Ji B T, Shu X O, Linet M S, Zheng W, Wacholder S, Gao Y T, Ying D M, Jin F
Division of Epidemiology, Columbia University, School of Public Health, New York, USA.
J Natl Cancer Inst. 1997 Feb 5;89(3):238-44. doi: 10.1093/jnci/89.3.238.
Cigarette smoking has been shown to increase oxidative DNA damage in human sperm cells. Assessment of the role of cigarette smoking in the etiology of childhood cancer has focused primarily on the effect of maternal smoking. Similar studies in relation to paternal smoking, however, have been inconclusive. Few studies have evaluated the effect of paternal smoking in the preconception period, and most of these could not disentangle the effects of paternal from maternal smoking.
We investigated the relationship of paternal smoking, particularly in the preconception period, with childhood cancer among offspring of the nonsmoking mothers.
We conducted a population-based, case-control study in Shanghai, People's Republic of China, where the prevalence of smoking is high among men but extremely low among women. The study included 642 childhood cancer case patients (<15 years of age) and their individually matched control subjects. Information concerning parental smoking, alcohol drinking, and other exposures of the index child was obtained by direct interview of both parents of the study subjects. Odds ratios (ORs), derived from conditional logistic regression models, were used to measure the association between paternal smoking and risk of childhood cancers.
Paternal preconception smoking was related to a significantly elevated risk of childhood cancers, particularly acute leukemia and lymphoma. The risks rose with increasing pack-years of paternal preconception smoking for acute lymphocytic leukemia (ALL) (P for trend = .01), lymphoma (P for trend = .07), and total cancer (P for trend = .006). Compared with children whose fathers had never smoked cigarettes, children whose fathers smoked more than five pack-years prior to their conception had adjusted ORs of 3.8 (95% confidence interval [CI] = 1.3-12.3) for ALL, 4.5 (95% CI = 1.2-16.8) for lymphoma, 2.7 (95% CI = 0.8-9.9) for brain tumors, and 1.7 (95% CI = 1.2-2.5) for all cancers combined. Statistically significant increased risks of cancer were restricted to children under the age of 5 years at diagnosis or those whose fathers had smoked during all of the 5 years prior to conception.
Further studies are needed to confirm the association of paternal smoking with increased risk of cancer in offspring, to clarify the pattern of risks in relation to the timing of cigarette smoking, and to elucidate the biologic mechanism involved in predisposing the offspring to cancer. For example, it may be that paternal smoking induces prezygotic genetic damage that, in turn, acts as the predisposing factor.
已有研究表明，吸烟会增加人类精子细胞中的氧化性DNA损伤。关于吸烟在儿童癌症病因学中的作用评估主要集中在母亲吸烟的影响上。然而，关于父亲吸烟的类似研究尚无定论。很少有研究评估父亲在受孕前吸烟的影响，而且其中大多数研究无法区分父亲吸烟与母亲吸烟的影响。
我们研究了父亲吸烟，尤其是受孕前吸烟，与不吸烟母亲后代儿童癌症之间的关系。
我们在中国上海进行了一项基于人群的病例对照研究，该地男性吸烟率高而女性吸烟率极低。该研究纳入了642例儿童癌症病例患者（年龄<15岁）及其个体匹配的对照对象。通过直接访谈研究对象的父母双方，获取有关父母吸烟、饮酒及指数儿童的其他暴露情况的信息。采用条件逻辑回归模型得出的比值比（OR）来衡量父亲吸烟与儿童癌症风险之间的关联。
父亲受孕前吸烟与儿童癌症风险显著升高有关，尤其是急性白血病和淋巴瘤。急性淋巴细胞白血病（ALL）（趋势P值=0.01）、淋巴瘤（趋势P值=0.07）和所有癌症（趋势P值=0.006）的风险随着父亲受孕前吸烟包年数的增加而上升。与父亲从不吸烟的儿童相比，父亲在受孕前吸烟超过5包年的儿童，ALL的调整后OR为3.8（95%置信区间[CI]=1.3 - 12.3），淋巴瘤为4.5（95%CI = 1.2 - 16.8），脑肿瘤为2.7（95%CI = 0.8 - 9.9），所有癌症合并为1.7（95%CI = 1.2 - 2.5）。癌症风险在统计学上显著增加仅限于诊断时年龄小于5岁的儿童或其父亲在受孕前的所有5年中都吸烟的儿童。
需要进一步研究来证实父亲吸烟与后代癌症风险增加之间的关联，阐明与吸烟时间相关的风险模式，并阐明使后代易患癌症的生物学机制。例如，可能是父亲吸烟诱导了合子前遗传损伤，进而成为易感因素。
