Trivers Katrina F, Mertens Ann C, Ross Julie A, Steinbuch Michael, Olshan Andrew F, Robison Leslie L
Department of Epidemiology, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599-7435, USA.
Paediatr Perinat Epidemiol. 2006 Mar;20(2):110-8. doi: 10.1111/j.1365-3016.2006.00700.x.
The aetiology of childhood acute myeloid leukaemia (AML) is largely unknown. Maternal marijuana use just before, or during pregnancy has been previously associated with childhood AML. This case-control investigation formally tested the hypothesis that parental marijuana use increases the risk of childhood AML in offspring. Incident cases of AML <18 years of age, diagnosed between 1989 and 1993, and registered with the Children's Cancer Group (a paediatric clinical co-operative group), were eligible for inclusion. Control children were selected via random digit dialling and individually matched 1:1 to cases on age, race and residential location, except for rare morphological subtypes that were matched 1:2. Parental telephone interviews were conducted to determine exposure and covariate information. Conditional logistic regression was used to estimate matched odds ratios (OR) and 95% confidence intervals [CI] adjusted for household income, parental education and parental age. The analysis included 517 cases and 610 matched controls. A series of sensitivity analyses examined the potential for recall bias. Ever lifetime use of marijuana by mothers was not associated with childhood AML [OR = 0.89; 95% CI = 0.66, 1.19]. Maternal marijuana use any time during the 3 months before, or during pregnancy was inversely associated with childhood AML [OR = 0.43; 95% CI = 0.23, 0.80]. Paternal use during the same time period was not associated with risk. Assuming a large degree of differential exposure misclassification was present, the corrected ORs ranged between 0.82 and 1.40. The previously reported positive association between maternal marijuana use before or during pregnancy and childhood AML was not confirmed. The decreased ORs observed in this study may be due to recall bias assuming plausibly low values of sensitivity.
儿童急性髓细胞白血病（AML）的病因在很大程度上尚不清楚。此前有研究表明，母亲在怀孕前或怀孕期间吸食大麻与儿童AML有关。本病例对照研究正式检验了父母吸食大麻会增加后代患儿童AML风险这一假设。1989年至1993年间确诊的18岁以下AML发病病例，并在儿童癌症组（一个儿科临床合作组）登记的，符合纳入条件。对照儿童通过随机数字拨号选择，并按年龄、种族和居住地点与病例进行1:1个体匹配，但罕见形态学亚型为1:2匹配。通过对父母进行电话访谈来确定暴露情况和协变量信息。采用条件逻辑回归来估计匹配比值比（OR）和针对家庭收入、父母教育程度和父母年龄进行调整的95%置信区间[CI]。分析包括517例病例和610例匹配对照。一系列敏感性分析检验了回忆偏倚的可能性。母亲终生吸食大麻与儿童AML无关[OR = 0.89；95% CI = 0.66, 1.19]。母亲在怀孕前3个月或怀孕期间任何时候吸食大麻与儿童AML呈负相关[OR = 0.43；95% CI = 0.23, 0.80]。同一时期父亲吸食大麻与风险无关。假设存在大量差异暴露错误分类，校正后的OR值在0.82至1.40之间。先前报道的母亲在怀孕前或怀孕期间吸食大麻与儿童AML之间的正相关未得到证实。本研究中观察到的OR值降低可能是由于假设敏感性值合理较低时的回忆偏倚所致。
