Abstract  14C-Di-2-ethylhexyl and 14C-diethyl phthalates were administered intraperitoneally to pregnant rats on either Day 5 or 10 of gestation. Rats were sacrificed at 24-hr intervals starting on Days 8 and 11, respectively; maternal blood, fetal tissue, amniotic fluid, and placentas (whenever possible) were obtained. The 14C-activity of each sample was determined by scintillation counting. It was found that both diesters and/or their metabolic products were present in each of these compartments throughout the gestation period, thus suggesting that the embryo-fetal toxicity and teratogenesis reported previously could be the results of a direct effect of the compound (or its metabolites) upon developing embryonic tissue. Additionally, the reduction in concentration of 14C from these tissues as a function of time was found to fit a first-order excretion curve. From this model curve, the half-life for both compounds was calculated; the average was about 2.33 days for di-2-ethylhexyl phthalate and 2.22 days for diethyl phthalate.

Abstract  Deodorants are one of the most frequently-used types of cosmetics and are a source of allergic contact dermatitis. Therefore, a gas chromatography - mass spectrometric analysis of 71 deodorants was performed for identification of fragrance and non-fragrance materials present in marketed deodorants. Furthermore, the sensitizing potential of these molecules was evaluated using structure activity relationships (SARs) analysis. This was based on the presence of 1 or more chemically reactive site(s), in the chemical structure, associated with sensitizing potential. Among the many different substances used to formulate cosmetic products (over 3500), 226 chemicals were identified in a sample of 71 deodorants. 84 molecules were found to contain at least 1 structural alert, and 70 to belong to, or be susceptible to being metabolized into, the chemical group of aldehydes, ketones and alpha,beta-unsaturated aldehydes, ketone or esters.

Abstract  Rate constants for reactions of the hydroxyl radical with 25 potential organic drinking water contaminants, including solvents, haloalkanes, esters, aromatics, and pesticides for example, aldicarb, atrazine, 1,2-dibromo-3-chloropropane, endrin, glyphosate, haloforms, lindane, picloram, etc.), have been measured in water using relative rate methods. A variety of HO.-generating techniques were used, including ozone decomposition, Fenton's reaction, and a convenient new method employing photo-Fenton's s chemistry. In addition, rate constants for 19 other compounds were estimated using structure-activity relationships. The present results are consistent with previous work that demonstrated that HO. is a relatively nonselective radical toward C-H bonds, but is least reactive with aliphatic polyhalogenated compounds. Olefins and aromatics all react at nearly diffusion-controlled rates in water, unlike the case in the gas phase where these compounds react more selectively. The rate constants are useful in estimating HO.-induced oxidation rates of organic compounds in a variety of aqueous systems including atmospheric water droplets, sunlit surface waters, supercritical and near-critical water reactors, and room temperature radical oxidation processes.

Abstract  Ozonation by‐products were analyzed for two surface water sources in Southern California—Los Angeles Aqueduct Water (LAAW) and State Project Water (SPW). Included are data obtained when LAAW was being treated at the Los Angeles Aqueduct Filtration Plant and similar data obtained during a two‐day experiment in which the plant was treating SPW. Some batch‐scale ozonation studies are also reported. Ozonation by‐products were monitored using three methods: closed‐loop stripping analysis, nonionic resin accumulation, and a direct aqueous derivatization method for low‐molecular‐weight aldehydes, each followed by gas chromatography–mass spectrometry analysis of the extracts. The major neutral by‐products appear to be aliphatic aldehydes, but the levels are unexpectedly low in SPW compared with LAAW treated under similar conditions. Low levels of several other compounds were found in ozonated water, including bromoform and some compounds tentatively identified as ketones.

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  In this study, we hypothesized that many of the reported effects of phthalate esters and other peroxisome proliferators (PPs) in the testis are mediated by members of the PP- activated receptor (PPAR) family of transcription factors through alterations in proteins involved in steroidogenesis. Exposure of Leydig cells to PPs prevented cholesterol transport into the mitochondria after hormonal stimulation and inhibited steroid synthesis, without altering total cell protein synthesis or mitochondrial and DNA integrity. PPs also reduced the levels of the cholesterol-binding protein peripheral-type benzodiazepine receptor (PBR) because of a direct transcriptional inhibition of PBR gene expression in MA-10 Leydig cells. MA-10 cells contain mRNAs for PPARalpha and PPARbeta/delta, but not for PPARgamma. In vivo treatment of mice with PPs resulted in the reduction of both testis PBR mRNA and circulating testosterone levels, in agreement with the proposed role of PBR in steroidogenesis. By contrast, liver PBR mRNA levels were increased, in agreement with the proposed role of PBR in cell growth/tumor formation in nonsteroidogenic tissues. However, PPs did not inhibit testosterone production and testis PBR expression in PPARalpha-null mice. These results suggest that the antiandrogenic effect of PPs is mediated by a PPARalpha-dependent inhibition of Leydig cell PBR gene expression.

Abstract  The absorption of undiluted phthalate diesters [dimethyl phthalate (DMP), diethylphthalate (DEP), dibutyl phthalate (DBP) and di-(2-ethylhexyl)phthalate (DEHP)] has been measured in vitro through human and rat epidermal membranes. Epidermal membranes were set up in glass diffusion cells and their permeability to tritiated water measured to establish the integrity of the skin before the phthalate esters were applied to the epidermal surface. Absorption rates for each phthalate ester were determined and a second tritiated water permeability assessment made to quantify any irreversible alterations in barrier function due to contact with the esters. Rat skin was consistently more permeable to phthalate esters than the human skin. As the esters became more lipophilic and less hydrophilic, the rate of absorption was reduced. Contact with the esters caused little change in the barrier properties of human skin, but caused marked increases in the permeability to water of rat skin. Although differences were noted between species, the absolute rates of absorption measured indicate that the phthalate esters are slowly absorbed through both human and rat skin.

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  It is important to know both the emission and the sorption behavior of materials when constructing or renovating buildings in order to avoid material related indoor climate problems. With a general, low-cost test method, the sink effect of materials under normal conditions can be incorporated as information in an indoor climate labeling system for materials. Reconditioned samples of waterborne paint applied on tinned steel plates and carpet were placed in small test chambers at a controlled air exchange rate and mean air velocity. The sorption behavior of the materials was studied, while ambient air from a recently renovated office environment was passed through the chambers. The desorption of VOCs from the test samples was analyzed chemically and by sensory evaluation. The results showed a correlation between the chamber concentration in the desorption phase expressed as the percentage of the concentration in the office air and the gas chromatographic retention times of the VOCs (using a semipolar column). The results are used to propose a general test method for assessing the sink effects of materials used in the indoor environment. A mixture of pollutants with affinities to indoor surfaces is proposed for adsorption testing under controlled environmental conditions. A mathematical model of the distribution of emitted VOCs between indoor air and sinks is proposed. It is possible to calculate the impact of the sinks on the indoor air quality by comparison within door relevant thresholds for odor and mucous membrane irritation.

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  The testicular effects produced by di(2-ethylhexyl) phthalate (DEHP) in the rat, characterized by a decrease in the relative organ weight and histological changes in the seminiferous tubules, can also be produced by di-n-butyl, di-n-pentyl and di-n-hexyl phthalates. The corresponding monoesters of these compounds, formed in vivo as a result of the action of nonspecific esterases in the intestinal mucosa and other tissues, were equally effective in inducing testicular damage. Phthalate-induced testicular injury was accompanied by a decrease in the zinc content in the gonads and in increased urinary excretion of this element. Exposure of preparations of rat seminiferous tubule cells in culture to monophthalates capable of producing testicular injury resulted in a dose-related detachment of germinal cells from Sertoli cells in a manner similar to the effect seen in the intact animal. This in vitro system may find application in the elucidation of the toxic mechanisms involved in phthalate-induced testicular injury and in screening compounds likely to act in a manner similar to phthalates.

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  Three kinds of particulate matter were collected: diesel and gasoline exhaust particles emitted directly from exhaust nozzle, and suspended particulate matter (SPM) near the traffic route. Soxhlet extraction was performed on each sample. By gas-chromatograph–mass spectrometer (GC–MS) analysis of these extracts, di-ethyl phthalate and di-n-butyl phthalate were detected from the extract of SPM and diesel exhaust particles (DEPs). Because these phthalates were sometimes suspected as contamination, time-of-flight secondary ion mass spectrometry (TOF-SIMS) measurements were also performed on the samples collected at the same environment. By comparing obtained spectra, it is clear that these environmental endocrine disrupters (EEDs) were adsorbed on DEP surface. Thus, we concluded that the combination of conventional method and TOF-SIMS measurement is one of the most powerful techniques for analyzing the toxic air pollutants adsorbed on SPM surface.

Abstract  BIOSIS COPYRIGHT: BIOL ABS. Some data on a newly developed filter/sorbent indoor air SVOC sampling device for thermal desorption analysis are described. Thermal desorption of SVOCs spiked on Tenax had response factors identical to on-column injection except for highly polar compounds like fatty acids. SVOCs spiked on quartz fiber filters had for non-oxygen compounds). Low nanogram on-tube amounts of lower desorption efficiency. In addition, it was indicated that the "memory" effect was an important source of background contaminations that might impair analysis of low nanogram on-tube amounts of some SVOCs. Polar SVOCs in the gas phase appear to adsorb to the quartz fiber filters. This functions as a precleaning of the sample and thus minimizes the problem with coeluting peaks. The relative standard deviations of air concentrations of 10 SVOCs in an office estimated from nine duplicate samples appeared to be sufficiently low to distinguish a day to day variation.

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  Effects of polyvinyl-chloride (9002862) (PVC) resins and their additives on human serum protein, guinea-pig complement, blood grouping antibodies (neutral and immune), human erythrocytes, tissue cultures, and developing chick embryos were studied. Additives included 46 heat stabilizers, 45 plasticizers, and 5 PVC resins. A total of 120 finished products was prepared from these ingredients. Various components had adverse reactions, and some which were used for finished plastics had no adverse effects. In general, many of the heat stabilizers and inhibitors with heavy metals had a destructive effect on guinea-pig complement. Among finished plastics those containing dimethylphthalate (131113), dibutyl-suberate (16090770), dimethyl-sebacate (106796), and butyl-oleate (142778) produced toxic changes in human red blood cells. Dibutyl-suberate and some phthalates also interfered with the blood grouping antibodies. Phthalates were found to produce reduced hatch rates, neurological abnormalities, and increased chick mortality. The data indicated possible harmful qualities of certain plastics components on stored biological material, such as serum proteins, red blood cells, and antiserum. The authors conclude that plastics used for containers, dispensers, and closures for biological products must be composed of ingredients that will not damage the product during storage.

Abstract  Phthalate esters with short alkyl chains, such as di-ethyl (DEP), di-n-propyl (DPP), and di-butyl phthalate (DBP), have adjuvant effects on an FITC-induced contact hypersensitivity mouse model. The adjuvant effects of DPP and DBP are associated with enhanced trafficking of FITC-presenting CD11b(+) dendritic cells (DC). DEP has relatively weak activity as to FITC-positive cell migration. Here we demonstrated that DBP and DPP also increased the number of FITC-positive CD8alpha(+) DC in draining lymph nodes. We also found enhanced production of interleukin-4 in draining lymph nodes after FITC sensitization with DEP, DPP, or DBP, suggesting an additional adjuvant mechanism of phthalate esters.

Abstract  This study was undertaken to observe the type of interaction that exists between polychlorinated biphenyls (Clophen A60) and diethyl phthalate (DEP) on the adrenal and thyroid glands of male and female Wistar rats. Animals were divided into four groups of six animals each, group I male and female rats were fed on a normal diet and water ad libitum. Groups II, III and IV male and female rats were given Clophen A60, DEP, or mixture of Clophen A60 and DEP, respectively, each dissolved in corn oil mixed with the diet at 50mg/kg of the diet/day. One hundred days after treatment, females were mated with males for 10 days. Exposure to the pollutants was continued throughout mating, gestation (21 days) until termination at weaning (21 days), which was 150 days of total treatment period of the parental generation. When the F1-generation pups (six males and six females of each group) were 75-100g in weight, they were treated in a similar manner to the parental generation, again for a period of 150 days, with the dose reduced to 25mg/kg of the diet/day in all treated groups. After 150 days of treatment, animals were sacrificed and histology of the adrenal and thyroid glands was asessed. An antagonistic interactive effect of treatment was seen in male parental and F1-generation rats, while an inhibitory type of interactive effect was observed in female rats. In the zona fasciculata region of the adrenal cortex of treated rats of both generations, vacuolations and degeneration were seen in samples from male animals and intracellular vacuolations in samples from females. A synergistic interactive toxic effect to the thyroid gland was observed in treated parental generation male rats, and mild changes in F1-generation-treated male rats, showing follicular shrinkage, loss of thyroglobulin and fibrosis of the interfollicular epithelium. In females, an antagonistic effect to the thyroid gland was observed in both parental and F1-generation-treated rats, showing similar effects as observed in males. From this study, we can conclude that combined administration of Clophen A60 and DEP shows an enhanced toxic effect on adrenal glands of F1-generation male and female rats, but the effect is much more marked in the thyroid gland of F1-generation male rats, and seen to a lesser extent in F1-generation female rats.

Abstract  A method has been developed for the separation and determination of dimethyl phthalate (DMP), diethyl phthalate (DEP), di-n-butyl phthalate (DBP), di-(2-ethylhexyl) phthalate (DEHP) and di-n-octyl phthalate (DnOP) by micellar electrokinetic chromatography (MEKC). The baseline separation of phthalates was achieved by using a buffer of 100 mM sodium cholate, 50 mM borate and 15% methanol (pH 8.5). The optimized MEKC method was used to quantify the concentrations of phthalates in 11 soil samples from different regions of China. The contents of DEP, DBP and DEHP in soils were ranged 0-0.42, 0-1.43, and 0.24-2.35 mg/kg, respectively, and no DMP and DnOP was detected. The limits of detection for DMP, DEP, DBP, DEHP, and DnOP were found to be 0.050, 0.051, 0.052, 0.054, and 0.063 mg/kg, respectively. The results obtained by the MEKC method were compared with those obtained by gas chromatography with flame ionization detector (GC-FID), and a good agreement was achieved.

Abstract  A previous in vitro study has indicated that four phthalate esters (PAEs) could damage hemocytes and decreases the cellular immunity of prawns [Sung, H.H., Kao, W.Y., Su, Y.J., 2003. Effects and toxicity of phthalate esters to hemocytes of giant freshwater prawn, Macrobranchium rosenbergii. Aquat. Toxicol. 64, 25-37]. The aim of this study was to investigate the in vivo effect of four PAEs, diethyl phthalate (DEP), dihexyl phthalate (DHP), dipropyl phthalate (DPrP) and diphenyl phthalate (DPP) on the defense system of the giant freshwater prawn, M. rosenbergii. PAE dissolved in corn oil was continuously fed to prawns for 8 days and five immune parameters (total hemocyte count, THC; ratio of granulocytes to hyalinocytes, G/H; intrahemocytic total phenoloxidase activity, PO(T); intracellular superoxide anion (O2-) production; transglutaminase (TGase) activity) were separately detected on days 1, 4 and 8. In addition, mortality was determined on days 4 and 8 after challenging the prawns with Lactobacillus garvieae. In comparison with untreated prawns, the results showed that DHP demonstrated the lowest toxicity in that it only influenced the PO activity and O2- production before 4 days after treatment and caused 6.6% mortality on day 8. DEP decreased G/H, PO(T) and TGase activity on day 1 and reduced THC, G/H and PO(T) and caused 16.6% mortality on day 4; however, on day 8, it increased O2- production and caused no mortality. In the DPrP-treated group, a reduction of all the immune reactions apart from TGase activity and 22.2% mortality were detected on day 4. As for the effect of DPP, results showed that it decreased all the immune parameters apart from THC on days 1 and 4, but caused no mortality on day 4; but on day 8, an increase of O2- production and 17.7% mortality were detected. These results indicated that the immune reactions of prawns were variable due to the different toxic effects of PAEs. In addition, it was found that, on day 8 after treatment, the three PAEs, DHP, DPrP and DPP increased O2- production and did not influence the other four reactions, but mortality was detected in these groups. These results suggest that other physiological responses may also be affected to increase the susceptibility of prawns to pathogens.

Abstract  A routine method which is simple, quick and precise has been set up and validated for phthalate analysis in environmental samples (tomato plants and sewage sludges). Six phthalates have been studied simultaneously: dimethylphthalate, diethylphthalate, di-n-butylphthalate, n-butylbenzylphthalate, di-2-ethyl-hexyl phthalate (DEHP) and di-n-octylphthalate. Optimization of sample, solvent extraction uses a Soxtec apparatus and extract purification with an a solid-phase extraction cartridge allows between 90 and 110% recovery of phthalates. Precise, sensitive and selective identification and quantifying of analytes is by GC-MS in the single ion monitoring mode. This protocol allows analytes with concentrations as low as 10 microg/kg dry matter (DM) to be determined from small (1-2 g DM) samples. This analytical method has been applied to the phthalate transfer study for agricultural recycling of sludges, where phthalate bioavailability has been studied in aquiculture using two types of experiments. Tomatoes have been grown in containers where the trace organics have been directly introduced as pure substances, and in a second experiment under the same growth conditions, sewage sludge has replaced the pure substances. Transfer of these trace organics has been followed into the various parts of the tomato plant and in general only the DEHP is worthy of note although its percentage transfer remains very low even in an experiment designed to maximize this.

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.