BACKGROUND:Individuals with lower socioeconomic status (SES) are at a higher risk of being exposed to adverse environmental factors. Children are more vulnerable to the harmful effects of air pollutants. Therefore, this study examined socioeconomic inequalities in air pollution exposure among children in Flanders, Belgium. METHODS:Data were used from 298 children (age range: 9-12 years), and from their parents who participated in the COGNition and Air pollution in Children study. Socioeconomic status was measured using highest parental education at the individual level and median income at the neighborhood (aggregated) level. Annual average outdoor concentrations of particulate matter with diameters <2.5 μm (PM2.5) and <10.0 μm (PM10), nitrogen dioxide (NO2), and black carbon (BC) in μg/m3 were estimated at the residential address. Mixed regression models were applied to examine the associations. RESULTS:Children from parents with a low education level were exposed to significantly higher levels of PM2.5, PM10, and BC compared to children from parents with a high education level. However, the associations were not significant when tested using regression models. Children who lived in areas with a lower median neighborhood income were exposed to significantly higher levels of air pollution; an interquartile range (IQR; €4505.00) decrease in income was associated with an increase in exposure to PM2.5 of 0.198 μg/m3, PM10 of 0.406 μg/m3, NO2 of 0.740 μg/m3, and BC of 0.063 μg/m3. Children of parents with a low/high education level had a higher exposure to PM2.5, PM10, NO2, and BC when living in a low income neighborhood. Exposure to all air pollutants was the highest for low parental education level and low neighborhood income. CONCLUSIONS:Low neighborhood income was significantly associated with higher levels of air pollution, while parental education level was not significantly associated. Children from parents with a low education and low income were exposed to the highest levels of air pollution.

To mitigate air pollution, source apportionment is a key element for the design of effective measures. However, source apportionment often involves complex model chains only accessible to expert users. In this paper we present a new web-application, the Concawe NO2 source apportionment viewer. It allows experts and non-expert users to evaluate the contributions of different sectors and the impact of measures in the road transport sector on current and future NO2 pollution in the EU27+UK in a fast and user-friendly way. The methodology behind the viewer was described in a previous paper by Degraeuwe et al. (2024). Here we describe the user interface and give some examples; the contribution of different sectors to the NO2 concentrations in the 3136 monitoring stations, and the impact of specific transport policies (e.g., Euro 7/VII standard, urban access regulations) on the NO2 concentrations in 948 European cities.

The deposition of active nitrogen on the special areas of conservation (SAC) is too high for several ecosystems in Flanders, Belgium. Therefore, in response to the 92/43/EEC (Habitats Directive) article 6 obligations of the member states, a policy to reduce nitrogen deposition is currently implemented in Flanders. Part of this policy are adjustments to the regulations for permitting new nitrogen (i.e. NH3, NOx) emitting installations. According to §3 of article 6, any plan or project that likely has a significant effect on the SAC, either individually or in combination with other plans or projects, is subject to an appropriate assessment of its implications for the site. It can only be approved if there is certainty that it will not adversely affect the integrity of the SAC. As is regularly done for permitting, this test is performed by using a model. The model chain in this case is the VLOPS-IFDM model. The model is well validated and based on these results, the uncertainty on the model results has been estimated. However, this uncertainty is quite large, in part due to the limited knowledge on the dry deposition process of reactive nitrogen. This study will first present the validation results for several validation cases. Thereafter, a discussion about the implications for policy related cases is initiated. At the moment the model uncertainty is ignored in the permitting procedure. However, one could state that this is not in agreement with the necessity of proving that the permit will not adversely affect the integrity of the SAC. Nevertheless, if the uncertainty was to be taken into account too rigorously, permitting new installations in Flanders would be impossible. The goal of this part is not to present the definite answer to this question but to initiate a discussion on how to take into account uncertainties in policy supporting cases.

In view of upcoming more stringent air quality limits and the ambition to align with the WHO guidelines, nitrogen dioxide (NO2) pollution from traffic and other sources will remain a problem in the EU. To assess the impact of traffic measures and emission reductions in other sectors on NO2-concentrations, an EU-wide high-resolution NO2 source apportionment web-application was developed. The application allows users to define scenarios in a user-friendly way and quickly visualize the NO2-concentrations at measurement stations and in cities. The user can configure a new Euro 7/VII emission standard and additionally define urban access regulations scenarios in cities. To capture the spatial scales of NO2 pollution, the SHERPA source-receptor model was used in combination with the QUARK kernel dispersion model. The first model considers long-distance impacts, the latter considers the strong concentration gradients close to roads. This paper focuses on the methodology, a follow-up paper describes the web-application.

Background The adverse effect of air pollution on mortality is well documented worldwide but the identification of more vulnerable populations at higher risk of death is still limited. The aim of this study was to evaluate the association between natural mortality (overall and cause-specific) and short-term exposure to five air pollutants (PM 2.5 , PM 10 , NO 2 , O 3 and black carbon) and identify potential vulnerable populations in Belgium. Methods We used a time-stratified case-crossover design with conditional logistic regressions to assess the relationship between mortality and air pollution in the nine largest Belgian agglomerations. Then, we performed a random-effect meta-analysis of the pooled results and described the global air pollution-mortality association. We carried out stratified analyses by individual characteristics (sex, age, employment, hospitalization days and chronic preexisting health conditions), living environment (levels of population density, built-up areas) and season of death to identify effect modifiers of the association. Results The study included 304,754 natural deaths registered between 2010 and 2015. We found percentage increases for overall natural mortality associated with 10 μg/m 3 increases of air pollution levels of 0.6% (95% CI: 0.2%, 1.0%) for PM 2.5 , 0.4% (0.1%, 0.8%) for PM 10 , 0.5% (-0.2%, 1.1%) for O 3 , 1.0% (0.3%, 1.7%) for NO 2 and 7.1% (-0.1%, 14.8%) for black carbon. There was also evidence for increases of cardiovascular and respiratory mortality. We did not find effect modification by individual characteristics (sex, age, employment, hospitalization days). However, this study suggested differences in risk of death for people with preexisting conditions (thrombosis, cardiovascular diseases, asthma, diabetes and thyroid affections), season of death (May–September vs October–April) and levels of built-up area in the neighborhood (for NO 2 ). Conclusions This work provided evidence for the adverse health effects of air pollution and contributed to the identification of specific population groups. These findings can help to better define public-health interventions and prevention strategies.

Mobile monitoring is used as an additional tool to collect air quality data at a high spatial resolution and to complement data from fixed air quality stations. Citizens are interested in contributing to air quality monitoring, and while the availability of low-cost air quality sensors can create opportunities to measure the air quality at a high spatial resolution, the data are often of lower quality, and sensors that measure combustion-related aerosols (like black carbon) are not commonly available. Mobile monitoring using a mid-range instrument can fill this gap. We present the results of a mobile BC (black carbon) monitoring campaign performed by citizens in Mechelen as part of a local citizen observatory (CO), Meet Mee Mechelen, initiated as part of the European H2020 project, Ground Truth 2.0. The goal of the study was two-fold: (1) to propose and evaluate a mobile monitoring method (data collection and data processing) to construct pollution maps of BC concentrations and (2) to demonstrate how to organize community-based air quality monitoring to measure both the spatial and temporal variations in air pollution levels. Measurements were taken during peak hours in four campaigns characterized by different meteorological conditions: October–November 2017, February–March 2018, June–July 2018 and September 2018. The results show large spatial and temporal variabilities. Spatial variability is influenced by traffic volume, stop-and-go traffic and also the building environment and the distance of biking paths from road traffic. The four different campaigns show similar spatial patterns, but due to background and meteorological influences, the absolute concentrations differ between seasons. A rescaling method using data from fixed stations in the air quality monitoring network (AQMN) was presented to construct maps representative of longer periods. This paper shows that mobile measurements can be used by CO to assess the spatial variability of air quality in a city. The data can be used to evaluate mobility plans, carry out hot spot detection, evaluate the exposure of cyclists as a function of cycling infrastructure and perform model validation. However, it is important to use high-quality instruments and apply the correct measurement methodology (number of repetitions, season) to obtain meaningful data.

Mitochondria are sensitive to oxidative stress, which can be caused by traffic-related air pollution. Placental mitochondrial DNA (mtDNA) mutations have been previously linked with air pollution. However, the relationship between prenatal air pollution and cord-blood mtDNA mutations has been poorly understood. Therefore, we hypothesized that prenatal particulate matter (PM2.5) and NO2 exposures are associated with cord-blood mtDNA heteroplasmy. As part of the ENVIRONAGE cohort, 200 mother-newborn pairs were recruited. Cord-blood mitochondrial single-nucleotide polymorphisms were identified by whole mitochondrial genome sequencing, and heteroplasmy levels were evaluated based on the variant allele frequency (VAF). Outdoor PM2.5 and NO2 concentrations were determined by a high-resolution spatial-temporal interpolation method based on the maternal residential address. Distributed lag linear models were used to determine sensitive time windows for the association between NO2 exposure and cord-blood mtDNA heteroplasmy. A 5 μg/m3 increment in NO2 was linked with MT-D-Loop16311T>C heteroplasmy from gestational weeks 17-25. MT-CYTB14766C>T was negatively associated with NO2 exposure in mid pregnancy, from weeks 14-17, and positively associated in late pregnancy, from weeks 31-36. No significant associations were observed with prenatal PM2.5 exposure. This is the first study to show that prenatal NO2 exposure is associated with cord-blood mitochondrial mutations and suggests two critical windows of exposure in mid-to-late pregnancy.

Background: Particulate matter (PM) is associated with aging markers at birth, including telomeres and mito-chondria. It is unclear whether markers of the core-axis of aging, i.e. tumor suppressor p53 (p53) and peroxisome proliferator-activated receptor gamma co-activator 1 alpha (PGC-1 alpha), are associated with prenatal air pollution and whether there are underlying mechanisms.Methods: 556 mother-newborn pairs from the ENVIRONAGE birth cohort were recruited at the East Limburg Hospital in Genk (Belgium). In placenta and cord blood, telomere length (TL) and mitochondrial DNA content (mtDNAc) were measured using quantitative real-time polymerase chain reaction (qPCR). In cord plasma, p53 and PGC-1 alpha protein levels were measured using ELISA. Daily ambient PM2.5 concentrations during gestation were calculated using a spatial temporal interpolation model. Distributed lag models (DLMs) were applied to assess the association between prenatal PM2.5 exposure and each molecular marker. Mediation analysis was performed to test for underlying mechanisms. Results: A 5 mu g/m3 increment in PM2.5 exposure was associated with-11.23 % (95 % CI:-17.36 % to-4.65 %, p = 0.0012) and-7.34 % (95 % CI:-11.56 % to-2.92 %, p = 0.0014) lower placental TL during the entire pregnancy and second trimester respectively, and with-12.96 % (95 % CI:-18.84 % to-6.64 %, p < 0.001) lower placental mtDNAc during the third trimester. Furthermore, PM2.5 exposure was associated with a 12.42 % (95 % CI:-1.07 % to 27.74 %, p = 0.059) higher cord plasma p53 protein level and a-3.69 % (95 % CI:-6.97 % to-0.31 %, p = 0.033) lower cord plasma PGC-1 alpha protein level during the third trimester. Placental TL mediated 65 % of the negative and 17 % of the positive association between PM2.5 and placental mtDNAc and cord plasma p53 protein levels, respectively.Conclusion: Ambient PM2.5 exposure during pregnancy is associated with markers of the core-axis of aging, with TL as a mediating factor. This study strengthens the hypothesis of the air pollution induced core-axis of aging, and may unravel a possible underlying mediating mechanism in an early-life epidemiological context.

Background: Early life exposure to ambient particulate matter (PM) may negatively affect neurobehavioral development in children, influencing their cognitive, emotional, and social functioning. Here, we report a study on prenatal PM 2.5 exposure and neurobehavioral development focusing on different time points in the first years of life. Methods: This study was part of the ENVIR ON AGE birth cohort that follows mother -child pairs longitudinally. First, the Neonatal Behavioral Assessment Scale (NBAS) was employed on 88 newborns aged one to two months to assess their autonomic/physiological regulation, motor organisation, state organisation/regulation, and attention/social interaction. Second, our study included 393 children between the ages of four and six years, for which the Strengths and Difficulties Questionnaire (SDQ) was used to assess the children 's emotional problems, hyperactivity, conduct problems, peer relationship, and prosocial behaviour. Prenatal PM 2.5 exposure was determined using a high -resolution spatial -temporal method based on the maternal address. Multiple linear and multinomial logistic regression models were used to analyse the relationship between prenatal PM 2.5 exposure and neurobehavioral development in newborns and children, respectively. Results: A 5 mu g/m 3 increase in first -trimester PM 2.5 concentration was associated with lower NBAS range of state cluster scores (-6.11%; 95%CI: -12.00 to -0.23%; p = 0.04) in one -to -two -month -old newborns. No other behavioural clusters nor the reflexes cluster were found to be associated with prenatal PM 2.5 exposure. Furthermore, a 5 mu g/m 3 increment in first -trimester PM 2.5 levels was linked with higher odds of a child experiencing peer problems (Odds Ratio (OR) = 3.89; 95%CI: 1.39 to 10.87; p = 0.01) at ages four to six. Additionally, a 5 mu g/m 3 increase in second -trimester PM 2.5 concentration was linked to abnormal prosocial behaviour (OR = 0.49; 95%CI: 0.25 to 0.98; p = 0.04) at four to six years old. No associations were found between in utero PM 2.5 exposure and hyperactivity or conduct problems. Conclusions: Our findings suggest that prenatal exposure to PM may impact neurobehavioural development in newborns and preschool children. We identified sensitive time windows during early -to -mid pregnancy, possibly impacting stage changes in newborns and peer problems and prosocial behaviour in children.

Background: Exposure to green spaces is associated with improved mental health and may reduce risk of suicide. Here, we investigate the association between long-term exposure to residential surrounding greenness and sui-cide mortality. Methods: We used data from the 2001 Belgian census linked to mortality register data (2001-2011). We included all registered individuals aged 18 years or older at baseline (2001) residing in the five largest urban areas in Belgium (n = 3,549,514). Suicide mortality was defined using the tenth revision of the World Health Organi-sation International Classification of Diseases (ICD-10) codes X60-X84, Y10-Y34, and Y870. Surrounding greenness was measured using the Normalized Difference Vegetation Index (NDVI) within a 300 m and 1,000 m buffer around the residential address at baseline. To assess the association between residential surrounding greenness and suicide mortality, we applied Cox proportional hazards models with age as the underlying time scale. Models were adjusted for age, sex, living arrangement, migrant background, educational attainment, neighbourhood socio-economic position. We additionally explored potential mediation by residential outdoor nitrogen dioxide (NO2) concentrations. Finally, we assessed potential effect modification by various socio-demographic characteristics of the population (sex, age, educational attainment, migrant background, and neighbourhood socio-economic position). Associations are expressed as hazard ratios and their 95% confidence intervals (CI) for an interquartile range (IQR) increase in residential surrounding greenness. Results: We observed a 7% (95%CI 0.89-0.97) and 6% (95%CI 0.90-0.98) risk reduction of suicide mortality for an IQR increase in residential surrounding greenness for buffers of 300 m and 1,000 m, respectively. Further-more, this association was independent of exposure to NO2. After stratification, the inverse association was only apparent among women, and residents of Belgian origin, and that it was stronger among residents aged 36 or older, those with high level of education, and residents of most deprived neighbourhoods. Conclusion: Our results suggest that urban green spaces may protect against suicide mortality, but this beneficial effect may not be equally distributed across all strata of the population.

Background: There is ample evidence that air pollution increases mortality risk, but most studies are based on modelled estimates of air pollution, while the subjective perception of air quality is scarcely assessed. We aimed to compare the effects of objective and subjective exposure to air pollution on cardiorespiratory mortality in Brussels, Belgium.Methods: Data consisted of the 2001 Belgian census linked to registry-based mortality data for the follow-up period 2001-2014. We included individuals aged >30 years of age residing in Brussels at baseline (2001). Air pollution exposure was assessed with objective (modelled annual mean concentrations of PM2.5 in micrograms per cubic metre, mu g/m3) and subjective indicators (poor self-reported air quality perception in the census). We used Cox Proportional Hazard models with age as the underlying time scale to evaluate associations with car-diovascular disease (CVD) and respiratory disease mortality, and separately, ischaemic heart disease (IHD), cerebrovascular disease, and COPD excluding asthma mortality. We specified single-and two-exposure models and evaluated effect modification by neighbourhood unemployment rate.Results: 437,340 individuals were included at baseline. During follow-up (2001-2014), 22,821 (5%) individuals had died from CVDs and 8572 (2%) from respiratory diseases. In single-exposure models, PM2.5 was significantly associated with an increased risk in CVD and IHD mortality (e.g. for IHD, per 5 mu g/m3 increase: Hazard Ratio, HR:1.22, 95%CI:1.08-1.37), and poor air quality perception with COPD excluding asthma mortality (HR:1.23, 95%CI:1.15-1.33). Associations remained significant in the two-exposure models, and additionally, perception was associated with respiratory disease mortality. Associations became gradually stronger with increasing neighbourhood unemployment rate [e.g. in the highest, Q3: PM2.5 and cerebrovascular disease mortality (HR:1.53, 95%CI:1.04-2.24)]. Conclusion: Our findings suggest that objective and subjective exposure to air pollution increased the risk of dying from cardiovascular and respiratory diseases respectively in Brussels. These results encourage policies reducing pollution load in Brussels whilst considering socio-economic inequalities.

Background Living in greener areas is associated with slower cognitive decline and reduced dementia risk among older adults, but the evidence with neurodegenerative disease mortality is scarce. We studied the association between residential surrounding greenness and neurodegenerative disease mortality in older adults. Methods We used data from the 2001 Belgian census linked to mortality register data during 2001–2014. We included individuals aged 60 years or older and residing in the five largest Belgian urban areas at baseline (2001). Exposure to residential surrounding greenness was assessed using the 2006 Normalized Difference Vegetation Index (NDVI) within 500-m from residence. We considered all neurodegenerative diseases and four specific outcomes: Alzheimer’s disease, vascular dementia, unspecified dementia, and Parkinson’s disease. We fitted Cox proportional hazard models to obtain hazard ratios (HR) and 95% confidence intervals (CI) of the associations between one interquartile range (IQR) increment in surrounding greenness and neurodegenerative disease mortality outcomes, adjusted for census-based covariates. Furthermore, we evaluated the potential role of 2010 air pollution (PM 2.5 and NO 2 ) concentrations, and we explored effect modification by sociodemographic characteristics. Results From 1,134,502 individuals included at baseline, 6.1% died from neurodegenerative diseases during follow-up. After full adjustment, one IQR (0.22) increment of surrounding greenness was associated with a 4–5% reduction in premature mortality from all neurodegenerative diseases, Alzheimer’s disease, vascular and unspecified dementia [e.g., for Alzheimer’s disease mortality: HR 0.95 (95%CI: 0.93, 0.98)]. No association was found with Parkinson’s disease mortality. Main associations remained for all neurodegenerative disease mortality when accounting for air pollution, but not for the majority of specific mortality outcomes. Associations were strongest in the lower educated and residents from most deprived neighbourhoods. Conclusions Living near greener spaces may reduce the risk of neurodegenerative disease mortality among older adults, potentially independent from air pollution. Socioeconomically disadvantaged groups may experience the greatest beneficial effect.

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.

BACKGROUND:Residing close to green spaces might reduce diabetes mellitus (DM) risk; however, evidence for diabetes mortality is limited. Moreover, individual and neighbourhood social factors may determine DM risk. Exposure to green spaces may also depend on socioeconomic position (SEP). This study examined the associations between residential greenness and diabetes-related mortality, and the role of the social environment in these associations.METHODS:We used the 2001 Belgian census linked to mortality register data for the period 2001-2014. We included individuals aged 40-79 years old and residing in the five largest Belgian urban areas at baseline. Exposure to residential greenness was assessed with surrounding greenness using the Normalized Difference Vegetation Index (NDVI) within 500-m of residence (objective indicator), and perceived neighbourhood greenness (subjective indicator). We conducted mixed-effects Cox proportional hazards models to obtain hazard ratios (HR) for diabetes-related mortality per interquartile range (IQR) increments of residential greenness. We assessed effect modification by social factors through stratification.RESULTS:From 2,309,236 individuals included at baseline, 1.2% died from DM during follow-up. Both residential greenness indicators were inversely associated with diabetes-related mortality after adjustment for individual social factors. After controlling for neighbourhood SEP, the beneficial association with surrounding greenness disappeared [HR 1.02 (95%CI:0.99,1.06)], but persisted with perceived neighbourhood greenness [HR 0.93 (95%CI:0.91,0.95)]. After stratification the inverse associations with perceived neighbourhood greenness were strongest for women, the lowest educated, and individuals residing in least deprived neighbourhoods.CONCLUSIONS:Our findings suggest that an overall positive perception of neighbourhood green spaces reduces independently the risk of diabetes-related mortality, regardless of the neighbourhood social environment. Nevertheless, neighbourhood SEP may be a strong confounder in the associations between diabetes-related mortality and greenness indicators derived from satellite images. Perception factors not captured by objective measurements of green spaces are potentially relevant in the association with DM, especially among disadvantaged groups.

Background Mitochondria play an important role in the energy metabolism and are susceptible to environmental pollution. Prenatal air pollution exposure has been linked with childhood obesity. Placental mtDNA mutations have been associated with prenatal particulate matter exposure and MT-ND4L 10550A>G heteroplasmy has been associated with BMI in adults. Therefore, we hypothesized that in utero PM 2.5 exposure is associated with cord blood MT-ND4L 10550A>G heteroplasmy and early life growth. In addition, the role of cord blood MT-ND4L 10550A>G heteroplasmy in overweight during early childhood is investigated. Methods This study included 386 mother-newborn pairs. Outdoor PM 2.5 concentrations were determined at the maternal residential address. Cord blood MT-ND4L 10550A>G heteroplasmy was determined using Droplet Digital PCR. Associations were explored using logistic regression models and distributed lag linear models. Mediation analysis was performed to quantify the effects of prenatal PM 2.5 exposure on childhood overweight mediated by cord blood MT-ND4L 10550A>G heteroplasmy. Results Prenatal PM 2.5 exposure was positively associated with childhood overweight during the whole pregnancy (OR = 2.33; 95% CI: 1.20 to 4.51; p = 0.01), which was mainly driven by the second trimester. In addition, prenatal PM 2.5 exposure was associated with cord blood MT-ND4L 10550A>G heteroplasmy from gestational week 9 – 13. The largest effect was observed in week 10, where a 5 µg/m 3 increment in PM 2.5 was linked with cord blood MT-ND4L 10550A>G heteroplasmy (OR = 0.93; 95% CI: 0.87 to 0.99). Cord blood MT-ND4L 10550A>G heteroplasmy was also linked with childhood overweight (OR = 3.04; 95% CI: 1.15 to 7.50; p = 0.02). The effect of prenatal PM 2.5 exposure on childhood overweight was mainly direct (total effect OR = 1.18; 95% CI: 0.99 to 1.36; natural direct effect OR = 1.20; 95% CI: 1.01 to 1.36)) and was not mediated by cord blood MT-ND4L 10550A>G heteroplasmy. Conclusions Cord blood MT-ND4L 10550A>G heteroplasmy was linked with childhood overweight. In addition, in utero exposure to PM 2.5 during the first trimester of pregnancy was associated with cord blood MT-ND4L 10550A>G heteroplasmy in newborns. Our analysis did not reveal any mediation of cord blood MT-ND4L 10550A>G heteroplasmy in the association between PM 2.5 exposure and childhood overweight.

Detailed validation of air quality models is essential, but remains challenging, due to a lack of suitable high-resolution measurement datasets. This is particularly true for pollutants with short-scale spatial variations, such as nitrogen dioxide (NO2). While street-level air quality model chains can predict concentration gradients at high spatial resolution, measurement campaigns lack the coverage and spatial density required to validate these gradients. Citizen science offers a tool to collect large-scale datasets, but it remains unclear to what extent such data can truly increase model performance. Here we use the passive sampler dataset collected within the large-scale citizen science campaign CurieuzeNeuzen to assess the integrated ATMO-Street street-level air quality model chain. The extensiveness of the dataset (20.000 sampling locations across the densely populated region Flanders, ∼1.5 data points per km2) allowed an in-depth model validation and optimization. We illustrate generic techniques and methods to assess and improve street-level air quality models, and show that considerable model improvement can be achieved, in particular with respect to the correct representation of the small-scale spatial variability of the NO2-concentrations. After model optimization, the model skill of the ATMO-Street chain significantly increased, passing the FAIRMODE model quality threshold, and thus substantiating its suitability for policy support. More generally, our results reveal how a “deep validation” based on extensive spatial data can substantially improve model performance, thus demonstrating how air quality modelling can benefit from one-off large-scale monitoring campaigns.

BACKGROUND Residing in greener areas may decrease the burden of chronic diseases, but the association with cancer is unclear. We studied the associations between residential green spaces and site-specific cancer mortality in urban Belgium. METHODOLOGY We linked the 2001 Belgian census, register mortality data for 2001-2014, and environmental information (green spaces and air pollution) at baseline residence (2001). We included residents from the largest Belgian urban areas aged ≥ 30 years at baseline. Exposure to residential green spaces was assessed using the Normalized Difference Vegetation Index (NDVI), Urban Atlas, and perceived neighbourhood greenness (from the census). We used Cox proportional hazards models to obtain hazard ratios (HR) and their 95 % confidence intervals (95 %CI) of the mortality risk from lung, colorectal, breast (in women) and prostate cancer (in men) per interquartile range increment in residential green spaces. We further analyzed the role of outdoor air pollution and effect modification by age and socioeconomic position (SEP) in main associations. RESULTS 2,441,566 individuals were included at baseline. During follow-up, 1.2 % died from lung cancer, 0.6 % from colorectal cancer, 0.8 % from breast cancer, and 0.6 % from prostate cancer. After adjustment, higher exposure to green spaces was associated with a reduced mortality risk from lung cancer and breast cancer [e.g., for NDVI within 300 m, HR:0.946 (95 %CI:0.924,0.970), and HR:0.927 (95 %CI:0.892,0.963), respectively], but not with colorectal or prostate cancer mortality. For the latter, a suggestive hazardous effect of green spaces was found. Air pollution seemed to have only a marginal role. Beneficial effects of greenspace were generally stronger in < 65-year-old, but no clear trend by SEP was found. CONCLUSIONS Our findings suggest that residing in green areas could decrease mortality risk from lung and breast cancer, potentially independent from air pollution. Future studies should consider different indicators of greenspace exposure and investigate potential pathways underlying the associations.

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 soiladjusted 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.

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) mu g/m(3), PM10 18.88 (16.64 - 21.13) mu g/m(3), PM2.5 13.67 (11.5 - 15.56) mu g/m(3) and NO2 18.39 (15.52 - 20.31) mu g/m(3). 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.

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.