Ito T, Ohyama K, Kusano T, Usuda Y, Nozawa A, Hayashi H, Ohji H, Kitamura H, Kanisawa M
Department of Pathology, Yokohama City University School of Medicine, Japan.
Exp Toxicol Pathol. 1997 Feb;49(1-2):65-70. doi: 10.1016/s0940-2993(97)80066-8.
We investigated the effect of intratracheal injections of an extract of suspended particulate matter (SPM) obtained from the urban ambient air of Tokyo, upon the development of proliferative lesions of pulmonary endocrine cells (PECs) in the rat. We also examined the modification effects of nitrogen dioxide, sulfur dioxide, or both of them on the PEC lesions. Male F344 rats were divided into six experimental groups of 5 animals each. Twenty animals were treated with intratracheal instillations of SPM admixed with carbon once a week for 4 weeks with or without additional gaseous exposure (6 ppm nitrogen dioxide or 4 ppm sulfur dioxide) 16 hrs a day for 11 months. Five animals were given intratracheal injections of carbon suspended in saline and the other five were untreated. The subcardiac lobes of the right lung were fixed with 4% paraformaldehyde, and embedded in paraffin. PEC hyperplasias and papillomas were counted in 200 serial sections, 4 microns thick. The average incidences of PEC hyperplasia in the untreated animals and in those treated with carbon were 194 and 200/cm3, respectively. The average incidences of PEC hyperplasia in the animals exposed to SPM tar only, SPM tar plus nitrogen dioxide and sulfur dioxide, SPM tar with nitrogen dioxide and SPM tar with sulfur dioxide were 376, 378, 372 and 349/cm3, respectively. These were significantly higher than the levels of the control animals, and additional gaseous stimuli had no effect on the incidence of PEC hyperplasia. Besides PEC hyperplasia, a few PEC papillomas were found in the animals treated with SPM tar, regardless of gaseous exposure, but in the control animals no papilloma was evident. Thus, compounds in airborne particulates are considered to be responsible for the development of PEC hyperplasias and papillomas.
我们研究了气管内注射从东京城市环境空气中获取的悬浮颗粒物（SPM）提取物对大鼠肺内分泌细胞（PEC）增殖性病变发展的影响。我们还研究了二氧化氮、二氧化硫或两者对PEC病变的修饰作用。将雄性F344大鼠分为6个实验组，每组5只动物。20只动物每周气管内滴注一次与碳混合的SPM，持续4周，同时或不同时每天16小时暴露于额外的气体环境（6 ppm二氧化氮或4 ppm二氧化硫）中，持续11个月。5只动物气管内注射盐水中悬浮的碳，另外5只未接受处理。右肺心下叶用4%多聚甲醛固定，然后石蜡包埋。在200个4微米厚的连续切片中计数PEC增生和乳头状瘤。未处理动物和接受碳处理动物中PEC增生的平均发生率分别为194个/cm³和200个/cm³。仅暴露于SPM焦油、SPM焦油加二氧化氮和二氧化硫、SPM焦油加二氧化氮以及SPM焦油加二氧化硫的动物中PEC增生的平均发生率分别为376个/cm³、378个/cm³、372个/cm³和349个/cm³。这些发生率显著高于对照动物的水平，额外的气体刺激对PEC增生的发生率没有影响。除了PEC增生外，在接受SPM焦油处理的动物中，无论是否暴露于气体环境，都发现了一些PEC乳头状瘤，但在对照动物中未发现明显的乳头状瘤。因此，空气中颗粒物中的化合物被认为是导致PEC增生和乳头状瘤发展的原因。
