Abstracts: ISEE 21st Annual Conference, Dublin, Ireland, August 25-29, 2009: Oral Presentations
*Department of Environmentaland Occupational Health, College of Medicine, National Cheng Kung University, Tainan, Taiwan; †Department of Industrial Safety and Health, Hung Kuang University, Taichung, Taiwan; ‡Department of Occupational and Environmental Medicine, National Cheng Kung University Hospital, Tainan, Taiwan; and §Research Center of Environmental Trace Toxic Substance, National Cheng Kung University, Tainan, Taiwan.
Abstracts published in Epidemiology have been reviewed by the organizations of Epidemiology. Affliate Societies at whose meetings the abstracts have been accepted for presentation. These abstracts have not undergone review by the Editorial Board of Epidemiology.
Background and Objective:
Insulin resistance and the dysfunction of pancreatic b-cells can occur several years before the development of type 2 diabetes. Dioxins and mercury can cause pancreatic endocrine dysfunction in experimental animals. Because humans are exposed to dioxins and mercury primarily in fish that they eat, it is necessary to investigate and clarify the effects of the interaction of these two pollutants on the homoeostasis model assessment-insulin resistance (HOMA-IR) and pancreatic β-cell function.
This cross-sectional study investigated 1449 non-diabetic residents near a deserted pentachlorophenol and chloralkali factory. Metabolic syndrome-related factors were measured to examine associations between serum dioxin and blood mercury levels. We also investigated associations between the risk of insulin resistance (HOMA-IR >75th percentile), pancreatic β-cell dysfunction (HOMA β-cell >75th percentile), serum dioxins, and blood mercury levels and their potential interaction.
After adjusting for confounding factors, residents with higher serum dioxin levels or blood mercury levels (reference: <25th percentile; higher: >75th percentile) were at a significant risk for insulin resistance (adjusted odds ratio [AOR] 4.0 [95% CI 2.3-7.3] for dioxins; AOR 2.3 [95% CI 1.5-3.5] for mercury) and HOMA β-cell dysfunction (AOR 2.5 [95% CI 1.4-4.3] only for dioxins). Residents with higher serum PCDD/F and blood mercury levels had a much greater risk of having insulin resistance (AOR 27.3 [95% CI 7.0-129.9]). In addition, participants with higher serum PCDD/F levels, but not for higher blood mercury levels, were at significant risk for having pancreatic β-cell dysfunction (AOR 2.3 [95% CI 1.3-3.9]) versus (AOR 1.0 [95% CI 0.7-1.6]), respectively.
We found a significant association between serum PCDD/Fs, blood mercury, and insulin resistance after adjusting for confounding factors: interaction between dioxins, mercury, and insulin resistance exists even in persons without diabetes. Accumulated dioxins and mercury may synergistically increase the risk of developing insulin resistance.