Congener-specific analyses for polychlorinated dioxins and dibenzofurans were performed on eighteen dairy, meat, and fish samples obtained from a supermarket in upstate New York. Dioxin toxic equivalents (TEqs) on a whole or wet weight basis for these food samples ranged from 0.02 to 1.5 parts per trillion (ppt). Data on American food consumption rates were used to estimate a U.S. range of dioxin intake from food. Based on these first congener-specific dioxin analyses of U.S. food, U.S. average daily intake of "International" dioxin toxic equivalents for an adult weighing 65 kilograms (kg) was estimated to be between 18 to 192 picograms TEq or 0.3 to 3.0 picograms per kilogram of body weight. Our previous results for cow's milk, human breast milk, and soy-based infant formula were used to calculate intake for infants. The relatively high level of dioxins commonly reported in human breast milk from America contributes from 35 to 53 picograms of dioxin toxic equivalents per kilogram of body weight to the nursing infant per day in its first year of life. This value greatly exceeds the U.S. Environmental Protection Agency estimated dose which would lead to one excess cancer per one million people of 0.006 pg of TCDD per kg of body weight per day over a seventy year lifetime or similar reference doses used by some other countries of up to 10/pg/kg/day over a 70 year lifetime.

Adult↗

PubMedDate not supplied

Elevated dioxin blood levels in Russian chemical workers and their children following maternal exposure.

Elevated dioxin levels in children of female workers with elevated dioxin body burden following workplace exposure has not been previously reported. We previously reported elevation of polychlorinated dibenzo-p-dioxins, particularly 2,3,7,8-TCDD, in Russia male and female chemical production workers' blood. Exposure is thought to have occurred in the early 1960s and blood was drawn in 1991. Among those with elevated dioxin levels were women with grown children. Since dioxins can be transferred transplacentally and by nursing, it was decided to see if a relationship existed between blood dioxin levels in mothers and their children. Individual samples were obtained from factory office workers, production workers and their now adult offspring. A pooled blood sample (n = 100) from adult Ufa residents was obtained for comparison. Samples were analyzed for polychlorinated dibenzo-p-dioxins (PCDDs), polychlorinated dibenzofurans (PCDFs) and coplanar polychlorinated biphenyls (CoPCBs). Office workers, production workers and workers' children 2,3,7,8-TCDD (TCDD) blood levels ranged from 11 to 273 parts per trillion (ppt) on a lipid basis, while the pooled blood sample (n = 100) from adult Ufa residents had a TCDD level of 12 ppt. Elevated TCDD was detected in all adult children of female production workers tested while two adult children of a male production worker had dioxin levels similar to the general population of Ufa. All children of workers had been nursed by their mothers for the first year of life and none have worked at a chemical plant. The data suggest that relatively large amounts of TCDD were transferred from mother to child approximately 18 to 28 years prior to blood collection. A sample of 2,4,-D amine salt produced at this factory was also analyzed to determine if its dioxin congeners might be contributing to dioxin contamination. 2,3,7,8-TCDD was not detected in the 2,4-D (detection limit of 0.02 ppb), although other dioxins were present, including some with 2,3,7,8- chlorine substitution.

Adult↗

PubMedDate not supplied

Comparison of dibenzodioxin levels in blood and milk in agricultural workers and others following pentachlorophenol exposure in China.

Substantial amounts of sodium pentachlorophenol (Na-PCP) salts have been sprayed in certain areas in central China since the 1960s for control of snail-borne schistosomiasis. A sample of Na-PCP used in the area of concern was analyzed and showed 2,3,7,8-substituted dibenzodioxin (PCDD) and dibenzofuran (PCDF) congeners as well as some non-2,3,7,8-substituted congeners. Dibenzodioxin analysis of two pooled blood samples from 100 persons living in sprayed areas and a pooled sample from 26 individuals who had direct contact with the Na-PCP showed elevations of PCDD/F congeners found in the Na-PCP. Total PCDD/Fs ranged from 631 to 1252 parts per trillion (ppt) lipid in the blood of those exposed to Na-PCP, while two general population age-matched pooled blood samples from 50 persons each had total PCDD/Fs of 147 and 178 ppt. Toxic equivalents calculated with International Toxic Equivalency Factors (I-TEqs) ranged from 9 to 16.3 ppt in the blood samples from exposed persons while the general population blood I-TEqs were 4.8 and 6.4 ppt. A pooled breast milk sample from 50 women living in the sprayed areas was compared with a pooled sample from 50 women living in unsprayed areas. Total PCDD/Fs was low in both exposed and general population samples (134 and 42 ppt lipid, respectively), however, the women living in sprayed areas had considerably higher PCDDs, 129 ppt versus 34 ppt. The mothers exposed to Na-PCP had a I-TEq of 5.4, which was about double that of the mothers from the general population, 2.6 ppt, lipid. Although human PCDD and PCDF tissue levels in China are low compared with those in more industrialized countries, the higher levels in exposed persons are cause for concern.

Adolescent↗

PubMedDate not supplied

Levels of dioxins, dibenzofurans, PCB and DDE congeners in pooled food samples collected in 1995 at supermarkets across the United States.

Food, particularly dairy products, meat, and fish, has been identified as the primary immediate source of intake of polychlorinated dibenzo-p-dioxins (PCDDs), polychlorinated dibenzofurans (PCDFs), and polychlorinated biphenyls (PCBs) for the general population. We previously reported PCDD/Fs in individual analyses of food samples from a number of countries, including the U.S., the former Soviet Union, and Vietnam. We also previously estimated daily intake of dioxins and related chemicals in Americans at various ages in these reports. In this paper, the levels of dioxins, dibenzofurans, dioxin toxic equivalents (TEQs), selected dioxin-like PCBs, and DDE (a persistent metabolite of DDT) were measured in 12 pooled food samples from over 90 individual specimens collected from supermarkets throughout the United States during 1995. Samples were pooled by food groups and then analyzed. Food samples were collected in Binghamton, New York; Atlanta, Georgia; Chicago, Illinois; San Diego, California; and Louisville, Kentucky. In addition to the meat, dairy, and fish samples, a vegan (all vegetable, fruit and grain, no animal product) diet, was simulated; this showed the lowest level of dioxins.

Benzofurans↗

PubMedDate not supplied

Dioxins, dibenzofurans, dioxin-like PCBs, and DDE in U.S. fast food, 1995.

Food, especially dairy products, meat, and fish, is the primary source of environmental exposure to dioxins in the general population. Little data exists on dioxin levels in the popular and widely consumed "fast foods". Data presented in a previously published pilot study was limited to measuring only the levels of dioxins and dibenzofurans in three types of U.S. fast food. This study adds to the previous paper by presenting data, in addition to dioxins and dibenzofurans, on the closely related dioxin-like polychlorinated biphenyls (PCBs), and the persistent metabolite of DDT, 1,1-dichloro-2,2-bis (p-chlorophenyl) ethylene (DDE), in four types of popular U.S. fast food. These include McDonald's Big Mac Hamburger, Pizza Hut's Personal Pan Pizza Supreme, Kentucky Fried Chicken (KFC) three piece original recipe mixed dark and white meat luncheon package, and Häagen-Daz chocolate-chocolate chip ice cream. Dioxin plus dibenzofuran dioxin toxic equivalents (TEQ) ranged from 0.03 to 0.28 TEQ pg/g wet or whole weight for the Big Mac, from 0.03 to 0.29 for the Pizza, from 0.01 to 0.31 for the KFC, and from 0.03 to 0.49 TEQ pg/g for the ice cream. Daily TEQ consumption per kilogram body weight (kg/BW), assuming an average 65 kg adult and a 20 kg child, from one serving of each of these fast food ranged between 0.046 and 1.556 pg/kg in adults whereas in children the values were between 0.15 and 5.05 pg/kg. Total measured PCDD/Fs in the Big Mac, Personal Pan Pizza, KFC, and the Häagen-Daz ice cream varied from 0.58 to 9.31 pg/g. Measured DDE levels in the fast foods ranged from 180 to 3170 pg/g. Total mono-ortho PCB levels ranged up to 500 pg/g or 1.28 TEQ pg/g for the KFC and for di-ortho PCBs up to 740 pg/g or 0.014 TEQ pg/g for the pizza sample. Total PCB values in the four samples ranged up to 1170 pg/g or 1.29 TEQ pg/g for the chicken sample.

Adult↗

PubMedDate not supplied

Cancer risk assessment using blood dioxin levels and daily dietary TEQ intake in general populations of industrial and non-industrial countries.

We previously measured polychlorinated dibenzo-p-dioxins (PCDDs) and polychlorinated dibenzofurans (PCDFs) in U.S. foods and estimated the daily dioxin toxic equivalent (TEQ) intake to be from 0.3 to 3.0 pg 1-TEQ/kg body weight for adults. These values are similar to values reported in Canada, Germany, England, and the Netherlands. The U.S. Environmental Protection Agency (EPA) Dioxin Reassessment Draft Documents currently propose a cancer risk-specific dose estimate of 0.01 pg TEQ/kg body weight/day (U.S. EPA, 1994). This risk-specific dose estimate represents a lifetime (70 years) dose which results in a plausible upper bound cancer risk of 1 x 10(-6) (the probability of one additional cancer per one million exposed population over a lifetime). The proximate source of almost all dioxin intake in the general population is from food. Using our data for daily dietary dioxin exposure and the EPA's proposed risk specific dose, we estimate that over a lifetime a maximum of 30 to 300 excess cancers per million could result from the ingestion of dioxin containing food products. In the U.S. population of 260 million, a maximum range of 7,800 to 78,000 excess cancers over a lifetime (70 years) or 111 to 1,114 cases/year might be directly linked to dioxin exposure from food. Because these calculations are based on conservative approaches to setting an upper bound, "true" risk is not likely to exceed this value. At present, one-third of all Americans will develop cancer over a lifetime and one in four Americans are likely to die from cancer. For 1995, it was estimated that there would be 1,252,000 new cancer cases in the U.S. From this, we calculate that a maximum between 0.009% and 0.09% (111-1,114 cases/year) of all cancer cases in the U.S. might be directly linked to dioxin intake in food, assuming intakes have remained constant over a lifetime. Previous studies have suggested that as much as 70% of the total cancer risk in humans may be attributable to diet, primarily as a function of caloric and synthetic chemicals in the diet. (NAS, 1996) These figures do not take into account the ingestion of more contaminated food products, other sources of exposure, possible interactions of PCDDs and PCDFs with other chemicals, or increased incidence of cancer from the cancer promoting actions of dioxins. In addition, we reviewed average U.S. general population blood TEQ (ppt, lipid) levels, which reflect body burden, with levels of persons living in less industrialized countries. These data were used to compare the cancer risk of individuals living in the U.S., an industrial country, to those living in selected less industrialized countries. With the assumption that similar populations were being compared, it is estimated that in the non-industrial region of north Vietnam there is one-third the risk of dioxin-related cancer compared with the United States, while Cambodians have a dioxin-related cancer risk that is 14 fold less than the U.S. at this time.

Adult↗

PubMedDate not supplied

A comparison of dioxins, dibenzofurans and coplanar PCBs in uncooked and broiled ground beef, catfish and bacon.

The primary source of dioxins (PCDDs), dibenzofurans (PCDFs) and coplanar PCBs for the general population is food, especially meat, fish, and dairy products. However, most data on the levels of these chemicals is from food in the raw or uncooked state. We report here the effect of one type of cooking (broiling) on the levels of PCDDs, PCDFs, and coplanar PCBs in ground beef (hamburger), bacon and catfish. Samples of hamburger, bacon, and catfish were broiled and compared to uncooked samples in order to measure changes in the amounts of dioxins in cooked food. The total amount of PCDD, PCDF, and coplanar PCB TEQ decreased by approximately 50% on average for each portion as a result of broiling the hamburger, bacon and catfish specimens. The mean concentration (pg TEQ/kg, wet weight) of PCDDs, PCDFs, and coplanar PCBs, however, remained the same in the hamburger, increased by 83% in the bacon, and decreased by 34% in the catfish. On average, the total measured concentration (pg/kg) of the congeners of PCDDs, PCDFs, and coplanar PCBs increased 14% in the hamburger, increased 29% in the bacon, and decreased 33% in the catfish.

Animals↗

PubMedDate not supplied

Concentrations of PCBs, PCDFs and PCDDs in the blood of Yusho patients and their toxic equivalent contribution.

Yusho blood and control serum were collected in around 1991 and analyzed for congeners of PCDDs, PCDFs and PCBs. In Yusho blood, TEQ was mainly contributed by 2,3,4,7,8-penta-CDF (77-248 ppt), 1,2,3,4,7,8-hexa-CDF (15-37 ppt) and 2,3,3',4,4',5-hexa-CB (16-77 ppt). Total TEQ in Yusho blood (185-441 ppt) was only 3-14 times higher than that of control serum (31-61 ppt). It is notable that the concentrations of 3,3',4,4',5-, 2,3,3',4,4'- and 2,3',4,4',5-penta-CBs in Yusho blood were comparable to or lower up to 3-5 times than those in control blood.

Benzofurans↗

PubMedDate not supplied

Decrease in levels and body burden of dioxins, dibenzofurans, PCBS, DDE, and HCB in blood and milk in a mother nursing twins over a thirty-eight month period.

This paper presents measured dioxin, dibenzofuran, PCB, DDE and HCB blood and milk levels and estimated body burdens in a mother who nursed twins for thirty-eight months. A total of thirteen milk samples and three blood samples were collected and analyzed. Measured PCDD and PCDF levels in milk decreased from 309 and 21 ng/kg (ppt) to 173 and 9 ng/kg, respectively, between March 1993 and September 1995. Based on the decrease in breast milk dioxin levels, we estimate that the nursing mother reduced her dioxin body burden from 310 to 96 ng dioxin toxic equivalents (TEQs), or approximately 69%. In two and one half years the level of HCB in the mother's milk decreased from 10.7 to less than 1.8 ng/g (ppb), the level of DDE decreased from 246 to 46 ng/g and the total level of non-coplanar PCBs decreased from 285 to 63 ng/g, on a lipid basis. We estimate that the twin's consumption of dioxins, dibenzofurans, and coplanar PCBs from breast feeding was approximately 115 ng TEQ per twin.

Adult↗

PubMedDate not supplied

Partitioning of dioxins, dibenzofurans, and coplanar PCBS in blood, milk, adipose tissue, placenta and cord blood from five American women.

Partitioning of dioxins, dibenzofurans and the dioxin-like coplanar PCBs was determined by congener-specific high resolution gc-ms analysis of compounds in 6 tissue samples each from 5 women. Samples were whole blood obtained prior to delivery; maternal adipose tissue, cord blood and placenta obtained during cesarean section delivery; and whole blood and milk taken at the time of first obstetrical follow-up examination, one to two months following delivery. All women lived in upstate New York. Specimens were collected in late 1995 and early 1996. Mean measured levels of total PCDDs, PCDFs and coplanar PCBs were 352 pg/g for adipose tissue, 526 pg/g for predelivery blood, 182 pg/g for placenta, 165 pg/g for cord blood, 352 pg/g for postpartum blood and 220 pg/g for milk. Mean total TEQ levels were 11.6 pg/g TEQ for adipose tissue, 12.1 pg/g TEQ for predelivery blood, 10.5 pg/g TEQ for placenta, 5.8 pg/g TEQ for cord blood, 10.0 pg/g TEQ for postpartum blood and 10.2 pg/g TEQ for milk.

Adipose Tissue↗