ASBESTOS RISKS

I wish to single out the problem of asbestos-induced cancers due to exposure to friction materials. In the Final Rule of 1989 (1), EPA attributes up to 144 projected cases of cancer to exposure to friction materials. These risks account for the majority of all risks in the Final Rule. These risk assessments were obtained using exposure-response relationships for cancer in different industries and in populations exposed to different asbestos materials of which the friction materials in only one.


In their study of more than 13,500 workers manufacturing friction materials in the period 1942-1980, Berry and Newhouse (67) found little excess cancer and the only excess mortality comprised 10 deaths from pleural mesothelioma, out of which 8 at least partly due to exposure to crocidolite.


The slope for increased lung cancer risk was only 0.00058 fibres /ml years. McDonald and co-workers (68) found practically no lung cancer risk and no mesothelioma in the group of long-term workers and in higher exposure categories in their study of more than 3,500 men employed in the manufacturing of friction products in the period 1938 Ð 1958. The slope for increased lung cancer risk was practically zero. The authors interpreted the results as 'doubtful whether there was any significant lung cancer excess".


I strongly disagreed (57) with the approach to the estimation of the projected number of cancers using the mean of slopes derived in all studies, of which only two (by far the lowest) were obtained in the friction products exposures. The population with expected exposure of asbestos fibres are garage mechanics, because of their work on the maintenance and repair of automobile asbestos containing brakes and clutches.


In a large case-control survey of all cases of mesothelioma diagnosed by pathologists in the USA and Canada during a defined period, McDonald (69) observed a substantial excess risk of mesothelioma in many occupations with exposure to asbestos, and particularly to amphiboles, but no excess was observed in the category of garage mechanics.


In 1988 (70), I analyzed all the available literature regarding asbestos risk in vehicle manufacture, maintenance and repair, and concluded that, provided good work practices are followed and no amphiboles are used, detectable risks in vehicle maintenance and repair are not to be expected.


As in 1991 (56) and 1993 (57), I still disagree with the EPAÕs approach to the estimation of the projected number of cancers due to exposure to friction materials by using a mean slope of 11 studies (1,36), of which only two (having by far the lowest slopes) were obtained in the friction products exposure.


It is hardly justifiable to estimate risks due to exposure to one type of fibre population by using the slopes obtained in exposure to completely different fibre populations, while being fully aware of the large variations among the slopes. This approach has resulted in an ungrounded overestimation of the projected number of cancers in exposure to friction materials.


Unfeasibility of practical application of risk assessments


As early as in 1988 and later in 1993, I pointed to the implications and practical unacceptability of the results of some well-known published asbestos risk estimates (55,57). Table 9 shows my calculations of exposure limits for asbestos in the atmosphere derived from some of these risk assessments.


A 1986 WHO Expert Meeting proposed the lifetime risk estimate for smokers (mesothelioma: 12 x 10 5, lung cancer: 16 x 10 5 as upper limits of the number of expected deaths per 100,000 population) at an assumed airborne asbestos fibre concentration of 500 f/m3 (71). Assuming that the acceptable risk, used for carcinogens in the WHO Water Quality Guidelines (72), is 1 x 10 5, the calculated exposure limit is 18 fibres per cubic meter of air.


Taking the risk estimate of 13.5 x 10 5 for nonsmokers and using the same acceptable risk (1 x 10 5), the obtained exposure limit is 37 fibres per cubic meter. Confronted with prevalent concentrations found in the air of rural areas with no specific asbestos sources (up to 100 f/m3) (7), these exposure limits seem to suggest that in areas without any specific source of asbestos emission, a nearly 6-fold reduction of current asbestos levels would be required, which is practically impossible to achieve.


Table 9 also illustrates that an exposure limit of 45 asbestos fibres per cubic meter can be derived from the asbestos risk estimate published in the WHO Air Quality Guidelines of 1987 (11 x 10 5 for a population with the hypothetical proportion of 30% smokers) (73). This value is lower or as low as the concentrations found in rural areas without specific asbestos emission. The table also shows prevalent asbestos fibre concentrations in urban areas (from fewer than 100 to 10,000 per cubic meter) (7).

EXPOSURE CONCERNS

Table 10 shows the same calculations on the basis of the risk assessment by the NRC/NAS (65). Applying the same level of acceptable risk (1 x 10 -5) and using the number of estimated deaths from mesothelioma and lung cancer for male smokers and nonsmokers at the assumed asbestos concentration of 400 fibres per cubic meter, the respective calculated exposure limits are 9 and 22 fibres per cubic meter.

In other words, these limits require a nearly 10-fold reduction of asbestos fibre levels in rural areas without specific asbestos emission! It is obvious that mathematical extrapolations

CONCLUSIONS There is no doubt that fibres of all the prevalent forms of asbestos can cause lung cancer and mesothelioma. The weight of evidence convincingly suggests that amphiboles are more potent carcinogens than chrysotile.

No threshold has been identified for any of the types of asbestos except possibly for chrysotile; a practical threshold was found in chrysotile mining operations, in the manufacturing of chrysotile friction products and in some cohorts of workers in asbestos-cement production.

The unit risks, estimated in studies acceptable as regards the number of examinees, the duration of follow-up and the quality of data vary by several orders of magnitude. To a large extent, this is the consequence of considerable uncertainty in the estimates of past exposure levels due to errors in conversion from weight (mg/m3) or count (mppcf) concentrations of total particles to the currently used count concentrations of defined fibres.

The practical application of unit risks of such uncertainty leads to unachievable exposure limits. In spite of hundreds of papers published on asbestos health effects, there are still important unresolved issues. The effects seen today are the consequence of uncertain exposure of 20-50 years ago.

It cannot be predicted with any degree of certainty what will the consequences of the current, incomparably lower exposure levels be in the future. Yet, there is no doubt that it is advisable to replace any potential carcinogen with noncarcinogenic or less carcinogenic material whenever possible.

At this point in time, however, there are few materials of known toxicity / carcinogenic and at least equal technological performance. There is a potential for the development of such materials, but their toxicological properties have not been evaluated sufficiently. This is the main problem the world is facing on the eve of the possible worldwide asbestos ban, which will be considered in the second part of this paper:

'The Asbestos Dilemma: II. The Ban". of asbestos risk lead to unfeasible threshold limit values.

WHERE'S THE ASBESTOS?

The TUC wants a public register of asbestos in workplaces, homes and public buildings.

In a submission to the HSC on new asbestos regulations, the TUC has welcomed the HSC proposals to require employers to survey their buildings for asbestos, but added the public and workers must have a right to know where there is asbestos in British buildings that contain the fatal fibre.

TUC general secretary John Monks said:

'Every year, 4,500 people die from asbestos-related diseases in Great Britain, and the main source of exposure in the future will be from the decay and disturbance of asbestos in premises across Britain. We welcome in particular the provisions for union safety reps to be involved in the management of asbestos risks. The protection promised by the new regulations rightly concentrates on those most at risk - workers engaged in repair, renovation and removal as well as workers in the emergency services. But the needs of others, such as the general public and workers in buildings with asbestos present, also need to be addressed.'
The public register should be freely accessible, for example on the internet, TUC said.

TUC news release.

TUC submission, Starting to clear out the fatal fibre - managing the risks of asbestos in premises.

Insurers refuse asbestos claims The insurance company Royal and Sun Alliance is refusing to pay compensation to victims of asbestos dust who worked in the Clyde shipyards. The company has denied claims that the law was broken when it issued insurance certificates to asbestos manufacturer Turner and Newall. Many former employees subsequently developed incurable diseases related to the dust.

Lawyers acting for sufferers say that from 1972 to 1977 Royal and Sun Alliance, formerly Royal Insurance, issued certificates to Turner and Newall, excluding asbestosis. They say this was illegal and Royal and Sun Alliance should now pay up. Royal, however, insists it has not broken the law, saying it excluded asbestos-related injury because it was a risk it was not willing to underwrite and Turner and Newall was self-insured against asbestosis.

The lawyer for those affected, Frank Maguire of Thompson's Solicitors, said they had already applied through the courts for documents that would prove Royal was liable. Asbestos compensation is becoming a highly contentious issue worldwide. Companies in the US are increasingly reporting financial difficulties due to the volume of claims.

BBC News Online.

For the international picture see the Financial Times and Hazards safety crimes webpages Victory for asbestos safety row worker An engineering consultant who lost his job after raising concerns about the handling of asbestos has been awarded more than ·40,000 compensation.

Making the award, a Glasgow employment tribunal ruled that Cadogan Consultants Ltd was wrong to dismiss Albert Wardle, who had continued to raise concerns about safety and training in relation to asbestos exposure. The warnings followed a serious incident at Perth Crematorium in which staff had been in contact with potentially harmful fibres.

The Scotsman

MOD 1: Asbestos victim's right to fight A dockyard worker has won the right to sue for damages over exposure to asbestos, despite bringing his action later than the law would normally allow. John Pope, 60, a former shipwright at Rosyth Naval Dockyard, worked alongside his brother, who died from the asbestos cancer mesothelioma. He submitted his claim years after being diagnosed with asbestos-related pleural plaques in 1997, but said he was so relieved to not have asbestosis he did not take in any other information. His employer, the Ministry of Defence (MoD), had argued the case was 'out of time.'

The Scotsman

MOD 2: Judgment paves way for forces asbestos payouts The High Court has paved the way for compensation claims by members of the armed forces who have previously been blocked from suing the government for death or injury. Mr Justice Keith backed the argument that the current immunity from action is incompatible with rights under the European Convention. The case was brought by Alan Matthews who claims that he developed an asbestos-related illness as a result of asbestos exposure in the course of his work in the Royal Navy.

He was employed as an electrical engineer between 1955 and 1968. He says it was not until some time in 1999 that he became aware that his illness was attributable to what he alleges were acts or omissions on the part of the Ministry of Defence (MoD). MoD was given permission to appeal.

Ananova

South Africa: Cape fear for compensation

South African asbestos victims have an anxious wait for hard-won compensation from London-listed Cape plc. Richard Meeran of Leigh Day & Co, the London lawyer for the South African victims, says Cape signed a settlement agreement last month in "good faith" and adds he has "every expectation" that Cape will meet its liability. However, Meeran concedes there is still a "risk" that Cape plc will go insolvent. Cape has agreed to pay ·21 million into a trust fund (Risks 33). The company has still to obtain approval from its bankers and shareholders for the deal. Meeran says if payouts are stalled the matter will proceed to trial. Business Day

CHRYSOTILE - AMPHIBOLES

Table 3 shows the EPAÕs inconsistency in the approach to carcinogenic potency of different asbestos fibres. It shows modified values of the coefficient KL, taken from an EPA publication (36), indicating considerable differences in the potency of different asbestos fibres.

The coefficient KL reflects the carcinogenic potential of the exposure to carcinogens; it is the estimated increase in lung cancer risk due to one-year exposure to the unit concentration of 1f/ml. The values presented in Table 3 clearly show that the carcinogenic risk is by far the lowest in the exposure to chrysotile only, with the exception of chrysotile in textile production.

Exposure to amosite fibres alone involves a much greater risk, as is the case with the combined exposure to amphiboles and chrysotile. The high KL value in pure chrysotile textile production is attributed to a significantly higher content of more carcinogenic long chrysotile fibres in textile production (37-40).

Rich evidence of the significant difference in the potencies between fibres of chrysotile and amphiboles gave grounds for introducing 'the chrysotile hypothesis" and 'the amphibole hypothesis". The first says that the human risk becomes acceptable at a sufficiently low exposure level to chrysotile, and the second that the carcinogenic risk at low concentrations of chrysotile is present only if amphiboles are also present.

These hypotheses are not generally accepted; they have particularly been rejected by the US regulatory agencies (1,33) and by the Ramazzini Society (12,41). The controversy about whether there is a difference in the carcinogenic potency between chrysotile and amphibole fibres is continued in more recent papers by most reputable authors in the field.

While Berry (42), Landrigan and co-workers (43), and Dement (44) believe that chrysotile is less potent than amphiboles in its ability to cause mesothelioma, and Hodgson and Darnton (45) conclude that specific risks of mesothelioma from chrysotile, amosite and crocidolite are in the ratio 1:100:500, respectively, Landrigan and coworkers and Dement consider that the lung cancer risk from chrysotile is at least as high as that from amphiboles, and Smith and Wright (46) regard chrysotile as the main cause of pleural mesothelioma in humans.

While McDonald and McDonald (50) and McDonald (53) state that the carcinogenic risk at present day levels of exposure to commercial chrysotile is vanishingly small and that the remaining risk is due to contamination of chrysotile by the amphibole tremolite, Dement (44) maintains that chrysotile should not be controlled differently than other asbestos types.

EXPOSURE CONCENTRATION

Errors in estimates of past asbestos exposure The current mortality from asbestos-related cancer is the consequence of exposures of 20- 50 years ago, or even longer. There is no doubt that the exposure levels in the distant past were considerably higher than those of today. As an example, Table 5 shows the concentrations measured in mines and towns of Canada in the period 1973 to 1995 (63).

Results in Parentheses Ð personal communication In the distant past, the techniques of exposure measurement did not specify asbestos fibres, but referred to either gravimetric concentration to particles in the air, expressed in grams or mg per m3 or, later, to count concentrations of particles (not fibres) expressed in million particles per cubic foot of air (mppcf). Thus, the early method measured all particles, of which fibres constituted only a minor fraction.

As exposure levels in the past must be taken into account in the quantitative risk assessment, various authors estimates assumed specific concentrations of airborne asbestos fibres converting the measured gravimetric or count concentrations of total particles to the currently defined fibres using a number of mathematical conversions.

These conversions relied on many dubious assumptions and approximations, and included errors of several orders of magnitude into the mathematical estimates of historical airborne fibre concentrations.

This is one of the main reasons why I cautioned Ð quite early Ð that the quantitative risk assessment equations and particularly low dose extrapolations used for predicting mortality or morbidity in populations exposed to considerably lower exposure levels were very uncertain (56,57).

Table 6 shows some errors in the conversion of such concentrations. The first part of the table shows the relationships between asbestos fibre diameter and length and the concentration expressed in fibres per ml for the gravimetric concentration of 10 ng/ml air [based on calculations by Pott (22)].

The table shows that the same air with weight concentration of 10 ng/ml may contain 32 f/ml if the fibre diameter is 2.0 mm and the length 40 mm, while it may contain 8,200,000 f/ml of fibres with the diameter of 0.03 mm and the length 0.63 mm.

The errors involved in the conversion of weight concentrations of total particles of unknown size distribution into the count concentrations of fibres of a defined size fraction are so great that the obtained results may be complete nonsense. Table 6 also shows an example of EPA's conversion in 1986 (36).

EPA took 30 (the geometric mean of conversion factors ranging 0.5-150 obtained in six studies) as the conversion factor to be used, introducing a possible error of more than 200 in the conversion.

Robock reported in 1984 (64) that the conversion factor for converting mppcf into f/ml obtained in a large number of samples was between 0.5 and 47.8, which introduces a hundredfold error into conversions.

Uncertainties and unspecifities of models Table 7 shows the estimation of lifetime risk due to lethality from mesothelioma (L: excess deaths per million population) induced by the asbestos concentration of 0.0004 f/ml for an age of 73 years, calculated by the well known equation of the National Research Council of the US National Academy of Sciences (NRC/NAS) L=C (conc.) (age) K (65).

Using the values of the coefficients C (0.85 Ð 7.22 x 10 8 ) and K (2.6-5.0), obtained in epidemiological investigations, the number of calculated excess deaths ranges from 0.2-60,000 per million population, yielding a ratio of up to 300,000 in estimated mortality per million population and rendering the risk assessment meaningless (56).

In 1991, I criticized (56) those EPA's uncertainties in risk assessments which led to their proposal of the asbestos ban. Table 8 shows the number of cancer cases expected by EPA to be avoided in 13 years following the proposed asbestos ban, as set forth by three consecutive EPA proposals. The very fact that the number of cancers varied from 1,000 in 1986 (36) to 315.8 in 1988 (66), ending with 148-202 in the Final Rule of 1989 (1), sheds strong doubt on EPA's risk estimates.

MESOTHELIOMA CANCER

The evaluation of IPCS/WHO in 1986 (7) was: In the general population the risks of mesothelioma and lung cancer attributable to asbestos cannot be quantified reliably and are probably undetectably low.

Cigarette smoking is the major etiological factor in the production of lung cancer in the general population. The risk of asbestosis is virtually zero. However, the latest IPCS /WHO evaluation in 1998 (31) stated that no threshold had been identified for carcinogenic risks from chrysotile asbestos.

There is an almost general consensus that no threshold exists for amphiboles. There is still a controversy as to whether there is a threshold, or at least a practical threshold, for chrysotile. Studies are limited to only two industrial cohorts with relatively pure exposure to chrysotile fibres containing sufficient high quality data for exposure-response analysis.

These studies include the Quebec miners and millers (47-53, 59) and South Carolina textile workers (37-40). Table 4 shows standard mortality from lung cancer in Quebec miners and millers (48), 1976-1988, in relation to exposure accumulated up to the age of 55 years, and the lung cancer mortality by cumulative exposure in South Carolina workers (39) employed between 1940 and 1990.

There is no indication of a trend in standard mortality over 7 lowest categories of exposure of miners and millers (<10 -<990 f/ml yrs). The standard mortality was elevated at the three highest levels, i.e. at the cumulative exposure of more than 990 f/ml yrs. A completely different result was obtained in South Carolina textile workers.

There was a consistent increase in the risk of lung cancer with increasing cumulative exposure in all the exposure categories of cumulative exposure more than 2.7 f/ml yrs. The proportional mortality from mesothelioma in the Quebec cohort was only 0.45% (33 deaths among 7,312 workers) by end of 1988.

Comparing the very high slope of 0.021 per f/ml yr in textile workers with the very low slope of 0.0005 per f/ml yr in Quebec miners and millers, the authors of the last exposure response analysis (40) attribute this large difference to the considerably higher proportion of carcinogenic long fibres in the textile production.

It was on the basis of the results obtained in Quebec workers that the authors (48, 50, 53) concluded that chrysotile was not the cause of lung cancer, except at very high levels of exposure above 25-30 f/ml, well above current exposure even under poor conditions. Can the finding that there was no trend in standard mortality over 7 lowest exposure categories of miners and millers be taken as the basis for the conclusion that there is a practical threshold for chrysotile (49)?

The situation with mesothelioma is somewhat different. The standard mortality rates in several countries show an increasing trend. The results of some evaluations caused panic. British (14, 19), French (17), New Zealand (15), and the US (12,18) data projected thousands of deaths per year of mesothelioma in the decades to come.

As a considerable proportion of diagnosed mesothelioma was believed to be the consequence of exposure to asbestos fibres, there is a tendency to attribute all these deaths to the effects of these fibres without an objective proof and without differentiating the type of fibres.

It is worth noting that the description of mesothelioma in literature preceded the exploitation of asbestos (59) and that other causes of mesothelioma have also been described (60). The role of Simian virus SV40 in the development of human mesothelioma has recently received more attention.

Some authors (60) assume that SV40 may contribute to the development of human mesotheliomas that occur in people not exposed to asbestos.

However, they state that the available epidemiological data are insufficient to explain the role that SV40 may have played in contributing to the increased incidence of mesothelioma currently recorded. Other authors (18,61,62) propose that asbestos and SV40 may be cocarcinogens.

The latency period for the development of mesothelioma is between 30 and 50 years, so that the current mesothelioma deaths are predominantly the consequence of exposure to mixtures of chrysotile and amphiboles in the far past when the exposure levels were incomparably higher than those of today. It is impossible to evaluate whether the current (considerably lower) exposures to pure chrysotile would bring about similar consequences.

MESOTHELIOMA MORTALITY

The current mortality from asbestos-related cancer is the consequence of exposures of 20- 50 years ago, or even longer. There is no doubt that the exposure levels in the distant past were considerably higher than those of today. As an example, Table 5 shows the concentrations measured in mines and towns of Canada in the period 1973 to 1995 (63).

Results in Parentheses Ð personal communication In the distant past, the techniques of exposure measurement did not specify asbestos fibres, but referred to either gravimetric concentration to particles in the air, expressed in grams or mg per m3 or, later, to count concentrations of particles (not fibres) expressed in million particles per cubic foot of air (mppcf). Thus, the early method measured all particles, of which fibres constituted only a minor fraction.

As exposure levels in the past must be taken into account in the quantitative risk assessment, various authors estimates assumed specific concentrations of airborne asbestos fibres converting the measured gravimetric or count concentrations of total particles to the currently defined fibres using a number of mathematical conversions.

These conversions relied on many dubious assumptions and approximations, and included errors of several orders of magnitude into the mathematical estimates of historical airborne fibre concentrations.

This is one of the main reasons why I cautioned Ð quite early Ð that the quantitative risk assessment equations and particularly low dose extrapolations used for predicting mortality or morbidity in populations exposed to considerably lower exposure levels were very uncertain (56,57).

Table 6 shows some errors in the conversion of such concentrations. The first part of the table shows the relationships between asbestos fibre diameter and length and the concentration expressed in fibres per ml for the gravimetric concentration of 10 ng/ml air [based on calculations by Pott (22)].

The table shows that the same air with weight concentration of 10 ng/ml may contain 32 f/ml if the fibre diameter is 2.0 mm and the length 40 mm, while it may contain 8,200,000 f/ml of fibres with the diameter of 0.03 mm and the length 0.63 mm.

The errors involved in the conversion of weight concentrations of total particles of unknown size distribution into the count concentrations of fibres of a defined size fraction are so great that the obtained results may be complete nonsense. Table 6 also shows an example of EPA's conversion in 1986 (36).

EPA took 30 (the geometric mean of conversion factors ranging 0.5-150 obtained in six studies) as the conversion factor to be used, introducing a possible error of more than 200 in the conversion.

Robock reported in 1984 (64) that the conversion factor for converting mppcf into f/ml obtained in a large number of samples was between 0.5 and 47.8, which introduces a hundredfold error into conversions.

Uncertainties and unspecifities of models Table 7 shows the estimation of lifetime risk due to lethality from mesothelioma (L: excess deaths per million population) induced by the asbestos concentration of 0.0004 f/ml for an age of 73 years, calculated by the well known equation of the National Research Council of the US National Academy of Sciences (NRC/NAS) L=C (conc.) (age) K (65).

Using the values of the coefficients C (0.85 Ð 7.22 x 10 8 ) and K (2.6-5.0), obtained in epidemiological investigations, the number of calculated excess deaths ranges from 0.2-60,000 per million population, yielding a ratio of up to 300,000 in estimated mortality per million population and rendering the risk assessment meaningless (56).

In 1991, I criticized (56) those EPA's uncertainties in risk assessments which led to their proposal of the asbestos ban. Table 8 shows the number of cancer cases expected by EPA to be avoided in 13 years following the proposed asbestos ban, as set forth by three consecutive EPA proposals. The very fact that the number of cancers varied from 1,000 in 1986 (36) to 315.8 in 1988 (66), ending with 148-202 in the Final Rule of 1989 (1), sheds strong doubt on EPA's risk estimates.

TREMOLITE - CHRYSOTILE

THE ASBESTOS DILEMMA

In the cohort of some 11,000 Quebec miners and millers (47,53), 25 cases of mesothelioma were identified from miners in the Thetford Mines region and 8 from the large mine at Asbestos. The proportion of tremolite in the chrysotile was 3 times higher in the former than in the latter region.

The analysis of deaths from mesothelioma in men employed in the Thetford Mines, with matched references, showed that odds ratios for work in the central mines, where the tremolite content was 3 times higher, were significantly elevated for mesothelioma and lung cancer.

By contrast, in the peripheral mines, where the tremolite content was 3 times lower, there was little or no evidence of increased risk. The authors conclude that these long-term studies Ð including data from as early as 1970Õs Ð show that chrysotile rarely caused mesothelioma and was not a major cause of lung cancer, except at very high levels of exposure.

They attribute the remaining risk to tremolite, because its biopersitence is much higher than that of chrysotile. However, the Mount Sinai group (54) in their analysis of the lung and mesothelial tissues taken from 151 human malignant mesothelioma cases, found asbestos fibres in almost all the lung tissues as well as in the mesothelial tissue, the most common asbestos types being an admixture of chrysotile and amphiboles, followed by amphiboles alone and chrysotile alone. The most common of asbestos types in the mesothelial tissues were chrysotile alone, followed by chrysotile plus amphibole, and amphibole alone.

They conclude that chrysotile can induce human malignant mesothelioma without the presence of amphiboles, since, in some of the mesothelioma cases, the fibres detected in the lung or mesothelial tissues were exclusively chrysotile fibres. The controversy continues.

Are health effects of asbestos fibres threshold or non-threshold effects?

All asbestos-related diseases are dose-related: the higher the concentration and duration of exposure, the higher the prevalence of the disease and mortality.

However, the form of the dose-response curve at low doses, typical for the exposure of general population, is not known. There are contradictory opinions as to whether the dose-response relationship in the region of low doses is linear or not. It is practically impossible to measure the effects at such low doses either epidemiologically or experimentally.

It is for this reason that mathematical extrapolations ('low-dose extrapolations"), which carry errors of several orders of magnitude, are used in the quantitative risk assessments. I criticized these extrapolations in 1988 (55) and again in 1991 (56) and in 1993 (57).

Recently, in 2001, Berman (58), reported that 'the published doseresponse coefficients for asbestos vary by more than a factor of 500 for lung cancer and more than a factor of 1,000 for mesothelioma".

Extrapolation of the most frequently used linear relationship into the origin of coordinates means that there is no exposure threshold, i.e. that even the lowest exposure to asbestos may carry some risk of disease and death.

Others, however, believe that there is an asbestos fibre exposure threshold for chrysotile below which there will be no pathologic effects (particularly asbestosis or lung carcinoma) or that the effects are so rare that they cannot be epidemiologically detected.

As negative effects cannot be proven in practical risk assessment, the issue remains unresolved. An expert group of the CEC concluded the following in 1977 (27): It is impossible to come to reliable quantitative assessment of the risk of malignancies for the general public. It is possible that there is a level of exposure (perhaps already achieved in the general public) where the risk is negligibly small.

ASBESTOS REFERENCES

1. U.S. Environmental Protection Agency (EPA). Asbestos manufacture, importation, processing, and distribution in commerce prohibitions. Final Rule. Federal Register 1989; 54/132:29462-29513.

2. EU Commission Directive 91/659/EEC. Official Journal L.363.31/12/1991, p.36-38.

3. EU Commission Directive 1999/77/EC. Official Journal L.207.06/08/1999, p.18-20.

4. International Labour Organization (ILO). Asbestos Recommendation, No. 172. Geneva: ILO, 1986.

5. Valic F. Asbestos and Health. Local authorities, Health and Environment Briefing Series 25. Copenhagen: WHO Regional office for Europe, 1998.

6. Landrigan PJ, Nicholson WJ, Suzuki Y, LaDou J. The hazards of chrysotile asbestos: a critical review. Industrial Health 1999; 37(3):271-80.

7. Interternational Programme on Chemical Safety/World Health Organization (IPCS/WHO). Asbestos and other natural mineral fibres. Environmental Health Criteria 53. Geneva: WHO; 1986.

8. IARC Monographs on Evaluation of Carcinogenic Risks to Humans. Suppl.7. Lyon: International Agency for Research on Cancer; 1987.

9. Commission of the European Communities (CEC). Official Journal of the European Communities, 1995; (C326/38).

10. World Health Organization (WHO) Guidelines for drinking water quality. Vol.2. Geneva: WHO; 1996.

11. Valic F, Beritic-Stahuljak D. Is chrysotile asbestos exposure a significant health risk to the general population? Central Eur J Publ Health 1993;1:26-30.

12. Collegium Ramazzini. Updating the epidemiology of asbestos disease. Proceedings, Annual Ramazzini Days. Med Lav 1995; 86(5):388-500.

13. Peto J, Henderson BE, Pike MC. Trends in mesothelioma incidence and the forecast epidemic due to asbestos exposure during World War II. In: Peto J, Schneiderman M, editors. Quantification of occupational cancer. Banbury Report 9. Cold Spring Harbor (NY): Cold Spring Harbor Laboratory; 1981. p. 51-72.

14. Peto J, Decarli A, La Vecchia C, Levi F, Negri E. The European mesothelioma epidemic. Br J Cancer 1999; 79:566-672.

15. Kjellstrom T. Smartt P. Increased mesothelioma incidence in New Zealand: the asbestos-cancer epidemic has started. New Zealand Med J 2000; 113:485-90.

16. Bourdes V, Boffetta P, Pisani P. Environmental exposure to asbestos and risk of pleural mesothelioma: review and meta-analysis. Eur J Epidemiol 2000; 16:411-7.

17. Banaei A, Auvert B, Goldberg M, Gueguen A, Luce D, Goldberg S. Future trends in mortality of Frenchmen from mesothelioma. Occup Environ Med 2000; 57:488-94.

18. Carbone M, Rizzo P, Pass H. Simian virus 40 : the link with human malignant mesothelioma is well established. Anticancer Res 2000; 20:875-7.

19. Coggon D. Occupational cancer in the United Kingdom. Environ Health Perspect 1999; 107 (Suppl.2): 239-44.

20. World Health Organization (WHO). A recommended method by phase-contrast optical microscopy (membrane filter method). Geneva: WHO; 1997.

21. Stanton MF, Layard D. The carcinogenicity of fibrous minerals. In: Proceedings of the Workshop on Asbestos: Definitions and Measurement Methods. Special publication 506. Washington (DC): US National Bureau of Standards; 1978. p.143- 151.

22. Pott F. Some aspects of the dosimetry and of carcinogenic potency of asbestos and other fibrous dusts. Staub-Reinhalt Luft 1978; 38:486-90.

23. Walton WH. The nature, hazards and assessment of occupational exposure to airborne asbestos dust Ð a review. Ann Occup Hyg 1982; 25:117-247.

24. Valic F, Skuric Z. Metodologija ocjenjivanja profesionalne izlozenosti vlaknima azbesta [Methodology of the evaluation of occupational exposure to asbestos fibres, in Croatian]. Arh Hig Rada Toksikol 1988; 39:169-81.

25. Kane AB, Boffetta P, Saracci R, Wilbourn JD, editors. Mechanisms of fibre carcinogenesis. IARC Scientific Publication No. 140. Lyon: International Agency for Research on Cancer; 1996.

26. Nicholson WJ, Landrigan PJ. The carcinogenicity of chrysotile asbestos. In: Mehlman MA, editor. Advances in modern environmental toxicology. Volume XXII. Princeton (NJ): Princeton Scientific Publication; 1994. p. 407-23.

27. Commission of the European Communities (CEC). Public health risks of exposure to asbestos. Bruxelles: CEC; 1977.

28. World Health Organization (WHO). Occupational exposure limits for asbestos. Geneva: WHO; 1989.

29. International Programme on Chemical Safety/World Health Organization (IPCS/WHO). Reduction of asbestos in the environment ICS/89.34). Geneva: International programme on Chemical Safety; 1989.

30. Commission of the European Communities (CEC). Communication 426. Bruxelles: CEC; 1996.

31. International Programme on Chemical Safety/World Health Organization (IPCS/WHO). Chrysotile Asbestos. Environmental Health Criteria 203. Geneva: WHO 1998.

32. American Conference of Governmental Industrial Hygienists (ACGIH). Occupational exposure limits 1995/1996. Cincinnati (OH): ACGIH; 1996.

33. Occupational Safety and Health Administration (OSHA). Occupational exposure to asbestos; Final Rule. Federal Register 1994; 59:40964-41158.

34. American Conference of Governmental Industrial Hygienists (ACGIH). 2001 threshold limit values for chemical substances and physical agents & biological exposure indices. Cincinnati (OH): ACGIH: 2001.

35. Pravilnik o maksimalno dopustivim koncentracijama stetnih tvari u atmosferi radnih prostorija i prostora i o bioloskim granicnim vrijednostima [Threshold limit values of hazardous materials in the air of work premises and biological threshold limits, in Croatian]. Narodne novine 1992/1993; (92): 2088-111.

36. US Environmental Protection Agency (US EPA). Airborne asbestos health assessment update. EPA/600/8-84/003F. Washington (DC): Environmental Protection Agency; 1986.

37. Dement JM, Wallingford KM. Comparison of phase contrast and electron microscopic methods for evaluation of occupational asbestos exposures. Appl. Occup Environ Hyg 1990;5:242-7.

38. Dement JM, Brown DP, Okun A. Follow-up study of chrysotile asbestos textile workers: cohort mortality and case control analyses. Am J Ind Med 1994;26:431-47.

39. Dement JM, Brown DP. Lung cancer mortality among asbestos textile workers: a review and update. Ann Occup Hyg 1994;38:525-532.

40. Stayner L, Smith R, Bailer J et al. Exposure Ð response analysis of respiratory disease associated with occupational exposure to chrysotile asbestos. Occup Environ Med 1997;54:646-652.

41. LaDou J, Landrigan P. Bailer J, Foa V, Frank A. on behalf of the Collegium Ramazzini. A call for an international ban on asbestos. Can Med Ass J 2001; 20:489- 490.

42. Berry G. Models for mesothelioma incidence following exposure to fibers in terms of timing and duration of exposure and the biopersistence of the fibers. Inhalation Toxicol 1999;11:11-30.

43. Landrigan PJ, Nicholson WJ, Suzuki Y, LaDou J. The hazards of chrysotile asbestos: a critical review. Indust Health 1999:37:271-80.

44. Dement J. Differences in carcinogenicity between asbestos types. 2001 EPA Asbestos Health Effects Conference; May 2001; Oakland (CA) [cited 10 March 2002]. Available from URL: http://www.epa.gov.swerrims/ahec/summary.htm

45. Hodgson JT, Darnton A. The quantitative risks of mesothelioma and lung cancer in relation to asbestos exposure. Ann Occup Hyg 2000; 44:565-601.

46. Smith AH, Wright CC. Chrysotile asbestos is the main cause of pleural mesothelioma. Am J Ind Med 1996;30:252-66.

47. McDonald JC, Liddell FDK, Dufresne A, McDonald AD. The 1891-1920 birth cohort of Quebec chrysotile miners and millers: mortality 1976-1988. Br J Ind Med 1993; 50:1072-81.

48. Liddell D. Cancer mortality in chrysotile mining and milling: exposure-response. Ann Occup Hyg 1994; 38:519-23.

49. Gibbs, GW, Valic F, Browne K, editors. Health risks associated with chrysotile asbestos. Ann Occup Hyg 1994; 38:399-426.

50. McDonald JC, McDonald AD. Chrysotile, tremolite, and carcinogenicity. Ann Occup Hyg 1997; 41:699-705.

51. McDonald AD, Case BW, Churg A et al. Mesothelioma in Quebec chrysotile miners and millers: epidemiology and aetiology. Ann Occup Hyg 1997; 41:707-19.

52. Liddell FDK, McDonald AD, McDonald JC. The 1891-1920 birth cohort of Quebec chrysotile miners and millers Ð development from 1904 and mortality to 1992. Ann Occup Hyg 1997; 41:13-36.

53. McDonald JC. Carcinogenicity of fibrous tremolite in workplace and general environments. 2001 EPA Asbestos Health Effects Conference; May 2001; Oakland (CA) [cited 10 March 2002]. Available from URL:http://www.epa.gov/swerrims/ahec

54. Suzuki Y, Yuen SR. Asbestos tissue burden study on human malignant mesothelioma. Indust Health 2001; 39:150-60.

55. Valic F. Risk assessment of non-occupational asbestos exposure Ð can it be done? Arh Hig Rada Toksikol 1988; 39:499-505.

56. Valic F. Some health aspects of environmental asbestos exposure. Proceedings of the AIA/NIOSH International Colloquium on Dust Measurement Techniques and Strategy. Budapest: National Institute of Occupational Health; 1991. p. 24-45.

57. Valic F. Influence of exposure conversions and activity-specific exposure Ð response relationships on the chrysotile asbestos risk assessment. In: Gibbs GW, Dunnigan J, Kido M. Higashi T, editors. Health Risks from exposure to mineral fibres: an international perspective. North York (NY) Ontario: Captus Press Inc.1993. p.129-35.

58. Berman DW. Assessing asbestos-related risk: new thinking / new protocol. 2001 EPA Asbestos Health Effects Conference; May 2001; Oakland (CA) [cited March 10 2002]. Available from URL: http://www.epa.gov/swerrims.ahec.

59. McDonald JC, McDonald AD. The epidemiology of mesothelioma in historical context. Eur Respir J 1996;9:1932-42.

60. Carbone M, Fisher S, Powers A, Pass HI, Rizzo P. New molecular and epidemiological issues in mesothelioma: role of SV40. J Cellul Physiol 1999; 180:167-72.

61. Mayall FG, Jacobson G, Wilkins R. Mutations of p53 gene and SV40 sequences in asbestos associated and non-asbestos associated mesothelioma. J Clin Pathol 1999;52:291-293.

62. Bocchetta M, Di Resta I, Powers A, Fresco R. Tosolini A, Testa JR, et al. Human mesothelial cells are unusually susceptible to simian virus 40 Ð mediated transformation and asbestos cocarcinogenicity. Proc Nat Acad Sci 2000;97:10214-9.

63. LeBel J. Review of fibre concentrations in asbestos mines and Quebec asbestos mining towns. Sherbrooke: Quebec Asbestos Mining Association; 1995.

64. Robock K. Comparison of different measuring procedures in relation to conditions at the work place. In: Fischer M, Meyer E, editors. Assessment of the cancer risk from asbestos. BBA Schriften No.2, 1984.

65. National Research Council, US National Academy of Sciences. Asbestiform fibers: non-occupational health risks. Washington (DC): National Academy Press, 1984.

66. US Environmental Protection Agency (US EPA). Regulatory impact analysis of controls on asbestos and asbestos products. Technical Report Vol. 1. Washington, DC; US EPA; 1988.

67. Berry G, Newhouse ML. Mortality of workers manufacturing friction materials using asbestos. Br J Indust Med 1983;40;1-7.

68. McDonald AD, Fry JC, Wooley AJ, McDonald JC. Dust exposure and mortality in an American chrysotile asbestos friction products plant. Br J Indust Med 1984:41:151-7.

69. McDonald JC. Health implications of environmental exposure to asbestos. Environ Health Perspect 1985;62:319-28.

70. Valic F, Asbestos risk in vehicle manufacture, maintenance and repair. In: Reduction of asbestos in the environment. Geneva: International Programme on Chemical Safety / World Health Organization, 1989, 73-99.

71. World Health Organization Regional Office for Europe (WHO/Europe). Asbestos. Final meeting on air quality guidelines for the European region. Copenhagen: WHO/Europe; 1986.

72. World Health Organization (WHO). Guidelines for drinking water quality, Geneva: WHO; 1984.

73. World Health Organization (WHO). Air quality guidelines for Europe. WHO Regional Publications, European Series No.23. Copenhagen: WHO/Europe;1987.

ASBESTOS REGULATIONS

Attention: Health and industrial editors, health, safety and personnel media
TUC wants legal right to know if the place where you live or work is contaminated with asbestos.

In a submission to the Health and Safety Commission (HSC) on new asbestos Regulations, published today (Saturday), the TUC has welcomed the HSC proposals to require employers to survey their buildings for asbestos, but calls for a public register of the asbestos in British buildings, such as homes, hospitals, schools and other workplaces.

The TUC believes that the public and workers should have a right to know where there is asbestos in the 850,000 commercial premises, 400,000 flats and 150,000 houses which contain the fatal fibre. The public register should be freely accessible, for example on the internet.

TUC General Secretary John Monks said:

'Every year, 4,500 people die from asbestos-related diseases in Great Britain, and the main source of exposure in the future will be from the decay and disturbance of asbestos in premises across Britain. The TUC has long campaigned on this issue and strongly welcomes the CommissionÕs proposals, although we would like to see them go further.

'We welcome in particular the provisions for union safety reps to be involved in the management of asbestos risks, and will be producing guidance for safety reps on how to make the most of the opportunities presented by the Regulations.

'The public and workers must have a legal right to know if they are living or working in the vicinity of asbestos through a public register of asbestos in buildings.

'The protection promised by the new regulations rightly concentrates on those most at risk - workers engaged in repair, renovation and removal as well as workers in the emergency services. But the needs of others, such as the general public and workers in buildings with asbestos present, also need to be addressed.

'In the long run, all asbestos in all British buildings needs to be removed. As a start, however, the regulations proposed by the Commission should be brought into force without delay.'

The TUC also wants to see:

more people protected

In addition to the groups of workers most at risk, there are new waves of workers and people who although less at risk, are still exposed to the possibility of disease, disablement and death. The TUC wants these people to be covered by the regulations and wants to see the proposed regulations strengthened to include accidental or potential, rather than simply planned, disturbance of asbestos.

faster implementation of the new Regulations

The TUC wants to see the changes set out in the Commission proposals introduced as soon as possible. A one-year implementation deadline is more appropriate than 18 months or two years, as suggested for different parts of the Regulations.

Notes to Editors:

All TUC press releases can be found at www.tuc.org.uk

A series of TUC rights leaflets are available on our website and from the know your rights line 0870 600 4 882. Lines are open every day from 8am-10pm. Calls are charged at the national rate.

The full TUC submission Ô Starting to clear out the fatal fibre - managing the risks of asbestos in premisesÕ , is available on the TUC website www.tuc.org.uk. The submission is in response to the HSE consultative document (CD 176) on ÔRevised proposals for amendments to the Control of Asbestos at Work Regulations and a new supporting Approved Code of Practice.Õ

Contacts:

Media enquiries: 020 7467 1248 or 07699 744115 (pager) or email media@tuc.org.uk

Other enquiries: Owen Tudor, Senior Policy Officer, on 020 7467 1325 or 07788 715261 or at otudor@tuc.org.uk