Hassett C, Mustafa M G, Coulson W F, Elashoff R M
J Natl Cancer Inst. 1985 Oct;75(4):771-7.
Inbred strain A/J mice, responsive to the chemical induction of pulmonary adenomas, were used to assess any of several roles that the photochemical air pollutant ozone might play in lung carcinogenesis. In separate experiments, animals were exposed to two concentrations of ozone (0.31 +/- 0.01 and 0.50 +/- 0.02 ppm) intermittently for a 6-month period, to evaluate the potential of ozone to act as either a pulmonary carcinogen, a tumor promoter, or an inhalant capable of increasing lung tumor yield when exposure was in conjunction with a pulmonary carcinogen, urethane. Statistical analyses of results indicated that ozone exposure at both concentrations caused an increase in lung tumor number relative to clean air controls, but that ozone was not an effective tumor promoter under the conditions of our protocol. When ozone exposure immediately preceded treatment with urethane (CAS: 51-79-6), animals were at increased risk for the development of lung adenomas.
对肺部腺瘤化学诱导有反应的近交系A/J小鼠，被用于评估光化学空气污染物臭氧在肺癌发生过程中可能扮演的几种角色。在单独的实验中，动物间歇性暴露于两种浓度的臭氧（0.31±0.01和0.50±0.02 ppm）下，为期6个月，以评估臭氧作为肺部致癌物、肿瘤促进剂或与肺部致癌物氨基甲酸乙酯联合暴露时能够增加肺部肿瘤发生率的吸入剂的可能性。结果的统计分析表明，相对于清洁空气对照组，两种浓度的臭氧暴露均导致肺部肿瘤数量增加，但在我们的实验方案条件下，臭氧不是一种有效的肿瘤促进剂。当臭氧暴露紧接着氨基甲酸乙酯（CAS：51-79-6）处理时，动物发生肺腺瘤的风险增加。
