Silica dust produces a distinctive reaction in the lung that eventually leads to the development of masses of fibrous tissue and distinctive nodules of dense fibrosis, which, by contracting, distort and damage the lung. Silicosis is a hazard in any occupation in which workers are exposed to silica dust, particularly rock drilling above or below ground, quarrying, or grinding with a wheel containing silica. Cases have also been reported in dental technicians, who use the material ground into a fine powder. Silicosisis usually fairly easy to detect on radiographs, and in its later stages itcauses considerable shortness of breath and reduction of the vital capacity (a maximal breath). Sandblasting without respiratory protection is exceedingly dangerous, and fatal cases of acute silicosiscaused by unprotected sandblasting have been reported. The dangers of silica are generally well recognized, and better protection has reduced the incidence of this condition. The disease may advance, with increasing disability, for years after the person has stopped inhaling the dust.
Coal dust alone, even if its silica content is very low, causes a distinctive pattern of change in the lung known as coalworker's pneumoconiosis (also called black lung). Initially the dust is deposited in the terminal bronchioles, where it causes a fibrotic reaction. At this stage there is little disability, but later the disease may progress to a more generalized form, and in some instances large masses of fibrotic tissue form in the lung. This condition, known as progressive massive fibrosis, is usually associated with severe disability and the risk of a secondary heart failure. It is not clear whether this stage is more likely to develop if pulmonary tuberculosis is superimposed on the respiratory damage caused by coal dust inhalation.
The widespread use of asbestos as an insulating material during World War II, and later in flooring,ceiling tiles, brake linings, and as a fire protectant sprayed inside buildings, led to a virtual epidemic of asbestos-related disease 20 years later. At first only the form of disease known as asbestosis, with radiographic changes and impaired function at an early stage, was recognized. Then it became apparent that exposure to much less asbestos than was needed to cause asbestosis led to thickening of the pleura, and, when both cigarette smoking and asbestos exposure occurred, there was a major increase in the risk for lung cancer. It is currently believed that the risks from smoking and from significant asbestos exposure are multiplicative in the case of lung cancer. Finally, a malignant tumour of the pleura known as mesothelioma was found to be caused almost exclusively by inhaled asbestos. Often a period of 20 years or more elapsed between exposure to asbestos and the development of the tumour.
As far as is known, all the respiratory changes associated with asbestos exposure are irreversible. Malignant mesothelioma is rare and unrelated to cigarette smoking, but survival after diagnosis is less than two years. Usually the pleural thickenings are not associated with disturbance of function or symptoms, although in occasional cases the pleuritis is more aggressive, in which case both may occur. It is not yet understood why asbestos causes such devastating changes. Furthermore, not all types of asbestos are equally dangerous; the risk of mesothelioma in particular appears to be much higher if crocidolite, a blue asbestos that comes from South Africa, is inhaled than if chrysotile is inhaled. But exposure to any type of asbestos is believed to increase the risk of lung cancer when associated with cigarette smoking. There has been much discussion of the advisability of removing asbestos from all buildings. It has been argued on the one hand that this is the only responsible policy, and on the other that more exposure might follow the careless removal of the material than would occur if it were left in place. All industrialized countries have imposed strict regulations for handling asbestos, and the work force is generally aware of the material's dangers.
The increasing use of man-made mineral fibres (as in fibreglass and rock wool) has led to concern that these may also be dangerous when inhaled; present evidence suggests that they do increase the risk of lung cancer in persons occupationally exposed to them. Standards for maximal exposure have been proposed.
The toxicity of beryllium was first discovered when it was widely used in the manufacture of fluorescent light tubes shortly after World War II. Beryllium causes the formation of granulomas in the lung and alveolar wall thickening, often with considerable disability as a result. Although beryllium is no longer used in the fluorescent light industry, it is still important in the manufacture of special steels and ceramics, and new cases of beryllium poisoning are occasionally reported.
It is not only inorganic minerals and dusts that may affect the lung. The dust produced in the processing of raw cotton may cause chronic obstructive lung disease. This does not have a characteristic pathology, however, and it does not give rise to emphysema. It is unclear whether cotton dust alone or the combination of cigarette smoke and cotton dust is particularly dangerous.The disease that results is known as byssinosis, or “brown lung.” Workers in cotton plants in England used to complain of “Monday morning fever” and were found to suffer an easily measurable decrement in ventilatory function when they returned to work after spending a weekend away from the plant. The active particle or contaminant in the cotton dust that is responsible for the syndrome has not yet been identified.
The dust from western red cedar may cause occupational asthma, and dust from the redwood andother trees may cause an acute hypersensitivity pneumonitis. Workers in the sugarcane industry may be affected by a similar syndrome, known as bagassosis; sisal workers also develop airflow obstruction.
Toluene diisocyanate, used in the manufacture of polyurethane foam, may cause occupational asthma at very low concentrations; in higher concentrations, such as may occur with accidental spillage, it causes a transient flulike illness associated with airflow obstruction. Prompt recognition of this syndrome has led to modifications in the industrial process involved.
Although the acute effects of exposure to many of these gases and vapours are well-documented, there is less certainty about the long-term effects of repeated low-level exposures over a long period of time. This is particularly the case when the question of whether work in a generally dusty environment has contributed to the development of chronic bronchitis or later emphysema—in other words, whether such nonspecific exposures increase the risk of these diseases in cigarette smokers. There is little unanimity on this question, but it is generally recognized that the differentiation is difficult.
Many chemicals can damage the lung in high concentration: these include oxides of nitrogen, ammonia, chlorine, oxides of sulfur, ozone, gasoline vapour, and benzene. In industrial accidents, such as occurred in 1985 in Bhopāl, India, and in 1976 in Seveso, near Milan, people in the neighbourhood of chemical plants were acutely exposed to lethal concentrations of these or other chemicals. The custom of transporting dangerous chemicals by rail or road has led to the occasional exposure of bystanders to toxic concentrations of gases and fumes. Although in many cases recovery may be complete, it seems clear that long-term damage may occur.
The assessment of disability and the writing of opinions on attributability have become important tasks for many respiratory specialists. Disability consequent upon a specific lung disease can be assessed by pulmonary function testing and in some cases by tests of exercise capability; these measures provide a good indication of the impact of the disease on the physical ability of the patient. It is much more difficult to decide how much of the disability is attributable to occupational exposure. If the exposure is historically known to cause a specific lesion in a significant percentage of exposed persons, such as mesothelioma in workers exposed to asbestos, attribution may be fairly straightforward. In many cases, however, the exposure may cause only generalized pulmonary changes leading to airflow obstruction or may cause lung lesions of multifactorial etiology, the precise cause of which cannot be determined by histological examination of the tissue. The question of attributability in these instances, already diffuse, may be complicated by a history of cigarette smoking, which may be mild or moderate, or of short or long duration. Physicians asked to give opinions on attributability in multifactorial disease processes before a legal body frequently must rely on the application of probability statistics to theindividual case, a not wholly satisfactory procedure to those who must assign compensation and disability benefits.
