Relationships between suicidal ideation and psychosocial factors among residents living in Nagano Prefecture of Japan.

OBJECTIVES: Feeling ashamed for seeking help when distressed is known to be a critical factor promoting suicidal behaviors. The objective of this study was to examine the relationship between suicidal ideation and psychosocial factors, including worries or anxieties, having a person to confide in, feeling ashamed for seeking help when distressed, and K6 score. METHODS: Fourteen out of 77 municipalities from Nagano Prefecture participated in this questionnaire survey. Participants of both sexes over 20 years of age were randomly selected according to age distribution in each municipality. Association between suicidal ideation and sociodemographic and psychosocial factors, including "feeling ashamed for seeking help", were determined by multiple logistic regression analysis. RESULTS: Among a total of 11,100 participants, 7394 (66.6%) returned the questionnaire. 2147 participants responded properly to essential study parameters and were submitted to the final analyses. The adjusted odds ratio of suicidal ideation was 2.09 (95% CI 1.49-2.94) among participants feeling ashamed for seeking help, compared to those not feeling ashamed. Although the rate of "no person to confide in" was 4.4%, participants who responded with "no person to confide in" had significantly increased odds ratio of suicidal ideation compared with those who responded with "having a person to confide in" (OR 1.97, 95% CI 1.12-3.47). CONCLUSIONS: Our findings suggest a need for tailored intervention targeting individuals at risk by gatekeepers to encourage individuals at risk to overcome feeling ashamed for seeking help and to cultivate an appropriate person to confide in.

Inhalation carcinogenicity and toxicity of 1,2-dichloropropane in rats.

The toxicity and carcinogenicity of 1,2-dichloropropane (DCP) were examined by inhalation exposure of male and female F344 rats to DCP for either 13 wk or 2 years. In the 13-wk study, the DCP concentrations used were 125, 250, 500, 1000, or 2000 ppm (v/v), and in the 2-year study the DCP concentrations were 80, 200, or 500 ppm (v/v). Thirteen-week exposure to DCP induced hyperplasia in the respiratory epithelium and atrophy of the olfactory epithelium at 125 ppm and above. At the higher levels of exposure, hemolytic anemia and lesions of liver and adrenal gland were observed. Two-year exposure to DCP significantly increased incidences of papilloma in the nasal cavity of male and female rats exposed to 500 ppm DCP. In addition, three cases of esthesioneuroepithelioma were observed in the DCP-exposed male rats. Total nasal tumors increased in a concentration-dependent manner. Hyperplasia of the transitional epithelium and squamous cell hyperplasia, both of which were morphologically different from the hyperplasia of the respiratory epithelium observed in the 13-wk exposure study, occurred in a concentration-dependent manner; these lesions are considered to be preneoplastic lesions. Atrophy of the olfactory epithelium, inflammation of the respiratory epithelium, and squamous cell metaplasia were also seen in the 2-year study. These results demonstrate that DCP is a nasal carcinogen in rats. Lifetime cancer risks for humans exposed to DCP in the ambient air and work environment were quantitatively estimated, using both nonthreshold and threshold approaches, with the data obtained from the 2-year study.

Two-year inhalation study of carcinogenicity and chronic toxicity of 1,4-dioxane in male rats.

Carcinogenicity and chronic toxicity of 1,4-dioxane were examined by inhalation exposure of 50 male F344 rats to 1,4-dioxane vapor at 0 (clean air), 50, 250, or 1250 ppm (v/v) for 6 h/day, 5 days/wk, and 104 wk. Survival rates of 250 and 1250 ppm-exposed groups were decreased near the end of the 2-yr exposure period, due probably to the occurrence of malignant tumors. A statistically significant but marginal decrement of terminal body weight (<10%) was found in the 1250 ppm-exposed group, suggesting slight systemic toxicity. Significant changes in plasma levels of AST, ALT, ALP, and gamma-GTP and relative weight of the liver occurred in the 1250 ppm-exposed group. Dose-dependent and statistically significant increases in incidences of nasal squamous cell carcinomas, hepatocellular adenomas, and peritoneal mesotheliomas were found primarily in the 1250 ppm-exposed group. The incidences of renal cell carcinomas, fibroadenomas in the mammary gland, and adenomas in the Zymbal gland were also increased dose-dependently. Preneoplastic lesions occurred in the nasal cavity and liver of the 1,4-dioxane-exposed groups. As nonneoplastic lesions, the significantly increased incidences of nuclear enlargement, atrophy, and respiratory metaplasia in the nasal cavity were noted at 50 ppm and above. A LOAEL (lowest observed adverse effect level) was determined at 50 ppm for the nasal endpoint of general chronic toxicity. This study provides clear evidence of carcinogenicity for 1,4-dioxane in male rats. A cytotoxic-proliferative and in vivo genotoxic mode of action is suggested to operate in 1,4-dioxane-induced carcinogenesis.

Evaluation of personal exposure of workers to indium concentrations in total dust and its respirable fraction at three Japanese indium plants.

This study aimed to evaluate personal exposures of 27 workers to indium compounds as "total" dust and its "respirable" fraction in their breathing zones at 3 Japanese indium plants. Eight-hour time-weighted average (TWA) indium concentrations of personal exposure to dust collected in sampling periods of 6 h or longer were determined by ICP-MS. The arithmetic means of exposure concentrations were 0.095 mg indium (In)/m3, when sampled as total dust, and 0.059 mg In/m3, as respirable fraction. ACGIH's TLV-TWA of 0.1 mg In/m3 for total particulate matter and Acceptable Exposure Concentration Limit (AECL) of 3×10-4 mg In/m3 for the respirable fraction notified by the Japanese Ministry of Health, Labour and Welfare were used to evaluate the exposure concentrations. Twenty-five out of 27 workers were exposed to indium concentrations lower than TLV-TWA, while all of the workers were exposed to the indium concentrations higher than AECL. We noted that there was a large discrepancy between the two occupational exposure limits referred to in this report, and these differences were attributed to the sampling strategies and health effects used as the prevention targets. Carcinogenicity of the respirable fraction of indium-containing particulates was considered in setting AECL, whereas it was not in ACGIH's TLV.

An improved system for exposure of cultured mammalian cells to gaseous compounds in the chromosomal aberration assay.

A gas exposure system using rotating vessels was improved for exposure of cultured mammalian cells to gaseous compounds in the chromosomal aberration assay. This system was composed of 12 square culture vessels, a device for preparation of air containing test gas, and positive and negative control gases at target concentrations and for supplying these gases to the culture vessels, and a roller apparatus in an incubator. Chinese hamster lung cells (CHL/IU) were grown on one side of the inner surface of the square culture vessel in the MEM medium. Immediately prior to exposure, the medium was changed to the modified MEM. Air in the culture vessel was replaced with air containing test gas, positive or negative control gas. Then, the culture vessels were rotated at 1.0 rpm. The monolayered culture cells were exposed to test gas during about 3/4 rotation at upper positions and alternatively immersed into the culture medium during about 1/4 rotation at lower positions. This system allowed the chromosomal aberration assay simultaneously at least at three different concentrations of a test gas together with positive and negative control gases with and without metabolic activations, and duplicate culture at each exposure concentration. Seven gaseous compounds, 1,3-butadiene, chlorodifluoromethane, ethyl chloride, methyl bromide, methyl chloride, propyne, and vinyl chloride, none of which has been tested to date, were tested on CHL/IU for the chromosomal aberration assay using this gas exposure system. All the compounds except chlorodifluoromethane showed positive responses of the structural chromosomal aberrations, whereas polyploidy was not induced by any of these gases. This improved gas exposure system proved to be useful for detecting chromosomal aberrations of gaseous compounds.

Control banding assessment of workers' exposure to indium and its compounds in 13 Japanese indium plants.

OBJECTIVES: This study aimed to assess workers' exposure to indium and its compounds in 55 indium-handling operations among 13 Japanese plants. The surveyed plants were selected from indium-manufacturing plants whose annual indium production exceeded 500 kg. METHODS: The Control of Substances Hazardous to Health (COSHH) Essentials control banding toolkit, which contains simple scales for hazard levels, quantities in daily use, and "dustiness" characteristics, was used to assess generic risks of indium-handling operations. The operations were then classified into one of four Control Approaches (CAs). RESULTS: There were 35 indium-handling operations classified into CA4 (requires expert advice) and 16 grouped into CA3 (requires containment). There were three operations classified into CA2 (requires engineering controls) and only one into CA1 (requires good general ventilation (GV) and working practices). Of the 51 operations classified as CA4 and CA3, 36 were found to be improperly equipped with local exhaust ventilation, and the remaining 15 operations solely relied on GV practices. Respiratory protective equipment (RPE) used in the 13 indium plants was examined with reference to the recommendations of the COSHH Essentials and Japan's Technical Guidelines. CONCLUSIONS: Our findings suggest that stringent engineering control measures and respiratory protection from indium dust are needed to improve indium-handling operations. Our results show that the most common control approach for Japanese indium-handling operations is to require expert advice, including worker health checks for respiratory diseases and exposure measurement by air sampling.

Quantitative assessment of occupational exposure to total indium dust in Japanese indium plants.

This study quantitatively assessed personal exposure of 86 workers to indium compounds as total dust at 11 Japanese indium plants. The personal exposures to indium concentrations in the breathing zone during an 8 h work-shift were determined by ICP-MS. The arithmetic mean indium concentration of all the workers was 0.098 mg Indium (In)/m3, with individual values ranging from 0.0001 to 1.421 mg In/m3. There were 11 workers whose exposure to indium concentrations exceeded the American Conference of Governmental Industrial Hygienists' Threshold Limit Value-Time Weighted Average (TLV-TWA) of 0.1 mg In/m3. Based on the condition TLV-TWA

Inhalation carcinogenicity and chronic toxicity of carbon tetrachloride in rats and mice.

Carcinogenicity and chronic toxicity of carbon tetrachloride were examined by inhalation exposure of 50 F344 rats and 50 BDF1 mice of both sexes to carbon tetrachloride at 0 (clean air), 5, 25, or 125 ppm (v/v) for 6 h/day, 5 days/wk, for 104 wk. Incidences of hepatocellular adenomas and carcinomas in rats and mice of both sexes and of adrenal pheochromocytomas in mice of both sexes were significantly increased dose-dependently. Hepatocellular carcinomas and cirrhosis significantly occurred in the 125-ppm-exposed rats of both sexes, and 3 cases of hepatocellular carcinomas and increased incidences of hepatic altered cell foci were noted in the 25-ppm-exposed female rats. Hepatocellular carcinomas were induced in mice of both sexes at 25 and 125 ppm, and hepatocellular adenomas occurred in females at 5 ppm without any degenerative or necrotic change in hepatocytes. Hepatocellular carcinomas metastasized to the lung. The chronic hepatotoxicity was characterized by cirrhosis, fibrosis, and fatty change in rats, and ceroid deposition, bile-duct proliferation, and hydropic change in mice. Survival rates were decreased in the 125-ppm-exposed rats and mice of both sexes and in the 25-ppm-exposed female mice, in association with decreased body weights. The decreased survival rates were considered to be causally related to both various tumors including hepatocellular carcinomas and severe chronic progressive nephropathy in rats and to hepatocellular carcinomas in mice. This study provided clear evidence of carcinogenicity for carbon tetrachloride in rats and mice. A cytotoxic-proliferative and genotoxic mode of action for carbon tetrachloride-induced hepatocarcinogenesis was suggested.

Thirteen-week inhalation toxicity of carbon tetrachloride in rats and mice.

Subchronic toxicity of carbon tetrachloride (CCl4) was examined by inhalation exposure of F344 rats and BDF1 mice of both sexes to 0, 10, 30, 90, 270 or 810 ppm (v/v) CCl4 vapor for 13 wk (6 h/d and 5 d/wk). In the high exposure levels at 270 and 810 ppm, altered cell foci in the livers of both rats and mice, and fibrosis and cirrhosis in the rat liver were observed. Hematoxylin and eosin-stained altered cell foci of rats were recognized as glutathione-S-transferase placental form (GST-P) positive foci, which are preneoplastic lesions of hepatocarcinogenesis. The most sensitive endpoint of CCl4-induced toxicity was fatty change with large droplets in rats of both sexes and male mice, and cytoplasmic globules in male mice, as well as increased relative liver weight in male rats. Those endpoints were manifested at 10 ppm and the LOAEL was determined as 10 ppm for the hepatic endpoints in rats and mice. Enhanced cytolytic release of liver transaminases into plasma in rats and mice and its close association with hepatic collapse in mice were observed at medium and high levels of inhalation exposure. Both CCl4-induced hematotoxicity and nephrotoxicity were observed in both rats and mice, but those toxicities were manifested at higher exposure concentrations than hepatotoxicity. The LOAEL for the hepatic endpoint and the GST-P-stained altered cell foci provide relevant animal data for reconsidering the occupational exposure limit val1ue of 5 ppm for CCl4 and strengthen the evidence of CCl4-induced hepatocarcinogenicity which is used in its carcinogenicity classification.

Dose- and time-dependent effects of 2,3,7,8-tetrabromodibenzo-p-dioxin on rat liver.

Dose- and time-dependent effects of 2,3,7,8-tetrabromodibenzo-p-dioxin (TBDD) on the liver were examined by single administration of TBDD by gavage to male and female rats. Fifteen Wistar rats of each sex per group received 0, 10, 30, 100 or 300 microg TBDD/kg body weight. Rats surviving to scheduled necropsy on Day 2, 7 or 36 after the TBDD administration were examined for hepatic histopathology, activities of hepatic microsomal enzymes and serum levels of lipids, total cholesterol and transaminases and hepatic concentrations of TBDD. Tigroid basophilic cytoplasm and hepatocellular hypertrophy were observed at 10 microg/kg on Day 2 or 7 through 36, whereas degenerative and aggressive lesions such as necrosis, fibrosis, multinucleated hepatocytes and disarrangement of hepatocytes occurred later at higher dose levels. Persistently increased activities of hepatic aryl hydrocarbon hydroxylase (AHH), ethoxycoumarin O-deethylase (ECOD) and ethoxyresorufin O-deethylase (EROD), increased serum levels of total cholesterol and phospholipid and increased relative liver weight were observed in all groups dosed 10 mug/kg and above, suggesting that hepatic microsomal monooxygenases and basophilic cytoplasm of hepatocytes were early and sensitive indicators among those TBDD-induced effects. A dose-dependent increase in liver concentrations of TBDD on Day 2 was followed by logarithmic decreases in TBDD concentrations against the days elapsed after the TBDD administration. An elimination half-life (t(1/2)) of TBDD from the liver was estimated to range from 12 to 16 days. It was suggested that females were more susceptible to TBDD than males, and that acute hepatotoxicity of TBDD was as potent as that of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD).

Assessment of workplace air concentrations of formaldehyde during and before working hours in medical facilities.

Workplace air concentrations of formaldehyde (FA) in medical facilities where FA and FA-treated organs were stored and handled were measured before and during working hours and assessed by the official method specified by Work Environment Measurement Law. Sixty-percent of the total facilities examined were judged as inappropriately controlled work environment. The concentrations of FA before working hours by spot sampling were found to exceed 0.1 ppm in some facilities, and tended to increase with increasing volume of containers storing FA and FA-treated materials. Regression analysis revealed that logarithmic concentrations of FA during working hours by the Law-specified analytical method were highly correlated with those before working hours by spot sampling, suggesting the importance for appropriate storing methods of FA and FA-treated materials. The concentrations of FA during working hours are considered to be lowered by effective ventilation of FA-contaminated workplace air and appropriate storage of FA and FA-treated materials in plastic containers in the medical facilities. In particular, such improvement by a local exhaust ventilation system and tightly-sealed containment of FA-treated material were urgently needed for the dissecting room where FA-treated cadavers were prepared and handled for a gross anatomy course in a medical school.

Carcinogenicity and chronic toxicity of para-chloronitrobenzene in rats and mice by two-year feeding.

Carcinogenicity and chronic toxicity of para-chloronitrobenzene (p-CNB) were examined by feeding diets containing p-CNB to rats and mice of both sexes for two years. The dietary concentration of p-CNB was 0 (control), 40, 200, or 1000 ppm (w/w) for rats and 0, 125, 500, or 2000 ppm for mice. Survival rates of the high-dosed male rats and male mice were significantly decreased compared with those of the respective controls, and this was attributed to the increased number of cancer deaths. Therefore, the high-dose levels were considered not to exceed the maximum tolerated dose. Significant decreases in red blood cell counts and hematocrit value and an increase in mean corpuscular volume were noted in the p-CNB-fed rats and mice. Nonneoplastic splenic lesions were characterized by capsule hyperplasia, fibrosis, fatty metamorphosis, and increased extramedullary hematopoiesis in rats, and congestion, increased extramedullary hematopoiesis, hemosiderin deposition, and ossification in mice. Incidences of fibromas, fibrosarcomas, osteosarcomas, sarcomas (NOS), and hemangiosarcomas in males and fibrosarcomas in females were significantly increased in the spleen of high-dosed rats. The most frequently observed splenic tumor was fibrosarcomas, followed by fibromas. The tumor incidences were increased in a dose-related manner and were more prevalent in males than in females. The malignant tumors metastasized mainly to the liver, peritoneum, and pancreas. Adrena/medullary hyperplasia and pheochromocytomas were significantly increased in the p-CNB-fed females. No tumor was induced in any of the p-CNB-fed mice of either sex except hepatic hemangiosarcomas in the 2000 ppm-fed females. Causative factors of p-CNB-induced carcinogenicity and chronic toxicity are discussed in light of the subchronic and chronic hematotoxicity reported in our present and previous studies and in the literature.

Enhancement of renal carcinogenicity by combined inhalation and oral exposures to chloroform in male rats.

Chloroform, ubiquitously present in indoor and outdoor air, drinking water, and some foodstuffs, enters the human body by inhalation, oral and dermal routes of exposure. In order to provide bioassay data for risk assessment of humans exposed to chloroform by multiple routes, effects of combined inhalation and oral exposures to chloroform on carcinogenicity and chronic toxicity in male F344 rats were examined. A group of 50 male rats was exposed by inhalation to 0 (clean air), 25, 50, or 100 ppm (v/v) of chloroform vapor-containing air for 6 h/d and 5 d/wk during a 104 w period, and each inhalation group was given chloroform-formulated drinking water (1000 ppm w/w) or vehicle water for 104 wk, ad libitum. Renal-cell adenomas and carcinomas and atypical renal-tubule hyperplasias were increased in the combined inhalation and oral exposure groups, but not in the oral- or inhalation-alone groups. Incidences of cytoplasmic basophilia and dilated tubular lumens in the kidney, as well as incidence of positive urinary glucose, were markedly increased by the combined exposures, compared with those after single-route exposures. It was concluded that combined inhalation and oral exposures markedly enhanced carcinogenicity and chronic toxicity in the proximal tubule of male rat kidneys, suggesting that carcinogenic and toxic effects of the combined exposures on the kidneys were greater than the ones that would be expected under an assumption that the two effects of single route exposures through inhalation and drinking were additive.

Carcinogenicity and chronic toxicity in rats and mice exposed by inhalation to 1,2-dichloroethane for two years.

Carcinogenicity and chronic toxicity of 1,2-dichloroethane (DCE) were examined by inhalation exposure of groups of 50 F344 rats and 50 BDF1 mice of both sexes to DCE vapor or clean air as control for 6 h/d, 5 d/wk and 104 wk. The rats were exposed to 10, 40 or 160 ppm (v/v) DCE, while the mice were exposed to 10, 30 or 90 ppm. The 2-yr exposure to DCE produced a dose-dependent increase in incidences of benign and malignant tumors, including subcutaneous fibroma, mammary gland fibroadenoma and peritoneal mesothelioma in male rats; subcutaneous fibroma and mammary gland adenoma, fibroadenoma and adenocarcinoma in female rats; and bronchiolo-alveolar adenoma and carcinoma, endometrial stromal polyp, mammary gland adenocarcinoma and hepatocellular adenoma in female mice. No exposure-related change in the incidence of non-neoplastic lesions or in any hematological, blood biochemical or urinary parameter occurred in any DCE-exposed rat or mouse group. The types of tumors and their target organs found in this study were consistent with those observed in rats and mice administered DCE by gavage in a NCI study. Selection of the exposure concentrations was considered appropriate with reference to the maximum tolerated dose for the highest doses and an occupational exposure limit of DCE for the lowest dose. The present findings suggest that those carcinogenic responses be primarily considered for standard setting of occupational and environmental exposure to DCE.

Effects of inhalation exposure to propylene oxide on respiratory tract, reproduction and development in rats.

Nasal, respiratory, reproductive and developmental toxicities of propylene oxide (PO) were examined by exposing male and female Sprague-Dawley rats to PO vapor by inhalation at a concentration of 0 (control), 125, 250, 500 or 1,000 ppm for 6 h/d, 7 d/wk, during a 5- to 6-wk period, including premating, mating and postmating or gestation. The inhalation exposure to 1,000 ppm PO seriously affected parental survival, the upper and lower respiratory tract, male and female reproductive systems, motor function, and fetal survival and development, whereas the exposure to 500 ppm or less primarily caused nasal lesions without any sign of reproductive or developmental toxicity. Because atrophy of the olfactory epithelium in the male rats exposed to 250 ppm was the most sensitive endpoint for PO toxicity, the NOAEL was determined to be 125 ppm for the nasal endpoint. An additional inhalation experiment was carried out to further examine developmental toxicity by exposing pregnant rats to 0, 125, 250, 500, 750 or 1,000 ppm PO during a 2-wk period of gestation, Day 6 through Day 19. The 2-wk inhalation experiment revealed that reduced fetal body weights and delayed ossification occurred in association with significantly reduced body weights of the dams exposed to 750 and 1,000 ppm, whereas neither fetal death nor teratogenicity occurred at those two exposure levels. It was concluded that the developmental toxicity of fetal death was manifested at parentally toxic exposure levels above 500 ppm, a level which seriously affected parental survival, the upper and lower respiratory tracts and reproductive system.

Developmental toxicity induced by inhalation exposure of pregnant rats to N,N-dimethylacetamide.

Developmental toxicity of N,N-dimethylacetamide (DMAC) was examined by exposing pregnant rats by inhalation to DMAC vapor at 0 (control), 100, 300, 450 or 600 ppm (v/v) for 6 h/d during Gestation Days 6 through 19. Fetal body weight and the number of male live fetuses were significantly decreased, along with a tendency of the number of intrauterine deaths to increase. The number of fetuses with visceral and skeletal malformations was significantly increased in the 450 and 600 ppm groups, while the number of fetuses with anasarca as an external malformation was increased at 600 ppm. Observed cardiovascular malformations included ventricular septum defect, persistent truncus arteriosus, malpositioned subclavian branch and retroesophageal subclavian artery. Persistent truncus arteriosus was accompanied by ventricular septal defect (VSD). Incidences of the persistent truncus arteriosus, which was classified as a serious congenital heart disease affecting postnatal survival, were increased at 450 and 600 ppm. Increased liver weights and hepatocellular swelling occurred in the dams exposed to 300 ppm and above, whereas neither hepatocellular necrosis nor increased serum activity of liver transaminases was observed in any of the exposed groups. Maternal body weights were decreased at 450 and 600 ppm. The most sensitive signs of developmental toxicity appeared at the exposure level of 300 ppm which was also the level of slight maternal toxicity. The No-Observed-Adverse-Effect-Level (NOAEL) was determined as 100 ppm for the endpoints of fetal and maternal toxicities. The NOAEL of 100 ppm and the induction of serious cardiovascular malformations occurring at 450 ppm and above were discussed with reference to the existing occupational exposure limit for DMAC.

Thirteen-week oral toxicity of para- and ortho- chloronitrobenzene in rats and mice.

Para- and ortho-chloronitrobenzene (p- and o-CNB) were compared for subchronic toxicity by feeding F344 rats and BDF(1) mice of both sexes p-CNB-or o-CNB-containing diets at 5 different concentrations for 13 weeks. The two isomers induced hematotoxicity and hepatotoxicity of different toxic potencies. p-CNB produced an anemic sign of external appearance in rats and mice, while o-CNB did not. Significant increases in the incidences of increased erythropoiesis in the bone marrow and increased extramedullary hematopoiesis in the spleen and liver, and in serum total bilirubin in rats and mice appeared at lower dose levels of p-CNB than o-CNB. A significant increase in serum ALT activity appeared at lower dose levels of o-CNB than p-CNB, together with appearance of both necrosis and hydropic degeneration of hepatocytes only in the o-CNB-fed rats and nuclear enlargement with atypia of hepatocytes only in the o-CNB-fed mice. BMDL(10)s of p- and o-CNB for the hematotoxic endpoint, substitutes for NOAELs, were 0.177 mg/kg/day and 1.03 mg/kg/day for the rats, respectively. For the mice, the NOAELs of p-and o-CNB for the hematotoxic endpoint were 10.5 mg/kg/day and 10.4 mg/kg/day, respectively. A NOEL of o-CNB for the hepatotoxic endpoint resulted in 13.8 mg/kg/day for the rats and 12.2 mg/kg/day for the mice. These results suggest that p-CNB is a more potent hematotoxicant than o-CNB, whereas o-CNB is a more potent hepatotoxicant than p-CNB, and that the rat hematopoietic system is more susceptible to p-CNB than the mouse hematopoietic system.

Carcinogenicity and chronic toxicity of 1,4-dichloro-2-nitrobenzene in rats and mice by two years feeding.

Carcinogenicity and chronic toxicity of 1,4-dichloro-2-nitrobenzene (DCNB) were examined by feeding each group of 50 F344 rats and 50 BDF1 mice of both sexes a DCNB-containing diet at a concentration of 0 (control), 320, 800 or 2,000 ppm (w/w) for 2 yr. In rats, incidences of hepatocellular adenomas and carcinomas and their combined incidence were increased in the 2,000 ppm-fed males, together with increased incidence of basophilic cell foci in the 800 and 2,000 ppm-fed males. A dose-related increase in combined incidences of renal cell adenomas and carcinomas was noted. Incidence of Zymbal gland adenomas tended to increase in the 2,000 ppm-fed males. In mice, incidences of hepatocellular adenomas in the 800 and 2,000 ppm-fed females and hepatocellular carcinomas in the 2,000 ppm-fed males and in the 800 and 2,000 ppm-fed females were increased. Incidence of hepatoblastomas was increased in all DCNB-fed males and in the 2,000 ppm-fed females. Signs of chronic toxicity were characterized by centrilobular hypertrophy of hepatocytes with nuclear atypia in mice, increased relative liver weight in rats, a dose-related increase in incidences of chronic progressive nephropathy with advanced grades of severity in male rats, and decreased hemoglobin concentration and hematocrit accompanied by increased bone marrow hematopoiesis in female rats. Carcinogenic activity of DCNB was evaluated for the three different tumors, and sensitive signs of the chronic toxicity were dis-

Control banding assessment of exposure of offset printing workers to organic solvents.

OBJECTIVES: We aimed to assess the exposure of offset printing workers to hazardous substances in the rinsing processes of small-sized companies using a control banding method. METHODS: We obtained half-year amounts of hazardous substances purchased through a questionnaire survey and the hazardous information from the safety data sheets (SDSs) and related literature. RESULTS: The amount of petroleum kerosine and carbon hydride markedly increased in 2013 compared with that in 2010. In contrast, the amount of dichloromethane (DCM) decreased in 2013, and 1,2-dichloropropane (DCP) was not used in either 2010 or 2013. Mineral oil and xylene were allocated to Hazard Group D and judged to require Control Approach 3. In addition to DCM with Global Harmonization System's carcinogenic category 1, mildly treated mineral oil and solvent naphtha, allocated into Hazard Group E, are carcinogenic to humans and were judged to require Control Approach 4. There are two limitations of the control banding assessment: first, only limited and scarce hazard information could be obtained from SDSs, and second, safe-sided judgment for control technology for industrial hygiene. CONCLUSION: Small-sized enterprises are encouraged to implement control banding assessment for hazardous substances and to access expert advice available from Regional Industrial Health Centers. Easy access to appropriate expert advice is important to compensate for the limited and scarce hazard information and safe-sided judgment for control technology for Control Approaches 3 and 4.

The Relationship between Attitudes toward Suicide and Family History of Suicide in Nagano Prefecture, Japan.

Certain attitudes toward suicide may be a risk factor for suicide among the bereaved. To explore this possibility, we examined the relationship between attitudes toward suicide and family history of suicide. We focused on two specific attitudes indicating resignation in a survey: #1 "When a person chooses to die by suicide, the suicide is inevitable" (i.e., inevitability belief); and #2 "A suicide cannot be stopped by any person, because suicide is unpreventable" (i.e., unpreventable belief). The data of 5117 fully completed questionnaires were analyzed. Logistic regression analysis revealed that the two attitudes of resignation were significantly associated with a family history of suicide. The adjusted odds ratio for #1 was 1.39 (95% CI, 1.07-1.79) for individuals having experienced suicide by a family member or relative, while that for #2 was 1.57 (95% CI, 1.27-1.95) for experiencing a suicide by a family member or relative and 1.25 (95% CI, 1.05-1.49) for experiencing a suicide by a friend, business associate, partner or other. These two attitudes of resignation toward suicide were significantly associated with a family history of suicide. These attitudes might increase suicide risk among the bereaved.