Birth defects research · 2026
Food-Borne Environmental Contaminants, Intestinal Injury, and Early Childhood Stunting: A Developmental Toxicology Perspective.
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Zhang Tian Kai, Qu Yan Xia, Li Jian Lin, Wang Jing Han, Ren Xing Long, Lu Zhi Tao
Аннотация
BACKGROUND: Childhood stunting (height-for-age z-score < -2 SD) remains a global developmental health burden. Traditional interventions centered on nutrition and infection have reached a bottleneck. Emerging evidence identifies chronic low-dose dietary environmental toxins as an independent, modifiable risk factor for early-life growth restriction.
METHODS: This review synthesizes cohort studies, meta-analyses, and in vivo toxicological models published over the past decade to characterize exposures to mycotoxins, toxic heavy metals, and food-borne endocrine disruptors that are closely associated with stunting.
RESULTS: Multi-layered mechanisms are elucidated, including environmental enteric dysfunction (EED), intestinal barrier disruption, persistent subclinical inflammation, GH-IGF-1 axis disturbance, gut microbiota dysbiosis, oxidative stress, and epigenetic alterations, which collectively impair linear growth. Critical surveillance gaps are identified, and integrated environment-nutrition-infection intervention strategies aligned with public health practice are proposed.
CONCLUSIONS: Dietary environmental toxins cause irreversible developmental deficits by damaging intestinal function and disrupting endocrine regulation. Strengthening developmental toxicology-oriented monitoring and source control will support precise prevention of early childhood stunting within the critical first 1000-day window.
METHODS: This review synthesizes cohort studies, meta-analyses, and in vivo toxicological models published over the past decade to characterize exposures to mycotoxins, toxic heavy metals, and food-borne endocrine disruptors that are closely associated with stunting.
RESULTS: Multi-layered mechanisms are elucidated, including environmental enteric dysfunction (EED), intestinal barrier disruption, persistent subclinical inflammation, GH-IGF-1 axis disturbance, gut microbiota dysbiosis, oxidative stress, and epigenetic alterations, which collectively impair linear growth. Critical surveillance gaps are identified, and integrated environment-nutrition-infection intervention strategies aligned with public health practice are proposed.
CONCLUSIONS: Dietary environmental toxins cause irreversible developmental deficits by damaging intestinal function and disrupting endocrine regulation. Strengthening developmental toxicology-oriented monitoring and source control will support precise prevention of early childhood stunting within the critical first 1000-day window.