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K Omae

Publications and source records attributed to K Omae.

At least 37 records · Page 2Linked to original sources
PubMed1998

Evidence on N-acetyltransferase allele-associated metabolism of hydrazine in Japanese workers.

Hydrazine (N2H4), which has been categorized as a weak carcinogen, is a chemical with the one of the largest production rates in Japan. We have investigated the effects of acetylation phenotypes on the metabolism of hydrazine. Genotypes of N-acetyl transferases, NAT2*, were determined using polymerase chain reaction for 297 male workers. Biological and exposure monitoring were also conducted. The rapid and intermediate acetylators accounted for 45% each, and the slow acetylators accounted for 10%. Biological half-lives were significantly different among the three acetylation phenotypes (analysis of variance, P < 0.05): 3.94+/-1.70 hours for slow acetylators, 2.25+/-0.37 hours for intermediate acetylators, and 1.86+/-0.67 hours for rapid acetylators. Among Japanese, rapid and intermediate acetylators are the major phenotypes, which is in sharp contrast with those among Caucasians. We conclude that biological monitoring should take genetic factors, which may vary dramatically among different populations, into account.

Adult↗
PubMed1998

Cross sectional observation of the effects of carbon disulphide on arteriosclerosis in rayon manufacturing workers.

OBJECTIVE: A prospective cohort study was designed to clarify the relations between occupational exposure to carbon disulphide (CS2) and its effects on arteriosclerosis in workers in 11 Japanese rayon manufacturing factories. This report is a cross sectional baseline observation in the first study year. METHODS: Study subjects were 432 male rayon workers (mean (range) age 35.5 (19.1-47.8); duration of exposure 13.4 (0.3-29.0)) and 402 male referent workers (age 35.8 (18.9-49.8)). Exposure to CS2 was assessed by determining the concentration of 2-thiothiazolidine-4-carboxylic acid (TTCA) in urine. Mean (SD) TTCA was 3.42 (2.73) mg/g creatinine (Cr) (n = 422). About a quarter of the urine samples were > 5 mg/g Cr, a biological exposure index recommended by the American Conference of Governmental Industrial Hygienists. Health effects on arteriosclerosis were evaluated by measuring blood pressure, serum lipids, pulse wave velocity of the aorta, stiffness and blood flow of the carotid artery, and blood coagulation and fibrinolysis indices, and by use of brain magnetic resonance imaging, electrocardiogram (at rest and after exercise), ophthalmograph, and Rose's questionnaire. Information on potential confounding factors was collected by self administered questionnaire. RESULTS: Prevalence of microaneurysm of the retinal artery was significantly higher in workers exposed to CS2 (8.1%) than in referent workers (3.4%), and increased with age. Other examinations did not show any differences between the two groups even after allowance for confounding factors. CONCLUSIONS: Significant effects of CS2 on arteriosclerosis were not found in current rayon manufacturing workers, with the exception of induction of microaneurysm of the retinal artery.

Adult↗
PubMed1998

Cross sectional observation of the effects of carbon disulphide on the nervous system, endocrine system, and subjective symptoms in rayon manufacturing workers.

OBJECTIVES: A prospective cohort study was initiated to clarify whether the current level of exposure to carbon disulphide (CS2) is low enough to prevent occurrence of subclinical health impairments or to ameliorate health effects due to past high exposure. This paper describes the effects of exposure to CS2 on the nervous and endocrine systems, and the subjective symptoms in a baseline observation. METHODS: The effects were evaluated of CS2 on the median nerve conduction velocity, neurobehavioural and psychological tests, and subjective symptoms related to solvents in 432 male workers exposed to CS2 and 402 reference workers from 11 rayon factories in Japan. Adjustment was made for potential confounding factors such as age or alcohol drinking. Exposure to CS2 was either dichotomised or categorised into three groups by job type. RESULTS: Reductions were observed in motor (-1.9 m/s) and sensory (-0.91 m/s for orthodromic and -1.1 m/s for antidromic) nerve conduction velocities in the workers exposed to CS2 at the spinning and refining processes. Small but significant increases were found in self rated depression scale score and decrease in digit span (backward) in the workers exposed to CS2. Of 54 subjective symptoms many were increased--namely, heavy feeling in the head, light headedness, fainting after suddenly standing up, tremor, dullness, and increased sensitivity of skin in the extremities, reduced grasping power, reduced sexual desire, and increased rough skin. The endocrinological indicator--the concentration of glycosylated haemoglobin--was also increased in the workers exposed to CS2. CONCLUSIONS: Subclinical effects on the nervous system and on glucose metabolism were found in the workers exposed to CS2. One interpretation is that relatively higher exposure to CS2 in the past may induce these, but the effects are still not entirely ameliorated under the current exposure to CS2. Another possibility is that the current exposure to CS2 may cause these positive findings. A follow up observation is necessary to clarify these questions.

Adult↗
PubMed1998

A cross-sectional observation of the health effects of hydrazine hydrate and differences of its metabolism by NAT2 polymorphism.

OBJECTIVES: To summarize the results of two studies that attempted to clarify: (1) the health effects of hydrazine hydrate (HH) (N2H4 x H2O: CAS No. 7803-57-8); and (2) the influence of allelic polymorphism of N-acetyltransferase (NAT2) on the metabolism of HH. METHODS: A cross-sectional survey was carried out on 172 male HH-exposed workers and 125 male referent workers at five factories in Japan. The biological half-lives of HH after 1 h of exposure were determined in 12 workers, four workers in each of three NAT2 phenotypes. Clinical examinations were performed and acute and chronic subjective symptoms related to HH were examined by self-administered questionnaires. NAT2 phenotypes were assessed. RESULTS: No hydrazine was detected in either the breathing zones or the urine of the referent workers. The mean hydrazine concentration in the breathing zones, hydrazine and acetylhydrazine in urine, and the cumulative exposure level were 0.0109 ppm, 0.8660 micromol/g x Cr, and 2.80 ppm-years, respectively. There was no difference and no dose-dependent change in the health examination items between HH-exposed and referent workers after adjusting confounding factors, nor in terms of the differences of NAT2 phenotypes. Of 90 subjective symptoms, complaints of nightmares were significantly related to HH exposure. The half-life of urinary hydrazine and acetylhydrazine on rapid, intermediate, and slow phenotypes was 1.68, 3.01, and 4.46 h, respectively. CONCLUSION: This study suggested that current and cumulative exposure to HH did not affect the workers' health, and the half-life of the slow phenotype was longer than those of the rapid and intermediate phenotypes.

Adolescent↗
PubMed1997

A simple method for carbon disulfide monitoring using a diffusive sampler, thermal desorption and a stain tube.

A simple sampling and analytical method for monitoring carbon disulfide (CS2) vapor was investigated to assess exposure to low levels of CS2 in a viscose rayon factory. CS2 vapor was adsorbed on polymer beads (poly (2,6-diphenyl-p-phenylene oxide)) packed in a diffusive sampling tube. The sampling tube was heated at 180 degrees C for 7 min using a Daily Exposure Limit Test Apparatus, and thermally desorbed CS2 was measured by a stain tube for CS2. In laboratory experiments, the indicated CS2 levels measured by this method were highly correlated with calibrated CS2 concentrations (1-40 ppm), exposure duration (1-8 hr) and cumulative exposure levels. The CS2 values were stable up to 7 days after sampling when the diffusive tubes were stored at 4 degrees C and 20 degrees C. The effects of relative humidity, wind velocity and hydrogen sulfide on the measured values were negligible. In a field survey, 65 workers in a viscose rayon factory wore both the diffusive sampling tube and a commercially available 3M 3500 organic vapor monitor on their collar during their 8-hr work period. CS2 concentrations obtained by the two methods were comparable and the correlation coefficient was 0.931. This method proved to be useful in determining the concentrations of CS2 to which workers were exposed.

Carbon Disulfide↗
PubMed1996

Evaluation of the subacute pulmonary and testicular inhalation toxicity of diborane in rats.

This study aimed to clarify the subacute pulmonary and testicular inhalation toxicity of diborane (B2H6, CAS: 19287-45-7) in rats. Male Wistar rats were exposed for 8 weeks to 0.11 or 0.96 ppm of diborane for 6 hr/day, 5 days/week. The control group was exposed to filtered air. Bronchoalveolar lavage fluid (BALF), hematological, biochemical, and histopathological examinations were conducted. Sperm counts and spermatic morphological changes were examined in epididymides, and histopathological examination was carries out in testes. BALF examinations revealed that the percentage of neutrophils increased in a dose-dependent manner and that of macrophages decreased in rats exposed to 0.96 ppm. Quantities of total and individual phospholipids in BALF increased in rats exposed to 0.96 ppm. The proportion of phosphatidylglycerol plus sphingomyelin decreased, and phosphatidylethanolamine and phosphatidylinositol increased in rats exposed to 0.96 ppm. LDH increased in rats exposed to 0.96 ppm, and ALP showed a dose-dependent increase. In serum, alpha 1-antitrypsin and superoxide dismutase activities increased in rats exposed to 0.11 or 0.96 ppm. These changes showed dose-dependent effects on the lung in rats exposed to diborane, possibly indicating that the hyperenergia of type II cells with proliferation and/or hypertrophy without histopathological changes occurred even in rats exposed to 0.11 ppm. Testicular examinations revealed no particular findings. The TLV-TWA of diborane (0.1 ppm) seems to be high and possibly unsafe, considering that the no-observed-effect level over 8 weeks for rat lung was under 0.11 ppm.

Administration, Inhalation↗
PubMed1996

Relationship between acetone exposure concentration and health effects in acetate fiber plant workers.

In order to clarify the effects of acetone (AC) exposure on health, a cross-sectional study was carried out in 110 male AC-exposed and 67 male nonexposed shift workers. The AC workers ranged in age from 18.7 to 56.8 years (mean: 37.6 years) and in length of AC exposure from 0.5 to 34.3 years (mean: 14.9 years). The nonexposed workers ranged in age from 20.7 to 57.5 years (mean: 41.9 years). AC exposure levels assessed by personal passive monitors and biological monitoring indices measured at the end of the workshift were 19.6-1018 ppm in the breathing zone (AC-E, mean: 364 ppm), 2.5-422 ppm in alveolar air (AC-A, mean: 97.3 ppm) 4-220 mg/l in blood (AC-B, mean 66.0 ppm), and 0.75-170 mg/l in urine (AC-U, mean: 37.8 mg/l). Symptoms at the end of the workshift with good exposure-response relationships were eye irritation, tearing, and acetone odor, and symptoms within the previous 6 months with good exposure-response relationships were heavy, vague, or faint feeling in the head, nausea, loss of weight, and slow healing of an external wound. In the 30-44 year age range, simple reaction time and digit span scores in a short computerized neuro-behavioral test battery were significantly lower in AC workers, but exposure-response relationships were not clear. Manifest Anxiety Scale scores, Self-rating Depression Scale scores, R-R interval variation on the ECG, hematological examinations, serum biochemistry examinations for liver function, and phagocytic activity of peripheral neutrophils did not show any AC-related differences between the two groups. In view of the reported findings, the current occupational exposure limit of 750 ppm recommended by many governmental and academic associations seems to be too high to prevent the health effects of AC observed in this study.

Acetone↗
PubMed1996

Acute and subacute inhalation toxicity of dichlorosilane in male ICR mice.

Using male ICR mice, the LC50 and acute and subacute inhalation toxicity of dichlorosilane (SiH2Cl2, DCS) and the fate of DCS released into the air were investigated. DCS resolved and minute particles including silicon and chloride were observed, when DCS was released into the air. Most particles were under 1 micron in diameter. The LC50 of DCS at 4-h exposure was 144 ppm (nominal concentration). In the acute inhalation study, ten mice in each group were exposed to 64 ppm (nominal concentration) DCS for 1, 2, 4 or 8 h. Body weight loss, wheezing and piloerection were observed in mice exposed for 2 h or more. Histopathologically, injury to the nasal mucosa and trachea were observed in all exposed mice. Mice exposed to 32 ppm (nominal concentration) DCS for 2 or 4 weeks also exhibited depression of body weight gain, wheezing and piloerection. Squamous metaplasia of the nasal mucosa and tracheal epithelium was observed in both 2- and 4-week exposure groups. Exposure to DCS was irritant or corrosive to the respiratory tract with both acute and subacute inhalation. Apart from silane (SiH4), toxic effects of DCS seem to be characterized by chloride compounds derived from DCS.

Administration, Inhalation↗
PubMed1995

Acetone excretion into urine of workers exposed to acetone in acetate fiber plants.

To develop a proper protocol for biological exposure monitoring of acetone, we evaluated whether exposure to acetone on the previous day affects the biological monitoring value at the end of a work day. One hundred and ten male workers exposed to acetone in three acetate fiber manufacturing plants were monitored using a liquid passive sampler on two consecutive working days after 2 days without exposure. Urine samples were collected at the start of the workshift and the end of the shift on both days for each subject. For ten exposed workers urine samples were collected approximately every 2 h during and after the first working day until the following morning. Acetone concentrations in urine (Cu) at the start of the first working day were 1.3 +/- 2.4 (range: ND-14.1) mg/l in nonexposed workers and 2.4 +/- 5.6 (range: ND-40.3) mg/l in exposed workers. The urinary acetone concentration at the beginning of the second working day indicated that urinary levels of acetone do not decline to background level by the following morning when exposure concentration exceeds 300 ppm. However, linear regression analysis demonstrated that the relationship between environmental exposure level and urine level was similar on the 1st day and the 2nd day. Thus, although urine acetone levels did not return completely to baseline after high exposures, under the present exposure levels the exposure on the previous day did not significantly affect urinary acetone at the end of the workshift of the next day.

Acetone↗
PubMed1995

Acute and subacute inhalation toxicity of diborane in male ICR mice.

To clarify the toxicity of diborane, we conducted acute (15 ppm for 1, 2, 4 or 8 h) and subacute (5 ppm for 2 or 4 weeks) inhalation studies on ICR mice. The concentration resulting in a 50% kill after 4 h exposure was 31.5 ppm. Body weight gain was suppressed and the lung weight was increased in diborane-exposed mice in both acute and subacute studies. In the acute study, diffuse pan bronchiolitis-like lesions developed in the lung in various degrees depending on exposure time, which can be pathologically characterized as infiltration of inflammatory cells into the terminal bronchioles and surrounding alveoli, pulmonary congestion and bleeding and/or edema. In the subacute study, we observed lymphoid hyperplasia in the perivascular and peribronchial areas, and infiltration of macrophage and plasma cells into the alveoli. In the mice exposed for 4 weeks, the lesions were more severe than in those exposed for 2 weeks, consisting of hyperplasia and desquamation of Clara cells. In the nasal cavity, we saw mucous exudate and inflammatory cells, suggesting irritation caused by diborane. The histopathological findings, except for the respiratory organs, did not reveal any exposure-related changes. No significant changes were seen in hematological and serum biochemical examinations either. In conclusion, the target organ of diborane inhalation is the respiratory organs, particularly the lung. Further inhalation experiments are essential to investigate the safety exposure levels of diborane.

Administration, Inhalation↗
PubMed1995

No-effect level of subacute tetraethoxysilane inhalation on the mouse kidney.

To determine safe exposure levels of tetraethoxysilane (TEOS) in the kidney, groups of male ICR mice (SPF grade) containing 10 animals each were exposed to TEOS, 100 ppm or 50 ppm, for 6 hours/day, 5 days/week, for 2 or 4 weeks. Tubulo-interstitial nephritis developed in mice exposed to 100 ppm for 2 and 4 weeks, but no kidney lesions or renal function changes were observed in mice exposed to 50 ppm. However, histopathological changes were detected in the nasal mucosa of mice exposed to 50 ppm TEOS. These results indicate that the occupational exposure level for TEOS should be strictly maintained below the current recommended exposure limit, 10 ppm, set by many countries and academic associations, and that renal tubular function of TEOS-exposed workers should be assessed and monitored for a long period.

Administration, Inhalation↗
PubMed1995

No-observed-effect level of diborane on the respiratory organs of male mice in acute and subacute inhalation experiments.

In order to clarify the acute and subacute toxicity of diborane (B2H6, CAS: 19287-45-7) at low concentrations, male ICR mice were exposed to diborane for 1, 2, 4 or 8 h at concentrations of 1 or 5 ppm (phase I study), and for 6 h/day, 5 days/wk, over 2 or 4 wk at concentrations of 0.02 or 0.7 ppm (phase II study). Hematological and biochemical tests, and histopathological examinations of the cornea, nasal mucosa, respiratory tract and lung were carried out. All mice in both studies survived until they were sacrificed. In the phase I study, lung weight increased significantly in mice exposed to 5 ppm of diborane for 8 h. Histopathologically diffuse panbronchiolitis-like lesion was observed in mice exposed to 5 ppm of diborane for 2, 4 or 8 h. In the phase II study, slight infiltration of polymorphous neutrophil was observed mainly in the peribronchiolar region in mice exposed to 0.2 ppm or 0.7 ppm of diborane for 2 or 4 wk. In both studies, hematological and biochemical examinations failed to reveal any exposure-related changes. These results suggest that no-observed-effect level of diborane inhalation on the respiratory organs were 1 ppm in acute exposure, but 0.2 ppm of diborane inhalation for 2 or 4 wk seems to be unsafe.

Acute Disease↗
PubMed1994

Acute and subchronic inhalation toxicity of tetraethoxysilane (TEOS) in mice.

To clarify the acute and subchronic inhalation toxicity of tetraethoxysilane [TEOS, Si(OC2H5)4], groups of ten male ICR mice (SPF grade) were exposed to 1000 ppm TEOS for 1,2,4 or 8 h (acute inhalation study), or to 200 ppm of TEOS for 6 h/day, 5 days/week, for 2 or 4 weeks (subchronic inhalation study). The numbers of mice that died during 2 weeks of observation were 0, 1, 1 and 6 in the 1-, 2-, 4- and 8-h inhalation experiments and zero in the subchronic inhalation study. In the acute inhalation study, body weight decreased after TEOS exposure and did not reach the level of control mice during 2 weeks of observation except in the 1-h inhalation study. In the subchronic exposure study, weight gain was suppressed during the exposure period. Body weight in mice exposed for 2 weeks reached the level of non-exposed mice during the 2-week observation period, but did not do so in mice exposed for 4 weeks. Acute tubular necrosis (ATN) and acute splenic atrophy (ASA) were observed in all dead mice in the acute inhalation study, and tubulointerstitial nephritis (TIN) was frequently found in the surviving mice in both the acute and subchronic studies. However, blood biochemical examinations revealed no evidence of renal dysfunction. The olfactory epithelium was necrotic in all dead mice. In the subchronic inhalation study, infiltration of polymorphonuclear neutrophils in the nasal mucosa was observed in all mice killed 1 day after exposure. These results indicate that the LCL0 for 1-h exposure to TEOS and LC50 for 4-h exposure are greater than 1000 ppm, and that the kidney and nasal mucosa are the target organs for TEOS inhalation.

Administration, Inhalation↗
PubMed1994

Work environment of plants manufacturing asbestos-containing products in Japan.

In 1985, a comprehensive study of asbestos-containing product plants (A/C, friction, textile) was performed. The data presented were based not on personal but on area sampling. A conversion equation from area sampling data to personal exposure values was developed. Exposure concentrations were 0.07-0.66 f ml-1. In workplaces which belonged to member companies of the Japan Asbestos Association, the percentage of workplaces whose exposure concentrations was less than 0.3 f ml-1 was 70% in 1985 (N = 510), but 98% in 1992 (N = 430). Concentrations in a new, well-controlled A/C plant were less than 0.1 f ml-1.

Asbestos↗
PubMed1994

[Cohort studies of effects of long-term toluene diisocyanate (TDI) exposure on pulmonary function].

Toluene diisocyanates (C6H3CH3 (NCO)2, TDIs) are synthetic low molecular-weight organic chemicals with two highly reactive isocyanate groups (-NCO). Exposure to TDI can cause irritation of the eyes, nose, and upper and lower respiratory tract, asthma-like responses, sensitive pneumonitis, and obstructive pulmonary function loss. In this paper, the exposure-effect relationships between long-term TDI exposure and its effect on pulmonary function are summarized by evaluating the results of cohort studies, including 2 cohort studies conducted by the author's research team, which were specially devoted to the exposure-effect relationships and were published at the end of 1992. By assessing the exposure-effect relationships, the current occupational exposure limit of TDI in Japan is discussed and a framework for the health checks on TDI-exposed workers is proposed.

Animals↗