What is Silicosis?
Silicosis, an occupational lung
disease, is a respiratory disease caused by inhalation
of silica dust. When crystalline silica (a component of silica
dust) is inhaled, it causes inflammation
of the lung tissue. This inflammation leads to scar tissue
formation on the lungs, also known as nodules, which obstructs
the flow of oxygen into the lungs and into the bloodstream.
Before it was identified and named in the 1930s, silicosis
was known by a variety of names, such as dust consumption,
grinder's asthma, grinder's rot, grit consumption, mason's
disease, miner's asthma, miner's phthisis, potter's rot, rock
tuberculosis, and stonemason's disease.
Types of Silicosis
There are three types of silicosis: chronic silicosis,
accelerated silicosis, and acute silicosis.
- Chronic silicosis - occurs due to
long-term exposure to low amounts of silica (10 to 20
years).
- Accelerated silicosis - also known as progressive
massive fibrosis; occurs more quickly than chronic silicosis,
usually due to exposure to larger amounts of silica over
a shorter period of time (five to 10 years).
- Acute silicosis - occurs due to short-term exposure
to extremely large amounts of silica. Acute silicosis can
develop within several weeks or up to five years after exposure.
Silicosis has also been linked to adverse health effects
such as tuberculosis and lung
cancer.
Silica Exposure
Silica, or silicon dioxide, is a naturally occurring mineral
that is composed of one silicon atom and two oxygen atoms.
When silica molecules line up and create a repeating pattern
they form a crystal (crystalline silica). Different crystal
patterns are given different names, such as quartz, cristobalite,
and tridymite, to name a few. People who work with quartz
and other types of crystalline silica are at an increased
risk of silica
exposure.
Silica exposure most often occurs in people who work in construction,
mining, sandblasting, stonecutting, abrasives manufacturing,
and in people who work with glass, pottery, and on railroads.
Silicosis Prevention
Although there is no cure for silicosis, it can be prevented
with occupational
safety measures. There has been a marked decrease in the
number of silicosis cases since the Occupational Safety and
Health Administration (OSHA) implemented regulations that
require the use of protective equipment when working with
silica dust.
Are Other Health Effects of
Silica Exposure Being Overlooked?
by
David F. Goldsmith, PhD
Public Health Institute
The National Conference to Eliminate Silicosis March 23-25,
1997 in Washington DC enjoyed a splendid turnout of over 600
attendees. In my opinion, the conference attention on silicosis
to the exclusion of discussion of other silica health effects
was very shortsighted . However, I was delighted by the opening
remarks by NIOSH Director, Dr. Linda Rosenstock, who pointed
out that we now know that silica exposure is a risk factor
for several "new" conditions, and that deliberations
should be expanded to consider other health problems such
as cancer, autoimmune diseases, nephritis and other kidney
diseases, and tuberculosis (TB).
What is the evidence for these other conditions? Last month
the International Agency for Research on Cancer (IARC) changed
the classification of silica from 2A (probable human carcinogen)
to 1 (known human carcinogen). The change to IARC Type 1 means
that occupational silica dust exposure is considered like
other known human carcinogens such as asbestos, vinyl chloride,
radon daughters, smoking, and DES. It means that companies
are likely to change their Material Data Safety Sheets (MSDS),
that workers need to be informed, and that where there are
alternatives to silica (such as sandblasting) that they need
to be sought out. The change in IARC status does not mean
that the controversy about carcinogencity is over, but it
does mean that the evidence is sufficient to convince a group
of IARC experts that silica increases the risk of lung cancer.
Furthermore, it goes a long way to meeting the criteria for
causation we use in epidemiology. There is other evidence
to suggest that silica is linked to stomach cancer, lymphatic
cancers, and skin cancer, though the IARC focus was on pulmonary
malignancies.
The other health effects are not "new," but we
now have good epidemiology studies of recent vintage showing
that silica exposure (with and without silicosis) is linked
with several autoimmune conditions which previously there
were only case studies: rheumatoid arthritis, scleroderma,
Sjogrens' syndrome, and lupus. There is also accumulating
epidemiology evidence that occupational silica exposure is
linked with kidney diseases such as nephritis and end-stage
renal disease.
With a narrow focus on silicosis, we tend to overlook serious
conditions that often accompany silicosis--silicoTB and cor
pulmonale (enlargement of the heart muscle). Although these
two secondary effects of silicosis are declining in the U.S.
(as is silicosis), they remain killers of relatively young
workers in developing countries and in China and former Soviet
Union. Sadly we also must acknowledge the epidemic of acute
and accelerated silicosis that descended upon Mexican workers
in the Midland-Odessa, Texas area in the early part of the
1990s, some 60(!!) years after the Gauley Bridge disaster.
These men were vastly overexposed to silica, without any protection,
in several oil pipe sandblasting operations, and they have
many of the autoimmune ailments as well as fatal silicosis.
Thus, the silicosis prevention we all hope to achieve should
include these other diseases: cancer, autoimmune illnesses,
kidney diseases, and TB. Furthermore, the employees we need
to communicate with about this hazard must receive information
in languages of the workers at risk, not in English only.
David F. Goldsmith, PhD
Public Health Institute
2001 Addison Street, 2nd Floor
Berkeley, CA 94704-1103 USA
davegold@publichealth.org
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