Browsing by Subject "DIBENZO-P-DIOXINS"
Now showing items 1-7 of 7
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(2016)A number of studies have found an association between the concentrations of persistent organic pollutants (POP) and type 2 diabetes. Causality has remained uncertain. This study describes the pharmacokinetic behavior of PCDD/Fs (polychlorinated dibenzo-p-dioxins and dibenzofurans) both in a theoretical model based on elimination rate constants, and in a group of 409 adult surgical patients with known PCDD/F concentrations and dietary information. A model assuming 10% annual decrease in past PCDD/F intake, predicted the measured profile of TEQ (toxic equivalents) in the patient population fairly well. The dominant determinant of PCDD/F level was age, and the level in patients was also associated with consumption of animal source products. Predicted daily intakes correlated with diet, but also with body mass index (BMI), indicating that high BMI was preceded by high consumption of foods containing PCDD/Fs. The results suggest that a third factor, e. g. high intake of animal source foods, could explain both higher levels of POPs in the body and higher incidence of type 2 diabetes, and BMI is not sufficient in describing the confounding caused by diet. Thus, to fully address the causality between POPs and type 2 diabetes, careful studies considering the pharmacokinetics of the studied compounds, and including the analysis of food consumption, are needed. (C) 2016 Elsevier Ireland Ltd. All rights reserved.
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(2017)Soft-tissue sarcoma is one of the few specific tumors thought to be caused by polychlorinated dibenzo-pdioxins and dibenzofurans (PCDD/Fs) and specifically TCDD. Evidence is, however, based on questionnaire-based case-control studies, and on very few cancer cases in cohort studies at high occupational exposures to chlorophenols or chlorophenoxy acid herbicides with dioxin impurities. Recall bias has been suspected to influence the reporting of exposure, but this possibility has never been adequately put to test. In the present study 87 cancer patients and 308 controls answered a questionnaire asking their exposure to wood preservatives, fungicides and herbicides, and insecticides, and their PCDD/ F concentrations were also measured. After matching for age and area 67-69 sarcoma patients and 153156 controls were available for the study depending on the chemical group, 1-3 controls for each sarcoma patient. Sarcoma patients reported exposure to these chemicals significantly more often than controls did, odds ratios were 6.7 for wood preservatives (p = 0.02), 16 for fungicides and herbicides (p = 0.01), and 4.9 for insecticides (p = 0.06). There was no association, when the analysis was based on measured PCDD/ F concentrations (odds ratios close to 1). Although it is not possible to exclude the role of the main chemical as the cause with certainty, the results indicate that recall bias is very likely in previous studies. Thus the causality between contaminant PCDD/Fs and soft tissue sarcoma cannot be considered proven. (C) 2017 Elsevier B.V. All rights reserved.
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(2020)Polychlorinated dibenzo-p-dioxins and furans (PCDD/Fs) and polychlorinated biphenyls (PCBs) are persistent organic pollutants that have detrimental health effects. As people are exposed to them mainly through the diet, EU has set maximum food dioxin and PCBs levels. EFSA CONTAM Panel made new risk assessment in 2018 that lowered the tolerable weekly intake (TWI) from 14 pg-TEQ/kg bw/week to 2 pgTEQ/kg bw/week. Critical effect was decreased semen count at the age of 18-19 years if serum total TEQ at the age of 9 years exceeded the No Observed Adverse Effect Level (NOAEL) of 7 pg/g lipid. However, it is largely unknown to what extent NOAEL is exceed in European boys currently. We thus measured PCBs from small volume of serum in 184 Finnish children 7-10 years of age. To estimate the TEQ levels of children from measured PCB levels, we used our existing human milk PCDD/F and PCB concentrations to create a hierarchical Bayesian regression model that was used to estimate TEQs from measured PCBs. For quality control (QC), three pooled blood samples from 18 to 20 year old males were measured for PCDD/Fs and PCBs, and estimated for TEQs. In QC samples measured and estimated TEQs agreed within 84% -106%. In our estimate for 7-10 year old children, PCDD/F TEQ exceeded NOAEL only in 0.5% and total TEQ in 2.7% of subjects. Risk management following the decreased TWI proposed by the CONTAM Panel should be carefully considered if total TEQ in children is already largely below the NOAEL. (C) 2020 Elsevier Ltd. All rights reserved.
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(2018)Humans and their associated microbiomes are exposed to numerous xenobiotics through drugs, dietary components, personal care products as well as environmental chemicals. Most of the reciprocal interactions between the microbiota and xenobiotics, such as halogenated compounds, occur within the human gut harboring diverse and dense microbial communities. Here, we provide an overview of the flux of halogenated compounds in the environment, and diverse exposure routes of human microbiota to these compounds. Subsequently, we review the impact of halogenated compounds in perturbing the structure and function of gut microbiota and host cells. In turn, cultivation-dependent and metagenomic surveys of dehalogenating genes revealed the potential of the gut microbiota to chemically alter halogenated xenobiotics and impact their fate. Finally, we provide an outlook for future research to draw attention and attract interest to study the bidirectional impact of halogenated and other xenobiotic compounds and the gut microbiota.
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(2018)The European Commission asked EFSA for a scientific opinion on the risks for animal and human health related to the presence of dioxins (PCDD/Fs) and DL-PCBs in feed and food. The data from experimental animal and epidemiological studies were reviewed and it was decided to base the human risk assessment on effects observed in humans and to use animal data as supportive evidence. The critical effect was on semen quality, following pre- and postnatal exposure. The critical study showed a NOAEL of 7.0 pg WHO2005-TEQ/g fat in blood sampled at age 9 years based on PCDD/F-TEQs. No association was observed when including DL-PCB-TEQs. Using toxicokinetic modelling and taking into account the exposure from breastfeeding and a twofold higher intake during childhood, it was estimated that daily exposure in adolescents and adults should be below 0.25 pg TEQ/kg bw/day. The CONTAM Panel established a TWI of 2 pg TEQ/kg bw/week. With occurrence and consumption data from European countries, the mean and P95 intake of total TEQ by Adolescents, Adults, Elderly and Very Elderly varied between, respectively, 2.1 to 10.5, and 5.3 to 30.4 pg TEQ/kg bw/week, implying a considerable exceedance of the TWI. Toddlers and Other Children showed a higher exposure than older age groups, but this was accounted for when deriving the TWI. Exposure to PCDD/F-TEQ only was on average 2.4- and 2.7-fold lower for mean and P95 exposure than for total TEQ. PCDD/Fs and DL-PCBs are transferred to milk and eggs, and accumulate in fatty tissues and liver. Transfer rates and bioconcentration factors were identified for various species. The CONTAM Panel was not able to identify reference values in most farm and companion animals with the exception of NOAELs for mink, chicken and some fish species. The estimated exposure from feed for these species does not imply a risk.
