Reducing dioxin formation by adding hydrogen in simulated fly ash.

In this study, simulated fly ash containing CuO/CuCl2 was heated at 350 °C in a flow of N2 and also in a nitrogen flow containing 10 vol% H2, to evaluate the influence of hydrogen adding on dioxin formation. The total polychlorinated dibenzo-p-dioxins and dibenzofurans (PCDD/F) output derived from the CuO sample under N2 and 10 % H2 was 7.382 and 0.708 ng/g, respectively. As for CuCl2, it was 589 and 46.1 ng/g, respectively. The results show that the hydrogen adding has a good inhibition effect on PCDD/F formation; the inhibition rate was higher than 90 % for PCDD/Fs. HCl and NH3 were detected by Gasmet in the flue gas; the probable inhibition mechanism of hydrogen reaction was proposed, based on our measurements and others' researches.

Neurodevelopmental retardation, as assessed clinically and with magnetoencephalography and electroencephalography, associated with perinatal dioxin exposure.

UNLABELLED: In 1980s Western Europe, human perinatal exposure to background levels of dioxins was rather high. We therefore evaluated the neurodevelopment of our cohort during the prepubertal period and in adolescence. At prepubertal age (7-12 years) 41 children were tested. Both neuromotor functioning and psychological testing were performed (Dutch version of the Wechsler Intelligence Scale for Children (WISC-R) and the Dutch version of the Child Behavior Checklist for ages 4-18 years (CBCL 4-18) and the Teacher Report Form (TRF)). Neurophysiological tests were performed using magnetoencephalography and electroencephalography. In adolescence (14-18 years) the behavior of 33 children was studied again (CBCL and TRF). And the levels of dioxins and dioxin-like PCBs (dl-PCBs) were measured in serum. RESULTS: At prepubertal age no association was found between perinatal dioxin exposure and verbal, performal and total IQ or with the Touwen's test for neuromotor development. There were behavioral problems associated with both prenatal and postnatal dioxin exposure. In adolescence there were problems associated with the current dioxin levels and dioxin-like-PCBs. Neurophysiological tests revealed clear negative dysfunction. An increase in latency time after a motion stimulus (N2b) of 13 ms (= a delay of 10%) is associated with the higher prenatal dioxin exposure. A similar delay was measured in testing cognitive ability by analyzing the odd ball measurements, N200 and P300, together with an amplitude decrease of 12 %. The delay is indicative of a defective myelinisation and the decrease in amplitude of a loss of neurons. CONCLUSION: We found effects on behavior in association with the perinatal dioxin exposure and in adolescence in association with the current dioxin levels. Neurophysiological testing is instrumental in the detection of effects of perinatal background levels of chemicals on brain development in normal, healthy children. The clinical, neurological and psychological tests commonly used are not sensitive enough to detect important effects.

Assessment of current serum levels of PCDD/Fs, dl-PCBs and PBDEs in a Dutch cohort with known perinatal PCDD/F exposure.

As part of a longitudinal cohort study, now in its second decade, we determined PCDDs/Fs dl-PCBs and PBDEs in serum of adolescents with known perinatal PCDD/F exposure. Of the original cohort, 33 adolescents aged 14-19 years, who had been studied previously during their neonatal (n=60), toddler and pre-pubertal period (n=41) agreed to participate in the current follow-up. PCDD/F-, dl-PCB- and PBDE congeners were measured using GC/MS. Current serum levels of PCDD/Fs determined in our cohort were relatively low (mean of 2.2 pg/g) compared to the perinatal exposure. No correlation between perinatal exposure and current serum PCDD/F was found. Planar PCB TEQ levels were 2.2 pg/g. Current summation operatorPBDE levels were 8.7 ng/g lipid. There was one outlier with a summation operatorPBDE of 74 ng/g lipid. The presence of this high value indicates that the exposure pathway is different from PCDD/F and PCB, most likely by dust and food contaminated with dust. Concluding we can say that current PCDD/F levels are quite low compared to the perinatal PCDD/F exposure of the cohort. PBDE levels however are relatively high compared to other European countries, more research on possible health effects of these levels, especially for subjects with outlier concentrations, should be performed.

Dioxin contamination in food. Bayreuth, Germany, from September 28 to October 1, 2000.

Dioxin and PCB monitoring programs for food and feeding stuff in most countries of the world, including many European Countries are currently inadequate. Better control of food production lines and food processing procedures is needed to minimize entry of dioxin to the food chain and will help to avoid dioxin contamination accidents. This would also improve the ability to trace back a possible contamination to its source. European guidelines for monitoring programs should be established to ensure comparable and meaningful results. These guidelines should define the minimum requirements for the design of monitoring programs, analytical methods, and quality assurance. Though data from Northern Europe shows that the general population exposure to dioxin and PCB has decreased during the last ten years these compounds continue to be a risk of accidental contamination of the food chain. The most prominent recent example is the Belgian dioxin contamination of feeding stuff in 1999. The Belgian dioxin contamination was not detected due to dioxin monitoring programs but by their direct biological effects seen in animals. Four other cases of dioxin contamination have been detected in Europe since 1997 due to local monitoring programs. One of them (citrus pulp pellets 1998) was in a much larger scale than the Belgian dioxin contamination. The general population's exposure to dioxins and PCBs is still in the same range (1-4 pg WHO-TEQ/kg body weight and day) as the recently revised WHO tolerable daily intake (TDI). There is concern that short-term high level exposure to dioxins, furans, and PCB may cause biological effects on the human fetal development and further research is required. Further actions to control sources building on considerable advances already made in many countries may need to be supplemented by measures to prevent direct contamination of feeding stuff or food to reduce general population exposure further.

Decreased lung function associated with perinatal exposure to Dutch background levels of dioxins.

UNLABELLED: Perinatal exposure to Dutch background dioxin levels is rather high. Studies of calamities have shown that dioxins negatively influence the respiratory system. It was hypothesized that perinatal exposure to background dioxin levels leads to lung suboptimality, probably through developmental interference. This study aimed to assess lung function in relation to perinatal dioxin exposure. Spirometry was performed in 41 healthy children (aged 7-12 y. mean 8.2 y) with known perinatal dioxin exposure. The ratio of forced expiratory volume in I s to forced vital capacity (FEV1/FVC ratio) was determined. A complete medical history was taken. The prenatal exposure ranged from 8.74 to 88.8 (mean 34.6) ng TEQ dioxin kg fat(-1), measured in breast milk. The postnatal exposure ranged from 4.34 to 384.51 (mean 75.4) ng TEQ dioxin. Twelve children had to be excluded. A significant decrease in lung function in relation to both prenatal (p = 0.045) and postnatal (p = 0.0002) dioxin exposure was seen in the 29 non-excluded children. A clinical association between chest congestion and perinatal dioxin exposure was seen. CONCLUSION: Perinatal background dioxin exposure may be inversely associated with the FEV1/ FVC ratio.

Blood lipid concentrations of dioxins and dibenzofurans causing chloracne.

Chloracne is caused by exposure to certain halogenated polycyclic hydrocarbons such as polychlorinated dibenzodioxins (PCDDs) and dibenzofurans (PCDFs). In chronic exposure it is not known what level of intoxication, represented by the level in blood lipids, is sufficient to cause chloracne. Blood levels of the congeners of PCDD/Fs were determined in four groups of humans. One group had clinically visible chloracne due to exposure in a hexachlorobenzene workshop of a large chemical factory. A second group was exposed in the same workshop, but had no skin changes. There were two control groups: one non-exposed group of maintenance workers from the same chemical factory, and one group of healthy individuals living elsewhere. Blood levels were converted to toxicity equivalents of tetrachlorodibenzo-p-dioxin (TCDD). In the chloracne group blood levels in toxicity equivalents (TEQs) ranged from 1168 to 22,308 pg/g blood lipid. In the exposed without chloracne this ranged from 424 to 662 pg/g. It is concluded that the level to develop chloracne is between 650 and 1200 pg/g TEQ. The contribution of TCDD was rather small, and the main causative congeners were the hexachlorinated dibenzodioxins and dibenzofurans (HxCDD/Fs); lipid-based blood levels in absolute amounts that may cause chloracne are in the range of 2-3.5 ng/g HxCDD, and 2-5 ng/g HxCDF.

Missing effects of background dioxin exposure on development of breast-fed infants during the first half year of life.

Fetal exposure to higher levels of PCBs can result in low birth weight and neurological disorders of the newborn. In this study the effects of exposure to the highly toxic dioxins and dibenzofurans, structurally related to PCBs, was investigated in a population of 38 healthy infants. The infants were divided into two groups, according to concentrations of dioxins and dibenzofurans in their mothers milk fat. Neonatal body weight, length, Quetelet index and liver size were determined at different time points during the first half year of life. Additionally neurological development was determined. Comparing these items between the high and low exposure groups did not show any statistically significant differences. The results of this study do not reveal any effect of exposure to background levels of dioxins and dibenzofurans, but in utero exposure to these toxic agents may result in symptoms later in life. Therefore follow-up study of this well defined group will be performed.

Monitoring and estimating concentrations of polychlorinated biphenyls, dioxins, and furans in cattle milk and soils of Rhine-Delta floodplains.

In the Rhine-Delta, accumulation of microcontaminants in floodplain foodwebs has received little attention in comparison with aquatic communities. Here, soil and cattle milk samples were taken from three floodplains and analyzed for polychlorinated biphenyls (PCBs), dibenzodioxins (PCDDs) and dibenzofurans (PCDFs). Based on 2,3,7, 8-tetrachlorodibenzodioxin equivalents, total PCDD and PCDF residues in milk did not exceed the quality standard of 0.006 microg/kg fat weight. This was still the case if non- and mono-ortho PCBs were added to the total. Yet, the floodplains investigated were only moderately polluted according to previous studies and one cannot exclude higher levels in milk from other floodplains. Bioconcentration ratios of milk fat vs soil organic matter were about 0.01 to 0.1 for persistent PCBs. These values are in accordance with a few literature data found for other persistent compounds. Yet, ratios are lower than expected from equilibrium partitioning. Ratios for PCDDs and PCDFs were even lower, possibly due to biotransformation.

Influence of short-term dietary measures on dioxin concentrations in human milk.

Breast-feeding may expose infants to high levels of toxic chlorinated dioxins. To diminish intake of these lipophilic compounds by the baby, two diets were tested for their ability to reduce concentrations of dioxins in human milk. The diets were a low-fat/high- carbohydrate/low-dioxin diet. (about 20% of energy intake derived from fat) and a high fat /low-carbohydrate/low-dioxin diet. These diets were tested in 16 and 18 breast-feeding women, respectively. The test diets were followed for 5 consecutive days in the fourth week after delivery. Milk was sampled before and at the end of the dietary regimen, and dioxin concentrations and fatty acid concentrations were determined. Despite significant influences of these diets on the fatty acid profiles, no significant influence on the dioxin concentrations in breast milk could be found. We conclude that short-term dietary measures will not reduce dioxin concentration in human milk.

Chloracne. Some recent issues.

Chloracne is an acneiform skin eruption that is still the most sensitive indicator of systemic poisoning caused by chemicals belonging to the group of chlorinated polycyclic aromatic hydrocarbons. Generally these chemicals are known as dioxins, dibenzofuranes, and PCBs. The cause of chloracne is probably interference of these chemicals with vitamin A metabolism in the skin, resulting in disturbances of the epithelial tissues of the pilosebaceous duct. A study of workers in a factory where chloracne is endemic is described. The product manufactured, pentachlorophenol, a wood preservative, was found to be contaminated with dioxins (congeners of TCDD) and dibenzofuranes. Blood levels of these chemicals in affected workers are given, along with supporting evidence of disturbances in vitamin A (retinoid) metabolism as demonstrated in skin biopsies.

Clinical laboratory manifestations of exposure to background levels of dioxins in the perinatal period.

The effects of exposure to low levels of dioxins in infants (intrauterine and via breast milk) were studied. In a group of 35 babies, specially selected, laboratory tests were performed in cord blood and in blood sampled at 7 days and 11 weeks of age. The outcome of these laboratory tests was related to dioxin concentrations in milk fat and cumulative dioxin intake. At 11 weeks of age, alanine aminotransferase and aspartate aminotransferase activities in plasma were significantly related to cumulative dioxin intake. A significant negative relation was found between platelet count and cumulative dioxin intake. The results of this study suggest that exposure to background levels of dioxins, both intrauterine and via breast milk, may have effects in newborns.

Effects of pre- and postnatal exposure to chlorinated dioxins and furans on human neonatal thyroid hormone concentrations.

Animal studies have shown that dioxins influence plasma thyroid hormone concentrations. To investigate the effect of chlorinated dioxins and furans on thyroid hormone concentrations in humans, we studied 38 healthy breast-fed infants. The study population was divided into two groups according to the dioxin concentrations in milk fat of their mothers. Blood samples were taken at birth and at the ages of 1 and 11 weeks. At birth a tendency to higher total thyroxine (tT4) concentrations was found in the high exposure group. At the ages of 1 and 11 weeks the increase of mean tT4 concentrations and tT4/thyroxine-binding globulin ratios in the high exposure group reached significance as compared to the low exposure group. At birth and 1 week after birth, mean thyrotropin (TSH) concentrations were similar in both groups, but at the age of 11 weeks the mean TSH concentrations were significantly higher in the high exposure group. We postulate that the observed plasma tT4 elevation in infants exposed to dioxins before and after birth is the result of an effect on the thyroid hormone regulatory system.

Placental transport of dioxins from mother to fetus. II. PCBs, dioxins and furans and vitamin K metabolism.

Placental transport of dioxins and furans from mother to fetus takes place. It is probably related to the fatty acid transport. Between 10 and 20% of fatty acids in a full-term baby are of maternal origin. In adipose tissue of children that died in the early neonatal period concentrations of +/- 25% were found of three dioxin and furan congeners 12378 P5CDD, 123678 H6CDD, and 23478 P5CDF in relation to a mean concentration of these congeners in the fat of 14 breastmilk samples. Data of concentrations are given as measured in liver and adipose tissue. In the placenta of a Dutch woman an accumulation of dioxins and furans is found in relation to blood. Animal studies support the hypothesis that polychlorobifenyls play a role in the cause of the late hemorrhagic disease in the newborn, in particular the 2, 4, 5, 2, 4, 5-hexachlorobifenyl that is present in relatively high concentrations in breastmilk.

Breast milk, dioxins and the possible effects on the health of newborn infants.

The concentration of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) in the fat of breast milk of 14 Dutch mothers varied from 5.35 to 17.0 ng kg-1 (nanograms per kilogram fat). Expressed as toxic equivalents the concentrations of the 17 different congeners of dioxin and furans in the fat of the breast milk were between 29.85 and 92.88 ng kg-1. These levels are sufficient to induce enzyme formation in the livers of infants. (The acceptable daily intake is 4 pg/kg bodyweight/day). Dioxin induces the same enzyme production in the liver as phenobarbital; therefore, because phenobarbital affects fat-soluble vitamins, such as vitamins D and K, a similar response was anticipated in response to exposure to dioxin. Consequently, one aim of this study was to investigate blood coagulation parameters. We found a statistically significant relationship with the mean concentration of TCDD in the breast milk of mothers whose babies suffered from bleeding problems. This association was not found for 2,3,4,7,8-pentachlorodibenzofuran concentrations, nor for the remaining congeners expressed as toxic equivalents. A simple laboratory test for measuring dioxins and furans is urgently needed.