South Africa was the third-largest exporter of asbestos in the world for more than a century. And because of particularly exploitative social conditions, former workers and residents of mining regions suffered – and continue to suffer – from a serious, yet still largely undocumented, burden of asbestos-related disease.
Mining operations of the asbestos industry not only exposed workers to high levels of asbestos but also extensively contaminated the environment. Even though the industry is aware of the hazardous properties of asbestos, it still remains a subject of intense controversy whether asbestos fibres cause asbestosis – a progressive fibrotic disease of the lungs – lung cancer and mesothelioma.
The incidence of mesothelioma in South Africa ranks among the highest in the world. The hefty mesothelioma count stems from the country’s extensive history of asbestos mining and production over more than a century.
On a positive note, in March 2008, South Africa prohibited the use, processing or manufacturing of any asbestos or asbestos-containing products – a decision welcomed by many concerned organisations. But was it too little, too late?
Occupational lung diseases are a broad group of diagnoses caused by the inhalation of dusts, chemicals, or proteins. The severity of the disease is related to the material inhaled and the intensity and duration of the exposure. Even individuals who do not work in the industry can develop occupational disease through indirect exposure.
Asbestos insulators expose their wives and children by bringing home their asbestos-covered clothing and asbestos factories and mines expose residents of nearby neighbourhoods. Different exposures result in different diseases.
These diseases are essentially man-made, resulting from inorganic dust exposure during mining, processing, or manufacturing.
Coal dust exposure can cause coal worker’s pneumoconiosis (CWP), also known as black lung. Simple CWP is largely only an abnormality on the chest X-ray; there are small spots in the upper lung zones that reflect inhalation of coal dust, but nothing more.
However, it can develop into complicated CWP, which is also called progressive massive fibrosis, a term and process shared with silicosis in which the smaller shadows join into large nodules. These lesions can distort and destroy normal lung architecture and result in shortness of breath and disability.
Exposure to coal dust has been found to result in airflow obstruction and chronic bronchitis and is also associated with the development of rheumatoid arthritis. An association with stomach cancer has also been described in coal miners, potentially related to ingestion of the coal dust. Other exposure-related diseases are “farmer’s lung,” or hypersensitivity pneumonitis (HP).
The well described at-risk populations are farmers and bird hobbyists but many other exposures can cause HP. The most recent addition is popcorn workers’ lung, noted in workers and consumers with a history of heavy exposure to microwave popcorn butter flavouring.
The illnesses have a great range of symptoms and many people with mild disease do not seek medical attention. HP, however, has been reported to be present in as many as 12% of farmers and 20%of bird hobbyists.
Sandblasters, miners, tunnellers, millers and potters – among many others – are exposed to these inhaled particles and are at risk.
SIGNS AND SYMPTOMS
The signs of chronic silicosis develop decades after exposure and are characterised by the silicotic nodule, predominantly in the upper lobes of the lungs, and “eggshell” calcification of the lymph nodes.
Higher intensity exposure can result in accelerated or acute silicosis, in which symptoms develop much earlier. Acute silicosis is the least frequent, but it also has the highest mortality rate.
When complicated, the silicotic nodules join into larger masses in the upper lobes of the lung and the patients develop increasing breathing difficulty.
Silicosis increases susceptibility to tuberculosis and there is also a link between silicosis and immune-mediated diseases, such as systemic sclerosis and rheumatoid arthritis. Silicosis patients also have an increased risk of lung cancer. There is also risk of airflow obstruction.
Many people who have occupational dust exposure also smoke, leading to chronic bronchitis.
PREVENTION & TREATMENT
For asbestos-, coal-, and silica-related disease, there is no treatment other than optimising the patient’s health and preventing further exposure. Prognosis varies depending on the severity of the disease.
People with simple CWP or classic silicosis may never experience symptoms, whereas complicated CWP results in severe respiratory debilitation and death. Since the use of asbestos has been banned only since 2008, the peak of disease incidence may lie ahead.
The prognosis for mesothelioma and lung cancer is very poor, with less than 20% five-year survival rates. For all individuals exposed to asbestos, there is the need for surveillance for development of malignancy. Aggressive regulations in the coal industry have resulted in reductions in the burden of disease.
Standards put in place ensure that cumulative exposure over the typical career span of 25 years would not exceed levels known to cause respiratory impairment.
In conjunction with these standards, secondary prevention measures also require all exposed workers to receive regular medical screening. And if a worker shows signs of developing disease, he or she has the option of transferring to a lower exposure area and receiving increased monitoring.
All patients are encouraged to stop smoking. Silica is the least regulated of the agents causing occupational lung diseases. Silicosis is an irreversible fibrotic process without a cure. Treatment rests on preventing further insult to the lungs.
Reduction in risk of tuberculosis is also critically important and all patients should be screened for latent or active tuberculosis infection and be evaluated for other tuberculosis risk factors, such as HIV infection.
In the case of hypersensitivity pneumonitis, treatment consists of removing the source of the exposure and eradicating any residual antigens to prevent re-exposure – for example, drying hay to prevent molding or removing stagnant water to prevent bacterial or fungal overgrowth.
Often, the most challenging part of care is convincing the patient that removal of the antigen is necessary or that he or she must leave the workplace. If the disease is severe at diagnosis, a short course of oral corticosteroids can help expedite recovery.
Each of the occupational diseases begins with the inhalation of disease-inducing particles. Therefore, the main goals have been to identify and regulate the industries that generate these particles on one hand and to determine ways to prevent or minimise their inhalation on the other.
In dealing with silica, coal, and asbestos, the significant latency period between exposure and diagnosis makes it difficult to determine dose–response relationships. here is no treatment for any of the occupational diseases that can reverse the damage already done.
