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Dietary microplastic exposure and lip–oral cavity cancer: a global ecological analysis with pre-specified spatial econometric sensitivity
Original title: Dietary microplastic exposure and lip–oral cavity cancer: a global ecological analysis with pre-specified spatial econometric sensitivity
Summary
Researchers looked at whether countries with higher estimated microplastic intake from food also had higher rates of mouth and lip cancer, but once they accounted for how nearby countries tend to share similar data patterns (a statistical checkpoint called spatial analysis), the link disappeared. In other words, this study doesn't show that microplastics in your diet cause oral cancer—it's more of an early clue that points scientists toward further research, not a reason to panic about your food right now.
To assess whether estimated dietary microplastic (MP) intake is linked to age-standardized lip and oral cavity cancer rates at the country level, independent of smoking, alcohol, socioeconomic status, and urbanization, we conducted a cross-sectional ecological study across 106 countries (2020 anchor year). While testing for effect modification by smoking, dietary MP intake showed a non-linear association with lip-oral cavity cancer incidence in unadjusted spline models. Smoking prevalence and urbanization were also positive predictors, although the evidence was inconsistent. Placebo/permutation testing, spatial residual diagnostics, and dietary-structure sensitivity analysis using fish/seafood supply as a proxy supported the stability and specificity of the association. We additionally performed a pre-specified spatial econometric sensitivity analysis: residual Moran's I on the refitted OLS model (n = 79) was 0.099 (p_sim = 0.082); Anselin's robust LM-lag test was significant (p = 0.003), identifying a Spatial Lag Model (SLM) as the appropriate primary spatial specification (ρ = 0.35; post-fit Moran's I = - 0.006, p_sim = 0.466 autocorrelation absorbed). Under SLM, the MP p90-vs-p10 exposure contrast was - 0.41 (p = 0.85); the pre-specified decision rule thereby classifies this result as null/hypothesis-generating (Path C). These findings generate hypotheses and do not establish causality, but encourage further individual-level exposure assessments and mechanistic studies to better understand the potential role of microplastics in oral carcinogenesis.