Liquid laundry detergent capsules (PODS): a review of their composition and mechanisms of toxicity, and of the circumstances, routes, features, and management of exposure.

Introduction: Liquid laundry detergent capsules (also called single-use detergent sacs; laundry pods; laundry packets) have become an increasingly popular household product worldwide. Objectives: To review the composition and mechanisms of toxicity of liquid laundry detergent, capsules, and the circumstances, routes, clinical features (and impact of packaging changes) and management of exposure. Methods: The databases PubMed and EMBASE were searched using the terms: "detergent" and "capsule", "pod", "pac" or "sac" combined with "poison", "ingest", "expos" but not "animal" or "in vitro" or "bacteria". The searches yielded 289 articles, of which 186 were excluded: 38 duplicates, 133 not relevant, 10 abstracts which had been published as a paper and 5 non-English language articles. The bibliographies of relevant articles were hand-searched which yielded 14 additional citations. Searching of abstracts from scientific meetings produced five additional citations. A total of 122 publications were relevant to the objectives of the review. Capsules and composition: Capsules typically contain anionic surfactants (20-35%), non-ionic surfactants (10-20%), propylene glycol (8-20%) and ethanol (2-5%) within a water-soluble polyvinyl alcohol membrane. Mechanisms of toxicity: Non-ionic surfactants are the primary mechanism, though anionic surfactants, ethanol and propylene glycol may also contribute. Circumstances of exposure: The majority (60%) of children are exposed when the capsule is removed from its original container. Routes of exposure: Ingestion is the most common (>85%); ocular (<15%) and dermal (<8%) exposure account for the remainder. Features following ingestion: Features develop in around half of all exposures, though >90% are minor. In those with features, vomiting occurs in some 50%; coughing and drowsiness are reported in <5%. Respiratory depression (<0.5%), central nervous system depression (<0.1%) esophageal or gastric injury (<0.5%), metabolic acidosis and hyperlactatemia (<0.05%) have been reported rarely. Of 17 deaths reported, 13 were adults and nine were suffering from cognitive impairment. Features following ocular exposure: Conjunctivitis, eye irritation and/or eye pain are commonly experienced; corneal injury is less common but complete recovery typically occurs within one week. Features following dermal exposure: Clinically important dermal toxicity seldom occurs, though skin burns can develop in <5% of cases when skin contact is prolonged. Impact of packaging changes on features: The implementation of packaging changes resulted in a fall in the number of exposures and their severity in the United States and in the number in Italy. Management-ingestion: Gut decontamination is not recommended, though small amounts of fluid can be administered orally to rinse out the mouth. Symptomatic and supportive care should be offered to all patients that develop features of toxicity. Supplemental oxygen should be administered for hypoxemia, and bronchodilators for laryngospasm/bronchospasm. Intubation and assisted ventilation may be required if CNS and respiratory depression develop. A chest radiograph should be performed if respiratory features develop. In patients with swallowing difficulties, drooling or oropharyngeal burns, endoscopy should be performed; if substantial mucosal damage is present MRI should be considered. In addition, intravenous fluids will be required if prolonged vomiting or diarrhea occur and acid-base disturbances should be corrected. Management-eye exposure: Thorough irrigation of the eye with sodium chloride 0.9% is required. Instillation of a local anesthetic will reduce discomfort and help more thorough decontamination. Due to the potential for corneal injury, fluorescein should be instilled. If ocular injury is present, the patient should be referred to an ophthalmologist. Management-skin exposure: Skin should be irrigated thoroughly with soap and water, and burns should be treated as a thermal burn. Conclusions: Accidental ingestion usually produces no or only minor features. Very rarely respiratory depression, central nervous system depression, esophageal or gastric injury, hyperlactatemia and metabolic acidosis occur. Ocular exposure results in corneal injury infrequently and skin burns can develop uncommonly following prolonged dermal contact. Of 17 deaths reported, 13 were adults and nine were suffering from cognitive impairment.

Iron overdose epidemiology, clinical features and iron concentration-effect relationships: the UK experience 2008-2017.

Background: Iron poisoning is potentially serious, but mortality has fallen worldwide since implementation of pack size and packaging restrictions, and changes in iron use during pregnancy. The management of individual cases of overdose remains problematic due to uncertainty about indications for antidote. We examine the epidemiology of iron overdose in hospital cases referred to the UK National Poisons Information Service (NPIS) and evaluate the toxicokinetics of iron in patients ingesting only iron preparations. Methods: Anonymized hospital referral patient data from the NPIS database were collated for the period 1 January 2008 to 31 July 2017. Information was extracted, where recorded, on type of ingestion [iron alone (single), or combined with other agents (mixed)], reported dose, iron salt, timed iron concentrations and symptoms. In single-agent ingestions, the relationships between reported elemental iron dose, early concentrations (4-6 h), and symptoms were evaluated in teenagers and adults (≥13 years) and children (≤12 years) using standard statistical techniques (correlation and unpaired nonparametric comparisons). In those patients with sufficient sample points (three or more), a simple kinetic analysis was conducted. Results: Of 2708 patients with iron overdoses referred by UK hospitals for advice during the 9.7 years study period, 1839 were single-agent ingestions. There were two peaks in age incidence in single-agent exposures; 539/1839 (28.4%) were <6 years (54.1% males) while 675/1839 (36.7%) were between 13 and 20 years (91% females), the latter a substantial excess over the proportion in the totality of hospital referrals to the NPIS in the same period (13-20 years: 23,776/144,268 16.5%; 67.5% female) (p < .0001 overall and for female %). In 475 teenagers and adults and 86 children, with at least one-timed iron concentration available, there was no correlation between stated dose and iron concentration measured 4-6 h post-ingestion. Observed peak iron concentrations were not related to reported symptoms in adults. Initial iron concentrations were significantly higher in 30 patients (25 adults, 5 children) who received desferrioxamine (DFO) compared to those that did not [no DFO: mean 63.8 µmol/L (95% CI 62.1-65.6), median 64; DFO: mean 78.5 µmol/L (95% CI 69.2-87.7), median 78.1; Mann-Whitney p < .0018). No significant differences in symptoms were observed pre-treatment between DFO-treated and untreated groups. No patients died in this cohort. Conclusion: Single-agent iron exposures reported from UK hospitals were most common in children <5 years and young people aged 13-20 years. Poisoning with organ failure was not identified and there were no fatalities. No correlations were observed between reported iron doses and early concentrations, or between iron concentrations and symptoms in this cohort of mild-to-moderate poisoning.

Diagnosis and treatment of polonium poisoning.

OBJECTIVES: Interest in the clinical toxicology of (210)polonium ((210)Po) has been stimulated by the poisoning of Alexander Litvinenko in 2006. This article reviews the clinical features, diagnosis, and treatment of acute radiation syndrome (ARS) resulting from the ingestion of (210)Po. PHYSICAL CHARACTERISTICS: (210)Po is a high-energy alpha-emitter (radioactive half-life 138 days) that presents a radiation hazard only if taken into the body, for example, by ingestion, because of the low range of alpha particles in biological tissues. As a result, external contamination does not cause radiation sickness. TOXICOKINETICS: Ingested (210)Po is concentrated initially in red blood cells and then the liver, kidneys, spleen, bone marrow, gastrointestinal (GI) tract, and gonads. (210)Po is excreted in urine, bile, sweat, and (possibly) breath and is also deposited in hair. After ingestion, unabsorbed (210)Po is present in the faeces. The elimination half-life in man is approximately 30-50 days. In the absence of medical treatment, the fatal oral amount is probably in the order of 10-30 microg. CLINICAL PRESENTATION: If the absorbed dose is sufficiently large (e.g., >0.7 Gy), (210)Po can cause ARS. This is characterized by a prodromal phase, in which nausea, vomiting, anorexia, lymphopenia, and sometimes diarrhea develop after exposure. Higher radiation doses cause a more rapid onset of symptoms and a more rapid reduction in lymphocyte count. The prodromal phase may be followed by a latent phase during which there is some clinical improvement. Subsequently, the characteristic bone marrow (0.7-10 Gy), GI (8-10 Gy), or cardiovascular/central nervous system syndromes (>20 Gy) develop, with the timing and pattern of features dependent on the systemic dose. The triad of early emesis followed by hair loss and bone marrow failure is typical of ARS. Those patients who do not recover die within weeks to months, whereas in those who survive, full recovery can take many months. INVESTIGATION AND DIAGNOSIS: Serial blood counts are important for assessing the rate of reduction in lymphocyte counts. Chromosome analysis, especially the dicentric count, may establish radiation effects and provides an estimation of dose. The diagnosis of (210)Po poisoning is established by the presence of (210)Po in urine and faeces and the exclusion of other possible causes. In the absence of a history of exposure, diagnosis is very difficult as clinical features are similar to those of much more common conditions, such as GI infections and bone marrow failure caused, for example, by drugs, other toxins, or infections. MANAGEMENT: Good supportive care is essential and should be directed at controlling symptoms, preventing infections but treating those that do arise, and transfusion of blood and platelets as appropriate. Gastric aspiration or lavage may be useful if performed soon after ingestion. Chelation therapy is also likely to be beneficial, with research in animals suggesting reduced retention in the body and improvements in survival, although increased activity in some radiosensitive organs has also been reported with some chelating agents. Dimercaprol (British Anti-Lewisite) (with penicillamine as an alternative) is currently recommended for (210)Po poisoning, but animal models also indicate efficacy for 2,3,-dimercapto-1-propanesulfonic acid, meso-dimercaptosuccinic acid, or N,N -dihydroxyethylethelene-diamine-N,N -bis-dithiocarbamate. CONCLUSIONS: Internal contamination with (210)Po can cause ARS, which should be considered in patients presenting initially with unexplained emesis, followed later by bone marrow failure and hair loss.