Previous studies have shown that vitamin E may be an integral part of lung surfactant and may function to protect this materialfrom oxidant damage Therefore we measured the vita min E levels in alveolar lavage materials from rats exposed to crystalline silica or treated with chlorphentermine CP two treatments that are known to increase surfactant phospholipids PL by different mechanisms Silica exposure leads to increased PL synthesis and CP treat ment causes a reduction in PL degradation Two different silica preparations HClwashed and unwashed silica were used because exposure to each of them leads to different degrees of phospholipidosis Exposure to HClwashed silica results in a more than 17 fold increase in lavage PL and protein levels and a 12 2 fold increase in the amount of vitamin E Exposure to unwashed silica leads to an approximately 7 fold increase in PL and proteins and a 5 8 fold increase in lavage vitamin E Following treatment of rats with CP there is a 15 to 19 fold increase in lavage PL and proteins and a 13 6 fold increase in vitamin E When the results are expressed as micrograms vitamin E per milligram of lavage PL or protein there is not much difference between controls and each treatment group Because surfactant synthe sis occurs in the endoplasmic reticulum we also measured vitamin E in lung microsomes Both silica exposure and CP treatment also lead to 1 8 to 2 5 fold increases respectively in the lung microsomal levels of vitamin E These results demonstrate that alveolar lavage vita min E levels are elevated along with lavage PL and proteins and lung microsomal vitamin E levels are increased following exposure of ratsto silica ortreatment ofthe animals with CP