Gunnison A F, Sellakumar A, Snyder E A, Currie D
Department of Environmental Medicine, New York University Medical Center, New York 10016.
Environ Res. 1988 Jun;46(1):59-73. doi: 10.1016/s0013-9351(88)80059-8.
In a previous study at this Institute, inhaled sulfur dioxide (SO2) was shown to enhance the induction by inhaled benzo[a]pyrene (BaP) of squamous cell carcinoma (SQCA) of the respiratory tract of rats (S. Laskin, M. Kuschner, A. Sellakumar, and G. V. Katz, 1976, In "Air Pollution and the Lung," pp. 190-213). We attempted to confirm and extend this finding by using an experimental protocol intended to illuminate the role of SO2. Rats were treated with BaP by 15 consecutive weekly intratracheal instillations. Some of these rats were simultaneously exposed either to SO2 by inhalation or to sulfite/bisulfite anions that accumulated systemically from endogenous generation in rats with induced sulfite oxidase deficiency. The total treatment period spanned 21 weeks, after which the rats were observed for the development of tumors. BaP-treated rats began to die with SQCA of the respiratory tract at approximately 200 days after the first BaP treatment and at 2 years after the first treatment nearly all rats in the BaP-treated groups had died, most with SQCA. Survival in the control groups was excellent and the health of all groups (aside from pulmonary SQCA in BaP-treated groups) was also excellent. The probability of dying with a pulmonary SQCA in the experimental groups treated with BaP, BaP plus inhaled SO2, and BaP plus systemic sulfite/bisulfite was calculated by the logrank analysis. The data sets of SQCA probability from these groups were not statistically different (i.e., P greater than 0.05) by the chi 2 test indicating that, in this experiment, neither inhalation exposure to SO2 nor systemic exposure to sulfite/bisulfite anions affected the induction of SQCA of the lung by intratracheally instilled BaP. We conclude that the results of this study do not support an etiological role for either SO2 or sulfite/bisulfite anions in the induction of SQCA of the respiratory tract by BaP.
在本研究所先前的一项研究中，吸入二氧化硫（SO₂）被证明可增强吸入苯并[a]芘（BaP）对大鼠呼吸道鳞状细胞癌（SQCA）的诱导作用（S.拉斯金、M.库施纳、A.塞拉库马尔和G.V.卡茨，1976年，载于《空气污染与肺部》，第190 - 213页）。我们试图通过使用一种旨在阐明SO₂作用的实验方案来证实并扩展这一发现。大鼠通过连续15周每周一次气管内滴注给予BaP。其中一些大鼠同时通过吸入暴露于SO₂，或暴露于因诱导亚硫酸盐氧化酶缺乏的大鼠内源性生成而全身累积的亚硫酸盐/亚硫酸氢盐阴离子。总治疗期为21周，之后观察大鼠肿瘤的发生情况。经BaP处理的大鼠在首次给予BaP治疗后约200天开始死于呼吸道SQCA，在首次治疗后2年，BaP处理组的几乎所有大鼠都已死亡，大多数死于SQCA。对照组的存活率很高，所有组（除BaP处理组的肺部SQCA外）的健康状况也很好。通过对数秩分析计算用BaP、BaP加吸入SO₂以及BaP加全身亚硫酸盐/亚硫酸氢盐处理的实验组死于肺部SQCA的概率。通过卡方检验，这些组的SQCA概率数据集无统计学差异（即P大于0.05），表明在本实验中，吸入暴露于SO₂或全身暴露于亚硫酸盐/亚硫酸氢盐阴离子均不影响气管内滴注BaP对肺部SQCA的诱导作用。我们得出结论，本研究结果不支持SO₂或亚硫酸盐/亚硫酸氢盐阴离子在BaP诱导呼吸道SQCA中起病因学作用。
