Perera F P
Columbia University School of Public Health, Division of Environmental Health Sciences, New York, NY 10032, USA.
J Natl Cancer Inst. 1996 Apr 17;88(8):496-509. doi: 10.1093/jnci/88.8.496.
Recent molecular epidemiologic research provides compelling new evidence that environmental factors are major contributors to human cancer and that their risks are strongly influenced by genetic and acquired susceptibility. In particular, molecular epidemiology has demonstrated substantial variability in biologic response to carcinogens and suggests that certain groups-such as the very young, those with predisposing genetic traits or nutritional deficits, and even certain ethnic groups-are likely to have greater risk from selected exposures than other members of the population. This work implies that major gains in prevention of cancer, which will claim more than 554 000 American lives this year, will necessitate health and regulatory policies that protect these more susceptible groups and individuals from risks of man-made and naturally occurring environmental carcinogens. The specific implication from this research is that, to be effective in prevention, risk assessments developed in support of these policies by regulatory bodies, such as the Environmental Protection Agency, should reflect the available scientific data on individual variability in both exposure and susceptibility.
最近的分子流行病学研究提供了令人信服的新证据，表明环境因素是人类癌症的主要促成因素，并且其风险受到遗传易感性和后天易感性的强烈影响。特别是，分子流行病学已经证明了对致癌物的生物学反应存在很大差异，并表明某些群体——如非常年幼的人、具有遗传易感性特征或营养缺乏的人，甚至某些种族群体——可能比其他人群更容易因特定暴露而面临更大风险。这项工作意味着，预防癌症（今年将夺去超过55.4万美国人的生命）取得重大进展将需要制定健康和监管政策，以保护这些更易受影响的群体和个人免受人为和自然环境致癌物的风险。这项研究的具体含义是，为了有效预防，监管机构（如环境保护局）为支持这些政策而开展的风险评估应反映有关暴露和易感性个体差异的现有科学数据。
