Our bodies have a variety of natural mechanisms to defend against inhaled minerals. The first of these is filtering of particles by the nasal cavities or upper respiratory tract [ Lehnert, 1990b], thereby preventing the particles from ever reaching the vulnerable lower respiratory tract and pleura (the membrane lining the lung cavity). The mucous lining much of the respiratory tract is another component of the defense system, trapping particles and transporting them up the trachea. Even after evading these defense systems, particles can be sequestered by some cell types (e.g., the macrophage) in a process called phagocytosis (an internalization of the particle by the cell). Once sequestered, the particle is transported by the macrophage out of the respiratory tract [ Lehnert, 1990b]. This process can remove particles effectively unless the system is overloaded by too many particles [ Lehnert, 1990a], the particles have a fibrous shape such that the macrophage cannot completely internalize the particle, or other factors (e.g., smoking) alter the clearance process. Finally, a potential geochemical defense mechanism is mineral dissolution: some minerals (e.g., chrysotile) are leached by [ Jaurand et al., 1984] and even dissolve rapidly in [ Hume and Rimstidt, 1992] lung fluids, resulting in low lung burdens relative to an individual's actual exposure [ Churg, 1993]. Interestingly, some minerals may actually precipitate in macrophages [ Galle et al., 1992].
Among the important mineralogical and geochemical issues immediately following exposure are the physical and chemical properties that allow a mineral to evade defense mechanisms: e.g., particle size and morphology and a mineral's dissolution characteristics. The former have been the focus of toxicity studies since the early investigations, as reflected, for example, by the numerous studies on the association of carcinogenicity with fibrous materials [ Stanton et al., 1981]. Mineral dissolution in physiological fluids has been investigated explicitly for over 15 years [ Huang et al., 1978; Thomassin et al., 1977], and such studies [ Hume and Rimstidt, 1992] have contributed to our understanding of the residence times for fibers in the absence of cellular and mechanical clearance mechanisms. In fact, these studies provide a geochemical explanation for the observation by pathologists that the amount of chrysotile typically found in human lungs is underrepresentative of the amount of chrysotile to which an individual is exposed [ Churg, 1993], i.e., chrysotile appears to dissolve rapidly in human lungs (although some chrysotile fibers appear to remain in the lung intact for long periods).
A continued effort by geochemists is essential to maintain
our understanding of minerals in physiological fluids at a
level commensurate with our understanding of minerals in
geological fluids. Although the dissolution of chrysotile in
physiological fluids is relatively well understood, the
physiological dissolution behavior for the majority of
potentially hazardous minerals is virtually unexplored. Even
when a mineral's dissolution characteristics have been
studied in simulated physiological environments, often only a
restricted set of physiological environments have been
addressed. Minerals encounter a wide range of fluid
compositions in the lung, including ranges in pH (
4-7) and
the types and concentrations of molecules such as chelating
and reducing agents. This fluid variability is known to
affect mineral dissolution [ Kreyling, 1992; Lund and Aust,
1990; Lundborg et al., 1992; Werner et al., 1994]. Mineral
dissolution data are essential in order to understand how
long minerals remain in the lung, how quickly minerals
release elements to the surrounding fluid, and, in general,
how minerals interact with physiological fluids and cells.