European Heart Journal (1988) 9 (Supplement L), 26-34

Chemical and physical agents of work-related cardiovascular diseases

L. PETRONIO

Istituto di Medicina del Lavoro, Department of Occupational Medicine, University of Trieste, Italy

KEY WORDS: Occupational cardiovascular disease, prevention, arsenic, carbon monoxide, lead, cadmium, cobalt, mercury, nitrates, carbon disulphide, freon, chlorinated hydrocarbons, vinyl chloride, heat, noise, vibration, electricity, non-ionizing and ionizing radiations. This article summarizes the state of the art in research on cardiovascular diseases (CVD) and occupational exposure. The major chemical and physical agents are considered and the methodological difficulties of epidemiological surveys are discussed. Work-related CVD, like all occupational disorders, are changing continuously as a consequence of modifications in industrial processes, improvements in preventative measures, and the tertiarization of the economy. The cornerstones of a preventative strategy of CVD are still based on environmental monitoring and medical surveillance, but at the same time on multidisciplinary and multicentred scientific research. Where possible, health promotion will include more general programmes directed at changing personal risk factors. In 1978 the American Heart Association formed a task force to review the data regarding environmental impact on cardiovascular diseases (CVD). The final report'1' stated: 'Surprisingly little medical or public health attention has been directed to the potential for general environmental effects on the cardiovascular system, and only one recent review has addressed this problem'. The authors were referring to the review of Rosenman'2'. In 1983 the NIOSH (National institute of Occupational Safety and Health) published a list of 10 leading work-related diseases and injuries as a guide for establishing a hierarchy in preventative intervention and for an effective allocation of resources'3'. In that decalogue, occupational CVD were in fifth place after lung diseases, musculoskeletal injuries, occupational cancers and severe occupational traumatic injuries. Despite this fact and the increased attention given by both cardiologists and occupational health physicians in recent years, the Excerpta Medico, in the section on occupational health and the cardiovascular system, has reviewed only 332 articles from the period 1983-87, an average of 70 articles per year. A brief classification of the main arguments has produced the following results: (a) the key words
Address for correspondence: Don. Lucio Petronio, Istituto di Medicina del Lavoro c/o Centra Tumori, via delta Pieta n. 19, 34129 Trieste, Italy. 0195-668X/88/9L0026 + 09 $02.00/0 Downloaded from http://eurheartj.oxfordjournals.org/ by guest on September 25, 2013

'physical activity' and 'sport' defined 27% of publications, followed by hypertension (15%), pharmacological trials and rehabilitation programmes (15% of the whole); (b) industrial toxic substances were the main topic in only 4% of publications and physical agents in another 7% (hand-arm vibration is the topic most often studied, with 20 publications); and (c) considering the occupational groups, aviation personnel and air-traffic controllers were the groups most often studied. Similar observations can be made after reviewing the Italian literature: in the last seven years (1980-86) one of the most prestigious journals (La Medicina del Lavoro) published 24 articles on work-related CVD, and the abstracts of two Italian seminars on the topic. However, even in 1983, an author entitled his article 'Occupational heart disease: absence of effects or absence of knowledge?''4'. The reasons for such difficulties in recognizing the causal relationship between occupational risks and CVD are well known'5', (i) The aetiology of CVD is multifactorial and not yet well understood; even in atherosclerotic disease, the known risk factors account for only 50% of cases. In this context, the role of occupational risk is often difficult to define, particularly when ambient concentrations of toxic substances are not known, (ii) The cardiovascular system is a classic stress-strain organ that reacts in a non-specific manner to various environmental noxae:
1988 The European Society of Cardiology

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therefore, there are no pathognomonic expressions in coronary arteriosclerotic heart disease (CAHD) of occupational origin, (iii) Epidemiological survey is often difficult because of the scarcity of sample (small worker cohorts) which impedes researchers from obtaining statistical significance (low power of study). There is also a need to improve study design: the bias called 'healthy worker effect' is well known: autoselection mechanisms in worker groups determine a deficit of cardiovascular mortality, (iv) One of the fundamental aspects of screening in occupational health is the acceptability and, therefore, the noninvasiveness of the test. At the present moment, such a test is not available for diagnosing CAHD. The chemical and physical agents of work-related CVD are thus considered separately. The complications of chronic obstructive lung diseases and/or pneumoconiosis and the acute events resulting from accidents (such as anoxic syndromes and other cardiovascular emergencies), will not be discussed in the present paper. Chemical agents
CARBON MONOXIDE

The effects of CO inhalation will be more severe in critical situations such as during exercise, in a hypobaric environment (altitude) and in subjects affected with CAHD. While there is a body of literature which confirms the effects of acute exposure to CO, the low-level, long-term effects have still not been determined or agreed upon, and, in particular, the role played in the genesis of atherosclerosis. Presently, with regard to workplace, the ACGIH propose a TLV-TWA value of 50 ppm'8'. The ambient air quality standard for the general population adopted by various countries is, on average, about 10 ppm'7'.
LEAD

Carbon monoxide is a colourless and odourless gas formed during incomplete combustion processes. Although smoking represents one of the most important sources of CO, we must not forget that natural and man-made sources produce at least 250 million tons of CO every year. The toxic effects of inhaled CO are due to tissue hypoxia and are closely related to the carboxyhaemoglobin (COHb) level'6'7'. The central nervous system and myocardium are the most vulnerable tissues; the cardiovascular effects are the following: (a) coronary flow and cardiac output increase with higher oxygen extraction; (b) reduced tolerance to exercisein CAHD patients, COHb at a concentration of 3-5% determines chest pain (also, in patients with chronic obstructive lung disease, the time for onset of exertional dyspnea is shortened); (c) transient ECG abnormalities and greater vulnerability to cardiac rhythm disturbancessupraventricular and ventricular extrasystoles, atrial fibrillation; (d) higher vascular permeability which can partially accelerate atherosclerotic lesions; (e) premature onset of claudication in subjects with arteriosclerosis obliterans in lower limbs; and (f) disturbances in cerebral functiona reduced performance in mental tests and a decrease in visual acuity has been reported at a COHb level of 3-5%.

Acute lead poisoning is characterized by saturnine colic and blood hypertension, secondary to diffuse arteriolar vasoconstriction. This is particularly evident in the kidneys, where lead causes a vasospasm of the afferent arterioles of glomeruli with a reduction in renal blood flow (and, consequently, in the filtration rate), and an activation of the reninangiotensin system. Chronic lead poisoning causes nephroangiosclerosis complicated by hypertension and, consequently, occasionally by severe abnormalities of the coronary and cerebrovascular beds. Higher standards of hygiene in the workplace, together with scrupulous biological monitoring in exposed workers, have contributed, at least in industrialized countries, to a sharp decline in the incidence of severe lead poisoning, although asymptomatic lead absorption is still present, not only in working groups, but also in the population (some reports regard children and a deficit of intellectual performance)'9"11'. Moreover, there are no definite answers to the following questions: Can long-term occupational exposure to low doses cause vascular damage? Can lead exposure in the community, due to industrial pollution, exhaust fumes (in the case of ethylated benzine), ingestion of lead in food, cause or be a co-factor in hypertension? A positive relationship between lead exposure and hypertension has been found'12"15], but has not always been confirmed by other authors'16'. Geographical studies have suggested, although controversies abound, that a higher incidence of CVD could be related to the hardness of the water. Soft water, low in calcium and magnesium salts, may transport more suspended lead than hard water and this metal could be responsible for hypertension and/or atherosclerosis. The problem is still being debated and the possible involvement of the following trace elements is periodically suggested: zinc,

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sure to trinitroglycerine and ethylene glycol dinitrate. (i) A syndrome of excessive nitrate absorption through the respiratory system and skin (cutaneous CADMIUM administration of nitroderivative drugs is also a Occupational exposure to cadmium is responsible means of therapy in CAHD): the typical effects for: (a) tubular and interstitial nephropathy, initially consist in vasodilatation with a facial flush, throbbing characterized by low molecular tubular proteinuria headache, dizziness, and orthostatic hypotension. If and then complicated with nephrosclerosis; (b) exposure continues, the above effects will be rechemical pneumonitis as a consequence of acute duced, but they reappear at each resumption of inhalation, and pulmonary emphysema after pro- work. longed exposure; and (c) bone metabolism disturb(ii) A withdrawal syndrome characterized by: (a) ances with osteomalacia in the most serious cases. anginal pain due to coronary vasospasm and to an The peculiar tropism for the kidneys may cause increase in oxygen uptake, as a consequence of renal hypertension. In kidney specimens obtained rebound effects (myocardial infarction is rarely from autopsies of patients suffering from hyperten- described); (b) 'Monday Morning Death', or sudden sion, cadmium, as well as lead, have been found in death on Monday morning awakening, before higher concentrations. However, the role of cad- reaching worksensitization to epinephrine lasts mium in the pathogenesis of hypertension is still from 24 to 48 h after the last nitrate exposure and can lead to ventricular fibrillation; (c) vasospastic Raynaud-like phenomena, more frequent in women. OTHER METALS AND METALLOIDS Subjects suffering from CVD may have a premaIatrogenic lesions of the heart caused by arsenical ture onset and a higher intensity of the above synderivatives and by antimony used once in syphilis and dromes. There is less evidence for long-term effects. schistosomiasis therapy, respectively, are now a thing Swedish authors'24' have reported a crude rate ratio of the past. More important is the acute arsine of 2-5 in the cardiovascular morbidity of workers (ASH3) poisoning, characterized by circulatory shock exposed to nitrates for at least 20 years. An excess of and renal failure due to haemolysis. ECG abnormali- mortality is also revealed in a 16-year follow-up ties are frequent and were well described in the 1950s study'25'. Recently, an American retrospective and 1960s. In a case-control study, Axelson et at. study'26', has shown an excess of ischaemic heart attributed the higher CAHD incidence in copper disease in two worker cohorts exposed to dinitrosmelters to trace arsenic. Vascular disorders and toluene in an ammunition plant. Despite these Raynaud's phenomenon have also been described'20'. reports, the evidence for the chronic effects of Cobalt is a heavy metal known to be a causal agent nitrates is not conclusive. in epidemic dilatated cardiomyopathy (beri-beri like) reported in the U.S.A., Canada and Belgium among heavy beer drinkers'21'. Cobalt has been used as a CARBON DISULPHIDE froth-stabilizing agent in beer. The role of cobalt in The most serious occupational exposure involved occupational exposure is less important, although rayon viscose workers, although carbon disulphide some cases of 'allergic' cardiomyopathy have been (CS2) is also used as a solvent in the rubber, chemical described among workers in the U.S.S.R.'22'. and pharmaceutical industries. Today, the manufacOccupational exposure to mercury (Hg) is ture of rayon is much rarer and preventative involved in causing hypertension with a prevalence measures have greatly modified occupational exporate which is double that of the general population. sure. Consequently, most of the information about Nowadays, in feltmaking, textile manufacture, and the toxic effects of CS2 is founded on the literature of caustic soda plants, the risk has almost disappeared the 1950s and 1960s; the whole vascular bed (the thanks to technical improvements and modifications cerebrovascular system, the heart, the splanchnic in processing methods'23'. organs and the kidneys, the limbs) is affected by a diffuse atherosclerosis, the exact pathogenetic mechanism of which is still unknown. The relative NITRATES risk of CAHD reported in numerous countries is 2-5 Workers in the explosives industry may suffer from times greater in exposed groups than in reference two cardiovascular disorders because of their expo-

cobalt, antimony, and cadmium (for a review of the epidemiology, see'17').

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groups'27'. Scandinavian authors estimate that exposure to CS2 has been reduced from 20-40 ppm in the 1950s, to 10-30 ppm in 1960s, and less than 10 ppm in 1970'28'. The TLV of the ACGIH is presently 30 mg m"3, or 10 ppm18'.

workers in dry-cleaningfirmsand in abusers (solvent sniffers)'3536'. In modern laundries, TRI has been substituted with less toxic compounds such as perchloroethylene. The ACGIH-TLV of TRI is 50 ppm.
VINYL CHLORIDE

ORGANIC SOLVENTS: HALOGENATED HYDROCARBONS

The first reports of sudden death in users of bronchodilatory aerosols, hair and deodorant sprays, etc., were published in the 1960s. In 1971, Reinhardt et a/.'29' listed 41 substances capable of sensitizing the heart to epinephrine and consequently with arrhythmogenic properties (including ventricular fibrillation). The most important compounds are fluorocarbons (freon), which are greatly used not only as propellants, but also as solvents and refrigerating fluids. Most reports of sudden death are related to abusers of these substances: 110 deaths of 'sniffers' were reported by Bass'30' in the period 1964-69 (fluorocarbons, benzene, trichloroethane and other agents were responsible). Among the personnel of a pathology department, who were working with freon to prepare cryostat sections, ECGs revealed a high incidence of arrhythmias'31'. Various mechanisms have been suggested as acting both directly and indirectly on the myocardium: cardiac sensitization to epinephrine, a depression of inotropism, a suppressive effect on sinus and atrioventricular nodes, and/or nervous reflexes due to irritation of upper airways. The experimental cardiotoxicity of different fluorocarbons varies, being higher for freon-11, freon-113, and freon-2l'32'. The chronic effects of fluorocarbons on low-level exposed occupational groups have not been confirmed. The chlorinated hydrocarbons include many compounds used as industrial solvents, cleaners and degreasers, and anaesthetic agents. Due to the latter use, the arrhythmogenic properties of chloroform, trichloroethylene (TRI) and halothane have been recognized'33'34'. Furthermore, cases of acute intoxication with TRI of an occupational origin or after a suicide attempt, have been reported, mainly involving commercial TRI containing other impurities (tetrachloroethylene, dichloroethane, dichloropropane, etc.). All the different arrhythmias have been recorded: premature atrial and ventricular beats, flutter and fibrillation, nodal rhythm, and atrioventricular dissociation. Apart from the cases of sudden death in the 1940s and 1950s due to TRI as an anaesthetic agent, other cases were registered among

Vinyl chloride is one of the most widely diffused plastic resins. Its narcotic effects on the central nervous system were described in the 1940s, but such acute intoxication is now a thing of the past. Between 1970 and 1973, the experimental and epidemiological evidence of vinyl chloride hepatic angiosarcoma'37' brought about an improvement in standards of hygiene; threshold limit values, which until 1974 had been 500 ppm. were consequently reduced to the present 5 ppm levelfixedby the ACGIH, with a limit of 1 ppm proposed by the U.S. Department of Labour. Therefore, long-term effects are also beginning to be seen more rarely. Vinyl chloride, in addition to osteolysis of the digital phalanges and scleroderma-like cutaneous lesions, causes vascular disturbances in the hands, which may cause an attack of Raynaud's phenomenon. It is likely that autoaggressive mechanisms produce antigen-antibody complexes which damage the microcirculation. In the literature, the prevalence of angioneurosis is extremely variable, being also related to different diagnostic approaches. Italian authors studying the blood flow in the hand with plethysmography found values of 3-4%, while a rate of 20% or higher is reported when vascular hyperreactivity to cold is considered a positive test'38'. Improved hygiene standards have greatly reduced the frequency of vascular disorders.
Physical agents
HEAT

Exposure to heat directly involves the cardiovascular system, because of the role of the latter in thermolysis'39'. In fact, the mechanisms which safeguard thermal equilibrium are made possible by a regional blood flow redistribution, particularly at the skin level. This guarantees a higher heat transfer to the air, supported by physical mechanisms of convection, irradiation and sweat evaporation (which determine 600 kcal dispersion per liter of sweat). As the temperature rises from 37 to 42-4C, cardiac output may double: this increase is due both to systolic output and to heart rate, which may reach 180-200 ml and 160-180 beats min~\ respectively (the latter is monitored because of its close relationship with O2

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L. Petronio factors such as acute or chronic exposure to noise, the fact that continuous noise exposure is not always clearly distinguished from intermittent noise exposure, and last but not least, that many epidemiological surveys have a weak study design (lack of reference groups and so on), there is great uncertainty about the extra-auditory effects of noise. The relationship between CVD, hypertension in particular, and chronic exposure to noise is even more disputed. The argument is of central importance because in Europe alone it is estimated that between 10 and 15 million subjects are exposed to a noise equivalent level in the workplace higher than 85 dB(A)'42'. The latter limit was recommended by a 1986 E.E.C. Directive which also, however, fixed a hazard threshold limit of 90 dB(A)'43'. The above limits were established with the sole aim of preventing hearing damage through occupational exposure. As regards the extra-auditory effects, no conclusions can be drawn at present but it is certain that workers suffering from CVD or subjects of 'A-type' personality are more susceptible to noise stress. These factors should be considered in the course of medical surveillance at work places.
VIBRATION

uptake). The redistribution of regional bloodflowto the skin, the skeletal muscles, and the myocardium is achieved to the detriment of the splanchnic and kidney regions. Therefore, the cardiovascular system may be subjected to excessive stresses, particularly when subjects are not only operating in extreme climatic conditions but also with a high working load, and without a period of acclimatization. Acute heat illness may then supervene, more frequently if certain predisposing factors exist, such as age, obesity, alcoholism or chronic diseases. Not only should these factors be evaluated accurately during periodical medical surveillance, but also, of course, the existence of CVD which may represent a contraindication to occupational heat exposure. The standards of hygiene in work places use various indices, based on physical factors or physiological parameters. One of the most frequently used is the WBGT proposed by the ACGIH(8). This index fixes the tolerable levels, reducing the duration of exposure under different working loads. Working in cold environments (arctic regions, deep-sea diving, refrigerated storage rooms, etc.) causes numerous physiological responses, principally consisting of vasoconstriction in the extremities and shivering. Severe cold exposure may cause hypothermia: when deep body temperature falls below 30C, lethargy, unconsciousness and death from ventricular fibrillation may supervene. Cold ambience represents a risk for subjects suffering from CVD, but are not known as causal agents of CAHD.
NOISE

The relationship between industrial noise and hearing loss is well established'40'41'. Moreover noise, as one of the most prevalent environmental stressors, acts on the pituitary adrenomedulla axis, thus activating various non-specific responses of the autonomic nervous system. In this way, a variety of extraauditory effects are brought about, consisting mainly of cardiovascular and digestive disturbances and, more generally, of negative effects on human performance. As a consequence of peripheral arterial vasoconstriction, easily measurable at the cutaneous level, heart rate and blood pressure increase. After a first series of 'direct' biological responses, there are then other effects on the heart, after early haemodynamic peripheral modifications. This sequence of effects and after-effects must be borne in mind in order to understand fully the mechanism involved, otherwise problems of 'incomparability' among different studies arise. Because of this, and other

Nowadays, exposure to mechanical vibration is extremely widespread, not only in industrial and agricultural occupations, but also in everyday life, because of the use of vehicles. The effects on the human body depend on how the vibration is transmitted: whole-body vibration or hand-arm vibration. Vibrations are characterized by frequency and amplitude (velocity, displacement or acceleration). Acceleration is the amplitude most commonly measured parameter, as equivalent frequency weighted acceleration, in an orthogonal triaxial system X, Y, Z. Whole-body vibration (WBV) The human body reacts to vibrations in a complex way, since it is composed of mass (skeletal segments) and of elastic and viscous elements (muscles, tendons and joints). This complex system can absorb or amplify vibration, according to body posture, muscular tension and resonance frequencies peculiar to various parts of the body'44'. Physiological reactions include increased muscular tone and tendon hyper-reflexia, with a resulting increase in oxygen uptake and cardiac output. Psychosensorial responses are non-specific because vibration behaves like other stressors and, therefore,

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may determine an alarm/adaption syndrome, as defined by Selye. The main chronic effects of WBV concern the skeletal and digestive systems. The most frequent disturbances reported in the cardiovascular system are: (a) Raynaud-like peripheral angiospastic disorders in the hands or feet; (b) varicose veins, haemorrhoids and varicocele; (c) ischaemic heart disease and hypertension; and (d) neuro-vascular symptoms, such as chest pain and cardiac neurosis. Since many of these disturbances have been reported in drivers, a prolonged sitting posture [in the case of (b)], and psychological stress [in the case of (c)], cannot be excluded as co-factors. Prevention criteria are reported in the ISO document 2631 of 1978, which defines acceptable levels of acceleration depending on exposure time'45'. Hand-arm vibration (HAV) Long-term use of hand-held vibrating tools often causes premature wrist and elbow osteoarthrosis, neurological symptoms, and vascular disturbances in the hands and arms'46'47'. A typical Raynaud's phenomenon may develop. These vasospastic symptoms are usually triggered by cold and are accompanied by numbness of the fingers ('dead fingers'). Because of its fundamental role, cold is the main tool in the provocative test for diagnosing vibrationinduced white finger. It seems that no observable anatomic changes in the digital arteries occur in mild and moderate cases of VWF. In advanced cases, subintimalfibrosisand medial layer hypertrophy may occur, but in only less than 1% of patients do these lesions reach the worst stage of tissue necrosis. The severity of the biological effects of HAV depends on the frequency spectrum of vibration, its magnitude (usually rms acceleration measured in an orthogonal coordinate system), the type and condition of the vibrating tool, the method of working, the hand posture and strength of grip, and the length of exposure (per day and cumulative). Vascular disorders may also be influenced by climatic conditions (cold), noise, smoking, and drug consumption. The risk of VWF is related to the dose of vibration, or energyequivalent, absorbed by the hand during the total time of exposure and can be calculated according to ISO guideline 5349 of 19861"8'. Depending primarily on the dose, and then on the diagnostic method adopted, the prevalence of VWF reported in the literature varies widely (see the reports of NIOSH)'49-50'. The majority of epidemiological surveys have been concerned with forestry workers (vibration generated by chain saws), stonecutters and

hard-rock miners (air hammers and rock drills), and foundry and shipyard workers (grinders, chipping hammers). In 1973, the NIOSH estimated that 1-2 million workers were exposed to occupational handarm vibration in the U.S.A. alone.
ELECTRICITY, NON-IONIZING AND IONIZING RADIATION

Electrocution may produce all the known ventricular arrhythmias: paroxysmal tachycardia, flutter, torsade de pointes, and fibrillation, which are usually fatal'39'. The nature and severity of electrical injuries and, in particular, the threshold of ventricular fibrillation, is influenced by many factors, such as the type of current, alternating current being the most dangerous, surface and duration of contact, age and size of subj ects, etc. In the case of less severe inj uries, heart ischaemia caused by coronary vasospasm and/or direct lesions on the myocardium have been described. Exposure to electric and magneticfieldsis reported as producing behavioural and cardiovascular effects, characterized by neurocirculatory asthenia, mainly reported by authors in the U.S.S.R.'5152'. At present, no convincing studies have been produced demonstrating measurable biological effects on the human body. The subject, however, is of great importance, not only for workers in electrical power plants and their substations, but also for people residing near high-tension power lines. Similarly, the literature on the biological effects of radiofrequency (RF) and microwave (MW) low-level exposure abounds in uncertainties and controversies'53'. RF and MW are extremely widespread nowadays: in the field of telecommuncations, in radar stations, in the wood and textile industries (because of glueing methods), in health services (i.e. diathermic treatments), and in domestic and industrial MW ovens. The thermal effects of exposure to high power density (100-200 mW cm"2) are by now well known. The non-thermal effects, on the other hand, have been the cause of disagreement, particularly in the Soviet and American literature. As a consequence of the exposure to low-power density (less than 1 mW cm"2), some authors have reported behavioural disturbances and a neurasthenic syndrome with bradycardia and h y p o t e n s i o n . Hyperhydrosis, hypertension, and vasospastic reactions have also been described. Although many authors propose the existence of a true radiowave sickness, the WHO in 1981 stressed the need for further research, especially to verify if all the effects are reversible and to study more precisely the dose-response relationship in the

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case of long-term, low-level exposure'53'. This subject is of interest in community medicine because it has been demonstrated that near radio and TV stations, the intensity of electromagneticfieldsis often 10-100 times higher than in other urban areas'54>S51. Finally, it should be remembered that electromagnetic fields may seriously disturb pacemaker activity. The cardiovascular effects of ionizing radiation include iatrogenic diseases and acute events. The first is represented by radiation-induced heart disease, which is a complication of tumour therapy'56'57'; the second follows an acute whole-body irradiation of more than 1000 Rad which causes a gastrointestinal syndrome resulting in hypovolemic shock and rapidly culminating in death. Conclusions Work-related cardiovascular diseases, like all occupational disorders, are changing continuously as a consequence of modifications in industrial processes, improvements in preventive measures, and the tertiarization of our economy. For this reason, acute occupational intoxication and most clinical forms of chronic ones are disappearing; for example, the more severe cases of lead and carbon disulfide poisoning are now a thing of the past, at least in the industrialized world. Moreover, the physical work load has been greatly reduced thanks to automation. Nowadays, the aetiology of work-related CVD is described differently, depending on the scientific approach. The first school of thought emphasizes the importance of the traditional chemical and physical cardiotoxic agents; these have been greatly reduced, however, in 'modern' industrial processes. The second underlines the role of psycho-social stress, taking into account personality factors, working and life styles. Both approaches are undoubtedly valid, but only if integrated with each other. In fact, it should be remembered that occupational exposure is almost always multiple, thus activating synergistic responses. This is particularly true of physical agents, often produced by the same source (i.e. noise and vibration). Furthermore, the cardiovascular system is a typical stress-strain organ. According to the NIOSH and the Association of Public Health Schools'58', the cornerstones of a preventive strategy for occupational CVD are mainly based on surveillance in the work environment, but at the same time on multidisciplinary and multicentred scientific research, in order to develop specific

knowledge and guide appropriate preventative solutions. Finally, it should be emphasized that the workplace provides access to more than half of the adult population, and therefore offers a unique opportunity for implementing health promotion and employee-assistance programmes. These programmes should represent a target for the cardiologist and specialist in occupational health and community medicine, because of longer life expectancies and a higher number of cardiovascular patients among young persons (50% of infarcted patients are under 60, and young patients represent more than 5% of all cases of infarction). A successful programme requires union and management cooperation, direct employee involvement, voluntary participation, confidentiality of medical records, and adequate allocation of private and public resources. In conclusion, a prevention policy for work-related CVD is based upon three classic areas of intervention: (i) health protectionactivities to reduce exposure to cardiotoxic agents and identify high-risk groups; (ii) health promotioneducating workers to better habits in the workplace and encouraging more healthy life styles (stopping smoking, losing surplus weight, etc.) in order to amplify and consolidate the results of prevention; and (iii) health servicesthe screening and rehabilitation of work-related (or not) CVD through specific programmes. References
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