Page 239 - Industrial Ventilation Design Guidebook

200 CHAPTER 5 PHYSIOLOGICAL AND TOXICOLOGICAL CONSIDERATIONS

each serve to represent airway branching. Recent studies have also suggested
7 8
a fractal pattern to the bifurcations. ' Whatever the overall bifurcation pat-
tern, the general structure can be most easily summarized by the Weibel "A"
4
model, in which successive bronchial generations are more numerous,
shorter, and have smaller individual cross-sectional areas than more proxi-
mal generations. According to the Weibel "A" model, the number of
branches in generation z is

and the mean diameter of airways in generation z, d(z), is given by

where d 0 = tracheal diameter (Table 5.5), Consequently, overall cross-
sectional area increases exponentially as a function of distance from the
2
nares, producing a predicted alveolar surface area of 43-80 m . Respira-
tion (exchanging O 2 for CO 2) depends on this large exchange surface to
provide sufficient gas exchange capacity during strenuous activity to ac-
commodate demands by active muscles for greater volumes of O -. and the
need to remove excess CO 2.
5.2.2.3 Airway Wall Anatomy
Airway cross-sections have the nominal anatomy shown in Fig. 5.16. Air-
way surface liquid (ASL), primarily composed of mucus gel and water, sur-
rounds the airway lumen with a thickness thought to vary from 5 to 10 mm.
ASL lies on the apical surface of airway epithelial cells (mostly columnar cili-
ated epithelium). This layer of cells, roughly two to three cells thick in proxi-
mal airways and eventually thinning to a single cell thickness in distal airways,
rests along a basement membrane on its basal surface. Connective tissue (col-
lagen fibers, basement membranes, elastin, and water) lies between the base-
ment membrane and airway smooth muscle. Edema occurs when the volume
of water within the connective tissue increases considerably. Interspersed
within the smooth muscle are respiratory supply vessels (capillaries, arterio-
venous anastomoses), nerves, and lymphatic vessels.
Certain respiratory diseases (e.g., asthma and emphysema) alter air-
way dimensions, thereby modifying airflow patterns and adversely affect-
ing gas exchange and particle deposition. Emphysema breaks down
alveolar walls, enlarging alveolar sac volume but significantly reducing
overall alveolar surface area. Assuming a constant gas exchange flux, re-
ducing alveolar surface area decreases gas exchange and diminishes the
body's ability to obtain oxygen from the inspired airstream. In addition,
eliminating alveolar walls reduces the number of alveoli and shortens over-
all path length. A shorter path may allow larger inhaled particles to reach
and deposit in the pulmonary airways, potentially leading to adverse clini-
cal consequences. Diseases that reduce bronchial diameter (asthma,
chronic bronchitis, and cystic fibrosis) increase airstream velocity in oc-
cluded airway regions, increasing heat and water vapor exchange and par-
ticle impaction while reducing sedimentation in the affected bronchi. This
results in a greater volume of fine inhaled particles [<3.0 fxm mean mass
aerodynamic diameter (MMAD)] passing to more distal (and potentially