Tipping the Balance of Autism Risk: Potential Mechanisms Linking Pesticides and Autism

被引:112
作者
Shelton, Janie F. [1 ]
Hertz-Picciotto, Irva [1 ,2 ]
Pessah, Isaac N. [2 ,3 ]
机构
[1] Univ Calif Davis, Dept Publ Hlth Sci, Grad Grp Epidemiol, Davis, CA 95616 USA
[2] UC Davis Med Invest Neurodev Disorders MIND Inst, Sacramento, CA USA
[3] Univ Calif Davis, Dept Mol Biosci, Davis, CA 95616 USA
关键词
autism spectrum disorders; carbamate; gene-environment interaction; immune; mitochondria; neuroexcitation; organochlorine; organophosphate; oxidative stress; pesticide; pyrethroid; DE-NOVO MUTATIONS; ORGANOCHLORINE PESTICIDES; CHLORPYRIFOS EXPOSURE; DEVELOPMENTAL NEUROTOXICITY; MITOCHONDRIAL DYSFUNCTION; SPECTRUM DISORDERS; PERINATAL EXPOSURE; PRENATAL EXPOSURE; PARAOXONASE PON1; OXIDATIVE STRESS;
D O I
10.1289/ehp.1104553
中图分类号
X [环境科学、安全科学];
学科分类号
083001 [环境科学];
摘要
BACKGROUND: Autism spectrum disorders (ASDs) have been increasing in many parts of the world and a portion of cases are attributable to environmental exposures. Conclusive replicated findings have yet to appear on any specific exposure; however, mounting evidence suggests gestational pesticides exposures are strong candidates. Because multiple developmental processes are implicated in ASDs during gestation and early life, biological plausibility is more likely if these agents can be shown to affect core pathophysiological features. OBJECTIVES: Our objectives were to examine shared mechanisms between autism pathophysiology and the effects of pesticide exposures, focusing on neuroexcitability, oxidative stress, and immune functions and to outline the biological correlates between pesticide exposure and autism risk. METHODS: We review and discuss previous research related to autism risk, developmental effects of early pesticide exposure, and basic biological mechanisms by which pesticides may induce or exacerbate pathophysiological features of autism. DISCUSSION: On the basis of experimental and observational research, certain pesticides may be capable of inducing core features of autism, but little is known about the timing or dose, or which of various mechanisms is sufficient to induce this condition. CONCLUSIONS: In animal studies, we encourage more research on gene x environment interactions, as well as experimental exposure to mixtures of compounds. Similarly, epidemiologic studies in humans with exceptionally high exposures can identify which pesticide classes are of greatest concern, and studies focused on gene x environment are needed to determine if there are susceptible subpopulations at greater risk from pesticide exposures.
引用
收藏
页码:944 / 951
页数:8
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