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dc.contributor.authorKuo, Chin-Chien_US
dc.contributor.authorSu, Pen-Huaen_US
dc.contributor.authorSun, Chien-Wenen_US
dc.contributor.authorLiu, Huei-Juen_US
dc.contributor.authorChang, Chaw-Liangen_US
dc.contributor.authorWang, Shu-Lien_US
dc.date.accessioned2018-08-21T05:53:51Z-
dc.date.available2018-08-21T05:53:51Z-
dc.date.issued2018-09-01en_US
dc.identifier.issn0160-4120en_US
dc.identifier.urihttp://dx.doi.org/10.1016/j.envint.2018.05.033en_US
dc.identifier.urihttp://hdl.handle.net/11536/145245-
dc.description.abstractBackground: Inorganic arsenic (iAs) exposure potentially causes diabetes and cardiovascular diseases in adults. However, its effect on glucose and lipid metabolism in early life remains unknown. Objective: We evaluated the associations between early-life arsenic exposure and profiles of glucose and lipids in a 15-year birth cohort in central Taiwan. Methods: We studied 237 adolescents through 5 waves of follow-up interviews and examinations at ages of approximately 2, 5, 8, 11, and 14 y. We obtained at least one follow-up urine measurement for arsenic species and blood sample collection up to 14 y of age and identified group-based trajectories of serial iAs by semi-parametric mixture modeling. Multiple linear and logistic regressions were performed to assess the effect of the arsenic exposure trajectory on serum fasting glucose, total cholesterol (TCHO), triglycerides (TGs), low-density lipoprotein cholesterol (LDL), and high-density lipoprotein cholesterol (HDL). Results: Three trajectories of postnatal arsenic exposure were identified, namely stable-low (31.4%), stable-high (48.2%), and rising-high (20.4%) groups. Compared with the stable-low trajectory group, the percent changes in TCHO and LDL was 14% (95% confidence interval 4-24%) and 23% (9-38%) for the group with "rising-high" trajectory and was 8% (-1-16%) and 16% (4-29%) for the group with "stable-high" trajectory. The rising-high group was also associated with an increase in the TCHO/HDL ratio by 14% (95% CI 3%-25%). The adjusted odds ratios of high developmental trajectories of TCHO, TG, LDL, and non-HDL levels were 4.0 (95% CI 1.2-13.7), 12.2 (2.2-67), 7.3 (1.8-30), and 3.6 (0.9-14.6), respectively, in the rising-high group (reference: stable-low group). Conclusion: Our findings suggest that conversion to an atherogenic lipid profile in adolescents may be associated with early-life exposure to environmental arsenic, particularly during the pre-adolescent period. An environmental modification approach for preventing As-related cardiovascular disease is recommended to begin early in life.en_US
dc.language.isoen_USen_US
dc.subjectArsenicen_US
dc.subjectLipid profileen_US
dc.subjectBirth cohorten_US
dc.subjectTrajectoryen_US
dc.subjectGlucose metabolismen_US
dc.subjectInsulin resistanceen_US
dc.titleEarly-life arsenic exposure promotes atherogenic lipid metabolism in adolescence: A 15-year birth cohort follow-up study in central Taiwanen_US
dc.typeArticleen_US
dc.identifier.doi10.1016/j.envint.2018.05.033en_US
dc.identifier.journalENVIRONMENT INTERNATIONALen_US
dc.citation.volume118en_US
dc.citation.spage97en_US
dc.citation.epage105en_US
dc.contributor.department生物科技學系zh_TW
dc.contributor.departmentDepartment of Biological Science and Technologyen_US
dc.identifier.wosnumberWOS:000438183000013en_US
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