A Churg and M Brauer
Department of Pathology, University of British Columbia, Vancouver, Canada.

There is extensive epidemiologic evidence that increased levels of the inhalable particulate fraction of air pollution (PM10) are associated with increased morbidity and mortality. The mechanisms of these effects are unknown, and the exact types and sizes of particles responsible are a matter of intense dispute. To obtain an idea of the sizes of particles retained in human lung parenchyma, we used analytical electron microscopy to count, size, and identify particles in the upper lobe apical segment parenchyma of autopsy lung tissue from 10 never- smoking long-term residents of Vancouver. The overall geometric mean particle diameter (GSD) was 0.38 microm (2.4); within this broad distribution, silica and silicate particles had a geometric mean diameter of 0.49 microm (2.2), whereas metals had a geometric mean diameter of 0.17 microm (2.0). Ultrafine particles (those with diameter < or = 0.1 microm) constituted less than 5% of the total, and most of these were metals. Translation of these projected area diameters into aerodynamic diameters (d(a)) revealed that 96% of the particles had d(a) less than 2.5. These data indicate that human lung parenchyma effectively retains PM2.5, suggesting that attempts to determine the particles responsible for chronic particulate pollutant effects should concentrate on this size range. These data also suggest that several different type/size classes of particle are present in human parenchyma, but that ultrafine particles make up only a small fraction of the total.

This article has been cited by other articles:

				D. Olivieri and E. Scoditti Impact of environmental factors on lung defences Eur. Respir. Rev., December 1, 2005; 14(95): 51 - 56. [Abstract] [Full Text] [PDF]

				U. C. Nygaard, M. Samuelsen, A. Aase, and M. Lovik The Capacity of Particles to Increase Allergic Sensitization Is Predicted by Particle Number and Surface Area, Not by Particle Mass Toxicol. Sci., December 1, 2004; 82(2): 515 - 524. [Abstract] [Full Text] [PDF]

				R. L. Johnson Jr Relative Effects of Air Pollution on Lungs and Heart Circulation, January 6, 2004; 109(1): 5 - 7. [Full Text] [PDF]

				H. Takizawa, S. Abe, H. Okazaki, T. Kohyama, I. Sugawara, Y. Saito, T. Ohtoshi, S. Kawasaki, M. Desaki, K. Nakahara, et al. Diesel exhaust particles upregulate eotaxin gene expression in human bronchial epithelial cells via nuclear factor-kappa B-dependent pathway Am J Physiol Lung Cell Mol Physiol, June 1, 2003; 284(6): L1055 - L1062. [Abstract] [Full Text] [PDF]

				G. D'Amato, G. Liccardi, M. D'Amato, and M. Cazzola Outdoor air pollution, climatic changes and allergic bronchial asthma Eur. Respir. J., September 1, 2002; 20(3): 763 - 776. [Abstract] [Full Text] [PDF]

				S. Kawasaki, H. Takizawa, K. Takami, M. Desaki, H. Okazaki, T. Kasama, K. Kobayashi, K. Yamamoto, K. Nakahara, M. Tanaka, et al. Benzene-Extracted Components Are Important for the Major Activity of Diesel Exhaust Particles . Effect on Interleukin-8 Gene Expression in Human Bronchial Epithelial Cells Am. J. Respir. Cell Mol. Biol., April 1, 2001; 24(4): 419 - 426. [Abstract] [Full Text]

				R. Sarangapani and A. S. Wexler The Role of Dispersion in Particle Deposition in Human Airways Toxicol. Sci., March 1, 2000; 54(1): 229 - 236. [Abstract] [Full Text] [PDF]

				S. H. GAVETT, S. L. MADISON, M. A. STEVENS, and D. L. COSTA Residual Oil Fly Ash Amplifies Allergic Cytokines, Airway Responsiveness, and Inflammation in Mice Am. J. Respir. Crit. Care Med., December 1, 1999; 160(6): 1897 - 1904. [Abstract] [Full Text]

				H. Takizawa, T. Ohtoshi, S. Kawasaki, T. Kohyama, M. Desaki, T. Kasama, K. Kobayashi, K. Nakahara, K. Yamamoto, K. Matsushima, et al. Diesel Exhaust Particles Induce NF-{kappa}B Activation in Human Bronchial Epithelial Cells In Vitro: Importance in Cytokine Transcription J. Immunol., April 15, 1999; 162(8): 4705 - 4711. [Abstract] [Full Text] [PDF]