Genotoxicity associated to exposure to Prestige oil during autopsies and cleaning of oil-contaminated birds.

After the accident involving the oil tanker Prestige in November 2002 near 63,000 tons of heavy oil reached Galician coast (Northwest of Spain). This unleashed a large movement of volunteers to collaborate in several cleaning tasks. The aim of this study was to determine whether handling of Prestige oil-contaminated birds during autopsies and cleaning may have resulted in genotoxic damage. We have also evaluated the possible influence of DNA repair genetic polymorphisms (XRCC1 codons 194 and 399, XRCC3 codon 241 and APE1 codon 148) on susceptibility to the genotoxic effects evaluated. Exposure levels were analysed by determining volatile organic compounds in air samples. Peripheral blood samples were obtained from 34 exposed and 35 controls, and comet assay and micronucleus (MN) test were carried out. Genotyping was performed following PCR-RFLP procedures. Results obtained have shown significantly higher DNA damage, but not cytogenetic damage, in exposed individuals than in controls, related to time of exposure. Among exposed individuals, carriers of the variant alleles XRCC1 399Gln and APE1 148Glu have shown altered DNA damage with regard to wild-type homozygotes, suggesting exposure-genotype interactions. No effect of the DNA repair genetic polymorphisms analysed was observed in the MN test.

Multiple organ failure after ingestion of pennyroyal oil from herbal tea in two infants.

BACKGROUND: Hepatic and neurologic injury developed in two infants after ingestion of mint tea. Examination of the mint plants, from which the teas were brewed, indicated that they contained the toxic agent pennyroyal oil. METHODS: Sera from each infant were analyzed for the toxic constituents of pennyroyal oil, including pulegone and its metabolite menthofuran. RESULTS: Fulminant liver failure with cerebral edema and necrosis developed in the first infant, who died. This infant was positive only for menthofuran (10 ng/mL). In the other infant, who was positive for both pulegone (25 ng/mL) and menthofuran (41 ng/mL), hepatic dysfunction and a severe epileptic encephalopathy developed. CONCLUSION: Pennyroyal oil is a highly toxic agent that may cause both hepatic and neurologic injury if ingested. A potential source of pennyroyal oil is certain mint teas mistakenly used as home remedies to treat minor ailments and colic in infants. Physicians should consider pennyroyal oil poisoning as a possible cause of hepatic and neurologic injury in infants, particularly if the infants may have been given home-brewed mint teas.

Mitigation of pennyroyal oil hepatotoxicity in the mouse.

OBJECTIVES: Pennyroyal oil ingestion has been associated with severe hepatotoxicity and death. The primary constituent, R-(+)-pulegone, is metabolized via hepatic cytochrome P450 to toxic intermediates. The purpose of this study was to assess the ability of the specific cytochrome P450 inhibitors disulfiram and cimetidine to mitigate hepatotoxicity in mice exposed to toxic levels of R-(+)-pulegone. METHODS: 20-g female BALB/c mice were pretreated with either 150 mg/kg of cimetidine intraperitoneal (IP), 100 mg/kg of disulfiram IP, or both. After one hour, mice were administered 300 mg/kg of pulegone IP and were killed 24 hours later. Data were analyzed using ANOVA. Post-hoc t-tests used Bonferroni correction. RESULTS: There was a tendency for lower serum glutamate pyruvate transaminase in the disulfiram and cimetidine groups compared with the R-(+)-pulegone group. The differences were significant for both the cimetidine and the combined disulfram and cimetidine groups compared with the R-(+)-pulegone group. Pretreatment with the combination of disulfiram and cimetidine most effectively mitigated R-(+)-pulegone-induced hepatotoxicity. CONCLUSIONS: Within the limitations of a pretreatment animal model, the combination of cimetidine and disulfiram significantly mitigates the effects of pennyroyal toxicity and does so more effectively than either agent alone. These data suggest that R-(+)-pulegone metabolism through CYP1A2 appears to be more important in the development of a hepatotoxic metabolite than does metabolism via CYP2E1.

Evaluating exposures to plants.

Exposures to plants generate an exceptional amount of public concern, especially plant ingestions by children. Most clinical problems, however, involve older age groups as a result of experimentation with or overt abuse of plant parts and extracts. Of mounting concern is the sometimes uninformed and massive use of herbal preparations, currently widely available and in popular vogue. Plant exposures, from whatever source, may present as complex pharmacologic problems that may challenge the diagnostic and therapeutic skills of the physician. Although specific physiologic antagonists (antidotes) may exist for specific intoxications, basic decontamination and supportive techniques are many times all that may be offered.

Pennyroyal oil toxicosis in a dog.

A dog was treated for fleas with the application of pennyroyal oil obtained by the owner at a health food store. Vomiting ensued within 2 hours, and despite emergency treatment, the dog died within 48 hours. At necropsy, pennyroyal oil was determined to be the cause of death.

Toxicity of Salvia officinalis in a newborn and a child: an alarming report.

Although it is widely believed that herbal products are beneficial to the health, some herbal products can result in serious adverse effects, such as epileptic seizures, especially in children who are particularly susceptible. Sage oil contains well-known convulsant substances such as thujone, camphor, and cineole in different proportions. We report 2 cases, those of a newborn and a toddler, who experienced generalized tonic-clonic seizures after accidental exposure to sage oil. No other causes of seizure were detected by our clinical inquiries in either of the patients. The seizures occurred as an isolated event in the toddler, but in a repeated manner in the newborn; both patients experienced good outcomes. In any case of a first seizure of unexplained origin, the possibility of exposure to a herbal product should be kept in mind. Parents should be informed about the pros and cons of these untested remedies, which are presented as an alternative to conventional medicine.

[Poisoning by anis oil]. / Forgiftning med anisolie.

Essential oils are used widespread by the Danish population. In Denmark a severe case of poisoning from anis oil has occurred.

Essential oil poisoning: N-acetylcysteine for eugenol-induced hepatic failure and analysis of a national database.

UNLABELLED: We present a 15-month-old boy who developed fulminant hepatic failure after ingesting 10 ml of clove oil. After 24 h, the ALT level was in excess of 13,000 U/l, with blood urea and creatinine of 11.8 mmol and 134 micromol/l respectively. The hepatic impairment resolved after intravenous administration of N-acetylcysteine so that 6 h later, the ALT level was approximately 10,000 U/l. His liver synthetic function and clinical status improved over the next 4 days. This is the first such case report of its kind in Europe. Analysis of a national database revealed a 14-fold increase in home accidents related to aromatherapy from 1994-1999. Clove oil has important hepatotoxic effects. CONCLUSION: Recent growth in aromatherapy sales has been accompanied by an unfortunate increase in accidental poisoning from these products. Clove oil warrants special attention. Ingesting as little as 10 ml causes hepatotoxicity which can be treated with N-acetylcysteine.

Management of oil of citronella poisoning.

The management for ingestion of oil of citronella, an essential oil, has traditionally been rigorous, including dilution with milk or oil, and gastric lavage or emesis, taking care to prevent aspiration. Recently our Centre handled five oil of citronella poisonings and their outcomes led us to review our management protocol which had been based on information from standard poisoning texts. The source data used to determine the human toxicity of oil of citronella and the appropriate management of poisoning included a case report of a fatal ingestion of oil of citronella in a child. On scrutiny, however, the management of this poisoning included now out-moded techniques, giving rise to uncertainties in establishing the true cause of the child's death. Our own experiences indicate that advice given in standard texts based on poisoning cases managed with out-moded techniques should be carefully evaluated.

Melaleuca oil poisoning.

A 23-month-old boy became confused and was unable to walk thirty minutes after ingesting less than 10 mL of T36-C7, a commercial product containing 100% melaleuca oil. The child was referred to a nearby hospital. His condition improved and he was asymptomatic within 5 hours of ingestion. He was discharged to home the following day. Melaleuca oil, extracted from the Melaleuca alternifolia, contains 50-60% terpenes and related alcohols. Clinical experience with products containing melaleuca oil is limited. This case report suggests that ingestion of a modest amount of a concentrated form of this oil may produce signs of toxicity.