Steady-state CO pulmonary diffusing capacity with alveolar CO measured from an endtidal sample (abbr. D_LCO SS₂) was evaluated in 250 patients with chronic pulmonary diseases. The normal range of D_LCO SS₂ was determined taking into consideration on ventilation (ATPS) when D_LCO SS₂ was measured. There is a good correlation between D_LCO SS₂ and ventilation when the D_LCO SS₂ was plotted against the ventilation in logarithmic scale. Coefficient of correlation r was 0.70. Regression formula, Y=31 log X-12.1 was obtained with the method of least squares. Using this equation, predicted values for D_LCO SS₂ were calculated and tabulated. The percentage of the observed D_LCO SS₂ to the predicted values gives % D_CO.
D_LCO SS₂ increases with increasing ventilation until D_LCO SS₂ reaches to a maximum value, which is the true pulmonary diffusing capacity. Voluntary hyperventilation or excercise is often too hard for patients with pulmonary disability to practice. Moreover, these patients are in fact making strenous efforts on breathing at rest. So we intended to use the % D_CO as a substitute for hyperventilation or excercise. Low D_LCO SS₂ with 100% D_CO indicates that ventilation, in other words, oxygen consumption, is low. Then the value is not a maximum and might be increased by voluntary hyperventilation and excercise. On the other hands, low D_LCO SS₂ with low % D_CO means that it can hardly be increased any more even by hyperventilation. It has already reached to a miximum value and can be considered as a real pulmonary diffusing capacity.
D_LCO SS₂ in bronchial asthma was within the normal ranges, even if D_LCO SS₂ value was 9.0ml/min/mmHg. Meanwhile, D_LCO SS₂ value in emphysema, pulmonary disability after pulmonary tuberculosis and fibrosis was not only low but also on the right of the normal range in our log V_E—D_LCO SS₂ diagram. Their D_LCO SS₂ values were 6-7ml/min/mmHg and % D_CO were lower than 50%. There were 52 patients whose D_LCO SS₂ values satisfied following condition; D_LCO SS₂ was below 9.0ml/min/mmHg, outside the normal range and less than 50% of the predicted values. 19 of them developed into acute exacerbation of respiratory failure. D_LCO SS₂ in the respiratory failure group lowered to as low as 5.6±1.7ml/min/mmHg and % D_CO was 35.4±8.2.

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Monoamine oxidase (MAO) activity in sera from patients with various pneumoconioses including asbestosis, silicosis, talcosis, graphitosis and arch welder's pneumoconiosis was estimated. This enzyme was also determined in other diseases such as liver cirrhosis, congenital heart disease and pulmonary tuberculosis for comparison. The total number of cases was 105, and the following results were obtained.
1) Serum MAO activity in pneumoconioses seemed to show high levels with the degree of diffuse or nodular fibrosis in lungs, which was assessed by roentgenographic manifestations. This enzyme in liver cirrhosis and congenital heart disease revealed also high value as in pneumoconiosis.
2) However MAO activity in sera from patients with pulmonary tuberculosis or silicosis, associated with tuberculosis who were given orally isoniazid (INH) was extremely inhibited and lowered until 4 weeks after INH discontinuation.
3) Since MAO is reported to be copper-pyridoxal phosphate dependent enzyme in beef serum, pyridoxal phosphate with the dosis of 60mg daily was administered to those patients with tuberculosis for 2 weeks. But this enzyme in their sera remained inactivated.
4) Mitochondrial MAO activity in tissues from a patient with asbestosis was measured. The activity of this enzyme in lungs revealed 22.3, while those in aorta and liver were 28.4 and 12.0mμmole/hr/mg protein respectively.

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For the purpose to clarify the mechanism of air pollution caused by ozone (O₃), the biochemical changes of lung tissue and bronchial washing were investigated. The effects of O₃ (10-20ppm) for various duration on Na⁺-K⁺, APTase activity and lipid metabolism in lung were observed, and following results were obtained:
1. Na⁺-K^K+, ATPase activity in normal lung tissue showed 26% of total ATPase activity and decreased about one-thirds of total activity in O₃ exposed lung.
2. Incorporation of ¹⁴C-palmitate into phospholipids in lung tissue was inhibited by 20ppm O₃ exposure for 2 hours.
3. Lipid composition in membrane component of lung tissue showed decreased of phospholipids and increase of triglyceride fraction after O₃ exposure.
4. Phospholipid, especially phosphatidyl choline, was decreased after O₃ exposure in bronchial washing.
5. Lipid peroxidation measured by TBA reaction was significantly increased, especially in triglyceride fraction, after O₃ exposure and inhibited following the administration of antioxidant (Vit. B₂-butyrate, Vit. E).
6. Fatty acids composition of phospholipid and triglyceride fractions in lung tissue and bronchial washing were not affected O₃ exposure.
In conclusion, the disturbance of lung metabolism by O₃ was suggested the inhibition of phospholipids synthesis and lipid peroxidation in lung tissue.

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