Rationale for assessment of risk from exposure to 2,3,7,8-TCDD

The human health risk assessment is supported by methodology for utilizing toxic effects in animals consisting of carcinogenic and noncarcinogenic responses as a result of chronic, subchronic and acute exposures. One of the initial steps in a risk assessment activity involves the estimation of exposure levels. These estimates are typically based on either direct environmental measurements or predictions obtained from fate and transport models. The decision to develop assessment of risk from chronic exposure based on a nonthreshold model is made if a chemical demonstrates carcinogenic activity in animal bioassays and/or in human epidemiological studies. In the absence of any positive human epidemiologic data, it is assumed that a substance which induces a statistically significant carcinogenic response in animals has the probability to cause cancer in humans. The carcinogenic potential of 2,3,7,8-TCDD has been established based on chronic exposure in rodents. In addition, 2,3,7,8-TCDD has also been shown to be a liver cancer promoter in rodents. In the risk assessment on dioxins based on chronic exposure in experimental animals, 2,3,7,8-TCDD is regarded as a carcinogenic substance. Carcinogenic data from animal bioassays are utilized for the assessment of risk for the purpose of estimating the likelihood of 2,3,7,8-TCDD being carcinogenic for humans and to determine the magnitude of the potential impact on public health.     

Qualitative and quantitative cancer risk assessment of 2, 3, 7, 8-tetrachloro-dibenzo-p-dioxin (2, 3, 7, 8-TCDD)

The carcinogenicity of 2,3,7,8-TCDD at multiple organ sites in animals has been well established by several cancer bioassays. Results of two of the most notable of these, the Kociba et al. (1978) rat feeding study and the National Toxicology Program (1980) gavage study in rats and mice showed hepatocellular carcinomas in two strains of female rats and male and female mice. Other tumor sites included carcinomas of the lung, tongue, hard palate and nasal turbinates, thyroid, and subcutaneous tissue. The evidence for carcinogenicity of 2,3,7,8-TCDD in animals is regarded as “sufficient” using the classification system of the International Agency for Research on Cancer (IARC).

Two Swedish epidemiologic case-control studies (Hardell and Sandstrom, 1979; Eriksson et al. 1979, 1981) reported a significant five- to sevenfold excess risk of soft-tissue sarcomas (STS) from occupational exposure to chlorinated phenoxyacetic acid herbicides and/or chlorophenols. Additionally, several small cohort studies collectively exhibited an unusual cluster of STS, significantly increased over combined expected incidence. Problems with these studies do not appear to be sufficient to discount this excess risk. The human evidence alone for the carcinogenicity of 2,3,7,8-TCDD is “inadequate” using the IARC classification. However, for 2,3,7,8-TCDD in combination with chlorinated phenoxyacetic acid herbicides and/or chlorophenols, the human evidence is considered to be “limited.” The overall evidence for carcinogenicity considering both animal and human studies would place 2,3,7,8-TCDD alone in the IARC category 2B, meaning that the substance is probably carcinogenic in humans. The overall weight of evidence for 2,3,7,8-TCDD in combination with chlorinated phenoxyacetic acid herbicides and/or chlorophenols is regarded as IARC category 2A, also meaning that they are probably carcinogenic for humans.

Using current EPA methodology for quantitatively estimating cancer risks, several animal data sets have been analyzed. Comparing the results, the upper-limit incremental unit risk estimate is 1.6 × 10⁻² for a lifetime exposure of 1 ng/kg/day. This estimate is derived from a lifetime feeding study (Kociba et al., 1978) in which 2,3,7,8-TCDD induced tumors of the liver, lungs, hard palate, and nasal turbinates in female rats. Incremental unit cancer risks are also extrapolated for lifetime 2,3,7,8-TCDD exposures in water and air. Based on continuous lifetime exposure to 1 ng/L 2,3,7,8-TCDD in drinking water, the upper-limit estimate of extra cancer risk per individual is 4.5 × 10⁻³. For lifetime exposure to 1 pg 2,3,7,8-TCDD/m³ in the ambient air, the upper-limit individual risk is 3.3 × 10⁻⁵.     

Levels of 2,3,7,8-Tetrachlorodibenzo- -dioxin (2,3,7,8-TCDD) in adipose tissue of U.S. Vietnam veterans seeking medical assistance

2,3,7,8-Tetrachlorodibenzo- -dioxin (2,3,7,8-TCDD) was detected in an earlier study in adipose tissue of U.S. veterans who were exposed to Agent Orange in Vietnam. The levels appear to be directly related to the intensity of exposure¹. We now report on a group of thirteen Vietnam veterans who were screened for 2,3,7,8-TCDD in adipose tissue. All the veterans had sought medical assistance and some had health effects that may be ascribed to exposure to 2,3,7,8-TCDD. Also included are control patients who were taken from the population of the U.S. 2,3,7,8-TCDD was detected in most of the adipose tissue samples at levels ranging from 2 to 14 ppt. No significant differences in the tissue levels of Vietnam veterans and the other persons were found in this preliminary study.     

Bald eagle mortality and chlorinated hydrocarbon contaminants in livers from British Columbia, Canada, 1989-1994

Between 1989 and 1994, we obtained 278 carcasses of bald eagles (Haliaeetus leucocephalus) found dead or dying in British Columbia, Canada. All specimens were necropsied and the cause of death determined wherever possible. Livers from a subset of 75 birds were analyzed for polychlorinated biphenyl (PCB) and organochlorine (OC) pesticide residues. A further subset of 19 eagles found dead around the Strait of Georgia, an area of known pulp mill pollution, in summer, and therefore presumably resident birds, were analyzed for polychlorinated dibenzo-p-dioxins (PCDDs) and polychlorinated dibenzofurans (PCDFs) and non-ortho PCBs. Liver concentrations ranged from less than 1 to 190 mg/kg for DDE, and up to 72 mg/kg for total PCBs. Concentrations of other OCs were generally less than 1 mg/kg, with the exception of chlordane-related compounds which were occasionally over 2 mg/kg. All birds analyzed for PCDDs and PCDFs contained detectable concentrations of the major 2,3,7,8-substituted isomers. Some birds were very contaminated; one eagle found near a kraft pulp mill site in 1990 contained: 400 ng/kg 2,3,7,8-TCDD, 1400 ng/kg 1,2,3,7,8-PnCDD and 4400 ng/kg 1,2,3,6,7,8-HxCDD. Birds with higher PCB and dichlorodiphenyldichloroethane (DDE) concentrations appeared to weigh less, and there was a significant negative relationship between both PCBs and DDE and numeric scoring of body condition, reflecting the well known process of starvation-induced mobilization of body lipids and contaminants. Birds with higher 2,3,7,8-TCDD concentrations tended to have unusually low concentrations of 2,3,7,8-TCDF, interpreted to indicate hepatic cytochrome P4501A-type induction by TCDD and subsequent metabolism of TCDF.     

Concentrations of polychlorinated dibenzo-p-dioxins in processed ball clay from the United States

Processed ball clays commonly used by the ceramic art industry in the United States were collected from retail suppliers and analyzed for the presence and concentration of the 2,3,7,8-Cl substituted polychlorinated dibenzo-p-dioxins and dibenzofurans (PCDDs/PCDFs). The average PCDD toxic equivalent (TEQ) concentrations of these processed ball clays was approximately 800 pg/g (TEQ-WHO) with characteristic congener profiles and isomer distributions similar to patterns of previously analyzed raw and processed ball clays. The PCDF concentrations were below the average limit of detection (LOD) of 0.5 pg/g. Correlation analyses reveal no significant relationship between total organic carbon (TOC) and either individual, homologues, and total tetra-through octa-chlorinated PCDD congeners, or TEQ concentrations of the processed ball clays. The results are consistent with earlier studies on levels of PCDDs in ball clays. Data from earlier studies indicated that dioxins may be released to the environment during the processing of raw clay or the firing process used in commercial ceramic facilities. The presence of dioxin in the clays also raises concerns about potential occupational exposure for individuals involved in the mining/processing of ball clay, ceramics manufacturing and ceramic artwork.     

Dioxin incinerator emissions exposure study Times Beach, Missouri

PURPOSE: To determine whether living in the vicinity of a hazardous waste incinerator that was burning material contaminated with 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) increased TCDD and toxicity equivalencies (TEQ) in individuals living near the incinerator. METHODS: Participants were randomly chosen from an area close to the incinerator and compared to participants outside of the exposure area. TCDD and related compounds were measured in blood serum before incineration, four months after incineration started, and at the end of incineration. RESULTS: Lipid adjusted serum levels of TCDD and TEQ decreased from pre-incineration to four months after incineration, and decreased further by the end of incineration. CONCLUSION: Incineration of TCDD did not result in any measurable exposure to the population surrounding the incinerator.     

Chlorinated dibenzo-p-dioxin and dibenzofuran levels in human adipose tissue and milk samples from the north and south of Vietnam

Although 2,3,7,8-TCDD has been found to be extremely toxic to a variety of laboratory aminals, human epidemiology studies, where exposure to 2,3,7,8-TCDD has been less well characterized than in animal toxicologic studies, have been less conclusive in characterizing the extent of toxicity. In order to determine whether the newly refined techniques of human adipose tissue biopsy including isomer specific and sensitive measurement of PCDDs and PCDFs might be able to assist in finding populations within the same country with high and low levels of dioxins, adipose tissue samples were taken and levels analyzed from the north and south of Vietnam. It seemed reasonable, based on previous work, that high levels of 2,3,7,8-TCDD might still be found in adipose tissue in selected patients living in areas sprayed with Agent Orange and other 2,3,7,8-TCDD containing herbicides, and that lower levels should be found in patients not exposed to 2,3,7,8-TCDD from herbicides or other sources, such as persons who had always resided in the north of Vietnam. Of 9 specimens from patients hospitalized in Hanoi who had never been south, none had detectable adipose tissue levels of 2,3,7,8-TCDD at a detection limit of 2 or 3 ppt on a wet weight basis. Of 15 specimens from Ho Chi Minh City hospitalized patients the mean of positive specimens (12 of 15) was 28 on a lipid basis. The mean of the positive values from the south is about 2 to 3 times higher than found in the North American Continent control patients where the mean is about 6–10 ppt and much higher than in the north of Vietnam. In the northern specimens, the levels were non-detectable with a sensitivity of between 2 and 3 ppt. Other PCDD and PCDF isomers not found in Agent Orange, the penta- through octachlorinated dibenzo-dioxins and dibenzofurans, were similar in isomer type and quantity in the south of Vietnam to what we previously reported in North America. Adipose tissue from the north of Vietnam contained the lowest levels of four through eight chlorinated dioxins and furans thus far reported. The initial data suggests that populations exist in the south of Vietnam with elevated levels of 2,3,7,8-TCDD at the present time, fourteen years after the last known 2,3,7,8-TCDD (Agent Orange) application, superimposed on a preexisting body burden of dioxins and dibenzofurans from sources other than Agent Orange such as technical grade pentachlorophenol or products of incineration contaminated with higher chlorinated PCDDs or PCDFs. In light of the recent finding that unexpected levels of PCDDs and PCDFs exist in the general adult population of industrialized countries, ca. 1,000 to 1,200 ppt, wet weight of total dioxin and furan isomers in adipose tissues, it seems reasonable that the extent of human toxicity of dioxins may be more readily characterized in Vietnam than in industrialized countries. Because 2,3,7,8-TCDD was applied in 1962–1970, although not yet cleaned up, the levels of 2,3,7,8-TCDD in the environment, the food chain, and in humans, would be expected to decrease with time. Therefore, if studies are not initiated in a timely fashion, the opportunity to better characterize the extent of the toxicity of TCDD to humans as well as the persistence of TCDD in the environment in Vietnam may be lost.     

Ambient air concentrations of polychlorinated dibenzo-p-dioxins and dibenzofurans in Ohio: Sources and health risk assessment

PCDD and PCDF were measured in air samples collected in Ohio in 1987. No 2,3,7,8-TCDD was detected in any of the samples with a detection limits of less than 240 fg/m³. Using a chemical mass balance model applied to PCDD/PCDF congener group profiles, major potential sources of these compounds to the atmosphere in Ohio were determined to be municipal solid waste combustion, and sewage sludge combustion. Cancer risk calculations for inhalation of PCDD/PCDF in ambient air in Ohio are approximately 10–6. Given the current knowledge of the health effects of exposure to PCDD/PCDF in air, there is no appreciable risk to public health for the levels of these compounds found in ambient air in Ohio.     

Polychlorinated dibenzo-p-dioxins and dibenzofurans in marine mammals in the Canadian North

Polychlorinated dibenzo-p-dioxins (PCDDs) and dibenzofurans (PCDFs) were determined in pooled samples of ringed seal (Phoca hispida) blubber, beluga (Delphinapterus leucas) blubber and polar bear (Ursus maritimus) liver and fat from several areas throughout the Canadian north and compared to mean PCB and HCB levels in the same samples. All seal samples, and all but one polar bear sample, had detectable 2,3,7,8-TCDD at concentrations ranging from 2 to 37 ng/kg, but TCDD was not found in beluga blubber (< 2 ng/kg). All seal samples and one of three beluga samples contained 2,3,7,8-TCDF at levels of 2 to 7 ng/kg, but TCDF was not found in any bear sample. TCDF must therefore be cleared rapidly by polar bears. No other PCDF congeners were found at detection limits of 4 to 8 ng/kg. OCDD concentrations in seal blubber and polar bear samples ranged from not detected (< 8 ng/kg) to 43 ng/kg. No apparent biomagnification of TCDD, OCDD or TCDF occurred from seal to bear fat, similar to previous findings for DDT, and unlike SigmaPCBs and HCB which biomagnified 6- to 17-fold. Highest concentrations of 2,3,7,8-TCDD and OCDD in seals and bears were found in the central Canadian Arctic Archipelago, and lowest were found in Hudson Bay, the reverse of PCB concentration distribution. The reason for higher levels of TCDD and OCDD in the Arctic than in the sub-Arctic is suggested to be trans-polar movement of aerosols with combustion-related origins in Eurasia. Levels of 2,3,7,8-TCDF were more evenly distributed throughout the North, and were positively correlated with PCB, but not with HCB or 2,3,7,8-TCDD levels in seals.     

Serum concentrations of chlorinated dibenzo-p-dioxins and dibenzofurans among former New Zealand trichlorophenol workers

This study examined serum levels of 2,3,7,8-substituted chlorinated dioxins and furans, and 15 PCBs for 346 New Zealand employees who worked at a site that manufactured 2,4,5-trichlorophenol (TCP) and 2,4,5-trichlorophenoxy acetic acid (2,4,5-T). Participants with potential TCP or 2,4,5-T exposures had mean lipid-adjusted 2,3,7,8-tetrachlorodibenzo-p-dioxin (2,3,7,8-TCDD) levels of 9.9 ng kg⁻¹ lipid compared to 4.9 ng kg⁻¹ for workers with no exposure at the site. Among exposed workers, we found evidence of differences in 2,3,7,8-TCDD levels by department and duties. Workers involved in an accidental release had the highest mean 2,3,7,8-TCDD levels, 37.9 ng kg⁻¹, followed by workers in the trichlorophenol plant, 23.4 ng kg⁻¹. Workers with potential intermittent exposures to 2,3,7,8-TCDD in construction, maintenance, mechanics, and transport had 2,3,7,8-TCDD levels above New Zealand background levels of 3.9 ng kg⁻¹, indicating workplace exposures. Among participants with work history indicating no 2,3,7,8-TCDD exposures, we observed some individuals with 2,3,7,8-TCDD levels above background levels. However, in most cases, these workers reported workplace exposures not recorded on their work histories or held other jobs with the potential for 2,3,7,8-TCDD exposures outside the plant. All other dioxin, furan, and PCB levels were similar among the exposed and unexposed workers.     

The influence of sewage sludge applications to agricultural land on human exposure to polychlorinated dibenzo-p-dioxins (PCDDs) and -furans (PCDFs)

Polychlorinated dibenzo-p-dioxins and furans (PCDD/Fs) are organic chemicals of suspected extreme toxicity. PCDD/Fs are ubiquitous in the environment and relatively enriched in sewage sludges. The deliberate application of sewage sludge to agricultural land can therefore potentially increase exposure of the human population to these compounds via transfers through the foodchain. This paper presents a protocol for assessing the background human exposure to all seventeen 2,3,7,8-substituted PCDD/Fs for which toxic equivalent factors (TEFs) are available. Background daily human exposure in the UK to 2,3,7,8-T(4)CDD and I-TEQ are calculated to be 0.0239 ng and 0.203 ng, respectively. The potential increases in crop plant and livestock tissue PCDD/F concentrations, and hence in human exposure, following applications of sewage sludge to agricultural land are quantified for different sludge application scenarios. The key role of PCDD/F transfer into livestock via ingestion of sludge adhered to vegetation in determining increases in human exposure is demonstrated.     

Polychlorinated dibenzothiophenes in Japanese environmental samples and their photodegradability and dioxin-like endocrine-disruption potential

Polychlorinated dibenzothiophenes (PCDTs) in sediment, soil, and fly ash samples collected in Japan were analyzed and their dioxin-like endocrine-disruption potential and photodegradability investigated. PCDTs were detected in all three types of sample, although the concentrations were lower than those of polychlorinated dibenzo-p-dioxins (PCDDs) and polychlorinated dibenzofurans (PCDFs). An Ah-immunoassay confirmed that 2,3,7,8-TeCDT, 1,2,3,7,8-PeCDT, 1,2,3,7,8,9-HxCDT, and 1,2,3,4,7,8,9-HpCDT had Ah receptor-binding activities, which means that these PCDTs have the potential to cause dioxin-like endocrine-disruption. Photodegradation of PCDTs by UV irradiation was accompanied by dechlorination. The photodegradation rates of 2,3,7,8-TeCDT and OCDT were lower than the rates for the corresponding PCDF isomers (2,3,7,8-TeCDF and OCDF), which indicates that PCDTs are more stable than PCDFs to photodegradation.     

A novel source for dioxins present in recycled fat from gelatin production

Within a survey on dioxins in animal fat used as feed ingredient, a sample originating from pigs offal was shown to contain 50 ng Toxic Equivalents (TEQ) PCDD/PCDFs kg(-1) fat. Further investigation revealed fat samples with levels as high as 440 ng TEQ kg(-1) fat and contaminated feed with a highest level of 8.4 ng TEQ kg(-1) feed. The congener pattern was dominated by 1,2,3,7,8-PeCDD and 2,3,7,8-TCDD, and was not recognized from any previous incident or known dioxin source. Remarkably, 2,3,7,8-substituted congeners were much more abundant than their non-2,3,7,8-substituted counterparts. The sampled fat was derived from a gelatin production plant. Broken filters, used to clean the hydrochloric acid (HCl) used in the process, caused the dioxin contamination. The fat was primarily used for pig feed. A new physiologically-based pharmacokinetic (PBPK) model for lipophilic contaminants in growing slaughter pigs predicted levels at slaughter varying between 40 pg TEQ g(-1) fat (worst-case) and 2.5-7pgTEQ g(-1) fat under more realistic scenarios. Almost 300 farms were temporarily blocked. Many fat samples of pigs were analyzed using a combined approach of DR CALUX and GC/HRMS. Levels in contaminated pig fat were around the EU-limit of 1 pg TEQ g(-1) fat, with some samples up to 2-3 pg TEQ g(-1) fat. Of 80 negative samples analyzed by DR CALUX and GC/HRMS no false-negatives were obtained, whereas 36 and 62 of the 80 samples classified suspected with the bioassay had GC/HRMS levels above respectively the tolerance and action limits. It is concluded that novel and unexpected dioxin sources remain a threat to the food chain and require the proper evaluation and monitoring of production processes, including chemicals used therein.     

Estimation of dioxin risk to Japanese from the past to the future

The transport processes of seventeen 2,3,7,8-chlorinated congeners of polychlorinated dibenzo-p-dioxins and dibenzofurans (PCDD/Fs) from their major sources to humans were modeled to estimate the time course, from the past to the future, of the human health risk to the Japanese population. The comparison between measured and estimated values showed that the present modeling approach represented the background levels of congeners in the environment, daily intake, and body burden reasonably well, except for in the case of 2,3,7,8-TCDF. Although PCDD/Fs in herbicides have contributed greatly to the daily intake and body burden to the Japanese population in the past, the main sources of the present intake and burden of PCDD/Fs is estimated to be incinerators. The margin of exposure (MOE) for the risk of morphological reproductive alteration in female offspring exposed prenatally was calculated based on the estimated maternal body burden. The results indicated that the MOE values were in the single digits, implying that these values may not be sufficiently large to guarantee the safety of female offspring of mothers born in the 1950s, whereas the MOE values for female offspring born in and after the latter half of the 1990s may be sufficiently large to guarantee safety.     

Priority assessment of toxic substances in life cycle assessment. Part II: assessing parameter uncertainty and human variability in the calculation of toxicity potentials

Toxicity potentials are standard values used in life cycle assessment (LCA) to enable a comparison of toxic impacts between substances. This paper presents the results of an uncertainty assessment of toxicity potentials that were calculated with the global nested multi-media fate, exposure and effects model USES-LCA. The variance in toxicity potentials resulting from input parameter uncertainties and human variability was quantified by means of Monte Carlo analysis with Latin Hypercube sampling (LHS). For Atrazine, 2,3,7,8-TCDD and Lead, variation, expressed by the ratio of the 97.5%-ile and the 2.5%-ile, ranges from about 1.5 to 6 orders of magnitude. The major part of this variation originates from a limited set of substance-specific input parameters, i.e. parameters that describe transport mechanisms, substance degradation, indirect exposure routes and no-effect concentrations. Considerable correlations were found between the toxicity potentials of one substance, in particular within one impact category. The uncertainties and correlations reported in the present study may have a significant impact on the outcome of LCA case studies.     

Blood dioxin biomonitoring to assess local residents' exposure from a large urban remediation project

Background

A total of 265 000 m³ of dioxin contaminated soil and sediments from past industrial activity was treated on site in an urban setting in Sydney, Australia. To respond to local community concerns about potential dioxin exposure from fugitive emissions a human biomonitoring study was undertaken.

Objective

To determine whether local residents were exposed to significant amounts of dioxin from the remediation process.Methods: Blood samples were collected from local residents around the site and a representative metropolitan control group. They were pooled within age and sex strata and the change in dioxin concentrations over the remediation period and a summary of the mid point and post remediation dioxin concentrations were compared between groups. Information on dietary intake was collected to look for possible confounding.

Results

The mean dioxin Toxic Equivalent concentrations (TeQ) decreased among both the local resident and control groups over the remediation period by 1.9 and 2.1 pg gm⁻¹ lipid respectively. Modelled blood concentrations adjusting for age and sex did not detect a significant difference between groups for changes in either TeQ or 2,3,7,8-tetrachlorodibenzo-p-dioxin (2,3,7,8 TCDD). The summary measure approach did however demonstrate that the 2,3,7,8 TCDD concentrations among the local resident group was approximately 0.7 pg g⁻¹ lipid higher compared to the control group post remediation. There were no significant changes in dietary intake sources of dioxin.

Conclusion

Biomonitoring demonstrated that local residents were not exposed to significant quantities of dioxin. Large scale remediation of dioxin contaminated land can be safely undertaken in an urban setting.     

Transcriptional profiles induced by the Aryl Hydrocarbon Receptor agonists 2,3,7,8-tetrachlorodibenzo-p-dioxin, 2,3,7,8-tetrachlorodibenzofuran and 2,3,4,7,8-pentachlorodibenzofuran in primary rat hepatocytes

Toxicogenomics was used to examine mRNA expression profiles obtained from primary rat hepatocytes treated for 24 h with 0.01 or 1.0 nM 2,3,7,8-tetrachlorodibenzo-p-dioxin (2,3,7,8-TCDD), 0.02 or 2.0 nM 2,3,4,7,8-pentachlorodibenzofuran (2,3,4,7,8-PeCDF) and 0.1 or 10 nM 2,3,7,8-tetrachlorodibenzofuran (2,3,7,8-TCDF). The concentrations of 2,3,4,7,8-PeCDF and 2,3,7,8-TCDF were chosen to be equivalent to 2,3,7,8-TCDD’s concentration based on the toxic equivalency factor/toxic equivalent (TEF/TEQ) method for estimating biological potency. 2,3,7,8-TCDD at 1.0 nM altered the expression of 533 genes; 2,3,4,7,8-PeCDF at 2.0 nM altered 182 genes, and 2,3,7,8-TCDF at 10 nM altered 154 genes. Of these, 57 genes were affected by all three congeners. Agglomerative hierarchical clustering revealed distinct congener-dependent gene subclusters. Principal components analyses of the microarray data revealed that these congeners cluster independently of one another. Data presented here demonstrate that equivalent TEQ concentrations of 2,3,7,8-TCDD, 2,3,4,7,8-PeCDF and 2,3,7,8-TCDF, while altering the expression of a small battery of genes in common, also produce substantial congener specific alterations in gene expression.     

Bioavailability of PCDDs and PCDFs on fly ash after semi-chronic oral ingestion by guinea pig and syrian golden hamster

Groups of guinea pigs and syrian golden hamster (n = 5) were fed 2.5% HCL pre-treated fly ash from the electrostatic precipitator of a municipal incinerator during one, two and three months, respectively, in the diet. The livers were analyzed for tetra-, penta- and hexa-chlorinated dibenzo(p)dioxins (PCDDs) and dibenzofurans (PCDFs).In the livers of the hamsters 2,3,7,8-substituted PCDDs and PCDFs were the major isomers retained. In the livers of the guinea pigs 2,3,7,8 substituted PCDDs and PCDF congeners were retained, but also a number of otherwise substituted PCDFs. These other PCDF congeners included some having a 2,3,6,7 or alternate chlorine substitution pattern. Those congeners retained in the livers were generally below 5% of the group dose. The PCDF congener which had the highest retention in the livers of guinea pig was 1,2,3,7,8-PnCDF, 11.3% after 95 days. In the livers of the hamsters highest retention was found for 2,3,4,7,8-PnCDF, 8.4% after 95 days. For most 2,3,7,8-substituted PCDDs and PCDFs the retention in the livers of the guinea pigs and hamsters was not significantly different during the whole period, which could indicate a bioconcentration approaching a linear relationship to the administered dose. Constant relative concentrations in the livers were found for the 2,3,7,8- substituted penta- and hexa-chlorinated PCDDs and PCDFs in both species during the three time periods.     

PCDD/Fs levels in indoor environments and blood of workers of three municipal waste incinerators in Taiwan

This study monitored ambient air concentrations of polychlorinated dibenzo-p-dioxins and polychlorinated dibenzofurans (PCDD/Fs) in three municipal waste incineration plants. Blood PCDD/Fs levels of 133 workers randomly selected from these plants were also measured. The associations between workers' blood PCDD/Fs concentrations and occupational exposures to PCDD/Fs were assessed. Means of air PCDD/Fs levels ranged from 0.08 to 3.01 pg/m3 in international toxic equivalents (I-TEQ). The geometric means of blood PCDD/Fs concentrations were 14.6, 15.8, 19.1 pg/g lipid in World Health Organization (WHO) TEQ, respectively, for workers from three plants. Air levels of total I-TEQ and all congeners, except 2,3,7,8-tetrachlorinated dibenzo-p-dioxin (TeCDD) and 1,2,3,4,7,8,9-heptachlorinated dibenzofuran (HpCDF), were significantly higher in plant B. However, blood concentrations of 2,3,7,8-TeCDD, 1,2,3,7,8-PeCDD, 2,3,7,8-TeCDF, 1,2,3,7,8-PeCDF and 1,2,3,4,7,8,9-HpCDF were significantly elevated in plant C workers. Although job contents, duration of employment and time spent in certain location were significantly different among incineration plants, they were not significantly associated with blood concentrations of any congener. Furthermore, results of the multiple regression analysis that assessed important occupational factors simultaneously and adjusted for potential confounders, showed significant associations between four congeners and incineration plant or job contents. However, the results were limited by small R-squares of the regression models. In conclusion, blood concentrations of several PCDD/Fs congeners were significantly different among three incineration plants. The differences were not explained by the discrepancy in job contents, duration of employment, and time activity in these plants.     

Chlorinated hydrocarbon contaminants in blood of black and turkey vultures from Savannah River Site,South Carolina,USA

Blood of adult and juvenile black and turkey vultures in the Savannah River Site of South Carolina, USA was analyzed for the presence of 2,3,7,8-chlorine substituted polychlorinated dibenzo-p-dioxins (2,3,7,8-PCDDs), dibenzofurans (2,3,7,8-PCDFs), -dioxin-like and -di-ortho polychlorinated biphenyls. Concentration ranges of 2,3,7,8-PCDD/DFs in blood of black and turkey vultures were 14.2-34.6 and 8.7-56.2 pg/ml wet wt., respectively. Dioxin-like PCBs were in the ranges of 815-4627 and 753-3611 pg/ml wet wt. respectively, in black and turkey vultures. Considerable concentrations of two congeners of di-ortho PCBs were noticed in the ranges of 1415-10325 and 663-7500 pg/ml respectively, in black and turkey vultures. Comparatively, greater toxic equivalency (TEQ) were observed in blood of turkey vultures with the ranges of 3.2-20, whereas black vulture contained 1.8-8.4 pgTEQ/ml wet wt. basis. The species-specific accumulation profiles of PCDD/DFs and dioxin-like PCBs may reflect the different feeding habits, ecology, metabolic capacity and migratory movements of these two scavenging species.