The expression pneumoconiosis, from the Greek pneuma (air, wind) and konis (dust) was coined in Germany by Zenker in 1867 to denote changes in the lungs caused by the retention of inhaled dust. Gradually, the need for distinction between the effects of various types of dust became evident. It was necessary to discriminate among mineral or vegetable dust and their microbiological component. Consequently, the Third International Conference of Experts on Pneumoconiosis, organized by the ILO in Sydney in 1950, adopted the following definition: “Pneumoconiosis is a diagnosable disease of the lungs produced by the inhalation of dust, the term ‘dust’ being understood to refer to particulate matter in the solid phase, but excluding living organisms.”
However, the word disease seems to imply some degree of health impairment which may not be the case with pneumoconioses not connected with the development of lung fibrosis/scarring. In general, the reaction of lung tissue to the presence of dust varies with different dusts. Non-fibrogenic dusts evoke a tissue reaction in lungs characterized by minimal fibrotic reaction and absence of lung function impairment. Such dusts, examples of which are finely divided dusts of kaolinite, titanium dioxide, stannous oxide, barium sulphate and ferric oxide, are frequently referred to as biologically inert.
Fibrogenic dust such as silica or asbestos causes a more pronounced fibrogenic reaction resulting in scars in the lung tissue and obvious disease. The division of dusts into fibrogenic and non-fibrogenic varieties is by no means sharp because there are many minerals, notably silicates, which are intermediate in their ability to produce fibrotic lesions in the lungs. Nevertheless, it proved useful for clinical purposes and is reflected in the classification of pneumoconioses.
A new definition of pneumoconioses was adopted at the Fourth International Conference on Pneumoconiosis, Bucharest, 1971: “Pneumoconiosis is the accumulation of dust in the lungs and the tissue reactions to its presence. For the purpose of this definition, ‘dust’ is meant to be an aerosol composed of solid inanimate particles.”
In order to avoid any misinterpretation, the expression non-neoplastic is sometimes added to the words “tissue reaction”.
The Working Group at the Conference made the following comprehensive statement:
The Definition of Pneumoconiosis
Earlier on, in 1950, a definition of pneumoconiosis was established at the 3rd International Conference of Experts on Pneumoconiosis and this has continued to be used until the present time. In the meantime, the development of new technologies has resulted in more occupational risks, particularly those related to the inhalation of airborne contaminants. Increased knowledge in the field of occupational medicine has enabled new pulmonary diseases of occupational origin to be recognized but has also demonstrated the necessity for a re-examination of the definition of pneumoconiosis established in 1950. The ILO therefore arranged for a Working Group to be convened within the framework of the IVth International Pneumoconiosis Conference in order to examine the question of the definition of pneumoconiosis. The Working Group held a general discussion on the matter and proceeded to examine a number of proposals submitted by its members. It finally adopted a new definition of pneumoconiosis which was prepared together with a commentary. This text is reproduced below.
In recent years a number of countries have included under pneumoconiosis, because of socio-economic reasons, conditions which are manifestly not pneumoconiosis, but are nevertheless occupational pulmonary diseases. Under the term “disease” are included for preventive reasons the earliest manifestations which are not necessarily disabling or life shortening. Therefore the Working Group has undertaken to redefine pneumoconiosis as the accumulation of dust in the lungs and the tissue reactions to its presence. For the purpose of this definition, “dust” is meant to be an aerosol composed of solid inanimate particles. From a pathological point of view pneumoconiosis may be divided for the sake of convenience into collagenous or non-collagenous forms. A non-collagenous pneumoconiosis is caused by a non-fibrogenic dust and has the following characteristics:
- the alveolar architecture remains intact
- the stromal reaction is minimal and consists mainly of reticulin fibres
- the dust reaction is potentially reversible.
Examples of non-collagenous pneumoconiosis are those caused by pure dusts of tin oxide (stannosis) and barium sulphate (barytosis).
Collagenous pneumoconiosis is characterised by:
- permanent alteration or destruction of alveolar architecture
- collagenous stromal reaction of moderate to maximal degree, and
- permanent scarring of lung.
Such collagenous pneumoconiosis may be caused by fibrogenic dusts or by an altered tissue response to a non-fibrogenic dust.
Examples of collagenous pneumoconiosis caused by fibrogenic dusts are silicosis and asbestosis, whereas complicated coalworkers’ pneumoconiosis or progressive massive fibrosis (PMF) is an altered tissue response to a relatively non-fibrogenic dust. In practice, the distinction between collagenous and non-collagenous pneumoconiosis is difficult to establish. Continued exposure to the same dust, such as coal dust, may cause transition from a non-collagenous to a collagenous form. Furthermore, exposure to a single dust is now becoming less common and exposures to mixed dusts having different degrees of fibrogenic potential may result in pneumoconiosis which can range from the non-collagenous to the collagenous forms. There are in addition occupational chronic pulmonary diseases which, although they develop from the inhalation of dust are excluded from the pneumoconiosis because the particles are not known to accumulate in the lungs. The following are examples of potentially disabling occupational chronic pulmonary diseases: byssinosis, berylliosis, farmers’ lung, and related diseases. They have one common denominator, namely the aetiologic component of dust has sensitized the pulmonary or bronchial tissue so that if the lung tissue responds, the inflammation tends to be granulomatous and if the bronchial tissue responds, there is apt to be bronchial constriction. Exposures to noxious inhaled materials in certain industries are associated with an increased risk of mortality from carcinoma of the respiratory tract. Examples of such materials are radioactive ores, asbestos and chromates.
Adopted at the IVth ILO International Conference on Pneumoconiosis. Bucharest, 1971.