Alison Elder

University of Rochester Medical Center

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Günter Oberdörster

University of Rochester Medical Center

Robert Gelein

University of Rochester Medical Center

Jacob N. Finkelstein

University of Rochester

David Chalupa

University of Rochester Medical Center

Iseult Lynch

University of Birmingham

Gunnar F. Nordberg

Umeå University

Wolfgang G. Kreyling

German Center for Lung Research

Uschi M. Graham

University of Kentucky

Christopher Cox

Johns Hopkins University

Robert A. Yokel

University of Kentucky

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University of Rochester

University of Rochester Medical Center

New York University

Harvard University

National Institutes of Health

Environmental Protection Agency

Research Triangle Park Foundation

Karolinska Institutet

National Institute of Environmental Health Sciences

Center for Environmental Health

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Systemic Effects of Inhaled Ultrafine Particles in Two Compromised, Aged Rat Strains

Inhalation Toxicology (2004)

Alison Elder Robert Gelein Mitra Azadniv Mark W. Frampton Jack Finkelstein

Epidemiological studies associate morbidity and mortality with exposure to particulate air pollution in elderly individuals with existing cardiopulmonary disease. These associations led to the hypothesis that inhaled particles can exert adverse effects outside of the lung, particularly on the cardiovascular system. We tested this hypothesis by examining the pulmonary and peripheral effects of inhaled ultrafine carbon particles in old rats that were injected with endotoxin (lipopolysaccharide, LPS) to model systemic gram-negative bacterial infection. Fischer 344 rats (23 mo) and spontaneously hypertensive (SH) rats (11–14 mo) were injected with LPS (2 mg/kg, ip) immediately before being exposed to inhaled ultrafine carbon particles for 6 h (150 μg/m3, CMD = 36 nm). Controls were injected with sterile saline or were sham exposed. Twenty-four hours after LPS injection, bronchoalveolar lavage (BAL) fluid, cells, and blood were obtained to assess endpoints of inflammation, oxidant stress, coagulability, and the acute-phase response. LPS did not cause an influx of neutrophils (PMNs) into the alveolar space, but did increase the number and percentage of circulating PMNs and the concentration of plasma fibrinogen in both rat strains. Inhaled ultrafine particles did not induce lung inflammation in either rat strain. In both strains, ultrafine particles (UFP) were found to decrease the number of blood PMNs, increase the intracellular oxidation of a fluorescent dye (DCFD) in blood PMNs, and affect plasma thrombin–anti-thrombin (TAT) complex and fibrinogen levels. UFP were also found to interact with ip LPS with respect to plasma TAT complex levels and blood PMN DCFD oxidation. Differences between the two rat strains were also found for TAT complex levels, BAL cell reactive oxygen species release, and DCFD oxidation in both BAL macrophages and blood PMNs. These results suggest that inhaled ultrafine carbon particles inhaled at concentrations mimicking high episodic increases in urban air can exert extrapulmonary effects in old rats and that they can change the systemic response to an inflammatory stimulus.

Ultrafine particle

Inhalation exposure

10.1080/08958370490439669

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Citations (75)

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Tian Xia Raymond F. Hamilton James C. Bonner Edward D. Crandall Alison Elder

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How do nanotubes suppress T cells?

Nature Nanotechnology (2009)

Alison Elder

10.1038/nnano.2009.167

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Effects of Surface Chemistry on the Generation of Reactive Oxygen Species by Copper Nanoparticles

ACS Nano (2012)

Miao Shi Hyun Soo Kwon Zhenmeng Peng Alison Elder Hong Yang

Mercaptocarboxylic acids with different carbon chain lengths were used for stabilizing uniform 15 nm copper nanoparticles. The effects of surface chemistry such as ligand type and surface oxidation on the reactive oxygen species (ROS) generated by the copper nanoparticles were examined. Transmission electron microscopy (TEM), powder X-ray diffraction (PXRD), UV–vis spectroscopy, and an acellular ROS assay show that ROS generation is closely related to the surface oxidation of copper nanoparticles. It was found that the copper nanoparticles with longer chain ligands had surfaces that were better protected from oxidation and a corresponding lower ROS generating capacity than did particles with shorter chain ligands. Conversely, the copper nanoparticles with greater surface oxidation also had higher ROS generating capacity.

10.1021/nn300445d

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Citations (157)

List of Contributors

Elsevier eBooks (2014)

Jan Aaseth Peter Aggett Antero Aitio Jan Alexander Shegufta Ameer

10.1016/b978-0-444-59453-2.01003-9

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Effects of On-Road Highway Aerosol Exposures on Autonomic Responses in Aged, Spontaneously Hypertensive Rats

Inhalation Toxicology (2006)

Alison Elder Jean‐Philippe Couderc Robert Gelein Shirley Eberly Christopher Cox

Alison Eldera*, Jean-Philippe Coudercb, Robert Geleina, Shirley Eberlyc, Christopher Coxc, Xiaojuang Xiab, Wojciech Zarebab, Philip Hopked, Winthrop Wattse, David Kittelsone, Mark Framptonf, Mark Utellf & Günter Oberdörsteraa Department of Environmental Medicine, University of Rochester, Rochester, New Yorkb Department of Cardiology, University of Rochester, Rochester, New Yorkc Department of Biostatistics, University of Rochester, Rochester, New Yorkd Department of Chemical Engineering, Clarkson University, Potsdam, New Yorke Department of Mechanical Engineering, University of Minnesota, Minneapolis, Minnesota, USAf Department of Pulmonary and Critical Care Medicine, University of Rochester, Rochester, New York

Ultrafine particle

Respiratory tract

Inhalation exposure

Geometric standard deviation

Respiratory Rate

Acute exposure

10.1080/08958370600985735

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Citations (77)

Formation of 8-oxo-7,8-dihydro-2′-deoxyguanosine in rat lung DNA following subchronic inhalation of carbon black

Toxicology and Applied Pharmacology (2003)

J Gallagher Reeder Sams Jeff Inmon Robert Gelein Alison Elder

Deoxyguanosine

10.1016/s0041-008x(03)00187-x

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Citations (63)

The outdoor air pollution and brain health workshop

NeuroToxicology (2012)

Michelle L. Block Alison Elder Richard L. Auten Staci D. Bilbo Honglei Chen

10.1016/j.neuro.2012.08.014

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Citations (494)

Acute pulmonary effects of ultrafine particles in rats and mice.

PubMed (2000)

Günter Oberdörster J. N. Finkelstein Carl J. Johnston Robert Gelein Christopher Cox

Ambient fine particles consist of ultrafine particles (< 100 nm) and accumulation-mode particles (approximately 100 to 1,000 nm). Our hypothesis that ultrafine particles can have adverse effects in humans is based on results of our earlier studies with particles of both sizes and on the finding that urban ultrafine particles can reach mass concentrations of 40 to 50 micrograms/m3, equivalent to number concentrations of 3 to 4 x 10(5) particles/cm3. The objectives of the exploratory studies reported here were to (1) evaluate pulmonary effects induced in rats and mice by ultrafine particles of known high toxicity (although not occurring in the ambient atmosphere) in order to obtain information on principles of ultrafine particle toxicology; (2) characterize the generation and coagulation behavior of ultrafine particles that are relevant for urban air; (3) study the influence of animals' age and disease status; and (4) evaluate copollutants as modifying factors. We used ultrafine Teflon (polytetrafluoroethylene [PTFE]*) fumes (count median diameter [CMD] approximately 18 nm) generated by heating Teflon in a tube furnace to 486 degrees C to evaluate principles of ultrafine particle toxicity that might be helpful in understanding potential effects of ambient ultrafine particles. Teflon fumes at ultrafine particle concentrations of approximately 50 micrograms/m3 are extremely toxic to rats when inhaled for only 15 minutes. We found that neither the ultrafine Teflon particles alone when generated in argon nor the Teflon fume gas-phase constituents when generated in air were toxic after 25 minutes of exposure. Only the combination of both phases when generated in air caused high toxicity, suggesting the existence of either radicals on the particle surface or a carrier mechanism of the ultrafine particles for adsorbed gas-phase compounds. We also found rapid translocation of the ultrafine Teflon particles across the epithelium after their deposition, which appears to be an important difference from the behavior of larger particles. Furthermore, the pulmonary toxicity of the ultrafine Teflon fumes could be prevented by adapting the animals with short 5-minute exposures on 3 days prior to a 15-minute exposure. This shows the importance of preexposure history in susceptibility to acute effects of ultrafine particles. Aging of the fresh Teflon fumes for 3.5 minutes led to a predicted coagulation resulting in particles greater than 100 nm that no longer caused toxicity in exposed animals. This result is consistent with greater toxicity of ultrafine particles compared with accumulation-mode particles. When establishing dose-response relationships for intratracheally instilled titanium dioxide (TiO2) particles of the size of the urban ultrafine particles (20 nm) and of the urban accumulation-mode particles (250 nm), we observed significantly greater pulmonary inflammatory response to ultrafine TiO2 in rats and mice. The greater toxicity of the ultrafine TiO2 particles correlated well with their greater surface area per mass. Ultrafine particles of carbon, platinum, iron, iron oxide, vanadium, and vanadium oxide were generated by electric spark discharge and characterized to obtain particles of environmental relevance for study. The CMD of the ultrafine carbon particles was approximately 26 nm, and that of the metal particles was 15 to 20 nm, with geometric standard deviations (GSDs) of 1.4 to 1.7. For ultrafine carbon particles, approximately 100 micrograms/m3 is equivalent to 12 x 10(6) particles/cm3. Homogeneous coagulation of these ultrafine particles in an animal exposure chamber occurred rapidly at 1 x 10(7) particles/cm3, so that particles quickly grew to sizes greater than 100 nm. Thus, controlled aging of ultrafine carbon particles allowed the generation of accumulation-mode carbon particles (due to coagulation growth) for use in comparative toxicity studies. We also developed a technique to generate ultrafine particles consisting of the stable isotope 13C by using 13C-graphite electrodes made in our laboratory from amorphous 13C powder. These particles are particularly useful tools for determining deposition efficiencies of ultrafine carbon particles in the respiratory tracts of laboratory animals and the translocation of particles to extrapulmonary sites. For compromised animals, we used acute and chronic pulmonary emphysema; a low-dose endotoxin inhalation aimed at priming target cells in the lung was also developed. Other modifying factors were age and copollutant (ozone) exposure. Exposure concentrations of the generated ultrafine particles for acute rodent inhalation studies were selected on the basis of lung doses predicted to occur in people inhaling approximately 50 micrograms/m3 urban ultrafine particles. Concentrations that achieved the same predicted lung burden per unit alveolar surface were used in rodents. (ABSTRACT TRUNCATED)

Ultrafine particle

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Pulmonary toxicity

Inhalation exposure

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Nanomaterials Versus Ambient Ultrafine Particles: An Opportunity to Exchange Toxicology Knowledge

Environmental Health Perspectives (2016)

Vicki Stone Mark R. Miller Martin J. D. Clift Alison Elder Nicholas L. Mills

Background: A rich body of literature exists that has demonstrated adverse human health effects following exposure to ambient air particulate matter (PM), and there is strong support for an important role of ultrafine (nanosized) particles. At present, relatively few human health or epidemiology data exist for engineered nanomaterials (NMs) despite clear parallels in their physicochemical properties and biological actions in in vitro models. Objectives: NMs are available with a range of physicochemical characteristics, which allows a more systematic toxicological analysis. Therefore, the study of ultrafine particles (UFP, <100 nm in diameter) provides an opportunity to identify plausible health effects for NMs, and the study of NMs provides an opportunity to facilitate the understanding of the mechanism of toxicity of UFP. Methods: A workshop of experts systematically analyzed the available information and identified 19 key lessons that can facilitate knowledge exchange between these discipline areas. Discussion: Key lessons range from the availability of specific techniques and standard protocols for physicochemical characterization and toxicology assessment to understanding and defining dose and the molecular mechanisms of toxicity. This review identifies a number of key areas in which additional research prioritization would facilitate both research fields simultaneously. Conclusion: There is now an opportunity to apply knowledge from NM toxicology and use it to better inform PM health risk research and vice versa. https://doi.org/10.1289/EHP424

Prioritization

Ultrafine particle

10.1289/ehp424

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Citations (336)