ArticleEnvironmental health perspectives2026
Multiomics Insights Linking Personal Care Products Exposure to Serum Lipid Profiles in Older Adults: The China BAPE Study.
Article in Environmental health perspectives, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Personal care products (PCPs) are widespread environmental exposures, yet their combined and system-wide effects on serum lipid profiles in the aging population remain poorly understood. This study aimed to comprehensively assess the association between exposure to multiple PCPs and serum lipid profiles in healthy older adults and to explore underlying molecular pathways and biological mechanisms. We conducted a prospective panel study with five monthly follow-up surveys between September 2018 and January 2019 among 76 healthy older adults (60-69 years) in Jinan, China. This study measured urinary concentrations of PCPs, serum lipid markers, and multiomics profiles (transcriptomics, lipidomics, and metabolomics). We employed linear mixed-effects models to analyze exposure-outcome associations and integrated multiomics data with causal inference testing and Ingenuity Pathway Analysis to identify mediating biomolecules and biological mechanisms. Additional analyses examined the relationships of PCP exposures with inflammatory cytokines, oxidative stress biomarkers, and electrocardiographic (ECG) parameters to provide functional support for the identified pathways and their associated phenotypic consequences. Four PCPs [Benzophenone-2 (BP-2), Benzophenone-3 (BP-3), 4-Hydroxy benzophenone (4-OHBP), and Ethyl p-Hydroxybenzoate (EtP)] were significantly associated with altered serum lipid profiles. Multiomics analyses suggested their convergence on a PPAR-centered immunometabolic network, with S100 signaling identified as a novel activation pathway. Specifically, BP-2 was associated with patterns consistent with IL-4/IL-13-mediated alternative macrophage activation, while PPAR appeared to be involved in inflammatory polarization and metabolic reprogramming. Cytokine analysis revealed associations between BP-2 and key inflammatory mediators (e.g., IL-1β), oxidative stress assessment linked BP-2 exposure to elevated markers of oxidative damage (e.g., 8-PGF2α), and ECG analysis associated BP-2 exposure with altered cardiac electrophysiology (e.g., QRS duration). These multifaceted findings suggest associations between PCP exposures and serum lipid profiles, and highlight the potential contribution to cardiovascular risk. Our findings provide integrated, multilayered evidence suggesting associations between exposure to PCPs and alterations in serum lipid profiles in older adults, bridging exposure profiles, biomolecular perturbations, and subclinical functional changes. These results serve as a hypothesis-generating theoretical foundation that, pending confirmation in larger studies or experimental validation, advances the understanding of environmental metabolic disruption in aging populations.
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