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Background Previous studies have reported associations between certain persistent organic pollutants (POPs) and type 2 diabetes mellitus (T2DM). Polybrominated diphenyl ethers (PBDEs) are a class of POPs that are found in increasing concentrations in humans. Although obesity is a known risk factor for T2DM and PBDEs are fat-soluble, very few studies have investigated associations between PBDEs and T2DM. No longitudinal studies have assessed associations between repeated measurements of PBDE and T2DM in the same individuals and compared time trends of PBDEs in T2DM cases and controls. Objectives To investigate associations between pre- and post-diagnostic measurements of PBDEs and T2DM and to compare time trends of PBDEs in T2DM cases and controls. Methods Questionnaire data and serum samples from participants in the Tromsø Study were used to conduct a longitudinal nested case-control study among 116 T2DM cases and 139 controls. All included study participants had three pre-diagnostic blood samples (collected before T2DM diagnosis in cases), and up to two post-diagnostic samples after T2DM diagnosis. We used logistic regression models to investigate pre- and post-diagnostic associations between PBDEs and T2DM, and linear mixed-effect models to assess time trends of PBDEs in T2DM cases and controls. Results We observed no substantial pre- or post-diagnostic associations between any of the PBDEs and T2DM, except for BDE-154 at one of the post-diagnostic time-points (OR = 1.65, 95% CI: 1.00, 2.71). The overall time trends of PBDE concentrations were similar for cases and controls. Discussion The study did not support PBDEs increasing the odds of T2DM, prior to or after T2DM diagnosis. T2DM status did not influence the time trends of PBDE concentrations.
2023
2001
2002
Polychlorinated n-alkanes (PCAs) are the main components of chlorinated paraffins (CPs) mixtures, that have been commonly grouped into short-chain (SCCPs, C10–13), medium-chain (MCCPs, C14–17), and long-chain (LCCPs, C18-30) CPs. PCAs pose a significant risk to human health as they are broadly present in indoor environments and are potentially persistent, bioaccumulative, and toxic. The lack of specific terminology and harmonization in analytical methodologies for PCA analysis complicates direct comparisons between studies. The present work summarizes the different methodologies applied for the analysis of PCAs in indoor dust, air, and organic films. The large variability between the reviewed studies points to the difficulties to assess PCA contamination in these matrices and to mitigate risks associated with indoor exposure. Based on our review of physicochemical properties of PCAs and previously reported sum of measurable S/M/LCCPs levels, the homologue groups PCAs–C10–13 are found to be mostly present in the gas phase, PCAs–C14–17 in particulate matter and organic films, and PCAs–C≥18 in settled dust. However, we emphasized that mapping PCA sources and distribution in the indoors is highly dependent on the individual homologues. To further comprehend indoor PCA distribution, we described the uses of PCA in building materials and household products to apportion important indoor sources of emissions and pathways for human exposure. The greatest risk for indoor PCAs were estimated to arise from dermal absorption and ingestion through contact with dust and CP containing products. In addition, there are several factors affecting indoor PCA levels and exposure in different regions, including legislation, presence of specific products, cleaning routines, and ventilation frequency. This review provides comprehensive analysis of available indoor PCA data, the physicochemical properties, applied analytical methods, possible interior sources, variables affecting the levels, human exposure to PCAs, as well as need for more information, thereby providing perspectives for future research studies.
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2015
2002