			Home About us Contact

Benzyl Butyl Phthalate (benzyl + butyl_phthalate)

Distribution by Scientific Domains

Medical Sciences	50%
Life Sciences	50%

Selected Abstracts

Substances with estrogenic activity in effluents of sewage treatment plants in southwestern Germany.

ENVIRONMENTAL TOXICOLOGY & CHEMISTRY, Issue 10 2001

Abstract A gas chromatography/mass spectrometry method for the simultaneous quantitative determination of natural and synthetic estrogens (17,-estradiol, estrone, 17,-ethinylestradiol, and mestranol), phytoestrogens (genistein and ,-sitosterol), and xenoestrogens (benzyl butyl phthalate, dibutyl phthalate, bisphenol A, 4-nonylphenol [NP], 4-nonylphenoxyacetic acid [NP1EC], 4-nonyl-phenol diethoxylate [NP2EO], and ,-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 ,-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 (17,-ethiny-lestradiol) and 1.6 ng/L (17,-estradiol). The metabolites of the nonylphenol polyethoxylates, NP, NP1EC, and NP2EO were found in concentrations ranging from the upper-ng/L-range (NP) to the lower-,g/L range (NP1EC). For all substances except mestranol and ,-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. [source]

A mixture of seven antiandrogens induces reproductive malformations in rats

INTERNATIONAL JOURNAL OF ANDROLOGY, Issue 2 2008
Cynthia V. Rider
Summary To date, regulatory agencies have not considered conducting cumulative risk assessments for mixtures of chemicals with diverse mechanisms of toxicity because it is assumed that the chemicals will act independently and the individual chemical doses are not additive. However, this assumption is not supported by new research addressing the joint effects of chemicals that disrupt reproductive tract development in the male rat by disrupting the androgen signalling pathway via diverse mechanisms of toxicity [i.e. androgen receptor (AR) antagonism in the reproductive tract vs. inhibition of androgen synthesis in the foetal testis]. In this study, pregnant rats were exposed to four dilutions of a mixture containing vinclozolin, procymidone, linuron, prochloraz, benzyl butyl phthalate, dibutyl phthalate and diethylhexyl phthalate during the period of sexual differentiation and male offspring were assessed for effects on hormone sensitive endpoints including: anogenital distance, infant areolae retention and reproductive tract tissue weights and malformations. The ratio of the chemicals in the mixture was based upon each chemical's ED50 for inducing reproductive tract malformations (hypospadias or epididymal agenesis). The observed responses from the mixture were compared with predicted responses generated with a toxic equivalency approach and models of dose addition, response addition or integrated addition. As hypothesized, we found that the mixture of chemicals that alter the androgen signalling pathway via diverse mechanisms disrupted male rat reproductive tract differentiation and induced malformations in a cumulative, dose-additive manner. The toxic equivalency and dose addition models provided the best fit to observed responses even though the chemicals do not act via a common cellular mechanism of action. The current regulatory framework for conducting cumulative risk assessments needs to consider the results, including those presented herein, which indicate that chemicals that disrupt foetal tissues during sexual differentiation act in a cumulative, dose-additive manner irrespective of the specific cellular mechanism of toxicity. [source]

Determination of phthalate esters in cosmetics by gas chromatography with flame ionization detection and mass spectrometric detection

INTERNATIONAL JOURNAL OF COSMETIC SCIENCE, Issue 4 2005
Huiming Chen
GC-FID; GC-MS; Produits cosmétiques; Esters Phtaliques Synopsis A gas chromatography coupled with flame ionization detection (GC-FID) and mass spectrometric detection (MSD) method was developed to determine the six kinds of phthalate esters [dimethyl phthalate (DMP), diethyl phthalate (DEP), di- n -butyl phthalate (DBP), benzyl butyl phthalate (BBP), di(2-ethylhexyl) phthalate (DEHP) and di- n -octyl phthalate (DOP)] in cosmetics (solid, cream and liquid cosmetics). The cosmetics were extracted with methanol by ultrasonic and then separated with high-speed centrifugation. The upper clear layer was dried and filtered through a 0.45 ,m pore diameter filter. The filtrate was injected into GC-FID/GC-MS for detection. GC-FID chromatogram was applied for qualitative analysis, external standard method was used for quantitative analysis. Confirmation of phthalate presence was undertaken by GC-EI-MS. The recovery range of all phthalates were between 92.0 and 110.0% with relative standard deviations between 1.95 and 5.92%. The low detection limits of the method were: 0.1 ng for DMP, DEP, DBP and BBP, 0.5 ng for DEHP and DOP. The method had advantages of high precision and sensitivity, simplicity of pretreatment. The method can be used to test the six kinds of phthalate esters in cosmetics. Resume Une méthode d'analyse par chromatographie gazeuse couplée à une détection par ionization de flamme (GC - FID) et une détection spectrométrique de masse (MSD) a été développée pour analyser 6 sortes d'esters phtaliques (phtalate de diméthyle (DMP), phtalate de diéthyle (DEP), phtalate de di- n -butyle (DBP), phtalate de benzylbutyle (BBP), phtalate de di-2-éthylhexyle (DEHP) et phtalate de di- n -octyle (DOP)) dans des produits cosmétiques (solides, crèmes et liquides). Les produits cosmétiques sont extraits au méthanol sous ultrason, puis séparés par ultracentrifugation. La phase supérieure limpide est déshydratée et filtrée sur un filtre de diamètre de pore moyen égal à 0,45 ,m. Le filtrat est injecté dans le système GC - FID/GC-MS pour analyse. Les chromatogrammes GC-FID sont utilisés pour l'analyse qualitative, des standards externes ont été utilisés pour l'analyse quantitative. La GC-EI-MS permet de confirmer la présence des esters phtaliques. Le taux de récupération de tous les esters est compris entre 92 et 110% avec une déviation standard allant de 1,95%à 5,92%. La limite de détection par cette méthode est de 0,1 ng pour DMP, DEP, DBP et BBP, 0,5 ng pour DEHP et DOP. Les avantages de cette méthode sont sa haute précision, sa sensibilité et la simplicité du prétraitement. Cette méthode peut être utilisée pour doser la présence des six sortes d'esters phtaliques dans des produits cosmétiques. [source]

Involvement of p53 in phthalate effects on mouse and rat osteoblasts,

JOURNAL OF CELLULAR BIOCHEMISTRY, Issue 2 2009
M.G. Sabbieti
Abstract The role of two estrogen-mimicking compounds in regulating osteoblast activities were examined. Previously, our attention was focused on benzyl butyl phthalate (BBP) and di- n -butyl phthalate (DBP) since previous works showed that they enter the cytoplasm, bioaccumulate, modify actin cytoarchitecture and exert mitogenic effects involving microfilament disruption, and nuclear actin and lamin A regulation in Py1a rat osteoblasts. In this study we showed that BBP and DBP cause DNA base lesions both in MT3T3-E1 osteoblasts and in mouse primary calvarial osteoblasts (COBs). In addition, treatment with the above effectors caused an increase of p53 and phospho-p53 (ser-15 and ser-20) as well as an increase of apoptotic proteins with consequent decrease of cell viability. Moreover, treatment with phthalates did not modified p53 and phospho-p53 expression in Py1a rat osteoblasts. It is of relevance that in p53 knockdown mouse osteoblasts a proliferative effect of phthalates, similar to that observed in rat Py1a osteoblasts, was found. In conclusion, our data demonstrated that phthalates induce osteoblast apoptosis, which is, at least in part, mediated by p53 activation, suggesting that the proliferative effects could be due to p53 missing activation or p53 mutation. J. Cell. Biochem. 107: 316,327, 2009. © 2009 Wiley-Liss, Inc. [source]