作者: G. Oberdörster , Z. Sharp , V. Atudorei , A. Elder , R. Gelein
DOI: 10.1080/08958370490439597
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摘要: Ultrafine particles (UFP, <100 nm) are ubiquitous in ambient urban and indoor air from multiple sources may contribute to adverse respiratory cardiovascular effects of particulate matter (PM). Depending on their particle size, inhaled UFP efficiently deposited nasal, tracheobronchial, alveolar regions due diffusion. Our previous rat studies have shown that can translocate interstitial sites the tract as well extrapulmonary organs such liver within 4 24 h postexposure. There were also indications olfactory bulb brain was targeted. objective this follow-up study, therefore, determine whether translocation ultrafine solid takes place, hypothesizing depositing mucosa nasal region will along nerve into bulb. This should result significant increases days following exposure opposed other areas central nervous system (CNS). We generated elemental 13 C (CMD = 36 nm; GSD 1.66) [ C] graphite rods by electric spark discharge an argon atmosphere at a concentration 160 µg/m 3 . Rats exposed for 6 h, lungs, cerebrum, cerebellum bulbs removed 1, 3, 5, 7 after exposure. concentrations determined isotope ratio mass spectroscopy compared background levels sham-exposed controls (day 0). The corrected pulmonary added day 1 postexposure 1.34 µg/lung. Lung decreased 1.39 µg/g 1) 0.59 persistent increase 0.35 which increased 0.43 7. Day cerebrum significantly but inconsistent, only one additional period, possibly reflecting across blood‐brain barrier certain regions. consistent with earlier nonhuman primates rodents demonstrated intranasally instilled axons CNS. conclude our study CNS be targeted airborne most likely mechanism is deposits nasopharyngeal subsequent via nerve.