Chronic exposure

There is a vast amount of literature on the chronic effects of carbon disulphide mainly generated from epidemiology studies on viscose rayon workers. A brief summary of the main points is given below with references for further reading.

Inhalation Cardiac effects

Chronic exposure to carbon disulphide has been associated with increased atherosclerosis and coronary atherosclerotic heart disease (CAHD). It is purported that carbon disulphide causes hypertension, hypercholesterolaemia and/or an antifibrinolytic effect (Rosenman, 1984). Specific electrocardiographic changes, including ST-T wave abnormalities, have also been noted by some workers (Davidson and Feinleib, 1972).

The atherosclerosis and ischaemic heart disease that has been reported from chronic carbon disulphide exposure are associated with vascular changes similar to those of artherosclerosis in older age groups (Vigliani, 1954), and these changes mainly affect the blood vessels supplying the brain and heart muscle (WHO, 1979). However, the current TLV (10 ppm) for carbon disulphide exposure should protect workers from development of carbon disulphide-induced cardiac effects. Studies in workers exposed to 10 ppm or less have found no increase in coronary heart disease or atherosclerotic findings (Franco et al., 1982; Drexler et al., 1996).

Tiller et al. (1968) undertook a study of deaths from cardiovascular diseases among employees of 5 British viscose rayon factories. They found a 2.5-3 fold excess mortality due to coronary heart disease, among workers who had worked primarily in the viscose spinning process, where exposure to carbon disulphide was greatest. Similar increased mortality rates have been demonstrated from epidemiological studies in other countries including Norway, Finland and the United States (Franco, 1982). Hernberg et al. (1976) in Finland, found an excess of coronary deaths among 48 men who had been exposed to carbon disulphide for at least 5 years, and who died under 65 years of age.

Examination of 343 viscose rayon workers who were matched with control subjects from a paper mill, demonstrated that the subjects exposed to carbon disulphide, had higher blood pressures and a slightly higher prevalence of ECG abnormalities. The authors concluded that their findings suggest that carbon disulphide may be an aetiological factor in the pathogenesis of coronary heart disease (Tolonen et al., 1975).

The pathological lesions observed on postmortem examination are those of atheromatous plaque formation, general atherosclerosis, glomerulosclerosis, and changes in the retinal arteries resembling those seen in hypertension (Davidson and Feinleib, 1972).

Animal studies investigating the effects of carbon disulphide on the myocardium showed alterations in the coronary arteries (capillary proliferation and vessel wall hypertrophy), plus vacuolar degeneration, fatty degeneration and haemorrhages of the myocardium.

Other reports investigating the cardiovascular effects of carbon disulphide include: Lieben et al., 1974; Oliver and Weber, 1984; Nurminen and Hernberg, 1985; Sweetnam et al., 1987; McMahon and Manson, 1988; Phillips, 1992; Liss and Finkelstein, 1996; Price et al., 1997; Guidotti and Hoffman, 1999.

Neurological effects

The most widely known and extensively studied aspect of carbon disulphide toxicity is its neurological effects. The nervous system is one of the main targets of carbon disulphide toxicity. Neurotoxicity manifests as psychological and behavioural changes followed by neurological changes, both in the brain and peripheral nerves (WHO, 1979).

Relatively short exposures are predominantly associated with psychiatric and neurological symptoms including extreme irritability, uncontrolled anger, rapid mood changes, hallucinations, paranoic and suicidal tendencies and manic delirium. Other symptoms include memory defects, severe insomnia, nightmares, fatigue, loss of appetite and gastrointestinal effects (Braceland, 1942; Davidson and Feinleib, 1972; Klemmer and Harris, 2000).

Long-term exposure over many years produces the syndrome of chronic poisoning characterised by signs and symptoms arising from adverse effects on different organ systems, including the nervous system and the cardiovascular system. Less frequently, there are symptoms suggesting involvement of the gastrointestinal and endocrine systems (WHO, 1979).

Measurable neurological changes have been demonstrated in workers who have never been exposed to more than 20 ppm (the occupational exposure limit at the time of the study) (Spyker et al., 1982). Symptoms of moderate to severe intoxication have appeared in individuals chronically exposed to vapour concentrations averaging slightly in excess of 20 ppm (Kleinfeld and Tabershaw, 1955). De Fruyt et al. (1998) studied the neuropsychological effects of occupational exposure to carbon disulphide. Only the study group exposed to values exceeding three times the recommended TLV for carbon disulphide (i.e., more than 30 ppm) had significant impairments in both the speed and quality of psychomotor performance. However, on evaluation of the effects of occupational carbon disulphide exposure in a sample of 156 male viscose rayon workers (maximum exposure concentration 7.6 ppm) small, but statistically significant, decreases in sensory and motor nerve conduction velocities were reported (Johnson et al., 1983). These findings suggest that even chronic low level exposure to carbon disulphide may result in neurological changes.

Aaserud et al. (1990) investigated the neurological symptoms of 24 men formerly and currently employed in the manufacture of viscose rayon. When clinical neurological examinations were performed with the 16 subjects still employed in rayon production, only one was considered normal. Nine had minor neurological deficits. Six had facial palsy, reduced coordination, asymmetrical reflexes, or a positive Romberg's test.

Chapman et al. (1991) studied index finger tremor in 19 age-matched control subjects and in 19 grain industry employees chronically exposed to carbon disulphide-based fumigants. The findings in this study suggest that amplitude and frequency abnormalities characterise finger tremor in subclinical and early clinical carbon disulphide parkinsonism. The authors suggest that tremor differences may be able to serve as an early warning in adverse chemical exposures, when overt manifestations are not present.

Peters et al. (1987) investigated the neurological effects of carbon disulphide fumigants in granary workers. They found that 50-80% exhibited a range of symptoms, including cogwheel rigidity, intention and resting tremulousness and conduction abnormalities. Hanninen et al. (1971; 1976) showed visual-perceptual, psychomotor and cognitive integration deficits in carbon disulphide exposed workers.

In observing workers in viscose rayon factories Vigliani (1954) concluded that chronic exposure to carbon disulphide may result in peripheral neuropathy characterised by a glove and stocking sensory impairment. Absence or a decrease of tendon reflexes, and muscle weakness was also observed. Polyneuropathy of workers in the viscose rayon industry has been studied by other authors (Alpers and Lewey, 1940; Vasilescu, 1976; Aaserud et al., 1990; Chu et al., 1995; Klemmer and Harris, 2000).

Huang et al. (1996) reported a detailed neurological investigation of 10 patients with polyneuropathy and various neuropsychiatric symptoms following carbon disulphide exposure. Clinical and laboratory examinations included electroencephalography (EEG), brain computerised tomography (CT), brain magnetic resonance images (MRI) and carotid duplex sonography. In four cases, brain MRI revealed lesions of the basal ganglia and corona radiata, 6 patients had mild atherosclerosis with plaques (<20% stenosis) of extracranial vessels. Clinically, headache, nightmares, memory impairment, fatigue, anorexia and emotional lability were common and two patients had stroke episodes. The authors concluded that encephalopathy, cerebrovascular disease, and polyneuropathy may all occur after chronic carbon disulphide exposure.

Psychiatric examination of 120 workers in the viscose rayon industry where the subjects had varying degrees of exposure to carbon disulphide concluded that the onset of psychosis was acute and frequently occurred when the patient was at work. However, this was usually preceded by gradual personality change observed first by family and friends (Braceland, 1942). Mancuso and Locke (1972) found an association between exposure to carbon disulphide and an increase in the suicide rate in viscose rayon workers employed between 1938 and 1948.

For a comprehensive review of the neuropsychological and psychological effects of carbon disulphide see Grasso et al. (1984) or Feldman (1999).

Renal effects

Klemmer and Harris (2000) reported nephropathy in a man occupationally exposed for 15 years to carbon disulphide. Ten years after his last carbon disulphide exposure, the patient developed end-stage renal disease (ESRD) due to the combined effect of focal segmental glomerulosclerosis (FSGS) and unilateral nephrectomy, necessitated by the presence of a renal mass.

Hepatic effects

Fatty degeneration of the liver was found in early animal studies by Lewey et al. (1941). In a control study, Vanhoorne et al. (1992) found hepatomegaly and raised y-glutamyltransferase in carbon disulphide exposed viscose rayon workers.

Gastrointestinal effects

Vanhoorne et al. (1992) reported a greater prevalence of gastrointestinal complaints (anorexia, nausea, vomiting, flatulence) in viscose rayon workers when compared to controls.

Ototoxicity

On auditory examination, Zenk (1970) concluded that workers exposed to carbon disulphide had a reduction of thresholds to high frequencies and that this should be regarded as an early symptom of intoxication.

Other effects

Diabetes mellitus is a risk factor for atherosclerosis, which is a feature of chronic carbon disulphide poisoning. Glucose tolerance testing in carbon disulphide exposed workers indicated an increased prevalence of decreased glucose tolerance (i.e., latent diabetes) in the carbon disulphide exposed workers (73%) compared to the control group (17%) (Franco et al., 1978).

Dermal

Prolonged contact with the skin produces second and third degree burns and a local neuritis (Gordy and Trumper, 1938). Carbon disulphide can be absorbed through the skin and cause toxicity.

The ocular manifestations of chronic carbon disulphide exposure are characterised by impaired colour vision and alterations in the retinal microvasculature. The retinal capillary anomalies are very similar to diabetic retinopathy, and although it has been postulated that the retinopathy had a possible aetiologic relationship with disturbed glucose metabolism due to carbon disulphide exposure, the pathogenesis is still unknown (Sugimoto et al., 1976a; 1976b).

Fundus anomalies, and subnormal or supranormal electroretinograms (ERGs) were found in viscose rayon workers chronically exposed to carbon disulphide. The fundus anomalies consisted of either discrete pigmentary changes in the posterior pole or microvascular retinal lesions (DeLaey et al., 1980).

A study of 338 workers of a viscose rayon plant demonstrated that the prevalence of retinopathy increased with both increasing carbon disulphide exposure and concentration (Sugimoto et al., 1976a). In a separate study the same authors repeated direct ophthalmoscopic/colour fundus photographic examinations (three times in five years) on 214 carbon disulphide exposed workers, to determine the effects of exposure cessation on the course of retinopathy, and develop a prognosis for retinopathy in workers continually exposed for years. Progression to a more developed stage of retinopathy occurred in 21.3% of the 134 workers still exposed to carbon disulphide. Among 80 workers no longer exposed to carbon disulphide, the prevalence of progression was 13.7%. Resolution or improvement to a milder stage of retinopathy occurred in 1.5% of the group still exposed to the chemical and in 11.3% of the group of workers removed from exposure. It was recommended that exposure to carbon disulphide should not continue for longer than 10 years and if retinopathy is found, the worker should immediately be transferred to work without exposure (Suigimoto et al., 1976b).

Raitta et al. (1981) studied the effect of chronic carbon disulphide exposure on the optic nerve in 62 workers (mean age 43.5 years) in a Finnish viscose rayon plant. The exposure history ranged from 6-36 years with a mean of 16 years. Carbon disulphide exposure did not relate to specific pattern defects in colour discrimination, but impaired colour discrimination occurred significantly more often in the exposed group compared to controls. The abnormal findings suggest impairment in the receptiveness of the ganglion cells or demyelination of the optic nerve fibres. However, in a later study, Ruijten et al. (1990) found no impairment of colour discrimination in their study group. Along with other peripheral and autonomic nervous system function tests, they evaluated colour discrimination in 45 workers (mean age 49 years) with an average of 20 years exposure to carbon disulphide in the viscose rayon industry. The mean cumulative exposure was calculated to be 165 ppm-years (a measure of exposure and duration). The difference in results between the two studies could be explained by differences in the sensitivity of testing methods (the method used by Riatta et al. was more sensitive), and the fact that subjects in the Riatta et al. study had higher mean exposure concentrations (generally below 20 ppm).

An ophthalmological examination of 123 male carbon disulphide exposed viscose rayon workers (with at least 1 year exposure) found strong associations between exposure and reduced colour vision discrimination, and an excess of microaneurysms. The findings were not thought significant enough to cause incapacity, but could serve as possible early indicators of serious ophthalmological, vascular or neurological damage (Vanhoorne et al., 1996).

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