We are what we breathe!

Dear Sir,

Having read the article by Cimrin et al.,[1] on pneumoconiosis, I would like to discuss my observations on the same. Silicosis, coal worker pneumoconiosis (CWP), asbestosis, berylliosis, heavy metal exposure, and talcosis have fibrotic form of pneumoconiosis, while siderosis, stannosis, and baritosis (barium sulfate) are nonfibrotic forms. In the predisposed, silicosis or CWP (inciting agent in coal being iron) may show reticulonodular lesions in a perilymphatic distribution with or without eggshell calcifications.

In a study, the time of progression in coal workers averaged 12.2 years from the last normal chest film until progressive massive fibrosis (PMF) was detected. Lung function declined sharply in both smokers and nonsmokers, averaging 87 ml/year, for FEV1 and 74 ml/year for FVC.[2]

Normal chest X-rays cannot exclude low grade silicosis as there is a seven-fold increased risk of simple (nodular) silicosis especially in those highly exposed. In ILO category 0/0, 8% HRCT round (in high quartz exposure), 22% irregular and/or linear opacities, and 41% HRCT emphysema were found.[3] SEM (scanning electron-microscope) and XRS (X-ray sedimentation) show that the number of mineral particles (silicates) is greater in the lungs of agricultural workers than in nonagricultural workers and is characterized by mineral-dust small-airways disease, pneumoconiosis, chronic bronchitis, emphysema, and interstitial fibrosis.

Miners from small mines (fewer than 50 workers) are five times more likely to have radiographic evidence of PMF (1.0% of miners) compared to miners from larger mines (0.2%).

Agate, a silicate quartz (used in beads and decorative items mainly in Khambhat, India) produces a fine dust when shaped and polished and has demonstrated a high risk of silicosis. Gujjar lung, a chronic lung disease caused by pinewood smoke inhalation in the Gujjar community is characterized by progressive fibrosis with anthracotic nodules and miliary mottling.

An Indian study quantified the amount of dust generation in 1993-94 as 869.4 kg/h (20,865 kg/day) which might have increased several folds by now. Areas in India like Lakhanpur, Lilari, and Belpahar opencast coal projects among others and the coal transport to nearby railway stations (Belpahar and Brajarajnagar) are notorious in adversely affecting the atmosphere.[4]

Serum matrix metalloproteinases (MMP-9) and tissue inhibitors of metalloproteinases TIMP-9 (high in silicosis and CWP) are shown to have a harmful role in pneumoconiosis.

Raised ferric heme and nitric oxide (FeNO) derived from stimulated inducible NO synthase by inflammatory cytokines such as TNF–alpha and IL–1 beta is incriminated and might correlate with the severity in pneumoconioses. FeNO negatively correlates with FVC and flow at 25% vital capacity/height. The microRNA-149 rs2292832 TT genotype and SMAD4 (rs10502913) AA genotype[5] are associated with a significantly increased risk of CWP. In pneumoconiosis, TNF-α-308 A allele is shown to elevate risk for pulmonary TB. Those dying with silicosis have 4.4-fold risk of dying with mycosis compared to those dying without pneumoconiosis.

MR can help distinguish lung cancer (high signal intensity and wash out in delayed image) from PMF in CWP.

Pneumoconiosis contributes to significant irreversible morbidity and stringent preventive measures at work places need to be taken to avert them.