Asbestos and the lung in the 21st century: an update


  • Silvie Prazakova,

    1. Faculty of Medicine, University of New South Wales, Sydney, NSW, Australia
    2. Respiratory Medicine Department, Prince of Wales Hospital, Sydney, NSW, Australia
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  • Paul S. Thomas,

    1. Faculty of Medicine, University of New South Wales, Sydney, NSW, Australia
    2. Respiratory Medicine Department, Prince of Wales Hospital, Sydney, NSW, Australia
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  • Alessandra Sandrini,

    1. Department of Thoracic Medicine, St Vincent's Hospital, Sydney, NSW, Australia
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  • Deborah H. Yates

    Corresponding author
    1. Department of Thoracic Medicine, St Vincent's Hospital, Sydney, NSW, Australia
    • Correspondence

      Deborah H Yates, MBBChir MSc Dip Occ Med AFOM MD FRACP FRCP, Department of Thoracic Medicine, Xavier 4, St. Vincent's Hospital, Victoria Street, Darlinghurst, NSW 2010, Australia.

      Tel: +61 (0)2 8382 2361

      Fax: +61 (0)2 8382 2359


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  • Authorship and contributorship

    Silvie Prazakova drafted the manuscript. Alessandra Sandrini, Deborah Yates and Paul Thomas edited it and contributed additions to the text.

  • Ethics

    The manuscript has been read and approved by all co-authors

  • Conflicts of interest

    The authors have stated explicitly that there are no conflicts of interest in connection with this article.


The asbestos-related disorders (ARDs) are currently of significant occupational and public health concern. Asbestos usage has been banned in most developed countries, but asbestos is still used in many developing countries and the number of cases of ARDs worldwide is rising. Many countries are now experiencing an epidemic of ARDs that is the legacy of occupational exposure in the 1960s–1980s because of the long latency period between asbestos exposure and manifestation of disease. It is likely that asbestos-related mortality and morbidity will continue to increase. Although the most feared complications of asbestos inhalation are the malignant conditions such as mesothelioma and lung cancer, asbestos inhalation more frequently results in benign conditions such as pleural plaques, diffuse pleural thickening, and asbestosis (pulmonary fibrosis due to asbestos exposure). Over recent years, there have been changes in the epidemiology of mesothelioma, in clinical management of ARDs and developments in new techniques for early detection of malignancy. This review provides an update on the respiratory manifestations of asbestos exposure and also considers advances in screening methods that may affect future management in the workplace.


Asbestos is the collective name for a group of fibrous silicates with high durability, tensile strength and heat resistance. Asbestos was extensively used in many products including thermal insulation, electrical wiring, building materials, friction products and others. All forms of asbestos are now banned in 52 countries, and safer materials have replaced many products that once contained it. However, asbestos mining still continues. Nowadays, asbestos is used mainly in developing countries, while in many countries where most types of asbestos have been banned, the controlled use of chrysotile asbestos is still allowed [1]. Annual world production remains at over 2 million tons with Russia as a leading producer of asbestos worldwide, followed by China, which is also the largest consumer [1]. As a consequence, an epidemic of asbestos-related disorders (ARDs) is expected in next decades in these countries.

Asbestos is a generic term for a group of fibrous silicates, and can be divided into two groups that differ in mineralogical and chemical properties: amphiboles and serpentines. Amphiboles include crocidolite, amosite, anthophyllite and tremolite. Chrysotile is the only serpentine and represents 95% of the commercial asbestos ever used around the world [1]. Crocidolite is recognized to be the most carcinogenic and fibrogenic, but there has been vigorous debate about the relative potency of chrysotile in carcinogenesis in the past 30 years. The general consensus currently is that chrysotile is capable of inducing malignant mesothelioma (MM), although it is less potent in this regard than other types of asbestos [2].

Asbestos produces the following lung disorders: asbestosis (diffuse interstitial pulmonary fibrosis due to asbestos inhalation), pleural plaques (PPs), diffuse pleural thickening (DPT), benign asbestos pleural effusion (BAPE), rounded atelectasis (RA), lung cancer (LC) and MM. The clinical characteristics of the ARDs are summarised in Table 1.

Table 1. Clinical characteristics of ARDs
DiseasePresenting symptomsChest X-ray findingsTreatment
  1. PP, pleural plaque; BAPE, benign asbestos pleural effusion; RA, rounded atelectasis; DPT, diffuse pleural thickening; LC, lung cancer; MM, malignant mesothelioma; ARD, asbestos-related disorder.
AsbestosisDyspnoea and dry coughBilateral, irregular reticulo-nodular opacities at the lung basesNo effective therapies, supportive and symptomatic care
PPsAsymptomaticDiscrete elevated areas of hyaline fibrosis from parietal pleura, white shaggy appearanceNo effective therapies
BAPEUsually asymptomaticSmall-to-moderate size and unilateral pleural effusion, may be massive or bilateralDrainage to alleviate symptoms, spontaneously resolve completely
RAUsually asymptomaticRounded mass-like opacity in the peripheral lungRestoring the pulmonary capacity/breathing comfort
DPTDyspnoeaContinuous, smooth pleural shadowing extending over at least one quarter of the chest wall with blunting of one or more costophrenic anglesNo effective therapies, supportive and symptomatic care
LCCough, dyspnoea and chest painA mass in the lungs +/- enlarged lymph nodesMultimodality treatment including surgery, radiotherapy and chemotherapy
MMChest pain, dyspnoea and coughUnilateral pleural effusion, occasionally multiple pleural masses or with pleural thickeningChemotherapy, multimodality treatment

Asbestos exposure

Asbestos usage peaked in 1950s, 1960s and 1970s in most developed countries. World Health Organisation officials estimate that 125 million people worldwide are annually exposed to asbestos in occupational settings, and more than 107 000 people die annually of diseases associated with asbestos exposure [3].

In Great Britain, at least 3500 people die from asbestos-related illnesses each year. The British mesothelioma death rate is now the highest in the world. According to the latest report from Cancer Research UK, mesothelioma accounts for 1% of all cancers with 2558 new cases of MM in 2009 [4]. The mesothelioma incidence rate is still rising with the current rate seven new cases for every 100 000 males and 1.4 for every 100 000 females (4.1 cases per 100 000 population) [4]. Tan and colleagues estimated mesothelioma deaths to peak in 2016 and approximately 91 000 deaths to occur from 1968 to 2050 [5]. Australia also has one of the highest incidences of ARDs in the world. The number of mesothelioma cases in Australia between years 1945 and 2002 has been reported as 7500 with an incidence of 40 cases per million for the total population [6]. There were 612 new cases of MM diagnosed in Australia in 2011, with the incidence rate 2.7 per 100 000 population overall (5.0 per 100 000 men and 0.8 per 100 000 women) [7]. Clements and colleagues used two different models to project the incidence of MM in men in New South Wales [8]. Using an age-cohort model, they predicted 6690 cases between 2004 and 2060, with peak annual numbers of 187 in 2021, and 6779 by the age and calendar year model, peaking in 2014 at 196 [8]. In the United States, the incidence rate of MM in 2009 was approximately 1 per 100 000 persons with 2500–3000 new cases annually [9], and the peak incidence of MM has already occurred [10].

Many developing countries, including some with extensive historical use of asbestos, do not report mesothelioma cases. After estimating reported and unreported numbers, Park et al. estimated the global burden of mesothelioma to be 213 200 (15-year cumulative mortality during 1994–2008) [11]. This is equivalent to an annual average of approximately 14 200 cases [11].

The phenomenon of para-occupational or ‘take home’ asbestos exposure has been recognised for over 50 years and can be described as exposure to asbestos that occurs in the worker's home generally because of dust that has accumulated on the worker's clothing or hair. Many studies have described cases of ARDs caused by para-occupational exposure [12-14]. However, the vast majority of the cases occurred among family members of workers in industries characterized by high exposures and nearly always to amphibole fibres.

Direct occupational exposure to raw asbestos or asbestos products remains the predominant cause of ARDs. However, recently attention has been focused on the potential dangers of non-occupational exposure associated with home renovation of asbestos-containing building products and car maintenance [7]. Asbestos-containing materials are present in many residential and commercial buildings built after World War II and may create an exposure hazard to the occupants or to the renovators. One study in Western Australia showed a marked increase of MM cases associated with home maintenance and renovation over the previous 10 years [15]. It is expected that MM cases as a result of non-occupational exposure to asbestos will continue to increase over next decades.


Asbestosis is defined as diffuse interstitial pulmonary fibrosis due to inhalation of asbestos fibres. The latency period for disease development is usually 15 years or more, and is influenced by duration and intensity of exposure. Relatively high levels of asbestos inhalation are required to produce asbestosis (cumulative exposure ≥25 fibres/mL-years), although there are some reports that record asbestosis following lower levels of asbestos exposure [16]. Asbestosis is interstitial fibrosis that is subpleural and initially affects the lung bases. Diagnostic criteria have been published [17] and include a compatible exposure history, clinical and radiographic features. It is very difficult to distinguish between idiopathic pulmonary fibrosis and asbestosis on the basis of investigations, and a thorough occupational history is needed. In asbestosis, there is less evidence of inflammation and fibroblastic change, but in general, only the presence of asbestos bodies permits the distinction of asbestosis from usual interstitial pneumonia [16].

Asbestosis usually presents with gradual and progressive dyspnoea and accompanying dry cough. Physical examination reveals fine end-inspiratory crackles at the lung bases that progress as disease advances. Clubbing of the fingernails occurs with severe disease. Pulmonary function tests demonstrate restriction with reduced lung volumes and forced vital capacity (FVC) and diminished gas transfer. In moderate-to-severe asbestosis, hypoxemia and reduced exercise tolerance are seen [18].

Classification of severity of chest X-ray (CXR) changes is made according to the International Labor Office (ILO) criteria, which correlate with disease stage and dyspnoea [19]. Bilateral, irregular parenchymal opacities occur at the lung bases, which coalesce with disease progression and become coarser with eventual honeycombing [17]. Involvement of middle and upper lobe is often seen in more advanced disease. CXRs are limited for detection of cases with early or mild asbestosis. The radiograph findings are normal in 10%–18% of patients with asbestosis confirmed by histopathological findings [20, 21]. The histological diagnosis of asbestosis requires an appropriate pattern of interstitial fibrosis and demonstration of asbestos bodies in histological section. High-resolution computed tomography (HRCT) is more sensitive and specific than chest radiography, and features include increased intralobular septal markings, subpleural curvilinear lines, parenchymal bands and small cysts [22].

Asbestosis resembles a variety of other inflammatory and fibrotic lung diseases. The differential diagnosis includes other pneumoconioses, idiopathic pulmonary fibrosis, respiratory bronchiolitis and sarcoidosis. There are no effective therapies for asbestosis. Treatment is primarily supportive following guidelines for treatment of interstitial lung disease. Management focuses on surveillance and prevention along with symptom abatement. Effect of pulmonary rehabilitation for patients with asbestosis has been recently evaluated with results showing positive effect on physical attributes and health-related quality of life [23, 24].


PPs are the commonest manifestation of asbestos exposure affecting up to 58% of asbestos-exposed workers and up to 8% of general environmentally exposed populations, with a latency period of 20–30 years. They are hypocellular lesions composed of thick collagen bundles arranged in a ‘basket-weave’ pattern covered by a single layer of normal mesothelial cells [25]. PPs are variable in size and number with white or pale yellow appearance, typically distributed on the posterolateral chest wall, the dome of the diaphragm and the mediastinal pleura (Fig. 1) [26]. They are sharply demarcated from subpleural tissue, and calcification is a common late finding [27].

Figure 1.

Computed tomography scan of the thorax demonstrating asbestos-related pleural plaques.

Most studies have demonstrated no significant association between PPs, and dyspnoea or abnormal pulmonary function tests, although there is still debate on this issue. One large scale study of patients with PPs using HRCT scans reported an association between isolated parietal and/or diaphragmatic PPs and a decrease in total lung capacity, FVC and forced expiratory volume in 1 s with a restrictive pattern [28]. Mukherjee et al. reported an association with chest pain [29], but this has not been found in a recent study [30].

The diagnosis relies on radiographic findings and a compatible history of exposure. The CXR is a standard diagnostic tool utilising ILO classification guidelines, although false-positive, false-negative and interobserver variability rates are relatively high. HRCT is more sensitive and specific for making the diagnosis, but because of its high radiation exposure and unavailability, it is inappropriate for screening [17]. American Thoracic Society guidelines recommend 3 yearly follow-up to monitor for subsequent development of DPT or MM [17], but according to British Thoracic Society guidelines, asymptomatic patients do not require further investigation [31].


BAPE is an exudative and often haemorrhagic pleural effusion following asbestos exposure and is a diagnosis of exclusion after other possible causes such as malignancies, tuberculosis and other infections [32]. It usually occurs within 10 years after exposure, earlier than other ARDs, although this is not invariable [17]. Typically, effusions are asymptomatic, but they can present acutely with fever, pleuritic-type chest pain, and raised inflammatory markers [32]. BAPE is often unilateral with a left-side predominance and usually resolve completely with a mean duration of 3–4 months, but may recur (30%–40%) [33]. Residual blunting of the costophrenic angle may occur or progress to DPT in approximately 50% of patients [33].


DPT is characterized by extensive thickening of the visceral pleura, often with adherence to the parietal pleura, and obliteration of the pleural space [17, 34]. Unlike PPs, DPT is not sharply demarcated and is often associated with fibrous strands known as ‘crow's feet’ or parenchymal bands [35]. DPT accounts for 22% of all ARDs [36]. It can develop within a year of exposure but can also take up to 40 years. A recent study showed that in about 40% of cases, DPT developed more than 40 years after onset of exposures with a median latency of 34 years [37]. In this study, 73% of patients presented with unilateral disease with a strong right-sided predominance and a quarter were shown to subsequently develop contralateral disease [37]. PPs often coexist.

DPT may be associated with dyspnoea and chest pain [34, 37]. Although symptoms are generally mild, severe restrictive lung disease with hypercapnic respiratory failure and death can rarely occur [35]. DPT can cause significant restrictive ventilatory impairment. A reduction in FVC, static lung volumes and diffusing capacity for carbon monoxide may occur, although an increased carbon monoxide transfer coefficient may result in the absence of parenchymal fibrosis [34, 38].

On a chest radiograph, DPT presents as continuous, irregular pleural shadowing that often extends up both chest walls and with blunting of one or more costophrenic angles (Fig. 2). According to the ILO classification, DPT is present only if there is obliteration of the costophrenic angle in continuity with ≥3 mm pleural thickening [19] using a chest radiograph. HRCT is more sensitive than CXR for detection of early pleural thickening (i.e. 1–2 mm in thickness) [17] (Fig. 3). The most commonly used classification system for HRCT is that of Lynch, defining DPT as a contiguous sheet of pleural thickening 5 cm wide on transverse images, 8 cm or greater on craniocaudal images, and more than 3 mm thick [39].

Figure 2.

Posteroanterior chest radiograph demonstrating asbestos-related diffuse pleural thickening.

Figure 3.

Computed tomography scan of the thorax demonstrating asbestos-related diffuse pleural thickening. Note the rounded atelectasis on the left and the subpleural interstitial pulmonary fibrosis bilaterally.

There are several important differential diagnoses; therefore, a thorough evaluation, including comprehensive occupational and environmental history, is essential. Treatment is largely limited to supportive and symptomatic care. Decortication may be beneficial in cases with progressive DPT when clinically significant parenchymal fibrosis is not present [27]. Rapidly progressive or severe chest pain should raise clinical suspicion of either malignancy or a non-malignant pleuritis [17].


RA (Blesovsky's syndrome) may occur with DPT. Pleural adhesions and fibrosis cause deformation of the lung with bending of some small bronchi [40]. On CXR, this presents as a rounded opacity in the peripheral lung adjacent to the thickened pleura, with curvilinear opacities (the comet tail sign) extending from the site of atelectasis towards the hilum [41]. Exposure to asbestos is the principal cause today, but any type of pleural inflammatory reaction can cause RA [40]. Difficulties may occur in excluding malignancy, and positron emission tomography (PET)/computed tomography (CT) scanning can be useful in this regard. RA is usually asymptomatic but may be accompanied by breathlessness.


MM is an aggressive and incurable tumour arising from mesothelial cells of the pleura, peritoneum and rarely elsewhere. Although cases due to environmental and para-occupational asbestos exposure have been described, most MMs are occupational in origin. MM can develop even after short and low exposure, but a dose–effect relationship has been demonstrated. Median latency is approximately 40 years (range 15–67). MM has a poor prognosis with median survival of 8–14 months [42, 43]. Patients who are younger, females and those with epithelioid histological subtype have been shown to have a survival benefit [43].

Patients usually present with chest pain (60–70%), dyspnoea (50–70%), cough (20–30%) [44] and restrictive gas exchange abnormality. The radiographic manifestation is usually a unilateral pleural effusion or pleural thickening. CT is the primary modality for the diagnosis, staging and response assessment of MM (Fig. 4). Features include a bulky pleural opacity with contraction of the hemithorax, extension along fissures, and invasion of the chest wall and mediastinal structures [45]. Fluorodeoxyglucose PET/CT (FDG-PET/CT) has been shown to be a useful diagnostic tool for detection of distant metastasis and to differentiate MM from benign pleural disease [46, 47]. It is also used for disease staging before surgery; however, understaging has been described, and the sensitivity in the detection of nodal disease is low [48]. In addition, previous surgery such as talc pleurodesis can cause an intense inflammatory reaction resulting in a confounding increased FDG uptake (false-positive result) [47]. Another possible roles of PET-CT may be in assessing response to treatment and post-treatment disease surveillance [47].

Figure 4.

(A) Posteroanterior chest radiograph of a patient with left-sided malignant mesothelioma. (B) Computed tomography scan of the thorax of a patient with left-sided malignant mesothelioma showing opacification and very little lung aeration.

Staging relies on the International Mesothelioma Interest Group TNM (tumour, nodes, metastases) staging system [49]. Survival depends on the stage of the disease when diagnosed. Stage I has approximately 12 months of survival, Stage II 4 months, and about 3 months in Stages III–IV [50]. The definitive diagnosis of MM requires a tissue sample; however, negative results do not exclude it as sampling problems can occur and the diagnosis is a difficult one histologically. MM occurs in three main histological subtypes: epithelioid, sarcomatoid and biphasic. These have prognostic significance, with epitheloid being the most common and sarcomatoid subtype predicting the worst outcome [7, 43].

Several tumour biomarkers measured in either the serum, plasma or the pleural fluid have been evaluated for diagnostic purposes. Biomarkers could also be useful to detect the development of MM at an early, potentially resectable stage, although no randomized data currently exist that confirm prolonged survival with surgical resection. Promising biomarkers include soluble mesothelin-related protein (SMRP) [51, 52], osteopontin [53, 54], and more recently, fibulin 3 [55] and integrin-linked kinase (ILK) [56]. Although initial results appear promising, most of these biomarkers have yet to be evaluated in prospective studies and primarily apply to epithelial type MM. SMRP has been evaluated in this manner and unfortunately was found to have a high rate of false-positives [52]. High SMRP levels have been shown to correspond with disease volume, suggesting that SMRP may be a useful for detecting the progression of MM and monitoring MM during treatment [51, 57]. Serum osteopontin levels are elevated in MM but also in patients with non-malignant ARDs [53, 54] resulting in rather low specificity and sensitivity [58, 59], limiting its value as a screening tool. A recent study investigated whether fibulin-3 in plasma and pleural effusions could be used to discriminate between early-stage MM and asbestos exposure without MM, with promising results. Plasma fibulin-3 levels discriminated between Stage I or II mesothelioma and asbestos exposure without MM, with a specificity of 94% and a sensitivity of 100% [55]. ILK serum levels have been shown to be significantly higher in patients with MM compared with healthy asbestos-exposed workers; however, the sensitivity and specificity for discrimination were rather low at 61.4% and 80.2%, respectively [56]. There is potential for the use of ILK as a marker of disease progression, as its levels are increased in advanced stages of MM in comparison with early stages [56], but more work in this area is needed. Novel biomarkers such as volatile organic compounds measured in exhaled breath [60], microRNAs [61] may prove useful in the future and/or a combination of biomarkers.

Many strategies have been tried for treating MM, including surgery, chemotherapy and radiation. Palliative surgical procedures include video-assisted thoracoscopic surgery (VATS) with pleurodesis and partial pleurectomy/decortication. Multimodality treatment appears theoretically to be the most effective therapeutic strategy, although the overall prognosis continues to be poor. There are two major surgical options: VATS pleurectomy/cytoreductive surgery and extrapleural pneumonectomy (EPP). Although it has been assumed in some countries that surgical therapy does improve morbidity and mortality, a benefit has not been confirmed in randomized trials [62, 63], and the only randomized trial of EPP with multimodal therapy ever performed actually showed shorter survival in those treated with surgery [64]. Thus, on current evidence, radical surgery should be used with caution in MM.

Retrospective studies suggest that radiotherapy can relieve pain in around half of the patients treated [65]. The principal role of radiotherapy is as an adjuvant following surgical resection [45]. Newer techniques such as intensity-modulated radiotherapy offer hope that targeted treatment will be of use, although these have yet to be fully evaluated. Chemotherapy plays an integral role in multimodality treatment and is also recommended alone as a treatment for inoperable patients [49], but no highly effective agents are yet available. A first-line regimen of pemetrexed or gemcitabine in combination with a platinum agent (cisplatin or carboplatin) is currently regarded as the best available treatment for MM [49]. Pemetrexed and raltitrexed in combination with cisplatin have been shown to improve survival, global quality of life and pulmonary function, when compared with cisplatin alone, but the survival effect is only approximately 12 weeks [66, 67]. This has provided indirect evidence that combination treatment might have a beneficial effect; however, there are no published randomised studies of single platinum drug vs best supportive care. Moreover, it is difficult to compare trial results because patients have different stages of disease and different histopathology subtypes, which are likely to influence the treatment outcome. Currently, chemotherapy has at best only a modest benefit for these patients. Further improvements in drug development and better designed clinical trials are strongly needed. In recent years, advances in knowledge of molecular and biological mechanisms of MM have led to development of immunologically based and targeted therapies, but these are still under evaluation.

LC associated with asbestos exposure

Heavy asbestos exposure produces an increased risk of LC, with a latency period of approximately 15–20 years. Asbestos-related LCs account for about 3–8% of all LCs and is similar in both the type of cancer and its signs and symptoms in asbestos-exposed and unexposed individuals. The risk of developing LC is linearly related to cumulative asbestos exposure. The issue of whether asbestosis is a necessary precursor for LC is still controversial, but recent consensus statements have concluded that heavy asbestos exposure of ≥25 fibres/mL-years rather than asbestosis is needed [68]. Epidemiological evidence indicates that the combined effect of smoking and asbestos exposures on LC incidence appears to be more than additive and is probably multiplicative. Smoking cessation has major health benefits and should be recommended in all patients with past asbestos exposure. One recent British study showed an inverse relationship between time since smoking cessation and LC mortality risk in asbestos workers [69]. Former smokers who had stopped smoking for 40 and more years had same risk of LC as asbestos workers who had never smoked [69].

The relative lack of symptoms during the early stages of LC frequently results in a delayed diagnosis. However, early diagnosis and treatment can result in long-term survival, improving the 5-year survival to approximately 70%. The treatment of LC and survival is very dependent on disease stage and the presence of co-morbidities and is identical in asbestos-exposed and non-exposed patients. Treatment includes surgical removal of the cancer, chemotherapy, radiotherapy or a combination, and several excellent reviews are available [70, 71]. Palliation is also important.

Recently, there has been a revival of interest in screening for LC. The National Lung Screening Trial showed a 20% lower risk of dying from LC in ex-smokers who had been screened with low-dose helical CT compared with CXR [72]. CT screening has been evaluated in a population exposed to asbestos and shown to be feasible, however, with a high incidence of incidental findings [73]. CT screening presents an opportunity for early diagnosis and treatment in asbestos-related LC and possibly also for MM. In future, a combination of screening techniques could increase specificity and potentially improve prognosis. However, this yet remains to be proved.


Paradoxically, asbestos was used because it is chemically inert, and yet with hindsight, it is clearly toxic and has produced a wave of ARDs. The United Kingdom and Australia have one of the highest incidences of ARDs in the world, and the general population is still potentially at risk from accidental domestic exposure. Care is needed in renovation and demolition of asbestos-containing buildings, and awareness of potential asbestos hazards needs to be high.

The benign ARDs are now well described and generally do not require specific treatment, although significant anxiety can occur because of lack of understanding of the differences between the different ARDs and because of the fear of developing mesothelioma. No new treatments have been developed for the benign ARDs. Significant advances have been made in chest imaging and nuclear medicine techniques, which have greatly assisted in diagnosis and treatment planning, and in thoracoscopic surgical techniques for diagnosing MM. Sadly, MM remains a deadly disease despite much research endeavour.

Early detection of LC or MM patients in asbestos-exposed subjects using screening programmes or biomarkers may eventually prove helpful for control or eradication of these neoplasms. This might certainly be the case in asbestos-related LC where early treatment can be curative, but in MM, better treatment options are needed. Advances in knowledge of molecular and biological mechanisms that regulate the growth and the spread of MM, as well as the identification of new tumour markers provides hope for the future. Until then, primary prevention still remains the key to control of the ARDs.