Intake and faecal excretion of chlorinated dioxins and dibenzofurans in breast-fed infants at different ages

Pluim, H.J.; Wever, J.; Koppe, J.G.; Slikke, J W van der; Olie, K.

doi:10.1016/0045-6535(93)90021-v

Cited by 32 publications

(14 citation statements)

References 4 publications

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“…In comparison, the levels in two non-breast-fed infants of 3.8 and 4.8 months of age were 2.8 and 2.1 ng TEQ/kg body wt, respectively. This cannot be explained by low absorption of dioxins in the breast-fed infant, since the bioavailability of dioxins from human milk has been shown to be about 95% (Pluim et al 1993a). In another work reported a study of portal absorption of dioxin using three 14 C-tagged compounds: 14 Cphenanthrene, 14 C-benzo[a]pyrene or 14 CTCDD (TCCD: 2 ,3,7,8-tetrachlorodibenzo-p-dioxin) in the growing pig.…”

Section: Human Health Risk By Dietary Dioxinsmentioning

confidence: 96%

Levels and congener distributions of PCDDs, PCDFs and dioxin-like PCBs in environmental and human samples: a review

Srogi

2007

Environ Chem Lett

180

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The term ''dioxins'' is often used in a confusing way. In toxicological considerations-and also in the present report-the term is used to designate the PCDDs, the PCDFs and the coplanar (''dioxin-like'') PCBs, since these classes of compounds show the same type of toxicity. Because of the large number of congeners, relevant individual congeners are assigned with a toxic equivalency factor (TEF) that relate their toxicity to that of tetrachlorodibenzo-p-dioxin (TCDD) (2,3,7,8-TCDD) and are to be evaluated as dioxins. Each concentration of an individual congener in a mixture is multiplied with its TEF, and the resulting TCDD equivalents are added up and expressed as WHO-endorsed toxic equivalents (WHO-TEQ). Polychlorinated dibenzo-p-dioxins (PCDDs) and polychlorinated dibenzofurans (PCDFs) are mainly the by-products of industrial processes (such as metallurgical processing, bleaching of paper pulp, and the manufacturing of some herbicides and pesticides) but they can also result from natural processes like volcanic eruptions and forest fires. Waste incineration, particularly if combustion is incomplete, is among the largest contributors to the release of PCDDs and PCDFs into the environment. Due to their persistence, PCDDs, PCDFs and PCBs are part of the socalled persistent organic pollutants group of compounds that also include some chlorinated pesticides. Since they have a high lipophilicity and resist transformation, they bio-accumulate in animal and human adipose tissues. Consumption of food is considered as the major source of non-occupational human exposure to PCDD/Fs with foodstuffs from animal origin accounting for more than 90% of the human body burden. With meat, dairy, and fish products being the main contributors. The aim of the present review was to summarize experimental data regarding dioxin emissions from contaminated and uncontaminated biological and environmental samples, from the available literature. The information will be presented chronologically with respect to distribution in human milk, serum; food, water, air, soils and sediments.

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Section: Human Health Risk By Dietary Dioxinsmentioning

confidence: 96%

Levels and congener distributions of PCDDs, PCDFs and dioxin-like PCBs in environmental and human samples: a review

Srogi

2007

Environ Chem Lett

180

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“…Bioavailability of dioxins from nursing seems to be more than 95%. 37 Mothers with a high body burden of dioxins could transmit these to their progeny through the placenta and breast milk, indicating that such babies are a highly exposed population. In laboratory animals, dioxins are excreted in the feces and urine by a variety of mechanisms.…”

Section: Toxicokineticsmentioning

confidence: 99%

Health Impact of Polychlorinated Dibenzo-p-dioxins: A Critical Review

Mukerjee

1998

Journal of the Air & Waste Management Association

122

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Polychlorinated dibenzo-p-dioxins (PCDDs), commonly known as dioxins, form as unwanted impurities in the manufacturing of chlorophenol and its derivatives-pulp and paper-and in the combustion of municipal, sewagesludge, hospital, and hazardous waste. Combustion, in presence of a chlorine donor, seems to be a major source of these compounds. High levels of dioxins are also emitted from metallurgical industries including copper smelters, electric furnaces in steel mills, and wire reclamation incinerators. Trace levels are detectable in emissions from motor vehicles using leaded gasoline or diesel fuel, in forest fires, and in residential wood burning.Extremely persistent and widely distributed in the environment, PCDDs have been detected in all three primary and many secondary media. Releases into the air occur mainly from combustor emissions. Atmospheric dispersion, deposition, and subsequent accumulation in the food chain seem to be the major pathways of exposure to the general population. Residues of these chemicals have been detected in soil, sediment, fish, meat, cow's milk, human adipose tissue, and mothers' milk. In general, these chemicals have high lipophilicity. The elimination half-life of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) in humans is approximately 7-11 years.Very little human toxicity data from exposure to PCDDs are available. Health-effect data obtained from occupational settings in humans are based on exposure to chemicals contaminated with TCDD. It produces a spectrum of toxic effects in animals and is one of the most toxic chemicals known. Most of the toxicity data available on TCDD are from high-dose oral exposures to animals. Very few percutaneous and no inhalation exposure data are available in the literature. There is a wide range of difference in sensitivity to PCDD lethality in animals. The signs and symptoms of poisoning with chemicals contaminated with TCDD in humans are analogous to those observed in animals. Dioxin exposures to humans are associated with increased risk of severe skin lesions such as chloracne and hyperpigmentation, altered liver function and lipid metabolism, general weakness associated with drastic weight loss, changes in activities of various liver enzymes, depression of the immune system, and endocrine-and nervous-system abnormalities. It is a potent teratogenic and fetotoxic chemical in animals. A very potent promoter in rat liver carcinogenesis, TCDD also causes cancers of the liver and other organs in animals.

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“…CDFs were reported in the liver and adipose tissue of a breast-fed infant bom to a mother with CDFs poisoning (Masuda et al, 1985). Studies in infants of mothers who were exposed to average environmental levels found in industrialized countries showed that some highly chlorinated congeners were more readily eliminated in infants' stools (Jbdicke et al, 1992;Pluim et al, 1993). In contrast, tetrachlorinated and hexachlorinated congeners were poorly eliminated (absorption was more than 90%).…”

Section: Exposurementioning

confidence: 93%

Breast-Feeding Exposure of Infants To Environmental Contaminants — a Public Health Risk Assessment Viewpoint: Chlorinated Dibenzodioxins and Chlorinated Dibenzofurans

Pohl¹,

Hibbs

1996

Toxicol Ind Health

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Exposure of children to chlorinated dibenzodioxins and chlorinated dibenzofurans via breast-feeding has been well-documented in industrialized countries. Recent studies indicate a possible link between development of subtle health effects in children and their exposure to dioxin-like chemicals from maternal milk. Some examples of the effects are lower vitamin K levels, increased thyroxine levels, and mild changes in liver enzymes. The projected daily intakes of chlorinated dibenzodioxins and chlorinated dibenzofurans are compared with minimal risk levels for intermediate duration oral exposure (15-365 days) derived for these chemicals. Public health recommendations for future actions related to infant intake of chlorinated dibenzodioxin- and chlorinated dibenzofuran-contaminated breast milk are also addressed.

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Intake and faecal excretion of chlorinated dioxins and dibenzofurans in breast-fed infants at different ages

Cited by 32 publications

References 4 publications

Levels and congener distributions of PCDDs, PCDFs and dioxin-like PCBs in environmental and human samples: a review

Levels and congener distributions of PCDDs, PCDFs and dioxin-like PCBs in environmental and human samples: a review

Health Impact of Polychlorinated Dibenzo-p-dioxins: A Critical Review

Breast-Feeding Exposure of Infants To Environmental Contaminants — a Public Health Risk Assessment Viewpoint: Chlorinated Dibenzodioxins and Chlorinated Dibenzofurans

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