Organotins. formation, use, speciation, and toxicology.

The speciation of organotin(IV) cations in natural waters, in sewage or in biofluids is strongly influenced by the complex formation with the available metal-binding compounds, i.e., both high and low molecular weight ligands of biological and environmental interest. The primary intention of this chapter is to discuss the aquatic solution chemistry of organotin cations and their complexes formed with low and high molecular weight bioligands. Besides, some synthetic aspects, applications and sources of organotin pollution, their destinations in the environment, and toxicology will be also shortly discussed.

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.

Unique cerebral dysfunction following triphenyltin acetate poisoning.

1. In animal studies, TPTA was found to be neurotoxic. In humans, variable CNS pictures have been described with or without significant EEG findings. Brain CT does not usually reveal any abnormalities. 2. Our patient presented with intermittent unique spontaneous involuntary movement of hands, facial twitching, silly smile and crying. Diplopia, drowsiness, giddiness, vertigo, bidirectional nystagmus, impairment of calculation ability, as well as disorientation to time, people and place also developed. EEG showed mild cortical dysfunction without seizures. MRI and Tc-99m HMPAO brain SPECT revealed no significant findings. TPTA may cause cellular dysfunction of brain without structural damage, which results in variable CNS clinical presentations. 3. Nadir of leucopenia was noted on the sixth day after consumption of TPTA. Liver impairment occurred on the ninth day. Borderline demyelinated neuropathy developed on the fifty-third day. CNS abnormalities, delayed peripheral neuropathy, hepatitis and leucopenia deserve monitoring for a prolonged period, even when the victim initially presents with GI upset only after consumption of TPTA.

Acute nephropathy of organotin compounds.

Three patients who developed acute nephropathy following ingestion of triphenyltin acetate (TPTA) are described. All of them had significant proteinuria, azotemia, and polyuria. Mild neurological manifestations in all patients were also noted. Hematuria and pyuria were noted in 1 severely poisoned patient. Evidence for hepatitis was present in 2 patients, and for pancreatitis in 1. Renal biopsy showed focal fusion of glomerular cell processes and proximal tubular damage with cellular necrosis. Two patients survived with complete recovery of renal functions. One old patient died of aspiration pneumonia. Acute nephropathy following organotin intoxication appears to result mainly from proximal renal tubular damage with a benign and reversible clinical course.

Occupational triphenyltin acetate poisoning: a case report.

A case of triphenyltin acetate (TPTA) poisoning is described. The patient, who had been exposed mainly to cutaneous absorption, showed acute stages of an urticarial eruption, signs of hepatic injury, slight glucose intolerance, and electroencephalographic abnormalities. Concomitant with the highest concentrations of tin in plasma and the peak of tin excretion in urine, neutrophils did not show the normal increase in actin polymerisation after stimulation with a chemotactic peptide (100 nM fMLP). The peak of urinary excretion of tin occurred between the fifth and the sixth day after poisoning; subsequently, the rate of excretion became slow, suggesting biphasic kinetics with the possibility of a cumulative trend.

Acute triphenyltin intoxication: a case report.

A 23 year old male developed abdominal pain, diarrhoea, and vomiting several hours after poisoning with acute triphenyltin intoxication in a suicide attempt. Severe ataxia, dysmetria, nystagmus, and blurring of vision soon supervened. Disturbance of consciousness and confusion developed 12 days later and lasted for two months. A delayed sensorimotor polyneuropathy was shown by electrophysiological studies to be due to axonal degeneration and demyelination. The neuropathy rapidly recovered after consciousness was regained.

Catecholamine levels in the brain and adrenals of rats poisoned with triphenyltin (Brestan 60).

The effects of organotin fungicide Brestan 60 and SnCl4 on rat brain and adrenal catecholamines (CA) were examined. Rats were treated with 0.5 LD50 of Brestan 60 (acute experiment) or 0.05 LD50 (subchronic experiment) and SnCl4 in equal dose of inorganic tin. Brestan 60 in both experiments decreased CA concentrations in the brain and adrenals. In contrast, SnCl4 did not alter brain CA but had greater effect on adrenal CA than Brestan 60 had. Effects of organotin fungicide may be related with inhibition of oxidative phosphorylation and membrane-bound ATP-ases.

Methyltin intoxication in six men; toxicologic and clinical aspects.

Neurologic and psychiatric symptoms such as headache, tinnitus, defective hearing, changing desorientation and aggressiveness are initial symptoms of methyltin chloride intoxication. Some patients also developed epileptic equivalents, such as dreamy attacks and central ventilation transaminases. Laboratory findings included low levels of serum potassium, leucocytosis and elevated transaminases. The excretion rate of tin in the urine correlated with the severity of the intoxication. There was no measurable effect of plasma separation or d-penicillamine therapy on tin excretion in the urine or on the clinical picture. The long-term prognosis of severely intoxicated persons is poor. Neurohistopathologic findings confirm the animal studies by Brown et al and the severe damage and cell necrosis in the hippocampus area. To prevent such events workers need to be warned of the risk and dangers of working with organo-metallic compounds. The effectiveness of protective clothes and gas masks should be checked. In exposed workers regular testing is advised of tin concentrations in the urine.

Technoeconomic and environmental assessment of industrial organotin compounds.

Current uses of organotins include heat stabilizers for polyvinyl chloride (PVC), catalysts for polyurethane foam and silicone rubber, biocides, and animal health products. Domestic production consumption in 1982 is about 28 million pounds, and overall growth is estimated at 7 percent per year. Physical properties of organotins, including solubility in water, octanol-water partition coefficients, and Freundlich adsorption isotherm constants, are not well characterized. Analytical methods for tin in environmental and biological matrices involve concentration, separation, and identification by chromatography, spectrometry, and spectroscopy. Environmental fate and effects of organotins are not well understood. Degradation reactions may yield a complex set of products, including inorganic tin oxide. The effects of exposure of workers and release of organotins to the environment at point sources have been documented. Nonpoint sources of environmental exposure include discard and sanitary landfill disposal of plastics and direct release of biocides to aquatic or marine environments. Other dissipative uses of organotins which pose potential human risk include PVC food wrapping and bottles and rigid potable water pipe. The long term health effects of low level exposure to organotins are not known. Toxic metal cycling in the environment, including biomethylation of inorganic tin by naturally occurring bacteria, is of rising concern.

Specificity of psychiatric manifestations in relation to neurotoxic chemicals.

Previous impressions of specificity of psychiatric manifestations in relation to particular chemical intoxications have been confirmed by comparisons of the symptoms and signs of two groups of individuals. Nine persons exposed to inorganic mercury had "erethism" and xenophobia in addition to non-specific features of central nervous system poisoning. Twelve men with heavy exposure to organotins, in contrast to ten men with light or no exposure, more frequently presented an unique alternation between outbursts of range and deep depression, the later lasting from a few hours to a few days. The more heavily exposed men also had a greater number of nonspecific symptoms from neurotoxins.