Tuesday, March 03, 2009

Fullerene Inhalation Impacts Immune Response - Another Nanoparticle Hazard ID

ToxicologyVolume 258, Issue 1, 5 April 2009, Pages 47-55
Gene expression profiles in rat lung after inhalation exposure to C60 fullerene particles

Katsuhide Fujitaa, , , Yasuo Morimotob, Akira Ogamib, Toshihiko Myojyob, Isamu Tanakab, Manabu Shimadac, Wei-Ning Wangc, Shigehisa Endohd, Kunio Uchidad, Tetsuya Nakazatod, Kazuhiro Yamamotoe, Hiroko Fukuia, Masanori Horiea, Yasukazu Yoshidaa, Hitoshi Iwahashia and Junko Nakanishif
aHealth Technology Research Center, National Institute of Advanced Industrial Science and Technology (AIST), Onogawa 16-1, Tsukuba, Ibaraki 305-8569, Japan
bInstitute of Industrial Ecological Sciences, University of Occupational and Environmental Health, Kitakyushu 807-8555, Japan
cGraduate School of Engineering, Hiroshima University, Higashi Hiroshima 739-8527, Japan
dResearch Institute for Environmental Management Technology, National Institute of Advanced Industrial Science and Technology (AIST), Tsukuba 305-8569, Japan
eResearch Institute of Instrumentation Frontier, National Institute of Advanced Industrial Science and Technology (AIST), Tsukuba 305-8568, Japan
fResearch Institute of Science for Safety and Sustainability, National Institute of Advanced Industrial Science and Technology (AIST), Tsukuba 305-8569, Japan

Concern over the influence of nanoparticles on human health has risen due to advances in the development of nanotechnology. We are interested in the influence of nanoparticles on the pulmonary system at a molecular level. In this study, gene expression profiling of the rat lung after whole-body inhalation exposure to C60 fullerene (0.12 mg/m3; 4.1 × 104 particles/cm3, 96 nm diameter) and ultrafine nickel oxide (Uf-NiO) particles (0.2 mg/m3; 9.2 × 104 particles/cm3, 59 nm diameter) as a positive control were employed to gain insights into these molecular events. In response to C60 fullerene exposure for 6 h a day, for 4 weeks (5 days a week), C60 fullerene particles were located in alveolar epithelial cells at 3 days post-exposure and engulfed by macrophages at both 3 days and 1 month post-exposures. Gene expression profiles revealed that few genes involved in the inflammatory response, oxidative stress, apoptosis, and metalloendopeptidase activity were up-regulated at both 3 days and 1 month post-exposure. Only some genes associated with the immune system process, including major histocompatibility complex (MHC)-mediated immunity were up-regulated. These results were significantly different from those of Uf-NiO particles which induced high expression of genes associated with chemokines, oxidative stress, and matrix metalloproteinase 12 (Mmp12), suggesting that Uf-NiO particles lead to acute inflammation for the inhalation exposure period, and the damaged tissues were repaired in the post-exposure period. We suggest that C60 fullerene might not have a severe pulmonary toxicity under the inhalation exposure condition.
BrooklynDodger(s) comment: There's a bit of "don't worry, be happy" in the final conclusion here. Fullerenes are really high tech carbon black, and carbon black is a 2A carcinogen. The study indicates that inhalation at 120 ug/cm3 affects immune response, but doesn't have the inflammatory response of nickel oxide, also a carcinogen. But, the nickel oxide exposure involved substantially more mass, more than twice the particle number, and substantially smaller particles. It would have been better to include an ultrafine carbon black to determine whether there was a differential with fullerenes.

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