Search PubMed⌕ Search

Biomedical subjects

W O Cookson

Publications and source records attributed to W O Cookson.

At least 91 records · Page 5Linked to original sources

Comparison of chest radiograph reading methods for assessing progress of pneumoconiosis over 10 years in Wittenoom crocidolite workers.

Thirty three pairs of chest radiographs taken up to 10 years apart were obtained for 33 subjects suffering from asbestosis who had applied for compensation to the Pneumoconiosis Medical Board of Western Australia. Multiple films from the period before the first radiograph in each pair, from the intervening period between the two, and from the period subsequent to the second radiograph were also available and all films were read by two independent readers according to the 1980 ILO classification of pneumoconiosis. Films were read twice as side by side pairs ten years apart, twice as two separate randomly ordered films ten years apart, and once as part of the full series of all available chest radiographs on each subject to assess which method provided the best consistency (between reader variation) and repeatability (within reader variation). Judging by consistency, the full series method performed as well as either of the other methods when assessing radiographic changes and significantly better when assessing the level of profusion of small opacities. There was little to choose between the other two methods either judging by consistency or repeatability, which could not be estimated for the full series method. Use of all available films for a subject is recommended for assessing single films, as in a prevalence study, as well as for documenting change in a longitudinal study.

Asbestos↗

Linkage between immunoglobulin E responses underlying asthma and rhinitis and chromosome 11q.

Family studies of IgE responses to common inhaled antigens have suggested dominant inheritance of atopy. Molecular genetic linkage analysis was used to confirm this proposal. In seven families the transmission of atopy was linked, with a maximum lod score of 5.58, to a DNA polymorphism defined by p lambda MS.51, which confirms dominant inheritance and assigns the gene locus to chromosome 11.

Asthma↗

Natural history of pleural thickening after exposure to crocidolite.

Serial plain chest radiographs of 384 men who worked at the Wittenoom crocidolite mine and mill between 1943 and 1966 and who applied for pneumoconiosis compensation between 1948 and 1982 have been examined independently by two trained observers for pleural disease using the 1980 ILO-UICC classification of radiographs to record width and extent of pleural disease. Radiographs covering follow up periods of from two to 38 years were examined (median number of films per subject was nine). The degree of crocidolite exposure was estimated from employment records and a survey of airborne fibre concentrations performed in 1966. Agreement between the observers on the presence and degree of pleural disease in the final film for each subject was moderately close (Kendall's tau B = 0.62) and was least for subjects with thickening less than 5 mm in width. Diffuse pleural thickening extending for greater than 50% of the lateral chest wall was the most common type recorded by both observers. Minor pleural thickening frequently progressed in extent along the lateral chest wall but progression beyond 5 mm in thickness was less common. Pleural plaques were not seen to progress beyond their initial thickness or extent. The rate of onset of thickening in this population increased continually from the time of first exposure and also increased slightly with age. There was evidence that the level of total cumulative exposure to crocidolite increased the rate of onset of pleural thickening in the period between five and 15 years after first exposure. Rate of progression of established thickening was greatest in subjects who first developed thickening early after first exposure. The relative rate of progression decreased slowly with time from first signs of thickening and there was no evidence of any progression more than 15 years after onset.

Asbestos↗

Diurnal variation in serum cortisol concentrations in asthmatic subjects after allergen inhalation.

To assess whether differences in the adrenal response to allergen are important in determining the magnitude of the allergen induced late responses in asthmatic subjects, we measured serum cortisol concentrations after inhalation challenge with allergen or control solution (phosphate buffered saline). The two challenges were performed in random order with an interval of 14 days. A normal diurnal decrease in serum cortisol concentrations was observed on both days. Mean blood cortisol concentrations three hours after inhalation of allergen (before the late response), nine hours afterwards (at the time of the late response), and 24 hours afterwards were virtually identical to those observed after inhalation of phosphate buffered saline. Serum cortisol concentrations before challenge and three, nine, and 24 hours after challenge were not related to the diurnal increase in blood eosinophils on the control day, or to the size of the late asthmatic response or accompanying changes in blood eosinophils after allergen challenge. It is concluded that serum cortisol concentrations show normal diurnal variation after allergen challenge and are unrelated to the size of the late response or associated changes in blood eosinophil counts.

Adult↗

Falls in peripheral eosinophil counts parallel the late asthmatic response.

Peripheral eosinophil counts were measured at intervals before and after control and allergen inhalation in 14 asthmatic subjects. A relative fall in eosinophil counts was noted 9 h after allergen challenge, in contrast to the diurnal increase seen on the control day (p = 0.005). This fall in eosinophil count correlated strongly with the magnitude of the late asthmatic response (r = -0.72, p = 0.003) and with the changes in bronchial responsiveness to histamine at 3 and 24 h after allergen was given (r = 0.54, p = 0.044 and r = 0.82, p less than 0.001, respectively). The findings demonstrate eosinophil kinetics are related to the occurrence of late-phase reactions and to the associated worsening of bronchial hyperreactivity.

Adult↗

Radiographic abnormalities and duration of employment in Western Australian iron-ore miners.

Plain chest radiographs of 788 Pilbara iron-ore miners from Western Australia have been examined by two independent observers for evidence of pneumoconiosis. The prevalence of any radiographic abnormality (a profusion grade of 0/1 or greater on the International Labour Office [ILO] scale) was 6.7% for Reader 1 and 9.9% for Reader 2. The prevalence of a definite radiographic abnormality (a profusion grade of 1/0 or greater on the ILO scale) was 1.9% for Reader 1 and 2.8% for Reader 2. The prevalence of any abnormality, as identified by either or by both observers, was significantly related to age. The relationship between a radiographic abnormality and the duration of employment was less clear. The results indicate a need for more detailed and comprehensive studies of the effects of iron-ore dust in this industry.

Adolescent↗

Dominant inheritance of atopic immunoglobulin-E responsiveness.

The familial occurrence of atopy, defined by skin prick test responses and serum immunoglobulin-E (IgE) titres to common inhaled allergens, was studied in 239 members of 40 nuclear and 3 extended families. 90% of the atopic children in the nuclear families had at least one demonstrably atopic parent. In each extended family, atopy was vertically transmitted, and 31 of 47 (66%) offspring of marriages between atopic and unaffected parents were atopic. Of the designated atopic subjects, 83% admitted to symptoms suggesting atopic disease but only 30% regarded themselves as having any such disorder. It is suggested that atopy, the propensity to produce IgE in response to common, usually inhaled, allergens, is inherited as an autosomal dominant character but that its clinical expression depends on interaction with other factors.

Adolescent↗

Increases in airway responsiveness to histamine precede allergen-induced late asthmatic responses.

Changes in airway responsiveness to histamine after allergen inhalation challenge were studied in 14 nonsmoking atopic adult subjects with asthma. Inhalation challenges with allergen and with phosphate-buffered saline (control challenge) were performed single blind in random order, with an interval of 14 days. The development of a late asthmatic response was accompanied by an increase in airway histamine responsiveness that was significant when it was compared with the airway histamine responsiveness after the control challenge at 3 hours (p less than 0.01), 24 hours (p less than 0.01), and 48 hours (p less than 0.02), with recovery at 2 weeks after allergen inhalation. The 3-hour changes in airway responsiveness occurred independently of changes in airway caliber and correlated with the magnitude of the subsequent late response (r = 0.86; p less than 0.001). These results suggest that the tissue events (possibly airway inflammation) that underlie the late asthmatic response may occur before this response becomes clinically apparent.

Adult↗

Dysgerminoma, gonadoblastoma, and testicular germ cell neoplasia in phenotypically female and male siblings with 46 XY genotype.

46 XY gonadal dysgenesis is a syndrome characterized by a female phenotype with streak gonads and complicated by the frequent occurrence of germ cell tumors. The syndrome and the risk of malignant disease occur in female siblings sharing the XY genotype, and screening of female siblings and prophylactic gonadectomy in those affected is generally recommended. A family of four siblings is described in which two phenotypically female XY children and one male each have developed germ cell tumors, demonstrating that brothers of affected sisters may also be at risk.

Child↗

Associations between asthma history, atopy, and non-specific bronchial responsiveness in young adults.

In 105 subjects taken from a student population and aged between 15 and 30 there was a strong positive association between the presence of the atopic state, defined by skin tests, and a high level of non-specific bronchial responsiveness to methacholine (chi 2 = 10.5, d.f. = 2, P = 0.01). Regression analysis showed a history of asthma, and the symptom of wheeze, to be predominantly predicted by the degree of bronchial responsiveness (R2 = 31%), with only a minor independent contribution from the degree of atopy (R2 a further 5%). The genetic or other reasons for the association between bronchial responsiveness and atopy may have importance in understanding the aetiology of allergic asthma.

Adolescent↗

Atopy, non-allergic bronchial reactivity, and past history as determinants of work related symptoms in seasonal grain handlers.

One hundred and five young subjects with little or no previous exposure to grain dust were studied before and after a seven week period of grain handling work to determine if there was an association between symptoms experienced at work and pre-employment respiratory symptoms, allergy skin test responses, and non-allergic bronchial reactivity. The incidence of work related symptoms was cough 18%, wheeze 13%, and dyspnoea 14%. The results showed that pre-employment history of respiratory symptoms, positive allergy skin test responses, and a high level of non-allergic bronchial reactivity were significantly associated with these symptoms. These measurements may be useful to predict symptoms associated with exposure to grain dust in new employees and the results suggest that these work related symptoms may be due to allergen induced asthma.

Adolescent↗

Prevalence of radiographic asbestosis in crocidolite miners and millers at Wittenoom, Western Australia.

An estimate has been made of the prevalence of unrecognised pneumoconiosis in former crocidolite workers from Wittenoom, Western Australia. All plain chest radiographs relating to a one in six random sample (1025 men) of all former Wittenoom workers who had never entered a compensation claim to the Pneumoconiosis Medical Board of Western Australia were sought from Perth teaching hospitals and from the Perth Chest Clinic where compulsory examination of all workers in the mining industry takes place. Radiographs were recovered for 83% of the men and read independently by two observers. By means of logistic regression analysis a current prevalence of parenchymal abnormality (defined as a radiographic profusion of small opacities of category 1/0 or greater on the ILO classification) of nearly 20% was calculated after adjustment for age, time since first exposure, and cumulative exposure level. One hundred men randomly selected from those known to be alive in the sample were invited to attend for a new radiographic examination. Seventy four men attended and the predicted prevalence was confirmed. It is estimated from these data that there were between 450 and 900 former Wittenoom workers in Australia at the end of 1980 who had radiographic abnormality consistent with pneumoconiosis but had not claimed compensation or had asbestosis diagnosed. The data are consistent with there being no threshold dose of crocidolite exposure for the development of radiographic abnormality in this group.

Adult↗

Symptoms and longitudinal changes in lung function in young seasonal grain handlers.

A total of 119 seasonal grain handlers (mean age 23) were assessed before and towards the end (mean work period 18 days) of the 1983 Western Australian grain harvest to determine if respiratory symptoms that occur with exposure to grain dust are associated with changes in ventilatory capacity or non-specific bronchial reactivity to methacholine. Eighteen per cent of subjects had wheeze, breathlessness, or chest tightness and 18% had cough or sputum production at work. Subjects complaining of wheeze, chest tightness, or breathlessness at work had a significantly greater decline in FEV1 than subjects who did not experience these symptoms (p less than 0.05). Symptoms were not associated with changes in bronchial reactivity. In young grain handlers who develop respiratory symptoms on short term exposure to grain dust changes in FEV1 but not in non-specific bronchial reactivity have been demonstrated.

Adolescent↗

Effect of monocrotaline ingestion on the distribution of protein and angiotensin converting enzyme activity in the rat lung.

The alveolar accumulation of protein and angiotensin converting enzyme activity was compared with the development of right ventricular hypertrophy in male rats after different periods of monocrotaline exposure. Total doses of monocrotaline were varied by dividing the animals into three groups in which ingestion was limited to three, seven, and 15 days. These groups were studied 21 days after the start of monocrotaline exposure and compared with a group treated continuously for 28 days. The total lung weight increased after three or more days of treatment, while after seven days there was significant alveolar accumulation of protein, which was paralleled by an increase in angiotensin converting enzyme activity in alveolar lavage fluid. Identical changes also occurred after 15 and 28 days of exposure to monocrotaline. Lung angiotensin converting enzyme activity was decreased after three days' ingestion of monocrotaline and did not alter further with longer periods of exposure. None of these effects of monocrotaline in the three and seven day treatment groups was associated with right ventricular hypertrophy, which occurred only in animals treated for 15 or more days. The effects of monocrotaline ingestion on the lung were dose related and had no causal relationship to the development of right ventricular hypertrophy.

Animals↗

Compensation, radiographic changes, and survival in applicants for asbestosis compensation.

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.

Asbestos↗