Consequences of Childhood Exposure to Asbestos
Robin Howie Associates, Edinburgh, Scotland
There has been concern for many years that young persons may be more
susceptible to damage by hazardous substances, as organs may be more susceptible
during growth. The Factories Acts and other legislation therefore restricted
the employment of children in hazardous work. For example, Section 77
of the Factories Act 1901 prohibited the employment of children and young
persons in process such as the silvering of mirrors using mercury or the
making of white lead. In the case of asbestos, the Asbestos Industry Regulations
1931 prohibited the employment of persons under 18 years of age in particularly
hazardous activities such as blending asbestos by hand, manufacturing
or repairing mattresses, cleaning sacks or cleaning out settling chambers.
Note that the school leaving ages in 1901 and 1931 were 12 and 14 respectively.
Concern about exposure at an early age is particularly relevant in the
case of carcinogens as critical organs may be susceptible to cell damage
when they are still growing. Fortunately, there is no evidence that asbestos
has such an effect. However, if children are exposed to asbestos at an
early age, their long life expectancy increases the probability that they
may live long enough to develop long latent period cancers such as asbestos-induced
lung cancer and mesothelioma. As one eminent doctor commented when asked
if all girls exposed to asbestos would develop asbestosis, he replied,
"Yes, if they live long enough"
The particular problem with the exposure of young children to asbestos
is that the risk of developing mesothelioma increases as the time since
exposure to the power about 4. Doll and Peto (1985) postulated that the
risk of developing mesothelioma from an exposure to asbestos could be
calculated from the equation:
R(tDP) = kL[(t-t1)4
HEI (1991) adopted a modified model:
R(tHEI) = kL[(t-t1-10)3
R(t) Mesothelioma Risk at age t
k constant depending on the type of asbestos
L Index of exposure
t Reference age
t1 Age at beginning of exposure
t2 Age at end of exposure
The consequences of such increase in risk with time can be seen in the
situation where a 3-year-old girl, her 25-year-old mother and her 55-year-old
grandmother all receive the same exposure to asbestos over the same period
of two years. If the risk of each developing mesothelioma by age 80 is
calculated, the child has 77 years from first exposure for the mesothelioma
to develop, the mother 55 years and the grandmother 25 years. From Doll
and Peto, if the grandmothers risk is taken as 1, the mothers
risk is 11 times greater and the childs risk is 32 times greater.
The HEI model gives relative risks of 1, 9.9 and 22 respectively, i.e.
compared with the Doll and Peto model, the same relative risk for the
mother and about 70% of the relative risk for the child. Both models therefore
underline the very substantially increased mesothelioma risk from asbestos
if exposure occurs early in life. Hodgson and Darnton (2000) consider
that the mesothelioma risk starts to decline after about 60 years from
first exposure. However, as discussed by this author in ARMB 25, Howie
(2001), the Scottish male mesothelioma rate continues to rise steeply
between ages 80-84 and 85+. It is therefore concluded that the Doll and
Peto (1985) and HEI (1991) models are more likely to be correct than Hodgson
and Darnton (2000) as regards increases in mesothelioma rates over 60
years after exposure, and therefore more relevant in the case of childhood
A further problem is that if the exposure to asbestos occurs in the home,
the child may be exposed to asbestos there for up to 20 hours per day
until she goes to school. The childs cumulative exposure could be
up to 140 hours per week, 52 weeks per year. Over a year, the childs
cumulative exposure would therefore be the same as that of a person occupationally
exposed to four times the childs fibre concentration for 40 hours
per week for 45 weeks per year.
Very stringent precautions must therefore be taken to prevent or minimise
childrens exposure to asbestos, particularly in the home.
The UK currently does not have a limit for environmental exposures to
Before an enclosure where work with asbestos has been undertaken can
be dismantled it must be demonstrated that airborne fibre levels inside
the enclosure do not exceed the Clearance Indicator of 0.01 fibres/ml.
This limit is the same for all types of asbestos. The Clearance indicator
is sometimes interpreted as an "Environmental Limit" For example;
one consultant in Scotland has assured clients that they should not be
concerned if airborne fibre concentrations on their premises do not exceed
Such interpretation is directly contrary to the Approved Code of Practice
L28, HSC (1999), paragraph 79 of which states "The threshold of less
than 0.01 fibres/ml should be taken only as a transient indication of
site cleanliness, in conjunction with visual inspection, and not
as an acceptable permanent environmental level" authors
italics. The same guidance was given the 1988 edition of the same Code,
What is the risk at 0.01 fibres/ml for children, particularly those under
From Peto (1989), the risk of a child developing mesothelioma or lung
cancer by age 80 from exposure to 0.01 fibres/ml of chrysotile for 40
hours per week between ages 0 and 5 is 750 per million for mesothelioma
and 370 per million for lung cancer. If the child spends an average of
20 hours per day in the home throughout childhood, the above risks would
be increased to 3,000 per million for mesothelioma and 1,500 per million
for lung cancer. Lung cancer risks would be further increased by about
50% if the child subsequently smokes or reduced by about 90% if he or
she never smokes. The consequences of secondary smoking on asbestos-induced
lung cancer have not been addressed.
The mesothelioma risk for low level exposures is about 7 times higher
with crocidolite than with amosite and about 20 times higher than with
chrysotile and the risk for lung cancer is about equal for all three types
of asbestos, Hodgson and Darnton (2000). That is, the above exposures
would generate mesothelioma risks of about 60,000 per million with crocidolite
and about 9,000 per million with amosite. These risks are in addition
to the 1,500 per million risks for lung cancer. Total risks are therefore
61,500 per million with crocidolite, 10,500 per million with amosite and
4,500 per million with chrysotile.
All above risk estimates substantially exceed HSEs (1989) "socially
tolerable" risk level of 10 per million per year.
To limit the total asbestos risk to below 10 per million per year for
children likely to be exposed to asbestos for up to 140 hours per week
from birth, their exposures must not exceed 0.00001 fibres/ml for crocidolite,
0.00005 fibres/ml for amosite or 0.0001 fibres/ml for chrysotile.
The Scottish consultants assurance that 0.01 fibres/ml is an acceptable
exposure is therefore dangerously misleading, particularly for residential
properties with children or schools.
It is generally asserted that the current techniques used for measuring
airborne fibre levels cannot quantify concentrations below 0.01 fibres/ml,
e.g. HSE (1995). However, increased sampling volumes and reduced filter
sizes can be used together to reduce the detection limit. For example,
a sample volume of 2 m3 through 6 mm diameter on a sampling
filter would permit a concentration of 0.0001 fibres/ml to be quantified
and a concentration of 0.00005 fibres/ml to be detected. From experience,
if the sampling filter is fitted into a size-selecting sampler, most of
the non-fibrous particulates which could otherwise obscure the fibres
of interest can be excluded, so increasing sensitivity in dusty situations.
Minimal changes to current sampling techniques can therefore reduce the
quantification limit to 0.0001 fibres/ml and the detection limit to 0.00005
fibres/ml. To measure below 0.00001 fibres/ml for crocidolite it will
probably be necessary to analyse samples using Electron Microscope techniques.
It is essential that such samples be collected during actual or simulated
occupation of the building throughout the sampling period so that any
fibres, which may be present, are disturbed and rendered airborne. Unless
any fibres present are disturbed fibre levels may be substantially underestimated.
In conclusion, children are at significant risk of developing mesothelioma
or asbestos-induced lung cancer unless airborne fibre concentrations are
reduced below 0.00001 fibres/ml for crocidolite, 0.00005 fibres/ml for
amosite or 0.0001 fibres/ml for chrysotile.
Doll R and Peto J (1985) Asbestos Effects on health of exposure to asbestos.
Health Effects Institute (1991) Asbestos in Public and Commercial Buildings.
Health Effects Institute Asbestos Research: Cambridge, MA, USA.
Health and Safety Commission (1999) Work with asbestos insulation, asbestos
coating and asbestos insulating board. L28. HSE Books: Sudbury.
Health and Safety Commission (1988) Work with asbestos insulation, asbestos
coating and asbestos insulating board. COP 3. HMSO: London
Health and Safety Executive (1995) Asbestos fibres in air. MDHS 39/4.
HSE Books: Sudbury.
Health and Safety Executive (1989) Risk criteria for land-use planning
in the vicinity of major industrial hazards. HMSO: London.
Hodgson and Darnton (2000) Quantitative risks of mesothelioma and lung
cancer in relation to asbestos exposure. Annals of Occupational Hygiene,
Howie (2001) Interpreting the mosthelioma tragedy Part 2. Asbestos
Risk Managing Briefing, No. 25: 5-8.
Peto J (1989) Fibre carcinogensis and environmental hazards. In: Non-occupational
exposure to mineral fibres. IARC Scientific Publication No. 90: 457-470.
4/16/05: Spectre to Introduce
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Joe Oliver, National Board Member and former President of the
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If you know anything about this horrific history or have documents
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The White Lung Association stands
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