PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Phthalic Acids”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources
PubMed1986

Phthalic acid excretion as an indicator of exposure to phthalic anhydride in the work atmosphere.

The concentration of phthalic acid was determined in the urine of nine subjects occupationally exposed to phthalic anhydride. For the determination, the urine samples were acidified, extracted with dimethyl ether, esterified with boron trifluoride/methanol and measured by electron capture gas chromatography. Environmental air samples were collected in Tenax tubes, eluted with methyl-t-butyl ether and assayed by electron capture gas chromatography. Significant correlations were found between the concentration in urine samples (range: 0.3-14.0 mumol/mmol creatinine), collected at different times of the day, and the time-weighed average atmospheric concentrations (range: 0.03-10.5 mg/m3). No conjugation of phthalic acid in the urine was observed. The detection limit for urine samples (10 ml) was 0.05 mumol/l) and that for air samples 0.4 microgram/m3. The method has potential for biological monitoring of workers exposed to phthalic anhydride. It was found that at atmospheric anhydride concentrations of about 30% of the hygienic reference value (6 mg/m3), which is applied in many market economies, a body-burden was caused which was not eliminated overnight.

Body Burden↗
PubMed1977

Asthma due to inhaled chemical agents--epoxy resin systems containing phthalic acid anhydride, trimellitic acid anhydride and triethylene tetramine.

Six workers with a diagnosis of occupational asthma and one with chronic bronchitis were examined for sensitivity to epoxy resin systems and certain of their components. In six cases the chemical agent responsible for their symptoms was identified by careful inhalation challenge testing, simulating their exposure at work and thus providing a precise aetiological diagnosis. In one worker asthma followed exposure to triethylene tetramine fume; four were sensitive to acid anhydrides, three to phthalic acid anhydride as a fume or powder and one to trimellitic anhydride. On worker thought to be sensitive to toluene di-isocyanate gave negative reactions to this and positive reactions to a phthalic acid anhydride epoxy resin and another thought to have asthma from acid anhydride fumes was found to be sensitive only to toluene di-isocyanate. Immediate, non-immediate or combined asthmatic reactions were elicited.

Adult↗
PubMed1976

Biodegradation of phthalic acid esters in river water and activated sludge.

The primary and ultimate biodegradability of phthalic acid, monobutyl phthalate, and five structurally diverse phthalic acid ester plasticizers in river water and activated sludge samples were determined via ultraviolet spectrophotometry, gas chromatography, and CO2 evolution. The compounds studied underwent rapid primary biodegradation in both unacclimated river water and acclimated activated sludge. When activated sludge acclimated to phthalic acid esters was used as the inoculum for the CO2 evolution procedure, greater than 85% of the total theoretical CO2 was evolved. These studies demonstrate that the phthalic acid ester plasticizers and intermediate degradation products readily undergo ultimate degradation in different mixed microbial systems at concentrations ranging from 1 to 83 mg/liter.

Bacteria↗
PubMed1992

Phthalic acid dermatitis caused by an organostannic compound, tributyl tin phthalate.

We report a case of primary irritant contact dermatitis caused by an organostannic insecticide, tributyl tin phthalate, which has been thought to be stable and safe. A factory worker has been in contact with raw tributyl tin phthalate on one leg. Soon after taking a hot-water bath, he developed severely painful erythema on this leg. Patch tests and chemical analysis revealed that hot water hydrolyzed tributyl tin phthalate and produced concentrated phthalic acid. Since phthalic acid, a weak acid, was then concentrated, an acute irritant reaction appeared in this patient.

Accidents, Occupational↗
PubMed1985

Determination of phthalic acid, mono-(2-ethylhexyl) phthalate and di-(2-ethylhexyl) phthalate in human plasma and in blood products.

Pretreatment for the determination of phthalic acid, mono-(2-ethylhexyl) phthalate (MEHP) and di-(2-ethylhexyl) phthalate (DEHP) in human serum or plasma, and the determination of these compounds in blood products by high-performance liquid chromatography was studied. The amount of phthalic acid, MEHP and DEHP, migrated into blood products from a flexible bag, was studied. About 0.1% of DEHP in a flexible bag was found to have migrated into human platelet plasma. Most of the MEHP and phthalic acid detected in human platelet plasma was not derived from the flexible bag but was produced by enzymatic hydrolysis of the migrated DEHP. The amount of DEHP eluted into blood products from the flexible bag differed, depending upon storage time, storage temperature, etc.

Acetonitriles↗
PubMed1977

Phthalic acid esters in various foodstuffs and biological materials.

Phthalic acid esters (PAEs) are ubiquitous environmental contaminants in Japan. Di-n-butyl phthalate (DNBP) and di-2-ethylhexyl phthalate (DEHP) are the most commonly found of nine PAEs examined. DNBP and DEHP residues in 22 kinds of commerical foodstuffs (55 examples), mostly in plastic containers, are recorded. The level is generally higher in powdered foodstuffs than in other materials and the content of PAEs increased sharply during their storage. A close correlation is found between the content of PAE residues in packing materials and those of foodstuffs. The levels of DNBP and DEHP in human blood samples are found to be much higher than those of PCBs.

Adult↗
PubMed1985

Circulating concentrations of di(2-ethylhexyl) phthalate and its de-esterified phthalic acid products following plasticizer exposure in patients receiving hemodialysis.

The degree of exposure to the plasticizer di(2-ethylhexyl) phthalate (DEHP) was assessed in 11 patients undergoing maintenance hemodialysis for the treatment of renal failure. The amount of DEHP leached from the dialyzer during a 4-hr dialysis session was estimated by monitoring the DEHP blood concentration gradient across the dialyzer. Circulating concentrations of the biologically active products of DEHP de-esterification, viz., mono(2-ethylhexyl) phthalate (MEHP) and phthalic acid, were also determined during the dialysis session. On the average, an estimated 105 mg of DEHP was extracted from the dialyzer during a single dialysis session, with a range of 23.8 to 360 mg. The rate of extraction of DEHP from the dialyzer was correlated with serum lipid content as expressed by the sum of serum cholesterol and triglyceride concentrations (r = +0.65, p less than 0.05). Time-averaged circulating concentrations of MEHP during dialysis (1.33 +/- 0.58 micrograms/ml) were similar to those of DEHP (1.91 +/- 2.11 micrograms/ml). Blood concentrations of phthalic acid (5.22 +/- 3.94 micrograms/ml) were higher than those of the esters. The length of time patients had been receiving regular dialysis treatment was not a determinant of circulating concentrations of DEHP or MEHP. In contrast, time-averaged circulating concentrations of phthalic acid correlated strongly with the duration (in years) of dialysis treatment (r = +0.92, p less than 0.001). The results indicated substantial exposure to DEHP during hemodialysis and that the de-esterified products of DEHP are present in significant concentrations in the systemic circulation. Further study is needed to assess the contribution of these metabolites to the biological actions of DEHP in man.

Adult↗
PubMed1990

[The breakdown of phthalic acid esters by microorganisms].

The distribution in environment of phthalic acid esters classified according to their inherent toxicity, teratogenic, mutagenic properties and cancerogenic activity into a group of priority pollutants of biosphere is described in this review. The role of microbial community in degradation of phthalate esters has been demonstrated. The effect of such environmental factors as pH of the medium, temperature, humidity, concentration of organic matter, the introduction of promising microbial strains in natural biocenoses has been examined. The pathways of phthalate ester metabolism have been analysed in representatives of active bacterial destructors belonging to genera Nocardia, Pseudomonas and Micrococcus. The decomposition rate of phthalate esters has been shown to be correlated with structure, concentration and culture conditions.

Bacteria↗
PubMed1986

Studies on the genetic effects of phthalic acid esters on cells in culture.

Mono(2-ethylhexyl) phthalate (MEHP) induced chromosome aberrations in cells of two culture lines, one derived from Chinese hamster ovary cells (CHO) and the other from rat liver cells (RL4). In CHO cells, the clastogenicity of MEHP was unaffected by the presence of an exogenous metabolic activation system (S-9 mix). 2-Ethylhexanol, o-phthalic acid, and phthalic anhydride were without effect. Cytochemical methods and assays for carnitine acetyltransferase and KCN-insensitive palmitoyl CoA oxidation were employed to determine whether chromosome damage was associated with peroxisome proliferation. No evidence of an increase in peroxisome numbers or of induction of marker enzymes was found in CHO cells treated with MEHP for up to 72 hr. Clofibric acid and BR931 were also ineffective. Observations on changes in CHO cell structure and permeability, and on the haemolytic effects of phthalate monoesters, suggest that the cytotoxicity of MEHP may be due primarily to its action on cell membranes. Since chromosome damage was observed only at cytotoxic concentrations, it is suggested that damage to lysosomal membranes and the release of endonucleases may be responsible for the observed clastogenicity of MEHP in vitro.

Animals↗
PubMed1986

Carcinogenic potential of phthalic acid esters and related compounds: structure-activity relationships.

Chronic toxicity and carcinogenicity studies of several phthalic acid esters (PAEs) and compounds containing a 2-ethylhexyl moiety were conducted in Fischer 344 rats and B6C3F1 (hybrid) mice. The compounds studied were phthalic anhydride, di(2-ethylhexyl) phthalate, butyl benzyl phthalate, diallyl phthalate, di(2-ethylhexyl) adipate, tris(2-ethylhexyl) phosphate, and 2-ethylhexyl sulfate (sodium salt). Estimated maximum tolerable doses and fractionally lower doses of each compound were administered to groups of 50 male and 50 female rats and mice for 2 years, followed by sacrifice, necropsy, and histopathological examination of major organs and tissues. The low toxic potencies of most of the compounds allowed for relatively high doses to be given during the chronic studies. In general, the toxic manifestations of the PAEs were closely correlated with their ester substituents. Although many of the PAEs possessed some carcinogenic activity, target sites for such effects were dissimilar, suggesting the absence of a common mode of action. In contrast, all of the 2-ethylhexyl-containing compounds studied possessed some hepatocarcinogenic activity, indicating that this moiety may have a propensity for causing hepatocarcinogenesis in mice, particularly those of the female sex. The 2-ethylhexyl compound that caused the greatest hepatocarcinogenic response in mice, di(2-ethylhexyl) phthalate, was also hepatocarcinogenic in rats. Similarly, those with a relatively greater effect in female mice were also active in male mice. Thus, sex and species differences in 2-ethylhexyl-induced hepatocarcinogenesis in rodents are probably quantitative rather than qualitative in nature.

Adipates↗
PubMed1986

Effects of phthalic acid esters (PAEs) on the neonate and aspects of teratogenic actions.

A review of the literature reveals that several different phthalic acid esters (PAEs) are capable of causing testicular damage. Phthalate-induced zinc deficiency is consistent with germinal epithelial damage. Among experimental animals, mice perhaps show the greatest sensitivity to phthalate-induced terata, but high doses/exposure are required. Little toxicologic information is available with regard to phthalate-induced effects upon the neonate.

Animals↗
PubMed1990

Anti-tumor promoting action of phthalic acid mono-n-butyl ester cupric salt, a biomimetic superoxide dismutase.

Skin tumor promotion induced by 12-O-tetradecanoylphorbol-13-acetate (TPA) was inhibited by a concurrent and topical application of phthalic acid mono-n-butyl ester cupric salt (PAMBCu) in CD-1 mice initiated with 7,12-dimethylbenz[a]anthracene. PAMBCu inhibited TPA-caused epidermal ornithine decarboxylase (ODC) induction and ear edema formation, i.e. skin inflammation. However, neither PAMBCu nor superoxide dismutase (SOD) inhibited TPA-caused ODC induction in primary cultured mouse epidermal cells. 7-Bromomethylbenz[a]anthracene (BrMBA) is known to be a non-TPA type of tumor promoting agent. Epidermal ODC induction and inflammation caused by BrMBA were not inhibited by a concurrent application of PAMBCu. When mice were topically treated twice with PAMBCu, i.e. concurrently with and 7 h after BrMBA treatment, BrMBA-caused ODC induction was markedly suppressed. The same dose regimen of PAMBCu, however, failed to inhibit tumor promotion and inflammation caused by BrMBA. PAMBCu showed SOD-mimetic activity in superoxide generating systems, i.e. xanthine-xanthine oxidase reaction and TPA-stimulated polymorphonuclear leukocytes (PMN). Mono-n-butyl phthalate, which lacks SOD-mimetic activity, failed to inhibit TPA-caused ODC induction and skin inflammation. Therefore, inhibition by PAMBCu of TPA-caused tumor promotion, epidermal ODC induction and inflammation may be attributable to its SOD-mimetic activity. The results also support the contention that a superoxide anion of non-epidermal cell origin, such as PMN and macrophages, plays a role (probably some enhancing role) in in vivo ODC induction and tumor promotion caused by TPA. Failure of PAMBCu to inhibit BrMBA-caused tumor promotion suggests that superoxide anion generation is not involved in the tumor promoting action of this agent and that the anti-tumor promoting action of PAMBCu is dependent on the nature of the tumor promoting agents.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1985

Mutagenicity evaluation of phthalic acid esters and metabolites in Salmonella typhimurium cultures.

The mutagenic potential of dimethyl phthalate (DMP), diethyl phthalate (DEP), dibutyl phthalate (DBP), and di-2-ethylhexyl phthalate (DEPH), as well as metabolites of DEHP--i.e., mono-2-ethylhexyl phthalate (MEHP), 2-ethylhexanol (2-EH), and phthalic acid (PA)--were tested in Salmonella typhimurium cultures using the Ames test procedure. The compounds were tested on strains TA98, TA100, TA1535, TA1537, TA1538, and TA2637 for base-pair substitution or frameshift-type mutations. Spot tests yielded negative responses for all compounds with the strains tested. Each compound was tested for a dose-effect relationship in the TA98, TA100, TA1535, and TA1538 systems. DEP and DBP exhibited a mildly positive response in both TA100 and TA1535 cultures, and DMP showed a similar response in TA1535. Normalization of the data for cytotoxicity of DMP suggests TA100 has a mildly positive effect. The higher doses of these compounds exhibited some cytotoxic effects. The mutagenic effects were apparently abolished by the addition of S9 fraction in TA100 and TA1535 cultures, while no effect, other than cytotoxicity, was observed in the TA98 and TA1538 systems. DEHP, MEHP, 2-EH, and PA exhibited no mutagenicity in any of the strains of Salmonella typhimurium tested, with or without S9 metabolic activation. MEHP and 2-EH, however, exhibited a moderate cytotoxic effect in most cultures.

Biotransformation↗