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ToxSci Advance Access originally published online on January 27, 2008
Toxicological Sciences 2008 103(1):108-115; doi:10.1093/toxsci/kfn014
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© The Author 2008. Published by Oxford University Press on behalf of the Society of Toxicology. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org
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Cellular Response to Diesel Exhaust Particles Strongly Depends on the Exposure Method

Amara L. Holder*,1, Donald Lucas{dagger}, Regine Goth-Goldstein{dagger} and Catherine P. Koshland{ddagger}

* Department of Mechanical Engineering, University of California Berkeley, Berkeley, California 94720-1740 {dagger} Environmental Energy Technologies Division, Lawrence Berkeley National Laboratory, Berkeley, California 94720-8168 {ddagger} Division of Environmental Health Sciences, School of Public Health, University of California Berkeley, Berkeley, California 94720-7360

1 To whom correspondence should be addressed at 1 Cyclotron Rd MS 70-108B, Berkeley, CA 94720-8168. Fax: (510) 486-7303. E-mail: aholder{at}lbl.gov.

Received November 2, 2007; accepted January 16, 2008


   Abstract

In vitro exposure to aerosols at the air–liquid interface (ALI) preserves the physical and chemical characteristics of aerosol particles. Although frequently described as being a more physiologic exposure method, ALI exposure has not been directly compared with conventional in vitro exposures where the particles are suspended in medium. We exposed immortalized human bronchial epithelial cells (16HBE14o) to aerosolized diesel exhaust particles at the ALI and to suspensions of collected particles. The response of the cells was determined from measurements of the cell viability and interleukin-8 (IL-8) secretion. The deposited size distribution at the cell surface was measured with transmission electron microscopy to obtain a dose for the ALI exposure. Although exposure by either method caused a slight decrease in cell viability and induced IL-8 secretion, the response to ALI exposure occurred at doses several orders of magnitude lower than exposure to particles in suspension. The most likely sources for the different dose responses are the artifacts introduced during the collection and resuspension of particles for conventional suspension exposures. The number concentration of particles deposited at the ALI is similar to the modeled deposition in the tracheal–bronchial region in a human lung, but the ALI size distribution is skewed toward particles larger than those deposited in the lung.

Key Words: air–liquid interface; particle deposition; ultrafine particles; nanoparticle toxicology.


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