Toolkit for the Elimination of Asbestos-Related Diseases
The Toolkit for the Elimination of Asbestos-Related Diseases (2013 Edition) was developed in the year 2013 to serve as a concise and easy-to-use reference source of knowledge, technologies and information that merit attention for the purpose of eliminating asbestos-related diseases (ARDs).
For this 2013 edition, the traditional public health approach of prevention was considered to be the basic means to tackle ARDs. Many countries, especially those which are rapidly developing, continue to use asbestos at alarming levels. The developing countries in Asia are at the forefront of this trait.
This edition focused on the asbestos hazard identification, asbestos exposure assessment, diagnostic tools for ARDs, the economic cost burden of asbestos exposure as well as risk communication. Our hope then was that any party with concern on ARDs can have something to benefit from this edition. Whoever the beneficiary, a core principle to bear in mind, is that the most effective means to prevent ARDs is to stop using asbestos. This position is unchanged as of today in 2020.
For a list of contributing Authors, click here.
* Please note: Factsheets 1C, 2A, 2B, 3A, 5A-D were exclusively written and published as Factsheets only.
- 1. Asbestos Exposure Assessment, Risk Identification, and Substitutes
- 2. Asbestos-Related Legislations and Regulations
- 3. Diagnostic Tools for ARDs
- 4. Economic Cost/Burden Incurred by Asbestos Exposure and ARDs
- 5. Risk Communication
- Appendix 1: Snapshot - Asbestos and Asbestos-related Diseases - Lessons and considerations for Asia
More than 30 different standard methods have been issued by various governmental agencies and standard organizations to standardize laboratory analysis results by using the same analytical procedures. Because positive identification of asbestos requires analysis of the morphology, chemical composition and crystal structure of fibers due to the attributes of asbestos minerals, various analytical techniques are used in these standard methods.
Among these analytical techniques, microscopy is the most important tool used for the detection of fibrous morphology. For the counting of airborne fibers, microscopic techniques such as phase contrast microscopy (PCM), transmission electron microscopy (TEM) and scanning electron microscopy (SEM) are widely used. For the analysis of bulk asbestos such as asbestos in commercial products and building materials, polarized light microscopy (PLM), TEM and SEM are generally used. As non-microscopic techniques, X-ray diffraction (XRD) and differential thermal analysis (DTA) have also been adopted in several standard methods.
Different techniques have their own strong and weak points and different methods have their own applications. Therefore, care should be taken to select and apply a standard method. The following present a review of existing standard testing methods related to asbestos in air or bulk materials for the monitoring of asbestos in occupational settings (not presented).
Substitute products, particularly fibers, are often more expensive than asbestos. However, this additional cost must be considered in the light of the enormous cost of asbestos-related diseases to society. The carcinogenicity of certain substitute fibers remains under close surveillance and the development of substitute products continues. Doubts remain as regards the health effects of certain fibers which up to now have not been fully examined, because they are not widely used (from ISSA technical report).
Considerable effort has been devoted to finding alternative fibers or minerals to replace asbestos fibers in their applications. Such efforts have been motivated by various reasons, typically, availability and cost, and more recently, health and liability concerns. The substitution of asbestos fibers by other types of fibers or minerals, must, in principle, comply with three types of criteria:
- the technical feasibility of the substitution;
- the gain in the safety of the asbestos-free product relative to the asbestos-containing product; and
- the availability of the substitute and its comparative cost (from USGS Asbestos).
It is important to know that safer substitutes for asbestos products of all kinds have become increasingly available. These include fiber-cement products using combinations of local vegetable fibers and synthetic fibers, as well as other products that serve the same purposes. The WHO is actively involved in evaluating alternatives (from WBG good practice note).
- The International Labour Organization (ILO) and the World Health Organization (WHO): Outline for the Development of National Programs for the Elimination of Asbestos-related Diseases (NPEAD), 2007
- WHO: Elimination of Asbestos-related Diseases, 2006
- ILO: Resolution concerning asbestos, 2006
- The United Nations Environmental Program (UNEP): Basel Convention on the Control of Transboundary Movements of Hazardous Wastes and their Disposal, 1989
- ILO: Convention concerning Safety in the Use of Asbestos, 1986 (No.162) and Recommendation concerning Safety in the Use of Asbestos, 1986 (No.172)
- UNEP and the Food Agriculture Organization (FAO): Rotterdam Convention on the Prior Informed Consent (PIC) Procedure for Certain Hazardous Chemicals and Pesticides in International Trade
- The European Parliament and the Council of the European Union: Council Directive on the Protection of Workers from the Risks related to Exposure to Asbestos at Work, 1983
Asbestosis is a type of pneumoconiosis that results from exposure to high levels of asbestos, developing into diffuse pulmonary fibrosis which begins at the peribronchiolar region.
Pathological changes in the pleura such as pleural plaque, diffuse pleural thickening, and hyperplasia of the visceral pleura that accompanies lung parenchyma with a band like shadow are useful in differentiating asbestosis from idiopathic interstitial pneumonia. However, there is more than a 5% chance that asbestosis will not combine with pleural plaque. There are cases in which calcified pleura plaque is present and even though there are findings of fibrosis in the lungs, they are not diagnosable asbestosis. Cases in which fibrosis is accompanied by chronic interstitial pneumonia or pulmonary emphysema are not uncommon, so it is important to obtain a detailed occupational history and ask if there was exposure to a high concentration of asbestos. In other words, we should take special note of pulmonary fibrosis with pleural plaque when the case is not asbestosis. The reason for this is that pleural plaque occurs even at exposure to low concentrations of asbestos, but also in many cases, it occurs in combination with asbestosis at exposure to high concentrations of asbestos. Therefore, the occurrence of pleural plaque is not a sufficient condition for the diagnosis of asbestosis.
Until some time ago, the definition of asbestos-related lung cancer was asbestosis complicated with primary lung cancer, and it was believed that fibrosis of the lung is important to the carcinogenesis mechanism. Recently, however, there have been asbestos-related lung cancer cases that were not complicated with asbestosis, and it is believed that asbestos itself is important for causing lung cancer.
Mesothelioma is a malignant tumor that originates from mesothelial cells or has the tendency to differentiate from the mesothelium, and occurs in the pleura, peritoneum, pericardium, or tunica vaginalis testis. Approximately 80% of mesothelioma cases originate in the pleura, and approximately 80% occur due to exposure to asbestos. Separately, SV40 virus, irradiation, and heredity have also been reported as other causes, but the frequency of these is low and lack consensus.
Mesothelioma is a malignancy located in the pleura, the peritoneum, the pericardium and the tunica vaginalis, all of which is normally lined by mesothelial cells.
In most mesothelioma cases, diffuse spread along the cavity is a characteristic feature. In the case of pleura, it is supposed that there are small nodules in the parietal pleura at the initial stage and immediately tumor begins to spread along the pleural surface, and as a result, diffuse pleural thickening is induced accompanied by adhesion between the parietal and visceral pleura. Finally, mesothelioma encloses the lung parenchyma, which is a classical gross feature of mesothelioma.
Occasionally (probably a few percent) mesothelioma forms a localized tumor with no diffuse spread pattern. Mesothelioma chiefly extends in the pleural cavity, however, sometimes it invades mainly to the chest wall, and as a result, it resembles a chest wall tumor. Although unusual, it is difficult to differentiate mesothelioma based on gross features, because the possibility that the tumor derives from chest wall (soft tissue or bone) or lung cannot be excluded.
In the case of peritoneum, most mesothelioma cases show diffuse thickening of the peritoneum or disseminated small nodules in the peritoneum. Rarely it may be noticed as a large nodule.
Among asbestos-related nonmalignant pleura lesions, inflammatory changes in the visceral pleura that accompany pleural effusions are called benign asbestos pleural effusions.
There are two types of pleural thickening due to asbestos: pleural plaque, which is a localized pleural thickening, and, diffuse pleural thickening. Diffuse pleural thickening is a visceral pleura lesion that spreads widely either unilaterally or bilaterally. The thickness ranges widely from less than 1 mm to more than 1 cm, and since the lesion reaches the parietal pleura, both pleura often adhere to each other.
There are three categories as to the origin of diffuse pleural thickening caused by asbestos exposure: Asbestosis extends from the visceral pleura to the parietal pleura, benign asbestos pleural effusion is involved as a preceding lesion, and neither asbestosis nor benign asbestos pleural effusion is the origin.
By being exposed to asbestos, a flat and irregular protrusion is formed under the mesothelium of the parietal pleura and is accompanied by hyperplasia. Histopathologically, the cell components show scarce fibrous lesions. The most common sites for pleural plaque to originate are the anterior chest wall, the sixth to eighth dorsal costal cartilage, lateral thorax, side of the of vertebra body, and the upper bifurcation tracheae (Figures. 7 and 8). Also, calcification often occurs in the convexity of the diaphragm. On the other hand, it does not occur in the costo-diaphragmatic recess or the apex area.
Mesothelial cells primarily have a potential of differentiation to an epithelioid cell lined at the serosal surface as well as a mesenchymal-spindle cell presented under the serosal lining. Therefore, mesothelioma has many histological subtypes, including carcinoma-like (epithelioid) tumor or sarcoma-like tumor (sarcomatoid) tumor, or mixed epithelioid and sarcomatoid tumor.
Mesothelioma is a rare type of malignancy, which is highly related to asbestos exposure. Eighty to 90% of the patients with mesothelioma have a history of occupational and/or environmental exposure to asbestos. It is known that mesothelioma is a highly aggressive malignancy, and average survival of the patients has been reported to be only 13 months. The incidence of mesothelioma is lower to those of lung cancer, therefore clinicians as well as pathologists have fewer experience of diagnosis, especially at the earlier stage.
When a small amount of pleurisy or ascites is found clinically with no significant thickening of pleura or peritoneum, the diagnosis of mesothelioma is very difficult. If the biopsy specimen consists of a small tissue sample, its pathological diagnosis is limited. A comprehensive judgement is warranted, including clinical examination, CT imaging as well as pathological findings, which in combination, contribute to an accurate diagnosis of mesothelioma.