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We studied the asbestos content of bronchoalveolar lavage fluid (BALF) from 9 patients with asbestosis, 17 asbestos exposed but without asbestosis, 15 with idiopathic pulmonary fibrosis (IPF) and 9 nonexposed volunteers. The cellular lavage pellet was digested and filtered for asbestos body (AB) quantification by light microscopy (LM) and analysis of numbers and types of uncoated fibers (UF) by scanning electron microscopy (SEM) and energy dispersive x-ray analysis. BALF of asbestosis patients had significantly higher AB content than that of the combined IPF and volunteer groups. The UF content as determined by SEM was similar in all four groups. Commercial amphiboles (amosite or crocidolite) were identified more frequently in BALF from patients with asbestosis than from the other groups. ABs were detected by SEM only in highly exposed individuals. We conclude that the findings of > 1 AB per 10(6) cells or 1 AB/mL BALF by LM and of ABs or commercial amphibole fibers by SEM are indicative of considerable exposure to asbestos in the majority of cases.

Lavage effluents from the lungs of patients with pulmonary alveolar proteinosis were analyzed for soluble constitutents. Antiserums monospecific for normal plasma components, C-reactive protein, and secretory piece were used to investigate the presence of these proteins in lavage effluent, wheras 2-dimensional polyacrylamide gel electrophoresis provided a comprehensive map of the major proteins that were present. The proteins of lung washing obtained from normal subjects and of patient and normal serums were similarly analyzed. Most of the soluble-phase proteins from lavage of patients with pulmonary alveolar proteinosis were also found in patient serum, and were present in amounts consistent with a theory that they originate from the plasma by passage through channels of approximately normal size and selectivity. This findings suggests that the abundant soluble protein found in the alveoli of the lungs of these patients does not arise by leakage through a serverly damaged blood-air barrier. Patients had in their lung lavage effluents 2 soluble proteins of molecular weights 47,000 and 52,000 daltons not found in their serum and not present in lung washings from normal subjects. Uniformly increased concentrations of immunoglobulins in patient lavage effluent, abnormal immunoglobulin concentrations in patient serum, and the presence of C-reactive protein in the serum from 4 of 5 patients indicate a response of the immune system to the disease process and suggest that an atypical hypersensitivity reaction may be involved.

The recovery of protein and two specific surfactant lipids, phosphatidylcholine and phosphatidylglycerol, from bronchoalveolar lavage fluid is altered in chronic and acute non-granulomatous interstitial lung disease. This study set out to determine whether the same is true for patients with sarcoidosis. The median value for recovery of protein from lavage fluid was significantly higher in 21 patients with sarcoidosis than in 19 normal subjects (18 v 11 mg), while the median value for phospholipid recovery was significantly lower (4 v 1.7 mg). There were no changes in the proportions of phosphatidylcholine and phosphatidylglycerol. In addition, significantly less of the neutral lipid, cholesterol, was recovered (3.2 v 1.5 mg). The combined values of three biochemical measurements, non-phospholipid polar lipid, non-polar lipid, and protein, correctly classified all 40 subjects in our series; in a further group of nine normal subjects and 11 patients with sarcoidosis it allowed all but one normal subject to be classified correctly. These results are discussed in terms of alterations in epithelial cell function in interstitial disease.

The appearances of the lungs on radiographs and computed tomographic (CT) scans were correlated with degree of uptake on gallium scans and results of pulmonary function tests (PFTs) in 27 patients with sarcoidosis. CT scans were evaluated both qualitatively and quantitatively. Patients were divided into five categories on the basis of the pattern of abnormality at CT: 1 = normal (n = 4); 2 = segmental air-space disease (n = 4); 3 = spherical (alveolar) masslike opacities (n = 4); 4 = multiple, discrete, small nodules (n = 6); and 5 = distortion of parenchymal structures (fibrotic end-stage sarcoidosis) (n = 9). The percentage of the volume judged to be abnormal (CT grade) was correlated with PFT results for each CT and radiographic category. CT grades were also correlated with gallium scanning results and percentage of lymphocytes recovered from bronchoalveolar lavage (BAL). Patients in CT categories 1 and 2 had normal lung function, those in category 3 had mild functional impairment, and those in categories 4 and 5 showed moderate to severe dysfunction. The overall CT grade correlated well with PFT results expressed as a percentage of the predicted value. In five patients, CT scans showed extensive parenchymal disease not seen on radiographs. CT grades did not correlate with the results of gallium scanning or BAL lymphocytes. The authors conclude that patterns of parenchymal sarcoidosis seen at CT correlate with the PFT results and can be used to indicate respiratory impairment.

We applied a two-stage random effects model to pulmonary function data from 31 sarcoidosis patients to illustrate its usefulness in analysing unbalanced longitudinal data. For the first stage, repeated measurements of percentage of predicted forced vital capacity (FVC%) from an individual were modelled as a function of time since initial clinical assessment. At the second stage, parameters of this function were modelled as a function of certain patient characteristics. We used three methods for estimating the model parameters: maximum likelihood; empirical Bayes; and a two-step least-squares procedure. Similar results were obtained from each, but we recommend the empirical Bayes, since it provides unbiased estimates of variance components. Results indicated that deterioration in FVC% is associated with a higher initial FVC% value and large numbers of both total cells and eosinophils in bronchoalveolar lavage at the initial assessment. Improvement is associated with higher values of pulmonary Gallium uptake at initial assessment and race. Blacks are more likely to improve than whites.

Two glycoproteins of Mr 62,000 and 36,000 have been isolated and purified from lung lavage of normal human and patients with sarcoidosis and bibasilar fibrosis. The two glycoproteins contained hydroxyproline, high amounts of glycine, and other amino acids in amounts comparable to those present in the same two glycoproteins isolated from lung lavage of patients with alveolar proteinosis. The antibody raised against the glycoprotein of Mr 36,000 isolated from lung lavage material of patients with alveolar proteinosis reacted with both the glycoproteins isolated from normal human as well as from patients with sarcoidosis and bibasilar fibrosis, indicating that these glycoproteins isolated from different sources are structurally related to each other.

Plasma proteins were measured in bronchoalveolar lavage effluents and serums from normal healthy nonsmokers and smokers, and their concentrations in the 2 fluids were compared. Two-dimensional polyacrylamide gel electropherograms suggested, and radial immunodiffusion assays confirmed, that the soluble proteins of the bronchoalveolar surface resemble serum in kind and amount with the following significant exceptions. Two immunoglobulins, IgG and IgA, were present in amounts that exceeded their concentrations in serum; of the 2, IgG was more abundant. Large nonimmunoglobulin proteins (greater than 300,000 daltons) were absent or present at very low concentrations compared with the amounts found in serum. Transferrin was the only nonimmunoglobulin with a concentration significantly higher at the bronchoalveolar surface than in serum. Smoking did not cause a significant change in the concentration of any protein in serum, but did cause an increase in IgG, C4, and C3 and a decrease in alpha 2-thioglycoprotein, alpha 1-acid glycoprotein, and Gc-globulin in lavage effluents from females.

The lungs of patients with pulmonary alveolar proteinosis were lavaged with saline. The lavage effluents were examined for the presence of unusual components which might be considered characteristic of the disease. Soluble proteins were resolved by electrophoresis on polyacrylamide linear gradient (2.5 to 27 per cent acrylamide) gel slabs and compared with proteins found in the patients' sera and lavage effluents from nondiseased human lungs. Many proteins in lavage effluents from both diseased and nondiseased lungs appeared similar to those found in serum. Several proteins from diseased lungs were not present in serum nor lavage effluents from nondiseased lungs. A number of proteins present in lavage effluents from nondiseased lungs appeared to be absent from lungs with alveolar proteinosis. Particulate components of lavage effluents from diseased and normal lungs were examined and compared using the electron microscope. Many particulate components including degenerate and disintegrating cells, ultrastructurally abnormal alveolar macrophages, and myelin-like structures were present in lavage effluents from diseased lungs but absent from normal lungs. Much of the particulate material resembled cell debris. The insoluble accumulations present in the pulmonary alveoli and airways of patients with alveolar proteinosis do not come from serum leakage nor from hypersecretion of materials normally found in these regions of the lungs. The major insoluble components appear to arise from cellular disintegration and the extracellular formation of myelin-like structures.

We studied the asbestos body (AB) content of bronchoalveolar lavage fluid from 20 patients with a history of occupational asbestos exposure, 31 patients with sarcoidosis and 5 patients with idiopathic pulmonary fibrosis. The cellular lavage pellet was digested in sodium hypochlorite and filtered onto Nuclepore filters for AB quantification by light microscopy. ABs were found in 15 of 20 asbestos-exposed individuals, 9 of 31 sarcoidosis cases and 2 of 5 patients with idiopathic pulmonary fibrosis. There was a statistically significant difference in the number of ABs per million cells recovered or per milliliter of recovered lavage fluid in the asbestos-exposed group as compared to the other categories of chronic interstitial lung disease. The highest levels occurred in patients with asbestosis. Large numbers of asbestos bodies in the lavage fluid (greater than 1 AB/10(6) cells) were indicative of considerable occupational asbestos exposure, whereas occasional bodies were a nonspecific finding.

A 61-yr-old woman was evaluated for dyspnea on exertion and interstitial lung disease. A unique association between inhaled particulates from wood burning and interstitial pneumonitis was demonstrated. Bronchoalveolar lavage revealed numerous particulates and fibers, as well as cellular and immunoglobulin abnormalities. The particles were shown to be carbonaceous by energy dispersive X-ray analysis (EDXA). Inflammation and fibrosis were found surrounding them on open biopsy. The particle source was traced to a malfunctioning wood-burning heater in the patient's home. We present this case to highlight the usefulness of BAL and EDXA in the elucidation of particle-associated lung disease.

We evaluated patterns of abnormal lung parenchyma on CT scans in six specific chronic lung diseases and then applied those findings in the differential diagnosis of these lung parenchymal patterns in 56 subjects. There were 48 patients with chronic lung diseases (43 with histologic proof) consisting of usual interstitial pneumonia (n = 20), sarcoidosis (n = 16), lymphangitic carcinomatosis (n = 7), lymphangioleiomyomatosis (n = 2), drug toxicity (n = 2), and eosinophilic granuloma (n = 1). Including eight CT scans of normal control subjects, 56 CT scans were assessed independently by two readers (R1 and R2). Chest radiographs, most of which were obtained within 1 week of CT examination, were available in 48 of the 56 subjects. CT scans were evaluated for specific parenchymal features including disease distribution, lung distortion, thickening of bronchovascular bundles and polygon walls, bronchiectasis, cysts, and nodules, to determine the association of each abnormal feature with the different diseases. Diagnosis was then made from the overall CT appearance of the lungs and, on a separate occasion, from the appearance of the chest radiograph. The correct diagnosis was made from the CT appearance in 54 of 56 patients (R1) and in 50 of 56 patients (R2). Correct diagnoses were made from the chest radiographs in 42 of 48 patients (R1) and 43 of 48 patients (R2). We have identified features that are reproducible and useful when describing CT scans of patients with chronic lung diseases. Interpretation of the appearance of the lung on CT scans was accurate in diagnosing usual interstitial pneumonia, sarcoidosis, and lymphangitic carcinomatosis.