Occupational Cancer:Occupational cancer can arise from various causes such as:
Consider the following case history:
In 1961 a man of 34 presented to his doctor with a history of having coughed up blood. He had never smoked. Nevertheless, after investigation he proved to have an oat cell carcinoma of the bronchus. Over the next 20 years, 11 other men aged between 41 and 67 also died of rapidly progressive undifferentiated carcinomas of the bronchus. Only 7 had been smokers but all had worked for the same chemical company making ion-exchange resins, which had a bad reputation for conditions in the workplace. Initially, no doctors made the connection, but the trade union at the factory pursued the matter and found out that one of the chemicals used was bischloromethyl ether (BCME). This had been found to be one of the most potent causes of bronchial carcinoma, in rats in 1967 and shortly thereafter accepted as a cause in humans. To date, some 16 men from this small factory have died of anaplastic lung cancer.If the index case and his colleagues had been smokers, do you think that their cancers could have been attributed to smoking?
Many people die of lung cancer every year - most due to smoking - yet in a proportion which is difficult to quantify the cause may have been occupational e.g. asbestos.
The following image shows an asbestos body which has not been successfully cleared by inflammatory cells in the lung.
The following image shows some cancerous lung cells:
To illustrate the complexity of causation of cancer, the
following account is an example based on respiratory disease:
Environmental Causes of Respiratory CancerUndeniably by far the biggest environmental cause of respiratory cancer for communities in the western world as a whole, is tobacco smoking. The discussion of smoking as a cause of lung cancer is a separate subject. However, other environmental causes of respiratory cancer deserve attention however because they are potentially preventable and because they can pose a high risk to certain small groups of people, notably in relation to work exposures. Thirdly, they may synergise with tobacco smoking in raising the lung cancer risk.
Physical factors, mainly radiation, are the first to be considered. Lung cancer is not an important consequence of external radiation as such. However, inhalation of alpha particle emitters can carry a very high risk. Thus, workers in the nuclear industry are classical occupational examples. For the community at large, the biggest concerns arise from inhalation of radon gas (and the closely related to thoron). Typically these arise from uranium bearing feldspars from some forms of pink granite of igneous origin but might arise in other circumstances as well. The gases decay to so-called "daughters" and it is these isotopes which release alpha particles in the lung. The national average radon activity in houses in the UK is 20 becquerels per cubic metre and this is associated with the life-time risk of lung cancer of 1 in 300. At the "action level" which is 10 times this national average (ie 200 becquerels per cubic metre), the life-time risk of lung cancer is similarly increased 10 fold (1 in 30). It is possible to measure exposures through appropriate dosemeters and to reduce the risk by adaptation of building techniques to prevent radon gas rising through the ground into the house.
The single most important occupational "chemical" cause is asbestos. There is evidence that because of the long latency of mesothelioma of the pleura (up to 40 years or so) the UK has not yet experienced its peak incidence of these cases. A similar rising incidence might be expected in other countries with comparable exposure patterns in the last few decades. While a histolological picture of mesothelioma of the pleura peritoneum can fairly confidently be clinically attributed to asbestos exposure, the same is not true of bronchogenic carcinoma. In most of these cases since the subject gives a history of smoking, this is clinically assumed to be the cause. In round figures, smokers may have a 10 fold risk of bronchogenic carcinoma when compared to non-smokers. If they have had a heavy occupational asbestos exposure this risk may rise to fifty-fold. Indeed the epidemiologic evidence suggests that to the order of twice as many cases of bronchogenic carcinoma are caused by asbestos as cases of mesothelioma from the same exposure.
Many other respiratory cancers have got occupational causes. Indeed estimates suggest that, depending on the exposures and how they are assessed, anything between 0.6 and 40% of lung cancers in occupational populations may be attributed to their work. Thus exposure to hard wood dusts and to certain compounds of nickel in its refining are associated with high risks of adeno-carcinoma and of squamous carcinoma respectively of the paranasal sinuses. Other occupational causes include mustard gas and some other organic compounds such as bis (chloromethyl) ether. Certain compounds of nickel, chromium and arsenic have also been important causes of occupational lung cancer, as have polycyclic aromatic hydrocarbons. This raises the question as to whether or not polycyclic aromatic hydrocarbons or other pollutants would explain the clear urban/rural gradient in the incidence of lung cancer. Epidemiologic studies are divided on this issue since smoking and other social factors might not necessarily explain all the difference.
Finally, mention should be made of the possible contribution of biological agents to lung cancer risk. Thus, for example, there is a small but increasing body of evidence suggesting an increased lung cancer risk in butchers or other meat workers. This might be related to an agent intrinsic to the meat or to a virus associated with it.
Acknowledgements: Part of this page has been adapted, with permission, from Practical Occupational Medicine (Copyright) - Arnold publishers.