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The clinical and neuropsychiatric features of seven workers from the grain storage industry are described. All were exposed to fumigants, especially carbon disulfide and malathion. Clinical manifestations included cogwheel rigidity, resting and action tremor, peripheral neuropathy, pyramidal tract signs, an EEG pattern of sleep apnea, and characteristic measurable neurobehavioral dysfunction. Similar signs and symptoms due to carbon disulfide exposure in the viscose rayon industry strongly supported the conclusion that these grain storage workers were suffering from carbon disulfide poisoning. Malathion exposure probably had a contributing role. We conclude that exposure to these fumigants poses a serious occupational risk to the nervous system.

The main purpose of this short review has been to present and evaluate the epidemiological evidence on CVD and environmental factors at work. It is indeed a difficult task to compare the scientific evidence in relation to the above mentioned risk factors. In some areas we find many studies, but with low overall methodological quality (noise is an example), while in others there are few, but good studies (e.g. carbon disulphide and nitroglycerine/glycol). We have to realize that in empirical sciences there is no such thing as a final proof. It would be easy if science dealt with what we know, while religion dealt with what we believe. It is more realistic however to say that science deals with what we believe we know, while religion deals with what we know we believe. Keeping this in mind the following classification of risk factors in the work environment seems to be well justified: Very probable causal relationships: Physical inactivity at work Nitroglycerine/nitroglycol Carbon disulphide Probable causal relationships: Monotonous high-paced work Shift work Noise Cobalt Arsenic Lead Possible causal relationships: Passive smoking Heat Dinitrotoluene Organophosphates Antimony Electromagnetic waves and fields No causal relationships: Cadmium Carbon monoxide One of the important questions raised by a list of this kind is whether we know enough to act, that is to use this knowledge in a preventive effort. Some might argue that we should wait until we have harder evidence. Another position would be that in many situations we have to act without such hard evidence. In my view fear of making mistakes should not prevent us from acting. If we always choose to wait until the evidence is 100% convincing, we will be very likely to make many - and often serious - mistakes.

A neurophysiological study was carried out to examine peripheral neurotoxicity of extremely low levels of CS2, that is, less than 2 ppm (TWA-8hr) among Chinese viscose rayon workers. From the subjects who participated in a 1981 cross-sectional medical survey, 70 male workers exposed to CS2 and age-matched unexposed workers were randomly selected for the present neurophysiological examination. The conduction velocities of motor, sensory and slower motor fibres of the right ulnar nerve were measured using the same methods as those in the study by Seppäläinen (1974). Skin temperature was measured at the middle of the volar surface of the right forearm with a Thermistor thermometer. According to an earlier occupational hygiene survey in the plant, current personal exposures determined by a passive dosimeter method were very low; the average of daily exposure of 7 jobs studied was 1.45 ppm (range 0.2-5.0). Past and current area sampling data also suggested that occupational hygiene conditions regarding CS2 exposure in the plant had been extremely good for the previous 6 years. The present neurophysiological study clearly showed that significant reduction in the conduction velocities of motor and slower motor fibres of the ulnar nerve was detected as a consequence of chronic exposure to low levels of CS2. In the previous cross-sectional medical survey, no retinopathy was found among Chinese workers exposed to CS2 at this level. These results suggested that an effect of CS2 on the peripheral nerve would appear earlier than that on the retina.

Cardiovascular effects of potential occupational hazards have received relatively little attention. The major inhalant occupational exposures of concern are carbon disulfide, nitrates, halogenated hydrocarbons and carbon dioxide. Occupational exposure to certain trace metals may also be associated with adverse cardiovascular effects. Of concern is potential toxicity from cobalt, antimony, lead, cadmium and arsenic. Potential physical hazards exist in association with noise, heat and radiofrequency radiation. In most instances, the data are suggestive rather than conclusive. Further epidemiologic studies with careful control for potentially complicating factors, such as baseline differences in blood pressure, cigarette smoking habits and age, are needed. In some areas where epidemiologic studies have provided clues, the mechanisms of action of potential occupational hazards require further basic scientific investigation.

An electromyographic (EMG) investigation was performed on 216 workers of a viscose rayon plant with different degrees of exposure to CS2. In the light of the data supplied by the survey the AA. maintain that meedle EMG is able to detect, probably better than other test, changes of PNS even if they are very slight, and to select subjects having a higher risk of suffering from neuropathies. Nevertheless, also because of its sensitivity, EMG seems to be less specific than other electrophysiological parameters such as maximal motor conductions velocity (MMCV), that is significantly altered in exposed people. Muscular changes may be connected to a specific effect of CS2 less surely than MMCV change. However, they might be considered as pointing to a predisposition to PNS illness and it seems advisable to eclude these subjects from CS2 exposure.

Serum levels of gonadotropins and testosterone were determined for 69 men exposed to CS2 in viscose rayon production and for 22 nonexposed male controls. Mean ages of the two groups were 40 and 39 yr, respectively. The duration of exposure to CS2 ranged from 1 to 36 yr (mean, 12.5). Follicle stimulating hormone (FSH) levels were significantly higher among the exposed men than among the controls (13.6 versus 10.0 IU/l). The level of sex hormone binding globulin (SHBG) was significantly lower among the exposed men than among the controls (44 versus 53 nmol/l). Luteinizing hormone (LH) values were significantly higher among the 24-31 yr old exposed men than the controls of the same age. Levels of SHBG, of the free testosterone index, and of FSH and LH in men under 39 yr who had been exposed to CS2 for 1-9 yr differed significantly from those of their controls, whereas only FSH differed significantly among those exposed for 10 or more years in the same age group. In men aged 40 yr or more, after at least 10 yr of exposure, only FSH and LH were significantly higher than in the controls. Although the observed alterations do not seem to have any overt clinical implications for the study groups, they indicate that overall levels of CS2 that are well below the current Finnish threshold limit value (30 mg/m3) may affect the hormonal balance in the pituitary-gonadal axis, favoring the view that there may be an increased risk of latent primary gonadal insufficiency.

The results of all the efforts made so far towards the reduction of CS2 concentrations at the workplaces of viscose rayon industry indicate that achievement of safe standards is little probable in the nearest future. Likewise, the preventive activities aimed at the reduction of the daily working time from 8 to 6 hours and referring workers to work with no exposure for several months are hardly effective. Basing on the results of clinical and epidemiological studies of the CS2 exposed population and relevant control groups the authors indicate their own solutions of decreasing the health risk. Pursuant to this suggestion the total time of work in exposure should not exceed 15 years and would be interrupted by so called periods of "health regeneration", consisting in the transfer to the production with no CS2 exposure for one year. This rotational system would apply to all those employed for over five years under CS2 concentrations exceeding the hygienic standards.

A cross sectional prevalence study of chest pain in 94 rubber chemical workers exposed to carbon disulphide (CS2) and methaemoglobin forming aromatic amines was carried out. The purpose of the study was to determine whether the prevalence of chest pain or coronary heart disease (CHD), or both, in exposed individuals exceeded that of a group of non-exposed individuals from the same plant. Cardiovascular, smoking, and occupational histories were obtained. Blood pressure, height, weight, serum cholesterol, and fasting blood glucose were measured. Resting electrocardiograms (ECGs) were obtained on all study participants, as were exercise stress tests on selected exposed individuals. Matching eliminated important known risk factors for coronary artery disease. Both chest pain and angina were significantly related to exposure, controlling for age and cigarette smoking. This association was not dependent on duration of exposure as defined by 10 or more years of employment in the department of interest. CHD as defined by angina, a history of myocardial infarction, or a coronary ECG or a combination of these occurred more frequently among exposed workers. The number of abnormal ECGs in the exposed group was twice that in the control group, but the difference was not statistically significant. Age rather than exposure appeared to be the important variable associated with raised blood pressure. Neither biological measures of exposure nor ECGs showed an acute effect of workplace exposures on the myocardium. Possible additive or multiplicative effects of individual chemical agents could not be evaluated. Appropriate modification of medical surveillance of rubber chemical workers with exposure to CS2 and aromatic amines is warranted.

A variety of industrial agents to which large segments of the population are exposed have been linked to the development of cardiovascular disease. These toxic agents, which include carbon monoxide, carbon disulphide, lead, and cadmium, are produced by a wide variety of industrial processes and so are ubiquitous in the modern industrial environment. Although the mechanisms by which such toxins may contribute to cardiovascular disease are not well defined, there are at least four possible theories that have received clinical and experimental support. The postulated mechanisms by which such toxins may play a role in vascular disease are: (1) an increase in blood pressure; (2) an increase in the levels of blood cholesterol and/or an induction of lipid accumulation in vessel walls; (3) an induction of a lipid peroxidation process thereby increasing the tendency of blood clotting; and (4) a promotion of a mutation in the arterial cell wall.

The cardiovascular mortality of a cohort of 343 Finnish men exposed for at least five years to carbon disulphide (CS2) in a viscose rayon plant has been monitored prospectively from 1967 to 1982. The results from the first five years of follow up in 1972 showed a 4.7-fold excess mortality for ischaemic and other heart diseases (ICD A83-A84) compared with a comparable reference cohort of paper mill workers. After 1972 a preventive intervention programme instituted at the rayon plant included removing all workers with coronary risk factors from exposure. Thus only 19% of the exposed cohort continued to be exposed in 1977 compared with 53% in 1972. Moreover, exposure levels were reduced after 1972 in compliance with the set hygienic standard of 10 ppm. These measures were reflected in a normalisation of the risk of cardiovascular death; the relative risk was 1.0 in the period after the intervention (1 July 1974 to 30 June 1982), whereas it had previously been 3.2 (from 1 July 1972 to 30 June 1974). The risk of a fatal heart attack remained at 11.6% throughout the 15 year follow up period (95% confidence limits 8.5%-15.4%) among the exposed compared with 7.8% (5.3%-11.2%) among the unexposed. The entire risk difference of 3.8% was accumulated during the first seven years of follow up. Thus we can estimate that 59 CS2-related cardiovascular deaths would have occurred during the next eight years (instead of the actual 19 deaths) had there been no preventive action. Calculations yielded a preventive fraction of 68%.

A comparative study was carried out between the divisions of one of the viscose industry plants where workers carry on shift work in CS2 exposure and shift workers of a wool industry plant--in the same town--with no chemical exposure. It appeared that more of the CS2 exposed workers became disabled at a younger age and after shorter employment duration. As to the diseases resulting in the untimely job leave most frequent were stenocardia, accidents and tumours; on the other hand no such observations referred to diabetes mellitus and obliterative inflammation of lower extremities arteries. Chronic obturative disease nervous system diseases and hypertension, and, to a lesser degree, predominated among wool industry workers.

The "dying back" process can be defined as a pathological changes affecting certain neurons in a number of systematized degenerative conditions. Examples exist to illustrate the nature of this process, which is unique to nervous tissue, and there is an association of this process with certain chronic vitamin-deficiency syndromes and some important neurotoxic chemicals. Albeit largely speculative, one can attempt to group the conditions showing the dying back process in terms of putative metabolic lesions. Although this attempt is admittedly only a first approximation, it enables us to look ahead to a future understanding of the metabolic problems of long neurons and how their selective degeneration comes about.

The investigation included 134 workers from a viscose rayon factory who were exposed to average concentrations of carbon disulphide exceeding MAC values (x = 119.3 mg/m3) for more than 75% of their working hours. Workers' chronic morbidity from carbon disulphide exposure was analysed over a three-year period, and results were compared with those for a control group of the same age but with a shorter exposure duration. The percentage of ill workers and the prevalence rate were both similar to those of the control group. However, as concerns the specific morbidity caused by carbon disulphide exposure, toxic polyneuropathy was present only among the exposed workers. In that group hypertension too reached a higher prevalence rate, statistically significant, although both groups consisted of younger workers of similar age. The prevalence of other diseases was comparable, possibly because of the selection bias, and the healthy worker effect. Owing to that effect workers with the most distinct symptoms had been removed from their jobs and, consequently, excluded from examinations. That could have been a reason for underestimating exposure effects.

Results are reported of a planned prospective longitudinal study of the early phases of angiopathy and other clinical, clinico-laboratory and functional changes in the early period of carbon disulphide effects. Subject of the study were 251 workers employed in artificial fiber production; in 73 of them the complex investigations were repeated within an interval of 3 years. The studies demonstrated the presence of distinct vascular, vegetative and irritative changes. They were low-grade ones, of no particular interest, especially the vascular ones, as they were demonstrable after comparatively short exposure to carbon disulphide and in young age.

This paper reviews the possible association between cardiovascular disease and occupational and environmental agents. The effects of carbon monoxide, fibrogenic dusts, carbon disulphide, heavy metals, noise, radiation, heat, cold, solvents and fluorocarbons are discussed. New directions for investigation are suggested.

We examined 81 men exposed for a long time to carbon disulphide (CS2) and tested the possible electrocardiographic (ECG) changes of ischemic heart disease (I.H.D.). The subjects were examined twice in two years. In order to make the ECG evaluation more objective, the Minnesota Code was applied. Two obligatory ECG examinations and only one submaximal effort test were carried out. For comparative evaluation, the control group was examined once. We proved that, in spite of the accepted opinion concerning the atheromatous action of CS2, this compound does not cause ECG symptoms of I.H.D. in a higher percentage of exposed persons. It also does not cause any significant increase in I.H.D. symptoms in dynamic ECG observations.

Three groups of pesticide-exposed grain workers from three different work facilities experienced chronic central and peripheral nervous system dysfunction that appeared to be exposure related. The grain inspectors, malt laboratory workers, and grain elevator workers displayed higher prevalence rates of atypical parkinsonism, cerebellar signs, hearing loss, and sensory changes than would be expected in a nonneurologic control population. The 21 self-selected patients included in this report exhibited cogwheel rigidity in 80% (17/21), decreased associated movements in 71% (15/21), distal sensory shading in 62% (13/21), intention tremulousness in 52% (11/21), resting tremulousness in 48% (10/21), and nerve conduction abnormalities in 44% (7/16). Carbon disulfide, a major component of the fumigant mixtures used, has been associated in the rayon industry, since the 1930s, with similar neurologic symptoms.

An investigation was made into the incidence of cardiovascular diseases in the Dutch viscose rayon industry. The first part of the article discusses a further study, complementary to a pilot study conducted in 1974, into the distribution of cardiovascular cases among the various departments of a rayon plant. No differences in the frequency of cardiovascular cases in departments with and departments without CS2 were observed. The second part deals with a case-control study in which the total number of patients per plant was matched with comparable individuals not suffering from cardiovascular disease. Here, too, it was not possible to demonstrate a significant correlation between CS2 exposure and cardiovascular diseases. The third part describes a cohort study. Three cohorts were formed: (1) a cohort of shift workers exposed to CS2; (2) a cohort of shift workers not exposed to CS2; and, (3) a cohort of non-shift workers not exposed to CS2. With a three-year interval, these cohorts were examined twice for cardiovascular diseases, with reference to a checklist of 39 variables. Again, no significant differences between the cohorts could be shown to exist.

An incidence of glucose tolerance disorders was investigated in the group of 47 employees of the viscose fibres of the mean duration of exposition exceeding 20 years. Control group included 31 employees uniform in the age and body weight. Carbohydrate metabolism was tested with the oral load with 100 g of glucose and intravenous glucose administration according to Conrad. Glucose tolerance disorders were noted in 11 employees (23.4%) chronically exposed to CS2 in the concentrations slightly exceeding acceptable levels whereas glucose intolerance was noted in 2 individuals (6.5%) of the control group. The difference was statistically significant. No difference in the glucose absorbability index was noted. Exposition time to the studied CS2 concentrations did not affect the incidence of the glucose tolerance disorders.

The iodine-azide test was performed on urine specimens of 28 workers exposed to CS2 (mean concentration 5-10 ppm) and of 17 control subjects. No significant difference between the two groups could be ascertained.