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Phthalate exposure and lipid disruption in Taiwanese children: Insights from serum lipidomic approach
Tzu-Hsin Yen1, Wei-Chen Tseng1, Sheng-Han Lee2,3
1Institute of Environmental and Occupational Health Sciences, College of Public Health, National Taiwan University, Taipei, Taiwan.
Insights
Phthalate exposure, specifically from di(2-ethylhexyl) phthalate (DEHP) metabolites like MEHHP, alters lipid profiles in children. This study reveals molecular insights into how environmental contaminants disrupt lipid metabolism during early development.
Area of Science:
- Environmental Health
- Metabolomics
- Pediatric Toxicology
Background:
- Phthalates are widespread environmental contaminants with higher exposure and susceptibility in children.
- Previous research suggests links between phthalate exposure and adverse health outcomes, but molecular mechanisms remain unclear.
Purpose of the Study:
- To investigate the molecular mechanisms of phthalate exposure in children by examining associations between phthalate metabolites and serum lipid profiles.
- To identify specific lipid alterations linked to phthalate exposure in early life.
Main Methods:
- Cross-sectional study of 256 Taiwanese children (aged 8-10 years) from two population-based cohorts.
- Serum phosphocholine-containing lipids were profiled using liquid chromatography-triple quadrupole mass spectrometry.
- Urinary levels of 12 phthalate metabolites were measured and associated with lipid profiles using multiple linear regression.
Main Results:
- Mono-(2-ethyl-5-hydroxyhexyl) phthalate (MEHHP), a di(2-ethylhexyl) phthalate (DEHP) metabolite, showed the strongest association with lipid alterations.
- Higher MEHHP levels were linked to increased diacyl- and lyso-phosphatidylcholines, and decreased sphingomyelins and ether-linked phosphatidylcholines.
- These findings suggest phthalate exposure disrupts lipoprotein metabolism, PPAR-related signaling, and sphingolipid balance.
Conclusions:
- This study identifies specific lipid perturbations associated with DEHP metabolite exposure in children.
- The findings provide molecular insights into how phthalates may disrupt lipid metabolic homeostasis during early development.
- These disruptions may underlie previously observed links between phthalate exposure and hepatic, cardiovascular, and neurological issues.
Abstract:
Phthalates are ubiquitous environmental contaminants that raise particular concern for children, who generally experience higher exposure levels and are more susceptible to environmental pollutants. To understand potential molecular mechanisms, we conducted a cross-sectional study of 256 Taiwanese children aged 8-10 years from two population-based cohorts: the Taiwan Birth Panel Study and the Taiwan Early-Life Cohort. Serum phosphocholine-containing lipids were profiled by liquid chromatography coupled with triple quadrupole mass spectrometry and associated with urinary levels of 12 phthalate metabolites. Multiple linear regression models, adjusted for demographic and socioeconomic factors, revealed that mono-(2-ethyl-5-hydroxyhexyl) phthalate (MEHHP), an oxidative metabolite of di(2-ethylhexyl) phthalate (DEHP), exhibited the strongest associations with lipid alterations. Specifically, higher urinary MEHHP was positively associated with several diacyl-phosphatidylcholines and lyso-phosphatidylcholines, while inversely related to sphingomyelins and ether-linked phosphatidylcholines. These lipid signatures suggest disturbances in lipoprotein metabolism, peroxisome proliferator-activated receptor-related signaling, and sphingolipid balance, offering mechanistic clues to previously observed links between phthalate exposure and hepatic, cardiovascular, and neurological outcomes. Overall, this study identifies lipid perturbations associated with metabolites of DEHP exposure in children and provides molecular insights into how phthalates may disrupt lipid metabolic homeostasis during early life.
