Council for Nutritional and Environmental Medicine (CONEM), Toften 24, Mo i Rana, 8610, Norway.
Department of Nutritional and Environmental Medicine, HP Medical Center, Bangkok 10540, Thailand.
Curr Med Chem. 2024;31(13):1620-1633. doi: 10.2174/0929867330666230409135310.
Lead (Pb) does not have any biological function in a human, and it is likely no safe level of Pb in the human body. The Pb exposure impacts are a global concern for their potential neurotoxic consequences. Despite decreasing both the environmental Pb levels and the average blood Pb levels in the survey populations, the lifetime redistribution from the tissues-stored Pb still poses neurotoxic risks from the low-level exposure in later life. The growing fetus and children hold their innate high-susceptible to these Pb-induced neurodevelopmental and neurobehavioral effects.
This article aims to evaluate cumulative studies and insights on the topic of Pb neurotoxicology while assessing the emerging trends in the field.
The Pb-induced neurochemical and neuro-immunological mechanisms are likely responsible for the high-level Pb exposure with the neurodevelopmental and neurobehavioral impacts at the initial stages. Early-life Pb exposure can still produce neurodegenerative consequences in later life due to the altered epigenetic imprints and the ongoing endogenous Pb exposure. Several mechanisms contribute to the Pb-induced neurotoxic impacts, including the direct neurochemical effects, the induction of oxidative stress and inflammation through immunologic activations, and epigenetic alterations. Furthermore, the individual nutritional status, such as macro-, micro-, or antioxidant nutrients, can significantly influence the neurotoxic impacts even at low-level exposure to Pb.
The prevention of early-life Pb exposure is, therefore, the critical determinant for alleviating various Pb-induced neurotoxic impacts across the different age groups.
铅(Pb)在人体内没有任何生物学功能,人体中可能不存在安全的 Pb 含量。Pb 暴露的影响是一个全球性的问题,因为它可能会产生潜在的神经毒性后果。尽管环境中的 Pb 水平和调查人群中的平均血 Pb 水平都在下降,但从组织中储存的 Pb 进行的终生再分布仍会对以后的低水平暴露造成神经毒性风险。不断发育的胎儿和儿童对这些由 Pb 引起的神经发育和神经行为影响具有先天的高易感性。
本文旨在评估 Pb 神经毒理学领域的累积研究和见解,同时评估该领域的新兴趋势。
Pb 诱导的神经化学和神经免疫机制可能是造成高水平 Pb 暴露导致神经发育和神经行为影响的原因,这些影响发生在初始阶段。由于表观遗传印记的改变和持续的内源性 Pb 暴露,早期生命 Pb 暴露仍可能在以后的生活中产生神经退行性后果。几个机制导致 Pb 诱导的神经毒性影响,包括直接的神经化学影响、通过免疫激活诱导的氧化应激和炎症,以及表观遗传改变。此外,个体的营养状况,如宏量、微量或抗氧化营养素,即使在低水平 Pb 暴露下,也能显著影响神经毒性影响。
因此,预防早期生命 Pb 暴露是减轻不同年龄段各种 Pb 诱导的神经毒性影响的关键决定因素。