thorax is the primary determinant of its pathogenicity: MVF must remain in the tissues long enough for chronic disease to occur (Berry 1999).

Given the importance of understanding biopersistence when determining protective exposure levels, the subcommittee found the Navy's discussion of the following aspects of biopersistence to be inadequate: critical target region, fiber size in relation to penetration and deposition, and in vivo dissolution of fibers.

In the Navy's discussion of the critical target region, it appears to assume that fibers that do not reach the alveoli are of no concern. However, the subcommittee believes that it is important for the Navy to consider very large (noninhalable) fibers that might be of concern for skin irritation, and thoracic fibers that deposit in the lung conductive airways and theoretically might be responsible for bronchitis and bronchogenic cancer in exposed occupational cohorts (Lippmann 1990a,b, 1993).

With regard to the Navy's discussion of fiber size in relation to penetration and deposition in lung regions, the subcommittee notes that in adults breathing orally, fibers with aerodynamic diameters of about 10 µm (physical diameter, about 3.3 µm) will penetrate only into the thorax, whereas most fibers with aerodynamic diameters less than 4 µm (physical diameter, about 1.3 µm) will penetrate into the deeper, gas-exchange regions of the lung (the alveoli) (Lippmann 1990a, 1993). However, nasal breathing would result in less penetration of fibers into the lung. The Navy's discussion of the influence of fiber length on regional fiber deposition should cite the work of Sussman et al. (1991a, 1991b), who showed that fiber length is an important determinant of fiber deposition in lung conductive airways, particularly for fibers longer than 10 µm. Also, the Navy's brief review of the biological effects of fibers longer than 15 µm should cite the stronger association of lung-cancer incidence with the number concentration of fibers longer than 10 or 20 µm with lung cancer incidence, rather than of fibers longer than 5 µm (Lippmann 1994). The subcommittee suggests that the association of lung cancer with fibers longer than 10 or 20 µm might stem from interception and preferential deposition of fibers longer than 10 µm at bifurcations of large airways. Fiber length might also be associated with disease because longer fibers, in general, are more biopersistent, more toxic to cells, and more mutagenic to chromosomes.

The Navy's review of relevant literature on in vivo fiber dissolution is fairly thorough for work conducted before the middle 1990s but is

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