Richard
Wilson
Department
of Physics and Energy and Environmental Policy Center
Harvard
University
Cambridge,
02138, MA
Risk
assessment for Asbestos and Management of Low Levels
Introduction:Medical
Effects of Asbestos
There
are a number of medical effects of asbestos with different locations (see
figure 1) which will be discussed in more detail below.
(1)Benign
conditions of the pleura, and in particular pleural plaques.
(2)Asbestosis.Observed
as early as 1906 by Auribault it was defined as fibrosis of the lung caused
by asbestos dust, and first called asbestos silicosis.It
was only defined as a separate disease after use of X rays became usual.According
to Doll and Peto (1982) the disease is indistinguishable from a rare "cryptogenic
fibrosing alveolitis", although asbestosis is usually assumed if there
has been evidence of exposure, simply from a weighing of probabilities.There
is in the literature some confusion as to what is to be called asbestosis.Most
reserve the term for interstitial fibrosis; others have separated pathological
reactions in the respiratory bronchioles and alveolar ducts, and called
them small airways disease.This
distinction is useful, because the small airways disease can be caused
by a wide variety of nonasbestos minerals, silica etc., which do not cause
interstitial fibrosis, or at least not frequently. (Churg 1983)
(3)
Lung Cancer. (Bronchial carcinoma)
(4)
Mesothelioma of the pleura or peritoneum.
(5)
Other cancers.A number of other
cancers have been suggested by Selikoff et al (1979) as being caused by
asbestos..Few of these other cancers
have been reliably attributed to asbestos, and even if they occur, are
negligible additions to the risk.
The
Risk Assessments
(1)Benign
conditions of the pleura may cause temporary problems, but are not usually
considered a danger at all.They
are often asymptomatic, however they are considered as indicators of exposure
(but not of risk), but are not definitive ones in all cases. (Churg 1982,1983),
(Hillerdahl 1978).
(2)The
risk assessment for asbestosis is very simple.It
seems to appear only after heavy accumulated exposure, and seems to have
a threshold-type effect.If exposure
is low, the accumulated dose will never exceed the threshold. This is shown,
for example in figure 2.The threshold
is higher than any environmental or occupational level of present concern,
so details are of no present interest.
Problems
arise in determining the exposure (defined as the concentration multiplied
by the occupancy) of the people in the cohort, and even worse of determining
the dose (the amount of asbestos that enters the lung).Different
studies do not agree.There are also
issues about what parameters of the dose are relavant, and whether all
forms of asbestos are the same.Rather
than discuss these in detail, I merely refer to a risk assessment carried
out for the EPA by William Nicholson.This
calculation agrees with numerical calculations of other authors, provided
similar assumptions are made (Hughes and Weill 1986)
For
lung cancer Nicholson assumes (following the work of Selikoff and Seidman
(19xx) that lung cancers begin to appear 20 years after start of exposure
but cease 40 years after exposure.He
assumes that in the study cohort that exposure was at the low end of what
was reasonable, and therefore derives a higher risk than many authors.
He assumes a linear (proportional) relationship between exposure (or dose)
and response.He assumes that the
relavanyt parameter of exposure is the exposure averaged over a long period
- of the oder of years rather than minutes, and then corrects for the fact
that people were exposed occupationally for only a portion of the day.He
does not distinguish between smokers and nonsmokers and therefore his risk
is applicable to a mix of persons (roughly half smokers and half non-smokerss).He
then presents a risk in tabular form for each age group and exposure period.
(4)For
risks of mesothelioma, I also take the calculations of Nicholson.However,
for mesothelioma the latent period is longer.Nicholson
used a formula developed by Peto et al. (1982) and fitted to the data that
describes the fact that mesotheliomas appear 30 years after exposure and
go on appearing till death from other causes.There
seems to be no indication that mesothelioma risk depends upon smoking history.For
non-smokers, and particularly for children, it dominates the calculated
risk.
Assumption
of Low dose linearity
The
actual data on lung cancers or mesotheliomas caused by asbestos arise from
workplace expsoure, with concentrations in the workplace of 1 fiber per
millilitre of air and above.This
is roughly equivalent to continuous exposure to a concentration of 0.1
fibers per millilitre and above.It
is important to realise that any assumption of a risk at concentrations
below this, does not rely upon direct data, but upon an INTERPOLATION (often,
even usually erroneously called an EXTRAPOLATION) between the cancer incidence
at the lowest measured increase and cancer incidence at zero concentration.
At
the time of the report of Mehir et al (1978) one of us was starting a campaign
among scientists in industry to persuade them to calculate risks for carcinogens
using a linear dose-response relationship.There
were several reasons for this.It
is possible that the linear relationship is correct and many academic scientists
believe so.It seemed to me unwise
for industrial leaders to take a rigid position where there were many academic
scientists"on the other side". Peto
(1979), an academic scientist, was arguing for a linear dose1response relationship
for asbestos.It was also clear that
very shortly scientists in the regulatory agencies would use it, largely
because they perceived it to be their duty "to be on the safe side."Indeed,
in 1984 a committee of the National Academy of Sciences stated, "This assumption
may not always be justified in application ... but it should lead to an
appropriate upper bound for the committee's risk assessments for asbestos.Furthermore,
and more importantly, ruling out a linear dose term for exposure does not
seem justified by the data now available."Doll
and Peto (1984), while adhering to the appropriateness of a linear dose-response
relationship for public policy purposes, point out that there is no model
for asbestos carcinogenesis that is as plausible as the model for cancer
produced by mutagens for which a linear dose-response relationship is strongly
suggested.However, this does not
mean that the linear dose-response relationship can be proven correct,
and as noted above, there can be no direct data on this question.
The
idea that asbestosis might exhibit a threshold and lung cancer might not
is not new.But a crucial question
is the mechanism.Thus the Chief
Inspector of Factories in the UK asked "Does silica or asbestos or the
fibrosis of the lung they produce tend to inhibit cancerof
the lung or to produce it?If the
latter, do either of these two substances act as specific carcinogenic
agents like tar, or is it that the disease they produce only prepares the
soil for the occurrence of cancer? ... With asbestosis, among 103 fatal
cases in which asbestosis or asbestosis with tuberculosis were present,
cancer of the lung was associated in 12 cases (11.6%)" (Merewether 1938).
Sine
the issue of linearity or non linearity is a matter of expert judgement,
expert elicitation may be appropriate.A
preliminary attempt at such a study has been done by D'Agostino and Wilson
(1990).We note that they failed
to find anyone who believed that the Nicholson calculation is an underestimate
of risk.
But
even if linearity is assumed, the distinction between a situation where
there is a measured small risk at low exposures (such as a risk of being
run down by a car even on an almost deserted road) and a risk that is merely
calculated may be important for some societal problems.Indeed
Crawford and Wilson (1995) argue that a low dose linearity can be calculated
for a very large number of societal issues, of which asbestos may not be
the most important.Here we argue
that an individual.Was a company
acting responsibly in installing asbestos in a school in 1955, and should
they be responsible for taking it out in 1988?A
company should be cautious about health effects, but they could not reasonably
be asked to predict vagaries of the regulatory
agencies.
If
it can be justified that the levels of asbestos in schools were not believed
to cause a hazard in 1955, and even now, if the risk is small enough that
the hazard is not large and not imminent, then the actions of the companies
in 1955 were not unreasonable. There is another reason for choosing a linear
dose-response for base-line risk estimations.The
appropriate measure of concentration is, in all linear models, the long-term
average. This remains an upper bound in other models. Then it becomes unnecessary
to make special allowance for occasional exposures to high concentrations,
provided that the average concentration is properly estimated.This
is important for addressing the concern of Selikoff (1990) and Brody (1990)
about intermittent high exposures of maintenance workers.
Are
all fibers the same?
The
reason for this reduction is less clear than the effect itself, but it
is generally considered to be due to a shorter clearance time for chrysotile
fibers in the lung, so that the ratio of dose to exposure is less.
Risk
at low doses
Example
of a detailed calculation:
the
risk of school exposure
The
present public interest is in reducing the risk at low doses.Recently
public policy has been addressed primarily to exposure in schools which
has raised a lot of emotion.We therefore
make a calculation for a "typical" school, in which chrysotile asbestos
was used for fire retardant or thermal insulation.In
this calculation, we will use the calculations of Nicholson for the EPA
(1985) and especially his table 6.3.However,
we note several important assumptions made by Nicholson.
Table
6.3 is calculated for continuous exposure, whereas exposure in a school
is only for part of the day.We assume
that in a typical school the exposure of the children to asbestos occurs
during 6 hours per day, and 150 days per year.This
is 1/10 of the total hours in the year.We
assume that this is for the ten year period 6 to 16 years.The
exposure for a teacher we assume to be for a thirty year period age 25
to 55.In the absence of specific
reliable measurements for the school, we take the reports on measurements
of concentrations in schools by Crump (1990), Corn (1991) or McCrone (1991)
that concentrations in schools are 0.0002 fibers/ml.
Following
the suggestion of Doll and Peto, we might allow a factor of 5 reduction
of mesothelioma risk if chrysotile is used, but since the correct reduction
factor may be much more, we may still be overestimating the risk. We assume
as Nicholson does, that there is a linear dose-response relationship at
low doses.
The
table does not differentiate between smokers and nonsmokers.For
the adults, we assume that his male risk is doubled for smokers, and is
negligible for nonsmokers.
Typical
lifetime risk due to asbestos in a school.
Based
upon Nicholson's table 6-3 and (where noted) a modified average school-time
exposure to chrysotile at 0.0002 fibers/ml (fibers greater than 5 microns):
Lifetime
Age
groupRisk
Mesothelioma
risk to females10-151
X 10-6
0-51.6
X 10-6
Interpolated
age group6-162.4
X 10-6
Adjusted
for chrysotile only6-165
X 10-7
(the
reduction by a factor of 5 noted in the text)
Mesothelioma
risk to males10-156
X 10-7
0-51
X 10-6
Interpolated
age group6-161.6
X 10-6
Adjusted
for chrysotile only6-163
X 10-7
Mesothelioma
risk any asbestos25-553
X 10-6
Adjusted
for chrysotile only25-556
X 10-7
Lung
cancer risk (smoker )25-554
X 10-6
Lung
cancer risk (non-smoker)25-554
X 10-7
Risk
if there is a threshold at 0.1 f/ml0
We
deliberately refrain from calculating the risk for smoking children because
of our belief that there should be no children who smoke, and that public
policy analysts should consider the problems of any who do in a different
way than the problems of those who do not.
These
risks are smaller than the risks that people regularly accept such as automobile
driving (200 X 10-6 per year or 15,000 X 10-6 per lifetime). Some people
reject such a comparison because automobile driving is voluntary, but the
average risk for pedestrians killed by automobile driving of 2,000 X 10-6
per lifetime is surely involuntary. So also is the risk of drinking chlorinated
surface water in a typical US city.This
is 200 X 10?6 calculated by the EPA methodology which may be expected to
be as conservative, but no more conservative than the calculations here.It
is also smaller than the risk of childhood death among blacks and minority
groups (5 X 10-2), to which many people believe that society should preferentially
pay attention.This comparison may
be taken as partial justification for the statements of many persons quoted
earlier that a concentration of 0.01 fiber/cc is safe.
It
has been assumed by advisory and regulatory bodies for 70 years that ionizing
radiation follows a linear (proportional) dose response and that radiation
exposure to a population should be reduced to As Low As Reasonably Achievable.
Individual exposures are to be kept below natural background, and if there
are a large number of people exposed, an integrated population exposure
in Man-Rem, now more correctly person-Sievert, is calculated.In
1974 after a two year long public hearing the Nuclear Regulatory Commission
(RM-30-2 and copied in federal regulations 10 CFR 50, appendix I) ruled
that if integrated exposures could be reduced for a cost of $1000 per Man
rem ($100,000 per person Sv) the expenditure should be made. More recently
this figure has been doubled to account for inflation (Kress 1995). On
a linear dose response relationship this corresponds to about $4,000,000
per calculated life saved.Other
organizations have used cost benefit analysis, often for situations (automobile
safety) where a linear dose response relationship is more certain.These
situations have been reviewed by Guenther and Thein (1997) who find an
average "Willingness To Pay (WTP)" of $4,000,000 per calculated life saved.
We suggest here that this concept be used for asbestos exposures.
It
is important to realize that background exposures are large. In the USA
they are about 0.3 Rem = 0.003 Sv of which radon gas in buildings forms
the largest part.Thus 250 million
Americans have an integrated population exposure of 75 million Man Rems
or 750,000 person Sv.The rule suggests
that if that background can be eliminated (which it cannot) it would be
worth an expenditure of $150 billion.We
spend far less than this even are exposed to
In
order to illustrate how this might work, we assume the above school where
500 children, 250 males and 250 females are exposed for the 50 year life
of the school buildings.5 groups
of children will spend 10 years there.Then
the probability that ONE will develop mesothelioma in the 50 year period
becomes:
5
X 250 (2.4 + 1.6) X 10-6 = 5 X 10 5 X 10-3 or
1
X 10-3 if a 5 fold reduction for chrysotile is assumed.
5/3
groups of 30 adults will be in the school, and if we pessimistically assume
that they are smokers, the probability that one will get lung cancer FROM
THIS CAUSE in the 50 year period is
5/3
X 30 X 4 X 10-6= 2 X
10--4.This is 10times
less for nonsmokers.
At
a cost to save a calculated life of $4,000,000 per calculated life, the
TOTAL amount that is justified to spend to reduce this concentration to
zero before the building reache=s the end of its natural 50 year life is:
$(5
X 10-3 + 2 X 10-4) X 4,000,000 = $20,800.
We
see at once that this number is dominated by the possibility of mesothelioma
in children.The societal preoccupation
with the risk to children is to this extent justified, and it becomes important
to be sure that we truly understand the model that extends the data to
the children.
Long-term
risk of worldwide asbestos use.
One
of the advantages of asbestos is that it is chemically stable and does
not disintegrate.One of the disadvantages
is that it is stable and lasts a long time!Further,
large asbestos fibers in the environment, perhaps with too large a diameter
to be airborne and cause health problems, can split into many fibers with
small diameters in the environment. This leads to a fear that continued
mining of asbestos can lead to a buildup of asbestos fibers with dangerous
shapes and sizes in the environment.If
this is coupled with a belief in a linear dose5response relationship, predictions
can be made of steadily rising background cancers from this cause.
This
concern is far from unique to asbestos; it follows for any stable material,
e.g. arsenic, which is stable, and for which a linear dose1response relationship
is suggested.These
predictions
lead to intense pressure for an absolute ban, even if it can be shown that
occupational exposures, and exposures in buildings, can be kept low.It
is impossible to disprove, in advance, the reality of such a concern for
any material.However, there is no
large increase of asbestos levels in rural communities and in urban communities
increases seem to be concentrated at busy intersections where automobile
brakes are widely used.Background
levels of mesothelioma have shown no increase among females, and the small
increase among males is attributed to occupational exposures.It
can therefore be argued that this problem is hypothetical, and while monitoring
might be appropriate, most remedial actions could be deferred without possibility
of disaster.Finally we note that
chrysotile asbestos is soluble in dilute acids, and asbestos in the environment
tends to be comprised of short fibers which are less carcinogenic.
Probability
of causation
Often,
when there is a victim of bronchial carcinoma, or of mesothelioma, or of
asbestosis or someone who has pleural plaques, the question arises, what
is the probability that his/her condition was caused by asbestos exposure,
and in particular, is it greater than 50% often demanded by law to allow
attribution of blame?The answer
to this question comes from a weighing of probabilities.The
usual approximate formula is that the probability of causation is the risk
calculated as above, divided by the probability of developing the same
disease from all other causes.
Risks
caused by other fibers
Although
we do not claim to be angels, risk assessors often
walk
where others fear to tread.In this
paragraph we address the risk due to exposure to an alternative fiber,
the man-made fiber, fiberglass.In
doing this we explore the consequences of the assumption that for equal
sizes of fiber, and after any correction for clearance time, fiberglass
is as potent in producing each of the ailments caused by asbestos as asbestos
itself.What is the risk, and what
precautions should we take to reduce it?Unless
we ask this question, we will fail to learn from the history of asbestos
use and we will be condemned to repeat it.A
whole journal once was addressed to this problem of man1made fibers (Walton
1987).
It
is evident that fiberglass is not used as carelessly as was asbestos. No
one sprays it on.Unlike asbestos,
fiberglass is not held in place by gypsum, which is subject to deterioration.We
must ensure that this is always the case; that fiberglass batts are secure
batts, and do not deteriorate.We
also note that it is possible and easy to make fiberglass with any dimension
of fibers we choose; in particular with a large enough diameter that effects
are unlikely.These seem obvious
criteria; but we know of no public health authority that watches these
matters; no regulation or standard for proper installation of fiberglass,
and no studies which confirm or deny our supposition that the fibers are
less likely to reach the environment than are the fibers of asbestos. Until
these are done, the claim can correctly be made, as we have heard it made
by more than one expert in the health effect of asbestos: "there exists
no substitute for chrysotile asbestos, properly applied, that is known
to be as safe".
Acknowledgements
References
Albelda
SM, DM Epstein, WB Gefter and WT Miller (1982), "Pleural thickening; its'
significance and relationship to asbestos
exposure",
AM Rev Respir Dis, 126, 621?624
Baris
YI, Sahin A, et al (1978) "An outbreak of pleural
mesothelioma
and chronic fibrosing pleurisy in the village of Karain/Unque in Australia",
Thorax 33, (8)
Breslow
L (Chairman) et al, 1984, "Asbestiform Fibers: non
occupational
health risks" National Academy of Sciences.
Brodeur
P. (1985) "The asbestos industry on trial"The
New Yorker Magazine, June 10th, 17th, 24th, and July 1st
Brody
A.R. (1990) "Asbestos, carcinogenicity, and public policy" Science, 248,
795 (letter)
Browne
K. (1986) "Is Asbestos or Asbestosis the cause of the increased risk of
lung cancer in asbestos workers?" (Editorial) British Journal of Industrial
Medicine, 43, 145?149
Craighead
JE (1987) "Eyes for the Epidemiologist: the pathologists role in shaping
our understanding of the asbestos-associated diseases "HP
Smith Award lecture Amer. Journ. Clin. Path. 89, 281
Churg
A. (1982) "Asbestos fibers and pleural plaques in a general autopsy population"
Amer Journal Pathology, 109, 88-96
Churg
A. (1983) "Current issues in the pathologic and mineralogic diagnosis of
asbestos-induced disease"Chest,
84 no 3, 275-280
Churg
A and Green FHY, Eds., (1987) "Pathology of occupational lung disease"Igagu-shoin,
NY and Tokyo, pp234-246
Churg
A (1988) private communication
McDonald
J.C. (1980) "Asbestos related disease:an epidemiological review" in Biological
effects of mineral fibers, vol 2 ed JC Wagner, IARC scientific publications,
Lyon France 30,590
CPSC
(1983) "Chronic hazards advisory panel on asbestos", Consumer Products
Safety Commission, Division of Health Sciences, July.
Davies
JMG (1985) "A review of recent experiments on the mechanisms of asbestos
pathogenicity"In proceedings of
Vthinternational colloquium on
dust measuring technique and strategyAsbestos
International Association p. 25
Doll
R (1955) "Mortality from lung cancer in asbestos workers" Brit J Ind Med
12, 81-86
Doll
R and Peto J (1982) "Effects on health of exposure to asbestos" Health
and Safety Commission, London (Her Majesty's Stationary Office)
Dupre
et al (1984) "Report of the Royal Commission on matters of health and safety
arising from the use of asbestos in Ontario" Ontario ministry of Public
services, 880 Bay St Toronto, Ontario, Canada
.
H.Druckrey,
R.Preussmann, S.Ivankovic und D.SchmahlAOrganotrope
carcinogene Wirkung bei 65 verscheidenen N-Nitroso- Verbindungen an BD-Ratten@Zeitschrift
fur Krebsforschung 69103-201;1967