Methodology for Conducting Risk Assessments at Asbestos Superfund Sites Part1:protocol Interim Version


EPA Contract No. 68-W9-0059
Work Assignment No. 59-06-D800
FINAL
METHODOLOGY FOR CONDUCTING RISK
ASSESSMENTS AT ASBESTOS SUPERFUND SITES
PART 1: PROTOCOL
INTERIM VERSION
Prepared for:
Kent Kitchingman
U.S. Environmental Protection Agency
Region 9
75 Hawthorne
San Francisco, California 94105
Prepared by:
D. Wayne Berman
Aeolus, Inc.
751 Taft St
Albany, CA 94706
and
Kenny Crump
ICF Kaiser Engineers, Inc.
602 E. Georgia Ave
Ruston, LA 71270
February 15,1999

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ACKNOWLEDGMENTS
This protocol was prepared by D. Wayne Berman of Aeolus, Inc., Albany, California
and Kenny Crump, ICF Kaiser Engineers, Inc., Ruston, Louisiana under USEPA
Contract No. 68-W9-0059, Work Assignment No. 59-06-D800 for the U.S.
Environmental Protection Agency (USEPA), Office of Emergency and Remedial
Response (OERR). The USEPA Task Manager for this project is Kent Kitchingman.
The USEPA project officer is Linda Ma.
This work could not have been completed without the assistance of John Davis and
Alan Jones (Institute of Occupational Medicine, Edinburgh, United Kingdom) and Eric
Chatfield (Chatfield Technical Consulting Limited, Mississauga, Ontario, Canada) and
their collaboration in several supporting studies. Support for data manipulation and
analysis were also provided by Chris Rambin and Tammie Covington of ICF Kaiser,
Ruston.
We would also like to thank Jean Chesson, John Dement, and Phil Cook for their
valuable and stimulating discussions on this work.
i

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DISCLAIMER
This report was prepared under contract to the U. S.
Environmental Protection Agency. Such support, however,
does not signify that the contents necessarily reflect the
views and policies of the U. S. Environmental Protection
Agency, nor does the mention of trade or commercial
products constitute endorsement of recommendations for
use.
ii

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Table of Contents
1.	INTRODUCTION	1-1
2.	PROTOCOL FOR ASSESSING ASBESTOS-RELATED RISKS	2-1
2.1	ESTIMATING RISKS USING RISK MODELS	2-1
2.1.1	Lung Cancer	2-2
2.1.2	Mesothelioma	2-4
2.2	ESTIMATING RISKS USING THE RISK TABLE	2-5
2.3	REQUIREMENTS FOR ASBESTOS MEASUREMENTS	2-8
2.3.1	Requirements for Measuring Airborne Asbestos
To Support Risk Assessment	2-8
2.3.2	Requirements for Estimating Airborne Exposure
from Soil or Bulk Measurements Combined with
Release and Transport Modeling	2-10
3.	REFERENCES	3-1
iii

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List of Tables
TABLE 2-1: RECOMMENDED RISK COEFFICIENTS
TABLE 2-2: ADDITIONAL RISK PER ONE HUNDRED THOUSAND
PERSONS FROM LIFETIME CONTINUOUS EXPOSURE
TO 0.0005 TEM f/cc LONGER THAN 5.0 pm AND THINNER
THAN 0.5 pm

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1.0 INTRODUCTION
This report presents a protocol for assessing potential human-health risks associated
with exposure to airborne asbestos, It is designed specifically for use in performing
risk assessments at Superfund sites; although it may be applicable to a broad range of
situations.
The protocol presented in this document was developed based on a detailed, critical
review of the literature and additional studies conducted to fill important knowledge
gaps in the record. Considerations addressed during the development of this protocol
are documented in Part 2 of this report (the Technical Background Document), under
separate cover.
In this protocol, the risk associated with asbestos exposure can be estimated using
either of two procedures. The first procedure, which is preferred when sufficient data
exist to support the required inputs, is to apply an appropriate risk model (selected from
among those presented, based on the end point health effect of interest) using case-
specific data as inputs. The models, the types of data required to support the models,
and the procedures to use for evaluating each model are defined within this protocol.
The second approach, which can be used when supporting data are limited, is to
estimate risk by extrapolation from a risk table. Both the table and instructions for its
use are provided. Limits to the validity of this approach are also discussed, so that the
user can evaluate the confidence that may be placed in risk estimates derived using
this latter technique.
This protocol also includes guidelines for collection and analysis of samples to be used
to support estimation of asbestos exposure. Estimates of asbestos exposure in a
particular setting can vary by orders of magnitude depending on the method(s)
employed to collect, prepare, and analyze samples and to report results (Berman and
Chatfield 1990). Therefore, both the method(s) to be used to develop exposure data
and the exposure index to be used to report results are specified in this protocol.
Correspondingly, the risk models and the risk table provided in the protocol have been
adapted for use with the specified exposure index.
Importantly, if the risk models or risk table presented in this document are
applied to exposure estimates derived using methods different from those
defined herein, the resulting risk estimates may not be valid.
The models employed for assessing asbestos-related risks in this protocol are adapted
from those proposed in the Airborne Asbestos Health Assessment Update (U.S. EPA
1986). The approach has been modified, however, to better account for the limitations
imposed by asbestos analytical techniques. Studies published since the appearance of
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the Update have also provided new insights into the relationship between asbestos
measurement and biological activity. Consequently, a review and evaluation of the
new studies and key studies published earlier are presented in the companion
Technical Background Document (Part 2 of this report).
The purpose for documenting the data and assumptions used to develop this protocol
is to facilitate critical evaluation while highlighting needs for additional research. Thus,
considerations addressed in the Technical Background Document that have been
documented in the literature are cited accordingly. Considerations that remain largely
a subject of conjecture are also noted. Due to the current level of interest and activity
provoked by asbestos, further improvements in asbestos sampling, analysis, and
evaluation are anticipated.
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2.0 PROTOCOL FOR ASSESSING ASBESTOS-RELATED RISKS
Exposure to asbestos dusts has been linked to several adverse health effects including
primarily asbestosis, lung cancer, and mesothelioma (U.S. EPA 1986). Asbestosis, a
chronic, degenerative lung disease, has been documented among asbestos workers
from a wide variety of industries. However, the disease is expected to be associated
only with the higher levels of exposure commonly found in workplace settings and is
not expected to contribute substantially to potential risks associated with environmental
asbestos exposure. The majority of evidence indicates that lung-cancer and
mesothelioma are the most important sources of risk associated with exposure to low
levels of asbestos.
Gastrointestinal cancers and cancers"of other organs (e:g; larynx, kidney, and ovaries)
have also been linked with asbestos exposures in some studies; However, such -
associations are not as compelling as those for the primary health effects listed above
and the potential risks from asbestos exposures associated with these other cancers
are much lower (U.S. EPA 1986). Consequently, this protocol is focused on risks
associated only with the induction of lung cancer and mesothelioma.
Because the hazard from asbestos exposure derives primarily from inhalation, the
protocol provided in this document is designed specifically to be applied to estimates of
airborne asbestos concentrations to which populations of interest are potentially
exposed. • Such estimates can be derived either by extrapolation from a well-designed
air sampling array or from release and transport modeling of asbestos concentrations
measured in representative samples of soils or bulk material, which may serve as
sources of airborne asbestos.
Depending on the specific scenario of interest, either estimates of long-term average
exposure concentrations or detailed estimates of time-dependent exposure may be
required. The latter can be used as inputs to the risk models described in this
document (Section 2.1) to assess risk. Risks associated with time-averaged exposure
can be derived using the risk table (Section 2.2).
As indicated previously, exposure estimates to be used with this protocol to assess risk
need to be representative of the exposure settings of interest and need to be
expressed in terms of a specific exposure index. Requirements for developing
exposure estimates are therefore highlighted in Section 2.3.
2.1 ESTIMATING RISK USING RISK MODELS
Models to be used for estimating lung cancer and mesothelioma risks are presented
below along with a description of the types of data required as inputs and a procedure
for evaluating the models.
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2.1.1 Lung Cancer
The Airborne Health Effects Assessment Update (U.S. EPA 1986) utilizes a model for
lung cancer in which the asbestos-related age-specific mortality from lung cancer at
age t is proportional to cumulative asbestos exposure at time t-10 years
(i.e., cumulative exposure lagged 10 years), multiplied by the age- and calendar year-
specific background mortality rate of lung cancer in the absence of asbestos exposure
(Equation 6.1 in Part 2 of this document). The same model is employed here except
that it has been modified to incorporate the recommended exposure index, Copt, rather
than the more traditional CpcMl which was employed in the original model.
In the lung cancer model, a linear relationship between cumulative dose and response
has been assumed based on the ten epidemiology studies identified (in the 1986 EPA
document) as containing sufficient information to establish a dose/response curve for
asbestos induced lung cancer:
lL= lE[1+KLCoptd(M0>]	(2.1)
where:
V is the overall lung cancer- mortality (expected lung cancer deaths per year
per person) adjusted for age and calendar year;
1E" is the corresponding lung cancer mortality in a population not exposed to
asbestos;	. ..
"Copt" is the concentration of asbestos expressed as the weighted sum of two
size categories of asbestos structures defined in Equation 2.2;
"t" is age;
"d(,.10)" is the duration of exposure up to age t, excluding the most recent 10
years; and
"Kl" is the proportionality constant between dose and response. This is the
risk coefficient that represents the potency of asbestos. Appropriate
values shall be selected as described below.
The above model is a relative risk model in that it assumes that the excess mortality of
lung cancer from asbestos is proportional to the mortality in an unexposed population.
Since smokers have a much higher mortality from lung cancer, if smoking-specific
mortality rates are applied, the model predicts a higher excess mortality from asbestos-
related lung cancer in smokers than in non-smokers. This is consistent with the
multiplicative relationships between smoking and asbestos that have been observed in
epidemiological studies. Note that the in the model pertains to an occupational
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pattern of exposure (e.g., 8 hours per day, 240 days per year) and must be modified
before application to environmental exposure patterns.
To apply the model described in Equation 2.1 for estimating lung cancer risks to a
specific population, the following data are required:
•	annualized (age-specific) smoking- and sex-specific mortality rates (both for total
mortality and mortality from respiratory cancer) for the specific population of
interest;		
•	time-dependent (rather than time-averaged) exposure estimates that can be
integrated to produce annualized (time-dependent) cumulative exposure; and
•	an appropriate value to use for the risk coefficient, KL.
As applied in this protocol, all exposure estimates to be used as inputs to the above
model must be expressed specifically in terms of Copt, which is the concentration of
asbestos expressed as a weighted sum of two size categories of asbestos structures
that are separately enumerated during analysis:
Copt = 0.003CS + 0.997Cl	(2.2)
where:
"Cs" is the concentration of asbestos structures between 5 and 10 pm in length
that are also thinner than 0.5 pm; and
UCL" is the concentration of asbestos structures longer than 10 pm that are
also thinner than 0.5 pm.
IMPORTANTLY, THE CONCENTRATIONS OF STRUCTURES REQUIRED FOR
DERIVING COPT MUST BE OBTAINED FROM APPROPRIATE ANALYSES OF
ASBESTOS SAMPLES OR THE RESULTING RISK ESTIMATES DERIVED USING
THIS PROTOCOL MAY NQI BE VALID. THIS PROTOCOL SHOULD NOT BE
APPLIED TO ASBESTOS MEASUREMENTS OBTAINED USING METHODS OTHER
THAN THOSE SPECIFIED IN SECTION 2.3.
The vaiue to be employed for in the above model shall be selected from the
following table, depending on whether the type of asbestos to which the population of
interest is exposed is chrysotile (serpentine asbestos) or one of the asbestiform
amphiboles (i.e. crocidolite, amosite, anthophyllite, tremolite, or actinolite):
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TABLE 2-1: RECOMMENDED RISK COEFFICIENTS1
Fiber Type	Kt Kw
	(x108)
Chrysotile	0.05 0.5
Amphiboles 0.3 50
1 Coefficients derived as described in Chapter 6 of the
Technical Background Document (Part 2 of this report).
IMPORTANTLY, THE RISK COEFFICIENTS PROVIDED IN TABLE 2-1 ARE ONLY
VALID WHEN USED IN CONJUNCTION WITH ASBESTOS EXPOSURE ESTIMATES
EXPRESSED AS DEFINED BY C0PT (EQUATION 2.2).
The recommended procedure for incorporating the data listed above and applying the
lung cancer model is described in Appendix A, which describes a lifetable analysis.
2.1.2 Mesothelioma
The model used here to describe mesothelioma mortality in relation to asbestos
exposure is the same model proposed in the Airborne Health Assessment Update
(U.S. EPA 1986 and Equation 6.7 of Part 2 of this report) except that it has been
modified to incorporate the recommended exposure index, Copt, in an identical manner
to that described for the lung cancer model (Section 2.1.1). This model assumes that
asbestos-induced mesothelioma mortality is independent of age at first exposure and
increases according to a power of time from onset of exposure, as described in the
following relationship:
Im = K« C^t(T-10}3 - (T-10-d)3] for T > 10+d (2.3)
= K^CopttT-IO)3	for 10+d > T > 10
= 0	for 10 > T
where:
"lM" is the mesothelioma mortality observed at'T* years from onset of
exposure to asbestos for duration "d" and concentration Copt of
fibrous asbestos structures;
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"Km" is the risk cofficient (proportionality constant between dose and
response) for mesothelioma and represents the potency of
asbestos;
T is the time since first exposure; and
all other factors have been previously defined.
This is an absolute risk model, which means thatthe incidence of mesothelioma
predicted by the model does not depend on the background incidence of the disease.
Background mesothelioma cases are rare in the general population in any case. This
model also assumes that mesothelioma risk from exposure in any increment of time
increases forever, even after exposure ceases. The validity and implications of this
latter assumption are addressed in Section 6.2.2 of Part 2 of this report.
To apply the model described in Equation 2.3 for estimating mesothelioma risks to a
specific population, the following data are required:
•	annualized (age-specific) smoking- and sex-specific total mortality rates for the
specific population of interest;
•	time-dependent (rather than time-averaged) exposure estimates that can be
integrated to produce annualized (time-dependent) cumulative exposure; and
•	an appropriate value to use for the risk coefficient, K„.
AS FOR THE LUNG CANCER MODEL DESCRIBED ABOVE, ALL EXPOSURE
ESTIMATES TO BE USED AS INPUTS TO THE MESOTHELIOMA MODEL MUST BE
EXPRESSED SPECIFICALLY IN TERMS OF C^ AS DEFINED IN EQUATION 2.2
AND SUCH ESTIMATES MUST BE DERIVED FROM MEASUREMENTS OBTAINED
AS DESCRIBED IN SECTION 2.3 OR RISK ESTIMATES MAY NOT BE VALID.
The value to be employed for Ku in Equation 2.3 shall be selected from the values
presented in Table 2-1, based on the type of asbestos being considered (i.e. chrysotile
or one of the amphiboles).
Procedures for evaluating Equation 2.3 are presented in Appendix A, which describes
a lifetable analysis.
2.2 ESTIMATING RISKS USING THE RISK TABLE
Because sufficient data will rarely be available to apply the models presented in
Section 2.1, a risk table (Table 2-2) is presented in this section to provide a simpler
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procedure for assessing asbestos risks. The only data required to assess risks using
the risk table are estimates of long-term average exposure (derived from appropriate
measurements, as described in Section 2.3) for each particular exposure scenario and
population of interest.
Table 2-2 presents estimates of the additional risk of death from lung cancer and
mesothelioma attributable to lifetime exposure to an asbestos concentration of
0.0005 f/ml (for fibrous structures longer than 5 pm and thinner than 0.5 pm) as
determined using the TEM methods recommended for use at Superfund sites
(ISO 10312 and Berman and Kolk 1997).
In Table 2-2, separate risk estimates are provided for males and females and for
smokers and non-smokers. Separate estimates are also presented for exposures
containing varying fractions (in percent) of fibrous structures greater than 10 pm in
length.
Separate estimates are presented for smokers and nonsmokers because the lifetime
asbestos-induced risk of both lung cancer and mesothelioma differ between smokers
and non-smokers. The asbestos-induced risk of lung cancer is higher among smokers
because the lung cancer model (Equation 2.1) assumes that the increased mortality
rate from lung cancer risk due to asbestos exposure is proportional to background lung
cancer mortality, which is higher among smokers.
The asbestos-induced risk of mesothelioma is smaller among smokers because the
mesothelioma model (Equation 2.3) assumes that risk from constant exposure
increases with the cube of age, with the result that the predicted mortality rate is
highest among the elderly. Thus, since smokers have a shorter life span than non-
smokers,-their risk of dying from mesothelioma is also predicted to be smaller.
Separate estimates are provided for different fractions of fibrous structures longer than
10 pm because the model assumes that structures longer than 10 pm are more potent
than structures between 5 and 10 pm in length (in a manner consistent with
Equation 2.2). The derivation of this model is described in detail in Chapters 5 and 6 of
the companion Technical Background Document.
Risks from lifetime exposures to asbestos levels other than 0.0005 may be estimated
from the appropriate entry in Table 2-2 by multiplying the value in the selected cell from
the Table by the airborne asbestos concentration of interest and dividing by 0.0005
(i.e., by assuming that the additional risk is proportional to the asbestos exposure
level). Airborne asbestos concentrations to be used in this manner must be estimates
of lifetime average exposure and must be expressed as structures longer than 5 pm
and thinner than 0.5 pm derived as described in Section 2.3. Estimates of the fraction
of these structures that are also longer than 10 pm must also be determined to select
the appropriate cell of the table from which to derive the risk estimate. Note that the
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TABLE 2-2:
ADDITIONAL RISK PER ONE HUNDRED THOUSAND PERSONS FROM LIFETIME
CONTINUOUS EXPOSURE TO 0.0005 TEM f/ml LONGER THAN 5.0 Jim
AND THINNER THAN 0.5
Percent of Fibers Greater Than 10 urn iri Length
0.5% 1% 2% 4% 6% 10% 15% 20% 30% 40% 50%
MALE NONSMOKERS
Lung Cancer	0.052 0.084 0.15
Mesotheliomas	0.057 0.093 0.16
FEMALE NONSMOKERS
Lung Cancer	0.039 0.063 0.11
Mesotheliomas	0.064 0.10 0.18
CHRYSOTILE
0.28
0.31
0,21
0.34
0.41
0.45
0.30
0.50
0.67
0.74
0.50
0.83.
0.99
1.1
0.74
1.2
1.3
1.4
0.98
1.6
2.0
2.2
1.5
2.4
2.6
2.9
1.9
3.2
3.3
3.6
2.4
4.0
MALE SMOKERS
Lung Cancer
Mesotheliomas
0.48 0.77 1.4 2.6 3.7 6.1 9.1 12 18 24 30
0.038 0.062 0.11 0.21 0.30 0.49 0.73 1.0 1.4 1.9 2.4
FEMALE SMOKERS
Lung Cancer
Mesotheliomas
0.32 0.52 0.93 1.7 2.5 4.2 6.2 8.2 12 16 20
0.057 0.093 0.16 0.31 0.45 0.74 1.1 1.5 2.2 2.9 3.6
MALE NONSMOKERS
Lung Cancer	0.51 0.82 1.5 2.7
Mesotheliomas	5.7 9.3 16 31
AMPHIBOLES
4,0
45
6.5
74
9.7
109
13
145
19
216
25
288
32
359
FEMALE NONSMOKERS
Lung Cancer
Mesotheliomas
0.38
6.4
0.61
10
1.1
18
2.0
34
3.0
50
4.8
83
7.2
123
9.6
163
14
243
19 24
323 403
MALE SMOKERS
Lung Cancer	4.7	7.6	13	25	37 60
Mesotheliomas	3.8	6.2	11	21	30	49
FEMALE SMOKERS
Lung Cancer	3.2	5.2	9.1	17	25	41
Mesotheliomas	5.7	9.3	16	31	45	74
89 118 176 235 293
73 97 144 192 239
61 81 120 .160 199
110 145 217 288 360

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two size fractions that are combined to determine Copt (Equation 2.2) are separately
enumerated (not combined) when they are to be used in conjunction with Table 2-2.
The procedure described above for estimating risks using Table 2-2 should provide
good approximations as long as the projected risk is no greater than 1,000 per
100,000. Risks greater than 1,000 per 100,000 (i.e. 1 in. 100) that are derived from the
Table are likely to be over-estimated.
Table 2-2 was derived using the approach described in Appendix A by incorporating
the age-, sex-, and smoking-specific death rates reported for the general U.S.
population and assuming that exposure is constant and continuous at the level
indicated in the table. The underlying models are provided in Section 2.1 for cases in
which exposure is either not constant or not continuous and for which sufficient data
exist to characterize the time-dependence of such exposure. If available, there may
also be cases in which it is advantageous to employ mortality data from a control
population that better matches the exposed population of interest than the U.S.
population as a whole.
2.3 REQUIREMENTS FOR ASBESTOS MEASUREMENTS
As indicated previously, estimates of airborne asbestos concentrations that are
required to support risk assessment can be derived either by extrapolation from
airborne measurements or by modeling release and dispersion of asbestos from
sources (soils or other bulk materials). In either case, exposure estimates must be
representative of actual (time-dependent or time-integrated) exposure and must provide
measurements of the specific size fractions of asbestos that are components of the
optimum exposure index defined by Equation 2.2. Additional considerations that need
to be addressed to assure the validity of risk estimates derived using this protocol are
indicated below.
2.3.1 Requirements for Measuring Airborne Asbestos to Support Risk
Assessment
Considerations that need to be addressed to assure the validity of risk estimates
derived from measurements of airborne asbestos include:
•	the array of samples collected for estimating airborne asbestos
concentrations must be representative of the exposure environment;
•	the time variation of airborne asbestos concentrations must be properly
addressed;
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airborne samples must to be collected on membrane filters that are
suitable for preparation for analysis by transmission electron microscopy
(TEM). Appropriate procedures for sample collection are described in
Chatfield and Barman (1990) or the ISO Method (ISO 10312)1;
sample filters must be prepared for analysis using a direct transfer
procedure (e.g. ISO 10312). Should indirect preparation be required
(due, for example, to problems with overloading of sample filters), a
sufficient number of paired samples will need to be collected and
analyzed to establish a site-specific correlation between directly and
indirectly prepared samples;
samples must be analyzed by TEM;
samples must be analyzed using the counting and characterization rules
defined in the ISO Method (ISO 10312) with one modification: only
structures longer than 5 pm need to be enumerated. Separate scans for
counts of total structures longer than 5 pm and longer than 10 pm are
recommended to increase the precision with which the longest structures
are enumerated. Importantly, ISO Method rules require separate
enumeration and characterization of component fibers and bundles that
are observed within more complex clusters and matrices. Such
components, if they meet the dimensional criteria defined in Equation 2.2
must be included in the structure count;
if risks are to be estimated using the risk models (Section 2.1), asbestos
concentrations derived from the above-described measurements must be
expressed as the weighted sum of structures between 5 and 10 pm in
length and structures longer than 10 pm in length, per the exposure index
defined in Equation 2.2. Only structures thinner than 0.5 pm are to be
included in these counts. Both fibers and bundles that are isolated
structures and fibers and bundles that are components of more complex
structures are to be included in structure counts (as long as each
structure counted satisfies the defined size criteria for the size category in
which it is included);
if risks are to be estimated using the risk models (Section 2.1), the risk
coefficient(s) selected from Table 2-1 must be appropriate for the fiber
Note that the ISO Method (ISO 10312) is a refinement of the method originally published
as the Interim Superfund Method (Chatfield and Bemnan 1990). It incorporates improved
rules for evaluating fiber morphology. Both methods derive from a common
development effort headed by Eric Chatfield.
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type (i.e. chrysotile or amphiboie) and the disease end point (i.e. lung
cancer or mesothelioma) relevant to the situation of interest; and
•	if risks are to be estimated using Table 2-2 (Section 2.2), rather than
deriving the weighted sum described in Equation 2.2, the concentration of
asbestos structures longer than 10 pm and thinner than 0.5 Mm must be
derived to determine the appropriate column of the Table from which to
estimate risk and the concentration of total asbestos structures longer
than 5 pm and thinner than 0.5 ym must be derived, divided by 0.0005,
and multiplied by the risk estimate listed in the appropriate cell of the
Table to generate the risk estimate of interest.
2.3.2 Requirements for Estimating Airborne Exposures from Soil or Bulk
Measurements Combined with Release and Transport Modeling
Considerations that need to be addressed to assure the validity of risk estimates
derived from soil or bulk measurements combined with release and transport modeling
include:
•	the array of samples collected for estimating source concentrations must
be representative of the surface area or volume of source material from
which asbestos is expected to be released and contribute to exposure;
•	samples must to be prepared and analyzed using the Superfund method
for soils and bulk materials (Berman and Kolk 1997), which is the only
method capable of providing bulk measurements that can be related to
risk;
•	membrane filters samples prepared using the tumbler and vertical
elutriator per the Superfund method must themselves be prepared for
TEM analysis using a direct transfer procedure;
•	TEM analysis must be conducted using the counting and characterization
rules defined in the ISO Method (ISO 10312) in precisely the same
manner that is described above for air measurements. Also, the same
size categories need to be evaluated in the same manner described in
Section 2.3.1, whether results are to be used to support assessment
using risk models or using the risk table; and
•	release and dispersion models that are selected for assessing risks must
be appropriate to the exposure scenario and environmental conditions of
interest. Such models must also be adapted properly so that they accept
input estimates expressed in terms of fiber number concentrations.
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Procedures suggested for adapting such models are illustrated in a recent
publication (Berman 1998).
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3.0 REFERENCES
Berman, D.W. "Asbestos Measurement in Soils and Bulk Materials: Sensitivity,
Precision, and Interpretation - You Can Have It All." Advances in Environmental
Measurement Methods for Asbestos, ASTM STP 1342, M.E. Beard, H.L Rook, Eds.,
American Society for Testing and Materials, 1998. In Press. -
Berman, D.W. and Chatfield, E.J.; Interim Superfund Method for the Determination of
Asbestos in Ambient Air. Part 2: Technical Background Document, Office of Solid
Waste and Remedial Response, U.S. EPA, Washington, D.C., EPA/540/2-90/005b,
May, 1990.
Berman, D.W. and Kolk, A. J.;. Superfund Method for the Determination of Asbestos in
Soils and Bulk Materials, Office of Solid Waste and Emergency Response, U.S. EPA,
Washington, D.C., EPA 540-R-97-028, 1997.
Chatfield, E.J. and Berman, D.W.; Interim Superfund Method for the Determination of
Asbestos in Ambient Air. Part 1: Method, Office of Solid Waste and Remedial
Response, U.S. EPA, Washington, D.C., EPA/540/2-90/005a, May, 1990.
ISO 10312: Ambient Air - Determination of Asbestos Fibres - Direct-Transfer
Transmission Electron Microscopy Method. (Developed by Chatfield, E.J. 1993).
U..S. EPA, Airborne Asbestos Health Assessment Update. Report 600/8-84-003F, U.S.
EPA, 1986.
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APPENDIX A:
DERIVATION OF LIFETIME RISKS FOR LUNG CANCER
AND MESOTHELIOMA FROM MODELS USING Kt AND K„ ESTIMATES
FOR POTENCY

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This appendix shows how additional lifetime risk of lung cancer or mesothelioma are calculated
from the models from which K^, the potency for lung cancer, and KM, the potency for mesotheliomas,
are derived. First a general model is developed that allows a variable exposure pattern, and the lung
cancer and mesothelioma models are shown to be special cases of the more general expression. Next
the procedure used to implement these models based on human mortality rates is explained. Finally,
the mortality rates used in these calculations are derived.
Let D = (D(t); t>aO} represent exposure to asbestos (i.e., exposure at age t is D(t) &ml), let
S0(tfx) be the probability of surviving to age t given survival to age x < t. Let M^(t) be the mortality
rate for a given cause at age t The probability of dying of the given cause during a small age interval
At at age t is the probability of surviving to age t times the probability of dying from the given cause
given survival to age I, or	• - • -•• 	-
SD(t|x)Mj>(t)At.	...... -
The probability of dying of the given cause is given survival to age x therefore given by the integral
Pd(*) = J SD(t|x)Mj,(t)dt.	(Bl)
x
The corresponding probability of dying of the given cause without any exposure to asbestos is given by
CD
PoM = / S0(t)M0(t)dt,	(B2)
x
where the subscript O indicates no exposure, and the additional probability of dying from the given
cause as a result of exposure pattern D is
?d(x) - Po(x).	(B3)
The lung cancer and mesothelioma models in Section 6.2 basically model the mortality rate
M0(t). It is shown below how expressions (Bl), (B2), and (B3) are used to convert estimates" from the
models in Section 6.2 into estimates of additional risk-
It will be assumed that the increase in the mortality rate at age t from an exposure of D(v)
between ages v and v+av, vet, is given by
D(v)g(t-v,t)Av.	•'
1

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Thus g(u,t) is an intensity function that relates an exposure u yean prior to age t to the resulting
mortality rate at age t. It is further assumed that the iota!-mortality rate at age t is the sum of the
contributions from all doses prior to age t, plus the background mortality rate Mq(i); i.e.,
t
MflO) = Mo(t) + J" D(v)g(l-v,t)dv/	(B4)
0
To obtain the relative risk model for lung cancer in Section 6.2.1, let
McCOKl	~ u > 10
g(u,t) =	(B5)
0	u < 10.
By applying (B5) to (B4) and performing the integration, it follows that
t-10
MD(l) = Mo(0 {I + Kt J* D(v)dv],	(B6)
0
Thus, the relative risk at age t, Mj>(t)/Mo(t), is given by
1 + K.£ * [total exposure up to 10 years prior to age t],	(B7)
which agrees with expression (E4) in Section 6.2.1. However (B7) holds generally for any exposure
pattern D(v), whereas (E.4) is more specialized in that it presupposes a constant exposure.
To obtain the absolute risk model for mesothelioma in Section 6.2.2 from (B4), define the
intensity function	...
(u-10)2 u > 10
g(u,t) =	(B8)
0	u < 10
Thus the intensity function is proportional to the square of elapsed time since exposure less 10 years, h
then follows that	_
MO
Mxj(t) - Mo(t) + 3Km J D(v)(t-v-10)2dv.	(B9)
0
;This expression assumes a linear dose response. For a non-lineir response, replace D(v) bf'
H(D(v)) where H is a non=linear function (e.g. H^sv2).

-------
If a constant exposure rate Is assumed over a fixed age interval,
f t; < v < tj	(BIO)
D(v) «
0 otherwise,
then
Mo(l) + KMf(Mr10)J	for t;+10t2+10,
which agrees with the mesothelioma model (E.5) in Section 6.22.
' i
To implement these models the integral (Bl) must be evaluated using the appropriate
expression for the morality.rate Mjp(t) (expression (B6) for lung cancer and (Bll) for mesothelioma).
Lei bj, b2f..., b18 be the mortality rates (expected number of deaths) for all causes per year per 100,000
persons for the age intervals 0-5, 5-10,...,80-85, and 85+ years, respectively, and let a^.-a^ be the
corresponding rates for lung cancer. Given survival to age x=5k, the probability of survival to t = 5i
years is estimated as
i
" SG(U) =1T [l-5b;/100,000].	(B12)
j*k+l
Given survival to age 5(1-1), the probability of dying of lung cancer by age 5i is estimated as
Sa;/100,000,	"	(B13)
The probability of dying of lung cancer given survival to age 85 is estimated as aw/b;S. Therefore, the
probability of dying of lung cancer in the absence of asbestos exposure, given survival to age x=5k is
estimated as
1?	i-1
PoOO - 2 ((5VI00,000) 7T(l-5b/100,000)]	(B14)
i-k+1	j«k+l
1?
+ (¦«/»>«) IT (l-5bj/100,000),
j«k+l
which represents a discrete approximation to the integral (B2).
To estimate the probability P^x) of dying of lung cancer when exposed to a particular pattern
D of asbestos exposure, expression (B14) is again used, but a, and b,- are replaced by a. + E, and b. +
E,-, where, following (B7),
3

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E, = a,KL * [total exposure up to 10 years prior	(B15j
to mid-point of ith age interval],
where % is the potency parameter (risk factor) for lung cancer. (Here a,+E; is playing the role of
MjjO) in equation (B6).) The additional lifetime risk of lung cancer is estimated by the difference
PnfxVPnM- For example, to estimate the future risk to a person presently 20 years of age, we would
use x=20 (i.e., k=4) in (B14).
The additional lifetime risk of death from mesothelioma is estimated using the same formulas,
except a,- is replaced by zero (background rate of mesothelioma is so small as to be unimportant), and
(following equation B9) E,- is replaced by a discrete approximation to
vio •• " '•	 " *" :t
3Km J D(v)(t,-v-10)2dv,
0	......
where t. is the mid-point of the ith age interval. Appropriate modifications are made to these
expressions when x is not a multiple of 5.
Sex- and smoking-specific estimates are used for the mortality rates required in the above
calculations (a,- and b,). Lung cancer mortality rates for nonsmokers arc obtained by averaging rates for
nonsmokers are obtained by averaging rates for three different lime periods calculated from the
American Cancer Society prospective study (Garfinkel 1981). Lung cancer mortality rates in smokers,
[P(LCFjS)], are calculated using the equation
P(LCD) = P(LCF(S)P(S) 4- P(LCD | NS)Jl-P(S)],	(B16)
where P(LCD) is a 1980 age- and sex-specific death rate from lung cancer in the general U.S.
population, P(S) is the fraction of smokers in the population, P(LCD | NS) is an age- and sex-specific
death rate from lung cancer in nonsmokers computed from Garfinkel (1981), and P(LCD | S) is a
corresponding rate in smokers. The proportion of smokers, P(S) is assumed to be 0.67 for males and
0.33 for females, which is consistent with the U.S. EPA (1986) approach. Smoking-specific rates for all
causes are calculated from 1980 U.S. rates for all causes assuming that the mortality rate in smokers is a
factor, f, times the mortality rate in nonsmokers. An age-specific mortality rate, P(AC| NS). in
nonsmokers is then calculated using the formula
P(AC) = fP(AC| NS)P(S) + P(AC|NS)[1-P(S)J,
where P(AC) is a 1980 age- and sex-specific death rate from all causes in the general U.S. population.
Following Hammond (1966), the factor f is taken as 1.83 for males and 1.26 for females. This
procedure is followed for all age groups despite the fact that smokers generally do not begin smoking
until teenage years and the effects upon mortality will not occur until still later. This makes little
difference in the risk calculations because mortality rates are relatively low at early ages.
The resulting mortality rates are listed in Table Bl.
4

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Table Bi
Smoking- and Sex-Specific Mortality Rates Per Year Per 100,000
Population for Respiratory Cancer and Total Mortality
Total Mortality
Respiratory Cancer
Aee
Smokers Nonsmokers

Smokers
Nonsmokers


Males


0-1
1679.0
918.0
.4
0
1-5
85.4
46.7
,0
0
5-10
41.2
215
.0
0
10-15
45.0
24.6
.0
0
15-20
166.3
90.9
.1
0
20-25
239.3 "
130.8
.4
0
25-30
230.7
126.1
.7
0
30-35
230.5
126.0
12
0
35-40
288.4
157.6
93
0
40-45
428.3
234.0
26.2
8.3
45-50
686.8
3753
76.1
3.1
50-55
1109.0
606.0
155.1
7.9
55-60
1717.8
938.7
263.2
10.2
60-65
2623.7
1433.7
4018
17.3
65-70
3991.2
2181.0
556.7
28.2
70-75
5972.2
3263.5
698.5
25.2
75-80
8796.8
4807.0
750.6
44.9
80-85
• 13218.0
7222.9
711.0
72.5
85+
22110.4
120812
527.1
100.5


Females


0-1
1324.9
1050
3
0
1-5
63.5
50.4
3
0
5-10
29.7
23.6
.3
0
10-15
26.6
21.1
.0
0
15-20
61.6
48,9
.0
0
20-25
71.8
57.0
3
0
25-30
79.1
618
.9
0 •
30-35
98.1
77.8
17
0
35-40
144.4
114.6
10.6
0
40-45
233.0
184.9
27.9
2.4
45-50
372.8
295.9
67.4
3.5
50-55
578.7
4593
124.0
5.2
55-60
869.2
689.8
178.8
7.0
60-65
1327.5
1053.6
234.8
13.6
65-70
1993.3
15810
2816
16.2
70-75
3101.6
2461.6
286.4
20.9
75-80
4939.5
3920.2
240.8
34.7
80-85
8424.9
6686.4
1812
45.5
85+
171118
13581.6
184.8
52.7


5

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