Pneumoconiosis

Pneumoconiosis
Asbestosis high mag.jpg
Micrograph of asbestosis (with ferruginous bodies), a type of pneumoconiosis. H&E stain.
Classification and external resources
Specialtypulmonology
ICD-10J60-J65
ICD-9-CM500-505
DiseasesDB31746
MeSHD011009

Pneumoconiosis is an occupational lung disease and a restrictive lung disease caused by the inhalation of dust, often in mines and from agriculture.[1][2]

In 2013, it resulted in 260,000 deaths globally, up from 251,000 deaths in 1990.[3] Of these deaths, 46,000 were due to silicosis, 24,000 due to asbestosis and 25,000 due to coal workers pneumoconiosis.[3]

Typology[]

Depending upon the type of dust, the disease is given different names:

Pathogenesis[]

The reaction of the lung to mineral dusts depends on many variables, including size, shape, solubility, and reactivity of the particles. For example, particles greater than 5 to 10 μm are unlikely to reach distal airways, whereas particles smaller than 0.5 μm move into and out of alveoli, often without substantial deposition and injury. Particles that are 1 to 5 μm in diameter are the most dangerous, because they get lodged at the bifurcation of the distal airways. Coal dust is relatively inert, and large amounts must be deposited in the lungs before lung disease is clinically detectable. Silica, asbestos, and beryllium are more reactive than coal dust, resulting in fibrotic reactions at lower concentrations. Most inhaled dust is entrapped in the mucus blanket and rapidly removed from the lung by ciliary movement. However, some of the particles become impacted at alveolar duct bifurcations, where macrophages accumulate and engulf the trapped particulates. The pulmonary alveolar macrophage is a key cellular element in the initiation and perpetuation of lung injury and fibrosis. Many particles activate the inflammasome and induce IL-1 production. The more reactive particles trigger the macrophages to release a number of products that mediate an inflammatory response and initiate fibroblast proliferation and collagen deposition. Some of the inhaled particles may reach the lymphatics either by direct drainage or within migrating macrophages and thereby initiate an immune response to components of the particulates and/or to self-proteins that are modified by the particles. This then leads to an amplification and extension of the local reaction. Tobacco smoking worsens the effects of all inhaled mineral dusts, more so with asbestos than with any other particle.[1]

Diagnosis[]

Positive indications on patient assessment:

Pneumoconiosis in combination with multiple pulmonary rheumatoid nodules in rheumatoid arthritis patients is known as Caplan's syndrome.[4]

Epidemiology[]

In 2013 pneumoconiosis resulted in 260,000 deaths up from 251,000 deaths in 1990.[3] Of these deaths 46,000 were due to silicosis, 24,000 due to asbestosis and 25,000 due to coal workers pneumoconiosis.[3]

Popular culture[]

See also[]

References[]

  1. ^ a b Kumar, MBBS, MD, FRCPath, Vinay (2013). Robbins Basic Pathology 9th Edition. Philadelphia, Pennsylvania: Elsevier Saunders. pp. 474–475. ISBN 978-1-4377-1781-5.
  2. ^ Schenker, Marc B.; Pinkerton, Kent E.; Mitchell, Diane; Vallyathan, Val; Elvine-Kreis, Brenda; Green, Francis H.Y. "Pneumoconiosis from Agricultural Dust Exposure among Young California Farmworkers". Environmental Health Perspectives. 117 (6): 988–994. doi:10.1289/ehp.0800144. PMC 2702418. PMID 19590695.
  3. ^ a b c d GBD 2013 Mortality and Causes of Death, Collaborators (17 December 2014). "Global, regional, and national age-sex specific all-cause and cause-specific mortality for 240 causes of death, 1990-2013: a systematic analysis for the Global Burden of Disease Study 2013". Lancet. 385: 117–71. doi:10.1016/S0140-6736(14)61682-2. PMC 4340604. PMID 25530442.
  4. ^ Andreoli, Thomas, ed. CECIL Essentials of Medicine. Saunders: Pennsylvania, 2004. p. 737.
  5. ^ "Zoolander (2001)". IMDb.com.

Further reading[]

External links[]