ABSTRACT
BACKGROUND: There is inconsistent evidence of the effects of exposure to ambient air pollution on the occurrence of lower respiratory tract infections (LRTIs) in early childhood. We assessed the effects of individual-level prenatal and early life exposure to air pollutants on the risk of LRTIs in early life. METHODS: We studied 2568 members of the population-based Espoo Cohort Study born between 1984 and 1990 and living in 1991 in the City of Espoo, Finland. Exposure assessment was based on dispersion modelling and land-use regression for lifetime residential addresses. The outcome was a LRTI based on data from hospital registers. We applied Poisson regression to estimate the incidence rate ratio (IRR) of LTRIs, contrasting incidence rates in the exposure quartiles to the incidence rates in the first quartile. We used weighted quantile sum (WQS) regression to estimate the joint effect of the studied air pollutants. RESULTS: The risk of LRTIs during the first 2 years of life was significantly related to exposure to individual and multiple air pollutants, measured with the Multipollutant Index (MPI), including primarily sulphur dioxide (SO2), particulate matter with a dry diameter of up to 2.5 µm (PM2.5) and nitrogen dioxide (NO2) exposures in the first year of life, with an adjusted IRR of 1.72 per unit increase in MPI (95% CI 1.20 to 2.47). LRTIs were not related to prenatal exposure. CONCLUSIONS: We provide evidence that ambient air pollution exposure during the first year of life increases the risk of LRTIs during the first 2 years of life. SO2, PM2.5 and NO2 were found to contribute the highest weights on health effects.
Subject(s)
Air Pollutants , Air Pollution , Environmental Exposure , Nitrogen Dioxide , Particulate Matter , Prenatal Exposure Delayed Effects , Respiratory Tract Infections , Sulfur Dioxide , Humans , Pregnancy , Female , Prenatal Exposure Delayed Effects/epidemiology , Finland/epidemiology , Particulate Matter/adverse effects , Respiratory Tract Infections/epidemiology , Respiratory Tract Infections/etiology , Air Pollutants/adverse effects , Air Pollution/adverse effects , Air Pollution/analysis , Infant , Male , Nitrogen Dioxide/analysis , Nitrogen Dioxide/adverse effects , Child, Preschool , Cohort Studies , Environmental Exposure/adverse effects , Sulfur Dioxide/adverse effects , Sulfur Dioxide/analysis , Infant, Newborn , Incidence , Risk Factors , Adult , Maternal Exposure/adverse effectsABSTRACT
OBJECTIVES: Air pollution and traffic noise are detrimental to cardiovascular health. However, the effects of different sources of these exposures on cardiovascular biomarkers remain unclear. We explored the associations of long-term exposure to source-specific air pollution (vehicular exhausts and residential woodsmoke) at low concentrations and road-traffic noise with systemic inflammation and cardiovascular disease biomarkers. MATERIAL AND METHODS: Modeled outdoor exposure to fine particulate matter (aerodynamic diameter ≤2.5 µm; PM2.5) from vehicular exhausts and residential woodsmoke, nitrogen dioxide (NO2) from road traffic, and road-traffic noise were linked to the home addresses of the participants (Finnish residents aged 25-74) in the FINRISK study 1997-2012. The participants were located in the cities of Helsinki, Vantaa, and the region of Turku, Finland. The outcomes were high-sensitivity C-reactive protein (CRP), a biomarker for systemic inflammation, and cardiovascular disease biomarkers N-terminal pro-B-type natriuretic peptide (NT-proBNP) and troponin I. We performed cross-sectional analyses with linear and additive models and adjusted for potential confounders. RESULTS: We found no association between PM2.5 from vehicular exhausts (% CRP difference for 1 µg/m3 increase in PM2.5: -0.9, 95% confidence interval, CI: -7.2, 5.8), or from residential woodsmoke (% difference: -8.1, 95% CI: -21.7, 7.9) and CRP (N = 4147). Road-traffic noise >70 dB tended to be positively associated with CRP (% CRP difference versus noise reference category of ≤45 dB: 18.3, 95% CI: -0.5, 40.6), but the association lacked significance and robustness (N = 7142). Otherwise, we found no association between road-traffic noise and CRP, nor between NO2 from road traffic and NT-proBNP (N = 1907) or troponin I (N = 1951). CONCLUSION: Long-term exposures to source-specific, fairly low-level air pollution from vehicular exhausts and residential woodsmoke, or road-traffic noise were not associated with systemic inflammation and cardiovascular disease biomarkers in this urban area.
ABSTRACT
BACKGROUND: Cold weather increases respiratory symptoms and provokes exacerbations of asthma, but there are no previous studies on its role in the aetiology of asthma. OBJECTIVE: We tested the hypothesis that a cold winter increases the risk of developing asthma during the following 1 to 2 years. METHODS: We conducted a case-crossover study of 315 newly diagnosed cases of asthma from the population-based Espoo Cohort Study from birth to the age of 27 years. The hazard period constituted 3 winter months preceding the onset of asthma and bidirectional reference periods of 1 year before hazard period and 1 year after onset of asthma. Exposure constituted average ambient temperature during the winter months of December, January and February. The outcome of interest was new doctor-diagnosed asthma. The measure of effect was OR of asthma estimated by conditional logistic regression analysis. RESULTS: The average winter temperature for the study period from winter 1983 to 2010 was -4.4°C (range -10.7 to 0.4). A 1°C decrease in the average winter temperature predicted a 7% increase in the risk of new asthma (OR=1.07, 95% CI 1.02 to 1.13). A cold winter with an average temperature below the climate normal value (-4.5°C; period 1981-2010) increased the risk of new asthma by 41% during the following year (OR: 1.41; 95% CI 1.04 to 1.90). CONCLUSIONS: This case-crossover study provides original evidence that a cold winter with below normal average temperatures increases the risk of developing new asthma during the following 1 to 2 years.
Subject(s)
Asthma , Cold Temperature , Humans , Adult , Cross-Over Studies , Finland/epidemiology , Cohort Studies , Seasons , Asthma/epidemiology , Asthma/etiologyABSTRACT
BACKGROUND: Residential wood combustion (RWC) is one of the largest sources of fine particles (PM2.5) in the Nordic cities. The current study aims to calculate the related health effects in four studied city areas in Sweden, Finland, Norway, and Denmark. METHODS: Health impact assessment (HIA) was employed as the methodology to quantify the health burden. Firstly, the RWC induced annual average PM2.5 concentrations from local sources were estimated with air pollution dispersion modelling. Secondly, the baseline mortality rates were retrieved from the national health registers. Thirdly, the concentration-response function from a previous epidemiological study was applied. For the health impact calculations, the WHO-developed tool AirQ + was used. RESULTS: Amongst the studied city areas, the local RWC induced PM2.5 concentration was lowest in the Helsinki Metropolitan Area (population-weighted annual average concentration 0.46 µg m- 3) and highest in Oslo (2.77 µg m- 3). Each year, particulate matter attributed to RWC caused around 19 premature deaths in Umeå (95% CI: 8-29), 85 in the Helsinki Metropolitan Area (95% CI: 35-129), 78 in Copenhagen (95% CI: 33-118), and 232 premature deaths in Oslo (95% CI: 97-346). The average loss of life years per premature death case was approximately ten years; however, in the whole population, this reflects on average a decrease in life expectancy by 0.25 (0.10-0.36) years. In terms of the relative contributions in cities, life expectancy will be decreased by 0.10 (95% CI: 0.05-0.16), 0.18 (95% CI: 0.07-0.28), 0.22 (95% CI: 0.09-0.33) and 0.63 (95% CI: 0.26-0.96) years in the Helsinki Metropolitan Area, Umeå, Copenhagen and Oslo respectively. The number of years of life lost was lowest in Umeå (172, 95% CI: 71-260) and highest in Oslo (2458, 95% CI: 1033-3669). CONCLUSIONS: All four Nordic city areas have a substantial amount of domestic heating, and RWC is one of the most significant sources of PM2.5. This implicates a substantial predicted impact on public health in terms of premature mortality. Thus, several public health measures are needed to reduce the RWC emissions.
Subject(s)
Mortality, Premature , Wood , Cities/epidemiology , Humans , Norway/epidemiology , Particulate Matter/toxicityABSTRACT
An operational urban air quality modelling system ENFUSER is presented with an evaluation against measured data. ENFUSER combines several dispersion modelling approaches, uses data assimilation, and continuously extracts information from online, global open-access sources. The modelling area is described with a combination of geographic datasets. These GIS datasets are globally available with open access, and therefore the model can be applied worldwide. Urban scale dispersion is addressed with a combination of Gaussian puff and Gaussian plume modelling, and long-range transport of pollutants is accounted for via a separate regional model. The presented data assimilation method, which supports the use of AQ sensors and incorporates a longer-term learning mechanism, adjusts emission factors and the regional background values on an hourly basis. The model can be used with reasonable accuracy also in urban areas, for which detailed emissions inventories would not be available, due to the data assimilation capabilities.
ABSTRACT
We analyzed pollution plumes originating from ships using liquefied natural gas (LNG) as a fuel. Measurements were performed at a station located on the Utö island in the Baltic Sea during 2015-2021 when vessels passed the station along an adjacent shipping lane and the wind direction allowed the measurements. The ratio of the measured concentration peaks ΔCH4/ΔCO2 ranged from 1% to 9% and from 0.1% to 0.5% for low and high pressure dual fuel engines, respectively. The ratio of the measured concentration peaks of ΔNOx/ΔCO2 varied between 0.5 and 8.7, which was not explained by engine type. The results were consistent with previously measured on-board or test-bed values for the corresponding ratios of emissions. While the methane emissions from high pressure dual fuel engines were found to fulfill the goal of reducing the climatic impacts of shipping, the emissions originating from low pressure dual fuel engines were found to be substantially high, with a potential for increased climatic impacts compared with using traditional marine fuels. Taking only the global warming potential into account, we can suggest a limit value for the methane emissions; the ratio of the emissions ΔCH4/ΔCO2 originating from LNG powered ships should not exceed 1.4%.
Subject(s)
Air Pollutants , Natural Gas , Air Pollutants/analysis , Baltic States , Methane , Ships , Vehicle Emissions/analysisABSTRACT
BACKGROUND: Previous studies have provided evidence that prenatal exposure to low-level air pollution increases the risk of preterm birth (PTB), but the findings of the effects of short-term exposure have been inconclusive. Moreover, there is little knowledge on potential synergistic effects of different combinations of air pollutants. OBJECTIVES: To assess independent and joint effects of prenatal exposure to air pollutants during the week prior to the delivery on the risk of PTB. METHODS: The study population included 2568 members of the Espoo Cohort Study, living in the City of Espoo, Finland, born between 1984 and 1990. We assessed individual-level prenatal exposure to ambient air pollutants of interest based on maternal residential addresses, while taking into account their residential mobility. We used both regional-to-city-scale dispersion modelling and land-use regression-based method to estimates the pollutant concentrations. We contrasted the risk of PTB in the highest quartile (Q4) of exposure to the lower exposure quartiles (Q1-Q3) during the specific periods of pregnancy. We applied Poisson regression analysis to estimate the adjusted risk ratios (RRs) with their 95% confidence intervals (CI), adjusting for season of birth, maternal age, sex of the baby, family's socioeconomic status, maternal smoking, and exposure to environmental tobacco smoke during pregnancy, single parenthood, and exposure to other air pollutants (this in multi-pollutant models). RESULTS: The risk of PTB was related to exposures to PM2.5, PM10 and NO2 during the week prior to the delivery with adjusted RRs of 1.67 (95%CI: 1.14, 2.46), 1.60 (95% CI: 1.09, 2.34) and 1.65 (95% CI: 1.14, 2.37), from three-pollutant models respectively. There were no significant joint effects for these different air pollutants (during the week prior to the delivery). CONCLUSION: Our results provide evidence that exposure to fairly low-level air pollution may trigger PTB, but synergistic effects of different pollutants are not likely.
Subject(s)
Air Pollutants , Air Pollution , Premature Birth , Prenatal Exposure Delayed Effects , Air Pollutants/adverse effects , Air Pollutants/analysis , Air Pollution/adverse effects , Cohort Studies , Female , Finland/epidemiology , Humans , Infant, Newborn , Maternal Exposure/adverse effects , Particulate Matter/adverse effects , Pregnancy , Premature Birth/chemically induced , Premature Birth/epidemiology , Prenatal Exposure Delayed Effects/chemically induced , Prenatal Exposure Delayed Effects/epidemiologyABSTRACT
BACKGROUND: There is some evidence that prenatal exposure to low-level air pollution increases the risk of preterm birth (PTB), but little is known about synergistic effects of different pollutants. OBJECTIVES: We assessed the independent and joint effects of prenatal exposure to air pollution during the entire duration of pregnancy. METHODS: The study population consisted of the 2568 members of the Espoo Cohort Study, born between 1984 and 1990, and living in the City of Espoo, Finland. We assessed individual-level prenatal exposure to ambient air pollutants of interest at all the residential addresses from conception to birth. The pollutant concentrations were estimated both by using regional-to-city-scale dispersion modelling and land-use regression-based method. We applied Poisson regression analysis to estimate the adjusted risk ratios (RRs) with their 95% confidence intervals (CI) by comparing the risk of PTB among babies with the highest quartile (Q4) of exposure during the entire duration of pregnancy with those with the lower exposure quartiles (Q1-Q3). We adjusted for season of birth, maternal age, sex of the baby, family's socioeconomic status, maternal smoking during pregnancy, maternal exposure to environmental tobacco smoke during pregnancy, single parenthood, and exposure to other air pollutants (only in multi-pollutant models) in the analysis. RESULTS: In a multi-pollutant model estimating the effects of exposure during entire pregnancy, the adjusted RR was 1.37 (95% CI: 0.85, 2.23) for PM2.5 and 1.64 (95% CI: 1.15, 2.35) for O3. The joint effect of PM2.5 and O3 was substantially higher, an adjusted RR of 3.63 (95% CI: 2.16, 6.10), than what would have been expected from their independent effects (0.99 for PM2.5 and 1.34 for O3). The relative risk due to interaction (RERI) was 2.30 (95% CI: 0.95, 4.57). DISCUSSION: Our results strengthen the evidence that exposure to fairly low-level air pollution during pregnancy increases the risk of PTB. We provide novel observations indicating that individual air pollutants such as PM2.5 and O3 may act synergistically potentiating each other's adverse effects.
Subject(s)
Air Pollutants , Air Pollution/statistics & numerical data , Maternal Exposure/statistics & numerical data , Ozone , Premature Birth/epidemiology , Cohort Studies , Female , Finland , Humans , Infant, Newborn , Particulate Matter , Pregnancy , Prenatal Exposure Delayed EffectsABSTRACT
UNLABELLED: We report on the analysis of contributions from road traffic emissions to fine particulate matter (PM2.5) concentrations within London for 2008 with the OSCAR Air Quality Assessment System. A spatiotemporal evaluation of the OSCAR system has been conducted with measurements from the London air quality network (LAQN). For the predicted and measured hourly time series of concentrations at 18 sites in London, the medians of correlation, mean absolute error, index of agreement, and factor of two (FAC2) of all stations were 0.80, 4.1 microg/m3, 0.86, and 74%, respectively. Spatial evaluation of modeled and observed annual mean concentrations also showed a fairly good agreement, with all the values falling within the FAC2 range. According to model predictions, the urban increment (including the contributions from urban traffic and other urban sources) was evaluated to be on the average 18%, 33%, 39%, and 43% of the total PM2.5 in suburban environments, in the urban background, near roads, and near busy roads, respectively. However, the highest values of the urban traffic increment can be around 50% of the total PM2.5 concentrations near motorways and major roads. The total concentrations (including regional background, and the contributions from urban traffic and other urban sources) can therefore be almost three times the regional background. The total urban increment close to busy roads was around 7-8 microg/m3, in which the estimated traffic contribution is more than 2 microg/m3. On the average, urban traffic contributes approximately 1 microg/m3 of PM2.5 to the urban background across London. According to modeling, approximately two-thirds of the traffic increment originated from exhaust emissions and most of the rest was due to brake and tire wear. IMPLICATIONS: The urban increment and traffic contribution to the total PM2.5 are significant and spatially heterogeneous across London. The highly heterogeneous distribution of PM2.5 hence requires detailed modeling studies to be carried out at high spatial resolution, which can be particularly important for exposure and health impact assessment. This type of information can be used to quantify health impacts resulting from specific sources of PM2.5 such as traffic emissions, to aid city and national decision makers when formulating pollution control strategies.
Subject(s)
Air Pollutants , Models, Theoretical , Particulate Matter/chemistry , Vehicle Emissions , Biomass , Environmental Monitoring , LondonABSTRACT
This study addresses the exhaust emissions of CO2, NO(x), SO(x), CO, and PM(2.5) originated from Baltic Sea shipping in 2006-2009. Numerical results have been computed using the Ship Traffic Emissions Assessment Model. This model is based on the messages of the automatic identification system (AIS), which enable the positioning of ships with a high spatial resolution. The NO(x) emissions in 2009 were approximately 7 % higher than in 2006, despite the economic recession. However, the SO(x) emissions in 2009 were approximately 14 % lower, when compared to those in 2006, mainly caused by the fuel requirements of the SO(x) emission control area (SECA) which became effective in May 2006, but affected also by changes in ship activity. Results are presented on the differential geographic distribution of shipping emissions before (Jan-April 2006) and after (Jan-April 2009) the SECA regulations. The predicted NO(x) emissions in 2009 substantially exceeded the emissions in 2006 along major ship routes and at numerous harbors, mostly due to the continuous increase in the number of small vessels that use AIS transmitters. Although the SO(x) emissions have been reduced in 2009 in most major ship routes, these have increased in the vicinity of some harbors and on some densely trafficked routes. A seasonal variation of emissions is also presented, as well as the distribution of emissions in terms of vessel flag state, type, and weight.
Subject(s)
Environmental Pollutants , Ships , Vehicle Emissions , Carbon Dioxide , Carbon Monoxide , Models, Theoretical , Nitrogen Oxides , Particulate Matter , Sulfur Oxides , Time FactorsABSTRACT
BACKGROUND: Shipping contributes to air pollution causing adverse health effects. We conducted for the first time a systematic review on the health and economic impacts of ambient air pollution from shipping emissions. METHODS: We performed a systematic search in PubMed, Web of Science, EBSCO (Medline), and Scopus of all time up to December 2023. We then inter-compared semi-quantitatively the results of the included eligible studies. RESULTS: We identified 23 eligible studies, 22 applying health impact assessment, and 1 using epidemiological methods. These studies used different methods for the evaluation of emissions, dispersion, and exposure, and for the exposure-mortality risk functions for exposure to shipping emissions for 1-2 years. The estimated excess global all-cause mortality from six studies ranged between 1 and 5 deaths per 100,000 person-years. However, the heterogeneity of the methods and critical gaps in the reporting seriously limited the synthesis of the evidence on health and economic effects of shipping emissions. Sufficient spatial and temporal resolutions in both dispersion and exposure modeling, as well as presentation of uncertainties is needed. Health impact assessment should present the results with all the main risk functions and population attributable risks, and the magnitude of the effect should be expressed in excess number per a given person-time or per population size. Economic effects should also cover work productivity, mental well-being, and cognitive functions. CONCLUSIONS: We recommend that future studies should properly evaluate and report the uncertainty ranges and the confidence limits of the results. Rigorous studies are needed on multipollutant exposures, exposures from various source categories, and exposures attributed to various particulate matter measures. Studies should report the health impact measures in a format that facilitates straightforward inter-study comparisons. Further research should also specifically report the used grid spacings and resolutions and evaluate whether these are optimal for the task.
Subject(s)
Air Pollutants , Air Pollution , Air Pollution/statistics & numerical data , Humans , Air Pollutants/analysis , Environmental Exposure/statistics & numerical data , Ships , Mortality , Particulate Matter/analysisABSTRACT
An evaluation of performance of the System for Integrated modeLling of Atmospheric coMposition (SILAM) in application to birch pollen dispersion is presented. The system is described in a companion paper whereas the current study evaluates the model sensitivity to details of the pollen emission module parameterisation and to the meteorological input data. The most important parameters are highlighted. The reference year considered for the analysis is 2006. It is shown that the model is capable of predicting about two-thirds of allergenic alerts, with the odds ratio exceeding 12 for the best setup. Several other statistics corroborate with these estimations. Low-pollen concentration days are also predicted correctly in more than two-thirds of cases. The model experiences certain difficulties only with intermediate pollen concentrations. It is demonstrated that the most important input parameter is the near-surface temperature, the bias of which can easily jeopardise the results. The model sensitivity to random fluctuations of temperature is much lower. Other parameters important at various stages of pollen development, release, and dispersion are precipitation and ambient humidity, as well as wind direction.
Subject(s)
Betula , Models, Theoretical , Pollen , Atmosphere , Europe , Flowers , WeatherABSTRACT
This article reviews interactions and health impacts of physical, chemical, and biological weather. Interactions and synergistic effects between the three types of weather call for integrated assessment, forecasting, and communication of air quality. Today's air quality legislation falls short of addressing air quality degradation by biological weather, despite increasing evidence for the feasibility of both mitigation and adaptation policy options. In comparison with the existing capabilities for physical and chemical weather, the monitoring of biological weather is lacking stable operational agreements and resources. Furthermore, integrated effects of physical, chemical, and biological weather suggest a critical review of air quality management practices. Additional research is required to improve the coupled modeling of physical, chemical, and biological weather as well as the assessment and communication of integrated air quality. Findings from several recent COST Actions underline the importance of an increased dialog between scientists from the fields of meteorology, air quality, aerobiology, health, and policy makers.
Subject(s)
Air Pollution , Weather , Environmental Monitoring , ForecastingABSTRACT
Urban dwellers are simultaneously exposed to several environmental health risk factors. This study aimed to examine the relationship between long-term exposure to fine particulate matter (PM2.5, diameter < 2.5 µm) of residential-wood-burning and road-traffic origin, road-traffic noise, green space around participants' homes, and hypertension. In 2015 and 2016, we conducted a survey of residents of the Helsinki Capital Region to determine their perceptions of environmental quality and safety, lifestyles, and health statuses. Recent antihypertensive medication was used as an indicator of current hypertensive illness. Individual-level exposure was estimated by linking residential coordinates with modelled outdoor levels of wood-smoke- and traffic-related PM2.5, road-traffic noise, and coverage of natural spaces. Relationships between exposure and hypertension were modelled using multi-exposure and single-exposure binary logistic regression while taking smooth functions into account. Twenty-eight percent of the participants were current users of antihypertensive medication. The odds ratios (95% confidence interval) for antihypertensive use were 1.12 (0.78-1.57); 0.97 (0.76-1.26); 0.98 (0.93-1.04) and 0.99 (0.94-1.04) for wood-smoke PM2.5, road-traffic PM2.5, road-traffic noise, and coverage of green space, respectively. We found no evidence of an effect of the investigated urban exposures on prevalent hypertension in the Helsinki Capital Region.
Subject(s)
Air Pollutants , Air Pollution , Hypertension , Air Pollutants/analysis , Air Pollution/analysis , Environmental Exposure/analysis , Finland/epidemiology , Humans , Hypertension/epidemiology , Hypertension/etiology , Particulate Matter/analysisABSTRACT
INTRODUCTION: Air pollution has been suggested to be associated with depression. However, current evidence is conflicting, and no study has considered different sources of ambient particulate matter with an aerodynamic diameter below 2.5 µm (PM2.5). We evaluated the associations of long-term exposure to PM2.5 from road traffic and residential wood combustion with the prevalence of depression in the Helsinki region, Finland. METHODS: We conducted a cross-sectional analysis based on the Helsinki Capital Region Environmental Health Survey 2015-2016 (N=5895). Modelled long-term outdoor concentrations of PM2.5 were evaluated using high-resolution emission and dispersion modelling on an urban scale and linked to the home addresses of study participants. The outcome was self-reported doctor-diagnosed or treated depression. We applied logistic regression and calculated the OR for 1 µg/m3 increase in PM2.5, with 95% CI. Models were adjusted for potential confounders, including traffic noise and urban green space. RESULTS: Of the participants, 377 reported to have been diagnosed or treated for depression by a doctor. Long-term exposure to PM2.5 from road traffic (OR=1.23, 95% CI 0.86 to 1.73; n=5895) or residential wood combustion (OR=0.78, 95% CI 0.43 to 1.41; n=5895) was not associated with the prevalence of depression. The estimates for PM2.5 from road traffic were elevated, but statistically non-significant, for non-smokers (OR=1.38, 95% CI 0.94 to 2.01; n=4716). CONCLUSIONS: We found no convincing evidence of an effect of long-term exposure to PM2.5 from road traffic or residential wood combustion on depression.
Subject(s)
Air Pollutants , Air Pollution , Air Pollutants/adverse effects , Air Pollutants/analysis , Air Pollution/adverse effects , Air Pollution/analysis , Cross-Sectional Studies , Depression/epidemiology , Environmental Exposure/adverse effects , Environmental Exposure/analysis , Humans , Particulate Matter/adverse effects , Particulate Matter/analysis , Prevalence , Wood/chemistryABSTRACT
A comprehensive modelling approach has been developed to predict population exposure to the ambient air PM2.5 concentrations in different microenvironments in London. The modelling approach integrates air pollution dispersion and exposure assessment, including treatment of the locations and time activity of the population in three microenvironments, namely, residential, work and transport, based on national demographic information. The approach also includes differences between urban centre and suburban areas of London by taking account of the population movements and the infiltration of PM2.5 from outdoor to indoor. The approach is tested comprehensively by modelling ambient air concentrations of PM2.5 at street scale for the year 2008, including both regional and urban contributions. Model analysis of the exposure in the three microenvironments shows that most of the total exposure, 85%, occurred at home and work microenvironments and 15% in the transport microenvironment. However, the annual population weighted mean (PWM) concentrations of PM2.5 for London in transport microenvironments were almost twice as high (corresponding to 13-20 µg/m3) as those for home and work environments (7-12 µg/m3). Analysis has shown that the PWM PM2.5 concentrations in central London were almost 20% higher than in the surrounding suburban areas. Moreover, the population exposure in the central London per unit area was almost three times higher than that in suburban regions. The exposure resulting from all activities, including outdoor to indoor infiltration, was about 20% higher, when compared with the corresponding value obtained assuming inside home exposure for all times. The exposure assessment methodology used in this study predicted approximately over one quarter (-28%) lower population exposure, compared with using simply outdoor concentrations at residential locations. An important implication of this study is that for estimating population exposure, one needs to consider the population movements, and the infiltration of pollution from outdoors to indoors.
Subject(s)
Air Pollutants , Air Pollution/statistics & numerical data , Environmental Exposure/statistics & numerical data , Air Pollution, Indoor , Environmental Monitoring , London , Particle Size , Particulate MatterABSTRACT
Marine traffic in harbors can be responsible for significant atmospheric concentrations of ultrafine particles (UFPs), which have widely recognized negative effects on human health. It is therefore essential to model and measure the time evolution of the number size distributions and chemical composition of UFPs in ship exhaust to assess the resulting exposure in the vicinity of shipping routes. In this study, a sequential modelling chain was developed and applied, in combination with the data measured and collected in major harbor areas in the cities of Helsinki and Turku in Finland, during winter and summer in 2010-2011. The models described ship emissions, atmospheric dispersion, and aerosol dynamics, complemented with a time-microenvironment-activity model to estimate the short-term UFP exposure. We estimated the dilution ratio during the initial fast expansion of the exhaust plume to be approximately equal to eight. This dispersion regime resulted in a fully formed nucleation mode (denoted as Nuc2). Different selected modelling assumptions about the chemical composition of Nuc2 did not have an effect on the formation of nucleation mode particles. Aerosol model simulations of the dispersing ship plume also revealed a partially formed nucleation mode (Nuc1; peaking at 1.5 nm), consisting of freshly nucleated sulfate particles and condensed organics that were produced within the first few seconds. However, subsequent growth of the new particles was limited, due to efficient scavenging by the larger particles originating from the ship exhaust. The transport of UFPs downwind of the ship track increased the hourly mean UFP concentrations in the neighboring residential areas by a factor of two or more up to a distance of 3600 m, compared with the corresponding UFP concentrations in the urban background. The substantially increased UFP concentrations due to ship traffic significantly affected the daily mean exposures in residential areas located in the vicinity of the harbors.
Subject(s)
Air Pollutants/analysis , Environmental Monitoring , Particulate Matter/analysis , Cities , Finland , Models, Theoretical , ShipsABSTRACT
Exposure to fine particles in ambient air has been estimated to be one of the leading environmental health risks in Finland. Residential wood combustion is the largest domestic source of fine particles, and there is increasing political interest in finding feasible measures to reduce those emissions. In this paper, we present the PM2.5 emissions from residential wood combustion in Finland, as well as the resulting concentrations. We used population-weighed concentrations in a 250 x 250 m grid as population exposure estimates, with which we calculated the disease burden of the emissions. Compared to a projected baseline scenario, we studied the effect of chosen reduction measures in several abatement scenarios. In 2015, the resulting annual average concentrations were between 0.5 and 2 µg/m3 in the proximity of most cities, and disease burden attributable to residential wood combustion was estimated to be 3400 disability-adjusted life years (DALY) and 200 deaths. Disease burden decreased by 8% in the 2030 baseline scenario and by an additional 63% in the maximum feasible reduction scenario. Informational campaigns and improvement of the sauna stove stock were assessed to be the most feasible abatement measures to be implemented in national air quality policies.
Subject(s)
Air Pollutants/adverse effects , Air Pollution/analysis , Environmental Monitoring/methods , Particulate Matter/adverse effects , Particulate Matter/analysis , Wood/adverse effects , Wood/chemistry , Air Pollutants/analysis , Air Pollution/statistics & numerical data , Environmental Exposure/statistics & numerical data , Finland , HumansABSTRACT
Air pollution has been estimated to be one of the leading environmental health risks in Finland. National health impact estimates existing to date have focused on particles (PM) and ozone (O3). In this work, we quantify the impacts of particles, ozone, and nitrogen dioxide (NO2) in 2015, and analyze the related uncertainties. The exposures were estimated with a high spatial resolution chemical transport model, and adjusted to observed concentrations. We calculated the health impacts according to Word Health Organization (WHO) working group recommendations. According to our results, ambient air pollution caused a burden of 34,800 disability-adjusted life years (DALY). Fine particles were the main contributor (74%) to the disease burden, which is in line with the earlier studies. The attributable burden was dominated by mortality (32,900 years of life lost (YLL); 95%). Impacts differed between population age groups. The burden was clearly higher in the adult population over 30 years (98%), due to the dominant role of mortality impacts. Uncertainties due to the concentration-response functions were larger than those related to exposures.
Subject(s)
Air Pollutants/economics , Air Pollution/economics , Nitrogen Dioxide/economics , Ozone/economics , Particulate Matter/economics , Adult , Air Pollutants/analysis , Air Pollution/analysis , Environmental Exposure/analysis , Environmental Exposure/economics , Finland/epidemiology , Humans , Models, Chemical , Nitrogen Dioxide/analysis , Ozone/analysis , Particulate Matter/analysis , Quality-Adjusted Life Years , Risk , Spatial AnalysisABSTRACT
BACKGROUND: Vegetation fires can release substantial quantities of fine particles (PM2.5), which are harmful to health. The fire smoke may be transported over long distances and can cause adverse health effects over wide areas. OBJECTIVE: We aimed to assess annual mortality attributable to short-term exposures to vegetation fire-originated PM2.5 in different regions of Europe. METHODS: PM2.5 emissions from vegetation fires in Europe in 2005 and 2008 were evaluated based on Moderate Resolution Imaging Spectroradiometer (MODIS) satellite data on fire radiative power. Atmospheric transport of the emissions was modeled using the System for Integrated modeLling of Atmospheric coMposition (SILAM) chemical transport model. Mortality impacts were estimated for 27 European countries based on a) modeled daily PM2.5 concentrations and b) population data, both presented in a 50 × 50 km2 spatial grid; c) an exposure-response function for short-term PM2.5 exposure and daily nonaccidental mortality; and d) country-level data for background mortality risk. RESULTS: In the 27 countries overall, an estimated 1,483 and 1,080 premature deaths were attributable to the vegetation fire-originated PM2.5 in 2005 and 2008, respectively. Estimated impacts were highest in southern and eastern Europe. However, all countries were affected by fire-originated PM2.5, and even the lower concentrations in western and northern Europe contributed substantially (~ 30%) to the overall estimate of attributable mortality. CONCLUSIONS: Our assessment suggests that air pollution caused by PM2.5 released from vegetation fires is a notable risk factor for public health in Europe. Moreover, the risk can be expected to increase in the future as climate change proceeds. This factor should be taken into consideration when evaluating the overall health and socioeconomic impacts of these fires. Citation: Kollanus V, Prank M, Gens A, Soares J, Vira J, Kukkonen J, Sofiev M, Salonen RO, Lanki T. 2017. Mortality due to vegetation fire-originated PM2.5 exposure in Europe-assessment for the years 2005 and 2008. Environ Health Perspect 125:30-37; http://dx.doi.org/10.1289/EHP194.