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Physiologic, biochemical, immunologic and pathologic changes following ozone exposure

A detailed study of physiologic, biochemical, immunologic and pathologic changes resulting from acute and repeated acute injuries due to inhalation of ozone is reported. This study defines the primary chemical reaction of ozone with constituents of the body, the response of the body to the presence of the toxic substance, the physiologic functional alterations produced by acute and repeated acute injuries due to inhalation of this gas and the pathology produced by these injuries in rabbits, mice and rats. The data presented show that ozone reacts with the proteins of lung tissue to produce a severe cellular irritation which alters cell wall permeability and leads to severe pulmonary edema. Repeated acute injuries are shown to cause the development of fibrosis of the bronchioles and alveolar ducts, which limits the reserve capacity of the lung by causing the Hering-Breuer reflex to stop inspiration before complete inhalation can take place. Immunologic and biochemical changes observed which are characteristic of this type of injury are reported. It has been shown that ozone reacts in a random fashion with proteins to produce a heterogeneous antigen which will stimulate an antibody response in rabbits. The antigen created was shown to have characteristics similar to denatured protein. The severe limitation of pulmonary function by reduced tidal volume and edema and the resulting pathologic changes are reported and discussed.

Submitted on July 7, 1958

Lester D. Scheel,

Olga J. Dobrogorski,

John T. Mountain,

Joseph L. Svirbely,

Herbert E. Stokinger,

1 JAN 1959

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