Imperial College London

Professor William Cookson

Faculty of MedicineNational Heart & Lung Institute

Professor of Genomic Medicine
 
 
 
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Contact

 

+44 (0)20 7594 2943w.cookson

 
 
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Location

 

400Guy Scadding BuildingRoyal Brompton Campus

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Summary

 

Publications

Publication Type
Year
to

396 results found

Cookson WO, De Klerk NH, Musk AW, Glancy JJ, Armstrong BK, Hobbs MSet al., 1985, Benign and malignant pleural effusions in former Wittenoom crocidolite millers and miners., Aust N Z J Med, Vol: 15, Pages: 731-737, ISSN: 0004-8291

Serial plain chest radiographs taken between 1943 and 1982 for 280 claimants for compensation for asbestosis and 32 claimants for malignant pleural mesothelioma from the Wittenoom asbestos industry were reviewed by two observers to identify diffuse pleural thickening and pleural effusion. A pleural effusion which appeared and resolved within two years without radiographic or clinical evidence of underlying malignancy, infection or cardiac failure was seen in 15 cases by reader 1 and 24 cases by reader 2. Eighteen cases of effusion, determined from clinical records to be caused by malignant pleural mesothelioma, were seen by reader 1 and 20 by reader 2. The latent periods between commencing work and the first radiograph showing effusion were much shorter for subjects with benign asbestos pleural effusion than for subjects with effusion due to malignant pleural mesothelioma, although there was considerable overlap in the range. The longest latent period for benign asbestos pleural effusion was 22 years and the shortest period for effusion due to malignant pleural mesothelioma was 12 years. The latent period for benign asbestos pleural effusion was inversely related to total cumulative exposure, whereas that for effusion due to malignant pleural mesothelioma was significantly shorter for subjects who had worked in the mill than for those who had worked in the mine. A long latent period and a history of working in the mill were significant discriminators for a malignant as opposed to a benign basis for an effusion. The appearance of a benign asbestos pleural effusion appeared to be a risk factor for the severity of subsequent diffuse pleural thickening.(ABSTRACT TRUNCATED AT 250 WORDS)

Journal article

Cookson WO, Wiseman MS, Shale DJ, 1985, Angiotensin converting enzyme and endotoxin induced lung damage in the mouse., Thorax, Vol: 40, Pages: 774-777, ISSN: 0040-6376

Acute pulmonary oedema can be induced by intraperitoneal injection of Escherichia coli endotoxin in the mouse. A fall in serum angiotensin converting enzyme activity is found in mice given endotoxin and in patients with septic adult respiratory distress syndrome, and has been proposed as an indicator of lung microvascular injury. Protein concentration and angiotensin converting enzyme activity in serum, lung, and bronchoalveolar lavage fluid were determined in male mice up to eight hours after injection of endotoxin. By six hours the serum protein concentration had increased and the bronchoalveolar lavage fluid protein concentration had fallen, suggesting fluid shift into the lung. Angiotensin converting enzyme activity fell in serum and lung but increased in bronchoalveolar lavage fluid. As these changes in enzyme activity were not paralleled by changes in protein concentration they are unlikely to be a result of fluid shift or protein leak, and may indicate an active role of the enzyme in the response to sepsis.

Journal article

Cookson WO, Musk AW, Glancy JJ, de Klerk NH, Yin R, Mele R, Carr NG, Armstrong BK, Hobbs MSet al., 1985, Compensation, radiographic changes, and survival in applicants for asbestosis compensation., Br J Ind Med, Vol: 42, Pages: 461-468, ISSN: 0007-1072

The survival of 354 claimants for compensation for pulmonary asbestosis among former workers of the Wittenoom crocidolite mine and mill in Western Australia has been examined. There were 118 deaths up to December 1982. The median time between start of work and claim for compensation was 17 years. The standardised mortality ratio (SMR) for deaths from all causes was 2.65 (p less than 0.0001). The SMR for pneumoconiosis was 177.2 (p less than 0.0001), bronchitis and emphysema 2.6 (p = 0.04), tuberculosis 44.6 (p less than 0.0001), respiratory cancer (including five deaths from malignant pleural mesothelioma) 6.4 (p less than 0.0001), gastrointestinal cancer 1.6 (p = 0.22), all other cancers 1.6 (p = 0.17), heart disease 1.4 (p = 0.07), and all other causes 2.18 (p = 0.004). Plain chest radiographs taken within two years of claiming compensation were found for 238 subjects and were categorised independently by two observers according to the International Labour Organisation criteria without knowledge of exposure or compensation details. Profusion of radiographic opacities, age at claiming compensation, work in the Wittenoom mill, and degree of disability awarded by the pneumoconiosis medical board were significant predictors of survival, but total estimated exposure to asbestos was not. Radiographic profusion and degree of disability were, however, predictable by total exposure. The median survival from claim for compensation was 17 years in subjects with ILO category 1 pneumoconiosis, 12 years in category 2, and three years in category 3.

Journal article

Cookson WO, Glancy JJ, Frost FA, 1985, Asymmetric rapidly progressive lung fibrosis: a cause of pseudotumour in asbestosis., Br J Ind Med, Vol: 42, Pages: 350-353, ISSN: 0007-1072

Journal article

Ryan G, Cookson WO, Musk AW, 1985, Allergy and nonallergic bronchial reactivity as determinants of work-related respiratory symptoms in seasonal grain handlers, Chest, Vol: 87, ISSN: 0012-3692

The authors studied a group of subjects with little or no previous grain dust exposure before and after a short period of grain handling work. The results suggest that preemployment atopy and increased bronchial reactivity are associated with an increased frequency of respiratory symptoms on exposure to grain dust. Second, preemployment history, allergy skin test response, and level of bronchial reactivity may be useful predictors of work-related symptoms. This supports the possibility that symptoms, particularly wheeze and dyspnea, that begin soon after starting work may respresent allergen-induced asthma. The weaker association with cough suggests that it may reflect a different mechanism.

Journal article

Cookson WO, Musk AW, Glancy JJ, 1984, Asbestosis and cryptogenic fibrosing alveolitis: a radiological and functional comparison., Aust N Z J Med, Vol: 14, Pages: 626-630, ISSN: 0004-8291

This study compares the relationship between lung function and radiological abnormality in 46 subjects with asbestosis and 38 subjects with cryptogenic fibrosing alveolitis. Radiographs were graded separately by two observers according to the 1980 International Labour Organisation criteria for classification of the pneumoconioses. The correlation between the transfer factor of the lungs and the radiographic profusion of small parenchymal opacities was found to be greater in subjects with asbestosis than in subjects with cryptogenic fibrosing alveolitis. At any level of radiological profusion transfer factor was higher in cases with asbestosis than in cases with fibrosing alveolitis. As pleural thickening is seen commonly in asbestosis and may influence lung volumes and the ratio of transfer factor to effective alveolar volume, the results of these measurements were compared only in the cases showing absent or minimal pleural thickening. Both of these variables were higher in the subjects with asbestosis. The results indicate that despite pathological, functional and radiographic similarities, lung function for a given degree of radiographic parenchymal abnormality is better in subjects with asbestosis than in subjects with cryptogenic fibrosing alveolitis, and that changes in the plain chest x-ray appearances in asbestosis correlate more closely with the results of lung function tests.

Journal article

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