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/SIGNS AND SYMPTOMS/ Sodium ricinoleate, as a surfactant, demonstrates predictable skin and mucus membrane irritant effects, and may induce a Type IV dermal sensitization response in those previously sensitized to it. However, food-grade castor oil and sodium ricinoleate are prepared in such a manner as to be free of the castor bean constituents that have been proven to be the source of reported Type I immediate hypersensitivity responses.

/SIGNS AND SYMPTOMS/ Castor oil is known for its purgative effects and can be used to induce labor. Both castor oil and ricinoleic acid are approved for use in food. The mechanistic basis for purgative actions likely includes the membrane-disruptive effects of detergent-like molecules, such as sodium ricinoleate (a "soap"). These effects have been shown to be dose-related and to exhibit a threshold below which no laxative response was evident, in both animals and in humans.

/ALTERNATIVE and IN VITRO TESTS/ ... The cytotoxicity of sodium ricinoleate and other fatty acid sodium salts in human saphenous vein endothelial cell cultures was evaluated. Cell count, trypan blue exclusion, and (3H)leucine incorporation into total cell-associated and released proteins were monitored. For the latter of the three, trichloroacetic acid precipitation of total cell extracts and cell supernates was performed. At concentrations less than or equal to 25 uM, sodium ricinoleate and other fatty acid sodium salts did not induce significant toxicity (based on cell count and trypan blue exclusion) for periods up to 72 hr prior to cytokine stimulation.

/ALTERNATIVE and IN VITRO TESTS/ ... The relationship between structural differences in fatty acids and the inhibition of endothelial activation, taking into consideration that dietary long-chain fatty acids may influence processes that involve endothelial activation (eg, inflammation and atherosclerosis) /were evaluated/. To test for a potential stimulatory effect of fatty acids on adhesion molecule expression, sodium salts of saturated, monounsaturated (sodium ricinoleate included), and n-6 and n-3 polyunsaturated fatty acids were each incubated alone (test concentration = 25 uM) with human saphenous vein endothelial cells (HSVECs) for 72 hr. The 72-hr incubation period was followed by 16 hr of stimulation with the cytokine interleukin (IL)-1alpha in the continuous presence of fatty acid salt. At the end of the incubation period, vascular cell adhesion molecule-1 (VCAM-1) expression was assessed using a cell surface enzyme immunoassay (EIA). Sodium ricinoleate significantly inhibited (considered modest; p < .05) cytokine-induced endothelial adhesion molecule expression. DHA inhibited VCAM-1 expression (p < .01) most potently. /Investigators/ also conducted an experiment to determine whether the fatty acid sodium salts may induce endothelial activation in the absence of cytokines. The salts were incubated with endothelial cell monolayers for 24 hr. Incubation periods prior to detection of adhesion molecule surface expression varied from 0 to 72 hr. Neither sodium ricinoleate (25 uM) nor any other fatty acid sodium salt induced adhesion molecule expression, as assessed by EIA.

/LABORATORY ANIMALS: Acute Exposure/ ... The effects sodium ricinoleate, castor oil, and ricinoleic acid on the digestive contractility of the canine small bowel using four male, mixed breed dogs (weights between 10 and 15 g) /were examined/. After feeding, each animal received a single bolus infusion of sodium ricinoleate (500 mg in 30 mL of saline) into the duodenum. Saline (30-mL volume) served as the control. A duodenal cannula was implanted in each animal, and circular muscle activity was recorded for 1 hr. Each animal was dosed with sodium ricinoleate in two experiments, and with isotonic saline (30 mL) in two control experiments. In additional experiments, alterations in digestive contractile patterns were monitored after administration (gastric tube) of castor oil or ricinoleic acid (volume=10 mL) one hr after feeding. Each treatment was repeated twice in each of two animals. Intraduodenal administration of sodium ricinoleate produced a biphasic response in the proximal and mid-jejunum consisting of brief initial stimulation, followed by inhibition of digestive contractility. Compared to the control experiments, these stimulatory and inhibitory effects on intestinal contractility were described as significant (p < .05) changes in the average force per contraction. The changes in mid-jejunal digestive contractility were similar to those observed in the proximal jejunum. The oral administration of ricinoleic acid (10 mL) induced alterations in digestive patterns that were qualitatively similar to those induced by the intraduodenal administration of sdium ricinoleate. Brief initial stimulation, followed by an apparent depression of intestinal contractility, was observed after oral dosing with castor oil (10 mL).

/LABORATORY ANIMALS: Acute Exposure/ ... The morphology of the colon after perfusion of the organ with sodium ricinoleate solution /was examined/ using 25 male New Zealand white rabbits. A Foley catheter was inserted and the colon was perfused with control solution (1.25 mL per minute) for 20 min. The colon was then flushed and perfused with the test solutions. Ten rabbits were perfused with 10 mM sodium ricinoleate and the remaining three groups of five were perfused with 2.5, 5.0, and 7.5 mM, respectively. The animals were killed and full thickness samples of colon were obtained and prepared for light or scanning electron microscopy. In additional experiments, tissue was obtained from animals that were not perfused and those perfused with control buffer (contained PEG 400) for 60 or 160 min. Using scanning electron microscopy, mucous membranes of colons perfused with control buffer for 60 min and unperfused colons appeared normal. After 1 hr of perfusion with 10 mM sodium ricinoleate, patchy loss of epithelial cells was apparent. The loss of epithelial cells was confirmed using light microscopy. A dose response-relationship for mucosal damage was noted. The most severe damage resulted from perfusion with 10 mM sodium ricinoleate. Lesser degrees of change and lesser areas of mucosal surface affected were associated with lower concentrations. Small amounts of DNA (due to loss of DNA into the lumen) accumulated in the control buffer, and perfusion with 2.5 mM sodium ricinoleate did not cause a significant increase in these amounts. However, DNA accumulation increased significantly after perfusion with 5.0, 7.5, and 10 mM sodium ricinolete, and a plateau was reached with 7.5 mM solutions.

/SRP:/ Immediate first aid: Ensure that adequate decontamination has been carried out. If patient is not breathing, start artificial respiration, preferably with a demand valve resuscitator, bag-valve-mask device, or pocket mask, as trained. Perform CPR if necessary. Immediately flush contaminated eyes with gently flowing water. Do not induce vomiting. If vomiting occurs, lean patient forward or place on the left side (head-down position, if possible) to maintain an open airway and prevent aspiration. Keep patient quiet and maintain normal body temperature. Obtain medical attention. /Poisons A and B/

/SRP:/ Basic treatment: Establish a patent airway (oropharyngeal or nasopharyngeal airway, if needed). Suction if necessary. Watch for signs of respiratory insufficiency and assist ventilations if needed. Administer oxygen by nonrebreather mask at 10 to 15 L/min. Monitor for pulmonary edema and treat if necessary ... . Monitor for shock and treat if necessary ... . Anticipate seizures and treat if necessary ... . For eye contamination, flush eyes immediately with water. Irrigate each eye continuously with 0.9% saline (NS) during transport ... . Do not use emetics. For ingestion, rinse mouth and administer 5 mL/kg up to 200 mL of water for dilution if the patient can swallow, has a strong gag reflex, and does not drool ... . Cover skin burns with dry sterile dressings after decontamination ... . /Poisons A and B/

/SRP:/ Advanced treatment: Consider orotracheal or nasotracheal intubation for airway control in the patient who is unconscious, has severe pulmonary edema, or is in severe respiratory distress. Positive-pressure ventilation techniques with a bag valve mask device may be beneficial. Consider drug therapy for pulmonary edema ... . Consider administering a beta agonist such as albuterol for severe bronchospasm ... . Monitor cardiac rhythm and treat arrhythmias as necessary ... . Start IV administration of D5W /SRP: "To keep open", minimal flow rate/. Use 0.9% saline (NS) or lactated Ringer's if signs of hypovolemia are present. For hypotension with signs of hypovolemia, administer fluid cautiously. Watch for signs of fluid overload ... . Treat seizures with diazepam or lorazepam ... . Use proparacaine hydrochloride to assist eye irrigation ... . /Poisons A and B/