AIRBORNE CARCINOGENS

被引:21
作者
LEWTAS, J
机构
[1] Health Effects Research Laboratory, U.S. Environmental Protection Agency, North Carolina, 27711, MD 68A, Research Triangle Park
来源
PHARMACOLOGY & TOXICOLOGY | 1993年 / 72卷
关键词
D O I
10.1111/j.1600-0773.1993.tb01670.x
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
Air pollution has been recognized as a cancer risk for many years. More than 2,800 different chemicals have been identified in the air or emission sources. Only about 10% of these chemicals have been evaluated in bioassays for genetic or carcinogenic effects. Hydrocarbons, nitrogen-containing organics, and halogenated organics account for nearly 60% of the airborne chemicals that have been studied in long term animal cancer bioassays or short-term genetic bioassays. The sources that emit the highest number of these potentially carcinogenic chemicals are sources involving combustion (e.g., tobacco smoke, automobile exhaust, and coal combustion). Quantitative estimates of the risk of airborne carcinogens in outdoor air consistently show that polycyclic organic matter (POM) from products of incomplete combustion (PICs) make the largest single contribution to human cancer risk. Although the POM emissions from various air pollution sources are chemically similar and induce cancer by a similar genotoxic mechanism, the cancer risk per unit of exposure of these emissions may vary by several orders of magnitude. Among these combustion sources motor vehicle emissions account for the greatest cancer risk in outdoor air. Environmental tobacco smoke (ETS) and radon are the major sources of cancer risk from indoor exposures. There are, however, many uncertainties in identifying the important airborne carcinogens and quantitating the human cancer risk of air pollution. One important uncertainty is the role of atmospheric transformation products in human cancer.
引用
收藏
页码:S55 / S63
页数:9
相关论文
共 44 条
[31]  
TOMATIS L, 1990, AIR POLLUTION HUMAN, P86
[32]  
VARMUS H, 1989, ONCOGENES MOL ORIGIN
[33]   THE GENE-TOX PROGRAM - GENETIC-ACTIVITY EVALUATION [J].
WATERS, MD ;
AULETTA, A .
JOURNAL OF CHEMICAL INFORMATION AND COMPUTER SCIENCES, 1981, 21 (01) :35-38
[34]   MITOGENESIS IS ONLY ONE FACTOR IN CARCINOGENESIS [J].
WEINSTEIN, IB .
SCIENCE, 1991, 251 (4992) :387-388
[35]   RESPONSE OF EXPERIMENTAL-ANIMALS TO HUMAN CARCINOGENS - AN ANALYSIS BASED UPON THE IARC MONOGRAPHS PROGRAM [J].
WILBOURN, J ;
HAROUN, L ;
HESELTINE, E ;
KALDOR, J ;
PARTENSKY, C ;
VAINIO, H .
CARCINOGENESIS, 1986, 7 (11) :1853-1863
[36]   MULTISTAGE CARCINOGENESIS - IMPLICATIONS FOR RISK-ESTIMATION [J].
YAMASAKI, H .
CANCER AND METASTASIS REVIEWS, 1988, 7 (01) :5-18
[37]  
1989, IARC MONOGRAPHS EVAL, V46
[38]  
1992, SAB EPA600690006B OF
[39]  
1990, EPA450190004 OFF AIR
[40]  
1986, FED REGISTER, V51, P33992