De B K, Majumdar D, Sen S, Guru Supriya, Kundu S
Department of Medicine and Chest, Institute of Post Graduate Medical Education and Research. 244, Acharya J.C. Bose Road, Kolkata - 700 020, India.
J Assoc Physicians India. 2004 May;52:395-400.
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.
由于饮用受污染的地下水导致的慢性砷中毒,是西孟加拉邦的一个主要公共卫生问题。它会造成多器官损害。本研究试图通过检查肺功能来客观地调查肺部受累情况。还评估了肺部变化的性质。
对107例慢性砷中毒患者(病例组)和52例无慢性砷中毒患者(对照组)进行了肺活量测定。测量了第1秒用力呼气容积(FEV1)、用力肺活量(FVC)和呼气峰值流速(PEFR)。对5例有肺部受累和5例无肺部受累的病例进行了支气管肺泡灌洗(BAL)。
33例(30.8%)病例和4例(7.6%)对照者(p<0.01)有呼吸系统受累。病例组的受累模式为:阻塞性-20例(68.9%)(包括3例(10%)支气管扩张),限制性-1例(3.5%),混合性-8例(27.6%),恶性肿瘤-4例(12.1%)(腺癌-1例,鳞状细胞癌-2例,未分化癌-1例)。病例组的FEV1(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)、FEV1/FVC(73.6±13.38[n=105] vs 79.1±18.65[n=52],p=0.007)和PEFR(53.9±21.52[n=103] vs 67.3±18.36[n=51],p=0.0002)(预测值百分比)均比对照组下降得更多。这些参数的恶化与砷中毒程度的增加相关。有肺部受累者的BAL液中炎症标志物(巨噬细胞、乳酸脱氢酶、一氧化氮)明显多于无肺部受累者,尽管砷含量无显著差异。
慢性砷中毒会导致肺部受累,主要为阻塞性,其程度随砷中毒程度的增加而加重。炎症而非直接毒性似乎是潜在机制。