Chemical name: Chrysotile asbestos

Final regulatory action has been taken for the category: Industrial

Final regulatory action: The chemical is Banned

Use or uses prohibited by the final regulatory action:

All uses are prohibited, except as stated in the exemptions following.

Use or uses that remain allowed:

If the intended use is subject to the provisions and exemptions of Annex 3.3 of the Ordinance relating to Environmentally Hazardous Substances.

Exemptions:

1. On reasoned request, the Federal Agency for the Environment, Forests and Landscapes my permit a manufacturer or trader to continue to supply certain products or articles or to import them as commercial goods after the dates laid down in Annex 3.3, Number 31 if:

1. according to the state of the art, there is no replacement substance for the asbestos and provided that no more than the minimum amount of asbestos for the desired purpose is employed, or

b. due to particular design conditions, only spare parts containing asbestos can be used.

Labeling:

Manufacturers may only supply packing drums and packaging for asbestos, product or articles containing asbestos, and unpackaged products containing asbestos if they carry a label giving the information laid out in Annex 3.3, Numbe 33 of the Ordinance relating to Environmentally Hazardous Substances.

The final regulatory action was based on a risk or hazard evaluation: Yes

Summary of the final regulatory action:

Asbestos shall no longer be used, except to manufacture products or articles which may be supplied or imported as commercial goods in accordance with Annex 3.3 of the Ordinance relating to Environmentally Hazardous Substances (SR 814.013)

The specified conditions are:

If the intended use is subject to the provisions and exemptions of Annex 3.3 of the Ordinance relating to Environmentally Hazardous Substances.

Exemptions:

1. On reasoned request, the Federal Agency for the Environment, Forests and Landscapes my permit a manufacturer or trader to continue to supply certain products or articles or to import them as commercial goods after the dates laid down in Annex 3.3, Number 31 if:

1. according to the state of the art, there is no replacement substance for the asbestos and provided that no more than the minimum amount of asbestos for the desired purpose is employed, or

b. due to particular design conditions, only spare parts containing asbestos can be used.

Labeling:

Manufacturers may only supply packing drums and packaging for asbestos, product or articles containing asbestos, and unpackaged products containing asbestos if they carry a label giving the information laid out in Annex 3.3, Numbe 33 of the Ordinance relating to Environmentally Hazardous Substances.

All other provisions stated in Annex 3.3 apply equally.

The reasons for the final regulatory action were relevant to: Human health

Summary of known hazards and risks to human health:

Chrysotile is an amphibole form of asbestos

There is general consensus amongst the scientific community that all types of asbestos fibres are carcinogenic and can cause asbestosis lung cancer and mesothelioma when inhaled.

Chrysotile is classified as a known human carcinogen. Exposure poses increased risks for asbestosis lung cancer and mesothelioma in a dose-dependent manner. It has been shown that smoking and asbestos act in a synergistic manner, increasing the overall risk of lung cancer.

In 1998, the EC Scientific Committee on Toxicity, Ecotoxicity and the Environment (CSTEE) concluded that chrysotile is a proven carcinogen and there is not sufficient evidence that it acts through a non-genotoxic mechanism.

The deposition of inhaled chrysotile asbestos is dependent upon the aerodynamic diameter, the length and the morphology of the fibre. Most airborne chrysotile fibres are considered respirable, because their fibre diameters are less than 3µm, equal to an aerodynamic diameter of about 10 µm. in laboratory rats, chrysotile fibres are deposited primarily at alveolar duct bifurcations. In the nasopharyngeal and tracheobronchial regions, chrysotile fibres are cleared via mucocilliary clearance. At the alveolar duct bifurcations the fibres are taken up by epithelial cells. Fibre length is an important determinant of alveolar clearance of chrysotile fibres. There is extensive evidence from animal studies that short fibres (less than 5 µm long) are cleared more rapidly than long fibres (longer than 5 µm). The mechanisms of the relatively more rapid clearance of chrysotile fibres compared to those of amphiboles are not completely known. It has been hypothesized that short chrysotile fibres are cleared through phagocytosis by alverloar macrophages, while long chrysotile fibres are cleared mainly by breakage and/or dissolution. To what extent chrysotile fibres are translocated to the interstitium, pleural tissue and other extrathoracic tissues is not fully understood. Analyses of human lungs of workers exposed to chrysotile asbestos indicate much greater retention of tremolite, an amphibole asbestos commonly associated with commercial chrysotile in small proportions, than of chrysotile. The more rapid removal of chrysotile fibres from the human lung is further supported by findings from animal studies showing that chrysotile is more rapidly cleared from the lung than are amphiboles including crocidolite and amosite.

Epidemiological studies, mainly on occupational groups, have established that all types of asbestos fibres are associated with diffuse pulmonary fibrosis (asbestosis), bronchial carcinoma and primary malignant tumours of the pleura and peritoneum (mesothelioma). Commercial grades of chrysotile have been associated with an increased risk of pneumoconiosis, lung cancer and mesothelioma in numerous epidemiological studies of exposed workers. That asbestos causes cancers at other sites is less well established. Cancers other than of the lung or mesothelioma have been considered in many studies. Some indicated an approximately two-fold risk with regard to gastrointestinal cancer in connection with shipyard work, and some increased risk was also seen in association with exposure to both chrysotile and crocidolite, to crocidolite or to chrysotile. Cancer of the colon and rectum was associated with asbestos exposure during chrysotile production, with an approximately two-fold risk; a similar excess was found for unspecified asbestos exposure.

Generally cases of malignant mesothelioma are rapidly fatal. The observed incidence of these tumours, which was low until about 30 years ago has been increasing rapidly in males in industrial countries. The long latency required for mesothelioma to develop after asbestos exposure has been documented in a number of publications. An increasing proportion of cases has been seen with increasing duration of exposure. As asbestos-related mesothelioma became more widely accepted and known to pathologists in western countries, reports of mesothelioma increased. The incidence of mesothelioma prior to, eg 1960, is not known. Mesotheliomas have seldom followed exposure to chrysotile asbestos only. Most, but not all, cases of mesothleioma have a history of occupational exposure to amphibole asbestos, principally crocidolite either alone or in amphibole-chrysotile mixtures. Mesotheliomas related to shipyard work and other exposures, including household contact with asbestos workers, have also been subject to epidemiological studies, resulting in risk ratios of about 3 to 15 in comparison with background rates not clearly referable to asbestos exposure. Exposure to crocidolite has been studies with regard to risk of lung cancer, and risk ratios of about 2 to 3 have been reported. Three lung cancers and two mesothleiomas occurred in 20 individuals after one year of high exposure to crocidolite; at least 17 of the cases had asbestos induced lung changes on X-ray films. It should be recognized that although the epidemiological studies of chrysotile-exposed workers have been primarily limited to the mining and milling, and manufacturing sector, there is evidence, based on the historical patterns of disease associated with exposure to mixed fibre types in western countries, that risks are likely to be greater among workers in construction and possibly other use industries.

Evidence for carcinogenicity to animals (sufficient) Asbestos has been tested for carcinogenicity by inhalation in rats, by intrapleural administration in rats and hamster, by intraperitoneal injection in mice, rats and hamsters and by oral administration in rats and hamsters. Chrysotile, crocidolite, amosite, anthophyllite and tremolite produced mesotheliomas and lung carcinomas in rats after inhalation exposure and mesotheliomas following intrapleural administration. Chrysotile, crocidolite, amosite and anthophyllite induced mesotheliomas in hamsters following intrapleural administration. Intraperitoneal administration of chrysotile, crocidolite and amosite induced peritoneal tumours, including mesotheliomas, in mice and rats. Given by the same route, crocidolite produced abdominal tumours in hamsters, and tremolite and actinolite produced abdominal tumours in rats. A statistically significant increase in the incidence of malignant tumours was observed in rats given filter material containing chrysotile orally. In more recent studies, tumour incidence was not increased by oral administration of amosite or tremolite in rats, of amosite in hamsters or of chrysotile in hamsters. In two studies in rats, oral administration of chrysotile produced a low incidence of benign adenomatous polyps of the large intestine in males (9/250 versus 3/524 pooled controls) and of mesenteric haemangiomas (4/22 versis 0/47 controls). Synergistic effects were observed following intratracheal administration of chrysotile and benzo[a] pyrene to rats and hamster and of intratracheal administration of chrysotile and subcutaneous or oral administration of N-nitrosodiethylamine to hamsters. Various experimental samples of chrysotile fibres have been shown in numerous long-term inhalation studies to cause fibrogenic and carcinogenic effects in laboratory rats. These effects include interstitial fibrosis and cancer of the lung and pleura. In most cases, there appears to be an association between fibrosis and tumours in the rat lung. Fibrogenic and carcinogenic effects have also been found in long-term animal studies (mainly in rats) using other modes of administration (eg intratracheal instillation and intrapleural or intraperitoneal injection). Exposure/dose-response relationships for chrysotile-induced pulmonary fibrosis, lung cancer and mesothelioma have not been adequately investigated in long-term animal inhalation studies. Inhalation studies conducted to date, mainly using a single exposure concentration, show fibrogenic nd carcinogenic responses at airborne fibre concentrations ranging from 100 to a few thousand fibres/ml. When data from various studies are combined, there appears to be a relationship between airborne fibre concentrations and lung cancer incidence. This type of analysis, however, may not be scientifically sound as different experimental conditions were used in available studies. In non-inhalation experiments (intrapleural and intraperitoneal injection studies), dose-response relationships for mesothelioma have been demonstrated for chrysotile fibres. Data from these types of studies, however, may not be suitable for the evaluations of human risk from inhalation exposure to fibres.

Other relevant data: Insulation workers exposed to asbestos 'displayed a marginal increase' in the incidence of sister chromatid exchange in lymphocytes in one study. Chrysotile did not induce micronuclei in bone marrow cells of mice or chromosomal aberrations in bone-marrow cells of rhesus monkeys treated in vivo. In cultured human cells, conflicting results were reported for the induction of chromosomal aberrations and negative results for the induction of sister chromatid exchanges by chrysotile and crocidolite; amosite and crocidolite did not induce DNA strand breaks, and crocidolite was not mutagenic. Amosite, anthophyllite, chrysotiel and crocidolite induced transformation of Syrian hamster embryo cells, chrysotile and crocidolite transformed BALB/c3T3 mouse cells, and chrysotile transformed rat mesothelial cells. Neither amosite nor crocidolite transformed CH3 10T1/2 cells. In cultured rodent cells, amosite, anthophyllite, chrysotile and crocidolite induced sister chromatid exchanges; chrysotile and crocidolite induced aneuploidy and micronuclei. Chrysotile did not induce unscheduled DNA synthesis in rat hepatocytes. Amosite, chrysotile and crocidolite were inactive or weakly active in induc ing mutation in rodent cells in vitro; none were mutagenic to bacteria.

Expected effect of the final regulatory action in relation to human health:

A reduction of exposure to asbestos for workers.

Date of entry into force of the final regulatory action: 09/06/1986