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Brominated dibenzo-p-dioxins and dibenzofurans (PBDD/Fs) are increasingly reported at significant levels in various matrices, including consumer goods that are manufactured from plastics containing certain brominated flame retardants. PBDD/Fs are known ligands for the aryl hydrocarbon receptor (AhR) but are not yet considered in the hazard assessment of dioxin mixtures. The aim of the present study was to determine if PBDD/Fs levels present in plastic constituents of toys could pose a threat to children's health. PBDD/Fs, unlike their chlorinated counterparts (PCDD/Fs), have not been officially assigned toxic equivalence factors (TEFs) by the WHO therefore, we determined their relative potency towards AhR activation in both human and rodent cell-based DR CALUX® bioassays. This allowed us to compare GC-HRMS PBDD/F congener levels, converted to total Toxic Equivalents (TEQ) by using the PCDD/F TEFs, to CALUX Bioanalytical Equivalents (BEQ) levels present in contaminated plastic constituents from children's toys. Finally, an estimate was made of the daily ingestion of TEQs from PBDD/Fs-contaminated plastic toys by child mouthing habits. It is observed that the daily ingestion of PBDD/Fs from contaminated plastic toys may significantly contribute to the total dioxin daily intake of young children.

Here, we characterized the dioxin-like activities of 42 polychlorinated naphthalenes (PCNs) and 6 technical Halowax formulations by using the DR-CALUX (dioxin-responsive chemically activated luciferase expression) assay with rat hepatoma luciferase-expressing H4IIE cells. Of the 42 PCNs examined, 31 showed dioxin-like activities, for which the mass-based REP-EC5TCDD (potency relative to that of 2,3,7,8-tetrachlorodibenzo-p-dioxin based on the 5% effective concentration determined from the dose–response curve for 2,3,7,8-TCDD) ranged from 0.00000012 to 0.0051, indicating that some of the PCNs (e.g., 1,2,3,6,7,8-HxCN and 1,2,3,4,6,7-HxCN) had dioxin-like activities that were equal to or higher than the WHO-TEFs and the mass-based REP-EC5TCDD reported for dioxins such as octachlorodibenzo-p-dioxin, octachlorodibenzofuran, 3,3′,4,4′-tetrachlorobiphenyl (PCB-77), 3,4,4′,5-tetrachlorobiphenyl (PCB-81), and 3,3′,4,4′,5,5′-hexachlorobiphenyl (PCB-169). For PeCNs to OCN with high dioxin-like activities, REPs determined in previous studies were comparable to the REP values obtained in the present study. The TCDD-EQs (2,3,7,8-TCDD equivalents) obtained experimentally for the Halowax formulations decreased in the order HW1051 (37 mg/kg) > HW1014 (30 mg/kg) > HW1013 (5.6 mg/kg) > HW1099 (2.9 mg/kg) > HW1001 (0.60 mg/kg) > HW1031 (

A study was performed to evaluate the dietary exposure of the Latvian population to polychlorinated naphthalenes (PCNs). Based on the toxicological characteristics, provisional levels of occurrence, congener patterns, and the availability of analytical standards, twenty-six congeners were included in the analysis. Considering the planar structure of PCNs, an analytical protocol on the basis of destructive clean-up and isolation of analytes on carbon was applied, while GC-HRMS and isotope dilution were used for the detection and quantification of analytes. Commonly consumed foods were analyzed for the content of PCNs, followed by per capita intake calculations. By applying the available in vitro relative potency (REP) factors, putative toxic equivalents (TEQ) were determined, in order to assess the “dioxin-like” effect arising from the presence of PCNs in food. The daily intake (EDI) for total PCNs (∑PCN) and PCN-TEQ for the general population were calculated to be 116 pg kg−1 body weight (b.w.) and 0.036 pg TEQ kg−1 b.w., respectively. Fish and fish products were found to provide the main contribution to the dietary “dioxin-like” burden of PCNs, constituting ∼60% of the total PCN-TEQ intake. For some fish samples, PCN-TEQ could additionally contribute up to ∼3% to the regulated PCDD/F-PCB-TEQ, while for other matrices this contribution could be lower by an order of magnitude. The obtained data indicated that the estimated dietary exposure to PCNs is likely to be of low concern, although PCN-TEQ could be recognized as a contributor to the overall “dioxin-like” TEQ loading that results from the exposure to halogenated aromatics.

Exposure to PM2.5-bound polycyclic aromatic hydrocarbons (PAHs) can elicit several types of cancer and non-cancer effects. Previous studies reported substantial burdens of PAH-induced lung cancer, but the burdens of other cancer types and non-cancer effects remain unknown. Thus, we estimate the cancer and non-cancer burden of disease, in disability-adjusted life years (DALYs), attributable to ambient PM2.5-bound PAHs exposure in Nagpur district, India, using risk-based approach. We measured thirteen PAHs in airborne PM2.5 sampled from nine sites covering urban, peri-urban and rural areas, from February 2013 to June 2014. We converted PAHs concentrations to benzo[a]pyrene equivalence (B[a]Peq) for cancer and non-cancer effects using relative potency factors, and relative toxicity factors derived from quantitative structure-activity relationships, respectively. We calculated time-weighted exposure to B[a]Peq, averaged over 30 years, and adjusted for early-life susceptibility to cancer. We estimated the DALYs/year using B[a]Peq exposure levels, published toxicity data, and severity of the diseases from Global Burden of Disease 2016 database. The annual average concentration of total PM2.5-bound PAHs was 458 ± 246 ng/m3 and resulted in 49,500 DALYs/year (0.011 DALYs/person/year). The PAH-related DALYs followed this order: developmental (mostly cardiovascular) impairments (55.1%) > cancer (26.5%) or lung cancer (23.1%) > immunological impairments (18.0%) > reproductive abnormalities (0.4%).

Ash samples collected from medical, municipal and small-scale domestic incinerators in Japan were tested for dioxin-like activity using bioassay technique (ethoxyresorufin-O-deethylase: EROD assay) and for extractable organohalogens (EOX) using instrumental neutron activation analysis in order to estimate potential toxicity and responsible chemicals in those samples. Crude extracts and fractions cleaned-up for dioxin analysis from the samples were used for the analysis. The ranges of dioxins in the ashes were between 2.23 and 12.29 ng TEQ/g (dry weight). Relative potency ranges estimated by EROD assay in the medical incinerator ashes were 3.8-17.6 times higher than the results of conventional chemical analysis. EOX analysis suggested that ash samples contained plenty of organochlorine compounds apart from chlorinated dioxins. In addition, medical waste incinerator ashes were considered to have relatively higher amount of organoiodine compounds. In the cleaned-up fractions, bioassay potency ranges were lower than those in the crude extracts. However, some samples still exhibited higher potency than expected from chemical analysis. Though some polycyclic aromatic hydrocarbons were found in the fractions, the amounts were relatively low (0.39-10.56 ng/g). The results imply that some bioactive organohalogens that cannot be detected in the conventional chemical analysis might have potential for dioxin-like toxicity, and contribute to higher bioassay activities. The combination of the chemical analysis with the bioassay and EOX provides rough figure of dioxin-like toxicity and suggests types of organohalogen compounds that should be identified as a part of dioxin analysis for control emission from an incineration plant.

The United States Environmental Protection Agency initiated a reassessment of the risk of exposure to dioxin in the spring of 1991 because of the evolution of scientific thinking as well as the publication of several key experimental studies. This involves a literature reevaluation as well as laboratory studies in both health and ecological risks. One of the major goals is development of a biologically based dose response model. Directed health research involves comparison of sensitive responses in rats and mice, following both acute and chronic exposure, such as enzyme induction in multiple tissues, phosphorylaton responses, tissue dosimetry, and effects on the immune system. The relative potency of 16 dioxin-like chemicals is being compared following chronic exposure in mice for a number of responses in several tissues to better estimate TEFs following low-level, respeated exposures. In addition, the levels of mRNA for induced enzymes is being correlated with the total TEQ in human livers from the general population.