Placental transfer of polychlorinated dibenzo-p-dioxins, dibenzofurans, and biphenyls in Taiwanese mothers in relation to menstrual cycle characteristics.

The aim was to determine the body burden of dioxins and polychlorinated biphenyls (PCBs) and whether they are associated with variables influencing reproduction. Our subjects were healthy women (mean age of 29 [SD=4.5]) from central Taiwan. The congeners of dioxins and dioxin-like PCBs in placentas (n=119) were identified using gas chromatography/high resolution mass spectrometry. The median levels of polychlorinated dibenzo-p-dioxins/dibenzofurans and PCBs were 10.2 (geometric mean [GM]: 9.8, 95% confidence interval [95% CI]: 8.8-10.9) and 2.7 (GM: 2.7, 95% CI: 2.3-3.1) pg WHO-TEQ/g lipid, respectively. Total TEQ level in placentas was significantly correlated with mothers' arm circumference (r=0.22, p=0.043). Increased body fat percentage was associated with higher total TEQ level in placentas. After adjustment for maternal age, pre-pregnant body mass index (BMI), and parity, placental dioxin-TEQ level higher in women (age 19 years) with irregular menstrual cycle than in those (age <18 years) with regular menstrual cycle (p=0.032) and placental PCB-TEQ level was higher in women with menstrual cycles longer than 33 days versus less than 33 days (p=0.006). Thus, environmental exposure to dioxins and PCBs may be related to changes in current menstrual cycle characteristics.     

Polychlorinated dibenzo-p-dioxins, polychlorinated dibenzofurans and dioxin-like polychlorinated biphenyls in cetaceans from Korean coastal waters

Data on levels and accumulation profiles of polychlorinated dibenzo-p-dioxins and dibenzofurans (PCDD/ Fs) and dioxin-like polychlorinated biphenyls (PCBs) in cetaceans are scarce. This paper presents data on the concentrations and accumulation features of PCDD/Fs and dioxin-like PCBs in muscle of minke whales (Balaenoptera acutorostrata) and long-beaked common dolphins (Delphinus capensis) collected from Korean coastal waters. The residue levels in cetaceans were in the order of mono-ortho PCBs> non-ortho PCBs>PCDFs>PCDDs. Total toxic equivalent (TEQ) concentrations in muscle of minke whales and common dolphins from Korea were lower than those reported for cetaceans and seals from other countries. The accumulation profiles of PCDD/Fs and dioxin-like PCBs were different between the cetacean species. Concentrations of PCDD/Fs and dioxin-like PCBs in common dolphins were significantly higher than those measured in minke whales, due to differences in the habitat and diet. The relative contribution of individual chemical groups to total TEQs was different between the cetacean species, suggesting different exposures and metabolic activity.     

Contamination of Russian Baltic fish by polychlorinated dibenzo-p-dioxins, dibenzofurans and dioxin-like biphenyls

Nineteen species of fish products caught and produced in the Russian economic zone of the Baltic region in 2002-2005 were analyzed for polychlorinated dibenzo-p-dioxins (PCDDs), dibenzofurans (PCDFs) and dioxin-like biphenyls (WHO-PCBs). Freshwater fish had significantly lower PCDD/PCDFs levels than most saltwater fish, except cod's fillet for which TEQ was comparable. In some cases pollutant levels of sea fish tissues essentially exceeded current regulatory values. Concentration of WHO(PCDD/F)-TEQ ranged from 0.06 to 0.57pg/g f.w. for freshwater fish, and from 0.16 to 17.83pg/g f.w. for sea fish. The special concern is caused by the high concentration of dioxin-like PCBs, whose contribution to the WHO-TEQ(PCDD/F,PCB) considerably exceeded that of PCDDs and PCDFs. Concentration of WHO(PCB)-TEQ ranged from 2.56 to 124.40pg/g f.w. Profiles of PCDD/Fs congeners in fish were rather similar: in our opinion, the most probable sources of pollution were chlorine bleaching and outflow of PCBs. There is no real reason to assume that fish contamination was affected by the fungicide Ky-5 or similar chlorophenols mixtures. Relative contributions of each dioxin-like PCBs congener to total TEQ in fish tissue are presented in Fig. 2. Profiles of dioxin-like PCBs in general are close to Aroclor 1254, though in some cases there are essential differences.     

Polychlorinated dibenzo-p-dioxins, polychlorinated dibenzofurans, and coplanar polychlorinated biphenyls in breast milk from two cities in Ukraine.

Substantial environmental pollution has been alleged in Ukraine, but little information is available to allow an assessment of the possible impact on humans. To help remedy this lack of information, it was of interest to investigate whether certain polychlorinated dibenzo-p-dioxins (PCDDs), polychlorinated dibenzofurans (PCDFs), or coplanar polychlorinated biphenyls (PCBs) were elevated in people from Ukraine. Samples of breast milk were obtained from 200 women from the cities of Kyiv and Dniprodzerzhinsk; Kyiv is the capital and Dniprodzerzhinsk is a highly industrialized city. The samples were combined into four pools by city and age, and analyzed for 7 PCDDs, 10 PCDFs, and 2 coplanar PCBs (126 and 169). The total of the measured PCDDs, expressed as toxic equivalent, ranged from 5.1 to 7.6 pg/g lipid; for PCDFs from 3.6 to 5.2, and for PCBs from 11 to 18 pg/g lipid. Results from the two cities were similar; older women had slightly higher concentrations than did younger women. Levels of these compounds seen in Ukraine were similar to or lower than those seen in other recent studies from European and Asian countries.     

Spatiotemporal patterns of polychlorinated dibenzo-p-dioxins and dibenzofurans and dioxin-like polychlorinated biphenyls in foodstuffs in air quality regions in Taiwan

High-fat food intake is the main source of dioxin-like compounds for humans, such as consumption of meat, dairy and eggs, and seafood products. Fruits, vegetables, and cereals have relatively low levels of dioxin-like compounds, but because of high consumption they also contribute to the food-borne intake. It is necessary to clarify dietary dioxin exposure affected by different food contamination levels and dietary habits among different geographic areas. We aimed to evaluate chronic dietary PCDD/Fs and DL-PCBs exposure in 725 individual foods in 14 categories in 6 Taiwan air quality regions (AQRs) and a total of 2441 foods from 2004 to 2018. We estimated daily PCDD/Fs + DL-PCBs intake on the basis of sex- and age-specific foodstuff ingestion rate and PCDD/Fs+ DL-PCBs concentrations using a probabilistic approach. PCDD/F+ DL-PCB levels among the different sampling periods exhibited a decreasing trend in fish and aquatic products (from 0.384 ± 0.764 to 0.206±0.223pgWHO₀₅-TEQg⁻¹ w.w.) (p for trend=0.043), livestock products (from 0.133±0.298 to 0.035±0.043 pgWHO₀₅-TEQ g⁻¹ w.w.), eggs (from 0.221 ± 0.373 to 0.056 ± 0.048 pgWHO₀₅-TEQ g⁻¹ w.w.) (p for trend = 0.002), and dairy samples (from 0.066 ± 0.075 to 0.024 ± 0.026 pgWHO₀₅-TEQ g⁻¹ w.w.) (p for trend= 0.001). All lifetime average daily doses (LADD) were below provisional tolerable monthly intake (PTMI) but higher than the TWI for PCDD/Fs and DL-PCBs in food. The percentages of the contribution of each food group to the total dietary intake of TEQ_PCDD/F+PCB in different ambient air dispersion areas and age groups. The total daily intake of PCDD/Fs and DL-PCBs by Taiwanese differed between AQRs (0.188–0.397 pgWHO₀₅-TEQ kg⁻¹ b.w. day⁻¹). The observed geographical variations were likely due to differences in food habits, cuisines, culture and levels of environmental contamination among various regions in Taiwan. By sensitivity analysis, we have identified the major contribution to LADD, which was the dioxin levels in marine fish, fresh water fish and fish related products, and followed by dioxin levels in duck eggs. In addition, marine and freshwater fish consumption rate accounts more than 10.2%. These major exposure variables was also consistent with the findings of total daily intake in different AQRs.     

Polychlorinated dibenzo-p-dioxins/polychlorinated dibenzofurans (PCDD/Fs), polychlorinated biphenyls (PCBs), and organochlorine pesticides in human blood of pregnant women from Germany

Blood samples from 226 pregnant women aged between 19 and 41 yr, living in an industrialized area of Germany (Duisburg birth cohort study), were collected between September 2000 and November 2002 and analyzed for their content of persistent organic pollutants (POPs). Levels of polychlorinated dibenzo-p-dioxins (PCDDs), polychlorinated dibenzofurans (PCDFs), and polychlorinated biphenyls (PCBs) were in the range of 4.34-97.3 pg WHO 1998 TEq/g(lipid base) (median: 25.96) or 3.77-63.56 pg WHO 2005 TEq/g(lipid base) (median: 19.38), respectively. Whole blood volume-based concentrations of organochlorine pesticides and their metabolites were 0.036-0.53 microg/L (median: 0.15) hexachlorobenzene (HCB), 4.5-1300 ng/L (median: 67) beta-hexachlorocyclohexane (HCH), 0.6-520 ng/L (median: 18) 4,4'-dichlorodiphenyltrichloroethane (DDT), and 0.1-9.1 microg/L (median: 0.54) 4,4'-dichlorodiphenyldichloroethene (DDE). Parameters influencing the POP levels in human blood were examined using multiple regression models. Levels and the levels scatter widths of most PCDD/F and PCB congeners and HCB increased significantly with age. Within the multiple regression model a weak age dependence was also found for beta-HCH and DDT, whereas blood levels of alpha- and gamma- HCH and DDE were not age dependent. The total lactation period for earlier born children decreased most POP blood levels, except for alpha- and gamma-HCH. Over the study period of 27 mo only a low decreasing effect on human POP blood levels was observed. The body mass index had in general no or a low positive influence on contaminant levels. Because exposure to PCDD/F and PCB is higher in most industrialized countries in comparison to less industrialized ones, lower levels of these substances were detected in blood samples of women who had lived outside Western Europe for a longer period. In contrast, these women showed higher blood levels of organochlorine pesticides, indicating that these chemicals are still in use outside Western Europe.     

Comparison of the concentrations of polychlorinated dibenzo-p-dioxins, dibenzofurans, and dioxin-like polychlorinated biphenyls in maternal and fetal blood, amniotic and allantoic fluids in cattle

To characterize the maternal-fetal transport of lipophilic endocrine disrupting chemicals, concentrations of polychlorinated (2,3,7,8-substituted) dibenzo-p-dioxins (PCDDs), dibenzofurans (PCDFs), and dioxin-like polychlorinated biphenyls (PCBs) were measured in maternal and fetal blood, and amniotic and allantoic fluids in cattle. Total toxicity equivalent quantity (TEQ) was highest in amniotic fluid on a fat-weight basis, whereas it was highest in maternal blood on a total weight basis. TEQ was lowest in allantoic fluid on either basis; 26 of 29 congeners analyzed in this experiment were detected in one or more samples. The largest number of congeners was detected in amniotic fluid. O8CDD, 2,3,4,7,8-P5CDF and 2,3',4,4',5-P5CB were the major congeners in PCDDs, PCDFs and PCBs, respectively. The O8CDD concentration was higher in fetal blood than in maternal blood on a fat-weight basis, whereas concentrations of other congeners were lower in fetal blood than in maternal blood. Furthermore, on a fat-weight basis, the O8CDD concentration was considerably higher in allantoic fluid compared with other samples. Concentrations of major PCB congeners were higher in amniotic fluid than in maternal and fetal blood on a fat-weight basis. In conclusion, it is suggested that lipophilic endocrine-disrupting chemicals contained in maternal blood are all transferred to the fetal circulation via the placenta in cattle. Furthermore, the results of this experiment imply that O8CDD has different transportation systems from other dioxins in the circulation, and that a considerable amount of PCBs is excreted and accumulated in amniotic fluid during the fetal stage in cattle.     

Comparative molecular field analysis of polyhalogenated dibenzo-p-dioxins, dibenzofurans, and biphenyls.

Comparative molecular field analysis (CoMFA) was performed on polyhalogenated dibenzo-p-dioxins, dibenzofurans, and biphenyls for Ah (dioxin) receptor binding and associated enzyme inducing activities determined by others using in vitro assays. Since various members of all three classes of compounds have been shown to produce qualitatively similar toxicities, a separate CoMFA was performed on each class of compounds and combinations of the different classes for each bioactivity which included combining all three classes of molecules in one CoMFA study. For the Ah receptor binding, the CoMFA-derived QSARs for all three classes of compounds and combinations thereof showed strong crossvalidated correlations indicating that they are highly predictive. For enzyme induction, the CoMFA-derived QSARs were highly predictive for the dibenzofurans but were only partially successful for the dioxins. For the biphenyls, the results were clearly unpredictive. The overall results of these CoMFA studies which include both steric and electrostatic considerations are compared and contrasted to other SAR models that have met with some success in making qualitative predictions about the potential for receptor binding and associated toxicity in these classes of compounds. The CoMFA-derived QSAR for the dioxin series of molecules in most cases significantly overestimates the enzyme inducing ability of the ortho-substituted biphenyls. This weak inducing activity of the o-biphenyls is, however, consistent with their relatively low dioxin-like toxicity as measured in other biological systems. Fundamentally different mechanisms may be operating in the expression of dioxin-like toxic responses for the o-biphenyls, and their direct, dioxin-like toxic equivalency perhaps needs to be reconsidered in this light.     

A review of the aquatic ecotoxicology of polychlorinated dibenzo-p-dioxins and dibenzofurans

This paper reviews published studies on polychlorinated dibenzo-p-dioxins and polychlorinated dibenzofurans that are relevant to an assessment of their aquatic ecotoxicology. The available data suggest that laterally substituted congeners containing altogether 4,5, or 6 chlorine atoms are highly toxic, particularly to the early life stages of fish, with reported effect concentrations in the ng L¹ range. These congeners are also the most readily bioaccumulated. An aquatic toxicity threshold concentration of 0.011–0.038 ng L^?1, applicable to natural ecosystems, was determined for 2,3,7,8-tetrachlorodibenzo-p-dioxin (or for mixtures of congeners expressed as 2,3,7,8-TCDD equivalents). This threshold corresponds to the no observed effect concentration/lowest-observed effect concentration determined for mortality, growth, and behavioral effects seen in rainbow trout early life stages, exposed to 2,3,7,8-TCDD in a flow-through system over a 28-day period, followed by 28 days of depuration. An investigation was also made into the potential for using mammalian-derived toxic equivalency factors (TEFs) in aquatic ecosystems. This revealed that such an approach may underestimate the aquatic toxicity of some congeners, and that the use of organism-specific TEFs may be more appropriate. © by John Wiley & Sons, Inc.     

Serum hormones in boys prenatally exposed to polychlorinated biphenyls and dibenzofurans

Polychlorinated biphenyls (PCBs) and dibenzofurans (PCDFs) are persistent environmental pollutants shown to adversely interact with several functions of the endocrine system. In 1978-1979, over 2000 Taiwanese people ingested rice oil accidentally contaminated with PCBs and PCDFs. This is one of the major toxic exposure episodes that occurred globally and was later called Yucheng (oil disease in Chinese). The children born to exposed Yucheng women were therefore exposed in utero to high doses of PCBs/PCDFs. In 1995, 60 Yucheng and 61 control boys participated in physical examination, and serum hormones were measured by radioimmunoassay (RIA). Age, body weight, body height, Tanner status, testicular size, serum luteinizing hormone (LH), prolactin (PRL), thyroxine (T4), triiodothyronine (T3), and thyroid-stimulating hormone (TSH) levels were not statistically different between Yucheng and control boys in the subgroups of before and at the age of puberty. However, the serum estradiol (E2) levels were significant higher in Yucheng boys at the age of puberty. Yucheng and control boys were further divided into two subgroups, those before (age <13 yr) and those at the age of puberty (age > or = 13 yr). There was a decrease of serum testosterone (TT) levels and increase of serum follicle-stimulating hormone (FSH) levels in Yucheng boys at the age of puberty as compared with controls. There was a significant decrease of the square root of TT/E2 and TT/FSH; however, the square root of E2/FSH was increased in Yucheng boys at the age of puberty as compared with controls. Data indicated that prenatal exposure to PCBs and PCDFs may have implications for boys' sex hormone homeostasis at puberty. Further studies are needed to identify the congeners of PCBs/PCDFs responsible for disruption of the endocrine system, as well as the mechanisms of such disruption.     

Level of polychlorinated dibenzo-p-dioxins, dibenzofurans and biphenyls (PCDD/Fs, PCBs) in human milk and the input to infant body burden.

This study determined PCDD/F and PCB levels in human milk, examined factors associated with levels of contamination, and assessed the infant body burden from breast-feeding. The congeners of PCDD/Fs, dioxin-like PCBs, and indicator PCBs were analyzed by HRGC/HRMS for 36 human milk samples from healthy women, aged 20-35 years, from December 2000 to November 2001 in central Taiwan. Mean levels of WHO-TEQs in human milk were 10.5 (95% CI=8.8-12.2) and 14.5 (95% CI=12.5-16.5) pg-TEQ/g lipid for those <29 and > or =29 years old, respectively. PCB 138 concentration significantly predicted total WHO-TEQs with r2=0.84 (p <0.001). Milk level of dioxin-TEQ was 9.63 pg-TEQ/g lipid (95% CI=7.0-13.2) in those with a yearly income $29,000 compared to 6.3 pg-TEQ/g lipid (95% CI=5.2-7.6) for those whose yearly income was $18,000 per year. Women who reported being Buddhist (64.3 ng/glipid) had significantly higher indicator PCB concentrations than did those who reported being Taoist (35.3 ng/g lipid). The monthly dioxin intake of exclusively breastfed infants decreased with increasing duration of lactation. The cumulative dose of exclusively breastfed infants (76.5 ng TEQ, 95% CI=69.7-83.3) was significantly greater compared to that of formula-fed infants (CI=16.4-17.0) at one year and to that of infants at birth (3.90 ng TEQ, 95% CI=3.6-4.2). Our findings suggest that breast-feeding should be strongly encouraged for infants in Taiwan.     

A comparative study of polychlorinated dibenzofurans,polychlorinated biphenyls and 2,3,7,8-tetrachlorodibenzo-p-dioxin on aryl hydrocarbon hydroxylase inducing potency in rats

The aryl hydrocarbon hydroxylase (AHH) inducing potency of toxic chlorinated aromatic hydrocarbons such as polychlorinated dibenzofurans (PCDFs), polychlorinated biphenyls (PCBs) and 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) was studied in the young male Wistar rats. Alternatively, a technical PCDF mixture, 15 individual PCDF isomers or TCDD were administered i.p. in doses of 5 g/kg; a PCB mixture was given in a dose of 50 mg/kg. The order of AHH inducing ability was TCDD > PCDFs PCBs in kidney, lung, and liver. In the prostate, thymus, and spleen, only TCDD enhanced the AHH activity. The AHH inducibility in the lung and liver, induced by 15 pure PCDF isomers with varying chlorine substitutions was also examined. Only 2,3,7,8-tetrachlorodibenzofuran (2,3,7,8-tetra-CDF) and 2,3,4,7,8-pentachlorodibenzofurans (2,3,4,7,8-penta-CDF) significantly induced the hepatic AHH activity (4- and 2-fold, respectively), while eight PCDF isomers, including these two, significantly enhanced the pulmonary AHH activity (6- to 30-fold). Taking into account both the potent AHH inducibility and the high bioaccumulation of these compounds, 2,3,7,8-tetra- and 2,3,4,7,8-penta-CDF should be given due attention with regard to environmental-related factors and the possibility of involvement in the etiology of Yusho disease.A part of this work was presented at the 51st annual meeting of the Japanese Society for Hygiene, May 1–3, 1981, Sapporo, Japan and the 52nd annual meeting of the Japanese Society for Hygiene, March 29–31, 1982, Tokyo, Japan     

Effects of polychlorinated dibenzofurans, biphenyls, and their mixture with dibenzo-p-dioxins on ovulation in the gonadotropin-primed immature rat: support for the toxic equivalency concept

Previous studies have shown that 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), 1,2,3,7,8-pentachlorodibenzo-p-dioxin (PeCDD), and 1,2,3,4,7, 8-hexachlorodibenzo-p-dioxin (HxCDD), and their equipotent mixture block ovulation, reduce ovarian weight gain and alter preovulatory hormone levels in a similar manner. The objective of the current experiment was to investigate the effect of other structurally related compounds such as chlorinated furans and biphenyls on ovulation and related hormonal endpoints. The gonadotropin-primed immature female rat model was used to study the effect of 2,3,4,7, 8-pentachlorodibenzofuran (PeCDF), 3,3',4,4',5-pentachlorobiphenyl (PeCB), and 2,2',5,5' tetrachlorobiphenyl (TCB) and their mixture with polychlorinated dibenzo-p-dioxins (PCDDs) on ovulation. Rats were dosed on Day 23 of age at 0900 h with individual congeners (PeCDF, PeCB, TCB) or a mixture of five compounds, which included TCDD, PeCDD, HxCDD, in addition to PeCDF and PeCB. Equine choronic gonadotropin (eCG; 5 IU) was injected 24 h later to induce follicular development. Blood and ovaries were harvested, and ovarian weights determined at various times after eCG. Serum concentrations of 17beta-estradiol (E(2)), progesterone (P(4)), luteinizing hormone (LH), and follicle-stimulating hormone (FSH) were determined by radioimmunoassay. At 72 h after injection of eCG, the number of ova shed was measured by irrigating the ova from oviducts. The slopes of the dose-responses for inhibition of ovulation generated by the individual PeCDF, PeCB, and/or their mixture with PCDDs were similar. PeCDF, PeCB, and the mixture increased serum concentrations of E(2) at 72 h after eCG injection, the day of expected ovulation; in contrast, serum P(4) and FSH were decreased at that same time point. Only the high doses of TCDD, PeCDF, and PeCB blocked LH and FSH surges at 58 h after eCG. The ovarian histology revealed that the effects of PeCDF, PeCB, and the mixture were very similar to those of PCDDs, consisting of ova in large preovulatory follicles and a lack of or reduced number of corpora lutea. Parallel dose-responses of the individual congeners (PeCDF and PeCB) and their equipotent mixture with PCDDs support the toxic equivalency (TEQ) concept for the blockage of ovulation. Thus, PCDDs, PCDFs, and PeCBs appear to block ovulation by the same or a very similar mechanism of action.     

Peroxidase-catalyzed in vitro formation of polychlorinated dibenzo-p-dioxins and dibenzofurans from chlorophenols.

Chlorophenols (CP) are transformed in vitro to polychlorinated dibenzo-p-dioxins and dibenzofurans (PCDD/F) by a peroxidase-catalyzed oxidation. This is shown for 2,4,5-tri-, 2,3,4,6-tetra- and pentachlorophenol with plant horseradish peroxidase and with myeloperoxidase recovered from human leukocytes, each in the presence of hydrogen peroxide. The yield, the reaction and the PCDD/F-pattern found are dependent on the CP. The amounts of PCDD/F formed within 4 or 24 h are in the micromol/mol-range for all substrates and both peroxidases. The experiments suggest that biochemical formation of PCDD/F from precursors such as CPs can take place in the human body and that this metabolic pathway may lead to a higher inner exposure to PCDD/F than up to now assumed based on intake data for PCDD/F.     

Impact of polychlorinated dibenzo-p-dioxins,dibenzofurans, and biphenyls on human and environmental health,with special emphasis on application of the toxic equivalency factor concept

A scientific evaluation was made of the mechanisms of action of polychlorinated dibenzo-p-dioxins, dibenzofurans and biphenyls. Distinction is made between the aryl-hydrocarbon (Ah) receptor-mediated and non-Ah receptor-mediated toxic responses. Special attention is paid to the applicability of the toxic equivalency factor (TEF) concept.     

Impact of polychlorinated dibenzo-p-dioxins, dibenzofurans, and biphenyls on human and environmental health, with special emphasis on application of the toxic equivalency factor concept.

A scientific evaluation was made of the mechanisms of action of polychlorinated dibenzo-p-dioxins, dibenzofurans and biphenyls. Distinction is made between the aryl-hydrocarbon (Ah) receptor-mediated and non-Ah receptor-mediated toxic responses. Special attention is paid to the applicability of the toxic equivalency factor (TEF) concept.     

Polychlorinated biphenyls, dibenzo-p-dioxins, and dibenzofurans and birth weight and immune and thyroid function in children

None of the publications reviewed provide clinical evidence that PCBs (polychlorinated biphenyls) and related chemicals adversely affect weight, immune, or thyroid function in infants or children born to healthy mothers. Birth weights of term infants fell within the normal range in all studies. The greatest difference between comparison groups was reported by G. G. Fein et al. (1984a, Intrauterine Exposure of Humans to PCBs: Newborn Effects, EPA-600/3-84-060, Environmental Protection Agency; 1984b, J. Pediatr. 105, 315-320). P. R. Taylor et al. (1989, Am. J. Epidemiol. 129, 395-406) reported smaller differences in occupationally exposed women and E. Dar et al. (1992, Environ. Res. 59, 189-201) found that women with higher PCB serum levels had larger babies. S. Patandin et al. (1998, Pediatr Res. 44, 538-545) found a negative association of PCB concentrations in maternal or cord plasma and birth weight of breast and formula-fed infants combined but not when breast-fed infants were analyzed separately. L. Rylander et al. (1995, Scand. J. Work Environ. Health 21, 368-375) reported decreased birth weights with higher dietary intake of contaminated fish. Thus, correlations between PCB exposure or polluted fish ingestion and birth weight were inconsistent. Thyroid and immune function were also within the normal range. In none of the papers were normal laboratory reference values provided and overall the statistically significant differences accounted for little of the variance.     

Elimination of various polychlorinated dibenzo-p-dioxins and dibenzofurans (PCDDs and PCDFs) in rat faeces

A defined mixture (of a composition characteristic of that present in incinerator fly ash) of polychlorinated dibenzo-p-dioxins and -furans (PCDDs and PCDFs) was subcutaneously administered to rats and the elimination of the unchanged congeners via faeces was measured. 1) All congeners administered could be found in faeces. 2) The rates of elimination via faeces were rather different for the different congeners. 3) The most toxic congeners, 2378-T4CDD and 12378-P5CDD, were present in unmetabolized form in faeces to < 4% and < 8% of the administered dose within the first week. Thus, parenteral administration clearly minimizes contamination of the animal quarters when compared with corresponding oral dosing. 4) The rate of unchanged elimination was apparently especially pronounced for the higher chlorinated PCDDs and PCDFs. The highest excretion rate was found for 1234678-H7CDD (up to 30% of administered dose). 5) No obvious differences were observed in the rates of elimination of the unchanged substances via faeces of the 2378-substituted or the non-2378-substituted isomers.Abbreviations Used PCDDs PCDFs polychlorinated dibenzo-p-dioxins, and -furans - T4CDDs T4CDFs tetra-chlorinated dibenzo-p-dioxins, and -furans - P5CDDs P5CDFs penta-chlorinated dibenzo-p-dioxins, and -furans - H6CDDs H6CDFs hexa-chlorinated dibenzo-p-dioxins, and -furans - H7CDDs H7CDFs hepta-chlorinated dibenzo-p-dioxins, and -furans - OCDD OCDF octa-chlorinated dibenzo-p-dioxin, and-furan - DMSO dimethyl-sulfoxide     

Docking and 3D-QSAR studies on the Ah receptor binding affinities of polychlorinated biphenyls (PCBs), dibenzo-p-dioxins (PCDDs) and dibenzofurans (PCDFs)

Polychlorinated biphenyls (PCBs), dibenzo-p-dioxins (PCDDs) and dibenzofurans (PCDFs) binding with the aryl hydrocarbon receptor (AhR) have been correlated with many toxic responses. Hence, it is very necessary to study the interactions between these ligands and AhR for further understanding of the mechanism of toxicity. In this study, an integrated molecular docking and 3D-QSAR approach was employed to investigate the binding interactions between PCBs, PCDDs, PCDFs and AhR. From molecular docking, hydrogen-bonding and hydrophobic interactions were observed to be characteristic interactions between compounds and AhR. Based on the mechanism of interactions, an optimum 3D-QSAR model with good robustness (Q(CUM)(2)=0.907) and predictability (Q(EXT)(2)=0.863) was developed by partial least squares. Additionally, the developed QSAR model indicated that the molecular size, shape profiles, polarizability and electropological states of compounds were related to the binding affinities to AhR.