Kalkbrenner Amy E, Schmidt Rebecca J, Penlesky Annie C
Zilber School of Public Health, University of Wisconsin-Milwaukee, Milwaukee, WI.
Department of Public Health Sciences, University of California Davis School of Medicine, Davis, CA; Medical Investigation of Neurodevelopmental Disorders (MIND) Institute, University of California Davis, Sacramento, CA.
Curr Probl Pediatr Adolesc Health Care. 2014 Nov;44(10):277-318. doi: 10.1016/j.cppeds.2014.06.001. Epub 2014 Sep 5.
In the past decade, the number of epidemiological publications addressing environmental chemical exposures and autism has grown tremendously. These studies are important because it is now understood that environmental factors play a larger role in causing autism than previously thought and because they address modifiable risk factors that may open up avenues for the primary prevention of the disability associated with autism. In this review, we covered studies of autism and estimates of exposure to tobacco, air pollutants, volatile organic compounds and solvents, metals (from air, occupation, diet, dental amalgams, and thimerosal-containing vaccines), pesticides, and organic endocrine-disrupting compounds such as flame retardants, non-stick chemicals, phthalates, and bisphenol A. We included studies that had individual-level data on autism, exposure measures pertaining to pregnancy or the 1st year of life, valid comparison groups, control for confounders, and adequate sample sizes. Despite the inherent error in the measurement of many of these environmental exposures, which is likely to attenuate observed associations, some environmental exposures showed associations with autism, especially traffic-related air pollutants, some metals, and several pesticides, with suggestive trends for some volatile organic compounds (e.g., methylene chloride, trichloroethylene, and styrene) and phthalates. Whether any of these play a causal role requires further study. Given the limited scope of these publications, other environmental chemicals cannot be ruled out, but have not yet been adequately studied. Future research that addresses these and additional environmental chemicals, including their most common routes of exposures, with accurate exposure measurement pertaining to several developmental windows, is essential to guide efforts for the prevention of the neurodevelopmental damage that manifests in autism symptoms.
在过去十年中,探讨环境化学物质暴露与自闭症关系的流行病学出版物数量大幅增长。这些研究很重要,因为现在人们认识到环境因素在自闭症成因中所起的作用比之前认为的更大,还因为它们涉及可改变的风险因素,这可能为自闭症相关残疾的一级预防开辟途径。在本综述中,我们涵盖了关于自闭症的研究以及对烟草、空气污染物、挥发性有机化合物和溶剂、金属(来自空气、职业、饮食、牙科汞合金和含硫柳汞疫苗)、农药以及有机内分泌干扰化合物(如阻燃剂、不粘化学品、邻苯二甲酸盐和双酚A)暴露的估计。我们纳入了具备以下条件的研究:有关于自闭症的个体层面数据、与孕期或生命第一年相关的暴露测量方法、有效的对照组、对混杂因素的控制以及足够的样本量。尽管许多此类环境暴露测量存在固有误差,这可能会削弱观察到的关联,但一些环境暴露显示出与自闭症有关联,尤其是与交通相关的空气污染物、某些金属和几种农药,一些挥发性有机化合物(如二氯甲烷、三氯乙烯和苯乙烯)以及邻苯二甲酸盐也有提示性趋势。这些因素是否起因果作用需要进一步研究。鉴于这些出版物的范围有限,不能排除其他环境化学物质,但尚未对其进行充分研究。未来针对这些及其他环境化学物质的研究,包括其最常见的暴露途径,并针对多个发育阶段进行准确的暴露测量,对于指导预防自闭症症状所表现出的神经发育损伤的努力至关重要。