Impact of exposure to environmental chemicals on the occurrence of molar incisor hypomineralisation and developmental enamel defects in children: a systematic review.

PURPOSE: Children are particularly susceptible to environmental toxins because of their immature metabolic and detoxification systems. Disturbances during enamel formation may result in molar incisor hypomineralisation (MIH) and developmental defects of enamel (DDE). This systematic review evaluated the association between exposure to environmental pollutants and the occurrence of MIH and DDE in children.

METHODS

The review followed PRISMA 2020 guidelines and was registered with PROSPERO (CRD420251149569). A comprehensive search of PubMed, Scopus, Embase, Ovid, EBSCO Host, and Web of Science identified observational studies published up to 2025.

RESULTS

Of 384 records identified, 9 studies met the eligibility criteria, including three cohort, one case-control, and five cross-sectional studies. Methodological quality was assessed using the Newcastle-Ottawa scale. Pollutants evaluated included polychlorinated biphenyls (PCBs), polychlorinated dibenzo-p-dioxins and furans (PCDD/Fs), per- and polyfluoroalkyl substances (PFAS), particulate matter (PM₂.₅ and PM₁₀), and phenols and phthalates. Studies investigating PCBs and PCDD/Fs generally reported positive associations between prenatal or early postnatal exposure and increased occurrence or severity of MIH and DDE. Higher dioxin concentrations in maternal milk were also associated with more frequent and severe enamel hypomineralisation, with dose-response relationships reported in some studies. Evidence regarding PFAS was congener- and sex-specific, whereas findings for ambient air pollution, phenols, and phthalates were limited and inconsistent.

CONCLUSION

Available evidence suggests an association between exposure to environmental pollutants and developmental enamel defects, particularly following exposure to persistent organic pollutants. However, heterogeneity in exposure assessment, diagnostic criteria, study design, and confounder adjustment limits the certainty of the evidence. Well-designed longitudinal studies using standardised diagnostic criteria and biomarker-based exposure assessment are needed to clarify these associations and determine potential causal relationships.