Wayne A. Temple

Diethylene glycol poisoning.

Introduction. Diethylene glycol (DEG) is a clear, colorless, practically odorless, viscous, hygroscopic liquid with a sweetish taste. In addition to its use in a wide range of industrial products, it has also been involved in a number of prominent mass poisonings spanning back to 1937. Despite DEGs toxicity and associated epidemics of fatal poisonings, a comprehensive review has not been published. Methods. A summary of the literature on DEG was compiled by systematically searching OVID MEDLINE and ISI Web of Science. Further information was obtained from book chapters, relevant news reports, and web material. Aim. The aim of this review is to summarize all main aspects of DEG poisoning including epidemiology, toxicokinetics, mechanisms of toxicity, clinical features, toxicity of DEG, diagnosis, and management. Epidemiology. Most of the documented cases of DEG poisoning have been epidemics (numbering over a dozen) where DEG was substituted in pharmaceutical preparations. More often, these epidemics have occurred in developing and impoverished nations where there is limited access to intensive medical care and quality control procedures are substandard. Toxicokinetics. Following ingestion, DEG is rapidly absorbed and distributed within the body, predominantly to regions that are well perfused. Metabolism occurs principally in the liver and both the parent and the metabolite, 2-hydroxyethoxyacetic acid (HEAA), are renally eliminated rapidly. Mechanisms of toxicity. Although the mechanism of toxicity is not clearly elucidated, research suggests that the DEG metabolite, HEAA, is the major contributor to renal and neurological toxicities. Clinical features. The clinical effects of DEG poisoning can be divided into three stages: The first phase consists of gastrointestinal symptoms with evidence of inebriation and developing metabolic acidosis. If poisoning is pronounced, patients can progress to a second phase with more severe metabolic acidosis and evidence of emerging renal injury, which, in the absence of appropriate supportive care, can lead to death. If patients are stabilized, they may then enter the final phase with various delayed neuropathies and other neurological effects, sometimes fatal. Toxicity of DEG. Doses of DEG necessary to cause human morbidity and mortality are not well established. They are based predominantly on reports following some epidemics of mass poisonings, which may underestimate toxicity. The mean estimated fatal dose in an adult has been defined as ∼1 mL/kg of pure DEG. Management. Initial treatment consists of appropriate airway management and attention to acid–base abnormalities. Prompt use of fomepizole or ethanol is important in preventing the formation of the toxic metabolite HEAA; hemodialysis can also be critical, and assisted ventilation may be required. Conclusions. DEG ingestion can lead to serious complications that may prove fatal. Prognosis may be improved, however, with prompt supportive care and timely use of fomepizole or ethanol.

Ricin as a weapon of mass terror — Separating fact from fiction

In recent years there has been an increased concern regarding the potential use of chemical and biological weapons for mass urban terror. In particular, there are concerns that ricin could be employed as such an agent. This has been reinforced by recent high profile cases involving ricin, and its use during the cold war to assassinate a high profile communist dissident. Nevertheless, despite these events, does it deserve such a reputation? Ricin is clearly toxic, though its level of risk depends on the route of entry. By ingestion, the pathology of ricin is largely restricted to the gastrointestinal tract where it may cause mucosal injuries; with appropriate treatment, most patients will make a full recovery. As an agent of terror, it could be used to contaminate an urban water supply, with the intent of causing lethality in a large urban population. However, a substantial mass of pure ricin powder would be required. Such an exercise would be impossible to achieve covertly and would not guarantee success due to variables such as reticulation management, chlorination, mixing, bacterial degradation and ultra-violet light. By injection, ricin is lethal; however, while parenteral delivery is an ideal route for assassination, it is not realistic for an urban population. Dermal absorption of ricin has not been demonstrated. Ricin is also lethal by inhalation. Low doses can lead to progressive and diffuse pulmonary oedema with associated inflammation and necrosis of the alveolar pneumocytes. However, the risk of toxicity is dependent on the aerodynamic equivalent diameter (AED) of the ricin particles. The AED, which is an indicator of the aerodynamic behaviour of a particle, must be of sufficiently low micron size as to target the human alveoli and thereby cause major toxic effects. To target a large population would also necessitate a quantity of powder in excess of several metric tons. The technical and logistical skills required to formulate such a mass of powder to the required size is beyond the ability of terrorists who typically operate out of a kitchen in a small urban dwelling or in a small ill-equipped laboratory. Ricin as a toxin is deadly but as an agent of bioterror it is unsuitable and therefore does not deserve the press attention and subsequent public alarm that has been created.

Lecithin:cholesterol acyltransferase activity, plasma and lipoprotein lipids and obesity in men and women

Lecithin:cholesterol acyltransferase (LCAT) activity, lipid concentration, lipoprotein lipid concentrations and cholesteryl ester linoleic acid proportion were determined in the plasma of 85 subjects randomly selected from a population during a health screen survey. Mean fractional LCAT rate was significantly higher in men than in women. Molar LCAT rate correlated with low density lipoprotein (LDL) cholesterol concentration in men and with nearly all lipoprotein lipid concentrations in women. Most of these relationships were dependent on plasma unesterified cholesterol (UC) concentration. Fractional LCAT rate was correlated only with HDL cholesterol concentration in women and this relation was dependent on the influence of obesity. An inverse relationship between plasma cholesteryl ester (PCE) linoleic acid proportion and molar LCAT rate in women was also explained by influences of obesity on the data. Both fractional and molar LCAT rates were positively correlated with obesity (Quetelets Index and subscapular skinfold thickness) in women but not in men. This study showed the influence of sex on nearly all correlations involving LCAT activity in combined groups of men and women.

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 childs death. Our own experiences indicate that advice given in standard texts based on poisoning cases managed with out-moded techniques should be carefully evaluated.

The adverse effects of hydrogen cyanamide on human health: an evaluation of inquiries to the New Zealand National Poisons Centre

Introduction. Hydrogen cyanamide is used in New Zealand to induce bud break in kiwifruit vines. The aim of this investigation was to evaluate the calls received by the New Zealand National Poisons Centre (NZNPC) attributed to acute hydrogen cyanamide exposure, and to ascertain the clinical effects of such exposures. Methods. Call data from the NZNPC telephone collection databases regarding human hydrogen cyanamide exposures were analyzed retrospectively for the years 1990–2006. Results. There were 68 human exposures, 69% were male and 22% female; 88% were adults and there were no suicide attempts. Common exposure routes were inhalation (56%) and skin contact (28%). The workplace accounted for 45% of calls. The predominant toxic effects were nausea and vomiting (29%), headache (22%), contact dermatitis (19%), and erythema (18%). Discussion. Reported symptoms and signs were consistent with the expected effects of hydrogen cyanamide exposure. Other reports of similar exposures describe higher degrees of illnesses among workers using hydrogen cyanamide, which might have been because of lack of training, inadequate access to personal protective equipment, and the absence of engineering controls. Conclusions. Based on the calls received by the NZNPC, acute exposure to hydrogen cyanamide in the workplace or acute exposure to those living within the vicinity of its use may not pose a significant immediate threat to human health.

Paediatric poisoning due to nicotine replacement therapy products: An emerging hazard

Dear Editor, PAEDIATRIC POISONING DUE TO NICOTINE REPLACEMENT THERAPY PRODUCTS: AN EMERGING HAZARD Nicotine replacement therapy (NRT) products are used as aids in smoking cessation and are available without a prescription in New Zealand. As they become increasingly popular, incidents of poisoning, particularly among young children, will theoretically become more common. Consequently, it is anticipated that poison information centres may be contacted with increasing frequency regarding inadvertent exposures. We retrospectively reviewed data from the New Zealand National Poisons Centre (NZNPC) call collection database to investigate the epidemiology of acute paediatric NRT exposures reported between 2003 and 2011 and compared this with New Zealand NRT sales data. For these years, the NZNPC received 185 enquiries associated with NRT exposures in children 6 years of age or less. From 2003 to 2007, enquiries were relatively steady with a mean of 8 (standard deviation (SD) + 2.5, range 4–10) calls per year. The