It is usually an occupational lung disease, typically from years of dust exposure during work in mining;[5] textile milling; shipbuilding, ship repairing, and/or shipbreaking; sandblasting; industrial tasks; rock drilling (subways or building pilings);[6] or agriculture.

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 stuck 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.

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.

To reduce the likelihood of developing pneumoconiosis, individuals working in affected industries should wear a mask, wash skin that comes in contact with dust, remove dust from clothing and wash the face and hands before eating or drinking.