Dynamic assessment of exposure to air pollution using mobile phone data

Background: Exposure to air pollution can have major health impacts, such as respiratory and cardiovascular diseases. Traditionally, only the air pollution concentration at the home location is taken into account in health impact assessments and epidemiological studies. Neglecting individual travel patterns can lead to a bias in air pollution exposure assessments. Methods: In this work, we present a novel approach to calculate the daily exposure to air pollution using mobile phone data of approximately 5 million mobile phone users living in Belgium. At present, this data is collected and stored by telecom operators mainly for management of the mobile network. Yet it represents a major source of information in the study of human mobility. We calculate the exposure to NO2 using two approaches: assuming people stay at home the entire day (traditional static approach), and incorporating individual travel patterns using their location inferred from their use of the mobile phone network (dynamic approach). Results: The mean exposure to NO2 increases with 1.27 mu g/m(3) (4.3 %) during the week and with 0.12 mu g/m(3) (0.4 %) during the weekend when incorporating individual travel patterns. During the week, mostly people living in municipalities surrounding larger cities experience the highest increase in NO2 exposure when incorporating their travel patterns, probably because most of them work in these larger cities with higher NO2 concentrations. Conclusions: It is relevant for health impact assessments and epidemiological studies to incorporate individual travel patterns in estimating air pollution exposure. Mobile phone data is a promising data source to determine individual travel patterns, because of the advantages (e.g. low costs, large sample size, passive data collection) compared to travel surveys, GPS, and smartphone data (i.e. data captured by applications on smartphones)

Projected heat-related mortality under climate change in the metropolitan area of Skopje

Abstract Background Excessive summer heat is a serious environmental health problem in Skopje, the capital and largest city of the former Yugoslav Republic of Macedonia. This paper attempts to forecast the impact of heat on mortality in Skopje in two future periods under climate change and compare it with a historical baseline period. Methods After ascertaining the relationship between daily mean ambient air temperature and daily mortality in Skopje, we modelled the evolution of ambient temperatures in the city under a Representative Concentration Pathway scenario (RCP8.5) and the evolution of the city population in two future time periods: 2026–2045 and 2081–2100, and in a past time period (1986–2005) to serve as baseline for comparison. We then calculated the projected average annual mortality attributable to heat in the absence of adaptation or acclimatization during those time windows, and evaluated the contribution of each source of uncertainty on the final impact. Results Our estimates suggest that, compared to the baseline period (1986–2005), heat-related mortality in Skopje would more than double in 2026–2045, and more than quadruple in 2081–2100. When considering the impact in 2081–2100, sampling variability around the heat–mortality relationship and climate model explained 40.3 and 46.6 % of total variability. Conclusion These results highlight the importance of a long-term perspective in the public health prevention of heat exposure, particularly in the context of a changing climate

FAIRMODE Intercomparison exercise - Dataset to assess the area of representativeness of Air Quality Monitoring Stations

A feasibility study for organizing an intercomparison exercise (IE) of the methods used for estimating of the area of representativeness of the Air Quality Monitoring Stations (SR) in Europe has been carried out. It showed that it should be possible to compare the extent of SR determined by the different methods. Moreover, at the FAIRMODE-Aveiro meeting in 2015, the participants agreed to carry out the intercomparison exercise assessing the SR estimates for PM10 and NO2 at one traffic station, and for PM10, NO2 and O3 at two urban background stations. This report presents a dataset suitable for the FAIRMODE IE of the area of representativeness of Air Quality Monitoring Stations in the urban area of Antwerp (Belgium) for the year 2012. Three monitoring stations, Borgerhout-Straatkant, Antwerpen-Linkeroever and Schoten, have been selected for the evaluation. The dataset includes the model results for interpolated annual means on a fine regular grid, hourly time series at a number of 341 virtual receptor points to which random noise have been added, data from measurements of the Antwerp automatic monitoring stations, individual sampling campaigns, emissions, traffic, population density, building information, gridded CORINE land cover data, a short summary of PM10 speciated data and daily time profiles for traffic.JRC.C.5-Air and Climat

Placental promoter methylation of DNA repair genes and prenatal exposure to particulate air pollution: an ENVIRONAGE cohort study

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. The work is supported by the European Research Council (ERC-2012-StG.310898 and ERC-2011-StG. 282413) and by the Flemish Scientific Fund (FWO,G073315N/G082317N)

A new method for fine-scale assessments of the average urban Heat island over large areas and the effectiveness of nature-based solutions

People living in cities experience extra heat stress due to the so-called Urban Heat Island (UHI) effect. To gain an insight into the spatial variability of the UHI for the Netherlands, a detailed map (10 m horizontal resolution) has been calculated that shows the summer-averaged daily maximal UHI situation. The map is based on a relationship between the UHI, mean wind speed at 10 m height and the number of people living within a distance of 10 km, derived from simulations of over 100 European cities with the extensively validated urban climate model UrbClim. The cooling effect of green and blue infrastructure is also taken into account in the map, based on these simulation results. The presented map will help local authorities in defining target areas for climate adaptation measures and estimate the impact of nature-based solutions

Impact of passenger car NOX emissions on urban NO2 pollution – Scenario analysis for 8 European cities

Residents of large European cities are exposed to NO2 concentrations that often exceed the established air quality standards. Diesel cars have been identified as a major contributor to this situation; yet, it remains unclear to which levels the NOX emissions of diesel cars have to decrease to effectively mitigate urban NO2 pollution across Europe. Here, we take a continental perspective and model urban NO2 pollution in a generic street canyon of 8 major European cities for various NOX emission scenarios. We find that a reduction in the on-road NOX emissions of diesel cars to the Euro 6 level can in general decrease the regional and urban NO2 concentrations and thereby the frequency of exceedances of the NO2 air quality standard. High NO2 fractions in the NOX emissions of diesel cars tend to increase the urban NO2 concentrations only in proximity of intense road traffic typically found on artery roads in large cities like Paris and London. In cities with a low share of diesel cars in the vehicle fleet such as Athens or a high contribution from the NO2 background to the urban NO2 pollution such as Krakow, measures addressing heavy-duty vehicles, and the manufacturing, energy, and mining industry are necessary to decrease urban air pollution. We regard our model results as robust albeit subject to uncertainty resulting from the application of a generic street layout. With small modifications in the input parameters, our model could be used to assess the impact of NOX emissions from road transport on NO2 air pollution in any European city

Prenatal Air Pollution and Newborns' Predisposition to Accelerated Biological Aging.

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

Sex-specific associations between particulate matter exposure and gene expression in independent discovery and validation cohorts of middle-aged men and women

BACKGROUND: Particulate matter (PM) exposure leads to premature death, mainly due to respiratory and cardiovascular diseases. OBJECTIVES: Identification of transcriptomic biomarkers of air pollution exposure and effect in a healthy adult population. METHODS: Microarray analyses were performed in 98 healthy volunteers (48 men, 50 women). The expression of eight sex-specific candidate biomarker genes (significantly associated with PM(10) in the discovery cohort and with a reported link to air pollution-related disease) was measured with qPCR in an independent validation cohort (75 men, 94 women). Pathway analysis was performed using Gene Set Enrichment Analysis. Average daily PM(2.5) and PM(10) exposures over 2-years were estimated for each participant’s residential address using spatiotemporal interpolation in combination with a dispersion model. RESULTS: Average long-term PM(10) was 25.9 (± 5.4) and 23.7 (± 2.3) μg/m(3) in the discovery and validation cohorts, respectively. In discovery analysis, associations between PM(10) and the expression of individual genes differed by sex. In the validation cohort, long-term PM(10) was associated with the expression of DNAJB5 and EAPP in men and ARHGAP4 (p = 0.053) in women. AKAP6 and LIMK1 were significantly associated with PM(10) in women, although associations differed in direction between the discovery and validation cohorts. Expression of the eight candidate genes in the discovery cohort differentiated between validation cohort participants with high versus low PM(10) exposure (area under the receiver operating curve = 0.92; 95% CI: 0.85, 1.00; p = 0.0002 in men, 0.86; 95% CI: 0.76, 0.96; p = 0.004 in women). CONCLUSIONS: Expression of the sex-specific candidate genes identified in the discovery population predicted PM(10) exposure in an independent cohort of adults from the same area. Confirmation in other populations may further support this as a new approach for exposure assessment, and may contribute to the discovery of molecular mechanisms for PM-induced health effects. CITATION: Vrijens K, Winckelmans E, Tsamou M, Baeyens W, De Boever P, Jennen D, de Kok TM, Den Hond E, Lefebvre W, Plusquin M, Reynders H, Schoeters G, Van Larebeke N, Vanpoucke C, Kleinjans J, Nawrot TS. 2017. Sex-specific associations between particulate matter exposure and gene expression in independent discovery and validation cohorts of middle-aged men and women. Environ Health Perspect 125:660–669; http://dx.doi.org/10.1289/EHP37