Idiopathic pulmonary fibrosis in asbestos-exposed workers.

Diffuse interstitial lung disease in asbestos-exposed workers is presumed to represent asbestosis. Among 176 asbestos-exposed persons for whom lung tissue was available, we found nine with clinical features consistent with asbestosis, but histologic sections failed to demonstrate asbestos bodies, the usual requirement for pathologic diagnosis of asbestosis (Group I). These nine were compared by analytic electron microscopy with nine persons with idiopathic pulmonary fibrosis (Group II), and with nine persons with all the criteria of asbestosis (Group III). The three groups did not differ significantly with respect to lung burden of chrysotile or tremolite and actinolite, but Group III had a lung burden of amosite and crocidolite that was three orders of magnitude greater than in Groups I and II, with no overlap. We conclude that (1) the American Thoracic Society criterion of "a reliable history of exposure" is sometimes difficult to define; (2) asbestos bodies are seen in tissue sections only when exposure has been reasonably high, and given the proper clinical setting, the presence of diffuse fibrosis and asbestos bodies in tissue sections are sensitive and specific criteria for a diagnosis of asbestosis; and (3) the prevalence here of 5.1% nonasbestos-induced interstitial lung disease among asbestos-exposed persons is artefactually high because of atypical case selection. However, because asbestosis is a disappearing disease, such cases will become more frequent. The identification of these other diseases is important because therapy and prognosis may differ from that of asbestosis.

Zirconium compound-induced pulmonary fibrosis.

Despite suspicion that inhalation of zirconium should be capable of causing human pulmonary disease, documentation of zirconium pneumoconiosis in humans has been lacking. We studied a likely case of zirconium compound-induced pulmonary fibrosis. The diagnosis was based on the following: (1) a history of gradual increase in symptoms and slowly progressing pulmonary fibrosis by chest roentgenogram compatible with a pneumoconiosis; (2) an appropriate history of exposure and a latency period of about 15 years before the onset of dyspnea and of roentgenographic changes; (3) analysis of open lung biopsy material revealing end-stage fibrosis and honeycombing, a moderate number of birefringent particles, and extremely high levels of a variety of zirconium compounds; and (4) no other potential cause of fibrosis. We conclude that zirconium should be considered a likely cause of pneumoconiosis and that appropriate precautions should be taken in the workplace.

Pulmonary fibrosis in aluminum oxide workers. Investigation of nine workers, with pathologic examination and microanalysis in three of them.

Epidemiologic surveys have indicated an excess of nonmalignant respiratory disease in workers exposed to aluminum oxide (Al2O3) during abrasives production. However, clinical, roentgenographic, histologic, and microanalytic description of these workers are lacking. This is a report of nine Al2O3-exposed workers with abnormal chest roentgenograms (profusion greater than or equal to 1/0, ILO/UC) from a plant engaged in the production of Al2O3 abrasives from alundum ore. Mean duration of exposure was 25 yr, and time since first exposure was 28 yr. in a subgroup of three, the severity of symptoms, reduction in the forced vital capacity (67% predicted) and diffusing capacity (51% predicted), and progressive roentgenographic changes (profusion greater than or equal to 2/2) prompted open lung biopsy. Lung tissue was analyzed by scanning electron microscopy and electron microprobe analysis. In each of the three biopsies, interstitial fibrosis with honeycombing was seen on routine section. In one biopsy, silica and asbestos fiber counts were at the low end of the range seen with silicosis and asbestosis; however, the absence of asbestos bodies and silicotic nodules suggested that the fibrosis was due to another cause. Metals occurred in amounts several orders of magnitude above background, and the majority was aluminum as Al2O3 and aluminum alloys. The findings in these nine workers suggests a common exposure as the possible cause. The nonspecific pathologic findings, absence of asbestos bodies and silicotic nodules, and the striking number of aluminum-containing particles suggest that Al2O3 is that common exposure. The possibility of "mixed dust" fibrosis should also be considered.

Pleural effusion in an asymptomatic patient. Spectrum and frequency of causes and management considerations.

We conducted retrospective chart and literature reviews to analyze the frequency and spectrum of causes of asymptomatic pleural effusion (APE). In our series, 16 percent of patients undergoing thoracentesis for PE were asymptomatic and the spectrum of causes was similar to that for symptomatic patients. Asymptomatic PEs were evenly distributed among transudates, exudates and indeterminate effusions. More symptomatic (S) PE were exudates, although the difference was not statistically significant (p greater than 0.1). In comparison to SPE, APE were more often free flowing and small. In both groups, the four most common diagnoses were malignancy, CHF, parapneumonic and postoperative effusions accounting for greater than 70 percent of each group. Review of the literature demonstrated the following associations with APE: recent childbirth or abdominal surgery, benign asbestos effusion, uremia, malignancy, and tuberculosis. In the uncomplicated postpartum or postoperative setting or in patients with typical findings of left ventricular failure, observation without diagnostic studies is appropriate. In all other situations, APE should be evaluated in traditional fashion. If thoracentesis is non-diagnostic and the effusion is an exudate, closed pleural biopsy and less often, fiberoptic bronchoscopy, should follow. Once malignant or granulomatous pleuritis has been excluded, it may be appropriate to observe for a period of time before proceeding to more invasive procedures.

Chronic eosinophilic pneumonia. A report of 19 cases and a review of the literature.

Clinical, roentgenographic and pathologic findings in patients with chronic eosinophilic pneumonia, including 19 additional cases, have been reviewed and summarized. Most patients present with subacute respiratory and constitutional symptoms and have failed to respond to therapy for presumptive pneumonia. A previous history of atopy, most often asthma, will be obtained in one-half. Eosinophilia occurs in most cases and its absence may be the major indication for lung biopsy. Although pulmonary infiltrates are more often peripheral than not, the classic "photographic negative of pulmonary edema" is seen in less than one-third of cases. Pathologic findings include an intra-alveolar and interstitial infiltrate which comprises eosinophils, histiocytes, and exudate. Bronchiolitis obliterans and eosinophilic microabscesses occur less frequently. Open-lung biopsy is preferable when atypical features prevent a confident clinical diagnosis. The exquisite responsiveness of CEP to corticosteroids should encourage use of a therapeutic trial when there is a strong clinical suspicion of the disorder. The rapid clinical response should not deter the clinician from giving a prolonged course of treatment. The differential diagnosis includes other diseases characterized by PIE and the more recently recognized bronchiolitis obliterans and organizing pneumonia, a disorder which is also marked by peripheral pulmonary infiltrates.

Congenital bronchial atresia. A report of 4 cases and a review of the literature.

The clinical, radiographic, and pathologic findings in 82 patients with congenital bronchial atresia (CBA) have been reviewed, and we have discussed 4 additional cases. Most patients are asymptomatic and come to attention because of abnormal radiographic findings of a round or lobulated perihilar, solid, or cystic mass--the mucoid impaction sign. Typically, the region distal to the mass is hyperinflated. Recently, computed tomography has been shown to be diagnostic and its use obviates the need for other more complex imaging modalities or surgical exploration. Excisional surgery has been performed to preserve lung function in younger patients, because of lack of familiarity with the entity or, as in 2 of our cases, to prevent recurrent infections. Pathologic findings include a cystic, blindly terminating, mucus-filled bronchocele without connection to the main bronchial tree, but with normal subsequent generations of bronchi. Distally there is noncollapsible hyperinflation of the corresponding lung segment or lobe as the result of collateral ventilation from the surrounding lung. The anomaly is the result of an insult to the growing bronchial tree in early development. The differential diagnosis most often includes allergic bronchopulmonary aspergillosis, but cystic bronchiectasis, bronchogenic cysts, and intrapulmonary sequestration should also be considered. Unusual features in our 4 cases included recurrent pulmonary infections in 2 patients and thoracic cage asymmetry in 1.

Patient work-up for bullectomy.

A localized area of hypertransradiance often leads to surgical referral. Among 608 cases, 115 were due to local lesions of airways, blood vessels, or parenchyma. Among the remaining 493 with bullae from diffuse emphysema, 21% underwent surgery. Good restoration of function occurred in patients with rapidly progressive dyspnea who did not have a bronchitic component, recurrent infections, or CO2 retention. Physiologically, preoperative findings suggestive of tension pneumothorax, including severe restriction, marked air trapping, and little ventilation/perfusion mismatch suggested good results. Favorable radiographic findings included well-defined, large air spaces without stigmata of diffuse emphysema, serial films showing rapid enlargement of bullae, and expiration films with good thoracic motion and obscuration of lung around bullae. Compressed but otherwise intact lung was best demonstrated by angiography and CT scans. Palliative bullectomy in severe diffuse emphysema sometimes had gratifying clinical results. Resection of small bullae never caused improvement. Localized giant bullae most often were associated with paraseptal or periacinar emphysema, and the best surgical results were obtained in this group.

EcoRI cleavage sites in the argECBH region of the Escherichia coli chromosome.

The EcoRI cleavage of deoxyribonucleic acids (DNAs) from lambdadarg phages, carrying argECBH, has been examined. The phages are derived from the heat-inducible, lysis-defective strain lambda y199, and their bacterial DNA, including argECBH, is derived from Escherichia coli K-12. Such cleavage of the phage DNAs, in each case, produces the D, E, and F segments of lambda. Additionally, these DNAs yield segments, ordered from left to right, of length (in kilobases [kb]) determined by electron microscopy and 0.7% agarose slab gel electrophoresis as follows: lambdadarg13 (ppc argECBH bfe), 13.9, 2.8, 1.5, and 5.6; lambdadarg14 (ppc argECBH), 3.0, 2.0, 17.3, and 6.2; and lambdadarg23 (argECBH), 18.4 and 6.2. For lambdadarg13 sup102 DNA, the segment analogous to the 13.9-kb segment measures 12.2 kb. The direction from left to right corresponds to the clockwise orientation of the E. coli genetic map. The EcoRI segments define five cleavage sites near the arg region of the E. coli chromosome. For each of the DNAs, the arg genes occur on the largest segment produced. The 17.3-kb segment, being entirely bacterial, represents the argECBH-bearing EcoRI segment of the E. coli chromosome. The location of the arg genes was demonstrated electron microscopically in heteroduplex experiments.