Rosin (pine resin) . This substance is used in many industries, in particular for the manufacture of glue, melting at high temperature, and solder for soldering tin and lead. 4 cases are described in which bronchial provocative tests caused immediate reactions [Fawcett et al., 1976].
Hardeners for epoxy resins . Epoxy resins (other than pine resins) are used in the manufacture of sticky materials, hardened plastics, paints and many other industrial processes. They consist of two main components: unpolymerized resin and hardener (or polymerization agent). While asthma caused by the epoxy itself has not yet been discovered, immediate, late and double reactions to a number of hardening chemicals, including phthalic anhydride, trimellitic acid and triethylenetetramine, have been observed [Fawcett et al., 1977].
The list of substances that are used in industry is constantly growing (many of them are chemicals with low molecular weight) and which can cause asthmatic symptoms. The type of reaction depends on the individual. Sometimes the reaction occurs immediately, in other cases, only after a few hours, and finally, sometimes the reactions are twofold. Some patients (but not all) have found direct indications of immunological mechanisms, i.e., specific antibodies. Of course, the preparation of material suitable for the study of antibodies is associated with technical difficulties and this may at least partially explain the lack of direct evidence of an immunological mechanism. However, until these technical problems are resolved, it is necessary to be critical of the mechanism that causes asthma when in contact with many chemicals.
Miner pneumoconiosis
At first glance, it seems unlikely that low molecular weight substances can induce asthma through immunological mechanisms. It is equally unlikely that inorganic dust can cause an immunological response. Nevertheless, there are quite a few indications of immunological reactions in various forms of pneumoconiosis caused by inorganic dust, although if they play a role in pathogenesis, this role is still unclear.
Kaplan syndrome and rheumatoid factors . Caplan (1953) described large nodular lesions seen on chest radiographs of miners with rheumatoid arthritis. These lesions differed from progressive massive fibrosis not only in shape, character and distribution, but also in that the background created by pneumocoiosis was significantly less noticeable. Histologically, these nodules are similar to subcutaneous rheumatoid nodules. They contain a central zone of necrosis, surrounded by a shaft of histiocytes, which in turn are surrounded by lymphocytes, plasma cells and fibroblasts [Gough et al., 1955]. Studies using immunofluorescence conducted by Wagner and McCormick (1967) showed that necrotic lesions in which rheumatoid factor was found are surrounded by plasma cells. Pernis (1969) found both IgG and complement in connection with these lesions. In a later paper, Caplan et al. (1962) noted an increased frequency of rheumatoid factor (57%) in miners suffering from arthritis, but having rounded nodular lesions such as Kaplan, detected by x-ray examination in 21% of miners without arthritis with g-lesion (JLO / IUCC classification).
Thus, apparently , there is convincing evidence that rheumatoid arthritis with a circulating rheumatoid factor somehow changes the tissue reactions of the lungs to coal dust in a certain group of miners. Kaplan nodules with a rheumatoid factor have also been found in patients in contact with other types of inorganic acne, including silica dust and asbestos [Richards, Barrett, 1958; Telleson, 1961; Morgan, 1964].
In Kaplan’s syndrome, rheumatoid factor titers are variable. The distribution of titers in the group of miners with Kaplan syndrome was the same as in patients with rheumatoid arthritis who worked in mines. Among individuals with progressive massive fibrosis (PMF), high titers were more common than with simple pneumoconiosis [Caplan et al., 1962]. Davies and Lindars (1967) found that the frequency of “rheumatoid” ppevmokoniosis (that is, lesions such as Kailap or r-type) in radiographs among 21 thousand miners in 5 different mines was greater than the frequency of the rheumatoid factor among the general population. These data suggest that contact with charcoal does not predispose to rheumatoid disease, however, in miners in whose body the rheumatoid factor circulates, pulmonary lesions have a slightly different character than in patients without this antiglobulin.
The volume of indications is constantly growing that pathological lesions in rheumatoid arthritis depend on local deposition of immune complexes and, possibly, in some individuals, antibodies contained in the complex (i.e., with a deformed molecule) may develop a rheumatoid factor. It is also known that coal dust easily adsorbs a wide variety of proteins. One can only speculate on the pathogenesis of Kaplan nodules, however, it is quite possible that immune complexes adhere to dust deposits and stimulate a local tissue reaction. The presence of complement in these lesions, apparently, supports this assumption [Pernis, 1968]. Dust deposition with immune complexes, in turn, could stimulate local rheumatoid factor formation. It was found in surrounding plasma cells [Wagner, McCormick, 1967]. There is no reason to share the assumption put forward several years ago that the formation of these lesions depends on the associated tuberculosis infection.