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Introduction
Study Background and Steering Committee
Delphi Method
First Round Questions
First Round Results
Second Round Questions
Second Round Results
Third Round Questions
Third Round Results
A Delphi Study of Asbestos Health Effects
A Consensus Report from the American College of Chest Physicians Delphi
Study of Asbestos Steering Committee
These pages contain the protocol and the data collected in the preparation of the
manuscript. This information is made available so that our methodology can be
considered open and transparent. Perhaps presentation of our work in this manner can serve as a model for others to explore the use of the Delphi process in
their research.
There are unresolved issues in the diagnosis of asbestos-related diseases. This study is
an attempt to resolve some of the important issues, using an expert panel with a webbased Delphi method, an iterative process developed by the RAND Corporation to aid in
reaching consensus on contentious issues. In this study, our expert panel was asked to
respond to three rounds of questions about the health effects of asbestos fiber inhalation. The questions, results, graphic and statistical analysis, expert comments and references for each round are available at the links below.
Many thanks to our participants and persevering expert panel.
Sponsored by the American College of Chest Physicians and the Workers Compensation Board - Alberta.
1
Study background
There is considerable disagreement over a number of the health issues associated with
respiratory exposure to asbestos. The goal of this protocol is to assess the health effects
of asbestos using the framework based on knowledge extracted from experts, i.e., the
Delphi method. This method allows for the resolution of “disputed” topics by polling experts and providing feedback to the experts regarding the responses elicited from other
experts. It is our intent to come to a conclusive opinion regarding specific questions associated with the health effects of asbestos.
The goal of this protocol is to assess the effects of asbestos using a framework based
on knowledge extracted from experts, i.e., the Delphi method. Despite its fundamentally
qualitative and subjective basis, this approach is a reasonable means of systematically
assessing expert opinions regarding asbestos health effects. This simple and operational methodology is proposed as a reliable and soundly based approach to assess the diverse opinions regarding the health effects of inhaled asbestos.
Members of the L.S.U. Coordinating Committee:
Daniel E. Banks, M.D., M.S.
Professor
Department of Medicine
L.S.U. School of Medicine
Shreveport, LA 71130
Runhua Shi, M.D., Ph.D.
Associate Professor
Department of Medicine
L.S.U. School of Medicine
Shreveport, LA 71130
Jerry McLarty, Ph.D.
Professor
Department of Medicine
L.S.U. School of Medicine Shreveport, LA 71130
2
Members of the American College of Chest Physicians Delphi Study of
Asbestos Steering Committee:
Daniel E. Banks, MD, MS
Chair, Steering Committee
LSU School of Medicine
P.O. Box 33932
1501 Kings Highway Shreveport, LA 71130
Clayton Cowl, MD, MS
Mayo Clinic
Baldwin Building 5A
200 First Street SW
Rochester, MN 55905
Michael H. Baumann, MD
University of Mississippi Medical Center
500 North State Street
Jackson, MS 39216-4505
Susan M. Tarlo, MD
Toronto Western Hospital, Suite EC4-009 399
Bathurst St. Toronto, ON, Canada M5T 2S8
Feroza Daroowalla, MD
T-17, Room 040
Stony Brook University Health Science Center
Stony Brook, NY 11794-8172
Dorsett D. Smith, MD
Chest Diseases, Inc.
4310 Colby Ave. Suite 201
Everett, WA 98203-23382
John R. Balmes, MD
UCSF School of Medicine
Box 0843 San Francisco, CA 94143-0843
3
Delphi Method
The Steering Committee was comprised of members from Occupational and Environmental Network of the American College of Chest Physicians. The questions
for the first round were developed by the Steering Committee. The members of the
L.S.U. Coordinating Committee structured the questionnaire from agreed upon
questions, set up the Web site, undertook the statistical analysis of data (including a graphic and tabular display of the answer to each question), produced interim documents, and guaranteed the general management of the process. The work
product generated at the completion of each of round was submitted to the Steering Committee for their review. Recommendations from the Steering Committee
based on collected data were implemented.
Introduction and description of the Delphi method:
The open interactive technique known as the Delphi method is a reasonable approach to
maximize the areas of agreement and minimize the areas of disagreement regarding the
role of asbestos in respiratory health. Consensus among experts is a central assumption
of Delphi methodology. This research methodology is used for problems that are difficult
to solve with conventional techniques.
The Delphi method structures communication in a way that allows a group of individuals
to deal with a complex problem and reach consensus. This method is particularly useful
for a topic with strong differences of opinion or high levels of uncertainty. The Delphi
method is suitable for areas of study where there is a lack of agreement, as is often the
case in defining the relationships between asbestos exposures and health outcomes. It
is a systematic and easily documented process that involves a series of questions designed by a monitor group.
One of the main advantages of the Delphi method is its ability to guide group opinion towards a final decision. This tendency to converge toward agreement is a unique aspect
of Delphi process and is a property considered to be of particular importance to this
study. The Delphi method as implemented in this study was cost-effective.
A strength of the Delphi method (as used in this protocol) was documentation of the
process. This included a graphic display of the answers, as well as all references and
comments by our experts for each question for each round. At end of the first round,
each reference was linked to the abstract or full text of the article. in addition, at end of
each round, each question whose answers did not reach consensus was reviewed. Revision of exisiting questions or addition of new questions to be used in the next round
was determined by the Steering Committee.
A Delphi method is considered complete when a convergence of opinion occurs or when
a point of diminishing returns is reached. The reliability of the Delphi method depends
largely on the selection of panel members, the size of the group, the response rate and
the number of rounds.
The number of experts may have a variable effect on the outcome of the project. With an
open-ended question, the greater the number of experts, the more the number of diverse
opinions may be. In such a situation, there is a lesser chance of convergence. However,
4
in our approach to the Delphi Method where the number of the answers are limited (we
used a scale of 0 to 10 in this protocol), the greater the number of experts, the better the
chance of convergence.
We assumed that all experts were equally knowledgeable. In reality, this assumption
might not be true. However, all expert were given the opportunity to present references
or additional evidence to educate and convince their colleagues about the validity of their
point of view.
A lack of agreement among our experts may be related to the fact that they have expertise in different aspects of asbestos-related health effects. Furthermore, even though
their backgrounds of our experts may be similar, they may judge outcomes differently.
Finally, since the answers to questions are obtained separately, the opportunity does not
exist for persuasion by discussion.
Under our protocol, the questionnaire was made available via the World Wide Web for
three rounds to a respondent group of experts who remained anonymous to each other,
thereby eliminating the possibility that the personality of one participant would dominate
or bias the rating of the statements under considered. Access to the Web-based questionnaire was sent by e-mail at the start of each round: access was password protected
and unique for each expert. The anonymity of answers allowed Delphi participants to
express their personal views freely. After each round, the results were summarized and
assessed and used to develop a questionnaire for the next round. This forced experts to
consider group opinion. The assessment document and new questionnaire, with supporting evidence (if available), were then sent to all who responded.
A detailed description of the methodology used in this report is presented in the manuscript.
Key characteristics of the Delphi method (as related to this protocol):
• Identification of a panel of experts;
• Participants who do not meet in face-to-face discussions nor know the identity of other
experts;
• Use of a series of questionnaires altered on the basis of collected information;
• Progressive convergence of opinions with administration of each questionnnaire;
• Anonymity of experts' responses;
• Quantification of the extent of agreement with statistical tools; and
• Summarization of the information collected from each round with direct feedback to our
expert panelists.
Reasons for implementing the Delphi method (as related to this protocol):
• Based on our method of determining of criteria for selection of experts, bias was minimized;
5
• Although we realize science is not driven by consensus, in some instances, disagreements among scientists can benefit from the use of consensus methods;
• Our experts may have diverse backgrounds in the context of asbestos related research; and
• The locations of our experts around the world makes internet communications the most
effective way to approach this project.
General references for the Delphi Method
1. Lindstone HA, Turoff M, eds. Introduction. In: The Delphi method: techniques and applications. Reading, MA, Addison-Wellsley, 1975, pages 3-12.
2. Monteagudo JL, Guillen C. Priorities for health professionals in education and training
in information technologies: results of a Delphi survey. Proc.of the 1st European Conf.
on Health Telematics Education. Corfu. 1996.
3. Fink A, et al. Consensus methods: characteristics and guidelines for use. Am J Public
Health. 1984; 74:979-983.
4. Goodman CM. The Delphi technique: a critique. J Advanced Nurs 1987; 12:729-734.
5. Dalkey N, Helmer O. An experimental application of the Delphi method to the use of
experts. Management Science 1963; 9:458-467.
6. Loughlin KG, Moore LF. Using Delphi to achieve congruent objectives and activities in
a Paediatrics department. J Med Ed 1979; 54:101-106.
7. Whitman NI. The committee meeting alternative: using the Delphi technique. J Nurse
Admin 1990, 20(7/8), 30-36.
8. Farrell P, Scherer K. The Delphi technique as a method for selecting criteria to evaluate nursing care. Nursing Papers (Canada) 1983; 15:51-60.
9. Reid NG. The Delphi technique, its contribution to the evaluation of professional practice. In Professional Competence and Quality Assurance in the Caring Professions (Ellis
R. ed.), Croom Helm, Beckenham, Kent.
10. Turoff M. The design of a policy Delphi. Technological Forecasting and Social
Change 1970; 2(2):17-26.
11. Lindeman CA. Delphi survey of priorities in clinical nursing research. Nurs Res 1975,
24(6):434-441.
12. Sackman H. Delphi Critique. D.C. Health, Lexington, Massachusetts 1975. Lyons H.
Solutions by consensus. Health Soc Serv Journal 1981; 2:1515-6.
13. Baumann MH, Strange C, Heffner JE, et al. Management of Spontaneous pneumo-
6
thorax - An American College of Chest Physicians Delphi Consensus Statement. Chest
2001; 119:590-602.
14. Clemen RT. Combining forecasts: A review and annotated bibliography. Int J Forecasting 1989; 5:559-584.
15. Mendel MB, Sheridan TB. Filtering information from human experts. IEEE Trnas.
Syst., Ma, Cybern., vol. SMC-19, 1989; 1:6-16.
16. Hau HY, Kashyap RL. Belief combination and propagation in a lattice-structured
network. IEEE Trans. Syst. Man Cybern 1990; 20:45-57.
17. McKenna HP. The selection and evaluationof an appropriate nursing model for longstay psychiatry patients. Unpublished D. Phil. thesis. University of Ulster, Coleraine, Ireland.
18. Duhan DF, Wilson RD. Prenotification and industrial survey response. Ind Marketing
Manag 1990; 19:95-105.
19. Faria AJ, Dickenson Jr, Filpic TV. The effect of telephone versus letter notification on
mail survey response rate, speed quality, and cost. J Market Res Soc 1990; 32:551-67.
20. Brennan M, Hoek J, Astridge C. The effects of monetary incentives on the response
rate and cost effectiveness of a mail survey. J Market Res Soc 1991; 33:229-41.
21. Mizes JS, Fleece EL, Roos C. Incentives for increasing return rates: magnitude levels, response bias, and format. Public Opinion Quarterly 1984; 48:794-800.
22. Conant JS, Smart DT, Walker BJ. Mail survey facilitation techniques: an assessment
and proposal regarding reporting techniques. J Market Res Soc 1990; 32:569-82.
23. Dillman D. Mail and telephone surveys: the total design method. New York, NY. John
Wiley & sons, 1978.
24. Albaum G, Strandskov J. Participation in a mail survey of international marketers:
effects of pre-contact and detailed project explanation. Journal of Global Marketing,
1986; 2(4):23.
7
First Round Questions:
Mark all that apply:
I. Participant Demographics:
My terminal degree is (mark all that are appropriate)
o M.D.
o Ph.D. (in basic medical sciences)
o Ph.D. (in medical sciences – not basic bench research {included epidemiology and statistics})
o Ph.D. (in non-medical services)
o M.D./Ph.D.
o J.D.
o M.D./J.D.
o J.D./Ph.D.
Other:_____________________________________
II. My current employment includes (mark that all are appropriate)
o The practice of clinical medicine
o Basic science research
o Epidemiology and statistical research
o Social historian
Other: _____________________________________
8
Questionnaire Round No. 1 Please rank (mark) the following statements with ranking scale from 0 to 10. You are invited
and encouraged to expand your answers in the space below and to provide references. If you do not feel qualified to answer this question please mark an “X” in parenthesis and go to the next question.
1. Pleural plaques alter lung function to a clinically significant degree (mark one).
Strongly Disagree
0
1
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
2
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3
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4
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5

6

7

8

Strongly agree
9
10


Please mark one:
o I do not feel qualified to answer this question.
o Expert opinion provided without references.
o Expert opinion provided with references (list below):
2. Workers with asbestos exposure and pleural plaques or diffuse pleural thickening (in the absence of fibrosis) are at increased risk of lung cancer (mark one).
Strongly Disagree
0
1
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
2
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3
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4
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5

6

7

8
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Strongly agree
9
10


Please mark one:
o I do not feel qualified to answer this question.
o Expert opinion provided without references.
o Expert opinion provided with references (list below):
9
3. Workers with asbestos exposure and pleural plaques or diffuse pleural thickening (in the absence of fibrosis) are at increased risk of mesothelioma (mark one).
Strongly Disagree
0
1
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2
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3
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4
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5
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6
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7
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8
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Strongly agree
9
10


7

8

Strongly agree
9
10


Please mark one:
o I do not feel qualified to answer this question.
o Expert opinion provided without references.
o Expert opinion provided with references (list below):
o
4. Asbestos exposure can cause diffuse pleural thickening (mark one).
Strongly Disagree
0
1
2
3
4
5






Please mark one:
o I do not feel qualified to answer this question.
o Expert opinion provided without references.
o Expert opinion provided with references (list below):
6

10
5. Asbestos exposure can cause pleural plaques (mark one).
Strongly Disagree
0
1
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2
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3
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4

5

6

7

8
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Strongly agree
9
10


Please mark one:
o I do not feel qualified to answer this question.
o Expert opinion provided without references.
o Expert opinion provided with references (list below):
6-11. In 1986, members of the American Thoracic Society authored an official statement entitled “The diagnosis of nonmalignant diseases related to asbestos” (Am Rev Resp Dis 1986; 134:363-368).
The authors wrote: “In the absence of pathologic examination of lung tissue, the diagnosis of asbestosis is a judgment
based on a careful consideration of all relevant clinical findings. In our opinion, it is necessary that there be:
A reliable history of exposure.
An appropriate time interval between exposure and detection (see text for details).
Furthermore, we regard the following clinical criteria to be of recognized value:
Chest roentgenographic evidence of “s”, “t”, “u” small irregular opacifications of a profusion of 1/1 or greater.
A restrictive pattern of lung impairment with a forced vital capacity below the lower limit of normal.
A diffusing capacity below the lower limit of normal.
11
Bilateral late or pan inspiratory crackles at the posterior lung bases not cleared by cough”.
A copy of this entire ATS statement is included as an attachment for your detailed review. We ask that you become thoroughly familiar with this document prior to answering these questions. Again, please rank your agreement with this Statement in the following questions (numbers 6 to 11) using a 0 to 10.
6. In the absence of pathologic examination of lung tissue, the diagnosis of asbestosis is a judgment based on a careful
consideration of all relevant clinical findings. In our opinion, it is necessary that there be: A reliable history of exposure
(mark one).
Strongly Disagree
0
1
2
3
4
5






Please mark one:
o I do not feel qualified to answer this question.
o Expert opinion provided without references.
o Expert opinion provided with references (list below):
6

7

8

Strongly agree
9
10


7. In the absence of pathologic examination of lung tissue, the diagnosis of asbestosis is a judgment based on a careful
consideration of all relevant clinical findings. In our opinion, it is necessary that there be: An appropriate time interval between exposure and detection (see ATS statement for details) (mark one).
Strongly Disagree
0
1
2
3
4
5






Please mark one:
o I do not feel qualified to answer this question.
o Expert opinion provided without references.
o Expert opinion provided with references (list below):
6

7

8

Strongly agree
9
10


12
8. Furthermore, we regard the following clinical criteria to be of recognized value: Chest roentgenographic evidence of “s”,
“t”, “u” small irregular opacifications of a profusion of 1/1 or greater (mark one).
Strongly Disagree
0
1
2
3
4
5






Please mark one:
o I do not feel qualified to answer this question.
o Expert opinion provided without references.
o Expert opinion provided with references (list below):
6

7

8

Strongly agree
9
10


9. Furthermore, we regard the following clinical criteria to be of recognized value: A restrictive pattern of lung impairment
with a forced vital capacity below the lower limit of normal (mark one).
Strongly Disagree
0
1
2
3
4
5






Please mark one:
o I do not feel qualified to answer this question.
o Expert opinion provided without references.
o Expert opinion provided with references (list below):
6

7

8

Strongly agree
9
10


10. Furthermore, we regard the following clinical criteria to be of recognized value: A diffusing capacity below the lower
limit of normal (mark one).
Strongly Disagree
0
1
2
3
4





Please mark one:
o I do not feel qualified to answer this question.
5

6

7

8

Strongly agree
9
10


13
o Expert opinion provided without references.
o Expert opinion provided with references (list below):
11. Furthermore, we regard the following clinical criteria to be of recognized value: Bilateral late or pan inspiratory crackles at the posterior lung bases not cleared by cough (mark one).
Strongly Disagree
0
1
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2
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3
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4
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5
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6

7
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8

Strongly agree
9
10


Please mark one:
o I do not feel qualified to answer this question.
o Expert opinion provided without references.
o Expert opinion provided with references (list below):
12. In an asbestos exposed individual, pulmonary fibrosis is a prerequisite to attribute the development of lung cancer to
asbestos (mark one).
Strongly Disagree
0
1
2
3
4
5

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


Please mark one:
o I do not feel qualified to answer this question.
o Expert opinion provided without references.
o Expert opinion provided with references (list below):
6

7

8

Strongly agree
9
10

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14
13. The extent of asbestos exposure correlates with the presence and extent of pleural abnormalities (mark one).
Strongly Disagree
0
1
2
3
4
5

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
o I do not feel qualified to answer this question.
o Expert opinion provided without references.
o Expert opinion provided with references (list below):
6

7
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8

Strongly agree
9
10


14. A reasonable scheme can be developed to apportion the individual attributability of smoking and exposure in a cigarette smoking asbestos-exposed worker with lung cancer (mark one).
Strongly Disagree
0
1
2
3
4
5

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


Please mark one:
o I do not feel qualified to answer this question.
o Expert opinion provided without references.
o Expert opinion provided with references (list below):
6

7

8

Strongly agree
9
10


15. Chest radiographs are a sensitive method to diagnose interstitial disease attributable to asbestos exposure (markone).
Strongly Disagree
0
1
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2
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3
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4
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5
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6
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7
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8
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Strongly agree
9
10


Please mark one:
o I do not feel qualified to answer this question.
o Expert opinion provided without references.
o Expert opinion provided with references (list below):
15
16. Chest radiographs are a sensitive method to measure pleural abnormalities attributable to asbestos exposure (mark
one).
Strongly Disagree
0
1
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2
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3
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4
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5
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6
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7
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8
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Strongly agree
9
10
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Please mark one:
o I do not feel qualified to answer this question.
o Expert opinion provided without references.
o Expert opinion provided with references (list below):
17. Asbestos exposure (in the absence of interstitial fibrosis) leads to chronic obstructive lung disease (mark one).
Strongly Disagree
0
1
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2
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3
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4
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5
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6
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7
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8
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Strongly agree
9
10

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Please mark one:
o I do not feel qualified to answer this question.
o Expert opinion provided without references.
o Expert opinion provided with references (list below):
18. A decline in small airway flow rates in a non-smoker can be attributed to asbestos exposure (mark one).
Strongly Disagree
0
1
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2
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3
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4
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5
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6
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7
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8
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Strongly agree
9
10
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
Please mark one:
16
o I do not feel qualified to answer this question.
o Expert opinion provided without references.
o Expert opinion provided with references (list below):
19. A decline in small airway flow rates in a smoker can be attributed to asbestos exposure (mark one).
Strongly Disagree
0
1
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2
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3
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4
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5

6

7
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8
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Strongly agree
9
10


Please mark one:
o I do not feel qualified to answer this question.
o Expert opinion provided without references.
o Expert opinion provided with references (list below):
20. A history of asbestos exposure is highly likely to be the cause of interstitial fibrosis in the absence of other explanations (mark one).
Strongly Disagree
0
1
2
3
4
5






Please mark one:
o I do not feel qualified to answer this question.
o Expert opinion provided without references.
o Expert opinion provided with references (list below):
6

7

8

Strongly agree
9
10


21. Asbestos exposure causes other neoplasms in addition to lung cancer and mesothelioma (mark one).
Strongly Disagree
0
1
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2
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3
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4
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5
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6
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7
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8
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Strongly agree
9
10
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17
Please mark one:
o I do not feel qualified to answer this question.
o Expert opinion provided without references.
o Expert opinion provided with references (list below):
22. Bronchoalveolar lavage (BAL) is a technique for accurately establishing lung fiber burden (mark one).
Strongly Disagree
0
1
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2
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3
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4
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5
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6
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7
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8
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Strongly agree
9
10


Please mark one:
o I do not feel qualified to answer this question.
o Expert opinion provided without references.
o Expert opinion provided with references (list below):
23. Identification of asbestos fibers in lung specimens is integral to the histologic diagnosis of asbestosis (mark one).
Strongly Disagree
0
1
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2
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3
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4
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5
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6
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7
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8
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Strongly agree
9
10


Please mark one:
o I do not feel qualified to answer this question.
o Expert opinion provided without references.
o Expert opinion provided with references (list below):
24. CT scanning of the chest should be used in screening populations at risk for asbestos-related diseases (mark one).
18
Strongly Disagree
0
1
2
3
4
5


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o I do not feel qualified to answer this question.
o Expert opinion provided without references.
o Expert opinion provided with references (list below):
6

7

8

Strongly agree
9
10


25. There should be initiatives to develop protocols to attempt therapy for asbestosis (mark one).
Strongly Disagree
0
1
2
3
4
5


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

Please mark one:
o I do not feel qualified to answer this question.
o Expert opinion provided without references.
o Expert opinion provided with references (list below):
6

7

8

Strongly agree
9
10


We welcome additional questions for consideration in the next round.
19
First Round Results: Question 1
Pleural plaques alter lung function to a clinically significant degree.
N
Median
Iqr
P-Value
Consensus
Decision
28
2
3
0.0003
Very Good
Accept
Expert Panel Suggested References for Question 1:
D. Bellis, A. Andrion, L. Delsedime and F. Mollo. Minimal pathologic changes of the lung and asbestos exposure. Hum Pathol, 1989,
20; 102-6 http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=2914698
N. Becker, J. Berger and U. Bolm-Audorff. Asbestos exposure and malignant lymphomas--a review of the epidemiological literature.
Int Arch Occup Environ Health, 2001, 74; 459-69
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=11697448
M. R. Becklake. Occupational lung disease--past record and future trend using the asbestos case as an example. Clin Invest Med,
1983, 6; 305-17
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=6671361
20
R. Begin, R. Boileau and S. Peloquin. Asbestos exposure, cigarette smoking, and airflow limitation in long-term Canadian chrysotile
miners and millers. Am J Ind Med, 1987, 11; 55-66
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=3028138
E. L. Baker, T. Dagg and R. E. Greene. Respiratory illness in the construction trades. I. The significance of asbestos-associated
pleural disease among sheet metal workers. J Occup Med, 1985, 27; 483-9
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=4032084
B. Jarvholm and A. Sanden. Pleural plaques and respiratory function. Am J Ind Med, 1986, 10; 41926http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=3788985
D. P. Loomis, G. W. Collman and W. J. Rogan. Relationship of mortality, occupation, and pulmonary diffusing capacity to pleural
thickening in the First National Health and Nutrition Examination Survey. Am J Ind Med, 1989, 16; 477-84
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=2589326
J. Bourbeau, P. Ernst, J. Chrome, B. Armstrong and M. R. Becklake. The relationship between respiratory impairment and asbestosrelated pleural abnormality in an active work force. Am Rev Respir Dis, 1990, 142; 837-42
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=2221591
K. H. Kilburn and R. H. Warshaw. Abnormal pulmonary function associated with diaphragmatic pleural plaques due to exposure to
asbestos. Br J Ind Med, 1990, 47; 611-4
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=2207032
S. P. Kouris, D. L. Parker, A. P. Bender and A. N. Williams. Effects of asbestos-related pleural disease on pulmonary function. Scand
J Work Environ Health, 1991, 17; 179-83
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=2068556
M. Garcia-Closas and D. C. Christiani. Asbestos-related diseases in construction carpenters. Am J Ind Med, 1995, 27; 115-25
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=7900729
B. Singh, P. R. Eastwood, K. E. Finucane, J. A. Panizza and A. W. Musk. Effect of asbestos-related pleural fibrosis on excursion of
the lower chest wall and diaphragm. Am J Respir Crit Care Med, 1999, 160; 1507-15
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=10556113
A. Miller. Pulmonary function in asbestosis and asbestos-related pleural disease. Environ Res, 1993, 61; 1-18
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=8472663
D. A. Schwartz, J. R. Galvin, S. J. Yagla, S. B. Speakman, J. A. Merchant and G. W. Hunninghake. Restrictive lung function and asbestos-induced pleural fibrosis. A quantitative approach. J Clin Invest, 1993, 91; 2685-92
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=8514875
N. al Jarad, N. Poulakis, M. C. Pearson, M. B. Rubens and R. M. Rudd. Assessment of asbestos-induced pleural disease by computed tomography--correlation with chest radiograph and lung function. Respir Med, 1991, 85; 203-8
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=1882109
21
C. G. Ohlson, L. Bodin, T. Rydman and C. Hogstedt. Ventilatory decrements in former asbestos cement workers: a four year follow
up. Br J Ind Med, 1985, 42; 612-6
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=3849974
G. Hillerdal, P. Malmberg and A. Hemmingsson. Asbestos-related lesions of the pleura: parietal plaques compared to diffuse thickening studied with chest roentgenography, computed tomography, lung function, and gas exchange. Am J Ind Med, 1990, 18; 627-39
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=2264562
Expert Panel Comments for Questions 1:
1. Agree in most cases. Extent of plaques correlates with decrease in FVC and can alter lung function in individual cases. Lesser effects can be clinically significant in pts with already reduced function. Diffuse pleural thickening can have marked effects.
… but Gaensler pleuritis with hyalinosis coplicata will reduce ventilation (VC).
2. Ordinary plaques have no significant effect. Occasionally one sees very extensive plaques in conjuction with marked pleural
fibrosis and this can alter function but these are exceptional cases
3. In epidemiologic surveys a mild restricive defect can be shown. In “clinical” practice the effect of pleural plaques is usually not
evident lung function is most often in the limits of theoric values.
4. This question is too simple. Although the vast majority of plaques are unlikely to affect function a very heavy plaque burden
may cause restriction. Plaques can be at least semi-quantified with CT.
5. This is a poor question - the real answer is “RARELY” but it does happen on occasion.
22
First Round Results: Question 2
Workers With Asbestos Exposure And Pleural Plaques Or Diffuse Pleural Thickening (In The Absence Of Fibrosis) Are At Increased Risk
Of Lung Cancer.
N
Median
Iqr
P-Value
Consensus
Decision
31
8
5
0.0031
None
2Nd Round
Expert Panel Suggested References for Question 2:
G. Hillerdal.Pleural plaques and risk for bronchial carcinoma and mesothelioma. A prospective study.Chest.105,144
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=8275722
G. Hillerdal and D. W. Henderson.Asbestos, asbestosis, pleural plaques and lung cancer.Scand J Work Environ Health.23,93103
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=9167232
A. Karjalainen, E. Pukkala, T. Kauppinen and T. Partanen.Incidence of cancer among Finnish patients with asbestos-related pulmonary or pleural fibrosis.Cancer Causes Control.10,51-7
23
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=10334642
B. T. Mossman and J. B. Gee.Asbestos-related diseases.N Engl J Med.320,1721-30
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=2659987
A. andrion, E. Pira and F. Mollo.Pleural plaques at autopsy, smoking habits, and asbestos exposure.Eur J Respir Dis.65,125-30
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=6698135
D. A. Edelman.Asbestos exposure, pleural plaques and the risk of lung cancer.Int Arch Occup Environ Health.60,389-93
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=3045007
F. Mollo, A. andrion, A. Colombo, N. Segnan and E. Pira.Pleural plaques and risk of cancer in Turin, northwestern Italy. An autopsy study.Cancer.54,1418-22
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=6467163
G. W. Gibbs.Etiology of pleural calcification: a study of Quebec chrysotile asbestos miners and millers.Arch Environ Health.34,7683
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=434935
P. Harber, Z. Mohsenifar, A. Oren and M. Lew.Pleural plaques and asbestos-associated malignancy.J Occup Med.29,641-4
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=3655947
E. A. Gaensler, P. J. Jederlinic and A. Churg.Idiopathic pulmonary fibrosis in asbestos-exposed workers.Am Rev Respir
Dis.144,689-96
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=1892312
W. Weiss.Asbestos-related pleural plaques and lung cancer.Chest.103,1854-9
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=8404113
D. D. Smith.Plaques, cancer, and confusion.Chest.105,8-9
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=8275791
G. Sheers.Asbestos-associated disease in employees of Devonport Dockyard.Ann N Y Acad Sci.330,281-7
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=294178
B. W. Robinson and A. W. Musk.Benign asbestos pleural effusion: diagnosis and course.Thorax.36,896-900
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=7336367
P. Wilkinson, D. M. Hansell, J. Janssens, M. Rubens, R. M. Rudd, A. N. Taylor and C. McDonald.Is lung cancer associated with
asbestos exposure when there are no small opacities on the chest radiograph?Lancet.345,1074-8
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=7715339
24
First Round Results: Question 3
Workers with asbestos exposure and pleural plaques or diffuse pleural thickening (in the absence of fibrosis) are
at increased risk of mesothelioma.
N
Median
Iqr
P-Value
Consensus
Decision
34
9.5
3
0.0001
Good
Accept
Expert Panel Suggested References for Question 3:
G. Hillerdal. Pleural plaques and risk for bronchial carcinoma and mesothelioma. A prospective study. Chest. 144-50.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=8275722
A. Karjalainen, E. Pukkala, T. Kauppinen and T. Partanen. Incidence of cancer among Finnish patients with asbestos-related pulmonary or pleural fibrosis. Cancer Causes Control. 517. ttp://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=10334642
25
Expert Panel Comments for Questions 3:
Again a badly worded question. Do you mean compared with the general public? In which case the answer is obviously Yes! Since
the probability is that they on the average had much higher exposure to amphibole asbestos. But if you mean compared with
others with identical exposures, the answer in both cases is No! See the references above. But the target organ is quite separate and there is no identified biological mechanism which would suggest any linkage apart from exposure.
Controversial area where scientific data are insufficient to assess, but plaques are seen in about only 30 % of subjects with mesothelioma. Hillerdal showed an approximately 11 fold increased risk of mesothelioma in patients with bilateral pleural plaques,
even more than for lung cancer. ANY exposure to asbestos increases the risk for mesothelioma.
If the question is whether exposed workers with plaques and diffuse pleural thickening (in absence of fibrosis) are at increased
risk of mesothelioma in comparison with workers without such pleural abnormalities, see item 2. Severe pleural changes
could be markers of severe exposure and then of definite (and probably greater) risk. Anyway direct malignant transformation
of these benign pleural changes has not been demonstrated. Risk of malignant pleural mesothelioma is high since substantially large numbers of carcinogen of mesothelioma (asbestos fibers) are present in the mesothelial tissues (the mother tissue
of malignant pleural mesothelioma).
26
First Round Results: Question 4
Asbestos exposure can cause diffuse pleural thickening.
N
Median
IQR
P-value
Consensus
Decision
34
10
0
0.0001
Very Good
Accept
No expert panel references or comments for question 4.
27
First Round Results: Question 5
Asbestos exposure can cause pleural plaques.
N
Median
IQR
P-value
Consensus
Decision
34
10
0
0.0001
Very Good
Accept
Expert Panel Suggested References for Question 5:
A. Andrion, A. Colombo, M. Dacorsi and F. Mollo. Pleural plaques at autopsy in Turin: a study on 1,019 adult subjects. Eur J
Respir Dis. 107-12.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=7067761
G. Hillerdal and A. Lindgren. Pleural plaques: correlation of autopsy findings to radiographic findings and occupational history. Eur
J Respir Dis. 315-9.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=7202602
B. Jarvholm and A. Sanden. Pleural plaques and respiratory function. Am J Ind Med. 419-26.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=3788985
G. Hillerdal and D. W. Henderson. Asbestos, asbestosis, pleural plaques and lung cancer. Scand J Work Environ Health. 93-103.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=9167232
B. T. Mossman and J. B. Gee. Asbestos-related diseases. N Engl J Med. 1721-30.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=2659987
28
Asbestos, asbestosis, and cancer: the Helsinki criteria for diagnosis and attribution. Scand J Work Environ Health. 311-6.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=9322824
Expert Panel Comments for Questions 5:
Personal data show that 95% of patients with pleural plaques but without asbestosis have an elevated pulmonary asbestos fiber burden. Pleural plaque is characteristically induced by exposure to asbestos (a marker of asbestos exposure). Pleural plaques have
been recognized as significant markers of asbestos exposure from the sixties (Meurman 1966) and bilateral plaques have been
considered as reliable indicators of occupational exposure (Medical Advisory Panel 1982). At present ‘the association with asbestos
is a firm one based on both epidemiological evidence and the identification of asbestos in underlying lung’ (Corrin 2000). As far as
the clinical-pathological experience in Turin, the predictive value of the post mortem finding of pleural plaques for previous occupational exposure of individual subjects was 76% when the plaques had a total surface > 100 cm2 reaching 100% when plaques of total
surface > 50 cm 2 were associated with a lung burden of uncoated mineral fibres (in light microscopy) >50.000 gram dry lung (Mollo
et al. 1987). In a previous study on more than 1 000 autopsies plaques with a total surface of 50 cm2 were nearly always bilateral
and both costal and diapragmatic (Andrion et al. 1982).
29
First Round Results: Question 6
In the absence of pathologic examination of lung tissue, the diagnosis of asbestosis is a judgment based on a careful consideration of all
relevant clinical findings. In our opinion it is necessary that there be a reliable history of exposure.
N
Median
IQR
P-value
Consensus
Decision
34
10
1
0.0001
Very Good
Accept
No expert panel references or comments for question 6.
30
First Round Results: Question 7
In the absence of pathologic examinaion of lung tissue, the diagnosis of asbestosis is a judgment based on a careful consideration of all
relevant clinical findings. In our opinion, it is necessary that there be an appropriate time interval between exposure and detection (see
ATS statement for details).
N
Median
IQR
P-value
Consensus
Decision
33
9
2
0.0001
Very Good
Accept
Expert Panel Suggested References for Question 7:
K. Browne. A threshold for asbestos related lung cancer. Br J Ind Med. 556-8.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=3730306
A. Andrion, A. Colombo, M. Dacorsi and F. Mollo. Pleural plaques at autopsy in Turin: a study on 1,019 adult subjects. Eur J
Respir Dis. 107-12.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=7067761
A. M. Goff and E. A. Gaensler. Asbestosis following brief exposure in cigarette filter manufacture. Respiration. 83-93.
31
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=5018998
W. Cookson, N. De Klerk, A. W. Musk, J. J. Glancy, B. Armstrong and M. Hobbs. The natural history of asbestosis in former crocidolite workers of Wittenoom Gorge. Am Rev Respir Dis. 994-8.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=3013058
M. R. Becklake. Occupational lung disease--past record and future trend using the asbestos case as an example. Clin Invest Med.
305-17. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=6671361
G. Hillerdal and D. W. Henderson. Asbestos, asbestosis, pleural plaques and lung cancer. Scand J Work Environ Health. 93-103.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=9167232
Asbestos, asbestosis, and cancer: the Helsinki criteria for diagnosis and attribution. Scand J Work Environ Health. 311-6.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=9322824
K. Donaldson and C. L. Tran. Inflammation caused by particles and fibers. Inhal Toxicol. 5-27.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=12122558
Expert Panel Comments for Questions 7:
Asbestosis is generally (even though not always in individual cases) associated with rather substantial levels of exposure. According to some authors, at least 25 ff ml years (see for example Browne 1986 1995 ) are requested. A latency habitually
ranging from 15 years to several decades has been reported (Roggli 1994 ) but a shorter period between the starting of a
very severe exposure and detection could not be excluded.
In a series of 195 subjects with pleural plaques studied in Turin 41 showed at autopsy a total extension > 50 cm 2 and 40 of
them were over the age of 40 years (Andrion et al. 1982 ). Since plaques of such an extension are habitually occupational
ones, this finding could be consistent with a latency of at least 2 decades.
The highest exposures are associated with the shortest latency. However, latency may be lower than 15 years.
It is well accepted that the development of asbestosis is a slow and long process. It is said that it takes 20 years and longer after
the first exposure to asbestos. Therefore, the duration after the first exposure to asbestos is an important factor for the diagnosis of pulmonary asbestosis. Latency is always a crucial issue in the diagnosis of asbestos-related diseases. The clinical
findings depend on the presence of lung fibrosis, which in turn depends on lung overload, which would take a time commensurate with the intensity of exposure. This is a complex issue.
It depends on level of exposure, in the document they consider 15 yrs which seems somewhat ad hoc as they refer to “present
levels”
32
First Round Results: Question 8
We regard the following clinical criteria to be of recognized value: Chest Roentgenographic evidence of "S" "T" "U" small irregular opacifications of a profusion of 1/1 or greater.
N
Median
IQR
P-value
Consensus
Decision
24
5
5
0.0991
None
2nd Round
Expert Panel Suggested References for Question 8:
N. al Jarad, B. Strickland, G. Bothamley, S. Lock, R. Logan-Sinclair and R. M. Rudd. Diagnosis of asbestosis by a time expanded
wave form analysis, auscultation and high resolution computed tomography: a comparative study. Thorax. 347-53.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=8511731
C. A. Staples, G. Gamsu, C. S. Ray and W. R. Webb. High resolution computed tomography and lung function in asbestosexposed workers with normal chest radiographs. Am Rev Respir Dis. 1502-8.
33
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=2729755
P. A. Gevenois, P. De Vuyst, S. Dedeire, J. Cosaert, R. Vande Weyer and J. Struyven. Conventional and high-resolution CT in
asymptomatic asbestos-exposed workers. Acta Radiol. 226-9.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=8192957
S. D. Rockoff and A. Schwartz. Roentgenographic underestimation of early asbestosis by International Labor Organization classification. Analysis of data and probabilities. Chest. 1088-91.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=3359826
W. B. Gefter and E. F. Conant. Issues and controversies in the plain-film diagnosis of asbestos-related disorders in the chest. J
Thorac Imaging. 11-28.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=3054135
J. A. Dick, W. K. Morgan, D. F. Muir, R. B. Reger and N. Sargent. The significance of irregular opacities on the chest roentgenogram. Chest. 251-60.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=1623762
D. C. Muir, J. Julian, N. Jadon, R. Roberts, J. Roos, J. Chan, W. Maehle and W. K. Morgan. Prevalence of small opacities in chest
radiographs of nickel sinter plant workers. Br J Ind Med. 428-31.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=8507595
34
First Round Results: Question 9
A restrictive pattern of lung impairment with a forced vital capacity below the lower limit of normal.
N
Median
IQR
P-value
Consensus
Decision
26
6
3
0.1036
None
2nd Round
Expert Panel Suggested References for Question 9:
B. T. Mossman and A. Churg. Mechanisms in the pathogenesis of asbestosis and silicosis. Am J Respir Crit Care Med. 1666-80.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=9603153
H. Weill, M. M. Ziskind, C. Waggenspack and C. E. Rossiter. Lung function consequences of dust exposure in asbestos cement
manufacturing plants. Arch Environ Health. 88-97.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=1115533
M. L. Thomson, A. M. Pelzer and W. J. Smither. The discriminant value of pulmonary function tests in asbestosis. Ann N Y Acad
Sci. 421-36. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=5219565
35
Expert Panel Comments for Questions 9:
Clearly of value, but does not have to be present in every case. Despite some confusion in literature (cf controverse in Chest. 1995
Jun;107(6) 1727-30)the pattern of impairment in asbestosis in clearly restrictive; however definite histological lesions can be
seen before significative impairment of VC. It is possible that very mild disease might be manifest on PA film and have equivocal functional changes. Many cases have normal lung function, or at least values within normal limits (which may represent a
significant loss!) Depends on the definition of “disease” or “radiological lesion “
See responses to Questions 1, 2, 3 plus 8 and 9.
There are different degrees of disease. What is your definition of an expert? I am not a pulmonary physiologist, but I am a clinician
with knowledge of the relevant scientific literature. Additionally a very relevant sign is reduced earning capacity in exercise
tests with low PO2. Reduced vital capacity is correct but not an early sign.
36
First Round Results: Question 10
We regard the following clinical criteria to be of recognized value: A diffusing capacity below the lower limit of normal.
N
Median
IQR
P-value
Consensus
Decision
27
7
4
0.0244
None
2nd Round
Expert Panel Suggested References for Question 10:
J. E. Cotes and B. King. Relationship of lung function to radiographic reading (ILO) in patients with asbestos related lung disease. Thorax. 777-83.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=3206385
Z. Dujic, J. Tocilj, S. Boschi, M. Saric and D. Eterovic. Biphasic lung diffusing capacity: detection of early asbestos induced changes in lung function. Br J Ind
Med. 260-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=1315153
Expert Panel Comments for Questions 10:
37
Only if other criteria are present viz. radiographic exposure prolonged etc. Clearly of value, but does not have to be present in every case. Furthermore, emphysema can result in a similar finding in the absence of asbestosis. It is possible that very mild disease might be manifest on PA film and have equivocal
functional changes (but DLCO is probably more sensitive than volumes and is more likely to be abnormal)
Same considerations for early lesions.
The measurement of CO diffusion capacity is not obligate if other criteria are fulfilled.
38
First Round Results: Question 11
Bilateral late or pan inspiratory crackles at the posterior lung bases not cleared by cough.
N
Median
IQR
P-value
Consensus
Decision
26
7.5
5
0.1583
None
2nd Round
Expert Panel Comments for Questions 11:
Only if incubation period long enough and there is radiographic evidence of s t and u opacities.
See prior references.
39
Clearly of value, but does not have to be present in every case, depends again on the definition of the disease.
Asbestosis (clinically relevant) is a disappearing disease. Note that rales are less sensitive
Such crackels are often difficult to recognize.
Expert Panel Suggested References for Question 11:
1.) N. al Jarad, B. Strickland, G. Bothamley, S. Lock, R. Logan-Sinclair and
R. M. Rudd. Diagnosis of asbestosis by a time expanded wave form analysis, auscultation and high resolution computed tomography: a comparative study. Thorax. 347-53.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=8511731
40
First Round Results: Question 12
In an asbestos exposed individual, pulmonary fibrosis is a prerequisite to attribute the development of lung cancer to asbestos .
N
Median
IQR
P-value
Consensus
Decision
34
1
4
0.0011
some
2nd Round
Expert Panel Suggested References for Question 12:
1.) D.Egilman and A. Reinert. Lung cancer and asbestos exposure: asbestosis is not necessary. Am J Ind Med. 398406.http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=8892544 2.) G. Hillerdal
and D. W. Henderson. Asbestos, asbestosis, pleural plaques and lung cancer. Scand J Work Environ Health. 93103.http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=9167232 3.) P. Wilkinson,
D. M. Hansell, J. Janssens, M. Rubens, R. M. Rudd, A. N. Taylor and C. McDonald. Is lung cancer associated with asbestos exposure when there are no small opacities on the chest radiograph? Lancet. 1074-
41
8.http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=7715339 4.) Asbestos, asbestosis, and cancer: the Helsinki criteria for diagnosis and attribution. Scand J Work Environ Health. 311-6.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=9322824 5.) R. N. Jones, J. M.
Hughes and H. Weill. Asbestos exposure, asbestosis, and asbestos-attributable lung cancer. Thorax. S9-15.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=8869346 6.) P. J. Borm. Munich
workshop on evaluation of fiber and particle toxicity: an introduction. Inhal Toxicol. 1-3.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=12122557 7.) P. T. Cagle. Criteria for attributing lung cancer to asbestos exposure. Am J Clin Pathol. 9-15.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=11789736 8.) J. M. Dement, D.
P. Brown and A. Okun. Follow-up study of chrysotile asbestos textile workers: cohort mortality and case-control analyses. Am J Ind
Med. 431-47. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=7810543 9.) E.
Imbernon, M. Goldberg, S. Bonenfant, A. Chevalier, P. Guenel, R. Vatre and J. Dehaye. Occupational respiratory cancer and exposure to asbestos: a case-control study in a cohort of workers in the electricity and gas industry. Am J Ind Med. 339-52.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=7485188 10.) G. Hillerdal. Pleural plaques and risk for bronchial carcinoma and mesothelioma. A prospective study. Chest. 144-50.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=8275722 11.) M. M. Finkelstein.
Radiographic asbestosis is not a prerequisite for asbestos-associated lung cancer in Ontario asbestos-cement workers. Am J Ind
Med. 341-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=9258387 12.) P.
Boffetta. Health effects of asbestos exposure in humans: a quantitative assessment. Med Lav. 471-80.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=10217936 13.) B. M. Haus, H.
Razavi and W. G. Kuschner. Occupational and environmental causes of bronchogenic carcinoma. Curr Opin Pulm Med. 220-5.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=11470978 14.) K. Browne. A
threshold for asbestos related lung cancer. Br J Ind Med. 556-8.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=3730306 15.) G. K. SluisCremer and B. N. Bezuidenhout. Relation between asbestosis and bronchial cancer in amphibole asbestos miners. Br J Ind Med.
537-40. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=2550049 16.) A. Churg.
Asbestos, asbestosis, and lung cancer. Mod Pathol. 509-11.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=8248104 17.) W. Weiss. Asbestosis: a marker for the increased risk of lung cancer among workers exposed to asbestos. Chest. 536-49.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=10027457 18.) M. L. Warnock
and W. Isenberg. Asbestos burden and the pathology of lung cancer. Chest. 20-6.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=3940784 19.) N. H. de Klerk, A.
W. Musk, J. L. Eccles, J. Hansen and M. S. Hobbs. Exposure to crocidolite and the incidence of different histological types of lung
cancer. Occup Environ Med. 157-
42
9.http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=8704855 20.) D. E. Banks, M.
L. Wang and J. E. Parker. Asbestos exposure, asbestosis, and lung cancer. Chest. 320-2.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=10027425 21.) H. H. Nelson, D.
C. Christiani, J. K. Wiencke, E. J. Mark, J. C. Wain and K. T. Kelsey. k-ras mutation and occupational asbestos exposure in lung adenocarcinoma: asbestos-related cancer without asbestosis. Cancer Res. 4570-3.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=10493509 22.) C. G. Billings
and P. Howard. Asbestos exposure, lung cancer and asbestosis. Monaldi Arch Chest Dis. 151-6.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=10949878 23.) P. De Vuyst and
P. Camus. The past and present of pneumoconioses. Curr Opin Pulm Med. 151-6.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=10741776 24.) N. Wikeley.
Compensation for asbestos-related lung cancer. Med Leg J. 17-25; discussion 25-8.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=11915572 25.) J. M. Hughes
and H. Weill. Asbestosis as a precursor of asbestos related lung cancer: results of a prospective mortality study. Br J Ind Med. 22933. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=2025587 26.) E. A. Gaensler, P. J. Jederlinic and A. Churg. Idiopathic pulmonary fibrosis in asbestos-exposed workers. Am Rev Respir Dis. 689-96.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=1892312 27.) B. W. Case and
A. Dufresne. Asbestos, asbestosis, and lung cancer: observations in Quebec chrysotile workers. Environ Health Perspect. 1113-9.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=9400709
Expert Panel Comments for Questions 12:
Again how is fibrosis diagnosed? The literature is conflicting, controversial area where scientific data are insufficient to assess.
First, the suitability of a given exposure for the development of a subsequent lung cancer must be assessed taking into account that 1) the latency must be at least 10 years (Helsinki Criteria 1997 ); 2) all types of commercial fibres are cancerogenic for the lung including chrysotile (IARC (1987 ); 3) a minimal threshold has not been defined (Doll e Peto 1985 ; Hillerdal and Henderson 1997 ; Boffetta 1998 ; Haus et al. 2001). Once these criteria are complied with the question remains whether pulmonary fibrosis (asbestosis) is a prerequisite or merely a marker of substantial exposure. Some authors
support the ‘asbestosis-cancer hypothesis’ (the asbestos cancer necessarily develops on a ground of asbestos fibrosis) see
for example Browne 1986 1995; Sluis Cremer and Bezuidenhout 1989 ; Churg 1993 ; Weiss 1999 . Other authors
43
support the ‘asbestos-cancer hypothesis’ (asbestos and not fibrosis gives rise to the cancer) see for example Warnock and
Isemberg 1986 ; Wilkinson et al. 1995; De Klerk et al. 1996; Egilman and Reinert 1996 ; Filkenstein 1997 ; Hillerdal
and Henderson 1997 ; Banks et al. 1999; Nelson et al. 1999; Billings and Howard 2000. I agree with the comment by
Henderson et al. 1997 ‘There has been a substantial change in the balance of evidence supporting the proposition that is
the asbestos fiber load itself in the lung tissue that is the main determinator for lung carcinogenesis though not the only factor’. Furthermore, it seems worthwhile to remind the mortality among asbestos workers has been reported as about 20%
since some decades ago (see for example Selikoff 1977 ) until now (see for example Kobzik 1999 ) whereas the incidence of asbestosis is clearly decreased (De Vuyst and Camus 2000 ). Many regulations are in substantial agreement
with the ‘asbestos-cancer hypothesis.’ Asbestosis is not required for the attribution of a lung cancer to a suitable asbestos exposure in Finland, Norway, Sweden, Denmark and neither is required in Germany in France in Great Britain and (according to
the ‘Georgine Criteria’) in USA provided that pleural plaques and or diffuse pleural fibrosis and or given levels of exposure are
ascertained (see Henderson et al. 1997; Wikely 2002 ). In our country, according to the ‘Guidlines for the Permanent Education and Accreditation in Occupational Medicine,’ (official document of the Italian Society of Occupational Medicine and Industrial Health) ‘the statement that the asbestos lung cancer is preceded by asbestosis is now disproved’ (Pira et al. 2002).
No rule of Italian law prescribes the asbestosis as prerequisite to attribute a lung cancer to a reliable asbestos exposure.
CONSENSUS REPORT. Asbestos asbestosis and cancer the Helsinki criteria for diagnosis and attribution. Scand J. Work
Environ. Health 23 311-316 1997.
If fibrosis is present; it means that exposure was important . I should certainly consider this as an important argument for attribution not a prerequisite. It is now well accepted that asbestosis is not a prerequisite to attribute the development of lung cancer. Pulmonary fibrosis of course greatly increases the excess of risk of lung cancer but is not a pre-requisite.
44
First Round Results: Question 13
The extent of asbestos exposure correlates with the presence and extent of pleural abnormalities.
N
Median
IQR
P-value
Consensus
Decision
33
5
5
0.474
None
2nd Round
Expert Panel Suggested References for Question 13:
C. Bianchi, A. Brollo and L. Ramani. Asbestos exposure in a shipyard area, northeastern Italy. Ind Health. 301-8.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=10943078
N. H. de Klerk, W. O. Cookson, A. W. Musk, B. K. Armstrong and J. J. Glancy. Natural history of pleural thickening after exposure
to crocidolite. Br J Ind Med. 461-7.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=2548564
B. Jarvholm. Pleural plaques and exposure to asbestos: a mathematical model. Int J Epidemiol. 1180-4.
45
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=1483825
A. Karjalainen, P. J. Karhunen, K. Lalu, A. Penttila, E. Vanhala, P. Kyyronen and A. Tossavainen. Pleural plaques and exposure to
mineral fibres in a male urban necropsy population. Occup Environ Med. 45660. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=8044244
J. R. Shepherd, G. Hillerdal and J. McLarty. Progression of pleural and parenchymal disease on chest radiographs of workers exposed to amosite asbestos. Occup Environ Med. 410-5.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=9245947
H. Ren, D. R. Lee, R. H. Hruban, J. E. Kuhlman, E. K. Fishman, P. S. Wheeler and G. M. Hutchins. Pleural plaques do not predict
asbestosis: high-resolution computed tomography and pathology study. Mod Pathol. 201-9.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=2047383
B. T. Mossman and A. Churg. Mechanisms in the pathogenesis of asbestosis and silicosis. Am J Respir Crit Care Med. 1666-80.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=9603153
E. Orlowski, J. C. Pairon, J. Ameille, X. Janson, Y. Iwatsubo, G. Dufour, J. Bignon and P. Brochard. Pleural plaques, asbestos exposure, and asbestos bodies in bronchoalveolar lavage fluid. Am J Ind Med. 349-58.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=7977408
S. Yazicioglu. Pleural calcification associated with exposure to chrysotile asbestos in southeast Turkey. Chest. 43-7.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=1277930
Expert Panel Comments for Questions 13:
In a series of 1 498 non-selected autopsies studied in Turin (Mollo et al. 1983) we obtained reliable occupational histories in 898
cases and 188 (20 9%) had plaques; definite occupational exposure was clearly ascertained in 17 subjects 13 out of which
had plaques. The mean duration of exposure was shorter in exposed workers without plaques (about 12 years range 6-20)
and longer in those with plaques (about 26 years range 10-39). The numbers are small, but some relationship between the
length of exposure and the presence of plaque could reasonably be suggested.
Individual susceptibility also seems to play a role.
Multiple studies have shown dose response for the presence and extent of pleural plaques.
Obviously there is some correlation since there is some dose-response, but by no means all of those who are heavily exposed,
develop plaques. But again the question doesn’t specify whether plain x-ray CT scan or autopsy findings are referred to. The
answers are different in each case. Pleural abnormalities, caused by exposure to asbestos, are dose related.
THIS QUESTION IS TOO IMPRECISE. ‘PLEURAL ABNORMALITES’ INCLUDE PLAQUES EFFUSION DIFFUSE FIBRSOIS
46
PLEURAL EXTENSION OF INTERSTITIAL FIBROSIS AND MESOTHELIOMA. THEY EACH MAY HAVE A DIFFERENT
RELATIONSHIP TO EXPOSURE. ALSO ‘EXTENT OF EXPOSURE’ IS A POOR TERM. DO YOU MEAN DOSE? THE
QUESTION DOES NOT CONSIDER DIFFERENT TYPES OF ASBESTOS.
There is some data that pleural fibrosis only occurs with moderately high fiber burdens (more than plaques not as much as asbestosis) but plaques clearly occur at burdens much lower than those that produce asbestosis many papers show that duration
is most important. Diffuse PT and plaques may be seen after seemingly minor exposure
47
First Round Results: Question 14
A reasonable scheme can be developed to apportion the attributability of smoking and asbestos exposure in a cigarette smoking asbestos-exposed worker with lung cancer.
N
Median
IQR
P-value
Consensus
Decision
32
5
5
0.5952
None
2nd Round
Expert Panel Suggested References for Question 14:
N. H. de Klerk, A. W. Musk, J. L. Eccles, J. Hansen and M. S. Hobbs.Exposure to crocidolite and the incidence of different histological types of lung cancer.Occup Environ Med.53,1579. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=8704855
G. K. Sluis-Cremer and B. N. Bezuidenhout.Relation between asbestosis and bronchial cancer in amphibole asbestos miners.Br J
Ind Med.46,537-
48
40. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=2550049
Expert Panel Comments for Questions 14:
The basis for my statement is a consequence of the fact that once a coal miner, asbestos worker, iron ore miner etc., has been
noted to be a smoker, there comes a time when a proportion of these will play down the number of cigarettes they smoke, or
much There are really 2 questions re: attributability: Can asbestos exposure be attributed as a cause at all? Sufficient info
Re: exposure and other stigmata of asbestos-related disease should allow an answer to this question in most cases. How to
attribute this question should not have been asked as it is not really answerable by this method. I am certainly as qualified
as anyone to answer this question, but it is far more complex than a numerical category can convey.
49
First Round Results: Question 15
Chest radiographs are a sensitive method to diagnose interstitial disease attributable to asbestos exposure.
N
Median
IQR
P-value
Consensus
Decision
32
4.5
4.5
0.1009
None
2nd Round
Expert Panel Suggested References for Question 15:
R. B. Reger, W. S. Cole, E. N. Sargent and P. S. Wheeler. Cases of alleged asbestos-related disease: a radiologic re-evaluation. J
Occup Med. 1088-90.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=2258763
50
C. E. Rossiter, K. Browne and J. C. Gilson. International classification trial of AIA set of 100 radiographs of asbestos workers. Br J
Ind Med. 538-43.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=3415919
N. al Jarad, A. R. Gellert and R. M. Rudd. Bronchoalveolar lavage and 99mTc-DTPA clearance as prognostic factors in asbestos
workers with and without asbestosis. Respir Med. 365-74.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=8209056
G. R. Epler, T. C. McLoud, E. A. Gaensler, J. P. Mikus and C. B. Carrington. Normal chest roentgenograms in chronic diffuse infiltrative lung disease. N Engl J Med. 934-9.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=642974
C. A. Staples, G. Gamsu, C. S. Ray and W. R. Webb. High resolution computed tomography and lung function in asbestosexposed workers with normal chest radiographs. Am Rev Respir Dis. 1502-8.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=2729755
F. Mollo, C. Magnani, P. Bo, P. Burlo and M. Cravello. The attribution of lung cancers to asbestos exposure: a pathologic study of
924 unselected cases. Am J Clin Pathol. 90-5.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=11789737
J. E. Craighead, J. L. Abraham, A. Churg, F. H. Green, J. Kleinerman, P. C. Pratt, T. A. Seemayer, V. Vallyathan and H. Weill. The
pathology of asbestos-associated diseases of the lungs and pleural cavities: diagnostic criteria and proposed grading schema. Report of the Pneumoconiosis Committee of the College of American Pathologists and the National Institute for Occupational Safety and Health. Arch Pathol Lab Med. 544-96.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=6897166
D. Bellis, A. Andrion, L. Delsedime and F. Mollo. Minimal pathologic changes of the lung and asbestos exposure. Hum Pathol. 1026. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=2914698
H. M. Kipen, R. Lilis, Y. Suzuki, J. A. Valciukas and I. J. Selikoff. Pulmonary fibrosis in asbestos insulation workers with lung cancer: a radiological and histopathological evaluation. Br J Ind Med. 96-100.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=3814551
S. Neri, A. Antonelli, F. Falaschi, P. Boraschi and L. Baschieri. Findings from high resolution computed tomography of the lung and
pleura of symptom free workers exposed to amosite who had normal chest radiographs and pulmonary function tests. Occup
Environ Med. 239-43.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=8199665
P. A. Gevenois, P. De Vuyst, S. Dedeire, J. Cosaert, R. Vande Weyer and J. Struyven. Conventional and high-resolution CT in
asymptomatic asbestos-exposed workers. Acta Radiol. 226-9.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=8192957
S. Lozewicz, R. H. Reznek, M. Herdman, J. E. Dacie, A. McLean and R. J. Davies. Role of computed tomography in evaluating
asbestos related lung disease. Br J Ind Med. 777-81.
51
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=2590642
Expert Panel Comments for Questions 15:
I am not a radiologist. Are you referring to clinical or pathological asbestosis? Differential diagnosis includes age, smoking, poor
inspiration, and obesity. There is also considerable observer variability.
At least serious disease CT scan ++++ Chest Xray is an essential approach to identify pulmonary asbestosis. However, Chest Xray’s sensitivity to detect asbestosis is weaker than that of histopathology. My own study indicated that 20 % of pulmonary
asbestosis detected by histopathology were overlooked by chest Xray examination. Chest radiographs are the best way to
detect functionally significant disease. It is possible that CT reliably detects early disease, but this is unproven and much of
the published data. It may depend on the employed technique the qualification of the radiologist in occupational chest diseases and the acquaintance of possible asbestos exposure. We recently published a survey on 924 surgical cases of lung cancer (Mollo et al. 2002) it was an unselected series from a general hospital without suspicions of possible occupational disease. We found 56 cases of histologic asbestosis 34 out of whom with minimal interstitial fibrosis according to the CAP and
NIOSH criteria (Craighead et al. 1982) and to our previous experience, (Bellis et al. 1989); the remaining 22 cases showed
more severe interstitial changes. From the clinical records no cases of interstitial fibrosis had been diagnosed or referred to
possible occupational disease. Furthermore, 22 additional cases of histologic asbestosis have been found in a new (unpublished) series of 232 surgical lung specimens and the results were the same.
See response to Question 13 and Gaensler paper. Sensitive but less sensitive than CT HRCT certain functional evaluations. Sensitivity is between 82 and 90%.
52
First Round Results: Question 16
Chest radiographs are a senstitive method to measure pleural abnormalities attributable to asbestos exposure.
N
Median
IQR
P-value
Consensus
Decision
29
4
4
0.0114
Some
2nd Round
Expert Panel Suggested References for Question 16:
P. A. Gevenois, P. De Vuyst, S. Dedeire, J. Cosaert, R. Vande Weyer and J. Struyven. Conventional and high-resolution CT in
asymptomatic asbestos-exposed workers. Acta Radiol. 226-9.
53
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=8192957
S. Neri, A. Antonelli, F. Falaschi, P. Boraschi and L. Baschieri. Findings from high resolution computed tomography of the lung and
pleura of symptom free workers exposed to amosite who had normal chest radiographs and pulmonary function tests. Occup
Environ Med. 239-43.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=8199665
A. C. Friedman, S. B. Fiel, M. S. Fisher, P. D. Radecki, A. S. Lev-Toaff and D. F. Caroline. Asbestos-related pleural disease and
asbestosis: a comparison of CT and chest radiography. AJR Am J Roentgenol. 26975.http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=3257311
N. al Jarad, N. Poulakis, M. C. Pearson, M. B. Rubens and R. M. Rudd. Assessment of asbestos-induced pleural disease by computed tomography--correlation with chest radiograph and lung function. Respir Med. 2038. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=1882109
G. F. Rubino, G. Piolatto, M. L. Newhouse, G. Scansetti, G. A. Aresini and R. Murray. Mortality of chrysotile asbestos workers at
the Balangero Mine, Northern Italy. Br J Ind Med. 187-94.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=500777
7.) G. Hillerdal and A. Lindgren. Pleural plaques: correlation of autopsy findings to radiographic findings and occupational history.
Eur J Respir Dis. 315-9.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=7202602
Expert Panel Comments for Questions 16:
?expert. An early investigation Hourihane DOB. Hyaline and calcified pleural plaques as an index
of exposure to asbestos, a
study of radiological and pathological features of 100 cases with a consideration of epidemiology found only 28% of plaques
found at autopsy had identifiable plaques on plain x-ray taken ante-mortem.
According to my own experiences histopathology is more sensitive to detect pleural abnormalities such as small pleural hyaline
plaque and mild pleural fibrosis.
Better with oblique projections along with pa and lateral projections
CT is much better especially for plaques
More sensitive is CT HRCT technology. My interpretation of the question will be interpretation of the sensitivity of conventionally
chest x-ray.
Pleural plaques are clearly visible by conventional radiography especially with oblique views, but in our experience they were well
identified by standard X rays mainly when their global surface was exceeding 100 cm2 at autopsy examination (Rubino et al.
1980). It is possible that at present better results may be achieved.
54
Sensitive but less than CT HRCT assuming chest radiograph does not include CT.
55
First Round Results: Question 17
Asbestos exposure (in the absence of interstitial fibrosis) leads to chronic obstructive lung disease.
N
Median
IQR
P-value
Consensus
Decision
28
3
4
0.0004
Some
2nd Round
Expert Panel Suggested References for Question 17:
R. N. Jones, H. W. Glindmeyer, 3rd and H. Weill. Review of the Kilburn and Warshaw Chest article--airways obstruction from asbestos exposure. Chest. 17279. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=7781375
A. Miller, R. Lilis, J. Godbold, E. Chan and I. J. Selikoff. Relationship of pulmonary function to radiographic interstitial fibrosis in 2,611 long-term asbestos insulators. An assessment of the International Labour Office profusion score. Am Rev Respir Dis. 263-70.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=1736729
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A. D. Oxman, D. C. Muir, H. S. Shannon, S. R. Stock, E. Hnizdo and H. J. Lange. Occupational dust exposure and chronic obstructive pulmonary disease. A
systematic overview of the evidence. Am Rev Respir Dis. 38-48.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=8317812
Expert Panel Comments for Questions 17:
“...leads to obstructive changes on physiologic testing.” This is not the same as COLD Asbestos interacts with smoking to increase the risk of airways obstruction.
Asbestos dust is also a general respiratory irritant that can, especially in combination with tobacco smoke and other pollutants, lead to COLD, but this is not a
specific entity related to asbestos exposure. In addition to cigarette smoking and a combination of cigarette smoking with asbestos exposure, asbestos
exposure alone may induce centrilobular emphysema associated with peri bronchiolar fibrosis.
Obstructive disease in asbestos exposure is due to peribronchiolar fibrosis, which is a form of interstitial fibrosis.
57
First Round Results: Question 18
A decline in small airway flow rates in a non-smoker can be attributed to asbestos exposure.
N
Median
IQR
P-value
Consensus
Decision
26
2
4
0.0017
Some
2nd Round
Expert Panel Suggested References for Question 18:
N. al Jarad, A. R. Gellert and R. M. Rudd. Bronchoalveolar lavage and 99mTc-DTPA clearance as prognostic factors in asbestos workers with and without asbestosis. Respir Med. 365-74. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=8209056
R. Begin, R. Boileau and S. Peloquin. Asbestos exposure, cigarette smoking, and airflow limitation in long-term Canadian chrysotile miners and millers. Am J
Ind Med. 55-66. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=3028138
D. Y. Sue, A. Oren, J. E. Hansen and K. Wasserman. Lung function and exercise performance in smoking and nonsmoking asbestos-exposed workers. Am
Rev Respir Dis. 612-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=4037534
D. McFadden, J. Wright, B. Wiggs and A. Churg. Cigarette smoke increases the penetration of asbestos fibers into airway walls. Am J Pathol. 95-9.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=3963152
S. Neri, P. Boraschi, A. Antonelli, F. Falaschi and L. Baschieri. Pulmonary function, smoking habits, and high resolution computed tomography (HRCT) early
58
abnormalities of lung and pleural fibrosis in shipyard workers exposed to asbestos. Am J Ind Med. 588-95.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=8909607
Expert Panel Comments for Questions 18:
More the combination
With extremely high exposure one could probably list both smoke and
asbestos as causes of airflow obstruction—however, with anything less than high exposure, smoking probably predominates.
59
First Round Results: Question 19
A decline in small airway flow rates in a smoker can be attributed to asbestos exposure.
N
Median
IQR
P-value
Consensus
Decision
26
5
4
0.895
None
2nd Round
Expert Panel Suggested References for Question 19:
J. L. Wright and A. Churg. Severe diffuse small airways abnormalities in long term chrysotile asbestos miners. Br J Ind Med. 556-9.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=2990526
P. Ernst, S. Shapiro, R. E. Dales and M. R. Becklake. Determinants of respiratory symptoms in insulation workers exposed to asbestos and synthetic mineral
fibres. Br J Ind Med. 90-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=3814550
N. al Jarad, A. R. Gellert and R. M. Rudd. Bronchoalveolar lavage and 99mTc-DTPA clearance as prognostic factors in asbestos workers with and without as-
60
bestosis. Respir Med. 365-74. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=8209056
X. R. Wang, E. Yano, K. Nonaka, M. Wang and Z. Wang. Pulmonary function of nonsmoking female asbestos workers without radiographic signs of asbestosis.
Arch Environ Health. 292-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=9709994
P. T. Macklem and J. Mead. Resistance of central and peripheral airways measured by a retrograde catheter. J Appl Physiol. 395-401.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=4960137
A. Miller. Pulmonary function in asbestosis and asbestos-related pleural disease. Environ Res. 1-18.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=8472663
A. Miller, R. Lilis, J. Godbold, E. Chan and I. J. Selikoff. Relationship of pulmonary function to radiographic interstitial fibrosis in 2,611 long-term asbestos insulators. An assessment of the International Labour Office profusion score. Am Rev Respir Dis. 263-70.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=1736729
Expert Panel Comments for Questions 19:
?expert. This is a complex question again with no simple yes no answer.
Asbestos exposure may in the initial phase lead to peribronchiolar inflammation and fibrosis.
Controversial area where scientific data are insufficient to assess.
Depending on other clinical info, high exposure and no confounders needed to make this association. Other fume dust exposures are serious confounders in
this setting. How do you define small airway flow rates? If there is a reliable and sufficient history of exposure and other causes of obstructive disease
can be eliminated. If the asbestosis is severe, also obstructive airway diseases can be found.
61
First Round Results: Question 20
A history of asbestos exposure is highly likely to be the cause of interstitial fibrosis in the absence of other explanations.
N
Median
IQR
P-value
Consensus
Decision
32
7
4.5
0.0011
None
2nd Round
Expert Panel Suggested References for Question 20:
1.) E. A. Gaensler, P. J. Jederlinic and A. Churg. Idiopathic pulmonary fibrosis in asbestos-exposed workers. Am Rev Respir Dis.
689-96. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=1892312
62
Expert Panel Comments for Questions 20:
Other etiological factors such as inflammation, congestion, sarcoidosis, and exposure to other type of dust should be excluded.
A history of exposure is not without details, such as intensity and duration and latency, which must be considered when determining whether it connotes a substantial present risk of asbestosis.
As a clinical diagnosis: yes. As a pathological diagnosis: obviously asbestos fibres and bodies must be in evidence.
It depends on intensity of cumulative exposure to asbestos ++++ Depends on history of exposure and clinical course. Also, biopsy
permits distinction between idiopathic pulmonary fibrosis and asbestosis, even if there is a history of exposure. It depends on
the intensity of exposure, if the fibrosis has a radiologically typical appearance. It depends entirely on the simultaneous existence of a history of adequate exposure or demonstration in tissue of that exposure. It is a probabilistic question. As far as I
know, this probability is very high. In asbestos workers the proportion of diffuse pulmonary fibrosis not attributable to asbestos
has been estimated as high as 5% even though it is likely to rise as the risk of asbestosis diminishes
See response to Question 12. The probability is linked with the intensity of exposure.
This really requires knowledge of specific occupation and years of exposure (i.e. high total exposure). As stated the proposition is
too vague and these days, is statistically probably unlikely.
63
First Round Results: Question 21
Asbestos exposure causes other neoplasms in addition to lung cancer and mesothelioma.
N
Median
IQR
P-value
Consensus
Decision
33
7
3
0.014
Good
Accept
Expert Panel Suggested References for Question 21:
Asbestos, asbestosis, and cancer: the Helsinki criteria for diagnosis and attribution.Scand J Work Environ Health.23,3116. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=9322824
N. Becker, J. Berger and U. Bolm-Audorff.Asbestos exposure and malignant lymphomas--a review of the epidemiological literature.Int Arch Occup Environ Health.74,459-69.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=11697448
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G. Berry, M. L. Newhouse and J. C. Wagner.Mortality from all cancers of asbestos factory workers in east London 1933-80.Occup
Environ Med.57,7825. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=11024203
C. Bianchi, L. Ramani and T. Bianchi.Concurrent malignant mesothelioma of the pleura and hepatocellular carcinoma in the same
patient: a report of five cases.Ind Health.40,383-7.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=12502242
K. Browne and J. B. Gee.Asbestos exposure and laryngeal cancer.Ann Occup Hyg.44,23950. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=10831728
P. Froom, N. Lahat, E. Kristal-Boneh, C. Cohen, Y. Lerman and J. Ribak.Circulating natural killer cells in retired asbestos cement
workers.J Occup Environ Med.42,19-24.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=10652684
M. Goodman, R. W. Morgan, R. Ray, C. D. Malloy and K. Zhao.Cancer in asbestos-exposed occupational cohorts: a metaanalysis.Cancer Causes Control.10,453-65.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=10530617
F. Mollo, A. Andrion, A. Colombo, N. Segnan and E. Pira.Pleural plaques and risk of cancer in Turin, northwestern Italy. An autopsy study.Cancer.54,141822. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=6467163
B. W. Robinson and A. W. Musk.Benign asbestos pleural effusion: diagnosis and course.Thorax.36,896900. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=7336367
D. Sali and P. Boffetta.Kidney cancer and occupational exposure to asbestos: a meta-analysis of occupational cohort studies.Cancer Causes Control.11,3747. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=10680728
G. F. Rubino, G. Piolatto, M. L. Newhouse, G. Scansetti, G. A. Aresini and R. Murray.Mortality of chrysotile asbestos workers at
the Balangero Mine, Northern Italy.Br J Ind Med.36,187-94.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=500777
V. L. Roggli, S. D. Greenberg, J. L. McLarty, G. A. Hurst, C. G. Spivey and L. R. Heiger.Asbestos body content of the larnyx in asbestos workers. A study of five cases.Arch Otolaryngol.106,533-5.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=7406758
I. J. Selikoff, E. C. Hammond and H. Seidman.Mortality experience of insulation workers in the United States and Canada, 1943-1976.Ann N Y Acad Sci.330,91-116.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=294225
14) I. J. Selikoff and H. Seidman.Asbestos-associated deaths among insulation workers in the United States and Canada, 19671987.Ann N Y Acad Sci.643,114. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=1809121
65
Expert Panel Comments for Questions 21:
Laryngeal cancer is in dispute. No others are attributable with reasonable certainty.
Larynx ++ Doll and Peto 1985 is the definitive reference showing that any other associations are due to the misclassification of
other tumors (principally lung cancer). There are many others. There is still in my view some question about laryngeal cancer, although it is fair to say there is a consensus that the strong confounders of alcohol and smoking make it difficult to assess. Epidemiologically, there are evidences that in addition to lung cancer and malignant mesothelioma, asbestos exposure
causes cancer in oropharynx, kidney, pancreas, colon and gallbladder.
In my opinion the cancer most likely attributable to asbestos, in addition to lung cancer and mesothelioma is the larynx cancer. In
our region (Piedmont, northwestern Italy) rather suggestive epidemiological and pathological data have been reported. In the
seventies, incidence of the larynx cancer among males in the area of the Balangero chrysotile mine (in province of Turin) was
as high as 51 5 100 000 year, whereas in the Turin province it was 12 6 100 000 year. Furthermore, a study on mortality of
workers at that mine showed a significant excess of laryngeal cancer (Rubino et al. 1979). An autopsy survey on general
hospital population (Mollo et al 1984) found a strong association of the larynx cancer with pleural plaques. The acknowledgment of the association with asbestos exposure is not easy or it is disproved mainly due to the confounding association with
smoking and alcohol (Browne 2000). Nevertheless, asbestos bodies have been found in the laryngeal mucosa of asbestos
workers (Roggli et al). In our laboratory an investigation in progress demonstrates asbestos bodies in the expectoration of
some subjects with larynx cancer. Further work is needed.
Laryngeal carcinoma and carcinoma of the esophagus and oropharynx can be contributed to by asbestos.
Many series show increased risk for esophageal colonic etc.
66
First Round Results: Question 22
Bronchoalveolar lavage (BAL) is a technique for accurately establishing lung fiber burden .
N
Median
IQR
P-value
Consensus
Decision
29
4
5
0.5444
None
2nd Round
Expert Panel Suggested References for Question 22:
A. Xaubet, R. Rodriguez-Roisin, J. A. Bombi, A. Marin, J. Roca and A. Agusti-Vidal.Correlation of bronchoalveolar lavage and clinical and functional findings in asbestosis.Am Rev Respir Dis.133,848
54. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=3706896
P. Sebastien, B. Armstrong, G. Monchaux and J. Bignon.Asbestos bodies in bronchoalveolar lavage fluid and in lung parenchyma.Am Rev Respir Dis.137,758. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=3337472
67
D. A. Schwartz, J. R. Galvin, S. J. Yagla, S. B. Speakman, J. A. Merchant and G. W. Hunninghake.Restrictive lung function and
asbestos-induced pleural fibrosis. A quantitative approach.J Clin Invest.91,268592. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=8514875
A. R. Gellert, J. Y. Kitajewska, S. Uthayakumar, J. B. Kirkham and R. M. Rudd.Asbestos fibres in bronchoalveolar lavage fluid from
asbestos workers: examination by electron microscopy.Br J Ind Med.43,1706. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=3947579
M. E. Turner-Warwick and P. L. Haslam.Clinical applications of bronchoalveolar lavage: an interim view.Br J Dis Chest.80,10521. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=3524646
P. De Vuyst, P. Dumortier, E. Moulin, N. Yourassowsky, P. Roomans, P. de Francquen and J. C. Yernault.Asbestos bodies in
bronchoalveolar lavage reflect lung asbestos body concentration.Eur Respir J.1,3627. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=3396675
P. Sartorelli, G. Scancarello, R. Romeo, G. Marciano, P. Rottoli, G. Arcangeli and S. Palmi.Asbestos exposure assessment by
mineralogical analysis of bronchoalveolar lavage fluid.J Occup Environ Med.43,87281. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=11665456
R. F. Dodson, J. G. Garcia, M. O'Sullivan, C. Corn, J. L. Levin, D. E. Griffith and R. S. Kronenberg.The usefulness of bronchoalveolar lavage in identifying past occupational exposure to asbestos: a light and electron microscopy study.Am J Ind
Med.19,61928. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=1647134
Asbestos, asbestosis, and cancer: the Helsinki criteria for diagnosis and attribution.Scand J Work Environ Health.23,3116. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=9322824
R. G. Crystal, J. E. Gadek, V. J. Ferrans, J. D. Fulmer, B. R. Line and G. W. Hunninghake.Interstitial lung disease: current concepts of pathogenesis, staging and therapy.Am J Med.70,54268. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=7011012
A. A. Hayes, A. H. Rose, A. W. Musk and B. W. Robinson.Neutrophil chemotactic factor release and neutrophil alveolitis in asbestos-exposed individuals.Chest.94,5215. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=3044701
B. W. Robinson, A. James, A. H. Rose, G. F. Sterrett and A. W. Musk.Bronchoalveolar lavage sampling of airway and alveolar
cells.Br J Dis Chest.82,4555. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=3166918
Expert Panel Comments for Questions 22:
68
Asbestos bodies in BAL are better markers of amphibole exposure than of chrysotile exposure. BAL can give an approximation of
the lung fiber burden which is not unreasonable. However, it can give negative results in some patients with substantial lung
fiber burden. In case the acute lung fiber burden. Deposition, but not retention. The mineralogic analysis of BAL for demonstration of asbestos fibers has been considered as a reliable biomarker of past asbestos exposure (Sartorelli et al. 2001). In
fact, the sensitivity of the elecron microscopic examination is higher than that attained by the search for asbestos bodies in
light microscopy. Nevertheless, the latter method is rather more standardized and many authors stated that a concentration of
1 asbestos body ml of BAL may reasonably be considered as an equivalent of the finding of 1 000 asbestos bodies per gram
of dry lung tissue that is of the concentration suggesting an occupational exposure.
69
First Round Results: Question 23
Identification of asbestos fibers in lung specimens is integral to the histologic diagnosis of asbestosis.
N
Median
IQR
P-value
Consensus
Decision
31
8
6
0.006
None
2nd Round
Expert Panel Suggested References for Question 23:
J. E. Craighead, J. L. Abraham, A. Churg, F. H. Green, J. Kleinerman, P. C. Pratt, T. A. Seemayer, V. Vallyathan and H. Weill.The
pathology of asbestos-associated diseases of the lungs and pleural cavities: diagnostic criteria and proposed grading schema. Report of the Pneumoconiosis Committee of the College of American Pathologists and the National Institute for Occupa-
70
tional Safety and Health.Arch Pathol Lab Med.106,54496. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=6897166
Asbestos, asbestosis, and cancer: the Helsinki criteria for diagnosis and attribution.Scand J Work Environ Health.23,3116. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=9322824
K. Rodelsperger and H. J. Woitowitz.Airborne fibre concentrations and lung burden compared to the tumour response in rats and
humans exposed to asbestos.Ann Occup Hyg.39,71525. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=8526402
Expert Panel Comments for Questions 23:
By light microscopy it is asbestos bodies not fibers that are found. The criteria are considered overly liberal by pathologists in the
United Kingdom (For example Commins B.) Id of fibers requires electron microscopy mineralogic analysis and is affected by
sampling passage of time etc. In my opinion the electron microscopy for identification of uncoated asbestos fibers is not indispensable when interstitial fibrosis and typical asbestos bodies are found in light microscopy. Otherwise (always in presence of interstitial fibrosis) an electron microscopic concentration of asbestos fibers in the range recorded in the same laboratory for the histologic asbestosis can be adequate.
It is particularly useful in asbestosis cases caused by short thin asbestos fibers (which are not easily identified by light microscopy)
and chrysotile fibers (unlike amphibole fibers, they are poorly transformed into asbestos bodies in the lung).
Some problems occur using these criteria, but not more than would occur using only identification by the use of lung fibres rather
than bodies. This has to be asbestos bodies visible in histologic sections, not just asbestos fibers (which can’t be seen by
light microscopy) found by some digestion technique. Everyone has asbestos fibers in their lungs! The definition of asbestosis
by histologic examination requires (1) a proper pattern of interstitial fibrosis (2) one or more asbestos bodies. With the exception of chrysotile and short amphiboles which can clear over time. As written-a poor question-by which method-certainly not
by light microscopy-but transmission em would be good.
71
72
First Round Results: Question 24
CT scanning of the chest should be used in screening populations at risk for asbestos-related diseases
N
Median
IQR
P-value
Consensus
Decision
29
5
6
0.8621
None
2nd Round
Expert Panel Suggested References for Question 24:
D. R. Aberle.High-resolution computed tomography of asbestos-related diseases.Semin Roentgenol.26,118-31.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=1853209
S. Lozewicz, R. H. Reznek, M. Herdman, J. E. Dacie, A. McLean and R. J. Davies.Role of computed tomography in evaluating asbestos related lung disease.Br J Ind Med.46,777-81.
73
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=2590642
Expert Panel Comments for Questions 24:
The criteria for early “asbestosis” by CT are controversial. Screening for benign pleural disease provides no obvious benefits.
Screening for lung cancer (whether one decides it requires fibrosis or not) will depend on whether spiral CT proves to be a
useful tool for lung cancer screening. CT not indicated to diagnose early lung fibrosis. Highly debated regarding cost sensitivity and especially specificity. What do you do with all the cases where small nodules are detected? Surgery on all? With what
yield of carcinoma? At what harm to those with benign nodules? I would have a greater degree of agreement with this were it
not so broadly stated. What exactly is meant by “populations at risk”? One has to take into account amount of exposure fiber
type age etc. For example it would be the height of irresponsibility to irradiate populations with low-level exposures to
chrysotile asbestos.
It depends on the reason for screening (if the reason is to pay everyone who has a pleural plaque which was the case in Sweden
in the 1980s, it could be of value) but not for detecting cancer. Only in randomized trials. No proof of any medical benefit.
Screening is by definition for symptom-free people. It also morally requires that a positive result may incur some benefit. The
only benefit in the past was from removal from further exposure. Since screening with such
an expensive procedure with its own possible health cost through the radiation exposure involved (>100 times the dose from a
plain chest film). Since no significant exposure to amphibole should be taking place and no unsustainable exposure to chrysotile.
There is no longer any place for such screening.
There is more danger from radiation than there is from asbestos now that the level of asbestos is less than 0.5 fibres cc. Though
more sensitive, I do not think that we in a screening will miss many serious cases by conventional chest x-rays.
74
75
First Round Results: Question 25
There should be initiatives to develop protocols to attempt therapy for asbestosis.
N
Median
IQR
P-value
Consensus
Decision
28
5.5
5
0.3682
None
2nd Round
No expert panel references for question 25.
Expert Panel Comments for Questions 25:
? expert. There should certainly be continuing research for progressive interstitial lung disease from whatever cause. The day for
specific treatment for asbestosis is past except perhaps in China, where effort should be into prevention. Asbestosis is in de-
76
cline in most of Europe and North America. Keep the TLV below 0.5 fibres cc and thre should be no asbestosis. At what
stage; with what? Don’t feel strongly about this one. Cases with progressive life threatening asbestosis are becoming quite rare. I think that prevention is the only choice. Most asbestosis diagnosed these days is mild and probably will not progress. Exceptions do occur but are rare. Given the failure to find a therapy for idiopathic pulmonary fibrosis, which is the closest approximation of severe
asbestosis looking for therapies for asbestosis is probably a waste of time. Where are your cases?
77
Round 2 questions:
1. Workers with asbestos-induced pleural abnormalities are at increased risk for lung cancer compared to workers with similar exposures without these pleural abnormalities.
2. From the 1986 ATS statement: With a reliable history of exposure and an appropriate time interval between exposure and detection, please rate your agreement with the following statement. In the absence of pathologic examination of lung tissue, we regard the
following clinical criteria to be of recognized value in the diagnosis of asbestosis: 'Chest roentgenographic evidence of 's', 't', 'u' small
irregular opacifications of a profusion of 1/1 or greater.
3. With a reliable history of exposure and an appropriate time interval between exposure and detection, please rate your agreement
with the following statement. In the absence of pathologic examination of lung tissue, chest radiographic changes of profusion 1/1
small irregular opacities or greater or high resolution CT scanning images in the prone position at lung bases indicating interstitial fibrosis are of value in detecting asbestosis. (New Question)
4. With a reliable history of exposure and an appropriate time interval between exposure and detection, please rate your agreement
with the following statement. In the absence of pathologic examination of lung tissue, chest radiographic changes of a profusion level
1/0 small irregular opacities are a good screening tool, but lack specificity for an accurate diagnosis of asbestosis. High resolution CT
scanning should be performed to increase the specificity of these chest radiographic findings -(New Question)
5. From the 1986 ATS statement: With a reliable history of exposure and an appropriate time interval between exposure and detection, please rate your agreement with the following statement. In the absence of pathologic examination of lung tissue, we regard the
following clinical criteria to be of recognized value in the diagnosis of asbestosis: 'A restrictive pattern of lungimpairment with a forced
vital capacity below the lower limit of normal.
6. From the 1986 ATS statement: With a reliable history of exposure and an appropriate time interval between exposure and detection, please rate your agreement with the following statement. In the absence of pathologic examination of lung tissue, we regard the
following clinical criteria to be of recognized value in the diagnosis of asbestosis: A diffusing capacity below the lower limit of normal.
7. From the 1986 ATS statement: With a reliable history of exposure and an appropriate time interval between exposure and detection, please rate your agreement with the following statement. In the absence of pathologic examination of lung tissue, we regard the
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following clinical criteria to be of recognized value in the diagnosis of asbestosis: Bilateral late or pan inspiratory crackles at the posterior lung bases not cleared by cough.
8. A heavy asbestos exposure (sufficient to cause asbestosis) with sufficient latency is necessary to establish asbestos exposure as
causative for lung cancer. (Clarified from Round 1 version)
9. The extent of asbestos exposure correlates with the presence and extent of pleural abnormalities.
10. A reasonable scheme can be developed to apportion the individual attributability of smoking and asbestos exposure in a cigarette
smoking asbestos-exposed worker with lung cancer .
11. In an asbestos exposed worker without asbestosis and with lung cancer, the recognition of asbestos is among co-workers with
similar exposures is sufficient to attribute the workers lung cancer to asbestos exposure.(New Question)
12. Chest radiographs are a sensitive method to diagnose interstitial disease attributable to asbestos exposure.
13. Compared to the chest radiograph, high resolution CT scan is a more sensitive method for detecting asbestos-related pleural and
parenchymal disease (New Question).
14. Chest radiographs are a sensitive method to measure pleural abnormalities attributable to asbestos exposure.
15. Asbestos exposure (in the absence of interstitial fibrosis) leads to chronic obstructive lung disease.
16. A decline in small airway flow rates in a non-smoker can be attributed to asbestos exposure.
17. A decline in small airway flow rates in a smoker can be attributed to asbestos exposure.
18. A history of asbestos exposure of sufficient duration, dose and latency is likely the cause of interstitial fibrosis in the absence of
other explanations (Clarified from Round 1 version).
19. Bronchoalveolar lavage (BAL) is a technique for accurately establishing lung fiber burden.
20. Identification of asbestos fibers in lung specimens is integral to the histologic diagnosis of asbestosis.
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21. CT scanning of the chest should be used to screen populations at risk for asbestos-related diseases.
22. There should be initiatives to develop protocols to attempt therapy for asbestosis.
23. Workers who have significant asbestos exposure (but who do not have asbestosis) are at increased risk of bronchogenic carcinoma. (New Question)
24. Non-smoking workers with significant asbestos exposure (without asbestosis) have at least double the risk of bronchogenic carcinoma compared to non-smoking workers with low level exposure. (New Question)
25. Workers who smoke cigarettes and have significant asbestos exposure (without asbestosis) have at least double the risk of bronchogenic carcinoma compared to non-exposed smokers-(New Question)
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The third and final round of the Delphi Study of Asbestos was conducted through email. Below are the final thirteen questions that had not yet reached consensus. As in the first two rounds, answers were based on a scale of
0-10.
Round 3 questions
1. Workers with asbestos-induced pleural abnormalities are at increased risk for lung cancer compared to workers with
similar exposures without these pleural abnormalities.
2. A heavy asbestos exposure (sufficent to cause asbestosis) with sufficient latency is necessary to establish asbestos
exposure as causative for lung cancer. (This question was clarified from round one.)
3. The extent of asbestos exposure correlates with th presence and extent of pleural abnormalities.
4. A reasonable scheme can be developed to apportion the individual attributability of smoking and asbestos exposure in
a cigarette smoking asbestos-exposed worker with lung cancer.
5. In an asbestos exposed worker without asbestosis and with lung cancer, the recognition of asbestosis among coworkers with similar exposures is sufficient to attribute the worker's lung cancer to asbestos exposure. (This question was
added in round two.)
6. Chest radiographs are a sensitive method to diagnose interstitial disease attributable to asbestos exposure.
7. Chest radiographs are a sensitive method to measure pleural abnormalities attributable to asbestos exposure.
8. A decline in small airway flow rates in a non-smoker can be attibuted to asbestos exposure.
9. Bronchoalveolar lavage (BAL) is a technique for accurately establishing lung fiber burden.
10. CT scanning of the chest should be used to screen populations at risk for asbestos-related diseases.
11. There should be initiatives to develop protocols to attempt therapy for asbestosis.
12. Non-smoking workers with significant asbestos exposure (without asbestosis) have at least double the risk of bronchogenic carcinoma compared to non-smoking workers with low level exposure (This question was added in round two).
13. Workers who smoke cigarettes and have significant asbestos exposure (without asbestosis) have at least double the
risk of bronchogenic carcinoma to non-exposed smokers. (This question was added in round two).
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