Industrial Exposures

Industrial workers are exposed to a wide range of organic and inorganic substances, which have different kinds of consequences on their health. Diseases can range from mere irritation of mucosa of airways due to organic fumes to lung cancer due to inorganic dusts and leukemia due to prolonged exposure to benzene and uranium. Pneumoconiosis is a typical example of the conditions which are brought by industrial exposures.

PNEUMOCONIOSES 

 Pneumoconiosis is a group of non-neoplastic pulmonary disease, which is due to inhalation of organic and inorganic particulates. The mineral dust pneumoconiosis, which is due to coal dust, asbestos, silicon and beryllium, almost always occur from exposure in work places.

Pathogenesis 

Pneumoconiosis is a result of lung reactions towards offending inhaled substances. The reaction depends on the size, shape, solubility and reactivity of the particles. Particles greater than 10μm are not harmful because they are filtered out before reaching distal airways. When they are less than 1μm in diameter they tend to move in and out of alveoli like gases so that they will not deposit and result in an injury.

Silica, asbestos & beryllium are more reactive than coal dust bringing about fibrotic reaction, while coal dust has to be deposited in huge amounts if it has to result in reaction because it is relatively inert. Most inhaled dust is removed out through the ciliary movement after being trapped in the mucus linings. When particles reach the alveoli they are in gulfed by macrophages. The more reactive particles activate macrophages to release fibrogenic factors, toxic factors and proinflammatory factors. The cumulative effect becomes lung injury and fibrosis. The important mediators released by macrophages are grouped in to three: -

1. Free radicals: reactive oxygen and reactive nitrogen species that induce lipid peroxidation and tissue damage

2.  chemotactic factors: leukotriene B4 (LTB4) interleukin 8 (IL-8 ) IL-6 ,and TNF which recruit and activate inflammatory cells and which in turn release damaging oxidants (free radicals ) 

3.  Fibrogenic cytokines: IL-1, TNF, fibronectin, platelet derived growth factor (PDGF), and insulin like growth factor (IG F-1), which recruit fibroblasts.

Figure.1 Pathogenesis of pneumoconiosis

Pneumoconiosis can be classified according to the substance incriminated.

A-  Coal workers Pneumoconiosis   _Due to coal dust

B- Silicosis    _Due to silica

C- Asbestosis    _Due to asbestos

D- Berylliosis    _Due to beryllium

Coal workers pneumoconiosis

Since earlier times of industrialization it has been noticed that coal miners were drying of “black lung” complicated by tuberculosis. Coal dust mainly contains carbon but has a variety of trace metals inorganic mineral and crystalline silica. Anthracite (hard) coal contains significantly more quartz than bituminous (soft) coal. Anthracite (hard) coal is more frequently associated with lesions in the lungs; hence the name pulmonary anthracosis is coined for coal induced pulmonary lesions. 

The disease has three distinct pathological entities:

i. Anthracosis:- Where pigments are accumulated without cellular reaction and symptoms

ii. Simple coal workers pneumoconiosis With minimal cellular reaction and little or no pulmonary dysfunction

iii. Progressive massive fibrosis:- With extensive fibrosis and compromised pulmonary function

Morphology

 •  Pulmonary anthracosis - Macrophages in the alveoli and interstitium are found laden with carbon pigments. These macrophages are also seen along the lymphatics including pleural lymphatics or lymphoid tissue along bronchi and lung hilus.

•  Simple Coal workers pneumoconiosis (CWP) characterized by coal macules and coal nodules. Coal macules constitutes of carbon-laden macrophages aggregated, coal nodule is when the macule additionally contains collagen fibers.

•   Complicated CWP - progressive Massive fibrosis (PMF) - occurring in the background of CWP after many years by coalescence of coal nodules. It is characterized by coal nodules intermingled with collagen fibers with central necrosis, size ranging from 2cm to 10cm.

Clinical course

 Pulmonary anthracosis and simple CWP result in no abnormalities in lung functions. When it progress to progressive massive fibrosis in minority of cases it results in pulmonary hypertension and corpulmonale. Progression from simple CWP to PMF has been linked to amount and duration of exposure to coal dust. Smoking also has been shown to have the same effects. Sometimes of course the progression does not need factors mentioned above.

Asbestos Related Disease

Asbestos is a generic name that embraces the silicate minerals that occur as long, thin fibers. Asbestosis refers to the pneumoconiosis that results from the inhalation of asbestos fibers

Pathogenesis

Asbestos fibers are thin and long so that they can reach the bifurcations of bronchioles and alveoli. There, they are engulfed by macrophages to induce the cascade of inflammatory process, which finally result in interstitial pulmonary fibrosis.

Pathology

1-Asbestosis:-is an interstitial fibrosis of the lung. At early stages, fibrosis is in and around the alveoli and terminal bronchioles. when disease progresses, gross examination of the lungs show gray streaks of fibrous tissue, which accentuate the interlobular septa, together with diffuse thickening of the visceral pleura. The asbestos body is the most diagnostic structure seen under the microscope, consisting of asbestos fiber beaded with aggregates of iron along its length.

2-Pleural plagues: - after a period of many years the inhalation of asbestos fibers will result in the appearance of plaques on the partial pleura.

They are 2 to 3 mm thick, and microscopically they are densely collagenous and hyalinized and sometimes calcified.

3-Mesothelioma:-a clear cut relationship between asbestos exposure and a maligment mesothelioma is now firmly established.

4-Other malignancies like lung and bladder cancers can also result from asbestos exposure.

References

Bezabeh ,M. ; Tesfaye,A.; Ergicho, B.; Erke, M.; Mengistu, S. and Bedane,A.; Desta, A.(2004). General Pathology. Jimma University, Gondar University Haramaya University, Dedub University.