Reduced pulmonary function is an important predictor of mortality in the general population, and antioxidant vitamins are thought to positively influence pulmonary function. Vitamin C, vitamin E, retinol, and carotenoids are powerful antioxidants but information about the joint relation of serum levels of these antioxidants to pulmonary function is limited. We analyzed the association of FEV(1) and FVC with serum vitamins C and E, retinol, and carotenoids (beta-cryptoxanthin, lutein/zeaxanthin, beta-carotene, and lycopene) in a cross-sectional study. The analysis was carried out in a sample of 1,616 randomly selected residents of Western New York, USA, age 35 to 79 yr and free of respiratory disease. Lung function was adjusted for height, age, sex, and race and expressed as percentage of predicted normal FEV(1) (FEV(1)%) and FVC (FVC%). Participants in the lowest quartile of each of the serum antioxidants had consistently lower FEV(1)% and FVC% than those in higher quartiles. Multiple linear regression analysis revealed significant associations of vitamin C, vitamin E, beta-cryptoxanthin, lutein/zeaxanthin, beta-carotene, and retinol with FEV(1)% when these variables were investigated individually after adjustment for other covariates (smoking status, pack-years of smoking, weight, eosinophil count, and education). When all of these antioxidant vitamins were analyzed simultaneously in a multivariate regression model, the strongest association was seen with vitamin E and beta-cryptoxanthin. Only retinol showed an independent effect on FEV(1)% after controlling for vitamin E and beta-cryptoxanthin. As for FEV(1)%, vitamin E and beta-cryptoxanthin were most strongly related to FVC% when all variables were considered in the multivariate regression model. The differences in FEV(1) associated with a reduction of one standard deviation of serum vitamin E or beta-cryptoxanthin were equivalent to the negative influence of approximately 1 to 2 yr of aging. Our findings support the hypothesis that antioxidant vitamins may play a role in respiratory health and that vitamin E and beta-cryptoxanthin appear to be stronger correlates of lung function than other antioxidant vitamins.

It has been suggested that lung function can be altered by both free radical and oxidant exposure, while antioxidant vitamin intake is positively related to lung function. However, the information on the relation of blood levels of oxidants and antioxidants to lung function is sparse. The present cross-sectional study, conducted from September 1995 to May 1996, analyzes the association between lung function measured as forced expiratory volume in 1 second (FEV1) with 1) levels of thiobarbituric acid-reactive substances in plasma (p-TBARS) and in low and very low density lipoprotein cholesterol (LDL cholesterol/VLDL cholesterol-TBARS) as indicators of lipid peroxidation and 2) compounds with antioxidant activity, erythrocytic glutathione, plasma glutathione peroxidase, trolox equivalent antioxidant capacity, and serum bilirubin, which may protect against lipid peroxidation. The analysis was carried out in 132 nonsmoking subjects aged 37-73 years who were randomly selected from the residents of Erie and Niagara counties, New York. FEV1 in percent of the predicted value (FEV1%) was negatively and statistical significantly associated with p-TBARS (r = -0.19). A negative association with borderline statistical significance was observed between FEV1% with low density lipoprotein cholesterol/very low density lipoprotein cholesterol-TBARS (r = -0.16) and glutathione (r = -0.16), while FEV1% was positively related to serum bilirubin (r = 0.15). Participants in the lowest quartile of FEV1% showed significantly higher levels of p-TBARS (p = 0.02) and lower levels of bilirubin (p = 0.04) than did those in the highest quartile. Our results suggest that increased lipid peroxidation is associated with pulmonary airway narrowing in the general population.

All indices of hypoxemia are affected by changes in FIO2 in patients with ARDS. PaO2/FIO2 ratio exhibits the most stability at FIO2 values of > or = 0.5 and PaO2 values of < or = 100 torr (< or = 13.3 kPa), and is a useful estimation of the degree of gas exchange abnormality under usual clinical conditions. Venous admixture varies substantially with alteration of FIO2 in patients who have clinically important ventilation/perfusion abnormalities. Under these circumstances, venous admixture is a poor indicator of the efficiency of pulmonary oxygen exchange, even if venous admixture is calculated from measured arterial and venous oxygen content values. Estimated venous admixture, based on an assumed arterial-venous oxygen content difference, is even more unreliable.

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