Presentation and evaluation of an integrated model chain to respond to traffic- and health-related policy questions

Lefebvre, Wouter; Degrawe, B.; Beckx, Carolien; Vanhulsel, Marlies; Kochan, Bruno; Bellemans, Tom; Janssens, Davy; Wets, Geert; Janssen, Stijn; Vlieger, Ina De; Panis, Luc Int; Dhondt, Stijn

doi:10.1016/j.envsoft.2012.09.003

Cited by 106 publications

(69 citation statements)

References 35 publications

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“…This method uses pollution data collected in the official fixed-site monitoring networks ( n = 34) and land cover data obtained from satellite images (CORINE land cover data set; http://www.eea.europa.eu/publications/COR0-landcover) in combination with a dispersion model as described by Lefebvre et al (2011, 2013). This model chain provides daily PM 2.5 values using data both from the Belgian telemetric air quality network, point sources, and line sources which then are interpolated to a high-resolution receptor grid (25 × 25 m).…”

Section: Methodsmentioning

confidence: 99%

Neonatal Cord Blood Oxylipins and Exposure to Particulate Matter in the Early-Life Environment: An ENVIR ON AGE Birth Cohort Study

Martens

Gouveia

Madhloum

et al. 2017

Environ Health Perspect

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Background:As part of the lipidome, oxylipins are bioactive lipid compounds originating from oxidation of different fatty acids. Oxylipins could provide a new target in the developmental origins model or the ability of early life exposure to change biology.Objectives:We studied the association between in utero PM2.5 (particulate matter with aerodynamic diameter < 2.5 μm) exposure and oxylipin profiles in newborns.Methods:Thirty-seven oxylipins reflecting the cyclooxygenase (COX), lipoxygenase (5-LOX and 12/15-LOX), and cytochrome P450 (CYP) pathways were assayed in 197 cord blood plasma samples from the ENVIRONAGE birth cohort. Principal component (PC) analysis and multiple regression models were used to estimate associations of in utero PM2.5 exposure with oxylipin pathways and individual metabolites.Results:A principal component representing the 5-LOX pathway (6 metabolites) was significantly positively associated with PM2.5 exposure during the entire (multiple testing–adjusted q-value = 0.05) and second trimester of pregnancy (q = 0.05). A principal component representing the 12/15-LOX pathway (11 metabolites) was positively associated with PM2.5 exposure during the second trimester of pregnancy (q = 0.05). PM2.5 was not significantly associated with the COX pathway during any time period. There was a positive but nonsignificant association between second-trimester PM2.5 and the CYP pathway (q = 0.16).Conclusion: In utero exposure to particulate matter, particularly during the second trimester, was associated with differences in the cord blood levels of metabolites derived from the lipoxygenase pathways. These differences may indicate an effect of air pollution during in utero life on the inflammatory state of the newborn at birth. Oxylipins may be important mediators between early life exposures and health outcomes later in life.Citation:Martens DS, Gouveia S, Madhloum N, Janssen BG, Plusquin M, Vanpoucke C, Lefebvre W, Forsberg B, Nording M, Nawrot TS. 2017. Neonatal cord blood oxylipins and exposure to particulate matter in the early-life environment: an ENVIRONAGE birth cohort study. Environ Health Perspect 125:691–698; http://dx.doi.org/10.1289/EHP291

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Section: Methodsmentioning

confidence: 99%

Neonatal Cord Blood Oxylipins and Exposure to Particulate Matter in the Early-Life Environment: An ENVIR ON AGE Birth Cohort Study

Martens

Gouveia

Madhloum

et al. 2017

Environ Health Perspect

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“…For the child's residence, we used a spatial temporal interpolation method to model the daily residential exposure levels (µg/m³) of PM2.5, PM10, and BC (Table 1). This method takes into account land-cover data obtained from satellite images (CORINE land-cover data set) 28 and pollution data of fixed monitoring stations in combination with a dispersion model 29,30 . The model calculates the daily interpolated exposure concentrations in a high resolution receptor grid based on information from the Belgian telemetric air quality networks, point sources, and line sources.…”

Section: Modeled Outdoor Air Pollution and Traffic Indicators At Resimentioning

confidence: 99%

Recent versus chronic exposure to particulate matter air pollution in association with neurobehavioral performance in a panel study of primary schoolchildren

Saenen

Provost

Viaene³

et al. 2016

Environment International

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Children's neuropsychological abilities are in a developmental stage. Recent air pollution exposure and neurobehavioral performance are scarcely studied. In a panel study, we repeatedly administered to each child the following neurobehavioral tests: Stroop Test (selective attention) and Continuous Performance Test (sustained attention), Digit Span Forward and Backward Tests (short-term memory), and Digit-Symbol and Pattern Comparison Tests (visual information processing speed). At school, recent inside classroom particulate matter ≤2.5 or 10μm exposure (PM2.5, PM10) was monitored on each examination day. At the child's residence, recent (same day up to 2days before) and chronic (365days before examination) exposures to PM2.5, PM10 and black carbon (BC) were modeled. Repeated neurobehavioral test performances (n=894) of the children (n=310) reflected slower Stroop Test (p=0.05) and Digit-Symbol Test (p=0.01) performances with increasing recent inside classroom PM2.5 exposure. An interquartile range (IQR) increment in recent residential outdoor PM2.5 exposure was associated with an increase in average latency of 0.087s (SE: ±0.034; p=0.01) in the Pattern Comparison Test. Regarding chronic exposure at residence, an IQR increment of PM2.5 exposure was associated with slower performances in the Continuous Performance (9.45±3.47msec; p=0.007) and Stroop Tests (59.9±26.5msec; p=0.02). Similar results were obtained for PM10 exposure. In essence, we showed differential neurobehavioral changes robustly and adversely associated with recent or chronic ambient exposure to PM air pollution at residence, i.e., with recent exposure for visual information processing speed (Pattern Comparison Test) and with chronic exposure for sustained and selective attention.

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“…For each mother's residential address, we interpolated the regional background levels of PM 2.5 (micrograms per cubic meter) using a spatial temporal interpolation method (Kriging) 41 that uses pollution data collected in the official fixed site monitoring network (n D 34) and land cover data obtained from satellite images (Corine land cover data set) in combination with a dispersion model (dispersion modeling described by Lefebvre et al 42,43 ). This model chain provides daily PM 2.5 values using data from the Belgian telemetric air quality network, point sources and line sources which are then interpolated to a high-resolution receptor grid.…”

Section: Exposure Measurementmentioning

confidence: 99%

Placental mitochondrial methylation and exposure to airborne particulate matter in the early life environment: An ENVIRONAGE birth cohort study

Janssen¹,

Byun²,

Gyselaers³

et al. 2015

Epigenetics

170

139

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Abbreviations: 12S rRNA, Mitochondrial ribosomal 12S rRNA; D-loop, Displacement loop; IQR, Interquartile range; mtDNA, Mitochondrial DNA; mtDNMT1, Mitochondrial isoform of nuclear-encoded DNA methyltransferase enzyme 1;MT-RNR1, Mitochondrial region RNR1; PM, Particulate matter.Most research to date has focused on epigenetic modifications in the nuclear genome, with little attention devoted to mitochondrial DNA (mtDNA). Placental mtDNA content has been shown to respond to environmental exposures that induce oxidative stress, including airborne particulate matter (PM). Damaged or non-functioning mitochondria are specifically degraded through mitophagy, exemplified by lower mtDNA content, and could be primed by epigenetic modifications in the mtDNA. We studied placental mtDNA methylation in the context of the early life exposome. We investigated placental tissue from 381 mother-newborn pairs that were enrolled in the ENVIRONAGE birth cohort. We determined mtDNA methylation by bisulfite-pyrosequencing in 2 regions, i.e., the D-loop control region and 12S rRNA (MT-RNR1), and measured mtDNA content by qPCR. PM 2.5 exposure was calculated for each participant's home address using a dispersion model. An interquartile range (IQR) increment in PM 2.5 exposure over the entire pregnancy was positively associated with mtDNA methylation (MT-RNR1: C0.91%, P D 0.01 and D-loop: C0.21%, P D 0.05) and inversely associated with mtDNA content (relative change of ¡15.60%, P D 0.001) in placental tissue. mtDNA methylation was estimated to mediate 54% [P D 0.01 (MT-RNR1)] and 27% [P D 0.06 (D-loop)] of the inverse association between PM 2.5 exposure and mtDNA content. This study provides new insight into the mechanisms of altered mitochondrial function in the early life environment. Epigenetic modifications in the mitochondrial genome, especially in the MT-RNR1 region, substantially mediate the association between PM 2.5 exposure during gestation and placental mtDNA content, which could reflect signs of mitophagy and mitochondrial death.

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Presentation and evaluation of an integrated model chain to respond to traffic- and health-related policy questions

Cited by 106 publications

References 35 publications

Neonatal Cord Blood Oxylipins and Exposure to Particulate Matter in the Early-Life Environment: An ENVIR ON AGE Birth Cohort Study

Neonatal Cord Blood Oxylipins and Exposure to Particulate Matter in the Early-Life Environment: An ENVIR ON AGE Birth Cohort Study

Recent versus chronic exposure to particulate matter air pollution in association with neurobehavioral performance in a panel study of primary schoolchildren

Placental mitochondrial methylation and exposure to airborne particulate matter in the early life environment: An ENVIRONAGE birth cohort study

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