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. 
: Biologic effects partly chemical partly physical.
Fiber configuration depends on handling during extraction/manufacture. 
: 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?