Abstract
The death of an adolescent after deliberate inhalation of the domestic fluorocarbon--lipid spray, PAM, triggered an investigation of the effects of this product on mammalian lung. Some of its constituents are known to destroy the lung-surfactant system, but death from its inhalation by earlier victims was usually attributed to the fluorocarbon's cardiac arrhythmogenic properties. In the present study, we applied methods and experimental models not previously used to study the effects of this aerosol material on the lung surfactant. We found morphological and functional acute disintegration of normal alveolar surfactant, leading to extensive alveolar collapse, with sustained and elevated surface tensions in vitro. This could result in fatal hypoxaemia at inspired concentrations of fluorocarbons insufficient to cause cardiac arrhythmias, and may explain at least partly the large number of deaths associated with inhalation of such product.
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