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An overview of Pneumoconiosis

  • Posted on- Aug 31, 2015
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The term Pneumoconiosis includes group of lung diseases caused by the inhalation of particulate matter occurring in certain occupations. Inorganic dusts such as silica, asbestos or coal dust and organic dusts such as mouldy hay, cotton dust or sugar cane dust may lead on to pneumoconiosis.

At present several occupations are known to be associated with this risk. More and more entities are likely to be recognized with the expansion of industry. Development of the pathological lesion depends upon several factors such as the nature of the substance inhaled, the concentration in the atmosphere, duration of exposure, particle size, and responsiveness of the individual. When the particles are below 10 micrometer in size, they reach the alveoli and are carried by alveolar macrophages to the interstitial spaces where inflammatory reaction sets in. In many cases, the process continues over the years and leads to gross functional and structural changes resulting in severe morbidity. Coarser particles are arrested by the air passages and they do not reach the alveoli.

Lesions caused by inorganic dusts ranging from minimal inflammatory reaction around the dust particle to more marked changes like focal emphysema, interstitial fibrosis and calcification. Some dusts like asbestos are carcinogenic. In some disorders such as silicosis the host's immune mechanism is altered, making the subject more susceptible to develop tuberculosis.

Organic dusts which tend to be more widely distributed in the agricultural belts of India exert their deleterious effects in different ways- Irritation by their presence, hypersensitisation to the components of the dust or sensitization to fungal contaminants in the dust play varying roles on the ultimate outcome. They cause damage principally on the alveolar ducts to produce extrinsic allergic alveolitis.

The factors which lead to pneumoconiosis are:

  • Mechanical blockage
  • Chemical irritation of the air passage, e.g., chlorine and acid fumes
  • Direct toxicity to the lung parenchyma, e.g. phosgene, methyl isocyanate
  • Fibrosis e.g., silica
  • Hypersensitisation, e.g., dander of animals, fungi, cotton dust
  • Chronic granulomatous process, e.g., beryllium
  • Predisposition to secondary infection, e.g., silicosi predisposes to tuberculosis and Neoplasia e.g., asbestos

Genetic factors probably modify the susceptibility to develop pneumoconiosis. Susceptible persons show early signs of ill health, whereas the others are relatively immune. Other factors such as tobacco smoking, nutrition, and infections also may have possible roles in determining the final outcome in individual subjects. Industrial legislation requires adequate protective steps to be undertaken by establishments to safeguard against the development of pneumoconiosis amongst workers.