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The presence of emphysema in silicosis is believed to be secondary to the development of progressive massive fibrosis (PMF). However, it is difficult to separate out other causative factors, particularly cigarette smoking. In order to attempt to distinguish these factors, we examined 30 patients with silicosis by means of pulmonary function testing and computed tomography (CT) scans of the chest. Eighteen of these patients were either exsmokers or current smokers, and 12 of them were nonsmokers. The CT scans were read independently by two observers on two separate occasions. Silicosis was graded on a 5-point scale from 0 to 4; emphysema was graded as a percentage of lung involved. Percent emphysema was associated with level of pulmonary function (FEV1, FVC, and DLCO) independent of its association with either cigarette smoking or silicosis grade (p less than 0.01). Silicosis grade was associated with DLCO (p less than 0.05) independent of its association with either cigarette smoking or percent emphysema, but was not associated with level of FEV1 or FVC. In the group without PMF (silicosis Grade 0, 1, or 2), smokers had worse emphysema than nonsmokers (p less than 0.01); there was no such difference among the patients with PMF (silicosis Grade 3 or 4). Only one of the nonsmoking subjects with silicosis but without PMF had any emphysema detected on CT. Our data suggest that silicosis, in the absence of PMF, does not cause significant emphysema, and that it is primarily the degree of emphysema rather than the degree of silicosis that determines the level of pulmonary function.

We used a CT program "density mask" outlining areas with attenuation values less than —910 HU, to indicate areas of emphysema on a chest CT and to provide an overall percentage of lung involvement by emphysema. The "density mask" quantitation of emphysema was previously shown to correlate well with the pathologic assessment of emphysema in patients undergoing lung resection. We compared the CT quantitation of emphysema with mean lung density, overall lung volume on CT and pulmonary function tests in 85 patients. There was a significant correlation between the extent of emphysema on CT and FEV 1 /FVC percent of predicted, functional residual capacity percent predicted and Dsb percent predicted. Determination of the percentage of lung with areas of low attenuation by CT provides a useful method for quantitating emphysema in life and correlates significantly with pulmonary function tests. (Cheat 1990; 97:315–321)

To assess the role of emphysema on the hyperinflation in chronic asthma, we studied 20 subjects with irreversible airflow limitation. Ten of the subjects had asthma and had never smoked; the other ten were cigarette smokers. Pulmonary function testing and chest computed tomography (CT) scans were performed on all subjects. Emphysema was graded using a score based on the percentage of lung involved on CT scan. There was good inter- and intra-observer agreement for the emphysema scores. The median emphysema score was 0 percent in the nonsmoking group and 10 percent in the smoking group. All smokers with a total lung capacity (TLC) of greater than 120 percent predicted had evidence of emphysema on the CT scan. None of the asthmatic subjects with a TLC greater than 120 percent predicted had emphysema identifiable on CT scan. We conclude that chronic asthma with severe hyperinflation does not result in emphysema.

Nasal washes before and at intervals after nasal challenge with mixed grass pollen extract were carried out in nine patients with allergic rhinitis and four control subjects. In the nasal wash, histamine was measured using the radioenzymatic method, prostaglandins (PGs) and leukotrienes (LTs) were measured by high pressure liquid chromatography. Control subjects did not react to allergen challenge. Small amounts of histamine (0.47 ± 0.23 ng/ml) and PGD2 were found in the nasal fluid before challenge with no increase in either mediator after challenge. Leukotrienes were not found before or after challenge. Subjects with allergic rhinitis developed sneezing, rhinorrhea, and stuffy nose after challenge. High levels of histamine (5.3 ± 7.0 ng/ml) and PGD2 (2.7 ± 3.2 ng/ml) were found in the first prechallenge wash even though the subjects were asymptomatic. The second prechallenge wash showed reduction of histamine (2.8 ± 5.2 ng/ml) and PGD2 (1.4 ± 1.8 ng/ml). Five to 15 minutes after antigen challenge, there was a rise in histamine and PGD2 in four of nine subjects. No LTs were detectable in the prechallenge wash. Five of nine subjects showed a rise in LTC4 and/or LTE4, immediately after challenge. Our results showed that although nasal challenge with antigen can induce the release of mediators in seven of nine subjects with allergic rhinitis, the profile of mediator release was variable, and there was no correlation between the type or amount of mediator released and the severity of the nasal symptoms. The pathogenetic role of these mediators in pollenallergic rhinitis needs further evaluation.

Plasma histamine levels were measured by radio-enzymatic technique in seven patients following 10 challenges: five methacholine challenge tests, four antigen inhalation challenge tests, and one oral aspirin challenge test. Baseline plasma histamine was the same in all patients except in the aspirin-challenged patient, who had a higher baseline histamine level. There was no statistical change in the level of histamine throughout the test in either the methacholine-challenged or the antigen-challenged patients, whereas there was a marked increase in histamine levels in the aspirin challenged patient. A possible explanation is that methacholine and antigen are inhaled and therefore have primarily local effects on the lung, whereas oral aspirin has a systemic effect with consequently systemic changes in histamine which are detectable as changes in plasma level.