報告書番号

U02006

タイトル（和文）

ディーゼル排気の健康・生物影響に関する文献調査

タイトル（英文）

Review of health and biological effects of diesel exhaust

概要 （図表や脚注は「報告書全文」に掲載しております）

ディーゼル排気の排出規制は年々強化されつつある。ディーゼル排気中のディーゼル排気微粒子は粒径が細かいために肺深部に沈着しやすく、微粒子表面には多くの化学物質が吸着しておりディーゼル排気毒性の中心である。疫学調査では職業暴露により肺がん発症・死亡率がやや増加したが、統計学的には有意ではない。しかし、動物を用いた生物研究においてディーゼル排気微粒子の発がん性が示唆され、肺の粒子体外排出能や呼吸生理機能、アレルギー疾患に対する影響も認められている。発がんのリスク評価については、国際がん研究機関によりディーゼル排気微粒子はヒト発がん物質である可能性が高いと分類されている。ディーゼル排気の毒性は主に排気中のディーゼル排気微粒子にあることから、セタン価が高く硫黄分の少ない燃料を用いたりディーゼル排気微粒子を触媒フィルターで除去することにより、生物・健康影響を低減させることが可能である。

概要 （英文）

Diesel exhaust (DE) is composed of diesel exhaust particulates (DEP), fine carbon core particulates and a mixture of various gases. Legal regulations of DEP, nitric oxides, carbon hydroxides, and monocarbon oxide from mobile diesel engine were issued in 1993 in Japan, and the regulation has been tightened since then. In view of comprehensive reduction of suspended particulate matter, immobile diesel facility including regional diesel engine power plants could be covered under the regulation in near future. This study aims at surveying research outcomes in epidemiology and toxicology of DE exposure. Epidemiological research revealed the mortality of lung tumor among railroad workers and truck drivers, who have been occupationally exposed to DE, rose 1.2- to 1.5-fold relative to the matched control cohort, although the difference is not statistically significant in most of these studies. Epidemiological results also indicated that respiratory functions were slightly but significantly affected by the DE exposure. Voluntary human exposure to DE altered the number of lung immune cells and lung physiological functions. DE and DEP inhalation in human strongly related to decreased particulate clearance in the lung and to aggravation of pulmonary allergic symptoms. Biological studies showed that the lethal dose 50 (LD50) of DEP in the mouse is 20 mg/kg body weight. DE inhalation caused inflammation, hyperplasia of airway epithelial cells and decreased lung clearance. Nose administration of DEP evoked increases of immunogloblins and cytokines production related to asthma. In the animal model of pollen allergy, respiratory functions were also changed by the DEP administration. Long term DE inhalation exposure was carcinogenic in the rat. Even though the lack of quantitative human data for health risk assessment, International Agency for Research Center classified DEP as a probable carcinogen to human based on animal exposure experiments. Fineness of DEP makes it difficult to be eliminated from the lung, which is thought to be one reason for cancer. Mutagenic substances absorbed on the DEP are also responsible for cancer. One way to decrease the potential health risk of DE is to reduce DEP in DE. Exclusion of DEP by filtering, decreasing sulfur content and aromatic compounds in diesel fuel, and using high cetan value fuel are considered to be effective. Results of our survey indicate that DE exposure adversely affect respiratory functions and deteriorates allergic status. Carcinogenicity of the DE is also suggested. Biological effects of DE are due to mainly the fineness of DEP and attached chemicals to the particulates. Because the DEP is largely responsible for DE toxicity, reducing DEP in DE should be effective to decrease suggested health effects of DE.

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