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The nature and extent of the acute injury due to toxic inhalants depend on the inhalant's solubility in water pH and chemical reactivity, on the aerodynamic diameter of particles (when the inhalant is an aerosol), and on the degree of exposure. Initial signs and symptoms indicate upper airways and bronchial irritation. Laryngeal oedema and (or) severe bronchospasm may be rapidly lethal. After cessation of exposure a transient improvement is generally observed; however a delayed pulmonary oedema may occur within the first 48 hours. On the following days, bacterial surinfection is a common complication. Possible long-term sequelae are reactive airways dysfunction syndrome and bronchiolitis obliterans.

To obtain objective measures of possible impairment due to organic solvents, auditory, visual and somatosensory evoked potentials and cognitive event related potentials were recorded in a group of 13 workers occupationally exposed to a mixture of various solvents. The patients were compared to healthy subjects and to chronic alcoholics seen during post-alcohol withdrawal. Auditory and visual evoked potentials were almost normal but somatosensory evoked potentials showed a slight decrease of peripheral conduction velocities and an increase of central conduction times more marked in the solvent exposed workers who were also alcoholics. The late "cognitive" components reflecting attention processes (N2 and P3) were normal. Solvent-exposed workers and alcoholics were both characterized by some difficulty in modulating their attentional resources according to task demands, as reflected by a tendency to responses (N1, N2 and P3) of similar amplitudes whether the stimulus was or was not the target. These findings support the presence, in solvent exposed workers, of minor dysfunction of the nervous system at both peripheral and cortical levels potentiated by alcohol as well as of mild cognitive impairments concerning attention processes.

Voluntary ingestion of concentrated anticoagulant rodenticides leads to prolonged hypocoagulability sometimes accompanied by haemorrhage. The authors report 11 cases referred to the Paris Anti-Poisons Centre. The products implicated were chlorophacinone, bromadiolone, and warfarin. The time interval before medical intervention ranged from 90 minutes to 3 weeks. The absence of early clinical signs probably explains the number of late admissions. Haemorrhage of variable severity was observed in 8 cases. The prothrombin time varied with the administered dose of Vitamin K and/or coagulation factors. Three patients were lost to follow-up at days 9, 24 and 68. The other patients were treated for several weeks (27 to 82 days). Massive overdose with these rodenticides justifies stomach washout when the patients are seen early, daily check-ups of coagulability and treatment with Vitamin K at a dosage adapted to the biochemical abnormalities. Severe haemorrhage requires transfusion and the administration of factors of coagulation. The duration of the abnormalities is unpredictable; the prothrombin time should therefore be checked 48 hours after stopping Vitamin K therapy to detect any recurrence.

Diethylene glycol (DEG) intoxication resembles that of ethylene glycol, with progressive inebriation, anion gap metabolic acidosis, renal failure, coma and death. DEG is oxidized by alcohol dehydrogenase (ADH) to more toxic byproducts, thus blockade of ADH might be beneficial. Triethylene glycol (TEG), also metabolized by ADH, is less toxic. A young female suicidally ingested DEG and TEG, presenting in metabolic acidosis with coma. Given 4-methylpyrazole (4-MP), an ADH inhibitor, the acidosis resolved, the patient recovered and was discharged without sequelae. 4-MP, if supported by further studies, may be useful in DEG poisoning.

Liver injury is the main feature of paracetamol poisoning. Early administration of N-acetylcysteine is an effective antidotal treatment. There are also effective treatments for salicylate poisoning and severe cases are always due to delayed diagnosis. Salicylate poisoning should be systematically suspected when several of the following features are observed in a poisoned patient: tinnitus, deafness, hyperventilation, respiratory alkalosis, metabolic acidosis. Diagnosis is readily confirmed by measuring plasma salicylate concentration.

The authors describe a high correlation between the plasma and urine Paraquat concentrations in 45 poisoned patients. The study of the plasma and urine kinetics asserts the importance and the rapidity of distribution processes and how it is necessary to quickly undertake the therapeutic means.

Thirty-one patients with isocyanate-induced asthma were studied 6-54 months after diagnosis. Four had the same work conditions and unchanged or worse respiratory symptoms; seven had an alternative job or safer work conditions at the same work-place and suffered from mild to severe symptoms. The remaining twenty subjects were definitely removed from exposure; of these, ten (50%) remained symptomatic after being removed from exposure for an average of 19 months. Asymptomatic patients appeared to be younger and to have shorter durations of total and symptomatic exposures, while symptomatic patients were more reactive to acetylcholine at diagnosis. For patients removed from isocyanate exposure and for those re-employed at the same work-place, quality of the new work site seems to play a role in the evolution of isocyanate-induced asthma.

The aim of this study was to evaluate air and surface contaminations, and internal contamination of healthcare workers during open-abdomen HIPEC using oxaliplatin. Platinum (Pt) was measured in urine of exposed workers and in multiple air and surface samples. Three successive HIPEC procedures were investigated in each of the two hospitals participating in the study. Analysis of air samples did not detect any oxaliplatin contamination. Heavy contamination of the operating table, the floor at the surgeon’s feet, and the surgeon’s overshoes were observed. Hand contamination was observed in surgeons using double gloves for intra-abdominal chemotherapy administration, but not in those using three sets of gloves. Pt was not detected in urine samples obtained after HIPEC (

Poisonings with industrial products represent approximately 7% of the cases reported to the poison centres. Ingestion of petroleum distillates induces irritation of the gastrointestinal tract, central nervous system depression and aspiration pneumonitis which may be severe; treatment is mainly supportive. Ethylene and diethylene glycol poisonings produce central nervous system depression, anion gap metabolic acidosis, osmolar gap and acute tubular necrosis; in severe cases, hypocalcaemia, cerebral oedema and heart failure may be observed; treatment often associates supportive measures, haemodialysis and administration of competitive inhibitors of alcohol dehydrogenase (ethanol or 4-methylpyrazole). Glycol ethers induce central nervous system depression and metabolic acidosis; in addition, ethylene glycol monobutyl ether produces haemolysis; monomethyl and monoethyl ethers are responsible for bone marrow and lymphoid organ toxicity, they adversely affect spermatogenesis and are teratogens.

Two cases of paraquat poisoning resulting from skin absorption are reported. One patient died from respiratory failure 26 d after deliberate application of the herbicide onto his whole body as a treatment for scabies. The other patient developed extensive dermatitis (probably a complication of pre-existing psoriasis). Only a moderate and transitory impairment of this latter patient's renal and respiratory functions were observed after repeated exposure of his damaged skin to a dilute paraquat spray.

Somatosensory, Brainstem Auditory and Pattern Reversal Evoked Potentials (SEPs, BAEPs, PREPs) are recorded in workers occupationally exposed to mixtures of organic solvents, in order to specify the levels of the nervous system affected by a long term exposure to solvents, and to analyze the effects of age and gender. The most significant differences are found for SEPs; they objectivate peripheral impairments magnifying the differential effects of age observed in the control subjects, and show the higher sensitivity of women. The central impairment is pointed out by the latency delay of P22 component mainly, whose age-related increase is amplified by solvent exposure.

A 43-year-old man, with no history of cardiac disease, deliberately ingested 4 tablets of a rodenticide containing 12 mg of scilliroside. Vomiting appeared a few minutes later and persisted for 48 hours. At the 20th hour, when he was admitted, EKG revealed a complete atrio-ventricular block which disappeared only on the 4th day. The repolarization abnormalities characteristic of digitalization persisted still further until the 12th day.

Only 7 cases of human poisoning with amitraz have been previously published and most of them are poorly documented. Four additional cases are now reported. The symptoms observed were remarkably similar in all cases: all patients experienced drowsiness; 3 presented with bradycardia, miosis and/or hyperglycemia; 2 developed hypotension and/or vomiting. These symptoms are compared to those observed in previous human or animal poisoning. Alpha 2-adrenoceptor stimulation could explain the clinical and laboratory features in most cases.

Seventy-five cases of acute poisoning with effervescent tablets of paracetamol have been recorded. No patients developed hepatitis. Ingested doses were low, and resulted only in minor manifestations. As each package contains only 6.6 g of paracetamol and effervescent tablets cannot be ingested in large quantities, the risk of serious overdosage is low.

Reports of acute human selenium toxicity are rare. We report 2 new cases. One patient ingested a mouthful of selenic acid (30 g/L); he only suffered mild gastrointestinal disturbances. Serial measurements of plasma selenium concentrations were performed. The first plasma level was obtained 3 h after ingestion and was the highest (931 micrograms/L); plasma concentrations subsequently decreased with a half-life of 17.5 h. The second patient ingested 1.7 g of sodium selenite. He suffered severe gastroenteritis, had transient electrocardiographic changes and developed a slight elevation of serum bilirubin. The first serum concentration measurement was performed 3 h after ingestion; the selenium level was 2.716 micrograms/L. These data are compared to those from other published cases. The prognostic significance of the blood selenium concentration is discussed.

4 cases of subcutaneous injection of metallic mercury are reported and compared with those recorded by others. Subcutaneous injection always causes local inflammatory reaction and granuloma formation. Systematic mercury absorption is the rule as it is proved by high mercury levels in blood and urine. Nevertheless this absorption is usually too small to be responsible for toxic manifestations. Surgical excision of all accessible contaminated subcutaneous areas should be performed. When residual mercury is roentgenographically detectable regular monitoring of CNS, renal function and urinary and/or blood mercury levels are necessary.

Epidemiological studies have provided evidence that neuropsychiatric symptoms are induced by long term exposure to solvents; individual diagnosis with psychometric tests, however, is not always possible (for example, when the patient has linguistic difficulties). Therefore evoked potentials and cerebral blood flow were studied in 50 patients occupationally exposed to solvents who were referred to our department and for whom a solvent induced psycho-organic syndrome was suspected. Degree of exposure was evaluated by its duration (mean 13.9, range 1 to 37 years) and its intensity (from an interview). At the group level, P22 and N35 latencies and amplitude N20-P22 of somatosensory evoked potentials were higher in cases than in controls (p < 0.05), whereas there was no difference for brainstem and visual evoked potentials, nor for hemispheric cerebral blood flow (but a higher distribution in the left occipital region was seen in patients, p < 0.05). Some parameters were linked to degree of exposure (amplitude N20-P22 of somatosensory evoked potentials, interpeak latency I-V of brainstem evoked potentials, distribution of cerebral blood flow in the internal frontal left region). At the individual level, these examinations were not of diagnostic value because sensitivity was low.

A retrospective study of 25 cases of cyanide poisoning has brought to light the following points: cardiorespiratory arrests are frequent (7/25) and often inaugural; in severe intoxications (7/25), deep metabolic acidosis is the rule, and cyanide poisoning should always be suspected in cases of coma with severe acidosis; mild intoxications are frequently symptomless. Anxiety and agitation should not be considered as evidence of cyanide poisoning; they are merely due to fear in most cases. The present treatment of acute cyanide poisoning relies basically on symptomatic measures: sodium bicarbonate, cardiac massage and, above all, assisted ventilation with 100% oxygen. Our experience does not support the concept of a lethal cyanide blood level when patients can rapidly be transferred by a medical team to an intensive care unit. Survival depends more on prompt medical care than on the accessibility to sophisticated antidotes.

One hundred and twenty nine children with chronic lead poisoning were followed from August 1985 to July 1989. Old lead paint was recognized as the contaminant source at home. Pica of paint flakes was the main mode of intoxication. Children were classified according to the Center for Disease Control 1985 as follows: class IV (39 cases), class III (45 cases), class II (30 cases), class I (15 cases). Nineteen of those in class IV had blood lead levels above 700 micrograms/l and received BAL + EDTA followed by EDTA alone for a mean of 4.6 +/- 3.5 courses. With this treatment, blood lead level decreases were 50 +/- 17%. Nine of these class IV children had an evaluation at last 3 months after the last chelation course: 5 became class I or II, and 2 class III with a negative provocative test. The remaining 20 children in class IV were given a mean of 2.7 +/- 1.4 courses of EDTA. Blood lead levels decreased by 52 +/- 15%; 11 children were evaluable at least 3 months after the last chelation course: 4 became class I, and 7 class II. Thus overall 80% of class IV moved under treatment to class I or II. Among those 45 children in class II, 30 underwent a provocative test and 24 one to three courses of EDTA: 8 were further studied: 3 became class I and 5 class II. Combination of screening, medical treatment and sociocultural approach led to avoid acute effects of severe chronic childhood lead poisoning. The efficacy of such an approach in preventing chronic effects has still to be evaluated.