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. National surveys in the past five years have shown a 7% increase in the number of workers sleeping six hours or less and a 9% decrease in those sleeping seven hours or more. 1 Decreased nocturnal sleep can lead to sleepiness, errors, and accidents during the daytime. 2 Even after a normal sleep at night, the mid-afternoon period (around 14:00) is characterized by decreased alertness, poor performance, and frequent errors in the workplace; or what has been recognized as the "post-lunch dip." 3-5 Thus, it is important to seek practical solutions to diminished daytime function resulting from less sleep.Recent research has documented that naps of less than 30 minutes are a promising strategy for counteracting the effects of a short sleep period of 4-5 hours the preceding night. [6][7][8][9] This research evaluated the roles of repeated (polyphasic) naps or a single nap taken in the morning or mid-afternoon. Such patterns of napping, however, seem unfeasible in most work settings, because of the obvious conflict with work schedules. In a previous study, we hypothesized that a post-lunch rest is an appropriate time to take a nap in the workplace, and therefore investigated the effects of a 15-minute nap taken at 12:30. 10 The results showed greater alertness and performance after the 15-min ute nap than after no nap or a 45-minute nap. These findings are in agreement with the latest evidence showing improved alertness after a 20-minute nap scheduled at 12:20 in a study in which the effects of meals and time cues were controlled. 11 However, since the subjects in both studies had a normal sleep the night before testing, the effects of a post-lunch nap following a short sleep remain to be determined.The purpose of the present study was to examine whether a 15-minute nap taken during post-lunch rest improves subsequent alertness and performance under prior sleep deficit. The effects of the nap were assessed by the P300 event-related potential (ERP) and neurobehavioral tasks. We also investigated the autonomic effects of the nap by measuring the electrocardiographic (ECG) R-R interval variability. METHODS SubjectsTwelve healthy students served as subjects for this experiment (7 males and 5 females, mean age 22.1±1.6 SD years). None of them reported sleep complaints or any history of medical disorders. Their habitual sleep duration was Abstract: We examined the effects of a 15-min nap after lunch on subsequent alertness, performance, and autonomic function following a short sleep the preceding night. Subjects were 12 healthy students who had slept for only 4 hours the night before being tested. They experienced both nap and no-nap conditions in a counterbalanced order, at least a week apart. The nap condition included a 15-min nap opportunity (12:30-12:45) in bed with polygraphic monitoring. We measured the P300 event-related potential, subjective sleepiness (Visual Analog Scale), and electrocardiogram (ECG) at 10:00, 13:15, and 16:15, and task performance (logical reasoning and digit span) at 10: 00, 11:30, 13:15, 14:45...

Genotoxicity and Cytotoxicity of Multiwall Carbon Nanotubes in Cultured ChineseHamster Lung Cells in Comparison with Chrysotile A Fibers: Masumi ASAKURA, et al. Japan Bioassay Research Center, Japan Industrial Safety and Health Association-Objectives: The potential applications and industrial production of multi-wall carbon nanotubes (MWCNT) have raised serious concerns about their safety for human health and the environment. The present study was designed to examine the in vitro cytotoxicity and genotoxicity of MWCNT and UICC chrysotile A (chrysotile). Methods: Cytotoxicity using both colony formation and lactate dehydrogenase (LDH) assays and genotoxicity including chromosome aberration, micronucleus induction and hgprt mutagenicity were examined by exposing cultured Chinese hamster lung (CHL/IU) cells to MWCNT or chrysotile at different concentrations. Results:The in vitro cytotoxicity of MWCNT depended on the solvent used for suspension of MWCNT and ultrasonication duration of the MWCNT suspension. A combination of DMSO/culture medium and 3-minute ultrasonication resulted in a well-dispersed medium with dispersion and isolation of agglomerated MWCNT by ultrasonication which manifested the highest cytotoxicity. The cytotoxicity was more potent for chrysotile than MWCNT. The genotoxicity of MWCNT was characterized by the formation of polyploidy without structural chromosome aberration, and an increased number of bi-and multi-nucleated cells without micronucleus induction, as well as negative hgprt mutagenicity. Chrysotile exhibited essentially the same genotoxicity as MWCNT, except for marginal but significant induction of micronuclei. MWCNT and chrysotile were incompletely internalized in the cells and localized in the cytoplasm. Conclusions: MWCNT and chrysotile were cytotoxic and genotoxic in Chinese hamster lung cells, but might interact indirectly with DNA. The results suggest that both test substances interfere physically with biological processes during cytokinesis. (J Occup Health 2010; 52: 155-166)

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Inhalation Carcinogenicity and ChronicToxicity of Indium-tin Oxide in Rats and Mice: Kasuke NagaNo, et al. Japan Bioassay Research Center, Japan Industrial Safety and Health Association-Objectives: Carcinogenicity and chronic toxicity of indium-tin oxide (ITO) were examined by inhalation exposure of rats and mice to ITO aerosol. Methods: Fifty mice of both sexes were exposed to ITO at 0 (control), 0.01, 0.03 or 0.1 mg/m 3 for 6 h/day, 5 day/wk for 104 wk, and 50 rats of both sexes were exposed to 0, 0.01 or 0.03 mg/m 3 ITO for the same time period. The repeated exposure of 50 rats of both sexes to 0.1 mg/m 3 ITO was discontinued at the 26th wk, followed by clean air exposure for the remaining 78 wk. Results: In rats, incidences of bronchiolo-alveolar adenomas and carcinomas, bronchiolo-alveolar hyperplasia, alveolar wall fibrosis and thickened pleural wall, alveolar proteinosis and infiltrations of alveolar macrophages and inflammatory cells were significantly increased. Combined incidences of malignant lung tumors in male rats and total lung tumors in male and female rats were significantly increased at exposure to 0.01 mg/m 3 ITO. In mice, no carcinogenic response occurred, but thickened pleural wall, alveolar proteinosis and alveolar macrophage infiltration were induced. Mice were less susceptible to ITO than rats. The lung content of indium was the greatest, followed by the spleen, kidney and liver. Blood indium levels increased dosedependently. Conclusions: There was clear evidence of carcinogenicity of inhaled ITO in male and female rats but not clear evidence in mice, together with occurrence of the chronic pulmonary lesions in both rats and mice. (J Occup Health 2011; 53: 175-187)