Search

Abiotic and biotic processes can be used to remediate DDX (DDT, DDD, DDE, and DDNS) contaminated soils; these processes can be fostered using specific carbon-amendments to stimulate particular soil indigenous microbial communities to improve rates or extent of degradation. In this study, toluene and glycerol were evaluated as cosubstrates under aerobic and anoxic conditions to determine the degradation efficiencies of DDX and to elucidate possible degradation mechanisms. Slurry microcosms experiments were performed during 60 days using pretreated soil with zero-valent iron (ZVI). Toluene addition enhanced the percentage of degradation of DDX. DDNS was the main compound degraded (around 86%) under aerobic conditions, suggesting cometabolic degradation of DDX by toluene-degrading soil bacteria. Glycerol addition under anoxic conditions favored the abiotic degradation of DDX mediated by sulfate-reducing bacteria activity, where DDT was the main compound degraded (around 90%). The 16S rDNA metagenomic analyses revealed Rhodococcus ruber and Desulfosporosinus auripigmenti as the predominant bacterial species after 40 days of treatment with toluene and glycerol additions, respectively. This study provides evidence of biotic and abiotic DDX degradation by the addition of toluene and glycerol as cosubstrates in ZVI pretreated DDX-contaminated soil., (Copyright © 2016 Elsevier B.V. All rights reserved.)

DDT, DDE and some additional lipophilic derivatives are recognized contaminants in sediments of Southern California Bight (SCB). Only about 10% of total DDTs discharged into the SCB are accounted for using available monitoring data (sediment, water, and biota). DDA represented up to 0.03% DDTs (DDT/DDE/DDD) in SCB surface sediments (top 2 cm) in amounts up to 76 μg DDA/kg dry weight. Highest DDA levels were found where DDT and DDD levels were maximal at the primary wastewater outfall indicating a natural precursor-product relationship for DDT and DDA. Still culture of SCB sediment revealed limited DDA formation following DDT fortification. DDA residues have also been found in contaminated Long Island, NY sediments provided by USGS. The formation of DDA and its potential release from sediments may be significant in resolution of uncertainties concerning the natural recovery of sediments in DDT-contaminated environments., (Copyright © 2012 Elsevier Ltd. All rights reserved.)

The organochlorine insecticide DDT (1,1,1-trichloro-2,2-bis(p-chlorophenyl)ethane) is still used for malaria vector control in certain areas of South Africa. The strict Stockholm Convention on Persistent Organic Pollutants (POPs) allows spraying on the inside of traditional dwellings with DDT. In rural villages contaminated dust presents an additional pathway for exposure to DDT. We present a new method for the determination of DDT in indoor air where separate vapour and particulate samples are collected in a single step with a denuder configuration of a multi-channel open tubular silicone rubber (polydimethylsiloxane (PDMS)) trap combined with a micro quartz fibre filter. The multi-channel PDMS trap section of the denuder concentrates vapour phase insecticide whereas particle associated insecticide is transferred downstream where it is collected on a micro-fibre filter followed by a second multi-channel PDMS trap to capture the blow-off from the filter. The multi-channel PDMS trap and filter combination are designed to fit a commercial thermal desorber for direct introduction of samples into a GC-MS. The technique is solvent-free. Analyte extraction and sample clean-up is not required. Two fractions, vapour phase and particulate phase p,p'-DDT, o,p'-DDT; p,p'-DDD, o,p'-DDD; p,p'-DDE and o,p'-DDE in 4 L contaminated indoor air, were each quantitatively analysed by GC-MS using isotopically labelled ring substituted (13)C(12) -p,p'-DDT as an internal standard. Limits of detection were 0.07-0.35 ng m(-3) for p,p'-DDT, o,p'-DDT, p,p'-DDD, o,p'-DDD, p,p'-DDE and o,p'-DDE. Ratios of airborne p,p'-DDD/p,p'-DDT and of o,p'-DDT/p,p'-DDT are unusual and do not match the ideal certified ingredient composition required of commercial DDT. Results suggest that the DDT products used for indoor residual spraying (IRS) prior to, and during 2007, may have been compromised with regards to insecticidal efficacy, demonstrating the power of this new environmental forensics tool., (Copyright © 2012 Elsevier B.V. All rights reserved.)

Previous studies of in utero exposure to dichlorodiphenyltrichloroethane (DDT) have shown mixed results for the harmful effects on fetal growth and development. This cross-sectional study was designed to: (1) examine the extent of DDT exposure in 1578 women, aged 28.5±6.0 who delivered between June 2005 and 2006 in the area of Al-Kharj, Saudi Arabia; and (2) assess its influence on neonatal anthropometric measurement of newly born babies. DDT and its metabolites, namely 1,1-dichloro-2,2-bis (p-chlorophenyl) ethylene (p,p'-DDE), 1,1-dichloro-2,2-bis (p-chlorophenyl) ethane (p,p'-DDD) and 1,1,1-trichloro-2,2' bis (p-chlorophenyl) ethane (p,p'-DDT) were measured in cord and maternal serum as well as placenta by Gas Chromatography coupled with an Electron Capture Detector (GC/ECD). p,p'-DDE was detected in 28.3% of cord and 54.4% of maternal serum, reflecting past exposure, whereas the p,p'-DDT was only found in 0.46% cord and 1.2% maternal samples. As expected the p,p'-DDE cord levels (0.197±0.961μg/L) were 2.8 times lower than the maternal levels (0.551±1.778μg/L), and both were significantly correlated (r=0.517) suggesting its transplacental transfer. The picture was different in placental tissues. p,p'-DDE and p,p'-DDT were detected in 84% and 99% of placental tissues, with the highest p,p'-DDT in placental tissues (29.62±158.282µg/kg dry wt.) compare to p,p'-DDE (10.167±18.851μg/kg dry wt.). In general, the presence of DDT metabolites in our participants indicates that these chemicals are still relevant despite the fact that they have been banned or restricted in the study area for many years. Our results support the view for an association between low in utero exposure to DDT and the anthropometric development of the fetus leading to a reduction in its head circumference, crown-heel length, birth weight and birth height. Since the reduction in these measures was independent of gestational age and/or preterm births, our findings suggest a detrimental effect of the DDT exposure on fetal growth. Neonatal anthropometric measures are considered as an important tool to detect newborns at higher risk of morbidity and impairment of growth. Efforts should be made to decrease exposure of women of reproductive age and to examine maternal DDT exposure in relation to long-term impact on health., (Copyright © 2011 Elsevier B.V. All rights reserved.)

The novel molecularly imprinted microsphere (MIM) that could be applied as special sorbent was synthesized by aqueous suspension polymerization using 1,1-bis(4-chlorophenyl)-1,2,2,2-tetrachloroethane (α-chloro-DDT) as the dummy template. The obtained MIM exhibited good recognition and selectivity to dicofol and it was successfully applied as selective sorbent of solid-phase extraction for the determination of dicofol from aquatic products. At the optimum conditions of the molecularly imprinted solid-phase extraction (MISPE) coupled with GC-ECD, good linearity for dicofol was achieved in a range of 0.4-100 ng g(-1) (r(2)=0.9995) and the recoveries at three spiked levels were ranged from 85.8% to 101.2% for aquatic products with the relative standard deviation (RSD) less than 5.6%. The presented MISPE-GC-ECD method exhibited the advantages of simplicity, selectivity and sensitivity, and could be potentially applied to the determination of dicofol in complicated aquatic products., (Copyright © 2011 Elsevier B.V. All rights reserved.)

Background Aims: Obesity is correlated with chronic low-grade inflammation. Thus the induction of inflammation could be used to stimulate adipose tissue formation in tissue-engineering approaches. As nitric oxide (NO) is a key regulator of inflammation, we investigated the effect of NO and its downstream signaling molecule guanosine 3',5'-cyclic monophosphate (cGMP) as well as adenosine 3',5'-cyclic monophosphate (cAMP) on preadipocytes in vitro., Methods: Preadipocytes were isolated from human subcutaneous adipose tissue, cultured until confluence, and differentiated. The NO donor diethylenetriamine (DETA)/NO (30-150 microm) was added during proliferation and differentiation. Additionally, cGMP/cAMP analogs 8-bromoguanosine 3',5'-cyclic monophosphate (8-Br-cGMP), 8-(4-chlorophenylthio)-guanosine 3',5'-cyclic monophosphate (8-pCPT-cGMP) and 8-bromoadenosine 3',5'-cyclic monophosphate (8-Br-cAMP), and the adenylyl cyclase activator forskolin, specific guanylyl cyclase inhibitor 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ) and adenylyl cyclase inhibitor 2'-5'-dideoxyadenosine (ddA), were applied. Proliferation and differentiation were evaluated., Results: DETA/NO in combination with the standard differentiation procedure significantly enhanced maturation of precursor cells to adipocytes. Proliferation, in contrast, was inhibited in the presence of NO. The application of cGMP and cAMP, respectively, increased pre-adipocyte differentiation to an even higher extent than NO. Inhibitors of the underlying pathways caused a significant decrease in adipogenic conversion., Conclusions: Our results support the application of NO donors during transplantation of preadipocytes in a 3-dimensional setting to accelerate and optimize differentiation. The results suggest that, instead of the rather instable and reactive molecule NO, the application of cGMP and cAMP would be even more effective because these substances have a stronger adipogenic effect on preadipocytes and a longer half-life than NO. Also, by applying inhibitors of the underlying pathways, the induced inflammatory condition could be regulated to the desired level.

Spatial distribution of selected contaminants in the surface sediments of Santa Monica Bay (SMB), California was investigated. Sediments were analyzed for DDTs (DDT and metabolites), polychlorinated biphenyls (PCBs), polycyclic aromatic hydrocarbons (PAHs), linear alkylbenzenes (LABs) and coprostanol. Effluent samples from the Hyperion Treatment Plant (HTP), which discharges treated municipal wastewater effluents into SMB, were also analyzed. The inter-correlation in the distribution trends of contaminants was examined. The concentrations of contaminants were interpolated in a geographic information system to visualize their spatial distribution in the Bay. Inventories of the contaminants were also estimated. The concentrations of coprostanol, LABs and PCBs are very high only in the vicinity of the sewage outfall whereas PAHs and DDTs occur widespread in the Bay. The poor correlation of DDTs with LABs, PAHs or coprostanol content confirms the historic origin of DDTs and their absence in the contemporary wastewaters. Moderate correlation of DDTs with PCBs implies historic deposits as a major origin of PCBs. There are hot spots of DDTs at water depths of 60 and 100m and the inventory of DDTs in Bay sediments is insignificant compared to that estimated in the Palos Verdes Shelf which extends from the southern edge of Redondo Canyon around Palos Verdes Peninsula. The concentration of toxic contaminants was examined according to published sediment quality guidelines. About 20 stations contain p, p'-DDE and/or total DDTs above ERM and, PCBs between ERL and ERM indicating potential for adverse biological effects.

In this work, a large-volume on-column injection method for the analysis of 21 organochlorine pesticides, including HCH isomers, DDT derivatives and cyclodiene derivatives, was optimized. The solvent selected to carry out the study was ethyl acetate and the injection volume was 100 microl. Some factors were introduced in a Plackett-Burman design to determine their influence in the vaporization efficiency. The significant factors were then studied by a univariate procedure and sorted according to their importance on the response. The effect of the injection conditions on the peak resolution was also noted. The conditions selected according to sensitivity and resolution were: initial oven temperature 75 degrees C, injection speed 20 microl s(-1), solvent vapor exit (SVE) valve closure time 60 s, initial pressure 100 kPa and isothermal oven time 1 min. Analytical characteristics expressed in terms of precision, linear range, and limit of detection have been determined and compared with those obtained by splitless injection. The degradation of endrin and p,p'-DDT thermolabile pesticides was evaluated for both injection techniques. Finally the developed method was successfully applied to the ultratrace analysis of pesticides in natural waters. With this purpose a micro liquid-liquid extraction method using 2 ml of ethyl acetate to extract 10 ml of water sample was proposed. Recoveries between 69 and 107% were obtained with a very good precision (0.2-1.3%) for the studied pesticides, except for p,p'-DDD. Detection limits between 0.3 and 25 ng l(-1), which fulfill the limits established by the new water directive 2008/105/EC, were achieved. The MLLE method was compared with the SPE method by the analysis of some water samples using both procedures, and good concordance was obtained.

DDT homologues and PCBs were determined in eggs of two stationary species, great crested grebe (Podiceps cristatus) and mallard (Anas platyrhynchos), in three breeding areas of Lake Maggiore in 1998. As expected, much higher contamination levels of both DDTs and PCBs were found in the fish-eating great crested grebe than in the mallard. In many eggs these values exceeded the safety thresholds proposed for aquatic bird protection. However, no significant correlation could be found between the two classes of pollutants and shell thickness in great crested grebe eggs. While a DDT manufacturer was detected as the main source of DDT pollution in the Lake Maggiore environment, the reason for the surprisingly high PCB level remains unknown.

The cardiovascular activity of 14-deoxy-11,12-didehydroandrographolide (DDA) from Andrographis paniculata (Burm.f.) Nees (Acanthaceae) was elucidated in anaesthetised Sprague-Dawley (SD) rats and isolated rat right atria. In anaesthetised rats, DDA produced significant falls in mean arterial blood pressure (MAP) and heart rate in a dose-dependent manner with the maximum decrease of 37.6 +/- 2.6% and 18.1 +/- 4.8%, respectively. The ED50 value for MAP was 3.43 mmol kg-1. Pharmacological antagonist studies were done using this dose. The hypotensive action of DDA was not mediated through effects on the alpha-adrenoceptor, muscarinic cholinergic and histaminergic receptors, for it was not affected by phentolamine, atropine as well as pyrilamine and cimetidine. However, it seems to work via adrenoceptors, autonomic ganglia receptor and angiotensin-converting enzyme, since the hypotensive effect of DDA was negated or attenuated in the presence of propranolol, hexamethonium and captopril. In the isolated right atria, DDA caused negative chronotropic action and antagonised isoproterenol-induced positive chronotropic actions in a non-competitive and dose-dependent manner. These results further supported the bradycardia-inducing and beta-adrenoceptor antagonistic properties of DDA in vivo.

2,2-Bis(4-chlorophenyl) acetic acid (DDA) was extracted from acidified urine at pH 2 by benzene. It was complexed by partitioning with crystal violet in acetic to yield a blue color which was quantitated at 610 nm. Its identity was confirmed by paper chromatographic separation. The DDA excretion in nine subjects ranged from 0.024 to 0.130 microgram/ml with a mean of 0.065 while that determined by gas chromatography ranged from 0.038 to 0.120 with a mean of 0.069.

The effects of 2,2,2-trichloro-1-(3,4-dichlorophenyl)ethyl acetate (Penfenate) on hepatic, renal and small intestinal drug-metabolizing enzyme activities, hepatic reduced glutathione content and urinary excretion of thioethers were studied in the rat. A single i.p. dose of Penfenate (500 mg/kg) decreased the body weight of the animals in 1-3 days, increased hepatic protein content at 2 days and increased urinary thioether excretion 12-24 h after the treatment. In liver a single i.p. dose (500 mg/kg) enhanced cytochrome P-450 content 1.7-fold, ethoxycoumarin O-deethylase activity 2.5-fold, 2,5-diphenyloxazole hydroxylase activity 1.6-fold, epoxide hydrolase activity 2.5-fold, glutathione S-transferase activity 1.4-fold and UDPglucuronosyltransferase (4-methylumbelliferone) activity 2.3-fold in 3 days. No effects could be seen 2 weeks after the treatment. Five consecutive daily doses (500 mg/kg) enhanced the drug metabolizing enzyme activities and caused a 50% mortality. A dose of 100 mg/kg had only minor effects on hepatic drug metabolizing enzyme activities. Renal and intestinal enzyme activities were only slightly affected by the administration of Penfenate. These data indicate that quite large doses of Penfenate are needed to bring about any significant effects and these effects are restricted mainly to the liver. However, the ability of Penfenate to change drug metabolizing enzyme activities must be considered when evaluating the advantages and disadvantages of this insecticide as a substitute for DDT.

The metabolites of 1,1,1-trichloro-2,2-bis(p-chlorophenyl)ethane (DDT) and 1,1-dichloro-2,2-bis(p-chlorophenyl)ethane (DDD) found in the urine of female Swiss mice are reported. The metabolites of DDT are DDD, 1-chloro-2,2-bis(p-chlorophenyl)ethene (DDMU), 1,1-dichloro-2-bis(p-chlorophenyl)ethene (DDE), 2,2-bis(p-chlorophenyl)acetic acid (DDA), 2-hydroxy-2,2-bis(p-chlorophenyl)acetic acid (alpha OH-DDA) and 2,2-bis(p-chlorophenyl)ethanol (DDOH), while DDD afforded DDMU, DDE, DDA, alpha OH-DDA and DDOH. The relative excreted levels of DDA and DDOH and the absence of 2,2-bis(p-chlorophenyl)acetaldehyde (DDCHO) are not consistent with the generally accepted pathway for DDA formation, which involves sequential metabolism of DDT and DDD via DDOH to afford DDA. The quantitative results are interpreted to mean that DDA is formed by hydroxylation at the chlorinated sp3-side chain carbon of DDD to give 2,2-bis(p-chlorophenyl)acetyl chloride (DDA-Cl), which in turn is hydrolyzed to DDA. The excretion of alpha OH-DDA from both DDT- and DDD-treated mice has never been previously observed. It is suggested that this metabolite arises from the initial epoxidation of DDMU, a metabolite of DDT and DDD, to yield 1,2-epoxy-1-chloro-2,2-bis(p-chlorophenyl)ethane (DDMU-epoxide). This chloroepoxide is then hydrolyzed and oxidized to produce the alpha OH-DDA.

The effect of certain DDT analogs on the binding of 3H-estradiol to the 8--9S estrogen binding protein of rat testicular cytosol was studied by sucrose sedimentation analysis. The binding of 3H-estradiol to testicular cytosol was inhibited by o,p'DDT, a DDT analog which is estrogenic in the intact female, but not by p,p'DDE which is a nonestrogen in the female. The pesticide methoxychlor, which is estrogenic in vivo in the female, failed to inhibit 3H-estradiol binding, presumably requiring metabolic activation for binding to the testicular cytosol. In fact, its di-demethylated metabolite 2,2-bis(p-hydroxyphenyl)-1,1,1-trichloroethane (HPTE), also estrogenic in vivo, caused marked suppression of 3H-estradiol binding.

The effects of DDT, some of its analogs, and selected cyclodiene insecticides on isolated spinach (Spinacea oleracea L.) thylakoids were identified, characterized, and compared to responses induced by selected herbicides. Except for endrin, the insecticides inhibited light-induced electron transport, altered chlorophyll fluorescence transients, and competitively displaced [14C]atrazine [2-chloro-4-(ethylamino)-6-(isopropylamino)-s-triazine], a known photosystem II inhibitor, from the membranes. The insecticides appeared to act at, or near B, the secondary electron acceptor of photo-system II. Binding of DDT and dieldrin was estimated at 900 and 2200 molecules, respectively, per photosynthetic unit (490 chlorophyll molecules). The insecticides also inhibited valinomycin-induced swelling of the thylakoid membrane. Whereas inhibition of electron transport can be attributed to interaction by the insecticides with a proteinaceous component of the thylakoid membrane, interference with the action of valinomycin may involve interaction with lipoidal constituents of the membrane.

Using a novel in vitro technique, whereby microsomal enzymes were embedded in an agar layer to prolong their viability, 1,1-bis(p-chlorophenyl) ethylene(DDNU), a mammalian metabolite of 1,1-bis(p-chlorophenyl)-2,2,2-trichloroethane (DDT), was converted by microsomal mono-oxygenases of mouse liver into 1,1-bis(p-chlorophenyl)-1,2-ethanediol (DDNU-diol). The putative epoxide intermediate, 1,1-bis(p-chlorophenyl)ethylene oxide (DDNU-oxide), a new compound, was synthesized; it showed weak alkylating activity with 4-(4-nitrobenzyl)pyridine but was not mutagenic in Salmonella typhimurium strains TA100 and TA98. DDT and 13 of its metabolites or putative synthetic derivatives, including 1,1-bis(p-chlorophenyl)-2,2-dichloroethylene (DDE), 1 1,1-bis(p-chlorophenyl)-2-chloroethylene (DDMU), 1,1-bis(p-chlorophenyl)-2-chloroethane (DDMS)-DDNU, 2,2-bis(p-chlorophenyl)ethanol (DDOH), bis(p-chlorophenyl)acetic acid (DDA) and 1,1-bis(p-chlorophenyl)-2,2,2-trichloroethanol (Kethane), caused no mutagenic effects in S. typhimurium strains TA100 or TA98, either in the presence or absence of a mouse-liver microsomal fraction. 1,1-Bis(p-chlorophenyl)-2,2,2-trichloroethyl acetate (Kelthane acetate) was a direct-acting mutagen in strain TA100, whereas 1,1-bis(p-chlorophenyl)-2,2-dichloroethane (DDD) was mutagenic in TA98, only in the presence of a mouse-liver microsomal system. The results are discussed in relation to possible pathways whereby DDT is activated to mutagenic and/or carcinogenic metabolites.

The effect of p,p'-isomers of DDT and its derivatives DDD, DDE and DDA on Chinese hamster cells in culture was studied. At different concentrations and various times of treatment the proliferation rate was inhibited most strongly by DDD and DDT, whereas DDE exhibited a markedly weaker influence. DDA was the least toxic compound of the four. The cytogenetic effects were also different. Again, DDA induced the least damage. Only enhanced gap rates but no chromosome breaks were observed. DDE was more active, and higher break rates occurred. DDD and DDT were by far the most damaging compounds, and they raised the gap and break rates markedly. However, no induction of configuration anomalies was found in any experiment. Chronic treatment of the cells for 3 months with DDT at 8 ppm did not alter the proliferation rate, the sensitivity to acute treatment with higher DDT concentrations or the chromosomal aberration rates. The results are discussed in relation to the relevance of differential pesticide effectivity in organs of higher animals and man.

In vitro inhibition of Ca2+-ATPase by DDT homologs was studied using maternal brush-border membranes from human term placentas as an enzyme source. At 10 microM concentration many of the compounds tested inhibited this enzyme. The order of effectiveness of inhibition was as follows: p,p'-DDE greater than p,p'-DDD greater than p,p'-DDT greater than methoxychlor(mec). Both p,p'-DDOH and p,p'-DDA did not inhibit the placental Ca2+-ATPase. Assays using varying concentrations (0.3 microM to 0.1 mM) of p,p'-DDT were also performed. The inhibition of human placental Ca2+-ATPase ranged from 12% for 0.3 microM p,p'-DDT to 69% for 30 microM p,p'-DDT. Higher concentrations of this pesticide failed to cause further enzyme inhibition.