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Patricia S. Grigson - One of the best experts on this subject based on the ideXlab platform.
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The role of dose and restriction state on morphine-, cocaine-, and LiCl-induced suppression of saccharin intake: A comprehensive analysis.
Physiology & behavior, 2016Co-Authors: Robert C. Twining, Robert A. Wheeler, Christopher S. Freet, Christian G. Reich, Dennie A. Tompers, Sarah E. Wolpert, Patricia S. GrigsonAbstract:Rats avoid intake of a taste cue when paired with a drug of abuse or with the illness-inducing Agent, lithium chloride (LiCl). Although progress has been made, it is difficult to compare the suppressive effects of abused Agents and LiCl on intake of a gustatory conditioned stimulus (CS) because of the cross-laboratory use of different CSs, different unconditioned stimuli (USs), and different doses of the drugs, different conditioning regimens, and different restriction states. Here we have attempted to unify these variables by comparing the suppressive effects of a range of doses of morphine, cocaine, and LiCl on intake of a saccharin CS using a common regimen in non-restricted, food restricted, or water restricted male Sprague-Dawley rats. The results showed that, while the putatively Aversive Agent, LiCl, was effective in suppressing intake of the taste cue across nearly all doses, regardless of restriction state, the suppressive effects of both morphine and cocaine were greatly reduced when evaluated in either food or water restricted rats. Greater sensitivity to drug was revealed, at very low doses, when testing occurred in the absence of need (i.e., when the rats were non-restricted). Together, these results provide the first uniform and comprehensive analysis of the suppressive effects of morphine, cocaine, and LiCl as a function of dose and restriction state. In the present case, the suppressive effects of morphine and cocaine are found to differ from those of LiCl and, in some respects, from one another as well.
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Drug-motivated behavior in rats with lesions of the thalamic orosensory area.
Behavioral neuroscience, 2015Co-Authors: Jennifer E. Nyland, Danielle N. Alexander, Patricia S. GrigsonAbstract:Rats suppress intake of a palatable taste cue when paired with a rewarding or an Aversive stimulus in appetitive or Aversive conditioning, respectively. A similar phenomenon occurs with drugs of abuse, but the nature of this conditioning has been subject for debate. While relatively little is known about the underlying neural circuitry, we recently reported bilateral lesions of the thalamic trigeminal orosensory area isolate drug-induced suppression of intake of a taste cue. The lesion blocks avoidance of the taste cue when paired with experimenter delivered drugs of abuse, yet has no effect on avoidance of the same cue when paired with an Aversive Agent or when it predicts access to a highly palatable sucrose solution. We hypothesize the lesion may blunt the rewarding properties of the drug. To test this, we used a runway apparatus, as running speed has been shown to increase with increasing reward value. Our hypothesis was supported by failure of the lesioned rats to increase running speed for morphine. Interestingly, lesioned rats did avoid intake of the drug-paired cue when presented in the runway apparatus and displayed naloxone-precipitated withdrawal. Using a partial crossover design, the lesion prevented avoidance of a cocaine-paired cue when presented in the home cage. We conclude that the lesion disrupts avoidance of a taste cue in anticipation of the rewarding properties of a drug but, at least in the presence of contextual cues, allows for avoidance of a taste cue as it elicits the onset of an Aversive conditioned state of withdrawal.
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Fischer rats are more sensitive than Lewis rats to the suppressive effects of morphine and the Aversive kappa-opioid agonist spiradoline.
Behavioral neuroscience, 2013Co-Authors: Christopher S. Freet, Robert A. Wheeler, Ellen Leuenberger, Nicole A. S. Mosblech, Patricia S. GrigsonAbstract:Data suggest that rats avoid intake of an otherwise palatable saccharin cue when paired with a drug of abuse, at least in part, because the value of the taste cue pales in anticipation of the availability of the highly rewarding drug. Earlier support for this hypothesis was provided by the finding that relative to the less sensitive Fischer rats, Lewis rats exhibit greater avoidance of a saccharin cue when paired with a rewarding sucrose or cocaine unconditioned stimulus (US), but not when paired with the Aversive Agent, lithium chloride (LiCl). More recent data, however, have shown that Fischer rats actually exhibit greater, not less, avoidance of the same saccharin cue when morphine serves as the US. Therefore, Experiment 1 evaluated morphine-induced suppression of intake of the taste cue in Lewis and Fischer rats when the morphine US was administered subcutaneously, rather than ip. Experiment 2 examined the effect of strain on the suppression of intake of the saccharin cue when paired with spiradoline, a selective κ-opioid receptor agonist. The results confirm that Fischer rats are more responsive to the suppressive effects of morphine than Lewis rats and that Fischer rats also exhibit greater avoidance of the saccharin cue when paired with spiradoline, despite the fact that spiradoline is devoid of reinforcing properties. Taken together, the data suggest that the facilitated morphine-induced suppression observed in Fischer rats, compared with Lewis rats, may reflect an increased sensitivity to the Aversive, κ-mediated properties of opiates.
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Bilateral lesions of the thalamic trigeminal orosensory area dissociate natural from drug reward in contrast paradigms.
Behavioral neuroscience, 2012Co-Authors: Jennifer E. Nyland, Danielle N. Alexander, Nu Chu Liang, Patricia S. GrigsonAbstract:Substance abuse and addiction are associated with an apparent devaluation of, and inattention to, natural rewards. This consequence of addiction can be modeled using a reward comparison paradigm where rats avoid intake of a palatable taste cue that comes to predict access to a drug of abuse. Evidence suggests rats avoid intake following such pairings, at least in part, because the taste cue pales in comparison to the highly rewarding drug expected in the near future. In accordance, lesions of the gustatory thalamus or cortex eliminate avoidance of a taste cue when paired with either a drug of abuse or a rewarding sucrose solution, but not when paired with the Aversive Agent, LiCl. The present study used bilateral ibotenic acid lesions to evaluate the role of a neighboring thalamic structure, the trigeminal orosensory area (TOA), in avoidance of a gustatory cue when paired with sucrose (experiment 1), morphine (experiment 2), cocaine (experiment 3), or LiCl (experiment 4). The results show that the TOA lesion disrupts, but does not eliminate avoidance of a taste cue that predicts access to a preferred sucrose solution and leaves intact the development of a LiCl-induced conditioned taste aversion. The lesion does, however, eliminate the suppression of intake of a taste cue when paired with experimenter-administered morphine or cocaine using our standard parameters. As such, this is the first manipulation found to dissociate avoidance of a taste cue when mediated by a sweet or by a drug of abuse.
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Ethanol-Induced Conditioned Taste Avoidance: Reward or Aversion?
Alcoholism clinical and experimental research, 2008Co-Authors: Chuang Liu, John W. Showalter, Patricia S. GrigsonAbstract:Background: Rats avoid intake of a palatable taste cue when paired with all drugs of abuse tested. Evidence suggests that, at least for morphine and cocaine, rats avoid the taste cue because they are anticipating the rewarding properties of the drug. Thus, the suppressive effects of a rewarding sucrose solution and cocaine, but not those of the putatively Aversive Agent, lithium chloride (LiCl), are exaggerated in drug-sensitive Lewis rats. Likewise, the suppressive effects of sucrose and morphine, but not those of LiCl, are eliminated by bilateral lesions of the gustatory thalamus. Unlike morphine and cocaine, it is less clear whether rewarding or Aversive drug properties are responsible for ethanol-induced suppression of intake of a taste cue. The present set of studies tests whether, like cocaine, ethanol-induced suppression of intake of a taste cue also is greater in the drug-sensitive Lewis rats and whether the suppressive effects of the drug are prevented by bilateral lesions of the taste thalamus. Methods: In Experiment 1, fluid-deprived Lewis and Fischer rats were given 5-minute access to 0.15% saccharin and then injected with saline or a range of doses of ethanol (0.5, 0.75, 1.0, or 1.5 g/kg). There was a total of 6 such pairings. In Experiments 2 and 3, Sprague–Dawley rats received bilateral electrophysiologically guided lesions of the gustatory thalamus. After recovery, suppression of intake of the saccharin cue was evaluated following repeated daily pairings with either a high (1.5 g/kg) or a low (0.75 g/kg) dose of ethanol. Results: Ethanol-induced suppression of intake of the saccharin conditioned stimulus (CS) did not differ between the drug-sensitive Lewis rats relative to the less-sensitive Fischer rats. Lesions of the taste thalamus, however, prevented the suppressive effect of the 0.75 g/kg dose of the drug, but had no impact on the suppressive effect of the 1.5 g/kg dose of ethanol. Conclusion: The results suggest that the suppressive effects of ethanol on CS intake are mediated by both rewarding and Aversive consequences, varying as a function of dose.
A Manoguerra - One of the best experts on this subject based on the ideXlab platform.
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comparison of pediatric poisoning hazards an analysis of 3 8 million exposure incidents a report from the american association of poison control centers
Pediatrics, 1992Co-Authors: T Litovitz, A ManoguerraAbstract:This analysis of life-threatening and fatal pediatric poisonings was conducted to aid poison prevention educational efforts, guide product reformulations and Aversive Agent use, reassess over-the-counter status for selected pharmaceuticals, and identify research areas for clinical advances in the treatment of pediatric poisonings. A hazard factor was devised to assess more objectively the pediatric poisoning hazard posed by pharmaceutical and nonpharmaceutical products. By considering the frequency and extent of injury following actual exposures, the hazard factor reflects more than the acute toxicity of individual ingredients and is also influenced by such variables as packaging, accessibility, availability (as a reflection of marketing), formulations, and closure types. Of the 3 810 405 exposures involving children younger than 6 years of age reported to poison centers in 1985 through 1989, 2117 patients experienced a major outcome (life-threatening effect or residual disability) and an additional 111 fatalities occurred. The three most commonly implicated substance categories, accounting for 30.4% of reported exposures, include cosmetics and personal care products, cleaning substances, and plants. All had low hazard factors, with significant hazards being limited to a small number of products identified herein. Thus this analysis of hazard factors demonstrates that frequent exposure does not imply toxicity. Iron supplements were the single most frequent cause of pediatric unintentional ingestion fatalities, accounting for 30.2% of reported pediatric pharmaceutical unintentional ingestion fatalities reported over an 8-year period. Antidepressants, cardiovascular medications, and methyl salicylate follow in frequency of pediatric pharmaceutical deaths. Hydrocarbons (including five lamp oil deaths) and pesticides were each implicated in 12 pediatric ingestion fatalities during the 8-year period. Selenious acid-containing gun bluing was involved in four deaths. These data allow a more informed approach to poison prevention efforts in the 1990s.
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Comparison of pediatric poisoning hazards: an analysis of 3.8 million exposure incidents. A report from the American Association of Poison Control Centers.
Pediatrics, 1992Co-Authors: T Litovitz, A ManoguerraAbstract:This analysis of life-threatening and fatal pediatric poisonings was conducted to aid poison prevention educational efforts, guide product reformulations and Aversive Agent use, reassess over-the-counter status for selected pharmaceuticals, and identify research areas for clinical advances in the treatment of pediatric poisonings. A hazard factor was devised to assess more objectively the pediatric poisoning hazard posed by pharmaceutical and nonpharmaceutical products. By considering the frequency and extent of injury following actual exposures, the hazard factor reflects more than the acute toxicity of individual ingredients and is also influenced by such variables as packaging, accessibility, availability (as a reflection of marketing), formulations, and closure types. Of the 3,810,405 exposures involving children younger than 6 years of age reported to poison centers in 1985 through 1989, 2117 patients experienced a major outcome (life-threatening effect or residual disability) and an additional 111 fatalities occurred. The three most commonly implicated substance categories, accounting for 30.4% of reported exposures, include cosmetics and personal care products, cleaning substances, and plants. All had low hazard factors, with significant hazards being limited to a small number of products identified herein. Thus this analysis of hazard factors demonstrates that frequent exposure does not imply toxicity. Iron supplements were the single most frequent cause of pediatric unintentional ingestion fatalities, accounting for 30.2% of reported pediatric pharmaceutical unintentional ingestion fatalities reported over an 8-year period. Antidepressants, cardiovascular medications, and methyl salicylate follow in frequency of pediatric pharmaceutical deaths. Hydrocarbons (including five lamp oil deaths) and pesticides were each implicated in 12 pediatric ingestion fatalities during the 8-year period.(ABSTRACT TRUNCATED AT 250 WORDS)
Mitchell F. Roitman - One of the best experts on this subject based on the ideXlab platform.
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the Aversive Agent lithium chloride suppresses phasic dopamine release through central glp 1 receptors
Neuropsychopharmacology, 2016Co-Authors: Samantha M Fortin, Elena H Chartoff, Mitchell F. RoitmanAbstract:Unconditioned rewarding stimuli evoke phasic increases in dopamine concentration in the nucleus accumbens (NAc) while discrete Aversive stimuli elicit pauses in dopamine neuron firing and reductions in NAc dopamine concentration. The unconditioned effects of more prolonged Aversive states on dopamine release dynamics are not well understood and are investigated here using the malaise-inducing Agent lithium chloride (LiCl). We used fast-scan cyclic voltammetry to measure phasic increases in NAc dopamine resulting from electrical stimulation of dopamine cell bodies in the ventral tegmental area (VTA). Systemic LiCl injection reduced electrically evoked dopamine release in the NAc of both anesthetized and awake rats. As some behavioral effects of LiCl appear to be mediated through glucagon-like peptide-1 receptor (GLP-1R) activation, we hypothesized that the suppression of phasic dopamine by LiCl is GLP-1R dependent. Indeed, peripheral pretreatment with the GLP-1R antagonist exendin-9 (Ex-9) potently attenuated the LiCl-induced suppression of dopamine. Pretreatment with Ex-9 did not, however, affect the suppression of phasic dopamine release by the kappa-opioid receptor agonist, salvinorin A, supporting a selective effect of GLP-1R stimulation in LiCl-induced dopamine suppression. By delivering Ex-9 to either the lateral or fourth ventricle, we highlight a population of central GLP-1 receptors rostral to the hindbrain that are involved in the LiCl-mediated suppression of NAc dopamine release.
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the Aversive Agent lithium chloride suppresses phasic dopamine release through central glp 1 receptors
Neuropsychopharmacology, 2016Co-Authors: Samantha M Fortin, Elena H Chartoff, Mitchell F. RoitmanAbstract:Unconditioned rewarding stimuli evoke phasic increases in dopamine concentration in the nucleus accumbens (NAc) while discrete Aversive stimuli elicit pauses in dopamine neuron firing and reductions in NAc dopamine concentration. The unconditioned effects of more prolonged Aversive states on dopamine release dynamics are not well understood and are investigated here using the malaise-inducing Agent lithium chloride (LiCl). We used fast-scan cyclic voltammetry to measure phasic increases in NAc dopamine resulting from electrical stimulation of dopamine cell bodies in the ventral tegmental area (VTA). Systemic LiCl injection reduced electrically evoked dopamine release in the NAc of both anesthetized and awake rats. As some behavioral effects of LiCl appear to be mediated through glucagon-like peptide-1 receptor (GLP-1R) activation, we hypothesized that the suppression of phasic dopamine by LiCl is GLP-1R dependent. Indeed, peripheral pretreatment with the GLP-1R antagonist exendin-9 (Ex-9) potently attenuated the LiCl-induced suppression of dopamine. Pretreatment with Ex-9 did not, however, affect the suppression of phasic dopamine release by the kappa-opioid receptor agonist, salvinorin A, supporting a selective effect of GLP-1R stimulation in LiCl-induced dopamine suppression. By delivering Ex-9 to either the lateral or fourth ventricle, we highlight a population of central GLP-1 receptors rostral to the hindbrain that are involved in the LiCl-mediated suppression of NAc dopamine release.
Robert A. Wheeler - One of the best experts on this subject based on the ideXlab platform.
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The role of dose and restriction state on morphine-, cocaine-, and LiCl-induced suppression of saccharin intake: A comprehensive analysis.
Physiology & behavior, 2016Co-Authors: Robert C. Twining, Robert A. Wheeler, Christopher S. Freet, Christian G. Reich, Dennie A. Tompers, Sarah E. Wolpert, Patricia S. GrigsonAbstract:Rats avoid intake of a taste cue when paired with a drug of abuse or with the illness-inducing Agent, lithium chloride (LiCl). Although progress has been made, it is difficult to compare the suppressive effects of abused Agents and LiCl on intake of a gustatory conditioned stimulus (CS) because of the cross-laboratory use of different CSs, different unconditioned stimuli (USs), and different doses of the drugs, different conditioning regimens, and different restriction states. Here we have attempted to unify these variables by comparing the suppressive effects of a range of doses of morphine, cocaine, and LiCl on intake of a saccharin CS using a common regimen in non-restricted, food restricted, or water restricted male Sprague-Dawley rats. The results showed that, while the putatively Aversive Agent, LiCl, was effective in suppressing intake of the taste cue across nearly all doses, regardless of restriction state, the suppressive effects of both morphine and cocaine were greatly reduced when evaluated in either food or water restricted rats. Greater sensitivity to drug was revealed, at very low doses, when testing occurred in the absence of need (i.e., when the rats were non-restricted). Together, these results provide the first uniform and comprehensive analysis of the suppressive effects of morphine, cocaine, and LiCl as a function of dose and restriction state. In the present case, the suppressive effects of morphine and cocaine are found to differ from those of LiCl and, in some respects, from one another as well.
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Fischer rats are more sensitive than Lewis rats to the suppressive effects of morphine and the Aversive kappa-opioid agonist spiradoline.
Behavioral neuroscience, 2013Co-Authors: Christopher S. Freet, Robert A. Wheeler, Ellen Leuenberger, Nicole A. S. Mosblech, Patricia S. GrigsonAbstract:Data suggest that rats avoid intake of an otherwise palatable saccharin cue when paired with a drug of abuse, at least in part, because the value of the taste cue pales in anticipation of the availability of the highly rewarding drug. Earlier support for this hypothesis was provided by the finding that relative to the less sensitive Fischer rats, Lewis rats exhibit greater avoidance of a saccharin cue when paired with a rewarding sucrose or cocaine unconditioned stimulus (US), but not when paired with the Aversive Agent, lithium chloride (LiCl). More recent data, however, have shown that Fischer rats actually exhibit greater, not less, avoidance of the same saccharin cue when morphine serves as the US. Therefore, Experiment 1 evaluated morphine-induced suppression of intake of the taste cue in Lewis and Fischer rats when the morphine US was administered subcutaneously, rather than ip. Experiment 2 examined the effect of strain on the suppression of intake of the saccharin cue when paired with spiradoline, a selective κ-opioid receptor agonist. The results confirm that Fischer rats are more responsive to the suppressive effects of morphine than Lewis rats and that Fischer rats also exhibit greater avoidance of the saccharin cue when paired with spiradoline, despite the fact that spiradoline is devoid of reinforcing properties. Taken together, the data suggest that the facilitated morphine-induced suppression observed in Fischer rats, compared with Lewis rats, may reflect an increased sensitivity to the Aversive, κ-mediated properties of opiates.
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Chronic morphine treatment exaggerates the suppressive effects of sucrose and cocaine, but not lithium chloride, on saccharin intake in Sprague-Dawley rats.
Behavioral neuroscience, 2001Co-Authors: Patricia S. Grigson, Robert A. Wheeler, Daniel S Wheeler, Sarah M. BallardAbstract:Three experiments examined the effect of chronic morphine treatment on cocaine-, sucrose-, and lithium chloride (LiCl)-induced suppression of saccharin intake in Sprague-Dawley rats. All rats were either water- or food-deprived and then implanted subcutaneously with 1 morphine (75 mg) or vehicle pellet for 5 days. They were then given brief access to 0.15% saccharin and soon thereafter injected with either cocaine (10 mg/kg s.c.), LiCl (0.009 M, 1.33 ml/100 g body weight i.p.), or saline, or, in Experiment 2, given a 2nd access period to either a preferred 1.0 M sucrose solution or the same 0.15% saccharin solution. There was 1 taste-drug or taste-taste pairing per day for a number of days. The results showed that a history of chronic morphine treatment exaggerated the suppressive effects of a rewarding sucrose solution and cocaine but not those of the Aversive Agent, LiCl. These data provide further support for the reward comparison hypothesis.
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Water-Deprivation Prevents Morphine-, but not LiCl-Induced, Suppression of Sucrose Intake
Physiology & behavior, 1999Co-Authors: Patricia S. Grigson, Polina Lyuboslavsky, Diana Tanase, Robert A. WheelerAbstract:Intake of a saccharin-conditioned stimulus (CS) can be suppressed following pairing with an Aversive Agent such as lithium chloride (LiCl) or x-rays (referred to as a conditioned taste aversion or CTA), a highly rewarding sucrose solution (referred to as an anticipatory contrast effect), or a drug of abuse such as morphine or cocaine. Although the suppressive effects of LiCl and sucrose are clear examples of Aversive and appetitive conditioning, respectively, it is not certain which properties (Aversive or appetitive) mediate the suppressive effects of drugs of abuse. It is known, however, that the suppressive effects of a rewarding sucrose US are attenuated when using a caloric sucrose CS in food deprived rats, while LiCl induced CTAs are much less effected. Standard CTA testing typically is conducted in water-deprived rather than food-deprived rats and, although LiCl is known to suppress intake of a sucrose CS in water-deprived rats, the suppressive effects of drugs of abuse have not been evaluated under these conditions. The present experiment, then, compared the suppressive effects of a standard dose of morphine (15 mg/kg) and a matched dose of LiCl (0.009 M) on intake of a sucrose CS in water-deprived and free-feeding rats. The results showed that both drugs suppressed intake in free-feeding subjects, but only the Aversive Agent, LiCl, reduced CS intake in the water-deprived rats. This finding dissociates the suppressive effects of morphine and LiCl and, in so doing, aligns the suppressive effects of morphine with those of an appetitive sucrose US.
T Litovitz - One of the best experts on this subject based on the ideXlab platform.
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comparison of pediatric poisoning hazards an analysis of 3 8 million exposure incidents a report from the american association of poison control centers
Pediatrics, 1992Co-Authors: T Litovitz, A ManoguerraAbstract:This analysis of life-threatening and fatal pediatric poisonings was conducted to aid poison prevention educational efforts, guide product reformulations and Aversive Agent use, reassess over-the-counter status for selected pharmaceuticals, and identify research areas for clinical advances in the treatment of pediatric poisonings. A hazard factor was devised to assess more objectively the pediatric poisoning hazard posed by pharmaceutical and nonpharmaceutical products. By considering the frequency and extent of injury following actual exposures, the hazard factor reflects more than the acute toxicity of individual ingredients and is also influenced by such variables as packaging, accessibility, availability (as a reflection of marketing), formulations, and closure types. Of the 3 810 405 exposures involving children younger than 6 years of age reported to poison centers in 1985 through 1989, 2117 patients experienced a major outcome (life-threatening effect or residual disability) and an additional 111 fatalities occurred. The three most commonly implicated substance categories, accounting for 30.4% of reported exposures, include cosmetics and personal care products, cleaning substances, and plants. All had low hazard factors, with significant hazards being limited to a small number of products identified herein. Thus this analysis of hazard factors demonstrates that frequent exposure does not imply toxicity. Iron supplements were the single most frequent cause of pediatric unintentional ingestion fatalities, accounting for 30.2% of reported pediatric pharmaceutical unintentional ingestion fatalities reported over an 8-year period. Antidepressants, cardiovascular medications, and methyl salicylate follow in frequency of pediatric pharmaceutical deaths. Hydrocarbons (including five lamp oil deaths) and pesticides were each implicated in 12 pediatric ingestion fatalities during the 8-year period. Selenious acid-containing gun bluing was involved in four deaths. These data allow a more informed approach to poison prevention efforts in the 1990s.
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Comparison of pediatric poisoning hazards: an analysis of 3.8 million exposure incidents. A report from the American Association of Poison Control Centers.
Pediatrics, 1992Co-Authors: T Litovitz, A ManoguerraAbstract:This analysis of life-threatening and fatal pediatric poisonings was conducted to aid poison prevention educational efforts, guide product reformulations and Aversive Agent use, reassess over-the-counter status for selected pharmaceuticals, and identify research areas for clinical advances in the treatment of pediatric poisonings. A hazard factor was devised to assess more objectively the pediatric poisoning hazard posed by pharmaceutical and nonpharmaceutical products. By considering the frequency and extent of injury following actual exposures, the hazard factor reflects more than the acute toxicity of individual ingredients and is also influenced by such variables as packaging, accessibility, availability (as a reflection of marketing), formulations, and closure types. Of the 3,810,405 exposures involving children younger than 6 years of age reported to poison centers in 1985 through 1989, 2117 patients experienced a major outcome (life-threatening effect or residual disability) and an additional 111 fatalities occurred. The three most commonly implicated substance categories, accounting for 30.4% of reported exposures, include cosmetics and personal care products, cleaning substances, and plants. All had low hazard factors, with significant hazards being limited to a small number of products identified herein. Thus this analysis of hazard factors demonstrates that frequent exposure does not imply toxicity. Iron supplements were the single most frequent cause of pediatric unintentional ingestion fatalities, accounting for 30.2% of reported pediatric pharmaceutical unintentional ingestion fatalities reported over an 8-year period. Antidepressants, cardiovascular medications, and methyl salicylate follow in frequency of pediatric pharmaceutical deaths. Hydrocarbons (including five lamp oil deaths) and pesticides were each implicated in 12 pediatric ingestion fatalities during the 8-year period.(ABSTRACT TRUNCATED AT 250 WORDS)
