Abstract  National Human Adipose Tissue Survey (NHATS) data and U.S. Environmental Protection Agency (U.S. EPA) STORET data were used to test for relationships between human exposure and environmental contamination according to census division. Regions were ranked according to the mean concentration of 43 toxic substances (pesticides, polychlorinated biphenyls, semi-volatiles, and volatiles) in human adipose tissue and environmental media (sediment, fish tissue, and groundwater). Correlation analyses between regional human and environmental ranks indicated that fish tissue data were good predictors of regional pesticide exposure, sediment data were good predicators of PCB exposure, and groundwater data were good predictors of exposure to semi-volatile compounds. None of the environmental data used were good predictors of exposure to volatile chemical compounds. Groundwater appeared to be a better predictor of overall regional toxics exposure than other types of environmental data.

Abstract  Human and environmental exposures to toxic substances may be evaluated by direct measurement (i.e., monitoring data), or by using surrogate measures (i.e., release data). The usefulness of surrogate measures is dependant upon their reliability as indicators of actual human exposure. The release of toxic substances into the environment may result in human and environmental exposures. Therefore, the recent creation of the Toxic Release Inventory (TRI) data base may provide suitable surrogate measures of regional human and environmental exposure. However, the reliability of these data as indicators of regional exposure has not been adequately tested. Previous studies using existing national monitoring data from the National Human Adipose Tissue Survey (NHATS) and the Environmental Protection Agency (EPA) STORET data base have demonstrated that regional differences in human and environmental exposures exist (Phillips and Birchard 1991a, 1991b). Regional correlations between NHATS and STORET data have a/so been observed (Phillips, 1991 ). In this study, regional relationships between the quantity of toxic substances released into the environment, and the magnitude of human and environmental exposures were evaluated using TRI data in conjunction with NHATS and STORET data. The results of this study provide: 1) a comprehensive assessment of regional correlations between the amount of toxics released via various emission pathways, and the levels of human exposure and environmental contamination; and 2) an evaluation of the reliability of toxic release data for predicting exposures.

Abstract  A two-generation reproductive toxicity study with extra parameters was performed for Butyl benzyl phthalate (BBP). The compound was administered orally by gavage with the doses of 0, 100, 200, or 400 mg/kg/day to groups of 24 Crj:CD (SD)IGS rats of both sexes to confirm the utility of the protocol for identification of non-steroid chemicals with endocrine activity by ssessing effects on parental animals and offspring. Softening of the testes, diffuse atrophy of testicular seminiferous tubules, decreased spermatozoa and/or residual germ cells in the epididymal lumina were observed in the F1generation after doses more than 100 mg/kg, lowering of the F1 epididymal weights at doses more than 200 mg/kg, along with low F0 epididymal weights, Leydig cell hyperplasia, residual germ cells in the epidimymal lumina, and low seminal vesicle weights, small testes and epididymes, partial aplasia or aplasia of the epididymes, and Leydig cell hyperplasia in the F1 generation with 400 mg/kg. With regard to effects on the reproductive capacity, F1 parents at the dose of 400mg/kg showed a reduced fertility index and delayed preputial separation of the penis. In the offspring, lowered body weights in the F1 case, and change in anogenital distance in the F1 females and F2 males were observed at doses more than 100 mg/kg, with low splenic weights at 400 mg/kg in both generations. Thus, the utility of this protocol was confirmed. In the parental animals, the no observed effect level (NOEL) and the no observed adverse effect level (NOAEL) were less than 100 mg/kg/day, and no serious effects on the reproductive capacity were induced at doses less than 200 mg/kg/day. The NOEL and NOAEL for the growth and development of offspring were concluded to be less than 100 mg/kg/day.

Abstract  People are exposed to a variety of chemicals throughout their daily lives. To protect public health, regulators use risk assessments to examine the effects of chemical exposures. This book provides guidance for assessing the risk of phthalates, chemicals found in many consumer products that have been shown to affect the development of the male reproductive system of laboratory animals. Because people are exposed to multiple phthalates and other chemicals that affect male reproductive development, a cumulative risk assessment should be conducted that evaluates the combined effects of exposure to all these chemicals. The book suggests an approach for cumulative risk assessment that can serve as a model for evaluating the health risks of other types of chemicals.

Abstract  Phthalates, e.g. dimethyl phthalate (DMP), diethyl phthalate (DEP), di-n-butyl phthalate (DBP), benzylbutyl phthalate (BBP), and di-(2-ethylhexyl) phthalate (DEHP) were measured in the atmosphere and sea water of the North Sea (German Bight). The air and water samples were collected during an expedition cruise with German research ship 'Gauss' in the North Sea from 29th February to 10th March 2004. The concentrations of phthalates in the atmosphere ranged from below the method detection limit to 3.4 ng m(-3). DBP, BBP, and DEHP were determined in the water phase with concentrations ranging from below the method detection limit to 6.6 ng L-1.

Air-sea vapour exchange of DBP, BBP, and DEHP was estimated using the two-film resistance model based upon relative air-water concentrations. The average of air-sea exchange fluxes was -338 ng m(-2) day(-1) for DBP and -13 ng m(-2) day(-1) for BBP, which indicates a net deposition is taking place. The air-sea exchange fluxes of DEHP were ranging from -95 to + 686 ng m(-2) day(-1). The average value of + 53 ng m(-2) day(-1) for DEHP suggested a net volatilization from the North Sea. Moreover, the particle-associated fractions were calculated as 2%, 46%, 75% and 78% for DEP, DBP, BBP and DEHP, respectively. These results indicate that the air-sea vapour exchanges is an important process that intervenes in the mass balance of phthalates in the North Sea. (c) 2005 Elsevier Ltd. All rights reserved.

Abstract  Five phthalate ester and related compounds (phthalic anhydride, phthalamide, di(2-ethylhexyl) phthalate, di(2-ethylhexyl) adipate and butyl benzyl phthalate) have been tested for carcinogenic effects in standard lifetime rodent feeding studies. Groups of 50 male and female rats and mice were fed diets containing various concentrations of the test chemicals for 102-106 consecutive weeks. The dietary concentrations were estimated to be maximally tolerated doses and half maximally tolerated doses. All animals that died during the study and all survivors at the end of two years were examined grossly and microscopically for the presence of tumors. The incidences of animals with tumors at a specific anatomic site in the treated groups and the controls were compared statistically. Neither phthalamide nor phthalic anhydride increased tumor incidences in rats or mice. Di(2-ethylhexyl) phthalate increased the incidences of liver tumors in rats and mice of both sexes, while di(2-ethylhexyl) adipate caused liver tumors in male and female mice, only. Butyl benzyl phthalate did not cause tumors in male or female mice, but the incidence of myelomonocytic leukemia in butyl benzyl phthalate-treated female rats was significantly greater than that in the controls. Chemically induced early deaths in the butyl benzyl phthalate-treated male rats precluded an evaluation of carcinogenic potential in this sex. Under the conditions of these tests, di(2-ethylhexyl) adipate was considered to be carcinogenic in both rats and mice and di(2-ethylhexyl) adipate was considered to be carcinogenic in mice. The evidence for carcinogenic effects of butyl benzyl phthalate in female rats was judged to be equivocal because of the variable nature of the incidence of myelomonocytic leukemia in Fischer 344 rats. Phthalamide and phthalic anhydride did not exhibit carcinogenic effects in these studies.

Abstract  In summary, the EPA has begun to look critically at the induction of certain types of tumors in certain species, including liver tumors in mice. The controversy over the use of such tumor data in assessing the cancer risk for humans has been going on for some time. The present agency policy is to downgrade the weight of evidence for such data under certain conditions. Review of the cancer risk assessments for the 109 chemicals that the agency has formally verified shows that a variety of chemicals yield liver tumors in mice. However, one group of substances that consistently produced such tumors was chlorinated compounds (84%). Many of these compounds not only induced liver tumors in mice but also induced liver tumors in rats and/or other types of tumors in mice and rats. However, several of the chlorinated compounds produced only mouse liver tumors. Another group of compounds that often induced liver tumors in mice was nitrogen-containing compounds (aromatic amines, hydrazines, nitrosamines). These latter substances tended to not only induce liver tumors in mice but also a variety of other tumor types in a variety of species. Mouse liver tumor data have played a major role in the classification of substances in categories B2 and C. Fifty-six percent of the chemicals in category B2 and 40% in category C were classified based at least partially on the use of mouse liver tumor data. In addition, 21 of the 29 category B2 chemicals that produced liver tumors in mice and 5 of the 8 category C chemicals are chlorinated compounds. These two results indicate the importance of chlorinated compounds to the agency, and therefore, the importance of mouse liver tumor data in agency cancer risk assessments.

Abstract  BACKGROUND: Exposure to endocrine disruptors (EDs), including some phthalates, phytoestrogens and phenols can be quantified using biomarkers of exposure. However, reliability in the use of these biomarkers requires an understanding of the timeframe of exposure represented by one measurement. Data on the temporal variability of ED biomarkers are sparse, especially among children. OBJECTIVE: To evaluate intraindividual temporal variability in 19 individual urinary biomarkers (eight phthalate metabolites from six phthalate diesters, six phytoestrogens (two lignans and four isoflavones) and five phenols) among New York City children. METHODS: Healthy Hispanic and Black children (N=35; 6-10 years old) donated several urine samples over 6 months. To assess temporal variability we used three statistical methods: intraclass correlation coefficient (ICC), Spearman correlation coefficients (SCC) between concentrations measured at different timepoints, and surrogate category analysis to determine how well the tertile categories based on a single measurement represented a 6-month average concentration. RESULTS: Surrogate category analysis indicated that a single sample provides reliable ranking for all analytes; at least three of four surrogate samples predicted the 6-month mean concentration. Of the 19 analytes, the ICC was >0.2 for 18 analytes and >0.3 for 10 analytes. Correlations among sample concentrations throughout the 6-month period were observed for all analytes; 14 analyte concentrations were correlated at 16 weeks. CONCLUSIONS: The reasonable degree of temporal reliability and the wide range of concentrations of phthalate metabolites, phytoestrogens and phenols suggest that these biomarkers are appropriate for use in epidemiologic studies of environmental exposures in relation to health outcomes in children.

Abstract  In our previous studies, butyl benzyl phthalate (BBP) was found to be teratogenic when administered to rats on days 7-9 and days 13-15 of pregnancy but not days 10-12. The present study was conducted to determine the phase specificity of the developmental toxicity of MBeP, which is one of the major metabolites of BBP, and to assess the role of MBeP in the developmental toxicity of BBP. Pregnant rats were given MBeP by gavage at a dose of 375, 500 or 625 mg/kg on days 7-9, days 10-12 or days 13-15 of pregnancy. A significant increase in embryolethality was noted in pregnant rats given MBeP at 500 mg/kg and above regardless of the days of treatment. No evidence of teratogenicity was found when MBeP was given on days 10-12. A significantly increased incidence of fetuses with external malformations was found after treatment on days 13-15 at 500 mg/kg. A significantly increased incidence of fetuses with skeletal malformations was observed after treatment on days 7-9 at 625 mg/kg and on days 13-15 at 375 mg/kg and above. Deformity of the vertebral column and ribs was predominantly observed after treatment on days 7-9. Cleft palate and fusion of the sternebrae were exclusively found after treatment on days 13-15. The dependence of gestational days of treatment on the manifestation of the developmental toxicity and the spectrum of fetal malformations induced by MBeP were similar to those induced by BBP. These findings suggest that MBeP and/or its further metabolites may be responsible for the production of the developmental toxicity of BBP.

Abstract  We investigated the effect of endocrine disrupting chemicals (EDCs), including medical, industrial, and agricultural chemicals, on 3,3',5-L-[125I]triiodothyronine ([125I]T3) binding to purified Japanese quail transthyretin (qTTR), a major thyroid hormone-binding protein in plasma, and to the ligand-binding domain of thyroid hormone receptor beta (qTR LBD). Scatchard plots of T3 binding to qTTR and qTR LBD revealed two classes of binding sites, with Kd values of 6.9 and 185 nM, and a single class of binding sites, with Kd value of 0.31 nM, respectively. Among the test chemicals, diethylstilbestrol was the most powerful inhibitor of [125I]T3 binding to qTTR (IC50 < 0.4 nM). Diethylstilbestrol, ioxynil (IC50 =1.1+/-0.5 nM) and pentachlorophenol (IC50 = 6.3+/-3.8 nM) displaced [125I]T3 from qTTR more effectively than unlabeled T3 (IC50 = 9.7+/-0.9 nM) did. Although malathion, 4-nonylphenol, bisphenol A and n-butylbenzyl phthalate were effective inhibitors of [125I]T3 binding to qTTR, their potency was two orders of magnitude less than that of T3. All test chemicals except for diethylstilbestrol had either a weak or no effect on [125I]T3 binding to qTR LBD. These results show that several EDCs tested in this study target qTTR rather than qTR LBD.

Abstract  Undescended testis is a common finding in boys, and the majority of cases have no discernible aetiology. There are unexplained geographical differences and temporal trends in its prevalence. Cryptorchidism, especially bilateral, is associated with impaired spermatogenesis and endocrine function and increases the risk of testicular cancer. There is an urgent need to identify factors that adversely affect testicular development and optimize treatment. Conclusion: Cryptorchidism may reflect a primary testicular maldevelopment with long-term consequences.

Abstract  It has been speculated that maternal phthalate exposure may affect reproductive development in human newborns. However, the mechanism awaits further investigation. The aim is to evaluate the association between maternal phthalate exposure and cord sex steroid hormones in pregnant women and their newborns from the general population. A total of 155 maternal and infant pair were recruited and analyzed. Levels of urinary phthalate metabolites and sex steroid hormones were determined using liquid chromatography/electrospray tandem mass spectrometry (LC-ESI-MS/MS) and radioimmunoassay (RIA), respectively. No significant correlation was found between each steroid hormones and phthalate metabolites for male newborns, except MMP was marginally significantly correlated with E(2). After adjusting for maternal age, estradiol (E(2)) levels in cord serum from male newborns were not correlated with maternal urinary phthalate metabolites. In female newborns, the maternal urinary levels of mono-(2-ethylhexyl) phthalate (MEHP) and mono-(2-ethyl-5-hydroxyhexyl) phthalate (5OH-MEHP) were negatively correlated with the free testosterone (fT) and fT/E(2) levels in cord serum with Pearson correlation coefficients ranging between -0.24 and -0.29 (p<0.05). Additionally, after gestational age was adjusted, the maternal urinary level of DEHP was negatively correlated with the free testosterone (fT) and fT/E(2) levels in cord serum. We suggest that maternal exposure to phthalates may affect sex steroid hormones status in fetal and newborn stage.

Abstract  Some phthalates are developmental and reproductive toxicants in animals. Exposure to phthalates is considered to be potentially harmful to human health as well. Based on a comprehensive literature research, we present an overview of the sources of human phthalate exposure and results of exposure assessments with special focus on human biomonitoring data. Among the general population, there is widespread exposure to a number of phthalates. Foodstuff is the major source of phthalate exposure, particularly for the long-chain phthalates such as di(2-ethylhexyl) phthalate. For short-chain phthalates such as di-n-butyl-phthalate, additional pathways are of relevance. In general, children are exposed to higher phthalate doses than adults. Especially, high exposures can occur through some medications or medical devices. By comparing exposure data with existing limit values, one can also assess the risks associated with exposure to phthalates. Within the general population, some individuals exceed tolerable daily intake values for one or more phthalates. In high exposure groups, (intensive medical care, medications) tolerable daily intake transgressions can be substantial. Recent findings from animal studies suggest that a cumulative risk assessment for phthalates is warranted, and a cumulative exposure assessment to phthalates via human biomonitoring is a major step into this direction.

Abstract  A gas chromatographic method for the identification and quantification of n-octyl esters (from n-octyl tetradecanoate to n-octyl hexa-cosanoate including dioctyl hexanedioate) and phthalates [dibutyl phthalate, benzyl butyl phthalate and di(2-ethylhexyl) phthalate] in sediments and biota from estuarine environments is described. Standards used for identification and quantification of some n-octyl esters were synthesized. The method has allowed the analysis of these compounds in polychaeta (Nereis diversicolor), oysters (Crassostea angulata), crabs (Carcinus maenas) and fish (Chelon labrosus, Platichtys flesus and Chondostroma polylepis) that were collected at different locations of the Urdaibai estuary (Bizkaia, Basque Country, Spain). Total phthalates and n-octyl esters ranged between 0.01 and 12 microg g(-1) and 0.05 and 9.4 microg g(-1), respectively, and were predominantly found in polychaeta and fish. Sediments did not contain these compounds in significant amount, only benzyl butyl phthalate, dioctyl hexanedioate and di(2-ethylhexyl) phthalate were found above limit of detection (0.01-0.05 microg g(-1)).

Abstract  GC/MS determinations on six phthalic acid esters (PAEs) in Ipomoea aquatic grown on potted paddy soil fertilized with municipal sludge and chemical fertilizers showed that the total contents of PAEs (sigma PAEs) in Ipomoea aquatic aboveground parts ranged from 2.129 mg.kg-1 to 7.111 mg.kg-1, decreasing in order of Guangzhou sludge + fertilizers (7.111 mg.kg-1) > Guangzhou sludge (4.767 mg.kg-1) > Foshan sludge (3.569 mg.kg-1) > Foshan sludge + fertilizers (3.305 mg.kg-1) > fertilizers (2.638 mg.kg-1) > control (2.129 mg.kg-1), indicating that compared with control, fertilization increased sigma PAEs in Ipomoea aquatica to a different extent. Only certain compounds of PAEs in different treatments of Ipomoea aquatica were dominant, e.g., butylbenzyl phthalate (BBP) in control, chemical fertilizers, Foshan sludge, and Guangzhou sludge accounted for 40% to 80% of sigma PAEs, di-n-butyl phthalate(DnBP) in foshan sludge + chemical fertilizers accounted for 56%, while di-n-octyl phthalate(DnOP), di(2-ethylhexyl)phthalate(DEHP) and BBP in Guangzhou sludge + chemical fertilizers accounted for approximately 30%. sigma PAEs and the contents of its most compounds were higher in the plants of Ipomoea aquatica than in its roots to a different extent.

Abstract  The sonochemical degradation of aqueous solutions containing low concentrations of six phthalate esters at an ultrasonic frequency of 80 kHz has been investigated. Ultrasonic treatment was found capable of removing the four higher molecular mass phthalates (di-n-butyl phthalate, butylbenzyl phthalate, di-(2-ethylhexyl) phthalate and di-n-octyl phthalate) within 30-60 min of irradiation. The rest (dimethyl phthalate and diethyl phthalate) were more recalcitrant and nearly complete removal could be achieved only after prolonged irradiation times. The relative reactivity of phthalates was explained in terms of their hydrophobicity. Experiments were carried out at an overall initial phthalate concentration of 240 microg l(-1), values of electric power of 75 and 150 W, temperatures of 21 and 50 degrees C and in the presence of NaCl to study the effect of various operating conditions on degradation. Solid-phase microextraction (SPME) coupled with GC-MS proved to be a powerful analytical tool to monitor the sonochemical degradation of phthalate esters at low microg l(-1) concentration levels, minimising the risk of secondary contamination during sample preparation, a major parameter to consider during phthalates analysis. The advantages as well as disadvantages of using SPME are also highlighted.

Abstract  Researchers have recently reported on the nongenomic action of estrogen via membrane receptors and ion channels, especially nicotinic acetylcholine receptors (nAChR). We studied the nongenomic effects of eight phthalates (an endocrine disrupter that expresses estrogen-like activity through estrogen receptors): di-n-ethyl (DEP), di-n-propyl (DPrP), di-n-butyl (DBP), benzyl-n-butyl (BBP), di-n-pentyl (DPP), di-n-hexyl (DHP), dicyclohexyl (DCHP), and di-(2-ethylhexyl) (DEHP). Specifically, we looked at their individual effects on cytosolic free calcium concentration rise induced by three nAChR agonists: carbachol, 1,1-dimethyl-4-phenyl-piperazinium iodide, and epibatidine. Results show that all of the tested phthalates suppressed nAChR-coupled Ca(2+) response. Strongest to weakest potencies were observed as DPP --> BBP --> DBP --> DCHP --> DHP --> DPrP --> DEHP --> DEP. DPP, DBP, and BBP were 10 times more potent than estradiol. We suggest that phthalate potency was associated with its chemical structure, since (a) the most effective phthalates had dialkyl group carbon numbers of C4 or C5, with shorter or longer numbers resulting in decreased potency, and (b) the presence of an alkyl ring or phenoic structure resulted in increasing potency. Because of the similarity between this relationship and estrogen receptor-binding potency, we suggest that the inhibitory effect of phthalates on nAChR-coupled Ca(2+) response is an indication of their nongenomic estrogen-like activity.

Abstract  Compared to yeast esterase, fungal cutinase degraded butyl benzyl phthalate (BBP) far more efficiently; i.e., almost 60% of the BBP disappeared within 7.5 h. Also, the final chemical composition significantly depended on the enzyme used. Toxicity monitoring using bioluminescent bacteria showed that butyl methyl phthalate, a major product of degradation by esterase, was an oxidative toxic hazard.

Abstract  Environmental chemicals with inherent estrogenic activity are supposed to be responsible for the decrease of quantity and quality of human sperms during the past 40 years. The current hypothesis is that estrogenic agents acting during fetal life may lead to impaired development of the testes and of the male reproductive tract in the human as well as in several wildlife species. However, from clinical and experimental data it is known, that estrogens may also lead to impairment of female reproductive functions. Perinatal application of DDT, octylphenol and benzylbutylphthalate resulted in persistent estrus in rats, in- and subfertility, respectively, and impaired sexual behaviour. Epidemiological and experimental data speak in favour of environmental estrogens to be one cause for the development of polycystic ovaries, being the most important reason for female infertility in the human.

Abstract  The plasma sex steroid-binding protein (SBP) is believed to be involved in regulating circulating endogenous sex steroids as well as cellular signal transduction to nuclear steroid receptors in sex steroid-sensitive tissues. In this study, a variety of estrogen mimics (EMs), which may contribute to the endocrine disrupting effects observed in fish, were tested for the ability to interact with the rainbow trout plasma sex steroid-binding protein (rtSBP) either singly or in binary combinations. The EMs ethynylestradiol, diethylstilbestrol, 4-hydroxytamoxifen, genistein, zearalenone, 4-t-octylphenol, bisphenol A and o,p'-DDT were all able to displace 1,2,4,6,7-[3H]estradiol from the sex steroid-binding site at the rtSBP (K(d)=2.1+/-0.5 nM, B(max)=2963+/-303 fmol estradiol/mg protein) in a dose-dependent and competitive manner. The plastizicer n-butyl benzyl phthalate only displayed weak binding affinity for the rtSBP, whereas the pesticide dieldrin was not able to compete for the high affinity estradiol-binding sites in plasma. None of the compounds tested was able to clearly promote the binding of the others when given in combination, indicating that synergy did not occur at the ligand-SBP binding level. The rtSBP binding affinity for EMs ranged over several orders of magnitude, but were consistently lower than those for the endogenous sex steroids (about 10(2)-10(6) less potent). The results suggest that the presence of rtSBP may potentially modulate the bioavailability of EMs to estrogen receptors relative to each other and to the endogenous sex steroids themselves. Since the binding of the endogenous ligands is reversible, SBP-bound estrogens (or androgens) potentially may also become displaced by potent EMs.

Abstract  The effects of ten endocrine disrupting chemicals, i.e., bisphenol A (BPA), p-nonylphenol (NP), p-octylphenol (OP), p-pentylphenol (PP), butyl benzyl phthalate (BBP), dicyclohexyl phthalate (DCHP), di-n-butyl phthalate (DBP), tetrabutyltin (TBT), tri-n-butyltin chloride (TBC), and di-n-butyltin dichloride (DBD), as well as 17 beta-estradiol (E(2)) as a positive control on the microtubule network in Chinese hamster V79 cells in culture were examined by the indirect immunofluorescence method using anti-beta-tubulin antibody. In the whole-animal system, the effects of BPA, NP, OP, BBP, DBD, and E(2) as well as vinblastine sulfate (VB) as a positive control on microtubules in the cytoplasm of Sertoli cells in rats were examined by electron microscopy. In Chinese hamster V79 cells, TBC and DBD showed higher microtubule-disruptive activity than E(2), while other chemicals had less activity than E(2). The ranking for efficiency on microtubule disruption was (TBC falling dots DBD) > (E(2) = TBT) > (BPA = alkylphenols, NP and OP) > (phthalate esters, BBP, DHP, and DBP). In rats as a whole-animal system, no disrupting effects on the microtubule network in the cytoplasm of Sertoli cells were observed under any environmental chemicals tested, whereas exposure to VB resulted in marked disruption of the microtubule network. The results of this study suggested that some endocrine disrupting chemicals have disrupting effects on the microtubule network in vitro, but no such effects in vivo.

Abstract  The objective of this study was to characterize recovered soil fines from construction and demolition (C&D) waste recycling facilities for trace organic pollutants. Over a period of 18 months, five sampling trips were made to 14 C&D waste recycling facilities in Florida. Screened soil fines were collected from older stockpiles and newly generated piles at the sites. The samples were analyzed for the total concentration (mg/kg) of a series of volatile organic compound (VOCs) and semi-volatile organic compounds (semi-VOCs). The synthetic precipitation leaching procedure (SPLP) test was also performed to evaluate the leachability of the trace organic chemicals. During the total analysis only a few volatile organic compounds were commonly found in the samples (trichlorofluoromethane, toluene, 4-isopropyltoluene, trimethylbenzene, xylenes, and methylene chloride). A total of nine VOCs were detected in the leaching test. Toluene showed the highest leachability among the compounds (61.3-92.0%), while trichlorofluoromethane, the most commonly detected compound from both the total and leaching tests, resulted in the lowest leachability (1.4-39.9%). For the semi-VOC analysis, three base-neutral semi-VOC compounds (bis(2-ethylhexyl)phthalate, butyl benzyl phthalate, and di-n-butyl phthalate) and several PAHs (acenaphthene, pyrene, fluoranthene, and phenanthrene) were commonly detected in C&D fines samples. These compounds also leached during the SPLP leaching test (0.1-25%). No acid extractable compounds, pesticides, or PCBs were detected. The results of this study were further investigated to assess risk from land applied recovered soil fines by comparing total and leaching concentrations of recovered soil fines samples to risk-based standards. The results of this indicate that the organic chemicals in recovered soil fines from C&D debris recycling facilities were not of a major concern in terms of human risk and leaching risk to groundwater under reuse and contact scenarios.

Abstract  A gas chromatography/mass spectrometry method for the simultaneous quantitative determination of natural and synthetic estrogens (17beta-estradiol, estrone, 17alpha-ethinylestradiol, and mestranol), phytoestrogens (genistein and beta-sitosterol), and xenoestrogens (benzyl butyl phthalate, dibutyl phthalate, bisphenol A, 4-nonylphenol [NP], 4-nonylphenoxyacetic acid [NP1EC], 4-nonylphenol diethoxylate [NP2EO], and alpha-endosulfan) in effluents of sewage treatment plants (STPs) was developed. Identification and quantification were carried out with the standard addition method using analyte-specific and, in some cases, deuterium-labeled internal standards. The effluents of 18 STPs were investigated. Apart from alpha-endosulfan and mestranol, all selected substances were detected in the majority of samples. The median concentrations of steroidal estrogens were between 0.4 ng/L (17alpha-ethinylestradiol) and 1.6 ng/L (17beta-estradiol). The metabolites of the nonylphenol polyethoxylates, NP, NPIEC, and NP2EO were found in concentrations ranging from the upper-ng/L-range (NP) to the lower-microg/L range (NP1EC). For all substances except mestranol and alpha-endosulfan, median values were calculated and compared to the results of other investigations in Europe and the United States. Possible dependencies of measured concentrations on the geographical location, the capacity, the influent composition, and the technical fitting of the STPs are discussed.