Shows progressive lung injury linked to contaminated aquatic environments in divers, indicating a need for early recognition and protection.
Chronic occupational exposure to contaminated aquatic environments is an underrecognized cause of progressive lung injury. Recurrent aspiration of sediment‐rich river water can lead to chronic inflammatory lung injury with possible environmental pathogen colonization and destructive lung disease, even in immunocompetent individuals. A 35‐year‐old non‐smoking professional diver in a tropical mangrove region of the Sundarban, Bangladesh, with 17 years of exposure performing 10–15 daily dives in muddy saline mangrove water, presented with 1 year of progressive exertional dyspnea and intermittent cough. Water aspiration during mud collection was frequent; four coworkers reported similar symptoms. SpO 2 was 93% at rest, dropping to 89% after 700 m on a 6‐min walk test, indicating exercise‐induced desaturation despite preserved walking distance. Digital clubbing and bilateral coarse crepitations were present. HRCT showed diffuse nodules and a left upper lobe cavitary lesion; Mantoux and Interferon gamma release assay were negative. Pulmonary function revealed severe restrictive defect (TLC 39%, FVC 25%, DLCO 36%, RV/TLC 48%). BAL grew Acinetobacter sensitive to meropenem and amikacin. After 7 days of IV therapy, symptoms improved, but domiciliary oxygen was not feasible. The patient died 1 month later. Muddy water pneumonitis can cause progressive necrotizing lung injury in divers, likely representing a multifactorial process involving environmental particulate exposure with superimposed infection. It was worsened by socioeconomic constraints and highlights the need for occupational protection and early recognition.
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Reshma et al. (2026) studied this question.
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