Dr. Cowie - Independent Medical Opinion
Condition | Pulmonary Fibrosis |
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Date of Production | May 28, 2012 |
Doctor's Name | Dr. R.L. (Bob) Cowie, MD, MB ChB, MSc, FCP(SA), MFOM (UK) |
Thank you so much for asking me to perform this independent medical opinion and thank you for your help when we spoke on the telephone earlier today. Having established that the bulk of the paper submitted did not relate directly to this case, my task was much simplified!
Notwithstanding the large amount of paper, the documentation regarding the Appellant's lung disease is quite sparse (but, probably, adequate). There is one rather brief report of a CT scan of his chest, a report on his lung function (but no data are provided) and a fragmented histology report of his open lung biopsy. Nevertheless, the available data supports and establishes a diagnosis of usual interstitial pneumonitis which is also known as idiopathic pulmonary fibrosis. The idiopathic relates to the absence of a known cause.
Characteristically, the features are predominantly peripheral (at the edges) of the lung and especially marked at the bases of the lung. Honeycombing, (traction) bronchiectasis (on the CT), fibroblastic foci and the surprising confluence of areas of grossly abnormal with areas of normal lung are all characteristic of and consistent with this diagnosis and included in the descriptors used in the histology and CT reports. The lung lining (the pleura) is characteristically not involved although the lung immediately beneath the lining is maximally involved.
A similar appearance has really only been described in one of the occupational (environmental) lung diseases - asbestosis. In asbestosis, it is usual to have a prolonged, extensive and obvious exposure to asbestos, to have associated pleural disease - usually pleural plaques - and to see so-called asbestos bodies when examining the lung histologically. None of these features were described in this case.
Lung fibrosis in association with other diseases such as rheumatoid arthritis may be similar to idiopathic pulmonary fibrosis when it reaches its end-stage. The underlying disease is almost always obvious at that stage and none is apparent in this case.
Other forms of lung fibrosis such as that associated with carbon black (graphite), coal etc. is quite distinct from the pattern seen with idiopathic pulmonary fibrosis.
There is a minority point of view that any respirable dust can aggravate or even cause 'idiopathic pulmonary fibrosis' but that view is not supported by current evidence.
Idiopathic pulmonary fibrosis is a disease of the elderly and as our populations age, we are seeing increasing numbers of cases. Familial associations are recognised but contribute to a very small proportion of the total cases of lung fibrosis. In individuals of the Appellant's age, the disease is thought to occur in approximately 250 per 100 000 people and it is more common in men than in women.
I would conclude that the evidence for a diagnosis of idiopathic pulmonary fibrosis (usual interstitital pneumonitis) is clear. None of the substances to which he was exposed as a member of the identity team are known to cause this pattern of lung fibrosis. It is thus improbable that his lung disease has an association with his former occupation.
To answer your questions:
1. No, the pulmonary fibrosis was not caused by his occupational exposure
- and
- Some of the material (carbon black) used for fingerprinting has the capacity in quantities far in excess of that used here to cause lung fibrosis but not of the type described in this case.
- Many of the substances which have the capacity to cause pulmonary fibrosis will not have any immediate effect and latent periods of decades may intervene before lung fibrosis is apparent.
- A latent period of 31 years is not inconceivable and has been documented in the example of asbestos exposure and the onset of asbestosis (lung fibrosis).
- The likelihood of his disease being related to other, non service-related causes is small.
- It is improbable that his disease is related to occupational chemical exposure.
- These are good studies which really fail to establish an association between these exposures and lung fibrosis. Aluminum was, at one time, given by inhalation to prevent lung fibrosis from silica! Some studies have shown that aluminum in some forms may cause lung fibrosis which has a different distribution and pattern from that seen here. No significant risk of lung fibrosis has been described from the small amounts of aluminum used here.
- In time, a cause for idiopathic pulmonary fibrosis might become apparent but extensive data has, to date, failed to reveal any cause or even a significant contribution from environmental exposure. This is an increasingly common disease and although there is an understandable enthusiasm for attributing it to a compensable cause, there are no data to support this approach.
Robert L. Cowie, MB ChB, FCP(SA), MD, MSc, MFOM - Respiratory Medicine
Eductation
- MB ChB: University of Cape Town, South Africa, 1962
- FCP (SA): College of Medicine of South Africa, 1968
- MSc: Epidemiology and Biostatistics, McGill University, Montreal, QC, 1987
- MD: University of Cape Town, South Africa, 1988
- MFOM: Faculty of Occupational Medicine, Royal College of Physicians, London, England, 1988
Academic Appointments
- Professor of Medicine, Division of Respiratory Medicine, University of Calgary, Calgary, AB, I995-present
- Professor, Department of Community Health Sciences, University of Calgary, Calgary, AB I995-present
- Head, Division of Respiratory Medicine, University of Calgary, Calgary, AB, 1997-2003.
Hospital Addiliations
- Foothills Hospital, Calgary, AB
Professional Affiliations
- American Thoracic Society
- British Thoracic Society
- Canadian Thoracic Society
- College of Medicine of South Africa
- European Respiratory Society
- Intemational Union Against Tuberculosis and Lung Disease
- Royal College of Physicians, Member of the Faculty of Occupational Medicine
Publications
Dr. Cowie has written numerous scientific research studies and textbooks focussing on asthma, tuberculosis, and occupational lung epidemiology. In 2002, he received the Alberta Lung Association Award of Excellence. a Lorraine Award.