Asbestos

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Timo Tuomi, Finnish Institute of Occupational Health

Introduction

Asbestos is a widely used constituent in buildings and building materials, machines, transport vehicles and consumer products. Asbestos has a known historic use going back at least 4500 years where it was added as a strengthening material into earthenware and cooking pots. Asbestos (Greek: inextinguishable) is the collective term for naturally occurring silicate minerals with a crystalline structure and a fibrous character. Inhalation of asbestos fibres may cause serious illnesses like lung cancer, mesothelioma and asbestosis. The European Union has banned all use of asbestos as well as extraction, manufacture and processing of asbestos products.

General description

Asbestos was given its name initially by the Greeks around 300 BC. More accurately the term asbestos is traceable to Rome. Legend has it that a Roman Emperor possessed a tablecloth made of asbestos and the Persians amazed the population by cleaning the cloth simply by exposing it to fire. There is some evidence that asbestos cloths and shrouds existed in Persia and China.

Modern day industrial use of asbestos dates from the second half of 19th century with many applications in insulation, fire retardant and acid resistant parts, pipe insulation etc. The First World War saw an enormous increase in shipbuilding and this further increased the use of asbestos as fire retardants were of critical importance for warships. At that time, the dangers of asbestos to shipyard workers were not even considered. The Second World War stimulated even more asbestos use and the production rose from that time.

In the 1970s, the manufacture and use of asbestos products were at their peak levels in Western Europe, Scandinavia, North America, and Australia when the worldwide production of asbestos exceeded five million tonnes every year. Even today levels amount to about two million tonnes with the largest producers being Russia, China, Canada, Kazakhstan, Brazil, and Zimbabwe. Most of the asbestos is used in Eastern Europe and Asia, i.e. the highest per-capita consumption occurs in Russia, Kazakhstan, Belorussia, Kyrgyzstan, and Thailand (over 2.0 kg/capita/year), whereas less than 0.1 kg/capita/year is still used in Western Europe or North America[1]. Asbestos cement accounts for about 85% of all commercial applications.

Asbestos minerals are not defined only on a mineralogical basis, but rather on the basis of their common properties which are the basis for their industrial uses. Asbestos minerals are fibrous in form and have many desirable properties such as high tensile strength, flexibility and chemical and physical durability. Asbestos minerals have been a valuable heat and fire insulation material for the construction industry and metal industry.

When asbestos was used for its fire/heat resistant properties, the fibres were often mixed with cement or woven into fabric or mats. Asbestos was also used in some domestic products in where heat and electric insulation was needed in hot environments e.g. ovens. Sprayed asbestos was used often as a layer of fire-protection and thermal insulation in industrial buildings, public buildings and domestic houses, on steel and concrete structures, especially on walls and ceilings, but also in boilers and chimneys[2]. Spraying of asbestos was one of the most dangerous forms of application, since sprayed asbestos is extremely friable and therefore its fibres are very likely to be emitted into the ambient air. A large amount of asbestos can be found in civilian and military ships which were built using this technique.

The term asbestos is applied to six naturally occurring minerals: chrysotile, which is a sheet silicate, grunerite asbestos (amosite), riebeckite asbestos (crocidolite), anthophyllite asbestos, tremolite asbestos and actinolite asbestos, which have a structure of double chain of silica tetrahedra, cross-linked by major cations, i.e. magnesium, iron, calcium and sodium[3].

Chrysotile is categorised to the serpentine group, with the remaining five types to the amphibole group of minerals. Chrysotile fibrils, about 30 nm in diameter, are flexible and form typically curvilinear bundles which break in the longitudinal direction into separate fibrils. Amphibole minerals are more brittle than chrysotile and divide along chrystallographic planes[4]. Chrysotile has always been the principal commercially used asbestos worldwide and it is the only currently mined asbestos. In 1989, about 4.2 million tonnes of chrysotile were produced at that time; this accounted for 99% of all asbestos production.

The fibrous form of the particles can become airborne and inhaled deep into the lungs. This is linked to the poor solubility of the fibres in human body fluids and this one is the main characteristics making asbestos and asbestos dust both carcinogenic and fibrogenic.

In addition to the six commercially exploited asbestos minerals, there are several other naturally occurring minerals which exist in a fibrous form, i.e. somewhere between 90 to 150 minerals may exist in a fibrous form. It has to be noted that these minerals are not defined as asbestos minerals. However, they do include some compounds with major use or with importance as they are present a contaminant of industrial minerals. From the group of nearly 40 zeolite minerals, four are fibrous: chabazite, clinoptilolite, erionite and mordenite. Two of the clay minerals, sepiolite and palygorskite (attapulgite), are fibrous. In addition, wollastonite, a calcium silicate mineral with an acicular form and nemalite, a fibrous magnesium hydroxide, can be regarded as being fibrous minerals[5]. The important group of non-asbestos fibrous minerals are the man-made mineral fibres (MMMF), which is a generic term for fibrous vitreous inorganic substances made from rock, clay, slag or glass. They are better known as glass wool, rock wool or slag wool. The nominal fibre diameter in bulk MMMF-products is 2-20 micrometers in wool and textile products. Due to their amorphous nature, unlike crystalline asbestos, man-made mineral fibres tend to break predominantly across the fibre axis and thus no thinner fibres are produced during their handling. In the evaluation of cancer risk following the exposure to man-made mineral fibres it has been stated that there was a risk of lung cancer in the early phases of MMMF production but no hazard of mesothelioma has been established[6].

Asbestos hazards

The proven adverse health effects related to asbestos are caused by inhalation of asbestos dust. There is no convincing evidence that other routes of exposure can increase the risk of asbestos diseases. There is some evidence however that small fractions of ingested asbestos fibres may be able to penetrate the gastrointestinal tract. Inhaled asbestos fibres with an aerodynamic diameter of up to 10 µm may pass down into the lower respiratory tract. Due to the small diameter of the asbestos fibres, which range from less than 0.1 µm up to several micrometers, the length of the fibres can be tens of micrometers even more than 300 µm but the aerodynamic diameter of this fibrous particle still remains smaller than 10 µm. The adverse health effects of asbestos fibres are as follows:

  • Pleural plaques are localised scars (fibrosis) consisting of collagen fibre deposits that form as a result of exposure to asbestos. They are the most common indication of significant exposure to asbestos. Pleural plaque is normally found in the parietal pleura, the lining of the inner wall of the chest. There are a few rare cases in which pleural plaques are found near a person’s rib cage.[7]
  • Pleural thickening is a type of pleural fibrosis that often extends over the area of an entire lobe or lung and causes a significant restrictive impairment of lung function.
  • Retroperitoneal fibrosis is characterised by a thick fibrotic mass covering the retroperitoneal structures.Retroperitoneal structures include the kidneys, the renal tract, the aorta, and other structures.
  • Asbestosis (pulmonary fibrosis) is a serious lung disease characterised by inflammation and scarring of lung tissue. Over time, lung tissues and the lining of the chest wall thicken and harden causing shortness of breath, persistent cough, fatigue, laboured and rapid breathing and chest pain. Asbestosis develops when asbestos fibres are inhaled and get stuck deep inside the lungs. Asbestosis can lead to illness and death.
  • Mesothelioma of pleura (membrane surrounding the lung) and peritoneum (membrane surrounding the abdominal cavity), is a rare form of cancer with a mean survival time of less than 12 months.
  • Lung cancer can be caused by all asbestos species. Smoking and asbestos act synergistically, i.e. smokers run a disproportionally higher risk to get of lung cancer when exposed to asbestos than non-smokers.

Carcinogenicity and fibrogenicity of asbestos

The role of the morphology of asbestos fibres is important in the carcinogenicity and fibrogenicity of them. The Stanton hypothesis states that long fibres (>8 µm in length) which are not easily engulfed by the macrophage cells (see below) in the lungs, and at the same time thin, i.e. less than 0.25 µm in diameter, have greater fibrinogenic and carcinogenic potential than shorter and thicker fibres[8]. However, there is also some evidence, based on the analysis of lung tissues of exposed cancer patients that also shorter and thinner fibres than postulated by the Stanton hypothesis may be important in carcinogenesis.

Alveolar macrophages, mobile cells that have the major responsibility of removing extra material from the lungs, can phagocytise (engulf) asbestos fibres. In the process of engulfing the fibres, the macrophages release active oxygen and nitrogen species, cytokines and growth factors (see below) and initiate inflammatory changes in the tissue. Other cell types like neutrophils, T-lymphocytes and mast cells also accumulate in lungs triggering detrimental processes ultimately leading to scarring of the lungs (fibrosis).

After entering the gas exchange region of the lungs, i.e. the bronchial alveoli, asbestos is able to evoke the production of reactive substances in the cells. There are many reactive oxygen species (ROS), e.g. hydrogen peroxide (H2O2), the superoxide anion (O2), the hydroxyl radical (HO), and reactive nitrogen species. In addition, nitric oxide (NO) production is induced in cells exposed to asbestos fibres. ROS and other reactive species attack DNA, some cellular proteins and lipid membranes and alter their function, and this is the reason why asbestos is mutagenic.

Some cell-signalling cytokines and growth factors like interleukin1 (IL-1), tumour necrosis factor α (TNF-α), transforming growth factor (TGF), platelet derived growth factor (PDGF), and interleukin 8 (IL-8) affect the cellular injury process and activate collagen deposition in the tissue as well as promoting fibroblast proliferation which leads to fibrosis (formation of scar tissue).

In animal experiments, some fibrous minerals other than asbestos have also been shown to be carcinogenic including palygorskite (attapulgite), erionite and nemalite[9]. The evidence of carcinogenicity was evaluated by IARC as sufficient for erionite, as well as for talc containing asbestiform fibres[10].

Asbestos and cancer

Mesothelioma

Malignant mesothelioma is a rare malignancy closely related to asbestos exposure. In the early 1950s, at the time when mesothelioma was recognised as a malignancy associated with asbestos, the disease was generally regarded as a pathological rarity. However, case reports in the medical literature had been published already in 1930s and 1940s. The findings of Dr C. Sleggs led to a report in which 33 cases of pleural mesothelioma and exposure to crocidolite in South Africa were described in 1960 by Wagner. This report is a landmark in associating asbestos with mesothelioma and it is now known that over 80% of mesothelioma patients have had some occupational exposure to asbestos and furthermore some of the exposures had been low. Mesothelioma is an invariably fatal disease with a median survival time of 9-12 months from diagnosis[11].

Lung cancer

After the first report[12] several studies have shown an elevated risk of lung cancer in association with asbestos exposure and today asbestos is a recognised carcinogen. There is sufficient evidence that not only the amphiboles but also chrysotile asbestos cause lung cancer[13]. A health study which followed a group of asbestos exposed workers showed cigarette smoking alone caused an 11-fold, and smoking and asbestos together a 53-fold increase in lung cancer risk[14].

Other cancers

Asbestos has been suspected of causing cancers in the pharynx, esophagus, stomach and intestine. However, only slightly increased risks have been shown for stomach and colorectal cancer, but there is some evidence that also laryngeal cancer may be caused by asbestos exposure[15].

Occupational and environmental exposure

The industrial use of asbestos is closely related to its subsequent health effects. The life cycle of asbestos containing products begins in the primary asbestos industry and continues with their secondary manufacture, installation, usage and disposal. In about 100 countries, asbestos-containing pipes and sheets are manufactured to be used as low-cost building materials. Other major uses include friction materials, floor tiles, gaskets, insulation boards and textiles.

The current use of asbestos consists solely of chrysotile. Before 1990, South Africa still produced crocidolite and amosite but has stopped after that time. Worldwide, millions of workers have been exposed to asbestos in the workplace, most often during handling, maintenance, repair, and replacement of asbestos-containing materials. In detailed interviews, about 20-40% of adult men reported past occupations and jobs that might have entailed asbestos exposures at work. Up to 20,000 asbestos-related lung cancers and 10,000 mesotheliomas occur annually within the population of Western Europe, Scandinavia, North America, Japan, and Australia. The ecologic relationship between past asbestos consumption and mesothelioma incidence is strongly indicated[16].

Asbestos, as dry material or embedded in hard material like concrete, readily produces dust and airborne particles when it is handled or ground up or the material is broken in some other way. Therefore, respirable asbestos fibres are released into the air easily, and in addition they stay airborne for a long time and travel long distances in the airstreams. Over time, the fibre burden in the lungs leads to serious health problems.

Analysis of the fibre concentration in lung tissue provides data which helps to estimate a person's past exposure to asbestos, and can serve as a supplement to work and exposure history. Lung fibre analysis is based on the fact that asbestos fibres remain in the lungs, and their chemical composition does not alter significantly. The maximum diameter for a fibre to be respirable has been estimated to be approximately 3 µm. Fibre length is of less importance for the aerodynamic behaviour in the penetration to lungs. Fibres up to 300 µm in length have been extracted from human lungs. The amount of retained fibres in the lungs can be even a better measure of the carcinogenic risk than the indirect exposure data. The lung fibre analysis is especially useful in detecting occult exposures, either occupational or non-occupational. The methods of lung fibre analysis are based on electron microscopy and elemental X-ray microanalysis of single fibres.

Lung fibre analysis is obviously possible only if a sample of lung tissue is available. The post mortem investigation is a routine procedure but also in connection with curative or diagnostic surgery, the biopsy sample of the lung tissue can serve as a useful specimen.

Everyone is exposed at least to low levels of asbestos at some time during their life. Asbestos is present in the air, water, and soil. People who become ill from asbestos are usually those who have been exposed in an occupation where they work directly with the material. In a recent study of 300 autopsied urban men between the ages of 33 and 69, fibre concentrations longer than 1 µm were found in a range from <0.3 to 163 million fibres per gram of dry tissue (f/g, dry tissue weight is about 10% of the weight of normal lung tissue). Asbestos fibre concentrations exceeding 1 million f/g were observed in 33% of the cases with probable occupational exposure to asbestos and in 1% of the cases with unlikely occupational exposure. In addition, concentrations between 0.3 to 1 million f/g, especially of crocidolite-amosite fibres, were rare among the men with unlikely occupational exposure. Fibre concentrations exceeding or equalling 1 million f/g were 10 times more frequent in the men more than 60 years of age as compared to those less than 40 years of age. Smoking habits had no significant effect on the pulmonary fibre counts. Asbestos fibre concentrations exceeding 1 million fibres per gram of dry tissue are highly indicative of past occupational exposure to asbestos. The distribution of fibre concentrations in the different age groups of this study was an indication of decreasing asbestos exposure in Finland since the 1970s[17].

There is probably no safe level of asbestos exposure, but health hazards have been recognised especially in people who have been exposed at work. Exposures to asbestos have taken place in the mining and milling of asbestos and in the primary and secondary manufacturing of asbestos products like friction materials (automobile and other machinery brake pads, shoes, and clutch discs), asbestos cement, asbestos textiles, floor tiles, roofing felts, insulating and building materials, heating equipment and industrial process furnaces. Occupational groups known to be exposed to asbestos, such as workers in the shipbuilding and repair sectors, and in the construction industry as well as several other groups such as insulation workers, car mechanics, ship engine room personnel, and maintenance workers in industry, are at risk of asbestos related diseases.

Asbestos abatement workers may be exposed to asbestos even though they are wearing high performance respirators. In addition, poorly operating (HEPA) filtration units and inadequate enclosures may contaminate the surroundings of the asbestos abatement site. A study of performance of full-face mask respirators with P3 filters and HEPA air filtration units at 21 work sites revealed that only 8 of the 21 tested respirators fully protected the workers against fibres. With the remaining 13 respirators, the fibre levels inside the respirator varied from 0.01 to 4.6 f/cm3, with a mean concentration of 0.46 f/ cm3 [18].

Asbestos fibres can be found in the outdoor air as well as in the indoor air in buildings where asbestos has been used in Construction. In addition, in geographical areas where asbestos is present in natural deposits, the health risk associated with this type of exposure is unclear. A striking cancer risk was revealed to be caused by environmental exposure to a fibrous mineral not classified as asbestos. Erionite, the fibrous zeolite, present in the Anatolian region of Turkey, is suspected of being responsible for the extremely high incidence of mesothelioma observed in this particular geographical region. Pleural or peritoneal mesothelioma was the cause of death in Karain village in 50% of the 217 deaths between 1970-87 and in Tuzköy in 33% of total deaths (277) between 1980-88[19].

Applicable legislation

The prohibition of asbestos use came into force at different times in the different EU Member States. Since 1st January 2005, the use of asbestos has been banned throughout the whole European Union. European legislation has set strict standards for the protection of workers in situation where they may be exposed. The following are some of the relevant directives:

  • Asbestos ban: Directive 1999/77/EC of the European Union bans all types of utilisation of asbestos from 1st January 2005[20]. In addition, the 2003/18/EC directive bans the extraction of asbestos and the manufacture and processing of asbestos products[21]. Thus, the exposure of the primary users of the asbestos-containing products and materials to asbestos is no longer a threat. However, the problems of exposure to asbestos in the removal, demolition, servicing and maintenance activities are still relevant and important.
  • Protection of workers: Council Directive 83/477/EEC of 19 September 1983 on the protection of workers from the risks related to exposure to asbestos at work[22], modified by Council Directive 91/382/EEC of 25 June 1991[23], and amended by Council Directive 98/24/EC of 7 April 1998[24] and Directive 2003/18/EC of the European Parliament and of the Council of 27 March 2003. Directive 2003/18/EC sets a single maximum limit value for airborne concentration of asbestos of 0.1 fibres per cm3 as an eight-hour time-weighted average (TWA) and prohibits activities exposing workers to asbestos fibres, with the exception of the treatment and disposal of products resulting from demolition and asbestos removal and updates the practical recommendations on the clinical surveillance of exposed workers in the light of the latest medical expertise, with a view to the early detection of pathologies linked to asbestos[21]. Because of the numerous amendments in the interests of clarity and rationality Directive 83/477/EEC and its amendments were released by the new asbestos Directive 2009/148/EC.[25]

Prevention of asbestos hazards

National bans of asbestos are already in place in 30 countries worldwide. However, the risk posed by asbestos has not disappeared especially for workers in maintenance and construction. Therefore it is important that managers of maintenance companies and workers should become better aware of the risks of asbestos, and develop the knowledge and skills to avoid exposure to the hazardous fibres[26]. In the construction industry, it is important to be aware of the national legislation and good practices in renovation work and have detailed guidance about how to work safely with asbestos containing materials[27][28]


In Europe, following the Dresden Declaration[29], the Senior Labour Inspectors’ Committee (SLIC) took in 2006 the initiative to create a common pan-European campaign in order to increase the attention to health and safety when dealing with built-in asbestos. The main focus of the campaign was on the protection of workers in maintenance/demolition/removal activities and waste disposal. European best practice guidelines were issued to labour inspectors competent for occupational safety and health issues and for employers and workers engaged in work exposing them to asbestos risks[30].

References

  1. Tossavainen, A., 'Global use of asbestos and the incidence of mesothelioma', Int J Occup Environ Health, Jan-Mar, 10(1), 2004, pp. 22-5
  2. U.S. EPA – U.S. Environmental Protection Agency, Asbestos (2011). Retrieved 22 June 2015, from: [1]
  3. Leake, B. E., 'Nomenclature of amphiboles', Can Mineral, 1978, 16, pp. 501-520.
  4. Pooley, F. D., 'Asbestos mineralogy', In: Antman, K., Aisner, J. (eds.), 'Asbestos related malignancy'. Grune&Stratton, Boston, 1987, pp. 3-27.
  5. Korhonen, K., Tossavainen, A., 'Wollastonite - a fibrous industrial mineral', Vuoriteollisuus/Bergshanteringen, 39, 1, 1981, pp. 38-45. (In Finnish with English abstract)
  6. Doll, R.,'Symposium on MMMF, Copenhagen, October 1986, overview and conclusions', Ann Occup Hyg, 4B, 1987, pp. 805-819.
  7. Mesothelioma Symptoms (2014). Pleural plaques. Retrieved 22 June 2015, from: [2]
  8. Stanton, M. F., Layard, M., Tegeris, A., Miller, E., May, M., Morgan, E., Smith, A., 'Relation of particle dimension to carcinogenicity in amphibole asbestos and other fibrous minerals', J Natl Cancer Inst, 67, 1981, pp. 965-975.
  9. Pott, F., Ziem, U., Reiffer, F. J., Huth, F., Ernst, H., Mohr, U., 'Carcinogenicity studies on fibres, metal compounds and some other dusts in rats', Exp Pathol , 32, 1987, pp. 129-152.
  10. IARC – International Agency for Research on Cancer, 'Monographs on the evaluation of carcinogenic risk to humans, Silica and some silicates', Vol 42, IARC, Lyon, 1987.
  11. Wagner, J. C., Sleggs, C.A., Marchand, P., 'Diffuse pleural mesothelioma and asbestos exposure in Cape Province', Br J Ind Med, 17, 1960, pp. 260-271.
  12. Doll, R., 'Mortality from lung cancer in asbestos workers', Br J Ind Med., 12, 1955, pp. 81-86.
  13. Berman, D. W., and Crump, K. S., 'Update on potency factors for asbestos-related lung cancer and mesothelioma', Crit Rev Toxicol, 38 Suppl 1, 2008, pp. 1-47.
  14. Selikoff, I. F., Hammond, E. C., 'Asbestos and smoking', JAMA, 242, 1979, pp. 458-459.
  15. Committee on Asbestos, Asbestos: Selected cancers, The National Academic Press, Washington D.C, 2006. Available at: [3]
  16. Takahashi, K, Huuskonen, M. S, Tossavainen, A., Higashi, T., Okubo, T., Rantanen, J., 'Ecological relationship between mesothelioma incidence/mortality and asbestos consumption in ten Western countries and Japan', J Occup Health, 41, 1999, pp. 8-11.
  17. Karjalainen, A., Vanhala, E., Karhunen, P. J., Lalu, K., Penttilä, A., and Tossavainen, A., 'Asbestos exposure and pulmonary fibre concentrations of 300 Finnish urban men', Scand J Work Environ Health, 1994, 20, pp. 34-41, 1994.
  18. Riala, R., Riipinen, H., 'Respirator and high efficiency particulate air filtration unit performance in asbestos abatement', Appl Occup Environ Hyg, 13(1), 1998, pp. 32-40.
  19. Baris, Y. I., 'Fibrous zeolite (erionite)-related diseases in Turkey', Am J Ind Med., 19, 1991, pp. 374-378.
  20. Directive 1999/77/EC of 26 July 1999 adapting to technical progress for the sixth time Annex I to Council Directive 76/769/EEC on the approximation of the laws, regulations and administrative provisions of the Member States relating to restrictions on the marketing and use of certain dangerous substances and preparations (asbestos), OJ L 207, 6.8.1999, pp. 18-20. Available at: [4]
  21. 21.0 21.1 Directive 2003/18/EC of the European Parliament and of the Council of 27 March 2003 amending Council Directive 83/477/EEC on the protection of workers from the risks related to exposure to asbestos at work, OJ L 97, 15.4.2003, pp. 48-52. Available at: [5]
  22. Council Directive 83/477/EEC of 19 September 1983 on the protection of workers from the risks related to exposure to asbestos at work (second individual Directive within the meaning of Article 8 of Directive 80/1107/EEC), OJ L 263, 24.9.1983. Available at: [6]
  23. Council Directive 91/382/EEC of 25 June 1991 amending Directive 83/477/EEC on the protection of workers from the risks related to exposure to asbestos at work (second individual Directive within the meaning of Article 8 of Directive 80/1107/EEC), OJ L 206 , 29/07/1991 P. 0016 - 0018. Available at: [7]
  24. Council Directive 98/24/EC of 7 April 1998 on the protection of the health and safety of workers from the risks related to chemical agents at work (fourteenth individual Directive within the meaning of Article 16(1) of Directive 89/391/EEC), OJ L 131, 5.5.1998, pp. 11-23. Available at: [8]
  25. Directive 2009/148/EC of the European Parliament and of the Council of 30 November 2009 on the protection of workers from the risks related to exposure to asbestos at work (Text with EEA relevance). Available at: [9]
  26. EU-OSHA – European Agency for Safety and Health at Work, 'Safe maintenance – asbestos in building maintenance', E-fact 48, 2010. Available at: [10]
  27. EU-OSHA – European Agency for Safety and Health at Work, 'Asbestos in construction', Factsheet 51, Bilbao, 2004, p. 1. Available at: [11]
  28. EU-OSHA – European Agency for Safety and Health at Work, European good practice Awards 2008-09 - prevention of risk in practice: good practice related to risk assessment, Healthy Workplaces. A European campaign on risk assessment, 2009, p. 21. Available at: [12]
  29. Asbestos - European Conference 2003, Dresdner Erklärung zum Schutz der Arbeitnehmer vor Asbest (German), 2003, pp. 1-3. Available at: [13]
  30. EU-OSHA – European Agency for Safety and Health at Work (2006), 'SLIC European Asbestos Campaign 2006'. Retrieved 22 June 2015, from: [14]


Links for further reading

Mesothelioma (2010). All about Mesothelioma. Retrieved 22 June 2015, from: [15]

Wikipedia – The Free Encyclopedia, Asbestos (6 July 2011). Retrieved 6 July 2011, from: [16] {{#jskitrating:view=score}}