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Laser desorption/ionization mass spectrometry of diesel particulate matter with charge-transfer complexes.

Polycyclic aromatic hydrocarbons (PAHs) are often associated with complex matrixes such as exhaust diesel particulate matter (DPM), which complicates their study. In that case, laser desorption/ionization mass spectrometry is one of the techniques which ensures their direct analysis in the solid state. We demonstrate in this paper that the use of charge-transfer pi-complexing agents allows us to selectively detect by Fourier transform ion cyclotron resonance mass spectrometry PAHs adsorbed on diesel particles with high sensitivity. 2,4,7-trinitro-9-fluorenone and 7,7',8,8'-tetracyanoquinodimethane pi-acceptor compounds form charge-transfer complexes with PAHs and prevent their evaporation in the mass spectrometer during analysis. Moreover, the production of PAH molecular ions is dramatically increased by laser irradiation of these complexes at short wavelength (221.7 nm) and low power density (5 x 10(6) W cm(-)(2)). This methodology is applied for the first time to the examination of DPM collected during the new European driving cycle for light-duty vehicles. Differentiation criteria may coherently be assigned to engine operating mode (engine temperature, driving conditions). DPM samples can also be easily distinguished in negative ions according to the high sensitivity of this detection mode to sulfate compounds.

Journal Article↗

The effect of particulate matter on resistance and conductance vessels in the rat.

Epidemiological and clinical studies suggest that air pollution, in particular ambient particulate matter (PM), increases mortality in patients with cardiovascular disease (CVD). Several in vivo studies have shown an increase of blood pressure by PM, but so far the mechanism or responsible particle-component has not been elucidated. We exposed small mesenteric rat artery (SMRA) and rat aorta to ambient particles (EHC-93) to test the ability of ambient particles to modify the vascular tone of different vessel types. PM suspensions (10-100 microg/ml) and filtrates containing only the water-soluble components failed to modify the resting tension of either the aorta or SMRA. However, PM did elicit a dose-dependent vasorelaxation in phenylephrine precontracted SMRA and aorta. The effect of the PM suspensions was higher than that of PM filtrate (without particles). The relaxation was already visible at 10 microg/ml, and the difference with filtrate became significant at 100 microg/ml for aorta (maximal relaxation E(max) = 18% vs. 12% PM filtrate) and as low as 30 microg/ml for SMRA (E(max) = 13% vs. 5% PM filtrate). Although the effect of PM was biggest in aorta, the concentration to cause half of the maximal effect (EC(50)) of suspension and filtrate was the same in both capacity (aorta) and resistance vessels (SMRA). The main difference seen between SMRA and aorta was that PM did not modify the phenylephrine-induced dose-response vasoconstriction in SMRA, while it did do so in the aorta. In conclusion, the in vitro exposure of precontracted blood vessels to ambient PM results in an acute vasorelaxation, which is in contrast to the observation that PM can cause increased blood pressure. Dose calculations show that the elevation of blood pressure observed in vivo is not likely due to direct effects of particles or constituents. We therefore suggest that the in vivo effect of PM on vasoconstriction acts through other pathways, such as the central nervous system.

Adrenergic alpha-Agonists↗

Vapor-phase and fine particulate matter concentrations of polycyclic aromatic hydrocarbons measured during the winter months in a northern Rocky Mountain urban airshed.

A fine particulate matter (PM2.5) sampling program was conducted in Missoula, MT, to investigate both the particle and vapor phases of PM2.5-associated polycyclic aromatic hydrocarbons (PAHs) found in a northern Rocky Mountain urban airshed. Twenty-four-hour samples were collected during the cold winter months of January through April 2002, when many of the more volatile organic components of PM2.5 were expected to be found in the condensed particle form. To meet analytical detection limits, each of the 12 individual sample days were aggregated into four total filter and polyurethane foam (PUF) samples, respectively, with each aggregate containing 3 sample days. Quartz filter (particle-phase PAHs) and PUF (vapor-phase PAHs) aggregates were analyzed separately for 18 individual PAHs and phenolics by gas chromatography/mass spectrometry. Results showed that 87% of the PM2.5-associated phenolics and PAHs measured in this study were found in the vapor phase. PM2.5-associated gas/particle partition coefficients (Kp,2.5) ranged from 0 for the lighter phenolics and PAHs to approximately 0.1 for some of the heavier PAHs, such as fluoranthene and pyrene. Calculating Kp,2.5 for the heaviest measured PAHs was not feasible because of low or undetectable concentrations in the vapor phases of these compounds. Phenolics and two-ringed and three-ringed PAHs were found almost exclusively in the vapor phase. Four-ringed PAHs were distributed between the particle and vapor phases, with more mass measured in the vapor phase. Very little five-ringed and higher PAHs were measured from either the filter or PUF sampling medium. These results provide information on both the concentrations and different phases of PM2.5-associated PAHs measured during the winter months in a northern Rocky Mountain urban airshed, when concentrations of PM2.5 are generally at their highest compared with the rest of the year.

Air Pollutants↗

Association between short term exposure to fine particulate matter and heart rate variability in older subjects with and without heart disease.

BACKGROUND: Short term increases in exposure to particulate matter (PM) air pollution are associated with increased cardiovascular morbidity and mortality. The mechanism behind this effect is unclear, although changes in autonomic control have been observed. It was hypothesised that increases in fine PM measured at the subjects' home in the preceding hour would be associated with decreased high frequency heart rate variability (HF-HRV) in individuals with pre-existing cardiac disease. METHODS: Two hundred and eighty five daily 20 minute measures of HRV (including a paced breathing protocol) were made in the homes of 34 elderly individuals with (n = 21) and without (n = 13) cardiovascular disease (CVD) over a 10 day period in Seattle between February 2000 and March 2002. Fine PM was continuously measured by nephelometry at the individuals' homes. RESULTS: The median age of the study population was 77 years (range 57-87) and 44% were male. Models that adjusted for health status, relative humidity, temperature, mean heart rate, and medication use did not find a significant association between a 10 microg/m3 increase in 1 hour mean outdoor PM2.5 before the HRV measurement and a change in HF-HRV power in individuals with CVD (3% increase in median HF-HRV (95% CI -19 to 32)) or without CVD (5% decrease in median HF-HRV (95% CI -34 to 36)). Similarly, no association was evident using 4 hour and 24 hour mean outdoor PM2.5 exposures before the HRV measurement. CONCLUSION: No association was found between increased residence levels of fine PM and frequency domain measures of HRV in elderly individuals.

Aged↗

The impact of particulate matter on daily mortality in Bangkok, Thailand.

Several studies conducted in U.S. cities report an association between acute exposures to particulate matter (PM), usually measured as PM10, and mortality. Evidence of high concentrations of PM10 in Eastern Europe and in large metropolitan areas outside of the United States, such as Mexico City and Bangkok, underscores the need to determine whether these same associations occur outside of the United States. In addition, conducting studies of mortality and air pollution in regions that have distinctly different seasonal patterns than those of the United States provides an effective opportunity to assess the potentially confounding aspects of seasonality. Over the last few years, daily measures of ambient PM10 have been collected in Bangkok, a tropical city of over 6 million people. In this metropolitan area, PM10 consists largely of fine particles generated from diesel- and gasoline-powered automobiles, and from two-stroke motorcycle engines. Our analysis involved the examination of the relationship between PM10 and daily mortality for 1992 through 1995. In addition to counts of daily natural mortality (total mortality net of accidents, homicides, and suicides), the data were compiled to assess both cardiovascular and respiratory mortality, and natural mortality by age group. A multivariate Poisson regression model was used to explain daily mortality while controlling for several covariates including temperature, humidity, day of the week, season, and time. The analysis indicated a statistically significant association between PM10 and all of the alternative measures of mortality. The results suggest a 10-microgram/m3 change in daily PM10 is associated with a 1-2% increase in natural mortality, a 1-2% increase in cardiovascular mortality, and a 3-6% increase in respiratory mortality. These relative risks are generally consistent with or greater than those reported in most studies undertaken in the United States.

Adolescent↗

Peroxides and macrophages in the toxicity of fine particulate matter in rats.

Epidemiologists have observed a positive association between human morbidity and mortality and the atmospheric concentrations of fine particulate matter (PM), but the mechanisms underlying the toxic effects of PM have not been elucidated. Various components of ambient PM have been implicated in toxicity (including ultrafine particles, transition metals, organics and oxidants). Our research focused on hydrogen peroxide (H2O2). We speculated that fine PM transports H2O2 into the lower lung, leading to tissue injury and to accumulation and activation of macrophages in these regions. The macrophages release cytotoxic mediators and proinflammatory cytokines that contribute to the pathogenesis of tissue injury. To test this hypothesis, we conducted studies to determine (1) whether tissue injury induced by aerosols is mediated by cytotoxic H2O2 carried into the lower lung by fine particles and (2) whether exposure of rats to fine PM leads to accumulation of activated macrophages in the lung. For our studies, systems were designed to generate model atmospheric fine PM and atmospheric peroxides consisting of an ammonium sulfate [(NH4)2SO4] aerosol (mass median diameter, 0.46 +/- 0.14 microm) and H2O2. We also constructed a 6-port nose-only exposure chamber. Female Sprague Dawley rats were exposed for 2 hours to aerosols consisting of (NH4)2SO4 (430 microg/m3), (NH4)2SO4 + 10, 20 or 100 ppb H2O2, vapor-phase H2O2 (10, 20 or 100 ppb), or particle-free air. Studies using oxygen-18 (18O)-labeled H2O2 were conducted to validate the transport of H2O2 into the lower lung with (NH4)2SO4. Rats were killed immediately (0 hours) or 24 hours after exposure. Compared with control animals, inhalation of (NH4)2SO4 and H2O2, alone or in combination, had no major effect on cell number or viability, protein content, or lactate dehydrogenase (LDH) levels in bronchoalveolar lavage (BAL) fluid collected either immediately or 24 hours after exposure. However, electron microscopy revealed that a larger number of neutrophils in pulmonary capillaries adhered to the vascular endothelium, especially in lungs of rats exposed to (NH4)2SO4 + H2O2. Inhalation of (NH4)2SO4 + H2O2 was also found to be associated with altered macrophage functional activity. Thus, exposing rats to (NH4)2SO4 + 20 ppb H2O2 or 20 ppb H2O2 alone caused a level of tumor necrosis factor alpha (TNF-alpha) production by lung macrophages that was higher than in controls. This higher level was observed immediately after exposure and persisted for at least 24 hours. Greater TNF-alpha production was also detected 24 hours after exposure to (NH4)2SO4 + 10 ppb H2O2. Immediately after rats inhaled (NH4)2SO4 + 10 ppb H2O2 or 20 ppb H2O2 alone, we also observed a transiently higher production of superoxide anion (O2-) by alveolar macrophages. Macrophages isolated 24 hours after exposure to 20 ppb H2O2 also produced larger quantities of superoxide anion. In contrast, immediately after exposure, macrophages from rats exposed to (NH4)2SO4 + 10 ppb H2O2 or to 20 ppb H2O2 alone generated less nitric oxide (NO). Reduced nitric oxide production was also observed 24 hours after exposure to (NH4)2SO4 + 10 ppb H2O2 or to 10 or 20 ppb H2O2 alone. Reduced nitric oxide production may have been due to superoxide anion-driven formation of peroxynitrite (ONOO-) anions. In this regard, nitrotyrosine, an in vivo marker of peroxynitrite, was detected in lung tissue immediately after rats were exposed to (NH4)2SO4 + H2O2 or to H2O2 alone (10 or 20 ppb). We also found that alveolar macrophages from rats exposed to (NH4)2SO4 + H2O2 showed a greater expression of the antioxidant enzyme heme oxygenase-1 (HO-1) when stimulated with lipopolysaccharide (LPS) and interferon-gamma (IFN-gamma). Similar results were observed after exposure of rats to an organic peroxide aerosol (cumene hydroperoxide). Taken together, the results of our studies demonstrate that biological effects of inhaled H2O2 are augmented by fine PM. Moreover, tissue injury induced by (NH4)2SO4 + H2O2 may be related to altered production of cytotoxic mediators by alveolar macrophages. Determining the relevance of these toxicologic results to human health will be important in future studies for evaluating the risk of exposure.

Aerosols↗

Source profiles of particulate matter emissions from a pilot-scale boiler burning North American coal blends.

Recent awareness of suspected adverse health effects from ambient particulate matter (PM) emission has prompted publication of new standards for fine PM with aerodynamic diameter less than 2.5 microm (PM2.5). However, scientific data on fine PM emissions from various point sources and their characteristics are very limited. Source apportionment methods are applied to identify contributions of individual regional sources to tropospheric particulate concentrations. The existing industrial database developed using traditional source measurement techniques provides total emission rates only, with no details on chemical nature or size characteristics of particulates. This database is inadequate, in current form, to address source-receptor relationships. A source dilution system was developed for sampling and characterization of total PM, PM2.5, and PM10 (i.e., PM with aerodynamic diameter less than 10 pm) from residual oil and coal combustion. This new system has automatic control capabilities for key parameters, such as relative humidity (RH), temperature, and sample dilution. During optimization of the prototype equipment, three North American coal blends were burned using a 0.7-megawatt thermal (MWt) pulverized coal-fired, pilot-scale boiler. Characteristic emission profiles, including PM2.5 and total PM soluble acids, and elemental and carbon concentrations for three coal blends are presented. Preliminary results indicate that volatile trace elements such as Pb, Zn, Ti, and Se are preferentially enriched in PM2.5. PM2.5 is also more concentrated in soluble sulfates relative to total PM. Coal fly ash collected at the outlet of the electrostatic precipitator (ESP) contains about 85-90% PM10 and 30-50% PM2.5. Particles contain the highest elemental concentrations of Si and Al while Ca, Fe, Na, Ba, and K also exist as major elements. Approximately 4-12% of the materials exists as soluble sulfates in fly ash generated by coal blends containing 0.2-0.8% sulfur by mass. Source profile data for an eastern U.S. coal show good agreement with those reported from a similar study done in the United States. Based on the inadequacies identified in the initial sampling equipment, a new, plume-simulating fine PM measurement system with modular components for field use is being developed for determining coal combustion PM source profiles from utility boiler stacks.

Air Movements↗

The influence of contrasting suspended particulate matter transport regimes on the bias and precision of flux estimates.

A large database (507 station-years) of daily suspended particulate matter (SPM) concentration and discharge data from 36 stations on river basins ranging from 600 km(2) to 600,000 km(2) in size (USA and Europe) was collected to assess the effects of SPM transport regime on bias and imprecision of flux estimates when using infrequent surveys and the discharge-weighted mean concentration method. By extracting individual SPM concentrations and corresponding discharge values from the database, sampling frequencies from 12 to 200 per year were simulated using Monte Carlo techniques. The resulting estimates of yearly SPM fluxes were compared to reference fluxes derived from the complete database. For each station and given frequency, bias was measured by the median of relative errors between estimated and reference fluxes, and imprecision by the difference between the upper and lower deciles of relative errors. Results show that the SPM transport regime of rivers affects the bias and imprecision of fluxes estimated by the discharge-weighted mean concentration method for given sampling frequencies (e.g. weekly, bimonthly, monthly). The percentage of annual SPM flux discharged in 2% of time (Ms(2)) is a robust indicator of SPM transport regime directly related to bias and imprecision. These errors are linked to the Ms(2) indicator for various sampling frequencies within a specific nomograph. For instance, based on a deviation of simulated flux estimates from reference fluxes lower than +/-20% and a bias lower than 1% or 2%, the required sampling intervals are less than 3 days for rivers with Ms(2) greater than 40% (basin size<10,000 km(2)), between 3 and 5 days for rivers with Ms(2) between 30 and 40% (basin size between 10,000 and 50,000 km(2)), between 5 and 12 days for Ms(2) from 20% to 30% (basin size between 50,000 and 200,000 km(2)), 12-20 days for Ms(2) in the 15-20% range (basin size between 200,000 and 500,000 km(2)).

France↗

A procedure for use in estimating human exposure to particulate matter of ambient origin.

Modern epidemiology has shown that fluctuations of mortality data are statistically significantly correlated with fluctuations of ambient particulate matter (PM) concentration data. This relation cannot be confounded by exposure to PM of indoor origin because the concentrations of ambient PM are not correlated with concentrations of PM of indoor origin. It has been suggested, given the above understanding, that modern PM exposure measurements and analysis should create separate estimates of exposure to all PM of ambient origin and exposure to all PM of nonambient origin (primarily of indoor origin), and not exposure to total PM. This paper reviews the developments of the form of the general microenvironmental mass balance equation that can be utilized for estimating human exposure to PM of ambient origin and for estimating the portion of total PM exposure that is attributable to nonambient origin PM. The equation is perfectly general and can be applied to conditions of time-varying factors that influence exposure, such as rapidly changing air-exchange rates in a home as doors and windows are opened and closed, and turning on and off air cleaners in a home. It is suggested that this procedure be applied in exposure assessment studies and validated using independent techniques of estimating exposure to PM of ambient origin available in the literature.

Air Pollution↗

Day-of-week patterns of particulate matter and its chemical components at selected sites in California.

This paper analyzes day-of-week variations in concentrations of particulate matter (PM) in California. Because volatile organic compounds (VOCs) and oxides of nitrogen (NOx) are not only precursors of ozone (O3) but also of secondary PM, it is useful to know whether the variations by day of week in these precursors are also evident in PM data. Concentrations of PM < or = 10 microm (PM10) and < or = 2.5 microm in aerodynamic diameter (PM2.5) were analyzed. PM concentrations exhibit a general weekly pattern, with the maximum occurring late in the workweek and the minimum occurring on weekends (especially Sunday); however, this pattern does not prevail at all sites and areas. PM nitrate (NO3-) data from Size Selective Inlet (SSI) samplers in the South Coast Air Basin (SoCAB) tend to be somewhat lower on weekends compared with weekdays. During 1988-1991, the weekend average was lower than the weekday average at 8 of 13 locations, with an average decrease of 1%. During 1997-2000, the weekend average was lower than the weekday average at 10 of 13 locations, with an average decrease of 6%. The weekend averages are generally lower than weekday averages for sulfates, organic carbon, and elemental carbon. Because heavy-duty trucks typically represent a major source of elemental carbon, the weekend decrease in heavy-duty truck traffic may also result in a decrease in ambient elemental carbon concentrations.

Air Pollutants↗

Seasonal and spatial variation of solvent extractable organic compounds in fine suspended particulate matter in Hong Kong.

The results of a 12-month study of more than 100 solvent extractable organic compounds (SEOC) in particulate matter (PM) less than or equal to 2.5 microm (PM2.5) collected at three air monitoring stations located at roadside, urban, and rural sites in Hong Kong are reported. The total yield of SEOC that accounts for approximately 8-18% of organic carbon (OC) determined by a thermal optical transmittance method was 125-2060 ng/m3, which included 14.6-128 ng/m3 resolved aliphatic hydrocarbons, 39.4-1380 ng/m3 unresolved complex mixtures, 0.6-17.2 ng/m3 polycyclic aromatic hydrocarbons, 41.6-520 ng/m3 fatty acids, and < 0.1-12.1 ng/m3 alkanols. Distinct seasonal variations (summer/winter differences) were observed with higher concentrations of the total and each class of SEOC in the winter and lower concentrations in the summer. Spatial variations are also obvious, with the roadside samples having the highest concentrations of SEOC and the rural samples having the lowest concentrations in all seasons. Characteristic ratios of petroleum hydrocarbons, such as carbon preference index, unresolved to resolved components, and carbon number with maximum concentration, suggest that PM2.5 carbon in Hong Kong originates from both biogenic and anthropogenic sources. The proportion of SEOC in PM2.5 from anthropogenic sources is estimated.

Air Pollutants↗

Hierarchical bivariate time series models: a combined analysis of the effects of particulate matter on morbidity and mortality.

In this paper we develop a hierarchical bivariate time series model to characterize the relationship between particulate matter less than 10 microns in aerodynamic diameter (PM10) and both mortality and hospital admissions for cardiovascular diseases. The model is applied to time series data on mortality and morbidity for 10 metropolitan areas in the United States from 1986 to 1993. We postulate that these time series should be related through a shared relationship with PM10. At the first stage of the hierarchy, we fit two seemingly unrelated Poisson regression models to produce city-specific estimates of the log relative rates of mortality and morbidity associated with exposure to PM10 within each location. The sample covariance matrix of the estimated log relative rates is obtained using a novel generalized estimating equation approach that takes into account the correlation between the mortality and morbidity time series. At the second stage, we combine information across locations to estimate overall log relative rates of mortality and morbidity and variation of the rates across cities. Using the combined information across the 10 locations we find that a 10 microg/m3 increase in average PM10 at the current day and previous day is associated with a 0.26% increase in mortality (95% posterior interval -0.37, 0.65), and a 0.71% increase in hospital admissions (95% posterior interval 0.35, 0.99). The log relative rates of mortality and morbidity have a similar degree of heterogeneity across cities: the posterior means of the between-city standard deviations of the mortality and morbidity air pollution effects are 0.42 (95% interval 0.05, 1.18), and 0.31 (95% interval 0.10, 0.89), respectively. The city-specific log relative rates of mortality and morbidity are estimated to have very low correlation, but the uncertainty in the correlation is very substantial (posterior mean = 0.20, 95% interval -0.89, 0.98). With the parameter estimates from the model, we can predict the hospitalization log relative rate for a new city for which hospitalization data are unavailable, using that city's estimated mortality relative rate. We illustrate this prediction using New York as an example.

Air Pollutants↗

Effects of atmospheric sulphur dioxide and particulate matter concentrations on emergency room admissions due to asthma in Ankara.

Recent studies have associated short-term exposure to respirable particulate matter (PM(10)) and sulphur dioxide (SO(2)) with peak flow decrements, increased symptoms of respiratory irritation, increased use of asthma medications, and increased admission and hospitalization for asthma. To further delineate the association between SO(2), PM(10) exposure and asthmatic response, we compiled daily records of asthma emergency room visits from our hospital and data of meteorological conditions, SO(2) and PM(10) concentrations in Ankara area. Weekly averages of daily counts of emergency room visits for asthma were significantly associated with average weekly SO(2) and PM(10) exposure on previous week (r= 0.328, p= 0.017 and r= 0.355, p= 0.009 respectively). Admission to emergency room for asthma count was also negatively correlated with ambient temperature (r= -0.496, p= 0.0001) and strong wind existence (X(2)= 3.930, p= 0.047) on previous days. It was also positively correlated with ambient relative humidity (r= 0.531, p= 0.0001). We observed that numbers of emergency visits due to asthma were higher in winter months, April and September. In winter and early spring period there was concordance between asthma emergency admissions with air pollutants levels. During this period ambient temperatures were low as well. There were two discordance points in monthly variation of air pollution and asthma visits. We thought that first asthma visits peak was related to allergic pollens during April and second peak was due to opening of schools and increasing of respiratory infections for this reason during September. The general pattern of our results confirms that even low levels of air pollution encountered in Ankara are linked to short-term increases in the number of people visiting emergency department for asthma.

Adult↗

Vanilloid (capsaicin) receptors influence inflammatory sensitivity in response to particulate matter.

The signs of airway inflammation and hyperresponsiveness that occur in animals exposed to air pollutants are often strain- and species-specific. To investigate the underlying causes of this phenomenon, BALB/c and C57bl/6 mice were exposed intratracheally to residual oil fly ash (ROFA, 3 mg/kg) and examined after 24 h for signs of airway inflammation. BALB/c showed significantly higher numbers of neutrophils and increased airway hyperresponsiveness in response to methacholine challenge, whereas B6 mice showed no significant change in either inflammatory endpoint. To determine the underlying cause of this strain specificity, cultures of dorsal root ganglion (DRG) sensory neurons, which innervate the upper airways in situ, were explanted from both BALB/c and B6 fetal mice. After 5-7 days in culture, they were exposed to ROFA, other urban and industrial particulate matter (PM; e.g., oil fly ash, woodstove, Mt. St. Helen, St. Louis, Ottawa, coal fly ash) or to prototype irritants (e.g., capsaicin 3-10 microM, pH 5.0 and 6.5). In all instances (except for woodstove), DRG neurons from BALB/c mice released significantly higher levels of the pro-inflammatory cytokine IL-6 into their nutrient media relative to neurons from B6 mice. This cytokine release could be significantly reduced for all PM treated cultures (except woodstove) by pretreatment of cultures with capsazepine (CPZ), a competitive antagonist of vanilloid receptors. DRG neurons, cultured from BALB/c and B6 neonates, were loaded with Fluo-3 AM and exposed to the prototype irritants, acid pH (5.0, 6.5), or capsaicin (3, 10 microM). Analysis of their increases in intracellular calcium showed that significantly higher numbers of BALB/c neurons responded to these prototype irritants, relative to B6 neurons. Morphometric analysis of BALB/c neurons, histochemically stained with cobalt to label neurons bearing capsaicin-sensitive receptors, showed a significantly higher level of stained neurons relative to B6 neurons. Finally, semiquantitative RT-PCR showed a higher expression of VR1 receptor mRNA in DRG and spinal cord taken from neonatal BALB/c mice relative to B6 mice. Taken together, these data suggest that capsaicin and acid-sensitive irritant receptors, located on somatosensory cell bodies and their nerve fiber terminals, subserve PM-induced airway inflammation and are quantitatively different in responsive and nonresponsive mouse strains.

Air Pollutants↗

Size fractions of ambient particulate matter induce granulocyte macrophage colony-stimulating factor in human bronchial epithelial cells by mitogen-activated protein kinase pathways.

Environmental pollutants, including ambient particulate matter (PM), increase respiratory morbidity. Studies of model PM particles, including residual oil fly ash and freshly generated diesel exhaust particles, have demonstrated that PM affects inflammatory airway responses. Neither of these particles completely represents ambient PM, and therefore questions remain about ambient particulates. We hypothesized that ambient PM of different size fractions collected from an urban environment (New York City air), would activate primary culture human bronchial epithelial cells (HBECs). Because of the importance of granulocyte-macrophage colony-stimulating factor (GM-CSF) on inflammatory and immunomodulatory processes, we focused our studies on this cytokine. We demonstrated that the smallest size fraction (ultrafine/fine; < 0.18 micro m) of ambient PM (11 micro g/cm(2)), upregulated GM-CSF production (2-fold increase). The absence of effect of carbon particles of similar size, and the day-to-day variation in response, suggested that the chemical composition, but not the particle itself, was necessary for GM-CSF induction. Activation of the extracellular signal-regulated kinase and the p38 mitogen-activated protein kinase was associated with, and necessary for, GM-CSF release. These studies serve to corroborate and extend those on model particles. Moreover, they emphasize the role of the smallest size ambient particles in airway epithelial cell responses.

Air Pollutants↗

Signal transduction pathways involved in particulate matter induced relaxation in rat aorta--spontaneous hypertensive versus Wistar Kyoto rats.

UNLABELLED: Previously we reported that in vivo exposure to ambient particulate matter (PM) induces vasodilatation in rat aorta. The purpose of the current study was to investigate the intracellular messengers involved in PM-elicited vasodilatation in aortas from spontaneous hypertensive (SHR) and normotensive (WKY) rats. METHODS: The contribution of three different intracellular pathways, i.e. (1) the NO-cGMP pathway, (2) prostanoids signaling and (3) endothelial hyperpolarisation factors were evaluated by using specific inhibitors (NS2028, Diclofenac and high K-concentration/17-ODYA, respectively). Using antagonists of capsaicin- or histamine receptors we tested potential interactions of PM with these receptors. Particle suspensions (EHC-93), particle filtrates (particle-free) and Cu(2+)- or Zn(2+)-containing solutions were used to obtain cumulative dose-response curves of relaxation in normal and endothelium-denuded rings. RESULTS: Our present data confirm that PM and its soluble components elicit an endothelium-independent vasodilatation in rat aorta rings. The response is mainly linked to the activation of soluble guanylate cyclase (sGC), since its inhibition by NS2028 almost abolished relaxation. Indeed PM suspensions stimulated cGMP production in purified isolated sGC. Neither the receptor nor their signaling pathways played a significant role in the direct relaxation by PM or metals. Vasodilatation responses were significantly higher in SHR than WKY control rats. CONCLUSION: Our data demonstrate that PM elicits a dose-dependent vasodilatation via activation of sGC in vascular smooth muscles. PM components, including soluble transition metals play a major role in this response. The stronger effect in SHR rats is in accordance with the observation that acute effects of PM are mainly seen in patients with underlying cardiovascular diseases.

Air Pollutants↗

Total arsenic and selenium levels in atmospheric particulate matter of La Coruña (Spain).

This paper presents a study concerning the degree of pollution due to arsenic and selenium in atmospheric particulates of La Coruña (NW Spain). Sampling of particulate matter was accomplished with high volume samplers equipped with glass microfibre filters; samples were collected in two different areas (one an industrial area and the other a rural area). For As and Se determination, hydride generation and electrothermal atomization atomic absorption spectrometry, respectively, were used.

Air Pollution↗

Ambient particulate matter, C-reactive protein, and coronary artery disease.

This article is a review of the scientific literature with respect to fine particulate matter (PM), 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors, and coronary artery disease (CAD). The association between air pollution and respiratory diseases has been extensively investigated for decades; however, the role of air pollution in exacerbating heart disease has only recently become a focus of attention. It has been shown that for every 10-microg/m(3) increase in fine PM in the air, there appears to be a 2.1% increase in the number of deaths related to ischemic heart disease. PM has been linked to increased levels of systemic inflammation biomarkers such as C-reactive proteins (CRP). Daily variation of ambient pollution is correlated with rises and falls in CRP levels. Increased CRP levels have been associated with increased morbidity and mortality in individuals with CAD. Seventy-five percent of patients with elevated CRP levels have reportedly experienced a major cardiac event despite low-density lipoproteins (LDL) levels that were below the threshold recommended for pharmacological intervention. HMG CoA reductase inhibitors (statins) have been shown to cause a reduction in coronary events by lowering LDL levels. However, recently it has been shown that statins have the effect of lowering CRP levels. This may explain why individuals with normal lipid levels may benefit from statin therapy. Ambient PM exposure levels and its effects on CRP are risk factors associated with coronary events and should be considered as a target for the treatment of CAD.

Air Pollutants↗