Tobacco smoking, harm reduction, and biomarkers

被引:62
作者
Shields, PG [1 ]
机构
[1] Georgetown Univ, Med Ctr, Lombardi Canc Ctr, Washington, DC 20057 USA
来源
JNCI-JOURNAL OF THE NATIONAL CANCER INSTITUTE | 2002年 / 94卷 / 19期
关键词
D O I
10.1093/jnci/94.19.1435
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
The only known way to reduce cancer risk in smokers is complete cessation, but many smokers are unable or unwilling to quit. Consequently, tobacco companies are now marketing products that purport to reduce carcinogen exposure, with the implication that such products provide a safer way to smoke. Moreover, researchers are exploring ways to reduce the amount of cigarette smoke carcinogens to which the smokers are exposed. Although these methods are, in theory beneficial, it is possible that the perceived availability of "safe" ways to smoke will cause some former smokers to resume smoking and some current smokers to delay quitting. Thus, the extent of exposure reduction and the impact on public health of these methods need to be considered carefully. However, risk reduction and its relation to exposure are not simple to estimate. The way people smoke and the way they respond to carcinogen exposure are both highly variable, as evidenced by the previous history of smokers who switched to light, or low-tar cigarettes. This can actually increase risk in some smokers. The evaluation of exposure reduction will therefore need to be multidisciplinary and include in vitro cell culture studies, animal studies, human clinical studies, and epidemiologic studies. Biomarkers will be critical for rapidly evaluating the effects of new strategies or products to reduce exposure to tobacco smoke carcinogens. No single biomarker will likely satisfy our assessment needs, and so a panel of biomarkers should be used that includes biomarkers of exposure, biologically effective dose, and potential harm. In addition, usefulness of new products will need to be tested in people of different susceptibilities (i.e., who vary in behavior, sex, age, genetics, and prior tobacco use). Even if the new products are shown to be effective at reducing lung carcinogens, they should not be used alone but rather be incorporated into a comprehensive tobacco control program.
引用
收藏
页码:1435 / 1444
页数:10
相关论文
共 150 条
[1]   GEOGRAPHIC-VARIATION OF P53 MUTATIONAL PROFILE IN NONMALIGNANT HUMAN LIVER [J].
AGUILAR, F ;
HARRIS, CC ;
SUN, T ;
HOLLSTEIN, M ;
CERUTTI, P .
SCIENCE, 1994, 264 (5163) :1317-1319
[2]  
[Anonymous], 1986, IARC MON EV CARC RIS
[3]  
[Anonymous], CLEAR SMOK ASS SCI B
[4]  
ASHURST SW, 1983, CANCER RES, V43, P1024
[5]  
Atawodi SE, 1998, CANCER EPIDEM BIOMAR, V7, P817
[6]   COMPENSATION AS A RISK FACTOR FOR LUNG-CANCER IN SMOKERS WHO SWITCH FROM NONFILTER TO FILTER CIGARETTES [J].
AUGUSTINE, A ;
HARRIS, RE ;
WYNDER, EL .
AMERICAN JOURNAL OF PUBLIC HEALTH, 1989, 79 (02) :188-191
[7]  
BADAWI AF, 1995, CANCER RES, V55, P5230
[8]   ANAPLASTIC WILMS-TUMOR, A SUBTYPE DISPLAYING POOR-PROGNOSIS, HARBORS P53 GENE-MUTATIONS [J].
BARDEESY, N ;
FALKOFF, D ;
PETRUZZI, MJ ;
NOWAK, N ;
ZABEL, B ;
ADAM, M ;
AGUIAR, MC ;
GRUNDY, P ;
SHOWS, T ;
PELLETIER, J .
NATURE GENETICS, 1994, 7 (01) :91-97
[9]   Aberrant methylation of p16INK4a is an early event in lung cancer and a potential biomarker for early diagnosis [J].
Belinsky, SA ;
Nikula, KJ ;
Palmisano, WA ;
Michels, R ;
Saccomanno, G ;
Gabrielson, E ;
Baylin, SB ;
Herman, JG .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1998, 95 (20) :11891-11896
[10]   GENETIC RISK AND CARCINOGEN EXPOSURE - A COMMON INHERITED DEFECT OF THE CARCINOGEN-METABOLISM GENE GLUTATHIONE-S-TRANSFERASE M1 (GSTM1) THAT INCREASES SUSCEPTIBILITY TO BLADDER-CANCER [J].
BELL, DA ;
TAYLOR, JA ;
PAULSON, DF ;
ROBERTSON, CN ;
MOHLER, JL ;
LUCIER, GW .
JOURNAL OF THE NATIONAL CANCER INSTITUTE, 1993, 85 (14) :1159-1164