Research Program Area: Health & Exposure
Topic Areas: Health Effects of Air Pollution
The investigation tested the effects of a variable daily dosage of 0.25ppm nitrogen dioxide (N02) on the lungs of weanling mice. Image analysis was used to quantitative Type 2 Cells, elastic tissue, and walls of alveoli. Effects of NO2 exposure were increases in Type 2 Cell number, Type 2 Cell field and mean areas, alveol; at alveolar wall area with and without the exclusion of Type 2 Cell area, and relationships (ratios) of Type 2 Cells to alveolar wall area, including numbers per wall area and area per wall area (with or without Type 2 Cell area excluded). There were also increases in elastic tissue fiber numbers, mean fiber area, and numbers of elastic fibers to alveolar wall area (minus elastic tissue area). A number of the statistically significant increases had not reversed by the final test period. The effects that have been produced are well recognized as early lesions and common denominators for diverse kinds of human lung disease. Type 2 Cell increases in number (hyperplasia) and size (hypertrophy) are generally responses to Type 1 Cell damage and loss. The Type 1 Cell is primarily responsible for gas exchange in the lung, and is also a major factor in the prevention of air space replacement by watery fluids (edema).
Hypertrophy and hyperplasia of Type 2 Cells not only implies damage to the Type 1 Cell but in addition may reflect damage to the Type 2 Cell itself. There may also be a need for in-creased Type 2 Cell work, in particular the secretion of detergent like substances (surfactants) that prevent the air spaces from collapsing (atelectasis and condensation fibrosis). Alterations of the alveolar wall impact on vital aspects of gas exchange. Integrity of the connective tissue of the wall is critical to appropriate expansion and recoil of the lung (compliance), to proper blood vessel perfusion and fluid drainage, and to the maintenance of a scaffolding that permits appropriate regeneration of alveolar lining cells when they are damaged and lost. The results of the elastic tissue and alveolar wall measurements imply suboptimal repair processes subsequent to NO2 exposure and thus a depletion of respiratory reserves. The persistence of the cell and wall alterations 32 weeks after NO2 exposure was stopped further implies some degree of irreversible depletion of structural and / or functional lung reserves.
For questions regarding this research project, including available data and progress status, contact: Research Division staff at (916) 445-0753
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