Department of Epidemiology, Columbia University Mailman School of Public Health, New York, NY, United States.
Neurotoxicol Teratol. 2013 Jul-Aug;38:1-5. doi: 10.1016/j.ntt.2013.04.001. Epub 2013 Apr 13.
Recent research emphasizes the contribution of environmental as well as genetic factors to the etiology of autism but studies testing associations between chemical exposures and autism have been limited. Prenatal exposure to persistent organic pollutants (POPs) has previously been associated with decrements in cognitive and developmental performance. We conducted a pilot study in the Finnish Prenatal Study of Autism (FiPS-A). Seventy-five cases with autism and 75 controls matched on sex, birth year, urbanization and maternal age were sampled from first-born children in the Finnish Maternity Cohort, which includes over 1million births. The study sample included births occurring from 1991 to 2000. Subjects were followed up for autism through 2007. DDT, DDE, PCB-118, PCB-138, PCB-153, PCB-156, PCB-170, PCB-180, hexachlorobenzene, and BDE-47 were measured in archived maternal serum samples taken during pregnancy using gas chromatography-high resolution mass spectrometry. Correlations between pollutant measures were assessed and mechanistically-related weighting schemes for summarizing PCB levels were compared. Case and control differences were assessed using graphical and statistical methods. All analytes, with the exception of DDT and BDE-47, were detected above the limit of quantification in all samples. The correlation between levels of individual PCB congeners and weighted summary measures was high (0.71-1.00). Paired t-tests revealed no significant differences between cases and controls for log-transformed mean values of any analyte; however, in an adjusted model the odds ratios for autism were 1.91 (p=0.29) and 1.79 (p=0.36) respectively, for subjects with total PCBs and DDE above the 90th percentile of control values. Levels of prenatal PCB exposure in FIPS-A were similar to the levels which previously correlated with poorer neurodevelopmental measures in other populations. Further study in a larger sample will be required to fully determine whether exposure to high POP levels is associated with autism diagnosis in the population.
最近的研究强调了环境和遗传因素对自闭症病因的贡献,但测试化学暴露与自闭症之间关联的研究一直受到限制。先前有研究表明,产前持续性有机污染物 (POPs) 暴露与认知和发育表现下降有关。我们在芬兰自闭症产前研究 (FiPS-A) 中进行了一项试点研究。从芬兰母婴队列的初生子中抽取了 75 例自闭症病例和 75 例性别、出生年份、城市化程度和母亲年龄相匹配的对照组。该研究样本包括 1991 年至 2000 年出生的婴儿。通过 2007 年对自闭症进行随访。在妊娠期间使用气相色谱-高分辨率质谱法从存档的母体血清样本中测量了滴滴涕、DDE、PCB-118、PCB-138、PCB-153、PCB-156、PCB-170、PCB-180、六氯苯和 BDE-47。评估了污染物测量之间的相关性,并比较了用于总结 PCB 水平的机制相关加权方案。使用图形和统计方法评估病例和对照组之间的差异。除了滴滴涕和 BDE-47 之外,所有分析物在所有样本中的定量限以上均有检出。单个 PCB 同系物水平与加权汇总测量之间的相关性很高(0.71-1.00)。配对 t 检验显示,在任何分析物的对数转换平均值方面,病例和对照组之间没有显著差异;然而,在调整后的模型中,对于总 PCBs 和 DDE 高于对照组值第 90 百分位数的个体,自闭症的比值比分别为 1.91(p=0.29)和 1.79(p=0.36)。FIPS-A 中的产前 PCB 暴露水平与先前与其他人群中较差的神经发育测量相关的水平相似。在更大的样本中进一步研究将需要确定人群中高水平 POP 暴露是否与自闭症诊断有关。