Terpenes and terpenoids in chemical sensitivity.

UNLABELLED: CONTEXT : Terpenes and terpenoids are a diverse class of organic compounds produced by a variety of plants, particularly conifers. Chemically sensitive patients can be targeted by terpenes and terpenoids, resulting in a triggering of symptoms and pathology. Often patients cannot clear their symptoms from exposure to chemicals unless terpenes and terpenoids are avoided and neutralized along with chemical avoidance and treatment. OBJECTIVE: This article evaluates the presence, diagnosis, and treatment of terpenes exposure in chemically sensitive patients. DESIGN: A double-blind, placebo-controlled, 2-part study was designed to establish the chemically sensitive state of the patients in part 1, followed by a second set of challenges to determine each patient's concurrent sensitivity to terpenes and terpenoids in part 2. In all of the challenges, normal saline was used as a control. A case report illustrates the history of 1 patient and describes the authors' treatment methods. SETTING: The study was developed and conducted at the Environmental Health Center of Dallas (EHC-D) because the environment within the center is 5 times less polluted than the surrounding environments, as determined by quantitative air analysis and particulate counts. PARTICIPANTS: A total of 45 chemically sensitive patients at EHC-D with odor sensitivity to terpenes. The cohort included 18 males and 27 females, aged 24-62 y.Intervention • Patients were deadapted (4 d) and evaluated in a 5-times-less-polluted environment, which was evaluated using air analysis and particulate counts. After deadaptation, the patients were challenged by inhalation in a controlled, less-polluted glass steel booth inside an environmentally controlled room with an ambient air dose of the toxics in the order of parts per billion (PPB) and parts per million (PPM). These toxics included formaldehyde, pesticide, cigarette smoke, ethanol, phenol, chlorine, new sprint, perfume, and placebo. They were also challenged intradermally with extracts of volatile organic compounds (VOCs), including formaldehyde, orris root, ethanol, phenol, cigarette smoke, chlorine, newsprint, perfume, terpenes, terpenoids, and placebo. OUTCOME MEASURES: Inhaled challenges recorded pulse, blood pressure, peak bronchial flow, and other signs and symptoms 30 min before and at 15-min intervals for 2 h postchallenge. Intradermal challenges recorded wheal size and the provocation of signs and symptoms. RESULTS : Different numbers of patients were tested for each terpenes source because of time-related factors or the cumulative effect of testing, which made patients unable to continue. Of 45 chemically sensitive patients in the study, 43 demonstrated sensitivity to terpenes. CONCLUSIONS: This particular patient group was positive for a number of toxic and nontoxic chemicals provoking their symptoms. This study shows there was a connection between VOCs, other chemicals, and terpenes in chemically sensitive patients in a prospective cohort study. It has also shown the potential for terpenes to exacerbate symptoms of chemical sensitivity. Further research on this topic is recommended.

"Herbal remedy is natural and safe"--truth or myth?

Neem oil is often used externally as a traditional medicine in India. Its ingestion, even in small doses produces toxic effects like severe metabolic acidosis, seizures, renal failure and encephalopathy. Management is supportive and prognosis is generally good but fatalities may occur. Herein we report an unusual case of neem oil toxicity in a previously normal adult.

Management of root lesion nematode, Pratylenchus delattrei in crossandra using oil cakes.

Selected oil cakes, neem, castor and mahua, were tried independently and in combination with a chemical nematicide (carbofuran 3G) for the management of Pratylenchus delattrei in crossandra under glass house conditions. The neem oil cake was effective compared to other oil cakes used and there was a synergistic effect when the neemcake was coupled with carbofuran 3G in the management of Pratylenchus delattrei. The treatment resulted in better establishment of seedlings, and with increased plant bio-mass and flower yield.

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.

Status spongiosis, optic neuropathy, and retinal degeneration in Helichrysum argyrosphaerum poisoning in sheep and a goat.

Lesions of natural Helichrysum argyrosphaerum poisoning were studied in eight sheep and one goat. Light microscopic examination revealed widespread, bilaterally symmetrical status spongiosis of the white matter of the brain consistently present in the subependymal area adjacent to the lateral ventricles, cerebellar peduncles, and brain stem in all animals. In three animals, the ultrastructural finding of intramyelinic vacuolation due to splitting of the myelin lamellae at the intraperiod lines indicated myelin edema. There was also mild distension of perivascular and extracellular spaces in the severely affected areas. Significant changes were absent in neurons, glial cells, axons, or blood vessel walls. Myelin edema associated with degeneration and loss of axons and myelin and astrocytic gliosis was present in the intraorbital and intracranial portions of the optic nerves. In the intracanalicular portions of the nerves in three animals that were studied, more chronic lesions consisting of fibrosis and atrophy of the nerve suggested that the optic neuropathy follows compression of the nerve in the optic canal as a result of myelin edema. The toxic principle of the plant also caused a degenerative retinopathy in five animals. The essential histopathologic change was degeneration and loss of the photoreceptor outer segments predominantly in the nontapetal retina. These retinal lesions were associated with hyperplasia and hypertrophy and with migration of the pigmented epithelium, focal retinal separation, and depletion and loss of the nuclear layers.

[Fatal poisoning caused by oil of epazote, Chenopodium graveolens]. / Envenenamiento mortal causado por el aceite de epazote, Chenopodium graveolens.

We present a case of acute lethal poisoning by oil of "epazote" (oil of chenopodium), in a 2 y 9 m female. The volatile oil was administered according to the advice of a "curandera" (female healer), in a total quantity of 40 ml. Clinical features of the poisoning were: vomiting, deep coma, seizures, mydriasis, apnea, metabolic acidosis, neurogenic shock and death. The EEG suggested a diffuse encephalopathy, the CT scan with an image of severe brain edema and ventricular collapse. Relevant postmortem findings were brain edema and neuronal necrosis, pneumonia, enteritis, pericholangitis, mild pancreatitis and tubular necrosis. The phytochemical analysis of volatile oil identified ascaridol, the main active compound of the chenopodium herbs, in a quantity of 39 mg/ml (1,560 mg in the dose administered), and Chenopodium graveolens as the plant employed to prepare it. According to the age of the patient, 60 mg of ascaridol would be the recommended dose formerly used in the treatment of parasitic disease. Thus 1,560 mg was 26 times higher than the recommended dose, and exceeded by 56% the dose of 1,000 mg reported as lethal in humans.

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.

Margosa oil poisoning as a cause of toxic encephalopathy.

Margosa Oil is an extract of the seed of the Neem tree and is widely used as a traditional medicine by Indians in India, Sri Lanka, Burma, Thailand, Malaysia and Indonesia. Used mainly for external applications, it is often administered orally to neonates and infants regularly in small amounts. Margosa Oil causes toxic encephalopathy particularly in infants and young children. The usual features are vomiting, drowsiness, tachypnea and recurrent generalised seizures. Leucocytosis and metabolic acidosis are significant laboratory findings. Management is aimed primarily towards the control of convulsions although supportive management is equally important. Prognosis is usually good but fatalities and neurological deficits have been reported. We report here two infants with Margosa Oil poisoning presenting with encephalopathy.

Toxicology of selected pesticides, drugs, and chemicals. D-limonene, linalool, and crude citrus oil extracts.

Cats are susceptible to poisoning by insecticidal products containing D-limonene, linalool, and crude citrus oil extracts. Signs of toxicosis include hypersalivation, muscle tremors, ataxia, depression, and hypothermia.

[Poisoning caused by the cutaneous application of camphorated balsam ointment in a nursing infant]. / Intossicazione da applicazione cutanea di unguento balsamico canforato in piccolo lattante.

We describe a case of camphor and balsamic oil poisoning observed in a 1-month-old infant. Because of toxic effects of camphor and volatile oils on central nervous system, these compounds show no therapeutical usefullness in children.

Reproduction of acute bracken poisoning in a calf with ptaquiloside, a bracken constituent.

Acute bracken fern toxicity in a calf was reproduced with ptaquiloside, a norsesquiterpene glucoside, isolated from the boiling water extract of bracken fern. Ptaquiloside was dissolved in 500 ml of saline and administered by drench at increasing dosages for six days out of every seven for the following periods: 400 mg/day for 24 days, 800 mg/day for 14 days and 1600 mg/day for four days. Neutrophilic granulocytes began to decrease markedly around 50 days after the start of the experiment, and granulocytopenia continued for a further 35 days until the autopsy, despite the discontinuance of ptaquiloside administration. Thrombocytes showed a relatively slow depression and reached 1 X 10(5)/mm3 at the lowest level. The calf was autopsied 86 days after the start of administration of ptaquiloside. Sternal bone marrow was found to be mostly replaced with fat marrow and only small foci of erythropoietic cells and a small number of megakaryocytes remained.

[Reactivity of the liver to administration of cholic acid to rats subjected to polychloropinene expsoure for a long time]. / Reaktivnost' pecheni na vvedenie kholevoi kisloty u krys, podvergavshikhsia dlitel'nomu vozdeistviiu polikhlorpinena.

It was found that in healthy rats cholic acid caused a moderately increased intensity of bile secretion and raised the content of bile acids in it. In animals with toxic hepatitis produced by a long-term action of the chemical poison polychlorpinene in a dose of 1/10 DL50 and following introduction to such rats of cholic acid in a dose of 30 mg/100 g an intensified elinination of cholates and cholesterol excretion were evident. Combined action of polychlorpinene and cholic acid was conductive to a reduced conjugation of cholic acid with taurine and to a greater conjugation with glycine, this being attended by an increased content of free bile acids in the bile.