Miller F J, Graham J A, Raub J A, Illing J W, Ménache M G, House D E, Gardner D E
J Toxicol Environ Health. 1987;21(1-2):99-112. doi: 10.1080/15287398709531005.
The study reported herein evaluates the influence of a chronic exposure to an urban pattern of NO2 (continuous baseline exposure of 0.2 ppm, on which were superimposed two 1-h spikes of 0.8 ppm NO2, 5 d/wk) as compared to the baseline exposure to determine the contribution of the spikes to toxicity. Mice were exposed for up to 52 wk with interim examinations. Multivariate analysis of variance revealed a statistically significant treatment effect on infectivity (p = 0.05) and pulmonary function (p = 0.03) parameters. Infectivity mortality of mice in the spiked exposure regimen was significantly greater than that in either the NO2-background-exposed mice or in control mice. Four of the pulmonary function variables exhibited the greatest differences among the treatment groups: end expiratory volume, vital capacity, respiratory-system compliance, and multiple-breath nitrogen washout. Results from the pulmonary-function analyses indicate that the spiked exposures to 0.8 ppm NO2 may have induced a subtle lesion. The chronic study results indicate that the presence of spikes of NO2 is contributing significantly to effects on antibacterial lung defenses and pulmonary function of mice.
本文报道的研究评估了长期暴露于城市模式的二氧化氮（持续基线暴露为0.2 ppm，在此基础上每周5天叠加两个1小时的0.8 ppm二氧化氮峰值）与基线暴露相比，峰值对毒性的贡献。小鼠暴露长达52周，并进行中期检查。多变量方差分析显示，在感染性（p = 0.05）和肺功能（p = 0.03）参数方面存在统计学上显著的治疗效果。在加标暴露方案中，小鼠的感染性死亡率显著高于二氧化氮背景暴露小鼠或对照小鼠。肺功能的四个变量在治疗组之间表现出最大差异：呼气末容积、肺活量、呼吸系统顺应性和多次呼吸氮洗脱。肺功能分析结果表明，加标至0.8 ppm二氧化氮的暴露可能诱发了细微病变。慢性研究结果表明，二氧化氮峰值的存在对小鼠的抗菌肺防御和肺功能有显著影响。
