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Human Exposure from Dioxins in Soil
Abstract
Dioxins are a family of chemical compounds that has received considerable attention, both historically and currently. This article reviews scientific field studies that examine the relationship between living on soil contaminated with dioxins and the level of dioxins in people's serum, with an emphasis on the University of Michigan Dioxin Exposure Study (UMDES), the largest and most comprehensive study of its kind. These studies conclude that the levels of dioxins in serum are most strongly correlated with age, gender, body mass index, weight loss, breast feeding, and smoking. Levels of dioxins in soil are not significant predictors for dioxin concentrations in serum. The increase in serum dioxin levels that is seen with age results from historic exposure and does not represent ongoing exposure. Based on the scientific field studies conducted to date, it appears that, in the absence of the consumption of contaminated animal products, there is little evidence of ongoing exposure from contaminated soil.
... "Matched" serum, residential soil, and house dust samples were collected from more than 700 subjects who were a representative sample of individuals living in the contaminated region, and also including control subjects living more than 100 miles from the contaminated area, making this the largest study of its kind. Regression models found that soil factors and dust factors were not predictive of serum TEQ or serum levels of key individual congeners (2,3,7,8-TCDD, octachlorodibenzodioxin (OCDD), 2,3,4,7,8-PCDF) [100]. It is notable that over 20% of subjects in the UMDES lived on soil with OCDD concentrations .1000 ...
... Though the TEF for OCDD is low (TEF 5 3 3 10 24 ), differences in gastrointestinal absorption among dioxin congeners only vary by about a factor of 2 [101,102], and so the regression model result for OCDD would indicate that the current USEPA Preliminary Remediation Goal (PRG) of 1000 ppt TEQ in soil is protective [103]. Regression models of major PCBs in serum (PCB 105, PCB 118, and PCB 126) showed small contributions to variance from residential soil and/or house dust (all about 1% [100]), but this was thought to reflect aerial exposure rather than direct exposure from soil or dust, as it is well known that many building materials and household furnishings have been demonstrated to be sources of PCBs in soil and in indoor air and dust [104À107]. p0235 A major criticism of the UMDES has been that it excluded subjects who were ,18 years of age, and therefore it did not provide information about exposure to dioxins in dust and/or soil to children. ...
This chapter first discusses the various aspects of human biomonitoring that are important to be able to use human data in a forensic context. Important aspects include: (1) toxicokinetics-absorption, distribution, metabolism, and elimination; (2) sensitive analytical chemistry methods; (3) characterizing normal background population levels such as in the US National Report on Human Exposure to Environmental Chemicals as well as in other countries; (4) development of reference values and biomonitoring equivalents; and (5) environmental exposure pathways, such as food, soil, dust, clay, and beef. Various human exposures are then discussed related to accidental exposures, poisonings, food contamination incidents, and occupational exposures such as e-waste and various manufacturing processes.
... Thus, dioxins are known as the "poisons of the century" and is one of the world's most toxic compounds [3]. According to previous reports, these poisonous pollutants are a historical problem in the environment, including soil, water, and air, mainly due to their slow decomposition, which ranges from decades to centuries, and bioaccumulative behavior [5][6][7][8][9]. Therefore, the effort to eliminate and degrade these recalcitrant pollutants still remains a challenge, particularly in water (surface water or groundwater). ...
Dioxins/furans are classified as highly toxic chemicals that seriously affect human health. To remove dioxin residues from contaminated water, CuZn-ZIFs, a material from bimetallic zeolitic imidazolate frameworks (ZIFs) has been synthesized and explored its efficacy treatment with dibenzofuran (DBF). The pristine structure of CuZn-ZIFs was confirmed using powder X-ray diffraction, Fourier-transform infrared, thermogravimetric analysis, energy-dispersive X-ray, Brunauer–Emmett–Teller, and scanning electron microscopy. CuZn-ZIFs exhibited its role as a heterogeneous catalyst promoting H 2 O 2 oxidation and as an adsorbent in DBF treatment. Herein, at room temperature, more than 86% of DBF adsorbed and 90% of DBF degraded in the presence of H 2 O 2 with 10 mg catalyst dosage, 30 ppm of DBF within 40 and 60 min, respectively. Remarkably, the CuZn-ZIFs’ reusability of each process showed a high efficacy removal with over 80% after five cycles. Therefore, CuZn-ZIFs synthesized could be a prospective candidate for the indirect or direct degradation of dioxins/DBF derivatives from contaminated water.
... In recent years, polychlorinated dibenzofurans (PCDFs) and polychlorinated dibenzo-p-dioxins (PCDDs) have been paid increasing attention due to the potential harm to the environment and human body (Demond et al. 2012;Fiedler et al. 1995). The dioxins are primarily emitted from the municipal solid waste incinerations (MSWIs) (Tang et al. 2013). ...
In this work, titania supported catalysts (V-W/Ti) with different vanadium-tungsten contents were prepared and evaluated in the catalytic oxidation of chlorobenzene, which was used as the model compound of dioxins. The results showed that V2O5 is the main active component for chlorobenzene oxidation, and doping of WO3 affects the valence distributions of vanadium, contributing a bimetallic synergistic effect. The catalysts were investigated by XRD, SEM–EDS mapping, Raman, and XPS, and the changes in V element valence state and chlorine content on fresh and used catalysts were observed by XPS. Moreover, in situ FTIR studies and chlorine balance were also conducted, the addition of WO3 is helpful to the breakage of C–Cl, and a reaction mechanism for the catalytic oxidation of chlorobenzene was proposed. 3 V-5 W/Ti catalyst with better catalytic activity was selected for catalytic oxidation of PCDD/Fs using a lab scale PCDD/Fs generating and decomposing system. The degradation efficiency was 66.5% at 200 °C and 62.2% at 300 °C, which indicated that the low reaction temperature of 200 °C was conducive to the catalytic degradation of PCDDs, while the high temperature of 300 °C was facilitated the degradation of PCDFs.
... Soils are known as collectors and sinks of PCDDs and PCDFs due to limited removal and long half-life of such chemicals (Brzuzy and Hites, 1996). The average background levels of dioxins in soils are estimated as 1 ng/g, mostly made of specific congeners as for instance the octachlorodibenzo-p-dioxins (OCDDs) (Demond et al., 2012). Soil pollution is challenging in almost every country worldwide and it calls for appropriate environmental risk assessment tools and management strategies. ...
The suitability of the AhR reporter gene bioassays to screen the presence of polychlorinated dibenzo-p-dioxins/furans (PCDD/Fs) and dioxin-like polychlorinated biphenyls (dl-PCBs) in sewage sludge (SL) and related hydrochar (HC) was here investigated. Samples of SL obtained from six WWTPs were processed by hydrothermal carbonization to obtain the resultant HCs and both tested with DR-CALUX® bioassay. Levels of PCDD/Fs and dl-PCBs were also determined analytically in the same samples by GC-MS/MS. Bioanalytical Toxicity Equivalent values (BEQ) resulted in one order of magnitude higher in HC compared to SL samples and those obtained from the dl-PCBs fraction higher than those from PCDD/Fs. BEQ and TEQWHO values, the latter obtained by GC-MS/MS analysis on the same matrices, were highly correlated showing also a similar trend in the six WWTPs (RS= 0.8252, p < 0.001; Pearson’s R RP=0.8029, p < 0.01). The suitability of AhR bioassays and in particular of the DR-CALUX® to screen the presence and biological activity of legacy organohalogen compounds in both SL and HC matrices was demonstrated for the first time which support their usage for the assessment of potential risks associated with their further environmental applications.
... In terms of the exposure pathway contribution, the ingestion and dermal contact routes played a more important role in the daily intakes and potential health risks of ash-bound PCDD/Fs, as compared with those of ash-emitted inhalation. It should be noted that these estimations focused only on the workplace ash, whereas food and other media such as indoor and outdoor air, soil, and house dust are considerable sources of human exposure to dioxins (Srogi 2008;Demond et al. 2012;Tue et al. 2013;Li et al. 2016). Therefore, a more comprehensive risk assessment of PCDD/Fs and other DRCs is needed, especially for the highrisk occupational groups. ...
The residue concentrations and congener profiles of polychlorinated dibenzo-p-dioxins/furans (PCDD/Fs) were examined in fly ash and bottom ash released from different thermal industrial processes in Vietnam. PCDD/F concentrations and toxic equivalents (TEQs) in the ash samples varied greatly and decreased in the following order: steel making > aluminum recycling > medical waste incinerator > boilers > municipal waste incinerator > tin production > brick production > coal-fired power plant. Both the precursor and de novo synthesis were estimated as possible formation mechanisms of dioxins in the ash, but the latter pathway was more prevalent. The highest emission factors were estimated for the ash released from some steel-making plants, aluminum-recycling facilities, and a medical waste incinerator. The emission factors of PCDD/Fs in ash released from some steel plants of this study were two to six times higher than the UNEP Toolkit default value. The annual emission amount of ash-bound dioxins produced by 15 facilities in our study was estimated to be 26.2 to 28.4 g TEQ year−1, which mainly contributed by 3 steel plants. Health risk related to the dioxin-containing ash was evaluated for workers at the studied facilities, indicating acceptable risk levels for almost all individuals. More comprehensive studies on the occurrence and impacts of dioxins in waste streams from incineration and industrial processes and receiving environments should be conducted, in order to promote effective waste management and health protection scheme for dioxins and related compounds in this rapidly industrializing country.
... The World Health Organization (WHO) assigned toxic equivalency factors (TEFs) to PCDD/Fs and dl-PCBs to allow the risks posed by these chemicals to be quantified ( Van den Berg et al., 2006). The toxic equivalents (TEQ) calculated using these TEFs can be used to estimate the total risk posed by PCDD/Fs and PCBs in the material of interest (Demond et al., 2012). We evaluated the risks posed by PCDD/Fs and PCBs to humans consuming crabs from the study area. ...
Polychlorinated dibenzo-p-dioxins and dibenzofurans (PCDD/Fs) and polychlorinated biphenyls (PCBs) in Chinese mitten crabs from several areas were determined. The toxic equivalents (TEQs) for the mean PCDD/F and total PCDD/F and dioxin-like PCBs were 2.9 ± 2.7 and 5.7 ± 4.0 pg TEQ g-1, respectively. The mean concentrations of PCBs and dl-PCBs were 282 and 59 times the concentrations of PCDD/Fs, respectively. PCDD/F and PCB sources in the crab food web were assessed. The total TEQ of PCDD/F and PCB supplied by crab compound feed was 2.1 times the TEQ in crab meat. Broken corn, aquatic biota, and water contributed around 12% of the total TEQ inputs for crab meat. The contribution from sediment was around 164 times that from crab meat, and sediment may be the most important source of PCDD/Fs and PCBs in cultured crabs. Principal component analysis (PCA) and stable isotope ratios for nitrogen (δ15N) and carbon (δ13C) supported the TEQ results. The mean total PCDD/F and dl-PCB TEQ exposure for humans consuming crabs was 3.4 pg TEQ per kilogram of body weight per day. The PCDD/Fs and PCBs in >80% of the crab samples would not cause the tolerable daily intake to be exceeded.
... Under the international treaty known as the Stockholm Convention, a number of persistent organic pollutants (POPs) have been banned or restricted in many countries. However, these types of pollutants still garner significant attention because of their persistence (Demond et al., 2011), bioaccumulation, movement over long distances and adverse health effects (Hänninen et al., 2014;Kang et al., 2008). ...
... Polychlorinated-dibenzo-p-dioxins (PCDDs), polychlorinated- dibenzofurans (PCDFs) and polychlorinated biphenyls (PCBs), or PCDDs/Fs/PCBs, are, under the ruling of the United Nations Stockholm 2009 Convention, well-established toxic persistent organic pollutants that persist as a worldwide issue of great con- cern [1,2]. These dangerous contaminants are released into the environment from numerous sources such as municipal and industrial waste incineration, and as by-products from the manu- facture of chlorinated chemical compounds and from engine exhaust [3,4]. ...
PCDDs, PCDFs, and PCBs present in soil can be hydrodechlorinated without a preliminary separation (extraction) step using a nano-size dispersed mixture of metallic Ca and CaO (206 nm average particle size). The treatment is quite simple: grinding in an electric mortar (100 rpm) at room temperature in open atmosphere for 24 h, producing up to 91, 99 and 97% hydrodechlorination yield for PCDDs, PCDFs and PCBs, respectively. The method is sensitive to soil moisture content, but because of its simplicity and low-cost, it can accommodate larger-scale adaptation. © 2015 American Institute of Chemical Engineers Environ Prog, 2015
... Unfortunately' mechanisms of varied toxicity are sti.ll no1 fulty characterised but there is a consensus that many of the toxic effects of dioxins and DL-pCBs result from their binding to the Ah receptor (Anonymous, 2003;Demond et al',2012;Denison et aL,2011;Poland and Glover' 1973;Safe et al"2013)' PCDDs' pcDFs and DL-PCBs are ubiquitously present in human tissues Although exPosure could occur through inhalation of air, dermal absorption, drinking water and food consumption' the latter is the predominant loute of exposure for the general population (Fiirst ef a\,,1993;Liemet al,,' 2000). They are readily absorbed following ingestion and they are distributed throughout the 409 Hqndbook of eggs in humon function body with highest accumulation in the liver and adipose tissue. ...
... The PBPK model demonstrated that exposures to DLCs in soils contributed very little to serum levels, even at soil concentrations of up to 2000 ppt, relative to the background sources of exposure included in this assessment. This finding is consistent with findings of recent community exposure studies (Garabrant et al., 2009a; Diliberto et al., 2010; Demond et al., 2011) where investigators found similar serum concentrations in both potentially exposed and unexposed individuals, indicating that soil exposures have little impact on body burden. Our findings are also consistent with PBPK modeling conducted by the US EPA to evaluate exposures to DLCs in Midland, MI, as part of the Agency's review of UMDES (US EPA, 2009b). ...
The need to remediate contaminated soils is typically accomplished by applying standard risk assessment methods followed by risk management to select remedial options. These human health risk assessments (HHRAs) have been largely conducted in a formulaic manner that relies heavily on standard deterministic exposure, toxicity assumptions and fixed mathematical formulas. The HHRA approach, with its traditional formulaic practice, does not take advantage of problem formulation in the same manner as is done in ecological risk assessment, and historically, has generally failed to emphasize incorporation of site-specific information. In response to these challenges, the National Academy of Sciences recently made several recommendations regarding the conduct of HHRAs, one of which was to begin all such assessments with problem formulation. These recommendations have since been extended to dose response assessment. In accordance with these recommendations, a group of experts presented and discussed findings that highlighted the importance and impact of including problem formulation when determining the need for remediation of dioxin contamination in soils, focusing in particular on exposure assessment is described.
... In 2004-5, the University of Michigan Dioxin Exposure Study (UMDES) gathered blood samples from residents, samples of their residential soil and house dust, and information about their behaviors that could influence their exposure. This information was then analyzed to determine whether and under what circumstances environmental concentrations of dioxins were correlated with resident body burdens (Demond et al., 2012;Garabrant et al., 2009aGarabrant et al., , 2009b, and the results were communicated to stakeholders and community residents through a variety of methods, including the study web site, public meetings, media contacts, and confidential communications to study participants (Franzblau et al., 2011). ...
Chemical properties of contaminants lead them to behave in particular ways in the environment and hence have specific pathways to human exposure. If residents of affected communities lack awareness of these properties, however, they could make incorrect assumptions about where and how exposure occurs. We conducted a mailed survey of 904 residents of Midland and Saginaw counties in Michigan, USA to assess to what degree residents of a community with known dioxin contamination appear to understand the hydrophobic nature of dioxins and the implications of that fact on different potential exposure pathways. Participants assessed whether various statements about dioxins were true, including multiple statements assessing beliefs about dioxins in different types of water. Participants also stated whether they believed different exposure pathways were currently significant sources of dioxin exposure in this community. A majority of residents believed that dioxins can be found in river water that has been filtered to completely remove all particulates, well water, and even city tap water, beliefs which are incongruous with the hydrophobic nature of dioxins. Mistrust of government and personal concern about dioxins predicted greater beliefs about dioxins in water. In turn, holding more beliefs about dioxins in water predicted beliefs that drinking and touching water are currently significant exposure pathways for dioxins. Ensuring that community residents' mental models accurately reflect the chemical properties of different contaminants can be important to helping them to adjust their risk perceptions and potentially their risk mitigation behaviors accordingly.
... Samples from each of three matrices were analyzed for the PCDD/F and PCB congeners included in the World Health Organization-designated 29 congeners [15] by Vista Analytical in El Dorado Hills, California, USA, using U.S. Environmental Protection Agency (U.S. EPA) methods 8290 and 1668 [16,17]. Details regarding respondent selection, sample collection, and summary statistical results for each matrix can be found in Garabrant et al. [14,18], Hedgeman et al. [19], and Demond et al. [10,20]. ...
As part of the University of Michigan Dioxin Exposure Study, soil, household dust, and serum samples were collected from more than 750 households in five populations around the city of Midland and in Jackson and Calhoun Counties, Michigan, USA. Polytopic vector analysis, a type of receptor model, was applied to better understand the potential sources of polychlorinated dibenzo-p-dioxins and polychlorinated dibenzofurans found in these samples and to quantify the contributions of the sources in each matrix across populations. The results indicated that source signatures found in soil are similar to those found in dust, reflecting various combustion profiles, pentachlorophenol, and graphite electrode sludge. The profiles associated with contamination in the Tittabawassee River, likely related to historical discharges from the Dow Chemical Company facility in Midland, exhibited the largest differences among the regional populations sampled. Differences in serum source contributions among the study populations were consistent with some of the regional differences observed in soil samples. However, the age trends of these differences suggested that they are related to past exposures, rather than ongoing sources. Environ. Toxicol. Chem. 2012; 31: 2191-2200. © 2012 SETAC.
This chapter is intended to provide a detailed weight of evidence scientific review on polychlorinated biphenyls (PCBs) and polybrominated biphenyls (PBBs). Notably, PCBs are among the most thoroughly studied chlorinated persistent organic pollutants to date; despite their discontinued commercial production in the 1970s, their environmental persistence and widespread distribution continue to garner research attention regarding potential impacts on human health. Due to the voluminous literature pertaining to exposure and toxicology of PCBs, for practical purposes, this chapter was written to capture the scientific highlights of greatest import with respect to knowledge on exposures and toxicological properties of these compounds.
Incidence of autoimmune disorders, birth defects, and neurological diseases rose over the past 50 years due to increasing variety and quantity of pollutants. To date, there appear few methods capable to evaluate and predict mixture effects. For the first time ever, we have developed calculus to determine mixture effects for all kinds of endocrine disrupting chemicals.
Our method uses the golden ratio φ and draws from bifurcation and chaos theory. From extensive analysis, and using the concept of molecular mimicry, we developed the equation: effect=(100%)/(1+e^5∙∑〖K_i [C_i]〗^(-n_i φ) ). We tested the equation for a range of cohort studies and biomarkers, and for different pollutants like heavy metals, thyroid hormone mimickants, chromate/chlorate, etc.
The equation is simple enough for use by a layman. The method is universal and calculation is data 'light', requiring only pollutant concentrations [C], potencies K and an integer n for endocrinal involvement. I envision far-reaching impact because all people and populations can be better assessed for their health effects from pollutant exposure. I provide useful examples and interpret results.
Dioxins and dioxin-like compounds comprise a group of chemicals including polychlorinated dibenzo-p-dioxins (PCDD) and polychlorinated dibenzofurans (PCDF), as well as certain dioxin-like polychlorinated biphenyls (dl-PCB), and potentially others. They act via a common mechanism, stimulation of aryl hydrocarbon receptor (AH receptor, AHR), a vital transcription factor in cells. There are very high differences in potency among these compounds, i.e. in the ability to stimulate the receptor. This leads to ten thousand fold or higher differences in doses causing similar toxic effects. Most of these compounds are eliminated very slowly in the environment, animals, or humans, which makes them persistent. They are much more soluble in fat than in water, and therefore they tend to accumulate in lipid or fatty tissues, and concentrate along the food web (bioaccumulation and biomagnification).
PCDD/PCDFs are formed mostly as side products in burning processes, but PCBs were oils manufactured for many purposes. Because of toxicity and persistence, dioxin-like compounds have been regulated strictly since 1980s, and their levels in the environment and animals have decreased by an order of magnitude or more. Therefore the effects on wildlife have clearly decreased, and even populations at the top of the food web such as fish-eating birds or seals have recovered after serious effects on their reproductive capacity and developmental effects in their young especially in 1970s and 1980s. This does not exclude the possibility of some remaining effects.
In humans the intake is mostly from food of animal sources, but because our diet is much more diverse than that of such hallmark animals as white-tailed eagles or seals, the concentrations never increased to similar levels. However, during 1970s and 1980s effects were probably also seen in humans, including developmental effects in teeth, sexual organs, and the development of immune systems.
Both scientists and administrative bodies debate at the moment about the importance of remaining risks. This is very important, because the AH receptors seem to be physiologically important regulators of growth and development of organs, immunological development, food intake and hunger, and in addition regulate enzymes protecting us from many chemicals. Thus a certain level of activation is needed, although inappropriate stimulation of the receptor is harmful. This dualism emphasizes the importance of benefit versus risk analysis. As a whole, regulating the emissions to the environment is still highly important, but one should be very cautious in limiting consumption of important and otherwise healthy food items and e.g. breast feeding.
Distinct toxic effects of high doses of dioxins in humans have been clearly demonstrated by frank poisonings and the highest occupational exposures. Hallmark effects have been skin lesions called chloracne, various developmental effects of children, and a slightly increased risk of total cancer rate. The highest dioxin levels have been ten thousand fold higher than those seen in the general population today.
Proximity to facilities emitting polychlorinated dibenzo-p-dioxins and polychlorinated dibenzofurans (PCDD/F) has been associated with increased risk of non-Hodgkin lymphoma (NHL). There is limited information about whether proximity to industrial sources leads to indoor PCDD/F contamination of homes. We measured carpet dust concentrations (pg/g) of 17 toxic PCDD/F congeners and calculated their toxic equivalence (TEQ) in 100 homes in a population-based case-control study of NHL in Detroit, Los Angeles, Seattle, and Iowa (1998-2000). We took global positioning system readings at residences and obtained coordinates and PCDD/F emissions (ng TEQ/yr) from an Environmental Protection Agency database for 6 facility types: coal-fired electricity generating plants, cement kilns burning non-hazardous waste, hazardous waste incinerators, medical waste incinerators, municipal solid waste incinerators, and sewage sludge incinerators. For each residence, we computed an inverse distance-squared weighted average emission index (AEI [pg TEQ/km(2)/yr]) for all facilities within 5km from 1983 to 2000. We also computed AEIs for each of the 6 facility types. We evaluated relationships between PCDD/F dust concentrations and the all-facility AEI or categories of facility-type AEIs using multivariable linear regression, adjusting for study center, demographics, and home characteristics. A doubling of the all-facility AEI was associated with a 4-8% increase in PCDD/F dust concentrations of 7 of 17 PCDD/F congeners and the TEQ (p-value<0.1). We also observed positive associations between PCDD/F dust concentrations and facility-type AEIs (highest vs. lowest exposure category) for municipal solid waste incinerators (9 PCDD/F, TEQ), and medical waste incinerators (7 PCDD/F, TEQ) (p<0.1). Our results from diverse geographical areas suggest that industrial PCDD/F emission sources contribute to residential PCDD/F dust concentrations. Our emissions index could be improved by incorporating local meteorological data and terrain characteristics. Future research is needed to better understand the links between nearby emission sources, human exposure pathways, and health risks.
Objective:
To determine if service members deployed to locations with open air burn pits have different serum microRNA (miRNA) profiles after deployment compared with length-of-service matched, non-deployed individuals. We also tested for correlations between miRNA and serum levels of Polychlorinated Dibenzo-p-Dioxins/Dibenzofurans (PCDD/PCDFs).
Methods:
MiRNAs were isolated and quantified by PCR array. Groups were analyzed for differences in miRNA expression. Correlations between serum miRNA and PCDD/PCDFs were assessed with a linear regression model.
Results:
Several miRNAs were differentially expressed after deployment and a partially overlapping set of miRNAs were identified between deployed and non-deployed individuals. Significant correlations between miRNAs and PCDD/PCDFs were identified.
Conclusions:
Serum miRNA levels show a link between deployment to locations with open burn pits and environmental exposures that can take place during deployment.
2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) (CAS No. 1704-01-6) is a colorless to white crystalline solid, which is the most toxic of a class of 75 structurally related congeners called chlorinated dibenzo-p-dioxins. TCDD is a waste byproduct, which did not exist prior to industrialization except in small amounts due to natural combustion and geological processes. The largest unintentional production of dioxins occurs through waste incineration, some metal production, and petroleum and wood combustion. TCDD is considered to be one of the most toxic chemicals known that interferes with biochemical, cellular, and tissue-level changes in normal biological processes by inducing microsomal enzymes in the liver primarily by binding to aryl hydrocarbon receptor.
The University of Michigan Dioxin Exposure Study provides extensive data on elevated residential soil and house dust concentrations of polychlorinated dioxins and dibenzofurans (PCDD/Fs) and adult body burdens among residents near a chemical manufacturing plant in Midland, Michigan. Recent reports found no significant contribution of residential soil/dust concentrations to serum lipid PCDD/Fs in adults. Although child body burdens were not studied by the University of Michigan, internal dose modeling that incorporates recent findings on demonstrated shorter elimination half life of PCDD/Fs in children (1-2year half life in children vs. ∼7years in older adults) can be applied to assess this important issue. The model examines children (ages 0-7years) with background dietary intake and exposure to residential soils at selected concentrations (10, 100 and 1000pg/g 2,3,7,8-tetrachlorodibenzo-p-dioxin toxic equivalents, TEQ) using the congener patterns observed in Midland. Model predictions assuming 50th percentile TEQ uptake from soil/dust-related dermal and ingestion exposures indicate no measurable changes in serum lipid TEQ concentrations up to 1000pg/g in soil/dust. Assuming 95th percentile uptake, the model shows no measurable serum lipid TEQ change up to 100pg/g in soil/dust, but serum lipid TEQ levels rose ∼2pg/g at 1000pg/g in soil/dust. Since the vast majority of soil/dust data were below 100pg/g, Michigan children exposed to such soil/dust TEQ concentrations are not reasonably expected to exhibit measurable changes in serum lipid TEQ concentrations when compared to typical background dietary exposures. With adequate data, this approach can be applied to evaluate child dose and risk for other persistent chemicals.
Octachlorodibenzodioxin (OCDD) forms spontaneously from pentachlorophenol (PCP) on the surfaces of Fe(III)-saturated smectite clay. (1) Here, we used in situ Fourier transform infrared (FTIR) methods and quantum mechanical calculations to determine the mechanism by which this reaction is initiated. As the clay was dehydrated, vibrational spectra showed new peaks that grew and then reversibly disappeared as the clay rehydrated. First-principle density functional theory calculations of hydrated Fe/PCP clusters reproduced these transient FTIR peaks when inner-sphere complexation and concomitant electron transfer produced Fe(II) and PCP radical cations. Thus, our experimental (FTIR) and theoretical (quantum mechanical) results mutually support the hypothesis that OCDD formation on Fe-smectite surfaces is initiated by the reversible formation of metastable PCP radical cations via single-electron transfer from PCP to Fe(III). The negatively charged clay surface apparently selects for this reaction mechanism by stabilizing PCP radical cations.
An assessment of community exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) was undertaken in Paritutu, New Zealand. The suburb lies adjacent to an agrichemical facility that produced 2,4,5-trichlorophenoxyacetic acid (2,4,5-T), between 1962 and 1987. Soil TCDD measurements from 73 nearby addresses demonstrated a pattern of TCDD deposition consistent with an aerial plume following the prevailing local wind patterns and the agrichemical plant as the point source. Blood samples were taken from 52 volunteers having lived for three or more years in Paritutu between 1962 and 1987. Candidate selection focused primarily on individuals who were most likely to show elevated TCDD blood lipid levels when compared to age and gender stratified national average blood concentrations, and secondarily on individuals that provided additional information about specific exposure periods, potential exposures of younger age groups, and specific dietary patterns. A multipathway exposure model was used to estimate serum TCDD levels in each participant. Age and gender-specific TCDD elimination kinetics were also considered. Historical TCDD environmental concentrations were back-calculated from soil concentrations at each residence assuming TCDD releases occurred pre-dominantly between 1962 and 1975. Serum was analysed for chlorinated dibenzodioxins and dibenzofurans, and a subset was analysed for dioxin-like polychlorinated biphenyls. TCDD in serum lipid exceeded two standard deviations above national background levels for 14 participants, and 3 standard deviations for 10 participants. The highest TCDD lipid concentration was 33.3 ng/kg-lipid, or 11 times higher than the comparative 1997 national average. Elevated TCDD concentrations were observed primarily, but not exclusively, in the older study participants who had been in residence in Paritutu before 1968. The study demonstrated TCDD exposure in this community, occurring most likely through the aerial route, and most probably from fugitive emissions during manufacture.
The soil of a residential area in Tokyo was found to contain dioxins, namely polychlorinated dioxins, furans, and dioxin-like biphenyls, the levels of which exceeded the environmental guideline [1,000 pg toxic equivalent (TEQ)/g] by up to 6.8 times. To assess the exposure levels of people living in this area and to study the possible relationship of blood dioxin concentrations of children with breast milk and/or formula feeding, a health survey was carried out in 2006, involving a total of 138 people, including 66 children aged 3-15 years, and blood dioxin concentrations and the characteristics and lifestyles of these people were analyzed. Mean ± standard error of the mean (SEM) of blood dioxin concentrations (pg/g-lipid) of group 1 (3-6 years old), group 2 (7-15 years old), and group 3 (≥16 years old) were 13 ± 1.9, 6.6 ± 0.65, and 10 ± 0.54, respectively. The congener/isomer profile of dioxins in blood samples differed markedly from that of the contaminated soil samples. According to the feeding mode of children, blood dioxin concentrations (pg/g-lipid) were 17 ± 2.9 for breast milk only, 7.4 ± 0.82 for both breast milk and formula, and 4.7 ± 1.1 for formula only, with a significant difference from one another. We conclude that people living in the dioxin-contaminated area are less likely to be exposed to excessive amounts of dioxins, and that blood dioxin concentrations of children aged 3-15 years seem to be strongly affected by breast feeding duration.
Polychlorinated dibenzo-p-dioxins, polychlorinated dibenzofurans, and dioxin-like polychlorinated biphenyls that have toxic equivalency factors (TEFs) were measured in serum of 946 subjects in five Michigan counties. The study was motivated by concerns about human exposure to dioxin-contaminated sediments in the Tittabawassee River (TR). Most of the toxic equivalency in TR sediments is from two furan congeners, 2,3,7,8-tetrachlorodibenzofuran and 2,3,4,7,8-pentachlorodibenzofuran (2,3,4,7,8-pentaCDF).
The individual with the highest adjusted (for age, age squared, and body mass index) serum level of 2,3,4,7,8-pentaCDF in the study (42.5 ppt) reported a unique history of raising cattle and vegetables in the floodplain of the TR. Interviews and serum samples were obtained from the index case and 15 other people who ate beef and vegetables raised by the index case. 2,3,4,7,8-pentaCDF in beef lipid was estimated to have been more than three orders of magnitude greater than background (1,780 vs. 1.1 ppt). The mean, median, and 95th percentile for serum 2,3,4,7,8-pentaCDF in the study control population were 6.0, 5.4, and 13.0 ppt, respectively, and were 9.9, 8.4, and 20.5 ppt among beef and vegetable consumers, respectively. Back extrapolation for the index case suggests that his increase in serum concentration of 2,3,4,7,8-pentaCDF above background may have been as high as 146 ppt.
Consumption of beef and/or vegetables raised on dioxin-contaminated soil may be an important completed pathway of exposure. RELEVANCE TO PUBLIC HEALTH PRACTICE: Animals and crops should not be raised for human consumption in areas contaminated with dioxins.
The main pathway for human exposure to the highly toxic polychlorinated-p-dioxins and polychlorinated furans [polychlorinated dibenzo-p-dioxins and dibenzofurans (PCDD/Fs)] is via dietary intake. Other exposure pathways may, however, be important in close proximity to point sources, such as wood preservation sites, where PCDD/F contaminated chlorophenols (CP) were previously used. In this study, a heavily PCDD/F contaminated CP saw mill site in Sweden was investigated. Human exposure through a broad spectrum of exposure pathways was assessed. Such studies are in demand since the question whether contaminated sites represent a current or future risk can only be answered by detailed site-specific risk assessments.
Sampling of exposure media (soil, air, groundwater, raspberries, carrots, potatoes, grass, milk, eggs, and chicken fodder) was made. Exposure media concentrations and congener distribution patterns were used to investigate the mobilization of PCDD/Fs from soil to the environment and to calculate exposure levels for adults. Blood serum levels from site-exposed and control individuals were also analyzed.
Congener distribution patterns at the site were generally dominated by a specific marker congener (1234678-HpCDF), which is highly abundant in the polluted soil. The dioxin toxic equivalents (TEQ) concentrations were notably elevated as compared to national reference samples for most exposure media, and the marker congener was a major contributor to increased TEQ levels. There were also indications of soil-to-air volatilization of tetra- and penta-CDD/Fs. People who participated in the restoration of a contaminated building showed higher levels of 1234678-HpCDF compared to controls, and calculated exposure levels suggest that several site-specific exposure routes may be of importance for the daily intake of PCDD/F. CONCLUSIONS, RECOMMENDATIONS, AND PERSPECTIVES: Despite low mobility of higher chlorinated PCDD/Fs, these contaminants were transferred from the polluted soil to the surroundings and into human tissue. The extent of increased exposure from contaminated sites depends on the PCDD/F source strength of the soil, composition of the pollution, human activities, and dietary patterns of the residents. Impact from the contaminated soil on other exposure media was seen also for areas with low to moderate soil contamination. In the future, not only the levels of PCDD/F soil pollution but also the composition must be considered in risk assessments of contaminated sites.
We conducted a population-based human exposure study in response to concerns among the population of Midland and Saginaw counties, Michigan, that discharges by the Dow Chemical Company of dioxin-like compounds into the nearby river and air had led to an increase in residents' body burdens of polychlorinated dibenzofurans (PCDDs), polychlorinated dibenzofurans (PCDFs), and dioxin-like polychlorinated biphenyls (PCBs), here collectively referred to as "dioxins."
We sought to identify factors that explained variation in serum dioxin concentrations among the residents of Midland and Saginaw counties. Exposures to dioxins in soil, river sediments, household dust, historic emissions, and contaminated fish and game were of primary interest.
We studied 946 people in four populations in the contaminated area and in a referent population, by interview and by collection of serum, household dust, and residential soil. Linear regression was used to identify factors associated with serum dioxins.
Demographic factors explained a large proportion of variation in serum dioxin concentrations. Historic exposures before 1980, including living in the Midland/Saginaw area, hunting and fishing in the contaminated areas, and working at Dow, contributed to serum dioxin levels. Exposures since 1980 in Midland and Saginaw counties contributed little to serum dioxins.
This study provides valuable insights into the relationships between serum dioxins and environmental factors, age, sex, body mass index, smoking, and breast-feeding. These factors together explain a substantial proportion of the variation in serum dioxin concentrations in the general population. Historic exposures to environmental contamination appeared to be of greater importance than recent exposures for dioxins.
As part of the University of Michigan Dioxin Exposure Study, the 29 congeners of polychlorinated dibenzo-p-dioxins, polychlorinated dibenzofurans, and dioxin-like polychlorinated biphenyls that have World Health Organization consensus toxic equivalency factors were measured in house dust from 764 homes using a population-based sampling design over selected regions in five Michigan counties. Twenty homes had a total toxic equivalency in house dust that was more than 2.5 standard deviations above the mean (i.e., defined to be outliers). This follow-up investigation describes the outlier house dust measurements and corresponding soil measurements and explores possible sources of these toxins in house dust. The congener distributions in the house dust outliers varied and were dominated (i.e., >50% of the total toxic equivalency) by either polychlorinated dibenzo-p-dioxins (n = 9), polychlorinated dibenzofurans (n = 1), or dioxin-like polychlorinated biphenyls (n = 9). Likely sources of contamination of house dust were identified in only three cases. In two cases, dust contamination appeared to be related to contaminated soil adjacent to the home; in one case, contamination was related to a source within the home (a carpet pad). In most cases, the source(s) of contamination of house dust could not be identified but appeared likely to be related to uncharacterized sources within the homes.
Several of the major incidents resulting in potential human exposures to polychlorinated dibenzodioxins (PCDDs) and/or polychlorinated dibenzofurans (PCDFs), polychlorinated biphenyls (PCBs) and related compounds which have occurred in the U.S. in recent periods have resulted from improper disposal of hazardous chemical wastes. Prominent examples of such environmental contamination episodes are the Love Canal, into which ton quantities of chlorinated organic compounds containing substantial concentrations of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) were deposited; numerous sites in the State of Missouri which were contaminated by the dumping of chlorinated organic wastes containing various PCDDs and possibly PCDFs, and PCBs; and the environs of a 2,4-D/2,4,5-T manufacturing plant site in Arkansas, which were contaminated with PCDDs. Environmental assessments of such sites have revealed extensive contamination of soils, waterways, fish and other biological species with these toxic compounds, which in turn could lead to human exposures. Other recently identified sources of PCDDs, PCDFs and related compounds in human environments include stack effluents from municipal refuse incineration, and fires and explosions involving electrical devices containing PCBs and polychlorinated benzenes. Data obtained in assessments of such incidents are presented, and the implications of these findings with respect to the distribution and persistence of PCDDs, PCDFs and related chemicals in the environment and possible effects on humans are discussed.
Food is the major source for polychlorinated biphenyl (PCB) and dioxin accumulation in the human body. Therefore, investigating food habits from early ages until reproductive age (25 years) is important in order to assess exposure risk for the next generation. The objective of this study was to assess the PCB/dioxin exposure and the relative contribution of different foods to total exposure during preschool age. Particularly, the importance of lactational PCB/dioxin exposure vs. dietary exposure until adulthood was investigated. A cohort of 207 children was studied from birth until preschool age. Based on 3 planar PCBs and 17 2,3,7,8-substituted dibenzo-para-dioxins (PCDDs) and dibenzofurans (PCDFs) measured in breast milk, a model was developed to calculate the cumulative toxic equivalent (TEQ) intake during breast-feeding (0-1 year). In 3. 5-year-old children, daily dietary intake of planar PCB-TEQ and dioxin-TEQ was measured with a validated food questionnaire. Cumulative TEQ intake from 1 to 5 years was estimated using the PCB- and dioxin-TEQ intake measured with the food questionnaire. Cumulative TEQ intake from 6 to 25 years was estimated using national food consumption and contamination data of PCB- and dioxin-TEQ intake. In toddlers, dairy products contributed 43% to PCB-TEQ and 50% to dioxin-TEQ intake. Meat and meat products contributed 14% and 19%, respectively, and processed foods 23% and 15%, respectively. Breast-feeding for 6 months contributed to the cumulative PCB/dioxin TEQ intake until 25 years of age, 12% in boys and 14% in girls. The daily TEQ intake per kilogram body weight is 50 times higher in breast-fed infants and three times higher in toddlers than in adults. Long-term dietary exposure to PCBs and dioxins in men and women is partly due to breast-feeding (12 and 14%, respectively). After weaning, dairy products, processed foods, and meat are major contributors of PCB and dioxin accumulation until reproductive age. Instead of discouraging breast-feeding, maternal transfer of PCBs and dioxins to the next generation must be avoided by enforcement of strict regulations for PCB and dioxin discharge and by reducing consumption of animal products and processed foods in all ages.
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We compared serum polychlorinated dibenzo-p-dioxins (PCDDs) and polychlorinated dibenzofurans (PCDFs) among residents of two homes to levels among age- and sex-matched comparison subjects. The residents of the two homes consumed contaminated eggs and beef from animals raised at the homes. The animals had greater soil contact than those raised with conventional commercial husbandry practices. The comparison subjects were from a similar rural area, but did not consume home-produced beef and eggs. Serum levels of 2,3,7, 8-substituted tetra-, penta-, and hexaCDDs and penta-, hexa-, and heptaCDFs were increased between 2- and 6-fold in residents from one home; contaminated eggs and beef were consumed by residents for 2-15 years. Elevations were less for those in the other index home, where only home-produced eggs were consumed for 2 years; a 3-fold elevation of 1,2,3,7,8,9-hexaCDD as compared to controls was most apparent. Very strong bivariate correlations among all of the 2,3,7, 8 penta- and hexaCDDs/CDFs were observed. The elevations observed verify that PCDD/PCDF-contaminated food contributed to the body burden of these compounds. The blood levels among the highest exposed participants are generally higher than those observed in other studies of U.S. contaminated-fish consumers and higher than average adipose tissue levels observed in U.S. urban populations. There are sufficient animal toxicologic and human epidemiologic data to recommend that exposures be reduced. In the study area, pentachlorophenol and pentachlorophenol incineration sources have been identified, and the animal contamination and blood elevations probably reflect these sources. Soil reference values and site-specific risk assessments should include estimates of exposures to contamination in home-produced animal products. Such estimates can be verified with limited PCDD/PCDF sampling of animals and humans.
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Data on lipid levels of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) in the general population in the United States, Canada, Germany, and France over the past 30 years were compiled from the literature. Mean lipid levels of TCDD exhibited a steady decrease by nearly a factor of 10 over this time period, with lipid-adjusted TCDD levels in 2000 about 2 parts per trillion (ppt). Pharmacokinetic modeling using a one-compartment model indicated that absorbed intake levels of TCDD must have decreased by more than 95% from levels in 1972 to result in the observed decrease in human lipid levels, with the bulk of this decrease occurring before 1980. Based on this modeling and the pharmacokinetic properties of TCDD in humans, we conclude that mean levels of TCDD in the general population are likely to decrease further over the next 15 years, to between 0.5 and 1 ppt, even if intake levels do not decrease further. Fewer data over a shorter time period are available for other dioxin and furan congeners in human lipid, but these data indicate substantial decreases as well, with general population TEQ lipid levels currently at least fourfold lower than in 1970 and still decreasing. Food sampling data are limited, but support these trends.
To evaluate the contribution of tobacco smoking to dioxin accumulation.
Dioxin (17 PCDD/F) concentrations in fasting blood from 251 subjects (161 never smokers, 54 past smokers, and 36 current smokers) were quantified.
Whereas serum dioxin concentrations of male smokers were on average 40% higher than those of non-smokers, in women, smoking was associated with significantly lower serum dioxin levels. A synergistic potentiation of dioxin metabolism by tobacco smoke in women is postulated to explain these paradoxical findings.
Current smoking is associated with gender dependent effects on dioxin body burden and is a potential source of confounding in human studies using blood dioxins as indicators of exposure.
In June 2005, a World Health Organization (WHO)-International Programme on Chemical Safety expert meeting was held in Geneva during which the toxic equivalency factors (TEFs) for dioxin-like compounds, including some polychlorinated biphenyls (PCBs), were reevaluated. For this reevaluation process, the refined TEF database recently published by Haws et al. (2006, Toxicol. Sci. 89, 4-30) was used as a starting point. Decisions about a TEF value were made based on a combination of unweighted relative effect potency (REP) distributions from this database, expert judgment, and point estimates. Previous TEFs were assigned in increments of 0.01, 0.05, 0.1, etc., but for this reevaluation, it was decided to use half order of magnitude increments on a logarithmic scale of 0.03, 0.1, 0.3, etc. Changes were decided by the expert panel for 2,3,4,7,8-pentachlorodibenzofuran (PeCDF) (TEF = 0.3), 1,2,3,7,8-pentachlorodibenzofuran (PeCDF) (TEF = 0.03), octachlorodibenzo-p-dioxin and octachlorodibenzofuran (TEFs = 0.0003), 3,4,4',5-tetrachlorbiphenyl (PCB 81) (TEF = 0.0003), 3,3',4,4',5,5'-hexachlorobiphenyl (PCB 169) (TEF = 0.03), and a single TEF value (0.00003) for all relevant mono-ortho-substituted PCBs. Additivity, an important prerequisite of the TEF concept was again confirmed by results from recent in vivo mixture studies. Some experimental evidence shows that non-dioxin-like aryl hydrocarbon receptor agonists/antagonists are able to impact the overall toxic potency of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and related compounds, and this needs to be investigated further. Certain individual and groups of compounds were identified for possible future inclusion in the TEF concept, including 3,4,4'-TCB (PCB 37), polybrominated dibenzo-p-dioxins and dibenzofurans, mixed polyhalogenated dibenzo-p-dioxins and dibenzofurans, polyhalogenated naphthalenes, and polybrominated biphenyls. Concern was expressed about direct application of the TEF/total toxic equivalency (TEQ) approach to abiotic matrices, such as soil, sediment, etc., for direct application in human risk assessment. This is problematic as the present TEF scheme and TEQ methodology are primarily intended for estimating exposure and risks via oral ingestion (e.g., by dietary intake). A number of future approaches to determine alternative or additional TEFs were also identified. These included the use of a probabilistic methodology to determine TEFs that better describe the associated levels of uncertainty and "systemic" TEFs for blood and adipose tissue and TEQ for body burden.
An adaptable model is presented for assessing the blood lipid concentrations of polychlorodibenzodioxins and polychlorodibenzofurans (PCDD/Fs) from dietary (breast milk, formula, milk, and other foods) and soil pathway exposures (soil ingestion and dermal contact) utilizing age-specific exposure and intake estimates for young children. The approach includes a simple one-compartment (adipose volume) toxicokinetic model that incorporates empirical data on age-dependent half-lives and bioavailability of PCDD/F congeners, child body size and intake rates, and recent data on breast milk and food dioxin levels. Users can enter site-specific soil concentration data on 2,3,7,8-chlorinated PCDD/F congeners for specific assessment of body burden changes from soil pathways in combination with background dietary exposures from birth through age 7 years. The model produces a profile of the estimated PCDD/F concentration in blood lipid (in World Health Organization 1998 dioxin toxic equivalents) versus time for a child from birth through age 7 years. The peak and time-weighted average (TWA) internal dose (defined as blood lipid dioxin toxic equivalents) for a variety of specific child exposure assumptions can then be compared to safe internal dose benchmarks for risk assessment purposes, similar to an approach taken by United States Environmental Protection Agency for assessing child lead exposures. We conclude that this adaptable toxicokinetic model can provide a more comprehensive assessment of potential health risks of PCDD/Fs to children because it integrates recent empirical findings on PCDD/F kinetics in humans and allows users to assess contributions from varied dietary and site-specific environmental exposure assumptions.
The Agency for Toxic Substances and Disease Registry (ATSDR) used a cross-sectional study to compare the serum dioxin toxic equivalent (TEQ) levels of a population-based representative sample of Calcasieu Parish residents aged 15 years and older to a similar group of residents of Lafayette Parish with less industrial facilities. Serum dioxins consisted of polychlorinated dibenzo-p-dioxins, polychlorinated dibenzofurans, and dioxin-like polychlorinated biphenyls. Overall, the mean and distribution of serum dioxin TEQ level in residents of both parishes were similar by age groups (15-29 years, 30-44 years, 45-59 years, and 60 year and older). When the Calcasieu Parish area was further divided based on distance to three industrial areas, the mean dioxin TEQ levels were similar. Serum dioxin TEQ levels in residents of both parishes increased with age. Calcasieu Parish residents who reported having eaten locally caught fish, smoked cigarettes, worked in an occupation with potential exposure, or used pesticides had dioxin levels similar to Lafayette Parish residents who reported these activities. African Americans had higher dioxin levels than Caucasians in Lafayette Parish and both races in Calcasieu Parish. The congener profiles were similar in residents of both parishes. When the combined Calcasieu and Lafayette Parish data were compared by age group to the National Health and Nutrition Examination Survey (NHANES) 2001-2002 data, the geometric means for the dioxin levels in the combined Parish data set were significantly lower than the NHANES data in all age groups (all P-values <0.0001), except the oldest age group where the significance level is marginal (P=0.067). The various percentiles of the youngest age group of the combined parish data were also significantly lower than those in NHANES. Since the combined parish dioxin levels were below a representative sampling of the US population, there is no increase in serum dioxin concentrations in both the parishes.
For the general population, the dominant source of exposure to dioxin-like compounds is food. As part of the University of Michigan Dioxin Exposure Study (UMDES), we measured selected polychlorinated dibenzo-p-dioxins (PCDDs), polychlorinated dibenzofurans (PCDFs), and dioxin-like polychlorinated biphenyls (PCBs) in serum of 946 subjects who were a representative sample of the general population in five Michigan counties.
The total toxic equivalency (TEQ; based on 2005 World Health Organization toxic equivalency factors) of serum from the index case was 211 ppt on a lipid-adjusted basis, which was the highest value observed in the UMDES study population. This subject had no apparent opportunity for exposure to dioxins, except that she had lived on property with soil contaminated with dioxins for almost 30 years, and had been a ceramics hobbyist for > 30 years. Soil from her property and clay that she used for ceramics were both contaminated with dioxins, but the congener patterns differed.
The congener patterns in this subject's serum, soil, and ceramic clay suggest strongly that the dioxin contamination in clay and not soil was the dominant source of dioxin contamination in her serum. RELEVANCE TO PUBLIC HEALTH PRACTICE: It appears that ceramic clay, in particular the process of firing clay with unvented kilns, can be a significant nonfood and nonindustrial source of human exposure to dioxins among ceramics hobbyists. The extent of human exposure from ceramic clay is unclear, but it may be widespread. Further work is needed to more precisely characterize the routes of exposure.
Today dioxin is a familiar word, but very few people in Italy had heard of it before the Seveso accident of July 10, 1976. Ever since, TCDD and related chemicals1,2 have been dealt with profusely by the domestic and international scientific communities. Because of the sensitizing effect it had, the Seveso case should be considered a turning point in environmental risk management. For instance, it is recalled here that, in February of 1988, the Commissione Consultiva Tossicologica Nazionale (CCTN)— Italy’s National Toxicology Commission—established a set of maximum tolerable limits (MTLs) for polychlorinated dibenzodioxins (PCDDs) and dibenzofurans (PCDFs) in several environmental matrices.3,4 These limits were based on the 1987 array of U.S. EPA toxicity equivalence factors (TEFs) to convert PCDD and PCDF analytical data into “toxicity equivalents of TCDD” (TE units),1 and also on much of the technical experience gained by dealing with the Seveso event.
The sources and pathways of food chain contamination of the persistent and toxic polychlorinated dibenzo-p-dioxins (PCDDs) and polychlorinated dibenzofurans (PCDFs) are unclear. PCDD/PCDF levels in eggs from chickens raised in backyards near Oroville, CA, near a former pentachlorophenol (PCP) wood treatment facility (WTF) and four former PCP waste burners, were previously reported to be elevated (above a level of significant cancer risk, i.e., 1 part per trillion (ppt) international toxicity equivalent (ITEQ) and above levels in eggs from a similar rural area with no such facilities). Limited sampling suggested associations with low ppt soil levels. Further investigations are reported here. Soil concentrations in samples (n = 26) collected from the foraging area of a single Oroville backyard have a geometric mean of 30 ppt ITEQ and are uniform, suggesting airborne deposition. Additional samples were collected from homes in Oroville and Stockton, CA also near a former PCP WTF. Geometric mean dioxin levels in eggs are 2.2 and 1.8 ppt ITEQ for Oroville (n = 35), and Stockton (n = 5), with 78% of samples above 1 ppt. Corresponding soil geometric means are 6.2 (n = 17) and 6.6 (n = 5) ppt ITEQ. Regression models estimate that soil concentrations of 0.38 and 2.7 ppt ITEQ, depending on whether chickens free-forage, predict an egg concentration of 1 ppt ITEQ. The combined evidence suggests that local industrial sources can contribute to environmental contamination. The soil concentrations associated with significant egg contamination are low, much lower than the dioxin level of 1000 ppt, frequently used for children's ingestion exposures, and potentially widespread. A broad and global concern for PCDD/PCDF sources and environmental levels, particularly with respect to human consumption of animal products, is underscored.
A comprehensive review of available PCDD/F time trend data is presented. This focuses on industrialized countries, drawing heavily on those countries that have been actively involved in PCDD/F monitoring and research, notably Germany, the United States, Sweden, The Netherlands, and the U.K. Information on temporal trends comes from the analysis of date able deposits (e.g., sediments), retrospective analysis of preserved or archived samples, and ongoing monitoring programs. The data on changes in air concentrations, deposition, sediments, soil, biota, food, and human tissues are reviewed. The evidence for natural input/formation of PCDD/Fs is also briefly reviewed and discussed. Human activity has dominated PCDD/F inputs to the environment this century. Conceptually, it is probably appropriate to consider a ‘pulse' of PCDD/Fs arising from human activities entering the environment in the 1930/1940s, peaking in the 1960/1970s, and continuing to a lesser degree today. A series of measures introduced in the past, recently, and anticipated for the future have reduced emissions to the atmosphere of industrialized countries and are projected to continue to reduce emissions over the coming decade. Comprehensive monitoring programs are required to confirm the interpretation of past changes and projected future declines presented here.
Ball clay was the source of dioxin contamination discovered in selected chickens analyzed as part of a joint U.S. Department of Agriculture/U.S. Environmental Protection Agency national survey of the U.S. poultry supply conducted in 1997. The affected animals, which had been raised in the southern United States, represented approximately 5% of the national poultry production. All of these chickens and other animal food sources (i.e., farm-raised catfish), similarly contaminated, were fed a diet of animal feed containing ball clay as an anti-caking additive. The clay was mined in northwestern Mississippi within a geological formation referred to as the Mississippi Embayment. Individual raw and processed ball clay samples were analyzed for the presence of the 2,3,7,8-PCDDs/ -PCDFs. The average toxic equivalents (TEQs) for the raw and processed samples were 1513 and 966 ppt dw, respectively. Other mined clay-based products used in animal feeds revealed lower TEQs. All of the products exhibited either an absence of detectable concentrations of 2,3,7,8-PCDFs or concentrations 2−3 orders of magnitude lower than the PCDDs. The isomer distribution, specific isomer identification, and congener profile of the PCDDs in the clay were established and compared to known sources of dioxin contamination. Several unique features of this isomer distribution are characteristic of the clays and are distinguishable from those of other known sources. These characteristics found in prehistoric clay deposits in the United States and Germany have led to speculation attributing their presence to natural geologic processes.
Dioxins are arguably one of the most notorious anthropogenic environmental toxicants. How this came to pass can be tied to a number of widely reported cases over the last several decades. Herein, Hites reviews the chemistry, prevalence, and environmental spread of dioxins to illustrate their links to environmental policy.
The aim of the current analysis was to examine the determinates of lipid-adjusted body levels of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) from occupational histories, age, body mass index, and self-reported information from a questionnaire. We collected serum from 346 workers at a New Zealand chemical plant that manufactured and formulated the herbicide, 2,4,5-trichlorophenoxyacetic acid (2,4,5-T). Age, body mass index, and employment history were significant determinates of TCDD. The self-reported data on occupation, residence, and general diet were not predictive of serum levels and we observed no evidence of increased TCDD levels from living close to the site. For participants with putative occupational exposure, employment history and personal factors were important to understand the range of TCDD serum levels. For employees without direct occupational exposure, and resulting lower dioxin levels, we recommend further efforts to develop and validate questionnaires to better evaluate environmental sources of dioxins.
The University of Michigan dioxin exposure study was undertaken to address concerns that the industrial discharge of dioxin-like compounds in the Midland, MI area had resulted in contamination of soils in the Tittabawassee River floodplain and downwind of the incinerator. The study was designed in a rigorously statistical manner comprising soil measurements of 29 polychlorinated dibenzo-p-dioxins (PCDDs), polychlorinated dibenzofurans (PCDFs), and polychlorinated biphenyls (PCBs) from 766 residential properties, selected probabilistically, in the Midland area and in Jackson and Calhoun Counties (Michigan) as a background comparison. A statistical comparison determined that the geometric mean toxic equivalent (TEQ) levels in samples from the target populations were statistically significantly above background. In addition, the probabilities of being above the 75th and 95th percentiles of background were also greater. Congener contributions to the TEQ were dominated by 2,3,4,7,8-PeCDF and 2,3,7,8-TCDF in the floodplain and by 2,3,7,8-TCDD in the incinerator plume. However, PCB 126 was the top congener contributing to the background TEQ. On the basis of statistical inference to the total population, it was estimated that about 36% of the properties in the floodplain and incinerator plume have at least one soil sample over the Michigan Department of Environmental Quality's soil direct contact criterion of 90 pg/g TEQ.
Interest in the potential sources of human exposure to TCDD (dioxins, TCDD and equivalents, or 2,3,7,8-tetrachlorodibenzo-p-dioxin) via foods has recently shifted from phenoxy herbicides to products of combustion and waste disposal. Proposals to locate municipal waste combustors in rural areas have raised concerns that emissions, which could contain TCDD, could contaminate animal feeds and such human foods as milk, meat, and vegetables. Important factors that can affect the results of an assessment of incinerator emissions include (1) the emission and deposition rates of TCDD from the source, (2) the fractional retention and half-life of fly ash on plants, (3) the environmental half-life of TCDD, (4) the animal feeding and management systems, (5) the bioavailability of TCDD and related compounds, (6) the metabolism and pharmacokinetics of TCDD in farm animals, (7) food consumption levels, (8) the half-life of TCDD in humans, and (9) the model selected to estimate cancer risk. For persons living in the area of highest deposition near an incinerator, a possible uptake of TCDD from foods of animal origin was estimated to be about 10-40 fg/kg.d, which was much greater than the 1-5 fg/kg.d uptake estimated for foods of plant origin. The total uptake of TCDD from foods by the maximally exposed population will usually be about 500- to 1000-fold greater than that due to inhalation. Although milk was assumed to be the most important food pathway in several previous assessments that evaluated the hazards of airborne emissions, we determined that the deposition-forage-cattle-beef pathway was the more important route of exposure. The previous assessments appear to have used inappropriate pharmacokinetic models for TCDD and to have overestimated pasture use for dairy cows. The amount of TCDD accumulated in soil from airborne emissions was found to be less important than the amount deposited in forage, a finding that is the opposite of the usual conclusions drawn for other routes of TCDD introduction into agricultural environments. Based on the assumption and parameters used in this assessment, the potential human health risks due to TCDD emissions from incinerators are insignificant compared to other background sources of TCDD. It would be desirable to measure TCDD in soil and crops around existing facilities to better evaluate this assessment, but it is likely that concentrations would be too low to reliably quantitate.
The PCDD/F levels were determined in the venous blood of 21 allotment gardeners in Duisburg (Germany). Soil analyses had shown elevated levels of PCDD/F in garden soil (range 16.4-77.6 ng I-TE/kg). Vegetable plants also had elevated levels of PCDD/F, mainly due to airborne contamination. The highest levels were found in kale (2.6-65.6 ng I-TE/kg d.w.) and endive (1.7-28.5 ng I-TE/kg d. w.). The study population consisted of 5 females and 16 males (mean age 57 years; range 43-67 years), who had been cultivating their allotment gardens for an average of 20 years (range 7-36 years). About 50% of their total vegetable consumption and 30% of their fruit consumption were from their own gardens. The mean 2.3.7.8-TCDD toxicity equivalents (TE) of PCDD/F in blood fat were 44.3 pg I-TE/g fat (range 29.2-81.1 pg I-TE/g fat). Compared to reference data these values are within the range of background PCDD/F-levels in the German population. The concentrations in individual gardeners as well as the congener pattern were not different from those of normal subjects. The present study shows that increased levels of PCDD/F in garden soil and garden products do not have a significant effect on the PCDD/F burden in gardeners, even if they consume homegrown vegetables and fruits from their own allotment gardens for many years in succession.
PCDD/PCDF/PCB concentrations were measured in samples from four mothers (at delivery and during lactation) and their infants (at birth and the end of first year of life). For two of these mothers it was the second delivery and breast-feeding period, and additional data were available from first lactation period and the first-born infant at the age of 11 to 12 months. Five of the six infants were fully breast-fed for at least 17 weeks. In four of them a distinct PCDD/PCDF/PCB accumulation was observed at the end of the first year of life: concentrations in blood fat were 1.5 to 3.6 times higher than maternal levels measured at the same time. Due to decreasing maternal body burdens during lactation, PCDD/PCDF concentrations at 11 to 12 months of life were only about half as high in the second infant as in the first one at the same age. During second pregnancy, no important change of the concentrations was observed in maternal blood.
We summarize temporal changes in the distribution of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) measurements made in serum drawn in 1987, 1992, and 1997 from 1419 Air Force Vietnam-era veterans who served as comparisons in a 20-year prospective study of health and exposure to herbicides and their TCDD contaminant in Air Force veterans of Operation Ranch Hand, the unit responsible for aerial spraying of Agent Orange and other herbicides in Vietnam. Among comparison veterans, TCDD levels decreased significantly with time at a rate of -- 0.25 parts per trillion per year. We also describe paired serum TCDD measurements in a subgroup of 33 veterans who had detectable levels in both 1987 and 1992. The paired measurements suggested that serum TCDD levels decreased with time, including those near the limit of detection.
The gastrointestinal exchange of polychlorinated biphenyls (PCBs), dibenzo-p-dioxins, and dibenzofurans (PCDD/Fs) as well as hexachlorobenzene was measured in five volunteers. The dietary intake and the fecal excretion of the chemicals were quantified and the net absorption/net excretion was calculated as the difference between these two fluxes. Experiments were conducted using an elevated dietary intake and a reduced dietary intake of chemical, and the results were compared with the absorption during normal dietary intake. The net absorption varied widely with the dietary intake for those compounds which bioaccumulate in humans; high dietary intake of chemical resulted in absorption approaching 100% of intake, while low dietary intake resulted in a net excretion several times greater than the dietary intake. In contrast to net absorption, the chemical flux in the feces was largely independent of the dietary intake of chemical for a given individual. Good agreement was found between the feces/blood distribution coefficients measured in this study and in a study with contaminated workers whose blood concentrations were several orders of magnitude higher, indicating that fecal excretion of chemical is linearly proportional to the blood concentration. The results suggest that gastrointestinal exchange can be viewed as two processes operating simultaneously: absorption of contaminant from the diet, and excretion of contaminant from the body's reservoirs via the feces. By subtracting that component of the fecal flux originating from the body, the maximum dietary absorption could be calculated. This was >95% for most of the compounds, decreasing to a minimum of 50-60% for the octachlorinated dioxins and furans. The maximum dietary absorption showed a Kow dependency consistent with the two film model of gastrointestinal absorption of persistent organic chemicals.
The Agency for Toxic Substances and Disease Registry (ATSDR) conducted biological testing to assess dioxin exposure in residents of a community who lived in an area with heavy chemical industry. Dioxin concentrations were measured in blood serum samples from 28 adult residents of the community. Fourteen of those tested had blood dioxin concentrations that exceeded the 95th percentile prediction level of an age-matched comparison population. Specific congener analyses indicated that the elevated dioxin concentrations were primarily due to high concentrations of 2,3,7,8 tetrachlorodibenzo-p-dioxin (TCDD), 1,2,3,7,8 pentachlorodibenzo-p-dioxin (PeCDD), and hexachlorodibenzo-p-dioxins (HxCDs). Principal components analysis (PCA) indicated that the profiles of dioxin congeners were different in people with elevated blood dioxin concentrations compared to those with background concentrations. Elevated blood dioxin concentrations were detected only in older members of the population, which suggests that dioxin exposures were higher in the past. The sources of the dioxin exposure have not been identified.
Concentrations of polychlorinated dibenzo-p-dioxins (PCDDs), polychlorinated dibenzofurans (PCDFs), polychlorinated biphenyls (PCBs), and organochlorine pesticides were measured in the serum of a sample of the New Zealand population aged 15 years and older. This was the first study to obtain representative measures of PCDDs, PCDFs and PCBs in the adult population of an entire country. Serum samples were obtained in 1996-1997. Potentially occupationally exposed individuals were excluded. Serum samples were pooled according to stratification criteria for area of residence, ethnicity, age, and sex. Of the 80 possible strata, sufficient serum for chemical analysis was available for 60, to which 1,834 individual samples contributed. For the PCDDs and PCDFs, most 2,3,7,8-chlorinated congeners were measured in all strata, with a mean toxic equivalents concentration across all strata of 12.8 ng TEQ kg(-1) lipid. Seven PCB congeners were frequently measured, including the coplanar congeners #126 and #169, quantified in all strata. Of the pesticides and their metabolites, only beta-HCH, dieldrin and pp'-DDE were consistently detected across strata. There was a general trend of increasing concentration with age. There were no consistent differences between the sexes, or between people of Maori (the indigenous people of New Zealand) and non-Maori ethnicity. Concentrations of PCDDs and PCDFs tended to increase in a North-South direction, possibly reflecting greater levels of industrialization and population concentration, and concentrations of the pesticide products were highest in the South, possibly reflecting historical use patterns. Results were consistent with a recent study of concentrations of these compounds in the milk of first-time mothers.
High levels of arsenic, cadmium, mercury and polychlorinated dibenzodioxins and dibenzofuranes (PCDD/PCDF) were detected in the soil of a residential area located at the river Elbe near Hamburg (Germany). Soil contamination resulted from sediments from the Hamburg harbour and from the Elbe that were deposited in this area up to the late 1950ies. The objective of this study was to evaluate whether the soil contamination in this area is associated with increased levels of arsenic, heavy metals and PCCD/PCDF in the blood and urine of selected residents living on highly contaminated grounds.
The blood levels of lead and PCDD/PCDF and the urine levels of arsenic, cadmium and mercury that were measured in 29 residents living on highly contaminated grounds were not elevated in relation to a control group. All individual values were in the range of the background exposure levels of the general population. There were no signs of an increased additional exposure related to soil contamination.
Based on the results of this study it was agreed to refrain from an expensive redevelopment of this area. As a preventive measure some recommendations were given to the residents to minimize possible exposure to soil contaminants. Human biological monitoring studies should be an essential part of exposure and risk assessment of soil contaminations in residential areas in future studies and as a basis for adequate risk management.
From the late 1950s to the early 1970s elastic polysulphide sealants were used in outdoor seams between concrete blocks in prefabricated buildings. The sealants contained 5-30% polychlorinated biphenyls (PCBs). Due to the weathering of sealants in general and the replacement of seams with new PCB-free materials in the 1990s, PCBs have drifted to the soil adjacent to buildings. The objectives of this study were to survey PCB contamination in the surroundings of former PCB-containing buildings and to evaluate the risks to human health. Samples from soil, and also from blood serum of residents, were collected to obtain data for exposure assessment. The health risk assessment was based on deterministic and probabilistic calculations for cancer and non-cancer risks. Soil ingestion and dermal contact were considered the main routes of exposure and children the most important exposed group. The mean total PCB concentration was 6.83 mg/kg within 2m of the buildings and 0.52 mg/kg within 3-10 m from of the buildings. The deterministic risk assessment with conservative parameters resulted in lifetime cancer risk estimates on the order of 10(-6)-10(-7). The lifetime average daily dose (LADD) for PCBs was less than 10% of the reference dose (RfD) 0.02 microg/kg day, which is based on immunosupression in monkeys. The LADD corresponding to the total site attributable exposure was less than 10% of the estimated average dietary PCB intake in Finland. Children can, however, in worst cases be exposed to daily doses near the level of the RfD. Low cost measures are recommended to reduce possible exposure of children.
Multivariate methods were used to predict levels of dichlorodiphenyldichloroethene (DDE) and polychlorinated biphenyl (PCB) concentrations in plasma from characteristics that included age, diet, race, reproductive history, socioeconomic status, and reported body mass index (BMI) at several decades of life before blood collection. Measurements were available for organochlorine compound (organochlorines), cholesterol, and triglycerides in plasma from 1,008 women participants in a population-based case-control study of breast cancer undertaken in 1996 to 1997 on Long Island, NY. Organochlorine compound levels were associated with age, race, lactation history, body size characteristics, and plasma lipids. PCB predictors also included fish consumption. DDE was correlated with current BMI, BMI at every decade of age from ages 20 to 60 years, and BMI-gain (from ages 20 or 30 years to 1997). In contrast, PCBs were correlated inversely with both BMI (fifth to seventh decades of age) and BMI-gain. After adjusting for covariates, DDE and PCB were both positively associated with BMI and inversely with BMI-gain; they were lowest with low BMI, high BMI-gain, and longer lactation. This pattern is consistent with a pharmacokinetic model that predicts higher body burdens during windows of highest uptake, faster elimination of organochlorine compounds in leaner women, and lowered levels accompanying BMI-gain. As a result, lifetime intake for specific organochlorine compound may lead to different plasma levels dependent on changes in body size, absolute intensity of intake, and whether exposure is ongoing (i.e., PCB) or long discontinued (i.e., DDE).
Animal studies have indicated that the oral bioavailability of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) in environmentally contaminated soil could range from 0.5 to 60%. To estimate the oral bioavailability of TCDD, and the 16 other 2,3,7,8-substituted dioxin/furan congeners, this study used a physiologically based extraction test, designed around the anatomic and physiologic characteristics of the human digestive tract. This test measures the fraction of dioxins/furans in soil that would be solubilized in the gastrointestinal tract (i.e., that would be bioaccessible) and therefore available for absorption. Eight soils from Midland, MI, were evaluated in this study and exhibited TCDD concentrations of 1.7-139 pg/g (ppt) and total TEQ concentrations of 6-340 ppt. Bioaccessibility of dioxins/furans from these soils ranged from 19 to 34% averaged across the 17 2,3,7,8-substituted dioxin/furan congeners), with an average of 25%. The total organic carbon in these soils was low--ranging from 1 to 4%--particularly for the soil series from which they were collected. Bioaccessibility of individual congeners did not appear to be correlated with degree of chlorination. Even though these dioxin/furan concentrations are much less than studied previously, these results are consistent with those from animal studies at other sites, which have generally yielded values of 20-60% relative bioavailability for TCDD in soil.
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