Chronic Toluene Research Articles

Severe dopaminergic pathways damage in a case of chronic toluene abuse

Introduction Toluene toxicity primarily affects central nervous system white matter, causing a characteristic brain MRI pattern. Case report A toluene addicted man, after an abstinence period and a treatment with neuroleptics, presented with severe worsening of preexisting generalized tremor, opsoclonus, dysarthria, gait inability, jerky tendon reflexes and behaviour disorders. Magnetic resonance imaging showed mild leukoencephalopathy and hypointensities in deep gray matter nuclei. The DaT-scan revealed a decrease in presynaptic dopamine reuptake. Conclusion Clinical and neuroradiological findings and the possible sensitivity to neuroleptics indicate dopaminergic impairment. Our case suggests that chronic toluene abuse causes presynaptic dopaminergic depletion.

Smaller Gray Matter Volumes in Frontal and Parietal Cortices of Solvent Abusers Correlate with Cognitive Deficits

Abuse of toluene-containing organic solvents by inhalation is a prevalent practice among adolescents. Long-term abuse of toluene causes cognitive deficits. The mechanism of cognitive deficits induced by long-term toluene abuse has not yet been defined. In the current study, we assessed the effects of chronic toluene abuse on cortical gray matter volume and the association between cognitive impairment and cortical gray matter volume distribution in chronic toluene abusers. Fifteen toluene abusers and 20 healthy control subjects matched in sex, age, education level, and handedness were investigated by structural MR imaging. The cognitive states of the subjects were assessed by using the third edition of the Wechsler Intelligence Scale for Children (WISC-III). The voxel-based comparison and correlation analyses of MR images were performed by using SPM5 software. The voxel-based morphometric analysis revealed that toluene abusers had significantly lower gray matter volumes in the bilateral frontotemporal and right parietal cortices. In addition, the lower gray matter volumes in the frontal and parietal regions correlated with the duration of toluene abuse. There was a positive correlation between the WISC performance scale scores and gray matter volumes in the frontal and parietal cortices of the abusers. The results of the current study demonstrate that chronic toluene abusers have smaller gray matter volumes than nonabusers in various regions of the brain. Moreover, the cognitive deficits are associated with the lower gray matter volumes in the frontal and parietal cortices of chronic toluene abusers.

Brain Magnetic Resonance Imaging in Chronic Trichloroethylene and Toluene Exposure

A 63-year-old woman with hypertension presented with amnesic episodes. The patient had no history of carbon monoxide intoxication or encephalitis, but she had been exposed to mixed solvents, including trichloroethylene and toluene, for 5 years for substrate treatment. The neurological examination was normal except for short-term memory disturbance. Fluid attenuated inversion recovery (FLAIR) and T2-weighted magnetic resonance imaging (MRI) of her brain revealed increased signal intensity in the bilateral thalamus, basal ganglia, internal and external capsule and white matter (Picture 1). Long-term occupational exposure to organic solvents can result in irreversible damage to the central nervous system. Approximately 30% of patients with chronic solvent encephalopathy showed abnormal MRI findings such as brain atrophy and white matter lesion (1). Chronic misuse of toluene has been reported to cause MRI changes, such as loss of grey-white matter differentiation and hypointensity in thala-

Pneumatosis intestinalis and hepatic portal venous gas

We report two cases of pneumatosis intestinalis and hepatic portal venous gas. The first case was in a 67-year-old woman who complained of strong right lower abdominal pain and high fever on the twelfth day after pancreatoduodenectomy (PD) with portal vein (PV) resection. Abdominal X-ray and computed tomography showed hepatic portal venous gas and pneumatosis intestinalis. The emergency laparotomy performed disclosed extensive necrosis of the bowel from the jejunum to the ascending colon. All necrotic parts of the bowel were resected and a jejunostomy was performed. The residual intact small intestine was 30 cm in length. Her postoperative course was stable. This is a rare complication after PD and cannot be cured by any other treatment but surgery. The second case was in a 45-year-old woman with the chief complaint of abdominal pain and constipation. She had a past history of chronic toluene inhalation. Abdominal X-ray and computed tomography also showed hepatic portal venous gas and pneumatosis intestinalis, as well as free air, but no physical examination or laboratory test results supported a diagnosis of bowel necrosis. Hyperbaric oxygen (HBO) therapy effectively controlled the symptoms and signs.

Protective Effects of Nigella sativa on the Neuronal Injury in Frontal Cortex and Brain Stem After Chronic Toluene Exposure

The goal of this study was designed to evaluate the possible protective effects of Nigella sativa (NS) on the neuronal injury in the frontal cortex and brain stem after chronic toluene exposure in rats. The rats were randomly alotted into one of three experimental groups: A (control), B (toluene treated) and C (toluene treated with NS); each group contain 10 animals. Control group received 1 ml serum physiologic and toluene treatment was performed by inhalation of 3,000 ppm toluene, in a 8 h/day and 6 day/week order for 12 weeks. The rats in NS treated group was given NS (in a dose of 400 mg/kg body weight) once a day orally by using intra gastric intubation for 12 weeks starting just after toluene exposure. Tissue samples were obtained for histopathological investigation. To date, no histopathological changes of neurodegeneration in the frontal cortex and brain stem after chronic toluene exposure in rats by NS treatment have been reported. In this study, chronic toluene exposure caused severe degenerative changes, shrunken cytoplasma, severely dilated cisternae of endoplasmic reticulum, markedly swollen mitochondria with degenerated cristae and nuclear membrane breakdown with chromatin disorganization in neurons of the frontal cortex and brain stem. The nerve cells showing the pathologic changes were almost absent in the NS-treated rats. We conclude that NS therapy causes morphologic improvement on neurodegeneration in frontal cortex and brain stem after chronic toluene exposure in rats. We believe that further preclinical research into the utility of NS may indicate its usefulness as a potential treatment on neurodegeneration after chronic toluene exposure in rats.

Effect of toluene exposure on the antioxidant status and apoptotic pathway in organs of the rat

The chronic abuse of the solvent toluene results in structural and functional impairment of various organs. However, the pathophysiological mechanisms that cause these impairments of function are not clearly understood. This study aims to assess the effect of chronic toluene exposure (15, 30 and 45 days) on the oxidative stress and antioxidant status of different organs in the rat. Also, cyclooxygenase-2 and caspase-3 activities (a marker of apoptosis) are studied. Forty male albino rats were used and divided into four groups: controls (group I) and three other groups receiving a single daily dose of toluene (650 mg/kg) for 15 days (group II), 30 days (group III) and 45 days (group IV). The animals were then sacrificed and the brain cortex, cerebellum, liver, kidney and testis were separated for the determination of thiobarbituric acid reactive substance (TBARS), GSH, glutathione disulphide (GSSG) and glutathione reductase (GR), glutathione peroxidase (GPx), glutathione-S-transferase (GST), superoxide dismutase (SOD), cyclooxygenase-2 (COX-2) and caspase-3 activity. Results showed a significant and time-dependent increase in the levels of TBARS, GSSG and in GST, SOD, COX-2 and caspase-3 activity, while GSH, GR and GPx showed a marked decline in most tissues. The brain (cortex and cerebellum) was the most affected organ, showing the greatest increase in one apoptotic marker (caspase-3), while the testis and kidneys were least affected. In conclusion, oxidative stress and derangement of the GSH:GSSG ratio, induced chronic inflammatory change and apoptosis may play an essential role in toluene toxicity.

Nigella sativa and Derived Thymoquinone Prevents Hippocampal Neurodegeneration After Chronic Toluene Exposure in Rats

The aim of this study was designed to investigate the possible beneficial effects of Nigella sativa (NS) and derived thymoquinone (TQ) on neurodegeneration in hippocampus after chronic toluene exposure in rats. The rats were randomly allotted into one of four experimental groups: A (control), B (toluene treated), C (toluene treated with NS) and D (toluene treated with TQ); each group contain 10 animals. Toluene treatment was performed by inhalation of 3,000 ppm toluene, in a 8 h/day and 6 day/week order for 12 weeks. Control group received 1 ml serum physiologic and the rats in NS and TQ treated groups (C and D) were given NS (in a dose of 400 mg/kg body weight) and TQ (50 mg/kg body weight) once a day orally by using intra gastric intubation for 12 weeks starting just after toluene exposure respectively. Tissue samples were obtained for histopathological investigation. To date, no histopathological changes of neurodegeneration in hippocampus after chronic toluene exposure in rats by NS and TQ treatment have been reported. In this study, chronic toluene exposure caused severe degenerative changes, shrunken cytoplasma, slightly dilated cisternae of endoplasmic reticulum, markedly swollen mitochondria with degenerated cristae and nuclear membrane breakdown with chromatin disorganization in neurons of the hippocampus. The distorted nerve cells were mainly absent in the TQ and NS-treated rats. We conclude that TQ and especially NS therapy causes morphologic improvement on neurodegeneration in hippocampus after chronic toluene exposure in rats. We believe that further preclinical research into the utility of NS and TQ may indicate its usefulness as a potential treatment on neurodegeneration after chronic toluene exposure in rats.

Immunochromatographic Analysis of Hippuric Acid in Urine

Toluene, a clear, colorless liquid with a distinctive smell, is the most commonly used industrial organic solvent. The adverse effects of chronic toluene exposure have been reported. The abuse of volatile substances is practiced mainly by adolescents and young adults. Chronic toluene abuse causes permanent changes in brain structure correlated with brain dysfunction; therefore, it is important to monitor the level of toluene exposure to prevent neurological damages. In this study, immunochromatographic analysis was performed to measure a level of the exposed toluene easily and accurately in urine. Inhaled toluene is metabolized to hippuric acid (HA) in the liver and secreted in urine. Therefore, the monoclonal antibodies against HA were generated and characterized by indirect competitive ELISA. The sensitivity was then monitored in order to adjust the cutoff concentration to 2 mg of HA/mL of urine. Using these monoclonal antibodies as raw materials, the immunochromatographic device was manufactured with the lateral flow system. The clinical studies were performed with suspected users' urine samples, and the results were confirmed by high-performance liquid chromatography.

EBSELEN PROTECTS AGAINST OXIDATIVE AND MORPHOLOGICAL EFFECTS OF HIGH CONCENTRATION CHRONIC TOLUENE EXPOSURE ON RAT SCIATIC NERVES

Aim: Neuroprotective effects of ebselen against free radical damage have been studied extensively. Toluene generates reactive oxygen species (ROS) and the toxic effects relating to these reactants. The aim of this study was designed to investigate the effects of chronic toluene inhalation in high concentration on lipid peroxidation, antioxidant enzyme activities and ultrastructural changes in the sciatic nerves of rats. Methods: We also examined the protective effects of ebselen against toluen exposure. Male Wistar albino rats (150-250 g) were divided in three experimental groups: the control, toluene and toluene+ebselen treated group (n=10 for each). Toluene treatment was performed by inhalation of 3000 ppm toluene, in a 8 hr/day and 6 day/week order for 16 weeks. Control group received 1ml serum physiologic and ebselen was given i.p. (10 mg/kg) to toluene+ebselen treated group just after toluene exposure per day. Blood and tissue samples were obtained for biochemical and histopathological investigation. The blood and sciatic nerves were assayed for toluene by gas chromatography. Results: Toluene significantly increased blood and tissue malondialdehyde (MDA), and decreased tissue superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px), but not tissue catalase (CAT) levels when compared with controls. Ebselen administration prevented to increase of blood and tissue MDA and decrease to SOD and GSH-Px levels induced by toluene inhalation. Electron micrographs of sciatic nerve in the toluene group shows myelin destructions with onion-bulb and bubble form protrusion on the myelin sheath and axolemma border of myelinated axons. Furthermore, ebselen salvaged the nerve fibers from toluene exposure. Conclusion: Ebselen treatment may provide neuroprotection against toluene neurotoxicity by directly scavenging ROS and by indirectly augmenting their antioxidant capacity.

D103 アルコール摂取とトルエン慢性曝露がNK細胞活性に及ぼす影響(有機溶剤中毒ほか,一般演題:口演,地方の時代の産業保健,第79回日本産業衛生学会)

D103 アルコール摂取とトルエン慢性曝露がNK細胞活性に及ぼす影響(有機溶剤中毒ほか,一般演題:口演,地方の時代の産業保健,第79回日本産業衛生学会)

The Oxidative and Morphological Effects of High Concentration Chronic Toluene Exposure on Rat Sciatic Nerves

This study was designed to investigate the effects of chronic toluene inhalation in high concentration on lipid peroxidation, antioxidant enzyme activities and ultrastructural changes in the sciatic nerves of rats. Male Wistar albino rats (150-250 g) were divided in two experimental groups: the control and the toluene treated group (n = 10 for each). Toluene treatment was performed by inhalation of 3000 ppm toluene, in a 8 h/day and 6 day/week order for 16 weeks. Blood and tissue samples were obtained for biochemical and histopathological investigation. The blood and sciatic nerves were assayed for toluene by gas chromatography. Toluene significantly increased blood and tissue malondialdehyde (MDA), and decreased tissue superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px), but not tissue catalase (CAT) levels when compared with controls. Electron micrographs of sciatic nerve in the toluene group shows myelin destructions with onion-bulb and bubble form protrusion on the myelin sheath and axolemma border of myelinated axons. The area of injury on the myelin sheath were measured by Image-Pro Plus. Mean of the injury area were estimated 34% each myelin. These findings indicate that chronic toluene inhalation might be involved with free radical processes.

Alterations in glutamatergic and gabaergic ion channel activity in hippocampal neurons following exposure to the abused inhalant toluene

Toluene, a representative member of the large class of abused inhalants, decreases neuronal activity and depresses behavior in both animals and humans. The sites of action of toluene are not completely known but recent studies suggest that ion channels that regulate neuronal excitability may be particularly sensitive. Previous studies with recombinant receptors showed that toluene decreases currents carried by N-methyl- d-aspartate (NMDA)-glutamate receptors without affecting those gated by non-NMDA receptors. In addition, toluene increases currents generated by GABA and glycine receptors. In the present study, primary cultures of rat hippocampal neurons were used to investigate the effects of acute and chronic toluene exposure on native excitatory and inhibitory ligand-gated ion channels. Toluene dose-dependently inhibited NMDA-mediated currents (IC 50 1.5 mM) but had no effect on responses evoked by the non-NMDA agonist kainic acid. Prolonged treatment of neurons with toluene (1 mM; 4 days) increased whole-cell responses to exogenously applied NMDA, reduced those evoked by GABA but did not alter responses generated by kainic acid. Immunoblot analysis revealed that prolonged toluene exposure increased levels of NR2A and NR2B NMDA receptor subunits with no change in NR1. Immunohistochemical analysis with confocal imaging showed that toluene-treated neurons had significant increases in the density of NR1 subunits as compared with control neurons. Toluene exposure increased the amplitude of synaptic NMDA currents and decreased those activated by GABA. The results from this study suggest that toluene induces compensatory responses in the functional expression of ion channels that regulate neuronal excitability.

Effects of prenatal exposure to chronic mild stress and toluene in rats

The aim of the present study was to elucidate whether prenatal chronic stress, in combination with exposure to a developmental neurotoxicant, would increase effects in the offspring compared with the effects of either exposure alone. Development and neurobehavioral effects were investigated in female offspring of pregnant rats (Mol:WIST) exposed to chronic mild stress (CMS) during gestational days (GD) 9–20, or 1500 ppm toluene, 6 h/day during gestational days 7–20, or a combination of the two. Prenatal CMS was associated with decreased thymic weight and increased auditory startle response. The corticosterone response to restraint seemed modified by prenatal exposure to toluene. Lactational body weight was decreased in offsprings subjected to CMS, primarily due to effects in the combined exposure group. Cognitive function was investigated in the Morris water maze, and some indications of improved function due to CMS were observed. In the present experimental setting, there was no indication of the two exposures potentiating each other with respect to adverse effects on the nervous system. However, the effects of prenatal CMS indicate that stress during fetal life may interfere with the development of the thymus and increase the reactivity (startle reflex) of the offspring.

The effects of toluene on the central nervous system.

In recent decades the organic solvent toluene (methylbenzene) has emerged as one of the best-studied neurotoxins. Long-term and intense exposure to toluene vapors in humans who abuse spray paint and related substances has led to the recognition that toluene has a severe impact on central nervous system myelin. Chronic toluene abuse produces a devastating neurological disorder, of which dementia is the most disabling component. The clinical syndrome, toluene leukoencephalopathy, can be detected by a combination of characteristic symptoms and signs, detailed neurobehavioral evaluation, and brain magnetic resonance imaging. In this paper, we consider the impact of toluene abuse on our society, describe the specific neurobehavioral deficits in toluene leukoencephalopathy, review the spectrum of neuroimaging findings in patients with this disorder, summarize the teratogenic effects of toluene in both humans and animal models, and offer possible explanations for the range of neuropathological damage seen in brains of individuals who chronically abuse toluene.

Single-voxel proton MR spectroscopy in toluene abuse.

Inhalation of toluene, which is an organic solvent, causes toxic encephalopathy characterized by cognitive impairment, cerebellar and extra-pyramidal symptoms. We studied cranial MR images and single-voxel MR spectroscopy of 22 toluene abusers and age-matched control subjects. The mean age of the abusers and mean duration of abuse were 18,1 years and 47 months, respectively. We got three MR spectra from the centrum semiovale, cerebellum and thalamus by using STEAM sequence with a TE value of 30 ms. N-acetyl aspartate (NAA)/Creatine (Cr), Choline (Cho)/Cr, myo-inositol (mI)/Cr peak integral ratios were calculated. NAA/Cr in the cerebellum and centrum semiovale of the abusers were significantly lower than those of the control subjects. mI/Cr in centrum semiovale and cerebellum were higher in toluene abusers. No significant difference was found in the metabolite ratios of the thalami. The association of NAA/Cr and mI/Cr ratios in cerebellum and centrum semiovale with the duration of abuse was significant. Normal level of NAA in thalamus, which was a neuron rich gray matter structure, might imply that toluene inhalation did not cause direct neuronal injury. Selective reduction of NAA and increased level of mI in white matter supported the theory of that axonopathy and gliosis were the main mechanisms of pathophysiology in chronic toluene encepholopathy. Insignificance of elevation of Cho/Cr ratios demonstrated that toluene inhalation did not cause active demyelination.

Behavioral and neurochemical effects induced by subchronic exposure to 40 ppm toluene in rats

Chronic toluene inhalation at concentrations above occupational exposure limits (e.g., 100 ppm; NIOSH) has been repeatedly shown to induce neurotoxic effects. In contrast, although few clinical and experimental data are available on the effects of toluene exposure at concentrations below occupational exposure standards, some of these data may support adverse effects of long-term exposure to low toluene concentrations. To test this hypothesis, we investigated the neurobehavioral and neurochemical effects of 40 ppm inhaled toluene in a rat model of 16-week subchronic exposure, examining locomotor and rearing activities; adaptation/sensitization to narcosis produced by acute exposure to toluene at high concentration; and tyrosine hydroxylase and tryptophan hydroxylase activities, and dopamine (DA) and serotonin (5-HT) turnovers in the caudate–putamen, nucleus accumbens, hippocampus, prefrontal cortex, and cerebellum. Our results mainly show that subchronic exposure to 40 ppm toluene significantly resulted in a sensitization to toluene-induced narcosis, a decrease in rearing activity, and alterations in DA and 5-HT transmissions. This demonstrates that subchronic toluene exposure at a low concentration may lead to adverse changes in neurobehavioral and neurochemical functioning, and further questions in a public health perspective the actual neurotoxic potential of toluene and other organic compounds, because deficits in functioning are generally viewed as precursors of more serious adverse effects.

Increased expression of transforming growth factor-β1 (TGF-β1) and loss of epithelial growth factor (EGFR)/TGF-β1 in chronic toluene diisocyanate (TDI)-induced asthma: Relationship to asthma symptoms

Increased expression of transforming growth factor-β1 (TGF-β1) and loss of epithelial growth factor (EGFR)/TGF-β1 in chronic toluene diisocyanate (TDI)-induced asthma: Relationship to asthma symptoms

Multicenter field trial on possible health effects of toluene. II. Cross-sectional evaluation of acute low-level exposure

Data on possible acute effects of today's relevant low-level exposure to toluene are contradictory, and information on possible effects of exposure under occupational conditions is largely lacking. In a controlled, multi-center, blinded field trial, effects possibly associated with acute toluene exposure were evaluated in workers of 12 German rotogravure factories. Medical examinations (inquiries on subjective symptoms, and standard tests of psycho-physiological and psycho-motor functions) were performed on almost 1500 volunteers, of whom 1290 were toluene-exposed (1178 men and 112 women), and about 200 participants served as references (157 men and 37 women), but the main aim of the trial was to reveal dose–response relationships. All volunteers were of the morning work-shift (6 h exposure). Both individual ambient air concentrations (time-weighted average) during the work-shift, as well as blood toluene concentrations after the work-shift were measured. Therefore, the medical data could for the first time be correlated with the actual individual body burden (blood toluene level) at the time of testing. In order to largely exclude confounding by chronic toluene exposure, kinetic measurements as well as the psycho-physiological and psycho-motoric tests were performed before and after the work-shift. Except for minor statistical deviations, neither convincing dose-dependent acute effects could be demonstrated with regression analyses in male volunteers at the exposure levels evaluated, nor were significant differences found when applying group statistics (highly toluene-exposed group versus volunteers with negligible exposure). Due to the rather large number of participants, the predictive power of the study is high, especially when compared with previous publications. In two psycho-physiological tests, a few more female volunteers with quite low toluene body burdens (<340 μg/l blood) showed relatively low scores when compared with participants of the reference group. Although evidence for a medical relevance is meager, the small numbers of participants, in both the exposure and the reference groups, hamper a reliable interpretation of the results concerning exposure levels above 85 μg toluene/l blood, and it is difficult to take confounding factors adequately into account. For the end points evaluated and under occupational conditions, neither blood toluene levels of 850 to 1700 μg/l (in the highest exposure group [EXPO-IV] with 56 participants), as measured 1/2 (±1/2) h after the work-shift, nor ambient air concentrations (time-weighted average over 6 h) between 50 and 100 ppm (188–375 mg/m 3) were convincingly associated with alterations in psycho-physiological and psycho-motoric performances or increased the frequency of subjective complaints in male volunteers. For higher dose ranges of toluene exposure (i.e. >1700 μg toluene/l blood [or >100 ppm in ambient air]), our data set is too small for far reaching conclusions. Our data are insufficient for conclusions on a possibly higher susceptibility to toluene of some female workers. Results of kinetic studies and possible effects of long-term exposure are discussed in two accompanying publications (Neubert et al., 2001; Gericke et al., 2001).

Effects of environmental and organizational factors on the health of shiftworkers of a printing company.

This study explored the effects of environmental and organizational stressors on the health of shiftworkers in a printing company (n = 124). A questionnaire was used to gather data on work history, organizational factors, psychosocial characteristics, medical history, present health, occupational and non-occupational exposures, and lifestyle factors. The perception of environmental and organizational conditions was associated (P < 0.05) with chronic back pain (odds ratio [OR], 1.29), varicose veins (OR, 1.35), allergic rhinitis (OR, 1.27), depression (OR, 1.45), and gastritis (OR, 1.15). Anxiety scores were associated with allergic rhinitis (OR, 1.14) and skin allergy (OR, 1.09). Shiftwork was a significantly risk factor for conjunctivitis (OR, 3.68), depression (OR, 0.23), cardiac arrhythmia (OR, 7.13), and gastritis (OR, 4.38). Other associations included tenure and chronic back pain (OR, 4.89), toluene exposure and skin allergy (OR, 3.76), worksite and conjunctivitis (OR, 7.0), and worksite and dermatitis (OR, 1.24 to 4.95). The number of hours of exercise per week was associated with varicose veins (OR, 4.33), and alcohol intake was associated with cardiac arrhythmia (OR, 6.74).

Chronic Occupational Exposure to Organic Solvents and Magnetic Resonance Signal Changes in the Brain White Matter —A Case Report—

Journal of Occupational HealthVolume 42, Issue 1 p. 47-49 Case StudyFree Access Chronic Occupational Exposure to Organic Solvents and Magnetic Resonance Signal Changes in the Brain White Matter —A Case Report— Michihiro Kamijima, Michihiro Kamijima Department of Occupational and Environmental Health, Nagoya University Graduate School of MedicineSearch for more papers by this authorEiji Shibata, Eiji Shibata Department of Medical Technology, Nagoya University School of Health SciencesSearch for more papers by this authorHisashi Tanaka, Hisashi Tanaka Division of Neurology, Kyoritsu General HospitalSearch for more papers by this authorGaku Ichihara, Gaku Ichihara Department of Occupational and Environmental Health, Nagoya University Graduate School of MedicineSearch for more papers by this authorYasuhiro Takeuchi, Yasuhiro Takeuchi Department of Occupational and Environmental Health, Nagoya University Graduate School of MedicineSearch for more papers by this author Michihiro Kamijima, Michihiro Kamijima Department of Occupational and Environmental Health, Nagoya University Graduate School of MedicineSearch for more papers by this authorEiji Shibata, Eiji Shibata Department of Medical Technology, Nagoya University School of Health SciencesSearch for more papers by this authorHisashi Tanaka, Hisashi Tanaka Division of Neurology, Kyoritsu General HospitalSearch for more papers by this authorGaku Ichihara, Gaku Ichihara Department of Occupational and Environmental Health, Nagoya University Graduate School of MedicineSearch for more papers by this authorYasuhiro Takeuchi, Yasuhiro Takeuchi Department of Occupational and Environmental Health, Nagoya University Graduate School of MedicineSearch for more papers by this author First published: 07 April 2006 https://doi.org/10.1539/joh.42.47 Correspondence to: M. Kamijima, Department of Occupational and Environmental Health, Nagoya University Graduate School of Medicine, 65 Tsurumai-cho, Showa-ku, Nagoya 466–8550, Japan AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL No abstract is available for this article. References World Health Organization European Office. Chronic effects of organic solvents on the central nervous system and diagnostic criteria. Copenhagen: World Health Organization European Office, 1985. Rosenberg N, Kleinschmidt-DeMasters B, Davis K, et al. Toluene abuse causes diffuse central nervous system white matter changes. Ann Neurol 1988; 23: 611– 614. Filley C, Heaton R, Rosenberg N. White matter dementia in chronic toluene abuse. Neurol 1990; 40: 532– 534. Aiba I, Indo T, Ichihara G, Takeuchi Y. Change in magnetic resonance imaging and clinical signs in a case of chronic toluene intoxication by sniffing. J Occup Health 1996; 38: 13– 19. Thuomas K, Möller C, Ödkvist L, Flodin U, Dige N. MR imaging in solvent-induced chronic toxic encephalopathy. Acta Radiologica 1996; 37: 177– 179. Ukai H, Inui S, Takeda S, et al. Types of organic solvents used in small- to medium-scale industries in Japan; a nationwide field survey. Int Arch Occup Environ Health 1997; 70: 385– 392. Lai P-H, Tien R, Chang M-H, et al. Chorea-ballismus with nonketotic hyperglycemia in primary diabetes mellitus. Am J Neuroradiol 1996; 17: 1057– 1064. Schrag A, Kingsley D, Phatouros C, et al. Clinical usefulness of magnetic resonance imaging in multiple system atrophy. J Neurol Neurosurg Psychiatry 1998; 65: 65– 71. Volume42, Issue1January 2000Pages 47-49 ReferencesRelatedInformation