RightAnswer Knowledge Solutions provides access to hundreds of data sources. Our premier and proprietary sources include fully-researched documents from well-established experts in the chemical and HazMat fields.
A search in our system for this chemical would return results – all in one place -- in the following categories from the listed data sources.
- Chemical Identification
- Environmental Hazards
- First Aid/Medical Treatment
- Handling/Storage/Shipping/Waste Management
- MSDS Documents
- Personal Protection
- Physical Hazards/Corrective Response Actions
- Physical/Chemical Properties
- Report Abstracts and Studies
- Reproductive Risk
- Toxicology/Health Hazards/Exposure
|Example of Acute Exposure data from MEDITEXT.|
RightAnswer Proprietary Data Sources:
Other Government Links Searched via RegsKnowledge:
State Environmental Regulations
Example Content from MEDITEXT for 57-24-9:
Please note: this is an extract of information from a larger document. Full document and details are available by subscription.
ACUTE EXPOSURE INFORMATION
- USES: Used mainly as a pesticide and a rodenticide. Also, used in some laboratories as a research tool to study glycine receptors.
- EPIDEMIOLOGY: Exposures to strychnine are becoming increasingly rare, though deaths still occur. It can be found in some Chinese herbal medicines, in the slang nut from Cambodia, and also as a street drug adulterant.
- TOXICOLOGY: Competitively inhibits glycine binding to the alpha-subunit of the glycine-regulated chloride channel in the spinal cord. Glycine acts as an inhibitory neurotransmitter in the spinal cord. It opens chloride channels allowing the influx of chloride into cells leading to hyperpolarization and inhibition. Thus, inhibition of glycine binding to this receptor causes excitation of the muscle directly stimulated by the spinal cord.
- WITH POISONING/EXPOSURE
- OVERDOSE: GASTROINTESTINAL: Nausea and vomiting occur uncommonly. CNS EFFECTS: Bilateral horizontal nystagmus and blurred vision have been reported. Muscle tightness/cramps, agitation, and heightened sensitivity to stimulation may precede severe neurologic toxicity. Neurologic symptoms occur quickly (within 15 to 30 minutes) and include agitation, severe hypertonicity of muscles, opisthotonos, and painful muscle spasms. Trismus and risus sardonicus are also reported. The patient usually remains alert throughout this convulsive activity. Auditory, tactile, or visual stimulation may trigger a violent motor response. OTHER: Tachycardia, hypertension, tachypnea, and hyperthermia are seen commonly secondary to neuromuscular hyperactivity. RESPIRATORY FAILURE: Patients may also present with bradycardia and hypotension in cases of respiratory failure/arrest. Involvement of the respiratory muscles leads to diaphragm paralysis resulting in hypoxia and hypercarbia. RENAL FAILURE: Acute renal failure can occur secondary to myoglobinuria, rhabdomyolysis, and crystalluria. METABOLIC: Additionally, a lactic acidosis can develop as a result of the neuromuscular hyperactivity and powerful muscle contractions. Respiratory acidosis is a terminal sign owing to diaphragmatic paralysis. FATALITIES: Early death are usually the result of respiratory failure. Late death are generally secondary to either anoxic brain injury or multiorgan system failure secondary to hyperthermia.
© 2011-2017 RightAnswer.com, Inc. and/or its licensors. All rights reserved. No claim to original U.S. Govt. works.