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Consequences of Childhood Exposure to Asbestos

Robin Howie
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 — (t-t2)4]

HEI (1991) adopted a modified model:

R(tHEI) = kL[(t-t1-10)3 — (t-t2-10)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 grandmother’s risk is taken as 1, the mother’s risk is 11 times greater and the child’s 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 exposures.

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 child’s cumulative exposure could be up to 140 hours per week, 52 weeks per year. Over a year, the child’s cumulative exposure would therefore be the same as that of a person occupationally exposed to four times the child’s fibre concentration for 40 hours per week for 45 weeks per year.

Very stringent precautions must therefore be taken to prevent or minimise children’s exposure to asbestos, particularly in the home.

The UK currently does not have a limit for environmental exposures to asbestos.

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 0.01 fibres/ml.

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" — author’s italics. The same guidance was given the 1988 edition of the same Code, HSC (1988).

What is the risk at 0.01 fibres/ml for children, particularly those under school age?

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 HSE’s (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 consultant’s 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. HMSO: London.

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, 44: 565-602.

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. IARC: Geneva.


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