Exposure assessment of carbon nanotube manufacturing workplaces.

Seven CNT (carbon nanotube) handling workplaces were investigated for exposure assessment. Personal sampling, area sampling, and real-time monitoring using an SMPS (scanning mobility particle sizer), dust monitor, and aethalometer were performed to characterize the mass exposure, particle size distribution, and particle number exposure. No workplace was found to exceed the current ACGIH (American Conference of Governmental Industrial Hygienists) TLVs (threshold limit values) and OELs (occupational exposure levels) set by the Korean Ministry of Labor for carbon black (3.5 mg/m(3)), PNOS (particles not otherwise specified; 3 mg/m(3)), and asbestos (0.1 fiber/cc). Nanoparticles and fine particles were most frequently released after opening the CVD (chemical vapor deposition) cover, followed by catalyst preparation. Other work processes that prompted nanoparticle release included spraying, CNT preparation, ultrasonic dispersion, wafer heating, and opening the water bath cover. All these operation processes could be effectively controlled with the implementation of exposure mitigation, such as engineering control, except at one workplace where only natural ventilation was used.

Inhibition of platelet aggregation by 1-methyl-4-phenyl pyridinium ion (MPP+) through ATP depletion: Evidence for the reduced platelet activities in Parkinson's disease.

Neuronal accumulation of 1-methyl-4-phenylpyridinium ion (MPP(+)), the metabolite of neural toxin, 1-methyl-4-phenyl-1,2,3,6-tetrahyropyridine (MPTP), induces a rapid depletion of cellular ATP level and loss of neuronal cell viability which simulates human Parkinson's disease (PD). Since ATP plays an important role in the physiology and function of platelets, which share many biochemical and physiological features with neuronal cells, we examined the effect of MPP(+) on platelet aggregation and viability using freshly isolated rat platelets. While the treatment of MPP(+) to platelets did not induce cytotoxicity, it significantly attenuated agonist-induced platelet aggregation in a concentration dependent manner. The inhibition of aggregation by MPP(+) was mediated by the depletion of the cytoplasmic ATP pool and resultant decreased ATP secretion. Different from the previous reports in neuronal cells, MPP(+) did not affect intracellular levels of glutathione and cytoplasmic Ca(2+) in platelets. The combined treatment with MPP(+) and 2-deoxyglucose, a glycolysis inhibitor, showed the additive effect in the decrease of ATP secretion and intracellular content. Consistent with these findings, inhibitory effects of MPP(+) on platelet aggregation was significantly enhanced by the treatment with 2-deoxyglucose. In conclusion, these results suggested that MPP(+) can induce ATP depletion in platelets and attenuate platelet aggregation providing a new theory on the reduced platelet activities in PD patients.

Comparison of lung asbestos fiber content in cancer subjects with healthy individuals with no known history of occupational asbestos exposure in Korea.

To evaluate the effects of environmental asbestos exposure on the inducement of lung cancer, pulmonary asbestos and non-asbestos fiber content was determined in 36 normal Korean subjects and 38 lung cancer subjects with no known occupational history of asbestos exposure. Pulmonary asbestos fiber content was measured by transmission electron microscopy (TEM) with energy-dispersive x-ray analysis after applying a low-temperature ashing procedure. Chrysotile fibers were the major fiber type found in the lungs of the Korean subjects. The asbestos fiber concentrations found in the lungs of normal males (25) and females (11) were 0.26 x 10(6) fibers/g of dry lung tissue and 0.16 x 10(6) fibers/g of dry lung tissue, respectively. The asbestos concentrations found in the lungs of cancer subjects were 0.16 x 10(6) fibers/g of dry lung tissue for 32 males and 0.44 x 10(6) fibers/g of dry lung tissue for 6 females. No statistical difference was found in pulmonary asbestos content between the normal and lung cancer subjects, whereas a statistical difference was noted between normal and lung cancer subjects with respect to lung non-asbestos content, indicating a potential role for non-asbestos fibers being associated with lung cancer.

Recurrent exposure to welding fumes induces insufficient recovery from inflammation.

Previous studies on welding-fume-induced lung fibrosis have indicated that recovery is possible when the degree of exposure is short-term and moderate. However, this study investigated the recovery after recurrent exposure to welding fumes, as welders are invariably re-exposed to welding fumes after recovering from radiographic pneumoconiosis. Thus, to investigate the disease and recovery processes of welding-fume-induced pneumoconiosis in the case of recurrent welding-fume exposure, rats were exposed to manual metal arc-stainless steel (MMA-SS) welding fumes with a total suspended particulate (TSP) concentration of 51.4 +/- 2.8 mg/m(3) (low dose) or 84.6 +/- 2.9 mg/m(3) (high dose) for 2 h/day in an inhalation chamber for 1 mo and then allowed to recover from the inflammation for 1 mo. Thereafter, the rats were exposed again to MMA-SS with a TSP concentration of 44.1 +/- 8.8 mg/m(3) (low dose) or 80.1 +/- 9.8 mg/m(3) (high dose) for another 30 d and then allowed to recover from the inflammation for 1 mo. The recovery from the first exposure was then compared with that from the second exposure. The first and second exposures to MMA-SS welding fumes were found to produce significant increases in the lung weights and inflammatory parameters, including total cell numbers, alveolar macrophages (AMs), polymorphonuclear cells (PMNs), lymphocytes, and lactate dehydrogenase (LDH) in the bronchoalveolar lavage fluid (BALF) when compared with the unexposed controls. Following the first and second recovery, a significant reduction in inflammatory parameters of BALF was observed between the exposure and recovery groups. Histopathological observations showed foamy or pigmented macrophage accumulation, cellular debris, or pigment from burst macrophages after the first or second exposure. Following the first or second recovery, cellular debris or pigment from burst macrophages was cleared away from the lungs and accumulation of foamy or pigmented macrophages was decreased when compared to previous exposure. Reactive hyperplasia was noticed after second exposure or either recovery. However, significant differences were observed between the first and second exposure or the first and second recovery. In particular, the number of PMNs was significantly higher after the second exposure than after the first exposure. Also, all cell types in the BALF were significantly elevated in the high-dose second recovery group than in the first recovery group, indicating an incomplete recovery from second exposure. In conclusion, these results indicated that the lung damage caused by the second welding-fume exposure was more difficult to recover from than the first exposure.

28-day inhalation toxicity of 3-methoxybutyl chloroformate in rats.

The 28-day repeated inhalation study was applied for hazard assessment of 3-methoxybutyl chloroformate (3-MBCF) in Sprague Dawley rats. Groups of five rats per sex were exposed 6 h/day, 5 days per week for 4 weeks to test substance concentration (ranging from 3 to 12 ppm) using a whole-body exposure system. At the terminal sacrifice, following blood collection and gross pathological examination, organ weights were determined and fixed organs were examined. The micronucleus test was performed using bone marrow cells. Exposure of 3-MBCF induced mortality at concentrations above 6 ppm. Decreases in body weight and food intake, hematologic alterations, organ weight changes, and gross and microscopic findings were seen even at the lowest concentrations of 3 ppm. Histopathology revealed principal test substance exposure correlated with lesions in the respiratory tract in both male and female rats above 3 ppm. Groups of male rats exposed above 6 ppm show microscopic lesions in spleens, livers, testes and epididymides; however, the micronucleated polychromatic erythrocytes frequency in bone marrow cells was not changed. Based on histopathology of the respiratory tract and other organs, the no observed adverse effect level (NOAEL) of 3-MBCF in the present study was less than 3 ppm.

Subacute Inhalation Toxicity of Cyclohexanone in B6C3F1 Mice.

Cyclohexanone (C6H10O, CAS No. 108-94-1) is a colorless oily liquid obtained through the oxidation of cyclohexane or dehydrogenation of phenol. It is used in the manufacture of adhesives, sealant chemicals, agricultural chemicals, paint and coating additives, solvent, electrical and electronic products, paints and coatings, photographic supplies, film, photochemicals, and as an intermediate in nylon production. Owing to the lack of information on repeated inhalation toxicity of cyclohexaone, in this study, we aimed to characterize the subacute inhalation toxicity. B6C3F1 mice were exposed to 0, 50, 150, and 250 ppm of cyclohexanone for 6 hr/day, 5 days/week for 4 weeks via whole-body inhalation in accordance with the OECD Test Guideline 412 (subacute inhalation toxicity: 28-day study). Mortality, clinical signs, body weights, food consumption, hematology, serum biochemistry, organ weights, as well as gross and histopathological findings were evaluated between the control and exposure groups. No mortality or remarkable clinical signs were observed during the study. No adverse effects on body weight, food consumption, hematology, serum biochemistry, and organ weights, gross or histopathological lesions were observed in any male or female mice in any of the exposure groups, although some statistically significant changes were observed in organ weights. We concluded that no observable adverse effect level (NOAEL) is above 250 ppm in mice exposed to cyclohexanone for 6 hr/day for 5 days/week.

Acute and repeated inhalation lung injury by 3-methoxybutyl chloroformate in rats: CT-pathologic correlation.

OBJECTIVES: To investigate the acute and repeated pulmonary damage in Sprague-Dawley rats caused by the inhalation of 3-methoxybutyl chloroformate (3-MBCF) using computed tomography (CT), and to correlate these results with those obtained from a pathological study. METHODS: Sixty, 7-week-old rats were exposed to 3-MBCF vapor via inhalation (6 h/day) for 1 day (N=20), 3 days (N=20), and 28 days (5 days/week) (N=20) using whole body exposure chambers at a concentration of 0 (control), 3, 6 and 12 ppm. CT examinations including densitometry and histopathologic studies were carried out. For the follow-up study, the rats exposed for 3 days were scanned using CT and their pathology was examined at 7, 14, and 28 days. RESULTS: There was a significant decrease in the parenchymal density in the groups exposed to the 3-MBCF vapors for 1 day at 3 ppm (p=0.022) or 6 ppm (p=0.010), compared with the control. The parenchymal density of the rats exposed to 12 ppm was significantly higher. The pathological findings in this period, the grades of vascular congestion, tracheobronchial exfoliation, and alveolar rupture were significant. In the groups exposed for 3 days, there was a large decrease in the parenchymal density with increasing dose (control: -675.48+/-32.82 HU, 3 ppm: -720.65+/-34.21 HU, 6 ppm: -756.41+/-41.68 HU, 12 ppm: -812.56+/-53.48 HU) (p=0.000). There were significant density differences between each dose in the groups exposed for 28 days (p=0.000). The CT findings include an irregular lung surface, areas of multifocal, wedge-shaped increased density, a heterogeneous lung density, bronchial dilatation, and axial peribronchovascular bundle thickening. The histopathology examination revealed the development of alveolar interstitial thickening and vasculitis, and an aggravation of the mainstem bronchial exudates and bronchial inflammation. The alveolar wall ruptures and bronchial dilatation became severe during this period. On the follow-up study, the groups exposed for 3 days showed diffusely increased parenchymal density on the 7 days study, but the lung densities were lower at 14 and 28 days than at 3 days. In the rats exposed to lowest concentration, the pulmonary parenchymal density and pathologic findings rapidly returned to normal within 1 week. CONCLUSIONS: Decreased parenchymal density of the lung was a common CT finding in acute and repeated inhalation injury. The air accumulation is believed to be the results of tracheolaryngeal inflammatory edema, bronchial dilatation, and alveolar rupture from the early period.

A 90-Day Inhalation Toxicity Study of Ethyl Formate in Rats.

Ethyl formate, a volatile solvent, has insecticidal and fungicidal properties and is suggested as a potential fumigant for stored crop and fruit. Its primary contact route is through the respiratory tract; however, reliable repeated toxicological studies focusing on the inhalation route have not been published to date. Therefore, the present study was conducted to investigate the safety of a 90-day repeated inhalation exposure in rats. Forty male and 40 female rats were exposed to ethyl formate vapor via inhalation at concentrations of 0, 66, 330, and 1,320 ppm for 6 hr/day, 5 days a week for 13 weeks. Clinical signs, body weights, food consumption, urinalysis, hematologic parameters, serum chemistry measurements, organ weights, necropsy, and histopathological findings were compared between the control and ethyl formate-exposed groups. Locomotor activity decreased during exposure and recovered afterward in male and female rats exposed to 1,320 ppm ethyl formate. Body weight and food consumption continuously decreased in both sexes exposed to 1,320 ppm ethyl formate from week 1 or 3 compared with the control values. The increases in adrenal weight and decreases in thymus weight were noted in both sexes exposed to ethyl formate at 1,320 ppm. Degeneration, squamous metaplasia of olfactory epithelium in the nasopharyngeal tissue, or both were noted in the male and female rats at 1,320 ppm and female rats at 330 ppm ethyl formate. Taken together, our results indicate that ethyl formate-induced changes were not observed in male and female rats at 330 and 66 ppm, respectively. This indicates that exposure to ethyl formate at concentrations below 66 ppm for 90 days is relatively safe in rats. This is the first report of a full-scale repeated inhalation toxicity assessment in rats and could contribute to controlling occupational environmental hazards related to ethyl formate.

[Effects of biophysical index, knowledge, and self management compliance of patients with primary hypertension by a self management compliance promotion program].

PURPOSE: This study was to develop and prove the effects of a self management compliance promotion program for primary hypertension patients who reside in rural communities. METHOD: The content of the self management compliance promotion program developed by this study was as follows: A leader trains patients as a group or individually, in walking, education and green tea therapy from the first to twelfth week. From the thirteenth to twenty fourth week, the patients should perform walking and green tea therapy by themselves. One hundred twenty subjects volunteered to participate in the study, who were among those registered as hypertension patients in the 14 community health clinics located in Chungcheongbuk-do. RESULT: Systolic blood pressure, total cholesterol, low-density lipoprotein cholesterol, triglyceride, step width, and degree of obesity decreased significantly. High-density lipoprotein cholesterol, step length, knowledge of hypertension, and self management compliance significantly increased. CONCLUSION: A self management compliance promotion program for primary hypertensive patients enhances biophysical index and knowledge on hypertension, thus ultimately suggesting a nursing intervention for promoting self management compliance.

Risk assessment of di(2-ethylhexyl) phthalate in the workplace.

OBJECTIVES: A hazard assessment of di(2-ethylhexyl) phthalate (DEHP), a commonly used workplace chemical, was conducted in order to protect the occupational health of workers. A literature review, consisting of both domestic and international references, examined the chemical management system, working environment, level of exposure, and possible associated risks. This information may be utilized in the future to determine appropriate exposure levels in working environments. METHODS: Hazard assessment was performed using chemical hazard information obtained from international agencies, such as Organization for Economic Cooperation and Development-generated Screening Information Data Set and International Program on Chemical Safety. Information was obtained from surveys conducted by the Minister of Employment and Labor ("Survey on the work environment") and by the Ministry of Environment ("Survey on the circulation amount of chemicals"). Risk was determined according to exposure in workplaces and chemical hazard. RESULTS: In 229 workplaces over the country, 831 tons of DEHP have been used as plasticizers, insecticides, and ink solvent. Calculated 50% lethal dose values ranged from 14.2 to 50 g/kg, as determined via acute toxicity testing in rodents. Chronic carcinogenicity tests revealed cases of lung and liver degeneration, shrinkage of the testes, and liver cancer. The no-observed-adverse-effect level and the lowest-observed-adverse-effect level were determined to be 28.9 g/kg and 146.6 g/kg, respectively. The working environment assessment revealed the maximum exposure level to be 0.990 mg/m(3), as compared to the threshold exposure level of 5 mg/m(3). The relative risk of chronic toxicity and reproductive toxicity were 0.264 and 0.330, respectively, while the risk of carcinogenicity was 1.3, which is higher than the accepted safety value of one. CONCLUSIONS: DEHP was identified as a carcinogen, and may be dangerous even at concentrations lower than the occupational exposure limit. Therefore, we suggest management of working environments, with exposure levels below 5 mg/m(3) and all workers utilizing local exhaust ventilation and respiratory protection when handling DEHP.

Exposure monitoring and risk assessment of biphenyl in the workplace.

This study was performed to assess exposure to and the risk caused by biphenyl in the workplace. Biphenyl is widely used as a heat transfer medium and as an emulsifier and polish in industry. Vapor or high levels of dust inhalation and dermal exposure to biphenyl can cause eye inflammation, irritation of respiratory organs, and permanent lesions in the liver and nervous system. In this study, the workplace environment concentrations were assessed as central tendency exposure and reasonable maximum exposure and were shown to be 0.03 and 0.12 mg/m³, respectively. In addition, the carcinogenic risk of biphenyl as determined by risk assessment was 0.14 × 10⁻4 (central tendency exposure) and 0.56 × 10⁻4 (reasonable maximum exposure), which is below the acceptable risk value of 1.0 × 10⁻4. Furthermore, the central tendency exposure and reasonable maximum exposure hazard quotients were 0.01 and 0.06 for oral toxicity, 0.05 and 0.23 for inhalation toxicity, and 0.08 and 0.39 for reproduction toxicity, respectively, which are all lower than the acceptable hazard quotient of 1.0. Therefore, exposure to biphenyl was found to be safe in current workplace environments. Because occupational exposure limits are based on socioeconomic assessment, they are generally higher than true values seen in toxicity experiments. Based on the results of exposure monitoring of biphenyl, the current occupational exposure limits in Korea could be reviewed.

Micronuclei induction by 13 week-inhalation of 1,1-dichloro-1-fluoroethane in Sprague-Dawley rats.

To investigate the genotoxic effect of l,1-dichloro-1-fluoroethane (HCFC-141b), which was currently widely used as a cleaning solvent in the electronic parts industry and suggested as a potential reproductive effector, in vivo micronucleus tests were performed. Groups of 10 male and 10 female Sprague-Dawley rats were exposed, by inhalation (6h/day, 5 days/week) to the vapors of HCFC-141b for 13 weeks using whole body exposure chambers at the concentrations of 0 (control), 1500, 3000, and 6000 ppm. The micronuclei frequencies among the polychromatic erythrocytes (PCEs) and the percentage of polychromatic erythrocytes among the total number of erythrocytes were counted in the bone marrow of rats, and body weights, organ weights, histopathology, clinical chemistry and hematologic changes were also observed. Statistically significant and dose-dependant increases were found in the micronuclei frequencies in the male rats (P<0.01), yet not in the females. The decreases in the percentage of polychromatic erythrocytes among the total number of erythrocytes were also statistically significant (P<0.05) in both sexes of the high concentration groups. However, no exposure-related effects of toxicological significance were noted with respect to organ weights, clinical chemistry and histopathology. Apart from it, only slightly decreased mean corpuscular hemoglobin concentration (MCHC) was noted in the females of 6000 ppm group (P<0.05). These results suggest that HCFC 141b can induce the genetic effects, micronuclei in the rat bone marrows, especially in males, at earlier stages before the other general clinical and histopathologic changes occur if with more prolonged exposure.

A histopathologic study of the nervous system after inhalation exposure of 1-bromopropane in rat.

1-Bromopropane (1-BP) has recently become known as an alternative cleaning material with less damage to the ozone layer. However, its toxicity is not fully evaluated. This study was designed to investigate the repeated inhalation toxicity of 1-BP on the nervous systems in Sprague-Dawley rats. The experiment was done by repeated exposure of the rats to 0, 200, 500, and 1250 ppm for 6 h per day, 5 days a week, for 13 weeks, respectively. Morphologic studies were done for the central nervous system, sacral and peroneal nerves. The serial sections of the brain and spinal cord of 1-BP inhalation groups revealed no pathological features either in the gray or white matter. The nerve fiber teasing, light and electron microscopic studies of the sacral and peroneal nerve fibers showed no significant difference between 1-BP inhalation groups and the control group. From these results, it is concluded that the nervous system is histologically resistant to the repeated inhalation of 1-BP up to 1250 ppm for 13 weeks. Experiments with higher concentrations of 1-BP and the functional studies are necessary to clarify the 1-BP toxicity.

Changes of 8-OH-dG levels in DNA and its base excision repair activity in rat lungs after inhalation exposure to hexavalent chromium.

According to the toxicological and epidemiological studies, hexavalent chromium (Cr) is associated with increase of lung cancer risk. Genotoxic effects, such as chromosomal aberrations, and cellular oxidative DNA damage by reactive oxygen species produced by hexavalent Cr exposure may play an important role in its carcinogenesis. To clarify whether reactive oxygen species are involved in its mechanism, we examined the levels of 8-hydroxydeoxyguanine (8-OH-dG) and its base excision repair activities in the lung tissues of rats that repeatedly inhaled a sodium chromate solution mist for 1, 2, and 3 weeks. The levels of 8-OH-dG increased significantly in the lung tissues of the rats exposed for 1 week at the low concentration (0.18 mg/m(3), P<0.05), as compared with the controls. However, there was no difference in the 8-OH-dG levels at the higher concentration or with more than 2 weeks of exposure. The 8-OH-dG repair activities decreased in a dose-dependent manner during 2 weeks of exposure, on the contrary they recovered at 3 weeks of repeated exposure. These results suggest that the DNA damage caused by hexavalent Cr inhalation is induced by the generation of reactive oxygen species and by inhibition of base excision repair activity during the earlier phase of exposure. However, the 8-OH-dG levels and its repair activities recovered to the level of the controls in the latter inhalation exposure period.

Evaluation of subchronic inhalation toxicity of methylcyclopentane in rats.

The aim of this study was to verify subchronic inhalation toxicity of methylcyclopentane (CAS No. 96-37-7) in Sprague-Dawley rats. Four groups of 10 rats of each gender were exposed to methylcyclopentane vapor by whole-body inhalation at concentrations of 0, 290, 1300, or 5870 ppm for 6h per day, 5 days/week over a 13-week period. During the study period, clinical signs, mortality, body weight, food consumption, ophthalmoscopy, urinalysis, hematology, serum biochemistry, gross pathology, organ weights, and histopathology were examined. Exposure-related clinical signs (salivation and rubbing) were observed in both genders of the 5870 ppm group. There was an increase in liver weight for both genders but the kidney weight was only higher in females than controls. However, no toxicologically significant changes were observed in body weight, food consumption, ophthalmoscopy, urinalysis, hematology, serum biochemistry, necropsy findings, or histopathology in any of the treatment groups. Under the present experimental conditions, the target organs were determined to be kidney and liver in rats. The no-observed-adverse-effect concentration was considered to be 1300 ppm/6h/day in rats.

Oxidative DNA damage from nanoparticle exposure and its application to workers' health: a literature review.

The use of nanoparticles (NPs) in industry is increasing, bringing with it a number of adverse health effects on workers. Like other chemical carcinogens, NPs can cause cancer via oxidative DNA damage. Of all the molecules vulnerable to oxidative modification by NPs, DNA has received the greatest attention, and biomarkers of exposure and effect are nearing validation. This review concentrates on studies published between 2000 and 2012 that attempted to detect oxidative DNA damage in humans, laboratory animals, and cell lines. It is important to review these studies to improve the current understanding of the oxidative DNA damage caused by NP exposure in the workplace. In addition to examining studies on oxidative damage, this review briefly describes NPs, giving some examples of their adverse effects, and reviews occupational exposure assessments and approaches to minimizing exposure (e.g., personal protective equipment and engineering controls such as fume hoods). Current recommendations to minimize exposure are largely based on common sense, analogy to ultrafine material toxicity, and general health and safety recommendations.

Toxicity of Methylcyclohexane and Its Effect on the Reproductive System in SD Rats.

OBJECTIVES: There is limited data regarding the toxicity of methylcyclohexane, despite its wide use in rubber adhesives, paint diluents, and cleansing agents. This study aimed to verify the toxicity and influence on the reproductive system of methylcyclohexane after its repeated injection in Sprague Dawley (SD) rats. METHODS: Methylcyclohexane was injected subcutaneously into male and female SD rats once a day, five times a week, for 13 weeks at different doses (0, 10, 100, and 1,000 mg/kg/day) for each group. The toxicity of testing material was verified by observing the change in body and organ weight, hematological change, pathological findings, and effect on the reproductive system at each different concentration. RESULTS: In the 1,000 mg/kg/day group, there were cases of animal deaths. In animals that survived, hematological changes, including a decrease in the red blood cell count, were observed. A considerable weight gain or loss and pathological abnormalities in the liver, kidney, and other organs were found. However, the 10 and 100 mg/kg/day groups did not cause deaths or other specific abnormalities. In terms of reproductive toxicity, there were changes in hormone levels, including a significant decrease in hormones such as estradiol and progesterone (p < 0.001) in male animals. Menstrual cycle change for female animals did not show concentration dependency. CONCLUSION: When injected repeatedly for 13 weeks, methylcyclohexane proved to be toxic for the liver, heart, and kidney at a high dose. The absolute toxic dose was 1,000 mg/kg/day, while the no observed adverse effect level was less than 100 mg/kg/day. The substance exerted little influence on the reproductive system.

Evaluation of the Genetic Toxicity of Cyclopentane and Ammonium Nitrate - In vitro Mammalian Chromosomal Aberration Assay in Chinese Hamster Ovary Cells.

OBJECTIVES: In this study, the in vitro mammalian chromosomal aberration (CA) assay was conducted to gain additional information concerning the hazards associated with the use of cyclopentane and ammonium nitrate. While these two chemicals had already been tested by many methods, they had not been studied in the CA test. METHODS: The assay was performed using the ovarian infantile cell (CHO-K1 cell), by the direct method (-S9) and by the metabolic activated method (+S9 mix). RESULTS: Using the direct method, the 7 dosages in a 48 hour treatment group did not show that the frequency of CA is proportion to the dosage addition. The frequency of CA is not proportion to the dosage addition for a 6 hour treatment using the metabolic activated method. CONCLUSION: From these findings, it was decided that the 2 chemicals do not induce chromosomal aberrations under the tested conditions.

Mutagenicity of octane and tetrasodium pyrophosphate in bacterial reverse mutation (Ames) test.

We investigated the genotoxicities or mutagenicities of 2 chemicals (octane and tetrasodium pyrophosphate) with limited toxicological data in spite of their common usage based on Ames reverse mutation test. In this test, treatment of 2 chemicals at each five dose did not induce mutagenicity in Salmonella typhimurium TA98, TA100, TA1535, TA1537, and in Escherichia coli WP2uvrA with and without metabolic activation. These results indicate that 2 chemicals do not have mutagenic potentials under the conditions examined in each study. Despite these results, it can affect by inducing inhalation, skin or eye contact, ingestion, and have affected central nervous system as a target organ. It is thus necessary to prepare the local exhaust system and personal protective equipments. Based on this study, we suggest that future studies should be directed toward chronic inhalation, carcinogenic test and so on.

Acute and Subchronic Inhalation Toxicity of n-Octane in Rats.

OBJECTIVES: We have investigated the toxic effects of the inhalation of subchronic and acute levels of n-octane. METHODS: The rats were exposed to n-octane of 0, 2.34, 11.68 and 23.36 mg/L (n = 5 rats/group/gender) in an acute inhalation test (Organization for Economic Co-operation and Development (OECD) TG 403), or to 0, 0.93, 2.62 and 7.48 mg/L (n = 10 rats/group/gender) for a subchronic inhalation test (OECE TG 413), to establish a national chemical management system consistent with the Globally Harmonized Classification System (GHS). RESULTS: Acutely-exposed rats became lethargic but recovered following discontinuation of inhalation. Other clinical symptoms such as change of body weight and autopsy finds were absent. The LC50 for the acute inhalation toxicity of n-octane was determined to exceed 23.36 mg/L and the GHS category was 'not grouping'. Subchronically-treated rats displayed no significant clinical and histopathological differences from untreated controls; also, target organs were affected hematologically, biochemically and pathologically. Therefore, the no observable adverse effect level was indicated as exceeding 7.48 mg/L and the GHS category was 'not grouping' for the specific target organ toxicity upon repeated exposure. CONCLUSION: However, n-octane exposure should be controlled to be below the American Conference of Industrial Hygienists recommendation (300 ppm) to prevent inhalation-related adverse health effects of workers.