Artificial snowmaking is used by winter recreation resorts to elongate the ski season in areas that lack sufficient snow, yet the occurrence of contaminants in artificial snow remains largely uncharacterized. Contaminants in artificial snow can lead to the introduction of pollutants into surrounding ecosystems (e.g., plants, water streams, soils) or create pathways for human exposure. Using the Arizona Snowbowl Ski Resort in Flagstaff, Arizona, as a case study, we characterized the chemical (organic and inorganic) profile of snow made from reclaimed water samples as compared to natural snow samples. Pharmaceuticals and anthropogenic compounds were identified in snowmaking from reclaimed water samples using nontargeted mass spectrometry paired with molecular networking, and identities of selected compounds were confirmed and quantified using targeted mass spectrometry alongside authentic chemical standards. Nineteen pharmaceuticals were found to be increased in high artificial snowmaking samples as compared to natural snow, including carbamazepine, fexofenadine, flecainide, and lamotrigine, which were present at low ng/L concentrations in one set of high artificial snowmaking samples. A suite of inorganic contaminants was also assessed and quantified using inductively coupled plasma mass spectrometry to reveal that nine metals(?)sodium, phosphorus, potassium, chromium, manganese, iron, zinc, arsenic, and barium(?)were increased in abundance in high artificial snowmaking samples compared to levels in normal snow. Taken together, this study suggests that snow made from reclaimed water may contain anthropogenic organic and inorganic analytes, warranting further study on their environmental and human health effects.

Atrial fibrillation is associated with a reduced quality of life, an increased risk of thromboembolic events and higher mortality. A fast and individualized treatment is essential, particularly to positively influence the progression. In addition to risk-adapted oral anticoagulation, early rhythm control is crucial for reducing the burden of symptoms as well as for decreasing hospitalization, ischemic stroke and cardiovascular death. Options for rhythm control include pharmacological strategies, electrical cardioversion, and catheter-based ablation procedures. Electrical cardioversion is particularly suitable for the acute treatment of hemodynamically unstable patients, while pharmacological treatment and catheter ablation represent long-term treatment approaches. Class IC antiarrhythmic drugs such as flecainide and propafenone are contraindicated in patients with structural heart disease.

Andersen-Tawil syndrome (ATS) is a rare autosomal dominant multisystem disorder characterised by ventricular arrhythmias, periodic paralysis, and dysmorphic features. However, marked phenotypic heterogeneity is observed, contributing to significant diagnostic delays. ATS is most commonly caused by loss-of-function variants in KCNJ2, which encodes the α-subunit of the inward rectifier potassium channel Kir2.1, resulting in impaired IK1 currents. Impaired IK1 destabilises terminal repolarisation and depolarisation kinetics, promoting prominent U waves, ventricular ectopy, and complex ventricular arrhythmias. Management remains challenging due to limited evidence and variable treatment response. β-blockers and flecainide are commonly used while implantable cardioverter-defibrillators are reserved for high-risk cases. Potassium supplementation and acetazolamide should be considered in selected patients with periodic paralysis. Given incomplete penetrance and absence of validated risk stratification tools, careful multidisciplinary evaluation and individualised management are essential.

Limited information indicates that maternal doses of flecainide up to 200 mg daily produce low levels in milk and would not be expected to cause any adverse effects in breastfed infants, especially if the infant is older than 2 months. Because of the relative lack of data concerning breastfeeding during maternal flecainide therapy, exclusively breastfed infants should be carefully monitored if this drug is used during lactation, possibly including measurement of serum levels to rule out toxicity if there is a concern.

Several studies have supported Dr Gideon Koren’s 1993 landmark article, “Medications Which Can Kill a Toddler with One Tablet or Teaspoonful.” Although each study has its own merits, most focus solely on pediatric overdoses, and few provide an exhaustive reference list for real-time evaluation of ingestions in children and adults. The following xenobiotics warrant special attention because of their potential to cause serious outcomes, even after exposure to small volumes. This list does not imply that all pediatric exposures to these agents result in fatality, and the absence of a xenobiotic from this list does not indicate that it is necessarily safe. α1-Adrenergic agonists and imidazoline receptor agonists: Clonidine, guanfacine, naphazoline, oxymetazoline, tetrahydrozoline, xylazine (veterinary). Sulfonylureas: Chlorpropamide, glyburide, glipizide, glimepiride. Calcium channel blockers: Verapamil, diltiazem, nifedipine, amlodipine, nicardipine, nimodipine; β-Blockers: Metoprolol, labetalol, propranolol, sotalol. Tricyclic antidepressants: Imipramine, desipramine, amitriptyline, nortriptyline. Opioids: Codeine, hydrocodone, methadone, morphine, heroin. Antidiarrheals: Diphenoxylate plus atropine, loperamide. Salicylates and methyl salicylate: Oil of wintergreen, bismuth subsalicylate, mentholated balms, paramao or lawang root oil . Antipsychotics: Loxapine, thioridazine, chlorpromazine. Antimalarials: Chloroquine, hydroxychloroquine, quinine, primaquine. Antiarrhythmics: Quinidine, disopyramide, procainamide, flecainide, amiodarone. Camphor: A terpenoid used as an analgesic, antipruritic agent, and component of cooling gels, ointments, balms, mothballs, household fragrances, and essential oils. Oral camphor use occurs in some regions for religious ceremonies, traditional remedies, aphrodisiacs, or lactation suppression. Nonalkaloid toxic lignan: Podophyllin, podofilox. Unique plant toxins: Colchicine. Oral acetylcholinesterase inhibitors: Rivastigmine, donepezil, galantamine, carbamate pesticides. Methylxanthines: Theophylline, 1,3-dimethylxanthine, caffeine. Other opioids: Buprenorphine, fentanyl. Toxic alcohols: Methanol, ethylene glycol, diethylene glycol. Caustics and other household products: Acidic or alkaline household products, hydrofluoric acid, selenious acid, acetonitrile, methylene chloride. Accidental overdoses continue to occur regularly despite the implementation of various safety measures, including widespread public education, the use of childproof containers, and easy access to poison control centers. In the US, poison control centers receive more than 2.4 million calls annually, with more than 50% involving children younger than 6 years. Most pediatric accidental ingestions involve household cleaning products and analgesics, followed by cosmetics, foreign objects, and dietary supplements. Adult overdoses may be unintentional but often involve larger total doses or high-risk medications, including opioids and sedative-hypnotics. America's Poison Centers identify the 5 most common substance classes as analgesics, household cleaners, antidepressants, cosmetic or personal care items, and cardiovascular drugs. The number of ingestions involving cleaning products increased sharply during the COVID-19 pandemic but has since declined.

Sex differences in drug metabolism and cardiac electrophysiology may influence the cardiovascular safety profiles of antiarrhythmic drugs (AADs). However, pharmacovigilance studies often pool data, potentially obscuring sex-specific cardiovascular adverse event (CV-AE) reporting patterns. We aim to investigate sex-specific CV-AE reporting profiles associated with commonly used antiarrhythmic drugs using pharmacovigilance data. We analyzed 122,853 medication-role records representing 38,430 unique FAERS reports involving eight AADs. Disproportionality analyses defined index-drug exposure by the primary-suspect role, whereas the report-level XGBoost pipeline separately encoded primary-suspect drugs and secondary-suspect or concomitant medications. Analyses included pooled and sex-stratified disproportionality, drug-adjusted common odds ratios, and a gradient-boosting machine learning model to assess ventricular arrhythmia (VA) reporting patterns. Sex-stratified analysis uncovered "hidden" associations undetected in pooled data, including propafenone-QT prolongation in men and amiodarone-QT prolongation in women. Adverse event profiles were often drug-specific and opposing: cardiogenic shock showed higher reporting odds among males for sotalol, whereas flecainide showed higher reporting odds in females. After adjustment, women had higher odds of torsade de pointes and men of ventricular arrhythmia. However, a machine learning model for VA demonstrated that sex contributed modestly (1.4% SHAP contribution) compared with co-medications and the primary drug, though drug-specific associations differed. Sex-specific CV-AE profiles reporting patterns are often masked in pooled analyses, underscoring the need for sex-stratified pharmacovigilance to guide personalized antiarrhythmic therapy. The identified associations should be considered hypothesis-generating and require validation in datasets with richer clinical information.

Sick sinus syndrome (SSS) presents significant challenges in psychiatric medication management because of the potential for worsening cardiac conduction and interactions with antiarrhythmic therapy. A 35-year-old woman with generalized anxiety disorder (GAD) and insomnia was treated with bupropion, hydroxyzine, melatonin, and intermittent quetiapine, alongside comorbid SSS and supraventricular tachycardia managed post-ablation with metoprolol. A review of her regimen identified several cardiac safety concerns: quetiapine's potential interference with flecainide, hydroxyzine-associated QT prolongation, and bupropion's CYP2D6 inhibition that could increase flecainide levels. Management prioritized minimizing arrhythmogenic risk by discontinuing quetiapine, restricting hydroxyzine to low doses, and continuing melatonin, supplemented by stress testing and reassessment of psychotropic options. This case highlights the importance of careful psychotropic selection in patients with SSS, favoring lower-risk agents, such as mirtazapine, which is one of the safest among several possible alternatives, while maintaining close ECG monitoring and coordinated cardiology and psychiatry collaboration to reduce drug-drug interactions and optimize safety.

As global demand for pharmaceuticals continues to grow, pharmaceutical pollution is becoming increasingly pervasive. Research on the occurrence and distribution of pharmaceuticals in marine ecosystems remains limited, however, with coastal sewage outfalls considered to be a major source of pharmaceutical pollutants in marine environments. Here, we investigated the distribution of pharmaceuticals across a wastewater gradient in Port Phillip Bay, Melbourne, Australia, using stable nitrogen isotope ratios (δ[15]N) as a signal of wastewater influence. Marine invertebrates, macroalgae and marine/terrestrial plants were sampled across four sites of varying distances from Melbourne's largest wastewater treatment plant and analyzed for δ[15]N and pharmaceuticals. Out of 95 target analytes, 15 were detected, with the most frequent detections being telmisartan (83%), flecainide (52%), memantine (37%), caffeine (28%) and tramadol (23%). Pharmaceutical concentration was positively associated with δ[15]N, supporting wastewater influence as a key driver of pharmaceutical pollution. Interestingly, concentrations were highest in primary producers, including terrestrial plants. Follow-up sampling revealed higher pharmaceutical concentrations in sea foam relative to seawater, suggesting enrichment within the air-water interface and potential transport to terrestrial environments via coastal aerosols. Overall, our findings demonstrate the role of wastewater in pharmaceutical pollution, with plants and algae emerging as potential bioindicators.