Address: Division of Respiratory Disease Studies, National Institute of Occupational Safety and Health, 1095 Willowdale Road, Morgantown, WV 26505-2888
Country: United States
Phone: 1 304 285 5714
Fax: 1 304 285 5861
Past position(s): Associate Professor of Medicine, West Virginia University School of Medicine
Education: MD, CM 1973, McGill University
Areas of interest: Airway hyper-responsiveness; occupational asthma
This article is devoted to a discussion of pneumoconioses related to a variety of specific non-fibrous substances; exposures to these dusts are not covered elsewhere in this volume. For each material capable of engendering a pneumoconiosis upon exposure, a brief discussion of the mineralogy and commercial importance is followed by information related to the lung health of exposed workers.
Aluminium is a light metal with many commercial uses in both its metallic and combined states. (Abramson et al. 1989; Kilburn and Warshaw 1992; Kongerud et al. 1994.) Aluminium-containing ores, primarily bauxite and cryolite, consist of combinations of the metal with oxygen, fluorine and iron. Silica contamination of the ores is common. Alumina (Al2O3) is extracted from bauxite, and may be processed for use as an abrasive or as a catalyst. Metallic aluminium is obtained from alumina by electrolytic reduction in the presence of fluoride. Electrolysis of the mixture is carried out by using carbon electrodes at a temperature of about 1,000°C in cells known as pots. The metallic aluminium is then drawn off for casting. Dust, fume and gas exposures in pot rooms, including carbon, alumina, fluorides, sulphur dioxide, carbon monoxide and aromatic hydrocarbons, are accentuated during crust breaking and other maintenance operations. Numerous products are manufactured from aluminium plate, flake, granules and castings—resulting in extensive potential for occupational exposures. Metallic aluminium and its alloys find use in the aircraft, boat and automobile industries, in the manufacture of containers and of electrical and mechanical devices, as well as in a variety of construction and structural applications. Small aluminium particles are used in paints, explosives and incendiary devices. To maintain particle separation, mineral oils or stearin are added; increased lung toxicity of aluminium flakes has been associated with the use of mineral oil.
Inhalation of aluminium-containing dusts and fumes may occur in workers involved in the mining, extraction, processing, fabrication and end-use of aluminium-containing materials. Pulmonary fibrosis, resulting in symptoms and radiographic findings, has been described in workers with several differing exposures to aluminium-containing substances. Shaver’s disease is a severe pneumoconiosis described among workers involved in the manufacture of alumina abrasives. A number of deaths from the condition have been reported. The upper lobes of the lung are most often affected and the occurrence of pneumothorax is a frequent complication. High levels of silicon dioxide have been found in the pot room environment as well as in workers’ lungs at autopsy, suggesting silica as a potential contributor to the clinical picture in Shaver’s disease. High concentrations of aluminium oxide particulate have also been observed. Lung pathology may show blebs and bullae, and pleural thickening is seen occasionally. The fibrosis is diffuse, with areas of inflammation in the lungs and associated lymph nodes.
Aluminium powders are used in making explosives, and there have been a number of reports of a severe and progressive fibrosis in workers involved in this process. Lung involvement has also occasionally been described in workers employed in the welding or polishing of aluminium, and in bagging cat litter containing aluminium silicate (alunite). However, there has been considerable variation in the reporting of lung diseases in relation to exposures to aluminium. Epidemiological studies of workers exposed to aluminium reduction have generally shown low prevalence of pneumoconiotic changes and slight mean reductions in ventilatory lung function. In various work environments, alumina compounds can occur in several forms, and in animal studies these forms appear to have differing lung toxicities. Silica and other mixed dusts may also contribute to this varying toxicity, as may the materials used to coat the aluminium particles. One worker, who developed a granulomatous lung disease after exposure to oxides and metallic aluminium, showed transformation of his blood lymphocytes upon exposure to aluminium salts, suggesting that immunologic factors might play a role.
An asthmatic syndrome has frequently been noted among workers exposed to fumes in aluminium reduction pot rooms. Fluorides found in the pot room environment have been implicated, although the specific agent or agents associated with the asthmatic syndrome has not been determined. As with other occupational asthmas, symptoms are often delayed 4 to 12 hours after exposure, and include cough, dyspnoea, chest tightness and wheeze. An immediate reaction may also be noted. Atopy and a family history of asthma do not appear to be risk factors for development of pot room asthma. After cessation of exposure, symptoms may be expected to disappear in most cases, although two-thirds of the affected workers show persistent non-specific bronchial responsiveness and, in some workers, symptoms and airway hyperresponsiveness continue for years even after exposure is terminated. The prognosis for pot room asthma appears to be best in those who are immediately removed from exposure when the asthmatic symptoms become manifest. Fixed airflow obstruction has also been associated with pot room work.
Carbon electrodes are used in the aluminium reduction process, and known human carcinogens have been identified in the pot room environment. Several mortality studies have revealed lung cancer excesses among exposed workers in this industry.
Deposits of diatomaceous earth result from the accretion of skeletons of microscopic organisms. (Cooper and Jacobson 1977; Checkoway et al. 1993.) Diatomaceous earth may be utilized in foundries and in the maintenance of filters, abrasives, lubricants and explosives. Certain deposits comprise up to 90% free silica. Exposed workers may develop lung changes involving simple or complicated pneumoconiosis. The risk of death from both nonmalignant respiratory diseases and lung cancer has been related to the workers’ tenure in dusty work as well as to cumulative crystalline silica exposures during the mining and processing of diatomaceous earth.
Aside from coal, the two common forms of elemental carbon are graphite (crystalline carbon) and carbon black. (Hanoa 1983; Petsonk et al. 1988.) Graphite is used in the manufacture of lead pencils, foundry linings, paints, electrodes, dry batteries and crucibles for metallurgical purposes. Finely ground graphite has lubricant properties. Carbon black is a partially decomposed form used in automotive tires, pigments, plastics, inks and other products. Carbon black is manufactured from fossil fuels through a variety of processes involving partial combustion and thermal decomposition.
Inhalation of carbon, as well as associated dusts, may occur during the mining and milling of natural graphite, and during the manufacture of artificial graphite. Artificial graphite is produced by the heating of coal or petroleum coke, and generally contains no free silica.
Pneumoconiosis results from worker exposure to both natural and artificial graphite. Clinically, workers with carbon or graphite pneumoconiosis show radiographic findings similar to those for coal workers. Severe symptomatic cases with massive pulmonary fibrosis were reported in the past, particularly related to the manufacture of carbon electrodes for metallurgy, although recent reports emphasize that the materials implicated in exposures leading to this sort of condition are likely to be mixed dusts.
Gilsonite, also known as uintaite, is a solidified hydrocarbon. (Keimig et al. 1987.) It occurs in veins in the western United States. Current uses include the manufacture of automotive body seam sealers, inks, paints and enamels. It is an ingredient of oil-well drilling fluids and cements; it is an additive in sand moulds in the foundry industry; it is to be found as a component of asphalt, building boards and explosives; and it is employed in the production of nuclear grade graphite. Workers exposed to gilsonite dust have reported symptoms of cough and phlegm production. Five of ninety-nine workers surveyed showed radiographic evidence of pneumoconiosis. No abnormalities in pulmonary function have been defined in relation to gilsonite dust exposures.
Gypsum is hydrated calcium sulphate (CaSO4·2H2O) (Oakes et al. 1982). It is used as a component of plasterboard, plaster of Paris and Portland cement. Deposits are found in several forms and are often associated with other minerals such as quartz. Pneumoconiosis has been observed in gypsum miners, and has been attributed to silica contamination. Ventilatory abnormalities have not been associated with gypsum dust exposures.
Oils and Lubricants
Liquids containing hydrocarbon oils are used as coolants, cutting oils and lubricants (Cullen et al. 1981). Vegetable oils are found in some commercial products and in a variety of foodstuffs. These oils may be aerosolized and inhaled when metals that are coated with oils are milled or machined, or if oil-containing sprays are used for purposes of cleaning or lubrication. Environmental measurements in machine shops and mills have documented airborne oil levels up to 9 mg/m3. One report implicated airborne oil exposure from the burning of animal and vegetable fats in an enclosed building.
Workers exposed to these aerosols have occasionally been reported to develop evidence of a lipoid pneumonia, similar to that noted in patients who have aspirated mineral oil nose drops or other oily materials. The condition is associated with symptoms of cough and dyspnoea, inspiratory lung crackles, and impairments in lung function, generally mild in severity. A few cases have been reported with more extensive radiographic changes and severe lung impairments. Exposure to mineral oils has also been associated in several studies with an increased risk of respiratory tract cancers.
Portland cement is made from hydrated calcium silicates, aluminium oxide, magnesium oxide, iron oxide, calcium sulphate, clay, shale and sand (Abrons et al. 1988; Yan et al. 1993). The mixture is crushed and calcined at high temperatures with the addition of gypsum. Cement finds numerous uses in road and building construction.
Silicosis appears to be the greatest risk in cement workers, followed by a mixed dust pneumoconiosis. (In the past, asbestos was added to cement to improve its characteristics.) Abnormal chest radiographic findings, including small rounded and irregular opacities and pleural changes, have been noted. Workers have occasionally been reported to have developed pulmonary alveolar proteinosis after the inhalation of cement dust. Airflow obstructive changes have been noted in some, but not all, surveys of cement workers.
Rare Earth Metals
Rare earth metals or “lanthanides” have atomic numbers between 57 and 71. Lanthanum (atomic number 57), cerium (58), and neodymium (60) are the commonest of the group. The other elements in this group include praseodymium (59), promethium (61), samarium (62), europium (63), gadolinium (64), terbium (65), dysprosium (66), holmium (67), erbium (68), thulium (69), ytterbium (70) and lutetium (71). (Hussain, Dick and Kaplan 1980; Sabbioni, Pietra and Gaglione 1982; Vocaturo, Colombo and Zanoni 1983; Sulotto, Romano and Berra 1986; Waring and Watling 1990; Deng et al. 1991.) The rare earth elements are found naturally in monazite sand, from which they are extracted. They are used in a variety of alloy metals, as abrasives for polishing mirrors and lenses, for high-temperature ceramics, in fireworks and in cigarette lighter flints. In the electronics industry they are used in electrowelding and are to be found in various electronic components, including television phosphors, radiographic screens, lasers, microwave devices, insulators, capacitors and semiconductors.
Carbon arc lamps are used widely in the printing, photoengraving and lithography industries and were used for floodlighting, spotlighting and movie projection before the wide-scale adoption of argon and xenon lamps. The rare earth metal oxides were incorporated into the central core of carbon arc rods, where they stabilize the arc stream. Fumes which are emitted from the lamps are a mixture of gaseous and particulate material composed of approximately 65% rare earth oxides, 10% fluorides and unburnt carbon and impurities.
Pneumoconiosis in workers exposed to rare earths has been exhibited primarily as bilateral nodular chest radiographic infiltrates. Lung pathology in cases of rare earth pneumoconiosis has been described as an interstitial fibrosis accompanied by an accumulation of fine granular dust particles, or granulomatous changes.
Variable pulmonary function impairments have been described, from restrictive to mixed restrictive-obstructive. However, the spectrum of pulmonary disease related to inhalation of rare earth elements is still to be defined, and data regarding the pattern and progression of disease and histological changes is available primarily only from a few case reports.
A neoplastic potential of the rare earth isotopes has been suggested by a case report of lung cancer, possibly related to ionizing radiation from the naturally occurring rare earth radioisotopes.
Sedimentary rock deposits form through the processes of physical and chemical weathering, erosion, transport, deposition and diagenesis. These may be characterized into two broad classes: Clastics, which include mechanically deposited erosion debris, and chemical precipitates, which include carbonates, shells of organic skeletons and saline deposits. Sedimentary carbonates, sulphates and halides provide relatively pure minerals that have crystallized from concentrated solutions. Due to the high solubility of many of the sedimentary compounds, they are rapidly cleared from the lungs and are generally associated with little pulmonary pathology. In contrast, workers exposed to certain sedimentary compounds, primarily clastics, have shown pneumoconiotic changes.
Phosphate ore, Ca5(F,Cl)(PO4)3, is used in the production of fertilizers, dietary supplements, toothpaste, preservatives, detergents, pesticides, rodent poisons and ammunitions (Dutton et al. 1993). Extraction and processing of the ore may result in a variety of irritant exposures. Surveys of workers in phosphate mining and extraction have documented increased symptoms of cough and phlegm production, as well as radiographic evidence of pneumoconiosis, but little evidence of abnormal lung function.
Shale is a mixture of organic material composed mainly of carbon, hydrogen, oxygen, sulphur and nitrogen (Rom, Lee and Craft 1981; Seaton et al. 1981). The mineral component (kerogen) is found in the sedimentary rock called marlstone, which is of a grey-brown colour and a layered consistency. Oil shale has been used as an energy source since the 1850s in Scotland. Major deposits exist in the United States, Scotland and Estonia. Dust in the atmosphere of underground oil shale mines is of relatively fine dispersion, with up to 80% of the dust particles under 2 mm in size.
Pneumoconiosis related to the deposition of shale dust in the lung is termed shalosis. The dust creates a granulomatous and fibrotic reaction in the lungs. This pneumoconiosis is similar clinically to coal workers’ pneumoconiosis and silicosis, and may progress to massive fibrosis even after the worker has left the industry.
Pathologic changes identified in lungs with shalosis are characterized by vascular and bronchial deformation, with irregular thickening of interalveolar and interlobular septa. In addition to interstitial fibrosis, lung specimens with shale pneumoconiosis have shown enlarged hilar shadows, related to the transport of shale dust and subsequent development of well-defined sclerotic changes in the hilar lymph nodes.
Shale workers have been found to have a prevalence of chronic bronchitis two and one-half times that of age-matched controls. The effect of shale dust exposures on lung function has not been studied systematically.
Slate is a metamorphic rock, made up of various minerals, clays and carbonaceous matter (McDermott et al. 1978). The major constituents of slate include muscovite, chlorite, calcite and quartz, along with graphite, magnetite and rutile. These have undergone metamorphosis to form a dense crystalline rock that possesses strength but is easily cleaved, characteristics which account for its economic importance. Slate is used in roofing, dimension stone, floor tile, flagging, structural shapes such as panels and window sills, blackboards, pencils, billiard tables and laboratory bench tops. Crushed slate is used in highway construction, tennis court surfaces and lightweight roofing granules.
Pneumoconiosis has been found in a third of workers studied in the slate industry in North Wales, and in 54% of slate pencil makers in India. Various lung radiographic changes have been identified in slateworkers. Because of the high quartz content of some slates and the adjacent rock strata, slateworkers’ pneumoconiosis may have features of silicosis. The prevalence of respiratory symptoms in slateworkers is high, and the proportion of workers with symptoms increases with pneumoconiosis category, irrespective of smoking status. Diminished values of forced expiratory volume in one second (FEV1) and forced vital capacity (FVC) are associated with increasing pneumoconiosis category.
The lungs of miners exposed to slate dust reveal localized areas of perivascular and peribronchial fibrosis, extending to macule formation and extensive interstitial fibrosis. Typical lesions are fibrotic macules of variable configuration intimately associated with small pulmonary blood vessels.
Talc is composed of magnesium silicates, and is found in a variety of forms. (Vallyathan and Craighead 1981; Wegman et al. 1982; Stille and Tabershaw 1982; Wergeland, Andersen and Baerheim 1990; Gibbs, Pooley and Griffith 1992.)
Deposits of talc are frequently contaminated with other minerals, including both fibrous and non-fibrous tremolite and quartz. Lung health effects of talc-exposed workers may be related to both the talc itself as well as the other associated minerals.
Talc production occurs primarily in Australia, Austria, China, France and the United States. Talc is used as a component in hundreds of products, and is used in the manufacture of paint, pharmaceuticals, cosmetics, ceramics, automobile tires and paper.
Diffuse rounded and irregular parenchymal lung opacities and pleural abnormalities are seen on the chest radiographs of talc workers in association with the talc exposure. Depending on the specific exposures experienced, the radiographic shadows may be ascribed to talc itself or to contaminants in the talc. Talc exposure has been associated with symptoms of cough, dyspnoea and phlegm production, and with evidence of airflow obstruction in pulmonary function studies. Lung pathology has revealed various forms of pulmonary fibrosis: granulomatous changes and ferruginous bodies have been reported, and dust-laden macrophages collected around the respiratory bronchioles intermingled with bundles of collagen. Mineralogical examination of lung tissue from talc workers is also variable and may show silica, mica or mixed silicates.
Since talc deposits may be associated with asbestos and other fibres, it is not surprising that an increased risk of bronchogenic carcinoma has been reported in talc miners and millers. Recent investigations of workers exposed to talc without associated asbestos fibres revealed trends for higher mortality from non-malignant respiratory disease (silicosis, silico-tuberculosis, emphysema and pneumonia), but the risk for bronchogenic cancer was not found to be elevated.
Exposure to hairsprays occurs in the home environment as well as in commercial hairdressing establishments (Rom 1992b). Environmental measurements in beauty salons have indicated the potential for respirable aerosol exposures. Several case reports have implicated hairspray exposure in the occurrence of a pneumonitis, thesaurosis, in heavily exposed individuals. Clinical symptoms in the cases were generally mild, and resolved with termination of exposure. Histology usually showed a granulomatous process in the lung and enlarged hilar lymph nodes, with thickening of alveolar walls and numerous granular macrophages in the airspaces. Macromolecules in hairsprays, including shellacs and polyvinylpyrrolidone, have been suggested as potential agents. In contrast to the clinical case reports, increased lung parenchymal radiographic shadows observed in radiological surveys of commercial hairdressers have not been conclusively related to hairspray exposure. Although the results of these studies do not allow definitive conclusions to be drawn, clinically important lung disease from typical hairspray exposures does appear to be an unusual occurrence.
Coal miners are subject to a number of lung diseases and disorders arising from their exposure to coal mine dust. These include pneumoconiosis, chronic bronchitis and obstructive lung disease. The occurrence and severity of disease depends on the intensity and duration of dust exposure. The specific composition of the coal mine dust also has a bearing on some health outcomes.
In the developed countries, where high prevalences of lung disease existed in the past, reductions in dust levels brought about by regulation have led to substantial drops in disease prevalence since the 1970s. In addition, major reductions in the mining work force in most of those countries over recent decades, partly brought about by changes in technology and resulting improvements in productivity, will result in further reductions in overall disease levels. Miners in other countries, where coal mining is a more recent phenomenon and dust controls are less aggressive, have not been so fortunate. This problem is exacerbated by the high cost of modern mining technology, forcing the employment of large numbers of workers, many of whom are at high risk of disease development.
In the following text, each disease or disorder is considered in turn. Those specific to coal mining, such as coal workers’ pneumoconiosis are described in detail; the description of others, such as obstructive lung disease, is restricted to those aspects that relate to coal miners and dust exposure.
Coal Workers’ Pneumoconiosis
Coal workers’ pneumoconiosis (CWP) is the disease most commonly associated with coal mining. It is not a fast-developing disease, usually taking at least ten years to be manifested, and often much longer when exposures are low. In its initial stages it is an indicator of excessive lung dust retention, and may be associated with few symptoms or signs in itself. However, as it advances, it puts the miner at increasing risk of development of the much more serious progressive massive fibrosis (PMF).
The classic lesion of CWP is the coal macule, a collection of dust and dust-laden macrophages around the periphery of the respiratory bronchioles. The macules contain minimal collagen and are thus usually not palpable. They are about 1 to 5 mm in size, and are frequently accompanied by an enlargement of the adjacent air spaces, termed focal emphysema. Though often very numerous, they are not usually evident on a chest radiograph.
Another lesion associated with CWP is the coal nodule. These larger lesions are palpable and contain a mixture of dust-laden macrophages, collagen and reticulin. The presence of coal nodules, with or without silicotic nodules (see below), indicates lung fibrosis, and is largely responsible for the opacities seen on chest radiographs. Macronodules (7 to 20 mm) in size may coalesce to form progressive massive fibrosis (see below), or PMF may develop from a single macronodule.
Silicotic nodules (described under silicosis) have been found in a significant minority of underground coal miners. For most, the cause may rest simply with the silica present in the coal dust, although exposure to pure silica in some jobs is certainly an important factor (e.g., among surface drillers, underground motormen and roof bolters).
The most useful indicator of CWP in miners during life is obtained using the routine chest radiograph. Dust deposits and the nodular tissue reactions attenuate the x-ray beam and result in opacities on the film. The profusion of these opacities can be assessed systematically by using a standardized method of radiograph description such as that disseminated by the ILO and described else in this chapter. In this method, individual posterior-anterior films are compared to standard radiographs showing increasing profusion of small opacities, and the film classified into one of four major categories (0, 1, 2, 3) based on its similarity to the standard. A secondary classification is also made, depending on the reader’s assessment of the film’s similarity to adjacent ILO categories. Other aspects of the opacities, such as size, shape and region of occurrence in the lung are also noted. Some countries, such as China and Japan, have developed similar systems for systematic radiograph description or interpretation that are particularly suited to their own needs.
Traditionally, small rounded types of opacity have been associated with coal mining. However, more recent data indicate that irregular types can also result from exposure to coal mine dust. The opacities of CWP and silicosis are often indistinguishable on the radiograph. However, there is some evidence that larger sized opacities (type r) more often indicate silicosis.
It is important to note that a substantial amount of pathologic abnormality related to pneumoconiosis may be present in the lung before it can be detected on the routine chest x ray. This is particularly true for macular deposition, but it becomes progressively less true with greater profusion and size of nodules. Concomitant emphysema may also reduce the visibility of lesions on the chest x ray. Computerized tomography (CT)—particularly high-resolution computerized tomography (HRCT)—may permit visualization of abnormalities not clearly evident on routine chest x rays, although CT is not necessary for routine clinical diagnosis of miners’ lung diseases and is not indicated for medical surveillance of miners.
The development of CWP, although a marker of excessive lung dust retention, in itself is often unaccompanied by any overt clinical signs. This should not, however, be taken to imply that the inhalation of coal mine dust is without risk, for it is now well known that other lung diseases can arise from dust exposure. Pulmonary hypertension is more often noted in miners who develop airflow obstruction in association with CWP. Moreover, once CWP has developed, it usually progresses unless dust exposure ceases, and may progress thereafter. It also puts the miner at greatly increased risk of development of the clinically ominous PMF, with the likelihood of subsequent impairment, disability and premature mortality.
Development of the earliest change of CWP, the dust macule, represents the effects of dust deposition and accumulation. The subsequent stage, that is, the development of nodules, results from the lung’s inflammatory and fibrotic reaction to the dust. In this, the roles of silica and non-silica dust have long been debated. On the one hand, silica dust is known to be considerably more toxic than coal dust. Yet, on the other hand, epidemiological studies have shown no strong evidence implicating silica exposure in CWP prevalence or incidence. Indeed, it seems that almost an inverse relationship exists, in that disease levels tend to be elevated where silica levels are lower (e.g., in areas where anthracite is mined). Recently, some understanding of this paradox has been gained through studies of particle characteristics. These studies indicate that not only the quantity of silica present in the dust (as measured conventionally using infrared spectrometry or x-ray diffraction), but also the bioavailability of the surface of the silica particles may be related to toxicity. For example, clay coating (occlusion) may play an important modifying role. Another important factor under current investigation concerns surface charge in the form of free radicals and the effects of “freshly fractured” versus “aged” silica-containing dusts.
Surveillance and epidemiology
The prevalence of CWP among underground miners varies with the kind of job, tenure and age. A recent study of US coal miners revealed that from 1970 to 1972 about 25 to 40% of working coal miners had category 1 or greater small rounded opacities after 30 or more years in mining. This prevalence reflects exposure to levels of 6 mg/m3 or more of respirable dust among coal face workers prior to that time. The introduction of a dust limit of 3 mg/m3 in 1969, with a reduction to 2 mg/m3 in 1972 has led to a decline in disease prevalence to about half of the former levels. Declines related to dust control have been noted elsewhere, for example, in the United Kingdom and Australia. Unfortunately, these gains have been counterbalanced by temporal increases in prevalence elsewhere.
An exposure-response relationship for prevalence or incidence of CWP and dust exposure has been demonstrated in a number of studies. These have shown that the primary significant dust exposure variable is exposure to mixed mine dust. Intensive studies by British researchers failed to disclose any major influence of silica exposure, as long as the percentage of silica was less than about 5%. Coal rank (percentage carbon) is another important predictor of CWP development. Studies in the United States, the United Kingdom, Germany and elsewhere have given clear indications that the prevalence and incidence of CWP increases markedly with coal rank, these being substantially greater where anthracite (high rank) coal is mined. No other environmental variables have been found to exert any major effects on CWP development. Miner age appears to have some bearing on disease development, since older miners appear to be at increased risk. However, it is not entirely clear whether this implies that older miners are more susceptible, whether it is a residence time effect, or is simply an artefact (the age effect might reflect underestimation of exposure estimates for older miners, for example). Cigarette smoking does not appear to increase the risk of CWP development.
Research in which miners were followed-up with chest radiographs every five years shows that the risk of developing PMF over the five years is clearly related to the category of CWP as revealed on the initial chest x ray. Since the risk at category 2 is much greater than that at category 1, conventional wisdom at one time was that miners should be prevented from reaching category 2 if at all possible. However, in most mines there are usually many more miners with category 1 CWP compared to category 2. Thus, the lower risk for category 1 compared to category 2 is offset somewhat by the larger numbers of miners with category 1. On this showing, it has become clear that all pneumoconiosis should be prevented.
Miners as a group have been observed to have increased risk of death from non-malignant respiratory diseases, and there is evidence that the mortality among miners with CWP is somewhat increased over those of similar age without the disease. However, the effect is smaller than the excess seen for miners with PMF (see below).
The only protection against CWP is minimization of dust exposure. If possible, this should be achieved by dust suppression methods, such as ventilation and water sprays, rather than by respirator use or administrative controls, for example, worker rotation. In this respect, there is now good evidence that regulatory actions in some countries to reduce the level of dust, taken around the 1970s, has resulted in greatly reduced levels of disease. Transfer of workers with early signs of CWP to less dusty jobs is a prudent action, although there is little practical evidence that such programmes have succeeded in preventing disease progression. For this reason, dust suppression must remain the primary method of disease prevention.
Ongoing, aggressive monitoring of dust exposure and the conscious exertion of control efforts can be supplemented by health screening surveillance of miners. If miners are found to develop dust-related diseases, efforts at exposure control should be intensified throughout the workplace and miners with dust effects should be offered work in low-dust areas of the mine environment.
Although several forms of treatment have been tried, including aluminium powder inhalation, and the administration of tetrandine, no treatment is known that effectively reverses or slows the fibrotic process in the lung. Currently, primarily in China, but elsewhere also, whole-lung lavage is being tried with the intent of reducing the total lung dust burden. Although the procedure can result in the removal of a considerable amount of dust, its risks, benefits and role in the management of miners’ health are unclear.
In other respects, treatment should be directed towards preventing complications, maximizing the miners’ functional status and alleviating their symptoms, whether due to CWP or to other, concomitant respiratory diseases. In general, miners who develop dust-induced lung diseases should evaluate their current dust exposures and utilize the resources of government and labour organizations to find the avenues available to reduce all adverse respiratory exposures. For miners who smoke, smoking cessation is an initial step in personal exposure management. Prevention of infectious complications of chronic lung disease with available pneumococcal and yearly influenza vaccines is suggested. Early investigation of symptoms of lung infection, with particular attention to mycobacterial disease, is also recommended. The treatments for acute bronchitis, bronchospasm and congestive heart failure among miners are similar to those for patients without dust-related disease.
Progressive Massive Fibrosis
PMF, sometimes referred to as complicated pneumoconiosis, is diagnosed when one or more large fibrotic lesions (whose definition depends on the mode of detection) are present in one or both lungs. As its name implies, PMF often becomes more severe over time, even in the absence of additional dust exposure. It can also develop after dust exposure has ceased, and may often cause disability and premature mortality.
PMF lesions may be unilateral or bilateral, and are most often found in the upper or middle lobes of the lung. The lesions are formed of collagen, reticulin, coal mine dust and dust-laden macrophages, while the centre may contain a black liquid which cavitates on occasion. US pathology standards require the lesions to be 2 cm in size or larger to be identified as PMF entities in surgical or autopsy specimens.
Large opacities >>1 cm) on the radiograph, coupled with a history of extensive coal mine dust exposure, are taken to imply the presence of PMF. However, it is important that other diseases such as lung cancer, tuberculosis and granulomas be considered. Large opacities are usually seen on a background of small opacities, but development of PMF from a category 0 profusion has been noted over a five-year period.
Diagnostic possibilities for each individual miner with large chest opacities must be appropriately evaluated. Clinically stable miners with bilateral lesions in the typical upper-lung distribution and with pre-existing simple CWP may present little diagnostic challenge. However, miners with progressive symptoms, risk factors for other disorders (e.g., tuberculosis), or atypical clinical features should undergo a thorough appropriate examination before the diagnostician attributes the lesions to PMF.
Dyspnoea and other respiratory symptoms often accompany PMF, but may not necessarily be due to the disease itself. Congestive heart failure (due to pulmonary hypertension and cor pulmonale) is a not infrequent complication.
Despite extensive research, the actual cause of PMF development remains unclear. Over the years, various hypotheses have been proposed, but none is fully satisfactory. One prominent theory was that tuberculosis played a role. Indeed, tuberculosis is often present in miners with PMF, particularly in the developing countries. However, PMF has been found to develop in miners in whom there was no sign of tuberculosis, and tuberculin reactivity has not been found to be elevated in miners with pneumoconiosis. Despite investigation, consistent evidence of the role of the immune system in PMF development is lacking.
Surveillance and epidemiology
As with CWP, PMF levels have been declining in countries which have strict dust control regulations and programmes. A recent study of US miners revealed that about 2% of coal miners working underground had PMF after 30 or more years in mining (although this figure may have been biased by affected miners leaving the work force).
Exposure-response investigations of PMF have shown that exposure to coal mine dust, category of CWP, coal rank and age are the primary determinants of disease development. As with CWP, epidemiological studies have found no major effect of silica dust. Although it was thought at one time that PMF developed only on a background of the small opacities of CWP, recently this has been found not to be the case. Miners with an initial chest x ray showing category 0 CWP have been shown to develop PMF over five years, with the risk increasing with their cumulative dust exposure. Also, miners may develop PMF after cessation of dust exposure.
PMF leads to premature mortality, the prognosis worsening with increasing stage of the disease. A recent study showed that miners with category C PMF had only one-fourth the rate of survival over 22 years compared to miners with no pneumoconiosis. This effect was manifested over all age groups.
Avoidance of dust exposure is the only way to prevent PMF. Since the risk of its development increases sharply with increasing category of simple CWP, a strategy for secondary prevention of PMF is for miners to undergo periodic chest x rays and to terminate or reduce their exposure if simple CWP is detected. Although this approach appears valid and has been adopted in certain jurisdictions, its effectiveness has not been evaluated systematically.
There is no known treatment for PMF. Medical care should be organized around ameliorating the condition and associated lung illnesses, while protecting against infectious complications. Although maintaining functional stability may be more difficult in patients with PMF, in other respects, management is similar to simple CWP.
Obstructive Lung Disease
There is now consistent and convincing evidence of a relationship between lung function loss and dust exposure. Various studies in different countries have looked at the influence of dust exposure on absolute values of, and temporal changes in, measurements of ventilatory function, such as forced expiratory volume in one second (FEV1), forced vital capacity (FVC) and flow rates. All have found evidence that dust exposure leads to a reduction in lung function, and the results have been strikingly similar for several recent British and US investigations. These indicate that over the course of a year, dust exposure at the coal face brings about, on average, a reduction in lung function equivalent to smoking half a pack of cigarettes each day. The studies also demonstrate that effects vary, and a given miner may develop effects equal to, or worse than, those expected from cigarette smoking, particularly if the individual has experienced higher dust exposures.
The effects of dust exposure have been found in both those who have never smoked and in current smokers. Moreover, there is no evidence that smoking exacerbates the dust exposure effect. Rather, studies have generally shown a slightly smaller effect in current smokers, a result that may be due to healthy worker selection. It is important to note that the relationship between dust exposure and ventilatory decline appears to exist independently of pneumoconiosis. That is, it is not a requirement that pneumoconiosis be present for there to be reduced lung function. To the contrary, it appears rather that the inhaled dust can act along multiple pathways, leading to pneumoconiosis in some miners, to obstruction in others and to multiple outcomes in yet others. In contrast to miners with CWP alone, miners with respiratory symptoms have significantly lower lung function, after standardization for age, smoking, dust exposure and other factors.
Recent work on ventilatory function changes has involved the exploration of longitudinal changes. The results indicate that there may be a non-linear trend of decline over time in new miners, a high initial rate of loss being followed by a more moderate decline with continued exposure. Furthermore, there is evidence that miners who react to the dust may choose, if possible, to remove themselves from the heavier exposures.
Respiratory symptoms, such as chronic cough and phlegm production, are a frequent consequence of work in coal mining, most studies showing an excess prevalence compared to non-exposed control groups. Moreover, the prevalence and incidence of respiratory symptoms has been shown to increase with cumulative dust exposure, after taking into account age and smoking. The presence of symptoms appears to be associated with a reduction in lung function over and above that due to dust exposure and other putative causes. This suggests that dust exposure may be instrumental in initiating certain disease processes that then progress regardless of further exposure. A relationship between bronchial gland size and dust exposure has been demonstrated pathologically, and it has been found that mortality from bronchitis and emphysema increases with increasing cumulative dust exposure.
Pathological studies have repeatedly found an excess of emphysema in coal miners compared to control groups. Moreover, the degree of emphysema has been found to be related both to the amount of dust in the lungs and to pathological assessments of pneumoconiosis. Furthermore, it is important to recognize that there is evidence that the presence of emphysema is related to dust exposure and to the percentage of predicted FEV1. Hence, these results are consistent with the view that dust exposure can lead to disability through causing emphysema.
The form of emphysema most clearly associated with coal mining is focal emphysema. This consists of zones of enlarged air spaces, 1 to 2 mm in size, adjacent to dust macules surrounding the respiratory bronchioles. The current thinking is that the emphysema is formed from tissue destruction, rather than from distension or dilation. Apart from focal emphysema, there is evidence that centriacinar emphysema has an occupational origin, and that total emphysema, (i.e., the extent of all types) is correlated with tenure in mining, in those who have never smoked as well as in smokers. There is no evidence that smoking potentiates the dust exposure/emphysema relationship. However, there are indications of an inverse relationship between the silica content of lungs and the presence of emphysema.
The issue of emphysema has long been controversial, with some stating that selection bias and smoking make interpretation of pathological studies difficult. In addition, some consider that focal emphysema has only trivial effects on lung function. However, pathological studies undertaken since the 1980s have been responsive to earlier criticisms, and indicate that the effect of dust exposure may be more significant for miners’ health than previously thought. This point of view is supported by recent findings that mortality from bronchitis and emphysema is related to cumulative dust exposure.
Silicosis, though associated more with industries other than coal mining, can occur in coal miners. In underground mines, it is found most frequently in workers in certain jobs where exposure to pure silica typically occurs. Such workers include roof bolters, who drill into the ceiling rock, which can often be sandstone or other rock with high silica content; motormen, drivers of rail transport who are exposed to the dust generated by sand placed on the tracks to lend traction; and rock drillers, who are involved in mine development. Rock drillers at surface coal mines have been shown to be at particular risk in the United States, with some developing acute silicosis after only a few years of exposure. Based on pathological evidence, as noted below, some degree of silicosis may afflict many more coal miners than just those working the jobs noted above.
Silicotic nodules in coal miners are similar in nature to those observed elsewhere, and consist of a whorled pattern of collagen and reticulin. One large autopsy study has revealed that about 13% of coal miners had silicotic nodules in their lungs. Although one job, (that of motorman) was notable for having a much higher prevalence of silicotic nodules (25%), there was little variation in the prevalence among miners in other jobs, suggesting that the silica in the mixed mine dust was responsible.
Silicosis cannot be reliably differentiated from coal workers’ pneumoconiosis on a radiograph. However, there is some evidence that the larger type of small opacities (type r) are indicative of silicosis.
Rheumatoid pneumoconiosis, one variant of which is called Caplan’s syndrome, is the term used for a condition affecting dust-exposed workers who develop multiple large radiographic shadows. Pathologically, these lesions resemble rheumatoid nodules rather than PMF lesions, and often arise over a short time interval. Active arthritis or the presence of circulating rheumatoid factor are generally found, but occasionally are absent.
Included in the occupational exposures suffered by coal miners are a number of substances that are potential carcinogens. Some of these are silica and benzo(a)pyrenes. Yet, there is no clear evidence of an excess of deaths from lung cancer in coal miners. One obvious explanation for this is that coal miners are forbidden to smoke underground because of the danger of fires and explosions. However, the fact that no exposure-response relationship between lung cancer and dust exposure has been detected suggests that coal mine dust is not a major cause of lung cancer in the industry.
Regulatory Limits on Dust Exposure
The World Health Organization (WHO) has recommended a “tentative health-based exposure limit” for respirable coal mine dust (with less than 6% respirable quartz) ranging from 0.5 to 4 mg/m3. WHO suggests a 2 in 1,000 risk of PMF over a working lifetime as a criterion, and recommends that mine-based environmental factors, including coal rank, percentage of quartz and particle size should be taken into account when setting limits.
Currently, among the major coal-producing countries, limits are based on regulating coal dust alone (e.g., 3.8 mg/m3 in the United Kingdom, 5 mg/m3 in Australia and Canada) or on regulating a mixture of coal and silica as in the United States (2 mg/m3 when the per cent quartz is 5 or less, or (10 mg/m3)/per cent SiO2), or in Germany (4 mg/m3 when the per cent quartz is 5 or less, or 0.15 mg/m3 otherwise), or on regulating pure quartz (e.g., Poland, with a 0.05 mg/m3 limit).
Asthma is a respiratory disease characterized by airway obstruction that is partially or completely reversible, either spontaneously or with treatment; airway inflammation; and increased airway responsiveness to a variety of stimuli (NAEP 1991). Occupational asthma (OA) is asthma that is caused by environmental exposures in the workplace. Several hundred agents have been reported to cause OA. Pre-existing asthma or airway hyper-responsiveness, with symptoms worsened by work exposure to irritants or physical stimuli, is usually classified separately as work-aggravated asthma (WAA). There is general agreement that OA has become the most prevalent occupational lung disease in developed countries, although estimates of actual prevalence and incidence are quite variable. It is clear, however, that in many countries asthma of occupational aetiology causes a largely unrecognized burden of disease and disability with high economic and non-economic costs. Much of this public health and economic burden is potentially preventable by identifying and controlling or eliminating the workplace exposures causing the asthma. This article will summarize current approaches to recognition, management and prevention of OA. Several recent publications discuss these issues in more detail (Chan-Yeung 1995; Bernstein et al. 1993).
Magnitude of the Problem
Prevalences of asthma in adults generally range from 3 to 5%, depending on the definition of asthma and geographic variations, and may be considerably higher in some low-income urban populations. The proportion of adult asthma cases in the general population that is related to the work environment is reported to range from 2 to 23%, with recent estimates tending towards the higher end of the range. Prevalences of asthma and OA have been estimated in small cohort and cross-sectional studies of high-risk occupational groups. In a review of 22 selected studies of workplaces with exposures to specific substances, prevalences of asthma or OA, defined in various ways, ranged from 3 to 54%, with 12 studies reporting prevalences over 15% (Becklake, in Bernstein et al. 1993). The wide range reflects real variation in actual prevalence (due to different types and levels of exposure). It also reflects differences in diagnostic criteria, and variation in the strength of the biases, such as “survivor bias” which may result from exclusion of workers who developed OA and left the workplace before the study was conducted. Population estimates of incidence range from 14 per million employed adults per year in the United States to 140 per million employed adults per year in Finland (Meredith and Nordman 1996). Ascertainment of cases was more complete and methods of diagnosis were generally more rigorous in Finland. The evidence from these different sources is consistent in its implication that OA is often under-diagnosed and/or under-reported and is a public health problem of greater magnitude than generally recognized.
Causes of Occupational Asthma
Over 200 agents (specific substances, occupations or industrial processes) have been reported to cause OA, based on epidemiological and/or clinical evidence. In OA, airway inflammation and bronchoconstriction can be caused by immunological response to sensitizing agents, by direct irritant effects, or by other non-immunological mechanisms. Some agents (e.g., organophosphate insecticides) may also cause bronchoconstriction by direct pharmacological action. Most of the reported agents are thought to induce a sensitization response. Respiratory irritants often worsen symptoms in workers with pre-existing asthma (i.e., WAA) and, at high exposure levels, can cause new onset of asthma (termed reactive airways dysfunction syndrome (RADS) or irritant-induced asthma) (Brooks, Weiss and Bernstein 1985; Alberts and Do Pico 1996).
OA may occur with or without a latency period. Latency period refers to the time between initial exposure and development of symptoms, and is highly variable. It is often less than 2 years, but in around 20% of cases is 10 years or longer. OA with latency is generally caused by sensitization to one or more agents. RADS is an example of OA without latency.
High molecular weight sensitizing agents (5,000 daltons (Da) or greater) often act by an IgE-dependent mechanism. Low molecular weight sensitizing agents (less than 5,000 Da), which include highly reactive chemicals like isocyanates, may act by IgE-independent mechanisms or may act as haptens, combining with body proteins. Once a worker becomes sensitized to an agent, re-exposure (frequently at levels far below the level that caused sensitization) results in an inflammatory response in the airways, often accompanied by increases in airflow limitation and non-specific bronchial responsiveness (NBR).
In epidemiological studies of OA, workplace exposures are consistently the strongest determinants of asthma prevalence, and the risk of developing OA with latency tends to increase with estimated intensity of exposure. Atopy is an important and smoking a somewhat less consistent determinant of asthma occurrence in studies of agents that act through an IgE-dependent mechanism. Neither atopy nor smoking appears to be an important determinant of asthma in studies of agents acting through IgE-independent mechanisms.
The symptom spectrum of OA is similar to non-occupational asthma: wheeze, cough, chest tightness and shortness of breath. Patients sometimes present cough-variant or nocturnal asthma. OA can be severe and disabling, and deaths have been reported. Onset of OA occurs due to a specific job environment, so identifying exposures that occurred at the time of onset of asthmatic symptoms is key to an accurate diagnosis. In WAA, workplace exposures cause a significant increase in frequency and/or severity of symptoms of pre-existing asthma.
Several features of the clinical history may suggest occupational aetiology (Chan-Yeung 1995). Symptoms frequently worsen at work or at night after work, improve on days off, and recur on return to work. Symptoms may worsen progressively towards the end of the workweek. The patient may note specific activities or agents in the workplace that reproducibly trigger symptoms. Work-related eye irritation or rhinitis may be associated with asthmatic symptoms. These typical symptom patterns may be present only in the initial stages of OA. Partial or complete resolution on weekends or vacations is common early in the course of OA, but with repeated exposures, the time required for recovery may increase to one or two weeks, or recovery may cease to occur. The majority of patients with OA whose exposures are terminated continue to have symptomatic asthma even years after cessation of exposure, with permanent impairment and disability. Continuing exposure is associated with further worsening of asthma. Brief duration and mild severity of symptoms at the time of cessation of exposure are good prognostic factors and decrease the likelihood of permanent asthma.
Several characteristic temporal patterns of symptoms have been reported for OA. Early asthmatic reactions typically occur shortly (less than one hour) after beginning work or the specific work exposure causing the asthma. Late asthmatic reactions begin 4 to 6 hours after exposure begins, and can last 24 to 48 hours. Combinations of these patterns occur as dual asthmatic reactions with spontaneous resolution of symptoms separating an early and late reaction, or as continuous asthmatic reactions with no resolution of symptoms between phases. With exceptions, early reactions tend to be IgE mediated, and late reactions tend to be IgE independent.
Increased NBR, generally measured by methacholine or histamine challenge, is considered a cardinal feature of occupational asthma. The time course and degree of NBR may be useful in diagnosis and monitoring. NBR may decrease within several weeks after cessation of exposure, although abnormal NBR commonly persists for months or years after exposures are terminated. In individuals with irritant-induced occupational asthma, NBR is not expected to vary with exposure and/or symptoms.
Recognition and Diagnosis
Accurate diagnosis of OA is important, given the substantial negative consequences of either under- or over-diagnosis. In workers with OA or at risk of developing OA, timely recognition, identification and control of the occupational exposures causing the asthma improve the chances of prevention or complete recovery. This primary prevention can greatly reduce the high financial and human costs of chronic, disabling asthma. Conversely, since a diagnosis of OA may obligate a complete change of occupation, or costly interventions in the workplace, accurately distinguishing OA from asthma that is not occupational can prevent unnecessary social and financial costs to both employers and workers.
Several case definitions of OA have been proposed, appropriate in different circumstances. Definitions found valuable for worker screening or surveillance (Hoffman et al. 1990) may not be entirely applicable for clinical purposes or compensation. A consensus of researchers has defined OA as “a disease characterized by variable airflow limitation and/or airway hyper-responsiveness due to causes and conditions attributable to a particular occupational environment and not to stimuli encountered outside the workplace” (Bernstein et al. 1993). This definition has been operationalized as a medical case definition, summarized in table 1 (Chan-Yeung 1995).
Table 1. ACCP medical case definition of occupational asthma
Criteria for diagnosis of occupational asthma1 (requires all 4, A-D):
(A) Physician diagnosis of asthma and/or physiological evidence of airways hyper-responsiveness
(B) Occupational exposure preceded onset of asthmatic symptoms1
(C) Association between symptoms of asthma and work
(D) Exposure and/or physiological evidence of relation of asthma to workplace environment (Diagnosis of OA requires one or more of D2-D5, likely OA requires only D1)
(1) Workplace exposure to agent reported to give rise to OA
(2) Work-related changes in FEV1 and/or PEF
(3) Work-related changes in serial testing for non-specific bronchial responsiveness (e.g., Methacholine Challenge Test)
(4) Positive specific bronchial challenge test
(5) Onset of asthma with a clear association with a symptomatic exposure to an inhaled irritant in the workplace (generally RADS)
Criteria for diagnosis of RADS (should meet all 7):
(1) Documented absence of preexisting asthma-like complaints
(2) Onset of symptoms after a single exposure incident or accident
(3) Exposure to a gas, smoke, fume, vapour or dust with irritant properties present in high concentration
(4) Onset of symptoms within 24 hours after exposure with persistence of symptoms for at least 3 months
(5) Symptoms consistent with asthma: cough, wheeze, dyspnoea
(6) Presence of airflow obstruction on pulmonary function tests and/or presence of non-specific bronchial hyper-responsiveness (testing should be done shortly after exposure)
(7) Other pulmonary diseases ruled out
Criteria for diagnosis of work-aggravated asthma (WAA):
(1) Meets criteria A and C of ACCP Medical Case Definition of OA
(2) Pre-existing asthma or history of asthmatic symptoms, (with active symptoms during the year prior to start of employment or exposure of interest)
(3) Clear increase in symptoms or medication requirement, or documentation of work-related changes in PEFR or FEV1 after start of employment or exposure of interest
1 A case definition requiring A, C and any one of D1 to D5 may be useful in surveillance for OA, WAA and RADS.
Source: Chan-Yeung 1995.
Thorough clinical evaluation of OA can be time consuming, costly and difficult. It may require diagnostic trials of removal from and return to work, and often requires the patient to reliably chart serial peak expiratory flow (PEF) measurements. Some components of the clinical evaluation (e.g., specific bronchial challenge or serial quantitative testing for NBR) may not be readily available to many physicians. Other components may simply not be achievable (e.g., patient no longer working, diagnostic resources not available, inadequate serial PEF measurements). Diagnostic accuracy is likely to increase with the thoroughness of the clinical evaluation. In each individual patient, decisions on the extent of medical evaluation will need to balance costs of the evaluation with the clinical, social, financial and public health consequences of incorrectly diagnosing or ruling out OA.
In consideration of these difficulties, a stepped approach to diagnosis of OA is outlined in table 2. This is intended as a general guide to facilitate accurate, practical and efficient diagnostic evaluation, recognizing that some of the suggested procedures may not be available in some settings. Diagnosis of OA involves establishing both the diagnosis of asthma and the relation between asthma and workplace exposures. After each step, for each patient, the physician will need to determine whether the level of diagnostic certainty achieved is adequate to support the necessary decisions, or whether evaluation should continue to the next step. If facilities and resources are available, the time and cost of continuing the clinical evaluation are usually justified by the importance of making an accurate determination of the relationship of asthma to work. Highlights of diagnostic procedures for OA will be summarized; details can be found in several of the references (Chan-Yeung 1995; Bernstein et al. 1993). Consultation with a physician experienced in OA may be considered, since the diagnostic process may be difficult.
Table 2. Steps in diagnostic evaluation of asthma in the workplace
Step 1 Thorough medical and occupational history and directed physical examination.
Step 2 Physiologic evaluation for reversible airway obstruction and/or non specific bronchial hyper-responsiveness.
Step 3 Immunologic assessment, if appropriate.
Assess Work Status:
Currently working: Proceed to Step 4 first.
Not currently working, diagnostic trial of return to work feasible: Step 5 first, then Step 4.
Not currently working, diagnostic trial of return to work not feasible: Step 6.
Step 4 Clinical evaluation of asthma at work or diagnostic trial of return to work.
Step 5 Clinical evaluation of asthma away from work or diagnostic trial of removal from work.
Step 6 Workplace challenge or specific bronchial challenge testing. If available for suspected causal exposures, this step may be performed prior to Step 4 for any patient.
This is intended as a general guide to facilitate practical and efficient diagnostic evaluation. It is recommended that physicians who diagnose and manage OA refer to current clinical literature as well.
RADS, when caused by an occupational exposure, is usually considered a subclass of OA. It is diagnosed clinically, using the criteria in Table 6. Patients who have experienced significant respiratory injury due to high-level irritant inhalations should be evaluated for persistent symptoms and presence of airflow obstruction shortly after the event. If the clinical history is compatible with RADS, further evaluation should include quantitative testing for NBR, if not contra-indicated.
WAA may be common, and may cause a substantial preventable burden of disability, but little has been published on diagnosis, management or prognosis. As summarized in Table 6, WAA is recognized when asthmatic symptoms preceded the suspected causal exposure but are clearly aggravated by the work environment. Worsening at work can be documented either by physiological evidence or through evaluation of medical records and medication use. It is a clinical judgement whether patients with a history of asthma in remission, who have recurrence of asthmatic symptoms that otherwise meet the criteria for OA, are diagnosed with OA or WAA. One year has been proposed as a sufficiently long asymptomatic period that the onset of symptoms is likely to represent a new process caused by the workplace exposure, although no consensus yet exists.
Step 1: Thorough medical and occupational history anddirected physical examination
Initial suspicion of possible OA in appropriate clinical and workplace situations is key, given the importance of early diagnosis and intervention in improving prognosis. The diagnosis of OA or WAA should be considered in all asthmatic patients in whom symptoms developed as a working adult (especially recent onset), or in whom the severity of asthma has substantially increased. OA should also be considered in any other individuals who have asthma-like symptoms and work in occupations in which they are exposed to asthma-causing agents or who are concerned that their symptoms are work-related.
Patients with possible OA should be asked to provide a thorough medical and occupational/environmental history, with careful documentation of the nature and date of onset of symptoms and diagnosis of asthma, and any potentially causal exposures at that time. Compatibility of the medical history with the clinical presentation of OA described above should be evaluated, especially the temporal pattern of symptoms in relation to work schedule and changes in work exposures. Patterns and changes in patterns of use of asthma medications, and the minimum period of time away from work required for improvement in symptoms should be noted. Prior respiratory diseases, allergies/atopy, smoking and other toxic exposures, and a family history of allergy are pertinent.
Occupational and other environmental exposures to potential asthma-causing agents or processes should be thoroughly explored, with objective documentation of exposures if possible. Suspected exposures should be compared with a comprehensive list of agents reported to cause OA (Harber, Schenker and Balmes 1996; Chan-Yeung and Malo 1994; Bernstein et al. 1993; Rom 1992b), although inability to identify specific agents is not uncommon and induction of asthma by agents not previously described is possible as well. Some illustrative examples are shown in table 3. Occupational history should include details of current and relevant past employment with dates, job titles, tasks and exposures, especially current job and job held at time of onset of symptoms. Other environmental history should include a review of exposures in the home or community that could cause asthma. It is helpful to begin the exposure history in an open-ended way, asking about broad categories of airborne agents: dusts (especially organic dusts of animal, plant or microbial origin), chemicals, pharmaceuticals and irritating or visible gases or fumes. The patient may identify specific agents, work processes or generic categories of agents that have triggered symptoms. Asking the patient to describe step by step the activities and exposures involved in the most recent symptomatic workday can provide useful clues. Materials used by co-workers, or those released in high concentration from a spill or other source, may be relevant. Further information can often be obtained on product name, ingredients and manufacturer name, address and phone number. Specific agents can be identified by calling the manufacturer or through a variety of other sources including textbooks, CD ROM databases, or Poison Control Centers. Since OA is frequently caused by low levels of airborne allergens, workplace industrial hygiene inspections which qualitatively evaluate exposures and control measures are often more helpful than quantitative measurement of air contaminants.
Table 3. Sensitizing agents that can cause occupational asthma
Examples of substances
Examples of jobs and industries
High-molecular-weight protein antigens
Laboratory animals, crab/seafood, mites, insects
Flour and grain dusts, natural rubber latex gloves, bacterial enzymes, castor bean dust, vegetable gums
Animal handlers, farming and food processing
Bakeries, health care workers, detergent making, food processing
Plasticizers, 2-part paints, adhesives, foams
Isocyanates, acid anhydrides, amines
Platinum salts, cobalt
Cedar (plicatic acid), oak
Auto spray painting, varnishing, woodworking
Platinum refineries, metal grinding
Sawmill work, carpentry
Pharmaceutical manufacturing and packaging
Chloramine T, polyvinyl chloride fumes, organophosphate insecticides
Janitorial work, meat packing
The clinical history appears to be better for excluding rather than for confirming the diagnosis of OA, and an open-ended history taken by a physician is better than a closed questionnaire. One study compared the results of an open-ended clinical history taken by trained OA specialists with a “gold standard” of specific bronchial challenge testing in 162 patients referred for evaluation of possible OA. The investigators reported that the sensitivity of a clinical history suggestive of OA was 87%, specificity 55%, predictive value positive 63% and predictive value negative 83%. In this group of referred patients, prevalence of asthma and OA were 80% and 46%, respectively (Malo et al. 1991). In other groups of referred patients, predictive values positive of a closed questionnaire ranged from 8 to 52% for a variety of workplace exposures (Bernstein et al. 1993). The applicability of these results to other settings needs to be assessed by the physician.
Physical examination is sometimes helpful, and findings relevant to asthma (e.g., wheezing, nasal polyps, eczematous dermatitis), respiratory irritation or allergy (e.g., rhinitis, conjunctivitis) or other potential causes of symptoms should be noted.
Step 2: Physiological evaluation for reversible airway obstruction and/or non-specific bronchial hyper-responsiveness
If sufficient physiological evidence supporting the diagnosis of asthma (NAEP 1991) is already in the medical record, Step 2 can be skipped. If not, technician-coached spirometry should be performed, preferably post-workshift on a day when the patient is experiencing asthmatic symptoms. If spirometry reveals airway obstruction which reverses with a bronchodilator, this confirms the diagnosis of asthma. In patients without clear evidence of airflow limitation on spirometry, quantitative testing for NBR using methacholine or histamine should be done, the same day if possible. Quantitative testing for NBR in this situation is a key procedure for two reasons. First, it can often identify patients with mild or early stage OA who have the greatest potential for cure but who would be missed if testing stopped with normal spirometry. Second, if NBR is normal in a worker who has ongoing exposure in the workplace environment associated with the symptoms, OA can generally be ruled out without further testing. If abnormal, evaluation can proceed to Step 3 or 4, and the degree of NBR may be useful in monitoring the patient for improvement after diagnostic trial of removal from the suspected causal exposure (Step 5). If spirometry reveals significant airflow limitation that does not improve after inhaled bronchodilator, a re-evaluation after more prolonged trial of therapy, including corticosteroids, should be considered (ATS 1995; NAEP 1991).
Step 3: Immunological assessment, if appropriate
Skin or serological (e.g., RAST) testing can demonstrate immunological sensitization to a specific workplace agent. These immunological tests have been used to confirm the work-relatedness of asthma, and, in some cases, eliminate the need for specific inhalation challenge tests. For example, among psyllium-exposed patients with a clinical history compatible with OA, documented asthma or airway hyper-responsiveness, and evidence of immunological sensitization to psyllium, approximately 80% had OA confirmed on subsequent specific bronchial challenge testing (Malo et al. 1990). In most cases, diagnostic significance of negative immunological tests is less clear. The diagnostic sensitivity of the immunological tests depends critically on whether all the likely causal antigens in the workplace or hapten-protein complexes have been included in the testing. Although the implication of sensitization for an asymptomatic worker is not well defined, analysis of grouped results can be useful in evaluating environmental controls. The utility of immunological evaluation is greatest for agents for which there are standardized in vitro tests or skin-prick reagents, such as platinum salts and detergent enzymes. Unfortunately, most occupational allergens of interest are not currently available commercially. The use of non-commercial solutions in skin-prick testing has on occasions been associated with severe reactions, including anaphylaxis, and thus caution is necessary.
If results of Steps 1 and 2 are compatible with OA, further evaluation should be pursued if possible. The order and extent of further evaluation depends on availability of diagnostic resources, work status of the patient and feasibility of diagnostic trials of removal from and return to work as indicated in Table 7. If further evaluation is not possible, a diagnosis must be based on the information available at this point.
Step 4: Clinical evaluation of asthma at work, or diagnostic trial of return to work
Often the most readily available physiological test of airway obstruction is spirometry. To improve reproducibility, spirometry should be coached by a trained technician. Unfortunately, single-day cross-shift spirometry, performed before and after the workshift, is neither sensitive nor specific in determining work-associated airway obstruction. It is probable that if multiple spirometries are performed each day during and after several workdays, the diagnostic accuracy may be improved, but this has not yet been adequately evaluated.
Due to difficulties with cross-shift spirometry, serial PEF measurement has become an important diagnostic technique for OA. Using an inexpensive portable meter, PEF measurements are recorded every two hours, during waking hours. To improve sensitivity, measurements must be done during a period when the worker is exposed to the suspected causal agents at work and is experiencing a work-related pattern of symptoms. Three repetitions are performed at each time, and measurements are made every day at work and away from work. The measurements should be continued for at least 16 consecutive days (e.g., two five-day work weeks and 3 weekends off) if the patient can safely tolerate continuing to work. PEF measurements are recorded in a diary along with notation of work hours, symptoms, use of bronchodilator medications, and significant exposures. To facilitate interpretation, the diary results should then be plotted graphically. Certain patterns suggest OA, but none are pathognomonic, and interpretation by an experienced reader is often helpful. Advantages of serial PEF testing are low cost and reasonable correlation with results of bronchial challenge testing. Disadvantages include the significant degree of patient cooperation required, inability to definitely confirm that data are accurate, lack of standardized method of interpretation, and the need for some patients to take 1 or 2 consecutive weeks off work to show significant improvement. Portable electronic recording spirometers designed for patient self monitoring, when available, can address some of the disadvantages of serial PEF.
Asthma medications tend to reduce the effect of work exposures on measures of airflow. However, it is not advisable to discontinue medications during airflow monitoring at work. Rather, the patient should be maintained on a constant minimal safe dosage of anti-inflammatory medications throughout the entire diagnostic process, with close monitoring of symptoms and airflow, and the use of short-acting bronchodilators to control symptoms should be noted in the diary.
The failure to observe work-related changes in PEF while a patient is working routine hours does not exclude the diagnosis of OA, since many patients will require more than a two-day weekend to show significant improvement in PEF. In this case, a diagnostic trial of extended removal from work (Step 5) should be considered. If the patient has not yet had quantitative testing for NBR, and does not have a medical contra-indication, it should be done at this time, immediately after at least two weeks of workplace exposure.
Step 5: Clinical evaluation of asthma away from work or diagnostic trial of extended removal from work
This step consists of completion of the serial 2-hourly PEF daily diary for at least 9 consecutive days away from work (e.g., 5 days off work plus weekends before and after). If this record, compared with the serial PEF diary at work, is not sufficient for diagnosing OA, it should be continued for a second consecutive week away from work. After 2 or more weeks away from work, quantitative testing for NBR can be performed and compared to NBR while at work. If serial PEF has not yet been done during at least two weeks at work, then a diagnostic trial of return to work (see Step 4) may be performed, after detailed counselling, and in close contact with the treating physician. Step 5 is often critically important in confirming or excluding the diagnosis of OA, although it may also be the most difficult and expensive step. If an extended removal from work is attempted, it is best to maximize the diagnostic yield and efficiency by including PEF, FEV1, and NBR tests in one comprehensive evaluation. Weekly physician visits for counselling and to review the PEF chart can help to assure complete and accurate results. If, after monitoring the patient for at least two weeks at work and two weeks away from it, the diagnostic evidence is not yet sufficient, Step 6 should be considered next, if available and feasible.
Step 6: Specific bronchial challenge or workplace challenge testing
Specific bronchial challenge testing using an exposure chamber and standardized exposure levels has been labelled the “gold standard” for diagnosis of OA. Advantages include definitive confirmation of OA with ability to identify asthmatic response to sub-irritant levels of specific sensitizing agents, which can then be scrupulously avoided. Of all the diagnostic methods, it is the only one that can reliably distinguish sensitizer-induced asthma from provocation by irritants. Several problems with this approach have included inherent costliness of the procedure, general requirement of close observation or hospitalization for several days, and availability in only very few specialized centres. False negatives may occur if standardized methodology is not available for all suspected agents, if the wrong agents are suspected, or if too long a time has elapsed between last exposure and testing. False positives may result if irritant levels of exposure are inadvertently obtained. For these reasons, specific bronchial challenge testing for OA remains a research procedure in most localities.
Workplace challenge testing involves serial technician-coached spirometry in the workplace, performed at frequent (e.g., hourly) intervals before and during the course of a workday exposure to the suspected causal agents or processes. It may be more sensitive than specific bronchial challenge testing because it involves “real life” exposures, but since airway obstruction may be triggered by irritants as well as sensitizing agents, positive tests do not necessarily indicate sensitization. It also requires cooperation of the employer and much technician time with a mobile spirometer. Both of these procedures carry some risk of precipitating a severe asthmatic attack, and should therefore be done under close supervision of specialists experienced with the procedures.
Treatment and Prevention
Management of OA includes medical and preventive interventions for individual patients, as well as public health measures in workplaces identified as high risk for OA. Medical management is similar to that for non-occupational asthma and is well reviewed elsewhere (NAEP 1991). Medical management alone is rarely adequate to optimally control symptoms, and preventive intervention by control or cessation of exposure is an integral part of the treatment. This process begins with accurate diagnosis and identification of causative exposures and conditions. In sensitizer-induced OA, reducing exposure to the sensitizer does not usually result in complete resolution of symptoms. Severe asthmatic episodes or progressive worsening of the disease may be caused by exposures to very low concentrations of the agent and complete and permanent cessation of exposure is recommended. Timely referral for vocational rehabilitation and job retraining may be a necessary component of treatment for some patients. If complete cessation of exposure is impossible, substantial reduction of exposure accompanied by close medical monitoring and management may be an option, although such reduction in exposure is not always feasible and the long-term safety of this approach has not been tested. As an example, it would be difficult to justify the toxicity of long-term treatment with systemic corticosteroids in order to allow the patient to continue in the same employment. For asthma induced and/or triggered by irritants, dose response may be more predictable, and lowering of irritant exposure levels, accompanied by close medical monitoring, may be less risky and more likely to be effective than for sensitizer-induced OA. If the patient continues to work under modified conditions, medical follow-up should include frequent physician visits with review of the PEF diary, well-planned access to emergency services, and serial spirometry and/or methacholine challenge testing, as appropriate.
Once a particular workplace is suspected to be high risk, due either to occurrence of a sentinel case of OA or use of known asthma-causing agents, public health methods can be very useful. Early recognition and effective treatment and prevention of disability of workers with existing OA, and prevention of new cases, are clear priorities. Identification of specific causal agent(s) and work processes is important. One practical initial approach is a workplace questionnaire survey, evaluating criteria A, B, C, and D1 or D5 in the case definition of OA. This approach can identify individuals for whom further clinical evaluation might be indicated and help identify possible causal agents or circumstances. Evaluation of group results can help decide whether further workplace investigation or intervention is indicated and, if so, provide valuable guidance in targeting future prevention efforts in the most effective and efficient manner. A questionnaire survey is not adequate, however, to establish individual medical diagnoses, since predictive positive values of questionnaires for OA are not high enough. If a greater level of diagnostic certainty is needed, medical screening utilizing diagnostic procedures such as spirometry, quantitative testing for NBR, serial PEF recording, and immunological testing can be considered as well. In known problem workplaces, ongoing surveillance and screening programmes may be helpful. However, differential exclusion of asymptomatic workers with history of atopy or other potential susceptibility factors from workplaces believed to be high risk would result in removal of large numbers of workers to prevent relatively few cases of OA, and is not supported by the current literature.
Control or elimination of causal exposures and avoidance and proper management of spills or episodes of high-level exposures can lead to effective primary prevention of sensitization and OA in co-workers of the sentinel case. The usual exposure control hierarchy of substitution, engineering and administrative controls, and personal protective equipment, as well as education of workers and managers, should be implemented as appropriate. Proactive employers will initiate or participate in some or all of these approaches, but in the event that inadequate preventive action is taken and workers remain at high risk, governmental enforcement agencies may be helpful.
Impairment and Disability
Medical impairment is a functional abnormality resulting from a medical condition. Disability refers to the total effect of the medical impairment on the patient’s life, and is influenced by many non-medical factors such as age and socio-economic status (ATS 1995).
Assessment of medical impairment is done by the physician and may include a calculated impairment index, as well as other clinical considerations. The impairment index is based on (1) degree of airflow limitation after bronchodilator, (2) either degree of reversibility of airflow limitation with bronchodilator or degree of airway hyper-responsiveness on quantitative testing for NBR, and (3) minimum medication required to control asthma. The other major component of the assessment of medical impairment is the physician’s medical judgement of the ability of the patient to work in the workplace environment causing the asthma. For example, a patient with sensitizer-induced OA may have a medical impairment which is highly specific to the agent to which he or she has become sensitized. The worker who experiences symptoms only when exposed to this agent may be able to work in other jobs, but permanently unable to work in the specific job for which she or he has the most training and experience.
Assessment of disability due to asthma (including OA) requires consideration of medical impairment as well as other non-medical factors affecting ability to work and function in everyday life. Disability assessment is initially made by the physician, who should identify all the factors affecting the impact of the impairment on the patient’s life. Many factors such as occupation, educational level, possession of other marketable skills, economic conditions and other social factors may lead to varying levels of disability in individuals with the same level of medical impairment. This information can then be used by administrators to determine disability for purposes of compensation.
Impairment and disability may be classified as temporary or permanent, depending on the likelihood of significant improvement, and whether effective exposure controls are successfully implemented in the workplace. For example, an individual with sensitizer-induced OA is generally considered permanently, totally impaired for any job involving exposure to the causal agent. If the symptoms resolve partially or completely after cessation of exposure, these individuals may be classified with less or no impairment for other jobs. Often this is considered permanent partial impairment/disability, but terminology may vary. An individual with asthma which is triggered in a dose-dependent fashion by irritants in the workplace would be considered to have temporary impairment while symptomatic, and less or no impairment if adequate exposure controls are installed and are effective in reducing or eliminating symptoms. If effective exposure controls are not implemented, the same individual might have to be considered permanently impaired to work in that job, with recommendation for medical removal. If necessary, repeated assessment for long-term impairment/disability may be carried out two years after the exposure is reduced or terminated, when improvement of OA would be expected to have plateaued. If the patient continues to work, medical monitoring should be ongoing and reassessment of impairment/disability should be repeated as needed.
Workers who become disabled by OA or WAA may qualify for financial compensation for medical expenses and/or lost wages. In addition to directly reducing the financial impact of the disability on individual workers and their families, compensation may be necessary to provide proper medical treatment, initiate preventive intervention and obtain vocational rehabilitation. The worker’s and physician’s understanding of specific medico-legal issues may be important to ensuring that the diagnostic evaluation meets local requirements and does not result in compromise of the rights of the affected worker.
Although discussions of cost savings frequently focus on the inadequacy of compensation systems, genuinely reducing the financial and public health burden placed on society by OA and WAA will depend not only on improvements in compensation systems but, more importantly, on effectiveness of the systems deployed to identify and rectify, or prevent entirely, workplace exposures that are causing onset of new cases of asthma.
OA has become the most prevalent occupational respiratory disease in many countries. It is more common than generally recognized, can be severe and disabling, and is generally preventable. Early recognition and effective preventive interventions can substantially reduce the risk of permanent disability and the high human and financial costs associated with chronic asthma. For many reasons, OA merits more widespread attention among clinicians, health and safety specialists, researchers, health policy makers, industrial hygienists, and others interested in prevention of work-related diseases.