Biology ETDs

Publication Date

12-14-1976

Abstract

With the expanding use of plutonium-239 (239Pu) as a nuclear reactor fuel and increased recycling of spent reactor fuel to recover 239Pu, the possibility of an accidental human exposure exists. Little information is available on the effects of inhaled 239Pu on immune mechanisms. This study was performed in order to examine the effects of 239Pu dioxide (239Pu02) inhalation on the ability of mice to be immunized against a bac­terial respiratory infection in which cell-mediated immunity is the primary mechanism of host resistance to infection. Groups of mice were exposed to 239Puo2 to achieve initial lung burdens (ILB) of 2.6 ± 0.7, 5.0 ± 1.3 and 11.9 ± 3.3 nanocuries (nCi) of 239Pu.

Pulmonary deposition of 239pu was observed in the lungs of mice immediately after exposure and retention at 3 to 4, 12, 18 and 26 weeks after exposure. At 3 to 4 and 26 weeks after 239puO2 inhalation, exposed mice and non- exposed control mice were divided into two subgroups, one to be immunized and the other to be non-immunized. Immunized animals received an intra­ venous injection of a sublethal dose of Listeria monocytogenes which was suspended in phosphate buffered saline. Non-immunized mice received only saline injections. One week after immunization, mice from the immunized and non-immunized subgroups of 239Pu exposed and control animals were chal­lenged with L. monocytogenes by the respiratory route. The pulmonary clearance of L. monocytogenes was observed through 4 hours after inhalation. Survival of mice was observed for 3 weeks following L. monocytogenes challenge. Body weights, hematological parameters and pulmonary lavage cell populations were observed in mice 3 to 4 and 26 weeks after 239PuO2 inhalation.

Results from these studies demonstrated that mice with ILB of 11.9 ± 3.3 nCi of 239pu has a suppression of pulmonary clearance of inhaled L. monocytogenes after 239PuO2 inhalation. This group of 239Pu exposed mice immunized at 26 weeks after exposure had a decreased survival when compared to non-exposed immunized mice. Body weight gain was not influenced by 239Pu exposure. The 11.9 ± 3.3 nCi ILB group of 239Pu exposed mice had elevated total white blood cell and absolute lymphocyte counts at 26 weeks after 239PuO2 inhalation. Also, the number of alveolar macrophages recoverable by saline lavage of the lung was reduced in this group of 239Pu exposed mice. Mice which had lower ILBs of 239Pu did not display any of the above effects with the exception of hematological alterations at 3 to 4 weeks after 239PuO2 inhalation.

It was concluded that mice with an 11.9 ± 3.3 nCi ILB of 239Pu had a suppressed clearance of inhaled L. monocytogenes from their lungs after 239Puo2 inhalation. An 11.9 nCi ILB of 239Pu resulted in a decreased survival of mice which had been immunized against L. monocytogenes, then challenged by the respiratory route, 26 weeks after 239PuO2 inhalation. The mechanism by which 239Pu exposure resulted in suppressed pulmonary clearance and decreased survival after L. monocytogenes respiratory challenge was not demonstrated but was related to a decreased number of alveolar macrophages, recoverable by saline lavage, from the lungs of 239Pu exposed mice.

Language

English

Document Type

Thesis

Degree Name

Biology

Level of Degree

Masters

Department Name

UNM Biology Department

First Committee Member (Chair)

David Lee Lundgren

Second Committee Member

Larry Lumir Barton

Third Committee Member

Paul Richard Kerkof

Fourth Committee Member

Roger Orville McClellan

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