Alveolar macrophage kinetics after inhalation of [sup 239]PuO[sub 2] by CBA/Ca mice: Changes in synthesis of DNA

Journal Article · Wed Jul 01 00:00:00 EDT 1992 · Environmental Health Perspectives; (United States)

DOI:https://doi.org/10.1289/ehp.929769· OSTI ID:7027422

Kellington, J P; Gibson, K; Buckle, T M; Talbot, R J; Hornby, S B ^[1]

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1. AEA Environment and Energy, Oxon (United Kingdom)

For workers in the nuclear industry, the primary route for the entry of radioactive materials into the body is by inhalation, and the rate of clearance of particles from the pulmonary region of the lung is an important factor in determining radiation dose. It is the function of alveolar macrophages (AM) to maintain the sterility of the lung and to remove insoluble particles from the respiratory surfaces and airways. The AM population is not static, and under normal conditions the loss of macrophages from the alvoli via the conducting airways is balanced by renewal. In this investigation the effects of inhaled [sup 239]PuO[sub 2] (plutonium dioxide) particles on the synthesis of DNA by AM were studied at times up to 77 days after exposure. We also measured the number of cells recovered by bronchoalveolar lavage and the incidence of AM with nuclear aberrations. The latter provides a sensitive indicator of the effects of radiation. One of the earliest effects observed after exposure to [sup 239]PuO[sub 2] is a reduction in the number of AM recovered by lavage. This reduction is associated with a 3-fold reduction in the proportion of AM undergoing DNA synthesis at early times after exposure. The overall mean pulse labeling index of AM recovered from sham-exposed mice is 1.68%, and no trends is observed with time. At later times after exposure there is a concurrent increase both in the number of AM recovered by lavage and the proportion of AM in the S-phase of the cell cycle. This repopulation of the AM pool is associated with an increase in the incidence of AM with nuclear aberrations. The results of this study are consistent with the theory of an intrapulmonary pool of proliferating macrophages. The depletion of the AM pool and the latency in the induction of nuclear aberrations after exposure to [sup 239]PuO[sub 2] can be attributed to a radiation-induced inhibition of cell division in addition to interphase death of AM. 57 refs., 4 figs.

• OSTI ID: 7027422
• Journal Information: Environmental Health Perspectives; (United States), Vol. 97; ISSN 0091-6765
• Country of Publication: United States
• Language: English

Related Subjects

63 RADIATION, THERMAL, AND OTHER ENVIRON. POLLUTANT EFFECTS ON LIVING ORGS. AND BIOL. MAT.
59 BASIC BIOLOGICAL SCIENCES
MACROPHAGES
BIOLOGICAL RADIATION EFFECTS
POPULATION DYNAMICS
PLUTONIUM DIOXIDE
INHALATION
LUNG CLEARANCE
BIOCHEMICAL REACTION KINETICS
DNA REPLICATION
LAVAGE
NUCLEAR INDUSTRY
OCCUPATIONAL EXPOSURE
RADIOACTIVE MATERIALS
ACTINIDE COMPOUNDS
ANIMAL CELLS
BIOLOGICAL EFFECTS
CHALCOGENIDES
CLEARANCE
CONNECTIVE TISSUE CELLS
EXCRETION
INDUSTRY
INTAKE
KINETICS
MATERIALS
NUCLEIC ACID REPLICATION
OXIDES
OXYGEN COMPOUNDS
PHAGOCYTES
PLUTONIUM COMPOUNDS
PLUTONIUM OXIDES
RADIATION EFFECTS
REACTION KINETICS
SOMATIC CELLS
TRANSURANIUM COMPOUNDS
560150* - Radiation Effects on Animals
550200 - Biochemistry
550300 - Cytology