This research endeavor seeks to delve into the potential mechanisms by which pharmaceutical and personal care products (PPCPs), recognized as emerging pollutants, could contribute to the human metabolic disorders and then trigger metabolic diseases. Therefore, we have selected lipid and atherosclerosis, Alzheimer's disease, and type Ⅱ diabetes mellitus as representative metabolic diseases, aiming to systematically explore the critical molecular pathways that may be disrupted by PPCPs for the metabolic disease development. By employing advanced network toxicology and molecular docking techniques, we have successfully elucidated the molecular mechanisms that trigger the three diseases. We pinpointed the potential targets associated with the disease by leveraging databases including PubChem, ADEMTlab2.0, SwissADME, and GeneCards. We further employed STRING analysis and Cytoscape software to pinpoint the core targets that were most significantly associated with these metabolic diseases. In addition, enrichment analysis of these core targets was conducted using Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways within the David database. To obtain the structural aspects of the target proteins, we also employed AlphaFold 3 for protein structure prediction. Finally, we validated the binding affinity of PPCPs to these target proteins using molecular docking with AutoDock Vina. Our findings suggested that PPCPs could potentially trigger metabolic diseases by modulating the expression of microRNAs, influencing cellular apoptosis and proliferation, and affecting signal transduction pathways. Interestingly, we also found the correlations among lipid and atherosclerosis, Alzheimer's disease, and type Ⅱ diabetes mellitus. Taken together, our study provides innovative insights into both the mechanisms of how environmental pollutants trigger human diseases and revealing the correlations among different diseases, thereby laying a theoretical foundation for disease prevention and treatment.