Special Articles on Asbestos,
A short summary of main points of some of the critical articles
written over the last 40 years which explain both the light and
the dark of occupational health policy and concerns about chemical
exposures in the workplace using asbestos as a model. All
the cited articles should be available in the Medical School
Library if you wish to delve further into this fascinating field.
Selikoff: The Landmark Article: Now 40 years old was:.
The First accepted epidemiologic survey in the U.S. linking
asbestos exposure and lung cancer. He reviewed past papers including an article
by Lynch & Smith in 1935 suggesting a link, with a particular attention to
a UK report on factory workers, asbestos and lung cancer reviewing
data from 1920 to 1950s.
Selikoff first studied pipe fitters, using union data on members
during 1942 to 1962. He showed a very significant risk to working
with asbestos. He reviewed the effects associated with
smoking then considered there was an excess risk beyond smoking.
Mossman: Noted the two main groups of Asbestos, Serpentines
and amphiboles. Chrysotile is the only serpentine
of commercial importance, it has curly fiber ( this may be
the most important physical aspect). Amphiboles are
straight fibers. 25% of asbestos is used for cement water
pipes ( recent and repeated concerns about stomach cancer
from drinking water distributed through such pipes) . Used
liberally in shipyards during WWII. Mesothelioma are
considered to be caused only by
exposure to asbestos. This article reviews
evidence that fiber characteristic may be more important
than chemistry. Peritoneal Mesothelioma are possibly secondary
to penetration of intestinal mucosa by fibers, or possibly
through lymphatics. Only associated with exposure to amphibole
asbestos. Bronchial Carcinoma: More prevalent among
Chrysotile miners. Cancer rare among non-smokers (despite
the EPA and its promotion of Radon as a major cause of lung
cancer!). Smokers >20 cig/day have an 80-90 fold increased
risk of bronchial cancer. Asbestos does not appear
to be a potent mutagen, it is more likely to be a promoter
than inhibitor.
Associated NEJM. Editorial: The major contribution of this editorial was
the emphasis on lack of knowledge about pathogenesis of disease. Most asbestos
in humans has a core of amphibole fibers. Little evidence for cases outside
industrial centers Note the lack of data on asbestos in relation to the known
effects of cigarette smoke causing bronchitis/emphysema. There is still a
need to clarify the role of smoking in lung cancer. Epidemiologic
evidence for effect of fiber size greatest for Mesothelioma. Crocidolite
is more important to Lung Ca than Chrysotile. Environmental factors such
as dose, fiber type and particle size are relevant.
Doll & Peto: Asbestos causes fibrosis of bronchial
passages, bronchial cancer and mesothelioma.
Asbestosis severity depends on: dose, length of exposure, time since exposure,
type of fiber.
Lung Ca is indistinguishable from that caused by smoking. Asbestos
effect seems to be synergistic. A very strong interaction between asbestos
and cigarette smoke. The best protection for asbestos workers is to stop
smoking, or never to start. However, intensity of exposure relates
more to incubation period, than to likelihood of developing CA. No
threshold has been shown to date. No long term cohort studies have
been done. They are now ethically impossible. (Think about
why , Ask Dr. Vance if you have a chance.) Mesothelioma are so rare
that development should indicate past exposure to asbestos. Dose increases
risk, but for mesothelioma does not affect incubation period.
Difficulties with assessment
First: Not a single compound.
Second: Biologic effects partly chemical partly physical.
Third: Fiber configuration depends on handling during extraction/manufacture.
Fourth: Commonly mixed with other materials so it may be only 5-20% of
total product.
Mossman 1990: Available data do not support the concept
that buildings and schools are health hazards from asbestos! (have
you any idea about how many $billions have been spent
removing asbestos?) He discusses some of the basic
actions at the molecular and cellular level that may
promote cancer. He also discusses the relevance
of public policy to scientific evidence.
Health Effects Monitoring and Health Hazard Assessment
Asbestos as a model.
Scientific Developments and implication for public policy can
be found in: Science. Vol 247, 19 Jan 1990 Pp 295‑301
Available data do not support concept that asbestos in low concentrations
is a health hazard.
(So why is there so much concern still?)
How hazardous is hazardous?
Problems of induction (initiator), promotion
Problem of epidemiologic models chosen. Costs for removal may
be $150 Bn.
Chrysotiles (90% world supply) vs. Amphiboles.
Diseases: Asbestosis, leads to benign thickening of pleura. May
cause no symptoms, symptoms, disability, or death.
Also causes Lung Cancer and Mesothelioma.
Some studies suggest that Erionite most harmful, Crocidolite medium,
Chrysotile least.
Problems with animal models include different protective and repair
mechanisms at the cellular levels for enzymes, DNA, RNA as well
as whole body effects. The evidence that human are different
to animals continues to mount.
To label a product as Carcinogenic
we need to find two or more animal models of cancer at different sites affected
by the same the chemical, plus evidence that these models
apply to humans.
Discuss the dangers of Asbestos on the lesson Discussion web.
Do you think the dangers have been overemphasized?
What role has politics played in what should be a scientific discussion?
Can you think of other chemicals whose hazard may not have been stated accurately?
How does the hazard assessment of exposure player into the strategic development
of public health policy? |