3 0 0 0 大気中微粒子の呼吸器内沈着と生体影響
本研究の主眼は、1.吸入粒子の呼吸器内沈着挙動の理論的実験的研究、2.呼吸器内に取り込まれた吸入粒子の種類、部位、沈着量、溶解量の評価、3.吸入粒子のフェイトアナリシスと生体影響評価である。第1のテーマに関して、人体呼吸器を16部に区別、これへの吸入エアロゾル粒子吸着とクリアランスを計算できる簡易式を開発し、その有効性を確認した、(高橋幹)、肺胞領域での吸入空気と肺内残存粒子の混合沈着機構をシミュレートできる不均一伸縮場ガラスシェル肺胞モデルを作成し、その影響が0.1μm付近の粒子に大きいことを明かにした。(江見)、第2のテーマに関して、化学形態の異なるNi化合物粒子吸入膜露実験を行ない、クリアランス期をおいて各臓器でのNi滞留量を比較した。(田中)、吸入エアロゾルスペーサーの効果をエアロゾル粒子数、粒径分布を測定し、4μm以下の小粒子を吸入させるためには大スペーサーが効果的であると結論した。(瀧島)病理解剖例を用い、人肺組織、肺門リンパ腺中の金属元素分析を行い、呼吸器病変、生活歴との相関を調査した。(竹本)気道鋳型モデル、微細気管内挿管法、吸入実験、培養肺マクロファージ試験管内実験など新手法を用い、NiO,石炭フライアッシュ,放射性BaSO_4,放射性Fe(OH)_3等微粒子の沈着量,毒性,溶解性,除去作用を明かにした。(高橋テ)、第3のテーマに関して、硫化ニッケル石炭フライアッシュの各種培養液への溶解挙動を明らかにした。(古谷)、フラッシュ脱離・質量分析法を開発し、ラット肺中数ngのPHAの定量に成功した。(飯田)レーザー励起蛍光・ミセル動電クロマト法を開発し、fgのPHA定量を可能とした。(今坂)モデル肺液へのPHA溶解度を測定する装置を開発し、生体影響評価に役立つ結果を得た。(坂本)本研究は、10名の相互の協力により、共通試料の提供、専門知識、設備の利用により、きわめて新しい成果を得ることが出来た。
- 著者
- 吉村 博之 竹本 和夫
- 出版者
- 公益社団法人日本産業衛生学会
- 雑誌
- 産業医学 (ISSN:00471879)
- 巻号頁・発行日
- vol.33, no.2, pp.81-93, 1991-03-20
- 被引用文献数
- 1
Occupationally induced lung cancer and mesothelioma have long been attributed to asbestos and moreover, several epidemiological studies have indicated a co-carcinogenic effect of cigarette smoking on the incidence of lung cancer in asbestos workers. The aim of the present study was to investigate the co-carcinogenic effects of asbestos and other carcinogens with emphasis placed on determining the effects of cigarette smoking on the incidence of asbestos induced carcinomas. Doses of 15mg of chrysotile asbestos were administered intratracheally to Wistar rats alone and in conjunction with N-bis(hydroxypropyl)nitrosamine (DHPN) and/or cigarette smoking. DHPN at dose of 1g/kg/B.W. was injected three times intraperitoneally, and the subject animals were exposed to smoke from 10 cigarettes per day, six days a week, for their entire life span. As a result, lung carcinomas were induced in one out of the 31 rats receiving only asbestos. Lung tumors were induced at a much higher incidence in the groups receiving DHPN alone and in conjunction with asbestos: of the 37 rats treated with DHPN alone 19 (51.4%) developed lung tumors, whereas those receiving asbestos as well showed an incidence of 68.4% (23/38) of carcinomas. The development of lung carcinomas (including adenocarcinomas, epidermoid carcinomas, anaplastic carcinomas, and combined carcinomas) was seen in 8 (21.6%) out of the 37 rats receiving DHPN alone and in 23 (60.5%) out of the 38 rats receiving asbestos as well. The incidence of lung carcinoma was significantly increased in combined treatment with asbestos than DHPN alone. In the group receiving asbestos in combination with cigarette smoke, 4 (13.8%) out of the 29 rats developed lung carcinomas, but these carcinomas were more common than in the group receiving only asbestos. Moreover, in the group administered asbestos, DHPN and smoking combined, lung tumors developed in 18 (62.1%) out of the 29, 15 (51.7%) of which proved to be malignant. Mesothelioma (pleura) was induced in three groups in the following combinations: DHPN plus asbestos, 8/38 (21.17%); smoking plus asbestos, 2/29 (6.9%); and smoking, DHPN and asbestos, 4/29 (13.8%). These tumors were extensively located, that is, on the parietal pleura, visceral pleura, epicardium and diaphragm surface. However, mesothelioma was not induced by asbestos alone nor by DHPN alone. Carcinogenicity of asbestos for pleural tumors was significantly promoted by combined treatment with DHPN to an extent greater than DHPN alone. It should be noted that asbestos plus smoking resulted in a higher incidence of mesothelioma than asbestos alone. The results of this study suggest that asbestos can induce lung cancer and that cigarette smoking has a promoting effect on asbestos-induced cancer and mesothelioma as well. Additionally, it was observed that the development of lung tumors and their malignancy and mesothelioma by asbestos is synergistic ally increased by the combined administration of DHPN. There were some histological differences in the carcinomas induced by DHPN alone and those induced in conjunction with asbestos.