Bioconcentration of polycyclic aromatic hydrocarbons in the adipose tissue of women with pelvic endometriosis and idiopathic infertility: A case-control study.

PURPOSE: Polycyclic aromatic hydrocarbons (PAHs), present in air and food, generated during energy production and waste incineration, are known for health toxicity. PAHs may activate the aryl hydrocarbon receptor, which could in turn modify estrogen-dependent inflammatory pathways in endometriosis. The possible role of PAHs in the pathogenesis of endometriosis remains unclear. The study aimed to evaluate the potential link between exposure to PAHs and the occurrence of peritoneal and ovarian endometriosis. METHODS: A prospective case-control tertiary-center study included 46 women aged 22-45 undergoing laparoscopy due to pelvic endometriosis (n â€‹= â€‹32; arm 1) and idiopathic infertility (n â€‹= â€‹14; arm 2). A sample of the greater omentum was collected intraoperatively for detection of 16 standard PAHs by gas chromatography-isotope dilution mass spectrometry method. PAHs concentrations were compared in both study arms. The associations between PAHs concentrations and selected variables were investigated. RESULTS: There were no significant differences between both arms in terms of reference PAHs concentrations, nor correlations between PAHs concentrations and the stage of endometriosis. However, notable differences were observed in specific PAHs concentrations related to certain conditions. The concentrations of acenaphthene (p â€‹= â€‹0.016) and fluorene (p â€‹= â€‹0.013) were significantly lower in women with peritoneal adhesions, while the concentrations of benz[a]anthracene, benzo[k]fluoranthene and indeno[1,2,3-cd]pyrene [ng/g] were higher in cigarette smokers. CONCLUSIONS: The study showed no differences in exposure to PAHs between women with and without pelvic endometriosis. Determining the toxicity of PAHs in endometriosis requires further research.

Seasonal variations of PCDD/Fs congeners in air, soil and eggs from a Polish small-scale farm.

The transfer of dioxin from the environment to the food is a problem in a consumers' health protection. The study aimed to determine the concentration of dioxins in free-range chicken eggs, air and soil samples, collected during 12 months on an individual small farm, located in Malopolska region, Poland. In the majority of analyzed eggs, the concentrations of dioxin exceeded several times the legal limit of 2.5 pg WHO-TEQ g-1fat. Seasonal changes in the PCDD/Fs congeners in egg, air and soil samples were studied. During the winter season, when the combustion processes of the solid fuel in domestic furnaces are intensive, the PM10 concentration in the Malopolska region exceeds the legal limit (50µg/m3) even eight times. In this period, eggs, air and soil samples showed a higher share of PCDFs with a specific contribution of 2,3,7,8-TCDF. During the summer months, in the egg, air and soil samples, the share of PCDDs is higher with dominant OCDD and 1,2,3,4,6,7,8-HpCDDs, showing the effect of other combustion processes such as grass utilization or burning plastic wastes in controlled fires. In August, the month of the highest average air temperature and lowest rainfall amount, the highest toxicity of PCDD/Fs in eggs (9.52pgWHO-TEQ g-1fat) was found. Due to the similarity of the shares of PCDD/Fs congeners in total WHO-TEQ value we can take into account the influence of toxicity of PCDD/Fs in the air and soil on the toxicity in the eggs.

Study on the impact of industrial flue gases on the PCDD/Fs congener profile in ambient air.

The aim of this study was to examine the impact of emissions from combustion processes from sinter, medical, waste and sewage waste incineration plants on the PCDD and PCDF congener profile in ambient air in Krakow (city in Poland). The subject matter of the study were air samples from the outskirts and the city center. It was found that in flue gases from industrial sources and in ambient air the share of PCDF congeners in relation to the total content of PCDD/Fs was higher than the share of PCDDs. However, in air samples collected in the city center, this relationship was reversed. The PCDD congener profiles in flue gases and in air samples are comparable. However, in the samples from the city centre, the share of OCDD is significantly higher and amounts to about 80%. The PCDF congener shares show higher spatial diversity, although in all the analyzed air samples, ODCF and 1,2,3,4,6,7,8 HpCDF dominated. Analyzing the share of congeners in regard to the sum of PCDDs/Fs a mutual resemblance of air from the suburbs, exhaust gases from the sinter ore and sewage sludge incinerator plant was observed. The study showed a similarity between the profile of congeners in air from the city centre and exhaust gases from the medical waste incinerator.

Tobacco smoke exposure and endothelial dysfunction in patients with advanced coronary artery disease.

INTRODUCTION:  Exposure to tobacco smoke is associated with a higher cardiovascular risk, especially in patients with coronary artery disease (CAD).  OBJECTIVES:  The aim of the study was to evaluate the effect of active and passive tobacco smoking on the activity of endothelial markers in advanced atherosclerosis. PATIENTS AND METHODS:  We studied 181 consecutive patients with advanced CAD (53 women and 128 men) aged 60 ±8 years, including 102 active self­declared smokers (56.3%). We determined plasma asymmetric dimethylarginine (ADMA), thrombomodulin (TM), and plasminogen activator inhibitor­1 (PAI­1) levels, along with serum cotinine concentrations as a marker of tobacco smoking.  RESULTS:  Plasma ADMA levels were higher in active smokers compared with nonsmokers (0.60 ±0.09 µmol/l vs. 0.49 ±0.08 µmol/l, P <0.001). There were similar intergroup differences in TM (4.60 ±2.11 ng/ml vs. 3.0 ±1.7 ng/ml, P <0.0001) and PAI­1 levels (30.3 ±12.4 ng/ml vs. 23.6 ±11.3 ng/ml, P <0.0001). We observed positive correlations between cotinine and ADMA (r = 0.71, P <0.0001), TM (r = 0.53, P <0.0001), and PAI­1 (r = 0.58, P <0.0001). In 21 patients (26.6%) who declared to be nonsmokers, cotinine levels (mean, 6.30 ±22.5 ng/ml) significantly correlated with ADMA, TM, and PAI­1 (all P <0.001). A multivariate regression analysis showed that cotinine was an independent predictor of ADMA, TM, and PAI­1 in the whole patient group.  CONCLUSIONS:  Despite long­lasting endothelial injury in advanced CAD, continued cigarette smoking is able to further enhance endothelial damage by increasing ADMA levels and resultant inhibition of fibrinolysis.

Study on the determination of PCDDs/Fs and HCB in exhaust gas.

The subject of this study was to develop a method of simultaneous determination of PCDDs/PCDFs and HCB in exhaust gases from industrial installations. Sampling to determine PCDDs/PCDFs was conducted using the method described in PN-EN 1948-1: 2006, where the sorption material is polyurethane foam (PUF). In order to simultaneously collect PCDDs/PCDFs and HCB and to avoid sorbent bed breakthrough, it was necessary to apply an additional polyurethane sorption layer. Twenty-seven samples of exhaust gases from various cement plants and 40 samples of exhaust gases from hospital and industrial waste incineration plants collected in 2009/2010 in the entire territory of Poland were examined. The average content of PCDDs/Fs in samples from cement plants amounted to 0.076 ng I-TEQ N m(-3) (range of 0.002-0.62 ng I-TEQ N m(-3)), while the average content of HCB amounted to 10 ng N m(-3) (range of 0.98-60.5 ng N m(-3)). In the case of samples collected from waste incineration plants, the average concentration of PCDDs/Fs was 0.39 ng I-TEQN m(-3) (range of 0.002-5.68 ng I-TEQ N m(-3)). In the case of HCB, the average concentration was 238 ng N m(-3) (range of 3.21-2500 ng N m(-3)). Also, the interdependence of the concentration of PCDDs/PCDFs and HCB was determined in the analysed samples, with the ranges of low and high content of PCDDs/PCDFs being examined separately. In all cases, the determined values of the r correlation coefficient were within the range of 0.7-1.0, which indicates a good correlation between the concentrations of PCDDs/PCDFs and HCB.

PBB levels in fish from the Baltic and North seas and in selected food products from Poland.

Recently, a significant amount of attention has been devoted to the determination of polybrominated biphenyls in food and the environment. In this study, PBB contamination of fish from the North and Baltic Seas, with a special focus on samples from Poland and France, was investigated. North Sea fish like salmon, herring, scarp, gilthead seabream and grey gurnard were collected from a French fish market. Baltic Sea fish like salmon, tunny, trout, herring, and freshwater fish such as carp were purchased from a Polish fish market. Cod livers in oil were also analyzed in this study. As additional food samples, butter, pork fat and beef fat were tested. Concentrations of PBBs in North Sea fish (except herring) were higher than in fish from the Baltic Sea. The highest total PBB concentration was measured in scarp muscle tissue (635+/-107 pg g(-1) wet weight), and the lowest was in carp samples (0.567+/-0.245 pg g(-1) wet weight). The PBB content in tunny oil samples was below the detection limits (0.45-1.05 pg g(-1)fat). Our study also demonstrated that PBBs may bioaccumulate in the liver, where PBB concentrations were 2116+/-351 pg g(-1) wet weight and 841+/-147 pg g(-1) wet weight. In fish species from Poland, the most dominant congeners were tetrabromobiphenyls, followed by pentabromobiphenyls and hexabromobiphenyls. In some species of fish from the North Sea, the most dominant groups were hexabromobiphenyls and tetrabromobiphenyls. Although the relative abundances of structurally known and unknown isomers varied from species to species, all fish (except tunny) were contaminated with PBBs.

Effects of dioxin (2,3,7,8-TCDD) and PCDDs/PCDFs congeners mixture on steroidogenesis in human placenta tissue culture.

OBJECTIVE: The aim was to compare the direct effect of most toxic 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) as well as of naturally occurring congener mixture of polychlorinated dibenzodioxins (PCDDs) and polychlorinated dibenzofurans (PCDFs) extracted from fly ash on the placental steroidogenesis. The concentration of all 17 toxic congeners was reported and the toxic equivalent (TEQ) was calculated as a 27.7 micrograms-TEQ/kg of fly ash. METHODS: Placental cotyledons were harvested immediately after expulsion of placenta. The cells were prepared according to KLIMAN et al. (1986). To examine TCDD and PCDDs/PCDFs mixture action on cytochrome P450 side change cleavage enzyme (P450 scc) and 3 beta-hydroxysteroid dehydrogenase (3 beta-HSD) activity the placental cells were cultured either in basal conditions or with the addition of 25-hydroxycholesterol (25-OH) or pregnenolone (P5). RESULTS: TCDD in all doses used decreased basal P4 secretion, while did not show any effect on 25-hydroxycholesterol (25-OH) and pregnenolone (P5) supplemented cultures. In all variants of culture PCDDs/PCDFs mixture was without effect on basal and substrate supplemented progesterone (P4) secretion suggesting a reduction in the activity of cytochrome P450scc or 3 beta-HSD. To examine TCDD and PCDDs/PCDFs mixture action on aromatase cytochrom P450 (P450 arom) activity the placental cells were cultured in basal condition or with the addition of dehydroepi-androsterone (DHEA) or testosterone (T). Significant increase of estradiol secretion under the influence of TCDD in DHEA and T supplemented cultures suggests its action on the activity of P450 arom. CONCLUSION: The discrepancy found between the action of pure TCDD and dioxin mixture on placental steroids secretion is possibly due to an additional effect of pentachlorodibenzo-p-dioxin (PeCDD) and pentachlorodibenzo-furan (PeCDF) which covered > 50% of the total toxic equivalents (TEQ) present in this mixture.