Exposure to metal(loid)s and glucose metabolism may influence the progression of gastric precancerous lesions (GPLs) or gastric cancer (GC), but their combined effects remain unclear. Our study aimed to elucidate the combined impact of metal (including metalloid and trace element) exposure and disturbances in glucose metabolism on the progression of GPLs and GC. From a prospective observational cohort of 1829 individuals, their metal(loid) levels and blood metabolism were analysed via inductively coupled plasma‒mass spectrometry and targeted metabolomics gas chromatography‒mass spectrometry, respectively. From healthy normal controls (NC) or GPLs to GC, we observed that the aluminum and arsenic levels decreased, whereas the vanadium, titanium and rubidium levels increased, but the iron, copper, zinc and barium levels initially decreased but then increased; these changes were not obvious from the NC to GPL group. With respect to glucose homeostasis, most metabolites decreased, except for phosphoenolpyruvate (PEP), which increased. Multiple logistic regression analysis revealed that titanium and phosphoenolpyruvate might be risk factors for GPLs, that barium is a protective factor for GC, and that D-glucaric acid might be a protective factor for GPLs and GC. Selenium, vanadium, titanium, succinate, maleate, isocitrate, PEP, and the tricarboxylic acid cycle (TCA) had good predictive potential for GPL and GC. Additionally, metal(loid)s such as arsenic, titanium, barium, aluminum, and vanadium were significantly correlated with multiple glucose metabolites involved in the TCA cycle in the GPL and GC groups. Our findings imply that metal(loid) exposure disrupts glucose metabolism, jointly influencing GPL and GC progression.