For definition of Groups, see Preamble Evaluation.
VOL.: 68 (1997) (p. 337)
5.1 Exposure data
Coal is a generic term for a heterogeneous, carbonaceous rock of varying composition and characteristics. It is mined in over 70 different countries around the world, and utilized in many more for electricity generation, heating, steel making and chemical processes. It varies in type from the soft and friable lignite to the hard and brittle anthracite. The term 'rank', which reflects the percentage carbon content, is used conventionally for its classification.
Coal typically contains variable but substantial amounts of mineral matter, of which quartz is an important component. The major exposures to coal dust occur during mining and processing of coal. In these operations the exposure includes dusts generated not only from the coal but also from adjacent rock strata and other sources. These may increase the quartz component of the airborne dust to about 10% of the total mixed dust, or to even greater levels if significant rock cutting is being undertaken.
Before 1970, in Germany, the United Kingdom and the United States, levels of respirable mixed dust in underground mines were typically 12 mg/m3 or less, depending on occupation and mine. More recently, regulations in some countries have brought these levels down to 3 mg/m3 or less. Dust concentrations in surface (strip, opencast) coal mines are generally lower than those found in underground mining. However, owing to the need to disturb overlying rock strata in surface mining, quartz exposures can be significant in some jobs, e.g. in rock drilling.
Exposure to coal dust also occurs during bulk loading and transfer, and at sites where coal is stored and used, such as power stations, steel and coke works, chemical plants, and during domestic use.
5.2 Human carcinogenicity data
There have been no epidemiological investigations on cancer risks in relation to coal dust per se. There is, however, a large body of published literature concerning cancer risks potentially associated with employment as a coal miner, including a small number of exposure-response associations with coal mine dust.
Cancers of the lung and stomach have been investigated most intensively among coal miners, with sporadic reports for other sites, such as urinary bladder. The absence of information on levels of the specific components of coal mine dust (e.g. coal, quartz, metals) further hindered interpretation of the epidemiological literature.
The evidence from occupational cohort studies for an association between coal mine dust and lung cancer has not been consistent; some studies revealed excess risks, whereas others indicated cohort-wide lung cancer deficits. There is no consistent evidence supporting an exposure-response relation for lung cancer with any of the customary dose surrogates, including duration of exposure, cumulative exposure or radiographic evidence of pneumoconiosis.
In contrast to the lung cancer findings, there have been reasonably consistent indications of stomach cancer excess among coal miners, detected both in occupational cohort studies and in community-based case-control studies. However, there is no consistent evidence supporting an exposure-response gradient for coal mine dust and stomach cancer.
5.3 Animal carcinogenicity data
Coal dust was tested for carcinogenicity both separately and in combination with diesel particle aerosols by inhalation in one adequate experiment in rats. The incidence of tumours was not increased compared to controls.
In one study in rats, single intrapleural injection of coal dust did not increase the incidence of thoracic tumours.
5.4 Other relevant data
The biological effects of coal mine dust in coal miners include simple coal workers' pneumoconiosis, progressive massive fibrosis, emphysema, chronic bronchitis and accelerated loss of lung function. Fibrotic endpoints in animals are attributable either to its quartz, clay or ash content; the age and dimensions of the particles probably also play a role. Human studies suggest that coal dust contains stable radicals and is able to induce reactive oxygen species that may cause DNA damage. Coal mine dust can cause cytotoxicity and induce the release of mediators from inflammatory cells; however, these effects are not predictable from its quartz content alone. In vitro, the cytotoxicity of quartz is clearly inhibited by the presence of coal dust, while the inflammatory activity is dependent on yet unidentified parameters. The release of cytokines and growth factors most probably contributes to pneumoconiosis development. Reactive oxygen species also can inactivate a-1-antitrypsin and bronchoalveolar leukocytes from rats inhaling coal mine dust had increased secretion of connective tissue proteases, leading to the development of emphysema.
Non-nitrosated extracts of a variety of coal dust samples were not mutagenic to Salmonella typhimurium. Non-nitrosated extracts of sub-bituminous coal dust induced mammalian cell transformation in one study; these extracts also induced chromosomal aberrations and sister chromatid exchange in human lymphocyte cultures. These extracts also induced sister chromatid exchange in Chinese hamster ovary cells.
Exposure of rodents to coal dust by inhalation or oral gavage did not produce any evidence of mutagenicity.
There is inadequate evidence in humans for the carcinogenicity of coal dust.
There is inadequate evidence in experimental animals for the carcinogenicity of coal dust.
Coal dust cannot be classified as to its carcinogenicity to humans (Group 3).
For definition of the italicized terms, see Preamble Evaluation.
See Also: Toxicological Abbreviations