TCDD Levels Research Articles

Assessment of Host Resistance to Trichinella spiralis in Mice Following Preinfection Exposure to 2,3,7,8-TCDD

2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) has been reported to decrease host resistance to a variety of infectious agents when exposure occurs prior to infection. Resistance to viral infection has been observed at doses as low as 0.1 μg TCDD/kg body wt, well below the thymolytic dose in mice. In the present study, female B6C3F1 mice were exposed to a single intraperitoneal injection of 0, 0.1, 1.0, 10.0, or 30.0 μg TCDD/kg 7 days prior to infection to determine the effects of TCDD exposure on resistance to the nematode parasite Trichinella spiralis. Exposure to 10 or 30 μg TCDD/kg delayed adult parasite elimination from the small intestine. Significantly more larvae were released by female parasites and greater numbers of encysted larvae were recovered from the muscle of mice exposed to TCDD. Proliferative responses of splenocytes and mesenteric lymph node cells stimulated with T. spiralis antigen were significantly suppressed at exposure levels of TCDD ≥ 1.0 μg/kg 7 days after infection and in splenocytes only at 14 days after infection, demonstrating the greater sensitivity of proliferative responses to TCDD exposure than actual host resistance to Ts infection. Suppressed proliferation was observed at doses which produced TCDD concentrations ≥ 0.2 pmol/g of lymphoid tissue on Day 7 of infection. In addition, it was determined that infected mice had higher TCDD levels than noninfected mice given the same dose. These results suggest an interaction between TCDD exposure and infection, i.e., that exposure to TCDD altered the host response to infection, while infection delayed elimination of TCDD from the host.

Relative Sensitivities of 2,3,7,8-Tetrachlorodibenzo-p-dioxin-lnduced Cypla-1 and Cypla-2 Gene Expression and Immunotoxicity in Female B6C3F1 Mice

Improvements in risk assessment require better linkage of exposure to response by the determination of target tissue dose. The relative sensitivity of several responses in female B6C3F1 mice was compared on the basis of administered and target tissue dose spanning 3 orders of magnitude. Twenty-four hours after administration, [3H]TCDD was detected in the heart, spleen, kidney, uterus, thymus, lung, and liver, and the highest concentrations were noted in the liver, uterus, and lung. At doses from 5 to 25 ng/kg, hepatic [3H]TCDD levels associated with the cytosolic and nuclear subcellular fractions increased from 12 to 62% of the total liver levels and then decreased at higher doses. At the two lowest doses used in the enzyme induction study, 5 and 10 ng/kg, the levels of specifically bound nuclear Ah receptor complex liganded with [3H]TCDD were 2.3 and 2.5 fmol/mg protein. Slightly higher levels of nuclear Ah receptor complex were observed at doses between 25 and 100 ng/kg (i.e., 3.6 to 4.2 fmol/mg protein) and a steep dose-dependent increase in nuclear Ah receptor levels was noted at doses of 500, 1000, and 5000 ng/kg (8.0, 39.3, and 92.8 fmol/mg protein, respectively). The dose-dependent effects of [3H]TCDD on hepatic Cypla-1 and Cypla-2 mRNA levels, ethoxyresorufin O-deethylase (EROD) activity, and the splenic antibody plaqueforming cell (PFC) response to sheep red blood cells were also determined; the latter response was determined 9 days after administration of TCDD. Statistically significant induction of hepatic Cypla-1 was observed at lower doses (25 ng/kg) than any other marker, followed by induction of EROD and PFCs expressed per spleen or per 106 cells which was observed at 100 ng TCDD/kg and at higher doses. Cypla-2 was elevated significantly relative to control at doses <1000 ng/kg. The ED50 value for PFCs/10 cells was the lowest of the variables analyzed and was not statistically significantly different from control (91 ± 92 ng/kg). A 50% increase in Cypla-2 and Cypla-1 mRNA levels was observed at doses of 736 ± 132 and 1630 ± 431 ng/kg, respectively. Due to variability in response in PFCs/spleen and the submaximal induction of EROD activity, ED50 values could not be calculated for these responses. The analyses indicate that the immunosuppressive response (when normalized for the number of spleen cells) may be depressed by administered doses as low as 90 ng TCDD/kg body weight. A 50% increase in Cypla-1 or Cypla-2 was observed at higher administered doses (1630 or 736 ng/kg, respectively). This suggests that the immunosuppressive response is depressed at lower doses of TCDD than the other variables studied.

Bioaccumulation of 2,3,7,8-tetrachlorodibenzo-P-dioxin in feral fish collected from a bleach-kraft paper mill receiving stream

Bleach-kraft mill (BKM) processes may result in the formation and release of a number of chlorinated organic compounds, including 2,3,7,8-tetrachIorodibenzo-p-dioxin (TCDD). Contamination of aquatic ecosystems by TCDD is of concern due to the chemical's toxicity, bioaccu-mulation potential, and persistence in the environment. Sediment samples and tissues from three species of fish and one invertebrate were collected downstream from a BKM facility and were analyzed for TCDD. Concentrations of TCDD were greatest in the bowfin, particularly in the ovary of a gravid female (46.1 pg/g). There appeared to be no correlation between either trophic position or habitat classification (i.e., epibenthic or pelagic) and TCDD tissue concentrations. Sediments collected near the mill outfall contained elevated levels of TCDD as great as 52.8 ppt. Sediment-based BAFs and lipid- and carbon-normalized bioavailability indexes (BI) were calculated for the fish livers and gonads, and blue crab hepatopancreas. BAF*s varied by a factor of 27, depending on species and organ, whereas Bis had an approximate seven-fold variation. It appears that organic carbon-and lipid-normalization factors may be more accurate predictors of the extent of bioaccumulation in resident biota from TCDD-contaminated sediments than either BAF*s or BCFs. As there is currently only a limited understanding of species variability in absorption and deposition of TCDD, a more accurate estimation of TCDD levels in feral fish tissues may not be possible.

Chlorinated dioxin, dibenzofuran, coplanar, mono-ortho, and di-ortho substituted PCB congener levels in blood and semen of Michigan Vietnam veterans compared with levels in Vietnamese exposed to Agent Orange

In the present study, conducted in 1991 and 1992, fifty Vietnam veterans from Michigan volunteered to have their blood analyzed for chlorinated dibenzo-p-dioxins (PCDDs), dibenzofurans (PCDFs), and polychlorinated biphenyls (PCBs). Seventeen of these veterans also contributed semen which was analyzed in three composite samples. Six of fifty Michigan veterans exhibited elevated TCDD blood levels ranging from 20.4 to 131 parts per trillion (ppt). The remaining forty-four had TCDD levels ranging from not detected to 8.3 ppt, with a mean level of 4.1 ppt lipid. Semen TCDD levels ranged from 0.00178 to 0.0034 ppt wet weight in the three composite samples. The veterans had total coplanar, mono- and di-ortho PCBs blood lipid levels ranging from 49,900 to 628,000 ppt, lipid. The PCB levels in these fifty veterans do not reflect exposure in Vietnam but do indicate that total dioxin-like toxicity in Americans, including Vietnam veterans, is greater than that from dioxins and dibenzofurans alone.

Bioaccumulation of 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) by Fish Downstream of Pulp and Paper Mills in Maine

Since 1988, the State of Maine has monitored dioxin levels in the tissues of predatory and bottom feeding species of fish taken from the state′s major water bodies, including five rivers which receive the effluent of bleached kraft paper mills. Data are also available on dioxin concentrations in the effluent of these mills. Monitoring results were analyzed using simple models to yield field bioaccumulation factors (BAFs) for 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) in Maine rivers. Three BAFs were computed for each fish species at each site to account for declining TCDD levels in mill effluents over time. Mean BAFs (across rivers) ranged from 11,500 to 24,600 for smallmouth bass fillets, from 17,900 to 28,300 for brown trout fillets, from 3000 to 7500 for white perch fillets, and from 78,500 to 106,000 for white sucker whole bodies. Field BAFs obtained in this analysis are similar to factors obtained in recent laboratory studies of TCDD accumulation in fish. Our results suggest that EPA′s currently recommended BCF value of 5000 is probably too low. Instead, a value between 15,000 and 25,000 is considered a reasonable estimate of the BAF to use for regulatory purposes in the state of Maine.

Interactions of 2,2′,4,4′,5,5′-hexachlorobiphenyl and 2,3,7,8-tetrachlorodibenzo-p-dioxin in a subchronic feeding study in the rat

Female (SD) rats were fed diets containing 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and 2,2′,4,4′,5,5′-hexachlorobiphenyl (PCB 153) in various concentrations for three months. PCB 153 had no significant effect on the body weight gain when given alone or in combination with TCDD. The increases in relative liver weights were additive. For thymic atrophy no interactive effects became apparent. PCB 153 had no effect on the EROD induction by TCDD. PROD induction by PCB 153 was diminished in the presence of TCDD. The level of TCDD in the liver was decreased by PCB 153. Increasing TCDD dosage led to an increase in PCB 153 levels.

Current Serum Levels of 2,3,7,8-Tetrachlorodibenzo-p- dioxin in Phenoxy Acid Herbicide Applicators and Characterization of Historical Levels

Workers who sprayed phenoxy acid herbicides, especially those who sprayed before 1975, may have been exposed to significant amounts of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), a potent animal carcinogen present in herbicide preparations as a contaminant. The aims of this study were (a) to determine serum levels of TCDD in a representative sample of workers occupationally exposed to the agent during the spraying of phenoxy acid herbicides; (b) to compare serum levels in workers exposed before 1965, when concentrations in herbicide products were unregulated and high, with levels in workers exposed after 1974, when concentrations were lower as a result of government regulations worldwide; and (c) to examine the correlation, if any, between serum levels and duration of employment in spraying. Thirty-seven subjects were randomly selected from a group of 654 men who had sprayed the herbicides 2,4,5-trichlorophenoxyacetic acid (2,4,5-T) and 2,4-dichlorophenoxyacetic acid (2,4-D) in Australia for at least 12 months. The workers were classified as follows: eight who sprayed only before 1965, nine who sprayed only during the period after 1964 and before 1975, and 20 who sprayed during the period after 1974 and before 1991. Serum from the workers was analyzed for TCDD by high-resolution gas chromatography and high-resolution mass spectrometry at a detection limit of 0.6 parts per trillion (ppt) on a lipid-weight basis. In addition, rates of exposure to TCDD were estimated, as were TCDD serum concentrations at termination of employment and intensity of herbicide use. Only one worker, with a serum TCDD level of 34 ppt, had a serum level higher than the maximum level of 26 ppt reported for the general population. Assuming a half-life of 7.1 years, we estimated the mean exposure rates to be 2.7, 2.3, and 0.06 ppt/mo for the three epochs, respectively. We found the highest serum level of TCDD at the time of cessation of employment to be 329 ppt. Calendar period and intensity of use of 2,4,5-T and 2,4-D were statistically significant determinants of rate of exposure to TCDD, but 2,4-D was associated with exposure rate only for the pre-1975 periods. Estimated rates prior to 1965 were more than an order of magnitude higher than those after 1974. The highest estimated exposure rate was 20.7 ppt/mo, which suggests that some sprayers may have been exposed to levels comparable with those that produce cancer in laboratory animals.

Dioxin and dibenzofuran levels in blood and adipose tissue of Vietnamese from various locations in Vietinam in proximity to Agent Orange Spraying

Polychlorinated dibenzodioxins (PCDDs) and dibenzofurans (PCDFs) are of concern in Vietnam because of contamination from Agent Orange and other dioxin-containing chemicals. To map out levels of dioxins in Vietnam, between 1987 and 1991 pooled samples were collected in hospitals from discarded blood of adults and analyzed for dioxin content. Locations represented include Hanoi in the north, and thirteen areas in southern and central Vietnam. Because humans are at the top of the food chain, human blood dioxin levels can be used to monitor the environment and to acquire data of public health concern. Vietnamese adults, usually over the age of 40, were selected to increase the probability that 2,3,7,8-TCDD from Agent Orange, sprayed from 1962–1970 over 10% of the south, would be detected. One special group was included, veterans of the North Vietnam Army who served in the jungles of the south where Agent Orange was used. In general, considerable variation in TCDD level was observed, with elevated levels from certain areas in the south and also in the soldiers from the north of Vietnam who had served in the south. Seven hundred and twenty-one Vietnamese tissue samples were collected and are reported from twenty dioxin analyses.

The Air Force health study: An epidemiologic investigation of health effects in Air Force personnel following exposure to herbicides, reproductive outcomes

This report investigates the relationship between birth defects and reproductive outcomes versus paternal TCDD levels among children and conceptions of members of Operation Ranch Hand, the unit responsible for the aerial spraying of herbicides in Vietnam and a comparison group. At a baseline physical examination in 1982 and again in 1985 and 1987, participants were asked to report occurrences of birth defects, miscarriages, stillbirths, infant deaths and neonatal deaths of their children. The birth defect status and outcome of all conceptions (N = 10,843) fathered by participants were verified by medical record review. Of these, 8,099 resulted in live births and birth defect status verified for 8,090 (99.9%). During the same period, the Air Force collaborated with the Centers for Disease Control to assay blood of the 1987 physical examination participants for 2,3,7,8 TCDD. The final interpretation of these data is deferred, pending further analyses.

Evaluation of Chronic Bronchitis, Chronic Obstructive Pulmonary Disease, and Ventilatory Function Among Workers Exposed to 2,3,7,8-Tetrachlorodibenzo-p-dioxin

2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) is produced as an undesirable contaminant in the manufacture of 2,4,5-trichlorophenol (TCP) and its derivatives. There is considerable concern about the health effects that may be associated with exposure to TCDD-contaminated substances. A cross-sectional medical study that included a comprehensive medical history, medical examination, and measurement of pulmonary function was conducted on workers employed more than 15 yr earlier in the manufacture of NaTCP and its derivatives at two chemical plants. The workers had substantial exposure to substances contaminated with TCDD, as evidenced by a mean serum TCDD level, lipid adjusted, of 200 ppt compared with a mean of 7 ppt in the unexposed reference group. The comparison group consisted of individuals with no occupational exposure to phenoxy herbicides who lived in the same communities as the workers. A total of 281 workers and 260 unexposed referents participated in the medical examination. Logistic and linear regression analyses, which contained categorical and continuous measures of TCDD exposure, were performed to control for important confounders, including cigarette and alcohol consumption. No difference was found between workers and referents in the risk for chronic bronchitis or COPD. Analysis of the ventilatory function data revealed no association between history of exposure to substances contaminated with TCDD and the forced expiratory volume at one second (FEV1), forced vital capacity (FVC), or the ratio of FEV1 to FVC (FEV1/FVC%).

Coplanar PCBs in human milk in the Province of Québec, Canada: Are they more toxic than dioxin for breast fed infants?

Different experimental studies have increased our understanding of toxic mechanisms of PCBs, PCDDs and PCDFs. Recently, coplanar PCBs which are approximate stereoisomers of 2,3,7,8-TCDD have been found to be the most toxic congeners of PCBs with a toxicity relative to that of 2,3,7,8 TCDD ranging from 0.001 for mono-ortho coplanars to 0.01, 0.1 and 0.05 respectively for tetra, penta and hexa non-ortho coplanar congeners. These congeners are present in different biological specimens at very high levels when compared with levels of TCDD. Therefore, coplanar PCBs determination is useful in evaluating the toxic potential of breast milk for infants. Moreover, the assessment of the relative importance of these compounds compared with other PCB congeners and PCDDs/PCDFs could be helpful in choosing the most suitable toxic parameters for the biomonitoring of human populations. This paper presents and discusses the levels of coplanar PCBs in the breast milk of a representative sample of 96 women from the general population of the province of Quebec - Canada.

Serum concentrations of 2,3,7,8‐tetrachlorodibenzo‐p‐dioxin and test results from selected residents of Seveso, Italy

2,3,7,8-Tetrachlorodibenzo-p-dioxin levels (TCDD) were measured in serum specimens from Seveso, Italy, residents, who were potentially highly exposed to the 1976 explosion, and in controls. The residents were chosen so as to represent those who did and did not develop chloracne. Levels of TCDD as high as 56,000 parts per trillion (ppt) were found in these serum specimens that were collected in 1976. These TCDD levels are the highest ever reported, and yet almost all clinical laboratory tests on these individuals were normal; any abnormal test result was only transitory in nature. These findings are unique in linking clinical histories to TCDD levels following an acute exposure.

Use of epidemiology data to assess the cancer risk of 2,3,7,8-tetrachlorodibenzo- p-dioxin

Most countries have assessed the human cancer risk of 2,3,7,8-tetrachlorodibenzo- p-dioxin (TCDD) by extrapolating from animal data. The 1600-fold variation for acceptable intakes estimated by the Americans, Canadians, and Europeans, however, indicates a large scientific uncertainty about TCDD toxicity. Regulators are attempting to use human epidemiology data to eliminate some of the limitations inherent in using animal data to quantitatively assess cancer risk in humans, particularly now that techniques for measuring TCDD levels in adipose tissue and serum are available. This paper presents an overview of the major epidemiologic studies that associate cancer with TCDD exposure. The actual exposures experienced by the study populations are emphasized. The TCDD serum levels of the Seveso, Italy, residents and of the NIOSH Dioxin Registry participants indicate that these populations hold the best promise for future assessment of the human carcinogenic risk of dioxin. Based on the animal data, however, the calculated risk from these exposures is still moderate compared with high background cancer incidence present in most industrialized countries.

Risk assessment for dioxin in Columbia River fish

The Columbia River, located in the Northwestern United States, supports active commercial and recreational fisheries. In addition to other industries, a number of bleached kraft pulp and paper mills are located along the river in the States of Washington and Oregon. To determine the impact that effluents from these mills have on residue levels of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) in fish, the most extensive field survey and health risk assessment ever conducted on a major river was undertaken. A total of 680 fish, including anadromous (salmon and steelhead trout) and resident (white sturgeon, carp, and largescale sucker) species were collected at 6 sampling stations located upstream and downstream of the mills. Eighty percent of the anadromous fish and 45% of all fish sampled had no detectable levels of TCDD. The geometric mean concentrations in fillet tissues of 3 subspecies of salmon ranged from 0.08 to 0.31 ppt; steelhead trout averaged 0.07 ppt. White sturgeon, largescale sucker, and carp collected in reaches impacted by mills averaged 0.55, 0.30, and 1.07 ppt, respectively, while fish collected upstream averaged 1.12, 0.24, and 1.12 ppt, respectively. These data indicate that mill effluents did not elevate fish TCDD residues above background. Lifetime average daily doses (LADDs) for residents, recreational fishermen, Asian Americans, and Native Americans were 0.0034, 0.056, 0.013, and 0.024 pg/kg-day. The theoretical upper-bound excess lifetime cancer risks associated with the consumption of Columbia River fish by recreational fishermen, the most sensitive consumers examined in this analysis, was below one in one million (5 × 10 −7).

Brominated and chlorinated dioxin blood levels in a chemist 34 years after exposure to 2,3,7,8-tetrachlorodibenzodioxin and 2,3,7,8-tetrabromodibenzodioxin

This paper reports, for the first time, 2,3,7,8-tetrabromodibenzodioxin (TBDD) detected in human tissue, a new potential health hazard for dioxin chemists. The patient had a co-existing, but much lower elevation of 2,3,7,8-tetrachlorodibenzodioxin (TCDD). The exposure thirty-four years ago caused acute illness and hospitalization at that time. The chemist had synthesized 20 to 30 grams of TCDD and a similar amount of TBDD 1 and became ill with chloracne, headaches, back and leg pain. Because of leg pain on exertion he experienced marked difficulty walking, and was hospitalized for these conditions. His measured 2,3,7,8-TBDD was 1100 ppt in serum lipid, 34 years after initial exposure. We estimate 11,606 or 122,450 ppt TBDD lipid blood level at time of exposure, assuming 10 or 5 year half-lives. We estimate a body burden of approximately 128-1,350 micrograms TBDD at time of exposure. This is the first report of a brominated dioxin in human tissue. We found 20 parts per trillion (ppt) TCDD in a blood sample taken 34 years after initial exposure, in comparison to the mean 2,3,7,8-TCDD level in the general U.S. population which is 5 ppt. We estimate a possible blood TCDD level of between 158 and 1670 ppt at time of exposure, assuming first order kinetics, a single compartment model, and using half lives of 10 or 5 years respectively. This corresponds to approximately 2 to 20 micrograms of 2,3,7,8-TCDD.

Relative distribution of 2,3,7,8-tetrachlorodibenzo- p-dioxin human hepatic and adipose tissues

Paired human hepatic and adipose tissues from 26 people were assayed for 2,3,7,8-tetrachlorodibenzo- p-dioxin (TCDD). On a whole tissue weight basis, TCDD concentration in the liver was about one-tenth that in the adipose tissue. When expressed in total tissue lipid basis, the TCDD concentrations in the liver and adipose tissue were about equal. At low levels of exposure, presumably below those necessary to cause hepatic enzyme induction, TCDD appeared to be partitioning into the human liver predominantly on the basis of its lipid solubility in that tissue store. The partitioning behavior of TCDD in the livers of humans exposed to higher levels of TCDD is currently unclear.

Concentration of TCDD in fish and the potential for human exposure

Levels of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) measured in fish from U.S. lakes and rivers confirm that TCDD is bioaccumulating in fish, and that low-level contamination of fish is widespread. As a result, many state and federal agencies have issued guidelines restricting or banning the consumption of TCDD-contaminated fish. This paper evaluates and interprets data on TCDD levels in fish collected as part of the EPA's National Dioxin Study and estimates the extent of human exposure due to ingestion of TCDD-contaminated fish. Results indicate that mean TCDD concentrations in whole fish and fish fillets from urban areas are low (0.4 and 0.3 pg/g, respectively) and that consumption of TCDD-contaminated fish is not a major pathway of human exposure, accounting for only 5% to 12.5% of total daily intake of TCDD. Assuming that the mean concentration of TCDD in whole fish is 0.4 pg/g, the steady-state bioconcentration factor for TCDD in fish is estimated to be approximately 140 000. The maximum concentration in fish fillets that does not pose an unacceptable health risk to average U.S. fish consumers is 81 pg/g.

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 ΣPCBs 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.

Medical evaluation of subjects with known body levels of 2,3,7,8-tetrachlorodibenzo-p-dioxin.

Forty-one persons with a history of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) exposure and measured adipose tissue TCDD levels were evaluated for potential health effects. No pattern of clinical abnormalities emerged related to TCDD levels.

2,3,7,8-tetrachlorodibenzo- p-dioxin (TCDD) persistence in the seveso (Milan, Italy) soil

Preliminary results of a new study on TCDD environmental persistence at Seveso (Milan, Italy) are presented. For this study, the most contaminated territory, Zone A, was divided into areas to fractionate the available TCDD levels in soil into data sets with reduced value spreads. In addition, various time subsets were defined for each area. Selected data were fitted with the exponential model y = y 0· e − k· t . It was estimated that at least 1.2 kg TCDD was present in Zone A shortly after the accident. On average, a considerable portion (23%) of this amount lay on vegetation; TCDD which was not photodegraded or volatilized before the heavy rains of fall 1976, was later washed off and transferred to ground by water action. From this study, mean analytical underestimations affecting January 1977 and March 1978 contamination map data were on the order of 30 and 24%. All the above figures are considered optimistic. A few years after the accident, mean TCDD half-life in soil appeared to be 9.1y(t 1 2 − 95% CLs, 6.2 − 17y ).