Robin J. Slaughter

Dear editor, In March 2020, nationwide restrictions on population movements were introduced in New Zealand due to the COVID-19 pandemic; the NZ Government adopted a four-level alert system to conta...

Sodium hypochlorite is used as a bleaching and disinfecting agent and is commonly found in household bleach. The objective is to review critically the epidemiology, mechanisms of toxicity, clinical features, diagnosis, and management of hypochlorite poisoning. PubMed was searched from January 1950 to June 2018 using the terms "Hypochlorite", "Sodium Hypochlorite", "Sodium Oxychloride", "Hypochlorous Acid", "Bleach", "Chlorine Bleach", in combination with the keywords "poisoning", "poison", "toxicity", "ingestion", "adverse effects", "overdose", and "intoxication". In addition, bibliographies of identified articles were screened for additional relevant studies including non-indexed reports. Non-peer-reviewed sources were also included. These searches produced 110 citations which were considered relevant. There is limited information regarding statistical trends on world-wide poisoning from sodium hypochlorite. In the United States of America, poison control center data have shown that enquiries regarding hypochlorite bleaches have ranged from 43,000 to 46,000 per year over the period 2012-2016. Mechanisms of toxicity: Hypochlorite's potential to cause toxicity is related to its oxidizing capacity and the pH of the solution. Toxicity arises from its corrosive activity upon contact with mucous membranes and skin. Features following ingestion: While small accidental ingestions are very unlikely to cause clinically significant toxicity, large ingestions may cause corrosive gastrointestinal injury and systemic effects, including metabolic acidosis, hypernatremia, and hyperchloremia. Features following dental exposure: Hypochlorite is used extensively by dentists for cleaning root canals and is safe if the solution remains within the root canal. Extrusions into the periapical area can result in severe pain with localized large and diffuse swelling and hemorrhage. Features following skin exposure: Prolonged or extensive exposure may cause skin irritation and damage to the skin or dermal hypersensitivity. Such exposures can result in either immediate or delayed-type skin reactions. High concentration solutions have caused severe chemical skin burns. Features following inhalation: Although there are only limited data, inhalation of hypochlorite alone is likely to lead to no more than mild irritation of the upper airways. Features following ocular exposure: Corneal injuries from ocular exposure are generally mild with burning discomfort and superficial disturbance of the corneal epithelium with recovery within 1 or 2 days. With higher concentration solutions, severe eye irritation can occur. The diagnosis can typically be made on the basis of a careful history, including details of the specific product used, its hypochlorite concentration, and the amount involved. As hypochlorite bleach produces a characteristic smell of chlorine, this may provide a diagnostic clue. In severe cases, corrosive injury is suggested on presentation because of hypersalivation, difficulty swallowing, retrosternal pain or hematemesis. Symptom-directed supportive care is the mainstay of management. Gastrointestinal decontamination is not beneficial. Local corrosive injury is the major focus of treatment in severe cases. Fiberoptic endoscopy and CT thorax/abdomen are complimentary and have been shown to be useful in corrosive injuries in assessing the severity of injury, risk of mortality and risk of subsequent stricture formation and should be performed as soon as possible after ingestion. Dental periapical extrusion injuries should be left open for some minutes to allow bleeding through the tooth and to limit hematoma development in tissue spaces. Once the bleeding has ceased, the canal can be dressed with non-setting calcium hydroxide and sealed coronally. Accidental ingestion of household bleach is not normally of clinical significance. However, those who ingest a large amount of a dilute formulation or a high concentration preparation can develop severe, and rarely fatal, corrosive injury so prompt supportive care is essential as there is no specific antidote. Treatment primarily consists of symptom-directed supportive care.

AIM: In autumn 2008, an outbreak of toxic honey poisoning was identified. The outbreak was not recognised initially until three cases from one family group presented to hospital, with a common factor of recent consumption of locally produced honey. The aim of this study was to investigate potential cases of this honey poisoning and determine which toxin was involved. METHOD: The incident was investigated retrospectively by Waikato District Health Board's Population Health unit and the New Zealand Food Safety Authority (NZFSA). Identified patients were followed up by questionnaire to gather case information. HortResearch (now Plant and Food Research) tested honey samples for toxins. RESULTS: The causative agent was identified as tutin, which comes from the New Zealand native plant tutu (Coriaria arborea) which has long been known as a potential source of contamination of honey produced in the warmer parts of New Zealand. Retrospective case investigation identified a total of 22 possible or probable cases, based on a clinical case definition. The spectrum of toxic effects reported were broadly similar to those previously described for tutin, derived either directly from the plant itself or indirectly from honey. There were 13 samples of honey, linked to symptomatic individuals, which were available for testing. Of these, 10 were positive for tutin and its hydroxy metabolite hyenanchin (hydroxytutin) and one was positive for hyenanchin alone. CONCLUSION: Toxic honey production is a significant risk in parts of New Zealand. Beekeepers and health professionals need to be informed of this risk and know how best to manage it. Due to this poisoning incident, public and professional awareness of honey poisoning has been substantially enhanced. This incident led to development of new food safety standards for New Zealand honey.

Objective: The New Zealand National Poisons Centre has, over a number of years, developed an electronic poisons information database. In 2002, this was released as toxin z™ (University of Otago, Dunedin, New Zealand), an Internet accessible version. The objective of this study is to describe New Zealand subscriber utilisation of TOXINZ with an emphasis on pharmaceutical monographs viewed.Methods: A retrospective review was conducted of records of New Zealand subscriber access to TOXINZ monographs during the period 1 January 2003 to 31 December 2012. Telephone enquiry data to the New Zealand National Poisons Centre was also obtained for the same time period.Results: Over the decade, 201 255 TOXINZ monographs were accessed, with annual numbers of documents viewed doubling from 13 718 in 2003 to 28 782 in 2012. Pharmaceuticals were the largest group viewed with 132 316 documents accessed (65.7% of all documents), followed by monographs relating to chemicals 46 061 (22.9%), substances of abuse 6698 (3.3%), plants 6563 (3.3%), supportive care 4668 (2.3%), animals 2553 (1.3%), and other 2396 (1.2%). In regard to the pharmaceuticals, high or rapidly increasing levels of enquiries were identified for venlafaxine, quetiapine, paracetamol, zopiclone and tramadol. Investigation of telephone enquiries to the New Zealand National Poisons Centre showed total poisoning calls increased slightly over the 10 year period, whereas telephone enquiries from hospitals halved.Conclusion: The TOXINZ Internet accessible poisons information database has proved to be a well‐utilised addition to the New Zealand National Poisons Centre's service.

To investigate poisoning exposures to chemicals that were unlabelled, mislabelled or not in their original containers in New Zealand over the last 10 years, based on calls to the New Zealand National Poisons Centre (NZNPC). Call data from the NZNPC between 2003 and 2012 were analysed retrospectively. Parameters reviewed included patient age, route and site of exposure, product classification and recommended intervention. Of the 324,411 calls received between 2003 and 2012, 100,465 calls were associated with acute human exposure to chemicals. There were 757 inquiries related to human exposure to mislabelled or unlabelled chemicals consisting of 0.75% of chemical exposures. Adults were involved in 51% of incidents, children, <5 years 32%, 5-10 years 10%, and adolescents 5%. Child exploratory behaviour was responsible for 38% of calls and adult unintentional exposures 61%. Medical attention was advised in 26% of calls. Inadvertent exposure to toxic products stored in unlabelled or mislabelled containers is a problem for all age groups. Although it represents a small proportion of total calls to the NZNPC it remains a potential risk for serious poisoning. It is important that chemicals are stored securely, in their original containers, and never stored in drinking vessels.

Synthetic cannabinoid use has become widespread, leading to increased burdens on health care providers. Symptoms range from agitation and psychosis to seizures and acute kidney injury. We report a case where a patient was assessed and treated twice within 12 h for seizures following synthetic cannabinoid intoxication. Blood sample determinations showed low concentrations of analogues not previously reported, some of which are legal. Clinicians should be aware that synthetic cannabinoids may cause an array of severe health consequences. Given the ever evolving structure of available analogues, clinicians must also be prepared for other unexpected adverse effects.