Published: Jan 1981
| ||Format||Pages||Price|| |
|PDF ()||30||$25||  ADD TO CART|
|Complete Source PDF (4.7M)||30||$72||  ADD TO CART|
The siliceous material which is the subject of this study has been produced commercially in the United States for approximately 30 years. Since both production and use of the material may result in human inhalation exposure, it was necessary to explore the biological potentials of the silica by exposing experimental animals to aerosols of the material. Since crystalline silica is able to augment the severity of tuberculosis, an infection phase was included. Nine component experiments involving 496 animals were conducted over a period of three years. Average dust concentrations were 3.57 mg/ft3 of air. Rats, guinea pigs, and rabbits were exposed. The tuberculous infection studies were limited to the guinea pigs. An elimination phase was included for each animal species. Deaths among control animals and exposed animals were approximately the same and were due to intercurrent infections or other natural causes. Lung weights increased pari passu with dust exposure, but returned to normal ranges after exposure stopped. Silica retention in the lung tissue ran parallel to this, and silica was relatively rapidly eliminated on cessation of exposure, with commensurate reduction of the lung ash. A transient type of alveolar hyperinflation of mild to moderate severity occurred in rats more particularly, but this was more related to intercurrent infection than to the silica itself. Macrophages accumulated in alveoli, in the bronchioles, and in lymphoid tissue. This remained a mild reaction in rats, but was more evident in guinea pigs and rabbits. In guinea pigs there was more infiltration of lymphoid tissue by these macrophages and far less alveolar hyperinflation. In rabbits the macrophage accumulation tended to be perivascular whereas in guinea pigs this response was more peribronchial. Almost complete reversal of all these responses occurred. Some reticulum deposition was noted in interstitial tissues. This disappeared on cessation of exposure. Bronchial and tracheal epithelia remained intact. No epithelization or pleural changes were noted and no neoplasia occurred. The tuberculogenic response was limited to a slight increase in size of some lesions and slightly longer persistence of the active cellular proliferation phase of the tubercles before resolution and calcifications. No extrapulmonary spread of the tuberculosis occurred. On the basis of the foregoing and by comparison with twenty-four other varieties of silica previously studied in comparable fashion, the precipitated submicron amorphous silica is the least biologically active of the synthetic silicas. Thus on a percentile scale its biological action may be rated at about five percent of the capability of the most injurious siliceous materials.
siliceous material, amorphous silica, emphysema
Veterans Administration Central Office, Washington, D.C.