Residential proximity to dioxin-emitting facilities and risk of non-Hodgkin lymphoma in the NIH-AARP Diet and Health Study.

BACKGROUND: Polychlorinated dibenzo-p-dioxins and dibenzofurans (PCDD/Fs) are persistent organic pollutants emitted from industrial sources. Residential proximity to these emissions has been associated with risk of non-Hodgkin lymphoma (NHL) in a limited number of studies. METHODS: We evaluated associations between residential proximity to PCDD/F-emitting facilities and NHL in the NIH-AARP Diet and Health Study (N = 451,410), a prospective cohort enrolled in 1995-1996 in 6 states and 2 U.S. cities. We linked enrollment addresses with a U.S. Environmental Protection Agency database of 4,478 historical PCDD/F sources with estimated toxic equivalency quotient (TEQ) emissions. We evaluated associations between NHL and exposures during a historical period prior to enrollment (1980-1995) using an average emissions index, weighted by toxicity, distance, and wind direction (AEI-W [g TEQ/km2]) within 3-, 5- and 10 km of residences. We also evaluated proximity-only metrics indicating the presence/absence of one or more facilities within each distance, and metrics calculated separately for each facility type. We used Cox regression to estimate associations (hazard ratio, HR; 95 % confidence interval, 95 %CI) with NHL and major subtypes, adjusting for demographic, lifestyle, and dietary factors. RESULTS: A total of 6,467 incident cases of NHL were diagnosed through 2011. Participants with an AEI-W ≥ 95th percentile had elevated risk of NHL compared to those unexposed at 3 km (HR = 1.16; 95 %CI = 0.89-1.52; p-trend = 0.24), 5 km (HR = 1.20;95 %CI = 0.99-1.46;p-trend = 0.05) and 10 km (HR = 1.15; 95 %CI = 0.99-1.34; p-trend = 0.04). We found a positive association at 5 km with follicular lymphoma (HR≥95vs.0 = 1.62; 95 %CI = 0.98-2.67; p-trend = 0.05) and a suggestive association for diffuse large B-cell lymphoma (HR≥95vs.0 = 1.40; 95 %CI = 0.91-2.14; p-trend = 0.11). NHL risk was also associated with high emissions from coal-fired power plants within 10 km (HR≥95vs.0 = 1.42; 95 %CI = 1.09-1.84; p-trend = 0.05). CONCLUSIONS: Residential proximity to relatively high dioxin emissions from industrial sources may increase the risk of NHL and specific subtypes.

Foraging animal origin food samples as passive indicators of dioxin-like POPs contamination in industry sites: Method development, characterisation and risk assessment.

Titanium dioxide (TiO2) is an important industrial chemical, and studies suggest its major production route - the chloride process could lead to the generation of unintentional dl-POPs. However, no relevant studies assessed the occurrence of dl-POPs associated with TiO2 production in the industrial zones, which is mostly due to the ultra-trace level distribution of these compounds in environmental compartments. The present study explored the novel possibility of utilising foraging animal-origin foods as sensitive indicators for addressing this challenge and generated a globally beneficial dataset by assessing the background levels of dl-POPs in the vicinity of a TiO2 production house in Southern India. Systematic sampling of foraging cow's milk and free-ranging hen's eggs was carried out from the study site, and the dl-POPs assessments were conducted utilising an in-house developed cost-effective GC-MS/MS-based analytical methodology. The median dl-POPs levels in milk and egg samples were about 3 times higher than the control samples collected from farm-fed animals and retail markets. The contaminant loads in the foraging animal-origin food samples were further traced to their presence in environmental compartments of soil and sediment and admissible degree of correlations were observed in congener fingerprints. Elevated health risks were inferred for the population in the industrial zones with weekly intakes weighing about 0.15-17 times the European Food Safety Authority-assigned levels. The consumption of foraging cow's milk was observed to have a higher contribution towards the hazard indices and cancer risk estimates and were significantly higher (p < 0.05) for children. The study also presents a critical validation of the GC-MS/MS-based method for the purpose of regulatory monitoring of dl-POPs, which could be of practical significance in economies in transition.

Halogenated aromatic pollutants in routine animal-derived food of south China: Occurrence, sources, and dietary intake risks.

Halogenated aromatic pollutants (HAPs) including polychlorinated dibenzo-p-dioxins/furans (PCDD/Fs), polychlorinated biphenyls (PCBs), polybrominated dibenzo-p-dioxins/furans (PBDD/Fs), and polybrominated diphenyl ethers (PBDEs) exhibit diverse toxicities and bio-accumulation in animals, thereby imposing risks on human via animal-derived food (ADF) consumption. Here we examined these HAPs in routine ADFs from South China and observed that PBDEs and PCBs showed statistically higher concentrations than PCDD/Fs and PBDD/Fs. PCDD/Fs and PCBs in these ADFs were mainly from the polluted feed and habitat of animals, except PCDD/Fs in egg, which additionally underwent selective biotransformation/progeny transfer after the maternal intake of PCDD/F-polluted stuff. PBDEs and PBDD/Fs were mostly derived from the extensive use of deca-BDE and their polluted environments. Significant interspecific differences were mainly observed for DL-PCBs and partly for PBDD/Fs and PBDEs, which might be caused by their distinct transferability/biodegradability in animals and the different living habit and habitat of animals. The dietary intake doses (DIDs) of these HAPs via ADF consumption were all highest for toddlers, then teenagers and adults. Milk, egg, and fish contributed most to the DIDs and risks for toddlers and teenagers, which results of several cities exceeded the recommended thresholds and illustrated noteworthy risks. Pork, fish, and egg were the top three risk contributors for adults, which carcinogenic and non-carcinogenic risks were both acceptable. Notably, PBDD/Fs showed the lowest concentrations but highest contributions to the total risks of these HAPs, thereby meriting continuous attention.

The aryl hydrocarbon receptor differentially modulates the expression profile of antibody isotypes in a human B-cell line.

2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) is a persistent environmental contaminant and high affinity ligand for the aryl hydrocarbon receptor (AhR). In animal models, AhR activation by TCDD generally inhibits antibody secretion. However, it is less clear if this translates to human antibody production. Using a human Burkitt lymphoma B-cell line (CL-01) that can be stimulated to secrete Ig and undergo class switch recombination to other Ig isotypes, the current study evaluated the effects of AhR activation or antagonism on the human Ig isotypic expression profile with CD40L+IL-4 stimulation. Our results suggest that AhR agonists (TCDD and indirubin) have little to no effect on IgM or IgA secretion, which were also not induced with stimulation. However, AhR activation significantly inhibited stimulation-induced IgG secretion, an effect reversed by the AhR antagonist CH223191. Evaluation of Ig heavy chain (IgH) constant region gene expression (ie Cµ, Cγ1-4, Cα1-2, and Cε that encode for IgM, IgG1-4, IgA1-2, and IgE, respectively) demonstrated differential effects. While Cµ and Cα2 transcripts were unaffected by stimulation or AhR agonists, AhR activation significantly inhibited stimulation-induced Cγ2-4 and Cε mRNA transcripts, which was reversed by AhR antagonism. Notably, AhR antagonism in the absence of exogenous AhR ligands significantly increased IgG and IgA secretion as well as the expression of Cγ2-4 and Cε. These results suggest that modulation of AhR activity differentially alters the IgH isotypic expression profile and antibody secretion that may be partly dependent on cellular stimulation. Since a variety of chemicals from anthropogenic, industrial, pharmaceutical, dietary, and bacterial sources bind the AhR, the ability of environmental exposures to alter AhR activity (i.e. activate or inhibit) may have a direct influence on immune function and antibody-relevant disease conditions.

The association between polychlorinated dibenzo-p-dioxin exposure and cancer mortality in the general population: a cohort study.

Introduction: Earlier research has indicated that being exposed to polychlorinated dibenzo-p-dioxins (PCDDs) in the workplace can heighten the likelihood of cancer-related deaths. Nevertheless, there is limited information available regarding the connection between PCDD exposure and the risk of cancer mortality in the general population (i.e., individuals not exposed to these substances through their occupation). Methods: The National Health and Nutrition Examination Survey (NHANES) detected PCDDs in the general population, and the death data were recently updated as of December 31, 2019. We conducted Cox regression analysis and controlled for covariates including age, gender, ethnicity, educational attainment, physical activity, alcohol intake, NHANES survey period, BMI category, cotinine concentration, and household earnings. Results: After accounting for confounding factors, the findings indicated that for each incremental rise of 1 log unit in 1,2,3,4,6,7,8,9-octachlorodibenzo-p-dioxin, there was a 76% rise in the likelihood of death from any cause, with a p value of 0.003. An increase of 1 log unit in the concentration of 1,2,3,4,6,7,8-heptachlorodibenzofuran could potentially lead to a 90% higher risk of cancer mortality, as indicated by a p value of 0.034 and a 95% confidence interval of 0.05-2.43. As the concentrations of 1,2,3,4,6,7,8-heptachlorodibenzofuran increased, the dose-response curve indicated a proportional rise in the risk of cancer mortality, accompanied by a linear p value of 0.044. The sensitivity analysis demonstrated that our findings were resilient. Discussion: In the general population, an elevated risk of cancer mortality was observed in PCDDs due to the presence of 1,2,3,4,6,7,8-heptachlorodibenzofuran. Mechanistic research is required to further confirm it.

Dietary intakes of dioxins and polychlorobiphenyls (PCBs) and mortality: EPIC cohort study in 9 European countries.

Dioxins and polychlorinated biphenyls (PCBs) are toxic, endocrine disruptors and persistent chemicals for which the main exposure source is diet due to their bioaccumulation and biomagnification in food chains. Cohort studies in the general populations have reported inconsistent associations between these chemicals in serum/plasma and mortality. Our objective was to study the association between dietary intake of 17 dioxins and 35 PCBs and all-cause, cancer-specific and cardiovascular-specific mortalities were assessed in the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort. Dietary intake of dioxins and PCBs was assessed combining EPIC food consumption data with European food contamination data provided by the European Food Safety Authority. We applied multivariable Cox regressions. The analysis included 451,390 adults (mean ± SD age:51.1 ± 9.7 years) with 46,627 deaths and a median follow-up of 17.4 years (IQR = 15.2-19.1). A U-shaped non-linear association with all-cause mortality for dietary intake of dioxins (Pnon-linearity<0.0001), DL-PCB (Pnon-linearity = 0.0001), and NDL-PCBs (Pnon-linearity<0.01) was observed. For example, the hazard ratios (95%Confidance interval) for all-cause mortality obtained with the spline model was equal to 1.03 (1.02-1.05) for low levels of intake to dioxins (7 pg TEQ/day), 0.93 (0.90-0.96) for moderate levels of intake (25 pg TEQ/day), while for high levels of intake (55 pg TEQ/day) it was 1.03 (0.97-1.09). Intake of dioxins, DL-PCBs and NDL-PCBs was not associated with cardiovascular mortality. There was no association between intakes of dioxins and cancer mortality, but a U-shaped association was observed for intake of DL-PCBs and intakes of NDL-PCBs and cancer mortality. The PCBs and dioxins are known to have endocrine disrupting properties which can lead to non-monotonic dose responses. These results need to be interpreted with caution and further studies are needed to better clarify the association between dietary intake of dioxins and PCB and mortality in the general population.

Health effects of future dioxins emission mitigation from Chinese municipal solid waste incinerators.

Dioxins (including 2,3,7,8-tetrachlorodibenzo-p-dioxin, as Group 1 Carcinogen) in the atmosphere mainly originate from incomplete combustion during municipal solid waste (MSW) incineration. To significantly reduce dioxins emission from the MSW incineration industry, China has promulgated a set of ambitious plans regulating MSW-related pollution; however, the emission reduction potentials and concomitant environmental and health impacts associated with the implementation of these programs on a national scale remain unknown. Here, we use real measurements from official environmental impact assessment systems and continuous emissions monitoring systems (covering 96.6% of national MSW incinerators) to estimate unit-level dioxins emission and concomitant environmental and health impacts. We find that in 2018, 99.3% and 66.7% of Chinese incinerators met such concentration and temperature standards, respectively, controlling the total emissions to 19.6 g toxic equivalency quantity and maintaining carcinogenic and noncarcinogenic risks significantly below safety levels nationwide. Fully achieving both current standards and future regulations will reduce emissions and health risks by 67.7% and 62.6%, respectively, with waste sorting program contributing the majority. This study reveals substantial benefits from curbing MSW-related dioxins pollution and underscores the promise of ongoing management.

Troubleshooting dioxins stack emissions in an industrial waste gas incinerator.

An important source of dioxins and furans at present is waste incineration, utmost formed during combustion processes and emitted to the environment without being fully captured by waste-gas treatment equipment. In this study, monitoring campaign of International Toxic Equivalents for dioxins and furans (I-TEQDF), was carried out at pharmaceutical industrial waste incinerator to find a correlation between combustion parameters and feed composition with potential emission. Principal Component Analysis (PCA) shows that high values of dioxin emission correlate with short residence time of the flue gas in the furnace as well as low oxygen concentration. These operating conditions were further investigated, using COMSOL Computational Fluid Dynamics (CFD) simulation to calculate the temperature profiles along the furnace. The results suggest that the flame temperature profile is anticipated to exhibit cold areas (cold spots), which may be used as a proxy for dioxin formation due to incomplete combustion. Additionally, the calculated congeners furan to dioxin concentration ratio, points to their formation via de novo mechanism. SEM-EDS analysis preformed on the bag filter upstream the feed following its filtration, have shown large amount of iron, which may have served as a metal catalytic source for dioxin formation. The iron origin is most likely from corrosion of the feeding pipe, drifted with the waste gas and trapped on the bag filter. The results of this study provide a better understanding of the parameters controlling dioxin formation and emission from the plant and may assist a planning of process optimization in such a plant.

Interpretable predictive models of genome-wide aryl hydrocarbon receptor-DNA binding reveal tissue-specific binding determinants.

The aryl hydrocarbon receptor (AhR) is an inducible transcription factor whose ligands include the potent environmental contaminant 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). Ligand-activated AhR binds to DNA at dioxin response elements (DREs) containing the core motif 5'-GCGTG-3'. However, AhR binding is highly tissue specific. Most DREs in accessible chromatin are not bound by TCDD-activated AhR, and DREs accessible in multiple tissues can be bound in some and unbound in others. As such, AhR functions similarly to many nuclear receptors. Given that AhR possesses a strong core motif, it is suited for a motif-centered analysis of its binding. We developed interpretable machine learning models predicting the AhR binding status of DREs in MCF-7, GM17212, and HepG2 cells, as well as primary human hepatocytes. Cross-tissue models predicting transcription factor (TF)-DNA binding generally perform poorly. However, reasons for the low performance remain unexplored. By interpreting the results of individual within-tissue models and by examining the features leading to low cross-tissue performance, we identified sequence and chromatin context patterns correlated with AhR binding. We conclude that AhR binding is driven by a complex interplay of tissue-agnostic DRE flanking DNA sequence and tissue-specific local chromatin context. Additionally, we demonstrate that interpretable machine learning models can provide novel and experimentally testable mechanistic insights into DNA binding by inducible TFs.

Developing an Improved Strategy for the Analysis of Polychlorinated Dibenzo-p-Dioxins/Furans and Dioxin-like Polychlorinated Biphenyls in Contaminated Soils Using a Combination of a One-Step Cleanup Method and Gas Chromatography with Triple Quadrupole Mass Spectrometry.

Soils contaminated with polychlorodibenzo-p-dioxins (PCDDs), polychlorodibenzofurans (PCDFs), and dioxin-like (dl) polychlorinated biphenyls (PCBs), known as persistent organic pollutants (POPs), have garnered global attention because of their toxicity and persistence in the environment. The standard method for target analytes has been used; however, it is an obstacle in large-scale sample analysis due to the comprehensive sample preparation and high-cost instrumental analysis. Thus, analytical development of inexpensive methods with lower barriers to determine PCDDs/Fs and dl-PCBs in soil is needed. In this study, a one-step cleanup method was developed and validated by combining a multilayer silica gel column and Florisil micro-column followed by gas chromatography with triple quadrupole mass spectrometry (GC-QqQ-MS/MS). To optimize the separation and quantification of 17 PCDDs/Fs and 12 dl-PCBs in soils, the sample cleanup and instrumental conditions were investigated. For quantification method validation, spiking experiments were conducted to determine the linearity of the calibration, recovery, and method detection limit of PCDDs/Fs and dl-PCBs using isotopic dilution GC-QqQ-MS/MS. The applicability of the simultaneous determination of PCDDs/Fs and dl-PCBs was confirmed by the recovery of native target congeners and labeled surrogate congeners spiked into the quality-control and actual soil samples. The results were in good agreement with the requirements imposed by standard methods. The findings in this work demonstrated the high accessibility of the sample cleanup and analysis methods for the efficient determination of PCDDs/Fs and dl-PCBs in contaminated soils.

Occurrence and carcinogenic potential of airborne PBDD/Fs and PCDD/Fs around a large-scale municipal solid waste incinerator: A long-term passive air sampling study.

Municipal solid waste incinerator (MSWI) not only is deemed one of the uppermost sources of polychlorinated dibenzo-p-dioxins/furans (PCDD/Fs), but also produces substantial amount of polybrominated dibenzo-p-dioxins/furans (PBDD/Fs) owing to the existence of brominated flame retardants (BFRs) in the waste. So far, however, PBDD/Fs in the vicinal environments of MSWI and their associated risks remain rarely studied. Based on a one-year passive air sampling (PAS) scheme, we investigated airborne PBDD/Fs and PCDD/Fs around a large-scale MSWI that has been operated for multi-years. Both the concentrations of PBDD/Fs and PCDD/Fs showed spatially decreasing trends with the distance away from the MSWI, confirming the influence of the MSWI on the dioxin levels in its ambient air. But its influence on PBDD/Fs was less because PBDD/Fs exhibit lower volatility and therefore lower gaseous concentrations than PCDD/Fs. Compared to the existing global data of airborne PCDD/Fs and PBDD/Fs, our data of the MSWI vicinity were at medium levels, despite PAS samples only represent the concentrations of gaseous dioxins in theory. The seasonal data suggest that meteorological conditions exerted apparent influences over the concentrations and sources of airborne dioxins around the MSWI. As for PCDD/Fs, the MSWI was diagnosed as their uppermost source, followed by local traffic and volatilization/deposition. Whereas the top three PBDD/F sources were related to PBDEs, bromophenol/bromobenzene, and traffic vehicles, respectively. The bioassay-derived TEQs based on the aryl hydrocarbon receptor activation of airborne dioxins around the MSWI were one or two orders of magnitudes higher than their concentration-based TEQs, and the corresponding carcinogenic risks at some MSWI-vicinal sites exceeded the acceptable threshold proposed by the U. S. EPA (10-6 âˆ¼ 10-4) and deserve continuous attention.

Is exposure to chemical pollutants associated with sleep outcomes? A systematic review.

Environmental exposures may influence sleep; however, the contributions of environmental chemical pollutants to sleep health have not been systematically investigated. We conducted a systematic review to identify, evaluate, summarize, and synthesize the existing evidence between chemical pollutants (air pollution, exposures related to the Gulf War and other conflicts, endocrine disruptors, metals, pesticides, solvents) and dimensions of sleep health (architecture, duration, quality, timing) and disorders (sleeping pill use, insomnia, sleep-disordered breathing)). Of the 204 included studies, results were mixed; however, the synthesized evidence suggested associations between particulate matter, exposures related to the Gulf War, dioxin and dioxin-like compounds, and pesticide exposure with worse sleep quality; exposures related to the Gulf War, aluminum, and mercury with insomnia and impaired sleep maintenance; and associations between tobacco smoke exposure with insomnia and sleep-disordered breathing, particularly in pediatric populations. Possible mechanisms relate to cholinergic signaling, neurotransmission, and inflammation. Chemical pollutants are likely key determinants of sleep health and disorders. Future studies should aim to evaluate environmental exposures on sleep across the lifespan, with a particular focus on developmental windows and biological mechanisms, as well as in historically marginalized or excluded populations.

Development of a Methodology for Determination of Dioxins and Dioxin-like PCBs in Meconium by Gas Chromatography Coupled to High-Resolution Mass Spectrometry (GC-HRMS).

An analytical strategy was applied to investigate polychlorinated dibenzo-p-dioxins (PCDDs), polychlorinated dibenzofurans (PCDFs), and dioxin-like polychlorinated biphenyls (dl-PCBs) in newborn meconium samples. The methodology includes extraction by selective pressurized liquid extraction (SPLE), followed by a clean-up multicolumn step. The samples were injected by gas chromatography coupled to a high-resolution mass spectrometer (GC-HRMS). The surrogate recoveries ranged from 68% to 95%, and the average of the limit of quantification (LOQ) ranged from 0.03 to 0.08 pg g-1 wet weight (ww) for PCDD/Fs and 0.2 to 0.88 pg g-1 ww for dl-PCBs. The strategy was applied to 10 samples collected in Valencia (Spain) in 2022. In total, 18 out of 29 analysed congeners were detected in at least one sample, whereas 6 of them were detected in all the samples (OCDD, PCB-123, PCB-118, PCB-105, PCB-167, and PCB-156). The levels for the sum of the 17 congeners of PCDD/Fs and 12 congeners of dl-PCBs in the upper-bound (UB), expressed as picograms of toxic equivalency quantity (TEQ) per gram of ww, ranged from 0.19 to 0.31 pg TEQ g-1 ww.

Exposure and Risk Assessment to Airborne dl-PCBs and Dioxins in the Population Living in the Neighborhood of a Cement Plant: A Pilot Study in the Valencian Region of Spain.

Emissions from cement manufacturing facilities may increase health risks in nearby populations. For this reason, dioxin-like PCB (dl-PCB), polychlorinated dibenzo-p-dioxin (PCDD), and polychlorinated dibenzofuran (PCDF) concentrations in PM10 samples were assessed in the vicinity of a cement manufacturing plant located in the Valencian Region (eastern Spain). The total concentrations of the sum of dl-PCBs, PCDDs, and PCDFs ranged between 1.85 and 42.53 fg TEQ/m3 at the assessed stations. The average daily inhalation dose (DID) for the sum in adults ranged from 8.93 · 10-4 to 3.75 · 10-3 pg WHO TEQ kg-1 b.w. d-1, and, for children, the DID ranged from 2.01 · 10-3 to 8.44 · 10-3 pg WHO TEQ kg-1 b.w. d-1. Risk assessment for adults and children was performed using both daily and chronic exposure. The hazard quotient (HQ) was calculated considering 0.025 pg WHO TEQ kg-1 b.w. d-1 to be the acceptable maximum permitted inhalation exposure. The HQ obtained was slightly higher than 1 for PCDD/Fs at one of the stations (Chiva), indicating a possible health risk for the population under study due to inhalation exposure. In the case of chronic exposure, cancer risk (>10-6) was observed for some samples in one of the assessed sampling sites (Chiva).

[Quantitative risk assessment of occupational exposure to PCDD/Fs in the waste incineration industry].

Objective: To analyze the level of PCDD/Fs exposure of occupational workers in the waste incineration industry and explore the risk of occupational exposure. Methods: In September 2021, literature on environmental PCDD/Fs exposure in waste incineration plants published from the establishment of the database to February 10, 2021 was retrieved from CNKI database. A total of 1365 literatures were retrieved, and 7 met the criteria for inclusion. The US Environmental Protection Agency (EPA) inhalation risk model was used to assess and analyze carcinogenic and non-carcinogenic risks of PCDD/Fs exposure among occupational workers in the waste incineration industry. Results: A total of 86 sampling sites were included in incineration plants in 7 regions. The study of Wuhan area showed that the concentration of working environment near the waste incinerator in the same factory was the highest, followed by the rest and office area in the factory. The concentration of PCDD/Fs in waste incinerators was the highest in Southwest China (4880.00-24880.00 pg TEQ/m(3)), and the lowest in Shenzhen (0.02-0.44 pg TEQ/m(3)). According to the cancer risk assessment, with the increase of exposure years, the risk of cancer increased. The highest risk of cancer was found in the waste incineration plants in Southwest China. When the exposure period was 1 year, the risk was moderate (22.40×10(-6)-114.20×10(-6)). When the exposure time was more than 5 years, the risk of cancer was high. In Jinan, workers working near the incinerator had a moderate risk of cancer after five years of exposure. In Zhejiang, workers were at medium risk of cancer after exposure for more than 20 years. Workers in Wuhan, Shanghai, Zhejiang Province, Shenzhen and the Pearl River Delta were still at low risk of cancer after 40 years of occupational exposure. HQ>1 of workers working near the waste incinerators in Jinan, Zhejiang Province and Southwest China, and the qualitative evaluation results showed that the non-carcinogenic risk was unacceptable. Conclusion: There are great differences in PCDD/Fs of occupational exposure in waste incineration industry, and the occupational exposure exceeding the occupational exposure limit has higher carcinogenic and non carcinogenic risks.

Effect of Hybrid Filler, Carbon Black-Lignocellulose, on Fire Hazard Reduction, including PAHs and PCDDs/Fs of Natural Rubber Composites.

The smoke emitted during thermal decomposition of elastomeric composites contains a significant number of carcinogenic and mutagenic compounds from the group of polycyclic aromatic hydrocarbons, PAHs, as well as polychlorinated dibenzo-p-dioxins and furans, PCDDs/Fs. By replacing carbon black with a specific amount of lignocellulose filler, we noticeably reduced the fire hazard caused by elastomeric composites. The lignocellulose filler reduced the parameters associated with the flammability of the tested composites, decreased the smoke emission, and limited the toxicity of gaseous decomposition products expressed as a toximetric indicator and the sum of PAHs and PCDDs/Fs. The natural filler also reduced emission of gases that constitute the basis for determination of the value of the toximetric indicator WLC50SM. The flammability and optical density of the smoke were determined in accordance with the applicable European standards, with the use of a cone calorimeter and a chamber for smoke optical density tests. PCDD/F and PAH were determined using the GCMS-MS technique. The toximetric indicator was determined using the FB-FTIR method (fluidised bed reactor and the infrared spectrum analysis).

Human 2,3,7,8-tetrachlorodibenzo-p-dioxin exposure and thyroid cancer risk.

Thyroid cancer incidence has been steadily rising since the 1970s and exposure to environmental pollutants, including persistent organic pollutants such as 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and other dioxins, has emerged as a potential explanation for this increase. This study aimed to summarize available human studies on the association between TCDD exposure and thyroid cancer. A systematic review of the literature was performed searching the National Library of Medicine and National Institutes of Health PubMed, Embase, and Scopus databases, through January 2022, using the following keywords: "thyroid", "2,3,7,8-tetrachlorodibenzo-p-dioxin", "TCDD", "dioxin", and "Agent Orange". Six studies were included in this review. Three studies evaluated the acute exposure to the chemical factory accident in Seveso, Italy, and found a non-significant increase in the risk of thyroid cancer. Two studies investigating Agent Orange exposure among United States Vietnam War veterans found a significant risk of thyroid cancer following exposure. No association was found in one study evaluating TCDD exposure through herbicides. The current study highlights the limited information on the potential association between TCDD exposure and thyroid cancer and thus the need for future human studies, especially considering the persistent human exposure to dioxins in the environment.

PCBs, PCNs, and PCDD/Fs in Soil around an Industrial Park in Northwest China: Levels, Source Apportionment, and Human Health Risk.

The concentrations of polychlorinated biphenyls (PCBs), polychlorinated naphthalenes (PCNs), and polychlorinated dibenzo-p-dioxins and dibenzofurans (PCDD/Fs) were determined in soil samples collected around an industrial park in Northwest China, to investigate the potential impacts of park emissions on the surrounding environment. The total concentration ranges of PCBs, PCNs, and PCDD/Fs in the soil samples were in 13.2-1240, 141-832, and 3.60-156 pg/g, respectively. The spatial distribution and congener patterns of PCBs, PCNs, and PCCD/Fs indicated that there might be multiple contamination sources in the study area, so source apportionments of PCBs, PCNs, and PCCD/Fs were performed by a positive matrix factorization model based on the concentrations of all target congeners together. The results revealed that these highly chlorinated congeners (CB-209, CN-75, and OCDF) might be derived from phthalocyanine pigments, the legacy of Halowax 1051 and 2,4-D products, which together contributed nearly half of the total concentration of target compounds (44.5%). In addition to highly chlorinated congeners, the local industrial thermal processes were mainly responsible for the contamination of PCBs, PCNs, and PCDD/Fs in the surrounding soil. The total carcinogenic risk of PCBs, PCNs, and PCDD/Fs in a few soil samples (0.22 × 10-6, 0.32 × 10-6, and 0.40 × 10-6) approached the threshold of potential carcinogenic risk (1.0 × 10-6). Since these pollutants can continuously accumulate in the soil, the contamination of PCBs, PCNs, and PCDD/Fs in surrounding soil deserves continuous attention.

Endocrine disruptors and endometriosis.

Endometriosis is a hormone-dependent inflammatory gynecological disease of reproductive-age women. It is clinically and pathologically characterized by the presence of functional endometrium as heterogeneous lesions outside the uterine cavity. The two major symptoms are chronic pelvic pain and infertility, which profoundly affect women's reproductive health and quality of life. This significant individual and public health concerns underscore the importance of understanding the pathogenesis of endometriosis. The environmental endocrine-disrupting chemicals (EDCs) are exogenous agents that interfere with the synthesis, secretion, transport, signaling, or metabolism of hormones responsible for homeostasis, reproduction, and developmental processes. Endometriosis has been potentially linked to exposure to EDCs. In this review, based on the robust literature search, we have selected four endocrine disruptors (i) polychlorinated biphenyls (PCB)s (ii) dioxins (TCDD) (iii) bisphenol A (BPA) and its analogs and (iv) phthalates to elucidate their critical role in the etiopathogenesis of endometriosis. The epidemiological and experimental data discussed in this review indicate that these four EDCs activate multiple intracellular signaling pathways associated with proinflammation, estrogen, progesterone, prostaglandins, cell survival, apoptosis, migration, invasion, and growth of endometriosis. The available information strongly indicates that environmental exposure to EDCs such as PCBs, dioxins, BPA, and phthalates individually or collectively contribute to the pathophysiology of endometriosis. Further understanding of the molecular mechanisms of how these EDCs establish endometriosis and therapeutic strategies to mitigate the effects of these EDCs in the pathogenesis of endometriosis are timely needed. Moreover, understanding the interactive roles of these EDCs in the pathogenesis of endometriosis will help regulate the exposure to these EDCs in reproductive age women.

Serum levels of polychlorinated dibenzo-p-dioxins and polychlorinated dibenzofurans in a sample of Lebanese pregnant women: The role of dietary, anthropometric, and environmental factors.

Polychlorinated dibenzo-p-dioxins (PCDDs) and polychlorinated dibenzofurans (PCDFs) are unintentionally produced, toxic environmental chemicals that persist for long years and bioaccumulate along the food chain, contaminating humans through diet. A particularly critical population subgroup is pregnant women given the adverse health effects on fetuses and newborns. Several anthropogenic sources of exposure to PCDD/Fs exist in Lebanon. Therefore, the aim of the present cross-sectional study is to measure the levels of PCDD/Fs in a sample of pregnant women in Lebanon and to explore potential associated factors. In this study, we measured serum concentrations of seven dioxins and ten furans, among 423 pregnant women recruited at delivery, using gas chromatography MS/MS. Among 269 participants, maternal sociodemographic information was collected including vicinity to landfills, incineration, pesticide use, industrial activity, and smoking. Anthropometric data were registered regarding pre-pregnancy body mass index (BMI), pre-pregnancy weight loss from restrictive diet, and gestational weight gain. Intake of major food groups generally related to PCDD/Fs was reported (fish, red meat, poultry, and dairy). Bivariate and multivariate analyses were performed to identify associations. PCDD/Fs were detected in 0 to 56.1% of the sample. Geometric mean concentrations were 75.5 (2.35) pg/g lipid and 2.25 (1.39) TEQ2005 pg/g lipid for total dioxins, and 2.66 (1.76) pg/g lipid and 0.34 (1.78) TEQ2005 pg/g lipid for total furans. Levels were relatively lower than levels previously observed in France, Germany, Mexico, Ghana, and Japan. Red meat consumption was the most consistently associated factor with a 2.38-2.57 fold increase in PCDD/F levels. Pre-pregnancy weight loss showed inverse associations with PCDD/F congeners. Vicinity to illegal incineration was also associated with a 2.32-2.43 fold increase in PCDD/F levels. In conclusion, results showed the importance of dietary, anthropometric, and environmental factors in the present sample's exposure to PCDD/Fs, in a region that contains anthropogenic sources of contamination.