Safety and ecotoxicology
Spinosad has high efficacy, a broad insect pest spectrum, low mammalian toxicity, and a good environmental profile, a unique feature of the insecticide compared to others currently used for the protection of grain products. It is regarded as natural product-based, and approved for use in organic agriculture by numerous national and international certifications. Spinosad residues are highly stable on grains stored in bins, with protection ranging from 6 months to 2 years.Ecotoxicology parameters have been reported for spinosad, and are:
in rat (Rattus norvegicus (Bergenhout, 1769)), acute oral: LD50 >5000 mg/kg (nontoxic)
in rat (R. norvegicus), acute dermal: LD50 >2000 mg/kg (nontoxic)
in California quail (Callipepla californica (Shaw, 1798)), oral toxicity: LD50 >2000 mg/kg (nontoxic)
in duck (Anas platyrhynchos domestica (Linnaeus, 1758)), dietary toxicity: LC50 >5000 mg/kg (nontoxic)
in rainbow trout (Oncorhynchus mykiss (Walbaum, 1792)), LC50-96h = 30.0 mg/L (slightly toxic)
in Honeybee (Apis mellifera (Linnaeus, 1758)), LD50 = 0.0025 mg/bee (highly toxic if directly sprayed on and of dried residues).Chronic exposure studies failed to induce tumor formation in rats and mice; mice given up to 51 mg/kg/day for 18 months resulted in no tumor formation. Similarly, administration of 25 mg/kg/day to rats for 24 months did not result in tumor formation. Further reading
The non‐target impact of spinosyns on beneficial arthropods
Spinosad toxicity to pollinators and associated risk

References
External links
"Spinosad". Drug Information Portal. U.S. National Library of Medicine. Monograph
A crush injury is injury by an object that causes compression of the body. This form of injury is rare in normal civilian practice, but common following a natural disaster. Other causes include industrial accidents, road traffic collisions, building collapse, accidents involving heavy plant, disaster relief or terrorist incidents. Presentation
Complications
Hypovolaemic Shock. Loss of plasma volume across damaged cell membranes and capillary walls can lead directly to severe hypovolaemia. Furthermore, shock can develop from myocardial depression following release of intracellular electrolytes. In addition, as a result of the mechanism of injury, blood loss from pelvic or long bone fractures may also co-exist. Hyperkalaemia and electrolyte imbalance. Disruption of cell membranes can result in a significant release of potassium, which is a largely intracellular cation that can precipitate cardiac arrest. Sequestration of plasma calcium into injured tissue can lead to a relative hypocalcaemia, which may worsen disruption of clotting abilities and shock. Metabolic acidosis may result from reperfusion injury and hypoperfusion related to shock. Compartment syndrome. Compartment syndrome is a common complication of crush injury as a consequence of oedematous tissue injury, redistribution of fluid into the intracellular compartment and bleeding. Established compartment syndrome may result in worsened systemic crush syndrome and irreversible muscle cell death. Acute Kidney Injury. Release of myoglobin by injured muscle leads to rhabdomyolysis coupled with shock leads to a significant rate of acute kidney injury, estimated as up to 15%. Acute kidney injury leads to a significantly higher mortality.