Chest pain in asbestos-exposed individuals with benign pleural and parenchymal disease

Many asbestos-exposed individuals complain of chest pain for which there is no clear explanation. To determine whether chest pain is associated with the presence of benign pleural or parenchymal disease on chest radiograph, we studied 1,280 subjects undergoing surveillance because of prior asbestos exposure at Wittenoom, Western Australia. All subjects completed the Rose questionnaire on chest pain and this revealed 556 subjects (43%) who experienced some chest pain. A posterior-anterior chest radiograph was performed at the same clinic visit and was subsequently graded independently by two experienced readers for diffuse parenchymal disease and pleural disease. Logistic regression models adjusted for sex, age, and cumulative asbestos exposure indicated that the presence of chest pain was significantly associated with the presence of both benign pleural disease and diffuse parenchymal disease. Further analysis after stratification of chest pain into nonanginal and anginal pain showed that there was a significant association between anginal pain and the presence of pleural and parenchymal asbestos-induced radiologic abnormalities and an association of nonanginal pain with parenchymal disease. We conclude that radiographic evidence of either parenchymal or pleural disease in subjects exposed to asbestos is significantly related to the presence of chest pain, particularly anginal pain.     

Immunologic heterogeneity of diffuse large cell lymphoma

The cellular lineage of 57 diffuse large-cell lymphomas (DLCLs) was determined using a panel of monoclonal antibodies directed against lineage-restricted and -associated T, B, and monocyte antigens. The majority (82%) were of B cell lineage as determined by the expression of sig and/or B1, with the remaining 16% being of T cell lineage and 2%, of monocyte-myeloid lineage. By the expression of other B cell- restricted and -associated antigens, two major and two minor subgroups could be identified. These subgroups expressed the following phenotypes: (1) B1+B4+sIG+B2- (51%); (2) B1+B4+sIg+B2+ (29%); (3) B1+B4+sIg-B2+ (10%); and (4) B1+B4-sIg+B2- (10)%. The morphology of transformed lymphocytes, the weak to absent expression of the early B cell antigens B2 and sIgD, and the absence of the late B cell differentiation antigens PCA-1 and PC-1 suggested that these tumors were the neoplastic counterparts of normal B cells at the mid-stages of differentiation. Further support for the notion that B-DLCLs correspond to transformed B lymphocytes was concluded from the observation that B cells could be identified in normal spleen that expressed the cell surface phenotype and morphological appearance of the majority of B- DLCLs.     

Colony-forming cell proliferation: a rapid and sensitive assay system for murine granulocyte and macrophage colony-stimulating factors

A microculture assay for murine granulocyte-macrophage colony- stimulating factor (GM-CSF) has been developed using fetal liver GM colony-forming cells (CFC) isolated by fluorescence-activated cell sorting. These GM-CFC are free of mature hemopoietic cells, such as granulocytes and macrophages, which may interfere with direct assays for GM-CSF. The assay procedure allows the quantitation of GM-CSF within 48 hr by measuring the number of cells produced from 50 GM-CFC in microcultures (15 microliter). The assay is particularly simple to set up and score and yet, because of the reduced volumes, this assay is still capable of detecting 0.2 pg (i.e., 0.2 U) of GM-CSF within 48 hr, i.e., 100 times less GM-CSF than the conventional soft agar assay. By allowing the microcultures to develop for 7 days, the extra proliferation allows a further tenfold increase in the sensitivity of CSF detection. The time and cost of setting up hundreds of GM-CSF assays for fractions from chromatographic columns, e.g., reverse phase high performance liquid chromatography, is reduced by at least five- fold. Enough GM-CFC can be isolated and stored frozen in one afternoon to provide sufficient cells for the daily assay of 200 samples of GM- CSF for several months. Microassay results for several sources of GM- CSF at different stages of purification are compared to the results obtained from the soft agar assay.     

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.     

Early life and later determinants of adult disease: a 50 year follow-up study of the Newcastle Thousand Families cohort

The relative contribution of socioeconomic, behavioural and biological factors operating in fetal and infant life, childhood and adulthood to risk for cardiovascular disease, respiratory diseases and non-insulin-dependent diabetes in middle age has become an important research issue. All 1142 babies born in Newcastle upon Tyne in May and June 1947 were recruited into a prospective cohort study of child health (the ‘Thousand Families’ study) and followed in great detail to the age of 15 y, with a brief further follow up at age 22 y. Children from poorer families were at greatest risk of severe respiratory tract infection in infancy. Children from professional and managerial families were on average taller and heavier throughout childhood than those from semi- and unskilled manual social classes. Repeated infections in early childhood greatly increased the risk of developing chronic respiratory disease by age 15 y. This paper outlines a new investigation designed to trace surviving members of this cohort and to chart the relationships between their socioeconomic circumstances, lifestyles, experiences and health from birth through to the present day. Existing data on socioeconomic circumstances and infections in infancy and childhood, infant nutrition, birthweight and physical development to age 22 y will be linked to information gained from a new study. This comprises a postal questionnaire survey of study members' adult health, socioeconomic circumstances and lifestyle, and a hospital based clinical examination including heart and lung function, glucose tolerance, blood lipids and anthropometric measurements at age 49–51 y. Out of a target sample of 979 people for whom sufficient data are available on the first year of life, 866 (88%) have been traced and 649 are still resident in the North of England. Those study members who have been traced are highly representative of the original cohort. The Thousand Families cohort provides a unique opportunity for detailed epidemiological study because of the wealth of data available on infant and childhood socioeconomic and family circumstances, all of which was collected prospectively. In addition, there has been comparatively little loss to follow-up since 1948.     

Exposure to grain dust and changes in lung function.

Respiratory symptoms and lung function were assessed in 41 seasonal grain handlers and related to duration of employment and level of exposure to grain dust. Ten public works department employees, not exposed to grain dust, were examined during the same period. Respiratory symptoms, forced expired volume in one second (FEV1), and bronchial responsiveness (dose of methacholine provoking a 20% fall in FEV1-PD20) were assessed before starting work and at weekly intervals during a period of employment lasting up to four weeks. Two atopic grainhandlers with pronounced bronchial hyperresponsiveness (PD20 less than 1 mumol) and a history of asthma withdrew from the study within two weeks because they developed severe asthma. Respiratory symptoms were more frequent and more often attributed to work in the grainhandlers than in the non-exposed subjects. In the grainhandlers the FEV1 decreased by a mean (95% confidence intervals) of 321 ml (198-444) (p less than 0.05) and the mean (95% confidence interval) PD20 decreased from 20.6 mumol (10.3-41.2) to 6.0 mumol (2.8-12.5) (p less than 0.05) after one week of work. Over the next three weeks the mean FEV1 returned towards the prestudy values. The mean PD20, however, remained significantly lower than the initial value. The mean FEV1 and PD20 did not change significantly in the non-exposed subjects. The frequency of symptoms and decreases in FEV1 were greater in grainhandlers when working in jobs where total exposure to dust was greater than 20 mg/m3 than when working in jobs where it was less than 10 mg/m3. The results indicate that occupational exposure to grain dust results in respiratory symptoms and changes in lung function, including increased airway responsiveness, within the first week of exposure to grain dust at work. These changes appear to be determined by the degree of dust exposure and suggest a direct effect of grain dust on the lung in these subjects.