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: Definition. 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.
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