Persistent DNA damage measured by comet assay of Sprague Dawley rat lung cells after five days of inhalation exposure and 1 month post-exposure to dispersed multi-wall carbon nanotubes (MWCNTs) generated by new MWCNT aerosol generation system.

Carbon nanotubes (CNTs) have specific physico-chemical properties that are useful for the electronics, automotive, and construction industries. Yet, despite their many advantages, there is a current lack of available information on the human health and environmental hazards of CNTs. For this reason, the current study investigated the inhalation toxicity potential of multiwall CNTs (MWCNTs). Eight-week-old rats were divided into four groups (10 rats in each group), the fresh-air control (0mg/m(3)), low-concentration group (0.16mg/m(3)), middle-concentration group (0.34mg/m(3)), and high-concentration group (0.94mg/m(3)), and the whole body was exposed to MWCNTs for 5 days (6h/day). Lung cells were then isolated from five rats in each group on day 0 and 1 month after the 5-day exposure, respectively. The MWCNTs were generated by a newly designed generation system, and the MWCNT concentrations in the exposure chambers monitored in accordance with National Institute for Occupational Safety and Health (NIOSH) 0500 using a membrane filter. The MWCNTs were also sampled for an elemental carbon concentration analysis using a glass filter. The animals exhibited no significant body weight changes, abnormal clinical signs, or mortality during the experiment. A single-cell gel electrophoresis assay (Comet assay) was conducted to determine the DNA damage in lung cells obtained from the right lung. As a result, the Olive tail moments were 23.00±1.76, 30.39±1.96, 22.96±1.26, and 33.98±2.21 for the control, low-, middle-, and high-concentration groups, respectively, on day 0 postexposure. Meanwhile, 1 month postexposure, the Olive tail moments were 25.00±2.71, 28.39±3.55, 22.56±1.36, and 31.97±3.16 for the control, low-, middle-, and high-concentration groups, respectively. Thus, the MWCNTs caused a statistically significant increase in lung DNA damage at high concentration (0.94mg/m(3)) when compared with the negative control group on day 0 and 1 month postexposure.