The Association Among Urinary Di-(2-ethylhexyl) Phthalate Metabolites, Serum Lipid Profiles, and Serum Apoptotic Microparticles in a Young Taiwanese Population

Prior research has suggested that exposure to Di-(2-ethylhexyl) phthalate (DEHP) may impact lipid metabolism. However, no previous studies have investigated the relationship between DEHP exposure and newly identified lipoprotein biomarkers. Additionally, the role of lipoproteins in the link between DEHP exposure and vascular endothelial cell apoptosis remains unexplored. A total of 867 Taiwanese individuals aged 12 to 30 years were enrolled in this study to examine the correlation between urinary DEHP metabolites, lipoprotein profiles (including low-density lipoprotein cholesterol (LDL-C), small dense low-density lipoprotein cholesterol (sdLDL-C), low-density lipoprotein triglyceride (LDL-TG), high-density lipoprotein cholesterol, lipoprotein(a), apolipoprotein A1, apolipoprotein B, and triglyceride), and apoptotic microparticles (CD31+/CD42a−, CD31+/CD42a+, and CD14). We reported elevated levels of mono-2-ethylhexyl phthalate (MEHP) that were found to be positively associated with higher levels of lipoproteins [LDL-C, sdLDL-C, LDL-TG, and lipoprotein(a)] with P values less than 0.001, less than 0.001, 0.010, and 0.006, respectively, as well as three types of apoptotic microparticles (all P values < 0.001). Additionally, increased levels of LDL-C, sdLDL-C, LDL-TG, and triglycerides were linked to higher levels of ln-CD31+/CD42a− with P values less than 0.001, less than 0.001, 0.002, and 0.014, respectively. Furthermore, increased levels of LDL-C and sdLDL-C were also linked to higher levels of ln-CD31+/CD42a+ with P values less than 0.001 and 0.001, respectively. The structural equation model demonstrated that MEHP had a direct correlation with CD31+/CD42a− and was also indirectly associated with it through LDL-C, sdLDL-C, and LDL-TG. Furthermore, MEHP was directly linked with CD31+/CD42a+, and indirectly associated with it through LDL-C and sdLDL-C. In conclusion, these novel findings have important implications for our understanding of the effects of DEHP exposure on cardiovascular health. The identification of DEHP as a contributor to lipoprotein alterations and apoptosis in vascular endothelial cells provides a valuable foundation for future research in the field of environmental cardiology. Further research is necessary to determine whether a causal relationship exists.