Toxic metal exposure and biomarkers of neurotoxic effects: A study in metal recycling workers

Background: Occupational exposure to toxic metals is a critical global health concern, particularly in the metal scrap recycling industry where simultaneous exposure to complex mixtures is common. Chronic exposure to these mixtures can disrupt redox homeostasis and trigger neuronal injury; however, human data on biomarkers reflecting early neural alterations in asymptomatic populations remain limited. Aims: This study evaluates biomarkers of neurotoxic effects in male recycling workers by measuring a comprehensive panel of neuronal and glial injury markers measure biomarkers indicative of possible neural damage associated with chronic toxic metal exposure. Study design: Cross-sectional study Methods: The study included 123 male subjects: 62 recycling workers employed in a metal scrap recovery facility (exposed group) and 61 healthy controls. Blood and urine concentrations of lead (Pb), cadmium (Cd), chromium (Cr), nickel (Ni), copper (Cu), manganese (Mn), cobalt (Co), iron (Fe), arsenic (As), and selenium (Se) were quantified using inductively coupled plasma mass spectrometry (ICP-MS). Serum levels of S100B, Neuron-specific enolase (NSE), Microtubule-associated protein 2 (MAP2), glial fibrillary acidic protein (GFAP), Myelin basic protein (MBP), and Calprotectin (CALPRO) were measured by ELISA. Statistical associations were examined using correlation and multivariate regression analyses. Results: Recycling workers exhibited markedly higher concentrations of Pb, Mn, Cd, Ni, Cu, Cr, Co, and Fe, alongside significantly decreased Se levels (p < 0.001), indicating substantial toxic metal overload and antioxidant depletion. Correspondingly, serum levels of S100B, NSE, MAP2, and GFAP were significantly elevated in the exposed group (p < 0.001), indicating subclinical neuronal and astroglial stress rather than established disease. Multivariate regression identified Pb, Fe, Cr, and Co as the most consistent independent predictors of biomarker alterations, with the NSE model demonstrating the highest explanatory power. Conclusion: Chronic occupational exposure to toxic metal mixtures is associated with significant alterations in neuronal biomarkers indicative of possible neurotoxic damage in an asymptomatic population, reflecting preclinical neural stress rather than established disease. The inverse relationship between selenium and neuronal injury markers suggests a potential protective role, although this requires further confirmation. These findings support the use of an integrated multi-biomarker approach as a sensitive early warning tool for monitoring neurotoxic risks in industrial populations.