The three-dimensional structure of 3,3',4,4'-tetrachlorobiphenyl, a dioxin-like polychlorinated biphenyl (PCB)

The crystal structure of PCB 77 (3,3',4,4'-tetrachlorobiphenyl, C(12)H(6)Cl(4)), a dioxin-like PCB congener, is described. The dihedral angle of PCB 77 is 43.94(6) degrees, which is slightly larger than calculated or experimental dihedral angles of biphenyl derivatives in solution but smaller than experimental dihedral angles in the gas phase.     

Accumulation pattern and biotransformation enzyme induction in rainbow trout embryos exposed to sublethal aqueous concentrations of 3,3',4,4'-tetrachlorobiphenyl

Accumulation pattern of 3,3',4,4'-tetrachlorobiphenyl (PCB 77) and the exposure time needed to activate the monooxygenase (EROD) and conjugation (GST) enzyme systems of fish at the advanced embryonic stage were studied. Eyed stage embryos of rainbow trout (Oncorhynchus mykiss) were exposed to sublethal doses (0, 1, 10, and 100 micrograms/l) of PCB 77. Results indicated direct accumulation of the chemical into the eggs, but the exposure time was not long enough for PCB 77 to reach constant steady state. However, at the two lowest test concentrations (1 microgram/l and 10 micrograms/l) a temporary plateau at chemical accumulation was reached at the third exposure day (185 and 1221 ng PCB/g egg w.w). At the highest concentration (100 micrograms/l) the decrease in the accumulation rate was already evident after the first day (2182 ng PCB/g egg w.w). The chemical uptake increased again at day 7 in all the exposure groups. That event could have been caused by the increased metabolic rate of the embryos in preparation for the upcoming hatching event. The microsomal CYP1A monooxygenase system (EROD) was shown to be a sensitive indicator of embryonic exposure, being induced at the low (1 microgram/l, 182 ng/g egg) PCB concentration and after a short (3 day) exposure time. The conjugation enzyme system (GST) was shown to be functioning already at the advanced embryonic stage, although no response to the studied chemical stress was detected.     

Vitamin and thyroid status in arctic grayling (Thymallus arcticus) exposed to doses of 3,3',4,4'-tetrachlorobiphenyl that induce the phase I enzyme system

Induction of phase I biotransformation enzymes is recognized as a hallmark response in fish exposed to coplanar PCBs. Depletions of vitamins A and E and disrupted thyroid hormone and glandular structure secondary to this induction have not yet been examined in an arctic fish species. Arctic grayling were exposed to a single oral dose of 0 (control), 10, 100 or 1000 ng 3,3',4,4'-tetrachlorobiphenyl (TCB) g(-1) bodyweight, a contaminant found in most arctic fish. After 30 and 90 days of exposure, TCB concentrations in tissues, hepatic phase I activity (as ethoxyresorufin-O-deethylase (EROD)), plasma and tissue vitamin A and E concentrations, plasma thyroid hormone levels and thyroid glandular structure were examined. Total plasma osmolality, as an indicator of overall fish health was also monitored. TCB recovery in tissues was low and extremely variable, making comparisons between intended dose groups inappropriate. Therefore, correlation analysis between actual recovered TCB concentrations and biochemical responses was employed. Hepatic EROD activity correlated strongly with liver TCB concentrations. Liver concentrations of vitamin A were altered as a function of TCB concentrations and EROD activity, but plasma vitamin A status was not affected. Vitamin E was depleted by TCB accumulation in blood and EROD induction in liver of males only at 90 days postexposure. Thyroid hormones status and glandular structure were not affected by the short duration TCB exposures used in this experiment. TCB concentrations were correlated with an elevation in plasma osmolality. Results from this experiment indicate that the vitamin status and osmoregulation of arctic grayling exposed to TCB can be compromised. Further studies of field populations exposed to this type of contaminant are warranted.     

Toxic and biochemical effects of 3,3',4,4'-tetrachlorobiphenyl (CB-77) and clophen A50 on eider duckling (Somateria mollissima) in a semi-field experiment

In this study the possible toxic and biochemical effects of one intraperitoneal dose of 5 or 50 mg kg(-1) of 3,3',4,4'-tetrachlorobiphenyl (CB-77) or 50 or 200 mg kg(-1) of Clophen A50 (CloA50) on 28-day-old eider ducklings (Somateria mollissima) were investigated. After ten days, no significant differences could be observed in any of the toxic and biochemical parameters studied, apart from ethoxyresorufin (EROD) activity, when comparing group average values of the dosed and control animals. However, significant correlations were observed at day 10 after exposure between the individual internal PCB concentration and body weight gain and beak length growth (negative correlations in the CloA50 groups); relative liver weight and cytochrome P4501A activity (positive correlations in CB-77 and CloA50 groups); plasma thyroid-hormone and hepatic retinoid levels (negative correlations in CB-77 groups); and plasma retinol levels and the ratio plasma retin/hepatic retinyl palmitate (positive correlations in CB-77 groups only). Animal activity was significantly reduced in the group that received 50 mg CB-77 kg(-1). These observations indicate that eider ducks are a sensitive species to PCB toxicity and may be at risk for development of adverse health effects in relatively highly contaminated areas such as the Waddenzee.     

Identification of hydroxylated metabolites in 2,2',4,4'-tetrabromodiphenyl ether exposed rats

Faeces from day 1-5 of orally administered 2,2',4,4'-tetrabromodiphenyl ether (BDE-47) in rat have been analysed for hydroxylated metabolites. Six hydroxylated tetrabrominated diphenyl ethers, as well as three hydroxylated tribrominated diphenyl ethers found, were structurally identified. They were 2'-hydroxy-2,4,4'-tribromodiphenyl ether, 3'-hydroxy-2,4,4'-tribromodiphenyl ether, 4'-hydroxy-2,2',4-tribromodiphenyl ether, 6-hydroxy-2,2',4,4'-tetrabromodiphenyl ether, 2'-hydroxy-2,3',4,4'-tetrabromodiphenyl ether, 3-hydroxy-2,2',4,4'-tetrabromodiphenyl ether, 5-hydroxy-2,2',4,4'-tetrabromodiphenyl ether, 4'-hydroxy-2,2',4,5'-tetrabromodiphenyl ether and 4-hydroxy-2,2',3,4'-tetrabromodiphenyl ether. The analysis was performed using gas chromatography-mass spectrometry (GC-MS). The identification of the hydroxylated polybrominated diphenyl ether (OH-PBDE) metabolites in the rat faeces was supported by similar relative retention times (RRTs) versus 2,2',3,4,4',5-hexabromodiphenyl ether (BDE-138) on two columns of different polarities compared to the authentic references. The identification of the OH-PBDE metabolites was also supported by full scan electron ionisation mass spectra. Two of the identified OH-PBDE metabolites have identical structures as natural products, which previously have been isolated from marine sponges and an ascidian.     

Disruption of thyroid hormone-mediated Xenopus laevis tadpole tail tip regression by hexabromocyclododecane (HBCD) and 2,2',3,3',4,4',5,5',6-nona brominated diphenyl ether (BDE206)

Thyroid hormone regulates amphibian metamorphosis, including the transformation of a tadpole into a froglet and regression of the tail. Xenopus laevis tadpole tail tips in organ culture (ex vivo) undergo regression when exposed to 3,3',5-triiodo-l-thyronine (T(3)) and interference by chemicals with this process was utilized as a bioassay to detect thyroid hormone disruption. In the present study the bioassay was further validated by investigating its response to compound induced T(3)-antagonism and - potentiation. Tadpole tail tips were exposed to two brominated flame retardants (BFRs) in presence or absence of T(3) at its EC(50) (20 nM). T(3)-induced tail tip regression was antagonized by 2,2',3,3',4,4',5,5',6-nona brominated diphenyl ether (BDE206) and potentiated by hexabromocyclododecane (HBCD) in a concentration dependent manner, which was consistent with results obtained with a in vitro T(3)-dependent proliferation bioassay termed the T-screen. Neither compound induced any effect in the absence of T(3). The results indicate that studying possible hormone disrupting effects of agonistic, antagonistic or potentiating compounds should include combined exposure with the natural hormone at around its EC(50) concentration. The results obtained with the tail tip exposures were in accordance with the T-screen predictions, and occurred at BFR-concentrations that were only 5-50 times those of T(3). The bioassay proved to be suitable not only for detecting T(3)-agonism, but also for antagonism and potentiation.     

Effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin or 2,2',4,4',5,5'-hexachlorobiphenyl on vitamin K-dependent blood coagulation in male and female WAG/Rij-rats

Newborns are susceptible to hemorrhages (hemorrhagic disease of the newborn or HDN) due to vitamin K deficiency. Induction of cytochrome P450 in the fetal liver by maternal anticonvulsant therapy such as phenobarbital or phenytoin is considered to be a major cause. An observed increase in late hemorrhagic disease (LHD) in breast fed neonates gave rise to the hypothesis that PCBs and dioxins, P450-inducing contaminants present in human milk, might effect vitamin K-dependent blood coagulation. This hypothesis was studied in rats. Administration of a single oral dose of 0.003, 0.03, 0.3, 3 or 30 nmol 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) per kg bodyweight or 0.75, 4, 20, 100 or 500 micromol 2,2',4,4',5,5'-hexachlorobiphenyl/kg bw (HxCB) to female and male rats resulted in dose-related reductions of the vitamin K-dependent coagulation factor VII. The highest factor VII reduction in female rats was 44%, observed after TCDD exposure. The Lowest Observed Adverse Effect Level (LOAEL) of TCDD on female factor VII levels was 0.3 nmol/kg bw (96 ng/kg). There was a significant inverse correlation between Factor VII levels and induction of hepatic ethoxyresorufin O-deethylating (EROD) activity, reflecting CYP1A1, and total P450 content. HxCB had no effect on female coagulation factors. In contrast, in male rats only exposure to HxCB, which induces mainly CYP2B1 and 2B2, decreased both coagulation factors dramatically up to 88%. The LOAEL of HxCB on factor VII in male rats was 100 micromol/kg bw (36 mg/kg). In general, effects on coagulation factors in male rats exceeded those in females. In addition, sex-dependent differences of TCDD and HxCB were observed on the hepatic vitamin K cycle enzyme activities in female and male rats. Vitamin K-dependent (gamma-glutamyl carboxylase activity was mainly induced in female rats; 2.3-fold in the highest dose group of TCDD. In male rats only vitamin K 2,3-epoxide reductase (KO-reductase) activity was induced 1.7-fold by the highest dose of HxCB. KO-reductase activity in female rats was also increased by TCDD, however, less pronounced than the carboxylase activity. Concluding, the hepatic vitamin K cycle still functions and is not blocked by TCDD or HxCB, thus explaining the observed reduction in factor VII. Finally, the possible role of P450 in vitamin K deficiency is discussed. Based on these results it is suggested to investigate the possible role of PCBs and dioxin-like compounds in LHD in more detail.     

Interaction between cadmium exposure and infection with the intestinal parasite Moniliformis moniliformis (Acanthocephala) on the stress hormone levels in rats

The impact of an infection with the acanthocephalan Moniliformis moniliformis and a simultaneous Cd-exposure on the stress hormone levels of rats was studied. Immediately after the application of cadmium to some rats, cortisol levels in all groups of rats, as quantified by radioimmunoassay (RIA), significantly increased. However, infections with M. moniliformis as well as the uptake of Cd reduced significantly the cortisol release compared to untreated controls. While catecholamine concentrations, as determined by high-performance liquid chromatography (HPLC), showed no clear tendency during the experimental period, the ratio of C(adrenaline)/C(noradrenaline) in the controls showed the significantly lowest value of all four groups after killing the animals. Thus, the acanthocephalan infection as well as the Cd-exposure and the combination of both treatments affect hormone homeostasis in the rats which probably lead to negative effects on the health of the rat. Therefore parasite infections must be carefully considered in environmental impact studies, as an important factor affecting the host's health.     

Determination of the toxic impurities 3,3′,4,4′-tetrachloroazobenzene and 3,3′,4,4′-tetrachloroazoxybenzent in commercial diuron, linuron and 3,4-dichloroaniline samples

Methods are described for the determination of 3,3′,4,4′-tetrachloroazobenzene (TCAB) and 3,3′,4,4′-tetrachloroazoxybenzene (TCAOB) in diuron and linuron formulations and in 3,4-dichloroaniline. The formulations were extracted with acetone, and after removal of solvent, the residue was partitioned between methanol-water and hexane. 3,4-Dichloroaniline products were partitioned between methanol-1M hydrochloric acid and hexane. The hexane extracts were purified by column chromatography on silica gel and analysed by gas chromatography with electron-capture detection. Detection limits for TCAB and TCAOB were around 0.1 ug/g using samples of one gram. Levels of 5.5 – 28 ug TCAB and 1.9 − < 0.05 ug TCAOB/g herbicide formulation and 2.4 – 460 ug TCAB/g TCAB/g 3,4-dichloroaniline have been found. TCAOB levels were below the detection limits in the 3,4-dichloroaniline samples. The presence of TCAB and TCAOB was confirmed by gas chromatography-mass spectrometry.     

An experimental design to probe the interactions of dissolved organic matter and xenobiotics: bioavailability of pyrene and 2,2',5,5'-tetrachlorobiphenyl to Daphnia magna

Experiments were conducted to probe the interactions between natural dissolved organic matter (DOM) and two xenobiotics, and to determine how DOM influences their bioavailability. The experimental set-up, using dialysis bags, was designed to expose test organisms to the same constant concentration of free dissolved chemical, while increasing the concentration of the bound-to-DOM fraction. Daphnia magna S. were exposed to pyrene or 2,2',5,5'-tetrachlorobiphenyl in the presence of 0, 1, 2, 5, 10 or 20 mg L(-1) of a reference riverine humic acid (Suwannee River Humic Acid). The physico-chemical parameters were well constrained in the microcosm, demonstrating its potential usefulness. However bioaccumulation by D. magna showed important variability between replicate treatments, sufficient to mask any trends as a function of DOM concentration. The organic-carbon-normalised partition coefficients (K(OC)) ranged from 52000 to 92000 L kg(-1) for pyrene and from 8200 to 89000 L kg(-1) for 2,2',5,5'-tetrachlorobiphenyl, with a marked "concentration effect" for the latter compound.     

Effects of chronic exposure to radiofrequency electromagnetic fields on energy balance in developing rats

The effects of radiofrequency electromagnetic fields (RF-EMF) on the control of body energy balance in developing organisms have not been studied, despite the involvement of energy status in vital physiological functions. We examined the effects of chronic RF-EMF exposure (900 MHz, 1 V?m^?1) on the main functions involved in body energy homeostasis (feeding behaviour, sleep and thermoregulatory processes). Thirteen juvenile male Wistar rats were exposed to continuous RF-EMF for 5 weeks at 24 °C of air temperature (T _a) and compared with 11 non-exposed animals. Hence, at the beginning of the 6th week of exposure, the functions were recorded at T _a of 24 °C and then at 31 °C. We showed that the frequency of rapid eye movement sleep episodes was greater in the RF-EMF-exposed group, independently of T _a (+42.1 % at 24 °C and +31.6 % at 31 °C). The other effects of RF-EMF exposure on several sleep parameters were dependent on T _a. At 31 °C, RF-EMF-exposed animals had a significantly lower subcutaneous tail temperature (?1.21 °C) than controls at all sleep stages; this suggested peripheral vasoconstriction, which was confirmed in an experiment with the vasodilatator prazosin. Exposure to RF-EMF also increased daytime food intake (+0.22 g?h^?1). Most of the observed effects of RF-EMF exposure were dependent on T _a. Exposure to RF-EMF appears to modify the functioning of vasomotor tone by acting peripherally through α-adrenoceptors. The elicited vasoconstriction may restrict body cooling, whereas energy intake increases. Our results show that RF-EMF exposure can induce energy-saving processes without strongly disturbing the overall sleep pattern.     

Prenatal and postnatal exposure to diazinon and its effect on spermatogram and pituitary gonadal hormones in male offspring of rats at puberty and adulthood

The objective of this research is to study the possible reproductive adverse effects of diazinon on rat offspring exposed in utero and during lactation. Twenty-four Sprague–Dawley female rats (10–12 week old) were randomly assigned to four groups, each consisting of six rats. Group 1 served as the control and these rats were given normal saline orally. Rats in groups 2, 3, and 4 were administered diazinon, dissolved in saline at 10, 15, 30 mg/ kg^?1 body weight, per oral, once daily, during mating, pregnancy and lactation. The male offsprings were examined at puberty and adulthood for body weight, testis weight, epididymis weight, sperm count, motility and morphology, pituitary-gonadal hormone levels. At 30 mg kg^?1 dose, the male offsprings showed a decrease in testicular weight, sperm count, motility, with an increase in abnormal sperm percentage and a decline in pituitary-gonadal hormones, at puberty. Upon attaining adulthood, there was a decrease in testicular weight, sperm count and motility with an increase in abnormal sperm percentage and a decrease in pituitary hormone level. There was evidence of some adverse reproductive effects on the male offspring at the 15 mg/ kg^?1 dose. Most of the adverse effects were irreversible and were evident at both puberty and adulthood in the offsprings, although a few parameters reverted to the normal growth pattern. Diazinon is a reproductive toxicant for male offsprings if exposed during prenatal and postnatal phases.     

Effects of sublethal exposure to a pesticide on levels of energetic compounds in Anguilla anguilla.

Abstract

The effect of two sublethal fenitrothion concentrations (0.02 and 0.04 mg/L) on the energy metabolism of the european eel Anguilla anguilla and its recovery from intoxication was investigated. Analysis of various parameters such as glycogen, proteins and total lipids was made on liver and muscle eel tissues after 2, 8, 12, 24, 32, 48, 56, 72 and 96 hr of fenitrothion (0,0‐dimethyl 0–3‐methyl‐4‐nitrophenyl phosphorothioate) exposure. Subsequently, the fish were allowed recovery periods of 8, 12, 24, 48, 72, 96, 144 and 192 hr in clean water, and the same parameters were again evaluated. The results obtained during the exposure to the pesticide as well as during the recovery phase were used to calculate the caloric content in both tissues of A. anguilla. A reduction in energy reserves in the selected tissues was observed after exposure to both fenitrothion concentrations and the caloric content in those animals was lower than in the controls. Most of the metabolic disorders did not persist after allowing recovery in clean water during a week.     

Reproductive impairment of sea urchin upon chronic exposure to cadmium. Part II: Effects on sperm development

Chronic pollution may impair the reproductive success of adult organisms through a decrease in the quality of gametes. Our parallel study on gamete quality, showed that male sea urchins were more sensitive than the females towards cadmium pollution. The effects of chronic exposure to 0.01 and 1 ppm Cd2+ on sperm development of the sea urchin Anthocidaris crassispina were studied. Despite the fact that no significant change in gonad index was observed when sea urchins were exposed to both levels of Cd2+ for 4 weeks, deposition of electron-dense materials was conspicuous at the wall and intracellular space of male gonads. Apparent cytological alterations were observed in sperm cells, including changes in morphology of nuage in spermatogonia. The discrete, granular bodies of nuage were replaced by a large electron-dense body. Spermatozoa with short, incomplete 'broken' tails (scanning electron microscope observation) or tails of spermatids/spermatozoa with extraordinary electron-density (transmission electron microscope observation) were more abundant in gonads exposed to both levels of Cd2+. Mitochondrial cristae deformation was observed for sperm cells at all stages of development. Sperm plasma membrane also became more convoluted but acrosome remained intact. The observed cytological distortion of sperm tails and mitochondria/midpiece could help to explain the decline in motility as well as poor perseverance in sperm produced by sea urchins exposed to cadmium observed in our earlier study.     

Effects of host plant exposure to cadmium on mycorrhizal infection and soluble carbohydrate levels of Pinus sylvestris seedlings

In a Cd-contaminated environment, not only mature trees but also their seeds and young seedlings can be exposed to Cd. Cadmium taken up by young seedlings may influence mycorrhizal infection, which might in turn influence resistance to Cd toxicity. In order to eliminate soil-mediated responses of mycorrhizal infection to Cd, Pinus sylvestris seedlings were exposed to Cd prior to fungal inoculation and replanted to clean substrates with fungal inoculum. Cadmium pretreatment reduced the proportion of living mycorrhizal short roots of seedlings inoculated with Paxillus involutus. However, no such effect was observed for seedlings inoculated with Suillus bovinus and Rhizopogon subcaerulescens. Therefore, infection by P. involutus appeared to be affected by Cd taken up by seedlings. Overall stem length and biomass of the seedlings were reduced by Cd pretreatment. Infection by S. bovinus and R. subcaerulescens increased stem length and biomass of the seedlings. Root soluble carbohydrate concentrations were lower in mycorrhizal seedlings than non-mycorrhizal seedlings.     

Effects of sodium arsenate exposure on liver fatty acid profiles and oxidative stress in rats

The present study aimed to evaluate the effect of arsenic on liver fatty acids (FA) composition, hepatotoxicity and oxidative status markers in rats. Male rats were randomly devised to six groups (n?=?10 per group) and exposed to sodium arsenate at a dose of 1 and 10 mg/l for 45 and 90 days. Arsenate exposure is associated with significant changes in the FA composition in liver. A significant increase of saturated fatty acids (SFA) in all treated groups (p?<?0.01) and trans unsaturated fatty acids (trans UFA) in rats exposed both for short term for 10 mg/l (p?<?0.05) and long term for 1 and 10 mg/l (p?<?0.001) was observed. However, the cis UFA were significantly decreased in these groups (p?<?0.05). A markedly increase of indicator in cell membrane viscosity expressed as SFA/UFA was reported in the treated groups (p?<?0.001). A significant increase in the level of malondialdehyde by 38.3 % after 90 days of exposure at 10 mg/l was observed. Compared to control rats, significant liver damage was observed at 10 mg/l of arsenate by increasing plasma marker enzymes after 90 days. It is through the histological investigations in hepatic tissues of exposed rats that these damage effects of arsenate were confirmed. The antioxidant perturbations were observed to be more important at groups treated by the high dose (p?<?0.05). An increase in the level of protein carbonyls was observed in all treated groups (p?<?0.05). The present study provides evidence for a direct effect of arsenite on FA composition disturbance causing an increase of SFA and TFAs isomers, liver dysfunction and oxidative stress. Therefore, arsenate can lead to hepatic damage and propensity towards liver cancer.     

Effect of acute exposure to PFOA on mouse liver cells in vivo and in vitro

Increasingly, epidemiological evidences indicate chemosynthetic perfluorooctanoic acid (PFOA), an environmental pollutant, induces potential adverse effect on human health after long-term exposure. However, less study has been performed for assessment of acute effect of PFOA exposure on metabolic homeostasis. In experimental designs, PFOA-exposed liver cells in vivo and in vitro were used to discuss underlying mechanism related to PFOA-induced metabolic dysfunction. In serological tests, PFOA-exposed mice showed increased treads of liver functional enzymes in alanine transaminase (ALT), aspartate transaminase (AST), and total bilirubin (T-BIL), trypsinase, low density lipoprotein-cholesterol (LDL-C), and insulin, while blood glucose, high density lipoprotein-cholesterol (HDL-C), and glucagon levels were reduced. In histocytological observations, PFOA-exposed liver showed visible cytoplasmic vesicles, and intact pancreatic islets were observed in PFOA-exposed pancreas. Additionally, increased insulin-positive cells and reduced glucagon-positive cells were detected in PFOA-exposed islets. As shown in immunoassays, PFOA-exposed liver resulted in elevations of cluster of differentiation 36 (CD36)-labeled cells and CD36 protein. In mouse liver cell study, PFOA-exposed cells showed increased cell apoptotic count, and increased phosphorylated levels of Bcl-2 and Bad in the cells. Furthermore, PFOA-exposed liver cells exhibited elevations of CD36-labeled cells and CD36 protein. Taken together, the present data demonstrate that acute exposure to PFOA-impaired liver function is associated with inducting CD36 expression and apoptosis, as well as disrupting key hormones in the pancreas.     

Comparison of semipermeable membrane device (SPMD) and large-volume solid-phase extraction techniques to measure water concentrations of 4,4'-DDT, 4,4'-DDE, and 4,4'-DDD in Lake Chelan, Washington

Semipermeable membrane devices (SPMDs) spiked with the performance reference compound PCB29 were deployed 6.1 m above the sediments of Lake Chelan, Washington, for a period of 27 d, to estimate the dissolved concentrations of 4,4'-DDT, 4,4'-DDE, and 4,4'-DDD. Water concentrations were estimated using methods proposed in 2002 and newer equations published in 2006 to determine how the application of the newer equations affects historical SPMD data that used the older method. The estimated concentrations of DDD, DDE, and DDD calculated using the older method were 1.5-2.9 times higher than the newer method. SPMD estimates from both methods were also compared to dissolved and particulate DDT concentrations measured directly by processing large volumes of water through a large-volume solid-phase extraction device (Infiltrex 300). SPMD estimates of DDD+DDE+DDT (SigmaDDT) using the older and newer methods were lower than Infiltrex concentrations by factors of 1.1 and 2.3, respectively. All measurements of DDT were below the Washington State water quality standards for the protection of human health (0.59 ng l(-1)) and aquatic life (1.0 ng l(-1)).