1 J Royal Naval Medical Service 2009, General Asbestos a legacy and a persistent problem F J H Brims Abstract Asbestos has been utilised by industrialised nations for over a century and its deleterious health effects have been reported for an almost equal length of time. Whilst developed countries have now reduced their asbestos use, developing nations are increasing their asbestos imports and consumption. Because of this, there is now a perceived risk to Non Government Organisation and military personnel involved in aid operations or conflict areas, where asbestos containing materials and buildings may have been disrupted. With significant asbestos exposures to UK military and dockyard personnel in the past, the health consequences are continuing to increase, with the incidence of malignant mesothelioma expected to continue to rise until between There is no effective cure or treatment for any of the lung or pleural asbestos related diseases; malignant mesothelioma has a median survival of just 6-12 months. Misconceptions about asbestos are widespread, contributed in part by a long latency between exposure and disease. Following diagnosis of an asbestos related disease, financial recompense for exservice personnel is limited, and the civilian legal implications continue to change. This review will encompass the historical usage of asbestos, its biological effects, the legal and financial implications of exposure, and establish that there may be a continuing threat of exposure to deployed military personnel Introduction Despite the recognised dangers of asbestos first documented in 1899 for a board of enquiry by a British physician , many industrial countries used and imported asbestos throughout most of the 20th Century; in the United Kingdom importation of asbestos only ceased in 1999 . Asbestos comes from a Greek adjective meaning inextinguishable. Historic records suggest asbestos has been used by man for over 4,000 years; it became increasingly popular throughout the 20th Century amongst manufactures and builders due to its resistance to heat, electricity and chemical damage, its sound absorption and tensile strength. Many of these properties made asbestos an ideal material for use in ship building, and vast tonnes of asbestos were used for this purpose during the second world war and beyond by the UK and other industrialised nations . Despite the recognised dangers, governments and societies failed to appreciate the true magnitude of the predicament and the range of hazards  and the use of asbestos in homes, schools, hospitals and indeed almost any building erected in the UK after 1960 became almost ubiquitous. In 2006 the French government were forced into an embarrassing position following widespread publicity and outcry after the 27,000 tonne former French flagship Clementeau, containing reportedly more than 1000 tonnes of asbestos, was sent to India for breaking up. Ship breaking remains a significant, mostly unregulated, lucrative business in India and Bangladesh . 4
2 Asbestos a legacy and a persistent problem 5 Asbestos is mined from the ground, and is still done so in a number of countries including South Africa, China, Brazil, Zimbabwe, Canada and Russia (currently the major supplier in the world) . The term asbestos refers to a group of crystallinehydrated silicate minerals that exist as fibres. It occurs in two forms: serpentine and amphibole. Chrysotile ( white asbestos) is the only serpentine form, whilst amphibole asbestos has several different forms, although the major commercial uses have largely only been with crocidolite ( blue) and amosite ( brown ). Chrysotile fibres are long, curly and pliable and have been mostly used to make fabrics and other flexible items. Amphibole fibres are short straight and stiff with superior chemical and physical stability and have been used to make asbestos cement, floor tiles and, when mixed with chrysotile, a vast array of products such as gaskets, roofing, insulation, lagging and fire proofing materials. Historical arguments with respect to different degrees of danger of carcinogenic potential by the different subtypes of asbestos are academic: man has often mixed different types together, and the World Health Organisation / International Agency for Research on Cancer classify all types of asbestos as carcinogenic to humans . Asbestos fibres enter the body usually by inhalation; airborne fibres are carried in the inspired airstream and lodge in small bronchioles, with smaller fibres (<3 Ìm) more likely to lodge in or around alveoli . Fibres lodged in larger airways are cleared by muco-cilliary clearance mechanisms. As lung tissue fibre burdens are correlated to cumulative exposure  it is thought that the natural pulmonary defence mechanisms can be overwhelmed by significant exposures. The softer, more pliable chrysotile fibres are cleared more easily than amphibole rods through phagocytic ingestion by macrophages or endocytosis by pneumocytes . Subsequent migration can occur via lymphatic drainage pathways to the pleural surface  where it is thought they can contribute to disease pathogenesis. Almost everyone in the western world has asbestos fibres in their lungs, and many individuals (in particular plumbers, builders, insulation fitters and military personnel) will recall specific asbestos exposures . Shipyard workers such as lagers, pipefitters, welders, sheet metal workers and painters have historically had significant asbestos exposures , although many workers performing other tasks will have been exposed because of working in close proximity, often in confined spaces, with others performing asbestos related tasks [11, 12]. A continuing danger In the 21st Century, the risks of asbestos exposure has not passed, particularly for military personnel, who may face exposure whilst deployed on disaster relief operations  or in conflict, where in both situations broken up building materials will be likely to contain asbestos. The importation and use of asbestos is increasing in many developing countries with consumption of asbestos between increasing by 20% in Indonesia, 31% in India, 48% in China and 51% in Thailand . The United Nations Environment Program has raised concerns about asbestos (and other toxic waste) exposure to locals and aid workers following the Asian tsunami of 2004 and Indonesian earthquake of 2005 . Similarly, there are risks from unnatural events such as building collapse from terrorist activity. There has been extensive investigation to try to characterise the risk to rescue workers following the attacks on the World Trade Centre and whilst it is clear that there was likely significant asbestos exposure to workers (amongst many other materials), quantification of risk is very difficult to reliably achieve [14, 15]. Time will tell if there are to be further victims of these attacks. Asbestos related Diseases With the exception of asbestos related pleural effusions, most asbestos related disease has a significant latency of more than twenty years following exposure before clinically
3 6 J Royal Naval Medical Service 2009, Vol 95.1 recognisable disease develops. Brief, intense exposures are capable of causing disease, however prolonged, greater cumulative exposures are more likely to manifest disease [9, 16]. The majority of asbestos related disease is within the lung and thoracic cavity, although peritoneal mesothelioma is a well recognised entity. Historically, asbestos corns were recognised on the hands of labourers handing large quantities of asbestos, with epidermal overgrowth due to intradermal deposition of asbestos fibres. The issue of whether lung cancer is caused by asbestos in the absence of other asbestos related disease is contentious [17, 18] and is beyond the realm of this article. Discussion of the major asbestos related diseases is provided below. Benign asbestos pleural effusion This benign pleural reaction is more likely with increased exposure [19, 20] and tends to occur with a shorter latency than the other major asbestos related diseases, at least with crocidolite with a study of workers in the Wittenoom Gorge mines in Western Australia identifying a median time of sixteen years following first exposure . Therefore, with significantly reduced rates of asbestos usage in the UK over the past years, this is likely to be a diagnosis largely confined to history and text books. Pleural plaques Pleural plaques are well circumscribed, discrete areas of hyaline or calcified pleural fibrosis. They occur mainly posteriorly and laterally, often following the eighth to tenth rib contours, although may affect the costophrenic angle, diaphragmatic or pericardial pleura . Pleural plaques can be visible on plain chest radiograph, although this tends to under estimate appearances . After crocidolite exposure they may become evident after ten years, but do not subsequently progress in size or extent [19, 23]. Pleural plaques are considered to be clinically benign and are often described as incidental findings on chest radiography. Whilst small reductions in vital capacity have been described in patients with pleural plaques , they are not thought to create sufficient physiological changes to induce dyspnoea. Rarely pleural plaques have been associated with an angina-like chest pain . Diffuse pleural thickening Diffuse pleural thickening is a condition of more extensive, active and progressive visceral pleural fibrosis. It is not necessarily specific to asbestos related disease as other conditions such as previous empyema or haemothorax may cause it . Never-theless, amphibole exposure is closely related to diffuse pleural thickening . In contrast to pleural plaques, diffuse pleural thickening can induce significant physiological abnormalities and dyspnoea. There is no proven beneficial therapy for diffuse pleural thickening, and associated chest pain should alert the clinician to the possibility of underlying malignancy. Asbestosis The term asbestosis is commonly misused to encompass all or any asbestos related lung disease. Strictly, it is pneumoconiosis and refers to a fibrotic parenchymal lung disease resulting from asbestos fibre inhalation. It is probably caused by the direct toxic effects of the fibres on the pulmonary parenchyma, as well as the release of various fibrotic mediators from inflammatory cells [28-30]. In time, there is gradual loss of alveolar pneumocytes and increases in inflammatory cells with progressive fibroblast proliferation and collagen accumulation [31-33]. The quantity of asbestos fibres in the lungs is generally ten to twenty fold higher in patients with asbestosis compared with unexposed individuals and correlates with the severity of fibrosis . Clinical presentation and course varies, however, most patients will present with increasing dyspnoea and perhaps dry cough. Clinically and radiologically, asbestosis can have very similar appearances to idiopathic pulmonary fibrosis (IPF: previously termed cryptogenic fibrosing alveolitis), although its clinical course is usually slower in contrast to the often rapid progression of IPF. To achieve
4 Asbestos a legacy and a persistent problem 7 a diagnosis the clinician must obtain a history of significant asbestos exposure, compatible clinical, laboratory and radiological signs, and an absence of other causes of similar appearances. There is currently no specific treatment for asbestosis and there may be an increased risk of primary lung malignancy . Malignant pleural mesothelioma Mesothelioma is linked to asbestos exposure but not to cigarette smoking . It is considered an occupational disease, although cases where families of workers have had sufficient exposure to cause mesothelioma from, for instance, washing overalls containing asbestos dust are becoming more common. The long incubation period of exposure to onset of disease (>30 years) means that the peak incidence in the UK is yet to be reached with predictions varying between [35-37]. Deaths in western Europe from mesothelioma are expected to approach nine thousand per year at this time . For individuals who have spent their working life in a trade with a high level of asbestos exposure, the lifetime risk of developing malignant mesothelioma can be up to one in five . Individuals can present with progressive breathlessness, chest pain and a pleural effusion. Life expectancy remains poor with a median survival estimated to be between six to twelve months [36, 40]. Metastatic spread is usually imperceptible clinically, although post mortem studies suggest local lymphatic spread is common . A recent study of US dockyard workers employed in the 1950s and 1960s reported a five-fold increase in lifetime risk of developing mesothelioma for all workers, with electricians (14-fold), sheet metal workers (16-fold) and woodworkers (18-fold increase in Standardised Mortality Ratios) at the highest risk . The treatment of mesothelioma remains difficult. The role of surgery is highly controversial and currently has no sound scientific evidence base. Equally, chemotherapy regimes are essentially a palliative treatment, with only small improvements in survival reported to date [43, 44]. The diffuse nature of the disease means that radical radiotherapy is not possible without significant damage to healthy lung. Local prophylactic radiotherapy to the chest wall where needles, chest drains or surgical instruments have crossed into the chest to obtain a diagnosis or therapeutic management is, however, recommended to prevent tumour seeding . There has been recent interest in the use of blood or pleural fluid biomarkers for the screening of asbestos exposed individuals for mesothelioma [45, 46], although a clear role for this test in screening for mesothelioma remains to be defined and validated . Legal and Compensation Implications for Service Personnel Crown Immunity Historically, no person could bring proceedings against the King in his own Courts. This position was gradually modified over the centuries until on the 4th March 1947 the Crown Proceedings Bill formally established for the first time a citizens right to sue the Crown. However, the Bill was to acknowledge that in certain matters, eg the defence of the realm and the maintenance of the Armed Forces, there involved responsibilities of a kind which no ordinary subject undertakes. Under Section 10 of the Crown Proceedings Act (CPA), members of the Armed Forces were to be denied the right to sue the Crown in tort actions for death or personal injury. Section 10 remained law until the passing of the Crown Proceedings (Armed Forces) Act 1987 which became law on 15th May The 1987 Act was not retrospective, thus preserving Crown immunity for all tort allegations up to 15th May The issues surrounding Crown Immunity have been tested in Court on a number of occasions with former Royal Navy personnel and asbestos exposure. Quinn v Ministry of Defence (1998) examined in the Court of Appeal the allegation that Section 10 did not provide immunity from the liability in tort for injury caused by an unsafe work system (i.e.
5 8 J Royal Naval Medical Service 2009, Vol 95.1 the exposure to asbestos from Crown equipment). This was dismissed. Matthews v Ministry of Defence (2003) held the contention that Section 10 infringed Article 6 of the Human Rights Act, namely Mr Matthew s civil right to claim damages against the MOD. This resulted in a House of Lords ruling in favour of the MOD: the 1947 Act states that Mr Matthews did not have this civil right in the first place, and the Act did not remove a civil right. This position was then tested in the European Court of Human Rights (ECHR) in October 2005 in Roche v The United Kingdom, a case where the plaintiff alleged links between participation in tests at Porton Down in the 1950s and various chronic illnesses diagnosed in the 1980s. An application for a War Pension (see below) was refused in 1992 on the grounds that the Secretary of State claimed that a causal link had not been demonstrated between the tests and his illnesses. The Secretary of State then issued a Certificate under Section 10 CPA 1947, which sought to block a Judicial Review of proceedings on the claim. Roche argued to the ECHR that Section 10 was in breach of his right to a fair trial under Article 6 of the Convention. This was rejected. There was no right Mr Roche had to which Article 6 could protect. As a result of these judgements, it is unlikely that former MOD personnel claimants will be in a position to recover any compensation for injuries sustained during Service prior to 15th May The only form of recompense available to these claimants is via a War Pension. The War Pension System War Pensions have been available only to former service personnel since they were introduced by Royal Warrant in 1911 (now the Naval, Military and Air Forces (Disablement and Death) Service Pensions Order 1983). The ex-service person submits a War Pension application for injury which must be attributable to service. For injuries occurring prior to 15th May 1987, the Secretary of State signs and issues a Certificate under Section 10, which conclusively attributes the injury to Crown employment. The War Pensions Tribunal deals with claims where there is a dispute as to entitlement to a pension and degree of disability. Pensions are now administered by the Veterans Agency (formerly the War Pensions Agency), an executive branch of the Department of Social Security. The scheme has its advantages. Applicants do not need to prove fault to obtain an award, the eligibility rules are generous and pensions are tax free and updated annually. Dependants and widows can also claim. The disadvantages of the war pension system are that its awards are woeful when compared to general damages awards made by the (civilian) Courts for the same injuries, and claimants must have demonstrable disability. Common Law Compensation and Industrial Injuries Benefit Clinicians diagnosing civilians with asbestos related diseases should advise the patient that if they are considering a compensation claim, they have three years from the date of knowledge to do so. Transgression beyond this may result in the case becoming statute barred, meaning the case may not be able to be heard in Court. Individuals may claim against a former employer s insurer, even if the employer is no longer in business, and must establish that the injuries and/or disability are due to the occupational exposure to asbestos, and that this exposure is attributable to the employer s negligence in not maintaining the standards required by common law. There have been two recent significant changes to the medico-legal issues of asbestos related disease in the last eighteen months in the UK. On 17th October 2007 the House of Lords ruled that asbestos related pleural plaques were no longer compensateable, as they do not cause demonstrable disease. Secondly, in a landmark ruling on 21st November 2008, the High Court ruled that insurers were liable from the point when victims were exposed
6 Asbestos a legacy and a persistent problem 9 to the asbestos dust not at the point at which the disease becomes apparent, as has previously been the case. For those whom neither an employer nor an insurer can be identified, claims may be pursued through the Department of Works and Pensions (DWP) under the Pneumoconiosis etc. (Workers Compensation) Act Furthermore, so long as individuals are not in receipt of a War Pension, individuals may be entitled to a weekly industrial injuries disablement benefit (IIDB), through the DWP. Particularly in mesothelioma cases, there have recent been efforts to fast track IIDB claims, and the Government has promised further future improvements into the way mesothelioma sufferers are compensated. A Future Threat? Carbon nanotubes are minute cylindrical structures that may be nanometers in diameter, with structural characteristics similar to asbestos. They exhibit extraordinary strength and unique electrical properties, which make them potentially useful in many applications in nanotechnology, electronics and optics. Recent reports have suggested that these nanotubes may have similar biological properties to asbestos  and in 2008 the Health and Safety Executive issued an advisory statement outlining potential health concerns with these new technologies . Conclusions After over a century of use, asbestos remains a preventable health hazard. Numerous military and dockyard personnel have had significant exposure, particularly in ship building, maintenance and refit. Furthermore, risks of exposure in theatres of conflict or disaster relief are a present danger. Appropriate awareness of the risks and prevention of exposure to military and other personnel in these operational theatres should be paramount. References 1. Tweedale G, Hansen P. Protecting the workers: the medical board and the asbestos industry, 1930s-1960s. Med Hist. 1998;42(4): PACE. Asbestos Regulations Revised. London: Central Advice Unit; te1200.pdf accessed 12 December Corn JK, Starr J. Historical perspective on asbestos: policies and protective measures in World War II shipbuilding. Am J Ind Med 1987;11(3): Rousmaniere P, Raj N. Shipbreaking in the developing world: problems and prospects. Int J Occup Environ Health. 2007;13(4): Virta R Minerals Yearbook. Washington: US Geological Survey; Monographs on the evaluation of carcinogenic risk to humans: IARC; Timbrell V. Deposition and retention of fibres in the human lung. Ann Occup Hyg 1982;26(1-4): Roggli VL, Sanders LL. Asbestos content of lung tissue and carcinoma of the lung: a clinicopathologic correlation and mineral fiber analysis of 234 cases. Ann Occup Hyg. 2000;44(2): Lippmann M. Effects of fiber characteristics on lung deposition, retention, and disease. Environ Health Perspect. 1990;88: Greenburg A. The North American experience with Malignant mesothelioma. In: Robinson B, editor. Mesothelioma. London Martin Dunitz p Phillips S. Ship and Dockyard Personnel. In: Greenburg M, Hamilton R, Phillips S, editors. Occupational, industrial and environmental toxicology. St Louis: Mosby Year Book Inc; Matthews C. Ship and boat building and repair: general profile. In: Stelman J, editor. Encyclopedia of occupational health and safety. Forth ed. Geneva: International labour Office p After the tsunami - rapid environmental assessment. In: United Nations Environment Programme; accessed 5 December Landrigan PJ, Lioy PJ, Thurston G, Berkowitz G, Chen LC, Chillrud SN, et al. Health and environmental consequences of the world trade center disaster. Environ Health Perspect.
7 10 J Royal Naval Medical Service 2009, Vol ;112(6): Moline J, Herbert R, Nguyen N. Health consequences of the September 11 World Trade Center attacks: a review. Cancer Invest. 2006;24(3): Roggli VL. Asbestos in lung tissue. Chest. 1990;97(6): Hessel PA, Gamble JF, McDonald JC. Asbestos, asbestosis, and lung cancer: a critical assessment of the epidemiological evidence. Thorax. 2005;60(5): Reid A, de Klerk N, Ambrosini GL, Olsen N, Pang SC, Berry G, et al. The effect of asbestosis on lung cancer risk beyond the dose related effect of asbestos alone. Occup Environ Med. 2005;62(12): Cookson WO, De Klerk NH, Musk AW, Glancy JJ, Armstrong BK, Hobbs MS. Benign and malignant pleural effusions in former Wittenoom crocidolite millers and miners. Aust N Z J Med. 1985;15(6): Epler GR, McLoud TC, Gaensler EA. Prevalence and incidence of benign asbestos pleural effusion in a working population. JAMA 1982;247(5): Evans AL, Gleeson FV. Radiology in pleural disease: state of the art. Respirology. 2004;9(3): Hillerdal G, Lindgren A. Pleural plaques: correlation of autopsy findings to radiographic findings and occupational history. Eur J Respir Dis. 1980;61(6): de Klerk NH, Cookson WO, Musk AW, Armstrong BK, Glancy JJ. Natural history of pleural thickening after exposure to crocidolite. Br J Ind Med. 1989;46(7): Hilt B, Lien JT, Lund-Larsen PG. Lung function and respiratory symptoms in subjects with asbestos-related disorders: a cross-sectional study. Am J Ind Med 1987;11(5): Mukherjee S, de Klerk N, Palmer LJ, Olsen NJ, Pang SC, William Musk A. Chest pain in asbestos-exposed individuals with benign pleural and parenchymal disease. Am J Respir Crit Care Med. 2000;162(5): Roach HD, Davies GJ, Attanoos R, Crane M, Adams H, Phillips S. Asbestos: when the dust settles an imaging review of asbestos-related disease. Radiographics. 2002;22 Spec No:S Hillerdal G, Musk AW. Pleural lesions in crocidolite workers from Western Australia. Br J Ind Med. 1990;47(11): Rom WN, Travis WD, Brody AR. Cellular and molecular basis of the asbestos-related diseases. Am Rev Respir Dis. 1991;143(2): Brody AR. Asbestos-induced lung disease. Environ Health Perspect. 1993;100: Kamp DW, Weitzman SA. The molecular basis of asbestos induced lung injury. Thorax. 1999;54(7): Chang LY, Overby LH, Brody AR, Crapo JD. Progressive lung cell reactions and extracellular matrix production after a brief exposure to asbestos. Am J Pathol. 1988;131(1): Hourihane DO, McCaughey WT. Pathological aspects of asbestosis. Postgrad Med J. 1966;42(492): Lemaire I. Characterization of the bronchoalveolar cellular response in experimental asbestosis. Different reactions depending on the fibrogenic potential. Am Rev Respir Dis. 1985;131(1): van Loon AJ, Kant IJ, Swaen GM, Goldbohm RA, Kremer AM, van den Brandt PA. Occupational exposure to carcinogens and risk of lung cancer: results from The Netherlands cohort study. Occup Environ Med. 1997;54(11): Peto J, Hodgson JT, Matthews FE, Jones JR. Continuing increase in mesothelioma mortality in Britain. Lancet. 1995;345(8949): Robinson BW, Lake RA. Advances in malignant mesothelioma. N Engl J Med. 2005;353(15): BTS statement on malignant mesothelioma in the UK, Thorax. 2007;62 Suppl 2:ii1-ii Peto J, Decarli A, La Vecchia C, Levi F, Negri E. The European mesothelioma epidemic. Br J Cancer. 1999;79(3-4): White C. Annual deaths from mesothelioma in Britain to reach 2000 by BMJ 2003;326(7404): Curran D, Sahmoud T, Therasse P, van Meerbeeck J, Postmus PE, Giaccone G. Prognostic factors in patients with pleural mesothelioma: the European Organization for Research and Treatment of Cancer experience. J Clin Oncol. 1998;16(1): Lumb PD, Suvarna SK. Metastasis in pleural mesothelioma. Immunohistochemical markers for disseminated disease. Histopathology.
8 Asbestos a legacy and a persistent problem ;44(4): Krstev S, Stewart P, Rusiecki J, Blair A. Mortality among shipyard Coast Guard workers: a retrospective cohort study. Occup Environ Med. 2007;64(10): Vogelzang NJ, Rusthoven JJ, Symanowski J, Denham C, Kaukel E, Ruffie P, et al. Phase III study of pemetrexed in combination with cisplatin versus cisplatin alone in patients with malignant pleural mesothelioma. J Clin Oncol. 2003;21(14): Nowak AK, Byrne MJ, Williamson R, Ryan G, Segal A, Fielding D, et al. A multicentre phase II study of cisplatin and gemcitabine for malignant mesothelioma. Br J Cancer. 2002;87(5): Robinson BW, Creaney J, Lake R, Nowak A, Musk AW, de Klerk N, et al. Mesothelin-family proteins and diagnosis of mesothelioma. Lancet. 2003;362(9396): Creaney J, Yeoman D, Naumoff LK, Hof M, Segal A, Musk AW, et al. Soluble mesothelin in effusions: a useful tool for the diagnosis of malignant mesothelioma. Thorax. 2007;62(7): Epub 2007 Mar Park EK, Sandrini A, Yates DH, Creaney J, Robinson BW, Thomas PS, et al. Soluble mesothelin-related protein in an asbestosexposed population: the dust diseases board cohort study. Am J Respir Crit Care Med. 2008;178(8): Epub 2008 Jun McEwen S. An update on the position concerning the hazards arising from Surgeon Lieutenant Commander F J H Brims MBChB MRCP MD Royal Navy Specialist Registrar in Respiratory & General Internal Medicine Institute of Naval Medicine. Surgeon Lieutenant Commander F Brims Royal Navy is currently undertaking an overseas fellowship in Sir Charles Gairdner Hospital, Perth, Western Australia, linked to the Australian National Centre for Asbestos Related Diseases.