Asbestos in drinking water
The WHO found "no convincing evidence of the carcinogenicity of ingested asbestos in epidemiological studies of populations with drinking water supplies containing high concentrations of asbestos." (Guidelines for Drinking Water Quality. World Health Organization Report, 1993.)

"Generally, it has been concluded that the concentrations of asbestos in drinking water resulting from the use of asbestos-cement pipes do not present a hazard to human health." (World Health Organization letter to Mr. N. Kouinis of the Greek municipality of Corinth, April 12, 1990)

Environmental risk
"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." (Asbestos and other natural mineral fibres. IPCS Environmental Health Criteria 53. Published under the joint sponsorship or UNEP, ILO and WHO, 1986.)

Fibre type differences
"There are differences between predicted risks by fibre type and by industrial process for the same fibre concentration and duration of exposure. These are relevant to interpretation of the evidence and for targeting of occupational control measures."

"It is also recommended that countries should move quickly to lower the occupational exposure limit for an individual worker to 1 f/ml or below, if they have not already done so. For crocidolite and amosite asbestos, on the basis of health, it is recommended that their use should be prohibited as soon as possible. (Occupational Exposure Limit for Asbestos. Report prepared by a WHO meeting, Oxford, UK, 10-11 April, 1989.)

Asbestos insulation in buildings
"Although public concern over asbestos in buildings has focused primarily on potential risks to general building occupants, there does not appear to be sufficient justification on the grounds of risk to the health of general occupants for arbitrarily removing intact asbestos-containing material (ACM) from well-maintained buildings." (Asbestos in Public and Commercial Buildings: A Literature Review and Synthesis of Current Knowledge. Health Effects Institute-Asbestos Research, Cambridge, MA, 1991.)

"Intact and undisturbed asbestos materials do not pose a health risk. The mere presence of asbestos in a building does not mean that the health of building occupants is endangered. Asbestos-containing material which is in good condition, and is not somehow damaged or disturbed, is not likely to release asbestos fibres into the air. Removal is often not a building owner's best course of action to reduce asbestos exposure. In fact, an improper removal can create a dangerous situation where none previously existed." (Managing Asbestos in Place: A Building Owner's Guide to Operations and Maintenance Programs for Asbestos-Containing Materials. United States Environmental Protection Agency, July 1990.)

Product risks
"High-density asbestos products such as asbestos cement and asbestos fire-board in normal condition and use should not create an unacceptable hazard, but care is needed to contain airborne dust during installation and maintenance of these products."

The Working Group concluded, therefore, that "provided good work practices were followed and that neither amphibole fibres nor substitute materials with similar potential to cause disease were used in friction products, detectable risks in vehicle maintenance and repair workers are not expected." (Report of an IPCS Group meeting on The reduction of asbestos in the environment, 12-16 December 1988, Rome, Italy. Published under the joint sponsorship of UNEP, ILO and WHO, 1989.)

Evidence of threshold
€ asbestosis
"In our judgement, asbestosis can be deemed a disease of past high exposure levels and will not occur in workers exposed to the regulated levels of occupational exposure now in force in Ontario." (Dupré J S, Mustard J F & Uffen R J. Report of the Royal Commission on Matters of Health and Safety Arising from the Use of Asbestos in Ontario. Ontario Ministry of the Attorney General, 1984:94-97.)

"It is concluded that there will be a threshold level of exposure below which no radiological or clinical manifestations of pulmonary fibrosis (asbestosis) will occur. The value for the threshold, and indeed the slope of the dose-response curve, depends on the fibre type and the fibre size-distribution in the workplace." (Health and Safety Executive, Review of Fibre Toxicology, 1996)

€ asbestosis as a precursor to lung cancer
"To me the available data indicate that the only scientifically established association of lung cancer and asbestos exposure is the association of asbestosis and lung cancer; thus, only the presence of asbestosis can be used to incriminate asbestos as a cause of lung cancer." (Churg A. Asbestos, Asbestosis and Lung Cancer, Modern Pathology 6: 1993; 6:509-511)

"Similarly to asbestosis, lung cancer shows a dose-response relationship with respect to asbestos exposure, suggesting that asbestos-induced lung cancer, like fibrosis, is a threshold phenomenon." (Health and Safety Executive, Review of Fibre Toxicology, 1996)

€ lung cancer
(i) mining
"There is no statistically significant evidence of increased lung cancer risk at <300 mpcf x years [ie. 50 f/cc for 20 years] in the chrysotile mine and mill workers of Quebec." (McDonald JC, Liddell FDK, Dufresne A, and McDonald AD, The 1891-1920 birth cohort of Quebec chrysotile miners and millers: mortality 1976-88, Br Jr Ind Med, 1993;50 1073-1081.)

"The significance of this study is that at current levels of occupational exposure any deaths from asbestosis or lung cancer are most unlikely." (study co-author J C McDonald)

(ii) Friction materials
"It is concluded that with good environmental control, chrysotile asbestos may be used in manufacture without causing excess mortality." (Berry G, Newhouse M L (1983). Mortality of workers manufacturing friction materials using asbestos. Br Jr Ind Med, 40(1):1-7.)

(iii) asbestos-cement
"Median exposure of 10-20 fibre€years does not seem to cause an increased risk of lung cancer" (Olsen CG and Hogstedt C. Lung Cancer among asbestos cement workers: A Swedish cohort study and review, Br J Ind Med 1985; 42(6):397-402.)

A cohort study carried out of 2,167 subjects employed between 1941 and 1983. No excess of lung cancers or other asbestos-related excess death is reported at mean fibre concentrations below 1 f/ml, although higher levels had probably occurred in certain areas of the asbestos-cement factory. (Gardner, MJ, Winter, PD, Pannett, B and Powell, CA. Follow-up study of workers manufacturing chrysotile asbestos-cement products. Br. J. Ind. Med. 1986; 43:726-732)

Three studies of asbestos-cement workers in Great Britain and Sweden using almost exclusively chrysotile are reviewed. No asbestos related mortality in meaningful excess of expected was found. "This is in contrast with most studies making similar products from mixed fibres containing mainly chrysotile but also amphiboles, crocidolite and amosite." (Gardner, MJ & Powell, CA. Mortality of asbestos-cement workers using almost exclusively chrysotile fibre, J. Soc. Occup. Med. 1986; 36:124-12)

A follow-up study of 1,970 workers in an asbestos-cement factory using chrysotile only, at low levels of exposure, showed no significant Standard Mortality Ratio (SMR) excesses. The causes of death investigated included neoplasms and cancers of the lung, pleura and gastrointestinal tract. (Thomas, HF, Benjamin, LT, Elwood, PC and Sweetnam, PM. Further follow-up study of workers from an asbestos cement factory. Br. J. Ind. Med., 1982; 39(3): 273-276.)

An investigation of 5,645 asbestos-cement manufacturing workers found no increased mortality resulting from chrysotile exposures of approximately 15 f/ml€years. (Weill, H, Hughes, J and Waggespack, C. Influence of dose and fibre type of respiratory malignancy risk in asbestos-cement manufacturing. American Review of Respiratory Disease, 1979; 120(2): 345-354.)

(iv) General public
This study of environmentally and domestically exposed women demonstrates that the general population exposed to chrysotile is not at a detectably increased risk of lung cancer, even when exposures have been very high (25-30 f/ml€years). Despite the fact that many of these women were exposed to doses which are significantly higher than today's occupational exposure limits (in France and elsewhere), and literally thousands of times higher than levels commonly found in public buildings - no excess lung cancer incidence was found. According to Michel Camus, one of the authors of the study, at the exposure levels he studied, the French risk model would have predicted 100 excess deaths due to lung cancer and there were none. (Camus & Siemiatycki, 1996 - in press)

€ mesothelioma
"...at present levels of environmental control, any mesothelioma risk from exposure in either area A or B [of Québec's chrysotile mines] would be far below the limits of epidemiological detection." (McDonald J C & McDonald A D. Chrysotile, tremolite and mesothelioma (Editorial). Science, January 10, 1995)

"As a practical matter, the data indicate that chrysotile will not produce mesothelioma in those exposed to any current or recent regulated numbers of fibres, and certainly not in those exposed to chrysotile encountered at environmental levels." (Churg A. Chrysotile, tremolite and malignant mesothelioma in man. Chest. 1988; 93(3). 621-628)

"Very few cases of mesothelioma can be reliably attributed to chrysotile, despite the many thousands of workers who have had massive and prolonged exposures to this type of asbestos. In contrast, mesotheliomas have been observed among some workers who experienced only brief exposures to amphiboles." (Health and Safety Executive, Review of Fibre Toxicology, 1996)

Biopersistence of chrysotile vs amphiboles
Wagner JC & Skidmore JW. (1965). Asbestos dust deposition and retention in rats, Ann NY Acad Sci, 132:77-86.

• In their inhalation exposure study on rats, Wagner & Skidmore reported that over a period of two months following a 6-week period of exposure to respirable dust, the rate of clearance for chrysotile was higher by a factor 3 than that for amosite or crocidolite. In addition, the retention of chrysotile, as measured a few days after the end of the 6-week exposure period was only about one third that of the amphiboles.

Wagner JC, Berry G, Skidmore JW & Timbrell V (1974). The effects of the inhalation of asbestos in rats, Br J Cancer, 28:173-185.

• This inhalation exposure study on rats found that while the lung burden of the amphibole fibres increased steadily over time, that of chrysotile appeared to reach a plateau after three months of exposure, and at a much lower level compared to the simultaneous amphibole level. The difference was attributed to the clearance rate of chrysotile.

Davis JMG, Bolton RE, Donglas A, Jones AD & Smith T (1988). The effects of electrostatic charge on the pathogeniciy of chrysotile asbestos. Br J Ind Med., 45: 337-345.

• In their series of rat inhalation studies, Davis & Jones found that amphibole levels at the end of a one year inhalation period was approximately 10 times those of chrysotile administered at the same mass dose.

Middleton AP, Beckett ST & Davis JMG (1979). Further observations on the short-term retention and clearance of asbestos in rats, using UICC reference samples, Ann occup Hyg, 22:141-152.

• This study exposed rats to chrysotile and amphibole fibres for a 6-week period and then estimated the amount of asbestos in the lung. It was concluded that the fractional deposition of chrysotile was lower than that of amosite and crocidolite, but that clearance patterns were similar. The overall retention of chrysotile was approximately one quarter that of amphiboles.

Le Bouffant L, Daniel H, Henin JP, Martin JC, Normand C, Tichoux G & Trolard F (1987). Experimental study on the long-term effects on inhaled MMMF on the lungs of rats, Ann occup Hyg, 31:765-790.

• In this study, rats were exposed to 5 mg/m3 of chrysotile B for 24 months, and found that most of the fibres had undergone splitting by the end of the inhalation period, and that chrysotile fibre numbers rapidly declined following inhalation.

Davis JMG (1989). Mineral fibres carcinogenesis: experimental data relating to the importance of fibre type, size, deposition, dissolution and migration. In Bignon J., Peto J. & Saracci R., eds. Non-occupational exposure to mineral fibres. Lyon: IARC, p. 33-45.

• This study compared the clearance of amosite and chrysotile. The author found that clearance rates over a 6-month period were 14% and 20% for long and short amosite respectively, compared to 55% and 90% for long and short Canadian chrysotile.

Oberdoerster G (1994). Macrophage-associated responses to chrysotile, Ann occup Hyg, 38:601-615.

• Using various types of published data, the author calculated that chrysotile clearance half-times are in the order of 90 to 100 days.

WHO/OCH (1989). Occupational exposure limit for asbestos, Geneva: World Health Organisation, Office of Occupational Health. WHO/OCH 89.1.

• "For those occupationally exposed to asbestos, amphibole asbestos concentrations in lung tissue correlate well with estimated workplace cumulative exposure. Chrysotile asbestos concentrations correlate less well. This poor correlation for chrysotile, together with the fact that there are much lower lung concentrations, exposure for exposure, suggests that much chrysotile is eliminated from the lung."

• "Lung burdens of amphibole, but not chrysotile asbestos, are higher in mesothelioma cases than controls."

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