Does the Harvard/U.S. Environmental Protection Agency Ambient Particle Concentrator Change the Toxic Potential of Particles?

Savage, Sara T; Lawrence, Joy; Katz, Tracy; Stearns, Rebecca C.; Coull, Brent A.; Godleski, John J.

doi:10.1080/10473289.2003.10466267

Cited by 12 publications

(8 citation statements)

References 27 publications

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“…Ambient fine particles were concentrated using the Harvard ambient particle concentrator (HAPC), the characteristics of which have been described in detail previously (Godleski et al, 2000;Lawrence et al, 2004;Savage et al, 2003). Briefly, the HAPC concentrates ambient fine particulate matter with an aerodynamic diameter ≤2.5 µm (PM 2.5 ) to ∼30× ambient levels without altering its size distribution or chemical composition.…”

Section: Exposure Technology and Characterizationmentioning

confidence: 99%

Effects of Ambient Particles and Carbon Monoxide on Supraventricular Arrhythmias in a Rat Model of Myocardial Infarction

Wellenius

Coull

Batalha³

et al. 2006

Inhalation Toxicology

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The association between short-term increases in particulate air pollution and increased cardiovascular morbidity and mortality is well documented. Recent studies suggest an association between particulate matter with aerodynamic diameter < 2.5 microm (PM2.5) and supraventricular arrhythmias (SVA), but the results have been inconsistent. We evaluated this hypothesis in a rat model of acute myocardial infarction (AMI). Diazepam-sedated Sprague-Dawley rats with AMI were exposed (1 h) to either filtered air (n = 16), concentrated ambient fine particles (CAPS; mean = 645.7 microg/m3; n = 23), carbon monoxide (CO; 35 ppm; n = 19), or CAPs and CO (n = 24). Each exposure was immediately preceded and followed by a 1-h exposure to filtered air (baseline and postexposure periods, respectively). Surface electrocardiograms were recorded and the frequency of supraventricular premature beats was quantified. Among rats in the CAPS group, the probability of observing any SVA decreased from baseline to the exposure and postexposure periods. This pattern was significantly different than that observed for the filtered air group during the exposure period (p = .048) only. In the subset of rats with one or more SVA during the baseline period, the change in SVA rate from baseline to exposure period was significantly lower in the CAPS (p = .04) and CO (p = .007) groups only, as compared to the filtered air group. No significant effects were observed in the group simultaneously exposed to CAPS and CO. Thus, the results of this study do not support the hypothesis that exposure to ambient air pollution increases the risk or frequency of supraventricular arrhythmias.

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Section: Exposure Technology and Characterizationmentioning

confidence: 99%

Effects of Ambient Particles and Carbon Monoxide on Supraventricular Arrhythmias in a Rat Model of Myocardial Infarction

Wellenius

Coull

Batalha³

et al. 2006

Inhalation Toxicology

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“…MSHA has been studied in the past and has shown no effect on breathing pattern during inhalation studies at higher doses than used in this study (Martin et al, 1986, Raub et al, 1985, Wiester et al, 1985). Some mild inflammatory effects have been shown after high dose instillation studies (Martin et al, 1986, Raub et al, 1985, Sanders et al, 1982, Vallyathan et al, 1983), but not after inhalation studies (Savage et al, 2003, Raub et al, 1985). Therefore, the breathing pattern changes produced by P+MSHA exposure are most likely the result of the tailpipe emissions rather than the MSHA.…”

Section: Discussionmentioning

confidence: 99%

“…Mt St Helens Ash (MSHA) (density, ρ p = 2.6 g/cm 3 ) was used as a seed particle because it is both chemically and toxicologically inert (Martin et al, 1986, Raub et al, 1985, Savage et al, 2003, Wiester et al, 1985). The seed aerosol was added to decrease the time required to form a stable accumulation mode size distribution, and to allow exposures to both types of atmospheres (primary and secondary) to be conducted with mass concentrations on the same order of magnitude.…”

Section: Methodsmentioning

confidence: 99%

Effects of fresh and aged vehicular exhaust emissions on breathing pattern and cellular responses – pilot single vehicle study

Diaz¹,

Chung

Papapostolou³

et al. 2012

Inhalation Toxicology

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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 five hours to either filtered room air (Sham) or one of two different atmospheres: 1. Diluted Car Exhaust (P) + Mt. Saint Helens Ash (MSHA); 2. P+MSHA+SOA (Secondary Organic Aerosol, formed during simulated photochemical aging of diluted exhaust). Primary and secondary gases were removed using a non-selective diffusion denuder. Continuous respiratory data was collected during the exposure, and broncho-alveolar lavage (BAL) and complete blood counts (CBC) were performed 24 hours 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.

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“…In the mid-1990s, the development of virtual impactor particle concentrators and centrifugal particle concentrators allowed inhalation exposures to ambient particles at concentrations 10 to 100-fold higher than found in ambient air. These concentrated ambient particles (CAPs) represent the naturally occurring PM mixture, and thus represent the most realistic PM exposure possible (Sioutas et al, 1995;Green and Armstrong, 2003;Demokritou et al, 2003;Savage et al, 2003). Airborne gases are not concentrated, allowing the researcher to test the effects of realtime exposures of animals to a particle mixture that maintains the physicochemical properties of ambient PM.…”

Section: Introductionmentioning

confidence: 99%

Cardiopulmonary Toxicity Induced by Ambient Particulate Matter (BI City Concentrated Ambient Particle Study)

Rohr¹,

Morishita²,

Keeler³

et al. 2010

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Does the Harvard/U.S. Environmental Protection Agency Ambient Particle Concentrator Change the Toxic Potential of Particles?

Abstract: ABSTRACT

Cited by 12 publications

References 27 publications

Effects of Ambient Particles and Carbon Monoxide on Supraventricular Arrhythmias in a Rat Model of Myocardial Infarction

Effects of Ambient Particles and Carbon Monoxide on Supraventricular Arrhythmias in a Rat Model of Myocardial Infarction

Effects of fresh and aged vehicular exhaust emissions on breathing pattern and cellular responses – pilot single vehicle study

Cardiopulmonary Toxicity Induced by Ambient Particulate Matter (BI City Concentrated Ambient Particle Study)

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