Bioavailability of 2,3,7,8-tetrachlorodibenzo-p-dioxin from municipal incinerator fly ash to freshwater fish

The bioavailability of 2,3,7,8-TCDD from municipal incinerator fly ash to freshwater fish was determined. It was observed that carp exposed to fly ash containing all 22 TCDD isomers, or the solvent extract of the fly ash, retain only 2,3,7,8-TCDD. Exposures with fly ash appears to follow a dose response relationship for bioconcentration, however, the bioavailability of 2,3,7,8-TCDD was not directly related to the level of 2,3,7,8-TCDD in fly ash for two fly ash samples studied.     

Some pharmacokinetic aspects of PCDDs and PCDFs in mammals after administration of a fly ash extract from a municipal incinerator

Fly ash extracts were fed to male hamster (single dose), male rat (single dose and multiple dose), pregnant and lactating female rat (multiple dose). The retention of four isomers, 2,3,7,8-TCDD, 2,3,7,8-TCDF, 1,2,3,7,8-PnCDD and 2,3,4,7,8-PnCDF, was studied in the liver of the adults, foetuses and liver of the sucklings.

Liver retention was structure dependent and different for both species. Transportation of the isomers via the mother milk was 50–100 times more effective than via the placenta.

After a single intravenous dose of fly ash extract to male rats the elimination of these four isomers was studied in the liver, during a period of 10 days. Elimination rates for 2,3,7,8-TCDD, 1,2,3,7,8-PnCDD and 2,3,4,7,8-PnCDF were in the same range. Pharmacokinetic calculations were done on both tetra congeners, to obtain information about the validity of the published K_e values in the multiple dose experiments with male rats.

For 2,3,7,8-TCDF the K_e value was applicable, but for 2,3,7,8-TCDD the validity of the K_e could not be determined.     

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.     

Study of PCDD/Fs distribution in fly ash,ash deposits,and bottom ash from a medical waste incinerator in China

Over the past decades in China, the number of medical waste incinerators (MWIs) has been rising rapidly, causing emissions of polychlorinated dibenzo-p-dioxins and dibenzofurans (PCDD/Fs). In this study, samples of fly ash, ash deposits, and bottom ash from typical MWIs were analyzed for PCDD/Fs and their distribution characteristics. Results showed international toxic equivalent (I-TEQ) values in the range of 6.9–67 ng I-TEQ/g in fly ash and ash deposits, whereas the concentration in bottom ash was extremely low (only 1.33 pg I-TEQ/g), yet the generation of PCDD/Fs was mostly de novo synthesis in fly ash and ash deposits according to the ratio of PCDFs to PCDDs; the major distribution differences of PCDD/Fs in fly ash was manifested by the content of toxic furan 2,3,7,8-TCDF, but other toxic PCDD/Fs showed similar distribution. Other findings are that 2,3,4,7,8-PeCDF had the most contribution to TEQ concentration, and that the most abundant toxic furan congener is 1,2,3,4,6,7,8-HpCDF. Correlation analysis showed that there was no significant correlation between PCDD/Fs concentration and several other physical and chemical parameters.

Implications: This paper is of interest because it presents the emission performances of PCDD/Fs in ash from medical waste incineration in China. PCDD/F contents in fly ash and ash deposits vary between 6.9 and 67.3 ng I-TEQ/g. However, the concentration in bottom ash was extremely low (only 1.33?×?10^?3 ng I-TEQ/g). The fingerprints of PCDD/Fs in fly ash are almost similar, except for 2,3,7,8-TCDF. There is no marked correlation between PCDD/Fs and other physicochemical properties.

Supplemental Materials: Supplemental materials are available for this paper. Go to the publisher's online edition of the Journal of the Air & Waste Management Association.     

Dioxin formation in pulp and paper mills of India

Samples of effluents, sludge, pulp, final products (paper) and soil were collected from the identified pulp and paper mills in India. The samples were analysed for 2,3,7,8-tetrachloro-dibenzo-p-dioxin (2,3,7,8-TCDD) and other dioxin congeners and precursors. Pulp and paper mills using chlorine for the bleaching process showed the presence of 2,3,7,8-TCDD in effluent samples. In the effluent and pulp samples from mills where chlorine dioxide was used as a bleaching agent, the 2,3,7,8-TCDD congener ranged from below the detection limit 0.05 to 0.12 ngL⁻¹/ngg⁻¹. The relative standard deviation of reproducibility and the percent recovery of 2,3,7,8-TCDD were 2.07 and 82.4% in pulp and 2.8 and 92% in effluent, respectively. The 1,3,6,8-TCDD was the only other major dioxin congener found in the treated and untreated effluent and sludge samples. However, dichlorobenzene, trichlorophenyl, and hexachlorobiphenyl were detected in all samples. The formation of dioxins can be minimised by replacing chlorine with chlorine dioxide in bleaching processes in pulp and paper mills.     

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.     

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.     

流化床垃圾焚烧炉产生的有毒二噁英同类物分布研究

测定了流化床垃圾焚烧炉焚烧产生的飞灰、烟尘和烟气中的2，3，7，8位氯取代二噁英同类物的含量及其毒性当量。结果表明，产生的二噁英主要存在于飞灰中，烟气中的含量很少。飞灰中二噁英总浓度和毒性当量分别为8.44ng／g和0．80ng／g，经过布袋除尘器后的烟尘和烟气中二噁英的浓度之和与毒性当量之和分别为0．34ng／m^3和0．02ng／m^3，而布袋除尘器前的烟尘和烟气中二噁英的浓度之和与毒性当量之和分别为40．78ng／m^3和3．0ng／m^3。飞灰和烟尘中2，3，7，8位氯取代二噁英同类物的分布相似，但是与烟气中2，3，7，8位氯取代二噁英同类物的分布差别较大。通过了解有毒二噁英同类物的分布，可以进一步优化流化床垃圾焚烧炉的焚烧条件，降低二噁英的排放量，减少垃圾焚烧对环境的污染。     

Development of GC capillary column for isomer-specific separation of toxic isomer of PCDDs and PCDFs in environmental samples

Analysis of polychlorinated dibenzo-p-dioxins (PCDD) and polychlorinated dibenzofurans (PCDF) has been performed using gas chromatography mass spectrometry (GC-MS). Analysis of the most toxic isomers, in particular, 2,3,7,8-substituted PCDD/PCDF in the presence of other isomers requires a special isomer specific capillary column or high performance liquid chromatography (HPLC) fractionation prior to GC-MS analysis. Commercially available long (>50 m) polar columns can separate 2,3,7,8-TCDD from other tetra isomers. However, those columns are not satisfactory for the analyses of total PCDD/PCDF in the environmental samples. Gas chromatography -high resolution mass spectrometry (GC-HRMS) and GC-MS/MS techniques are not helpful in the analysis of 2,3,7,8-TCDD unless it is separated from the other tetra isomers. The analysis of 2,3,7,8-TCDD and total PCDD and PCDF in a single GC-MS run can ease the laborious techniques presently used. In this study we have developed a new stationary phase for the GC capillary column. The capillary column developed using this new stationary phase showed unsurpassed selectivity for the separation of 2,3,7,8-TCDD from other tetra isomers. There are several advantages of the newly developed GC capillary column.     

Levels and congener profiles of PCBs and PCDD/Fs in blue shark (Prionace glauca) liver from the South-Eastern Mediterranean Sea (Italy)

Liver of blue shark (Prionace glauca) specimens from the South-Eastern Mediterranean Sea were analyzed for the presence of polychlorinated biphenyls (PCBs), including coplanar congeners, polychlorinated dibenzo-p-dioxins (PCDDs) and dibenzofurans (PCDFs). PCBs were the dominant chemicals, followed by PCDFs and PCDDs. The pattern of PCB congener concentrations in the hepatic tissue was dominated by higher chlorinated compounds. The specific profile of toxic PCDD/F congeners was characterized mainly by 2,3,7,8-TCDF and 2,3,7,8-TCDD, followed by 1,2,3,6,7,8-HxCDD and 2,3,4,6,7,8-HxCDF. The total 2,3,7,8-TCDD toxic equivalent (TEQs) was 149 pg g⁻¹ lipid wt. The profile of TEQ shows that PCDDs present the greatest risk to this species contributing to total toxicity with a percentage approximately of 60%, while the contribution of PCDFs and DL-PCBs is almost the same being 22.4% and 21.6%, respectively. Further investigations are urgently needed to characterize the PCDD/Fs contamination levels not only in elasmobranch fish but in all Mediterranean marine biota.     

Determination of 2,3,7,8-TCDD toxic equivalent factors (TEFs): support for the use of the in vitro AHH induction assay

The in vitro induction of the cytochrome P₁-450-dependent monooxygenases, aryl hydrocarbon hydroxylase (AHH) or ethoxyresorufin O-deethylase (EROD) by 2,3,7,8-TCDD and related toxic halogenated aryl hydrocarbons in rat hepatoma H-4-II E cells has been developed as a short term quantitative bioassay for these toxic chemicals. There was a linear correlation between the -log EC₅₀ (in vitro) AHH induction vs the -log ED₅₀ (in vivo) for body weight loss, thymic atrophy, hepatic AHH and EROD induction in the rat for several polychlorinated biphenyl, dibenzo-p-dioxin and dibenzofuran congeners and mixtures. These data clearly support the utility of the in vitro AHH induction assay as a short term test system for quantitating the “toxic or 2,3,7,8-TCDD equivalents” in an extract containing toxic halogenated aromatics. The bioassay method is rapid, relatively accurate and much more cost effective than conventional analytical methods such as gas-chromatography-mass spectrometry from which it is difficult to determine the levels of 2,3,7,8-TCDD equivalents in specific analytes.     

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.     

Adsorption and thermal reactions of 1,2,3,4-tetrachlorodibenzo-p-dioxin on fly ash from a municipal incinerator

Adsorption and thermal reactions of 1,2,3,4-tetrachlorodibenzo-p-dioxin (TCDD) on fly ash from a municipal incinerator were determined for temperatures between 100 to 300°C in air and in helium atmospheres. Results show 1,2,3,4-TCDD undergoes partial irreversable adsorption or decomposition in air at these temperatures. However, no decomposition products in air atmosphere were detected using gas chromatographic/mass spectrometric analysis of fly ash extracts and effluent.     

Chlorination reactions of 1,2,3,4-tetrachlorodibenzo-p-dioxin on fly ash with HC1 in air

Chlorine substitution reactions of 1,2,3,4-TCDD to higher chlorinated PCDD occurred on fly ash between 50°C to 250°C with an HC1 in air atmosphere in a laboratory reaction apparatus used to simulate emission conditions in municipal incinerators. Percent conversion of 1,2,3,4-TCDD through such reactions was as high as 66% by mass corrected for losses to irreversable absorption. Production of penta-, hexa-, hepta- and octa-CDD was evident and a maximum in production of P₅CDD and H₆CDD was reached in 10 to 30 min. Results showed that these reactions may involve complex mechanisms which include several states of adsorption with different reactivities of 1,2,3,4-TCDD on fly ash.     

Polychlorinated dibenzo-p-dioxins and dibenzofurans in eggs of eight avian species from Dongting Lake, China

Concentrations of polychlorinated dibenzo-p-dioxins (PCDDs) and dibenzofurans (PCDFs) were determined in eggs of eight avian species collected from Dongting Lake of China to assess residue levels, accumulation patterns, and toxic potential in different avian species. Concentrations of total 2,3,7,8-substituted PCDD/Fs were in the range of 10.8-182pgg(-1) lipid weight. Eggs of great egret and lesser pied kingfisher contained higher levels of PCDD/Fs than eggs of other species, indicating the specific exposure and accumulation of PCDD/Fs relating to feeding habits and the life span. PCDD/Fs congener patterns varied among species. The patterns of PCDD/Fs in the eggs may be influenced by feeding habits, specific elimination, and metabolism. In general, concentrations of PCDDs were higher than those of PCDFs in avian eggs. On basis of lipid weight, total 2,3,7,8-TCDD toxic equivalents (TEQs) calculated based on the WHO TEFs for birds ranged from 2.04 to 42.0pgg(-1); and on basis of wet weight, total WHO-TEQs ranged from 0.19 to 1.59pgg(-1). 2,3,7,8-TCDF, 2,3,4,7,8-PeCDF, 2,3,7,8-TCDD, 1,2,3,7,8-PeCDD were the major contributors to TEQ concentration in most avian eggs, whereas 1,2,3,4,7,8-HxCDD also accounted for a major portion of TEQs in eggs of azure-winged magpie. Values of TEQs in avian eggs were lower than toxic threshold values, implying risk reduction and natural restoration of PCDD/Fs contamination in Dongting Lake region.     

Dioxins and their fingerprint in size-classified fly ash fractions from municipal solid waste incinerators in China—Mechanical grate and fluidized bed units

The distribution of polychlorinated dibenzo-p-dioxins/dibenzofurans (PCDD/Fs), in brief dioxins, has seldom been addressed systematically in fly ash from municipal solid waste incinerators (MSWIs). This study shows the amount and fingerprint of PCDD/Fs in fly ash from four different Chinese MSWIs, that is, three mechanical grate units and one circulating fluidized bed unit. In these fly ash samples, dioxins-related parameters (international toxic equivalent quantity, total amount of PCDD/Fs, individual isomer classes, and 17 toxic 2,3,7,8-substituted congeners) all tend to increase with decreasing particle size for mechanical grate incinerators, yet only for the finest fraction for fluidized bed units. Moreover, the fluidized bed incinerator seems superior to grate incineration in controlling dioxins, yet a comparison is hampered by internal differences in the sample, for example, the fluidized bed fly ash has much lower carbon and chlorine contents. In addition, the presence of sulfur from mixing coal as supplemental fuel to the MSW may poison the catalytic steps in dioxins formation and thus suppress the formation of dioxins. With more residual carbon and chlorine in the fly ash, it is easier to form dioxins during cooling. Nevertheless, there is no apparent relation between Fe, Cu, and Zn contents and that of dioxins in fly ash.

Implications This paper is of interest because it presents the amounts and distribution of PCDD/Fs in fly ash samples from some typical waste incineration plants in China, featuring distinct incinerator types, combustion conditions, fuel composition, or residual carbon, chloride, and heavy metal contents in fly ash.     

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.     

Dioxins and their fingerprint in size-classified fly ash fractions from municipal solid waste incinerators in China--mechanical grate and fluidized bed units

The distribution of polychlorinated dibenzo-p-dioxins/dibenzofurans (PCDD/Fs), in brief dioxins, has seldom been addressed systematically in fly ash from municipal solid waste incinerators (MSWIs). This study shows the amount and fingerprint of PCDD/Fs in fly ash from four different Chinese MSWIs, that is, three mechanical grate units and one circulating fluidized bed unit. In these fly ash samples, dioxins-related parameters (international toxic equivalent quantity, total amount of PCDD/Fs, individual isomer classes, and 17 toxic 2,3,7,8-substituted congeners) all tend to increase with decreasing particle size for mechanical grate incinerators, yet only for the finest fraction for fluidized bed units. Moreover, the fluidized bed incinerator seems superior to grate incineration in controlling dioxins, yet a comparison is hampered by internal differences in the sample, for example, the fluidized bed fly ash has much lower carbon and chlorine contents. In addition, the presence of sulfur from mixing coal as supplemental fuel to the MSW may poison the catalytic steps in dioxins formation and thus suppress the formation of dioxins. With more residual carbon and chlorine in the fly ash, it is easier to form dioxins during cooling. Nevertheless, there is no apparent relation between Fe, Cu, and Zn contents and that of dioxins in fly ash.     

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.     

Fast extraction of polychlorinated dibenzo-p-dioxin and polychlorinated dibenzofuran in sewage sludge and soil samples

The current environmental legislations recommend monitoring chemical contaminants such as polychlorinated dibenzo-p-dioxins and polychlorinated dibenzofurans before the use of sewage sludge on the agricultural land. In this study, a solid–liquid extraction with low-temperature purification (SLE-LTP) was optimized and validated to determine 2,3,7,8-tetrachlorodibenzo-p-dioxin and 2,3,7,8-tetrachlorodibenzofuran in sewage sludge and soil samples. The analyses were performed by gas chromatography-mass spectrometry operating in the selective ion mode (GC-MS-SIM). Acetonitrile:ethyl acetate 6.5:1.5 (v/v) was the best extraction phase, and the recoveries percentages were close to 100%. The linearity was demonstrated in the range of 1.25–25 µg L^?1 of 1.25–20 µg L^?1 for sewage sludge and soil, respectively. Matrix effect was proved for the two compounds and in the two matrices studied. Extraction percentages were between 78 and 109% and relative standard deviations ≤ 19%. The proposed method is faster than methods described in the literature because showed a few steps. The quantification limits (LOQ) in sewage sludge were 6.4 and 32 ng TEQ kg^?1 for 2,3,7,8-TCDF and 2,3,7,8-TCDD, respectively. In soil, LOQs were 0.8 and 8.0 ng TEQ kg^?1 for 2,3,7,8-TCDF and 2,3,7,8-TCDD, respectively. These values are lower than the maximum residue limits established by European Legislation. The method was applied to 22 agricultural soil samples from different Brazilian cities and 2,3,7,8-TCDF was detected in one of these samples.