Lung Dust Content and Response in Guinea Pigs Inhaling Three Forms of Silica

Abstract

Guinea pigs were exposed by inhalation to atmospheric suspensions of crystalline free silica (cristobalite), amorphous free silica (diatomaceous earth), and amorphous silicate (volcanic glass). Randomly selected animals were killed at 2-month intervals and their lungs were examined. Tissue samples were collected and analyzed for total silica content and total ash. Total silica content per lung increased linearly throughout at least 21 months in each experiment and total ash weight increased more rapidly than dust was accumulating. Crystalline silica produced a greater increment in ash weight that did the amorphous free silica and the silicate produced the least increase. Furthermore, although atmospheric dust concentrations were roughly comparable for the three preparations, the total amount of silica accumulated varied inversely with the degree of tissue damage occurring. Thus, the maximum total content of the crystalline silica reached only 68 mg per lung, while that of the amorphous silica and silicate was 120 mg and 465 mg, respectively. This suggests that a silicious dust that produces cell damage may be cleared more effectively from the lung than is an innocuous dust.

The global variability of diatomaceous earth toxicity: a physicochemical and in vitro investigation

“…In vivo studies of unprocessed, amorphous DE show it has the potential to be pathogenic, causing acute/sub-acute inflammation in rats 60 days after a single intratracheal injection of 10 mg DE, an effect that decreased with time [ 29 ]. While inhalation of unprocessed DE (170 million particles per cubic foot (mppcf)) by guinea pigs for 39–44 h/week for 24 months resulted in fibrosis, calcined, cristobalite-rich DE was seen to cause more severe fibrosis more rapidly [ 30 ]. However, in a separate study, exposure via inhalation to 5–50 mppcf flux-calcined DE, consisting of 61 % cristobalite, for 30 h/week up to 30 months caused no body weight loss or pulmonary fibrosis in rats, guinea pigs or dogs [ 31 ].…”

Acute Pulmonary Toxicity Caused by Exposure to Colloidal Silica: Particle Size Dependent Pathological Changes in Mice

“…There are several types of amorphous silica including fumed silica, colloidal silica, diatomaceous earth and precipitated silica. A number of studies have reviewed the adverse effects of amorphous silica; this silica has potential to induce transient pulmonary inflammation but changes may regress during the recovery period compared to persistent pulmonary inflammation by crystalline silica (Pratt, 1983;Reuzel et al, 1991;Warheit et al, 1995). In humans, an epidemiologic investigation in occupational exposure to amorphous silica generally showed no evidence of silicotic effect and any potential for carcinogenicity (McLaughlin et al, 1997).…”

Was there sufficient justification for the 10-fold increase in the TLV for silica fume? A critical review

“…In the 1983 Supplement, various forms of amorphous silicas were recognized including diatomaceous earth, precipitated silica, silica gel, fumed silica, and fused silica. At this stage (ACGIH 1980:1983, silica fume was not included.…”

“…Such collectivization is exemplified in Table II where health effects of amorphous silica subchronic inhalation were assessed from studies on colloidal silica, Ludox [Warheit, 1991;Kelly and Lee, 1990] and health effects of amorphous silica chronic inhalation were assessed solely from studies on fused silica, silica gel, and precipitated silica [Groth et al, 1981;Schepers, 1981]. Amorphous silica and crystalline silica are contrasted in studies in which the only amorphous silica used is (a) fumed silica [Reutzel et al, 1991], (b) colloidal silica [Warheit et al, 1991b], (c) fused silica [Rosenbruch et al, 1990], (d) diatomaceous earth [Pratt, 1983], (e) Ludox, Zeofree 80 [Warheit et al, 1995].…”