EXCERPTS FROM THE EPA ASBESTOS HEALTH EFFECTS CONFERENCE
Oakland, California
May 24-25, 2001
The recent EPA Asbestos Health Effects Conference offered a state-of-the-art analysis
of the medical implications of asbestos exposure, as well as a re-evaluation of
asbestos risk assessment. The international panel of chairpersons and speakers was
comprised of the "best of the best" among the experts in these fields. The following
review summarizes conference highlights of relevance to asbestos litigators.
The EPA Asbestos Health Effects Conference was co-sponsored by the Environmental
Protection Agency, National Institute of Occupational Safety and Health, Agency
for Toxic Substances and Disease Registry, California Office of Environmental Health
Hazard Assessment, and the Mining Safety and Health Administration. The seminar
attempted to identify lessons to be learned from today’s asbestos medicine and risk
assessment "sound science." Key questions and controversies regarding the health
effects of asbestos exposure stimulated by research conducted in the 1970’s and
80’s were revisited to identify present day areas of multidisciplinary agreement.
In addition, the conference hoped to generate a re-appraisal of existing EPA health
assessment criteria for asbestos exposure to bring these protocols in line with
contemporary scientific evidence.
Peter Grevatt, EPA’s Senior Science Advisor for the National Hazardous Waste Cleanup
Program, opened the meeting with the observation that the current approach by the
EPA and other Federal agencies to asbestos exposure management continues to be driven
by a health risk assessment policy statement that is fifteen years old. He noted
that at the time, this analysis had treated all asbestos fiber types and dimensions
equally. Furthermore, this document recommended that asbestos risk assessment be
based upon phase contrast microscopic (PCM) fiber counts, because studies utilizing
electron microscopy were still in the investigational phase. A number of policy
shortcomings resulted from the fact that asbestos science prior to 1986 had not
yet advanced to the point where health effects could be distinguished according
to asbestos types and fiber dimensions. Non-cancerous asbestos health issues also
were not well addressed by this early report.
The first morning of the conference was devoted to mineralogy and exposure assessment.
Panel Chairperson, Bruce Case of McGill University, Canada, asserted that the terms
“environmental” and “occupational” exposures must be carefully applied, and that
investigators should refine their language to talk more about levels versus categories
of exposure. For example, it is entirely possible that a particular occupational
exposure might be "trivial," while a given environmental (i.e. non-occupational)
exposure might be "massive."
John Addison, a mineralogist with John Addison Consultancy, Scotland, defined crystalloid
and other chemical properties that distinguish various asbestos forms from those
of other minerals with which these might be confused. Addison clarified the meaning
and health implications of the term “asbestiform” by explaining this label is actually
an adjective signifying only that a mineral resembles asbestos. In reality, there
are a number of minerals that are asbestiform, but which are not toxicologic if
inhaled.
Addison also opined that most of the U.S. and European definitions of asbestos as
a health problem-causing mineral are currently inadequate. He noted that fiber shape
criteria have been mistakenly included as part of the definition and that the use
of such terms as “fibrous” tremolite are ambiguous. Furthermore, Addison sees the
present definition of “asbestos-containing material” as inappropriate, with the
U.S. definition of one percent as far too high to be of any value and the United
Kingdom standard of “zero” as impossible to prove.
Other lecturers the first morning included Patrick Sebastien of McGill University,
who addressed the matter of exposure assessment in environmental circumstances,
and Gunnar Hillerdal of Karolinska Hospital in Sweden, who considered radiological
changes as markers of environmental asbestos exposure. Hillerdal discussed several
controversial aspects relating to pleural plaque formation and relevance. He indicated
that in terms of latency it was unusual to observe plaques on chest x-rays during
the first ten to twenty years of asbestos exposure, but that these radiographic
findings were typically well seen at the thirty-year point.
The afternoon of the first day considered developments in the field of asbestos
epidemiology and was chaired by Julian Peto, Institute of Cancer Research in England.
John Dement of Duke University compared differences in carcinogenicity among differing
types of asbestos fibers. He explained that existing data indicates the lung cancer
risk for chrysotile exposure is at least as high as that observed for amphiboles,
and that while chrysotile can cause mesotheliomas, epidemiological data reveals
the proportional yield in terms of percentage of deaths to be less than that for
amphiboles.
Marcel Goldberg, of INSERM, France, reviewed studies pertaining to the health effects
of non-occupational exposures to asbestos. Such types of exposures are varied and
can include non-occupational building, asbestos-containing soil, industrial pollution,
and other environmental exposures. Key determinants of environmental risk were listed
as fiber type, exposure intensity, and total accumulated exposure.
The second day of the meeting considered the basic science aspects pertaining to
how asbestos fibers interact at the cellular level to elicit adverse effects. The
morning panel was chaired by Kevin Driscoll, Proctor & Gamble Pharmaceuticals,
who indicated that the critical next step in understanding these cellular interactions
was to precisely identify the target (i.e., DNA, phagocytes) of asbestos and then
to relate this understanding to an application of exposure dosage principles.
To this end, Gunter Oberdorster, Professor of Toxicology and Environmental Medicine
at the University of Rochester, presented an algorithm for various pathogenic sequences
for the interaction of asbestos fibers in the respiratory tract. These pathways
traced such interactions from the time of airborne asbestos fiber exposure through
cellular transformation and ultimate development of bronchogenic carcinoma, pleural
mesothelioma, or lung fibrosis. Oberdorster indicated that asbestos fiber dimensions
and biopersistence were the most important determinants of toxicity, with long fibers
more carcinogenic than short. However, it should be noted that short fibers contribute
to risk, especially if respiratory clearance is retarded for some reason.
A number of other noteworthy talks were presented at this conference beyond what
can be summarized in this brief review. Synoptic statements offered during the final
roundtable discussion noted that the lower biopersistence of chrysotile asbestos
fibers is now believed to result in relatively lower risk for mesothelioma, as compared
to amphibole fibers. Pre-existing disease conditions and genetic factors may increase
ones susceptibility to develop asbestos-related pathology. Different, distinct mechanisms
are now believed to lead to the development of either lung cancer or mesothelioma.
Visitors to the EPA’s Internet site at
www.epa.gov/swerrims/ahec/summary.htm can still attend this conference,
as most of the speakers’ slide presentations are available for download in PDF format.
Because of the size and complexity of some of these presentations, visitors may
experience sporadic difficulties printing the actual slides; however, they can still
be viewed directly on screen.
Visitors who possess Microsoft Windows Media can access the audio portion of many
of these sessions. At times, the quality of these audio presentations has been compromised,
seemingly due to technological difficulties during the recording process.
Over twenty abstracts of conference poster displays are also available at this site.
Most of these exhibits present findings from recently conducted mineralogic, geologic,
toxicologic, and epidemiologic research associated with the health effects and risk
exposure of asbestos.
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