[Trend of PCB/PCDF concentrations in the blood of Yusho patients for 38 years after the incidence].

Concentrations of 2,3',4,4',5-pentaCB (PCB118), 2,2',4,4',5,5'-hexaCB (PCB153), 2,3,3',4, 4',5-hexaCB (PCB156) and total PCB congeners (PCBs) in the blood of Yusho patients, surveyed by the annual medical examination in Fukuoka Prefecture, have been gradually decreased from 1974 (7 ppb) to 2006 (3 ppb). The patients are classified into 3 types of Yusho, namely, Yusho A: having typical Yusho gas chromatogram (GC) pattern, Yusho B: between Yusho A and Yusho C, and Yusho C: having GC pattern similar to those of Controls. The concentrations of PCB153, PCB156 and PCBs in the blood of Yusho A were higher than those of Yusho B and Yusho C in order. However, the concentrations of PCB118 in the blood of Yusho A were lower than those of Yusho B and Yusho C in order. Simple correlation coefficients between the concentrations of PCB118, PCB153, PCB156 and PCBs in the blood of Yusho patients and their ages at the blood sampling were examined from 1974 to 2006. The significant correlations were rather rare among them from 1974 to 1991, increasing number to 2000, and finally almost all to 2006, as observed in the blood of Fukuoka Controls in 1999 in which all the correlations are significant. However, the correlation coefficients between the concentrations of PCB118 and PCB156 in the blood of Yusho patients have been insignificant throughout from 1974 to 2006 with a few exceptions. By the use of the data of 3 Taiwan Yucheng patients and 5 Fukuoka Yusho patients, chronological concentrations of PCB118, PCB153, PCB156, 2,3,4,7,8-pentaCDF (23478F) and 1,2,3,4,7,8-hexaCDF (123478F) in the blood of Yusho patients were figured out from the outbreak of the poisoning to the present for 38 years. Very high concentrations of PCBs (20-90 ppb) and PCDFs (100-500 ppt) just after the onset were gradually decreased to 0.04-1.3 ppb of PCBs and 0.3-5 ppt of PCDFs in 2005 with the biological half-lives of 3.84, 6.31, 7.24, 4.98 and 4. 30 years, respectively. The particular declining mode of the PCB congeners during 38 years and the correlation coefficients between the concentrations of PCB118, PCB153, PCB156, 23478F and 123478F in the blood of Yusho patients indicated that PCB118 concentrations have been decreased by the coexisting PCB156, 23478F and others which have very strong enzyme inducing activities and the PCB118 has been metabolized by the enzyme inducers to hydroxyl-PCBs which firmly bind to transthyretin (thyroxin transport protein) in the blood and disturb the hormonal effects.

Sex ratios of children of Russian pesticide producers exposed to dioxin.

We investigated the sex ratio of children of pesticide workers who produced the biocide trichlorophenol and the herbicide 2,4,5-trichlorophenoxy acetic acid from 1961 to 1988 in the city of Ufa, Bashkortostan, Russia. We measured exposure of the two related cohorts to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and other dioxins by analyzing 84 blood samples, which produced median TCDD toxic equivalents blood lipid values of 240 ng/kg, which are more than 30 times higher than background or normal exposure from the region. The sex ratio (fraction male) of the combined cohort of 227 children from 150 male and 48 female workers was 0.40, significantly lower (z-test for proportions = 3.21; p < 0.001) than those for the city of Ufa (0.512) and elsewhere worldwide. When we analyzed the sex ratio of the children according to maternal or paternal exposure, we observed a decrease in the number of boys (ratio 0.38) for fathers and a normal number (ratio 0.51) for the mothers. Human exposure of these pesticide producers to high levels of dioxins is associated with the birth of more girls, but only for paternal exposures.

Polybrominated diphenyl ethers (PBDEs) in U.S. mothers' milk.

No previous reports exist on polybrominated diphenyl ether (PBDE) congeners in human milk from individual U.S. mothers. This article on PBDEs is an extension of our previous studies on concentrations of dioxins, dibenzofurans, polychlorinated biphenyls, and other chlorinated organic compounds in human milk in a number of countries. PBDE commercial products are used as flame retardants in flexible polyurethane foam (penta-BDE), in acrylonitrile-butadiene-styrene resins (octa-BDE), and in high-impact polystyrene resins (deca-BDE). Their use is permitted in the United States but is banned in some European countries because of presumed toxicity, demonstrated persistence, and bioaccumulation. Different commercial products can be found in various consumer products such as television sets, computers, computer monitors and printers, carpets, and upholstery. Analyses of human levels of these compounds suggest low but rising levels in European human milk, which may have peaked, at least in Sweden, in the late 1990s. Very few data exist on levels of PBDEs in humans in the United States, and none from milk from individual nursing mothers. To address this issue, we analyzed 47 individual milk samples from nursing mothers, 20-41 years of age, from a milk bank in Austin, Texas, and a community women's health clinic in Dallas, Texas. Up to 13 PBDE congeners were measured. The concentrations of the sum of PBDE congeners varied from 6.2 to 419 ng/g (or parts per billion) lipid, with a median of 34 ng/g and a mean of 73.9 ng/g lipid. The PBDE levels in breast milk from Texas were similar to levels found in U.S. blood and adipose tissue lipid from California and Indiana and are 10-100 times greater than human tissue levels in Europe. Their detection in breast milk raises concern for potential toxicity to nursing infants, given the persistence and bioaccumulative nature of some of the PBDE congeners. These results indicate a need for more detailed investigation of the levels of PBDE in people and food, as well as determining if animal fat in food is the major route of exposure of the general U.S. population. Other routes of intake may also be significant.

Polybrominated diphenyl ethers in retail fish and shellfish samples purchased from Canadian markets.

Fish and shellfish retail samples (n = 122) were purchased from three Canadian cities in the winter of 2002 and analyzed for a total of 18 polybrominated diphenyl ether (PBDE) congeners. The samples (salmon, trout, tilapia, Arctic char, mussels, oysters, shrimp, and crab) represented the range of fish and shellfish commercially available to Canadian consumers at the time of purchase. Trout and salmon (geometric mean SigmaPBDE = 1600 and 1500 pg/g, wet weight, respectively) were found to contain significantly higher amounts of PBDEs than the mussel, tilapia, and shrimp groups (geometric mean SigmaPBDE = 260, 180, and 48 pg/g, wet weight, respectively). These differences in SigmaPBDE concentrations among fish and shellfish products were partly driven by differences in lipid content among the samples. Mean SigmaPBDE concentrations in domestic samples were also significantly greater than in imported samples, possibly reflecting global environmental distribution of PBDEs. These concentration differences will contribute to variations in dietary exposure to PBDEs when assorted fish and shellfish items from various origins are consumed.

Are Vietnamese food exports contaminated with dioxin from Agent Orange?

In this study the levels of dioxins and dioxinlike compounds, dibenzofurans, and polychlorinated biphenyls (PCBs) were measured in food exported from Vietnam to the United States. In the past, some Vietnamese fish was found to be contaminated with dioxin, 2,3,7,8-TCDD, or TCDD, from Agent Orange. U.S. commercial catfish farmers recently claimed that exported Vietnamese food, especially catfish, was contaminated with dioxin from Agent Orange and was thus a matter of concern to the U.S. Congress. In 2001, twenty-two exported Vietnamese food samples (mostly fish) were purchased in the United States and Laos to evaluate possible contamination with dioxin from Agent Orange. Dioxin, dibenzofuran, and coplanar PCB congeners were measured by high-resolution gas chromatography-high-resolution mass spectrometry by laboratories in Germany and Canada certified for dioxin analysis by the World Health Organization (WHO). In the current study, only low levels of dioxins and dioxinlike compounds were present in all exported Vietnamese food analyzed, despite recent findings of elevated levels of one dioxin, 2,3,7,8-TCDD, from Agent Orange exposure in some Vietnamese individuals, presumably due to food consumption. It appears unlikely that exported Vietnamese food is, in general, contaminated with large amounts of dioxin (TCDD) from Agent Orange or other sources. Further food sampling from areas of heavy Agent Orange spraying in Vietnam is warranted to map out where the source of TCDD contamination of food may be originating.

Dioxin, dibenzofuran, and coplanar PCB levels in Laotian blood and milk from agent orange-sprayed and nonsprayed areas, 2001.

Agent Orange, a phenoxyherbicide contaminated with 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), was used by American military forces during the United States-Vietnam war between 1962 and 1971 primarily as a defoliant to destroy forests where enemy troops might find cover. Agent Orange was used mainly in Vietnam, but also to a lesser extent in Laos and Cambodia. In Laos, there have been no prior studies of TCDD contamination from Agent Orange, despite known defoliation and documented records of Agent Orange spraying. This article presents findings of TCDD in human blood and milk from two geographic areas in Laos: Vientiane, a nonsprayed area, and Sepone, an Agent Orange-sprayed area. German and Canadian laboratories used high-resolution gas chromatography-mass spectrometry to measure 7 dioxin, 10 dibenzofuran, and 4 non-ortho or coplanar polychlorinated biphenyls in Laotian blood and milk samples. Most subjects tested in this Laos Ministry of Health Study showed low dioxin and dibenzofuran levels, consistent with what would be expected in a primarily rural nonindustrial country. These findings are consistent with relatively low dioxin and dibenzofuran levels recently found in food from these same areas. The chemically and toxicologically related non-ortho PCBs were measured but were found at low levels compared to specimens from other countries, presumably because of less industrialization and industrial pollution in Laos.

Dioxin, dibenzofuran, and polychlorinated biphenyl (PCB) levels in food from Agent Orange-sprayed and nonsprayed areas of Laos.

During the Vietnam War, a phenoxy-herbicide mixture called Agent Orange, which was contaminated with 2,3,7,8-tetrachlorodibenzodioxin, or TCDD, was used primarily for destruction of forest and other foliage in order to prevent enemy troop movement and protect American and allied troops and military bases in the south of Vietnam. Smaller areas of Laos and Cambodia were also sprayed with Agent Orange between 1962 and 1971 from fixed-wing aircraft. In 2001, 28 food samples consisting of meat, fish, and dairy products were collected in sprayed and nonsprayed areas of Laos and analyzed for dioxins, dioxinlike dibenzofurans, and selected polychlorinated biphenyl (PCB) congeners by high-resolution gas chromatography/high-resolution mass spectrometry at laboratories in Germany and Canada. Low levels of dioxin and other dioxinlike substances were found in Laotian food, similar to levels present in recent exported Vietnamese food to United States. Vietnam is geographically adjacent to Laos. Total dioxin toxic equivalent (TEQ) levels were similar in samples from sprayed and non-sprayed areas, ranging from 0.009 to 0.851 pg/g or parts per trillion (ppt) in sprayed Sepone, and from 0.022 to 0.537 pg/g or ppt wet weight in non sprayed Vientiane. However, the Laotian fish samples from the Agent Orange-sprayed area had, on average, a higher proportion of total TEQ from TCDD (31.7% vs. 9.4%) compared to the nonsprayed area. Some other food items, duck eggs and pork liver from Sepone, also had severalfold higher TCDD levels than similar food samples from Vientiane, 0.029 vs. 0.011 pg/g and 0.070 vs. 0.004 pg/g wet weight, respectively. There were no substantial differences in levels of dibenzofuran and PCB congeners. In general, elevated TCDD levels were not found in Laotian food samples. It is possible that dioxin-contaminated areas, or "hot spots," exist in Laos as they do in Vietnam, although they have not yet been identified.

Patterns of PCBs and PCDD/PCDFs in chicken and pork fat following a Belgian food contamination incident.

A food contamination incident involving polychlorobiphenyls (PCBs) and PCDD/Fs occurred in 1999 in Belgium. On heavily affected farms, concentrations of PCBs in chicken or pork fat exceeded the Belgium tolerance limit of 200 ng/g lipid weight for the sum of seven marker PCBs. Analysis of contaminated samples showed that the patterns for PCB and PCDD/F congeners differed among feed, chicken fat and pork fat. Lower chlorinated PCBs and polychlorodibenzofurans (PCDFs) including those with high TEFs (PCBs 105, 118, 126 and 2,3,4,7,8-PeCDF) were shown to either bioaccumulate more in chicken fat or to be eliminated more readily in pork. This leads to the possibility that consumption of chicken would result in a higher TEQ human body burden than that from the same consumption of pork. In addition, PCDF congeners with non-2,3,7,8-substitution (e.g., 1,2,4,7,8-PeCDF) were present in chicken fat but absent in pork fat. Since the residue pattern in this commercial episode changes less in the avian species, these results reinforce the value of birds rather than mammals as markers of the source of contamination with persistent organochlorine pollutants.

The brominated flame retardants, PBDEs and HBCD, in Canadian human milk samples collected from 1992 to 2005; concentrations and trends.

Human milk samples were collected from individuals residing in various regions across Canada mostly in the years 1992 to 2005. These included five large cities in southern Canada as well as samples from Nunavik in northern Quebec. Comparative samples were also collected from residents of Austin, Texas, USA in 2002 and 2004. More than 300 milk samples were analysed for the brominated flame retardants (BFRs), PBDEs and HBCD, by extraction, purification and quantification using either isotope dilution gas chromatography-mass spectrometry (GC-MS) or liquid chromatography-MS. The Canadian total PBDE values in the years 2002-2005 show median levels of about 20µg/kg on a lipid basis; a value significantly higher than in the 1980s and 1990s. Milk samples from Inuit donors in the northern region of Nunavik were slightly lower in PBDE concentrations than those from populated regions in the south of Quebec. Milk samples from Ontario contained slightly lower amounts of PBDEs in two time periods than those from Texas. HBCD levels in most milk samples were usually less than 1ppb milk lipid and dominated by the α-isomer. This large data set of BFRs in Canadian human milk demonstrates an increase in the last few decades in human exposure to BFRs which now appears to have stabilized.

Polychlorinated dioxins, furans (PCDD/Fs), and polychlorinated biphenyls (PCBs) and their trends in Canadian human milk from 1992 to 2005.

More than 300 samples of human milk were collected from individuals residing in various regions across Canada in the years 1992 to 2005. The milks were taken from the main populated areas east to west in southern Canada as well as from the region of Nunavik in northern Quebec and analysed for polychlorinated dibenzo-p-dioxins (PCDDs), polychlorinated dibenzofurans (PCDFs), and polychlorinated biphenyls (PCBs). The concentrations, expressed in ng kg(-1) milk lipid, show an overall decrease of virtually all compounds examined including 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), World Health Organization 2005 toxic equivalents (WHO2005-TEQ) PCDD/PCDFs, WHO2005-TEQ dioxin-like PCBs (dl-PCBs), and total PCBs. Median values of 2,3,7,8-TCDD changed from about 1.5 ng kg(-1) milk lipid in 1992 to 0.8 ng kg(-1) in 2005 while the median WHO2005-TEQ PCDD/F fell from about 14-7 ng kg(-1) milk lipid in the same period. The concentrations of PCDD/Fs and PCBs in samples from Nunavik, which is in Arctic Quebec, were higher than those observed in milk from southern Quebec although this difference was not large. Over two time periods, milk samples from Hamilton, Ontario showed slightly higher levels of PCBs than Austin, Texas, USA--a North American city of similar size and development but with more than twice the PBDE exposure. When compared with earlier human milk data going back to the early 1980s, this large data set shows a steady decline of human exposure to POPs in Canada by a factor of about four times.

Dioxins, furans and non-ortho-PCBs in Canadian total diet foods 1992-1999 and 1985-1988.

In the period from 1985 to 1999, about 600 samples of total diet foods from Canadian cites were analysed for dioxins, furans and non-ortho-PCBs. Toxic equivalent (TEQ) concentrations on a lipid basis were found to be the highest in dairy and beef products followed by poultry and pork. These levels decreased over the 15-year period of sampling, particularly those for fluid milk, less so for poultry and pork and little or no change for beef. Calculation of the human daily intake for the years 1985-1988 showed values a little less than 1 pg of TEQ(2005) polychlorinated dibenzo-p-dioxin/polychlorinated dibenzofuran per kg body weight, falling progressively to less than 0.5 pg of TEQ in 1999. These estimates are lower than the 2.3 pg of TEQ currently recommended by the WHO. The main categories of foods contributing to the TEQ were animal meats and dairy products, with lesser amounts from fish and other foods.

Higher accumulation of polybrominated diphenyl ethers in infants than in adults.

Pooled serum samples collected from 8132 residents in 2002/ 03 and 2004/05 were analyzed to assess human polybrominated diphenyl ether (PBDE) concentrations from specified strata of the Australian population. The strata were defined by age (0-4 years, 5-15 years, < 16 years, 16-30 years, 31-45 years, 46-60 years, and > 60 years); region; and gender. For both time periods, infants and older children had substantially higher PBDE concentrations than adults. For samples collected in 2004/ 05, the mean +/- standard deviation sigmaPBDE (sum of the homologue groups for the mono-, di-, tri-, tetra-, penta-, hexa-, hepta-, octa-, nona-, and deca-BDEs) concentrations for 0-4 and 5-15 years were 73 +/- 7 and 29 +/- 7 ng g(-1) lipid, respectively, while for all adults > 16 years, the mean concentration was lower at 18 +/- 5 ng g(-1) lipid. A similar trend was observed for the samples collected in 2002/03, with the mean sigmaPBDE concentration for children < 16 years being 28 +/- 8 ng g(-1) lipid and for the adults >16 years, 15 +/- 5 ng g(-1) lipid. No regional or gender specific differences were observed. Measured data were compared with a model that we developed to incorporate the primary known exposure pathways (food, air, dust, breast milk) and clearance (half-life) data. The model was used to predict PBDE concentration trends and indicated that the elevated concentrations in infants were primarily due to maternal transfer and breast milk consumption with inhalation and ingestion of dust making a comparatively lower contribution.

Is house dust the missing exposure pathway for PBDEs? An analysis of the urban fate and human exposure to PBDEs.

Polybrominated diphenyl ether (PBDE) body burdens in North America are 20 times that of Europeans and some "high accumulation" individuals have burdens up to 1-2 orders of magnitude higher than median values, the reasons for which are not known. We estimated emissions and fate of sigma PBDEs (minus BDE-209) in a 470 km2 area of Toronto, Canada, using the Multi-media Urban Model (MUM-Fate). Using a combination of measured and modeled concentrations for indoor and outdoor air, soil, and dust plus measured concentrations in food, we estimated exposure to sigma PBDEs via soil, dust, and dietary ingestion and indoor and outdoor inhalation pathways. Fate calculations indicate that 57-85% of PBDE emissions to the outdoor environment originate from within Toronto and that the dominant removal process is advection by air to downwind locations. Inadvertent ingestion of house dust is the largest contributor to exposure of toddlers through to adults and is thus the main exposure pathway for all life stages other than the infant, including the nursing mother, who transfers PBDEs to her infant via human milk. The next major exposure pathway is dietary ingestion of animal and dairy products. Infant consumption of human milk is the largest contributor to lifetime exposure. Inadvertent ingestion of dust is the main exposure pathway for a scenario of occupational exposure in a computer recycling facility and a fish eater. Ingestion of dust can lead to almost 100-fold higher exposure than "average" for a toddler with a high dust intake rate living in a home in which PBDE concentrations are elevated.

Determination of persistent organohalogenated pollutants in human hair reference material (BCR 397): an interlaboratory study.

A human powdered hair material (BCR 397) was tested for its content in persistent organic pollutants (POPs), such as polychlorinated biphenyls (PCBs), organochlorine pesticides (OCPs) and polybrominated diphenyl ethers (PBDEs). Using different methods, three laboratories (two from Canada and one from Belgium) analysed a powdered hair sample to evaluate some methodologies and to obtain consensus values for selected POPs. Measured values for all PCB congeners and p,p'-DDE were within a relative standard deviation (RSD) of 15%. These first results contribute to the accuracy and precision for POPs quantification in hair and render test results more comparable among different laboratories.

Determination of polybrominated diphenyl ethers and polychlorinated biphenyls in human adipose tissue by large-volume injection-narrow-bore capillary gas chromatography/electron impact low-resolution mass spectrometry.

A new analytical method has been developed for the quantification of polybrominated diphenyl ethers (PBDEs) in human adipose tissue samples. After Soxhlet extraction and a cleanup procedure using two successive solid-phase extraction cartridges containing acid silica and acid silica: neutral silica:deactivated basic alumina (from top to bottom), detection can been achieved by narrow-bore (0.10-mm i.d.) capillary gas chromatography/electron impact low-resolution mass spectrometry using a large-volume injection technique. Using narrow-bore capillaries, it is possible to analyze complex mixtures in a short time (up to 10 min), saving 50% or more of the analysis time of conventional columns while maintaining a similar resolution power. The method allows the determination of five major PBDE congeners (BDE 28, 47, 99, 100, and 153) at concentrations below 1 ng/g lipid weight. Detection limits in the selected ion mode varied between 0.05 and 0.30 ng/g lipid weight, depending on the degree of bromination. The sensitivity of this method can compete with low-resolution mass spectrometry with electron capture ionization, while a much better selectivity is obtained. Levels of PBDEs in 20 Belgian human adipose tissue samples ranged between 2.18 and 11.70 ng/g lipid weight and were similar to previously reported values from Europe.

Distribution of organobrominated and organochlorinated contaminants in Belgian human adipose tissue.

We have measured the levels of flame retardants, polybrominated diphenyl ethers (PBDEs), in 20 recent human adipose tissues from Belgium and compared them to other organohalogen compounds such as polychlorinated biphenyls (PCBs), hexachlorobenzene, 2,2-bis(4-chlorophenyl)-1,1,1-trichloroethane (p,p'-DDT), and its metabolite, 2,2-bis(4-chlorophenyl)-1,1-dichloroethylene (p,p'-DDE). After Soxhlet extraction and cleanup on acidified silica solid-phase extraction cartridges, analysis was achieved by capillary gas chromatography/electron impact mass spectrometry. The method allowed the determination of 5 PBDE and 35 PCB congeners. Concentrations of PBDEs (sum of congeners IUPAC Nos. 28, 47, 99, 100, and 153) ranged between 2.2 and 11.7 ng/g lipid weight and were on the lower end of reported PBDE concentrations in European countries. The median value for the sum of PCBs (35 congeners) was 841 ng/g lipid weight and ranged from 286 to 1802 ng/g lipid weight. The median value for the sum of DDTs (calculated from p,p'-DDE and p,p'-DDT) was 290 ng/g lipid weight and ranged from 47 to 2802 ng/g lipid weight. The sum of PCBs showed a good correlation with the sum of DDTs (r=0.77, P<0.05), while the correlation with the sum of PBDEs was weaker (r=0.56, P<0.05). No age dependency was found for PBDEs (r=0.09), while PCBs and DDTs showed higher correlation coefficients with age (r=0.59 and 0.40, respectively, P<0.05).