Annual decline in lung function determined longitudinally is often compared with predicted decline determined cross-sectionally. To test this comparison, spirometric data were collected 5 times over 5 yr from 52 adult male Caucasians. The age regression coefficient for FEV1 and FVC, determined cross-sectionally at each visit, was more than twice the longitudinal annual change computed from the same data as the mean of the slopes of each subject's regression lines. The discrepancy persisted even when the first visit was deleted to reduce learning effects on longitudinal estimates. This discrepancy may be partly explained by the sensitivity of cross-sectional analyses to past noxious influences, whereas longitudinal analyses are sensitive only to influences that continue to affect annual decline during the study period. We also found historical evidence of an increase in height-specific VC, which would artifactually steepen cross-sectionally determined regression lines. Thus, observed longitudinal changes of study cohorts should be compared with control longitudinal data.
Workers at a toluene-diisocyanate manufacturing plant were studied longitudinally to determine the effects of the chemical on their health. Studies included health questionnaire, pulmonary function, environmental monitoring, and immunologic testing. Workers reporting increased lower respiratory symptoms were from the nonsmoker group. Environmental monitoring showed frequent excursions of toluene-diisocyanate concentrations above the threshold limiting value. There was poor correlation between area and personal exposure levels. No exposure-related decline of pulmonary function was demonstrable. Immunologic studies showed development of a positive skin test to a toluene-diisocyanate-human serum albumin conjugate by some persons and an increasing incidence of toluene-diisocyanate-specific IgE antibodies as measured by a radioallergosorbent test. Toluene-diisocyanate did not induce histamine release from leukocytes in vitro but did diminish the in vitro stimulation of cyclic adenosine monophosphate by isoproterenol. Most of the clinically sensitive persons demonstrated adverse bronchial response when challenged by inhalation of toluene-diisocyanate. This response was dose dependent in some persons. When challenged with Mecholyl, clinically sensitive persons showed greater reactivity of airways than nonsensitive persons.
From an original prospective cohort of 244 current and ex-workers in two asbestos cement plants, longitudinal radiographic data covering ten years were available for 165 and lung function data covering about six years for 150. Estimates of average and cumulative dust exposure were available for each participant, all men. Radiographic progression (onset or worsening) was assessed by comparing earliest and latest films side by side. Annual changes in lung function were computed by fitting regression lines to all the data points. Small opacities (ILO category 1/0 or higher) were found in 16% of initial films, and progression of small opacities occurred in 13% of film pairs. Average and cumulative dust exposure were each significant determinants of the initial presence of small opacities, and were determinants of the progression of both parenchymal and pleural abnormalities. There was greater likelihood of progression if an abnormality was initially present, and a greater likelihood ofprogression in the plant that had systematic use of some crocidolite. Initial levels of lung function were related to smoking, exposure to dust, and initial radiographic status. Mean annual declines in lung function were modest (FVC -0-017 l/y, FEV, -0-020 l/y) and were related to smoking but not exposure to dust, initial radiographic status, or radiographic progression. Both plants used mainly chrysotile asbestos and exposure levels declined severalfold after 1960. Our findings suggest a waning effect of the larger remote dust exposures on recent annual change in lung function. This accords with human and experimental pathology data showing the relatively low resistance of chrysotile fibres to chemical alteration and clearance.Asbestosis and asbestos induced pleural thickening and calcification share several characteristics. By definition, they are caused by exposures to asbestos (usually, occupational), and they are normally diagnosed with a chest radiograph. They each show exposure radiographic response relations, although they have different slopes and different prevalences. With the exception of organisation after asbestos pleural effusion,' they have long latent periods between first exposure and detectable manifestations. Each is chronic and tends to progress, even after exposure has ceased. Since the late onsets and subsequent worsenings both reflect gradual advance of
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