Abstract：
Autism spectrum disorder (ASD) is a developmental disorder with symptoms that range from social and communication impairments to restricted interests and repetitive behavior and is the 4th most disabling condition for children aged 5-14. Risk factors of ASD are not fully understood. Environmental risk factors are believed to play a significant role in the ASD epidemic. Research focusing on air pollution exposure as an early-life risk factor of autism is growing, with numerous studies finding associations of traffic and industrial emissions with an increased risk of ASD. One of the possible mechanisms linking autism and air pollution exposure is metabolic dysfunction. However, there were no consensus about the key metabolic pathways and corresponding metabolite signatures in mothers and children that are altered by air pollution exposure and cause the ASD. Therefore, we performed a review of published papers examining the metabolomic signatures and metabolic pathways that are associated with either air pollution exposure or ASD risk in human studies. In conclusion, we found that dysregulated lipid, fatty acid, amino acid, neurotransmitter, and microbiome metabolisms are associated with both short-term and long-term air pollution exposure and the risk of ASD. These dysregulated metabolisms may provide insights into ASD etiology related to air pollution exposure, particularly during the perinatal period in which neurodevelopment is highly susceptible to damage from oxidative stress and inflammation.
摘要：
自闭症谱系障碍（ASD）是一种发育障碍，其症状范围从社交和沟通障碍到兴趣受限和重复行为，是5-14岁儿童的第四大致残疾病。ASD的危险因素尚未完全了解。环境风险因素被认为在ASD流行中起着重要作用。关注空气污染暴露作为自闭症早期风险因素的研究正在增长，大量研究发现交通和工业排放与ASD风险增加有关。将自闭症与空气污染暴露联系起来的可能机制之一是代谢功能障碍。然而,对于因暴露于空气污染而改变并导致ASD的母亲和儿童的关键代谢途径和相应的代谢物特征,目前尚无共识.因此,我们对已发表的研究人体研究中与空气污染暴露或ASD风险相关的代谢组学特征和代谢途径的论文进行了综述.总之,我们发现脂质失调，脂肪酸，氨基酸,神经递质,微生物组代谢与短期和长期空气污染暴露以及ASD风险相关。这些失调的代谢可能提供有关空气污染暴露的ASD病因的见解。特别是在围产期，神经发育极易受到氧化应激和炎症的损害。
