Wood stove use and other determinants of personal and indoor exposures to particulate air pollution and ozone among elderly persons in a Northern Suburb.

A six-month winter-spring study was conducted in a suburb of the northern European city of Kuopio, Finland, to identify and quantify factors determining daily personal exposure and home indoor levels of fine particulate matter (PM2.5 , diameter <2.5 µm) and its light absorption coefficient (PM2.5abs ), a proxy for combustion-derived black carbon. Moreover, determinants of home indoor ozone (O3 ) concentration were examined. Local central site outdoor, home indoor, and personal daily levels of pollutants were monitored in this suburb among 37 elderly residents. Outdoor concentrations of the pollutants were significant determinants of their levels in home indoor air and personal exposures. Natural ventilation in the detached and row houses increased personal exposure to PM2.5 , but not to PM2.5abs , when compared with mechanical ventilation. Only cooking out of the recorded household activities increased indoor PM2.5 . The use of a wood stove room heater or wood-fired sauna stove was associated with elevated concentrations of personal PM2.5 and PM2.5abs , and indoor PM2.5abs . Candle burning increased daily indoor and personal PM2.5abs , and it was also a determinant of indoor ozone level. In conclusion, relatively short-lasting wood and candle burning of a few hours increased residents' daily exposure to potentially hazardous, combustion-derived carbonaceous particulate matter.

Impact of wood combustion for secondary heating and recreational purposes on particulate air pollution in a suburb in Finland.

Little information is available on the concentrations of ambient fine particles (PM2.5) in residential areas where wood combustion is common for recreational purposes and secondary heating. Further, the validity of central site measurements of PM2.5 as a measure of exposure is unclear. Therefore, outdoor PM2.5 samples were repeatedly collected at a central site and home outdoor locations from a panel of 29 residents in a suburb in Kuopio, Finland. Source apportionment results from the central site were used to estimate the contributions from local sources, including wood combustion, to PM2.5 and absorption coefficient (ABS) at home outdoor locations. Correlations between the central and home outdoor concentrations of PM2.5, ABS, and their local components were analyzed for each home. At the central site, the average PM2.5 was 6.0 µg m(-)(3) during the heating season, and the contribution from wood combustion (16%) was higher than the contribution from exhaust emissions (12%). Central site measurements predicted poorly daily variation in PM2.5 from local sources. In conclusion, wood combustion significantly affects air quality also in areas where it is not the primary heating source. In epidemiological panel studies, central site measurements may not sufficiently capture daily variation in exposure to PM2.5 from local wood combustion.

Source-specific fine particulate air pollution and systemic inflammation in ischaemic heart disease patients.

OBJECTIVE: To compare short-term effects of fine particles (PM2.5; aerodynamic diameter <2.5 µm) from different sources on the blood levels of markers of systemic inflammation. METHODS: We followed a panel of 52 ischaemic heart disease patients from 15 November 2005 to 21 April 2006 with clinic visits in every second week in the city of Kotka, Finland, and determined nine inflammatory markers from blood samples. In addition, we monitored outdoor air pollution at a fixed site during the study period and conducted a source apportionment of PM2.5 using the Environmental Protection Agency's model EPA PMF 3.0. We then analysed associations between levels of source-specific PM2.5 and markers of systemic inflammation using linear mixed models. RESULTS: We identified five source categories: regional and long-range transport (LRT), traffic, biomass combustion, sea salt, and pulp industry. We found most evidence for the relation of air pollution and inflammation in LRT, traffic and biomass combustion; the most relevant inflammation markers were C-reactive protein, interleukin-12 and myeloperoxidase. Sea salt was not positively associated with any of the inflammatory markers. CONCLUSIONS: Results suggest that PM2.5 from several sources, such as biomass combustion and traffic, are promoters of systemic inflammation, a risk factor for cardiovascular diseases.

Exhaled nitric oxide and atherosclerosis.

BACKGROUND: Fractional exhaled nitric oxide concentration (FENO) measurement has been proposed to be an important adjunct in the diagnosis and management of asthma, pulmonary hypertension and cystic fibrosis. But do we understand how other diseases influence the FENO values? In particular, atherosclerosis is one of the pathological conditions, in which nitric oxide (NO) production is inhibited and its degradation enhanced. Therefore, hypothesis of the current study was that FENO is inversely associated with risk markers of atherosclerosis and with diseases leading secondarily to the progression of atherosclerosis. MATERIALS AND METHODS: A long-term FENO value (median of biweekly measurements over a 24-week period) of 53 patients with ischaemic heart disease (IHD) was compared with the results of clinical and biochemical analyses. RESULTS: Fractional exhaled NO was inversely associated with the plasma concentration of triglycerides (P = 0·01) and with the blood concentration of glycated haemoglobin A1c (P = 0·03). It also tended to be inversely associated with the plasma glucose concentration (P = 0·10). However, there were no statistically significant associations with inflammatory or other biochemical markers, health status, lifestyle or other personal determinants. CONCLUSIONS: In accordance with the hypothesis, FENO is inversely associated with some of risk markers of atherosclerosis in patients with stable IHD (triglycerides and haemoglobin A1c, a marker of hyperglycaemic metabolism). A potential explanation is that, at hyperglycaemia and with higher triglyceride concentrations, atherosclerosis leads to endothelial dysfunction and, subsequently, to decreased production and increased degradation of NO.

Low-level exposure to ambient particulate matter is associated with systemic inflammation in ischemic heart disease patients.

Short-term exposure to ambient air pollution is associated with increased cardiovascular mortality and morbidity. This adverse health effect is suggested to be mediated by inflammatory processes. The purpose of this study was to determine if low levels of particulate matter, typical for smaller cities, are associated with acute systemic inflammation. Fifty-two elderly individuals with ischemic heart disease were followed for six months with biweekly clinical visits in the city of Kotka, Finland. Blood samples were collected for the determination of inflammatory markers interleukin (IL)-1ß, IL-6, IL-8, IL-12, interferon (IFN)γ, C-reactive protein (CRP), fibrinogen, myeloperoxidase and white blood cell count. Particle number concentration and fine particle (particles with aerodynamic diameters <2.5 µm (PM(2.5))) as well as thoracic particle (particles with aerodynamic diameters <10 µm (PM(10))) mass concentration were measured daily at a fixed outdoor measurement site. Light-absorbance of PM(2.5) filter samples, an indicator of combustion derived particles, was measured with a smoke-stain reflectometer. In addition, personal exposure to PM(2.5) was measured with portable photometers. During the study period, wildfires in Eastern Europe led to a 12-day air pollution episode, which was excluded from the main analyses. Average ambient PM(2.5) concentration was 8.7 µg/m(3). Of the studied pollutants, PM(2.5) and absorbance were most strongly associated with increased levels of inflammatory markers; most notably with C-reactive protein and IL-12 within a few days of exposure. There was also some evidence of an effect of particulate air pollution on fibrinogen and myeloperoxidase. The concentration of IL-12 was considerably (227%) higher during than before the forest fire episode. These findings show that even low levels of particulate air pollution from urban sources are associated with acute systemic inflammation. Also particles from wildfires may exhibit pro-inflammatory effects.

Toxicological properties of emission particles from heavy duty engines powered by conventional and bio-based diesel fuels and compressed natural gas.

BACKGROUND: One of the major areas for increasing the use of renewable energy is in traffic fuels e.g. bio-based fuels in diesel engines especially in commuter traffic. Exhaust emissions from fossil diesel fuelled engines are known to cause adverse effects on human health, but there is very limited information available on how the new renewable fuels may change the harmfulness of the emissions, especially particles (PM). We evaluated the PM emissions from a heavy-duty EURO IV diesel engine powered by three different fuels; the toxicological properties of the emitted PM were investigated. Conventional diesel fuel (EN590) and two biodiesels were used - rapeseed methyl ester (RME, EN14214) and hydrotreated vegetable oil (HVO) either as such or as 30% blends with EN590. EN590 and 100% HVO were also operated with or without an oxidative catalyst (DOC + POC). A bus powered by compressed natural gas (CNG) was included for comparison with the liquid fuels. However, the results from CNG powered bus cannot be directly compared to the other situations in this study. RESULTS: High volume PM samples were collected on PTFE filters from a constant volume dilution tunnel. The PM mass emission with HVO was smaller and with RME larger than that with EN590, but both biofuels produced lower PAH contents in emission PM. The DOC + POC catalyst greatly reduced the PM emission and PAH content in PM with both HVO and EN590. Dose-dependent TNFα and MIP-2 responses to all PM samples were mostly at the low or moderate level after 24-hour exposure in a mouse macrophage cell line RAW 264.7. Emission PM from situations with the smallest mass emissions (HVO + cat and CNG) displayed the strongest potency in MIP-2 production. The catalyst slightly decreased the PM-induced TNFα responses and somewhat increased the MIP-2 responses with HVO fuel. Emission PM with EN590 and with 30% HVO blended in EN590 induced the strongest genotoxic responses, which were significantly greater than those with EN590 + cat or 100% HVO. The emission PM sample from the CNG bus possessed the weakest genotoxic potency but had the strongest oxidative potency of all the fuel and catalyst combinations. The use of 100% HVO fuel had slightly weaker and 100% RME somewhat stronger emission PM induced ROS production, when compared to EN590. CONCLUSIONS: The harmfulness of the exhaust emissions from vehicle engines cannot be determined merely on basis of the emitted PM mass. The study conditions and the engine type significantly affect the toxicity of the emitted particles. The selected fuels and DOC + POC catalyst affected the PM emission from the heavy EURO IV engine both qualitative and quantitative ways, which influenced their toxicological characteristics. The plain HVO fuel performed very well in emission reduction and in lowering the overall toxicity of emitted PM, but the 30% blend of HVO in EN590 was no better in this respect than the plain EN590. The HVO with a DOC + POC catalyst in the EURO IV engine, performed best with regard to changes in exhaust emissions. However some of the toxicological parameters were significantly increased even with these low emissions.

A novel particle sampling system for physico-chemical and toxicological characterization of emissions.

Several studies have shown that combustion-derived fine particles cause adverse health effects. Previous toxicological studies on combustion-derived fine particles have rarely involved multiple endpoints and a detailed characterization of chemical composition. In this study, we developed a novel particle sampling system for toxicological and chemical characterization (PSTC), consisting of the Dekati Gravimetric Impactor (DGI) and a porous tube diluter. Physico-chemical and toxicological properties of the particles emitted from various combustion sources were evaluated in two measurement campaigns. First, the DGI was compared with the High-Volume Cascade Impactor (HVCI) and to the Dekati Low-Pressure Impactor (DLPI), using the same dilution system and the same sampling conditions. Only small differences were observed in the mass size distributions, total particulate matter (PM), and particulate matter with diameter smaller than 1 um (PM(1)) concentrations and geometric mass mean diameters (GMMD) between these three impactors. Second, the PSTC was compared with the HVCI sampling system, which has been optimal for collection of particulate samples for toxicological and chemical analyses. Differences were observed in the mass size distributions, total PM and PM(1) emissions, and GMMDs, probably due to the different sampling and dilution methods as well as different sampling substrates which affected the behavior of semi-volatile and volatile organic compounds. However, no significant differences were detected in the in vitro measurements of cytotoxicity between the samples collected with the PSTC and the HVCI systems. In measurements of genotoxicity, significant differences between the two sampling systems were seen only with the particles emitted from the sauna stove. In conclusion, due to compact size, PSTC is an applicable method for use in particle sampling as part of the toxicological and chemical characterization of particulate emissions from different combustion sources. It offers some advantages compared to the previously used high-volume sampling methods including compactness for field measurements, simple preparation of sample substrates and high extraction efficiency.

Toxicological effects of emission particles from fossil- and biodiesel-fueled diesel engine with and without DOC/POC catalytic converter.

There is increasing demand for renewable energy and the use of biodiesel in traffic is a major option when implying this increment. We investigated the toxicological activities of particulate emissions from a nonroad diesel engine, operated with conventional diesel fuel (EN590), and two biodiesels: rapeseed methyl ester (RME) and hydrotreated fresh vegetable oil (HVO). The engine was operated with all fuels either with or without catalyst (DOC/POC). The particulate matter (PM(1)) samples were collected from the dilution tunnel with a high-volume cascade impactor (HVCI). These samples were characterized for ions, elements, and polycyclic aromatic hydrocarbon (PAH) compounds. Mouse RAW264.7 macrophages were exposed to the PM samples for 24 h. Inflammatory mediators, (TNF-α and MIP-2), cytotoxicity, genotoxicity, and oxidative stress (reactive oxygen species [ROS]) were measured. All the samples displayed mostly dose-dependent toxicological activity. EN590 and HVO emission particles had larger inflammatory responses than RME-derived particles. The catalyst somewhat increased the responses per the same mass unit. There were no substantial differences in the cytotoxic responses between the fuels or catalyst use. Genotoxic responses by all the particulate samples were at same level, except weaker for the RME sample with catalyst. Unlike other samples, EN590-derived particles did not significantly increase ROS production. Catalyst increased the oxidative potential of the EN590 and HVO-derived particles, but decreased that with RME. Overall, the use of biodiesel fuels and catalyst decreased the particulate mass emissions compared with the EN590 fuel. Similar studies with different types of diesel engines are needed to assess the potential benefits from biofuel use in engines with modern technologies.

Associations of urban air particulate composition with inflammatory and cytotoxic responses in RAW 246.7 cell line.

Epidemiological studies show heterogeneities in the particulate pollution-related exposure-effect relationships among cardiorespiratory patients, but the connection to chemical composition and toxic properties of the inhaled particles is largely unknown. To identify the chemical constituents and sources responsible for the diverse inflammatory and cytotoxic effects of urban air, fine (PM(2.5-0.2)) and coarse (PM(10-2.5)) particulate samples were collected during contrasting air pollution situations. We exposed mouse RAW 246.7 macrophages for 24 hrs to PM(2.5-0.2) and PM(10-2.5) samples from six European cities. The concentrations of proinflammatory cytokines (IL-6, TNFalpha), chemokine (MIP-2), and nitric oxide were measured from the cell culture medium, and the cytotoxicity was assayed. Spearman's correlations between the chemical constituents and cellular responses were analyzed. In the PM(2.5-0.2) size range, the tracers of photo-oxidation of organics in the atmosphere (oxalate, succinate, malonate), some transition metals (Ni, V, Fe, Cu, Cr), and insoluble soil constituents (Ca, Al, Fe, Si) correlated positively with the response parameters. In contrast, the tracers of incomplete biomass (monosaccharide anhydrides) and coal (As) combustion, and polycyclic aromatic hydrocarbons (PAHs), had negative correlations with the inflammatory activity. The compositions of PM(10-2.5) samples were more uniform and there were only occasional high correlations between the chemical constituents, endotoxin, and the response parameters. The present results suggest that the local sources of incomplete combustion and resuspended road dust are important producers of harmful fine particulate constituents that may, however, operate via diverse toxicity mechanisms. The results agree well with our recent findings in the mouse lung.

Health risk assessment of indoor air pollution in Finnish ice arenas.

Poor indoor air quality and epidemic carbon monoxide (CO) and nitrogen dioxide (NO(2)) poisonings due to exhaust emissions from ice resurfacers have been continuously reported from enclosed ice arenas for over 30 years. The health risks in users of Finnish ice arenas were analysed in three ways: (1) evaluation of four cases of epidemic CO poisonings, (2) modelling the association between NO(2) exposure and respiratory symptoms among junior ice hockey players, and (3) estimation of the number of arena users at risk of breathing poor quality air due to non-compliance of ice arenas with recommended abatement measures. The common causes for the CO poisonings involving over 300 subjects were large emissions from propane-fuelled ice resurfacer, small arena volume, negligible ventilation, and very recent opening of the arena. Rhinitis (prevalence 18.3%) and cough (13.7%) during or after training or game were significantly associated with the estimated personal NO(2) exposure of young hockey players (n=793) to average concentrations ranging from 21 to 1176 microg/m(3) in their home arena. During a 6-year follow-up of an intensive information campaign the portion of electric resurfacers increased from 9% to 27%, and that of emission control technology on propane-fuelled resurfacers increased from 13% to 84%. The portion of inadequately ventilated arenas decreased from 34% to 25%. However, 48% of the investigated Finnish ice arenas (n=125) did not fully comply with the non-regulatory recommendations. Consequently, 20000 daily users of ice arenas were estimated to remain in 2001 at risk of breathing poor quality air. Modern small and inadequately ventilated ice arenas pose their users (mostly children and young adults) at risk of breathing poor quality air and suffering from acute adverse health effects. Governmental regulations are needed worldwide to ensure safe sports in enclosed ice arenas.

Chemical compositions responsible for inflammation and tissue damage in the mouse lung by coarse and fine particulate samples from contrasting air pollution in Europe.

Inflammation is regarded as an important mechanism in mortality and morbidity associated with exposures of cardiorespiratory patients to urban air particulate matter. We investigated the association of the chemical composition and sources of urban air fine (PM(2.5-0.2)) and coarse (PM(10-2.5)) particulate samples with the inflammatory activity in the mouse lung. The particulate samples were collected during selected seasons in six European cities using a high-volume cascade impactor. Healthy C57BL/6J mice were intratracheally instilled with a single dose (10 mg/kg) of the particulate samples. At 4, 12, and 24 h after the exposure, the lungs were lavaged and the bronchoalveolar lavage fluid (BALF) was assayed for indicators of inflammation and tissue damage: cell number, total protein, and cytokines (tumor necrosis factor [TNF]-alpha, interleukin [IL]-6, and KC). Dicarboxylic acids and transition metals, especially Ni and V, in PM(2.5-0.2) correlated positively and some secondary inorganic ions (NO3(-), NH4(+)) negatively with the inflammatory activity. Total organic matter and SO4(2-) had no consistent correlations. In addition, the soil-derived constituents (Ca2+, Al, Fe, Si) showed positive correlations with the PM(2.5-0.2)-induced inflammatory activity, but their role in PM(10-2.5) remained obscure, possibly due to largely undefined biogenic material. Markers of poor biomass and coal combustion, i.e., monosaccharide anhydrides and As, were associated with elevated PAH contents in PM(2.5-0.2) and a consistent immunosuppressive effect. Overall, our results support epidemiological findings that the local sources of incomplete combustion and resuspended road dust are important in urban air particulate pollution-related health effects.

Heterogeneities in inflammatory and cytotoxic responses of RAW 264.7 macrophage cell line to urban air coarse, fine, and ultrafine particles from six European sampling campaigns.

We investigated the cytotoxic and inflammatory activities of size-segregated particulate samples (particulate matter, PM) from contrasting air pollution situations in Europe. Coarse (PM10-2.5), fine (PM2.5-0.2), and ultrafine (PM0.2) particulate samples were collected with a modified Harvard high-volume cascade impactor (HVCI). Mouse RAW 264.7 macrophages were exposed to the samples for 24 h. Selected inflammatory mediators, nitric oxide (NO) and cytokines (tumor necrosis factor alpha [TNFalpha], interleukin 6 [IL-6], macrophage inflammatory protein-2 [MIP-2]), were measured together with cytotoxicity (MTT test), and analysis of apoptosis and cell cycle (propidium iodide staining). The PM10-2.5 samples had a much higher inflammatory activity than the PM2.5-0.2 and PM0.2 samples, but the PM2.5-0.2 samples showed the largest differences in inflammatory activity, and the PM0.2 samples in cytotoxicity, between the sampling campaigns. The PM2.5-0.2 samples from traffic environments in springtime Barcelona and summertime Athens had the highest inflammatory activities, which may be related to the high photochemical activity in the atmosphere during the sampling campaigns. The PM0.2 sample from wintertime Prague with proven impacts from local coal and biomass combustion had very high cytotoxic and apoptotic activities and caused a distinct cell cycle arrest. Thus, particulate size, sources, and atmospheric transformation processes affect the toxicity profile of urban air particulate matter. These factors may explain some of the heterogeneity observed in particulate exposure-response relationships of human health effects in epidemiological studies.

Mortality due to Vegetation Fire-Originated PM2.5 Exposure in Europe-Assessment for the Years 2005 and 2008.

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.

Effects of particulate matter on the pulmonary and vascular system: time course in spontaneously hypertensive rats.

BACKGROUND: This study was performed within the scope of two multi-center European Commission-funded projects (HEPMEAP and PAMCHAR) concerning source-composition-toxicity relationship for particulate matter (PM) sampled in Europe. The present study aimed to optimize the design for PM in vivo toxicity screening studies in terms of dose and time between a single exposure and the determination of the biological responses in a rat model mimicking human disease resulting in susceptibility to ambient PM. Dust in thoracic PM size-range (aerodynamic diameter <10 mum) was sampled nearby a road tunnel (RTD) using a high volume cascade impactor. Spontaneously hypertensive rats were exposed to urban dust collected in Ottawa, Canada (EHC-93 10 mg/kg of body weight; reference PM) or different RTD doses (0.3, 1, 3, 10 mg/kg of body weight) by intratracheal instillation. Necropsy was performed at 4, 24, or 48 hr after exposure. RESULTS: The neutrophil numbers in bronchoalveolar lavage fluid increased tremendously after exposure to the highest RTD doses or EHC-93. Furthermore, PM exposure slightly affected blood coagulation since there was a small but significant increase in the plasma fibrinogen levels (factor 1.2). Pulmonary inflammation and oxidative stress as well as changes in blood coagulation factors and circulating blood cell populations were observed within the range of 3 to 10 mg PM/kg of body weight without significant pulmonary injury. CONCLUSION: The optimal dose for determining the toxicity ranking of ambient derived PM samples in spontaneously hypertensive rats is suggested to be between 3 and 10 mg PM/kg of body weight under the conditions used in the present study. At a lower dose only some inflammatory effects were detected, which will probably be too few to be able to discriminate between PM samples while a completely different response pattern was observed with the highest dose. In addition to the dose, a 24-hr interval from exposure to sacrifice seemed appropriate to assess the relative toxic potency of PM since the majority of the health effects were observed one day after PM exposure compared to the other times examined. The aforementioned considerations provide a good basis for conducting PM toxicity screening studies in spontaneously hypertensive rats.

Chemical composition, mass size distribution and source analysis of long-range transported wildfire smokes in Helsinki.

Special episodes of long-range transported particulate (PM) air pollution were investigated in a one-month field campaign at an urban background site in Helsinki, Finland. A total of nine size-segregated PM samplings of 3- or 4-day duration were made between August 23 and September 23, 2002. During this warm and unusually dry period there were two (labelled P2 and P5) sampling periods when the PM2.5 mass concentration increased remarkably. According to the hourly-measured PM data and backward air mass trajectories, P2 (Aug 23-26) represented a single, 64-h episode of long-range transported aerosol, whereas P5 (Sept 5-9) was a mixture of two 16- and 14-h episodes and usual seasonal air quality. The large chemical data set, based on analyses made by ion chromatography, inductively coupled plasma mass spectrometry, X-ray fluorescence analysis and smoke stain reflectometry, demonstrated that the PM2.5 mass concentrations of biomass signatures (i.e. levoglucosan, oxalate and potassium) and of some other compounds associated with biomass combustion (succinate and malonate) increased remarkably in P2. Crustal elements (Fe, Al, Ca and Si) and unidentified matter, presumably consisting to a large extent of organic material, were also increased in P2. The PM2.5 composition in P5 was different from that in P2, as the inorganic secondary aerosols (NO3-, SO4(2-), NH4+) and many metals reached their highest concentration in this period. The water-soluble fraction of potassium, lead and manganese increased in both P2 and P5. Mass size distributions (0.035-10 microm) showed that a large accumulation mode mainly caused the episodically increased PM2.5 concentrations. An interesting observation was that the episodes had no obvious impact on the Aitken mode. Finally, the strongly increased concentrations of biomass signatures in accumulation mode proved that the episode in P2 was due to long-range transported biomass combustion aerosol.

Chemical and microbial components of urban air PM cause seasonal variation of toxicological activity.

The chemical and microbial composition of urban air particulate matter (PM) displays seasonal variation that may affect its harmfulness on human health. We studied the in vitro inflammatory and cellular metabolic activity/cytotoxicity of urban air particulate samples collected in four size-ranges (PM10-2.5, PM2.5-1, PM1-0.2, PM0.2) during four seasons in relatively clean urban environment in Helsinki, Finland. The composition of the same samples were analyzed, including ions, elements, PAH compounds and endotoxins. In addition, microbial contribution on the detected responses was studied by inhibiting the endotoxin-induced responses with Polymyxin B both in the PM samples and by two different bacterial strains representing Gram-positive and -negative bacteria. Macrophage cell line (RAW 264.7) was exposed to the size segregated particulate samples as well as to microbe samples for 24h and markers of inflammation and cytotoxicity were analyzed. The toxicological responses were dependent on the dose as well as size range of the particles, PM10-2.5 being the most potent and smaller size ranges having significantly smaller responses. Samples collected during spring and autumn had in most cases the highest inflammatory activity. Soil components and other non-exhaust particulate emissions from road traffic correlated with inflammatory responses in coarse particles. Instead, PAH-compounds and K(+) had negative associations with the particle-induced inflammatory responses in fine particles, suggesting the role of incomplete biomass combustion. Endotoxin content was the highest in PM10-2.5 samples and correspondingly, the largest decrease in the responses by Polymyxin B was seen with the very same samples. We found also that inhibitory effect of Polymyxin B was not completely specific for Gram-negative bacteria. Thus, in addition to endotoxin, also other microbial components may have a significant effect on the toxicological responses by ambient particulate matter.

Chemical and in vitro toxicologic characterization of wintertime and springtime urban-air particles with an aerodynamic diameter below 10 microm in Helsinki.

OBJECTIVES: The chemical composition and toxicity of wintertime urban-air particulate matter with an aerodynamic diameter of <10 microm (PM10), derived mostly from long-range transport and local combustion sources, were compared with those of springtime PM10 derived mostly from the resuspension of road dust. METHODS: Water-soluble ions and elements and polycyclic aromatic hydrocarbons (PAH) were analyzed from seasonally pooled PM10 samples collected at a busy traffic site in Helsinki in 1999. These PM10 samples were also tested for cytotoxicity [3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-tetrazolium bromide test] and the production of proinflammatory cytokines [tumor necrosis factor alpha (TNF-alpha) and interleukin 6 (IL-6)] and nitric oxide (NO) in the mouse macrophage cell line RAW 264.7. Their oxidative capacity and the associated DNA (deoxyribonucleic acid) damage were investigated by electron paramagnetic resonance and the formation of 8-hydroxy-2'-deoxyguanosine (8-OH-DG) in isolated calf thymus DNA, respectively. RESULTS: The late wintertime and springtime PM10 had similar compositions of water-soluble ions and elements, but the winter PM10 had a higher content of PAH. The spring PM10 was a much more potent inducer of TNF-alpha and IL-6 production than the winter PM10 was, but there were no consistent differences in cytotoxic potency. In contrast, the winter PM10 was a significantly more potent inducer of NO production and 8-OH-DG formation. The large cytokine responses to the spring PM10 were caused by its insoluble fraction and largely inhibited by the endotoxin antagonist polymyxin B. The transition metal chelator deferoxamine did not modify the proinflammatory or cytotoxic responses to the PM10 samples. CONCLUSIONS: The toxicity profile of urban-air PM10 changed with season in a subarctic climate. Particulate-bound endotoxin from soil gram-negative bacteria is suggested as a highly proinflammatory constituent of springtime resuspended road dust.

Non-accidental health impacts of wildfire smoke.

Wildfires take a heavy toll on human health worldwide. Climate change may increase the risk of wildfire frequency. Therefore, in view of adapted preventive actions, there is an urgent need to further understand the health effects and public awareness of wildfires. We conducted a systematic review of non-accidental health impacts of wildfire and incorporated lessons learned from recent experiences. Based on the literature, various studies have established the relationship between one of the major components of wildfire, particulate matter (particles with diameter less than 10 µm (PM10) and less than 2.5 µm (PM2.5)) and cardiorespiratory symptoms in terms of Emergency Rooms visits and hospital admissions. Associations between wildfire emissions and various subclinical effects have also been established. However, few relationships between wildfire emissions and mortality have been observed. Certain segments of the population may be particularly vulnerable to smoke-related health risks. Among them, people with pre-existing cardiopulmonary conditions, the elderly, smokers and, for professional reasons, firefighters. Potential action mechanisms have been highlighted. Overall, more research is needed to better understand health impact of wildfire exposure.

Mortality among population with exposure to industrial air pollution containing nickel and other toxic metals.

OBJECTIVE: To assess disease mortality among people with exposure to metal-rich particulate air pollution. METHODS: We conducted a cohort study on mortality from 1981 to 2005 among 33,573 people living near a nickel/copper smelter in Harjavalta, Finland. Nickel concentration in soil humus was selected as an indicator for long-term exposure. Relative risks--adjusted for age, socioeconomic status, and calendar period--were calculated for three exposure zones. RESULTS: The relative risks for diseases of the circulatory system by increasing exposure were 0.93 (95% confidence interval = 0.79 to 1.09), 1.20 (1.04 to 1.39), and 1.18 (1.00 to 1.39) among men and 1.01 (0.88 to 1.17), 1.20 (1.04 to 1.38), and 1.14 (0.97 to 1.33) among women. Exclusion of smelter workers from the cohort did not materially change the results. CONCLUSIONS: Long-term environmental exposure to metal-rich air pollution was associated with increased mortality from circulatory diseases.

Serum myeloperoxidase is independent of the risk factors of atherosclerosis.

OBJECTIVES: The main hypothesis of the study was that as serum myeloperoxidase (MPO) concentration is known to indicate the progression of the atherosclerotic process, MPO may be associated with common risk factors of atherosclerosis. Therefore, the presence of these risk factors (especially elevated glucose and lipid concentrations) should predict an increased MPO level during the subsequent months. We also hypothesized an association of MPO with markers of other chronic diseases involving inflammation. METHODS: Fifty-three patients with ischemic heart disease were followed for 24 weeks by biweekly visits, during which the basic MPO level was measured (500 measurements in total, 2-12 per patient). The association of the patients' typical MPO with the risk factors of atherosclerosis and other personal determinants was examined by trend analysis and analysis of variance. RESULTS: MPO was statistically significantly associated with blood leukocyte, neutrophil, and lymphocyte concentrations of the patients (P=0.001-0.003). MPO was also associated with high-sensitivity C-reactive protein (P=0.02). MPO was not associated with markers of lipid and glucose metabolism, of atherosclerosis, or of other chronic diseases. CONCLUSION: Contradictory to our hypotheses, the results indicate that the serum MPO level is independent of the commonly measured risk factors of atherosclerosis and markers of other chronic diseases. Consequently, the findings suggest that MPO-related acute pathologic events (such as plaque destabilization) are not associated with the preceding glucose or lipid values. However, the results support the third hypothesis and previously reported view that MPO is a marker of inflammation in patients of ischemic heart disease.