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Sensors (Basel, Switzerland) 2011Dioxins and dioxin-like polychlorinated biphenyls (DL-PCBs) are hazardous toxic, ubiquitous and persistent chemical compounds, which can enter the food chain and... (Review)
Review
Dioxins and dioxin-like polychlorinated biphenyls (DL-PCBs) are hazardous toxic, ubiquitous and persistent chemical compounds, which can enter the food chain and accumulate up to higher trophic levels. Their determination requires sophisticated methods, expensive facilities and instruments, well-trained personnel and expensive chemical reagents. Ideally, real-time monitoring using rapid detection methods should be applied to detect possible contamination along the food chain in order to prevent human exposure. Sensor technology may be promising in this respect. This review gives the state of the art for detecting possible contamination with dioxins and DL-PCBs along the food chain of animal-source foods. The main detection methods applied (i.e., high resolution gas-chromatography combined with high resolution mass-spectrometry (HRGC/HRMS) and the chemical activated luciferase gene expression method (CALUX bioassay)), each have their limitations. Biosensors for detecting dioxins and related compounds, although still under development, show potential to overcome these limitations. Immunosensors and biomimetic-based biosensors potentially offer increased selectivity and sensitivity for dioxin and DL-PCB detection, while whole cell-based biosensors present interpretable biological results. The main shortcoming of current biosensors, however, is their detection level: this may be insufficient as limits for dioxins and DL-PCBs for food and feedstuffs are in pg per gram level. In addition, these contaminants are normally present in fat, a difficult matrix for biosensor detection. Therefore, simple and efficient extraction and clean-up procedures are required which may enable biosensors to detect dioxins and DL-PCBs contamination along the food chain.
Topics: Animals; Biosensing Techniques; Dioxins; Eggs; Food Chain; Meat; Milk; Polychlorinated Biphenyls
PubMed: 22247688
DOI: 10.3390/s111211692 -
Arhiv Za Higijenu Rada I Toksikologiju Dec 2010The term dioxins usually refers to polychlorinated dibenzo-dioxins (PCDDs) and polychlorinated dibenzofurans (PCDFs). As 2,3,7,8-tetrachloro-dibenzo-p-dioxin (TCDD) has... (Review)
Review
The term dioxins usually refers to polychlorinated dibenzo-dioxins (PCDDs) and polychlorinated dibenzofurans (PCDFs). As 2,3,7,8-tetrachloro-dibenzo-p-dioxin (TCDD) has the highest toxic potential, the toxic potentials of other PCDDs and PCDFs are defined in comparison with it. Human exposure to dioxins can be environmental (background), occupational, or accidental pollution. In the human body, dioxins are in part metabolised and eliminated, and the rest is stored in body fat. People vary in their capacity to eliminate TCDD, but it is also dose-dependent; the elimination rate is much faster at higher than lower levels. The liver microsomal P4501A1 enzyme oxygenates lipophilic chemicals such as dioxins. It is encoded by the CYP1A1 gene. Cytosolic aryl hydrocarbon receptor (AhR) mediates their carcinogenic action. It binds to dioxin, translocates to nucleus and together with hydrocarbon nuclear translocator (ARNT) and xenobiotic responsive element (XRE) increases the expression of CYP1A1.Dioxins are classified as known human carcinogens, but they also cause noncancerous effects like atherosclerosis, hypertension, and diabetes. Long-term exposures to dioxins cause disruption of the nervous, immune, reproductive, and endocrine system. Short-term exposure to high levels impairs the liver function and causes chloracne. The most sensitive population to dioxin exposure are the foetuses and infants.A large number of health effects have been documented in the scientific literature, and they all place dioxins among the most toxic chemicals known to man.
Topics: Cytochrome P-450 Enzyme System; Dioxins; Environmental Exposure; Food Contamination; Humans; Occupational Exposure; Polychlorinated Dibenzodioxins
PubMed: 21183436
DOI: 10.2478/10004-1254-61-2010-2024 -
Chimia Oct 2018Polychlorinated dibenzodioxins (PCDDs) and polychlorinated dibenzofurans (PCDFs) summarized as dioxins, as well as polychlorinated biphenyls (PCBs) are persistent,... (Review)
Review
Polychlorinated dibenzodioxins (PCDDs) and polychlorinated dibenzofurans (PCDFs) summarized as dioxins, as well as polychlorinated biphenyls (PCBs) are persistent, bio-accumulative and toxic environmental contaminants. Over 95% of human exposure to these problematic chemicals occurs the ingestion of fatty rich food like meat and meat products, fatty fish, as well as milk and dairy products. Several major food and feed contamination incidents in Europe during the years 1997 and 2010 revealed the necessity of establishing food and feed monitoring programs for dioxins and PCBs. Various monitoring programs carried out by the Federal Office of Public Health (FOPH) and the Federal Food Safety and Veterinary Office (FSVO), suggest that cattle from extensive farming (suckler cow husbandry) exhibited higher levels of dioxin-like PCBs (dl-PCBs) and exceeded with higher frequency the permitted maximum levels (ML) when compared to conventional raised cattle. The reasons for the higher levels are possibly due to higher levels of PCBs in green fodder (pasture, silage, and hay) when compared to the concentrated feed used in conventional farming. Additionally, an increased uptake of soil, which is known to be a risk matrix for the uptake of dioxins and PCBs in grazing animals, leads to elevated contaminant levels in the suckler cows and hence their calves. Furthermore, PCB point sources present on a farm from older building and construction materials ( PCB-containing wall paints) might result in very high contamination of the animals and the meat produced from them.
Topics: Agriculture; Animal Feed; Animals; Cattle; Dioxins; Food Contamination; Humans; Meat; Polychlorinated Biphenyls
PubMed: 30376917
DOI: 10.2533/chimia.2018.690 -
International Journal of Molecular... Jul 2014The rotation of the earth on its axis creates the environment of a 24 h solar day, which organisms on earth have used to their evolutionary advantage by integrating this... (Review)
Review
The rotation of the earth on its axis creates the environment of a 24 h solar day, which organisms on earth have used to their evolutionary advantage by integrating this timing information into their genetic make-up in the form of a circadian clock. This intrinsic molecular clock is pivotal for maintenance of synchronized homeostasis between the individual organism and the external environment to allow coordinated rhythmic physiological and behavioral function. Aryl hydrocarbon receptor (AhR) is a master regulator of dioxin-mediated toxic effects, and is, therefore, critical in maintaining adaptive responses through regulating the expression of phase I/II drug metabolism enzymes. AhR expression is robustly rhythmic, and physiological cross-talk between AhR signaling and circadian rhythms has been established. Increasing evidence raises a compelling argument that disruption of endogenous circadian rhythms contributes to the development of disease, including sleep disorders, metabolic disorders and cancers. Similarly, exposure to environmental pollutants through air, water and food, is increasingly cited as contributory to these same problems. Thus, a better understanding of interactions between AhR signaling and the circadian clock regulatory network can provide critical new insights into environmentally regulated disease processes. This review highlights recent advances in the understanding of the reciprocal interactions between dioxin-mediated AhR signaling and the circadian clock including how these pathways relate to health and disease, with emphasis on the control of metabolic function.
Topics: Animals; Circadian Clocks; Dioxins; Environmental Illness; Homeostasis; Humans; Receptors, Aryl Hydrocarbon; Signal Transduction
PubMed: 24987953
DOI: 10.3390/ijms150711700 -
Bioscience, Biotechnology, and... Oct 2002In the last decade, extensive investigation has been done on the bacterial degradation of dioxins and its related compounds, because this class of chemicals is highly... (Comparative Study)
Comparative Study Review
In the last decade, extensive investigation has been done on the bacterial degradation of dioxins and its related compounds, because this class of chemicals is highly toxic and has been widely distributed in the environment. These studies have revealed the primary importance of a novel dioxygenation reaction, called angular dioxygenation, in the aerobic bacterial degradation pathway of dioxin. Accompanied by the electron transport proteins, Rieske nonheme iron oxygenase catalyzes the incorporation of oxygen atoms to the ether bond-carrying carbon (the angular position) and an adjacent carbon, resulting in the irreversible cleavage of the recalcitrant aryl ether bond. The 2,2',3-trihydroxybiphenyl or 2,2',3-trihydroxydiphenyl ether derivatives formed are degraded through meta cleavage. In addition to the degradation system of dibenzofuran and dibenzo-p-dioxin (the nonchlorinated model compounds of dioxin), those of fluorene and carbazole were shown to function in dioxin degradation. Some dioxin degradation pathways have been studied biochemically and genetically. In addition, feasibility studies have shown that some dioxin-degrading strains can function in actual dioxin-contaminated soil. These studies provide useful information for the establishment of a bioremediation method for dioxin contamination. This review summarizes recent progress on molecular and biochemical bases of the bacterial aerobic degradation of dioxin and related compounds.
Topics: Aerobiosis; Animals; Bacteria; Biodegradation, Environmental; Child; Dioxins; Guinea Pigs; Humans; Oxidation-Reduction; Rats
PubMed: 12450109
DOI: 10.1271/bbb.66.2001 -
Environment International Dec 2018Autism spectrum disorder (ASD) has emerged as a major public health concern due to its fast-growing prevalence in recent decades. Environmental factors are thought to... (Review)
Review
Autism spectrum disorder (ASD) has emerged as a major public health concern due to its fast-growing prevalence in recent decades. Environmental factors are thought to contribute substantially to the variance in ASD. Interest in environmental toxins as causes of ASD has arisen due to the high sensitivity of the developing human brain to toxic chemicals, particularly to dioxin and certain dioxin-like compounds (dioxins). As a group of typical persistent organic pollutants, dioxins have been found to exert adverse effects on human brain development. In this paper, we review the evidence for association of exposure to dioxins with neurodevelopmental abnormalities related to ASD based on both human epidemiological and animal studies. It has been documented that exposure to dioxins during critical developmental periods increased risk for ASD. This notion has been demonstrated in different populations exposed to high or background level of dioxins. Furthermore, the effects and mechanisms of action of dioxins relevant to the pathophysiology and pathogenesis of ASD are summarized, describing potential underlying mechanisms linking dioxin exposure with ASD onset. Further studies focusing on effects of prenatal/perinatal exposure to individual dioxin congeners or to mixtures of dioxins on ASD-associated behavioral and neurobiological consequences in animal models, and on the mechanisms of actions of dioxins, are needed in order to better understand how dioxin exposure might contribute to increased risk for ASD.
Topics: Animals; Autism Spectrum Disorder; Dioxins; Environmental Exposure; Environmental Pollutants; Humans; Risk Factors
PubMed: 30347373
DOI: 10.1016/j.envint.2018.10.028 -
Environmental Health Perspectives Mar 2011
Topics: Air Pollutants; Air Pollution; China; Dioxins; Environmental Exposure; Environmental Policy; History, 20th Century; History, 21st Century; Humans; Refuse Disposal
PubMed: 21356622
DOI: 10.1289/ehp.1103535 -
Scientific Reports Nov 2016The objective of the present study was to systematically assess the association between dioxin/2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and cancer incidence and... (Meta-Analysis)
Meta-Analysis
The objective of the present study was to systematically assess the association between dioxin/2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and cancer incidence and mortality. Systematic literature searches were conducted until July 2015 in Pubmed, Embase and Cochrane library to identify relevant studies. A random-effects model was applied to estimate the pooled odds ratio (OR), risk ratio (RR), standard incidence ratio (SIR) or standard mortality ratio (SMR) for cancer incidence or mortality. In addition, dose-response, meta-regression, subgroup, and publication bias analyses were conducted. Thirty-one studies involving 29,605 cancer cases and 3,478,748 participants were included. Higher external exposure level of TCDD was significantly associated with all cancer mortality (pooled SMR = 1.09, 95% CI: 1.01-1.19, p = 0.04), but not all cancer incidence (pooled RR = 1.01, 95% CI: 0.97-1.06, p = 0.49). Higher blood level of TCDD was both significantly associated with all cancer incidence (pooled RR = 1.57, 95% CI: 1.21-2.04, p = 0.001) and all cancer mortality (pooled SMR = 1.45, 95% CI: 1.25-1.69, p < 0.001). Subgroup analysis suggested that higher external exposure and blood level of TCDD were both significantly associated with the mortality caused by non-Hodgkin's lymphoma. In conclusion, external exposure and blood level of TCDD were both significantly associated with all cancer mortality, especially for non-Hodgkin's lymphoma.
Topics: China; Dioxins; Humans; Incidence; Neoplasms; Prognosis; Risk Factors; Survival Rate
PubMed: 27897234
DOI: 10.1038/srep38012 -
Environmental Pollution (Barking, Essex... Nov 2018The gut microbiome is sensitive to diet and environmental exposures and is involved in the regulation of host metabolism. Additionally, gut inflammation is an...
The gut microbiome is sensitive to diet and environmental exposures and is involved in the regulation of host metabolism. Additionally, gut inflammation is an independent risk factor for the development of metabolic diseases, specifically atherosclerosis and diabetes. Exposures to dioxin-like pollutants occur primarily via ingestion of contaminated foods and are linked to increased risk of developing cardiometabolic diseases. We aimed to elucidate the detrimental impacts of dioxin-like pollutant exposure on gut microbiota and host gut health and metabolism in a mouse model of cardiometabolic disease. We utilized 16S rRNA sequencing, metabolomics, and regression modeling to examine the impact of PCB 126 on the microbiome and host metabolism and gut health. 16S rRNA sequencing showed that gut microbiota populations shifted at the phylum and genus levels in ways that mimic observations seen in chronic inflammatory diseases. PCB 126 reduced cecum alpha diversity (0.60 fold change; p = 0.001) and significantly increased the Firmicutes to Bacteroidetes ratio (1.63 fold change; p = 0.044). Toxicant exposed mice exhibited quantifiable concentrations of PCB 126 in the colon, upregulation of Cyp1a1 gene expression, and increased markers of intestinal inflammation. Also, a significant correlation between circulating Glucagon-like peptide-1 (GLP-1) and Bifidobacterium was evident and dependent on toxicant exposure. PCB 126 exposure disrupted the gut microbiota and host metabolism and increased intestinal and systemic inflammation. These data imply that the deleterious effects of dioxin-like pollutants may be initiated in the gut, and the modulation of gut microbiota may be a sensitive marker of pollutant exposures.
Topics: Animals; Dioxins; Gastrointestinal Microbiome; Homeostasis; Inflammation; Intestines; Male; Metabolomics; Mice; Microbiota; Polychlorinated Biphenyls; Polychlorinated Dibenzodioxins; RNA, Ribosomal, 16S; Toxicity Tests
PubMed: 30373033
DOI: 10.1016/j.envpol.2018.07.039 -
Chemosphere Feb 2022In the two rounds of the UNEP-coordinated 'Biennial interlaboratory assessments of POPs laboratories, which were implemented in 2016/2017 and 2018/2019, 56 and 46...
In the two rounds of the UNEP-coordinated 'Biennial interlaboratory assessments of POPs laboratories, which were implemented in 2016/2017 and 2018/2019, 56 and 46 laboratories submitted results for dioxin-like persistent organic pollutants (dl-POPs). Test matrices consisted of solutions of analytical standards and naturally contaminated sediment, air extract, fish and human milk. Performance assessment using z-scores so that satisfactory performance corresponded to 2 z = ±25%, which is recommended for laboratories submitting data to the global monitoring plan of the Stockholm Convention on POPs. Participation has shown that analytical capacity for analyzing dl-POPs exist in all UN regions; however, in Africa and Central and Eastern European countries capacities are (very) limited; in Latin America capacity is increasing. The presence of dioxin laboratories is not limited to industrialized or OECD countries but also present in developing countries such as China, Brazil, Egypt, Thailand, or Vietnam. Laboratories using established methods based on gas chromatographs coupled to high-resolution mass spectrometers (sector field instruments only) by far had the best results. Among the test samples, human milk and especially fish in the last round posed severe problems to all laboratories so that performance must improve, especially in foodstuffs at (very) low concentrations.
Topics: Animals; Dibenzofurans, Polychlorinated; Dioxins; Environmental Monitoring; Fishes; Humans; Milk, Human; Polychlorinated Biphenyls; Polychlorinated Dibenzodioxins
PubMed: 34606892
DOI: 10.1016/j.chemosphere.2021.132449