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.

The effect of parathyroid hormone (1-84) treatment on serum bone morphogenetic protein 4 and vascular endothelial growth factor in postmenopausal women with established osteoporosis.

PURPOSE: To investigate the effect of 18 months' parathyroid hormone 1-84 (PTH 1-84) treatment on serum levels of bone morphogenetic protein 4 (BMP4) and vascular endothelial growth factor (VEGF), in postmenopausal women with established osteoporosis. METHODS: Thirty-seven postmenopausal women with osteoporosis (mean age 72.9 ± 8.1 years old) and 23 healthy controls (mean age 68.9 ± 9.9 years old) were enrolled. Patients were treated with daily subcutaneous injections of PTH (1-84) 100 mcg for 18 months, plus calcium 1 gr and vitamin D 800 IU per os daily. Blood samples were taken every 6 months during the study. RESULTS: At baseline, there were no differences considering anthropometric parameters, co-morbidities, current medications used between patients and controls. Mean serum VEGF levels were significantly higher in osteoporotic patients compared to controls (436.7 ± 259.7 vs. 260.3 ± 184.3 pg/ml, p = 0.006), while there were no differences in mean serum values of BMP4 (5.3 ± 1.7 vs. 5.7 ± 1.6 pg/ml, p = 0.40). Serum VEGF levels increased by approximately 20% after 12 months of PTH (1-84) treatment compared to baseline (p = 0.03) and by 22% after 18 months (p = 0.01). A significant increase of 10% in mean serum BMP4 levels was observed after 18 months of PTH (1-84) treatment compared to baseline (p = 0.02). In the control group we found no differences after 18 months compared to baseline in BMP4 (5.7 ± 1.6 vs. 6.0 ± 1.5 pg/ml, p = 0.53) and VEGF (260.3 ± 184.3 vs. 257.4 ± 107.1 pg/ml, p = 0.94). CONCLUSIONS: PTH (1-84) treatment increased serum levels of VEGF and BMP4 in postmenopausal women with severe osteoporosis.

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.

Insulin resistance is associated with poorer verbal fluency performance in women.

AIMS/HYPOTHESIS: Type 2 diabetes is an independent risk factor for cognitive decline. Insulin resistance occurring during midlife may increase the risk of cognitive decline later in life. We hypothesised that insulin resistance is associated with poorer cognitive performance and that sex and APOE*E4 might modulate this association. METHODS: The association of insulin resistance and APOE*E4 genotype on cognitive function was evaluated in a nationwide Finnish population-based study (n = 5,935, mean age 52.5 years, range 30-97 years). HOMA-IR was used to measure insulin resistance. Cognitive function was tested by word-list learning, word-list delayed-recall, categorical verbal fluency and simple and visual-choice reaction-time tests. Linear regression analysis was used to determine the association between HOMA-IR and the results of the cognitive tests. RESULTS: Higher HOMA-IR was associated with poorer verbal fluency in women (p < 0.0001) but not in men (p = 0.56). Higher HOMA-IR was also associated with poorer verbal fluency in APOE*E4 -negative individuals (p = 0.0003), but not in APOE*E4 carriers (p = 0.28). Furthermore, higher HOMA-IR was associated with a slower simple reaction time in the whole study group (p = 0.02). CONCLUSIONS/INTERPRETATION: To our knowledge, this is the first comprehensive, population-based study, including both young and middle-aged adults, to report that female sex impacts the association of HOMA-IR with verbal fluency. Our study was cross-sectional, so causal effects of HOMA-IR on cognition could not be evaluated. However, our results suggest that HOMA-IR could be an early marker for an increased risk of cognitive decline in women.

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.

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.

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.

Effect of risedronate in osteoporotic HIV males, according to gonadal status: a pilot study.

The aim of the study was to evaluate the effect of risedronate on bone mineral density (BMD) and bone turnover markers in HIV-infected osteoporotic males, according to their gonadal status. HIV patients were followed up for 24 months and divided into two groups: patients with osteoporosis or osteopenia with fractures (group A, n = 20) and those without (group B, n = 21). Group A and B were further divided according to the presence of reduced androgenizations. Both groups were treated with cholecalciferol 800 I.U. and calcium (Ca) 1,000 mg orally every day for the first 12 months. Risedronate 75 mg for two consecutive days a month orally was then added in group A, for another 12 months. Group B continued treatment with Ca and vitamin D. Every 6 months each patient underwent biochemical evaluation, and BMD measurement. A significant increase in lumbar BMD was observed in HIV males with adequate androgenization after 12 months of risedronate treatment in group A together with a reduction of bone turnover markers. BMD remained stable with a concomitant significant slight reduction of bone turnover markers in group B. Risedronate increased BMD and reduced bone turnover markers to a greater extent in patients with adequate androgenization compared to osteoporotic HIV males with symptomatic hypoandrogenization.

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.

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.

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.

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.

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.

[Effect of treatment with selective serotonin reuptake inhibitors on lipid profile: state of the art]. / Effetto del trattamento con inibitori selettivi del reuptake della serotonina sul profilo lipidico: stato dell'arte.

Selective Serotonin Reuptake Inhibitors (SSRI) are an effective treatment for depressive disorder. Nevertheless, there is evidence suggesting a negative effect of these drugs on the lipid profile of the patients. We carried out a systematic review of the literature evaluating the influence of therapy with SSRI on lipid profile. Data source was MEDLINE. Clinical trials, prospective studies, retrospective studies and reviews published until November 2011 were considered. We identified twelve studies published from 1994 to 2011, of which four were randomized clinical trials, six were prospective studies and two were retrospective studies. Sertraline and Paroxetine seemed to have negative effects on the serum levels of Total and LDL Cholesterol. Citalopram did not demonstrate any influence on Total and LDL Cholesterol blood levels, being conversely associated with a slight increase of the HDL Cholesterol levels. Few data were found about the effects of Fluoxetina e Fluvoxamina on lipid profile and no data were found about Escitalopram. Sertaline and Paroxetine, two effective and widely used drugs for the treatment of major depression, seem to have a negative effect on the lipid profile; Citalopram, with its neutral or positive effect on lipid profile, should be considered the treatment of choice for depressive patients affected by dyslipidemia.

Health effects of black carbon

Black carbon is a good indicator of combustion-related air pollution and was only recently recognized as a short-lived climate-forcer, which contributes to warming the Earth’s atmosphere. This report presents the results of a systematic review of evidence of the health effects of black carbon in ambient air. Epidemiological studies provide sufficient evidence of the association of cardiopulmonary morbidity and mortality with exposure to black carbon. Toxicological studies suggest that black carbon may operate as a universal carrier of a wide variety of chemicals of varying toxicity to the human body. Although black carbon may not be a major, directly toxic component of fine particulate matter, reducing people’s exposure to particulate matter containing black carbon should reduce its effects on their health, as well as helping to mitigate climate change. This review is of particular interest to environmental health professionals concerned with assessing and reducing the health effects of air pollution, as well as to those who use scientific evidence in support of climate change mitigation policies.

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.

Particle induced toxicity in relation to transition metal and polycyclic aromatic hydrocarbon contents.

Exposure to ambient particulate matter (PM) is statistically significantly associated with morbidity and mortality. The objectives of this study were (a) to investigate in vivo pulmonary and systemic cytotoxicity and inflammatory activity in compromised animals exposed to PM and (b) to investigate the relationships of the outcomes to the chemical compositions of particular polycyclic aromatic hydrocarbons (PAH) and transition metals in the PM. The PM samples were collected in European cities representing contrasting situations. Exposure of spontaneously hypertensive rats (7 mg of PM/kg) resulted in pulmonary inflammation, cellular toxicity and the induction of blood fibrinogen. Coarse PM generally caused stronger effects per mg than fine particles. Positive correlations between lactate dehydrogenase, proteins, and some inflammation parameters and the particle metal and PAH content were found. PM rich in PAH also led to increased blood fibrinogen. Removal of particles but not the organics (i.e., PAH) of a sample led to reduced inflammation in the lungs. The present study highlights the importance of metals as well as PM-bound PAH in particle biological outcomes. It supports the hypothesis that, on an equal mass basis, particle health effects differ due to differences in compositions and size.