanders, Belgium between February 2010 and December 2014, all with a singleton full-term birth (≥37 weeks of gestation). For statistical analysis, participants with full data on both cord blood and placental telomere lengths were included, resulting in a final study sample size of 641. Exposures: Maternal residential PM2.5 (particles with an aerodynamic diameter ≤2.5 µm) exposure during pregnancy. Main Outcomes and Measures: In the newborns, cord blood and placental tissue relative telomere length were measured. Maternal residential PM2.5 exposure during pregnancy was estimated using a high-resolution spatial-temporal interpolation method. In distributed lag models, both cord blood and placental telomere length were associated with average weekly exposures to PM2.5 during pregnancy, allowing the identification of critical sensitive exposure windows. Results: In 641 newborns, cord blood and placental telomere length were significantly and inversely associated with PM2.5 exposure during midgestation (weeks 12-25 for cord blood and weeks 15-27 for placenta). A 5-µg/m3 increment in PM2.5 exposure during the entire pregnancy was associated with 8.8% (95% CI, -14.1% to -3.1%) shorter cord blood leukocyte telomeres and 13.2% (95% CI, -19.3% to -6.7%) shorter placental telomere length. These associations were controlled for date of delivery, gestational age, maternal body mass index, maternal age, paternal age, newborn sex, newborn ethnicity, season of delivery, parity, maternal smoking status, maternal educational level, pregnancy complications, and ambient temperature. Conclusions and Relevance: Mothers who were exposed to higher levels of PM2.5 gave birth to newborns with shorter telomere length. The observed telomere loss in newborns by prenatal air pollution exposure indicates less buffer for postnatal influences of factors decreasing telomere length during life. Therefore, improvements in air quality may promote molecular longevity from birth onward.


Assuntos
Envelhecimento/genética , Material Particulado/efeitos adversos , Efeitos Tardios da Exposição Pré-Natal , Encurtamento do Telômero/fisiologia , Adulto , Poluição do Ar/efeitos adversos , Poluição do Ar/análise , Feminino , Sangue Fetal/fisiologia , Idade Gestacional , Humanos , Recém-Nascido , Masculino , Exposição Materna/efeitos adversos , Material Particulado/análise , Placenta/fisiologia , Gravidez , Estações do Ano
18.
Environ Health ; 16(1): 87, 2017 08 18.
Artigo em Inglês | MEDLINE | ID: mdl-28821289

RESUMO

BACKGROUND: Due to their lack of repair capacity mitochondria are critical targets for environmental toxicants. We studied genes and pathways reflecting mitochondrial responses to short- and medium-term PM10 exposure. METHODS: Whole genome gene expression was measured in peripheral blood of 98 adults (49% women). We performed linear regression analyses stratified by sex and adjusted for individual and temporal characteristics to investigate alterations in gene expression induced by short-term (week before blood sampling) and medium-term (month before blood sampling) PM10 exposure. Overrepresentation analyses (ConsensusPathDB) were performed to identify enriched mitochondrial associated pathways and gene ontology sets. Thirteen Human MitoCarta genes were measured by means of quantitative real-time polymerase chain reaction (qPCR) along with mitochondrial DNA (mtDNA) content in an independent validation cohort (n = 169, 55.6% women). RESULTS: Overrepresentation analyses revealed significant pathways (p-value <0.05) related to mitochondrial genome maintenance and apoptosis for short-term exposure and to the electron transport chain (ETC) for medium-term exposure in women. For men, medium-term PM10 exposure was associated with the Tri Carbonic Acid cycle. In an independent study population, we validated several ETC genes, including UQCRH and COX7C (q-value <0.05), and some genes crucial for the maintenance of the mitochondrial genome, including LONP1 (q-value: 0.07) and POLG (q-value: 0.04) in women. CONCLUSIONS: In this exploratory study, we identified mitochondrial genes and pathways associated with particulate air pollution indicating upregulation of energy producing pathways as a potential mechanism to compensate for PM-induced mitochondrial damage.


Assuntos
Poluentes Atmosféricos/toxicidade , Exposição Ambiental , Genes Mitocondriais/efeitos dos fármacos , Material Particulado/toxicidade , Transcriptoma/efeitos dos fármacos , Idoso , Bélgica , Estudos de Coortes , Monitoramento Ambiental , Feminino , Perfilação da Expressão Gênica , Humanos , Masculino , Pessoa de Meia-Idade , Reação em Cadeia da Polimerase em Tempo Real , Fatores Sexuais
19.
Am J Respir Crit Care Med ; 196(7): 873-881, 2017 10 01.
Artigo em Inglês | MEDLINE | ID: mdl-28686472

RESUMO

RATIONALE: Ambient air pollution, including black carbon, entails a serious public health risk because of its carcinogenic potential and as climate pollutant. To date, an internal exposure marker for black carbon particles that have cleared from the systemic circulation into the urine does not exist. OBJECTIVES: To develop and validate a novel method to measure black carbon particles in a label-free way in urine. METHODS: We detected urinary carbon load in 289 children (aged 9-12 yr) using white-light generation under femtosecond pulsed laser illumination. Children's residential black carbon concentrations were estimated based on a high-resolution spatial temporal interpolation method. MEASUREMENTS AND MAIN RESULTS: We were able to detect urinary black carbon in all children, with an overall average (SD) of 98.2 × 105 (29.8 × 105) particles/ml. The urinary black carbon load was positively associated with medium-term to chronic (1 mo or more) residential black carbon exposure: +5.33 × 105 particles/ml higher carbon load (95% confidence interval, 1.56 × 105 to 9.10 × 105 particles/ml) for an interquartile range increment in annual residential black carbon exposure. Consistently, children who lived closer to a major road (≤160 m) had higher urinary black carbon load (6.93 × 105 particles/ml; 95% confidence interval, 0.77 × 105 to 13.1 × 105). CONCLUSIONS: Urinary black carbon mirrors the accumulation of medium-term to chronic exposure to combustion-related air pollution. This specific biomarker reflects internal systemic black carbon particles cleared from the circulation into the urine, allowing investigators to unravel the complexity of particulate-related health effects.


Assuntos
Poluentes Atmosféricos/urina , Poluição do Ar/estatística & dados numéricos , Carbono/urina , Biomarcadores/urina , Criança , Feminino , Humanos , Masculino , Reprodutibilidade dos Testes
20.
Eur J Prev Cardiol ; 24(13): 1416-1428, 2017 09.
Artigo em Inglês | MEDLINE | ID: mdl-28617090

RESUMO

Background In view of the increasing heart failure epidemic and awareness of the adverse impact of environmental pollution on human health, we investigated the association of left ventricular structure and function with air pollutants in a general population. Methods In 671 randomly recruited Flemish (51.7% women; mean age, 50.4 years) we echocardiographically assessed left ventricular systolic strain and strain rate and the early and late peak velocities of transmitral blood flow and mitral annular movement (2005-2009). Using subject-level data, left ventricular function was cross-sectionally correlated with residential long-term exposure to air pollutants, including black carbon, PM2.5, PM10 (particulate matter) and nitrogen dioxide (NO2), while accounting for clustering by residential address and confounders. Results Annual exposures to black carbon, PM2.5, PM10 and NO2 averaged 1.19, 13.0, 17.7, and 16.8 µg/m3. Systolic left ventricular function was worse ( p ≤ 0.027) with higher black carbon, PM2.5, PM10 and NO2 with association sizes per interquartile interval increment ranging from -0.339 to -0.458% for longitudinal strain and from -0.033 to -0.049 s-1 for longitudinal strain rate. Mitral E and a' peak velocities were lower ( p ≤ 0.021) with higher black carbon, PM2.5 and PM10 with association sizes ranging from -1.727 to -1.947 cm/s and from -0.175 to -0.235 cm/s, respectively. In the geographic analysis, the systolic longitudinal strain sided with gradients in air pollution. The path analysis identified systemic inflammation as a possible mediator of associations with black carbon. Conclusions Long-term low-level air pollution is associated with subclinical impairment of left ventricular performance and might be a risk factor for heart failure.


Assuntos
Poluição do Ar/efeitos adversos , Ecocardiografia Doppler/métodos , Monitoramento Ambiental/métodos , Insuficiência Cardíaca/etiologia , Ventrículos do Coração/fisiopatologia , Material Particulado/efeitos adversos , Função Ventricular Esquerda/fisiologia , Bélgica/epidemiologia , Feminino , Seguimentos , Insuficiência Cardíaca/epidemiologia , Ventrículos do Coração/diagnóstico por imagem , Humanos , Incidência , Masculino , Pessoa de Meia-Idade , Estudos Retrospectivos , Fatores de Risco
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