Unusual cause of palpable mass in upper abdomen--giant gastric trichobezoar: report of a case.

A trichobezoar is a ball of swallowed hair that accumulates in the stomach and fails to pass through the intestines. Usually a trichobezoar presents in early satiety and malnutrition. Obstructive symptoms and manifestations of gastric outlet obstruction may occur. While small gastric trichobezoars may be removed via gastroscopy, large trichobezoars require surgical removal by gastrotomy through abdominal incision. We present a case of a successful mini-laparotomy removal of a giant gastric trichobezoar in a 15-year-old girl with a history of trichophagia for a long time and marginal psychological disturbances.

Persistent organic pollutant patterns in grey seals (Halichoerus grypus).

The aim of this paper is to examine the patterns of polychlorinated biphenyls (PCB) in the grey seals (Halichoerus grypus) from the Baltic, Northeast and Eastern England, and the St. Lawrence Estuary (Canada). In fact, the feeding habits of the ringed seal (Phoca hispida) include ingestion of major quantities of benthic crustaceans that might cause observed differences obtained in PCBs, whereas the grey seal feed mainly on fish. The profile (percent in mixture) of polychlorinated biphenyls (PCB) 101, 118, 138, 153, and 180, and the total of their concentrations in mg/kg lipid in grey seals from the Baltic, from Northeast and Eastern England, and from the St. Lawrence estuary (Canada), were examined by principal component analysis (PCA). When considering the possible effects of consuming seafood by the grey seal, it is necessary to characterize populations and individuals according to the amounts they consume, since populations in different parts of the world are likely to show big differences in their consumption of seafood. The patterns differ between juveniles and adult animals, but the gender of adults and geography do not appear to play a role.

Polycyclic aromatic musk compounds in sewage treatment plant effluents of Canada and Sweden--first results.

Polycyclic musk fragrances (PMF) are widely used fragrances for cosmetics and other personal and household care products. Quantitative data on PMF (HHCB-Galaxolide, AHTN-Tonalide, ATTI-Traseolide, AHMI-Phantolide, ADBI-Celestolide, and DPMI-Cashmeran) and the most prominent nitro musks (Musk Xylene-MX, and Musk Ketone-MK) in different wastewater treatment effluents in Canada and Sweden are presented to provide preliminary information on the variations within the emission pattern of these compounds. In all samples HHCB and AHTN were detected at concentrations of up to 1300 and 520 ngl(-1), respectively. ADBI, AHMI were also present, but close to the detection limit. The other PMF DPMI, ATTI, and more surprisingly musk ketone and musk xylene were not detected in any sample analysed. In comparison the samples from Canada were contaminated at a higher level than the Swedish samples, by a maximum factor of ca 10 for HHCB and AHTN.

Distribution of PACs in surficial sediments and bioavailability to mussels, Mytilus edulis of Halifax Harbour.

Surficial sediments and blue mussels were collected around the perimeter of Halifax Harbour. Samples were analysed for the levels and fingerprint of polycyclic aromatic compounds (PACs). The objective was to explore the relationship between contaminant profiles in sediments and in mussels and to explore the possibility of deducing their sources, pattern of deposition and circulation in the harbour. Combustion derived compounds predominated in both sets of samples, with more variability observed in the level of petroleum derived hydrocarbons in mussel samples. Biota-sediment accumulation factors (BSAF, dry/dry wt.) varied throughout the harbour, ranging from means of 0.006 to 1.26, where generally fluoranthene displayed the highest BSAF. Sediments and mussels give complementary views of the geographical distribution of contaminants, they reflect the state of benthic and pelagic habitats. Results observed for Halifax Harbour are discussed from the perspective of published data.

First derivative UV spectra of surface water as a monitor of chlorination in drinking water treatment.

Many countries require the presence of free chlorine at about 0.1 mg/l in their drinking water supplies. For various reasons, such as cast-iron pipes or long residence times in the distribution system, free chlorine may decrease below detection limits. In such cases it is important to know whether or not the water was chlorinated or if nonchlorinated water entered the system by accident. Changes in UV spectra of natural organic matter in lakewater were used to assess qualitatively the degree of chlorination in the treatment to produce drinking water. The changes were more obvious in the first derivative spectra. In lakewater, the derivative spectra have a maximum at about 280 nm. This maximum shifts to longer wavelengths by up to 10 nm, decreases, and eventually disappears with an increasing dose of chlorine. The water treatment system was monitored by this technique for over 1 year and changes in the UV spectra of water samples were compared with experimental samples treated with known amounts of chlorine. The changes of the UV spectra with the concentration of added chlorine are presented. On several occasions, water, which received very little or no chlorination, may have entered the drinking water system. The results show that first derivative spectra are potentially a tool to determine, in the absence of residual chlorine, whether or not surface water was chlorinated during the treatment to produce potable water.

The lethality of Salmosan (Azamethiphos) to American lobster (Homarus americanus) larvae, postlarvae, and adults.

The pesticide formulation Salmosan (47.5% w/w azamethiphos) is currently registered for use, in Canada, to treat salmonids for infestations of the copepod parasites, Lepeophtheirus salmonis and Caligus elongatus (sea lice). Determination was made of the acute lethality of this product to the three larval stages, the first postlarval stage, and the adult of the American lobster (Homarus americanus), a species of significant economic importance in Eastern Canada. The 48-h LC50 (as azamethiphos) is 3.57 microg/liter for Stage I, 1.03 microg/liter for Stage II, 2.29 microg/liter for Stage III, 2.12 microg/liter for Stage IV (the first postlarval stage), and 1.39 microg/liter for adults. These concentrations are not significantly different from each other, although the variability in response is greater in the larval stages than in the postlarvae or adults. These data when interpreted in conjunction with known physical oceanographic data and chemical dispersion studies indicate that single anti-louse treatments are unlikely to result in mortality among lobsters in the vicinity of salmon farms. However, the sublethal effects of this product and the effects of repeated exposures have yet to be determined.

Qualitative determination of 10,10'-oxybisphenoxarsine and decabromodiphenyl ether in plastics.

Plastics destined for facilities holding aquatic fauna, such as aquaculture and aquatic toxicology laboratories, were studied. The plastics were extracted with dichloromethane. The fungicide 10,10'-oxybisphenoxarsine (OBPA) was detected by silver nitrate after cleanup on a silica cartridge and TLC in petroleum ether-diethyl ether-acetic acid 80:20:1. The flame retardant decabromodiphenyl ether (DBDPO) was crystallized from dichloromethane and confirmed by IR spectrum. A UV-spectrophotometric method is suggested for the estimation of the leaching potential of additives from plastics.

Levels of organochlorine and polycyclic aromatic compounds in harp seal beaters (Phoca groenlandica).

Chlorinated dibenzo-p-dioxins, dibenzofurans, chlorobiphenyls, organochlorine pesticides and polycyclic aromatic hydrocarbons were measured in blubber, liver, kidney and muscle of five male and five female, 8-month-old harp seals (Phoca groenlandica). Levels of organochlorine contaminants were lowest in muscle, nearly 100 times higher in blubber and intermediate in kidney and liver. Only 2,3,7,8-tetrachlorodibenzofuran was detected in all liver and blubber samples (0.45 and 3.15 pg/g wet wt., respectively). Concentrations of chlorobiphenyls expressed as Aroclor 1254 were 3.8 and 8.2, 8.6 and 21.5, 23 and 73, and 945 and 890 ng/g wet wt. in the muscle, kidney, liver and blubber of female and male seals, respectively. p,p'-DDE, trans-nonachlor, oxychlordane and alpha-HCH were the additional predominant organochlorine compounds at 460 and 460, 415 and 530, 300 and 390, and 190 and 230 ng/g wet in the blubber of female and male seals, respectively. Concentrations of chlorobiphenyls and pesticides in muscle, liver and kidney were two-three times higher in males compared to females, whether expressed on a wet weight or a lipid weight basis, and approximately equal in blubber, even though the blubber layer of females was 30% thicker than that of males. Naphthalene and its C1-C3 homologues were detected in all tissues, generally at concentrations below 10 ng/g wet wt. The concentrations of PCBs and DDTs in blubber are considerably lower than those reported for juvenile seals from the same area 20 years ago. PCB and organochlorine pesticide concentrations and profiles are discussed in relation to those reported from other areas, as well as to sex and age of the seals.

The relevance of aquatic organisms' lipid content to the toxicity of lipophilic chemicals: toxicity of lindane to different fish species.

The acute toxicity (48-hr LC50) of lindane (gamma-HCH) to 16 fish species, belonging to eight families, ranges from 22 to 900 micrograms/liter (mean: 150 micrograms/liter). A significant positive linear relationship between the lipid content (% on a wet weight basis) of the fishes and their toxicity to gamma-HCH was found. If the toxicity is referred to 1% lipid, 48-hr LC50 values range between 13.2 and 32 micrograms/liter, and thus the coefficient of variation of the mean is reduced from 139 to 22%. It is concluded that the lipids of aquatic organisms serve as a protective reservoir against the toxic effects of lindane and other lipophilic, relatively persistent organic chemicals, because they are bioconcentrated mainly in the body lipids. Therefore, in organisms with high lipid content, only a relatively small fraction of the hydrophobic chemical can reach target organs (nerves, liver, etc.) and/or receptors. For comparing toxicity data of organic chemicals to aquatic organisms, the total lipid content of the organisms must be considered. The results of this investigation are important in comparative environmental toxicology for risk assessment of freshwater and marine organisms.

Patterns of polynuclear aromatic hydrocarbons (PAH) in sediments.

The patterns of polynuclear aromatic hydrocarbons (PAH) in sediments were studied by Principal Component Analysis (PCA). Phenanthrene (P), fluoranthene (Fl), pyrene (Py), benzo[a]anthracene (BaA), chrysene (Chr), and benzo[a]pyrene (BaP) were used. Three patterns were found: type P, associated primarily with petroleum hydrocarbons, type Fl, from relatively clean marine sediments, and type Py+BaA+Chr+BaP, from industrialized areas. Aerial fallout appears to be the major source of PAH for the latter. There is a considerable variation in the PAH patterns obtained in different laboratories. PCA is a good tool for the study of PAH patterns.

Domoic acid-containing toxic mussels produce neurotoxicity in neuronal cultures through a synergism between excitatory amino acids.

In 1987, an intoxication by cultured mussels produced neurological problems, such as headache, confusion, and loss of memory, particularly severe at times. Neuronal damage was found in the hippocampus and amygdala of four patients. The intoxication was attributed to the presence in mussels of domoic acid, a rare excitatory amino acid acting at the non-NMDA receptor. We now report that a domoic acid-containing mussel extract is more neurotoxic for cultured neurons than purified domoic acid. Moreover, we show that this increase in neurotoxicity is selectively due to domoic acid potentiation of the excitotoxic effect of glutamic acid and aspartic acid present in high concentrations in mussel tissue. We also show that subtoxic concentrations of domoic acid are sufficient to potentiate glutamic acid and aspartic acid neurotoxicity, and we present evidence suggesting that the neurotoxic synergism may occur through a reduction of the voltage-dependent Mg2+ block at the NMDA receptor-associated channel, following activation of non-NMDA receptors by domoic acid. Thus, based on our results, we suggest that the contemporary presence in the brain of concentrations of domoic acid insufficient alone to be toxic, together with excitatory amino acids, of endogenous and eventually of diet-related origin, may have been relevant in the occurrence of the neurological problems reported.

Effects of excitotoxins on free radical indices in mouse brain.

Excitotoxins and free radicals individually have been implicated in several neurological disorders including those associated with aging. We observed that systemically administered domoic acid enhanced mouse brain superoxide dismutase activity with either an associated decrease or no change in mouse brain lipid peroxidation. These findings reflect a state of adequately compensated oxidative stress induced by excitotoxins. In homogenates containing disrupted cells from various regions of mouse brain, however, kainic acid produced a 2 to 5-fold increase in lipid peroxidation. This suggests that excitotoxins cause lipid peroxidation possibly by acting at intracellular loci which become more accessible following disruption of cells in vitro and by extrapolation, possibly in vivo due to cellular permeability changes during the edematous stage of ischemic and other related neuropathological conditions.

The amnesic shellfish poison domoic acid enhances neurotoxicity by excitatory amino acids in cultured neurons.

A recent episode of human intoxication by cultured mussels containing a rare excitatory amino acid named domoic acid, received particular attention for its neurological implications. The intoxication produced neurological problems, such as headache, confusion, and loss of memory, particularly severe at times. Neuronal damage was found in the hippocampus and amygdala of four patients. We now report that in neuronal cultures the neurotoxicity of a domoic acid-containing mussel extract is the result of domoic acid potentiation of the excitotoxic effect of glutamic acid and aspartic acid present in high amounts in mussel tissue. Moreover, we show that subtoxic concentrations of domoic acid are sufficient to potentiate glutamic acid and aspartic acid neurotoxicity. We present evidence suggesting that the neurotoxic synergism may be due to a reduction of Mg(+ +) block at the NMDA receptor-associated channel, following activation of NON-NMDA receptors by domoic acid.

The marine toxin okadaic acid is a potent neurotoxin for cultured cerebellar neurons.

The tumor promoter okadaic acid (OKA), is a marine toxin of algal origin, identified as a potent inhibitor of protein phosphatases 1 and 2A, and possibly enhancing calcium influx through voltage dependent calcium channels (VSSC). We now report that OKA at concentrations as low as 0.5 nM produced neurotoxicity, characterized first by the desintegration of the neurites and swelling of cell bodies, and later by cellular death. Non-neuronal cells viability and morphology were unaffected up to at least 5 nM OKA. Neurons sensitivity to the toxin changed with age in culture. Maximum neurotoxicity was observed in neurons at 9 DIC, when the OKA concentration producing half of the maximum reduction in neuronal survival (EC50) was approximately 0.65 nM. At 5 DIC or 19 DIC (EC50 approximately 2.5 nM and approximately 4.5 nM respectively), neurons appeared to be less sensitive to OKA. Neurotoxicity by OKA was not reduced by VSCC antagonists such as nifedipine and verapamil, nor by antagonists of excitatory aminoacid (EAA) receptors including APV, MK801 or CNQX. VSCC antagonists and EAA receptors antagonists fully protected from neurotoxicity induced by depolarization with KCl. These results suggest that OKA mechanism of neurotoxicity may not directly involve VSCC, endogenous EAA release and EAA receptors, but may depend upon other neurochemical events.