RISK ASSESSMENT
Risky Business:
Out of the Sandbox
The Silica Story
BY FRANK MIRER
Back in the day (that is, the 1970s), we used to wonder why
asbestos caused lung fibrosis and lung cancer, while crystalline silica caused lung fibrosis but not cancer, and amorphous silica and (most) silicates caused neither. “Asbestos” is a
collection of minerals that can be thought of (by non-mineral-ogists) as fibrous forms of silicates. Now, both the International Agency for Research on Cancer (since 1995) and the
U.S. National Toxicology Program (since 2000) classify silica
as “known” to be carcinogenic to humans. Prior to the 1995
and 2000 assessments, the agencies described silica’s carcinogenicity as “probable” (IARC, in 1987) and “reasonably anticipated” (NTP, in 1991).
This article claims to be timely because silica will likely be
the first chemical PEL to emerge from OSHA under new, sci-ence-based leadership. The proposed new PEL is unrevealed, but
the ACGIH® TLV® for silica is now 25 µg/m3. ACGIH still classi-fies silica as a “suspected,” rather than “known,” carcinogen.
Practitioners would do well to find the range of silica exposures
in their territory with 10 µg/m3—a rounded-down action level—
as a benchmark. The silica story illustrates the power of paradigm shifts in science to spur changes in our understanding of
health risk, and it explains why I abandoned my opposition to
using quantitative exposure-response assessment in setting
chemical exposure standards.
Paradigm Lost: Silica and the Stanton Hypothesis
Back to the 1970s. The putative disparate carcinogenic potential
of silica and asbestos supported the Stanton Hypothesis—that
long, thin fibers possessed toxic potential because they penetrated the bronchial tree by streamlining, then deposited in
alveoli but were indigestible by macrophage, and also penetrated into the pleural and peritoneal cavities. The Stanton Hypothesis had the virtue of indicting the whole spectrum of
durable fibers, although none were convicted of carcinogenicity
or fibrogenicity on structure. No exposure limits for non-as-bestos fibers were set based on this understanding.
The Stanton Hypothesis also had a downside: it supported
arguments to acquit, without trial or convincing evidence,
asbestos cleavage fragments and various fibrous materials
because of shortness and low durability. Stanton also didn’t
account for the fibrogenicity of granular crystalline silica particles, or the alleged differing toxic potential of so-called amorphous but actually microcrystalline silica or silicates. Likely,
Risky Business will return to this subject in a future commentary examining the ABC (anything but chrysotile) campaign on
asbestos risks.
Hazard Identification: How Silica Became a Carcinogen
The history of silica’s toxic potential and potency is most authoritatively reviewed by IARC Monographs on the Evaluation
of Carcinogenic Risks to Humans Volume 68, published in 1997
and available in full text at http://monographs.iarc.fr/ENG/
Monographs/vol68/ index.php. The previous review (in Volume
42, 1987) is unfortunately not available in full text. In addition,
the summary evaluation for silica in Volume 42 has departed
down the memory hole on the IARC website.
The 1997 monograph answers the two questions most pertinent to scientific history: what new evidence appeared between
1987 and 1997 to change peoples’ minds about human carcinogenicity, and how did silica become classified as probable only
in 1987?
I’ve repeatedly told people that despite many studies finding
increased lung cancer among workers exposed to silica, a “best
