Overview
Jocsak and co-authors reviewed mechanisms by which environmental endocrine disruptors (EDCs), including lead, cadmium, arsenic, manganese, and mercury, disrupt synaptic plasticity and contribute to cognitive and behavioral dysfunction. The review identifies five mechanistic axes: receptor-mediated disruption, calcium signaling disruption, oxidative stress and mitochondrial dysfunction, epigenetic reprogramming, and network-level and barrier dysfunction. This is a mechanistic review without primary food concentration data.
Key findings
Lead disrupts calcium ion homeostasis and alters the balance between long-term potentiation and long-term depression. Arsenic alters glutamatergic transmission. Cadmium disrupts calcium signaling at neuronal membranes. Manganese disrupts dopaminergic signaling. Mercury causes mitochondrial dysfunction in neurons. The review notes that heavy metals are among the most environmentally prevalent EDCs and that prenatal exposure during sensitive developmental windows is particularly damaging. Effects can be transgenerational via epigenetic mechanisms.
Methods (brief)
Narrative review. No primary experiment. Evidence class: mechanistic review; no food concentration data applicable to contamination profiling.
Evidence fitness
Supports: mechanistic context for why lead, arsenic, cadmium, manganese, and mercury are toxicologically significant at the nervous system level; relevant to the toxicology sections of metal pages. Does not support: food occurrence values, dose-response thresholds, or regulatory limit derivation.
Related evidence
Update history
No substantive edit history is available in this build. The full commit record is available in git.