Table 5.
Species | |||
---|---|---|---|
Rat | Mouse | Hamster | Primate/human |
Likelihood for developing particle overload (slow lung clearance) | |||
+++ | +++ | + | Not determined* |
Alveolar macrophage participation | |||
Active (accumulation in alveolar ducts) | Active (accumulation in alveolar ducts) | Extensive (rapid clearance) | Not as extensive (translocation to interstitial sites) |
Pulmonary (neutrophilic) inflammation | |||
+++ | +++ | + | + |
Epithelial and interstitial cell proliferation | |||
+++ | + | (+) | (+) |
Septal fibrosis | |||
+++ | + | (+) | (+) |
Anatomical location of retained particulates | |||
Primarily alveolar (some increased translocation at overload) | Primarily alveolar (some translocation at overload) | Rapid clearance | Primarily interstitial |
Lung tumours following chronic exposure | |||
Yes | No | No | No |
aSeverity low +, moderate ++, high +++, or questionable (+), reprinted with permission from ([34], p. 52)**.
*This should be + (see p. 53 in [34]) because particle overload is typified by an impairment in alveolar particle clearance (see p. 1 and 4 in [34]).
**There may be a variance of opinion about the extent/degree of some of the endpoints in the table (e.g., alveolar macrophage participation, septal fibrosis) and there is continuing research to refine these findings.