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Introduction
Published in Frank A. Barile, Barile’s Clinical Toxicology, 2019
Descriptive toxicology is a comprehensive attempt at explaining the toxic agents and their applications. Descriptive toxicology developed principally as a method for bridging the vacuum between the science and the public’s understanding of the field, especially when it became necessary for nonscientific sectors to comprehend the importance of toxicology. For instance, the study of metals in the environment (metal toxicology) has become a popular description for toxicologists interested in examining the role of heavy or trace metals in the environment. Clinical toxicology may also be considered as a descriptive category that involves the analysis of drugs or chemicals whose exposure is associated with pathological consequences, therapeutic intervention, known signs and symptoms, and public health involvement. Other descriptive areas in the field are defined in Table 1.1. More recently, research areas have intensified in toxicology and have blossomed into several broad descriptive fields, including, but not limited to, the study of apoptosis, receptor-mediated signal transduction, gene expression, proteomics, oxidative stress, and toxicogenomics.
Toxicology
Published in Aruna Bakhru, Nutrition and Integrative Medicine, 2018
There are several subdisciplines of toxicology, which focus on particular aspects of toxicology. These include: ToxicogenomicsChemical toxicologyClinical toxicologyEcotoxicologyEnvironmental toxicologyForensic toxicologyMedical toxicologyOccupational toxicologyRegulatory toxicology
Cyanides: Toxicology, Clinical Presentation, and Medical Management
Published in Brian J. Lukey, James A. Romano, Salem Harry, Chemical Warfare Agents, 2019
Gary A. Rockwood, Gennady E. Platoff Jr., Harry Salem
The most commonly available cyanides (CNs) are hydrogen cyanide (HCN), a highly volatile liquid, and sodium, potassium, and calcium cyanides, which are solids. They are widely used industrially and commercially; examples are in manufacturing processes (includes dyes, pigments, chelating agents, various nitriles, monomers, resins, and fibers), case hardening, electroplating, the extraction of precious metals, and fumigation (Allen et al., 2015; Ballantyne, 1988; Ballantyne and Salem, 2005; Homan, 1987). In addition, due to their rapid lethal toxicity, they have been used for suicide, homicide, judicial execution, assassinations, and chemical warfare operations, and there exists a possibility for use by terrorists (Ballantyne, 1987a, 1987b; Ballantyne et al., 2006; Gee, 1987; Pita, 2015; WHO, 2004). Additionally, CN-related toxicity and pathology may result from exposure to man-made and to naturally occurring cyanogens (Ballantyne, 1987b; Brimer, 1988). In addition, HCN is a product of combustion, and inhalation of smoke from fires may cause CN intoxication (Ballantyne, 1987c; Ballantyne and Salem, 2005; Marrs, 2016; Norris and Ballantyne, 1999; Purser, 2016). As discussed later (Section 12.11.2), HCN has been employed by the military in chemical warfare operations because of its lethal and incapacitating effects. In addition, because of their known toxicity and comparatively ready availability, CNs are candidates for use as psychological and lethal agents by terrorist organizations. CN, as a terrorist weapon, has been used in various ways, including the contamination of over-the-counter medication. Additionally, CN has been used for extortion, in state and non-state terrorism, and potentially by jihadi terrorists. A detailed study of incidents with chemical warfare agents (CWAs) linked to al‐Qaeda shows that the nefarious use of CN is of great interest among jihadi terrorists (see Pita, 2015 for review). This chapter discusses the experimental and human clinical toxicology of CNs with particular reference to their potential for application as chemical warfare weapons and use by terrorists.
Medication errors in inquiries to the Poison Information Center Erfurt — a systematic analysis
Published in Clinical Toxicology, 2022
Mandy Gollmann, Martina P. Neininger, Michael Deters, Dagmar Prasa, Thilo Bertsche
The estimated risk of toxicity describes the potential harm to the patients that may occur. The Society for Clinical Toxicology (Germany) defined the estimated risk as the expected severity of symptoms over time if no therapeutic measures were taken; they classified the risk into nontoxic, minor, moderate, and severe according to the PSS [8]. Additionally, the following category was used: unknown — missing or insufficient information, both a symptom-free and symptomatic course is possible or expected symptoms are of unknown extent. The risk was assessed by a physician or pharmacist on duty in the PIC based on all available information, especially type and dose of drug, time of exposure, and clinical signs and symptoms. The causality assessment was based on the data from comment databases on drug toxicity. The assessment was then subjected to an internal plausibility check by another staff member.
Population pharmacokinetics of Pseudechis porphyriacus (red-bellied black snake) venom in snakebite patients
Published in Clinical Toxicology, 2021
Suchaya Sanhajariya, Stephen B. Duffull, Geoffrey K. Isbister
Population pharmacokinetic analysis has previously been used in clinical toxicology to investigate the time course of drugs in overdose, and determine if specific treatments such as activated charcoal influence drug exposure [5–7]. In addition, population pharmacokinetic-pharmacodynamic analysis has been used to describe the toxic effects of drugs in overdose and estimate the effect of treatments [8–10]. In a similar way, population-based modelling is an ideal tool for investigating the PK of snake venom, and the effect of antivenom. Similar to overdose patients, the dose is poorly defined, blood collection is often after the absorption period, due to travel time to hospital following the bite. For many types of snake envenomation, antivenom is given to all patients, after which venom concentrations are usually reduced to undetectable concentrations. However, antivenom is not always administered in RBBS envenomation, so we have the unique opportunity to investigate venom exposure in patients with and without antivenom, with sufficient serial venom concentrations in patients not given antivenom.
Bupropion associated seizures following acute overdose: who develops late seizures
Published in Clinical Toxicology, 2020
Steve Offerman, Jasmin Gosen, Stephen H. Thomas, Angie Padilla-Jones, Anne-Michelle Ruha, Michael Levine
This study also is limited by reported ingestion histories from patients, family members, or other witnesses, which is a problem inherent in most clinical toxicology research. It is possible histories may be inaccurate. To reduce some of the limitation of unknown time of ingestion, we opted to define late seizures as being more than 8 h after emergency department arrival, rather than from the time of ingestion. It is likely the length of time from ingestion to ED arrival may vary. However, clinically, we feel that having a clear time of observation in the emergency department is not only more clinically useful to the practicing provider, but also reduces the inherent difficulty associated with ambiguous or inaccurate histories. Lastly, confirmatory testing, which is not routinely available at most centers, was not an inclusion criterion. Thus, it is possible a patient reported taking bupropion but actually took a different medication. If this happened, it could underestimate the number of patients with seizures, including late seizures. However, given the relatively high percentage of patients who exhibited toxicity consistent with bupropion ingestion, we feel this is unlikely to have significantly altered our findings.