Autism spectrum disorder (ASD) has emerged as a major public health concern due to its fast-growing prevalence in recent decades. Environmental factors are thought to contribute substantially to the variance in ASD. Interest in environmental toxins as causes of ASD has arisen due to the high sensitivity of the developing human brain to toxic chemicals, particularly to dioxin and certain dioxin-like compounds (dioxins). As a group of typical persistent organic pollutants, dioxins have been found to exert adverse effects on human brain development. In this paper, we review the evidence for association of exposure to dioxins with neurodevelopmental abnormalities related to ASD based on both human epidemiological and animal studies. It has been documented that exposure to dioxins during critical developmental periods increased risk for ASD. This notion has been demonstrated in different populations exposed to high or background level of dioxins. Furthermore, the effects and mechanisms of action of dioxins relevant to the pathophysiology and pathogenesis of ASD are summarized, describing potential underlying mechanisms linking dioxin exposure with ASD onset. Further studies focusing on effects of prenatal/perinatal exposure to individual dioxin congeners or to mixtures of dioxins on ASD-associated behavioral and neurobiological consequences in animal models, and on the mechanisms of actions of dioxins, are needed in order to better understand how dioxin exposure might contribute to increased risk for ASD.

自闭症谱系障碍（ASD）由于最近几十年的快速流行而已成为主要的公共卫生问题。环境因素被认为是对ASD差异的重要贡献。由于发展中的人类大脑对有毒化学物质（特别是对二恶英和某些二恶英类化合物（二恶英））的高度敏感性，引起人们对引起ASD的环境毒素的关注。作为一组典型的持久性有机污染物，已发现二恶英对人脑发育产生不利影响。在本文中，我们根据人类流行病学和动物研究综述了二恶英暴露与与ASD相关的神经发育异常相关的证据。有文献证明，在关键的发育时期接触二恶英会增加ASD的风险。这一概念已在暴露于高或背景二恶英水平的不同人群中得到了证明。此外，总结了ASD的发病机理，描述了将二恶英暴露与ASD发作联系起来的潜在潜在机制。为了更好地了解二恶英如何暴露，需要进一步研究集中在产前/围产期暴露于单独的二恶英同类物或二恶英混合物对动物模型中与ASD相关的行为和神经生物学后果，以及二恶英的作用机制。可能会增加ASD的风险。