Fact-checked by Grok 2 weeks ago

Acute toxicity

Acute toxicity refers to the adverse effects occurring following oral or dermal administration of a single dose of a substance, or multiple doses given within a 24-hour period, or an exposure of 4 hours. This is central to and hazard assessment, distinguishing it from , which involves prolonged or repeated exposures over extended periods. Acute toxicity evaluates the immediate potential for harm from chemicals, pharmaceuticals, pesticides, and other agents, guiding regulatory classifications for safe handling and emergency response. The Globally Harmonized System (GHS) of Classification and Labelling of Chemicals provides a standardized framework for categorizing acute toxicity into five hazard levels based on median lethal dose (LD50) for oral and dermal routes or median lethal concentration (LC50) for inhalation. Category 1 represents the highest toxicity (e.g., oral LD50 ≤ 5 mg/kg), escalating to Category 5 for the lowest (e.g., oral LD50 > 2000 mg/kg), with specific thresholds varying by exposure route—such as dermal LD50 ≤ 50 mg/kg for Category 1 or inhalation LC50 ≤ 100 ppm (gas) for the same category. These categories inform pictograms, signal words like "Danger" or "Warning," and precautionary statements on labels, ensuring global consistency in communicating risks. In the United States, the Environmental Protection Agency (EPA) aligns with GHS but uses four toxicity categories for pesticides, where Category I denotes the most toxic products (e.g., oral LD50 ≤ 50 mg/kg) and Category IV the least (e.g., oral LD50 > 5000 mg/kg). Acute toxicity testing typically involves animal models to determine LD50/LC50 values, though with regulatory agencies like the FDA now accepting alternative methods such as in vitro assays and computational models under the FDA Modernization Act 2.0 to replace traditional animal testing, including plans announced in 2025 to phase out requirements for certain pharmaceuticals. For pharmaceuticals, the Food and Drug Administration (FDA) defines acute toxicity as effects from one or more doses within 24 hours, emphasizing endpoints like mortality, behavioral changes, or organ damage observed over 14 days. Key routes of exposure—oral, dermal, and inhalation—determine the relevant tests, with factors such as dose, substance structure, and individual susceptibility influencing outcomes.

Definition and Classification

Core Definition

Acute toxicity refers to serious adverse health effects occurring following a single exposure or multiple exposures to a substance within a 24-hour period, with effects typically manifesting within 14 days of exposure. These effects can arise through various routes, including , dermal contact, or , and may range from mild irritation to severe outcomes such as organ damage or death. The scope of acute toxicity encompasses immediate physiological disruptions caused by high-dose exposures, distinguishing it from , which involves prolonged or repeated low-level exposures over weeks or months. It focuses on the rapid onset of harm from substances like chemicals, pharmaceuticals, or pesticides, excluding cumulative effects from ongoing environmental or occupational exposures. The concept of acute toxicity originated in early 20th-century toxicology studies on poisons, with the development of standardized tests like the LD50 assay in the to quantify lethal doses in animal models. It was formalized in U.S. regulations through the 1947 Federal Insecticide, Fungicide, and Rodenticide Act (FIFRA), which mandated acute toxicity data for pesticide registration to assess risks to humans and the . Due to ethical prohibitions on direct human testing, acute toxicity assessments rely on animal models or alternatives, as established by the 1938 Federal Food, Drug, and Cosmetic Act, which required safety demonstrations without endangering human subjects. This approach prioritizes the 3Rs principle—replacement, reduction, and refinement—of animal use to minimize suffering while ensuring reliable hazard identification.

Hazard Categories

The Globally Harmonized System of Classification and Labelling of Chemicals (GHS) provides a standardized framework for categorizing acute toxicity hazards based on the median lethal dose (LD<sub>50</sub>) for oral and dermal routes or median lethal concentration (LC<sub>50</sub>) for inhalation, using data from animal studies or equivalent estimates. Categories range from 1 (most severe) to 5 (least severe), with severity decreasing as the dose or concentration required to produce lethality increases; Category 5 is optional and not implemented in all jurisdictions. These categories guide the use of pictograms (e.g., skull and crossbones for Categories 1-3), signal words ("Danger" for Categories 1-3, "Warning" for Category 4), and hazard statements such as "Fatal if swallowed" for oral Category 1. The following table summarizes the GHS acute toxicity categories for key exposure routes, based on approximate LD<sub>50</sub>/LC<sub>50</sub> values in rats or equivalent species:
RouteCategory 1Category 2Category 3Category 4Category 5 (optional)
Oral (LD<sub>50</sub>, mg/kg body weight)≤ 5> 5 and ≤ 50> 50 and ≤ 300> 300 and ≤ 2000> 2000 and ≤ 5000
Dermal (LD<sub>50</sub>, mg/kg body weight)≤ 50> 50 and ≤ 200> 200 and ≤ 1000> 1000 and ≤ 2000> 2000 and ≤ 5000
Inhalation - Gases (LC<sub>50</sub>, ppmV/4 hours)≤ 100> 100 and ≤ 500> 500 and ≤ 2500> 2500 and ≤ 20,000Not established
Inhalation - Vapors (LC<sub>50</sub>, mg/L/4 hours)≤ 0.5> 0.5 and ≤ 2.0> 2.0 and ≤ 10.0> 10.0 and ≤ 20.0> 20.0 and ≤ 50.0
Inhalation - Dusts/Mists (LC<sub>50</sub>, mg/L/4 hours)≤ 0.05> 0.05 and ≤ 0.5> 0.5 and ≤ 1.0> 1.0 and ≤ 5.0Not established
The European Union's Classification, Labelling and Packaging (CLP) Regulation aligns closely with GHS, adopting the same 1-4 for acute toxicity but excluding Category 5 to focus on higher-risk substances. Older systems, such as the U.S. (EPA) framework for pesticides, use four toxicity based on similar LD<sub>50</sub> thresholds (e.g., I: LD<sub>50</sub> ≤ 50 mg/kg oral, signal word "Danger"; II: >50-500 mg/kg, "Warning"; III and IV: progressively less toxic with "Caution"). These EPA categories predate full GHS adoption and emphasize signal words for labeling but are being phased toward GHS harmonization. GHS categories are applied in Safety Data Sheets (SDS) for chemicals, pesticides, and pharmaceuticals to communicate risks and inform handling, storage, and emergency response. For example, aspirin (acetylsalicylic acid), with an oral LD<sub>50</sub> of approximately 1100-2000 mg/kg in rats, falls into Category 4, indicating it may be harmful if swallowed but not highly toxic. As of 2025, GHS revisions since the 2017 update (Revision 7) have incorporated guidance on using , , and read-across methods alongside or instead of animal LD<sub>50</sub>/LC<sub>50</sub> data for classification, aiming to reduce while maintaining reliability; this builds on post-2015 efforts to promote alternative approaches. The 2024 OSHA Hazard Communication Standard update further emphasizes integrating human-relevant data, including non-animal sources, into acute toxicity assessments.

Assessment and Measurement

Experimental Metrics

The lethal dose 50 (LD<sub>50</sub>) is defined as the dose of a substance that causes death in 50% of a test population, typically determined through dose-response experiments in animal models. This metric quantifies acute oral or dermal toxicity and is calculated using statistical methods such as probit analysis or the Reed-Muench method. In probit analysis, a seminal approach for dose-response modeling, the probit value (inverse cumulative normal distribution) is regressed against the log-transformed dose, yielding the equation for the probit as: \text{probit}(P) = 5 + \frac{\log(D) - \log([\text{LD}_{50}](/page/Median_lethal_dose))}{\text{slope}} where P is the mortality proportion, D is the dose, [\text{LD}_{50}](/page/Median_lethal_dose) is the , and the slope reflects the response steepness; the LD<sub>50</sub> is solved at 5 (50% mortality). The Reed-Muench method, an arithmetical alternative for quantal data from multiple dose levels, estimates the LD<sub>50</sub> via on the log-dose scale between the doses bracketing 50% mortality: \log_{10}(\text{LD}_{50}) = \log_{10}(D_{\text{low}}) + \frac{50 - \% \text{ mortality low}}{ \% \text{ mortality high} - \% \text{ mortality low} } \left( \log_{10}(D_{\text{high}}) - \log_{10}(D_{\text{low}}) \right) where D_{\text{low}} and \% \text{ mortality low } &lt; 50\% are at the lower dose, and D_{\text{high}} and \% \text{ mortality high } &gt; 50\% at the higher dose. The lethal concentration 50 (<sub>50</sub>) measures the concentration of a substance in air or that kills 50% of the test population, primarily for or assessments. In , such as rats, <sub>50</sub> tests involve a 4-hour under dynamic conditions, followed by observation for delayed effects. For , like or are exposed for 96 hours under static, semi-static, or flow-through systems to derive the <sub>50</sub>, with mortalities recorded at 24, 48, 72, and 96 hours. Standardized testing protocols for acute toxicity, particularly oral, follow OECD guidelines to minimize animal use while ensuring reliable metrics, aligning with the 3Rs principle (Replacement, Reduction, Refinement). Recent advancements as of 2025 include Integrated Approaches to Testing and Assessment (IATA) combining in vitro, in silico, and read-across methods for predicting acute toxicity and gaining regulatory acceptance. OECD Guideline 420, the fixed dose procedure, employs young adult rats (typically females) administered single oral doses of 5, 50, 300, or 2000 mg/kg body weight via gavage after fasting; up to five animals per dose level are used sequentially based on outcomes, with observation for 14 days to monitor mortality, clinical signs, body weight, and pathology. Similarly, OECD Guideline 423, the acute toxic class method, uses groups of three female rats per step in a stepwise fashion across the same fixed dose levels, classifying the substance into toxicity categories via mortality patterns, also with a 14-day observation period for comprehensive endpoint evaluation. Both protocols prioritize evident toxicity signs over death to reduce animal numbers. In vitro alternatives to animal-based metrics are increasingly adopted to assess acute , reducing reliance on LD<sub>50</sub>/LC<sub>50</sub> tests. The Neutral Red Uptake (NRU) assay quantifies viable cells by their lysosomal accumulation of neutral red dye, measuring at 540 nm; is indicated by reduced uptake in exposed cells (e.g., HepG2 hepatocytes) relative to controls, providing IC<sub>50</sub> values for hazard screening. By 2025, organ-on-chip models simulating human tissues (e.g., liver or lung chips) have advanced under REACH updates, enabling predictive assessments that further minimize through standardized, physiologically relevant platforms.

Regulatory Standards

Regulatory standards for acute toxicity establish enforceable exposure limits and classification requirements to protect workers, consumers, and the environment from short-term high-level exposures to hazardous substances. These standards translate experimental toxicity data, such as LD50 values, into practical thresholds for safe handling and use. Key exposure limits include the Short-Term Exposure Limit (STEL), defined as a 15-minute time-weighted average (TWA) concentration that should not be exceeded to prevent acute effects from brief peaks, and the Ceiling Value (CV), an absolute maximum concentration not to be surpassed at any time during exposure. For instance, the Occupational Safety and Health Administration (OSHA) sets a Permissible Exposure Limit (PEL) for hydrogen cyanide as a TWA of 10 ppm (11 mg/m³) over an 8-hour shift, with a skin notation indicating potential absorption through the skin; the National Institute for Occupational Safety and Health (NIOSH) recommends a STEL of 4.7 ppm (5 mg/m³). In the United States, the Environmental Protection Agency (EPA) defines the Acute Reference Dose (ARfD) for s as the maximum single-day oral exposure level anticipated to be without appreciable health risk to the general population, including sensitive subgroups like children and pregnant women, typically derived by applying uncertainty factors to no-observed-adverse-effect levels from . Internationally, the World Health Organization's (WHO) International Programme on Chemical Safety (IPCS) provides guidelines for assessing and preventing acute toxic exposures, including recommendations for based on oral LD50 values to identify highly hazardous formulations and promote safer alternatives in and . Compliance with these standards mandates standardized hazard communication through the Globally Harmonized System of Classification and Labelling of Chemicals (GHS), which requires pictograms, signal words, and statements on labels for substances with acute toxicity s, ensuring consistent global understanding of risks. The ' GHS Revision 10, effective as of 2023 with ongoing implementations into 2025, includes updates such as guidance on non-animal testing methods for health s. Material Safety Data Sheets (MSDS) or Safety Data Sheets (SDS) serve as primary data sources for acute toxicity information, detailing exposure limits, handling precautions, and test results like LD50 values to inform regulatory compliance. For example, benzene's dermal LD50 exceeds 8,200 mg/kg in rabbits, leading to its classification under GHS as having low acute dermal toxicity hazard (Category 5 or unclassified), though it carries other warnings for carcinogenicity.

Mechanisms and Influencing Factors

Toxicological Mechanisms

Acute toxicity arises from various primary mechanisms at the cellular level, including direct damage to cellular structures and interference with critical biochemical processes. Corrosive substances, such as strong acids, induce by denaturing proteins and desiccating superficial tissues, leading to rapid upon contact. Alkaline corrosives, in contrast, cause through protein denaturation and of , effectively melting tissues in their path. inhibition represents another key mechanism, exemplified by , which binds to the a3-CuB binuclear center of in the mitochondrial , halting ATP production and . At the systemic level, acute toxicants can disrupt organ-specific functions through targeted biochemical pathways. often occurs via inhibition of by organophosphates, resulting in accumulation at synapses and overstimulation of receptors across the central and peripheral nervous systems. , as seen in acetaminophen overdose, involves the cytochrome P450-mediated formation of the reactive N-acetyl-p-benzoquinone imine (), which depletes stores and binds to cellular proteins, lipids, and nucleic acids, triggering hepatocyte . These mechanisms highlight how acute toxicants overwhelm endogenous pathways, such as conjugation or enzymatic breakdown, leading to rapid onset of cellular dysfunction. The dose-response relationship in acute toxicity typically follows a threshold model, where no observable adverse effects occur below a certain dose due to sufficient detoxification capacity, but toxicity manifests as the dose exceeds this threshold, saturating protective mechanisms. This can be mathematically described using a simple hyperbolic dose-response equation derived from Michaelis-Menten kinetics: \text{Effect} = \frac{E_{\max} \cdot \text{Dose}}{EC_{50} + \text{Dose}} Here, E_{\max} represents the maximum effect, Dose is the administered amount, and EC_{50} is the dose producing half-maximal effect, illustrating the sigmoidal curve shift from subthreshold to toxic regimes. Illustrative examples underscore these mechanisms' diversity. exerts toxicity by binding to with an affinity 200–300 times greater than oxygen, forming and impairing oxygen delivery to tissues, which exacerbates cellular . Recent research on nanoparticles reveals acute toxicity primarily through induction of , where generation disrupts antioxidant defenses, leading to , protein damage, and in exposed cells.

Modifying Factors

The severity of acute toxicity from a chemical is profoundly influenced by variables related to the itself, the host, and the surrounding environment, which can alter , , , and of the toxicant. Key variables include the , dose, and duration. The route determines rates and systemic ; for instance, typically allows rapid entry into the bloodstream via the lungs, often faster than oral , which requires gastrointestinal processing and first-pass , resulting in lower overall for some substances. In acute cases, oral accounts for approximately 80% of exposures, primarily due to accidental or intentional , while poses risks in occupational or environmental settings with airborne contaminants. Dose-response relationships are fundamental, where higher doses generally increase severity, but even sublethal doses can cause harm depending on duration; standard acute assessments, such as those outlined in Test Guideline 403, evaluate effects over a 4-hour to simulate short-term high-concentration scenarios. Host factors, including , , , and pre-existing conditions, significantly modulate individual susceptibility to acute toxic effects. Age-related differences arise from variations in metabolic capacity and function; children may experience heightened vulnerability due to higher relative doses per weight and immature pathways, while the elderly often face reduced clearance rates. influences toxicity through hormonal and physiological differences, with females showing a 1.5- to 1.7-fold greater risk of drug-induced from acute exposures compared to males. Genetic polymorphisms, particularly in () enzymes like and , affect metabolism; for example, variants can lead to rapid or deficient bioactivation of s, increasing risk in susceptible individuals. Pre-existing conditions such as exacerbate outcomes by impairing ; chronic liver impairment reduces activity, prolonging circulation and amplifying acute damage. Environmental interactions further modify toxicity through chemical synergism and physicochemical alterations. Synergistic effects occur when co-exposures enhance toxicity; alcohol, for instance, potentiates acetaminophen-induced by inducing , shifting metabolism toward the toxic metabolite even at therapeutic doses. Changes in and can destabilize chemicals or alter their ; lower increases acute toxicity of pharmaceuticals like acetaminophen and by enhancing ionization and membrane permeability, while elevated temperatures boost toxicity by accelerating metabolic rates and evaporation in aquatic or dermal exposures. These interactions underscore the need to consider co-occurring stressors in risk evaluation. Recent insights as of 2025 emphasize emerging roles of biological and global factors in acute toxicity modulation. The gut influences oral toxicity by metabolizing xenobiotics through enzymatic activities that can activate or detoxify compounds, with potentially heightening susceptibility to ingested toxins via altered barrier function and metabolite production. amplifies volatile exposures by increasing temperatures and altering atmospheric dynamics, enhancing and of volatile organic compounds, as noted in interlinkage assessments between chemical releases and environmental shifts.

Clinical Manifestations and Management

Signs and Symptoms

Acute toxicity often presents with general signs and symptoms that appear rapidly, typically within hours of exposure, including nausea, vomiting, and dizziness, which reflect initial gastrointestinal and central nervous system involvement. In more severe cases, these can progress to seizures, coma, or multi-organ dysfunction as the toxic agent dissociates and affects broader physiological systems. These manifestations arise from mechanisms such as cellular disruption and oxidative stress, but vary by the toxin's properties and route of exposure. System-specific symptoms further characterize acute toxicity depending on the affected organ. Respiratory effects, such as dyspnea and violent coughing, are common with irritant gases like , which cause immediate airway constriction and . Cardiovascular symptoms, including arrhythmias and irregular pulse, predominate in cases of poisoning, leading to or . Neurological signs, like and , occur with heavy metal exposures such as , resulting from direct neurotoxic effects on peripheral nerves and the . Severity of acute toxicity is graded based on clinical presentation, with mild cases involving local (e.g., redness or mild resolving quickly), moderate cases featuring systemic (e.g., persistent and ), and severe cases progressing to organ failure (e.g., or ). For instance, opioid overdoses exemplify severe toxicity through respiratory depression, pinpoint pupils (), and altered mental status, often requiring urgent intervention to prevent fatality. Diagnostic clues include elevated biomarkers such as levels indicating from substances like or cardiotoxic drugs, providing early evidence of myocardial injury. Symptoms typically align with a 14-day window post-exposure, during which acute effects like or organ damage are monitored to assess the toxin's impact.

Treatment Strategies

Treatment of acute toxicity begins with decontamination to minimize toxin absorption, tailored to the route of exposure. For oral ingestions, activated charcoal is administered as a single dose (50-100 g for adults) within 1 hour of ingestion to adsorb toxins and reduce systemic absorption, with efficacy persisting up to 4 hours for certain substances like acetaminophen. Multiple doses may be used for drugs undergoing enterohepatic recirculation, such as . is considered within 1 hour for life-threatening ingestions of substances with slow gastric emptying or sustained-release formulations, though it is rarely recommended due to risks like . For dermal exposures, immediate removal of contaminated clothing reduces contamination by 50-70%, followed by thorough irrigation with water or mild soap for lipid-soluble agents like organophosphates, ideally initiated within 1 minute and continuing for at least 90 seconds. Specific antidotes are employed when available to counteract toxin effects, selected based on the identified agent. serves as a competitive to reverse respiratory depression in overdoses, administered intravenously at 0.4-2 mg doses. For , atropine blocks muscarinic receptors to alleviate symptoms, while regenerates enzyme activity, typically given as 2-5 mg atropine IV followed by 30 mg/kg . In heavy metal toxicities such as lead or mercury, chelating agents like succimer bind metals to facilitate urinary excretion, dosed at 10 mg/kg orally for mild cases. Supportive care forms the cornerstone of management, addressing immediate life threats regardless of toxin identity. Airway protection via rapid-sequence with sedatives like (0.1 mg/kg IV) and muscle relaxants such as succinylcholine (1-2 mg/kg IV) is prioritized for patients with altered mental status or risk of . Intravenous fluids, using normal saline or lactated Ringer's in boluses of 500-1000 mL for adults, correct and maintain hydration. Continuous monitoring of , including cardiac rhythm, , , and neurological status, guides ongoing interventions and detects complications like . Enhanced elimination techniques are utilized for select toxins to accelerate removal. effectively clears low-molecular-weight substances (<300 Da) such as , , , and salicylates in cases of severe or renal failure, employing intermittent sessions via double-lumen . Treatment choices are informed by presenting to optimize efficacy.

References

  1. [1]
    Overview of the GHS Classification Scheme in Hazard ... - NCBI - NIH
    The GHS defines acute “toxicity as adverse effects occurring following oral or dermal administration of a single dose of a substance, or multiple doses given ...
  2. [2]
    Toxicology | National Institute of Environmental Health Sciences
    Mar 19, 2025 · Toxicology is the study of the harmful effects of chemicals, substances, or environmental agents on living systems.
  3. [3]
    Pesticide Labels and GHS: Comparison and Samples | US EPA
    Oct 8, 2025 · Currently, EPA uses two pictograms: a version of the skull and crossbones for the most severe categories of acute toxicity and a flame symbol ...Missing: authoritative | Show results with:authoritative<|control11|><|separator|>
  4. [4]
    [PDF] Hazard Classification Guidance for Manufacturers, Importers ... - OSHA
    ▫ OECD Test Guideline 423: Acute Oral Toxicity – Acute Toxic Class Method provides a ... concept of toxicology, i.e., all substances are potentially toxic, and ...
  5. [5]
    40 CFR 156.62 -- Toxicity Category. - eCFR
    This section establishes four Toxicity Categories for acute hazards of pesticide products, Category I being the highest toxicity category.Missing: GHS | Show results with:GHS
  6. [6]
    Advances in acute toxicity testing: strengths, weaknesses and ... - NIH
    It is used for estimating the potential hazards of chemicals on humans. Although its major endpoint is death, non-lethal acute effect may occur as signs of ...Missing: key facts
  7. [7]
    [PDF] Single Dose Acute Toxicity Testing for Pharmaceuticals - FDA
    Aug 26, 1996 · DEFINITION. Acute toxicity is the toxicity produced by a pharmaceutical when it is administered in one or more doses during a period not ...Missing: authoritative sources
  8. [8]
    [PDF] Module One Introduction to Toxicology
    The toxicity depends on a variety of factors: dose, duration and route of exposure (see Module Two), shape and structure of the chemical itself, and individual ...Missing: key facts
  9. [9]
  10. [10]
    [PDF] Appendix A. Glossary of Useful Terms
    EPA routinely uses. SARs to estimate toxicity of chemicals submitted as Pre-Manufacture Notices mandated by Section 5 of the Toxic Substances Control Act (TSCA) ...
  11. [11]
    7.7.1 Toxic Effects - Cornell EHS
    Acute toxicity is generally thought of as a single, short-term exposure where effects appear immediately and are often reversible. An example of acute toxicity ...Missing: authoritative | Show results with:authoritative
  12. [12]
    A Review of the LD50 and Its Current Role in Hazard Communication
    Dec 21, 2020 · Toxicity is generally divided into multiple categories based on exposure duration, including acute, subacute, subchronic, and chronic. Acute ...History Of The Ld50 · Modern Ld Methods · Acute Toxic Class Procedure
  13. [13]
    Summary of the Federal Insecticide, Fungicide, and Rodenticide Act
    Apr 25, 2025 · The Federal Insecticide, Fungicide, and Rodenticide Act (FIFRA) authorizes the EPA to regulate the distribution, sale, production, and use of pesticides and ...
  14. [14]
    [PDF] EPA Health Effects Test Guidelines: Acute Toxicity Testing
    The purpose of this guideline-by-guideline review was to identify those factors that most frequently cause toxicology studies required for pesticide.Missing: key facts
  15. [15]
    [PDF] History of the 3Rs in Toxicity Testing: From Russell and Burch to ...
    Jul 10, 2012 · The 3Rs, proposed by Russell and Burch, advocate for replacing, reducing, and refining animal use in toxicity testing. Refinement means less ...
  16. [16]
    [PDF] Label Review Manual - Chapter 7: Precautionary Statements
    If so, the recommended signal word, regardless of the toxicity categories noted in the acute toxicity review, is “DANGER.” 3. Location and prominence. The ...
  17. [17]
    Aspirin | C9H8O4 | CID 2244 - PubChem - NIH
    LD50: 250 mg/kg (Oral, Mouse) (A308) LD50: 1010 mg/kg (Oral, Rabbit) (A308) LD50: 200 mg/kg (Oral, Rat) (A308). Toxin and Toxin Target Database (T3DB). 12.1 ...
  18. [18]
    What is a LD₅₀ and LC₅₀? - CCOHS
    Oral LD50 (rat): 56 mg/kg · Dermal LD50 (rat): 75 mg/kg · Intraperitoneal LD50: (rat) 15 mg/kg · Inhalation LC50 (rat): 1.7 ppm (15 mg/m3); 4-hour exposure · Oral ...
  19. [19]
    Probit Analysis - an overview | ScienceDirect Topics
    This results in a regression line with the formula y = ax + b, where y is the expected mortality, a the slope, x the log dose/concentration, and b the intercept ...
  20. [20]
    Determination of 50% endpoint titer using a simple formula - PMC
    Two commonly used methods for calculating 50% endpoint using serial dilutions are Spearman-Karber method and Reed and Muench method.
  21. [21]
    Test No. 203: Fish, Acute Toxicity Test | OECD
    Mortalities are recorded at 24, 48, 72 and 96 hours and the concentrations which kill 50 per cent of the fish (LC50) are determined where possible. One or more ...Missing: rodents | Show results with:rodents
  22. [22]
    Test No. 420: Acute Oral Toxicity - Fixed Dose Procedure | OECD
    The test substance is administered in a single dose by gavage using a stomach tube or a suitable intubation canula. Animals should be fasted prior to dosing. A ...
  23. [23]
    Test No. 423: Acute Oral toxicity - Acute Toxic Class Method | OECD
    Abstract. This is a test guideline for testing for Acute Oral Tosxidity using the Acute Toxic Class Method.
  24. [24]
    Neutral Red Uptake Assay to Assess Cytotoxicity In Vitro - PubMed
    The neutral red uptake (NRU) assay is a cell viability assay that can be used for the assessment of compound-induced cytotoxicity.
  25. [25]
    Setting out a roadmap for standardisation of organ-on-chip technology
    Jan 13, 2025 · Standardisation of Organ-on-chip technology is an important step towards personalised medicine and animal-free testing.
  26. [26]
    ECHA & REACH: Shifting to animal-free chemical assessments
    Jul 24, 2025 · ECHA progresses toward animal-free chemical testing with REACH regulations, embracing innovation, ethics, and industry transformation.
  27. [27]
    Hydrogen cyanide - NIOSH Pocket Guide to Chemical Hazards - CDC
    Hydrogen cyanide ; Exposure Limits. NIOSH REL. ST 4.7 ppm (5 mg/m3) [skin]. OSHA PEL. TWA 10 ppm (11 mg/m3) [skin] See Appendix G ; Measurement Methods. NIOSH ...
  28. [28]
    Guidelines on the prevention of toxic exposures
    Apr 13, 2004 · These Guidelines have been prepared by IPCS to help governments, national agencies and urban and rural communities plan, carry out and evaluate education ...
  29. [29]
    The WHO Recommended Classification of Pesticides by Hazard and ...
    May 1, 2020 · This document sets out a classification system to distinguish between the more and the less hazardous forms of selected pesticides based on acute risk to human ...
  30. [30]
    Globally Harmonized System of Classification and ... - UNECE
    Jul 27, 2023 · You will find below the electronic version of GHS Rev.10, available for free, for consultation purposes, in the six UN official languages.
  31. [31]
    Caustic & Corrosive agents (acid or base) - TMedWeb
    May 31, 2012 · Acids: Acid ingestion causes tissue injury by coagulation-type necrosis (desiccation or denaturation of superficial tissue proteins).
  32. [32]
    [PDF] “The solution to the pollution is dilution”
    Alkalis damage tissue by liquefaction necrosis and protein denaturation; essentially melting any tissue in their path (alkalis react with lipids to form soaps) ...
  33. [33]
    Interaction of Cyanide and Nitric Oxide with Cytochrome c Oxidase
    Cyanide binds to the cytochrome c oxidase (CcOX) heme a3-CuB binuclear center to inhibit both cellular oxygen utilization and ATP production (Way, 1984).Abstract · MATERIALS AND METHODS · RESULTS · DISCUSSION
  34. [34]
    Mechanisms of Organophosphate Toxicity and the Role of ...
    Oct 18, 2023 · The primary mechanism, common among all OPs, that initiates their toxic effects is the inhibition of acetylcholinesterase. In acute OP exposure, ...
  35. [35]
    Mechanisms of acetaminophen-induced liver injury and its ...
    In general, NAPQI is detoxified by conjugating with GSH. However, excessive NAPQI depletes GSH following APAP overdose, leading to formation of APAP-ADs through ...
  36. [36]
    [PDF] Dose-Response Curves - Toxicology MSDT
    The point at which toxicity first appears is known as the threshold dose level. From that point, the curve increases with higher dose levels. In this ...
  37. [37]
    Dose-Response Curve | Definition and Applications
    ... dose-response curve that a classical Hill equation mathematical model can formulate. ... Evaluating Toxicity Through Dose-Response Relationships. In toxicology, ...Understanding Ec50 And Ic50... · Evaluating Toxicity Through... · The Impact Of Antagonists On...
  38. [38]
    Physiology, Oxygen Transport And Carbon Dioxide Dissociation Curve
    Hemoglobin binds carbon monoxide (CO) 200 to 300 times more than with oxygen, forming carboxyhemoglobin and preventing the binding of oxygen to hemoglobin due ...Introduction · Mechanism · Clinical Significance
  39. [39]
    Exploring Oxidative Stress Mechanisms of Nanoparticles Using ...
    This review synthesizes current findings on NP-induced oxidative stress in zebrafish, highlighting key toxicity mechanisms and case studies.2.2. Surface Charge And... · 3.3. Genotoxicity And Lipid... · 5.1. Nanoparticles As...<|control11|><|separator|>
  40. [40]
    Poisoning: First aid - Mayo Clinic
    Symptoms · Burns or redness around the mouth and lips. · Breath that smells like chemicals, such as gasoline or paint thinner. · Vomiting. · Difficulty breathing.Poisoning: First Aid · When To Seek Emergency Help · Treatment
  41. [41]
    Acute Toxicity - an overview | ScienceDirect Topics
    Acute toxicity manifests primarily in the CNS, cardiovascular system, and gastrointestinal system. CNS signs include restlessness, tremor, nervousness, headache ...
  42. [42]
    Toxicity, mechanism and health effects of some heavy metals - PMC
    This review gives details about some heavy metals and their toxicity mechanisms, along with their health effects.Missing: denaturation | Show results with:denaturation
  43. [43]
    Chlorine Gas Toxicity - StatPearls - NCBI Bookshelf - NIH
    Acute exposure at high levels causes dyspnea, violent cough, nausea, vomiting, lightheadedness, headache, chest pain, abdominal discomfort, and corneal burns, ...Continuing Education Activity · Introduction · Pathophysiology · History and Physical
  44. [44]
    Arsenic Toxicity - StatPearls - NCBI Bookshelf - NIH
    Jun 12, 2023 · Gastrointestinal: Gastroenteritis is the most common symptom seen with acute toxicity. Doses under 5mg results in nausea, vomiting, diarrhea ...
  45. [45]
    [PDF] POISONING SEVERITY SCORE (PSS) IPCS/EAPCCT
    The PSS is a classification scheme for cases of poisoning in adults and children. This scheme should be used for the classification of acute poisonings ...
  46. [46]
    Opioid Toxicity - StatPearls - NCBI Bookshelf
    Jan 22, 2025 · Additional signs of opiate overdose include euphoria, drowsiness, altered mental status, fresh needle marks, seizures, and conjunctival ...Opioid Toxicity · Toxicokinetics · Treatment / Management<|control11|><|separator|>
  47. [47]
    Cardiac troponins as biomarkers of drug- and toxin ... - PubMed
    Cardiac troponin T and I (cTnT, cTnI) are sensitive biochemical markers of myocardial cell necrosis and have been adopted as the gold standard tests for acute ...
  48. [48]
    Gastrointestinal decontamination in the acutely poisoned patient - NIH
    This article will review the current recommendations, guidelines and data on gastrointestinal (GI) decontamination in the poisoned patient.Missing: strategies | Show results with:strategies
  49. [49]
    Chemical Decontamination - StatPearls - NCBI Bookshelf - NIH
    Jun 12, 2023 · Dry decontamination can be performed using an absorptive material such as Fuller's earth, activated charcoal, talcum powder, or absorptive ...
  50. [50]
    Antidotes - StatPearls - NCBI Bookshelf - NIH
    Cyanide: Treatment of cyanide toxicity depends on the rapid administration of one of the three currently available antidotes. The first is hydroxycobalamin ...Missing: decontamination | Show results with:decontamination
  51. [51]
    Emergency Management of Poisoning - PMC - PubMed Central - NIH
    The general approach to the poisoned patient can be divided into six phases: (1) stabilization; (2) laboratory assessment; (3) decontamination of the ...
  52. [52]
    Artificial Intelligence Applications in Emergency Toxicology
    Aug 22, 2025 · Background and importance Emergency toxicology is a complex field requiring rapid and precise decision-making to manage acute poisonings ...Missing: AAPCC | Show results with:AAPCC
  53. [53]
    Initial Management of Poisoned Patient - PMC - PubMed Central - NIH
    The plan of management is to provide supportive care, prevention of poison absorption, use of antidote wherever is indicated, and enhancement of elimination ...