Translocation and potential neurological effects of fine and ultrafine particles a critical update

Annette Peters¹^,2 , Bellina Veronesi³ , Lilian Calderón-Garcidueñas⁴^,5 , Peter Gehr⁶ , Lung Chi Chen⁷ , Marianne Geiser⁶ , William Reed⁸ , Barbara Rothen-Rutishauser⁶ , Samuel Schürch⁶^,9 and Holger Schulz²^,10

¹Institute of Epidemiology, GSF-National Research Center for Environment and Health, Neuherberg, Germany

²Focus Network of Aerosols and Health, GSF-National Research Center for Environment and Health, Neuherberg, Germany

³National Health and Environmental Effects Research Laboratory, Neurotoxicology Division, US Environmental Protection Agency, RTP, NC, USA

⁴Instituto Nacional de Pediatría, Mexico City 14410, Mexico

⁵The Center for Structural and Functional Neurosciences, University of Montana, Missoula, MT 59812, USA

⁶Institute of Anatomy, University of Bern, 3012 Bern, Switzerland

⁷New York University School of Medicine, Department of Environmental Medicine, Tuxedo, NY, USA

⁸Department of Pediatrics and Center for Environmental Medicine, Asthma and Lung Biology, University of North Carolina, 27599-7310, USA

⁹Department of Physiology and Biophysics, University of Calgary, Canada

¹⁰Institute for Inhalation Biology, GSF-National Research Center for Environment and Health, Neuherberg, Germany

author email corresponding author email

Particle and Fibre Toxicology 2006, 3:13doi:10.1186/1743-8977-3-13


Published:	8 September 2006

Abstract

Particulate air pollution has been associated with respiratory and cardiovascular disease. Evidence for cardiovascular and neurodegenerative effects of ambient particles was reviewed as part of a workshop. The purpose of this critical update is to summarize the evidence presented for the mechanisms involved in the translocation of particles from the lung to other organs and to highlight the potential of particles to cause neurodegenerative effects.

Fine and ultrafine particles, after deposition on the surfactant film at the air-liquid interface, are displaced by surface forces exerted on them by surfactant film and may then interact with primary target cells upon this displacement. Ultrafine and fine particles can then penetrate through the different tissue compartments of the lungs and eventually reach the capillaries and circulating cells or constituents, e.g. erythrocytes. These particles are then translocated by the circulation to other organs including the liver, the spleen, the kidneys, the heart and the brain, where they may be deposited. It remains to be shown by which mechanisms ultrafine particles penetrate through pulmonary tissue and enter capillaries. In addition to translocation of ultrafine particles through the tissue, fine and coarse particles may be phagocytized by macrophages and dendritic cells which may carry the particles to lymph nodes in the lung or to those closely associated with the lungs. There is the potential for neurodegenerative consequence of particle entry to the brain. Histological evidence of neurodegeneration has been reported in both canine and human brains exposed to high ambient PM levels, suggesting the potential for neurotoxic consequences of PM-CNS entry. PM mediated damage may be caused by the oxidative stress pathway. Thus, oxidative stress due to nutrition, age, genetics among others may increase the susceptibility for neurodegenerative diseases. The relationship between PM exposure and CNS degeneration can also be detected under controlled experimental conditions. Transgenic mice (Apo E -/-), known to have high base line levels of oxidative stress, were exposed by inhalation to well characterized, concentrated ambient air pollution. Morphometric analysis of the CNS indicated unequivocally that the brain is a critical target for PM exposure and implicated oxidative stress as a predisposing factor that links PM exposure and susceptibility to neurodegeneration.

Together, these data present evidence for potential translocation of ambient particles on organs distant from the lung and the neurodegenerative consequences of exposure to air pollutants.