Characteristics of short sleeping time and eating behaviors related to obesity.

OBJECTIVE: To clarify the relation between short sleeping time, obesity and eating behaviors in male workers. METHODS: A self-completed questionnaire survey of 680 male daytime workers (age 19-60 years, mean age 42.9 ± 12.5 years) at a manufacturing plant was conducted in 2005. Subjects were divided into two groups by body mass index (BMI): 480 non-obese men with BMI of <25.0 kg/m(2) (mean age 42.8 ± 12.8 years) and 200 obese men with BMI of ≥25.0 kg/m(2) (mean age 43.3 ± 11.7 years). Basic attributes and living habits were then investigated, and the relation of eating behavior to each BMI level was analyzed. BMI and eating behaviors were also investigated in relation to sleeping time. RESULTS: Sleeping time was significantly shorter in obese men than in non-obese men. Multiple regression analysis showed that sleep time as well as living with family were independent factors for greater BMI. BMI increased as sleeping hours became shorter in the order of ≥9 h, 8 h, 7 h, and ≤6 h. With shorter sleeping time, the mean eating behaviors scores also increased for cognition of constitution, substitution eating and drinking, feeling of satiety, meal contents, eating rhythm abnormalities, and eating style. The mean scores for these eating behaviors all increased with level of obesity, and these behaviors were characteristic of the obese men. CONCLUSIONS: This study showed that people with short sleeping times tended to have eating behaviors of eating more, which can lead to obesity. Short sleeping time may contribute to eating much and then obesity.

Eating behavior related to obesity and job stress in male Japanese workers.

OBJECTIVE: We examined a possible relation among obesity, eating behavior, and job stress in male Japanese workers. METHODS: A questionnaire survey on lifestyle, eating behavior, and job stress was conducted with 595 male daytime workers (19-60 y of age, mean +/- SD 41.8 +/- 12.6 y of age) in a synthetic-fiber manufacturing plant. The 431 non-obese men (body mass index <25.0 k/m(2), mean age 41.7 +/- 12.9 y) and 164 obese men (body mass index > or = 25.0 k/m(2), mean age 42.0 +/- 11.9 y) were examined in relation to obesity, eating behavior, and job stress. Body mass index was calculated from height and weight measured in an annual health check. RESULTS: Obesity was associated with eating behaviors such as eating to satiety, eating fast, and substitution eating from irritability. These eating behaviors were related to high job demands of quantitative workload. The eating behaviors were also correlated with psychological stress responses of fatigue, tension/anxiety, and depression, which were associated with quantitative workload. CONCLUSION: The present study suggests that high job demands of quantitative workload may be a factor related to eating behavior to eat a lot among male Japanese workers. Increased workplace stress from job strain may affect the workers through eating behaviors to eat a lot that contribute to obesity.

Pulmonary effects and biopersistence of deposited silicon carbide whisker after 1-year inhalation in rats.

Silicon carbide whisker (SiCW) is a durable asbestos substitute. To clarify the biopersistence, the changes of geometrical configurations of deposited whiskers, and potential carcinogenicity and fibrogenicity, 42 Wistar male rats were exposed to SiCW for 6 h/day, 5 days/wk for 1 yr by inhalation. The mass median aerodynamic diameter (geometric standard deviation, GSD), the geometric mean fiber diameter (GSD), and the geometric mean fiber length (GSD) were 2.4 microm (2.4), 0.5 microm (1.5) and 2.8 microm (2.3), respectively. The daily average exposure concentrations were 2.6 +/- 0.4 mg/m3 (98 +/- 19 fibers/ml) and the rats were sacrificed at 6 days and 3, 6, and 12 mo after the exposure. The SiCW amount deposited in each rat lung at 6 days after the exposure, determined by an x-ray diffraction method, was 5.3 +/- 1.4 mg. The biological half-time (BHT) was 16 mo calculated from the deposited SiCW at 6 days and 3, 6, and 12 mo. The BHT was more prolonged than normal physiological clearance. The diameter of SiCW in the lung at each sacrificed time during 12 mo of clearance after the inhalation did not change. However, as for the length of SiCW in the lung, longer SiCW tended to be retained in the lung as the clearance time increased, especially after 6 mo. The histopathological examination revealed bronchoalveolar hyperplasia (BAH) in 2 rats at 1 yr after the exposure and severe fibrotic changes around aggregated SiCW.

The effect of lung burden on biopersistence and pulmonary effects in rats exposed to potassium octatitanate whiskers by intratracheal instillation.

In our previous inhalation studies on health effects of the asbestos substitute, potassium octatitanate whiskers (POW), we showed that an excess amount of POW deposition in the rat lung increased biopersistence resulting in fibrotic changes. The critical deposition amount which induced the higher biopersistence was estimated to lie between 1.5 mg and 2.4 mg. In order to find the exact amount, the relationship between the lung POW burden and biopersistence was investigated by the intratracheal instillation method. The chemical formula of POW is K2Ti8O17 and the geometric mean fiber diameter (geometric standard deviation, GSD) and geometric mean fiber length (GSD) are 0.35 microm (1.6) and 4.4 microm (2.7), respectively. Rats were intratracheally instilled with 0.5 mg, 1.0 mg, 2.0 mg or 5.0 mg of POW and sacrificed at 1 day and 1, 3, 6 and 12 months after the instillation. The POW amount in each lung was chemically analyzed by ICP-AES after microwave digestion and the biological half time (BHT) of each POW dose was calculated. The BHTs of each group were 10, 15, 20 and 42 months for 0.5, 1.0, 2.0 and 5.0 mg of POW, respectively, and BHT showed a linear dose-dependent increase, but without a threshold within the range of 0.5 mg to 5.0 mg, which was recognized in our earlier inhalation studies. In the histopathological photograph just after the instillation, many macrophages, which had phagocytized many more fibers, existed around the bronchiole compared with the earlier inhalation study at almost the same deposited amount. The relationship between POW amount and biopersistence in this intratracheal instillation study was different from that of our previous inhalation studies, probably due to the unnatural method of the fiber introduction to the lung, which in turn led to a different fiber distribution. It is suggested that an intratracheal instillation study is not an appropriate method for estimating excess deposition amounts of POW and an inhalation study will be needed. However, this intratracheal instillation study clarified that the clearance of POW was delayed as compared with previous inhalation studies at similar deposition amounts and this result has importance for the hazard assessment of dusts in animal experiments.

The effect of lung burden on biopersistence and pulmonary effects in rats exposed to potassium octatitanate whiskers by inhalation.

The effect of lung burden on biopersistence and histopathological changes caused by potassium octatitanate whiskers (POW) which is one of the asbestos substitutes were investigated for 1-yr and 4-wk inhalation periods. In the 1-yr inhalation experiment, male Wistar rats were exposed to POW (TW) for 6 h/d, 5 d/wk under the same conditions as a previous study of POW (PT1, JFM fiber) which is made by different manufacturer. The exposure concentration was 1.9 +/- 0.7 mg/m(3) and the mass median aerodynamic diameter (MMAD) and geometric standard deviation (GSD) in the chamber were 1.6 microm and 2.9. Rats were sacrificed at 3 d and 1 yr after the inhalation experiment and TW deposits in the lungs were determined by ICP-AES. Lung burden at 3 d and 1 yr after the inhalation was 2.39 +/- 0.50 mg and 1.37 +/- 0.96 mg, respectively, the deposition fraction was 8.1% and biological half time (BHT) was 15 months. Aggregated dust cells and mild fibrotic changes around these dust cells were observed in the exposed rat lung. These results were almost the same as those obtained in the previous 1-yr PT1 study. In the 4-wk inhalation experiment, to investigate the effect of lung burden on biopersistence and histopathological change, male Wistar rats were exposed to PT1. The exposure concentration was 102 +/- 21 mg/m(3), MMAD (GSD), the geometiric mean length and diameter (GSD) of the PT1 in the chamber were 1.6 microm (3.0), 2.2 microm (1.8) and 0.33 microm (1.5), respectively. Rats were sacrificed at 3 d, 1 wk, and 1, 3, 6 and 12 months after the inhalation experiment. The lung burden of POW at 3 d after 4 wk inhalation was 1.49 +/- 0.19 mg, which was close to the estimated amount of overload. The BHT of the total mass (4.1 months) was not prolonged, but aggregated dust cells were observed in the subpleural region and around the bronchioles and mild fibrotic changes were observed only around the dust cells at one year after the 4-wk inhalation. It is considered that the excessive exposure which impairs the function of alveolar macrophage mediated clearance may cause the aggregation of dust cells and fibrotic changes.

[Method for installing an effective smoking room and the effectiveness of real-time monitoring].

We investigated the methodology for installing effective smoking rooms in workplaces. It is absolutely necessary to install exhaust ventilation in smoking rooms. There are two bases for deciding the exhaust ventilation rate. The most important is to eliminate the leakage of environmental tobacco smoke (ETS) from the smoking room. An airflow rate of more than 0.2 m/s at the opening of the smoking room is required by the Guidelines for Smoking Control in Workplaces (Ministry of Labour, Welfare and Health) to eliminate the leakage. This ventilation rate is decided by multiplying the opening area by 0.2 m/s. The second important point is to keep the concentration of ETS in the smoking room less than control concentration (0.15 mg/m3). This ventilation rate is decided by dividing the rate of generation of ETS by the control concentration. It is confirmed that an effective smoking room can be installed by following these guidelines. We used real-time monitoring to evaluate the leakage of ETS from the smoking room and the ETS concentration in the smoking room before and after the improvement. It is concluded that real-time monitoring of ETS is a useful method for evaluating the effectiveness of the smoking room.

Gene expression of surfactant protein-A and thyroid transcription factor-1 in lungs of rats exposed to silicon-carbide whisker in vivo.

Intratracheal instillation studies have shown that exposure to silicon carbide whisker (SiCW), an asbestos substitute, produces pulmonary fibrotic changes, suggesting that SICW might have a fibrogenic potential. It is thought that surfactant protein is a good biomarker of lung injury and pulmonary fibrotic activity. In order to explore whether or not surfactant protein is associated with lung disorder through exposure to SiCW, we examined the expression of SP-A, SP-C and thyroid transcription factor-1 (TTF-1), a common transcription factor of SP-A and SP-C mRNA in lungs exposed to SiCW. Male Wistar rats were administered 2 mg or 10 mg of SiCW suspended in saline by a single intratracheal instillation, and were sacrificed at 3 d, 1 wk, 1 month, 3 months and 6 months after the intratracheal instillation. RNA was subsequently extracted from the lungs, and expression of SP-A, SP-C and TTF-1 mRNA from the lungs was observed by reverse transcription-polymerase chain reaction (RT-PCR). Exposure to 2 mg of SiCW showed a decrease in mRNA of SP-A and TTF-1 at 6 months, but exposure to 10 mg of SiCW showed decreased levels of SP-A and TTF-1 mRNA at 3 d and 6 months. On the other hand, 2 mg of SiCW increased the level of SP-C mRNA from 3 d to 3 months, and 10 mg of SiCW decreased the levels of SP-C mRNA in the rat lungs at 3 d, 1 month and 6 months. No clear tendency to the expression of SP-C was observed, but the patterns of expression of TTF-1 and SP-A were similar. These data suggest that SP-A and TTF-1 are associated with not only the acute phase but also the chronic phase in lungs exposed to SiCW.

Clearance of deposited silicon carbide whisker from rat lungs inhaled during a 4-week exposure.

Pulmonary deposition and the clearance of deposited fiber particles from lungs are key determinant factors in assessing potential carcinogenicity and fibrogenicity. Forty-two Wistar male rats (9 wk old) were exposed to silicon carbide whisker (SiCW) for 6 h/d, 5 d/wk for 4 wk. The mass median aerodynamic diameter was 2.5 microm as detected by an Andersen sampler, and the geometric mean fiber diameter and length determined by a scanning electron microscope were 0.4 and 2.2 microm, respectively. The daily average exposure concentrations were 10.4 0.5 mg/m(3) (214 +/- 31 fibers/ml ) during the exposure period. The rats were sacrificed after 3 d, 2 wk, 1, 2, 3, 6 and 12 months after 4-wk exposure. At the time of sacrifice, the wet lung weights and the deposited SiCW amounts in the lungs were measured by an X ray reference method. The amount of SiCW deposited was 0.60 +/- 0.09 mg 3 d after a 4-wk exposure. The apparent deposition fraction was 4.8 +/- 0.7 (%). During the clearance period, the amount of SiCW deposited in the rat lungs decreased exponentially with the increasing duration of the clearance period. The biological half time in the one-compartment model was determined to be 4.0 months which is similar to the values for glass fiber, potassium titanate whisker and aluminium-silicate ceramic fiber under similar exposure conditions.

Expression of Clara cell secretory protein in the lungs of rats exposed to silicon carbide whisker in vivo.

Intratracheal instillation studies have shown that exposure to silicon carbide whiskers (SiCW), an asbestos substitute, produces pulmonary fibrotic changes, suggesting that SiCW might have fibrogenic potential. It has been theorized that Clara cell secretory protein (CCSP) plays a critical role in regulating the acute inflammatory response in the lung. The present study was conducted to investigate the time course of the expression of CCSP in lungs exposed to SiCW in vivo. Male Wistar rats were administered 2 mg or 10 mg of SiCW suspended in saline by a single intratracheal instillation and were sacrificed at 3 days, 1 week, 1 month, 3 months and 6 months of recovery time. The expression of CCSP was observed by reverse transcriptase-polymerase chain reaction (RT-PCR), Western blot and immunostaining. Exposure to 10 mg of SiCW decreased in levels of CCSP mRNA at 3 days, 1 week, 1 month and 6 months following intratracheal instillation. The protein level of CCSP in SiCW-exposed rats was decreased at 1 day, 3 days and 1 month after a single instillation of 2 and 10 mg. These findings suggest that CCSP are involved not only in the acute injury but also in the chronic injury of the lung exposed to SiCW.