1. We have developed a method for non-invasive measurement of lung tissue mass, thoracic blood and interstitial volumes by a combination of transmission and emission scanning with technetium isotope ( 99m Tc). 2. In a lung model we demonstrated that emission counts could be successfully corrected for attenuation with data obtained by transmission scanning, despite an uneven distribution of radioactivity and attenuation in the model. 3. In dogs we compared regional transthoracic tissue thickness, measured by transmission scanning, and regional ‘thickness’ of blood measured by transmission/emission scanning with direct gravimetric measurements made post mortem. Scanning and direct measurements correlated significantly. 4. In man we used a [ 99m Tc]pertechnetate ( 99m TcO 4 ) flood source to obtain antero–posterior transmission scans with a gamma-camera. The thickness of attenuating tissue was estimated in each pixel. Scans were obtained of thoracic blood (by labelling erythrocytes with 99m TcO 4 ) and of interstitium (with 99m Tc-labelled diethylene-triaminepenta-acetic acid and subtraction of the blood image). We used a computer program to correct the emission scans for attenuation using the transmission scan derived tissue thickness, pixel by pixel. Finally we took a lateral chest radiograph to estimate chest wall thickness. 5. In normal man lung tissue thickness at hilar level was 3.1 ± 0.5 cm ( n = 8). Thoracic blood thickness increased from the apex downwards in the upright lung, being 1.2 ± 0.1 cm at the hilar level and 2.0 ± 0.3 cm at the lung base. Interstitial thickness was 0.8 ± 0.3 cm at the hilum and 0.85 ± 0.2 at the base. These values compare well with data in the literature. 6. In emphysema ( n = 5) lung tissue and blood thickness were decreased; interstitial thickness was normal. In patients with interstitial pneumonitis ( n = 7) lung tissue thickness was approximately doubled, and interstitial thickness similarly increased. In two patients with acute pulmonary sarcoidosis interstitial thickness was not increased despite a marked increase in lung tissue thickness. 7. In conclusion, this technique gives information not readily obtainable by other methods, which may be of clinical utility. Further evaluation and development is warranted.

1. Unrestrained proteolysis in the lung is believed to initiate emphysema, a disease common among tobacco smokers. However, few studies have found extracellular protease activity in human lung lavage. 2. In this investigation, elastase and serine protease activities were measured in broncho-alveolar lavage supernatants (BAL) from patients undergoing routine investigations. Significantly more elastolytic activity (against insoluble [ 3 H]-elastin) was recovered in the lavage of smokers than that of non-smokers. However, no significant difference was found when the levels of serine proteolytic activity (against N -succinyl-L-trialanyl- p -nitroanilide) were compared. 3. The elastolytic component of the protease activity rose from 5% in non-smokers’ BAL to over 30% in that of smokers, suggesting that elastase activity is selectively enhanced by smoking. In lavages from most smokers, 80% or more of the elastase activity was serine-dependent, whereas lavages from non-smokers contained variable proportions of serine elastase. 4. Both α 1 -proteinase inhibitor (α 1 -PI) and a low molecular weight antiprotease, bronchial mucus proteinase inhibitor (BMPI) were detectable in the lavage samples, the latter contributing up to 76% of the total antiprotease quantified in the lavage. Functional antiprotease was detected in 85% of the lavages. 5. Since there were no differences in either antiprotease levels or functional inhibitory capacities between lavages from smokers and controls, it is concluded that the imbalance in the protease/antiprotease profile of the smokers’ lung results from an enhancement of proteases, specifically of elastolytic activity, rather than a reduction in inhibitory capacity.