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K Olie

Publications and source records attributed to K Olie.

18 recordsLinked to original sources

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.

Animal Feed↗

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.

Adult↗

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.

Acne Vulgaris↗

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.

Animals↗

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.

Adult↗

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.

Adult↗

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.

Adult↗

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.

Acne Vulgaris↗

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.

Adult↗

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.

Dioxins↗

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.

Adult↗

[Breast feeding, PCBs and dioxins].

In breastmilk of 14 Dutch mothers and 5 Polish mothers the content of dioxins and furans is measured. The study in Dutch mothers is started to relate the level of these xenobiotics to bleeding in the perinatal and late neonatal period. Interference with coagulation is hypothesized in analogon to phenobarbital. A relation is seen between bleeding in four babies and the mean content of 2, 3, 7, 8 TCDD (= tetrachloordibenzodioxin) (P = 0.02) in their breastmilk. This relation however is not found for the content of 2, 3, 4, 7, 8 PnCDF (= pentachloordibenzofuran) or the total amount of toxic equivalents. The fact that the prenatal gradient from mother to baby is different for T4CDD and PnCDF, respectively 2:1 and 10:1, may be an explanation for the dissociation between T4CDD on one side and PnCDF and total amount of toxic equivalents on the other side. Polish breastmilk was significantly lower (about four times) for dioxins and furans than Dutch breastmilk. This means that for these chemicals pollution in Holland is much higher than in Poland.

Adult↗

Transfer of polychlorinated dibenzo-p-dioxins and dibenzofurans to fetal and neonatal rats.

A fly ash extract from a municipal incinerator, containing polychlorinated dibenzo-p-dioxins (PCDDs) and dibenzofurans (PCDFs), was orally administered to rats on Days 10 to 17 of the pregnancy and during the first 10 days of the lactation period. PCDD and PCDF congeners retained in the fetuses and livers of the offspring had a 2,3,7,8-chlorine substitution pattern. The only non-2,3,7,8-substituted congener retained in the liver of the offspring and females was 2,3,4,6,7-pentachlorodibenzofuran (PnCDF). In the fetuses 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) had the highest retention (0.13% of total dose) and a decrease in retention was found with increasing number of chlorine atoms. In the livers of the offspring, the highest retention was found for 2,3,7,8-TCDD and the three 2,3,7,8-substituted hexachlorodibenzo-p-dioxins (HxCDDs) (5.26-8.12%). In the livers of the pregnant and lactating females penta- and hexachlorinated congeners had the highest retention (53.91-80.20%). For both groups the liver retention of the tetra- to octachlorinated congeners was similar, but the lactating females stored less PCDDs and PCDFs in their adipose tissue. A linear relationship was found between the retention of congeners in the livers of the females and offspring.

Adipose Tissue↗

Effects of pentachlorophenol on rat liver changes induced by hexachlorobenzene, with special reference to porphyria, and alterations in mixed function oxygenases.

Hexachlorobenzene (HCB, 1000 ppm) and 500 ppm pentachlorophenol (PCP) were fed separately or in combination to female Wistar rats. A control group was provided with standard food without HCB or PCP. Subgroups of 4 rats were killed after 1, 2, 4, 6 and 8 weeks. No significant difference was found between the amounts of HCB accumulated in the livers of the HCB and HCB + PCP fed rats. Administering HCB together with PCP caused a noticeable accumulation of PCP in the liver, compared to the results after administering HCB and PCP separately. In the HCB and HCB + PCP fed groups liver weight increased continuously during the experiments. Microsomal cytochrome P-450, NADPH-cytochrome c reductase, ethoxyresorufin O-de-ethylase, aminopyrine N-demethylase, and glucuronyl transferase increased to a maximum in 2-4 weeks in HCB and HCB + PCP fed rats. Pentachlorophenol accelerates the onset of HCB porphyria, in other words it increases the total urinary porphyrin excretion and causes an earlier disturbance of the porphyrin pattern.

Animals↗

Organochlorine contaminants in human milk from Slavonia Province, Yugoslavia, 1978.

Organochlorine residues were determined in human milk samples from an agricultural area of Slavonia, Yugoslavia. Concentrations of pentachlorobenzene, hexachlorobenzene, alpha-, beta-, gamma-isomers of benzene hexachloride, heptachlor, aldrin, DDE, TDE, and DDT were determined by gas chromatography (GC). Confirmation was carried out by computerized GC-mass spectrometry. The most abundant contaminant was p,p'-DDE (range, 42.0-418.5 microgram/kg (ppb)).

Humans↗

Identification of hydroxyhalobiphenyls as their methyl ethers by gas chromatography mass spectrometry.

The mass spectra and gas chromatographic properties of 17 synthetic fluoro-, chloro- and bromomethoxy-biphenyls and 12 dichlorodimethoxybiphenyls have been examined. From this representative series it appears that the position of the methoxy group (ortho, meta and para to the biphenyl bond) in all monomethoxy compounds examined, and the positions of the two methoxy groups in most of the dimethoxy compounds, can be assigned unambiguously by their difference in fragmentation pattern. The value of this method was shown by metabolism experiments in which 4,4'-difluoro- and 4,4'-dibromobiphenyl were fed to rats and 4,4'-dichlorobiphenyl was administered to plants. All hydroxylated metabolites found were identified by gas chromatography mass spectrometry. Relationships between structure and gas chromatographic retention time of these compounds are discussed.

Animals↗