Kristensen P, Andersen A, Irgens L M, Bye A S, Vagstad N
National Institute of Occupational Health, Oslo, Norway.
Cancer Epidemiol Biomarkers Prev. 1996 Jan;5(1):3-9.
Testicular cancer incidence is increasing rapidly in several countries. Environmental causes acting early in life are suspected but have not yet been identified. We conducted a cohort study to identify parental risk factors for testicular cancer among farmers' sons. Children born in 1952-1991 to parents who were farm holders at the time of the agricultural censuses in 1969-1989 were identified in the Central Population Register (Oslo, Norway). The resulting cohort of male offspring (n = 166,291) were followed up in the Cancer Registry of Norway (Oslo, Norway) for 1965-1991. Exposure indicators were derived from census information on activities on the farm. The cancer incidence was compared with that of the total rural population, and potential risk factors were analyzed by Poisson regression. In a follow-up of 2,924,663 person-years, 158 incident cases of testicular cancer were identified. The study population had a higher incidence of testicular cancer than did the total rural population, particularly at ages 15-19 years and in western Norway. Specific fertilizer regimens on the farm were associated with testicular cancer (rate ratio = 2.44; 95% confidence interval = 1.66-3.56), in particular nonseminoma (rate ratio = 4.21; 95% confidence interval = 2.13-8.32). The rate ratio estimates were highest for boys ages 15-19 years and for a subset of study subjects who were considered more likely to have grown up on a farm. Nondifferential misclassification and bias toward unity are likely because exposure information was available only at the farm level and only for census years. The fertilizer indicators were not available early in life for most subjects, and precise interpretations are difficult. A hypothesis worth considering is that excess nutrient run-off from agriculture constitutes a risk. However, inferences concerning the biological basis of our observations can scarcely be made.
在一些国家,睾丸癌的发病率正在迅速上升。人们怀疑生命早期的环境因素是病因,但尚未确定。我们进行了一项队列研究,以确定农民儿子患睾丸癌的父母风险因素。在挪威中央人口登记处(奥斯陆,挪威)中识别出1969 - 1989年农业普查时为农场主的父母在1952 - 1991年所生的子女。由此产生的男性后代队列(n = 166,291)于1965 - 1991年在挪威癌症登记处(奥斯陆,挪威)进行随访。暴露指标来自关于农场活动的普查信息。将癌症发病率与整个农村人口的发病率进行比较,并通过泊松回归分析潜在风险因素。在2,924,663人年的随访中,识别出158例睾丸癌新发病例。研究人群的睾丸癌发病率高于整个农村人口,特别是在15 - 19岁年龄段以及挪威西部。农场特定的施肥方案与睾丸癌相关(率比 = 2.44;95%置信区间 = 1.66 - 3.56),尤其是非精原细胞瘤(率比 = 4.21;95%置信区间 = 2.13 - 8.32)。对于15 - 19岁的男孩以及被认为更有可能在农场长大的一部分研究对象,率比估计值最高。由于暴露信息仅在农场层面且仅针对普查年份可用,所以可能存在无差异错误分类和向一致性的偏差。大多数研究对象在生命早期无法获得施肥指标信息,因此难以进行精确解释。一个值得考虑的假设是农业中过量的养分径流构成风险。然而,几乎无法对我们观察结果的生物学基础进行推断。