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Abstract Background In Korea, Carbon disulfide (CS2) toxicity was an important social problem from the late 1980s to the early 1990s but there have been few large-scale studies examining the prevalence of diseases after CS2 exposure discontinuance. So we investigated past working exposure to CS2 characteristics from surviving ex-workers of a rayon manufacturing plant including cumulative CS2 exposure index. Furthermore, we studied the prevalence of their chronic diseases recently after many years. Methods We interviewed 633 ex-workers identified as CS2 poisoning-related occupational diseases to determine demographic and occupational characteristics and reviewed their medical records. The work environment measurement data from 1992 was used as a reference. Based on the interviews and foreign measurement documents, weights were assigned to the reference concentrations followed by calculation of individual exposure index, the sum of the portion of each time period multiplied by the concentrations of CS2 during that period. Results The cumulative exposure index was 128.2 ppm on average. Workers from the spinning, electrical equipment repair, and motor repair departments were exposed to high concentrations of ≥10 ppm. Workers from the maintenance of the ejector, manufacturing of CS2, post-process, refining, maintenance and manufacturing of viscose departments were exposed to low concentrations below 10 ppm. The prevalence for hypertension, coronary artery disease, cerebrovascular disease, diabetes, arrhythmia, psychoneurotic disorder, disorders of the nervous system and sensory organ were 69.2%, 13.9%, 24.8%, 24.5%, 1.3%, 65.7%, 72.4% respectively. Conclusions We estimated the individual cumulative CS2 exposure based on interviews and foreign measurement documents, and work environment measurement data. Comparing the work environment measurement data from 1992, these values were similar to them. After identified as CS2 poisoning, there are subjects over 70 years of average age with disorders of the nervous system and sensory organs, hypertension, psychoneurotic disorder, cerebrovascular disease, diabetes, coronary artery disease, and arrhythmia. Because among ex-workers of the rayon manufacturing plant, only 633 survivors recognized as CS2 poisoning were studied, the others not identified as CS2 poisoning should also be investigated in the future.

Background: To investigate the clinicopathological characteristics of renal damage caused by long-term exposure to carbon disulfide (CS2) in nine patients., Methods: All the patients underwent ultrasound-guided renal biopsy. All specimens were examined by light microscopy and immunohistochemistry (IHC). Samples form one patient were further analyzed using transmission electron microscopy., Results: Similar pathological changes were observed in all patients, but the degrees of lesions were different. All cases had moderate to severe nodular mesangial hyperplasia; among these, type "Kimme1stie1-Wi1son" (K-W nodule for short) was observed in four cases, type "K - W nodule" refer to nodular hyperplasia of mesangial membrane like letter K or W. four cases had proliferative extracapillary glomerulonephritis (GN), while there were no concomitant changes in one patient. Besides, six cases had diffuse basement membrane thickening, focal segmental sclerosis or bulbar sclerosis; two cases had diffuse glomerular sclerosis, and one case had focal segmental capillary hyperplasia. Moreover, all patients had renal tubular atrophy/interstitial fibrosis with less to moderate chronic inflammatory cell infiltration, as well as renal arteriosclerosis. IHC showed that the depositions of IgA, IgM, C3d, C4d, C1q and Fib were not specific; while IgG, type III collagen, Fibronectin, Amyloid A, Igκ, Igλ, HBsAg and HBcAg were all negative., Conclusion: Diffuse nodular mesangial hyperplasia/sclerosing glomerular nephropathy is characterized by nodular mesangial hyperplasia with type "K-W nodules" formation, which we speculate is a special pathological manifestation of renal damage caused by carbon disulfide (CS2).

Background: In Korea, Carbon disulfide (CS 2 ) toxicity was an important social problem from the late 1980s to the early 1990s but there have been few large-scale studies examining the prevalence of diseases after CS 2 exposure discontinuance. So we investigated past working exposure to CS 2 characteristics from surviving ex-workers of a rayon manufacturing plant including cumulative CS 2 exposure index. Furthermore, we studied the prevalence of their chronic diseases recently after many years., Methods: We interviewed 633 ex-workers identified as CS 2 poisoning-related occupational diseases to determine demographic and occupational characteristics and reviewed their medical records. The work environment measurement data from 1992 was used as a reference. Based on the interviews and foreign measurement documents, weights were assigned to the reference concentrations followed by calculation of individual exposure index, the sum of the portion of each time period multiplied by the concentrations of CS 2 during that period., Results: The cumulative exposure index was 128.2 ppm on average. Workers from the spinning, electrical equipment repair, and motor repair departments were exposed to high concentrations of ≥10 ppm. Workers from the maintenance of the ejector, manufacturing of CS 2, post-process, refining, maintenance and manufacturing of viscose departments were exposed to low concentrations below 10 ppm. The prevalence for hypertension, coronary artery disease, cerebrovascular disease, diabetes, arrhythmia, psychoneurotic disorder, disorders of the nervous system and sensory organ were 69.2%, 13.9%, 24.8%, 24.5%, 1.3%, 65.7%, 72.4% respectively., Conclusions: We estimated the individual cumulative CS 2 exposure based on interviews and foreign measurement documents, and work environment measurement data. Comparing the work environment measurement data from 1992, these values were similar to them. After identified as CS 2 poisoning, there are subjects over 70 years of average age with disorders of the nervous system and sensory organs, hypertension, psychoneurotic disorder, cerebrovascular disease, diabetes, coronary artery disease, and arrhythmia. Because among ex-workers of the rayon manufacturing plant, only 633 survivors recognized as CS 2 poisoning were studied, the others not identified as CS 2 poisoning should also be investigated in the future.

Objective: To analyze the clinical characteristics of 267 cases with occupational chronic carbon disulfide (CS(2)) poisoning and to provide the basis for revising the items of periodical medical examination of workers occupationally exposed to CS(2)., Methods: The subjects of present study were 267 patients with mild CS(2) poisoning diagnosed according to "Diagnostic Criteria of Occupational Chronic Carbon Disulfide Poisoning (GBZ4-2002)" from April in 2006 to May in 2010. All patients were from the same chemical fiber factory. When a subject was diagnosed as patient with CS(2) poisoning, who should interview with questionnaire which included the illness and occupational history, symptoms, individual habits. The physical examination, nervous test, cardiovascular test, biochemical test and electromyogram were performed., Results: The rate of decreased motor conduction velocity was 87.3% (233/267 roots). The highest detection rate of slowing conduction velocity was the common peroneal motor nerve which was 48.6% (138/248 roots) and the second was median motor nerve with delay rate of 37% (155/419 roots). The main symptoms of the patients were neurasthenia, numbness and paresthesia. The rates of abnormal achilles tendon reflex and knee jerk reflex in patients were were 79.4% and 49.8%, respectively. The detected rates of patients with ST-segment changes and hypertension were 19.1% and 27.5%, respectively. The rates of hypertension, systolic pressure and diastolic pressure were 27.3%, 22.5% and 21.1%, respectively. The rates of lactate dehydrogenase (LDH), triglycerides (TG) and low density lipoprotein (LDL) were high. The detected rates of urine acid, indirect bilirubin and total bilirubin in male patients were higher than those in female patients. In addition, the abnormal detected rate of urea nitrogen and indirect bilirubin increased with exposure years., Conclusion: Occupational chronic CS(2) poisoning mainly affects the nervous system, as well as liver and kidney function. Detecting the median and common peroneal motor nerve conduction velocities could be the screening indicators for the peripheral nerve injury induced by CS(2) in the occupational exposure population during the periodical occupational medical examinations.

Preventive injection of "Kalifen" extract of high cranberry before and during intoxication with carbon bisulphide appeared to preserve lipid component of RBC membrane in rats.

Objectives: Telomeres are critical to maintain the integrity of the chromosomes, and telomere abnormalities are important features of carcinogenesis. Telomere length differs among individuals due to genetic and environmental factors. Aiming to examine the relationship between DNA-damaging agents and average telomere length in peripheral blood, we conducted a cross-sectional study among 157 workers working in the rubber industry in Sweden., Methods: N-nitrosamines were measured in air by personal sampling on Thermosorb/N tubes and analyzed by liquid chromatography tandem mass spectrometry (LC/MS/MS) for 60 individuals. Based on a similar working situation, the exposure was estimated for all workers. Polycyclic aromatic hydrocarbons (PAH) were measured as the metabolite 1-hydroxypyrene (1-HP) in urine by LC. Carbon disulphide (CS2) was measured as the metabolite 2-thiothiazolidine-4-carboxylic acid (TTCA) in urine by LC/MS/MS. Toluidines (orto-, meta-, and para-) were measured in urine by gas chromatography (GC)/MS. The average telomere length in peripheral blood was determined by quantitative polymerase chain reaction (PCR)., Results: There was a reduction in telomere length with increasing exposure to N-nitrosamines in air [measured (N=60) N-nitrosamines β-coefficient= -10, (95% confidence interval [95% CI] -17- -1.9) P=0.016; estimated (N=157) N-nitrosamines β-coefficient = -5.3, (95% CI -9.5- -0.97) P=0.016]. Also, there were negative associations between para-toluidine [β-coefficient= -0.031 (95% CI -0.055- -0.0063) P=0.014], as well as age β-coefficient= -0.005 (95% CI -0.007- -0.002) P=0.001] and telomere length. There were no strong associations between other exposures and telomere length nor did smoking modify the effect., Conclusion: N-nitrosamines exposure may lead to telomere shortening.

Introduction. The objective was to evaluate the toxicity of poisoning by metam sodium, a dithiocarbamate fumigant, the breakdown products of which are methyl isothiocyanate (MITC), carbon disulphide (CS2), and dihydrogen sulphide (H2S). Methods. This is a retrospective, observational case series of metam sodium exposure cases reported to the Angers Poison and Toxicovigilance Centre from 1992 through 2009. Results. A total of 106 cases of metam sodium exposure were recorded and 102 cases were included in this study. All cases of exposure were unintentional. Occupational poisoning occurred in eight cases. The most common route of exposure was inhalation (n = 96). In 79 cases, the patients were people living near fields where metam sodium had recently been applied. Most of the reported symptoms involved irritation of the eyes (n = 76), throat and nose (n = 65), attributable to MITC. Cough and dyspnoea occurred in four cases but no persistent, irritant-induced asthma or persistent exacerbation of asthma was observed. Sixteen patients at two different sites of pollution were exposed to emanations from the drainage system in their homes following the illicit discharge of metam sodium into the sewers. Most presented with nausea and headaches, but only four experienced eye or throat irritation. A breakdown product other than MITC was involved: air analysis at one site revealed the presence of CS2 (337 mg/m(3)) and no H2S. Two of these patients, who had consumed some alcohol, experienced dysgeusia but no disulfiram-like reaction. The only lethal case recorded was a truck driver who was found dead of acute lung injury after falling into a tank that had previously contained metam sodium. Two patients who ingested a dilute solution, presented with mild epigastric pain. Four skin exposures caused erythema (n = 2), moderate burns (n = 1), and urticaria (n = 1). According to the poisoning severity score, their symptoms were minor in 99% of cases. Conclusion. Acute metam sodium exposure usually causes minor symptoms. They vary as a function of the circumstances of exposure, which determine the degradation product that forms. On contact with moist soil, metam sodium decomposes into MITC and causes irritant symptoms. Under specific conditions, such as a spillage in the drainage system, metam sodium can degrade into CS2 and cause neurological signs.

Experimental studies were conducted on 4 groups of 10 rats each: 1) intact animals (a control group); 2) inhalation of carbon disulfide at a concentration of 2.0 mg/m3 for 7 days; 3) prophylactic administration of the hepatoprotective agent Legalon (100 mg/kg of total polyphenols), followed by carbon disulfide inhalation for 7 days; 4) prophylactic administration of the biologically active additive Kalifen (100 mg/kg of total polyphenols for 7 days), followed by carbon disulfide inhalation. Animal survival after carbon disulfide inhalation was 80%; preadministration of Legalon or Kalifen increased survival up to 100%. Carbon disulfide inhalation was attended by abnormal size features of red blood cells, impairments in the antioxidant defense system and the ratio of phospholipid fractions to neutral lipids. Preadministration of Legalon or Kalifen before inhalation contributes to less abnormalities in the study physiological and biochemical parameters of erythrocyte membranes.

Objective: Mass carbon disulfide (CS(2)) poisoning was reported at a viscose rayon factory in Korea. We evaluated the association between CS(2) poisoning and the prevalence of metabolic syndrome., Methods: The cases (n = 170) involved CS(2)-poisoned subjects, who participated in a health examination conducted at a hospital in Korea in 2005. The controls (n = 170) were selected randomly from the participants in the third Korean National Health and Nutrition Examination Survey. Metabolic syndrome was defined as having at least three of following metabolic abnormalities: abdominal obesity, elevated triglyceride, reduced high-density lipoprotein cholesterol, elevated blood pressure, and elevated fasting glucose levels., Results: After adjusting for covariates (age, gender, education, marital status, alcohol consumption, and smoking), CS(2)-poisoned subjects had an increased risk of metabolic syndrome (prevalence ratio 1.57, 95% CI 1.25-1.98)., Conclusions: The findings suggest that CS(2) poisoning may increase the risk of metabolic syndrome.

Objective: Mass poisoning by carbon disulfide (CS(2)) was reported at a viscose rayon factory in Korea in the late 1980s; the factory was subsequently closed in 1993. In this study, we evaluated the late electrocardiographic features in the CS(2) poisoned subjects., Methods: The cases were composed of 198 retired workers with a history of CS(2) poisoning. An age- and sex-matched reference group was randomly selected from people visiting a hospital for regular health checkups. Intervals, amplitudes and abnormal findings from the electrocardiograms (ECGs) of the two groups were compared., Results: Except for the PQ interval, there were no significant ECG differences between the two groups. The cases exhibited ECG abnormalities more frequently than the reference group. Multiple logistic regression analysis revealed that CS(2) poisoning was positively associated with the presence of abnormal ECG findings (OR = 1.603; 95% CI, 1.008-2.549)., Conclusion: This study suggests that CS(2) poisoned subjects may have an increased risk of ECG abnormalities even after the exposure to CS(2) is no longer present.

Objective: To investigate whether the alterations of microtubule and microfilament expression are responsible for the neurotoxicity of carbon disulfide., Methods: Wistar rats were administered with carbon disulfide by gavage at a dosage of 300 or 500 mg/kg for continuous 12 weeks (five times per week). Spinal cords of carbon disulfide-intoxicated rats and their age-matched controls were Triton-extracted and ultracentrifuged to yield a pellet and a corresponding supernatant fraction. Then, the contents of alpha-tubulin, beta-tubulin, and beta-actin in both fractions were determined by immunoblotting. In the meantime, their mRNA levels in spinal cords were quantified using reverse transcriptase-polymerase chain reaction (RT-PCR)., Results: In the supernatant fraction, the contents of beta-tubulin and beta-actin in both treated groups increased significantly (P < 0.01) the content of beta-tubulin increased by 141% and 158% respectively, and the content of beta-actin increased by 19% and 32% respectively. In the pellet fraction, the content of beta-tubulin in both groups increased by 107%(P < 0.01) and 118%(P < 0.01) respectively, and the others keep unaffected. In the meantime, the levels of of mRNA expression of beta-tubulin and beta-actin gene were elevated consistently in CS(2)-treated groups (P < 0.01) the levels of mRNA expression of beta-tubulin increased by 207% and 212% respectively, and the levels of mRNA expression of beta-actin increased by 94% and 91% respectively., Conclusion: Carbon disulfide intoxication results in alternations of microtubule and microfilament expression, and the alternations might be related to its neurotoxicity.

Objective: This study investigated electrocardiography (ECG) manifestations for male workers with carbon disulfide exposure at rayon manufacturing plants., Methods: A total of 251 men in the exposure group and 226 administrative clerks in the reference group received physical examinations and completed questionnaires., Results: The prevalence of ECG abnormalities was much higher in the carbon disulfide exposure group (25.9%, n = 65) than in the reference group (2.7%, n = 6), with an odds ratio (OR) of 12.8 (95% confidence interval [CI] = 5.4-30.2). The foremen were at the highest risk of abnormal ECG (OR = 20.6, 95% CI = 6.5-65.2), followed by filament-spinning workers (OR = 14.2, 95% CI = 5.7-35.3), viscose-manufacturing workers (OR = 11.3, 95% CI = 4.3-30.1), and carbon disulfide-manufacturing workers (OR = 8.1, 95% CI = 2.7-25.6). The multivariate logistic regression analysis based on cumulative exposure index also showed a dose-response relationship with the exposure, and the risk of ECG abnormality could be initiated at the exposure history of 31 to 57 year-ppm with an OR of 7.2 (95% CI = 1.5-36.7)., Conclusions: In general, the ECG abnormalities observed in workers at the permissible exposure level of carbon disulfide implicate the importance of environmental control of the chemical and of workers' education in exposure prevention at work.

Objective: To evaluate the association between hand dermatitis (HD) and occupational exposure to CS(2) and to determine whether combined exposure to CS(2) and H(2)SO(4) exhibits a higher risk of HD., Methods: In all, 110 subjects from a rayon factory were recruited and their exposure was classified into CS(2) exclusively, H(2)SO(4) exclusively, combined exposure, and nonexposure control based on workers' job characteristics. A dermatologist was designated in the diagnosis of HD on palm and dorsal sites for each subject. Other confounding factors including detergent, glove wearing, and participation in wet work were determined using a person-to-person questionnaire interview from 37 randomly selected subjects., Results: Significant elevated odds ratios (ORs) for HD were found in CS(2) exclusively (44.8, P < 0.01) and combined exposure (49.0, P < 0.001) compared with control. Dose-response trends of ORs for HD were found across control, single exposure, and combined exposure for both CS(2) and H(2)SO(4)., Conclusions: HD could occur resulting from occupational exposure to CS(2) alone. This study was unable to affirm that the exposure to H(2)SO(4) alone is associated with HD due to limited H(2)SO(4) exposure subjects. The combined exposure to both CS(2) and H(2)SO(4) simultaneously could increase the risk of HD. The control remedy in preventing dermal contact with either CS(2) or H(2)SO(4) among the rayon workers should be performed immediately.

To evaluate the effects of the occupational exposure to rayon manufacturing chemicals (RMC, containing predominantly carbon disulfide (CS(2)) and minor sulfuric acid) in a rayon factory on the basal transepidermal water loss (TEWL), barrier integrity (BI), and sequential increasing TEWL profiles. Six Thais and five Chinese workers in the spinning department of a rayon manufacturing plant and five healthy unexposed controls were recruited as the test subjects. An area of 4.5 x 5.5 cm on the mid-side of the volar forearm on the right hand was stripped by means of moderate pressure with commercially available adhesive tape by the same technician throughout the experiment. The skin was progressively stripped until glistening. TEWL was measured at every three and five tape strips on the right hand. The corresponding site on the left hand was measured parallel as the self-control. We found significant differences in basal TEWL and in BI between Chinese workers and Chinese controls, and between Thai workers and Chinese workers, respectively. Two-stage patterns of progressive TEWL profiles were found in such a chronic and repeated occupational exposure to RMC containing CS(2). The occupational exposure to RMC could result in the perturbation of the skin barrier function. Basal TEWL might be more sensitive to chronic skin irritant exposure. The TEWL profile achieved to the glistening stage might be necessary to avoid erroneous pattern estimation. Due to the lack of Thais control in this study, the racial difference in response to the RMC warrants further study.

Objective: This cross-sectional study investigates the cardiovascular effects among Chinese workers who were occupationally exposed to carbon disulfide (CS2), and evaluates the protective value of the current Chinese Maximum Allowable Concentration (MAC) of CS2 against cardiovascular effects., Methods: The measurements of exposure were performed by personal sampling and gas chromatography. The biological monitoring was performed by HPLC. Three hundred and sixty-seven exposed workers and 125 reference workers (never exposed to CS2,) were included in this study. The exposed workers were divided into 2 sub-groups according to their cumulative exposure indices, the cut-off point being at 100 which means 10 years exposure to the Chinese Maximum Allowable Concentration in the workplace (10 mg/m3). All subjects were examined using a self-administered questionnaire including medical and job history, clinical complaints in the previous three months, and underwent a clinical check-up and a 12 lead electrocardiography (ECG) at rest, coded according to the Minnesota code. Blood pressure (BP) was recorded and blood samples were collected for lipid measurements., Results: The personal monitoring showed that the exposures levels (15.47 +/- 2.34 mg/m3) were below the Threshold Limit Value (TLV, 31 mg/m3), and most of the samples analyzed still showed higher values than the Chinese MAC (10 mg/m3). Clinical complaints and abnormal electrocardiograms were not significantly increased in exposed workers. No significant effect of CS2 on blood pressure, cholesterol, HDL and LDL cholesterol or triglycerides was found. Further studies are recommended to elucidate the mechanism of cardiac intoxication after CS2 exposure., Conclusion: This study showed that Chinese workers exposed to CS2 did not have more clinical complaints, nor more ECG abnormalities than controls and no adverse effects were found in their lipids at an exposure level below the current TLV. The present results indicate that differences of health effects reported worldwide are possibly due to different exposure levels. They also indicate that the current Chinese MAC (10 mg/m3) sufficiently protects workers against negative cardiovascular effects.

Carbon disulfide (CS2) intoxication may induce peripheral neuropathy, encephalopathy, and cardiovascular diseases. In our studies, abnormalities of the peripheral nerves including clinical symptoms and electrophysiological findings were still present 3 years after cessation of CS2 exposure. The data indicate that CS2 neuropathy may persist for a period of time. The involvement of central nervous system may continue even longer. Brain magnetic resonance images usually show multiple high signal intensities in the basal ganglia and subcortical white matter suggesting a vascular event particularly in the small vessels. In addition, a patient with diffuse demyelination in the cerebral hemispheres also showed a diffuse decrease of regional cerebral blood flow indicating a microangiopathy. Therefore, CS2 exposure should be considered as a risk factor for strokes and one of the causes for diffuse leucoencephalopathy. Because CS2 may induce parkinsonian features, a differential diagnosis between CS2 parkinsonism and idiopathic parkinsonism is important. In our study, dopamine transporter with 99mTc-TRODAT-1 brain single photon emission computed tomography showed a normal uptake in the corpus striatum. The data suggest a normal presynaptic dopaminergic pathway function and provide useful information in differentiation. The involvement of cardiovascular systems may be due to thrombotic effects rather than atherogenic effects. In addition, absorption of CS2 through skin is also significant particularly in workers with skin lesions.

Objective: DNA damage in human buccal cells of workers occupationally long-term exposed to carbon disulfide (CS(2)) was monitored with comet assay., Methods: Ninety workers exposed to CS(2) were randomly selected as exposure group from a large-scale chemical fiber manufacturer in Hubei and 81 workers not exposed to CS(2) as control group. DNA damage in their buccal cells was detected with comet assay., Results: Rate of DNA tail was 0.51% in exposure group, significantly higher than that in control group (0.23%), with very statistical significance. Rate of DNA tail was 0.50% in male exposure group and 0.56% in exposure group with short length of employment, significantly higher than that in control group (0.08% and 0.25%, respectively). Multivariate unconditional logistic regression analysis showed that possibility of DNA damage was significantly higher in exposure group than that in control group (P < 0.05)., Conclusion: Long-term exposure to lower concentration of carbon disulfide could cause certain damage to human buccal cell DNA.

Objectives: Mass poisoning by carbon disulfide (CS(2)) occurred in a viscose-rayon factory in Korea. Including 38 who had died, 830 employees were diagnosed as CS(2) poisoned. We evaluated the heart-rate variability (HRV) among CS(2)-poisoned subjects, to discover whether CS(2) may affect HRV and whether its toxic effect persists after exposure has ceased., Methods: The case group comprised 71 retired male workers with CS(2) poisoning. The control group comprised 127 public officials of the same age-range who had no history of organic-solvent exposure and cardiovascular diseases. Information on individual age, height, weight, cigarette smoking, alcohol drinking, regular exercise, medical and occupational history, and ECG recordings of the two groups were collected through medical examination and self-administered questionnaire. Time (maximum, average, minimum RR interval) and frequency domain measures [low (LF), high (HF), and total power spectrum (TPS)] of the two groups were analyzed., Results: In univariate analysis, time domain measures of the two groups did not differ significantly, while frequency domain measures in the case group was significantly lower than in the control group except for HF power. In multivariate analysis, previous history of CS(2) poisoning was inversely related to all frequency domain measures and significantly affected LF power., Conclusions: This study suggests that CS(2) may cause heart-rate impairment and its toxic effect persists after exposure has ceased. Based on this study, HRV measurement can be considered as a useful tool to assess toxic effects of CS(2) both in current and retired workers.

Long-term exposure to carbon disulfide (CS(2)) may induce diffuse encephalopathy with parkinsonism, pyramidal signs, cerebellar ataxia, and cognitive impairments, as well as axonal polyneuropathy. The pathogenic mechanisms of diffuse encephalopathy are unclear, although vasculopathy and toxic demyelination have been proposed. Recently, we have encountered a patient who developed headache, limb tremors, gait disturbance, dysarthria, memory impairment, and emotional lability after long-term exposure to CS(2). The brain magnetic resonance images (MRI) showed diffuse hyperintensity lesions in T(2)-weighted images in the subcortical white matter, basal ganglia, and brain stem. The brain computed tomography perfusion study revealed a diffusely decreased regional cerebral blood flow and prolonged regional mean transit time in the subcortical white matter and basal ganglion. To our knowledge, there have been few reports demonstrating diffuse white matter lesions in chronic CS(2) encephalopathy using brain MRI. In addition, the (99m)Tc-TRODAT-1 single photon emission computed tomography showed a normal uptake of the dopamine transporter, indicating a normal presynaptic dopaminergic pathway. We conclude that diffuse white matter lesions may develop after chronic exposure to CS(2), possibly through microangiopathy. In addition, CS(2) poisoning can be considered as one of the causes of chronic leukoencephalopathy., (Copyright 2003 S. Karger AG, Basel)

A 70-year-old man developed a slowly progressive cerebellar syndrome after having been exposed to carbon disulfide (CS2) in a viscose rayon plant for 27 years. Ataxia, dysmetria, dysarthria and adiadochokinesia appeared 7 years after retirement from work (at age 54), and were later accompanied by cognitive deterioration, dysmnesia, spatio-temporal disorientation, emotional lability, and paranoid-obsessive disturbances. Brain computed tomography (CT) and magnetic resonance imaging (MRI) showed advanced global cerebellar atrophy, and a picture of less severe cerebrocortical atrophy. The case illustrates the possibility of chronic toxic encephalopathy among patients with previous long-term exposure to CS2. In such instances, cerebellar damage may develop as an exceptional, delayed manifestation of neurotoxicity: brain imaging techniques can significantly contribute to the diagnosis and follow-up, in addition to occupational anamnesis and neuropsychiatric evaluation. The patient presented also serves as a remainder that neurodegenerative disorders of apparently unknown origin sometimes derive from occupational toxic exposures suffered in the past. The clinical manifestations may appear several years after retirement from work, when the effects of toxic damage combine with age-related neuronal loss to overcome the brain functional reserve.

Objectives: To evaluate the long-term neuropsychological effects and magnetic resonance imaging (MRI) findings among retired patients with a history of exposure to carbon disulfide (CS2)., Material and Methods: Seventy-four patients with a history of exposure to CS2 were divided into two equal groups according to their level of exposure, and they completed a questionnaire and were evaluated for neuropsychological symptoms using the Korean version of the revised Wechsler Adult Intelligence Scale. Thirty-one MRI images were reviewed retrospectively., Results: There were no statistically significant differences in total, verbal and performance IQs between high- and low-exposure groups. MRI findings revealed a significantly larger number of cerebral lacunae (five of 12 subjects) in the high-exposure group. Periventricular hyperintensities were mostly located in frontal and occipital areas, and white-matter hyperintensities were mostly in frontal and parietal areas., Conclusion: The higher prevalence of lacunae in the high-exposure group as revealed by MRI suggests that further MRI studies are needed into long-term neuropsychological effects induced by CS2.

Objective: To evaluate the findings of brain MRI in patients with carbon disulfide poisoning., Materials and Methods: Ninety-one patients who had suffered carbon disulfide poisoning [male:female=87:4; age, 32-74 (mean 53.3) years] were included in this study. To determine the extent of white matter hyperintensity (Grade 0-V) and lacunar infarction, T2-weighted MR imaging of the brain was performed., Results: T2-weighted images depicted white matter hyperintensity in 70 patients (76.9%) and lacunar infarcts in 27 (29.7%)., Conclusion: In these patients, the prevalent findings at T2-weighted MR imaging of the brain were white matter hyperintensity and lacunar infarcts. Disturbance of the cardiovascular system by carbon disulfide might account for these results.

The natural course of clinical manifestations and electrophysiological changes were studied in six patients with carbon disulfide (CS(2)) induced polyneuropathy. All of the six patients worked in the cutting-machine department of a viscose rayon plant. The environmental monitoring was also conducted in the initial stage and followed up 3 years later. In the 3-year follow-up period, the neurological symptoms and signs persisted. The highest concentration of CS(2) in the cutting machine where these patients worked was about 100-200 ppm. Three years later, the highest concentration was decreased to between 10 and 20 ppm in the cutting machine of the new production line after the engineering control had been improved. Nerve conduction velocity (NCV) studies revealed persistent abnormality in motor and sensory NCVs. Although, a tendency to improvement was noted, it did not reach a statistical significance except for conduction velocity of sural nerve in sensory NCV. Sural nerve biopsy from one patient, 2 years after diagnosis showed degeneration of both axon and myelin and a predominant loss of large myelinated fibers. A remyelination process was also noted. We concluded that CS(2) intoxication may induce a persistent damage to the peripheral nerves even after CS(2) exposure had ceased for 3 years.

We present the clinical manifestations of 4 male patients with acute stroke-like symptoms and polyneuropathy after long-term exposure to carbon disulfide (CS2) in a viscose rayon plant. The ages of onset of polyneuropathy ranged from 42 to 45 years with a duration of CS2 exposure between 6 and 21 years. The ages of onset of stroke were from 42 to 48 years. The risk factors for stroke including heart disease and diabetes were denied, except for smoking in 4, hyperlipidemia in 2 and hypertension in 1. At the initial visit in 1992, only 2 patients developed sudden onset of hemiparesis suggesting a lacunar stroke before the diagnosis of CS2 intoxication. Brain computed tomography (CT) scans showed low-density lesions in the basal ganglia in 2 patients, cortical atrophy in 1 and normal in 1. Brain magnetic resonance image (MRI) study disclosed multiple lesions in the corona radiata and basal ganglia on T(2)-weighted images in 3 patients and cortical atrophy in 1. After the diagnosis, they left their jobs for a CS2-free environment, and improvement of the working conditions was noted. During 5 years follow-up period, another 2 patients also developed an acute episode of stroke with hemiparesis. Brain CT and/or MRI follow-up studies in these 2 patients revealed new lesions in the basal ganglia and corona radiata. Intriguingly, a patient with previous stroke also developed new lesions in the bilateral thalami and brainstem. Carotid Doppler scan, transcranial Doppler scan and/or cerebral angiography did not show any prominent stenosis or occlusion in the major intracranial large arteries. We conclude that encephalopathy may occur in patients after long-term CS2 exposure, probably due to impaired cerebral perfusion. The lesions tend to occur in the basal ganglia, corona radiata and even brainstem, particularly involving the small-sized vessels. In addition, the cerebral lesions may progress even after cessation of CS2 exposure. Therefore, we suggest that CS2 exposure may be a risk factor for stroke., (Copyright 2001 S. Karger AG, Basel)