Shell thickening and chambering in the oyster Crassostrea gigas: natural and anthropogenic influence of tributyltin contamination.

Abnormal thickening and chambering in Crassostrea gigas oysters have been adopted for many years as bioindicators of available tributyltin (TBT) in coastal waters. Nevertheless, since natural causes can also induce the formation of multiple chambers, a field study and laboratory experimentation has been conducted with 72 examples of C. gigas in successive culture media. This work has enabled differences to be established between natural fine sediment-induced characteristics and the influence of TBT on the shells. External shell deformities have been assessed using three biometric indices, shell thickness index, weight index and volume index. Internal differences have been observed in longitudinal sections of the shell: retraction of growth, stagnation of the adductor muscle scar and thinning of the chambers in the TBT-polluted shell secretion. A new index, the opening chambers index, has been proposed, with a value of less than 1 in the TBT-polluted environment and greater than 1 in shells secreted in an unpolluted production site. These conclusions should be borne in mind when C. gigas is used in biomonitoring programmes.

Hydrobia ulvae imposex levels at Ria de Aveiro (NW Portugal) between 1998 and 2007: a counter-current bioindicator?

Imposex expression in prosobranch gastropods has been widely used as a biomarker of tributyltin (TBT) pollution. Estuaries have been described as the most affected areas by this problem since they usually enclose the main TBT sources--ports, dockyards and marinas--resulting from the compound's application as a biocide in antifouling paints on ships. Using Hydrobia ulvae as a bioindicator, the current work addresses the most reliable methods to reduce the influence of critical variables, such as the animals' size, on imposex levels assessment for TBT pollution monitoring and presents its temporal trends from 1998 to 2007 in Ria de Aveiro (NW Portugal) to evaluate the effectiveness of recent legislation applied to reduce TBT environmental levels. H. ulvae imposex levels did not decrease in this estuarine system during the last decade despite the implementation of the EU Regulation No. 782/2003. Instead, there was a global significant increase in the percentage of females affected by imposex and a slight increase of the vas deferens sequence index (VDSI), contrasting with what has been described for other bioindicators in the same study area. These results show that different biology/ecology traits determine distinct routes of TBT uptake and/or bioaccumulation, pointing the importance of choosing the bioindicator depending on the compartment that is being monitored (sediment vs. water). Sediment ingestion as feeding habit is discussed and pointed as a reason to choose H. ulvae as a bioindicator of TBT pollution persistence in sediment. It is therefore predicted that the response of different prosobranch species around the world may diverge according to the compartment that is being monitored and that female masculinisation may not be completely eradicated in the near future due to TBT persistence in sediments.

Imposex and surface sediment speciation: a combined approach to evaluate organotin contamination in Guanabara Bay, Rio de Janeiro, Brazil.

An integrated biological-chemical survey of organotin compounds was carried out in Guanabara Bay, the second most important Brazilian harbor complex. The biological survey revealed high levels of imposex in Stramonita haemastoma populations. Inside the bay values of relative penis length index from 42.7 to 107.6 and vas deferens sequence index from III to VI were found, while organisms collected outside the bay had values ranging from <0.1 to 35.2 and from 0 to II. None of the females sampled inside the bay were normal and imposex was found in all stations. Surface sediments in the bay are contaminated by tributyltin (10-522 ng/g d.w.) and triphenyltin (<3.9-39.4 ng/g d.w.) with greater concentrations close to shipyards and marinas. The observed predominance of parent compounds (TBT and TPT) is commonly found when recent inputs occur, but may also indicate slow degradation processes in the anoxic conditions of these sediments. To our knowledge, this is the first report of a combined imposex-sediment approach to evaluate organotin contamination in marine environments of South America, and also the first report of TPT detection in environmental matrices in this region.

Imposex and butyltin contamination off the Oporto Coast (NW Portugal): a possible effect of the discharge of dredged material.

Imposex in the gastropod Hinia reticulata, a bioindicator for tributyltin (TBT) contamination, was investigated in locations at different distances from the Oporto harbour-dredged material discharge site. The degree of imposex found was inversely related to the distance to the discharge site, the highest imposex frequency being found closest to the discharge area. However, the levels of imposex found were low when compared with those reported for H. reticulata populations from moderately TBT-contaminated areas. Despite detectable levels of dibutyltin (DBT) and monobutyltin (MBT) in snail tissues (total butyltins ranging from 84 to 410 ng/g Sn dry wt.), TBT was below detection limit in all snail samples collected in open sea.

Contamination of organotin compounds and imposex in molluscs from Vancouver, Canada.

Gastropods and bivalves were collected at 15 sites at Vancouver and Victoria, Canada between 24 May and 7 June, 1999, to establish tissue concentrations of butyltin and phenyltin compounds, to record imposex symptoms in gastropods, and to assess the present status of organotin contamination around Vancouver. No neogastropods (such as Nucella lima) were found around Vancouver. Neogastropod populations could have been extirpated by severe TBT contamination in Vancouver, as relatively high concentrations of TBT were detected in tissues of Mytilus trossulus from Vancouver, and the neogastropods distributed in Vancouver might be sensitive to TBT. Recovery from imposex, however, was observed in neogastropod populations from three sites at Victoria and Mission Point. TBT contamination has continued around Vancouver, arising from continuous use of TBT in antifouling paints for vessels larger than 25 m in length; however, TBT has decreased around Victoria and Mission Point. Different patterns of TBT accumulation in tissue were observed among the bivalve species from Vancouver. The highest TBT concentration detected in Tresus capax suggested some possible adverse effects. TBT was the most predominant butyltin component in almost all bivalve specimens surveyed, suggesting a low rate of TBT metabolism. Phenyltin compounds were not detected in any molluscan specimens in this study.

Vancouver workshop: overview and synthesis.

Investigators from the six PICES member nations conducted a May, 1999 interdisciplinary research assessment of Vancouver Harbour, BC, Canada. Sediment contaminants were analyzed at several sites along an assumed pollution gradient extending eastward into the harbour from the relatively less-impacted Howe Sound area (located outside and seaward, to the west). Subsets of a few representative benthic biota (English sole for general contaminants; specific mollusks for TBT) at the sampling sites were concurrently assessed for specific tissue contaminants. Measurements of biotic response to contaminants-across a wide spectrum of biological and ecosystem organization, and ranging from selected biomarkers and tissue responses, to observations at the organism and community level-were likewise conducted. Parameters examined included: P-450 expression, EROD induction and histopathologic assessment of toxicopathic liver lesions in English sole; prevalence and frequency of imposex in neogastropods; perturbations in benthic community responses to pollutants; tissue assays of various bivalve shellfish species for PSP. Results affirmed a consistent east-to-west trend in declining contaminant-associated effects, across a range of biological assessments, thus providing strong evidence that these effects are pollution-related. Specific findings revealed a significant distortion of benthic community structure along the pollution gradient, as well as biomarker evidence of histological and biochemical stress in English sole from central and inner harbour sites. Although the study reaffirms prior assumptions that various species of neogastropods have been extirpated from the harbour, most likely from the antifoulant uses of tributyltin, some of the adverse impacts from TBT may be declining. Also noted were strong biochemical inferences that sediments in the relatively "uncontaminated" Howe Sound, may well contain significant P450-inducing pollutants which were not included as analytes in the design of this limited and preliminary assessment. During the brief sampling period, PSP contamination did not appear to be a significant issue for the harbour.

Tributyltin use in interior paints: a continuing health hazard.

We report on five patients who developed mucous membrane irritation after inhalational exposure to an interior use latex paint containing the organotin compound bis(tributyltin) oxide. Stricter regulations regarding the use of bis(tributyltin) oxide with interior paint would most likely have prevented these cases of tributyltin toxicity. Bis(tributyltin) oxide should not be used with paint intended for interior use.

Acute effect of indoor exposure to paint containing bis(tributyltin) oxide--Wisconsin, 1991.

In January 1991, a woman in Wisconsin contacted her local public health department to report that she and her two children had become ill after her landlord painted the walls and ceilings of two rooms of her apartment. Reported symptoms included a burning sensation in the nose and forehead, headache, nose bleed, cough, loss of appetite, nausea, and vomiting. The woman, who was in the third trimester of pregnancy, also complained of a persistent odor from the paint and provided an empty bottle of a paint additive used for mildew control. The label indicated that this product contained 25% bis(tributyltin) oxide (TBTO) as its only active ingredient.

Dose-specific effects of trimethyltin poisoning on learning and hippocampal corticosterone binding.

The organometal neurotoxin trimethyltin (TMT) damages limbic forebrain, and impairs acquisition of lever-directed behaviors in an autoshaping task, in which a lever is presented according to a random time schedule, and rats learn to associate its presentation/retraction with food delivery (Cohen et al., 1987). This impairment is evident only if a sufficiently long delay of reinforcement is interposed between lever retraction (which occurs either automatically after 15 sec, or immediately upon a touch response) and food pellet delivery. Paradoxically, rats given a higher (7.5 mg/kg) dose show a smaller acquisition impairment, perhaps because they are generally more reactive to the lever than controls. These rats sustain a larger hippocampal lesion (measured by wet weight of the structure). The experiment reported here was done to investigate (1) an autoshaping deficit related to hippocampal weight loss, and (2) biochemical changes in hippocampus which might be related to behavioral impairments. Rats were treated with water vehicle or TMT four weeks before autoshaping using a 6 sec reinforcement delay. In addition to lever touching, touches of the food trough were measured. The timing of trough-touching behaviors within a trial was used as an indication of the strength of the association formed between the lever and the site of food delivery. Following autoshaping rats were adrenalectomized and killed for measurement of cytosolic [3H]corticosterone binding in hippocampus. As before, rats treated with 6.0 mg TMT/kg showed a deficit in acquisition of lever-directed behaviors. Also, as hypothesized, the proportion of total trough-directed behaviors made during the 6 sec reinforcement delay intervals (when reinforcement probability was high) diverged significantly from control values as learning progressed. These rats also showed a reduction in hippocampal weight compared with controls, but significant decreases in hippocampal steroid binding were observed only in groups given the low and median dose of TMT. Further, steroid binding was correlated with lever-directed behaviors. It thus appears that lever and trough behaviors can be used to simultaneously assess different aspects of impairment in associative learning which are accompanied by differential cell loss and biochemical deficit.

[Anti-cerebral edema properties of PEG 300 in triethyltin poisoning]. / Propriété antioedémateuse cérébrale du PEG 300 LORS de l'intoxication par le triéthylétain.

The polyethylene glycols (PEG) frequently used as solvents of non hydrosoluble molecules present toxic and pharmacodynamic properties. The effect of PEG 300 (10 ml/kg) on the modifications of the central nervous system (CNS) previously induced by a subchronic intoxication with triethyltin salt (TEE) (2 mg/kg p.o. for 5 days) has been studied in rat. The following parameters are recorded: measure of brain edema, concentration of the aminergic neurotransmitters in four different brain areas, neurological status, behaviour, mortality. The PEG 300 antagonizes or reduces some of the effects of the TEE: edema, behavioral disturbances, mortality. On the opposite, no change in the amines and their metabolites induced modifications is observed. This selective antagonism towards some of the components of TEE brain toxicity brings more information on pharmacological properties of this solvent and opens a discussion on the role of neurotransmitters on brain edema.

Effect of triethyltin chloride on the central aminergic neurotransmitters and their metabolites: relationship with pathophysiology of aging.

Triethyltin (TET) salt intoxication provokes a myelinic vacuolisation associated with a white matter cerebral edema. The central nervous system disturbances accompanying these phenomena (Na-K-ATPase activity, neurological symptoms, water and sodium cerebral content) can be counteracted by drugs used in age-related brain failure; consequently, TET intoxication could be suggested as an experimental model for studying the aging process. The aim of the present study is to follow-up the biogenic amine concentrations in different brain areas of TET treated rats, knowing that modifications of cerebral amines exist throughout the aging process. The following results are obtained: the cerebral water content of the TET treated rats is significantly increased, confirming the existence of a brain edema. Monoamine concentrations are significantly decreased, specifically noradrenaline (in hypothalamus, mesencephalon, cerebellum); serotonin (in striatum, hypothalamus, mesencephalon); dopamine only in hypothalamus; these are accompanied by an increase of the metabolites 5 HIAA (in striatum and mesencephalon) and HVA (striatum). These modifications are compared to those occurring in physiological aging, and hypothetical mechanisms are reviewed. We conclude that TET intoxication must not be considered as a pathophysiological model of brain aging, but may be considered as a useful pharmacological tool for studying experimental drugs liable to counteract brain age-induced disturbances.

Neuropathology of trimethyltin intoxication. IV. Changes in the spinal cord.

Young C57BL/6N mice were injected (ip) with trimethyltin chloride at a dosage of 3.0 mg/kg body wt. Animals were sacrificed between 48 to 72 hr postinjection by means of intracardial perfusion of saline solution followed by 2.5% buffered glutaraldehyde. For light microscopy, the cords were further fixed in 10% buffered formalin and embedded in Paraplast. For electron microscopy, tissue samples were obtained from the cord levels at L1-L4, further fixed in glutaraldehyde and osmium tetroxide, and embedded in Epon. Chromatolytic and vacuolar changes involving neurons mainly in the medial and lateral motor nuclei of the anterior horns were observed. Electron microscopy revealed lysosomal accumulation and extensive dilatation of the cytoplasmic membrane systems (endoplasmic reticulum, Golgi complex). Large intraneuronal vacuoles were formed as a result of extensive intraneuronal edema. Progressive distention of the cytoplasmic membranes resulted in severe vacuolation, disintegration, and total breakdown of the neurons.

Behavioral toxicity of trialkyltin compounds: a review.

Triethyltin (TET) and trimethyltin (TMT) are neurotoxic organotin compounds which produce different patterns of toxicity in adult animals. Exposure to TET produces behavioral toxicity (decreased motor activity, grip strength, operant response rate and startle response amplitude) which reflects impaired neuromotor function. These deficits are consistent with the reported myelin vacuolation and cerebral edema produced by TET, and with its direct effects on muscle. Exposure to TMT produces both hyperactivity and impaired learning and performance. These impairments are consistent with reported neuronal cell death produced by TMT, particularly in limbic system structures. While the behavioral deficits produced by repeated exposure to TET are reversible when dosing is terminated, the behavioral impairments produced by a single exposure to TMT appears to be irreversible.

The pattern of myelin proteins in triethyltin (TET) intoxication.

Myelin proteins isolated from the brain of Wistar rats intoxicated chronically with triethyltin sulfate (TET) according to the technique of ETO et al. (1971) were investigated. Among the various protein fractions, the Agraval protein happened to be most evidently affected, demonstrating considerably reduced percentages. However the results did not prove that any of the individual myelin proteins was specifically affected by TET intake. The interesting point in chronic TET poisoning was that some clinical symptoms as well as disturbances in myelin proteins demonstrated a clear tendency to retrogression despite of the continued intoxication. These observations indicate obviously that during chronic TET intake, some kind of biochemical adaptation to the noxious action of the poison on the myelin sheath takes place.