Van Larebeke Nicolas A, Birnbaum Linda S, Boogaerts Marc A, Bracke Marc, Davis Devra Lee, Demarini David M, Hooper Kim, Huff James, Kleinjans Jos C, Legator Marvin S, Schoeters Greet, Vähäkangas Kirsi
Study Center for Carcinogenesis and Primary Prevention of Cancer, Ghent University, Ghent, Belgium.
Int J Occup Environ Health. 2005 Apr-Jun;11(2):199-201. doi: 10.1179/oeh.2005.11.2.199.
Epidemiologic methods only seldom identify causes of childhood cancer associated with relative risks below a factor of 1 1/2-2. Children are at risk of exposure to over 15,000 high-production-volume chemicals and are certainly exposed to many carcinogens. The individual impacts of most of these agents are too small to be detected, but collectively these unrecognized factors are potentially important. Infants and children are exposed to higher levels of some environmental toxicants and may also be more sensitive. During intrauterine development and childhood, cells divide frequently, and the mutant frequency rises rapidly. Endocrine-related cancers or susceptibility to cancer may result from developmental exposures rather than from exposures existing at or near the time of diagnosis. That environmental exposures may be important causes of childhood cancers is indicated by associations of enzyme polymorphisms with risk.
流行病学方法很少能识别出相对风险低于1.5至2倍的儿童癌症病因。儿童面临接触超过15000种高产量化学品的风险,并且肯定接触过许多致癌物。这些物质中的大多数对个体的影响太小而无法检测到,但这些未被认识到的因素总体上可能很重要。婴儿和儿童接触某些环境毒物的水平较高,而且可能也更敏感。在子宫内发育和儿童期,细胞频繁分裂,突变频率迅速上升。与内分泌相关的癌症或癌症易感性可能源于发育过程中的接触,而非诊断时或诊断前后存在的接触。酶多态性与风险的关联表明,环境接触可能是儿童癌症的重要病因。