Pulmonary involvement in chronic arsenic poisoning from drinking contaminated ground-water

• Published in: Journal of the Association of Physicians of India Vol. 52; p. 395
• Main Authors: De, B K, Majumdar, D, Sen, S, Guru, Supriya, Kundu, S
• Format: Journal Article
• Language: English
• Published: India 01.05.2004
• Subjects: Adolescent; Adult; Arsenic Poisoning - complications; Bronchoalveolar Lavage Fluid - chemistry; Bronchoalveolar Lavage Fluid - immunology; Chronic Disease; Diagnostic Techniques, Respiratory System; Female; Humans; India; Lung Diseases - chemically induced; Lung Diseases - diagnosis; Male; Middle Aged; Rural Population; Water Pollution, Chemical - adverse effects; Water Supply; India
• ISSN: 0004-5772

Chronic arsenic poisoning, due to ingestion of contaminated ground-water, is a major public health problem in West Bengal. It causes multiorgan damage. The present study attempts to objectively investigate the pulmonary involvement by examining the lung function. The nature of lung changes was also evaluated. One hundred and seven subjects with (cases) and 52 subjects without (controls) chronic arsenic poisoning were examined by spirometry. Forced expiratory volume-I second (FEVI), forced vital capacity (FVC) and peak expiratory flow rate (PEFR) were measured. Bronchoalveolar lavage (BAL) was performed in five cases with and five cases without pulmonary involvement. Thirty three (30.8%) cases and four (7.6%) controls (p<0.01) had respiratory involvement. The pattern of involvement in cases was: obstructive- 20(68.9%) (including three (10%) with bronchiectasis), restrictive- 1(3.5%), mixed- 8(27.6%), malignancy- 4(12.1%) (adenocarcinoma-I, squamous cell- 2, undifferentiated- I). FEVI (69.7+/-25.9 [n=105] vs 83.7+/-15.19 [n=51], p=0.0005), FVC (77.4+/-22.7 [n=105] vs 85.6+/-18.23 [n=51], p=0.025), FEVI/FVC (73.6+/-13.38 [n=105] vs 79.1+/-18.65 [n=52], p=0.007) and PEFR (53.9+/-21.52 [n= 103] vs 67.3+/-18.36 [n=51], p=0.0002) (percent of predicted) were all reduced more in cases compared to controls. Worsening of these parameters correlated with increasing degree of arsenic toxicity. Markers of inflammation (macrophage, lactate dehydrogenase, nitric oxide) were apparently more in the BAL fluid of those with lung involvement than in those without, though the arsenic content did not differ significantly. Chronic arsenic poisoning causes pulmonary involvement, predominantly obstructive, the degree of which worsens with increasing degree of arsenic toxicity. Inflammation, rather than direct toxicity, appears to be the underlying mechanism.