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PubMed2004

Metal particulate matter components affect gene expression and beat frequency of neonatal rat ventricular myocytes.

Soluble particulate matter (PM) components (e.g., metals) have the potential to be absorbed into the bloodstream and transported to the heart where they might induce the expression of inflammatory cytokines and remodel electrical properties. We exposed cultured rat ventricular myocytes to similar concentrations of two metals [zinc (Zn) and vanadium (V)] found commonly in PM and measured changes in spontaneous beat rate. We found statistically significant reductions in spontaneous beat rate after both short-term (4-hr) and long-term (24-hr) exposures, with a more substantial effect seen with Zn. We also measured the expression of genes associated with inflammation and a number of sarcolemmal proteins associated with electrical impulse conduction. Exposure to Zn or V (6.25-50 microM) for 6 hr produced significant increases in IL-6, IL-1 alpha, heat shock protein 70, and connexin 43 (Cx43). After 24 hr exposure, Zn induced significant changes in the gene expression of Kv4.2 and KvLQt (potassium channel proteins), the alpha 1 subunit of the L-type calcium channel, and Cx43, as well as IL-6 and IL-1 alpha. In contrast, V produced a greater effect on Cx43 and affected only one ion channel (KvLQT1). These results show that exposure of rat cardiac myocytes to noncytotoxic concentrations of Zn and V alter spontaneous beat rate as well as the expression of ion channels and sarcolemmal proteins relevant to electrical remodeling and slowing of spontaneous beat rate, with Zn producing a more profound effect. As such, these data suggest that the cardiac effects of PM are largely determined by the relative metal composition of particles.

Animals↗

PubMed2003

Proinflammatory and cytotoxic effects of Mexico City air pollution particulate matter in vitro are dependent on particle size and composition.

Exposure to urban airborne particulate matter (PM) is associated with adverse health effects. We previously reported that the cytotoxic and proinflammatory effects of Mexico City PM10 (less than or equal to 10 micro m mean aerodynamic diameter) are determined by transition metals and endotoxins associated with these particles. However, PM2.5 (less than or equal to 2.5 micro m mean aerodynamic diameter) could be more important as a human health risk because this smaller PM has the potential to reach the distal lung after inhalation. In this study, we compared the cytotoxic and proinflammatory effects of Mexico City PM10 with those of PM2.5 using the murine monocytic J774A.1 cell line in vitro. PMs were collected from the northern zone or the southeastern zone of Mexico City. Elemental composition and bacterial endotoxin on PMs were measured. Tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6) production by J774A.1 cells was measured in the presence or absence of recombinant endotoxin-neutralizing protein (rENP). Both northern and southeastern PMs contained endotoxin and a variety of transition metals. Southeastern PM10 contained the highest endotoxin levels, 2-fold higher than that in northern PM10. Northern and southeastern PM2.5 contained the lowest endotoxin levels. Accordingly, southeastern PM10 was the most potent in causing secretion of the proinflammatory cytokines TNF-alpha and IL-6. All PM2.5 and PM10 samples caused cytotoxicity, but northern PMs were the most toxic. Cytokine secretion induced by southeastern PM10 was reduced 50-75% by rENP. These results indicate major differences in PM10 and PM2.5. PM2.5 induces cytotoxicity in vitro through an endotoxin-independent mechanism that is likely mediated by transition metals. In contrast, PM10 with relatively high levels of endotoxin induces proinflammatory cytokine release via an endotoxin-dependent mechanism.

Air Pollutants↗

PubMed2000

Ozone and particulate matter air pollution in Wisconsin: trends and estimates of health effects.

OBJECTIVES: Ozone and particulate matter 10 microns in diameter or less (PM10) are associated with increased risk of morbidity and mortality. This paper will report ozone and PM10 trends in Wisconsin and provide estimates of potentially susceptible populations and adverse health outcomes associated with current levels of these pollutants. METHODS: Ozone and PM10 monitoring data is provided by Department of Natural Resources (DNR) air monitors. Exposure-response modeling and data, provided by the United States Environmental Protection Agency (US EPA), was used to estimate hospital admissions associated with ozone and PM10 pollution. RESULTS: Days with high ozone concentrations have become less frequent and the annual PM10 levels have decreased over the 1990s. However, the potentially susceptible population has increased, the number of children who could experience a lung function decrement due to ozone is between 12,978 and 38,653, and high PM10 concentrations are estimated to have resulted in 43 hospital admissions. CONCLUSION: Despite decreasing ozone and PM10 levels, the burden of respiratory and cardiovascular disease affected by these pollutants remains significant.

Air Pollutants↗

PubMed2002

Effect of concentrated ambient particulate matter on blood coagulation parameters in rats.

Epidemiologic studies have shown that exposure to particulate air pollution is associated with short-term increases in cardiovascular morbidity and mortality. These adverse effects of inhaled particulate matter (PM*) may be the indirect result of a PM-induced increase in blood coagulability. This explanation is biologically plausible because prospective studies have shown that increases in blood coagulation parameters are significantly associated with risk of adverse cardiovascular events. We examined the hypothesis that acute exposure to elevated levels of PM causes prothrombotic changes in blood coagulation parameters. Rats with indwelling jugular vein catheters were exposed for 6 hours to filtered air or concentrated ambient PM in New York City air (n = 9 per group per experiment). PM less than 2.5 microm in mass median aerodynamic diameter (PM2.5) was concentrated for animal exposures using a centrifugal concentrator. Blood samples were taken at four time points: before and immediately after exposure and at 12 and 24 hours after the start of exposure. At each time point, six coagulation parameters (platelet count, fibrinogen level, factor VII activity, thrombin-antithrombin complex [TAT] level, tissue plasminogen activator [tPA] activity, and plasminogen activator inhibitor [PAI] activity) were measured as well as all standard blood count parameters. Five concentrated-PM exposure experiments were performed over a period of 8 weeks in the summer of 1999. PM exposure concentrations ranged from 95 to 341 microg/m3. Statistical significance was determined by two-way analysis of variance (ANOVA) on the postexposure data with time and exposure status as main effects. There were no consistent exposure-related effects on any of the end points across the five experiments and no indication of any dose-dependent effects. Most of the statistically significant differences that were observed do not represent adverse effects. Therefore, the results of this study do not indicate that exposure to concentrated ambient PM causes adverse effects on blood coagulation in healthy rats.

Air Pollutants↗

PubMed2006

Exposures to airborne particulate matter and adverse perinatal outcomes: a biologically plausible mechanistic framework for exploring potential effect modification by nutrition.

OBJECTIVES: The specific objectives are threefold: to describe the biologically plausible mechanistic pathways by which exposure to particulate matter (PM) may lead to the adverse perinatal outcomes of low birth weight (LBW), intrauterine growth retardation (IUGR), and preterm delivery (PTD); review the evidence showing that nutrition affects the biologic pathways; and explain the mechanisms by which nutrition may modify the impact of PM exposure on perinatal outcomes. METHODS: We propose an interdisciplinary conceptual framework that brings together maternal and infant nutrition, air pollution exposure assessment, and cardiopulmonary and perinatal epidemiology. Five possible albeit not exclusive biologic mechanisms have been put forth in the emerging environmental sciences literature and provide corollaries for the proposed framework. CONCLUSIONS: Protecting the environmental health of mothers and infants remains a top global priority. The existing literature indicates that the effects of PM on LBW, PTD, and IUGR may manifest through the cardiovascular mechanisms of oxidative stress, inflammation, coagulation, endothelial function, and hemodynamic responses. PM exposure studies relating mechanistic pathways to perinatal outcomes should consider the likelihood that biologic responses and adverse birth outcomes may be derived from both PM and non-PM sources (e.g., nutrition). In the concluding section, we present strategies for empirically testing the proposed model and developing future research efforts.

Air Pollutants↗

PubMedDate not supplied

[Real-time measurement of indoor particulate matter originating from environmental tobacco smoke: a pilot study].

Short-term measurement of suspended particulate matter has been recently made possible since the release of laser-operating portable instruments. Data of a pilot study of field evaluation of environmental tobacco smoke (ETS) with a portable instrument are reported. We analysed the concentrations of total suspended particle (TSP) and of the fine particles PM10, PM7, PM2.5 and PM1 released indoor from a single cigarette, and their levels inside smoking- and non-smoking-areas of a restaurant. The results indicate that ETS creates high level indoor particulate pollution, with concentrations of PM10 exceeding air quality standards. This kind of field evaluation could allow a more careful assessing of short-term exposure to ETS and its relevance to public health.

Air Pollution, Indoor↗

PubMed2004

Quantifying hazardous species in particulate matter derived from fossil-fuel combustion.

An analysis protocol that combines X-ray absorption near-edge structure spectroscopy with selective leaching has been developed to examine hazardous species in size-segregated particulate matter (PM) samples derived from the combustion of fossil fuels. The protocol has been used to identify and determine quantitatively the amounts of three important toxic species in combustion-derived PM: viz., nickel sulfides in residual oil fly ash (ROFA) PM, and Cr(VI) and As(III) species in coal fly ash PM. Although it has been assumed that these toxic species might exist in PM derived from fossil-fuel combustion, the results presented here constitute the first direct determination of them in combustion-derived PM and their potential bioavailability. Detailed information on the presence of these toxic species in PM samples is of significant interest to epidemiological and toxicological studies of the health effects of both source and ambient PM. Additionally, information is obtained on insoluble forms that may be useful for source attribution and on the distribution of phases between size fractions that may be related to formation mechanisms of specific toxic species during combustion.

Air Pollutants↗

PubMed2006

Airborne particulate matter and premature deaths in urban Europe: the new WHO guidelines and the challenge ahead as illustrated by Spain.

Twenty first century epidemiological publications on urban air pollution are confirming that inhalation of fine, airborne particulate matter (PM) has serious chronic human health effects and is a major cause of premature death worldwide. Recently updated recommendations by WHO identify three "Interim Targets" for the stepped reduction in PM levels within world cities in the quest to achieve an annual mean Air Quality Guideline (AQG) concentration of 20 mug/m(3) for particles less than 10 microns in size (PM(10)). In this paper we offer a perspective from Spain, a country with the longest record of reporting pollution data from large numbers of urban traffic sites to a central European database (AIRBASE). We can demonstrate that average annual PM concentrations at urban traffic monitoring stations in many European cities continue to be 50-100% above the WHO AQG, a situation exacerbated by high urban PM(2.5/10) ratios which indicate a dominance of finer, more deeply inhalable particles potentially more detrimental to health. Given that WHO has estimated in 2000 there were well over 250,000 premature deaths in Europe attributable to PM inhalation, such continuing high urban pollution levels are placing a huge burden on European medical resources.

Air Pollution↗

PubMed2005

Comparative study of the formation of oxidative damage marker 8-hydroxy-2'-deoxyguanosine (8-OHdG) adduct from the nucleoside 2'-deoxyguanosine by transition metals and suspensions of particulate matter in relation to metal content and redox reactivity.

An association between exposure to ambient particulate matter (PM) and increased incidence of mortality and morbidity due to lung cancer and cardiovascular diseases has been demonstrated by recent epidemiological studies. Reactive oxygen species (ROS), especially hydroxyl radicals, generated by PM, have been suggested by many studies as an important factor in the oxidative damage of DNA by PM. The purpose of this study was to characterize quantitatively hydroxyl radical generation by various transition metals in the presence of H2O2 in aqueous buffer solution (pH 7.4) and hydroxylation of 2'-deoxyguanosine (dG) to 8-hydroxy-2'-deoxyguanosine (8-OHdG) under similar conditions. The order of metals' redox reactivity and hydroxyl radical production was Fe(II), V(IV), Cu(I), Cr(III), Ni(II), Co(II), Pb(II), Cd(II). Then, we investigated the generation of hydroxyl radicals in the presence of H2O2 by various airborne PM samples, such as total suspended particulate (TSP), PM10, PM2.5 (PM with aerodynamic diameter 10 and 2.5 microm), diesel exhaust particles (DEP), gasoline exhaust particles (GEP) and woodsmoke soot under the same conditions. When suspensions of PMs were incubated with H2O2 and dG at pH 7.4, all particles induced hydroxylation of dG and formation of 8-OHdG in a dose-dependent increase. Our findings demonstrated that PM's hydroxyl radical (HO radical) generating ability and subsequent dG hydroxylation is associated with the concentration of water-soluble metals, especially Fe and V and other redox or ionizable transition metals and not their total metal content, or insoluble metal oxides, via a Fenton-driven reaction of H2O2 with metals. Additionally, we observed, by Electron paramagnetic resonance (EPR), that PM suspensions in the presence of H2O2 generated radical species with dG, which were spin-trapped by 2-methyl-2-nitroso-propane (MNP).

8-Hydroxy-2'-Deoxyguanosine↗

PubMed2002

Use of a stratified oxidative stress model to study the biological effects of ambient concentrated and diesel exhaust particulate matter.

Although several epidemiological studies have shown a positive relationship between exposure to ambient air particulate matter (PM) and adverse health effects in humans, there is still a fundamental lack of understanding of the most toxic particle components and the biological mechanisms through which they act. Since our studies on the biological effects of diesel exhaust particles (DEP) have highlighted the role of reactive oxygen species (ROS), catalyzed by organic chemical compounds, we set out to establish whether this constitutes an oxidative stress model that can be used to study the biological effects of ambient coarse and fine PM. We demonstrate that organic DEP extracts induce a stratified oxidative stress response, leading to heme oxygenase 1 (HO-1) expression at normal GSH/ GSSG ratios, proceed to Jun kinase activation and interleukin 8 (IL-8) production at intermediary oxidative stress levels, and culminate in cellular apoptosis in parallel with a sharp decline in GSH/GSSG ratios. We demonstrate that ambient concentrated air particulates, collected with a particle concentrator and a liquid impinger, mimic the effects of organic DEP extracts at lower oxidative stress levels. While fine PM consistently induced HO-1 expression in all most of the samples collected over a 9-mo survey period, coarse particulates were effective at inducing that effect during fall and winter. Moreover, HO-1 expression was positively correlated to the higher organic carbon (OC) and polyaromatic hydrocarbons (PAHs) content of fine versus coarse PM, as well as the rise in PAH content that occurs in coarse PM during the winter months. Although coarse and fine PM lead to a decrease in cellular glutathione (GSH)/GSSG ratios, oxidative stress did not increase to cytotoxic levels. Taken together, these data demonstrate that it is possible to use the stratified oxidative stress model developed for DEP to interpret the biological effects of coarse and fine PM. This work has important implications for the selection of relevant biological endpoints for in vivo studies.

Air Pollutants↗

PubMed2002

Systemic inflammatory response induced by particulate matter air pollution: the importance of bone-marrow stimulation.

The relationship between the level of particulate air pollution (PM(10)) and the mortality and morbidity rates from respiratory and cardiovascular diseases is well established, but the biological mechanisms responsible for these associations are still unclear. The injurious effects of particulate air pollution may be either local (in the lung) or systemic. Bone-marrow release of leukocytes and platelets is an important component of the systemic inflammatory response. We have developed methods to quantify bone-marrow stimulation and showed in animals that acute exposure to ambient particles accelerates the transit of polymorphonuclear leukocytes (PMN) through the marrow whereas chronic exposure expands the size of the bone marrow pool of PMN. Human studies showed that an episode of severe air pollution stimulates the bone marrow in a manner similar to that observed in animals. In vitro and in vivo studies suggest that alveolar macrophage produce the mediators implicated in the bone marrow response to ambient particles. Cytokines produced in the lung due to deposition of ambient particles also appear in the circulation. In vitro and in vivo studies have shown that PMN recently released from the bone marrow preferentially sequester in pulmonary capillaries, are less chemotactic, and contain more damaging granular enzymes, all factors that potentate their ability to damage alveolar tissue. In animals that naturally develop atherosclerosis, deposition of ambient particles in the lung causes progression of atherosclerotic plaques with phenotypic changes in atherosclerotic plaques characteristic of lesions vulnerable to rupture. We conclude that exposure to ambient particulate matter air pollution induces a systemic inflammatory response that includes the release of inflammatory mediators into the circulation that stimulate the bone marrow to release leukocytes and platelets. We postulate that this systemic response to particulate air pollution augments lung inflammation and changes the phenotype of atherosclerotic plaques to make them more vulnerable to rupture.

Air Pollutants↗

PubMed2001

On-road particulate matter (PM2.5 and PM10) emissions in the Sepulveda Tunnel, Los Angeles, California.

Total and speciated particulate matter (PM2.5 and PM10) emission factors from in-use vehicles were measured for a mixed light- (97.4% LD) and heavy-duty fleet (2.6% HD) in the Sepulveda Tunnel, Los Angeles, CA. Seventeen 1-h test runs were performed between July 23, 1996, and July 27, 1996. Emission factors were calculated from mass concentration measurements taken at the tunnel entrance and exit, the volume of airflow through the tunnel, and the number of vehicles passing through the 582 m long tunnel. For the mixed LD and HD fleet, PM2.5 emission factors in the Sepulveda Tunnel ranged from 0.016 (+/-0.007) to 0.115 (+/-0.019) g/vehicle-km traveled with an average of 0.052 (+/-0.027) g/vehicle.km. PM10 emission factors ranged from 0.030 (+/-0.009) to 0.131 (+/-0.024) g/vehicle. km with an average of 0.069 (+/-0.030) g/vehicle.km. The PM2.5 emission factor was approximately 74% of the PM10 factor. Speciated emission rates and chemical profiles for use in receptor modeling were also developed. PM2.5 was dominated by organic carbon (OC) (31.0 +/- 19.5%) and elemental carbon (EC) (48.5 +/- 20.5%) that together account for 79% (+/-24%) of the total emissions. Crustal elements (Fe, Mg, Al, Si, Ca, and Mn) contribute approximately 7.8%, and the ions Cl-, NO3-, NH3+, SO4(2-), and K+ together constitute another 9.8%. In the PM10 size fraction the particulate emissions were also dominated by OC (31 +/- 12%) and EC (35 +/- 13%). The third most prominent species was Fe (18.5 +/- 9.0%), which is greater than would be expected from purely geological sources. Other geological components (Mg, Al, Si, K, Ca, and Mn) accounted for an additional 12.6%. PM10 emission factors showed some dependence on vehicle speed, whereas PM2.5 did not. For test runs in which the average vehicle speed was 42.6 km/h a 1.7 times increase in PM10 emission factor was observed compared to those runs with an average vehicle speed of 72.6 km/h. Speciated emissions were similar. However, there is significantly greater mass attributable to geological material in the PM10, indicative of an increased contribution from resuspended road dust. The PM2.5 shows relatively good correlation with NOx emissions, which indicates that even at the low percent of HD vehicles, which emit significantly more NOx than LD vehicles, they may also have a significant impact on the PM2.5 levels.

Air Movements↗

PubMed2006

Thermal desorption/pyrolysis coupled with photoionization time-of-flight mass spectrometry for the analysis of molecular organic compounds and oligomeric and polymeric fractions in urban particulate matter.

Atmospheric aerosols are subject to be responsible for human health effects. In this context, besides mass and number concentration of particles, their chemical composition has gained interest recently. However, knowledge about the organic content of particulate matter is still relatively scarce; i.e., only 10-40% of compounds present in the aerosol are as yet identified. By means of a newly developed measurement technique, thermal desorption/photoionization time-of-flight mass spectrometry (TOFMS), organic species evolved from urban aerosol samples collected at Augsburg, Germany, are analyzed. Thereby, compounds desorbed according to a temperature protocol following procedures for OC/EC analysis (120, 250, and 340 degrees C as desorbing temperatures) are ionized by soft, fragmentationless resonance multiphoton ionization (REMPI) and single photon ionization (SPI), respectively. With REMPI-TOFMS, a large variety of PAH is detectable. A comprehensive analysis is enabled by adding SPI-TOFMS, which gives access to aliphatic and carbonylic hydrocarbons as well as alkanoic acids and esters. Analysis of the data showed a high abundance of phenol and guiacol as well as retene, which are known markers for wood combustion. Similar patterns were found with ash from spruce wood combustion. An increase of volatile substances at 340 degrees C gave rise to the suggestion that these compounds are re-formed by pyrolytic decomposition reactions from oligomeric, polymeric, and polyfunctional oxygenated species. This was corroborated by the investigation of the behavior of cellulose acetate, which exhibited a similar pattern in its SPI-TOFMS spectrum at 340 degrees C as the aerosol. More thorough investigations of urban aerosol and source material with respect to problems such as the mass closure of carbonaceous material, indications for source apportionment, and allotment of organic species on a molecular level to fractions of organic and elemental carbon seem feasible with this measurement method.

Adsorption↗

PubMed2005

Characterisation of particulate matter for toxic metals in ambient air of Kochi city, India.

Measurement of respirable suspended particulate matter (RSPM) and analysis of toxic metals in air of Kochi city was carried out for a period of one year, 1997. Seasonal variations of RSPM and toxic metals are analysed to identify the influence of meteorological parameters. The air pollution problem with respect to RSPM and lead is moderately significant especially in winter season. The profile of other toxic metals in RSPM is not much significant. Domestic fuel used mainly coal/wood and petrol/diesel fueled motor vehicles are the major contributors to the RSPM and toxic metals. Various control strategies are delineated for reduction of ambient RSPM and toxic metals in air of Kochi city.

Air Pollutants↗

PubMed2005

Toxic metal content of particulate matter (PM10), within the Greater Area of Athens.

This study presents results from a yearlong particulate matter measurement campaign, conducted across the Greater Athens Area, at four locations, between 1st June 2001 and 31st May 2002. The collected PM(10) 24-h samples were analyzed for nine toxic metals and metalloids (Pb, As, Cd, Ni, Cr, Mn, V, Cu, Hg). Concerning the five elements regulated by the European Union, annual average concentrations of Pb were found below the limit values at all sites, Cd and Ni concentrations were lower than the prospective assessment thresholds at all sites, concentrations of As exceeded the assessment threshold at two sites, while concentrations of Hg were found below detection limits in all samples. Concentration levels of Mn and V were in compliance with the values proposed by the World Health Organization. The seasonal and spatial variability of metal concentrations was examined and site-specific correlation analysis was conducted for the identification of metals with similar origin. The association between trace metals and NO(x) concentrations was explored to account for the impact of automotive sources, at two traffic-impacted sites. Cu was the metal most closely linked with the road transport sector. The relation of concentration levels with the prevalence of winds from different sectors was studied in an effort to investigate the transport of metal particles from various zones of the city. Finally, factor analysis was carried out to extract the main components responsible for the variance of the dataset and to attribute them to specific source categories, with vehicle-related sources being important in all cases.

Air Pollutants↗

PubMed2003

The effects of Asian Dust on particulate matter fractionation in Seoul, Korea during spring 2001.

The concentrations of three different fractions of particulate matter (PM) including PM2.5, PM10, and TSP were determined concurrently during March-May 2001. Measurements of three PM fractions were made at hourly intervals from four different observatory sites located within the city boundary of Seoul. On the basis of this study, we attempted to describe relationships between the occurrences of the Asian Dust (AD) event and its influences on the PM distribution characteristics. The results of our study demonstrated distinct differences between concentrations of PM fractions at AD and non-AD (NAD) periods. The increase of PM observed during the AD episode appeared to be dominated by the coarse, rather than fine, fraction of PM. In addition, it was found that TSP/PM10 ratios were almost constant, while the coarse/fine or TSP/PM2.5 ratios changed noticeably between AD and NAD periods. In most cases, differences in environmental conditions between AD and NAD periods were prominent and proven to be statistically significant. Moreover, the regression relationships between PM and N-oxides indicate that the source processes governing PM levels between the AD and NAD period can be different. The overall results of our analysis were hence helpful enough to distinguish competing processes in AD and NAD periods, while suggesting indirectly the possible control of different source processes on PM fractionation.

Air Pollutants↗

PubMed1998

Pulmonary and cardiovascular effects of acute exposure to concentrated ambient particulate matter in rats.

To examine the biological plausibility of the adverse health effects of ambient particulate matter (PM), we have studied the cardio-pulmonary effects of PM in an animal model of pulmonary hypertension. Normal and monocrotaline-treated rats were exposed, nose-only, for 3 h to filtered air or concentrated ambient PM. At 3 h--but not 24 h--post-exposure, the percentage of neutrophils in peripheral blood was significantly elevated in PM-exposed animals while the percentage of lymphocytes was decreased with no change in white blood cell counts. These changes in white blood cell differential occurred in both normal and monocrotaline-treated animals. Small, but consistent changes in heart rate, but not core temperature, were observed after exposure to concentrated ambient PM. Pulmonary injury, as evidenced by increased protein levels in lavage fluid, occurred only in monocrotaline-treated animals exposed to > 360 microg/m3 PM. The observed pattern of hematological and cardiac changes suggests an activation of the sympathetic stress response.

Air Pollutants↗

PubMed2003

Determination of chloroacetates in atmospheric particulate matter.

Chloroacetates (CAAs) are ubiquitous in the environment. This study presents chloroacetates level in atmospheric particulate matter (APM) collected at Athens center. CAAs have been derivatized to their respective propyl esters and determined by gas chromatography (GC) with electron capture detection (ECD). Monochloroacetate (MCA) was the most abundant, followed by dichloroacetate (DCA) and trichloroacetate (TCA). Concentration values range from 3.0 to 8240 ng g(-1) (0.6-2010 pg m(-3)). Correlations to meteorological and pollution parameters are discussed, indicating that car exhausts may be a direct or indirect source of MCA, but origin from natural marine sources may also be relevant.

Acetates↗