Noise

Hearing loss due to workplace noise has been recognized as an occupational disease for many years. Cardiovascular diseases are at the centre of the discussion on possible chronic extra-aural effects of noise. Epidemiological studies have been done within the workplace noise field (with high-level noise indicators) as well as in the surrounding noise field (with low-level noise indicators). The best studies to date were done on the relationship between exposure to noise and high blood pressure. In numerous new survey studies, noise researchers have assessed the available research results and summarized the current state of knowledge (Kristensen 1994; Schwarze and Thompson 1993; van Dijk 1990).

Studies show that the noise risk factor for diseases of the cardiovascular system is less significant than behavioural risk factors like smoking, poor nutrition or physical inactivity (Aro and Hasan 1987; Jegaden et al. 1986; Kornhuber and Lisson 1981).

The results of epidemiological studies do not permit any final answer on the adverse cardiovascular health effects of chronic workplace or environmental noise exposure. The experimental knowledge on hormonal stress effects and changes in peripheral vasoconstriction, on the one hand, and the observation, on the other, that a high workplace noise level >85 dBA) promotes the development of hypertension, allow us to include noise as an non-specific stress stimulus in a multi-factored risk model for cardiovascular diseases, warranting high biological plausibility.

The opinion is advanced in modern stress research that although increases in blood pressure during work are connected to noise exposure, the blood pressure level per se depends on a complex set of personality and environmental factors (Theorell et al. 1987). Personality and environmental factors play an intimate role in determining the total stress load at the workplace.

For this reason it appears all the more urgent to study the effect of multiple burdens at the workplace and to clarify the cross effects, mostly unknown up to now, between combined influencing exogenous factors and diverse endogenous risk characteristics.

Experimental studies

It is today generally accepted that noise exposure is a psychophysical stressor. Numerous experimental studies on animals and human subjects permit extending the hypothesis on the pathomechanism of noise to the development of cardiovascular diseases. There is a relatively uniform picture with respect to acute peripheral reactions to noise stimuli. Noise stimuli clearly cause peripheral vasoconstriction, measurable as a decrease in finger pulse amplitude and skin temperature and an increase in systolic and diastolic blood pressure. Almost all studies confirm an increase in heart rate (Carter 1988; Fisher and Tucker 1991; Michalak, Ising and Rebentisch 1990; Millar and Steels 1990; Schwarze and Thompson 1993; Thompson 1993). The degree of these reactions is modified by such factors as the type of noise occurrence, age, sex, state of health, nervous state and personal characteristics (Harrison and Kelly 1989; Parrot et al. 1992; Petiot et al. 1988).

A wealth of research deals with the effects of noise on metabolism and hormone levels. Exposure to loud noise almost always results fairly quickly in changes such as in blood cortisone, cyclical adenosinmonophosphate (CAMP), cholesterol and certain lipoprotein fractions, glucose, protein fractions, hormones (e.g., ACTH, prolactin), adrenalin and noradrenalin. Increased catecholamine levels can be found in the urine. All of this clearly shows that noise stimuli below the noise-deafness level can lead to hyperactivity of the hypophyseal adrenal cortex system (Ising and Kruppa 1993; Rebentisch, Lange-Asschenfeld and Ising 1994).

Chronic exposure to loud noise has been shown to result in a reduction of magnesium content in serum, erythrocytes and in other tissues, such as the myocardium (Altura et al. 1992), but study results are contradictory (Altura 1993; Schwarze and Thompson 1993).

The effect of workplace noise on blood pressure is equivocal. A series of epidemiological studies, which were mostly designed as cross-sectional studies, indicate that employees with long-term exposure to loud noise show higher systolic and/or diastolic blood pressure values than those who work under less noisy conditions. Counterpoised, however, are studies that found very little or no statistical association between long-term noise exposure and in- creased blood pressure or hypertension (Schwarze and Thompson 1993; Thompson 1993; van Dijk 1990). Studies that enlist hearing loss as a surrogate for noise show varied results. In any case, hearing loss is not a suitable biological indicator for noise ex- posure (Kristensen 1989; van Dijk 1990). The indications are mounting that noise and the risk factors—increased blood pres- sure, increased serum cholesterol level (Pillsburg 1986), and smoking (Baron et al. 1987)—have a synergistic effect on the de- velopment of noise-induced hearing loss. Differentiating between hearing loss from noise and hearing loss from other factors is difficult. In the studies (Talbott et al. 1990; van Dijk, Veerbeck and de Vries 1987), no connection was found between noise exposure and high blood pressure, whereas hearing loss and high blood pressure have a positive correlation after correction for the usual risk factors, especially age and body weight. The relative risks for high blood pressure range between 1 and 3.1 in com- parisons of exposure to loud and less loud noise. Studies with qualitatively superior methodology report a lower relationship. Differences among the blood pressure group means are relatively narrow, with values between 0 and 10 mm Hg.

A large epidemiological study of women textile workers in China (Zhao, Liu and Zhang 1991) plays a key role in noise effect research. Zhao ascertained a dose-effect relationship between noise levels and blood pressure among women industrial workers who were subject to various noise exposures over many years. Using an additive logistical model the factors “indicated cooking salt use”, “family history of high blood pressure” and “noise level” (0.05) significantly correlated with the probability of high blood pressure. The authors judged that no confounding was present due to overweight. The noise level factor nevertheless constituted half the risk of hypertension of the first two named factors. An increase in the noise level from 70 to 100 dBA raised the risk for high blood pressure by a factor of 2.5. The quantification of the risk of hypertension by using higher noise exposure levels was possible in this study only because the offered hearing protection was not worn. This study looked at non-smoking women aged 35 ±8 years, so according to v. Eiff’s results (1993), the noise-related risk of hypertension among men could be significantly higher.

Hearing protection is prescribed in western industrialized countries for noise levels over 85-90 dBA. Many studies carried out in these countries demonstrated no clear risk at such noise levels, so it can be concluded from Gierke and Harris (1990) that limiting the noise level to the set limits prevents most extra-aural effects.

Heavy Physical Work

The effects of “lack of movement” as a risk factor for cardiovascular disease and of physical activity as promoting health were elucidated in such classic publications as those by Morris, Paffenbarger and their co-workers in the 1950s and 1960s, and in numerous epidemiological studies (Berlin and Colditz 1990; Powell et al. 1987). In previous studies, no direct cause-and-effect relationship could be shown between lack of movement and the rate of cardiovascular disease or mortality. Epidemiological studies, however, point to the positive, protective effects of physical activity on reducing various chronic diseases, including coronary heart disease, high blood pressure, non insulin dependent diabetes mellitus, osteoporosis and colon cancer, as well as anxiety and depression. The connection between physical inactivity and the risk of coronary heart disease has been observed in numerous countries and population groups. The relative risk for coronary heart disease among inactive people compared to active people varies between 1.5 and 3.0; with the studies using qualitatively higher methodology showing higher relationship. This increased risk is comparable to that found for hypercholesterolemia, hypertension and smoking (Berlin and Colditz 1990; Centers for Disease Control and Prevention 1993; Kristensen 1994; Powell et al. 1987).

Regular, leisure-time physical activity appears to reduce the risk of coronary heart disease through various physiological and metabolic mechanisms. Experimental studies have shown that with regular motion training, the known risk factors and other health-related factors are positively influenced. It results, for example, in an increase in the HDL-cholesterol level, and a decrease in the serum-triglyceride level and blood pressure (Bouchard, Shepard and Stephens 1994; Pate et al. 1995).

A series of epidemiological studies, spurred on by the studies of Morris et al. on coronary risk among London bus drivers and conductors (Morris, Heady and Raffle 1956; Morris et al. 1966), and the study of Paffenbarger et al. (1970) among American harbour workers, looked at the relationship between the difficulty level of physical work and the incidence of cardiovascular diseases. Based on earlier studies from the 1950s and 1960s the prevailing idea was that physical activity at work could have a certain protective effect on the heart. The highest relative risk for cardiovascular diseases was found in people with physically inactive jobs (e.g., sitting jobs) as compared to people who do heavy physical work. But newer studies have found no difference in the frequency of coronary disease between active and inactive occupational groups or have even found a higher prevalence and incidence of cardiovascular risk factors and cardiovascular diseases among heavy labourers (Ilmarinen 1989; Kannel et al. 1986; Kristensen 1994; Suurnäkki et al. 1987). Several reasons can be given for the contradiction between the health-promoting effect of free-time physical activities on cardiovascular morbidity and the lack of this effect with heavy physical labour:

• Primary and secondary selection processes (healthy worker effect) can lead to serious distortions in occupational medical epidemiological studies.
• The relationship found between physical work and the onset of cardiovascular diseases can be influenced by a number of confounding variables (like social status, education, behavioural risk factors).
• Assessing the physical load, often solely on the basis of job descriptions, must be seen as an inadequate method.

Social and technological development since the 1970s has meant that only a few jobs with “dynamic physical activity” remain. Physical activity in the modern workplace often means heavy lifting or carrying and a high proportion of static muscle work. So it is not surprising that physical activity in occupations of this type lacks an essential criterion for coronary-protective effect: a sufficient intensity, duration and frequency to optimize the physical load on big muscle groups. The physical work is, in general, intensive, but has less of a workout effect on the cardiovascular system. The combination of heavy, physically demanding work and high free-time physical activity could establish the most favourable situation with respect to the cardiovascular risk-factor profile and the onset of CHD (Saltin 1992).

The results of studies to date are also not consistent on the question of whether heavy physical work is related to the onset of arterial hypertension.

Physically demanding work is related to changes in blood pressure. In dynamic work that utilizes big muscle masses, blood supply and demand are in balance. In dynamic work that requires the smaller and middle muscle masses, the heart may put out more blood than is needed for the total physical work and the result can be considerably increased systolic and diastolic blood pressure (Frauendorf et al. 1986).

Even with combined physical-mental strain or physical strain under the effects of noise, a substantial increase in blood pressure and heart rate are seen in a certain percentage (approximately 30%) of people (Frauendorf, Kobryn and Gelbrich 1992; Frauendorf et al. 1995).

No studies are presently available on the chronic effects of this increased circulatory activity in local muscle work, with or without noise or mental strain.

In two recently published independent studies, by American and German researchers (Mittleman et al. 1993; Willich et al. 1993), the question was pursued as to whether heavy physical work can be a trigger for an acute myocardial infarction. In the studies, of 1,228 and 1,194 people with acute myocardial infarction respectively, the physical strain one hour before the infarction was compared with the situation 25 hours before. The following relative risks were calculated for the onset of a myocardial infarction within one hour of heavy physical strain in comparison with light activity or rest: 5.9 (CI 95%: 4.6-7.7) in the American and 2.1 (CI 95%: 1.6-3.1) in the German study. The risk was highest for people not in shape. An important limiting observation is, however, that the heavy physical strain occurred one hour before the infarction in only 4.4 and 7.1% of the infarction patients respectively.

These studies involve questions of the significance of physical strain or a stress-induced increased output of catecholamines on the coronary blood supply, on triggering coronary spasms, or an immediately harmful effect of catecholamines on the beta adrenergic receptors of the heart muscle membrane as a cause of the infarction manifestation or acute cardiac death. It can be assumed that such results will not ensue with a healthy coronary vessel system and intact myocardium (Fritze and Müller 1995).

The observations make clear that statements on possible causal relationships between heavy physical labour and effects on cardiovascular morbidity are not easy to substantiate. The problem with this type of investigation clearly lies in the difficulty in measuring and assessing “hard work” and in excluding preselections (healthy worker effect). Prospective cohort studies are needed on the chronic effects of selected forms of physical work and also on the effects of combined physical-mental or noise stress on selected functional areas of the cardiovascular system.

It is paradoxical that the result of reducing heavy dynamic muscle work—until now greeted as a significant improvement in the level of strain in the modern workplace—possibly results in a new, significant health problem in modern industrial society. From the occupational medicine perspective, one might conclude that static physical strain on the muscle-skeleton system with lack of movement, presents a much greater health risk than previously assumed, according to the results of studies to date.

Where monotonous improper strains cannot be avoided, counterbalancing with free-time sports activities of comparable duration should be encouraged (e.g., swimming, bicycling, walking and tennis).

Heat and Cold

Exposure to extreme heat or cold is thought to influence cardiovascular morbidity (Kristensen 1989; Kristensen 1994). The acute effects of high outside temperatures or cold on the circulatory system are well documented. An increase in mortality as a result of cardiovascular diseases, mostly heart attacks and strokes, was observed at low temperatures (under +10°C) in the winter in countries at northern latitudes (Curwen 1991; Douglas, Allan and Rawles 1991; Kristensen 1994; Kunst, Looman and Mackenbach 1993). Pan, Li and Tsai (1995) found an impressive U-shaped relationship between outside temperature and mortality rates for coronary heart disease and strokes in Taiwan, a subtropical country, with a similarly falling gradient between +10°C and +29°C and a sharp increase thereafter at over +32°C. The temperature at which the lowest cardiovascular mortality was observed is higher in Taiwan than in countries with colder climates. Kunst, Looman and Mackenbach found in the Netherlands a V-shaped relationship between total mortality and outside temperature, with the lowest mortality at 17°C. Most cold-related deaths occurred in people with cardiovascular diseases, and most heat-related deaths were associated with respiratory tract illnesses. Studies from the United States (Rogot and Padgett 1976) and other countries (Wyndham and Fellingham 1978) show a similar U-shaped relationship, with the lowest heart attack and stroke mortality at outside temperatures around 25 to 27°C.

It is not yet clear how these results should be interpreted. Some authors have concluded that a causal relationship possibly exists between temperature stress and the pathogenesis of cardiovascular diseases (Curwen and Devis 1988; Curwen 1991; Douglas, Allan and Rawles 1991; Khaw 1995; Kunst, Looman and Mackenbach 1993; Rogot and Padgett 1976; Wyndham and Fellingham 1978). This hypothesis was supported by Khaw in the following observations:

• Temperature proved to be the strongest, acute (day to day) predictor for cardiovascular mortality under the parameters which were handled differently, such as seasonal environmental changes and factors like air pollution, sunlight exposure, incidence of flu and nutrition. This speaks against the assumption that temperature acts only as a substitute variable for other detrimental environmental conditions.
• The consistency of the connection in various countries and population groups, over time and in different age groups, is furthermore convincing.
• Data from clinical and laboratory research suggests various biologically plausible pathomechanisms, including effects of changing temperature on haemostasis, blood viscosity, lipid levels, the sympathetic nervous system and vasoconstriction (Clark and Edholm 1985; Gordon, Hyde and Trost 1988; Keatinge et al. 1986; Lloyd 1991; Neild et al. 1994; Stout and Grawford 1991; Woodhouse, Khaw and Plummer 1993b; Woodhouse et al. 1994).

Exposure to cold increases blood pressure, blood viscosity and heart rate (Kunst, Looman and Mackenbach 1993; Tanaka, Konno and Hashimoto 1989; Kawahara et al. 1989). Studies by Stout and Grawford (1991) and Woodhouse and co-workers (1993; 1994) show that fibrinogens, blood clotting factor VIIc and lipids were higher among older people in the winter.

An increase in blood viscosity and serum cholesterol was found with exposure to high temperatures (Clark and Edholm 1985; Gordon, Hyde and Trost 1988; Keatinge et al. 1986). According to Woodhouse, Khaw and Plummer (1993a), there is a strong inverse correlation between blood pressure and temperature.

Still unclear is the decisive question of whether long-term exposure to cold or heat results in lasting increased risk of cardiovascular disease, or whether exposure to heat or cold increases the risk for an acute manifestation of cardiovascular diseases (e.g., a heart attack, a stroke) in connection with the actual exposure (the “triggering effect”). Kristensen (1989) concludes that the hypothesis of an acute risk increase for complications from cardiovascular disease in people with underlying organic disease is confirmed, whereas the hypothesis of a chronic effect of heat or cold can neither be confirmed nor rejected.

There is little, if any, epidemiological evidence to support the hypothesis that the risk of cardiovascular disease is higher in populations with an occupational, long-term exposure to high temperature (Dukes-Dobos 1981). Two recent cross-section studies focused on metalworkers in Brazil (Kloetzel et al. 1973) and a glass factory in Canada (Wojtczak-Jaroszowa and Jarosz 1986). Both studies found a significantly increased prevalence of hypertension among those subject to high temperatures, which increased with the duration of the hot work. Presumed influences of age or nutrition could be excluded. Lebedeva, Alimova and Efendiev (1991) studied mortality among workers in a metallurgical company and found high mortality risk among people exposed to heat over the legal limits. The figures were statistically significant for blood diseases, high blood pressure, ischemic heart disease and respiratory tract diseases. Karnaukh et al. (1990) report an increased incidence of ischemic heart disease, high blood pressure and haemorrhoids among workers in hot casting jobs. The design of this study is not known. Wild et al. (1995) assessed the mortality rates between 1977 and 1987 in a cohort study of French potash miners. The mortality from ischemic heart disease was higher for underground miners than for above-ground workers (relative risk = 1.6). Among people who were separated from the company for health reasons, the ischemic heart disease mortality was five times higher in the exposed group as compared to the above-ground workers. A cohort mortality study in the United States showed a 10% lower cardiovascular mortality for heat-exposed workers as compared to the non-exposed control group. In any case, among those workers who were in heat-exposed jobs less than six months, the cardiovascular mortality was relatively high (Redmond, Gustin and Kamon 1975; Redmond et al. 1979). Comparable results were cited by Moulin et al. (1993) in a cohort study of French steel workers. These results were attributed to a possible healthy worker effect among the heat-exposed workers.

There are no known epidemiological studies of workers exposed to cold (e.g., cooler, slaughterhouse or fishery workers). It should be mentioned that cold stress is not only a function of temperature. The effects described in the literature appear to be influenced by a combination of factors like muscle activity, dress, dampness, drafts and possibly poor living conditions. Workplaces with exposure to cold should pay special attention to appropriate dress and avoiding drafts (Kristensen 1994).

Vibration

Hand-arm vibration stress

It is long known and well documented that vibrations transmitted to the hands by vibrating tools can cause peripheral vascular disorders in addition to damage to the muscle and skeletal system, and peripheral nerve-function disorders in the hand-arm area (Dupuis et al. 1993; Pelmear, Taylor and Wasserman 1992). The “white finger disease”, first described by Raynaud, appears with higher prevalency rates among exposed populations, and is recognized as an occupational disease in many countries.

Raynaud’s phenomenon is marked by an attack with vasospastic reduced fusion of all or some fingers, with the exception of the thumbs, accompanied by sensibility disorders in the affected fingers, feelings of cold, pallor and paraesthesia. After the exposure ends, circulation resumes, accompanied by a painful hyperaemia.

It is assumed that endogenous factors (e.g., in the sense of a primary Raynaud’s phenomenon) as well as exogenous exposures can be held responsible for the occurrence of a vibration-related vasospastic syndrome (VVS). The risk is clearly greater with vibrations from machines with higher frequencies (20 to over 800 Hz) than with machines that produce low-frequency vibrations. The amount of static strain (gripping and pressing strength) appears to be a contributing factor. The relative significance of cold, noise and other physical and psychological stressors, and heavy nicotine consumption is still unclear in the development of the Raynaud’s phenomenon.

The Raynaud’s phenomenon is pathogenetically based on a vasomotor disorder. Despite a large number of studies on functional, non-invasive (thermography, plethysmography, capillaroscopy, cold test) and invasive examinations (biopsy, arteriography), the pathophysiology of the vibration-related Raynaud’s phenomenon is not yet clear. Whether the vibration directly causes damage to the vascular musculature (a “local fault”), or whether it is a vasoconstriction as a result of sympathetic hyperactivity, or whether both these factors are necessary, is at present still unclear (Gemne 1994; Gemne 1992).

The work-related hypothenar hammer syndrome (HHS) should be distinguished in the differential diagnosis from vibration-caused Raynaud’s phenomenon. Pathogenetically this is a chronic-traumatic damage to the artery ulnaris (intima lesion with subsequent thrombosization) in the area of the superficial course above the unciform bone (os hamatum). HHS is caused by long-term mechanical effects in the form of external pressure or blows, or by sudden strain in the form of mechanical partial body vibrations (often combined with persistent pressure and the effects of impacts). For this reason, HHS can occur as a complication or in connection with a VVS (Kaji et al. 1993; Marshall and Bilderling 1984).

In addition to the early and, for exposure against hand-arm vibration, specific peripheral vascular effects, of particular scientific interest are the so-called non-specific chronic changes of autonomous regulations of the organ systems—for example, of the cardiovascular system, perhaps provoked by vibration (Gemne and Taylor 1983). The few experimental and epidemiological studies of possible chronic effects of hand-arm vibration give no clear results confirming the hypothesis of possible vibration-related endocrine and cardiovascular function disorders of the metabolic processes, cardiac functions or blood pressure (Färkkilä, Pyykkö and Heinonen 1990; Virokannas 1990) other than that the activity of the adrenergic system is increased from exposure to vibration (Bovenzi 1990; Olsen 1990). This applies to vibration alone or in combination with other strain factors like noise or cold.

Whole-body vibration stress

If whole-body mechanical vibrations have an effect on the cardio- vascular system, then a series of parameters such as heart rate, blood pressure, cardiac output, electrocardiogram, plethysmo- gram and certain metabolic parameters must show corresponding reactions. Conclusions on this are made difficult for the method- ological reason that these circulation quantifications do not react specifically to vibrations, but can also be influenced by other simultaneous factors. Increases in heart rate are apparent only under very heavy vibration loads; the influence on blood pressure values shows no systematic results and electrocardiographic (ECG) changes are not significantly differentiable.

Peripheral circulatory disorders resulting from vasoconstriction have been less researched and appear weaker and of shorter duration than those from hand-arm vibrations, which are marked by an effect on the grasping strength of the fingers (Dupuis and Zerlett 1986).

In most studies the acute effects of whole-body vibrations on the cardiovascular system of vehicle drivers were found to be relatively weak and temporary (Dupius and Christ 1966; Griffin 1990).

Wikström, Kjellberg and Landström (1994), in a comprehensive overview, cited eight epidemiological studies from 1976 to 1984 that examined the connection between whole-body vibrations and cardiovascular diseases and disorders. Only two of these studies found a higher prevalence of such illnesses in the group exposed to vibrations, but none where this was interpreted as the effect of whole-body vibrations.

The view is widely accepted that changes of physiological functions through whole-body vibrations have only a very limited effect on the cardiovascular system. Causes as well as mechanisms of the reaction of the cardiovascular system to whole-body vibrations are not yet sufficiently known. At present there is no basis to assume that whole-body vibrations per se contribute to the risk of diseases of the cardiovascular system. But attention should be paid to the fact that this factor very often is combined with exposure to noise, inactivity (sitting work) and shift work.

Ionizing Radiation, Electromagnetic Fields, Radioand Microwaves, Ultra- and Infrasound

Many case studies and a few epidemiological studies have drawn attention to the possibility that ionizing radiation, introduced to treat cancer or other diseases, may promote the development of arteriosclerosis and thereby increase the risk for coronary heart disease and also other cardiovascular diseases (Kristensen 1989; Kristensen 1994). Studies on the incidence of cardiovascular diseases in occupational groups exposed to ionizing radiation are not available.

Kristensen (1989) reports on three epidemiological studies from the early 1980s on the connection between cardiovascular diseases and exposure to electromagnetic fields. The results are contradic- tory. In the 1980s and 1990s the possible effects of electrical and magnetic fields on human health have attracted increasing atten- tion from people in occupational and environmental medicine. Partially contradictory epidemiological studies that looked for cor- relations between occupational and/or environmental exposure to weak, low-frequency electrical and magnetic fields, on the one hand, and the onset of health disorders on the other, aroused considerable attention. In the foreground of the numerous experi- mental and few epidemiological studies stand possible long-term effects such as carcinogenicity, teratogenicity, effects on the im- mune or hormone systems, on reproduction (with special atten- tion to miscarriages and defects), as well as to “hypersensitivity to electricity” and neuro-psychological behavioural reactions. Poss- ible cardiovascular risk is not being discussed at present (Gamber- ale 1990; Knave 1994).

Certain immediate effects of low-frequency magnetic fields on the organism that have been scientifically documented through in vitro and in vivo examinations of low to high field strengths should be mentioned in this connection (UNEP/WHO/IRPA 1984; UNEP/WHO/IRPA 1987). In the magnetic field, such as in the blood stream or during heart contraction, charged carriers lead to induction of electrical fields and currents. Thus the electrical voltage that is created in a strong static magnetic field over the aorta near the heart during coronary activity can amount to 30 mV at a flow thickness of 2 Tesla (T), and induction values over 0.1 T were detected in the ECG. But effects on the blood pressure, for example, were not found. Magnetic fields that change with time (intermittent magnetic fields) induce electrical eddy fields in biological objects that can for example arouse nerve and muscle cells in the body. No certain effect appears with electrical fields or induced currents under 1 mA/m². Visual (induced with magnetophosphene) and nervous effects are reported at 10 to 100 mA/m². Extrasystolic and heart chamber fibrillations appear at over 1 A/m². According to currently available data, no direct health threat is to be expected for short-term whole-body exposure up to 2 T (UNEP/WHO/IRPA 1987). However, the danger threshold for indirect effects (e.g., from the magnetic field force action on ferromagnetic materials) lies lower than that for direct effects. Precautionary measures are thus required for persons with ferromagnetic implants (unipolar pacemakers, magnetizable aneurysm clips, haemoclips, artificial heart valve parts, other electrical implants, and also metal fragments). The danger threshold for ferromagnetic implants begins at 50 to 100 mT. The risk is that injuries or bleeding can result from migration or pivotal motions, and that functional capacities (e.g., of heart valves, pacemakers and so on) can be affected. In facilities in research and industry with strong magnetic fields, some authors advise medical surveillance examinations for people with cardiovascular diseases, including high blood pressure, in jobs where the magnetic field exceeds 2 T (Bernhardt 1986; Bernhardt 1988). Whole-body exposure of 5 T can lead to magnetoelectrodynamic and hydrodynamic effects on the circulatory system, and it should be assumed that short-term whole-body exposure of 5 T causes health hazards, especially for people with cardiovascular diseases, including high blood pressure (Bernhardt 1988; UNEP/WHO/ IRPA 1987).

Studies that examine the various effects of radio and microwaves have found no detrimental effects to health. The possibility of cardiovascular effects from ultrasound (frequency range between 16 kHz and 1 GHz) and infrasound (frequency range >>20 kHz) are discussed in the literature, but the empirical evidence is very slight (Kristensen 1994).

Back

Despite numerous studies, the role of chemical factors in causing cardiovascular diseases is still disputed, but probably is small. The calculation of the aetiological role of chemical occupational factors for cardiovascular diseases for the Danish population resulted in a value under 1% (Kristensen 1994). For a few materials such as carbon disulphide and organic nitrogen compounds, the effect on the cardiovascular system is generally recognized (Kristensen 1994). Lead seems to affect blood pressure and cerebrovascular morbidity. Carbon monoxide (Weir and Fabiano 1982) undoubtedly has acute effects, especially in provoking angina pectoris in pre-existing ischaemia, but probably does not increase the risk of the underlying arteriosclerosis, as was long suspected. Other materials like cadmium, cobalt, arsenic, antimony, beryllium, organic phosphates and solvents are under discussion, but not sufficiently documented as yet. Kristensen (1989, 1994) gives a critical overview. A selection of relevant activities and industrial branches can be found in Table 1.

Table 1. Selection of activities and industrial branches that may be associated with cardiovascular hazards

The exposure and effect data of important studies for carbon disulphide (CS₂), carbon monoxide (CO) and nitroglycerine are given in the chemical section of the Encyclopaedia. This listing makes clear that problems of inclusion, combined exposures, varying consideration of compounding factors, changing target sizes and assessment strategies play a considerable role in the findings, so that uncertainties remain in the conclusions of these epidemiological studies.

In such situations clear pathogenetic conceptions and knowledge can support the suspected connections and thereby contribute to deriving and substantiating the consequences, including preventive measures. The effects of carbon disulphide are known on lipids and carbohydrate metabolism, on thyroid functioning (triggering hypothyroidism) and on coagulation metabolism (promoting thrombocyte aggregation, inhibiting plasminogen and plasmin activity). Changes in blood pressure such as hypertension are mostly traceable to vascular-based changes in the kidney, a direct causal link to high blood pressure due to carbon disulphide has not yet been excluded for certain, and a direct (reversible) toxic effect is suspected on the myocardium or an interference with the catecholamine metabolism. A successful 15-year intervention study (Nurminen and Hernberg 1985) documents the reversibility of the effect on the heart: a reduction in exposure was followed almost immediately by a decrease in cardiovascular mortality. In addition to the clearly direct cardiotoxic effects, arteriosclerotic changes in the brain, eye, kidney and coronary vasculature that can be considered the basis of encephalopathies, aneurysms in the retina area, nephropathies and chronic ischaemic heart disease have been proven among those who are exposed to CS₂. Ethnic and nutritionally related components interfere in the pathomechanism; this was made clear in the comparative studies of Finnish and Japanese viscous rayon workers. In Japan, vascular changes in the area of the retina were found, whereas in Finland the cardiovascular effects dominated. Aneurysmatic changes in the retinal vasculature were observed at carbon disulphide concentrations under 3 ppm (Fajen, Albright and Leffingwell 1981). Reducing the exposure to 10 ppm clearly reduced cardiovascular mortality. This does not definitively clarify whether cardiotoxic effects are definitely excluded at doses under 10 ppm.

The acute toxic effects of organic nitrates involve widening of the vasa, accompanied by dropping blood pressure, increased heart rate, spotty erythema (flush), orthostatic dizziness and headaches. Since the half-life of the organic nitrate is short, the ailments soon subside. Normally, serious health considerations are not to be expected with acute intoxication. The so-called withdrawal syndrome appears when exposure is interrupted for employees with long-term exposure to organic nitrate, with a latency period of 36 to 72 hours. This includes ailments ranging from angina pectoris up to acute myocardial infarction and cases of sudden death. In the investigated deaths, often no coronary sclerotic changes were documented. The cause is therefore suspected to be “rebound vasospasm”. When the vasa-widening effect of the nitrate is removed, an autoregulative increase in resistance occurs in the vasa, including the coronary arteriae, which produces the above-mentioned results. In certain epidemiological studies, suspected associations between exposure duration and intensity of organic nitrate and ischaemic heart disease are considered uncertain, and pathogenetic plausibility for them is lacking.

Concerning lead, metallic lead in dust form, the salts of diva- lent lead and organic lead compounds are toxicologically impor- tant. Lead attacks the contractile mechanism of the vasa muscle cells and causes vascular spasms, which are considered causes for a series of symptoms of lead intoxication. Among these is tem- porary hypertension that appears with lead colic. Lasting high blood pressure from chronic lead intoxication can be explained by vasospasms as well as kidney changes. In epidemiological studies an association has been observed with longer exposure times between lead exposure and increased blood pressure, as well as an increased incidence of cerebrovascular diseases, whereas there was little evidence of increased cardiovascular diseases.

Epidemiological data and pathogenetic investigations to date have produced no clear results on the cardiovascular toxicity of other metals like cadmium, cobalt and arsenic. However, the hypothesis that halogenated hydrocarbon acts as a myocardial irritant is considered certain. The triggering mechanism of occasionally life-threatening arrhythmia from these materials presumably comes from myocardial sensitivity to epinephrine, which works as a natural carrier for the autonomic nervous system. Still being discussed is whether a direct cardiac effect exists such as reduced contractility, suppression of impulse formation centres, impulse transmission, or reflex impairment resulting from irrigation in the upper airway region. The sensitizing potential of hydrocarbons apparently depends on the degree of halogenation and on the type of the halogen contained, whereas chlorine-substituted hydrocarbons are supposed to have a stronger sensitizing effect than fluoride compounds. The maximum myocardial effect for hydrocarbons containing chlorine occurs at around four chlorine atoms per molecule. Short chain non-substituted hydrocarbons have a higher toxicity than ones with longer chains. Little is known about the arrhythmia-triggering dosage of the individual substances, as the reports on humans predominantly are case descriptions with exposure to high concentrations (accidental exposure and “sniffing”). According to Reinhardt et al. (1971), benzene, heptane, chloroform and trichlorethylene are especially sensitizing, whereas carbon tetrachloride and halothane have less arrhythmogenic effect.

The toxic effects of carbon monoxide result from tissue hypoxaemia, which results from the increased formation of CO-Hb (CO has 200-times greater affinity to haemoglobin than does oxygen) and the resulting reduced release of oxygen to the tissues. In addition to the nerves, the heart is one of the organs that react especially critically to such hypoxaemia. The resulting acute heart ailments have been repeatedly examined and described according to exposure time, breathing frequency, age and previous illnesses. Whereas among healthy subjects, cardiovascular effects first appear at CO-Hb concentrations of 35 to 40%, angina pectoris ailments could be experimentally produced in patients with ischaemic heart disease already at CO-Hb concentrations between 2 and 5% during physical exposure (Kleinman et al. 1989; Hinderliter et al. 1989). Deadly infarctions were observed among those with previous afflictions at 20% CO-Hb (Atkins and Baker 1985).

The effects of long-term exposure with low CO concentrations are still subject to controversy. Whereas experimental studies on animals possibly showed an atherogenic effect by way of hypoxia of the vasa walls or by direct CO effect on the vasa wall (increased vascular permeability), the flow characteristics of the blood (strengthened thrombocyte aggregation), or lipid metabolism, the corresponding proof for humans is lacking. The increased cardiovascular mortality among tunnel workers (SMR 1.35, 95% CI 1.09-1.68) can more likely be explained by acute exposure than from chronic CO effects (Stern et al. 1988). The role of CO in the cardiovascular effects of cigarette smoking is also not clear.

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