No full-text available
To read the full-text of this research,
you can request a copy directly from the authors.
Development and characterization of an exposure generation system to investigate the health effects of particles from fresh and aged traffic emissions
Abstract
Atmospheric photochemical reactions of vehicular primary emissions result in the formation of secondary organic aerosol (SOA). This is the first study that has investigated the toxicity of secondary particles based on fleet vehicular emissions. We developed methods for photochemical oxidation of traffic primary emissions to produce mixtures of primary and/or secondary particles suitable for animal exposures. The exposure generation system produced test atmospheres of primary (P), aged primary plus SOA (P + SOA), or SOA particles suitable for animal exposures. The system consists of (1) a sampling system to extract the traffic emissions from the plenum of a highway tunnel ventilation stack, (2) a photochemical chamber to simulate atmospheric aging, and (3) a nonselective diffusion denuder to remove gaseous pollutants prior to exposure. In the presence of traffic primary particles (P + SOA), a longer mean residence time resulted in a higher SOA yield. Higher baseline plenum primary particle mass concentration resulted in lower SOA yield. In the absence of primary particles (SOA), higher plenum gas concentrations resulted in higher SOA yield. Secondary aerosol was largely organic but contained some nitrate and sulfate. Formation of secondary aerosol is influenced significantly by reaction of primary gases with ·OH. The system (1) provides adequate flow and stable chamber output of P, P + SOA, and SOA for characterization and animal exposures and (2) generates reproducible exposure atmospheres of P, P + SOA, and SOA, all at consistent mass concentrations.
... As noted earlier, these chambers are not fully represen- tative of the ambient environment due to the reduced complexity of the atmosphere. Both sets of studies utilized the same equipment, and methodological papers have been published for both ( Papapostolou et al. 2011Papapostolou et al. , 2013Ruiz et al. 2007a,b). The power plant experimental results were published in a special issue of Inhalation Toxicology; an introduction/overview and results summary are provided by Godleski et al. (2011a) and (2011b), respectively. ...
... In the full-scale mobile source component of TERESA, primary emissions from a highway tunnel ventilation stack were withdrawn, aged in a photochemical cham- ber, and used for experimental exposures in Sprague- Dawley rats. About 35 000 vehicles per day traveled through the tunnel, of which approximately 6% were heavy-duty diesel vehicles ( Papapostolou et al. 2013). It is important to note that emissions did not contain only vehicle exhaust, but also brake wear PM, tire wear PM, and road dust. ...
... It is important to note that emissions did not contain only vehicle exhaust, but also brake wear PM, tire wear PM, and road dust. Methods were developed to photochem- ically oxidize the primary emissions to form SOA ( Papapostolou et al. 2013) and to denude gases from the exposure atmospheres ( Papapostolou et al. 2011). Effects on respiratory pattern, inflammation, and in vivo oxidative stress were evaluated by Diaz et al. (2013), while blood pressure effects were reported by Lamoureux et al. (2013). ...
Air pollution is a complex mixture of gas-, vapor-, and particulate-phase materials comprised of inorganic and organic species. Many of these components have been associated with adverse health effects in epidemiological and toxicological studies, including a broad spectrum of carbonaceous atmospheric components. This paper reviews recent literature on the health impacts of organic aerosols, with a focus on specific sources of organic material; it is not intended to be a comprehensive review of all the available literature. Specific emission sources reviewed include engine emissions, wood/biomass combustion emissions, biogenic emissions and secondary organic aerosol (SOA), resuspended road dust, tire and brake wear, and cooking emissions. In addition, recent findings from large toxicological and epidemiological research programs are reviewed in the context of organic PM, including SPHERES, NPACT, NERC, ACES, and TERESA. A review of the extant literature suggests that there are clear health impacts from emissions containing carbon-containing PM, but difficulty remains in apportioning responses to certain groupings of carbonaceous materials, such as organic and elemental carbon, condensed and gas phases, and primary and secondary material. More focused epidemiological and toxicological studies, including increased characterization of organic materials, would increase understanding of this issue.
... The gaseous fraction of traffic-derived air pollution (specifically Carbon Monoxide) has mainly been utilized as a marker of the exposure . Indeed, a number of recent studies show low levels of carbon monoxide (Wellenius et al. 2004; Dolinay et al. 2004; Kim et al. 2006; Morse and Choi 2008; Ryter et al. 2004) and nitric oxide (Gianetti et al. 2002; Sethi et al. 2008) to have anti-inflammatory, vasorelaxant, and other potentially beneficial effects The companion papers in this series describe the development and characterization of the exposure generation system (Papapostolou et al. 2012) and the cardiovascular results from the exposure study (Lamoureux et al. 2012). ...
... Experimental set-up These studies were carried out in a field laboratory inside the ventilation building of a traffic tunnel in the Northeastern USA. The tunnel and the exposure generation system are described in detail in a companion publication (Papapostolou et al. 2012) and are summarized here. Briefly, the exposure generation system consists of three major components: a sampling system to extract vehicular emissions from the tunnel plenum, a photochemical reaction chamber to simulate atmospheric photochemical oxidation, and a non-selective denuder to remove gaseous pollutants prior to exposure (Papapostolou et al. 2011a). ...
... The aerosol was then diluted with clean air and mixed inside the chamber with sufficient O 3 to titrate NO. The lamps were turned on and the emissions were photochemically oxidized to generate a mixture of aged primary particles and secondary aerosol, mostly organic but also containing a small fraction of sulfate and nitrate (Papapostolou et al. 2012). c. ...
Air pollution is comprised of a complex mixture of gaseous and particulate pollutants emitted from multiple sources. During transport in the atmosphere, emissions undergo photochemical reactions, which may change their toxicity. Toxicological and epidemiological studies have linked vehicular emissions to respiratory and cardiovascular health effects. The aim of this study was to investigate the toxicity of primary and secondary traffic particles. Male Sprague–Dawley rats were exposed to either filtered air (control group) or one of three types of atmospheres: fresh primary particles from a major traffic tunnel plenum (P); secondary organic aerosol formed from photochemical oxidation of primary tunnel gases after filtration of primary particles (SOA); or photochemically aged primary particles plus secondary organic aerosols (P + SOA). In each exposure, 80–90 % of pollutant gases were removed using a non-selective denuder. Animals were exposed for 5 h per day, with varying number of days of exposure. Outcomes included: breathing pattern, broncho-alveolar lavage (BAL), complete blood count, and in vivo chemiluminescence (IVCL). Consistent mass concentration (approximately 50 μg/m3) was achieved for all exposures. Respiratory data showed many changes with each exposure type. All exposures produced decreases in tidal volume, minute volume, inspiratory and expiratory flows. There were mild inflammatory changes in BAL, with increased neutrophils for the SOA and P + SOA exposures and lymphocytes for the P and P + SOA exposure, with no changes in any test exposure for total protein, β-NAG or IVCL. All exposures produced changes compared to filtered air. Exposures containing particles (P and P + SOA) had stronger effects than SOA.
... Then, if there are more reactive gases inside the chamber, more products are formed. These shape of the size distribution of secondary particles in these chamber experiments is similar to the shape found in the chamber experiments for exhaust escape gases in tunnel experiments according to [31,46]. ...
... Then, if there are more reactive gases inside the chamber, more products are formed. These shape of the size distribution of secondary particles in these chamber experiments is similar to the shape found in the chamber experiments for exhaust escape gases in tunnel experiments according to [31,46]. In the chamber, non-refractory PM1.0 was measured during the UV irradiation with the ACSM. Figure 5 shows the results. ...
The main emission source in Central and Southern Chilean cities is biomass combustion from residential heating and cooking due to old combustion technologies that are still widely utilized. In order to improve our understanding of biomass burning pollution and how it ages in the atmosphere, emissions from a pellet and wood stoves were studied with the aid of a photochemical chamber. Firewood combustion is an inefficient process that produces higher chamber loading of primary emission (gases and particles) compared to pellets. When these emissions are exposed to UV irradiation secondary particles are formed. However, with both fuels the secondary particle concentration was negligible with regards to the primary initial particle concentration. Observations show that when the initial mass is the same, firewood combustion emissions are more rapidly oxidized compared to emissions from pellet combustion. Particle aging evolution inside the chamber was evaluated using fragment tracer signals, via the mass fractions f44 vs f43 and f44 vs f60 triangles plots. For the same UV irradiation time, it was found that primary particles emitted form from firewood combustion show a slower aging rate compared to those emitted from pellet combustion, but this is due to high primary loading from wood combustion. Particle aging observed inside the chamber was similar to that found it in ambient urban air of Santiago de Chile in spring of 2011, indicating that chamber measurements can be a good indicator for some atmospheric processes. Levoglucosan, a well-known tracer for biomass combustion was also studied. It was found that wood stoves yielded higher levels than pellet stoves. This is due to the higher fuel combustion efficiency in pellet stoves, which yield low levoglucosan levels, making it difficult to use it for evaluation of the impact of pellet emissions on pollution.
... In order to fully understand the behavioral consequences of near roadway exposures during early life, we leveraged an innovative real-time rodent exposure facility to expose developing rats. Since composition, dose, duration, intensity, mixtures, and timing of air pollution exposures can influence biological outcomes [40][41][42] , we designed our study to be translationally relevant by representing human TRAP exposure and combined realworld composition of pollutants and dosing in an animal model. The detailed components of the exposure can be found in our Supplementary Information and are reported in comprehensive detail in Bein et al. (under review) 43 . ...
Epidemiological studies consistently implicate traffic-related air pollution (TRAP) and/or proximity to heavily trafficked roads as risk factors for developmental delays and neurodevelopmental disorders (NDDs); however, there are limited preclinical data demonstrating a causal relationship. To test the effects of TRAP, pregnant rat dams were transported to a vivarium adjacent to a major freeway tunnel system in northern California where they were exposed to TRAP drawn directly from the face of the tunnel or filtered air (FA). Offspring remained housed under the exposure condition into which they were born and were tested in a variety of behavioral assays between postnatal day 4 and 50. To assess the effects of near roadway exposure, offspring of dams housed in a standard research vivarium were tested at the laboratory. An additional group of dams was transported halfway to the facility and then back to the laboratory to control for the effect of potential transport stress. Near roadway exposure delayed growth and development of psychomotor reflexes and elicited abnormal activity in open field locomotion. Near roadway exposure also reduced isolation-induced 40-kHz pup ultrasonic vocalizations, with the TRAP group having the lowest number of call emissions. TRAP affected some components of social communication, evidenced by reduced neonatal pup ultrasonic calling and altered juvenile reciprocal social interactions. These findings confirm that living in close proximity to highly trafficked roadways during early life alters neurodevelopment.
... Most animal studies published to date, however, have employed exposure paradigms that do not capture the complexity or spatiotemporal dynamics of real-world TRAP exposures. Since composition, dose, and timing of air pollution exposures may influence biological outcomes [25][26][27] , translating the relevance of much of the published animal literature to the human condition is problematic. To better represent human TRAP exposures in an animal model, we developed an exposure paradigm that preserves the gaseous and particulate components of real-world TRAP and captures daily fluctuations in pollutant levels. ...
Epidemiological studies link traffic-related air pollution (TRAP) to increased risk for various neurodevelopmental disorders (NDDs); however, there are limited preclinical data demonstrating a causal relationship between TRAP and adverse neurodevelopmental outcomes. Moreover, much of the preclinical literature reports effects of concentrated ambient particles or diesel exhaust that do not recapitulate the complexity of real-world TRAP exposures. To assess the developmental neurotoxicity of more realistic TRAP exposures, we exposed male and female rats during gestation and early postnatal development to TRAP drawn directly from a traffic tunnel in Northern California and delivered to animals in real-time. We compared NDD-relevant neuropathological outcomes at postnatal days 51–55 in TRAP-exposed animals versus control subjects exposed to filtered air. As indicated by immunohistochemical analyses, TRAP significantly increased microglial infiltration in the CA1 hippocampus, but decreased astrogliosis in the dentate gyrus. TRAP exposure had no persistent effect on pro-inflammatory cytokine levels in the male or female brain, but did significantly elevate the anti-inflammatory cytokine IL-10 in females. In male rats, TRAP significantly increased hippocampal neurogenesis, while in females, TRAP increased granule cell layer width. TRAP had no effect on apoptosis in either sex. Magnetic resonance imaging revealed that TRAP-exposed females, but not males, also exhibited decreased lateral ventricular volume, which was correlated with increased granule cell layer width in the hippocampus in females. Collectively, these data indicate that exposure to real-world levels of TRAP during gestation and early postnatal development modulate neurodevelopment, corroborating epidemiological evidence of an association between TRAP exposure and increased risk of NDDs.
... Its contribution to global warming (GW) and climate change (CC) through greenhouse gas (GHG) emissions is indeed substantial (European Commission 2018), whereas another important environmental impact is the degradation of air quality at local levels from emissions of various air pollutants (Amin et al. 2017;Chin 1996;Danielis and Chiabai 1998;Rayfield et al. 1998). Because road transport is "the mode of transport of proximity," its emissions-close to human receptors-directly expose populations to higher risks of respiratory diseases related to urban air pollution (Papapostolou et al. 2013;Vouitsis et al. 2017). Therefore, the transport sector in general and road transport in particular must reduce or even eliminate these environmental impacts to ensure the sustainable mobility of goods and people. ...
Emissions reduction has emerged as one of the principal targets in the planning and designing of road alignment today, and intelligent design methods can help optimize road alignment as a response toward more sustainable road infrastructures. The largest share of emissions in road transport occurs in the use phase; hence, considering vehicles’ behavior already in the early stages of the planning process is crucial. This study compares earthwork costs, fuel costs, and tank-to-wheel emissions of alternative road vertical alignments using a spline linear programming (LP) optimization method. The traditional minimal earthwork cost model is tailored and augmented with a fuel item to account for vehicle fuel costs. Three options are considered, including an earthwork-based (EW) optimal road alignment, a balanced earthwork-and-fuel cost (EW-FC) optimal alignment, and a minimal fuel cost (FC) alignment. Calculations are done for a reference test heavy-duty vehicle assumed to operate at uniform speed. The results exhibited that, although leading to some increase in earthwork costs, a design for balanced EW-FC cost yields substantial fuel budget and related emissions savings.
... Ozone may react with organic compounds on the surface of particles, potentially changing both the composition and reactivity of the aged particles compared to the unaltered primary particles . Furthermore, primary traffic-derived particles include a larger mass fraction of non-polar water-insoluble organic compounds compared to oxidized aged particles which form more polar compounds (Lovett et al., 2018;Papapostolou et al., 2013). The non-polar components, such as polycyclic aromatic hydrocarbons, may more readily permeate the hydrophobic lipid-bilayer of cell membranes, resulting in greater overall toxicity (Lovett et al., 2018). ...
Epidemiology studies over the past five decades have provided convincing evidence that exposure to air pollution is associated with multiple adverse health outcomes, including increased mortality. Air pollution is a complex mixture of particles, vapors and gases emitted from natural and anthropogenic sources as well as formed through photochemical transformation processes. In metropolitan areas, air pollutants from combustion emissions feature a blend of emitted particles, oxides of carbon, sulfur and nitrogen, volatile organic compounds, and secondary reaction products, such as ozone, nitrogen dioxide, and secondary organic aerosols. Because many of the primary and transformed pollutants track together, their relative contributions to health outcomes are difficult to disentangle. Aside from the criteria pollutants O3 and NO2 and some of the simpler aldehydes (e.g. formaldehyde and acrolein), other products from photochemical processes are a particularly vexing class of chemicals to investigate since they comprise a dynamic ill-defined complex mixture in both particulate and gas phases. The purpose of this review was to describe and compare health effects of freshly emitted versus oxidatively or photochemically aged air pollutants. In some cases, (e.g. single volatile organic compounds) photochemical transformation resulted in marked enhancements in toxicity through formation of both known and unidentified reaction products, while in other examples (e.g. aging of automobile emissions) the potentiation of effect was variable. The variation in experimental design, aging system employed, concentration and type of starting agent, and toxicity endpoints make comparisons between different studies exceedingly difficult. A more systematic approach with a greater emphasis on higher throughput screening and computational toxicology is needed to fully answer under what conditions oxidatively- or photochemically-transformed pollutants elicit greater health effects than primary emissions.
... Teflon filter media (47 mm, 2.0 µm pore, Pall Corporation Inc., US) 8 was used to collect SOA for toxicological analysis. After sampling, the filters were stored at -20° 154 In order to establish methodology for the Biofuel Toxicology Study, primary particles (PM) were 185 collected on Teflon filters at a field laboratory in an urban tunnel as a source of traffic related air 186 pollution rich in organic components (Papapostolou et al, 2013). These were used as a surrogate 187 for the biofuel samples in order to determine methods of optimal extraction from the filters, to 188 confirm that published methods used for resuspension of organic rich particulate were optimal, to 189 establish dose ranges to be used, and to determine the optimal time after instillation for incidental food aspiration, food was removed 4 hours before the procedure. ...
Background:
Ethanol vehicles release exhaust gases that contribute to the formation of secondary organic aerosols (SOA).
Objective:
To determine in vivo toxicity resulting from exposure to SOA derived from vehicles using different ethanol-gasoline blends (E0, E10, E22, E85W, E85S, E100).
Methods:
Exhaust emissions from vehicles using ethanol blends were delivered to a photochemical chamber and reacted to produce SOA. The aerosol samples were collected on filters, extracted, and dispersed in an aqueous solutions and intratracheally instilled into Sprague Dawley rats in doses of 700 μg/0.2 ml. After 45 min and 4 h pulmonary and cardiac chemiluminescence (CL) was measured to estimate the amount of reactive oxygen species (ROS) produced in the lungs and heart. Inflammation was measured by differential cell count in bronchoalveolar lavages (BAL).
Results:
Statistically and biologically significant differences in response to secondary particles from the different fuel formulations were detected. Compared to the control group, animals exposed to SOA from gasoline (E0) showed a significantly higher average CL in the lungs at 45 min. The highest CL averages in the heart were observed in the groups exposed to SOA from E10 and pure ethanol (E100) at 45 min. BAL of animals exposed to SOA from E0 and E85S had a significant increased number of macrophages at 45 min. BAL neutrophil count was increased in the groups exposed to E85S (45 min) and E0 (4 h). Animals exposed to E0 and E85W had increased BAL lymphocyte count compared to the control and the other exposed groups.
Discussion:
Our results suggest that SOA generated by gasoline (E0), followed by ethanol blends E85S and E85W, substantially induce oxidative stress measured by ROS generation and pulmonary inflammation measured by the recruitment of white blood cells in BAL.
... Environmental chambers have been an indispensable tool in studying gas-phase atmospheric chemistry (Cocker et al., 2001) and pollutant exposure (Papapostolou et al., 2013) because they can provide controlled environments. Over the past years, there have been several studies on sensor performance evaluation that involved environmental chambers. ...
A state-of-the-art integrated chamber system has been developed for evaluating the performance of low-cost air quality sensors. The system contains two professional grade chamber enclosures. A 1.3 m³ stainless-steel outer chamber and a 0.11 m³ Teflon-coated stainless-steel inner chamber are used to create controlled aerosol and gaseous atmospheres, respectively. Both chambers are temperature and relative humidity controlled with capability to generate a wide range of environmental conditions. The system is equipped with an integrated zero-air system, an ozone and two aerosol generation systems, a dynamic dilution calibrator, certified gas cylinders, an array of Federal Reference Method (FRM), Federal Equivalent Method (FEM), and Best Available Technology (BAT) reference instruments and an automated control and sequencing software. Our experiments have demonstrated that the chamber system is capable of generating stable and reproducible aerosol and gas concentrations at low, medium, and high levels. This paper discusses the development of the chamber system along with the methods used to quantitatively evaluate sensor performance. Considering that a significant number of academic and research institutions, government agencies, public and private institutions, and individuals are becoming interested in developing and using low-cost air quality sensors, it is important to standardize the procedures used to evaluate their performance. The information discussed herein provides a roadmap for entities who are interested in characterizing air quality sensors in a rigorous, systematic and reproducible manner.
... Especially in the densely-built environment of city centres, vehicle exhaust pollutants are trapped within road canyons, forming local concentration hot-spots. For these reasons, traffic and its associated emissions have been directly linked to adverse health effects (HEI, 2010;Papapostolou et al., 2013). ...
This work presents a new set of exhaust particulate emission factors for light and heavy duty vehicles and different driving conditions (urban, rural and highway). The emission factors, building upon COPERT methodology, are expressed in terms of particulate mass (PM), particle number (PN) and as particle size distributions, addressing current and future vehicle technologies, as well as conventional and alternative fuels. All emission factors correspond to fine particles (PM2.5), as the coarse fraction (PM2.5-10) is negligible in primary vehicle emissions. PN emission factors refer to both total and solid particles to cover typical engine exhaust. The set of emission factors is a consistent set of information and can be useful to inventory compilers, air quality researchers and as input to impact assessment studies for policy options.
... Exposure tubes were maintained at 1.5 L/min continuous air flow and monitored with plethysmographic transducers (Buxco Electronics, Wilmington, NC) as previously described along with the exposure system [11,13]. Aerosol was oxidized in a photochemical reaction chamber with enough ozone (O 3 ) added to titrate vehicular nitric oxide (NO) exhaust and expedite stable secondary particulate generation [14]. After a 4-h residence, aerosol was delivered continuously via two parallel denuders [15]-reducing gaseous pollutant concentrations by 80-90%-to animal exposure tubes. ...
Background
Epidemiological studies have linked exposures to ambient fine particulate matter (PM2.5) and traffic with autonomic nervous system imbalance (ANS) and cardiac pathophysiology, especially in individuals with preexisting disease. It is unclear whether metabolic syndrome (MetS) increases susceptibility to the effects of PM2.5. We hypothesized that exposure to traffic-derived primary and secondary organic aerosols (P + SOA) at ambient levels would cause autonomic and cardiovascular dysfunction in rats exhibiting features of MetS. Male Sprague Dawley (SD) rats were fed a high-fructose diet (HFrD) to induce MetS, and exposed to P + SOA (20.4 ± 0.9 μg/m3) for 12 days with time-matched comparison to filtered-air (FA) exposed MetS rats; normal diet (ND) SD rats were separately exposed to FA or P + SOA (56.3 ± 1.2 μg/m3). ResultsIn MetS rats, P + SOA exposure decreased HRV, QTc, PR, and expiratory time overall (mean effect across the entirety of exposure), increased breathing rate overall, decreased baroreflex sensitivity (BRS) on three exposure days, and increased spontaneous atrioventricular (AV) block Mobitz Type II arrhythmia on exposure day 4 relative to FA-exposed animals receiving the same diet. Among ND rats, P + SOA decreased HRV only on day 1 and did not significantly alter BRS despite overall hypertensive responses relative to FA. Correlations between HRV, ECG, BRS, and breathing parameters suggested a role for autonomic imbalance in the pathophysiologic effects of P + SOA among MetS rats. Autonomic cardiovascular responses to P + SOA at ambient PM2.5 levels were pronounced among MetS rats and indicated blunted vagal influence over cardiovascular physiology. Conclusions
Results support epidemiologic findings that MetS increases susceptibility to the adverse cardiac effects of ambient-level PM2.5, potentially through ANS imbalance.
... The contribution of SOC to the total amount of OC showed an analogous monthly variation, ranging from 30 % in July, to ∼70 % in February. Initially, an increase in SOC levels from winter to summer was expected since volatile and semivolatile organic compounds are mainly oxidized in the atmosphere by OH radicals and ozone yielding less volatile products and thus increasing the formation of secondary organic aerosols (Donahue et al. 2006;Papapostolou et al. 2013). In fact, several previous studies have shown an increase in SOC concentrations during periods of maximum photochemical activity (Grivas et al. 2012;Kim et al. 2012;Na et al. 2004;Plaza et al. 2011;Russel and Allen 2004). ...
The aim of the present study is to evaluate the possible influence of cement works on carbonaceous aerosol concentrations in the western Mediterranean. A PM2.5 and PM10 sampling campaign was performed between September 2005 and August 2006 in a suburban area close to two cement plants in southeastern Spain. All the samples were analyzed for elemental carbon (EC) and organic carbon (OC) using a thermal-optical method. The percentage contribution of total carbon to annual PM mass concentrations was 20 % for PM2.5 and 10 % for PM10. These values were lower than those reported for other European urban and industrial locations because of a higher proportion of crustal matter and secondary inorganic aerosols in the study area. The seasonal cycle of OC concentrations, with higher values in winter than in summer, was influenced by the transport of cement plants' emissions to the sampling site, as corroborated by the results obtained from the CPF analysis. In contrast, no clear effect of cement plants' emissions on EC concentrations could be established. The concentrations of secondary organic carbon (SOC) in the PM2.5 fraction were estimated using the EC tracer method. The contribution of SOC to the annual OC concentration was 50 %, varying between 30 % in July and 70 % in February. Contrary to expectations, SOC levels also exhibited a summer minimum, suggesting that photochemistry cannot be considered to be the leading factor in the formation of secondary organic aerosols in the research area.
Associations between exposure to fine particulate matter and blood pressure responses have been reported in epidemiological studies but findings have proven inconsistent. The objective of this study was to measure effects of primary and secondary components of traffic-derived fine particulate matter (PM2.5) on blood pressure (BP). Sprague–Dawley rats were exposed to fresh primary vehicular particles (P), secondary organic aerosol (SOA), photochemically aged primary plus secondary organic aerosols (P + SOA) or filtered air for 5 h per day for three consecutive weeks. Particle concentration target was 50 μg/m3 for all exposures. Blood pressure parameters were measured continuously using implanted transmitters. Systolic (SBP) and diastolic blood pressure (DBP), mean pressure, pulse pressure, and heart rate responses were assessed using mixed effects models. Exposure to P resulted in increased SBP (p = 0.03) and DBP (p = 0.05) that was sustained across weeks. SOA exposure resulted in increases in SBP (p = 0.07) and DBP (p = 0.01) on the first day with this effect decreasing significantly across exposure days (p < 0.0001). P + SOA showed significant increases in SBP (p = 0.002) and DBP (p < 0.0001) across weeks with a magnitude of effect equaling the approximate average of the effect estimates of the P and SOA exposures. Double Sham exposures following SOA and P + SOA showed compensatory decreases in SBP and DBP. No exposure had a significant effect on heart rate. Primary and secondary traffic derived aerosols can substantially increase SBP and DBP, but these increases are lost with continued exposures. Compensatory BP responses resulting after exposure to secondary particles require further investigation to define BP control mechanisms.
Air pollution is comprised of a complex mixture of gaseous and particulate pollutants emitted from multiple sources. During transport in the atmosphere, emissions undergo photochemical reactions, which may change their toxicity. Toxicological and epidemiological studies have linked vehicular emissions to respiratory and cardiovascular health effects. The aim of this study was to investigate the toxicity of primary and secondary traffic particles. Male Sprague–Dawley rats were exposed to either filtered air (control group) or one of three types of atmospheres: fresh primary particles from a major traffic tunnel plenum (P); secondary organic aerosol formed from photochemical oxidation of primary tunnel gases after filtration of primary particles (SOA); or photochemically aged primary particles plus secondary organic aerosols (P + SOA). In each exposure, 80–90 % of pollutant gases were removed using a non-selective denuder. Animals were exposed for 5 h per day, with varying number of days of exposure. Outcomes included: breathing pattern, broncho-alveolar lavage (BAL), complete blood count, and in vivo chemiluminescence (IVCL). Consistent mass concentration (approximately 50 μg/m3) was achieved for all exposures. Respiratory data showed many changes with each exposure type. All exposures produced decreases in tidal volume, minute volume, inspiratory and expiratory flows. There were mild inflammatory changes in BAL, with increased neutrophils for the SOA and P + SOA exposures and lymphocytes for the P and P + SOA exposure, with no changes in any test exposure for total protein, β-NAG or IVCL. All exposures produced changes compared to filtered air. Exposures containing particles (P and P + SOA) had stronger effects than SOA.
The study presented here is a laboratory pilot study using diluted car exhaust from a single vehicle to assess differences in toxicological response between primary emissions and secondary products resulting from atmospheric photochemical reactions of gas phase compounds with O₃, OH and other radicals. Sprague Dawley rats were exposed for 5 h to either filtered room air (sham) or one of two different atmospheres: (i) diluted car exhaust (P)+Mt. Saint Helens Ash (MSHA); (ii) P+MSHA+secondary organic aerosol (SOA, formed during simulated photochemical aging of diluted exhaust). Primary and secondary gases were removed using a nonselective diffusion denuder. Continuous respiratory data was collected during the exposure, and bronchoalveolar lavage (BAL) and complete blood counts (CBC) were performed 24 h after exposure. ANOVA models were used to assess the exposure effect and to compare those effects across different exposure types. Total average exposures were 363 ± 66 μg/m³ P+MSHA and 212 ± 95 µg/m³ P+MSHA+SOA. For both exposures, we observed decreases in breathing rate, tidal and minute volumes (TV, MV) and peak and median flows (PIF, PEF and EF50) along with increases in breathing cycle times (Ti, Te) compared to sham. These results indicate that the animals are changing their breathing pattern with these test atmospheres. Exposure to P+MSHA+SOA produced significant increases in total cells, macrophages and neutrophils in the BAL and in vivo chemiluminescence of the lung. There were no significant differences in CBC parameters. Our data suggest that simulated atmospheric photochemistry, producing SOA in the P+MSHA+SOA exposures, enhanced the toxicity of vehicular emissions.
The toxicological evaluation of realistic emissions of source aerosols (TERESA) study seeks to delineate health effects of aerosols formed from emissions of particulate matter sources. This series of papers reports the findings of experiments using coal-fired power plants as the source of emissions and this paper summarizes the findings and knowledge acquired from these studies. Emissions were drawn directly from the stacks of three coal-fired power plants in the US, and photochemically aged in a mobile laboratory to simulate downwind power plant plume processing. The power plants used different sources of coal and had different emission controls. Exposure scenarios included primary particles, secondary particles and mixtures of these with common atmospheric constituents (α-pinene and ammonia). Extensive exposure characterization was carried out, and toxicological outcomes were evaluated in Sprague-Dawley rats exposed to different emission scenarios. Breathing pattern, pulmonary inflammatory responses, in vivo pulmonary and cardiac chemiluminescence and cardiac response in a model of acute myocardial infarction were assessed. The results showed no response or relatively mild responses to the inhaled aerosols studied; complex scenarios which included oxidized emissions and α-pinene to simulate biogenic secondary organic aerosol tended to induce more statistically significant responses than scenarios of oxidized and non-oxidized emissions alone. Relating adverse effects to specific components did not consistently identify a toxic constituent. These findings are consistent with most of the previously published studies using pure compounds to model secondary power plant emissions, but importantly add substantial complexity and thus have considerable merit in defining toxicological responses.
Laboratory experiments simulating atmospheric aging of motor vehicle exhaust emissions were conducted using a single vehicle and a photochemical chamber. A compact automobile was used as a source of emissions. The vehicle exhaust was diluted with ambient air to achieve carbon monoxide (CO) concentrations similar to those observed in an urban highway tunnel. With the car engine idling, it is expected that the CO concentration is a reasonable surrogate for volatile organic compounds (VOCs) emissions. Varying the amount of dilution of the exhaust gas to produce different CO concentrations, allowed adjustment of the concentrations of VOCs in the chamber to optimize production of secondary organic aerosol (SOA) needed for animal toxicological exposures. Photochemical reactions in the chamber resulted in nitric oxide (NO) depletion, nitrogen dioxide (NO₂) formation, ozone (O₃) accumulation, and SOA formation. A stable SOA concentration of approximately 40 μg m⁻³ at a chamber mean residence time of 30 min was achieved. This relatively short mean residence time provided adequate chamber flow output for both particle characterization and animal exposures. The chamber was operated as a continuous flow reactor for animal toxicological tests. SOA mass generated from the car exhaust diluted with ambient air was almost entirely in the ultrafine mode. Chamber performance was improved by using different types of seed aerosol to provide a surface for condensation of semivolatile reaction products, thus increasing the yield of SOA. Toxicological studies using Sprague-Dawley rats found significant increases of in vivo chemiluminescence in lungs following exposure to SOA.
Determining the health impacts of sources and components of fine particulate matter (PM(2.5)) is an important scientific goal. PM(2.5) is a complex mixture of inorganic and organic constituents that are likely to differ in their potential to cause adverse health outcomes. The Toxicological Evaluation of Realistic Emissions of Source Aerosols (TERESA) study focused on two PM sources--coal-fired power plants and mobile sources--and sought to investigate the toxicological effects of exposure to emissions from these sources. The set of papers published here document the power plant experiments. TERESA attempted to delineate health effects of primary particles, secondary (aged) particles, and mixtures of these with common atmospheric constituents. TERESA involved withdrawal of emissions from the stacks of three coal-fired power plants in the United States. The emissions were aged and atmospherically transformed in a mobile laboratory simulating downwind power plant plume processing. Toxicological evaluations were carried out in laboratory rats exposed to different emission scenarios with extensive exposure characterization. The approach employed in TERESA was ambitious and innovative. Technical challenges included the development of stack sampling technology that prevented condensation of water vapor from the power plant exhaust during sampling and transfer, while minimizing losses of primary particles; development and optimization of a photochemical chamber to provide an aged aerosol for animal exposures; development and evaluation of a denuder system to remove excess gaseous components; and development of a mobile toxicology laboratory. This paper provides an overview of the conceptual framework, design, and methods employed in the study.
The Toxicological Evaluation of Realistic Emission Source Aerosols (TERESA) project assessed primary and secondary particulate by simulating the chemical reactions that a plume from a source might undergo during atmospheric transport and added other atmospheric constituents that might interact with it. Three coal-fired power plants with different coal and different emission controls were used. Male Sprague-Dawley rats were exposed for 6 h to either filtered air or aged aerosol from the power plant. Four exposure scenarios were studied: primary particles (P); primary + secondary (oxidized) particles (PO); primary + secondary (oxidized) particles + SOA (POS); and primary + secondary (oxidized) particles neutralized + SOA (PONS). Exposure concentrations varied by scenario to a maximum concentration of 257.1 ± 10.0 μg/m(3). Twenty-four hours after exposure, pulmonary cellular responses were assessed by bronchoalveolar lavage (BAL), complete blood count (CBC), and histopathology. Exposure to the PONS and POS scenarios produced significant increases in BAL total cells and macrophage numbers at two plants. The PONS and P scenarios were associated with significant increases in BAL neutrophils and the presence of occasional neutrophils and increased macrophages in the airways and alveoli of exposed animals. Univariate analyses and random forest analyses showed that increases in total cell count and macrophage cell count were significantly associated with neutralized sulfate and several correlated measurements. Increases in neutrophils in BAL were associated with zinc. There were no significant differences in CBC parameters or blood vessel wall thickness by histopathology. The association between neutrophils increases and zinc raises the possibility that metals play a role in this response.
Hourly concentrations of ambient fine particle sulfate and carbonaceous aerosols (elemental carbon [EC], organic carbon [OC], and black carbon [BC]) were measured at the Harvard-U.S. Environmental Protection Agency Supersite in Boston, MA, between January 2007 and October 2008. These hourly concentrations were compared with those made using integrated filter-based measurements over 6-day or 24-hr periods. For sulfate, the two measurement methods showed good agreement. Semicontinuous measurements of EC and OC also agreed (but not as well as for sulfate) with those obtained using 24-hr integrated filter-based and optical BC reference methods. During the study period, 24-hr PM2.5 (particulate matter [PM] < or = 2.5 microm in aerodynamic diameter) concentrations ranged from 1.4 to 37.6 microg/m3, with an average of 9.3 microg/m3. Sulfate as the equivalent of ammonium sulfate accounted for 39.1% of the PM2.5 mass, whereas EC and OC accounted for 4.2 and 35.2%, respectively. Hourly sulfate concentrations showed no distinct diurnal pattern, whereas hourly EC and BC concentrations peaked during the morning rush hour between 7:00 and 9:00 a.m. OC concentrations also exhibited nonpronounced, small peaks during the day, most likely related to traffic, secondary organic aerosol, and local sources, respectively.
The hypothesis of this study was that exposing diesel exhaust (DE*) to the atmosphere transforms its composition and toxicity. Our specific aims were (1) to characterize the gas- and particle-phase products of atmospheric transformations of DE under the influence of daylight, ozone (O3), hydroxyl (OH) radicals, and nitrate (NO3) radicals; and (2) to explore the biologic activity of DE before and after the transformations took place. The study was executed with the aid of the EUPHORE (European Photoreactor) outdoor simulation chamber facility in Valencia, Spain. EUPHORE is one of the largest and best-equipped facilities of its kind in the world, allowing investigation of atmospheric transformation processes under realistic ambient conditions (with dilutions in the range of 1:300). DE was generated on-site using a modern light-duty diesel engine and a dynamometer system equipped with a continuous emission-gas analyzer. The engine (a turbocharged, intercooled model with common-rail direct injection) was obtained from the Ford Motor Company. A first series of experiments was carried out in January 2005 (the winter 2005 campaign), a second in May 2005 (the summer 2005 campaign), and a third in May and June 2006 (the summer 2006 campaign). The diesel fuel that was used closely matched the one currently in use in most of the United States (containing 47 ppm sulfur and 15% aromatic compounds). Our experiments examined the effects on the composition of DE aged in the dark with added NO3 radicals and of DE aged in daylight with added OH radicals both with and without added volatile organic compounds (VOCs). In order to remove excess nitrogen oxides (NO(x)), a NO(x) denuder was devised and used to conduct experiments in realistic low-NO(x) conditions in both summer campaigns. A scanning mobility particle sizer was used to determine the particle size and the number and volume concentrations of particulate matter (PM) in the DE. O3, NO(x), and reactive nitrogen oxides (NO(y)) were monitored using chemiluminescence and Fourier transform infrared instruments. At the end of the exposures, samples of particle-associated and semivolatile organic compounds (SVOCs) were collected from the chamber for chemical analysis using an XAD-coated annular denuder followed by a filter and XAD cartridge. (XAD is an adsorbent polystyrene divinylbenzene resin used in sampling cartridges.) Samples for toxicity testing were collected using Teflon filters followed by two XAD cartridges. The chemical analyses included determination of organic carbon (OC), elemental carbon (EC), carbon fractions, inorganic ions (e.g., sulfate and nitrate), and speciated organic compounds (polycyclic aromatic hydrocarbons [PAHs], nitro-PAHs, polar compounds, alkanes, hopanes, and steranes). The toxicity tests were performed with extracts of PM combined with the SVOCs. The biologic activity of these extracts was evaluated in vivo by instilling them into the tracheas of rodents and measuring pulmonary toxicity, inflammation, and oxidative-stress responses. Results from the chemical analyses indicated that aging DE in the dark with added NO3 radicals and aging DE in daylight with and without additions led to the formation of additional particles and SVOC mass caused by reactions of VOCs, SVOCs, and inorganic gases. The greatest increase in mass occurred with the addition of VOCs as co-reactants. The proportions of the pyrolized OC (POC) fraction increased in the organic mass, which suggested that highly polar and oligomeric compounds had been formed. Results from the toxicity testing were consistent with the hypothesis that the toxicity of the samples had been affected by changes in their composition (caused both by the atmospheric aging and by changes in the initial composition of the DE presumably associated with changes in the engine, which was new at the outset and accrued wear during the study).
Emissions from motor vehicles are a significant source of fine particulate matter (PM) and gaseous pollutants in urban environments. Few studies have characterized both gaseous and PM emissions from individual in-use vehicles under real-world driving conditions. Here we describe chase vehicle studies in which on-road emissions from individual vehicles were measured in real time within seconds of their emission. This work uses an Aerodyne aerosol mass spectrometer (AMS) to provide size-resolved and chemically resolved characterization of the nonrefractory portion of the emitted PM; refractory materials such as elemental carbon (EC) were not measured in this study. The AMS, together with other gas-phase and particle instrumentation, was deployed on the Aerodyne Research Inc. (ARI) mobile laboratory, which was used to “chase” the target vehicles. Tailpipe emission indices of the targeted vehicles were obtained by referencing the measured nonrefractory particulate mass loading to the instantaneous CO2 measured simultaneously in the plume. During these studies, nonrefractory PM1.0 (NRPM1) emission indices for a representative fraction of the New York City Metropolitan Transit Authority (MTA) bus fleet were determined. Diesel bus emissions ranged from 0.10 g NRPM1/kg fuel to 0.23 g NRPM1/kg, depending on the type of engine used by the bus. The average NRPM1 emission index of diesel-powered buses using Continuously Regenerating Technology (CRT™) trap systems was 0.052 g NRPM1/kg fuel. Buses fueled by compressed natural gas (CNG) had an average emission index of 0.034 g NRPM1/kg Fuel. The mass spectra of the nonrefractory diesel aerosol components measured by the AMS were dominated by lubricating oil spectral signatures. Mass-weighted size distributions of the particles in fresh diesel exhaust plumes peak at vacuum aerodynamic diameters around 90 nm with a typical full width at half maximum of 60 nm.
Particulate matter (PM) air pollution has been associated with cardiovascular morbidity and mortality, and elevated blood pressure (BP) is a known risk factor for cardiovascular disease. A small number of studies have investigated the relationship between PM and BP and found mixed results. Evidence suggests that traffic-related air pollution contributes significantly to PM-related cardiovascular effects.
We hypothesized that black carbon (BC), a traffic-related combustion by-product, would be more strongly associated with BP than would fine PM [aerodynamic diameter < or = 2.5 microm (PM(2.5))], a heterogeneous PM mixture, and that these effects would be larger among participants with genetic variants associated with impaired antioxidative defense.
We performed a repeated-measures analysis in elderly men to analyze associations between PM(2.5) and BC exposure and BP using mixed-effects models with random intercepts, adjusting for potential confounders. We also examined statistical interaction between BC and genetic variants related to oxidative stress defense: GSTM1, GSTP1, GSTT1, NQO1, catalase, and HMOX-1.
A 1-SD increase in BC concentration was associated with a 1.5-mmHg increase in systolic BP [95% confidence interval (CI), 0.1-2.8] and a 0.9-mmHg increase in diastolic BP (95% CI, 0.2-1.6). We observed no evidence of statistical interaction between BC and any of the genetic variants examined and found no association between PM(2.5) and BP.
We observed positive associations between BP and BC, but not between BP and PM(2.5), and found no evidence of effect modification of the association between BC and BP by gene variants related to antioxidative defense.
The species and chemistry responsible for secondary organic aerosol (SOA) formation remain highly uncertain. Laboratory studies of the oxidation of individual, high-flux SOA precursors do not lead to particles with mass spectra (MS) matching those of ambient aged organic material. And, the complexity of real organic particles challenges efforts to identify their chemical origins. We have previously hypothesized that SOA can form from the atmospheric oxidation of a large suite of precursors with varying vapor pressures. Here, we support this hypothesis by using an aerosol mass spectrometer to track the chemical evolution of diesel exhaust as it is photochemically oxidized in an environmental chamber. With explicit knowledge of the condensed-phase MS of the primary emissions from our engine, we are able to decompose each recorded MS into contributing primary and secondary spectra throughout the experiment. We find that the SOA MS becomes increasingly oxidized as a function of time, eventually reaching a final MS that closely resembles that of ambient aged organic particulate matter. This observation is consistent with the idea that lower vapor pressure, semi-volatile organic emissions can form condensable products with fewer generations of oxidation, and therefore, they form relatively less oxidized SOA very quickly.
Diesel exhaust particulate (DEP) is a key arbiter of the adverse cardiovascular effects of air pollution.
We assessed the in vitro effects of DEP on vascular function, nitric oxide (NO) availability, and the generation of oxygen-centered free radicals.
We assessed the direct vascular effects of DEP (10-100 microg/mL) in isolated rat aortic rings using myography. We investigated NO scavenging and oxygen-centered free radical generation using an NO electrode and electron paramagnetic resonance (EPR) with the Tempone-H (1-hydroxyl-2,2,6,6-tetramethyl-4-oxo-piperidine) spin trap, respectively.
Acetylcholine-induced relaxation was attenuated by DEP (maximum relaxation reduced from 91 +/- 4% to 49 +/- 6% with 100 microg/mL DEP; p < 0.001) but was restored by superoxide dismutase (SOD; maximum relaxation, 73 +/- 6%; p < 0.001). DEP caused a modest inhibition of relaxation to NO donor drugs, an effect that could be reversed by SOD (p < 0.01). At 10 microg/mL, DEP did not affect verapamil-induced relaxation (p = 0.73), but at 100 microg/mL DEP inhibited relaxation (p < 0.001) by a mechanism independent of SOD. NO concentrations generated by 2-(N,N-diethylamino)-diazenolate-2-oxide (DEA/NO; 10 microM) were reduced by DEP (100 microg/mL; from 5.2 +/- 0.4 to 3.3 +/- 0.4 microM; p = 0.002). Free radical generation was increased by DEP (10 microg/mL; 9-fold increase in EPR spectra; p = 0.004) in a manner that could be attenuated by SOD (p = 0.015).
DEP caused oxidative stress through the generation of oxygen-centered free radicals that reduced the bioavailability of endothelium-derived NO without prior interaction with the lung or vascular tissue. These findings provide a mechanism for the adverse cardiovascular effects of particulate air pollution.
Although a number of studies have documented the relationship between lung function and traffic-related pollution among children, few have focused on adult lung function or examined community-based populations.
We examined the relationship between black carbon (BC), a surrogate of traffic-related particles, and lung function among women in the Maternal-Infant Smoking Study of East Boston, an urban cohort in Boston, Massachusetts.
We estimated local BC levels using a validated spatiotemporal land-use regression model, derived using ambient and indoor monitor data. We examined associations between percent predicted pulmonary function and predicted BC using linear regression, adjusting for sociodemographics (individual and neighborhood levels), smoking status, occupational exposure, type of cooking fuel, and a diagnosis of asthma or chronic bronchitis.
The sample of 272 women 18-42 years of age included 57% who self-identified as Hispanic versus 43% white, and 18% who were current smokers. Mean +/- SD predicted annual BC exposure level was 0.62 +/- 0.2 microg/m3. In adjusted analysis, BC (per interquartile range increase) was associated with a 1.1% decrease [95% confidence interval (CI), -2.5% to 0.3%] in forced expiratory volume in 1 sec, a 0.6% decrease (95% CI, -1.9% to 0.6%) in forced vital capacity, and a 3.0% decrease (95% CI, -5.8% to -0.2%) in forced mid-expiratory flow rate. We noted differential effects by smoking status in that former smokers were most affected by BC exposure, whereas current smokers were not affected.
In this cohort, exposure to traffic-related BC, a component of particulate matter, independently predicted decreased lung function in urban women, when adjusting for tobacco smoke, asthma diagnosis, and socioeconomic status.
Previously we reported that fine particle mass (particulate matter [less than and equal to] 2.5 microm; PM(2.5)), which is primarily from combustion sources, but not coarse particle mass, which is primarily from crustal sources, was associated with daily mortality in six eastern U.S. cities (1). In this study, we used the elemental composition of size-fractionated particles to identify several distinct source-related fractions of fine particles and examined the association of these fractions with daily mortality in each of the six cities. Using specific rotation factor analysis for each city, we identified a silicon factor classified as soil and crustal material, a lead factor classified as motor vehicle exhaust, a selenium factor representing coal combustion, and up to two additional factors. We extracted daily counts of deaths from National Center for Health Statistics records and estimated city-specific associations of mortality with each source factor by Poisson regression, adjusting for time trends, weather, and the other source factors. Combined effect estimates were calculated as the inverse variance weighted mean of the city-specific estimates. In the combined analysis, a 10 microg/m(3) increase in PM(2.5) from mobile sources accounted for a 3.4% increase in daily mortality [95% confidence interval (CI), 1.7-5.2%], and the equivalent increase in fine particles from coal combustion sources accounted for a 1.1% increase [CI, 0.3-2.0%). PM(2.5) crustal particles were not associated with daily mortality. These results indicate that combustion particles in the fine fraction from mobile and coal combustion sources, but not fine crustal particles, are associated with increased mortality.
Pulmonary inflammatory and hematologic responses of canines were studied after exposure to concentrated ambient particles (CAPs) using the Harvard ambient particle concentrator (HAPC). For pulmonary inflammatory studies, normal dogs were exposed in pairs to either CAPs or filtered air (paired studies) for 6 hr/day on 3 consecutive days. For hematologic studies, dogs were exposed for 6 hr/day for 3 consecutive days with one receiving CAPs while the other was simultaneously exposed to filtered air; crossover of exposure took place the following week (crossover studies). Physicochemical characterization of CAPs exposure samples included measurements of particle mass, size distribution, and composition. No statistical differences in biologic responses were found when all CAPs and all sham exposures were compared. However, the variability in biologic response was considerably higher with CAPs exposure. Subsequent exploratory graphical analyses and mixed linear regression analyses suggested associations between CAPs constituents and biologic responses. Factor analysis was applied to the compositional data from paired and crossover experiments to determine elements consistently associated with each other in CAPs samples. In paired experiments, four factors were identified; in crossover studies, a total of six factors were observed. Bronchoalveolar lavage (BAL) and hematologic data were regressed on the factor scores. Increased BAL neutrophil percentage, total peripheral white blood cell (WBC) counts, circulating neutrophils, and circulating lymphocytes were associated with increases in the aluminum/silicon factor. Increased circulating neutrophils and increased BAL macrophages were associated with the vanadium/nickel factor. Increased BAL neutrophils were associated with the bromine/lead factor when only the compositional data from the third day of CAPs exposure were used. Significant decreases in red blood cell counts and hemoglobin levels were correlated with the sulfur factor. BAL or hematologic parameters were not associated with increases in total CAPs mass concentration. These data suggest that CAPs inhalation is associated with subtle alterations in pulmonary and systemic cell profiles, and specific components of CAPs may be responsible for these biologic responses.
The objectives of this study were (1) to determine whether short-term exposures to concentrated air particles (CAPs) cause pulmonary inflammation in normal rats and rats with chronic bronchitis (CB); (2) to identify the site within the lung parenchyma where CAPs-induced inflammation occurs; and (3) to characterize the component(s) of CAPs that is significantly associated with the development of the inflammatory reaction. Four groups of animals were studied: (1) air treated, filtered air exposed (air-sham); (2) sulfur dioxide treated (CB), filtered air exposed (CB-sham); (3) air treated, CAPs exposed (air-CAPs); and (4) sulfur dioxide treated, CAPs exposed (CB-CAPs). CB and normal rats were exposed by inhalation either to filtered air or CAPs during 3 consecutive days (5 hours/day). Pulmonary inflammation was assessed by bronchoalveolar lavage (BAL) and by measuring the numerical density of neutrophils (Nn) in the alveolar walls at the bronchoalveolar junction and in more peripheral alveoli. CAPs (as a binary exposure term) and CAPs mass (in regression correlations) induced a significant increase in BAL neutrophils and in normal and CB animals. Nn in the lung tissue significantly increased with CAPs in normal animals only. Greater Nn was observed in the central compared with peripheral regions of the lung. A significant dose-dependent association was found between many CAPs components and BAL neutrophils or lymphocytes, but only vanadium and bromine concentrations had significant associations with both BAL neutrophils and Nn in CAPs-exposed groups analyzed together. Results demonstrate that short-term exposures to CAPs from Boston induce a significant inflammatory reaction in rat lungs, with this reaction influenced by particle composition.
The objective of this study was to determine whether short-term exposures to concentrated ambient particles (CAPs) alter the morphology of small pulmonary arteries in normal rats and rats with chronic bronchitis (CB). Sprague-Dawley male rats were exposed to CAPs, using the Harvard Ambient Particle Concentrator, or to particle-free air (sham) under identical conditions during 3 consecutive days (5 hr/day) in six experimental sets. CB was induced by exposure to 276 +/- 9 ppm of sulfur dioxide (5 hr/day, 5 days/week, 6 weeks). Physicochemical characterization of CAPs included measurements of particle mass, size distribution, and composition. Rats were sacrificed 24 hr after the last CAPs exposure. Histologic slides were prepared from random sections of lung lobes and coded for blinded analysis. The lumen/wall area (L/W) ratio was determined morphometrically on transverse sections of small pulmonary arteries. When all animal data (normal and CB) were analyzed together, the L/W ratios decreased as concentrations of fine particle mass, silicon, lead, sulfate, elemental carbon, and organic carbon increased. In separate univariate analyses of animal data, the association for sulfate was significant only in normal rats, whereas silicon was significantly associated in both CB and normal rats. In multivariate analyses including all particle factors, the association with silicon remained significant. Our results indicate that short-term CAPs exposures (median, 182.75 micro g/m3; range, 73.50-733.00 micro g/m3) can induce vasoconstriction of small pulmonary arteries in normal and CB rats. This effect was correlated with specific particle components and suggests that the pulmonary vasculature might be an important target for ambient air particle toxicity.
The discovery that nitric oxide (NO) has powerful vasoactive properties identical to those of endothelial-derived relaxing factor spawned a vast body of research investigating the physiological actions of small gas molecules. NO, which arises endogenously through the action of nitric oxide synthase (NOS) enzymes, is a highly reactive gas that plays important roles in the regulation of vascular and immune function. Carbon monoxide (CO), a similar yet much more chemically stable gas, occurs in nature as a product of the oxidation or combustion of organic materials. CO also arises in cells and tissues as a byproduct of heme oxygenase (HO) activity, which degrades heme to biliverdin-IXalpha. Like NO, CO acts as a vasorelaxant and may regulate other vascular functions such as platelet aggregation and smooth muscle proliferation. CO has also been implicated as a neurotransmitter in the central nervous system. HO-1, the inducible form of HO, confers cytoprotection against oxidative stress in vitro and in vivo. CO, when applied at low concentration, exerts potent cytoprotective effects mimicking those of HO-1 induction, including down-regulation of inflammation and suppression of apoptosis. Many of the effects of CO depend on the activation of guanylate cyclase, which generates guanosine 3',5'-monophosphate (cGMP), and the modulation of mitogen-activated protein kinase (MAPK) signaling pathways. This review highlights new advances in the interaction of CO with cellular signaling processes.
An association between exposure to vehicular traffic in urban areas and the exacerbation of cardiovascular disease has been suggested in previous studies. This study was designed to assess whether exposure to traffic can trigger myocardial infarction.
We conducted a case-crossover study in which cases of myocardial infarction were identified with the use of data from the Cooperative Health Research in the Region of Augsburg Myocardial Infarction Registry in Augsburg, in southern Germany, for the period from February 1999 to July 2001. There were 691 subjects for whom the date and time of the myocardial infarction were known who had survived for at least 24 hours after the event, completed the registry's standardized interview, and provided information on factors that may have triggered the myocardial infarction. Data on subjects' activities during the four days preceding the onset of symptoms were collected with the use of patient diaries.
An association was found between exposure to traffic and the onset of a myocardial infarction within one hour afterward (odds ratio, 2.92; 95 percent confidence interval, 2.22 to 3.83; P<0.001). The time the subjects spent in cars, on public transportation, or on motorcycles or bicycles was consistently linked with an increase in the risk of myocardial infarction. Adjusting for the level of exercise on a bicycle or for getting up in the morning changed the estimated effect of exposure to traffic only slightly (odds ratio for myocardial infarction, 2.73; 95 percent confidence interval, 2.06 to 3.61; P<0.001). The subject's use of a car was the most common source of exposure to traffic; nevertheless, there was also an association between time spent on public transportation and the onset of a myocardial infarction one hour later.
Transient exposure to traffic may increase the risk of myocardial infarction in susceptible persons.
Nitric oxide (NO) and carbon monoxide (CO) in exhaled breath are considered obtainable biomarkers of physiologic mechanisms. Therefore, obtaining their measures simply, non-invasively, and repeatedly, is of interest, and was the purpose of the current study.
Expired NO (ENO) and CO (ECO) were measured non-invasively using a gas micro-analyzer on several strains of mice (C57Bl6, IL-10-/-, A/J, MKK3-/-, JNK1-/-, NOS-2-/- and NOS-3-/-) with and without allergic airway inflammation (AI) induced by ovalbumin systemic sensitization and aerosol challenge, compared using independent-sample t-tests between groups, and repeated measures analysis of variance (ANOVA) within groups over time of inflammation induction. ENO and ECO were also measured in C57Bl6 and IL-10-/- mice, ages 8-58 weeks old, the relationship of which was determined by regression analysis. S-methionyl-L-thiocitrulline (SMTC), and tin protoporphyrin (SnPP) were used to inhibit neuronal/constitutive NOS-1 and heme-oxygenase, respectively, and alter NO and CO production, respectively, as assessed by paired t-tests. Methacholine-associated airway responses (AR) were measured by the enhanced pause method, with comparisons by repeated measures ANOVA and post-hoc testing.
ENO was significantly elevated in naïve IL-10-/- (9-14 ppb) and NOS-2-/- (16 ppb) mice as compared to others (average: 5-8 ppb), whereas ECO was significantly higher in naïve A/J, NOS-3-/- (3-4 ppm), and MKK3-/- (4-5 ppm) mice, as compared to others (average: 2.5 ppm). As compared to C57Bl6 mice, AR of IL-10-/-, JNK1-/-, NOS-2-/-, and NOS-3-/- mice were decreased, whereas they were greater for A/J and MKK3-/- mice. SMTC significantly decreased ENO by ~30%, but did not change AR in NOS-2-/- mice. SnPP reduced ECO in C57Bl6 and IL-10-/- mice, and increased AR in NOS-2-/- mice. ENO decreased as a function of age in IL-10-/- mice, remaining unchanged in C57Bl6 mice.
These results are consistent with the ideas that: 1) ENO is associated with mouse strain and knockout differences in NO production and AR, 2) alterations of ENO and ECO can be measured non-invasively with induction of allergic AI or inhibition of key gas-producing enzymes, and 3) alterations in AR may be dependent on the relative balance of NO and CO in the airway.
The exposure of mice to irradiated automobile exhaust prior to mating significantly impaired reproductive function in male members of sexual pairs. The impairment was expressed at various stages of reproduction: conception, fecundity, and infant survival. These effects imply that the chromatin content of the sperm was altered. This experiment suggests mutational effects on mammalian cells from components or subsequent products of irradiated automobile exhaust. Significantly, the concentrations of these pollutants were similar to those present in many urban communities today. A direct toxic effect on infant mice was noted during postnatal exposure to irradiated automobile exhaust. Death rates during the first 8 days of life were higher compared to those for controls.
Associations between exposure to fine particulate matter and blood pressure responses have been reported in epidemiological studies but findings have proven inconsistent. The objective of this study was to measure effects of primary and secondary components of traffic-derived fine particulate matter (PM2.5) on blood pressure (BP). Sprague–Dawley rats were exposed to fresh primary vehicular particles (P), secondary organic aerosol (SOA), photochemically aged primary plus secondary organic aerosols (P + SOA) or filtered air for 5 h per day for three consecutive weeks. Particle concentration target was 50 μg/m3 for all exposures. Blood pressure parameters were measured continuously using implanted transmitters. Systolic (SBP) and diastolic blood pressure (DBP), mean pressure, pulse pressure, and heart rate responses were assessed using mixed effects models. Exposure to P resulted in increased SBP (p = 0.03) and DBP (p = 0.05) that was sustained across weeks. SOA exposure resulted in increases in SBP (p = 0.07) and DBP (p = 0.01) on the first day with this effect decreasing significantly across exposure days (p < 0.0001). P + SOA showed significant increases in SBP (p = 0.002) and DBP (p < 0.0001) across weeks with a magnitude of effect equaling the approximate average of the effect estimates of the P and SOA exposures. Double Sham exposures following SOA and P + SOA showed compensatory decreases in SBP and DBP. No exposure had a significant effect on heart rate. Primary and secondary traffic derived aerosols can substantially increase SBP and DBP, but these increases are lost with continued exposures. Compensatory BP responses resulting after exposure to secondary particles require further investigation to define BP control mechanisms.
Gas-phase oxidation of SO2 in the ozone-olefin reactions was studied, and the yield of sulfuric acid aerosol was determined for various types of olefins under atmospheric pressure. No sulfur-containing compound other than sulfuric acid was detected. Pressure dependence of the yield of H2SO4 was studied for the first time for trans-2-butene. The yield decreased to zero as the total pressure of air was decreased. This fact supports the contention that only a stabilized Criegee intermediate can undergo bimolecular reactions. Stabilized fractions of CH2OO and CH3CHOO in the ozone reaction of ethylene and trans-2-butene under atmospheric pressure are 0.390 +/- 0.053 and 0.185 +/- 0.028, respectively. The yield of H2SO4 was as low as 0.052 +/- 0.013, 0.032 +/- 0.024, and 0.029 +/- 0.015 for cyclopentane, cyclohexene, and cycloheptene, respectively. The yield of H2SO4 for alpha- and beta-pinene was 0.125 +/- 0.040 and 0.249 +/- 0.024, respectively. The rate constant ratio of decomposition of the initially formed hot Criegee intermediate to its collisional stabilization was obtained to be (3.9 +/- 0.8) x 1018 molecules/cm³ for trans-2-butene.
As part of the 1993 Lower Fraser Valley Oxidants Study, measurements of mobile source emission factors were performed in the Cassiar Tunnel on the Trans-Canada Highway to measure the on-road contribution to the ozone-forming precursors (NOx and speciated hydrocarbons) along with CO. Observed emission factors were compared to the Canadian versions of the U.S. Environmental Protection Agency's MOBILE models, MOBILE4.1C and MOBILE5C, to assess uncertainty in the predicted mobile source contributions to the Vancouver emissions inventory.A total of 16 1-h runs were made. The timing of the individual runs was designed to encompass different traffic volumes, driving conditions, and times of day. A total of 24,513 vehicles traversed the tunnel during the study, with approximately 91% light-duty vehicles, 4% heavy-duty spark ignition vehicles, and 5% heavy-duty diesel vehicles. MOBILE5C overpredicted the observed value of CO by ∼2%, NMHC by 24%, and NOx by 13%, while MOBILE4.1C underpredicted the observed values by 36, 29, and 23% for CO, NMHC, and NOx respectively.
This paper presents the design and development of a compact high volume cascade impactor (HVCI). The HVCI operates at a è ow rate of 900 l/min and consists of 4 impaction stages equipped with circular slit-shaped acceleration nozzles and a backup é l- ter. The backup é lter is placed downstream of the fourth stage and is used to collect the ultraé ne particles (dp < 0.1 πm). The major feature of this novel sampler is its ability to collect relatively large amounts of particles (mg-g levels) onto relatively small polyurethane foam substrates without using adhesives. As previously reported, the capacity of the impaction substrate is 2.15 g of collected particles per cm 2 of foam. Although the im- paction substrates are not coated with adhesives such as grease or mineral oil, particle bounce and re-entrainment losses were found not to be signié cant. Particles can be easily recovered from the foam substrates using aqueous extraction. The impactor was calibrated using polydisperse particles. The 50% cutpoints of the 4 stages were 9.90, 2.46, 1.0, and 0.1 πm, respectively. In- terstage losses of ultraé ne and é ne particles were
This paper synthesizes data on aerosol (or particulate matter, PM) chemical characteristics, which were obtained in European aerosol research activities at natural, rural, near-city, urban, and kerbside sites over the past decade. It includes only two (nearby) sites in the semi-arid Mediterranean area, and lacks data from Eastern Europe. PM chemical compositions are compared with the PM mass concentrations in PM10, PM2.5, and further size resolved PM fractions (chemical mass closure). Such data sets are more comprehensive than those currently provided by air quality monitoring networks (e.g. EMEP, EUROAIRNET). Data available from 24 sites in Europe were reviewed. They were processed and plotted to allow comparisons in spite of differences in the sampling and analytical techniques used in various studies. A number of conclusions are drawn among which are the following.
Gas phase oxidation of SO2 in the ozone-olefin reactions was studied, and the yield of sulfuric acid aerosol was determined for various types of olefins under atmospheric pressure. No sulfur-containing compounds other than sulfuric acid was detected. Pressure dependence of the yield of H2SO4 was studied for the first time for trans-2-butene. The yield decreased to zero as the total pressure of air was decreased. This fact supports the contention that only a stabilized Criegee intermediate can undergo bimolecular reactions. Stabilized fractions of CH2OO and CH3CHOO in the ozone reaction of ethylene and trans-2-butene under atmospheric pressure are 0.390+-0.053 and 0.185+-0.028, respectively. The yield of H2SO4 was as low as 0.052+-0.013, 0.032+-0.024, and 0.029+-0.015 for cyclopenten, cyclcohexene, and cycloheptene, respectively. The yield of H2SO4 for a- and b-pinene was 0.125+-0.040 and 0.249+-0.024, respectively. The rate constant ratio of deconposition of the initially formed hot Criegee intermediate to its collisional stabilization was obtained to be (3.9+-0.8)x1018 molecule/cm3 for trans-2-butene.
The thermal/optical reflectance method of carbon analysis developed by Huntzicker et al. (in Particulate Carbon, Atmospheric Life Cycle, edited by Wolff G. T. and Klimisch R. L., pp. 79–88, Plenum Press, New York, 1982) has been adapted by several laboratories for the quantification of organic and elemental carbon on quartz-fiber filter deposits. While the principle used by these laboratories is identical to that of Huntzicker et al., the details differ with respect to calibration standards, analysis time, temperature ramping and volatilization/combustion temperatures. This paper reports a variation on this method which has been applied to over 27,000 samples taken in more than a dozen urban and regional air quality studies in the U.S.A. In this variation, a 0.5 cm² punch from a dozen urban and regional air quality studies in 120, 250, 450 and 550°C in a pure helium atmosphere, then to combustion at temperatures of 550, 700 and 800°C in a 2% oxygen and 98% helium atmosphere. The carbon which evolves at each temperature is converted to methane and quantified with a flame ionization detector. The seven separate carbon fractions facilitate evaluation of the method and increase the information content concerning the samples.
Diffusion denuders have been commonly used to remove trace gases from an aerosol (mixture of gases and particles), while allowing the particles to remain suspended in air. We present the design and evaluation of a high-flow (16.7 L min⁻¹) countercurrent parallel-plate membrane diffusion denuder that has high removal efficiencies for both non-reactive gases such as carbon monoxide (89%), as well as volatile organic compounds (80-85%) from an automobile exhaust. Particle losses were approximately 15% for particles around 100 nm in diameter. This denuder is suitable for toxicological tests involving both human and animal exposures to combustion aerosols. The denuder may also be used for other applications, for example, to reduce the effect of gas-phase sampling artifacts on particle composition.
Particulate pollution has been linked to risk for cardiac death; possible mechanisms include pollution-related increases in cardiac electrical instability. T-wave alternans (TWA) is a marker of cardiac electrical instability measured as differences in the magnitude between adjacent T waves. In a repeated-measures study of 48 patients aged 43 to 75 years, associations of ambient and home indoor particulate pollution, including black carbon (BC) and reports of traffic exposure, with changes in 0.5-hourly maximum TWA (TWA-MAX), measured by 24-hour Holter electrocardiographic monitoring, were investigated. Each patient was observed up to 4 times within 1 year after percutaneous intervention for myocardial infarction, acute coronary syndromes without infarction, or stable coronary artery disease, for a total of 5,830 0.5-hour observations. Diary data for each 0.5-hour period defined whether a patient was home or not home, or in traffic. Increases in TWA-MAX were independently associated with the previous 2-hour mean ambient BC (2.1%, 95% confidence interval 0.9% to 3.3%) and with being in traffic in the previous 2 hours (6.1%, 95% confidence interval 3.4% to 8.8%). When subjects were home, indoor home BC effects were largest and most precise; when subjects were away from home, ambient central site BC effects were strongest. Increases in pollution increased the odds of TWA-MAX > or =75th percentile (odds ratio 1.4, 95% confidence interval 1.2 to 1.6 for a 1 microg/m(3) increase in 6-hour mean BC). In conclusion, after hospitalization for coronary artery disease, being in traffic and short-term ambient or indoor BC exposure increased TWA, a marker of cardiac electrical instability.
Particulate air pollution has been consistently linked to increased risk of arterial cardiovascular disease. Few data on air pollution exposure and risk of venous thrombosis are available. We investigated whether living near major traffic roads increases the risk of deep vein thrombosis (DVT), using distance from roads as a proxy for traffic exposure.
From 1995 through 2005, we examined 663 patients with DVT of the lower limbs and 859 age-matched controls from cities with population >15 000 inhabitants in Lombardia Region, Italy. We assessed distance from residential addresses to the nearest major traffic road using geographic information system methodology. The risk of DVT was estimated from logistic regression models adjusting for multiple clinical and environmental covariates. The risk of DVT was increased (odds ratio=1.33; 95% confidence interval, 1.03 to 1.71; P=0.03 in age-adjusted models; odds ratio=1.47; 95% confidence interval, 1.10 to 1.96; P=0.008 in models adjusted for multiple covariates) for subjects living near a major traffic road (index distance of 3 meters, 10th centile of the distance distribution) compared with those living farther away (reference distance of 245 meters, 90th centile). The increase in DVT risk was approximately linear over the observed distance range (from 718 to 0 meters) and was not modified after adjusting for
=0.008 for 10th versus 90th distance centile in models adjusting for area levels of particulate matter <10 mum in aerodynamic diameter in the year before diagnosis).
Living near major traffic roads is associated with increased risk of DVT.
Mice, rats, guinea pigs, and hamsters were exposed to four levels of uv-irradiated or nonirradiated auto exhaust (CO: 20 to 100 ppM). Irradiated exhaust increased post-middle-age susceptibility to disease and infection and decreased mouse fertility and infant survival. Both exhaust types caused stress-adaptation response as measured by decreased spontaneous activity, increased bone lead concentrations, and increase in nonfunctional lung tissue. No significant affect on mortality, histopathology, growth, some hematology, immunology, oxygen consumption, or permanent pulmonary function was noted.
Particulate matter emissions from the California in-use vehicle fleet were measured as 37,500 vehicles traveled through two bores of the Caldecott Tunnel located in the San Francisco Bay area. Microorifice cascade impactors and filter-based samplers were used to determine the particle chemical composition as a function of particle size. Ammonia emissions from the vehicle fleet were measured as well. Concentrations of aerosol mass, organic carbon, elemental carbon, sulfate ion, nitrate ion, and ammonium ion, as well as 13 elements are reported. The particle mass distribution peaks in the particle size range 0.1-0.18 microm aerodynamic diameter (Da). Elemental carbon and organic matter were the largest components of particle mass in all the size ranges studied. The Caldecott Tunnel bores studied include one which carries light-duty vehicle traffic and one which carries a mixture of light- and heavy-duty vehicle traffic. From experiments conducted in both bores, estimates are made of the size distribution and chemical composition of particulate matter emissions extrapolated to the 100% light-duty and 100% heavy-duty vehicle fleets. The heavy-duty vehicle fleet emitted 1285 +/- 237 mg of fine particulate matter (Da < 1.9 microm)/kg of C contained in the fuel burned (corresponding to approximately 430 +/- 79 mg/km driven). Light-duty vehicles emitted less than 85 +/- 6 mg/kg of C in the fuel burned (corresponding to less than approximately 5.5 +/- 0.4 mg/km driven). Emissions of gas-phase ammonia in the Caldecott Tunnel were measured to be 194 and 267 mg/L of gasoline-equivalent fuel burned in the tunnel. The ammonia emissions are attributed to automobiles that were equipped with 3-way catalysts and operating fuel rich.
Because of its high diffusing capacity through the alveolar–blood barrier and its high selectivity for the pulmonary vasculature, inhaled nitric oxide (NO) has been recently shown to be a viable and efficient approach to restore pulmonary NO deficiency.
The most relevant applications of inhaled NO are in infants with primary pulmonary hypertension or hypoxia. In these patients, inhaled NO improves gas exchange and ventilation-perfusion matching, reduces the length of hospitalization and is without severe detrimental effects. The use of inhaled NO has also been extended to adults with pulmonary hypertension and the acute respiratory distress syndrome. In addition, recent clinical evidence supported by data from animal models, shows beneficial extra-pulmonary effects of inhaled NO, including protection against myocardial ischaemia-reperfusion injury.
Ventilator-induced lung injury (VILI) is a major cause of morbidity and mortality in intensive care units. The stress-inducible gene product, heme oxygenase-1, and carbon monoxide (CO), a major by-product of heme oxygenase catalysis of heme, have been shown to confer potent antiinflammatory effects in models of tissue and cellular injury. In this study, we observed increased expression of heme oxygenase-1 mRNA and protein in a rat model of VILI. To assess the physiologic function of heme oxygenase-1 induction in VILI, we determined whether low concentration of inhaled CO could serve to protect the lung against VILI. Low concentration of inhaled CO significantly reduced tumor necrosis factor-alpha levels and total cell count in lavage fluid, while simultaneously elevating levels of antiinflammatory interleukin-10 levels. To better characterize the mechanism of CO-mediated antiinflammatory effects, we examined key signaling pathways, which may mediate CO-induced antiinflammatory effects. We demonstrate that inhaled CO exerts antiinflammatory effects in VILI via the p38 mitogen-activated protein kinase pathway but independent of activator protein-1 and nuclear factor-kappaB pathways. Our data lead to a tempting speculation that inhaled CO might be useful in minimizing VILI.
Diesel exhaust is a public health concern and contributor to both ambient and occupational air pollution. As part of a general health assessment of multiple anthropogenic source emissions conducted by the National Environmental Respiratory Center (NERC), a series of health assays was conducted on rats and mice exposed to environmentally relevant levels of diesel exhaust. This article summarizes the study design and exposures, and reports findings on several general indicators of toxicity and carcinogenic potential. Diesel exhaust was generated from a commonly used 2000 model 5.9-L, 6-cylinder turbo diesel engine operated on a variable-load heavy-duty test cycle burning national average certification fuel. Animals were exposed to clean air (control) or four dilutions of whole emissions based on particulate matter concentration (30, 100, 300, and 1000 microg/m(3)). Male and female F344 rats and A/J mice were exposed by whole-body inhalation 6 h/day, 7 days/wk, for either 1 wk or 6 mo. Exposures were characterized in detail. Effects of exposure on clinical observations, body and organ weights, serum chemistry, hematology, histopathology, bronchoalveolar lavage, and serum clotting factors were mild. Significant exposure-related effects occurring in both male and female rats included decreases in serum cholesterol and clotting Factor VII and slight increases in serum gamma-glutamyl transferase. Several other responses met screening criteria for significant exposure effects but were not consistent between genders or exposure times and were not corroborated by related parameters. Carcinogenic potential as determined by micronucleated reticulocyte counts and proliferation of adenomas in A/J mice were unaffected by 6 mo of exposure. Parallel studies demonstrated effects on cardiac function and resistance to viral infection; however, the results reported here show few and only modest health hazards from subchronic or shorter exposures to realistic concentrations of contemporary diesel emissions.
Many biological functions of heme oxygenase (HO), such as cytoprotection against oxidative stress, vasodilation, neurotransmission in the central or peripheral nervous systems, and anti-inflammatory, anti-apoptotic, or anti-proliferative potential, have been attributed to its enzymatic byproduct carbon monoxide (CO), although roles for biliverdin/bilirubin and iron have also been proposed. In addition to these well-characterized effects, recent findings reveal that HO-derived CO may act as an oxygen sensor and circadian modulator of heme biosynthesis. In lymphocytes, CO may participate in regulatory T cell function. A number of the known signaling effects of CO depend on stimulation of soluble guanylate cyclase and/or activation of mitogen-activated protein kinases (MAPK). Furthermore, modulation of caveolin-1 status may serve as an essential component of certain aspects of CO action, such as growth control. In this review, we summarize recent findings of the beneficial or detrimental effects of endogenous CO with an emphasis on the signaling pathways and downstream targets that trigger the action of this gas.
Diluted exhaust from a diesel engine was photo-oxidized in a smog chamber to investigate secondary organic aerosol (SOA) production. Photochemical aging rapidly produces significant SOA, almost doubling the organic aerosol contribution of primary emissions after several hours of processing at atmospherically relevant hydroxyl radical concentrations. Less than 10% of the SOA mass can be explained using a SOA model and the measured oxidation of known precursors such as light aromatics. However, the ultimate yield of SOA is uncertain because it is sensitive to treatment of particle and vapor losses to the chamber walls. Mass spectra from an aerosol mass spectrometer (AMS) reveal that the organic aerosol becomes progressively more oxidized throughout the experiments, consistent with sustained, multi-generational production. The data provide strong evidence that the oxidation of a wide array of precursors that are currently not accounted for in existing models contributes to ambient SOA formation.
acute lung injury is characterized by the loss of barrier function of the alveolar epithelial and pulmonary capillary endothelial cells along with acute inflammation ([19][1]). Epidemiological studies suggest that aspiration of gastric contents is a major clinical risk factor for the development of
Atmospheric transformation of diesel emissions. Research report. Health Effects Institute no
- B S Samy
- Mcdonald Jd
- Seagrave
- Jc
B, Samy S, McDonald JD, Seagrave JC (2010) Atmospheric transformation of diesel emissions. Research report. Health Effects Institute no. 147 Air Qual Atmos Health (2013) 6:419–429
The DRI thermal/optical reflectance carbon analysis system: description, evaluation and applications in U.S. air quality studies Inhaled concentrated ambient particles are associated with hematologic and bronchol-veolar lavage changes in canines
- Jc
- Jg Watson
- Pritchett
- Lc
- Pierson
- Wr
- Ca Frazier
- Purcell Rg Clarke Rw
- Reinisch B U Coull
- P Catalano
- Koutrakis P Killingsworth Cr
- Kavouras I Murthy
- Lawrence J Ggk
- E Lovett
- Wolfson Jm
- Verrier Rl
- Godleski
- Jj
JC, Watson JG, Pritchett LC, Pierson WR, Frazier CA, Purcell RG (1993) The DRI thermal/optical reflectance carbon analysis system: description, evaluation and applications in U.S. air quality studies. Atmos Environ 27A:1185–1201 Clarke RW, Coull B, Reinisch U, Catalano P, Killingsworth CR, Koutrakis P, Kavouras I, Murthy GGK, Lawrence J, Lovett E, Wolfson JM, Verrier RL, Godleski JJ (2000) Inhaled concentrated ambient particles are associated with hematologic and bronchol-veolar lavage changes in canines. Environ Health Perspect 108 (12):1179–1187
Gas-phase oxidation of SO 2 in the ozone-olefin reactions Engineering the chronic exposure of animals to laboratory produced automobile exhaust Biological effects of atmospheres contaminated by auto exhaust
- S H Kobayashi
- Akimoto
S, Kobayashi H, Akimoto H (1984) Gas-phase oxidation of SO 2 in the ozone-olefin reactions. J Phys Chem 88:4736–4739 Hinners RG (1962) Engineering the chronic exposure of animals to laboratory produced automobile exhaust. J Air Pollut Contr Assoc 12:527–530 Hueter FG et al (1966) Biological effects of atmospheres contaminated by auto exhaust. Arch Environ Health 12:553
Effects of fresh and aged traffic-related particles on breathing pattern, cellular responses and oxidative stress Inhaled carbon monoxide confers anti-inflammatory effects against ventilator-induced lung injury
- Chung Y Lamoureux
- D P Ms Long
- Lawrence V J Papapostolou
- V Mazzaro
- H Buonfiglio
- J P Oliveira
- Koutrakis R P Sato
- Godleski
- T Dolinay
- M Szilasi
- M Siu
- Choi
E A, Chung Y, Lamoureux D P, Long MS, Papapostolou V, Lawrence J, Mazzaro V, Buonfiglio H, Oliveira J P, Sato R, Koutrakis P, Godleski JJ (2012b) Effects of fresh and aged traffic-related particles on breathing pattern, cellular responses and oxidative stress. Air Quality Atmosphere and Health (in press) Dolinay T, Szilasi M, Siu M, Choi AMK (2004) Inhaled carbon monoxide confers anti-inflammatory effects against ventilator-induced lung injury. Am J Respir Crit Care Med 170:613–620
Living near major traffic roads and risk of deep vein thrombosis Concentrated ambient air particles induce vasoconstriction of small pulmonary arteries in rats Chase studies of particulate emissions from in-use
- A I Martinelli
- Melly V S Pegoraro
- P Grillo
- A Zanobetti
- L Kou
- A Bertazzi
- Pm Manucci
- Schwartz
- Batalha Jrf
- Saldiva
- Clarke Rw Phn
- Ba Coull
- Lawrence Rc J Stearns
- Krishna Murthy Gg
- Koutrakis P Godleski Jj Canagaratna
- Jayne Jt Mr
- Da Ghertner
- S Herndon
- Q Shi
- Jimenez
- Jl
- Silva
- Williams P Pj
- Lanni T F Drewnick
- Kl Demerjian
- Kolb Ce
- Wornshop
- Dr
A, Martinelli I, Pegoraro V, Melly S, Grillo P, Zanobetti A, Kou L, Bertazzi A, Manucci PM, Schwartz J (2009) Living near major traffic roads and risk of deep vein thrombosis. Circulation 119:3118–3124 Batalha JRF, Saldiva PHN, Clarke RW, Coull BA, Stearns RC, Lawrence J, Krishna Murthy GG, Koutrakis P, Godleski JJ (2002) Concentrated ambient air particles induce vasoconstriction of small pulmonary arteries in rats. Env Health Perspect 110:1191–1197 Canagaratna MR, Jayne JT, Ghertner DA, Herndon S, Shi Q, Jimenez JL, Silva PJ, Williams P, Lanni T, Drewnick F, Demerjian KL, Kolb CE, Wornshop DR (2004) Chase studies of particulate emissions from in-use New York City vehicles. Aerosol Sci Technol 38:555–573