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).

Pathology

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).

Radiography

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.

Clinical aspects

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.

Disease mechanisms

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.

Mortality

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).

Prevention

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.

Treatment

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.

Pathology

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.

Radiology

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.

Clinical aspects

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.

Disease mechanisms

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.

Mortality

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.

Prevention

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.

Treatment

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.

Chronic Bronchitis

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.

Emphysema

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

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

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.

Lung Cancer

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).

Back

Historical Perspective

Asbestos is a term used to describe a group of naturally occurring fibrous minerals which are very widely distributed in rock outcrops and deposits throughout the world. Exploitation of the tensile and heat-resistant properties of asbestos for human use dates from ancient times. For instance, in the third century BC asbestos was used to strengthen clay pots in Finland. In classic times, shrouds woven from asbestos were used to preserve the ashes of the famous dead. Marco Polo returned from his travels in China with descriptions of a magic material which could be manufactured into a flame resistant cloth. By the early years of the nineteenth century, deposits were known to exist in several parts of the world, including the Ural Mountains, northern Italy and other Mediterranean areas, in South Africa and in Canada, but commercial exploitation only started in the latter half of the nineteenth century. By this time, the industrial revolution created not only the demand (such as that of insulating the steam engine) but also facilitated production, with mechanization replacing hand cobbing of fibre from the parent rock. The modern industry began in Italy and the United Kingdom after 1860 and was boosted by the development and exploitation of the extensive deposits of chrysotile (white) asbestos in Quebec (Canada) in the 1880s. Exploitation of the also extensive deposits of chrysotile in the Ural mountains was modest until the 1920s. The long thin fibres of chrysotile were particularly suitable for spinning into cloth and felts, one of the early commercial uses for the mineral. The exploitation of the deposits of crocidolite (blue) asbestos of the northwest Cape, South Africa, a fibre more water-resistant than chrysotile and better suited to marine use, and of the amosite (brown) asbestos deposits, also found in South Africa, started in the early years of this century. Exploitation of the Finnish deposits of anthophyllite asbestos, the only important commercial source of this fibre, took place between 1918 and 1966, while the deposits of crocidolite in Wittenoom, Western Australia, were mined from 1937 to 1966.

Fibre Types

The asbestos minerals fall into two groups, the serpentine group which includes chrysotile, and the amphiboles, which include crocidolite, tremolite, amosite and anthophyllite (figure 1). Most ore deposits are heterogeneous mineralogically, as are most of the commercial forms of the mineral (Skinner, Roos and Frondel 1988). Chrysotile and the various amphibole asbestos minerals differ in crystalline structure, in chemical and surface characteristics and in the physical characteristics of their fibres, usually described in terms of the length-to-diameter (or aspect) ratio. They also differ in characteristics which distinguish commercial use and grade. Pertinent to the current discussion is the evidence that the different fibres differ in their biological potency (as considered below in the sections on various diseases).

Figure 1. Asbestos fibre types.

Seen on election microscopy together with energy dispersive x-ray spectra which enables identification of individual fibres. Courtesy of A. Dufresne and M. Harrigan, McGill University.

Commercial Production

The growth of commercial production, illustrated in figure 2, was slow in the early years of this century. For instance, Canadian production exceeded 100,000 short tons per annum for the first time in 1911 and 200,000 tons in 1923. Growth between the two World Wars was steady, increased considerably to meet the demands of the Second World War and spectacularly to meet peacetime demands (including those of the cold war) to reach a peak in 1976 of 5,708,000 short tons (Selikoff and Lee 1978). After this, production faltered as the ill-health effects of exposure became a matter of increasing public concern in North America and Europe and remain at approximately 4,000,000 short tons per annum up to 1986, but decreased further in the 1990s. There was also a shift in the uses and sources of fibre in the 1980s; in Europe and North America demand declined as substitutes for many applications were introduced, while on the African, Asian and South American continents, demand for asbestos increased to meet the needs of a cheap durable material for use in construction and in water reticulation. By 1981, Russia had become the world’s major producer, with an increase in the commercial exploitation of large deposits in China and Brazil. In 1980, it was estimated that a total of over 100 million tons of asbestos had been mined worldwide, 90% of which was chrysotile, approximately 75% of which came from 4 chrysotile mining areas, located in Quebec (Canada), Southern Africa and the central and southern Ural Mountains. Two to three per cent of the world’s total production was crocidolite, from the Northern Cape, South Africa, and from Western Australia, and another 2 to 3% was amosite, from the Eastern Transvaal, South Africa (Skinner, Ross and Frondel 1988).

Figure 2. World production of asbestos in thousands of tons 1900-92

Asbestos-Related Diseases and Conditions

Like silica, asbestos has the capability of evoking scarring reactions in all biological tissue, human and animal. In addition, asbestos evokes malignant reactions, adding a further element to the concern for human health, as well as a challenge to science as to how asbestos exerts its ill effects. The first asbestos-related disease to be recognized, diffuse interstitial pulmonary fibrosis or scarring, later called asbestosis, was the subject of case reports in the United Kingdom in the early 1900s. Later, in the 1930s, case reports of lung cancer in association with asbestosis appeared in the medical literature though it was only over the next several decades that the scientific evidence was gathered establishing that asbestos was the carcinogenic factor. In 1960, the association between asbestos exposure and another much less common cancer, malignant mesothelioma, which involves the pleura (a membrane that covers the lung and lines the chest wall) was dramatically brought to attention by the report of a cluster of these tumours in 33 individuals, all of whom worked or lived in the asbestos mining area of the Northwest Cape (Wagner 1996). Asbestosis was the target of the dust control levels introduced and implemented with increasing rigour in the 1960s and 1970s, and in many industrialized countries, as the frequency of this disease decreased, asbestos-related pleural disease emerged as the most frequent manifestation of exposure and the condition which most frequently brought exposed subjects to medical attention. Table 1 lists diseases and conditions currently recognized as asbestos-related. The diseases in bold type are those most frequently encountered and for which a direct causal relationship is well established, while for the sake of completeness, certain other conditions, for which the relationship is less well established, are also listed (see footnote to Table 16) and the sections which follow in the text below that expand upon the various disease headings).

Table 1. Asbestos-related diseases and conditions

¹ The diseases or conditions indicated in bold type are those most frequently encountered and the ones for which a causal relationship is well established and/or generally recognized.

² Fibrosis in the walls of the small airways of the lung (including the membranous and respiratory bronchioles) is thought to represent the early lung parenchymal response to retained asbestos (Wright et al. 1992) which will progress to asbestosis if exposure continues and/or is heavy, but if exposure is limited or light, the lung response may be limited to these areas (Becklake in Liddell & Miller 1991).

³ Included are bronchitis, chronic obstructive pulmonary disease (COPD) and emphysema. All have been shown to be associated with work in dusty environments. The evidence for causality is reviewed in the section Chronic Airways Diseases and Becklake (1992).

⁴ Related to direct handling of asbestos and of historical rather than current interest.

⁵ Data not consistent from all studies (Doll and Peto 1987); some of the highest risks were reported in a cohort of over 17,000 American and Canadian asbestos insulation workers (Selikoff 1990), followed from January 1, 1967 to December 31, 1986 in whom exposure had been particularly heavy.

Sources: Becklake 1994; Liddell and Miller 1992; Selikoff 1990; Doll and Peto in Antman and Aisner 1987; Wright et al. 1992.

Uses

Table 2 lists the major sources, products and uses of the asbestos minerals.

Table 2. Main commercial sources, products and uses of asbestos

¹ A list such as this is obviously not comprehensive and the readers should consult the sources cited and other chapters in this Encyclopedia for more complete information.

² No longer in operation.

Sources: Asbestos Institute (1995); Browne (1994); Liddell and Miller (1991); Selikoff and Lee (1978); Skinner et al (1988).

Though necessarily incomplete, this table emphasizes that:

1. Deposits are found in many parts of the world, most of which have been exploited non-commercially or commercially in the past, and some of which are currently commercially exploited.
2. There are many manufactured products in current or past use which contain asbestos, particularly in the construction and transport industries.
3. Disintegration of these products or their removal carries with it the risk of the resuspension of fibres and of renewed human exposure.

A figure of over 3,000 has been commonly quoted for the number of uses of asbestos and no doubt led to asbestos being dubbed the “magic mineral” in the 1960s. A 1953 industry list contains as many as 50 uses for raw asbestos, in addition to its use in the manufacture of the products listed in Table 17, each of which has many other industrial applications. In 1972, the consumption of asbestos in an industrialized country like the United States was attributed to the following categories of product: construction (42%); friction materials, felts, packings and gaskets (20%); floor tiles (11%); paper (9%); insulation and textiles (3%) and other uses (15%) (Selikoff and Lee 1978). By contrast, a 1995 industry list of the main product categories shows major redistribution on a worldwide basis as follows: asbestos cement (84%); friction materials (10%); textiles (3%); seals and gaskets (2%); and other uses (1%) (Asbestos Institute 1995).

Occupational Exposures, Past and Current

Occupational exposure, certainly in industrialized countries, has always been and is still the most likely source of human exposure (see Table 17 and the references cited in its footnote; other sections of this Encyclopaedia contain further information). There have, however, been major changes in industrial processes and procedures aimed at diminishing the release of dust into the working environment (Browne 1994; Selikoff and Lee 1978). In countries with mining operations, milling usually takes place at the minehead. Most chrysotile mines are open cast, while amphibole mines usually involve underground methods which generate more dust. Milling involves separating fibre from rock by means of mechanized crushing and screening, which were dusty processes until the introduction of wet methods and/or enclosure in most mills during the 1950s and 1960s. The handling of waste was also a source of human exposure, as was transporting bagged asbestos, whether it involved loading and unloading trucks and railcars or work on the dockside. These exposures have diminished since the introduction of leak-proof bags and the use of sealed containers.

Workers have had to use raw asbestos directly in packing and lagging, particularly in locomotives, and in spraying walls, ceilings and airducts, and in the marine industry, deckheads and bulkheads. Some of these uses have been phased out voluntarily or have been banned. In the manufacture of asbestos cement products, exposure occurs in receiving and opening bags containing raw asbestos, in preparing the fibre for mixing in the slurry, in machining end-products and in dealing with waste. In the manufacture of vinyl tiles and flooring, asbestos was used as a reinforcing and filler agent to blend with organic resins, but has now largely been replaced by organic fibre in Europe and North America. In the manufacture of yarns and textiles, exposure to fibre occurs in receiving, preparing, blending, carding, spinning, weaving and calendaring the fibre—processes which were until recently dry and potentially very dusty. Dust exposure has been considerably reduced in modern plants through use of a colloidal suspension of fibre extruded through a coagulant to form wet strands for the last-mentioned three processes. In the manufacture of asbestos paper products, human exposure to asbestos dust is also most likely to occur in the reception and preparation of the stock mix and in cutting the final products which in the 1970s contained from 30 to 90% asbestos. In the manufacture of asbestos friction products (dry mix-moulded, roll-formed, woven or endless wound) human exposure to asbestos dust is also most likely to occur during the initial handling and blending processes as well as in finishing the end product, which in the 1970s contained from 30 to 80% of asbestos. In the construction industry, prior to regular use of appropriate exhaust ventilation (which came in the 1960s), the high-speed power sawing, drilling and sanding of asbestos-containing boards or tiles led to the release of fibre-containing dust close to the operator’s breathing zone, particularly when such operations were conducted in closed spaces (for instance in high-rise buildings under construction). In the period after the Second World War, a major source of human exposure was in the use, removal or replacement of asbestos-containing materials in the demolition or refurbishing of buildings or ships. One of the chief reasons for this state of affairs was the lack of awareness, both of the composition of these materials (i.e., that they contained asbestos) and that exposure to asbestos could be harmful to health. Improved worker education, better work practices and personal protection have reduced the risk in the 1990s in some countries. In the transport industry, sources of exposure were the removal and replacement of lagging in locomotive engines and of braking material in trucks and cars in the automobile repair industry. Other sources of past exposure leading to, in particular, pleural disease, continue to attract notice, even in the 1990s, usually on the basis of case reports, for instance those describing workers using asbestos string in the manufacture of welding rods, in the formation of asbestos rope for grouting furnaces and maintaining underground mine haulage systems.

Other Sources of Exposure

Exposure of individuals engaged in trades which do not directly involve use or handling of asbestos but who work in the same area as those who do deal with it directly is called para-occupational (bystander) exposure. This has been an important source of exposure not only in the past but also for cases presenting for diagnosis in the 1990s. Workers involved include electricians, welders and carpenters in the construction and in the ship building or repair industries; maintenance personnel in asbestos factories; fitters, stokers and others in power stations and ships and boiler houses where asbestos lagging or other insulation is in place, and maintenance personnel in post-war high-rise buildings incorporating various asbestos-containing materials. In the past, domestic exposure occurred primarily from dust-laden workclothes being shaken or laundered at home, the dust so released becoming entrapped in carpets or furnishings and resuspended into the air with the activities of daily living. Not only could levels of airborne fibre reach levels as high as 10 fibre per millilitre (f/ml), that is, ten times the occupational exposure limit proposed by a WHO consultation (1989) of 1.0 f/ml but the fibres tended to remain airborne for several days. Since the 1970s, the practice of retaining all work clothes at the worksite for laundering has been widely but not universally adopted. In the past also, residential exposure occurred from contamination of air from industrial sources. For instance, increased levels of airborne asbestos have been documented in the neighbourhood of mines and asbestos plants and are determined by production levels, emission controls and weather. Given the long lag time for, in particular, asbestos-related pleural disease, such exposures are still likely to be responsible for some cases presenting for diagnosis in the 1990s. In the 1970s and 1980s, with the increase in public awareness of both the ill-health consequences of asbestos exposure and of the fact that asbestos containing materials are used extensively in modern construction (particularly in the friable form used for spray-on applications to walls, ceilings and ventilation ducts), a major cause of concern centred on whether, as such buildings age and are subject to daily wear and tear, asbestos fibres may be released into the air in sufficient numbers to become a threat to the health of those working in modern high-rise buildings (see below for risk estimates). Other sources of contamination of the air in urban areas include the release of fibre from brakes of vehicles and rescattering of fibres released by passing vehicles (Bignon, Peto and Saracci 1989).

Non-industrial sources of environmental exposure include naturally occurring fibres in soils, for instance in eastern Europe, and in rock outcrops in the Mediterranean region, including Corsica, Cyprus, Greece and Turkey (Bignon, Peto and Saracci 1989). An additional source of human exposure results from the use of tremolite for whitewash and stucco in Greece and Turkey, and according to more recent reports, in New Caledonia in the South Pacific (Luce et al. 1994). Furthermore, in several rural villages in Turkey, a zeolite fibre, erionite, has been found to be used both in stucco and in domestic construction and has been implicated in mesothelioma production (Bignon, Peto and Saracci 1991). Finally, human exposure may occur through drinking water, mainly from natural contamination, and given the widespread natural distribution of the fibre in outcrops, most water sources contain some fibre, levels being highest in mining areas (Skinner, Roos and Frondel 1988).

Aetiopathology of Asbestos-Related Disease

Fate of inhaled fibres

Inhaled fibres align themselves with the airstream and their capability of penetrating into the deeper lung spaces depends on their dimension, fibres of 5mm or less in aerodynamic diameter showing an over 80% penetration, but also less than 10 to 20% retention. Larger particles may impact in the nose and in major airways at bifurcations, where they tend to collect. Particles deposited in the major airways are cleared by the action of ciliated cells and are transported up the mucus escalator. Individual differences associated with what appears to be the same exposure are due, at least in part, to differences between individuals in the penetration and retention of inhaled fibres (Bégin, Cantin and Massé 1989). Small particles deposited beyond the major airways are phagocytosed by alveolar macrophages, scavenger cells which ingest foreign material. Longer fibres, that is, those over 10mm, often come under attack by more than one macrophage, are more likely to become coated and to form the nucleus of an asbestos body, a characteristic structure recognized since the early 1900s as a marker of exposure (see figure 3). Coating a fibre is considered to be part of the lungs’ defense to render it inert and non-immunogenic. Asbestos bodies are more likely to form on amphibole than on chrysotile fibres, and their density in biological material (sputum, bronchoalveolar lavage, lung tissue) is an indirect marker of lung burden. Coated fibres may persist in the lung for long periods, to be recovered from sputum or bronchoalveolar lavage fluid up to 30 years after last exposure. Clearance of non-coated fibres deposited in the lung’s parenchyma is towards the lung periphery and subpleural regions, and then to lymph nodes at the root of the lung.

Figure 3. Asbestos body

Magnification x 400, seen on microscopic section of the lung as a slightly curved elongated structure with a finely beaded iron protein coat. The asbestos fibre itself can be identified as the thin line near one end of the asbestos body (arrow). Source: Fraser et al. 1990

Theories to explain how fibres evoke the various pleural reactions associated with asbestos exposure include:

1. direct penetration into the pleural space and drainage with the pleural fluid to pores in the pleura lining the chest wall
2. release of mediators into the pleural space from subpleural lymphatic collections
3. retrograde flow from lymph nodes at the root of the lung to the parietal pleura (Browne 1994)

There may also be retrograde flow via the thoracic duct to the abdominal lymph nodes to explain the occurrence of peritoneal mesothelioma.

Cellular effects of inhaled fibres

Animal studies indicate that the initial events which follow asbestos retention in the lung include:

1. an inflammatory reaction, with accumulation of white blood cells followed by a macrophagic alveolitis with release of fibronectin, growth factor and various neutrophil chemotactic factors and, over time, the release of superoxide ion and
2. proliferation of alveolar, epithelial, interstitial and endothelial cells (Bignon, Peto and Saracci 1989).

These events are reflected in the material recovered by bronchoalveolar lavage in animals and humans (Bégin, Cantin and Massé 1989). Both fibre dimensions and their chemical characteristics appear to determine biological potency for fibrogenesis, and these characteristics, in addition to surface properties, are also thought to be important for carcinogenesis. Long, thin fibres are more active than short ones, although the activity of the latter cannot be discounted, and amphiboles are more active than chrysotile, a property attributed to their greater biopersistence (Bégin, Cantin and Massé 1989). Asbestos fibres may also affect the human immune system and change the circulating population of blood lymphocytes. For instance, human cell mediated immunity to cell antigens (such as is exhibited in a tuberculin skin test) may be impaired (Browne 1994). In addition, since asbestos fibres appear to be capable of inducing chromosome abnormality, the view has been expressed that they can also be considered capable of inducing as well as promoting cancer (Jaurand in Bignon, Peto and Saracci 1989).

Dose versus exposure response relationships

In biological sciences such as pharmacology or toxicology in which dose-response relationships are used to estimate the probability of desired effects or the risk of undesired effects, a dose is conceptualized as the amount of agent delivered to and remaining in contact with the target organ for sufficient time to evoke a reaction. In occupational medicine, surrogates for dose, such as various measures of exposure, are usually the basis for risk estimates. However, exposure-response relationships can usually be demonstrated in workforce-based studies; the most appropriate exposure measure may, however, differ between diseases. Somewhat disconcerting is the fact that although exposure-response relationships will differ between workforces, these differences can be explained only in part by the fibre, particle size and industrial process. Nevertheless, such exposure-response relationships have formed the scientific basis for risk assessment and for setting permissible exposure levels, which were originally focused on controlling asbestosis (Selikoff and Lee 1978). As the prevalence and/or incidence of this condition has decreased, concern has switched to assure protection of human health against asbestos-related cancers. Over the last decade, techniques have been developed for the quantitative measurement of lung dust burden or biological dose directly in terms of fibres per gram of dry lung tissue. In addition, energy dispensive x-ray analysis (EDXA) permits precise characterization of each fibre by fibre type (Churg 1991). Though standardization of results between laboratories has not yet been achieved, comparisons of results obtained within a given laboratory are useful, and lung burden measurements have added a new tool for case evaluation. In addition, the application of these techniques in epidemiological studies has

1. confirmed the biopersistence of amphibole fibres in the lung compared to chrysotile fibres
2. identified fibre burden in the lungs of some individuals in whom exposure was forgotten, remote or thought to be unimportant
3. demonstrated a gradient in lung burden associated with rural and urban residence and with occupational exposure and
4. confirmed a fibre gradient in the lung dust burden associated with the major asbestos-related diseases (Becklake and Case 1994).

Asbestosis

Definition and history

Asbestosis is the name given to the pneumoconiosis consequent on exposure to asbestos dust. The term pneumoconiosis is used here as defined in the article “Pneumoconioses: Definitions”, of this Encyclopaedia as a condition in which there is “accumulation of dust in the lungs and tissue responses to the dust”. In the case of asbestosis, the tissue reaction is collagenous, and results in permanent alteration of the alveolar architecture with scarring. As early as 1898, the Annual Report of Her Majesty’s Chief Inspector of Factories contained reference to a lady factory inspector’s report on the adverse health consequences of asbestos exposure, and the 1899 Report contained details of one such case in a man who had worked for 12 years in one of the recently established textile factories in London, England. Autopsy revealed diffuse severe fibrosis of the lung and what subsequently came to be known as asbestos bodies were seen on subsequent histologic re-examination of the slides. Since fibrosis of the lung is an uncommon condition, the association was thought to be causal and the case was presented in evidence to a committee on compensation for industrial disease in 1907 (Browne 1994). Despite the appearance of reports of a similar nature filed by inspectors from the United Kingdom, Europe and Canada over the next decade, the role of exposure to asbestos in the genesis of the condition was not generally recognized until a case report was published in the British Medical Journal in 1927. In this report, the term pulmonary asbestosis was first used to describe this particular pneumoconiosis, and comment was made on the prominence of the associated pleural reactions, in contrast, for instance, to silicosis, the main pneumoconiosis recognized at the time (Selikoff and Lee 1978). In the 1930s, two major workforce-based studies carried out among textile workers, one in the United Kingdom and one in the United States, provided evidence of an exposure-response (and therefore likely causal) relationship between level and duration of exposure and radiographic changes indicative of asbestosis. These reports formed the basis of the first control regulations in the United Kingdom, promulgated in 1930, and the first threshold limit values for asbestos published by the American Conference of Government and Industrial Hygienists in 1938 (Selikoff and Lee 1978).

Pathology

The fibrotic changes which characterize asbestosis are the consequence of an inflammatory process set up by fibres retained in the lung. The fibrosis of asbestosis is interstitial, diffuse, tends to involve the lower lobes and peripheral zones preferentially and, in the advanced case, is associated with obliteration of the normal lung architecture. Fibrosis of the adjacent pleura is common. Nothing in the histological features of asbestosis distinguish it from interstitial fibrosis due to other causes, except the presence of asbestos in the lung either in the form of asbestos bodies, visible to light microscopy, or as uncoated fibres, most of which are too fine to be seen except by means of electron microscopy. Thus, the absence of asbestos bodies in images derived from light microscopy does not rule out either exposure or the diagnosis of asbestosis. At the other end of the spectrum of disease severity, the fibrosis may be limited to relatively few zones and affect mainly the peribronchiolar regions (see figure 4), giving rise to what has been called asbestos-related small airways disease. Again, except perhaps for more extensive involvement of membranous small airways, nothing in the histologic changes of this condition distinguishes it from small airways disease due to other causes (such as cigarette smoking or exposure to other mineral dusts) other than the presence of asbestos in the lung. Small airways disease may be the only manifestation of asbestos-related lung fibrosis or it may coexist with varying degrees of interstitial fibrosis, that is, asbestosis (Wright et al. 1992). Carefully considered criteria have been published for the pathological grading of asbestosis (Craighead et al. 1982). In general, the extent and intensity of the lung fibrosis relates to the measured lung dust burden (Liddell and Miller 1991).

Figure 4.  Asbestos-related small airways disease

Peribronchiolar fibrosis and infiltration by inflammatory cells is seen on a histologic section of a respiratory bronchiole (R) and its distal divisions or alveolar ducts (A). The surrounding lung is mostly normal but with focal thickening of the interstitial tissue (arrow), representing early asbestosis. Source: Fraser et al. 1990

Clinical features

Shortness of breath, the earliest, most consistently reported and most distressing complaint, has led to asbestosis being called a monosymptomatic disease (Selikoff and Lee 1978). Shortness of breath precedes other symptoms which include a dry, often distressing cough, and chest tightness—which is thought to be associated pleural reactions. Late inspiratory rales or crackles which persist after coughing are heard, first in the axilla and over the lung bases, before becoming more generalized as the condition advances, and are thought to be due to the explosive opening of airways which close on expiration. Coarse rales and rhonchi, if present, are thought to reflect bronchitis either in response to working in a dusty environment, or due to smoking.

Chest imaging

Traditionally, the chest radiograph has been the most important single diagnostic tool for establishing the presence of asbestosis. This has been facilitated by the use of the ILO (1980) radiological classification, which grades the small irregular opacities that are characteristic of asbestosis on a continuum from no disease to the most advanced disease, both for severity (described as profusion on a 12-point scale from –/0 to 3/+) and extent (described as the number of zones affected). Despite between reader differences, even among those who have completed training courses in reading, this classification has proved particularly useful in epidemiological studies, and has also been used clinically. However, pathological changes of asbestosis can be present on lung biopsy in up to 20% of subjects with a normal chest radiograph. In addition, small irregular opacities of low profusion (e.g., 1/0 on the ILO scale) are not specific for asbestosis but can be seen in relation to other exposures, for instance to cigarette smoking (Browne 1994). Computer tomography (CT) has revolutionized the imaging of interstitial lung disease, including asbestosis, with high resolution computer tomography (HRCT) adding increased sensitivity to the detection of interstitial and pleural disease (Fraser et al. 1990). Characteristics of asbestosis which can be identified by HRCT include thickened interlobular (septal) and intralobular core lines, parenchymal bands, curvilinear subpleural lines and subpleural dependent densities, the first two being the most distinctive for asbestosis (Fraser et al. 1990). HRCT can also identify these changes in cases with pulmonary function deficit in whom the chest radiograph is inconclusive. Based on postmortem HRCT, thickened intralobular lines have been shown to correlate with peribronchiolar fibrosis, and thickened interlobular lines with interstitial fibrosis (Fraser et al. 1990). As yet, no standardized reading method has been developed for the use of HRCT in asbestos-related disease. In addition to its cost, the fact that a CT device is a hospital installation makes it unlikely that it will replace the chest radiograph for surveillance and epidemiological studies; its role will likely remain limited to individual case investigation or to planned studies intended to address specific issues. Figure 21 illustrates the use of chest imaging in the diagnosis of asbestos-related lung disease; the case shown exhibits asbestosis, asbestos-related pleural disease and lung cancer. Large opacities, a complication of other pneumoconioses, in particular silicosis, are unusual in asbestosis and are usually due to other conditions such as lung cancer (see the case described in figure 5) or rounded atelectasis.

Figure 5. Chest imaging in asbestos-related lung disease.

A posteroanterior chest radiograph (A) shows asbestosis involving both lungs and assessed as ILO category 1/1, associated with bilateral pleural thickening (open arrows) and a vaguely defined opacity (arrow heads) in the left upper lobe. On HRCT scan (B), this was shown to be a dense mass (M) abutting onto the pleura and transthoracic needle biopsy revealed an adenocarcinoma of the lung. Also on CT scan (C), at high attenuation pleural plaques can be seen (arrow heads) as well as a thin curvilinear opacity in the parenchyma underlying the plaques with interstitial abnormality in the lung between the opacity and the pleura. Source: Fraser et al. 1990

Lung function tests

Established interstitial lung fibrosis due to asbestos exposure, like established lung fibrosis due to other causes, is usually but not invariably associated with a restrictive lung function profile (Becklake 1994). Its features include reduced lung volumes, in particular vital capacity (VC) with preservation of the ratio of forced expiratory volume in 1second to forced vital capacity (FEV₁/FVC%), reduced lung compliance, and impaired gas exchange. Air flow limitation with reduced FEV₁/FVC may, however, also be present as a response to a dusty work environment or to cigarette smoke. In the earlier stages of asbestosis, when the pathological changes are limited to peribronchiolar fibrosis and even before small irregular opacities are evident on the chest radiograph, impairment of tests reflecting small airway dysfunction such as the Maximum Mid-expiratory Flow Rate may be the only sign of respiratory dysfunction. Responses to the stress of exercise may also be impaired early in the disease, with increased ventilation in relation to the oxygen requirement of the exercise (due to an increased breathing frequency and shallow breathing) and impaired O₂ exchange. As the disease progresses, less and less exercise is required to compromise O₂ exchange. Given that the asbestos-exposed worker may exhibit features of both a restrictive and an obstructive lung function profile, the wise physician interprets the lung function profile in the asbestos worker for what it is, as a measure of impairment, rather than as an aid to diagnosis. Lung functions, in particular vital capacity, provide a useful tool for the follow-up of subjects individually, or in epidemiological studies, for instance after exposure has ceased, to monitor the natural history of asbestosis or asbestos-related pleural disease.

Other laboratory tests

Bronchoalveolar lavage is increasingly used as a clinical tool in the investigation of asbestos-related lung disease:

1. to rule out other diagnoses
2. to assess the activity of the pulmonary reactions under study such as fibrosis or
3. to identify the agent in the form of asbestos bodies or fibres.

It is also used to study disease mechanisms in humans and animals (Bégin, Cantin and Massé 1989). The uptake of Gallium-67 is used as a measure of the activity of the pulmonary process, and serum antinuclear antibodies (ANA) and rheumatoid factors (RF), both of which reflect the immunological status of the individual, have also been investigated as factors influencing disease progression, and/or accounting for between individual differences in response to what appears to be the same level and dose of exposure.

Epidemiology including natural history

The prevalence of radiological asbestosis documented in workforce-based surveys varies considerably and, as might be expected, these differences relate to differences in exposure duration and intensity rather than differences between workplaces. However, even when these are taken into account by restricting comparison of exposure response relationships to those studies in which exposure estimates were individualized for each cohort member and based on job history and industrial hygiene measurements, marked fibre and process related gradients are evident (Liddell and Miller 1991). For instance, a 5% prevalence of small irregular opacities (1/0 or more on the ILO classification) resulted from a cumulative exposure to approximately 1,000 fibre years in Quebec chrysotile miners, to approximately 400 fibre years in Corsican chrysotile miners, and to under 10 fibre years in South African and Australian crocidolite miners. By contrast, for textile workers exposed to Quebec chrysotile, a 5% prevalence of irregular small opacities resulted from a cumulative exposure to under 20 fibre years. Lung dust burden studies are also consistent with a fibre gradient for evoking asbestosis: in 29 men in Pacific shipyard trades with asbestosis associated with mainly amosite exposure, the average lung burden found in autopsy material was 10 million amosite fibres per gram of dry lung tissue compared to an average chrysotile burden of 30 million fibres per gram of dry lung tissue in 23 Quebec chrysotile miners and millers (Becklake and Case 1994). Fibre size distribution contributes to but does not fully explain these differences, suggesting that other plant-specific factors, including other workplace contaminants, may play a role.

Asbestosis may remain stable or progress, but probably does not regress. Progression rates increase with age, with cumulative exposure, and with the extent of existing disease, and are more likely to occur if exposure was to crocidolite. Radiological asbestosis can both progress and appear long after exposure ceases. Deterioration of lung functions may also occur after exposure has ceased (Liddell and Miller 1991). An important issue (and one on which the epidemiological evidence is not consistent) is whether continued exposure increases the chance of progression once radiological changes have developed (Browne 1994; Liddell and Miller 1991). In some jurisdictions, for example in the United Kingdom, the number of cases of asbestosis presenting for worker’s compensation have decreased over the last decades, reflecting the workplace controls put in place in the 1970s (Meredith and McDonald 1994). In other countries, for instance in Germany (Gibbs, Valic and Browne 1994), rates of asbestosis continue to rise. In the United States, age-adjusted asbestos-related mortality rates (based on mention of asbestosis on the death certificate as either the cause of death or as playing a contributory role) for age 1+ increased from under 1 per million in 1960 to over 2.5 in 1986, and to 3 in 1990 (US Dept. of Health and Human Services, 1994).

Diagnosis and case management

Clinical diagnosis depends on:

1. establishing the presence of disease
2. establishing whether exposure occurred and
3. evaluating whether the exposure was likely to have caused the disease.

The chest radiograph remains the key tool to establish the presence of disease, supplemented by HRCT if available in cases where there is doubt. Other objective features are the presence of basal crackles, while lung function level, including exercise challenge, is useful in establishing impairment, a step required for compensation evaluation. Since neither the pathology, radiological changes, nor the symptoms and lung function changes associated with asbestosis are different from those associated with interstitial lung fibrosis due to other causes, establishing exposure is key to diagnosis. In addition, the many uses of asbestos products whose content is often not known to the user makes an exposure history a much more daunting exercise in interrogation than was previously thought. If the exposure history appears inadequate, identification of the agent in biological specimens (sputum, bronchoalveolar lavage and when indicated, biopsy) can corroborate exposure; dose in the form of lung burden can be assessed quantitatively by autopsy or in surgically removed lungs. Evidence of disease activity (from a gallium-67 scan or bronchoalveolar lavage) may assist in estimating prognosis, a key issue in this irreversible condition. Even in the absence of consistent epidemiological evidence that progression is slowed once exposure ceases, such a course may be prudent and certainly desirable. It is not, however, a decision easy to take or recommend, particularly for older workers with little opportunity for job retraining. Certainly exposure should not continue in any workplace not in conformity with current permissible exposure levels. Criteria for the diagnosis of asbestosis for epidemiological purposes are less demanding, particularly for cross-sectional workforce-based studies which include those well enough to be at work. These usually address issues of causality and often use markers that indicate minimal disease, based either on lung function level or on changes in the chest radiograph. By contrast, criteria for diagnosis for medicolegal purposes are considerably more stringent and vary according to the legal administrative systems under which they operate, varying between states within countries as well as between countries.

Asbestos-Related Pleural Disease

Historical perspective

Early descriptions of asbestosis mention fibrosis of the visceral pleura as part of the disease process (see “Pathology”, page 10.55). In the 1930s there were also reports of circumscribed pleural plaques, often calcified, in the parietal pleura (which lines the chest wall and covers the surface of the diaphragm), and occurring in those with environmental, not occupational, exposure. A 1955 workforce-based study of a German factory reported a 5% prevalence of pleural changes on the chest radiograph, thereby drawing attention to the fact that pleural disease might be the primary if not the only manifestation of exposure. Visceroparietal pleural reactions, including diffuse pleural fibrosis, benign pleural effusion (reported first in the 1960s) and rounded atelectasis (first reported in the 1980s) are now all considered interrelated reactions which are usefully distinguished from pleural plaques on the basis of pathology and probably pathogenesis, as well as clinical features and presentation. In jurisdictions in which the prevalence and/or incidence rates of asbestosis are decreasing, pleural manifestations, increasingly common in surveys, are increasingly the basis of detection of past exposure, and increasingly the reason for an individual seeking medical attention.

Pleural plaques

Pleural plaques are smooth, raised, white irregular lesions covered with mesothelium and found on the parietal pleura or diaphragm (figure 6). They vary in size, are often multiple, and tend to calcify with increasing age (Browne 1994). Only a small proportion of those detected at autopsy are seen on the chest radiograph, though most can be detected by HRCT. In the absence of pulmonary fibrosis, pleural plaques may cause no symptoms and may be detected only in screening surveys using chest radiography. Nevertheless, in workforce surveys, they are consistently associated with modest but measurable lung function impairment, mainly in VC and FVC (Ernst and Zejda 1991). In radiological surveys in the United States, rates of 1% are reported in men without known exposure, and 2.3% in men which include those in urban populations, with occupational exposure. Rates are also higher in communities with asbestos industries or high usage rates, while in some workforces, such as sheet metal workers, insulators, plumbers and railroad workers, rates may exceed 50%. In a 1994 Finnish autopsy survey of 288 men aged 35 to 69 years who died suddenly, pleural plaques were detected in 58%, and exhibited the tendency to increase with age, with the probability of exposure (based on history), with the concentration of asbestos fibres in lung tissue, and with smoking (Karjalainen et al. 1994). The aetiologic fraction of plaques attributable to a lung dust burden of 0.1 million fibres per gram of lung tissue was estimated at 24%, (this value is considered to be an underestimate). Lung dust burden studies are also consistent with fibre gradient in potency for evoking pleural reactions; in 103 men with amosite exposure in Pacific shipyard trades, all with pleural plaques, the average autopsy lung burden was 1.4 million fibres per gram of lung tissue, compared to 15.5 and 75 million fibres per gram of lung tissue for chrysotile and tremolite respectively in 63 Quebec chrysotile miners and millers examined in the same way (Becklake and Case 1994).

Figure 6.  Asbestos-related pleural disease

A diaphragmatic pleural plaque (A) is seen in an autopsy specimen as a smooth well defined focus of fibrosis on the diaphragm of a construction worker with incidental exposure to asbestos and asbestos bodies in the lung. Visceral pleural fibrosis (B) is seen on an inflated autopsy lung specimen, and radiates from two central foci on the visceral pleura of the lung of a construction worker with asbestos exposure who also exhibited several parietal pleural plaques. Source: Fraser et al. 1990.

Visceroparietal pleural reactions

Though the pathology and pathogenesis of the different forms of visceroparietal reaction to asbestos exposure are almost certainly interrelated, their clinical manifestations and how they come to attention differs. Acute exudative pleural reactions may occur in the form of effusions in subjects whose lungs do not manifest other asbestos-related disease, or as an exacerbation in the severity and extent of existing pleural reactions. Such pleural effusions are called benign by way of distinguishing them from effusions associated with malignant mesothelioma. Benign pleural effusions occur typically 10 to 15 years after first exposure (or after limited past exposure) in individuals in their 20s and 30s. They are usually transient but may reoccur, may involve one or both sides of the chest simultaneously or sequentially, and may be either silent or associated with symptoms including chest tightness and/or pleural pain and dyspnoea. The pleural fluid contains leucocytes, often blood, and is albumin-rich; only rarely does it contain asbestos bodies or fibres which may, however, be found in biopsy material of the pleura or underlying lung. Most benign pleural effusions clear spontaneously, though in a small proportion of subjects (of the order of 10% in one series) these effusions may evolve into diffuse pleural fibrosis (see figure 6), with or without the development of lung fibrosis. Local pleural reactions may also fold in upon themselves, trapping lung tissue and causing well defined lesions called rounded atelectasis or pseudotumour because they may have the radiological appearance of lung cancer. In contrast to pleural plaques, which seldom cause symptoms, visceroparietal pleural reactions are usually associated with some shortness of breath as well as lung function impairment, particularly when there is obliteration of the costophrenic angle. In one study, for instance, average FVC deficit was 0.07 l when the chest wall was involved and 0.50 l when the costophrenic angle was involved (Ernst and Zejda in Liddell and Miller 1991). As already indicated, the distribution and determinants of pleural reactions vary considerably between workforces, with prevalence rates increasing with:

1. estimated residence time of fibre in the lung (measured as time since first exposure)
2. exposures primarily to or including amphibole and
3. possibly intermittence of exposure, given the high rates of contamination in occupations in which use of asbestos materials is intermittent, but exposure probably heavy.

Lung Cancer

Historical perspective

The 1930s saw the publication of a number of clinical case reports from the United States, the United Kingdom and Germany of lung cancer (a condition much less common then than it is today) in asbestos workers, most of whom also had asbestosis of varying degrees of severity. Further evidence of the association between the two conditions was provided in the 1947 Annual Report of His Majesty’s Chief Inspector of Factories, which noted that lung cancer had been reported in 13.2% of male deaths attributed to asbestosis in the period 1924 to 1946 and in only 1.3% of male deaths attributed to silicosis. The first study to address the causal hypothesis was a cohort mortality study of a large United Kingdom asbestos textile plant (Doll 1955), one of the first such workforce-based studies, and by 1980, after at least eight such studies in as many workforces had confirmed an exposure-response relationship, the association was generally accepted as causal (McDonald and McDonald in Antman and Aisner 1987).

Clinical features and pathology

In the absence of other associated asbestos disease, the clinical features and criteria for the diagnosis of asbestos-associated lung cancer are no different from those for lung cancer not associated with asbestos exposure. Originally, asbestos-associated lung cancers were considered to be scar cancers, similar to lung cancer seen in other forms of diffuse lung fibrosis such as scleroderma. Features which favoured this view were their location in the lower lung lobes (where asbestosis is usually more marked), their sometimes multicentric origin and a preponderance of adenocarcinoma in some series. However, in most reported workforce-based studies, the distribution of cell types was no different from that seen in studies of non-asbestos-exposed populations, supporting the view that asbestos itself may be a human carcinogen, a conclusion reached by the International Agency for Research on Cancer (World Health Organization: International Agency for Research on Cancer 1982). Most but not all asbestos-related lung cancers occur in association with radiologic asbestosis (see below).

Epidemiology

Cohort studies confirm that lung cancer risk increases with exposure, though the fractional rate of increase for each fiber per milliliter per year exposed varies, and is related both to fibre type and to industrial process (Health Effects Institute—Asbestos Research 1991). For instance, for mainly chrysotile exposures in mining, milling and friction product manufacture, the increase ranged from approximately 0.01 to 0.17%, and in textile manufacture from 1.1 to 2.8%, while for exposure to amosite insulation products and some cement product exposures involving mixed fibre, rates of as high as 4.3 and 6.7% have been recorded (Nicholson 1991). Cohort studies in asbestos workers also confirm that cancer risk is demonstrable for non-smokers and that risk is increased (closer to multiplicative than additive) by cigarette smoking (McDonald and McDonald in Antman and Aisner 1987). The relative risk for lung cancer declines after exposure ceases, although the decline appears slower than that which occurs after quitting smoking. Lung dust burden studies are also consistent with a fibre gradient in lung cancer production; 32 men in Pacific shipyard trades with mainly amosite exposure had a lung dust burden of 1.1 million amosite fibres per gram of dry lung tissue compared to 36 Quebec chrysotile miners with an average lung dust burden of 13 million chrysotile fibres per gram of lung tissue (Becklake and Case 1994).

Relationship to asbestosis

In the 1955 autopsy study of causes of death in 102 workers employed in the United Kingdom asbestos textile factory referred to above (Doll 1955), lung cancer was found in 18 individuals, 15 of whom also had asbestosis. All subjects in whom both conditions were found had worked for at least 9 years before 1931, when national regulations for asbestos dust control were introduced. These observations suggested that as exposure levels decreased, the competing risk of death from asbestosis also decreased and workers lived long enough to exhibit the development of cancer. In most workforce-based studies, older workers with long service have some pathological evidence of asbestosis (or asbestos-related small airways disease) at autopsy even though this may be minimal and not detectable on the chest radiograph in life (McDonald and McDonald in Antman and Aisner 1987). Several but not all cohort studies are consistent with the view that not all excess lung cancers in populations exposed to asbestos are related to asbestosis. More than one pathogenetic mechanism may in fact be responsible for lung cancers in individuals exposed to asbestos depending on the site and deposition of the fibres. For instance, long thin fibres, which are deposited preferentially at airway bifurcations, are thought to become concentrated and to act as inducers of the process of cancerogenesis through chromosomal damage. Promoters of this process may include continued exposure to asbestos fibres or to tobacco smoke (Lippman 1995). Such cancers are more likely to be squamous cell in type. By contrast, in lungs which are the site of fibrosis, cancerogenesis may result from the fibrotic process: such cancers are more likely to be adenocarcinomas.

Implications and attributability

While determinants of excess cancer risk can be derived for exposed populations, attributability in the individual case cannot. Obviously, attributability to asbestos exposure is more likely and credible in an exposed individual with asbestosis who has never smoked than in an exposed individual without asbestosis who smokes. Nor can this probability be modelled reasonably. Lung dust burden measurements may supplement a careful clinical assessment but each case must be evaluated on its merits (Becklake 1994).

Malignant Mesothelioma

Pathology, diagnosis, ascertainment and clinical features

Malignant mesotheliomas arise from the serous cavities of the body. Approximately two-thirds arise in the pleura, about one-fifth in the peritoneum, while the pericardium and tunica vaginalis are much less frequently affected (McDonald and McDonald in Lidell and Miller 1991). Since mesothelial cells are pluripotential, the histological features of mesothelial tumours may vary; in most series, epithelial, sarcomatous and mixed forms account for approximately 50, 30 and 10% of cases respectively. Diagnosis of this rare tumour, even in the hands of experienced pathologists, is not easy, and mesothelioma panel pathologists often confirm only a small percentage, in some studies less than 50% of cases submitted for review. A variety of cytological and immunohistochemical techniques have been developed to assist in differentiating malignant mesothelioma from the main alternative clinical diagnoses, namely, secondary cancer or reactive mesothelial hyperplasia; this remains an active research field in which expectations are high but findings inconclusive (Jaurand, Bignon and Brochard 1993). For all these reasons, ascertainment of cases for epidemiological surveys is not straightforward, and even when based on cancer registries, may be incomplete. In addition, confirmation by expert panels using specified pathological criteria is necessary to assure comparability in criteria for registration.

Clinical features

Pain is usually the presenting feature. For pleural tumours, this starts in the chest and/or shoulders, and may be severe. Breathlessness follows, associated with pleural effusion and/or progressive encasement of the lung by tumour, and weight loss. With peritoneal tumours, abdominal pain is usually accompanied by swelling. Imaging features are illustrated in figure 7. The clinical course is usually rapid and median survival times, six months in a 1973 report and eight months in a 1993 report, have changed little over the last two decades, despite the greater public and medical awareness which often leads to earlier diagnosis and despite advances in diagnostic techniques and an increase in the number of treatment options for cancer.

Figure 7. Malignant mesothelioma

Seen on an overpenetrated chest roetngenogram (A) as a large mass in the axillary region. Note the associated reduction in volume of the right haemothorax with marked irregular nodular thickening of the pleura of the whole right lung. CT scan (B) confirms the extensive pleural thickening involving parietal and mediastinal pleura (closed arrows) in and around the ribs. Source: Fraser et al. 1990

Epidemiology

In the 15 years which followed the 1960 report of the mesothelioma case series from the Northwest Cape, South Africa (Wagner 1996), international confirmation of the association came from reports of other case series from Europe (United Kingdom, France, Germany, Holland), the United States (Illinois, Pennsylvania and New Jersey) and Australia, and of case control studies from the United Kingdom (4 cities), Europe (Italy, Sweden, Holland) and from the United States and Canada. Odds ratios in these studies ranged from 2 to 9. In Europe in particular, the association with shipyard occupations was strong. In addition, proportional mortality studies in asbestos-exposed cohorts suggested that risk was associated both with fibre type and with industrial process, with rates attributable to mesothelioma ranging from 0.3% in chrysotile mining to 1% in chrysotile manufacturing, compared with 3.4% in amphibole mining and manufacturing and as high as 8.6% for exposure to mixed fibre in insulation (McDonald and McDonald in Liddell and Miller 1991). Similar fibre gradients are shown in cohort mortality studies which, given the short survival times of these tumours, are a reasonable reflection of incidence. These studies also show longer latent periods when exposure was to chrysotile compared to amphiboles. Geographical variation in incidence has been documented using Canadian age-and sex-specific rates for 1966 to 1972 to calculate expected rates (McDonald and McDonald in Liddell and Miller 1991); rate ratios (values actually observed over expected) were 0.8 for the United States (1972), 1.1 for Sweden (1958 to 1967), 1.3 for Finland (1965 to 1969), 1.7 for United Kingdom (1967 to 1968), and 2.1 for the Netherlands (1969 to 1971). While technical factors including ascertainment may obviously contribute to the variation recorded, the results do suggest higher rates in Europe than in North America.

Time trends and gender differences in mesothelioma incidence have been used as a measure of the health impact of asbestos exposure on populations. The best estimates for overall rates in industrialized countries before 1950 are under 1.0 per million for men and women (McDonald and McDonald in Jaurand and Bignon 1993). Subsequently, rates increased steadily in men and either not at all or less in women. For instance, overall rates in men and women per million were reported at 11.0 and under 2.0 in the United States in 1982, 14.7 and 7.0 in Denmark for 1975-80, 15.3 and 3.2 in the United Kingdom for 1980-83, and 20.9 and 3.6 in the Netherlands for 1978-87. Higher rates in men and women, but excluding younger subjects, were reported for crocidolite mining countries: 28.9 and 4.7 respectively in Australia (aged 2+) for 1986, and 32.9 and 8.9 respectively in South African Whites (aged 1+) for 1988 (Health Effects Institute—Asbestos Research 1991). The rising rates in men are likely to reflect occupational exposure, and if so, they should level off or decrease within the 20-to 30-year “incubation” period following the introduction of workplace controls and reduction of exposure levels in most workplaces in most industrialized countries in the 1970s. In countries in which the rates in women are rising, this increase may reflect their increasing engagement in occupations with risk exposure, or the increasing environmental or indoor contamination of urban air (McDonald 1985).

Aetiology

Environmental factors are clearly the main determinants of mesothelioma risk, exposure to asbestos being the most important, though the occurrence of family clusters maintains interest in the potential role of genetic factors. All asbestos fibre types have been implicated in mesothelioma production, including anthophyllite for the first time in a recent report from Finland (Meurman, Pukkala and Hakama 1994). However, there is a substantial body of evidence, from proportional and cohort mortality studies and lung burden studies, which suggests the role of a fibre gradient in mesothelioma production, risk being higher for exposures to mainly amphiboles or amphibole chrysotile mixtures, compared with mainly chrysotile exposures. In addition, there are rate differences between workforces for the same fibre at what appears to be the same exposure level; these remain to be explained, though fibre size distribution is a likely contributing factor.

The role of tremolite has been widely debated, a debate sparked by the evidence of its biopersistence in lung tissue, animal and human, compared to that of chrysotile. A plausible hypothesis is that the many short fibres which reach and are deposited in peripheral lung airways and alveoli are cleared to subpleural lymphatics where they collect; their potency in mesothelioma production depends on their biopersistence in contact with pleural surfaces (Lippmann 1995). In human studies, mesothelioma rates are lower for populations exposed at work to chrysotile relatively uncontaminated by tremolite (for instance, in Zimbabwean mines) compared to those exposed to chrysotile which is so contaminated (for instance, in Quebec mines), and these findings have been replicated in animal studies (Lippmann 1995). Also, in a multivariate analysis of lung fibre burden in material from a Canada-wide mesothelioma case control study (McDonald et al. 1989), the results suggested that most if not all mesotheliomas could be explained by tremolite lung fibre burden. Finally, a recent analysis of the mortality in the cohort of over 10,000 Quebec chrysotile miners and millers born between 1890 and 1920, and followed to 1988 (McDonald and McDonald 1995), supports this view: in almost 7,300 deaths, the 37 mesothelioma deaths were concentrated in certain mines from the Thetford area, yet the lung burden of 88 cohort members from the mines implicated did not differ from that of miners from other mines in terms of chrysotile fibre burden, only in terms of tremolite burden (McDonald et al. 1993).

What has been called the tremolite question is perhaps the most important of the currently debated scientific issues, and it also has public health implications. Note must also be made of the important fact that in all series and jurisdictions, a certain proportion of cases occur without reported asbestos exposure, and that only in some of these cases do lung dust burden studies point to previous environmental or occupational exposure. Other occupational exposures have been implicated in mesothelioma production, for instance in talc, vermiculite and possibly mica mining, but in these, the ore contained either tremolite or other fibres (Bignon, Peto and Saracci 1989). An open search for other exposures, occupational or non-occupational, to fibres, inorganic and organic, and to other agents which may be associated with mesothelioma production, should continue.

Other Asbestos-Related Diseases

Chronic airways disease

Usually included under this rubric are chronic bronchitis and chronic obstructive pulmonary disease (COPD), both of which can be diagnosed clinically, and emphysema, until recently diagnosed only by pathological examination of lungs removed at autopsy or otherwise (Becklake 1992). A major cause is smoking, and, over the past decades, mortality and morbidity due to chronic airways disease has increased in most industrialized countries. However, with the decline of pneumoconiosis in many workforces, evidence has emerged to implicate occupational exposures in the genesis of chronic airways disease, after taking into account the dominant role of smoking. All forms of chronic airways disease have been shown to be associated with work in a variety of dusty occupations, including those occupations in which an important component of the dust contaminating the workplace was asbestos (Ernst and Zejda in Liddell and Miller 1991). Total pollutant burden, rather than exposure to any of its particular components, in this case asbestos dust, is thought to be implicated, in much the same way as the effect of smoking exposure on chronic airways diseases is viewed, that is, in terms of total exposure burden (e.g., as pack-years), not exposure to any one of the over 4,000 constituents of tobacco smoke. (see elsewhere in this volume for a further discussion of the relationship between occupational exposures and chronic airways disease).

Other cancers

In several of the earlier cohort studies of asbestos exposed workers, mortality attributable to all cancers exceeded that expected, based on national or regional vital statistics. While lung cancer accounted for most of the excess, other cancers implicated were gastro-intestinal cancers, laryngeal cancer and cancer of the ovaries, in that order of frequency. For gastro-intestinal cancers, (including those affecting the oesophagus, the stomach, the colon and the rectum), the relevant exposure in occupational cohorts is presumed to be via swallowing asbestos-laden sputum raised from the major airways in the lung, and in earlier times, (before protection measures were taken against exposure at lunch sites) direct contamination of food in workplaces which had no lunch areas separate from working areas of plants and factories. Retrograde flow via the thoracic duct from lymph nodes draining the lung might also occur (see “Fate of inhaled fibres”, page 10.54). Because the association was inconsistent in the different cohorts studied, and because exposure response relationships were not always seen, there has been a reluctance to accept the evidence of the association between occupational exposure and asbestos exposure as causal (Doll and Peto 1987; Liddell and Miller 1991).

Cancer of the larynx is much less common than gastro-intestinal or lung cancer. As early as the 1970s, there were reports of an association between cancer of the larynx and asbestos exposure. Like lung cancer, a major risk factor and cause of laryngeal cancer is smoking. Laryngeal cancer is also strongly associated with alcohol consumption. Given the location of the larynx (an organ exposed to all the inhaled pollutants to which the lungs are exposed) and given the fact that it is lined by the same epithelium that lines the major bronchi, it is certainly biologically plausible that cancer of the larynx occurs as a result of asbestos exposure. However, the overall evidence available to date is inconsistent, even from large cohort studies such as the Quebec and Balangero (Italy) chrysotile miners, possibly because it is a rare cancer and there is still reluctance to regard the association as causal (Liddell and Miller 1991) despite its biological plausibility. Cancer of the ovaries has been recorded in excess of expected in three cohort studies (WHO 1989). Misdiagnosis, in particular as peritoneal mesothelioma, may explain most of the cases (Doll and Peto 1987).

Prevention, Surveillance and Assessment

Historical and current approaches

Prevention of any pneumoconiosis, including asbestosis, has traditionally been through:

1. engineering and work practices to maintain airborne fibre levels as low as possible, or at least in conformity with permissible exposure levels usually set by law or regulation
2. surveillance, conducted to record trends of markers of disease in exposed populations and monitor the results of control measures
3. education and product labelling aimed at assisting workers as well as the general public in avoiding non-occupational exposure.

Permissible exposure levels were originally directed at controlling asbestosis and were based on industrial hygiene measurements in million particles per cubic foot, gathered using the same methods as were used for the control of silicosis. With the shift in biological focus to fibres, in particular long thin ones, as the cause of asbestosis, methods more appropriate to their identification and measurement in air were developed and, given these methods, the focus on the more abundant short fibres which contaminate most workplaces was minimized. Aspect (length to diameter) ratios for most particles of milled chrysotile asbestos fall within the range 5:1 to 20:1, going up to 50:1, in contrast to most particles of milled amphibole asbestos (including cleavage fragments) whose values fall below 3:1. The introduction of the membrane filter for fibre counting of air samples led to an arbitrary industrial hygiene and medical definition of a fibre as a particle at least 5μm long, 3μm or less thick, and with a length to width ratio of at least 3:1. This definition, used for many of the studies of exposure-response relationships, forms the scientific basis for setting environmental standards.

For instance, it was used in a meeting sponsored by the World Health Organization (1989) to propose occupational exposure limits and has been adopted by agencies such as the US Occupational Safety and Health Administration; it is retained mainly for reasons of comparability. The WHO meeting, chaired by Sir Richard Doll, while recognizing that the occupational exposure limit in any country can only be set by the appropriate national body, recommended that countries having high limits should take urgent steps to lower the occupational exposure for an individual worker to 2 f/ml (eight-hour time-weighted average) and that all countries should move as quickly as possible to 1 f/ml (eight-hour time-weighted average) if they had not already done so. With the decrease in asbestosis rates in some industrialized countries, and concern over asbestos-related cancers in all, attention has now shifted to determining whether the same fibre parameters—that is, at least 5mm long, 3mm or less thick, and with a length to width ratio of at least 3:1—are also appropriate for controlling carcinogenesis (Browne 1994). A current theory of asbestos carcinogenesis implicates short as well as long fibres (Lippmann 1995). In addition, given the evidence for a fibre gradient in mesothelioma and lung cancer production, and to a lesser extent, for asbestosis production, an argument could be made for permissible exposure levels taking fibre type into account. Some countries have addressed the issue by banning the use (and thus the import) of crocidolite, and setting more stringent exposure levels for amosite, namely 0.1 f/l (McDonald and McDonald 1987).

Exposure levels in the workplace

Permissible exposure levels embody the hypothesis, based on all available evidence, that human health will be preserved if exposure is maintained within those limits. Revision of permissible exposure levels, when it occurs, is invariably towards greater stringency (as described in the paragraph above). Nevertheless, despite good compliance with workplace controls, cases of disease continue to occur, for reasons of personal susceptibility (for instance, higher-than-average fibre retention rates) or because of failure of workplace controls for certain jobs or processes. Engineering controls, improved workplace practices and the use of substitutes, described elsewhere in the chapter, have been implemented internationally (Gibbs, Valic and Browne 1994) in larger establishments through industry, union and other initiatives. For instance, according to a 1986 worldwide industry review, compliance with the current recommended standard of 1 f/ml had been achieved at 83% of production sites (mines and mills) covering 13,499 workers in 6 countries; in 96% of 167 cement factories operating in 23 countries; in 71% of 40 textile factories covering over 2,000 workers operating in 7 countries; and in 97% of 64 factories manufacturing friction materials, covering 10,190 workers in 10 countries (Bouige 1990). However, a not unimportant proportion of such workplaces still do not comply with regulations, not all manufacturing countries participated in this survey, and the anticipated health benefits are evident only in some national statistics, not in others (“Diagnosis and case management”, page 10.57). Control in demolition processes and small enterprises using asbestos continues to be less than successful, even in many industrialized countries.

Surveillance

The chest radiograph is the main tool for asbestosis surveillance, cancer registries and national statistics for asbestos-related cancers. A commendable initiative in international surveillance of mining, tunnelling and quarrying, undertaken by the ILO through voluntary reporting from governmental sources, focuses on coal and hard-rock mining but could include asbestos. Unfortunately, follow-through has been poor, with the last report, which was based on data for 1973-77, being published in 1985 (ILO 1985). Several countries issue national mortality and morbidity data, an excellent example being the Work-related Lung Disease Surveillance Report for the United States, a report referred to above (USDHSS 1994). Such reports provide information to interpret trends and evaluate the impact of control levels at a national level. Larger industries should (and many do) keep their own surveillance statistics, as do some unions. Surveillance of smaller industries may require specific studies at appropriate intervals. Other sources of information include programmes such as the Surveillance of Work-related Respiratory Diseases (SWORD) in the United Kingdom, which gathers regular reports from a sample of the country’s chest and occupational physicians (Meredith and McDonald 1994), and reports from compensation boards (which often, however, do not provide information on workers at risk).

Product labelling, education and the information highway

Mandatory product labelling together with worker education and education of the general public are powerful tools in prevention. While in the past, this took place within the context of worker organizations, worker management committees, and union education programmes, future approaches could exploit electronic highways to make available databases on health and safety in toxicology and medicine.

Exposure in buildings and from water supplies

In 1988, a review of potential health risks associated with working in buildings constructed using asbestos-containing materials was mandated by the US Congress (Health Effects Institute—Asbestos Research 1991). The results of a large number of indoor sampling studies from Europe, the United States and Canada were used in risk estimates. The lifetime risk for premature cancer death was estimated to be 1 per million for those exposed for 15 years in schools (for estimated exposure levels ranging from .0005 to .005 f/ml) and 4 per million for those exposed for 20 years working in office buildings (for estimated exposure levels ranging from .0002 to .002 f/ml). For comparison, the risk for occupational exposure to 0.1 f/ml (i.e., in compliance with the permissible exposure limit proposed by the US Occupational Safety and Health Administration) for 20 years was estimated at 2,000 per million exposed. Measurements in drinking water in urban communities show considerable variation, from undetectable levels to high levels ranging from 0.7 million f/l in Connecticut, USA, to levels ranging from 1.1 million to 1.3 billion f/l in the mining areas of Quebec (Bignon, Peto and Saracci 1989). Some contamination may also occur from the asbestos cement pipes which must service most urban water reticulation services in the world. However, a working group which reviewed the evidence in 1987 did not discount the potential associated hazard, but did not regard the health risks associated with asbestos ingestion as “one of the most pressing public health hazards” (USDHHS 1987), a view concordant with the concluding remarks in an IARC (WHO) monograph on non-occupational exposure to mineral fibres (Bignon, Peto and Saracci 1989).

Asbestos and other fibres in the 21st century

The first half of the twentieth century was characterized by what could be described as gross neglect of asbestos-related ill health. Before the Second World War, the reasons for this are not clear; the scientific basis for control was there but perhaps not the will and not the worker militancy. During the war, there were other national and international priorities, and after the war, pressures of urbanization by a rapidly increasing world population took precedence, and perhaps fascination in an industrial age with the versatility of the “magic” mineral diverted attention from its dangers. Following the first International Conference on the Biological Effects of Asbestos in 1964 (Selikoff and Churg 1965), asbestos-related disease became a cause célèbre, not only on its own account, but also because it marked a period of labour-management confrontation concerning the rights of the worker to knowledge about workplace hazards, health protection and fair compensation for injury or illness. In countries with no-fault worker’s compensation, asbestos-related disease on the whole received fair recognition and handling. In countries where product liability and class action suits were more usual, large awards have been made to some affected workers (and their lawyers) while others have been left destitute and without support. While the need for fibres in modern societies is unlikely to diminish, the role of the mineral fibres vis-à-vis other fibres may change. There has already been a shift in uses both within and between countries (see “Other sources of exposure”, page 10.53). Though the technology exists to diminish workplace exposures, there remain workplaces in which it has not been applied. Given the current knowledge, given international communication and product labelling, and given worker education and industry commitment, it should be possible to use this mineral to provide cheap and durable products for use in construction and water reticulation on an international basis without risk to user, worker, manufacturer or miner, or to the general public at large.

Back

Shortly after the end of the First World War, while doing research to find a material able to replace diamond in metal-drawing nozzles, Karl Schoeter patented in Berlin a sintering process (pressurization plus heating at 1,500°C) of a mixture of fine tungsten carbide (WC) powder with 10% of cobalt to produce “hard metal”. The main characteristics of this sinter are the extreme hardness, only slightly inferior to that of diamond, and the maintenance of its mechanical properties at high temperatures; these characteristics make it suitable for use in drawing metal, for welded inserts, and for high-speed tools for machining of metals, stone, wood and materials with high resistance to wear or to heat, in the mechanical, aeronautical and ballistic fields. The use of hard metal is continually expanding all over the world. In 1927 Krupp extended the use of hard metal into the cutting tools field, calling it “Widia” (wie Diamant—like diamond), a name still in use today.

Sintering remains the basis of all hard metal production: techniques are improved by the introduction of other metallic carbides—titanium carbide (TiC) and tantalum carbide (TaC)—and by treatment of hard metal parts for mobile cutting inserts with one or more layers of titanium nitride or aluminium oxide and of other very hard compounds applied with chemical vapour deposition (CVD) or physical vapour deposition (PVD). The fixed inserts welded to the tools cannot be plated, but are repeatedly sharpened by a diamond grinding wheel (figures 1 and 2).

Figure 1. (A) Examples of some hard metal drawing mobile inserts, plated with golden-yellow tungsten nitride; (B) insert welded to the tool and working in steel drawing.

Figure 2. Fixed inserts welded to (A) stone drill and (B) saw disk.

The hard metal sinter is formed by particles of metallic carbides incorporated in a matrix formed by cobalt, which melts during sintering, interacting and occupying the interstices. Cobalt is therefore the structure gluing material, which assumes metal-ceramic characteristics (figures 3, 4, and 5).

Figure 3. Microstructure of a WC/Co sintering; WC particles are incorporated into the Co light matrix (1,500x).

Figure 4. Microstructure of a WC + TiC + TaC + Co sintering. Along with WC prismatic particles, globular particles formed by a solid solution of TiC + TaC are observed.  The light matrix is formed by Co (1,500x).

Figure 5. Sintering microstructure plated by multiple very hard layers (2,000x).

The sintering process uses very fine metallic carbide powders (average diameters from 1 to 9μm) and cobalt powders (average diameter from 1 to 4μm) which are mixed, treated with paraffin solution, die-pressed, de-waxed at low temperature, pre-sintered at 700 to 750°C and sintered at 1,500°C (Brookes 1992).

When sintering is done with inadequate methods, improper techniques and poor industrial hygiene, the powders can pollute the atmosphere of the work environment: workers are therefore exposed to the risk of inhalation of metallic carbide powders and cobalt powders. Along with the primary process there are other activities which can expose the workers to the risk of aerosol inhalation of hard metal. Sharpening of fixed inserts welded to tools is normally carried out by dry diamond grinding or, more frequently, cooled with liquids of different kinds, producing powders or mists formed by very small drops containing metallic particles. Particles of hard metal are also used in the production of a high-resistance layer on steel surfaces subjected to wear, applied through methods (plasma coating process and others) based on the combination of a powder spray with an electric arc or a controlled explosion of a gas mixture at high temperature. The electric arc or the explosive flow of the gas determines the fusion of the metallic particles and their impact on the surface being plated.

First observations on “hard metal diseases” were described in Germany in the 1940s. They reported a diffuse, progressive pulmonary fibrosis, called Hartmetallungenfibrose. During the next 20 years parallel cases were observed and described in all industrial countries. The workers affected were in the majority of cases in charge of the sintering. From 1970 to the present, several studies indicate that the pathology to the breathing apparatus is caused by the inhalation of hard metal particles. It affects only susceptible subjects, and consists of the following symptoms:

• acute: rhinitis, asthma
• subacute: fibrosant alveolitis
• chronic: diffuse and progressive interstitial fibrosis.

It affects not only workers in charge of sintering, but anyone inhaling aerosol containing hard metal and particularly cobalt. It is mainly and perhaps exclusively caused by cobalt.

The definition of hard metal disease now includes a group of pathologies of the breathing apparatus, different from each other in clinical gravity and prognosis, but having in common a variable individual reactivity to the aetiological factor, cobalt.

More recent epidemiological and experimental information agree on the causal role of cobalt for acute symptoms in the upper respiratory tract (rhinitis, asthma) and for subacute and chronic symptoms in the bronchial parenchyma (fibrosing alveolitis and chronic interstitial fibrosis).

The pathogenic mechanism is based on the induction by Co of a hypersensitive immunoreaction: in fact, only some of the subjects present pathologies after short exposures to relatively low concentration, or even after longer and more intense exposures. Co concentrations in biological samples (blood, urine, skin) are not significantly different in those who have the pathology and those who do not; there is no correlation of dose and response at the tissue level; specific antibodies have been individuated (immunoglobins IgE and IgG) against a Co-albumin compound in asthmatics, and the Co patch test is positive in the subjects with alveolitis or fibrosis; the cytological aspects of the giant-cellular alveolitis are compatible with immunoreaction, and acute or subacute symptoms tend to regress when the subjects are removed from exposure to Co (Parkes 1994).

The immunological basis of hypersensitivity to Co has not yet been satisfactorily explained; it is not possible, therefore, to identify a reliable marker of individual susceptibility.

Identical pathologies to those found in the subjects exposed to hard metals were also observed in diamond cutters, who use disks formed by microdiamonds cemented with Co and who therefore inhale only Co and diamond particles.

It is not yet fully demonstrated that pure Co (all other inhaled particles excluded) is capable alone of producing the pathologies and above all the diffused interstitial fibrosis: the particles inhaled with Co could have a synergistic as well as modulating effect. Experimental studies seem to demonstrate that the biological reactivity to a mixture of Co particles and of tungsten is stronger than that caused by Co alone, and significant pathologies are not to be observed in the workers in charge of the production of pure Co powder (Science of the Total Environment 1994).

Clinical symptoms of hard metal disease, which, on the basis of current aetiopathogenic knowledge should be more precisely called “cobalt disease”, are, as mentioned before, acute, subacute and chronic.

Acute symptoms include a specific respiratory irritation (rhinitis, laryngo-tracheitis, pulmonary oedema) caused by exposure to high concentrations of Co powder or Co smoke; they are observable only in exceptional cases. Asthma is observed more frequently. It appears in 5 to 10% of the workers exposed to cobalt concentrations of 0.05 mg/m³, the current US threshold limit value (TLV). Symptoms of thoracic constriction with dyspnoea and cough tend to appear at the end of the work shift or during the night. The diagnosis of occupational allergic bronchial asthma due to cobalt can be suspected on the basis of case history criteria, but it is confirmed by a specific bronchial stimulation test which determines the appearance of an immediate, delayed or dual bronchospastic response. Even respiratory capacity tests carried out at the beginning and at the end of the work shift can help the diagnosis. Asthmatic symptoms due to cobalt tend to disappear when the subject is removed from exposure, but, similarly to all other forms of occupational allergic asthma, symptoms can become chronic and irreversible when the exposure continues for a long time (years), despite the presence of respiratory disturbances. Highly bronchoreactive subjects can present non-allergic aetiological asthmatic symptoms, with a non-specific response to inhalation of cobalt and other irritating powders. In a high percentage of cases with allergic bronchial asthma, specific reaction towards a human Co-seroalbumin compound was found in the IgE serum. The radiological finding does not vary: only in rare cases can mixed forms of asthma plus alveolitis with radiological alteration specifically caused by alveolitis be found. Bronchodilator therapy, along with an immediate end of the work exposure, leads to complete recovery for cases that are of recent onset, not yet chronic.

Subacute and chronic symptoms include fibrosant alveolitis and chronic diffuse and progressive interstitial fibrosis (DIPF). The clinical experience seems to indicate that the transition from alveolitis to interstitial fibrosis is a process which evolves gradually and slowly in time: one can find cases of pure initial alveolitis reversible with withdrawal from the exposure plus corticosteroid therapy; or cases with an already present fibrosis component, which can improve but not reach complete recovery by removing the subject from exposure, even with additional therapy; and finally, cases in which the predominant situation is that of an irreversible DIPF. The occurrence of such cases is low in the exposed workers, very much lower than the percentage of allergic asthma cases.

Alveolitis is easy to study today in its cytological components through broncho-alveolar lavage (BAL); it is characterized by a large increase of the total cell number, mainly formed by macrophages, with numerous multinuclear giant cells and the typical aspect of foreign-body giant cells containing at times cytoplasmic cells (figure 6); even an absolute or relative increase of lymphocytes is frequent, with a decreased CD4/CD8 ratio, associated with a large increase of eosinophiles and mast cells. Rarely, alveolitis is mainly lymphocytic, with CD4/CD8 ratio inverted, as it occurs in the pneumopathies due to hypersensitivity.

Figure 6. Cytological BAL in a macrophagic mono-nuclear giant-cellular alveolitis case caused by hard metal. Between the mononuclear macrophages and the lymphocyte, a giant foreign-body type of cell (400x) is observed.

Subjects with alveolitis report dyspnoea linked with fatigue, loss of weight and dry cough. Crepitation is present in the lower lung with functional alteration of a restrictive kind and diffused round or irregular radiological opacity. The patch test for cobalt is positive in the majority of cases. In the susceptible subjects, alveolitis is revealed after a relatively short period of workplace exposure, of one or a few years. In its initial phases this form is reversible up to complete recovery with the simple removal from exposure, with better results if this is combined with cortisone therapy.

The development of diffuse interstitial fibrosis aggravates the clinical symptoms with a worsening of the dyspnoea, which appears even after minimal strain and then even at rest, with worsening of the restrictive ventilatory impairment which is linked to a reduction of the capillary-alveolar diffusion, and with appearance of radiographic opacities of a linear type and of honeycombing (figure 7). The histological situation is that of a fibrosing alveolitis of a “mural type”.

Figure 7. Thoracic radiograph of a subject affected by interstitial fibrosis caused by hard metal. Linear and diffused opacity and honeycombing aspects are observed.

The evolution is rapidly progressive; therapies are ineffective and the prognosis doubtful. One of the cases diagnosed by the author eventually required a lung transplant.

The occupational diagnosis is based on case history, BAL cytological pattern and cobalt patch test.

Prevention of hard metal disease, or, more precisely, of cobalt disease, is now mainly technical: protecting the workers through the elimination of powder, smokes or mists with adequate ventilation of the work areas. In fact, the lack of knowledge about the factors which determine individual hypersensitivity to cobalt makes the identification of susceptible people impossible, and the maximum effort must be made to reduce the atmospheric concentrations.

The number of people at risk is underestimated because many sharpening activities are carried out in small industries or by craftspeople. In such workplaces, the US TLV of 0.05 mg/m³ is frequently exceeded. There is also some question as to the adequacy of the TLV for protecting workers against cobalt disease since dose-effect relationships for disease mechanisms involving hypersensitivity are not completely understood.

Routine surveillance must be accurate enough to identify cobalt pathologies in their earliest stages. An annual questionnaire aimed mainly at temporary symptoms must be administered, along with a medical examination that includes pulmonary function testing and other appropriate medical examinations. Since it has been demonstrated that there is a good correlation between cobalt concentrations in the work environment and the urinary excretion of the metal, it is appropriate to carry out semi-annual measurement of cobalt in urine (CoU) on samples taken at the end of the work week. When the exposure is at the level of the TLV, the biological exposure index (BEI) is estimated to be equal to 30μg Co/litre urine.

Pre-exposure medical examinations for the presence of pre-existing respiratory disease and bronchial hypersensitivity can be useful in the counselling and placement of workers. Metacholine tests are a useful indicator of non-specific bronchial hyperreactivity and may be useful in some settings.

International standardization of environmental and medical surveillance methods for workers exposed to cobalt is highly recommended.

Back

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

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.

Lung health

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.

Diatomaceous Earth

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.

Elemental Carbon

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.

Lung health

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

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

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.

Lung health

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

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.

Lung health

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.

Lung health

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 Compounds

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.

Phosphates

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

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.

Lung health

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

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.

Lung health

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

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.

Lung health

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.

Hairspray

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.

Back