Groundnut Consumption Emerges as the Strongest Predictor of Aflatoxin Exposure in Southwestern Nigeria
Serum aflatoxin-albumin adducts offered an objective window into exposure among gastroenterology patients in tertiary hospitals across southwestern Nigeria, where aflatoxin remains a persistent hepatocarcinogenic threat. In this cross-sectional cohort of 573 patients, the median AF-ALB concentration reached 3.5 pg/mL, a level that reflects systemic exposure rather than the self-reported dietary recall that often blurs environmental risk assessment. The study population was predominantly male, with 405 men accounting for 70.7% of participants and 168 women making up 29.3%.
The pattern that emerged was straightforward and clinically important. Daily groundnut consumption carried the strongest dietary association with high AF-ALB levels, with an adjusted odds ratio of 9.7 and a 95% confidence interval of 4.3 to 21.9. The p value was below 0.001. In practical terms, frequent groundnut intake was not a background detail in this cohort; it was the dominant exposure signal. Groundnuts are a well-recognized vehicle for aflatoxin contamination when storage, drying, or handling conditions allow fungal growth, and the biomarker findings here align with that biological pathway.
AF-ALB concentrations also shifted with the time period of sampling. The sampling period remained significantly associated with adduct levels, again with p < 0.001, suggesting that exposure is not static in this setting. Seasonal food storage practices, market supply chains, rainfall patterns, and post-harvest contamination can all change the burden of contaminated staple foods over time. In a region where exposure is intertwined with food security, the biomarker signal likely reflects the intersection of habit, availability, and storage conditions rather than a single fixed source.
Why the Biomarker Matters More Than Exposure Recall
AF-ALB is an unusually useful marker because it captures internal dose. Unlike questionnaire-based exposure estimates, it records the biologically absorbed mycotoxin burden after ingestion and hepatic processing. For a toxin such as aflatoxin, which exerts its major clinical harm through chronic liver injury and carcinogenesis, that distinction matters in the clinic. A patient may deny or under-recognize risk foods, but the albumin adduct profile still documents what reached the circulation.
Aflatoxin’s relevance extends beyond hepatology. Gastroenterology clinics in endemic regions often sit at the front end of a broader disease spectrum that includes chronic liver injury, cirrhosis, and hepatocellular carcinoma risk. The presence of measurable AF-ALB in this patient group suggests that the exposure burden is not confined to the general community; it is visible in patients already engaged with specialty care. That raises the possibility that routine clinical contact could be leveraged for exposure counseling, food-safety education, and earlier prevention messaging.
The model also showed a more nuanced result for urban residence. Urban living appeared linked to high AF-ALB levels in some analyses, but the association was model-dependent rather than truly independent. In other words, once other variables entered the regression framework, urban residence did not hold as a stable standalone predictor. This is a useful reminder that location can stand in for several overlapping exposures, including socioeconomic patterns, food sourcing, storage conditions, and purchasing habits. The apparent urban signal should not be overread as a direct causal relationship.
Age, sex, education, occupation, marital status, and aflatoxin awareness status were not significantly associated with AF-ALB levels. Those null findings matter because they narrow the field of plausible predictors and point back toward food exposure rather than demographic background. Awareness alone also did not track with lower biomarker levels, suggesting that knowledge without structural access to safer food storage and lower-risk staples may have little effect on actual exposure.
Disease Differences and the Clinical Meaning of High Variability
AF-ALB median levels differed significantly across gastroenteric diseases, with p < 0.001 and Cramer’s V of 0.478. The size of that association indicates meaningful heterogeneity across diagnostic groups, although the abstract does not provide the disease-by-disease breakdown. Even without those subgroup details, the finding suggests that aflatoxin exposure is not evenly distributed across gastroenterology diagnoses in this tertiary care population. It may track with underlying nutritional patterns, liver vulnerability, referral mix, or other disease-specific factors that were not fully resolved in the abstract.
The broader public health message is direct. Aflatoxin exposure in southwestern Nigeria remains measurable, common enough to be clinically relevant, and tightly linked to a staple food that many households consume regularly. Groundnuts are nutritionally valuable and culturally embedded, but they also represent a contamination pathway when storage quality falters. The size of the association in this study makes clear that prevention cannot rest on generic advice alone.
Food safety interventions would need to reach the points where exposure is created: drying, storage, inspection, and supply-chain handling. In the clinic, biomarker-informed counseling could help identify patients whose diets place them at higher risk, especially in gastroenterology settings where liver-related consequences already cluster. The study does not show cancer outcomes, fibrosis progression, or mortality, and it does not establish whether lowering exposure would reverse disease risk. It does, however, provide a strong biologic rationale for linking dietary practice to objective toxin burden in a region where aflatoxin remains a persistent carcinogenic threat.
The most clinically actionable signal in the dataset is the same one that appeared first and strongest in the regression model: daily groundnut consumption. In a setting where a single dietary habit can multiply the odds of high biomarker-defined exposure, prevention starts long before the first abnormal liver test.