Saul R L, Archer M C
Toxicol Appl Pharmacol. 1983 Feb;67(2):284-91. doi: 10.1016/0041-008x(83)90235-1.
Sprague-Dawley rats exposed to atmospheres containing low levels of nitrogen dioxide (NO2) for 24 hr had increased levels of nitrate in their urine on the day of exposure and on the 3 subsequent days. The total increase in urinary nitrate was linearly related to the nitrogen dioxide concentration administered. We recovered in urine 8.4 +/- 1.1 mumol nitrate/ppm NO2/24-hr exposure (slope +/- 95% confidence limits) for 185-g rats. Both the linearity and magnitude of this effect imply that reaction with respiratory tract water is not a major pathway of NO2 absorption in the lung. Instead, our observations support the hypothesis that the major interaction of NO2 in the lung is with readily oxidizable tissue components to form nitrite. We estimate that 9.6 mumol of nitrite is formed in the respiratory tract of the rat per ppm NO2 per 24-hr exposure. We also estimate that humans breathing air containing 0.1 ppm NO2 have about 3.6 mg of nitrite formed in their respiratory tract per day.
将斯普拉格-道利大鼠暴露于含有低水平二氧化氮（NO₂）的环境中24小时，在暴露当天及随后3天，其尿液中的硝酸盐水平升高。尿中硝酸盐的总增加量与所给予的二氧化氮浓度呈线性相关。对于185克的大鼠，每ppm NO₂/24小时暴露，我们在尿液中回收了8.4±1.1微摩尔硝酸盐（斜率±95%置信区间）。这种效应的线性和程度都表明，与呼吸道水分的反应不是二氧化氮在肺部吸收的主要途径。相反，我们的观察结果支持这样的假设，即二氧化氮在肺部的主要相互作用是与易于氧化的组织成分反应形成亚硝酸盐。我们估计，每ppm NO₂每24小时暴露，大鼠呼吸道中会形成9.6微摩尔亚硝酸盐。我们还估计，呼吸含0.1 ppm NO₂空气的人类，每天呼吸道中会形成约3.6毫克亚硝酸盐。
