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A Schecter

Publications and source records attributed to A Schecter.

At least 19 recordsLinked to original sources

Levels of dioxins and dibenzofurans in breast milk of women residing in two cities in the Irkutsk Region of Russian Siberia compared with American levels.

The presence of dioxins, dibenzofurans, and polychlorinated biphenyls (PCBs) in human tissue, food, and environmental samples from Russia has been monitored since 1988 as part of a research collaboration between a number of countries including Finland, the United States, Germany, the former Soviet Union, and Canada. Although elevated TCDD and PnCDD levels have previously been found in blood of male and female Russian chemical manufacturing workers and in their children, dioxin levels in the general population have usually been found to be lower than in Americans and Europeans. This study continues earlier work in the Irkutsk region of Russian Siberia, where we report levels of dioxin, dibenzofurans, and PCBs in human milk samples taken from general population women living in the industrialized cities of Angarsk and Usolye-Sibirskoye, near Lake Baikal. Total polychlorinated dibenzo-p-dioxin (PCDD) toxic equivalents (TEQs) compared in this paper for the industrialized regions of Siberia, Ukraine, and the US are similar, ranging from 6.1 to 7 parts per trillion (ppt). Recent 1998 milk samples from Angarsk and Usolye-Sibirskoye have total mean polychlorinated dibenzofuran (PCDF) TEQs of 10 and 21.7 ppt, respectively, with the other industrialized countries ranging from 2.3 to 6.7 ppt. Although dioxin-like PCBs were not measured for the city of Usolye-Sibirskoye (1998), total mean PCDD/F TEQ from Angarsk and Usolye-Sibirskoye (1998) were the two highest levels in this study, with 26.9 and 28.5 ppt, respectively, followed by 1993-1994 Ukraine samples with 24 ppt, 1989 Siberian samples with 13.6 ppt, and 1996 USA with 11.4 ppt total TEQ. In this study, higher levels of dioxins are noted in milk from Angarsk and Usolye-Sibirskoye than found in earlier Russian studies, with mean levels also exceeding 1996 and 1999 US breast milk dioxin levels.

Adult↗

Characterization of dioxin exposure in firefighters, residents, and chemical workers in the Irkutsk Region of Russian Siberia.

The goal of this study was to characterize body burdens of polychlorinated dioxins (PCDDs), polychlorinated dibenzofurans (PCDFs), and polychlorinated biphenyls (PCBs) in three groups of Siberians living in the Irkutsk Region of Russia. These groups included firefighters exposed to a mixture of toxic substances extinguishing a large fire at the Shelekhovo Cable Factory in 1992, chemical workers from the Khimprom chemical plant, and residents living in proximity to large chemical factories in Sayansk and Angarsk. Blood samples from all groups were obtained in the fall of 1998. Dioxin analyses of samples were performed in Germany, Canada, and in a Russian dioxin laboratory in Ufa, Bashkortostan Republic. The average levels of dioxin toxic equivalents (TEQs) are 23.6 parts per trillion (ppt) total TEQ (PCDD/F only) in the disabled firefighters, 25.0 in the non-disabled firefighters, 28.7 in residents, and 45.6 in the Khimprom workers blood. Two workers did have elevated total TEQs of 91.4 and 102.2 ppt. Dibenzofurans and coplanar PCBs substantially contribute to the total elevated TEQ seen here. The average TEQs suggest levels of dioxin exposure in this part of the former Soviet Union not dissimilar to levels measured in industrialized countries of Europe and Northern America.

Adult↗

Intake of dioxins and related compounds from food in the U.S. population.

The first U.S. nationwide food sampling with measurement of dioxins, dibenzofurans, and coplanar, mono-ortho and di-ortho polychlorinated biphenyls (PCBs) is reported in this study. Twelve separate analyses were conducted on 110 food samples divided into pooled lots by category. The samples were purchased in 1995 in supermarkets in Atlanta, GA, Binghamton, NY, Chicago, IL, Louisville, KY, and San Diego, CA. Human milk also was collected to estimate nursing infants' consumption. The food category with highest World Health Organization (WHO) dioxin toxic equivalent (TEQ) concentration was farm-grown freshwater fish fillet with 1.7 pg/g, or parts per trillion (ppt), wet, or whole, weight. The category with the lowest TEQ level was a simulated vegandiet, with 0.09 ppt. TEQ concentrations in ocean fish, beef, chicken, pork, sandwich meat, eggs, cheese, and ice cream, as well as human milk, were in the range O.33 to 0.51 ppt, wet weight. In whole dairy milk TEQ was 0.16 ppt, and in butter 1.1 ppt. Mean daily intake of TEQ for U.S. breast-fed infants during the first year of life was estimated at 42 pg/kg body weight. For children aged 1-11 yr the estimated daily TEQ intake was 6.2 pg/kg body weight. For males and females aged 12-19 yr, the estimated TEQ intake was 3.5 and 2.7 pg/kg body weight, respectively. For adult men and women aged 20-79 yr, estimated mean daily TEQ intakes were 2.4 and 2.2 pg/kg body weight, respectively. Estimated mean daily intake of TEQ declined with age to a low of 1.9 pg/kg body weight at age 80 yr and older. For all ages except 80 yr and over, estimates were higher for males than females. For adults, dioxins, dibenzofurans, and PCBs contributed 42%, 30%, and 28% of dietary TEQ intake, respectively. DDE was also analyzed in the pooled food samples.

Adolescent↗

Recent dioxin contamination from Agent Orange in residents of a southern Vietnam city.

Marked elevation of dioxin associated with the herbicide Agent Orange was recently found in 19 of 20 blood samples from persons living in Bien Hoa, a large city in southern Vietnam. This city is located near an air base that was used for Agent Orange spray missions between 1962 and 1970. A spill of Agent Orange occurred at this air base more than 30 years before blood samples were collected in 1999. Samples were collected, frozen, and sent to a World Health Organization--certified dioxin laboratory for congener-specific analysis as part of a Vietnam Red Cross project. Previous analyses of more than 2200 pooled blood samples collected in the 1990s identified Bien Hoa as one of several southern Vietnam areas with persons having elevated blood dioxin levels from exposure to Agent Orange. In sharp contrast to this study, our previous research showed decreasing tissue dioxin levels over time since 1970. Only the dioxin that contaminated Agent Orange, 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), was elevated in the blood of 19 of 20 persons sampled from Bien Hoa. A comparison, pooled sample from 100 residents of Hanoi, where Agent Orange was not used, measured blood TCDD levels of 2 parts per trillion (ppt). TCDD levels of up to 271 ppt, a 135-fold increase, were found in Bien Hoa residents. TCDD contamination was also found in some nearby soil and sediment samples. Persons new to this region and children born after Agent Orange spraying ended also had elevated TCDD levels. This TCDD uptake was recent and occurred decades after spraying ended. We hypothesize that a major route of current and past exposures is from the movement of dioxin from soil into river sediment, then into fish, and from fish consumption into people.

2,4,5-Trichlorophenoxyacetic Acid↗

Exposure of Russian phenoxy herbicide producers to dioxins.

Russian workers who manufactured phenoxy herbicides and related compounds in the 1960s in the city of Ufa, Bashkortostan, a republic of the former Soviet Union, were studied for exposure to polychlorinated dibenzo-p-dioxins (PCDDs) and dibenzofurans. Sixty whole blood samples were drawn in September 1992 and analyzed by gas chromatography-mass spectrometry. Thirty-four workers who manufactured the herbicide 2,4,5-trichlorophenoxyacetic acid (2,4,5-T) had median blood lipid 2,3,7,8-tetrachlorodibenzo-p-diozin (TCDD) concentrations of 166 ng per kg (parts per trillion) and 1,2,3,7,8-pentachloro-p-dioxin (PnCDD) levels of 52 parts per trillion with several TCDD values greater than 500 ng/kg. These 1992 values are 10 to 30 times greater than contemporary normal or background blood levels from the Baskortostan region of Russia and were at least 10-fold higher 25 years earlier in the late 1960s. Six workers who produced the herbicide 2,4-dichlorophenoxyacetic acid also had elevated levels in 1992, with 1,2,3,7,8-PnCDD blood lipid levels higher than 2,3,7,8-TCDD. Even children of some of the workers and factory administrative personnel had blood levels of TCDD higher than most general population groups from other parts of Russia or from other countries. The patterns of the PCDDs and dibenzofurans (as defined by the specific congeners and their relative amounts) were distinctive for the type of chemical produced, with notable contributions to the TCDD toxic equivalents from the 2,3,7,8-TCDD and 1,2,3,7,8-PnCDD congeners. No correlation was found between chloracne status in 1965 to 1967 and TCDD or toxic equivalent blood lipid concentrations in 1992. These Russian phenoxy herbicide and related chemical producers have some of the highest occupational exposure to dioxins of any cohort studied to date and seem to be unique with respect to the presence of appreciable amounts of 1,2,3,7,8-PnCDD.

Adolescent↗

Levels of methyleugenol in a subset of adults in the general U.S. population as determined by high resolution mass spectrometry.

We developed a sensitive and accurate analytical method for quantifying methyleugenol (ME) in human serum. Our method uses a simple solid-phase extraction followed by a highly specific analysis using isotope dilution gas chromatography-high resolution mass spectrometry. Our method is very accurate; its limit of detection is 3.1 pg/g and its average coefficient of variation is 14% over a 200-pg/g range. We applied this method to measure serum ME concentrations in adults in the general U.S. population. ME was detected in 98% of our samples, with a mean ME concentration of 24 pg/g (range < 3.1-390 pg/g). Lipid adjustment of the data did not alter the distribution. Bivariate and multivariate analyses using selected demographic variables showed only marginal relationships between race/ethnicity and sex/fasting status with serum ME concentrations. Although no demographic variable was a good predictor of ME exposure or dose, our data indicate prevalent exposure of U.S. adults to ME. Detailed pharmacokinetic studies are required to determine the relationship between ME intake and human serum ME concentrations.

Adolescent↗

Quantitation of the extracellular domain of epidermal growth factor receptor in the plasma of dioxin-exposed individuals.

Animal models suggest that dioxins have a negative effect on the level of expression of the epidermal growth factor receptor in cells. In vivo the level of expression in tissue of the epidermal growth factor receptor can be monitored by assaying for the extracellular domain in blood using an enzyme linked immunosorbent assay. We have determined the levels of the extracellular domain of the epidermal growth factor receptor in the plasma of 30 individuals: 10 with high blood dioxin levels (TEQ range = 318-673 ppt), 10 with medium blood dioxin levels (TEQ range = 16-60 ppt), and 10 with low background blood dioxin levels (TEQ range = 3-10 ppt). The levels of the epidermal growth factor receptor extracellular domain were lower in the high blood dioxin group (mean +/- SD = 45 +/- 26 fmol/ml) and the medium blood dioxin group (mean +/- SD = 41 +/- 23 fmol/ml) compared with the low blood dioxin group (mean +/- SD = 73 +/- 43 fmol/ml). These results suggest that the extracellular domain of the epidermal growth factor receptor may be a marker of the biological effect of dioxin exposure.

Dioxins↗

Human exposure assessment and the National Toxicology Program.

The National Institute of Environmental Health Sciences/National Toxicology Program (NIEHS/NTP) is developing a new interagency initiative in exposure assessment. This initiative involves the NIEHS, the Centers for Disease Control and Prevention through its National Center for Environmental Health, the National Institute for Occupational Safety and Health, the EPA, and other participating institutes and agencies of the NTP. This initiative will benefit public health and priority setting in a number of ways. First, as discussed above, it will strengthen the scientific foundation for risk assessments by the development of more credible exposure/response relationships in people by improving cross-species extrapolation, the development of biologically based dose-response models, and the identification of sensitive subpopulations and for "margin of exposure" based estimates of risk. Second, it will provide the kind of information necessary for deciding which chemicals should be studied with the limited resources available for toxicological testing. For example, there are 85,000 chemicals in commerce today, and the NTP can only provide toxicological evaluations on 10-20 per year. Third, we would use the information obtained from the exposure initiative to focus our research on mixtures that are actually present in people's bodies. Fourth, we would obtain information on the kinds and amount of chemicals in children and other potentially sensitive subpopulations. Determinations of whether additional safety factors need to be applied to children must rest, in part, upon comparative exposure analyses between children and adults. Fifth, this initiative, taken together with the environmental genome initiative, will provide the science base essential for meaningful studies on gene/environment interactions, particularly for strengthening the evaluation of epidemiology studies. Sixth, efficacy of public health policies aimed at reducing human exposure to chemical agents could be evaluated in a more meaningful way if body burden data were available over time, including remediation around Superfund sites and efforts to achieve environmental justice. The exposure assessment initiative is needed to address public health needs. It is feasible because of recent advances in analytical technology and molecular biology, and it is an example of how different agencies can work together to better fulfill their respective missions.

Environmental Exposure↗

A selective historical review of congener-specific human tissue measurements as sensitive and specific biomarkers of exposure to dioxins and related compounds.

Estimating internal exposure or dose of dioxins and related chemicals such as dibenzofurans and dioxinlike polychlorinated biphenyls is relatively straightforward in laboratory animals because a known dose is given and the amount absorbed can be measured. In wildlife, direct tissue measurement and measurement of environmental samples have both recently been used to estimate exposure. Until recently, human studies used only indirect indicators such as skin lesions to qualitatively estimate exposure to these chlorinated organic compounds. Environmental measurements have also sometimes been used to estimate human exposure. Dioxins in human tissue were not measured until the 1970s, when 2,3,7,8-tetrachlorodibenzo-p-dioxin was measured in mothers' milk; congener-specific measurement of dioxins and dibenzofurans in tissues (blood, milk, and adipose tissue) of the general population and exposed workers was first performed in the United States in the 1980s. Measurement in a sensitive and specific fashion of the 17 toxic dioxin and dibenzofuran congeners currently found in human tissue from industrial countries began in the 1980s. The use of known chemical standards, capillary columns, high resolution gas chromatography and mass spectrometry (GC-MS) has now become relatively common. GC-MS analysis of blood is currently accepted as the gold standard for estimating human exposure to dioxins. However, analyses are still costly and time consuming, and worldwide there are few qualified laboratories. There is currently a lack of knowledge concerning kinetics at higher and lower exposure levels for most of the toxic dioxin congeners and of levels in target tissues of concern.

Benzofurans↗

Blood levels of DDT and breast cancer risk among women living in the north of Vietnam.

A positive association has been reported between elevated tissue organochlorines (p,p'-DDT/p,p'-DDE, PCBs, dioxins) and breast cancer in some case-control studies and occupational cohort studies. We previously reported high serum levels of p,p'-DDT and its metabolite p,p'-DDE in women living throughout Vietnam. We report here the results of a small hospital-based case-control study examining the association between blood levels of p,p'-DDT/p,p'-DDE and the risk of invasive breast cancer among residents of the north of Vietnam-an area where insecticides such as p,p'-DDT have been heavily used in the recent past. The study was conducted among patients admitted to a single hospital in the capital city of Hanoi in 1994. Study subjects were 21 women newly diagnosed with invasive adenocarcinoma of the breast, who served as cases, and 21 women of similar age with fibrocystic breast disease, who served as controls. No increase was evident in the relative risk of breast cancer with increasing tertiles of serum concentration of the compounds of interest, even after adjustment for major potential confounders, such as age at menarche, parity, history of lactation, and body weight. These results suggest that recent and past exposure to p,p'-DDT does not play an important role in the etiology of breast cancer among women living in a country with a tropical climate where insecticide use for mosquito control is common.

Adult↗

[The condition of PCBs and PCDFs in the blood of Yusho patients 20 years after the onset].

Blood samples of Yusho and control persons were analyzed for individual congeners of PCDDs, PCDFs, and PCBs by high resolution GC/MS. Concentrations of 2,3,4,7,8-penta-CDF, 1,2,3,4,7,8-hexa-CDF and 2,3,3',4,4',5-hexa-CB in Yusho blood were up to 56 times higher than the corresponding concentrations in the control blood. These high concentrations have persisted for 23 years after the incident. Concentrations of 3,3',4,4',5-penta-CB and 2,3',4,4',5-penta-CB in some Yusho blood were lower than the control blood. In Yusho blood, 2,3,4,7,8-penta-CDF contributed the highest toxicity (TEQ 77-248 ppt in lipid) among the congeners determined and toxic contribution of PCDFs was very large (41-77%) in the chlorinated pollutants. Thirty PCB congeners were identified in the blood of Yusho patients in 1996 by GC/MS. The average total PCB concentration in Yusho blood were 4.9 times higher than that of the controls. Characteristic PCB congeners in Yusho patients were 2,2',3,4,4',5-hexa-CB, 2,3,3',4,4',5-hexa-CB and 2,3,3',4,4',5'-hexa-CB and their concentration ratios to the controls were 8-19.

Adult↗

Dioxins and dioxin-like chemicals in blood and semen of American Vietnam veterans from the state of Michigan.

This exposure assessment pilot study tested the hypothesis that elevated blood levels of the dioxin congener 2,3,7,8-TCDD ("TCDD"), due to Agent Orange exposure, in American Vietnam veterans could be demonstrated two to three decades after Vietnam service. A second objective was to determine if dioxins, including TCDD, are present in the semen of adult males. In the early 1990s, blood samples from 50 Vietnam veterans and three pooled semen samples from 17 of them were analyzed by high-resolution gas chromatography-mass spectroscopy for dioxins, dibenzofurans, and the dioxin-like PCBs. Fifty volunteers from the Michigan Vietnam veteran bonus list, which documented Vietnam service, were invited to participate based on their self-reported exposure to Agent Orange in Vietnam. Screening of military and medical records was performed by an epidemiologist and a physician to assure that Agent Orange exposure was possible based on job description, location of service in Vietnam, and military Agent Orange spray records. Elevated 2,3,7,8-TCDD levels, over 20 ppt on a lipid basis, could still be detected in six of the 50 veterans in this nonrandomly selected group. The dioxin and dibenzofuran congeners commonly found in the U.S. population, including TCDD, were also detected in the three pooled semen samples. Quantification and comparison on a lipid basis were not possible due to low lipid concentrations where levels were below the detection limit. Therefore, semen samples were measured and reported on a wet-weight basis. Elevated blood TCDD levels, probably related to Agent Orange exposure, can be detected between two and three decades after potential exposure in some American veterans. Original levels were estimated to be 35-1,500-fold greater that that of the general population (4 ppt, lipid) at the time of exposure. In addition, the detection of dioxins in semen suggests a possible mechanism for male-mediated adverse reproductive outcomes following Agent Orange or other dioxin exposure.

2,4,5-Trichlorophenoxyacetic Acid↗

Conclusions from Ufa, Russia, drinking water dioxin cleanup experiments involving different treatment technologies.

The city of Ufa, in the Bashkortostan Republic of Russia, is believed to have dioxin contamination of its water supply from 30 years of gas ejections, sewage and buried sludge from the Chimprom industrial factory, and possibly other sources. A project was developed to provide technology at relatively low cost for treating dioxin contaminated water in routine and also in emergency situations. This paper describes the results of the 15-year research project to remove dioxins from drinking water. Three different methods were experimentally tested for efficiency at removing dioxins from tap water. The methods used were: (1) ozonization plus filtration through powder sorbents, (2) filtration through sand, and (3) filtration through granulated sorbents. It was found that the method of filtration through granulated sorbents was most effective at removing dioxins from water: 90-95% of all PCDD and PCDF isomers were removed from water samples. This research also shows that the most toxic congener, 2,3,7,8-TCDD, can be removed effectively and efficiently. In addition, there are no significant differences between the extractability of PCDDs and PCDFs. Reductions in exposure to humans from contaminated drinking water can be accomplished via sorptive water treatments for relatively reasonable cost, making this a practical approach. This method of decreasing toxic chemicals is being implemented in Ufa, Russia.

Benzofurans↗

Decrease in milk and blood dioxin levels over two years in a mother nursing twins: estimates of decreased maternal and increased infant dioxin body burden from nursing.

This study addresses the issue of breast-feeding and its reduction of maternal dioxin body burden. Nursing is also a source of infant dioxin exposure. This study extends our previous efforts to investigate a nursing mother's milk and blood dioxin levels. We report polychlorinated dibenzo-p-dioxin (PCDD) and polychlorinated dibenzofuran (PCDF) dioxin toxic equivalents (TEQs) in milk (M) and blood (B) both before and also after two years of nursing twins to be 16.9 ppt (M), 14.9 ppt (B), and 3.1 ppt (M) and 4.9 ppt (B), respectively. The ratios of measured congeners comparing milk to whole blood from a nursing mother taken initially and after two years of nursing vary from 0.36 to 8.40 in 1992 and 0.17 to 1.0 in 1994. The mother's body burden was initially calculated to be 329 ng TEQ from milk levels and 291 ng TEQ from blood levels using samples taken in February 1992 and decreased to 60.1 ng TEQ from milk and 96 ng TEQ from measured blood using samples collected in December 1994. We calculate that the excretion of dioxin TEQ by the mother through breast-feeding is 269 ng TEQ, which is similar to the 303 ng TEQ estimated total dioxin intake by the twins over two years. The average daily dioxin intake from nursing is 66 pg TEQ/kg-BW/day for each twin over the two years.

Benzofurans↗

Concentrations of polychlorinated dibenzo-p-dioxins and dibenzofurans in human placental and fetal tissues from the U.S. and in placentas from Yu-Cheng exposed mothers.

We report the concentrations of polychlorinated dibenzo-p-dioxins (PCDDs) and polychlorinated dibenzofurans (PCDFs) found in human placentas and fetal tissue from the U.S. and in placentas from Yu-Cheng mothers. In placental material from sources in the U.S. we found concentrations, expressed as dioxin toxic equivalence (TEQ) values and on a lipid basis, between 8.4 and 17.6 ng/kg. In a pooled sample of fetal tissue (8-14 week) the concentration, 5.3 ng/kg, was somewhat smaller. In placental material from Taiwanese Yu-Cheng subjects much higher concentrations were found, in the range 610 to 9010 TEQ ng/kg, again on a lipid basis.

Benzofurans↗

Dioxin concentrations in the blood of workers at municipal waste incinerators.

OBJECTIVES: Increased concentrations of polychlorinated dibenzo-p-dioxins (PCDDs) and polychlorinated dibenzo-furans (PCDFs) in pooled blood samples from workers at municipal waste incinerators have been reported. This study was undertaken to confirm these results in individual blood samples from potentially exposed and unexposed workers at municipal waste incinerators compared with matched unexposed controls and compared with concentrations in the slag and fly ash from the municipal waste incinerators. METHODS: Concentrations of PCDDs and PCDFs were determined in the blood of 10 workers from an old municipal waste incinerator without adequate pollution controls, 11 workers from a newer incinerator with modern pollution controls, and 25 controls from the general population group matched for age (+/- 10 years), sex, and race, and in the slag and fly ash from the older incinerator. RESULTS: Significant increases of certain PCDDs and PCDFs were found in the blood of the workers from the older incinerator compared with the controls as follows: octaCDD (1051 (438) v 637 (344), P < 0.001), hexaCDF (52.3 (28.7) v 30.2 (18.2), P < 0.01), heptaCDF (43.9 (30.4) v 22.7 (12.4), P < 0.001), total PCDDs (1262 (484) v 825 (454), P < 0.001), total PCDFs (133.0 (68.1) v 93.7 (36.7), P < 0.05), and total PCDD/Fs (1395 (537) v 918 (437), P < 0.001). The workers from the older incinerator with the greatest exposure were found to have the most significant increases of the blood PCDDs and PCDFs, and the pattern of increased PCDD and PCDF congeners in the blood corresponded to the pattern in the incinerator slag and ash. No significant differences were found between the blood concentrations of the workers at the newer incinerator and the controls. CONCLUSION: Occupational exposure to slag and fly ash from municipal waste incinerators may increase the blood concentrations of PCDDs and PCDFs. Modern pollution control technology in new incinerators may be able to minimise potential exposure to slag and fly ash and thus the absorption of PCDDs and PCDFs from this source.

Adult↗

Agent Orange and the Vietnamese: the persistence of elevated dioxin levels in human tissues.

OBJECTIVES: The largest known dioxin contamination occurred between 1962 and 1970, when 12 million gallons of Agent Orange, a defoliant mixture contaminated with a form of the most toxic dioxin, were sprayed over southern and central Vietnam. Studies were performed to determine if elevated dioxin levels persist in Vietnamese living in the south of Vietnam. METHODS: With gas chromatography and mass spectroscopy, human milk, adipose tissue, and blood from Vietnamese living in sprayed and unsprayed areas were analyzed, some individually and some pooled, for dioxins and the closely related dibenzofurans. RESULTS: One hundred sixty dioxin analyses of tissue from 3243 persons were performed. Elevated 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) levels as high as 1832 ppt were found in milk lipid collected from southern Vietnam in 1970, and levels up to 103 ppt were found in adipose tissue in the 1980s. Pooled blood collected from southern Vietnam in 1991/92 also showed elevated TCDD up to 33 ppt, whereas tissue from northern Vietnam (where Agent Orange was not used) revealed TCDD levels at or below 2.9 ppt. CONCLUSIONS: Although most Agent Orange studies have focused on American veterans, many Vietnamese had greater exposure. Because health consequences of dioxin contamination are more likely to be found in Vietnamese living in Vietnam than in any other populations, Vietnam provides a unique setting for dioxin studies.

2,4,5-Trichlorophenoxyacetic Acid↗