Asbestos General information Key Points Fire Non flammable and non combustible under normal conditions Chemically inert under normal conditions. Resistant to most solvents, acids and alkalis In the event of a fire involving asbestos, use fine water spray and liquid-tight protective clothing with breathing apparatus Health The most common route of exposure is by inhalation Toxic and carcinogenic In general asbestos is not considered to be acutely toxic Short-term high level exposure may cause pleural disorders, mesothelioma or lung cancer after a long latency period Long-term low level inhalation exposure may cause pleural disorders, mesothelioma or lung cancer; long-term high dose exposure may cause asbestosis Asbestos is a category 1 carcinogen i.e. is carcinogenic to humans Asbestos has not been linked with any adverse reproductive outcomes in humans Environment Environmentally hazardous substance Inform Environment Agency of substantial release incidents Prepared by S Bull CHAPD HQ, HPA 2007 Version 1
ASBESTOS GENERAL INFORMATION Background Asbestos is a general name given to several naturally occurring fibrous minerals that have crystallised to form long thin fibres. They are divided into two sub-groups: serpentine (chrysotile (white asbestos)), which is the most commonly used type of asbestos and amphiboles, which includes crocidolite (blue asbestos), amosite (brown asbestos), tremolite, actinolite and anthophyllite, of which crocidolite was the most commonly used in the past. Asbestos minerals are widespread in the environment. They may be found in the soil due to erosion of asbestos-bearing rock. Asbestos fibres are strong, heat and chemical resistant and they do not evaporate into the air or dissolve in water. Such properties made it an ideal material for use in a number of products, including insulation material for buildings, boilers and pipes; insulating board to protect buildings and ships against fire; asbestos cement for roofing sheets and pipes. Due to the risk to health following exposure to asbestos, importation, supply and use of all asbestos products have been banned in the UK since 1999. People however, may still be exposed to existing asbestos-containing materials in buildings etc due to the widespread use in the past. Asbestos in air may arise from natural weathering of asbestos-containing ores or damage and breakdown of asbestoscontaining products. People may also be exposed to asbestos in drinking water. Although asbestos does not dissolve, fibres may enter water after being eroded from natural sources, from asbestos-cement or from asbestos-containing filters People who work with asbestos or with asbestos-containing products such as miners or those producing asbestoscontaining products are likely to be exposed to much higher levels of asbestos fibres in air than the general public. In addition, as asbestos has been widely used in building for fire-proofing, insulation or floor and ceiling tiles, those involved in demolition work, asbestos abatement, building repair and maintenance may be exposed to higher levels as disturbing such materials releases fibres into the air. Breathing in high concentrations of asbestos for a long period of time mainly affects the lungs, causing a disease called asbestosis where breathing becomes difficult and the heart enlarges. People breathing in lower concentrations may get pleural plaques, mesothelioma or lung cancer. Most asbestos products pose little risk if they are intact. However, if asbestoscontaining products are damaged in some way, fibres may be released into the air and may be breathed in. The health effects of swallowing asbestos in water or food are unclear. The International Agency for Research on Cancer (IARC) has classified asbestos as being carcinogenic to humans. General information: Page 2 of 6
ASBESTOS GENERAL INFORMATION Production and Uses Key Points Asbestos fibres do not dissolve in water or evaporate, they are resistant to heat, fire, chemical and biological degradation and are mechanically strong Due to their physical properties they are used in many products, including insulation for houses, ceiling and floor tiles and car brakes, as well as many others Asbestos is a general name given to several naturally occurring fibrous silicate minerals. Such silicate minerals are characterised by fine, long parallel fibres or bundles. Overall, asbestos fibres do not dissolve in water or evaporate, they are resistant to heat, fire, chemical and biological degradation and are mechanically strong. Such properties make it an ideal material for use in a number of products, including insulation material for buildings, boilers and pipes, sprayed coating/lagging, insulating boards, asbestos cement, ropes, cloth, car brakes and clutches, ceiling and floor tiles, coated metal, textured paints and reinforced plastic amongst others. Serpentine asbestos: Chrysotile is the most common and abundant form of asbestos. It is a magnesium silicate mineral, often referred to as white asbestos. Chrysotile fibres are soft, flexible and curved that may be separated easily into small bundles and individual fibrils. Chrysotile fibres naturally occur in lengths < 5 m. Due to their structure they may be woven and can withstand mechanical treatment better than the amphibole fibres. Amphibole asbestos: This group includes crocidolite, amosite, anthophyllite, tremolite and actinolite (figure 1). Amphibole asbestos fibres include silicates of magnesium, iron, calcium and sodium. Fibres are brittle and have a rod- or needle shaped appearance. They are more heat and chemical resistant than serpentine fibres. Crocidolite is a sodium iron silicate, commonly known as blue asbestos. Crocidolite fibre bundles can disperse into smaller fibres (5-10 m), although such fibres are generally not as small as those of chrysotile. Fibres of crocidolite are relatively flexible, have a poor resistance to heat, but are highly resistant to acid. Amosite is made up of iron magnesium silicate, often referred to as brown asbestos. The fibres are usually yellow-grey to dark brown and are very coarse. Amosite fibres are approximately 5-10 m. Anthophyllite is another fibrous form of iron magnesium silicate. Fibres are grey or brown grey and have similar properties to amosite but have no commercial value. In general, anthophyllite fibres are approximately 5-10 m. Tremolite is a grey-white, yellow, green or blue calcium magnesium silicate. It is found as a contaminant with other fibres such as chrysotile and has no industrial applications. Tremolite fibres range in size (5 10 m). Actinolite asbestos occurs as a contaminant of both chrysotile and talc deposits. General information: Page 3 of 6
ASBESTOS GENERAL INFORMATION ASBESTOS Serpentine Amphibole Chrysotile Crocidolite Amosite Anthophyllite Tremolite Actinolite Figure 1. Types of serpentine and amphibole asbestos fibres General information: Page 4 of 6
ASBESTOS GENERAL INFORMATION Frequently Asked Questions What is asbestos? Asbestos is a general name given to several naturally occurring fibrous minerals that have crystallised to form long thin fibres. They are divided into two sub-groups: serpentine (chrysotile (white asbestos)), which was the most commonly used type of asbestos and amphiboles, which includes crocidolite (blue asbestos), amosite (brown asbestos), tremolite, actinolite and anthophyllite, of which crocidolite was the most commonly used. Blue and brown asbestos are considered to be the most dangerous. The importation, supply and use of blue and brown asbestos have been banned in the UK since 1985 and this ban was extended to include white asbestos in 1999. Chrysotile asbestos fibres are soft, flexible and curved whereas amphibole asbestos fibres are brittle and often are rod- or needle-like in appearance. Asbestos fibres do not dissolve in water or evaporate, they are resistant to heat, fire, chemical and biological degradation and are mechanically strong, hence it has been used in a wide number of products such as car brakes and insulation. How does asbestos get into the environment? Asbestos fibres may enter the atmosphere due to the erosion of natural asbestos-containing ores or damage to asbestos-containing products including insulation, car brakes and clutches, ceiling and floor tiles and cement. How will I be exposed to asbestos? Asbestos minerals are widespread in the environment due to naturally occurring sources or from the damage of products containing asbestos. The asbestos fibres from damaged asbestos-containing products can break down into smaller fibres. People are most likely to be exposed to asbestos by breathing in fibres that are suspended in air, or may swallow small amounts of the fibres if the asbestos enters the soil or water. Indoor air may contain small levels of asbestos from insulation, ceiling or floor tiles, or other purposes. Levels depend on the state of the products, as more fibres will be released from materials that are damaged. People who worked with asbestos or with asbestos-containing products were likely to be exposed to much higher levels of asbestos fibres in air than the general public. However, as the use of new asbestos products is now banned only those involved in demolition work, asbestos abatement, building repair and maintenance may be exposed to higher levels as disturbing such materials releases fibres into the air. If there is asbestos in the environment will I have any adverse health effects? The presence of asbestos in the environment does not always lead to exposure as you must come into contact with the chemical. You may be exposed by breathing, eating, or drinking the substance or by skin contact. Following exposure to any hazardous chemical, the adverse health effects you may encounter depend on several factors, including the amount to which you are exposed (dose), the duration of exposure, the way you are exposed, the form of asbestos and if you were exposed to any other chemicals. All forms of asbestos are hazardous as they induce cancer, but amphibole forms of asbestos are considered to be somewhat more hazardous to health than chrysotile. General information: Page 5 of 6
ASBESTOS GENERAL INFORMATION Breathing in high concentrations of asbestos for a long period of time mainly affects the lungs, causing a disease called asbestosis where breathing becomes difficult and the heart enlarges. People breathing in lower concentrations for a long period of time may get pleural plaques, mesothelioma or lung cancer. Can asbestos cause cancer? The International Agency for Research on Cancer (IARC) has classified asbestos as being carcinogenic to humans. Does asbestos affect children or damage the unborn child? Several experimental studies have suggested that asbestos does not cause adverse pregnancy outcomes or birth defects. If children are exposed to asbestos by inhalation they may develop lung cancer or mesothelioma after a prolonged latent period. However, this may occur at a younger age than when exposure occurs in adults. What should I do if I am exposed to asbestos? It is very unlikely that the general population will be exposed to a level of asbestos high enough to cause adverse health effects. This document from the HPA Centre for Radiation, Chemical and Environmental Hazards reflects understanding and evaluation of the current scientific evidence as presented and referenced in this document. General information: Page 6 of 6
Asbestos Incident management Fire Key Points Non flammable and non combustible under normal conditions Chemically inert under normal conditions. Resistant to most solvents, acids and alkalis In the event of a fire involving asbestos, use fine water spray and liquid-tight protective clothing with breathing apparatus Health The most common route of exposure is by inhalation Acute inhalation may cause local irritation Skin and eye irritation may occur from fibres Environment Environmentally hazardous substance Inform Environment Agency of substantial release incidents CRCE HQ, HPA 03/2012 Version 2
ASBESTOS INCIDENT MANAGEMENT Hazard Identification Standard (UK) Dangerous Goods Emergency Action Codes (a) 2212 Crocidolite (blue asbestos) UN EAC 2212 Amosite (brown asbestos) 2590 Chrysotile (white asbestos) 2X Use fine water spray. Wear liquid-tight chemical protective clothing in combination with breathing apparatus*. Spillages and decontamination run-off should be prevented from entering drains and watercourses. APP - Hazards Class 9 Miscellaneous dangerous substances and articles Sub risks HIN 90 - Environmentally hazardous substance; miscellaneous dangerous substances UN United Nations number; EAC Emergency Action Code; APP Additional Personal Protection; HIN - Hazard Identification Number * Liquid-tight chemical protective clothing (BS 8428) in combination with self-contained open circuit positive pressure compressed air breathing apparatus (BS EN 137). a Dangerous Goods Emergency Action Code List 2011. National Chemical Emergency Centre (NCEC). The Stationary Office, London. Incident management: Page 2 of 11
ASBESTOS INCIDENT MANAGEMENT Chemical Hazard Information and Packaging for Supply Classification (a) Carc. cat 1 Category 1 carcinogen Classification T Toxic Risk phrases Safety phrases R45 R48/23 S45 S53 May cause cancer Toxic: danger of serious harm to health by prolonged exposure through inhalation In case of accident or if you feel unwell seek medical advice immediately (show label where possible) Avoid exposure obtain special instructions before use a Annex VI to Regulation (EC) No 1272/2008 on Classification, Labelling and Packaging of Substances and Mixtures- Table 3.2. http://esis.jrc.ec.europa.eu/index.php?pgm=cla (accessed 03/2012) Incident management: Page 3 of 11
ASBESTOS INCIDENT MANAGEMENT Globally Harmonised System of Classification and Labelling of Chemicals (GHS) (a) Carc 1A Carcinogenicity, category 1A Hazard Class and Category STOT RE 1 Specific target organ systemic toxicity following repeated exposure, category 1 Hazard Statement Signal Words H350 H372 DANGER Implemented in the EU on 20 January 2009. May cause cancer Causes damage to organs through prolonged or repeated exposure a Annex VI to Regulation (EC) No 1272/2008 on Classification, Labelling and Packaging of Substances and Mixtures- Table 3.1. http://esis.jrc.ec.europa.eu/index.php?pgm=cla (accessed 03/2012) Incident management: Page 4 of 11
ASBESTOS INCIDENT MANAGEMENT Physicochemical Properties Serpentine asbestos Chrysotile CAS number 12001-29-5 Molecular weight Variable Empirical formula Mg 3 (Si 2 O 5 )(OH) 4 Common synonyms State at room temperature White asbestos; serpentine asbestos White, grey or green fibrous solid Volatility Non-volatile at 20 C Specific gravity 2.55 (water = 1) Flammability Lower explosive limit Upper explosive limit Water solubility Reactivity Reaction or degradation products Odour Non flammable Data not available Data not available Insoluble in water and organic solvents Stable under normal conditions. Incompatible with strong oxidisers, strong acids and bases Thermal decomposition may release toxic and/or hazardous gases Odourless Structure Incident management: Page 5 of 11
ASBESTOS INCIDENT MANAGEMENT Amphibole asbestos Crocidolite Amosite Anthophyllite Tremolite Actinolite CAS number 12001-28-4 12172-73-5 77536-67-5 77536-68-6 77536-66-4 Molecular weight Empirical formula Common synonyms State at room temperature Variable Variable Variable Variable Variable NaFe 3 2+ Fe 2 3+ Si 8 O 22 (OH) 2 Blue asbestos Lavender, blue or green fibrous solid (Mg,Fe) 7 Si 8 O 22 (OH) 2 Brown asbestos; mysorite Brown or grey fibrous solid Mg 7 (Si 8 O 22 ) (OH) 2 Azbolen asbestos; ferroanthophyllite Grey or browngrey fibrous solid Volatility Non-volatile at 20 C Specific 3.37 3.43 2.9 3.1 gravity (water = 1) (water = 1) (water = 1) Flammability Lower explosive limit Upper explosive limit Water solubility Reactivity Reaction or degradation products Odour Non flammable Data not available Data not available Ca 2 Mg 5 (Si 8 O 22 )(OH) 2 Silicic acid; calcium magnesium salt (8:4) White to pale green fibrous solid 2.9-3.2 (water = 1) Insoluble in water and organic solvents Ca 2 Mg 3 Si 8 O 22 (OH) 2 Fe 2+ 2 Stralite White to green fibrous solid 3.0-3.2 (water = 1) Stable under normal conditions. Incompatible with strong oxidisers, strong acids and bases Thermal decomposition may release toxic and/or hazardous gases Odourless Structure References (both tables) (a,b,c,d,e) a Asbestos (HAZARDTEXT Hazard Management). In: Klasco RK (Ed): TOMES System, Thomson Micromedex, Greenwood Village, Colorado, USA. (electronic version). RightAnswer.com, Inc., Midland, MI, USA, Available at: http://www.rightanswerknowledge.com/data/dt/dt204.htm (03/2012). b International Chemical Safety Card (ICSC) entry for asbestos (Chrysotile). ISCS 0014. International Occupational Safety and Health Information Centre (CIS), 1999. c The Merck Index (14 th Edition). Entry 826: Asbestos, 2006. d IARC. Some inorganic and organometallic compounds. Asbestos. Vol 2. Summary of data reported and evaluation. 1998. e ATSDR. Case studies in environmental medicine. Asbestos toxicity, 1997. Incident management: Page 6 of 11
ASBESTOS INCIDENT MANAGEMENT Threshold Toxicity Values EXPOSURE VIA INGESTION mg SIGNS AND SYMPTOMS REFERENCE - Asbestos is thought to be of low acute toxicity a TOXBASE - http://www.toxbase.org (accessed 03/2012) a TOXBASE: Asbestos, 2005. Incident management: Page 7 of 11
ASBESTOS INCIDENT MANAGEMENT Published Emergency Response Guidelines Emergency Response Planning Guideline (ERPG) Values ERPG-1* ERPG-2** ERPG-3*** Listed value (ppm) Data not available Calculated value (mg m -3 ) * Maximum airborne concentration below which it is believed that nearly all individuals could be exposed for up to 1 hr without experiencing other than mild transient adverse health effects or perceiving a clearly defined, objectionable odour. ** Maximum airborne concentration below which it is believed that nearly all individuals could be exposed for up to 1 hr without experiencing or developing irreversible or other serious health effects or symptoms which could impair an individual's ability to take protective action. *** Maximum airborne concentration below which it is believed that nearly all individuals could be exposed for up to 1 hr without experiencing or developing life-threatening health effects. Acute Exposure Guideline Levels (AEGLs) AEGL-1 AEGL-2 AEGL-3 mg m -3 10 min 30 min 60 min 4 hr 8 hr Data not available The level of the chemical in air at or above which the general population could experience notable discomfort. The level of the chemical in air at or above which there may be irreversible or other serious longlasting effects or impaired ability to escape. The level of the chemical in air at or above which the general population could experience lifethreatening health effects or death. Incident management: Page 8 of 11
ASBESTOS INCIDENT MANAGEMENT Exposure Standards, Guidelines and Regulations Occupational standards WEL (a,b) http://www.hse.gov.uk/ Control Limit: 0.1 f cm -3 Short term exposures (10 min reference period): 0.6 f cm -3 WEL Workplace exposure limit; Control limit: a maximum concentration of asbestos fibres in the air (averaged over any continuous 4 hour period) that must not be exceeded. Short term exposures: worker exposure must not exceed 0.6 f cm -3 of air averaged over any continuous 10 minute period using respiratory protective equipment if exposure cannot be reduced sufficiently by other means. This is an Approved Code of Practice (ACoP) standard. Public health guidelines DRINKING WATER QUALITY GUIDELINE AIR QUALITY GUIDELINE No guideline value specified No guideline value specified SOIL GUIDELINE VALUE AND HEALTH CRITERIA VALUES No guideline value specified a The Control of Asbestos Regulations 2006. SI 2006/2739. The Stationery Office. 2006 b Control of Asbestos Regulations 2006 General Enforcement Guidance and Advice http://www.hse.gov.uk/foi/internalops/fod/oc/200-299/265-50.htm (accessed 03/2012). Incident management: Page 9 of 11
ASBESTOS INCIDENT MANAGEMENT Major route of exposure (a,b) Health Effects The most common route of exposure is by inhalation. Immediate Signs or Symptoms of Acute Exposure (b) Asbestos is thought to be of low acute oral toxicity. Acute inhalation of asbestos dust is likely to cause only local irritation. No signs of toxicity expected after ingestion. Possibility of obstruction. Skin and eye irritation may arise from acute exposure to fibres. TOXBASE - http://www.toxbase.org (accessed 03/2012) a TOXBASE: Asbestos, 2005. b TOXBASE: Eye irritants, 2002. Incident management: Page 10 of 11
ASBESTOS INCIDENT MANAGEMENT Decontamination and First Aid Important Notes Ambulance staff, paramedics and emergency department staff treating chemicallycontaminated casualties should be equipped with Department of Health approved, gas-tight (Respirex) decontamination suits based on EN466:1995, EN12941:1998 and pren943-1:2001, where appropriate. Decontamination should be performed using local protocols in designated areas such as a decontamination cubicle with adequate ventilation. Prevent dispersal of dust and avoid all contact. Damp down any friable/exposed areas to avoid dust cloud. Dermal exposure (a) Remove patient from exposure. The patient should remove all clothing and personal effects. Double-bag soiled clothing and place in a sealed container clearly labelled as a chemical hazard. Brush away any adherent solid particles from the patient. Wash hair and all contaminated skin with copious amounts of water (preferably warm) and soap for at least 10-15 minutes. Decontaminate open wounds first and avoid contamination of unexposed skin. Pay special attention to skin folds, axillae, ears, fingernails, genital areas and feet. Ocular exposure (b) Remove patient from exposure. Remove contact lenses if necessary and immediately irrigate the affected eye thoroughly with water or 0.9% saline for at least 10-15 minutes. Patients with corneal damage or those whose symptoms do not resolve rapidly should be referred for urgent ophthalmological assessment. Inhalation (a) Remove patient from exposure. Treatment other than symptomatic unlikely to be required after acute exposure. Ingestion (a) Treatment unlikely to be required following acute ingestion. This document from the HPA Centre for Radiation, Chemical and Environmental Hazards reflects understanding and evaluation of the current scientific evidence as presented and referenced in this document. TOXBASE - http://www.toxbase.org (accessed 03/2012) a TOXBASE: Asbestos, 2005. b TOXBASE: Eye irritants, 2002. Incident management: Page 11 of 11
Asbestos Toxicological overview Kinetics and metabolism Key Points Short asbestos fibres are deposited in the upper respiratory tract where they are cleared by mucociliary action Longer fibres are carried into the alveolar regions and are cleared much slower thereby being retained in the lungs for longer periods Some fibres may be swallowed during inhalation due to the mucociliary action The properties of the fibres play a role in their toxicity; shorter fibres such as chrysotile are generally less potent than amphibole fibres Health effects of acute exposure The major route of exposure is through inhalation and to a lesser extent ingestion In general asbestos is not considered acutely toxic Acute high level exposure may cause pleural disorders, mesothelioma or lung cancer after a long latency period Health effects of chronic exposure Chronic low level inhalation exposure may cause pleural disorders, mesothelioma or lung cancer; chronic high dose exposure may cause asbestosis Asbestos is a category 1 carcinogen i.e. is carcinogenic to humans Asbestos has not been linked with any adverse reproductive outcomes in humans Prepared by S Bull CHAPD HQ, HPA 2007 Version 1
ASBESTOS TOXICOLOGICAL OVERVIEW Toxicological Overview Summary of Health Effects The main route of exposure of asbestos fibres is through inhalation and to a lesser extent ingestion. Short thick fibres are deposited in the upper respiratory tract and are cleared by mucociliary action to the pharynx where they are swallowed. Longer thinner fibres are carried deeper into the distal airways and alveolar regions and are cleared at a much slower rate, thereby being retained in the lung for longer periods. The size and shape of the asbestos fibres can therefore determine the effect caused by their inhalation, as asbestosis is related to the number of shorter, thicker fibres, whereas mesothelioma and lung cancer are related to longer thinner fibres. Chrysotile fibres (white asbestos) are generally < 5 m and crocidolite (blue asbestos), amosite (brown asbestos), anthophyllite and tremolite fibres are approximately 5 10 m. In general, chrysotile is recognized recognised to be less potent regarding carcinogenicity than amosite or crocidolite. Asbestos is generally not considered to be acutely toxic, as few immediate effects are observed following exposure. Short-term high level inhalation exposure to asbestos has been associated with lung cancer, mesothelioma and pleural disorders such as pleural plaques. Such effects may be observed following a latency period of approximately 30 years. Epidemiology studies have shown that chronic inhalation of all types of asbestos fibres is associated with asbestosis, pleural abnormalities, mesothelioma and lung cancer. Parenchymal asbestosis is considered to be a feature of high occupational exposure whereas pleural disorders, mesothelioma and lung cancers are more commonly associated with long-term to low levels. Clinical signs and symptoms of asbestosis include basal crackles on auscultation, dyspnoea, rales, cough and abnormal gaseous exchange, which may ultimately lead to death. Hypoxia with cor pulmonale may occur in severe cases. Although asbestosis is non-malignant, its occurrence increases the risk of lung cancer, especially in smokers. Mesothelioma is a rare malignant tumour of the pleura or the peritoneum, induced mainly by amphibole asbestos and to a lesser extent chrysotile. Signs and symptoms of pleural mesothelioma include weight loss, fever, chest pain, breathlessness on exertion and pleural effusion whereas peritoneal mesothelioma may cause abdominal pain, change in bowel habit and weight loss. Both are usually incurable when diagnosed. The incidence of mesothelioma appears to be independent of smoking. Lung cancer may be caused by chronic inhalation of chrysotile, amosite, anthophyllite, and mixed fibres containing crocidolite, tremolite and actinolite or tremolite with anthophyllite, although it is unknown if different fibres differ in their potency. As with mesothelioma, a latency period of approximately 30 years may occur between the initial exposure and onset of disease. Unlike mesothelioma, the incidence of lung cancer is related to smoking as asbestos and smoking act synergistically to exert their carcinogenic effect. Conflicting data exist regarding whether the inhalation of asbestos fibres may also cause cancer at other sites, such as stomach, oesophagus, colon or rectum. Overall, following a Toxicological overview: Page 2 of 15
ASBESTOS TOXICOLOGICAL OVERVIEW meta-analysis it was concluded that a causal relationship between asbestos exposure and gastrointestinal cancers could not be established. The World Health Organisation (WHO) concluded that there was little evidence that ingested asbestos is hazardous to health and therefore did not feel it necessary to establish a healthbased guideline value for drinking water. The International Agency for Research on Cancer (IARC) reviewed available data on the carcinogenicity of asbestos. Overall, there was sufficient evidence for carcinogenicity and asbestos was classified as group 1, namely carcinogenic to humans. Although not entirely established, asbestos may be considered a genotoxic carcinogen hence is thought not to exhibit a threshold under which adverse effects are seen. There is evidence that chrysotile is less potent than the amphiboles, but as a precaution chrysotile has been attributed the same risk estimates, although no threshold has been identified for carcinogenic risks of chyrsotile. Toxicological overview: Page 3 of 15
ASBESTOS TOXICOLOGICAL OVERVIEW Kinetics and metabolism Asbestos consists largely of fibres that are generally insoluble and do not undergo absorption, distribution and metabolism as do most other non-fibrous chemicals. The main route of exposure of asbestos fibres is through inhalation and to a lesser extent ingestion. It is unlikely that appreciable amounts of asbestos will be absorbed following dermal exposure [1]. Following inhalation, asbestos fibres are deposited on the epithelial surface of the respiratory tract. The fate of the asbestos fibres depends on the site of deposition and the aerodynamic characteristics [1-2]. Shorter thicker fibres (> 3m) are deposited in the upper respiratory tract, whereas longer thinner fibres are carried deeper into the distal airways and alveolar regions [1-2]. Most of the fibres that are deposited in the upper airway are transported by mucociliary action to the pharynx, where they are swallowed. Fibres that are short enough to be ingested by macrophages are thought to be removed through phagocytosis [3]. Longer fibres are cleared at a much slower rate and may undergo fragmentation, splitting or dissolution. Therefore a higher proportion of longer fibres is retained in the lungs [3]. Due to the differences in structure and its longer fibre length, chrysotile is more likely to be deposited in the upper airways of the respiratory tract and is therefore cleared more efficiently from the lungs compared with amphibole fibres [2-3]. A small fraction of shorter fibres may also remain in the lungs for a longer period of time, and may penetrate through the epithelial layer of the lungs into the lymphatic system or the blood. Fibres that reach the lymphatic system are then able to reach other tissues of the body and those that that enter the gastrointestinal tract, either by ingestion following inhalation or mucociliary transport from the lungs are mostly excreted in the faeces [1-2]. Ingestion of asbestos is not a major route of exposure. Ingestion of asbestos may accompany inhalation due to fibres being cleared from the respiratory tract by mucocilliary action. Few ingested fibres pass through the wall of the gastrointestinal tract and reach the blood, lymph and urine hence most will be excreted in the faeces. Therefore the risk of noncarcinogenic injury to the lungs, heart, liver, kidney or skin following absorption from the GI tract is minimal [2, 4]. However, animal studies reported fibres in kidney, liver, brain, heart and spleen of rats fed only an asbestos-containing diet, supporting the hypothesis that fibres may pass though the gastrointestinal tract [1]. Asbestos fibres can pass through the skin. However, no studies have shown that fibres enter systemic circulation following dermal exposure [2]. Sources and route of human exposure Asbestos is a group of naturally occurring fibrous serpentine (chrysotile) or amphibole (crocidolite, amosite, anthophyllite, tremolite and actinolite) minerals. Asbestos minerals are widely spread throughout the earth s crust. Chrysotile, the most abundant and commercially important form, is present in most serpentine rock formations and in many soils [5]. The main route of exposure of asbestos fibres is through inhalation and to a lesser extent ingestion [4, 6]. Toxicological overview: Page 4 of 15
ASBESTOS TOXICOLOGICAL OVERVIEW Human exposure to asbestos underwent a rapid increase over the past 100 years as it was used, due to its specific characteristics, in >3000 products. Therefore asbestos fibres are ubiquitous in the environment. Commercial use of asbestos peaked in the 1970s but bans on importation, supply and use of blue and brown fibres in 1985 and chrysotile in 1999 have contributed to the declining presence of asbestos. However, insulating materials in buildings and products manufactured before the ban may still exist [4, 6]. Asbestos is prevalent in the three main environmental media, namely air, water and soil. The majority of asbestos exposure arises from air due to natural weathering of asbestoscontaining rock, which may be enhanced by human activity. It has been suggested that the amount emitted from natural sources may be greater than that emitted form industrial sources but overall, very little is known about the amounts arising from natural sources [4-6]. Emission of asbestos from human activities in the past resulting in potential human exposure may be separated into four main categories [5-6]: Product manufacture (thermal insulation, brake shoes, floor tiles, cement); Construction activities (removal or maintenance of previously installed asbestos in buildings and demolition of such buildings); Transport, use and disposal of products containing asbestos. Indoor air may become contaminated with asbestos fibres from building materials, especially if damaged, including asbestos pipe insulation, boiler coverings and floor and ceiling tiles [4]. A summary of asbestos in air measurements reported asbestos concentrations in different environments [4]; Rural areas (outdoors remote form asbestos emission sources): below 0.0001 fibres ml -1 Urban areas (outdoors) general levels may vary from below 0.0001 fibres ml -1 In buildings without specific asbestos sources generally below 0.001 fibres ml -1 Drinking water may become contaminated with asbestos fibres from natural sources such as erosion of rock, or man-made sources such as industrial effluents, atmospheric pollution, disintegration of asbestos-containing products and asbestos cement pipes in the distribution system [5, 7]. Exfoliation of asbestos from asbestos-cement pipes is related to the aggressiveness of the water supply [7]. Surveys of asbestos concentrations in raw and treated water in the United Kingdom suggest that most drinking water contains asbestos fibres, the concentration of which varies between none detectable and 1 million fibres L -1 [8]. The limited data available suggest that exposure to airborne asbestos released from tap water during showering and bathing is negligible [7]. Soil may also be contaminated with asbestos due to the weathering of natural asbestos deposits or by land-based disposal of waste materials containing asbestos, although current regulations now restrict the disposal into landfills [1]. Once liberated in the environment asbestos persists for an unknown period of time [5]. Toxicological overview: Page 5 of 15
ASBESTOS TOXICOLOGICAL OVERVIEW Health Effects of Acute / Single Exposure Human Data General toxicity The size and shape of the asbestos fibre appear to play a major role in the toxicity, as both affect the capacity of the lung to effectively remove them from the body. Asbestosis is related to the number of shorter, thicker fibres, whereas mesothelioma and lung cancer are related to longer thinner fibres (table 1). Chrysotile fibres (white asbestos) are generally < 5 m whereas crocidolite (blue asbestos), amosite, anthophyllite and tremolite fibres are approximately 5 10 m. It is recognized that chrysotile is generally less potent than amosite or crocidolite [3-4, 9]. Table 1. Effect of inhalation of different size asbestos fibres Asbestosinduced Length of fibre (m) Width of fibre (m) effect Asbestosis > 2 m > 0.15 m Mesothelioma > 5 m < 0.1 m Lung cancer > 10 m < 0.15 m Acute, high level exposure to asbestos fibres can cause pleural disorders, mesothelioma and lung cancer after a long latency period, whereas chronic exposure to higher doses (concentrations not given) are more likely to be related to parenchymal asbestosis as well as lung cancer [4]. Inhalation Acute exposure to asbestos fibres does not produce immediate acute effects other than some irritancy of skin, eyes and lungs with high concentrations. Temporary breathing difficulties have been reported in individuals exposed to high concentrations of asbestos dust [2]. Short-term high level exposure to asbestos has been associated with lung cancer, mesothelioma and pleural disorders such as pleural plaques although risks are likely to be very low [4]. Ingestion No data on acute toxicity in humans following oral exposure was available. Toxicological overview: Page 6 of 15
ASBESTOS TOXICOLOGICAL OVERVIEW Dermal / ocular exposure Asbestos fibres may penetrate the skin and cause benign lesions around the implanted fibres, such as warts and corns, known as asbestos corns. Approximately 60 % of workers installing amosite insulation in the past reported lesions on the hands within 10 days [2]. Delayed effects following an acute exposure Most health effects caused by asbestos occur after a latent period following exposure. Asbestos is carcinogenic by inhalation, and does not produce acute effects, but lung toxicity (the target organ) may be manifest after many years. Clinical manifestations often occur approximately 30 years after the first exposure. However, the risks of serious long-term health effects from a single exposure are judged to be very low [6]. Animal and In-Vitro Data Inhalation Rats exposed to asbestos (concentration not stated) for 14 days developed local inflammatory lesions in the terminal bronchioles and progressive fibrosis occurred within a few weeks of exposure [2]. Ingestion A single oral exposure of rats to chrysotile (5 100 mg kg -1 ) produced an increase in thymidine in the stomach, jejunum and duodenum, suggestive of an immediate response of cellular proliferation and DNA synthesis [2]. Dermal / ocular exposure No data on acute toxicity in animals following dermal or ocular exposure was available. Toxicological overview: Page 7 of 15
ASBESTOS TOXICOLOGICAL OVERVIEW Health Effects of Chronic / Repeated Exposure Human Data Inhalation Chronic inhalation of all types of asbestos fibres can cause a number of abnormalities such as; pleural asbestosis (now called asbestosis-related pleural abnormalities) parenchymal asbestosis mesothelioma of the pleura and peritoneum and bronchial carcinoma [3, 7, 10]. Pleural asbestosis (asbestosis-related pleural abnormalities) Inhalation of asbestos can cause irreversible diffuse interstitial fibrosis of the lung, known as asbestosis. Pleural asbestosis or asbestosis-related pleural abnormalities include pleural plaques, mainly involving the parietal pleura, and pleural thickening involving the visceral pleura. Pleural plaques are discrete fibrous or calcified thickened areas that arise from the surface of the parietal pleura. They are usually asymptomatic without clinical important findings and may be observed without parenchymal asbestosis. Pleural plaques are not precursors of lung cancer, although many affected people have an increased incidence of lung cancer. Pleural plaques may be observed in 20 60 % of individuals occupationally exposed to asbestos and are most likely caused by the migration of inhaled asbestos to the pleura [4, 10]. Pleural thickening by definition is a homogeneous uninterrupted plural density. It can occur with or without pleural effusion and may or may not be associated with asbestosis. It is usually asymptomatic but in severe cases can cause signs and symptoms of restrictive lung disease [10-11]. Parenchymal asbestosis Parenchymal asbestosis results from a prolonged inflammatory response stimulated by the presence of fibres in the lung, leading to fibrosis of the lung parenchyma or the pleural tissue [2]. Asbestos fibres are resistant to breakdown in the lungs, thereby initiating a continual inflammatory response, even after exposure has ceased. It is estimated that cumulative exposure of 17-75 fibres-year ml -1 could cause fibrotic lesions and 3.5-300 fibres-year ml -1 could be fatal [2, 10]. Clinical symptoms may take up to approximately 30 years to develop after onset of exposure, although radiological differences may be observed earlier [2, 4-5]. The main clinical symptoms of asbestosis are basal crackles on auscultation, dyspnoea, rales, cough, abnormal gaseous exchange and enlargement of the heart, which may ultimately lead to death [2, 10]. Hypoxia with cor pulmonale may occur in severe cases [6]. In a recent review of epidemiological data of asbestosis exposure-response relationships for chrysotile, it was concluded that asbestotic changes are common following prolonged exposures of 5 20 fibres ml -1, corresponding to cumulative exposures of 50 200 fibres Toxicological overview: Page 8 of 15
ASBESTOS TOXICOLOGICAL OVERVIEW year ml -1 for a 10-year exposure, and that the risk at lower exposure levels is not known [1, 5]. Parenchymal asbestosis is considered to be a feature of high occupational exposure although cases have been reported following an acute exposure to high concentrations of asbestos (concentrations not specified) [4, 6]. In contrast, parietal pleural plaques are more commonly seen following low occupational exposure, or those that have undergone environmental exposure. However, as asbestosis is rarely observed in relation to nonoccupational asbestosis exposure WHO concluded that environmental concentrations of asbestos are not sufficient to cause asbestosis [6]. Although asbestosis is non-malignant, its occurrence increases the risk of lung cancer, especially in smokers. There is some disagreement as to whether asbestosis is merely a marker of high-dose exposure or whether the interstitial fibrosis seen in asbestosis induces cancer, although lung cancer may develop without asbestosis [6]. Mesothelioma Mesothelioma is a rare malignant tumour of the pleura or the peritoneum. The majority of cases reported are a result of occupational or para-occupational exposure to asbestos [3, 6, 10]. The majority of cases of mesothelioma arise following exposure to crocidolite and less frequently to amosite. Chrysotile only seldom causes mesothelioma, unless mixed with amphibole fibres [12]. This is mainly due to the long, thin dust fibres that are produced during technical processes involving amphiboles. When inhaled, such fibres are more resistant in the body and have a lower lung clearance than chrysotile. It is interesting to note that one study of a large group of workers occupationally exposed to chrysotile alone showed no incidence mesothelioma [3, 6, 9, 12-13]. Mesothelioma, in general, may occur following chronic low asbestos exposure, and peritoneal mesothelioma is associated with higher levels of asbestos exposure than pleural mesothelioma. In some cases, a very short exposure period may be sufficient to initiate the onset of the tumour [4]. Pleural mesothelioma initially causes few or non-specific symptoms such as weight loss and fever. As the disease progresses chest pain, breathlessness on exertion and pleural effusion may occur. Peritoneal mesothelioma may cause abdominal pain, change in bowel habit and weight loss [10]. Both are usually incurable when diagnosed [6, 9]. As with asbestosis, mesothelioma has a long latency period. A minimum of ten years from initial exposure is usually required. In most cases however the latency period is between approximately 30 years, although higher exposures may shorten the time frame [4, 9]. Bronchial carcinoma. Many studies have been carried out to investigate the carcinogenicity of inhaled asbestos fibres. Occupational exposure to chrysotile, amosite, anthophyllite and mixed fibres containing crocidolite has been reported to cause lung cancer, as have minerals containing tremolite and actinolite or tremolite mixed with anthophyllite [12]. Although all types of asbestos can cause lung cancer, it is unclear whether they differ in their potency. In some studies, exposure to chrysotile resulted in no increase in risk ratio or only a slightly elevated risk ratio for lung cancer [12]. In contrast, some studies have reported that fibres found in the lung are predominately amphibole fibres although a few cases reported that mainly or only chrysotile fibres were found [3-4, 12-13]. Toxicological overview: Page 9 of 15
ASBESTOS TOXICOLOGICAL OVERVIEW Exposure to asbestos fibres may cause all four major types of lung cancer, namely squamous cell carcinoma, adenocarcinoma, large-cell carcinoma and small-cell carcinoma [4]. A latency period of approximately 30 years or more may occur between the time of initial exposure and tumour occurrence [4, 12-13]. Both asbestos and smoking independently increase the incidence of lung cancer, but together they act in a synergistic manner, whereas the risk of mesothelioma appears to be independent of smoking [12-13]. Carcinoma of other sites Several mortality studies have also revealed that inhalation of asbestos may cause small increases in the incidence of death due to cancer of the stomach, oesophagus, colon or rectum. Other mortality studies however, failed to showed a significantly increased risk of cancer incidence [1]. Following a meta-analysis of available studies, it was concluded that the available data do not establish a causal relationship between occupational exposure to asbestos and the development of gastrointestinal cancers [1]. Excess cases of kidney, brain, bladder, larynx or haematopoietic cancers have also been noted in a number of studies. However, overall it was concluded that the evidence for such cancers was not strong [1]. Cardiovascular effects Asbestos does not exert a direct effect on the cardiovascular system following inhalation. However, increased cardiovascular disease in asbestos workers has been reported. Lung fibrosis (asbestosis) following asbestos inhalation may cause an increased resistance to capillary blood flow in the lungs, resulting in pulmonary hypertension and cor pulmonale. Such heart failure may also arise with less severe fibrosis in patients with chronic obstructive pulmonary disease (COPD) or those that smoke. Pulmonary hypertension can also arise, in most cases prior to the decreased lung function being clinically detectable. Chronic constrictive pericarditis has also been reported [1, 4, 11]. Gastrointestinal effects The gastrointestinal tract is directly exposed to asbestos, as fibres which are deposited in the respiratory tract following inhalation, may be swallowed. However, there is no evidence to suggest that asbestos increases the risk of non-carcinogenic and carcinogenic effects in the gastrointestinal system following inhalation [1]. Immunologic effects Immunological changes have been reported following occupational, but also environmental exposure [4]. As asbestos-induced fibrosis progresses, patients may have an altered immune response as they exhibit antinuclear antibodies and rheumatoid factors. In addition, cell-mediated immunity is commonly decreased in patients with asbestosis, including a progressive decrease in lymphocytes. Although not well understood, it is thought that such a depression in immune function may play a role in the aetiology of asbestos-induced carcinoma [1, 4]. Ingestion Various studies in humans have reported that ingestion of asbestos causes little or no risk of non-carcinogenic illness [1]. Conflicting data have been reported regarding the carcinogenicity of ingested asbestos fibres. Mortality studies of asbestos workers have shown an increased incidence of cancer of the larynx, kidneys and gastrointestinal system, including the oesophagus, stomach, colon Toxicological overview: Page 10 of 15
ASBESTOS TOXICOLOGICAL OVERVIEW and rectum. Authors hypothesised such an increase to be due to ingestion of fibres. In contrast, other epidemiological studies failed to show any significant association between asbestos exposure and extrathoracic tumours [4, 12]. Many epidemiology studies have also been carried out in populations that drink water with high concentrations of asbestos. Overall, there has been little convincing evidence of the carcinogenicity of ingested asbestos. The WHO concluded that there is no consistent evidence that ingested asbestos is hazardous to health and hence did not feel the need to establish a health-based guideline value for asbestos in drinking water [7]. Dermal Small warts or corns may develop on the skin following dermal contact. Such lesions are thought to be due to penetration of the skin by a macroscopic spicule, although fibres could not be identified on histological examination of the corns [1]. Genotoxicity Epidemiology studies of asbestos workers, residents in asbestos-rich areas and patients with mesothelioma or lung cancer suggest that asbestos is genotoxic as chromosomal aberrations and sister chromatid exchange were significantly higher in peripheral blood lymphocytes of exposed individuals, compared with non-exposed controls in a number of studies [1]. Carcinogenicity The International Agency for Research on Cancer (IARC) reviewed available data. Overall, there was sufficient evidence for carcinogenicity and asbestos was classified as group 1, namely carcinogenic to humans [13]. Several authors have produced estimates indicating that a population, of which 30% are smokers, with a lifetime exposure to asbestos at concentrations of 1000 F m -3 (0.0005 F ml -1 or 500 F m -3, optically measured) would have an excess risk of lung cancer in the order of 10-6 - 10-5 and the risk of mesothelioma would be in the range of 10-5 - 10-4. These ranges were proposed to provide adequate health protection [6]. A WHO Task Group expressed concern over the reliability of estimating the risk to human health from asbestos. Risk estimates are based on a large set of epidemiology data from occupational studies. Such data have been extrapolated to concentrations found in the environment. It was felt that the risk estimates proposed could be used only to obtain an approximation of the risk of lung cancer or mesothelioma from environmental exposures to asbestos [6]. Although there is evidence that chrysotile is less potent than the amphiboles, as a precaution chrysotile has been attributed the same risk estimates. No threshold has been identified for carcinogenic risk of chrysotile [6]. Toxicological overview: Page 11 of 15
ASBESTOS TOXICOLOGICAL OVERVIEW Reproductive and developmental toxicity Female workers exposed to asbestos cement dust via inhalation experienced reproductive disorders. In addition, male railway builders who inhaled asbestos had sex organ abnormalities. However, such workers were also exposed to other chemicals including carbon monoxide, nitrogen dioxide, acrolein and formaldehyde as well as asbestos [11]. Few studies were identified regarding the reproductive effects following oral exposure to asbestos [1]. Chrysotile fibres have been reported in lung, liver and placenta of still born infants hence transplacental transfer of asbestos is thought to occur, although this has not been linked with any adverse reproductive outcomes in humans [11]. Animal and In-Vitro Data Inhalation Many chronic inhalation studies have been carried out to investigate the toxicity of different asbestos fibres in laboratory animals. Several species such as rats, hamsters, guinea pigs and monkeys developed fibrosis following exposure to chrysotile and amphibole asbestos, the incidence and severity of which were dose-related. In general, it was observed that shorter fibres were generally less fibrogenic [3]. Guinea pigs and monkeys were exposed to chrysotile and amosite dust (30000 particles ml - 1 ), for 8 hours day -1, 5 days week -1 for 49 weeks year -1. Both chrysotile and amosite produced pulmonary fibrosis, interstitial pneumonitis, metaplasia of the epithelium of alveolar ducts and cor pulmonale in guinea pigs. Three of the monkeys died after exposure to both chrysotile and amosite [2]. In a further study, rats were exposed to amosite, anthophyllite, crocidolite and chrysotile dust (9.7 14.7 mg m -3 ) for 7 hours day -1, 5 days week -1 for 3, 6, 12 or 24 months. Results showed an increase in severity of asbestosis with increasing dose [2]. Other studies, in which rats were exposed to chrysotile, crocidolite or amosite at 2 or 10 mg m -1 for 12 months reported that all malignant pulmonary tumours occurred due to the chrysotile fibres, predominantly those over 20 m in length [3]. Several studies induced fibrosis in animals by inhalation or intratracheal exposure to chrysotile, amosite, anthophyllite, crocidolite or tremolite (concentrations not stated). Results showed that crocidolite causes more severe inflammation than chrysotile and is retained in the lungs for longer periods [1]. Although fibrosis has been reported in several animal species an increased incidence of bronchial carcinoma and mesothelioma has only been documented in the rat [3]. Overall, data have shown that fibrosis, bronchial carcinoma and pleural mesothelioma may arise following inhalation of chrysotile and amphibole fibres, but there was no increase in tumours at other sites [3]. Toxicological overview: Page 12 of 15
ASBESTOS TOXICOLOGICAL OVERVIEW Ingestion Several studies investigating the toxic potential of ingested asbestos have been carried out. In a National Toxicology Program (NTP) study, male and female rats and Syrian Golden hamsters were administered 1% short and intermediate length chrysotile in the diet over their lifetime, equating to approximately 500 or 830 mg kg -1 day -1 for rats and hamsters, respectively. A similar study was also carried out by exposing male and female rats to 1% crocidolite, amosite or tremolite for life. None of the different forms of asbestos affected survival or induced any signs of toxicity [1-2]. Similarly, rats were administered 0.5 or 50 mg chrysotile for 14 months, after which time no adverse effects were observed in the gastrointestinal tract, although structural changes in the villi of the ileum were noted. Moreover, following a significant increase in [ 3 H] thymidine incorporation in the gastrointestinal tract it was suggested that asbestos interferes with DNA metabolism in the rat [2]. Rats fed margarine containing 5 mg g -1 amosite, crocidolite or chrysotile (250 mg week -1 ) for 25 months did not show signs of gastrointestinal damage, although occasional asbestos fibres were seen in several tissues [2]. Most ingested asbestos fibres are not absorbed into the body hence the GI epithelium is the most directly exposed. A few studies in rats showed biochemical changes in cells following chronic oral exposure to 20 140 mg kg -1 day -1 chrysotile. However, no non-neoplastic regions were identified in several animal studies, including the NTP studies on lifetime exposure of rats and hamsters to asbestos [1]. Overall, there was no conclusive evidence from the toxicological studies carried out that ingested asbestos is carcinogenic [3, 5]. Genotoxicity Many studies have been carried out to investigate whether asbestos fibres interact with DNA directly or indirectly via the induction of oxidative stress. Cell free assays have demonstrated that chrysotile, amosite and crocidolite all cause lipid peroxidation. Moreover, chrysotile causes the breakage of isolated DNA but it has been hypothesised that this may be due to the generation of reactive oxygen species attributed to the surface area of the fibres [5]. Data from several in-vitro assays demonstrated sister chromatid exchanges, chromosomal aberrations and anaphase abnormalities in Chinese hamster cells thus authors reported chrysotile, amosite and crocidolite to be weakly mutagenic. In contrast, chrysotile and crocidolite did not cause DNA breakage in tracheal epithelial cells [3, 5]. In-vivo and in-vitro mutagenicity studies have given equivocal results. Asbestos was not mutagenic in Salmonella typhimurium and Escherichia coli, but gave a mutagenic response in the S. typhimurium TA 102 strain, which is sensitive to reactive oxygen species. Similarly, in-vitro genotoxicity assays using mammalian cells reported both negative and positive data [1]. Moreover, the UICC reference samples of asbestos did not show mutagenic activity in bacterial assays [3]. Overall, data suggest that asbestos may have mutagenic potential. Asbestos was assessed by WHO Europe as part of the work on air quality guidelines. It was noted that it is prudent to assume that there is no threshold below which effects are not observed and hence exposure should be kept as low as reasonably practicable [6]. Toxicological overview: Page 13 of 15
ASBESTOS TOXICOLOGICAL OVERVIEW Carcinogenicity The NTP study in which male and female rats and Syrian Golden hamsters were administered 1% short and intermediate length chrysotile in the diet over their lifetime, or 1% crocidolite, amosite or tremolite (see ingestion ), reported mainly negative results. Some increased frequencies of tumours were seen in the large intestine of male rats exposed to intermediate length chrysotile (500 mg kg -1 day -1 ). However, the significance of this is unclear [1]. The carcinogenic mechanism induced by asbestos fibres is not completely understood. Fibres may induce reactive oxygen species that may damage DNA; physical interactions between fibres and target cells may occur, causing DNA damage; fibres may induce cell proliferation or fibres may induce chronic inflammatory reactions. It is likely that several mechanisms contribute to the carcinogenicity [5]. Overall, data from inhalation studies provide adequate evidence that asbestos fibres are a carcinogenic hazard to humans. However, the data are not adequate to provide quantitative estimates of the risk to humans, as the exposure-response data from inhalation studies are not sufficient and the sensitivity of animals to predict risk to humans is uncertain [5]. Reproductive and developmental toxicity In a National Toxicology Program study, male and female rats were administered 1% short and intermediate length chrysotile in the diet over their lifetime, equating to approximately 500 mg kg -1 day -1 starting with the dams of the test animals. Neither fibre affected the fertility of the dams or the litter size [1-2]. In a similar study male and female rats were fed 1% crocidolite in feed, beginning with the dams before and during gestation [2]. Exposure to crocidolite did not affect fertility or litter size, but average weight gain of the pups at weaning was lower compared to offspring from non-exposed rats. Similar results were also observed in other NTP studies with tremolite and amosite [1-2]. Offspring from mice given up to 33 mg kg -1 day -1 chrysotile during gestation did not show any teratogenic abnormalities [1-2]. Asbestos given to rats in drinking water (concentration not specified) did not cause any effects on embryo survival or any teratogenic effects [11]. Asbestos was shown to cross the placenta in rats following maternal intravenous injection [11]. Mice given chrysotile asbestos in drinking water (20 mg kg -1 abnormalities in sperm [11]. day -1 ) did not show any Toxicological overview: Page 14 of 15
ASBESTOS TOXICOLOGICAL OVERVIEW References [1] Agency for Toxic Substances and Disease Registry (ATSDR) (2001). Toxicological profile for asbestos. US department of Health and Human Services. Atlanta, US. [2] Risk Assessment Information System (RAIS) (1995). Toxicity summary for asbestos. Chemical Hazard Evaluation and Communication Group, Biomedical and Environmental Information Analysis Section, Health and Safety Research Division. [3] International Programme on Chemical Safety (IPCS) (1986). Asbestos and other natural mineral fibres. Environmental Health Criteria 53. WHO. Geneva. [4] Agency for Toxic Substances and Disease Registry (ATSDR) (1997). Case studies in environmental medicine: Asbestos toxicity. US Department of Health and Human Services. Atlanta, US. [5] International Programme on Chemical Safety (IPCS) (1998). Chrysotile asbestos. Environmental Health Criteria 203. WHO. Geneva. [6] World Health Organisation (WHO) (2000). Air quality guidelines for Europe. WHO Regional Publications, European Series, No. 91. 2nd edition.. WHO Regional Office for Europe. [7] World Health Organisation (WHO) (2004). Guidelines for Drinking-Water Quality: Third edition. Vol 1. Recommendations.. WHO. geneva. [8] World Health Organisation (WHO) (2003). Asbestos in drinking water.. WHO. Geneva. [9] International Agency for the Research on Cancer (IARC) (1998). Some inorganic and organometallic compounds. Asbestos. Vol 2. Summary of data reported and evaluation. IARC. Lyon. [10] Health and Safety Executive (HSE) (2005). Asbestos: Medical guidance note MS13. [11] MEDITEXT Medical Management Asbestos. [12] International Agency for the Research on Cancer (IARC) (1987). Asbestos (Actinolite, amosite, anthophyllite, chrysolite, crocidolite, tremolite). Suppl. 7. Overall evaluations of carcinogenicity: An updating of IARC monographs, volumes! to 42.. IARC. Lyon. [13] International Agency for the Research on Cancer (IARC) (1998). Asbestos. Vol 14. Summary of data reported and evaluation. IARC. Lyon. This document from the HPA Centre for Radiation, Chemical and Environmental Hazards reflects understanding and evaluation of the current scientific evidence as presented and referenced in this document. Toxicological overview: Page 15 of 15