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Chronic low-level exposure to nickel (Ni), copper (Cu), and arsenic (As) may contribute to myocardial injury via oxidative stress. This study investigated the effects of these metals in male Sprague–Dawley rats exposed to aerosols of Ni (0.106 mg/m 3 ), Cu (0.048 mg/m 3 ), and As (0.025 mg/m 3 ) at environmental and 10-fold concentrations for 3 mo. Blood metal levels were analyzed using inductively coupled plasma–mass spectrometry (ICP–MS), and oxidative stress and myocardial injury biomarkers were measured with enzyme-linked immunosorbent assay (ELISA). Blood As levels showed a dose-dependent increase in both exposure groups. Myocardial ultrastructural damage, including mitochondrial swelling, disorganized myofibrils, and increased autolysosomes, was observed. Biomarkers of oxidative stress, including catalase (CAT), superoxide dismutase (SOD), and glutathione (GSH), were significantly elevated in both exposure groups, while malondialdehyde (MDA) levels were notably higher in the 10-fold group. Myocardial injury markers (TNNI3, LDHA, and α-HBDH) were elevated in both exposure groups. Significant correlations were found between Cu and As levels and oxidative stress and myocardial injury biomarkers. These findings demonstrate that prolonged low-level exposure to Ni, Cu, and As induces oxidative stress and myocardial injury in rats. The results highlight the potential cardiovascular risks associated with environmental exposure to mixed heavy metals and emphasize the importance of stricter regulatory measures to limit such pollutants.

Effects of combined exposure to low levels of aerosolised nickel, copper and arsenic on myocardial injury in rats