Project at a Glance

Title: Health effects from the inhalation of oxidant air pollutants as related to the immune system : final report, California Air Resources Board, contract number A1-054-32

Principal Investigator / Author(s): Osebold, John W.

Contractor: Department of Veterinary Microbiology and Immunology, UC Davis

Contract Number: A1-054-32

Research Program Area: Health & Exposure

Topic Areas: Health Effects of Air Pollution


These investigations dealt with links between ozone inhalation and lung diseases. Increases in allergic lung disease occurred among our test populations of mice following inhalation of ozone at levels as low as 0.13 ppm, thus establishing a cause and effect relationship between the toxic inhalant and enhancement of a specific health problem. When the ozone exposure was made intermittent by removing the 0.18 ppm of ozone for nine hours each day during the four-day ozone cycles, this also reduced the total ozone exposure to 60 hours per cycle rather than the previously used 96-hour cycles. Under these conditions there continued to be more allergically sensitized animals when compared to those maintained in ambient air.

An adjuvant substance was used to augment the immunological responses against the antigen (allergen). The adjuvant was inactivated Bordetella pertussis cells. This is the same material that is used to immunize against whooping-cough in children. In mice receiving adjuvant, there was a significant enhancing effect for allergic sensitization from ozone at the level of 0.10 ppm. The adjuvant effect of whooping cough vaccine could still be detected in mice when they received only 1/49th or 1/24th of a dose used for childhood immunization. In this circumstance the environmental influence of periodic exposure to 0.15 or 0.18 ppm of ozone significantly increased the number of animals developing allergy.

Guinea pigs were used to see if they would show enhanced allergic sensitization from ozone exposure by a reaction similar to human asthma. This trial was not definitive and the factors involved would require additional investigation. Ozone inhalation reduced the severity of pneumonia in mice from influenza virus infection. When infected lungs were examined for the presence of influenza virus, it was found that the lining cells of the airways were less affected by virus replication in animals that had inhaled 0.16 ppm of ozone. Both ozone inhalation and influenza virus infection cause edema fluid to collect in the lungs. In an experiment designed so that maximum edema from both causes would occur simultaneously, the effect persisted wherein fewer deaths occurred in ozone exposed animals than in infected mice maintained in ambient air.

For questions regarding this research project, including available data and progress status, contact: Research Division staff at (916) 445-0753

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