- LAST MODIFIED: 22 February 2018
- DOI: 10.1093/obo/9780199756797-0187
- LAST MODIFIED: 22 February 2018
- DOI: 10.1093/obo/9780199756797-0187
The first use of the pneumoconiosis term dates back to 1866; Zenker coined the term “pneumokoniosis,” derived from Greek pneuma (air, wind) and konis (dust). Later, in 1874, Proust modified that term as “pneumoconiosis” to connote “dusty lung.” Pneumoconiosis is a general term and refers to a spectrum of tissue reactions developing against inhaled and accumulated dusts in the lungs; however, the spectrum has varied time to time by definition for some purposes. The entities under this umbrella term have a unique name, mostly derived from and implies the exposed dust, such as asbestosis due to asbestos dust, fiber, exposure, or silicosis due to crystalline silica exposure. The International Labour Organization (ILO) defines pneumoconiosis as “the accumulation of dust in the lungs and the tissue reactions to its presence.” The dust, in this definition, infers “an aerosol composed of solid inanimate particles” (Pneumoconioses: Defintion. In Encyclopedia of Occupational Health and Safety. Geneva, Switzerland: International Labour Organization, 1998). Sometimes, the expression of nonneoplastic has been added avoid any misinterpretation. Some dust-related chronic occupational diseases, such as asthma, chronic obstructive pulmonary disease, byssinosis, berylliosis, and hypersensitivity pneumonitis, are beyond the scope of this definition because dust accumulation is not required in their development. This definition does not include the word of “disease” because it may add up to some degree of health impairment, which may not be the case with all pneumoconiosis, that is, the ones caused by non-fibrogenic dusts, and is less likely to develop fibrogenic reaction. Dusts, causing pneumoconiosis, have a spectrum that fibrogenic ones are on one side and non-fibrogenic, or inert ones, are on the other side. From a pathological view, pneumoconiosis can be divided as collagenous and non-collagenous. In collagenous pneumoconiosis, alveolar architecture changes or becomes destructed, having a moderate to maximal degree collagenous stromal reaction and permanent scarring of lung. Collagenous pneumoconiosis may occur due to fibrogenic dust, such as silicosis and asbestosis, exposure or by altered tissue response to a non-fibrogenic dust, such as coal dust, which is considered relatively less fibrogenic than silica and asbestos. As a response to repeated exposure to a single non-fibrogenic dust, such as coal dust, a non-collagenous pneumoconiosis at the beginning (simple coal worker’s pneumoconiosis, or CWP) may evolve to a collagenous one (complicated CWP) in progress of time. Furthermore, mixed dust exposure is becoming more common than a single dust exposure, which may result in the coexistence of non-collagenous and collagenous forms at the same time.
Several factors—including the characteristics of the inhaled dust, being fibrogenic or inert; the dust size and density; the duration and intensity of exposure; the latency period, or time elapsed since the first exposure; individual susceptibility; personal protection; age; and smoking status—are associated with the manifestation of pneumoconiosis. The exposure to these dusts mainly occurs in occupational settings, but environmental exposure has also been reported, that is, environmental asbestos exposure in some rural areas. The classical and common forms of pneumoconiosis include asbestosis, silicosis, and coal worker’s pneumoconiosis, which are caused by inhalation of asbestos, silica, and coal dust, respectively. They represent the fibrogenic or collagenous side of pneumoconioses, which usually progress to massive fibrosis, even after cessation of dust exposure, whereas other mineral dusts and silicates usually cause non-fibrogenic or non-collagenous forms, which usually remain silent or cause mild disease. Meiklejohn 1949 provides a brief historical perspective. Nemery 2007 and Barber and Fishwick 2016 provide a nice basis for the ones who are not familiar to the topic. Nemery 2007 describes the traditional pneumoconioses and focus on diagnosis of occupational causes of parenchymal diseases and important points for clinicians, such as taking occupational history. Barber and Fishwick 2016 focuses on the most common types but also mentions the other pneumoconioses due to non-fibrogenic dusts. Laney and Weissman 2012 is a more comprehensive one for the inorganic dusts and the classical pneumoconioses caused by exposure to these dusts. Karkhanis and Joshi 2013 gives more detailed information on all the types of pneumoconiosis, including inert dust pneumoconiosis, that is, siderosis, stannosis, and baritosis, as well as uncomplicated, that is, aluminosis, talcosis, and berylliosis, and the complicated ones. Cowie 2010 handles the subject from the viewpoint of mining but from a broader perspective by addressing mining-associated problems and diseases in addition to pneumoconioses. Cowie, et al. 2010 provides an all-in-one and comprehensive evaluation of pneumoconioses and other mineral dust-related diseases. Van Sprundel 1990 draws attention to high and also increasing trends of pneumoconiosis in developing countries. Moitra, et al. 2015 discusses occupational and environmental diseases, with a special focus on pneumoconiosis, from a global perspective, and Cullinan, et al. 2017 draws attention to the global burden of occupational lung diseases, including pneumoconiosis, and provides recommendations to reduce the burden.
Barber, C., and D. Fishwick. 2016. Pneumoconiosis. Medicine 44.6: 355–358.
It is a concise review and briefly summarizes epidemiology, clinical features, management, and prevention of the most common pneumoconioses.
Cowie, R. L. 2010. Mining. In Occupational and environmental lung diseases. Edited by S. M. Tarlo, P. Cullinan, and B. Nemery, 177–189. Chichester, UK: Wiley-Blackwell.
This chapter deals with pneumoconioses and the broad range of thoracic disorders and diseases, which may be associated with mining.
Cowie, R. L., J. Murray, and M. R. Becklake. 2010. Pneumoconioses and other mineral dust-related diseases. In Murray and Nadel’s textbook of respiratory medicine. 5th ed. Edited by R. J. Mason, V. C. Broaddus, and T. R. Martin, 1554–1586. Philadelphia: Saunders Elsevier.
It provides a comprehensive evaluation of common pneumoconioses and other mineral dust-related diseases, including beryllium lung disease and hard-metal disease.
Cullinan, P., X. Munoz, H. Suojalehto, et al. 2017. Occupational lung diseases: From old and novel exposures to effective preventive strategies. Lancet Respiratory Medicine 5.5: 445–455.
In this review, they discuss the causes of the global burden of occupational diseases and provide recommendations for research, surveillance, and other actions for reducing the burden of occupational lung diseases.
Karkhanis, V. S., and J. M. Joshi. 2013. Pneumoconioses. Indian Journal of Chest Diseases and Allied Sciences 55.1: 25–34.
A comprehensive review of all causes of pneumoconioses, including inert dust and uncomplicated and complicated pneumoconioses as well as hard metal disease and mixed-dust fibrosis. It provides a useful classification of pneumoconioses that makes it easier to understand biological behavior of exposed dusts.
Laney, A. S., and D. N. Weissman. 2012. The classic pneumoconioses: New epidemiological and laboratory observations. Clinics in Chest Medicine 33.4: 745–758.
The aim of this review is to provide information on selected issues related to three inorganic mineral dust exposures—asbestos, crystalline silica, and coal—that cause classic forms of pneumoconiosis and adverse health effects due to exposure of these dusts. Additionally, it addresses new imaging modalities.
Meiklejohn, A. 1949. Pneumoconiosis. Postgraduate Medical Journal 25.290: 599–610.
It summarizes the evolution of the definition of and approach to pneumoconiosis from the “Epidemics of Hippocrates” (460–370 BCE) and the “Treatise of the Diseases of Tradesmen” by Ramazzini (1633–1714) to the mid-20th century.
Moitra, S., R. Puri, D. Paul, and Y. C. Huang. 2015. Global perspectives of emerging occupational and environmental lung diseases. Current Opinion in Pulmonary Medicine 21.2: 114–120.
This review discusses environmental and occupational lung diseases and exposures from a global perspective and gives some examples of emerging causes of pneumoconiosis, such as environmental exposure as the cause of asbestos, accelerated silicosis in denim sandblasters, and coal worker’s pneumoconiosis in surface coal miners.
Nemery, B. 2007. Occupational lung disorders of the parenchyma: Important points for clinicians. Breathe 4.1: 33–36.
It describes the main causes of the mineral pneumoconioses and remarks on the importance of taking a detailed occupational history in making the diagnosis, and it suggests considering the possibility of any occupational or environmental exposures in the etiology of a wide range of interstitial lung diseases.
Van Sprundel, M. P. 1990. Pneumoconioses: The situation in developing countries. Experimental Lung Research 16.1: 5–13.
It outlines the high and increasing trend of incidence and prevalence of pneumoconioses in developing countries and presents some data from Africa, Asia, and South America. It also discusses the causes of the increasing trends in those countries and absence of reliable information about the real magnitude of the problem as well as effective dust control and medical surveillance.
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