Silica dust exposure and associated pulmonary dysfunction among mine workers.

This study assessed the impact of silica exposure on 145 mine workers in Mianwali, Punjab, Pakistan, compared to 45 non-exposed individuals. Pulmonary function tests revealed significantly reduced lung function in exposed workers (P < 0.05), with declines in Forced Expiratory Volume in one second (FEV1), Forced Vital Capacity (FVC), FEV1/FVC ratio, Peak Expiratory Flow, and Forced Expiratory Flow at 25-75% of FVC (FEF25-75). Radiological evaluations confirmed extensive lung damage (P < 0.05), including pleural effusion, reticular shadowing, and lung consolidation. Oxidative stress markers demonstrated increased lipid peroxidation, Fenton's Oxidative Stress, and Oxidative Stress Index (P < 0.05), along with reduced antioxidant enzyme activities, including Catalase, Superoxide Dismutase, Total Antioxidant Capacity, and Glutathione Peroxidase. Hematological analysis showed elevated White Blood Cells, Lymphocyte percentage, Hemoglobin, Hematocrit, Mean Corpuscular Volume, and Mean Corpuscular Hemoglobin (P < 0.05), reflecting systemic inflammation. Silica's piezoelectric properties contributed to oxidative stress and cellular damage, exacerbating pulmonary dysfunction. These findings highlight silica exposure as a severe occupational hazard, causing irreversible lung impairment and systemic oxidative imbalance. Implementing strict safety protocols, personal protective measures, and regular health monitoring is crucial to safeguarding workers.