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Retrospective analysis of ingestions of iron containing products in the United States: Are there differences between chewable vitamins and adult preparations?1
The Journal of Emergency Medicine, Vol. 19, No. 3, pp. 255–258, 2000 Copyright © 2000 Elsevier Science Inc. Printed in the USA. All rights reserved 0736-4679/00 $–see front matter
PII S0736-4679(00)00234-7
Selected Topics: Toxicology RETROSPECTIVE ANALYSIS OF INGESTIONS OF IRON CONTAINING PRODUCTS IN THE UNITED STATES: ARE THERE DIFFERENCES BETWEEN CHEWABLE VITAMINS AND ADULT PREPARATIONS? Bruce D. Anderson,* Steven G. Turchen,‡,§ Anthony S. Manoguerra,†,‡,§ and Richard F. Clark†,§ *Maryland Poison Center, University of Maryland, School of Pharmacy, Baltimore, Maryland; †San Diego Division of the California Poison Control System, San Diego, California; ‡University of California School of Pharmacy, San Francisco, California; and §Division of Medical Toxicology, Department of Emergency Medicine, UCSD Medical Center, San Diego, California Reprint Address: Richard F. Clark, MD, Department of Emergency Medicine, UCSD Medical Center, 200 W. Arbor Dr., San Diego, CA 92103-8676
e Abstract—Iron is the one of the leading causes of pediatric poisoning deaths in the United States. Most cases of serious iron overdose reported in the medical literature have resulted from adult formulations of iron. To begin evaluating the possibility that differences in toxicity exist between iron preparations, we performed a retrospective evaluation of all exposures to pediatric and adult iron products reported to the American Association of Poison Control Centers’ (AAPCC) Toxic Exposure Surveillance System (TESS) from 1983 to 1998. We attempted to determine the incidence of fatal iron poisoning for each group. A total of 195,780 ingestions of children’s vitamins containing iron were reported to the TESS between 1983 and 1998 with no resulting fatalities. During the same twelve-year study period, 147,079 exposures to adult forms of iron were reported with 60 fatalities (p < 0.0001). A prospective study is required to assess whether differences may exist in the toxicity of these two iron preparations. © 2000 Elsevier Science Inc.
numerous case series and reports of serious or fatal iron overdose cited in the medical literature, including five toddler deaths in Los Angeles county during 7 months in 1992 (1– 4). Most of this literature involves ingestions of adult preparations of iron, and we were unable to find any reported deaths from ingestion of children’s vitamins containing iron (CVI). One retrospective review of ingestions involving CVI describes no serious toxicity in 113 exposures (5). Most textbooks consider the possibility of systemic iron poisoning based on the quantity of elemental iron ingested. CVI are known to contain less iron than adult preparations, and possibly require more pills to cause systemic toxicity. Unfortunately, no prospective human studies have been performed to date comparing clinical findings in poisonings from these two preparations. Therefore, to begin studying these two forms of iron, we conducted a retrospective review of poison center records to examine outcome after exposures to CVI and adult iron products (AIP).
e Keywords—iron; poisoning; overdose; absorption
INTRODUCTION
MATERIALS AND METHODS
Acute iron poisoning is one of the leading causes of pediatric poisoning death in the United States. (1) There are
All exposures to CVI and AIP reported to the American Association of Poison Control Centers’ Toxic Exposure Surveillance System (TESS) from 1983 through 1998 were retrospectively reviewed. The CVI group included any type of pediatric multivitamin containing iron, such
Presented in part at the International Congress of Clinical Toxicology, Sep 13, 1993; New York, New York.
Selected Topics: Toxicology is coordinated by Kenneth Kulig,
RECEIVED: 4 October 1999; FINAL ACCEPTED: 5 April 2000
SUBMISSION RECEIVED:
MD,
3 April 2000; 255
of Denver, Colorado
256
B. D. Anderson et al.
as Flintstones® Brand. The AIP group would include compounds such as ferrous sulfate and ferrous gluconate, as well as standard generic prenatal vitamins. The data elements of TESS were searched to identify all exposures to these products with an outcome coded as “death.” Cases were only reviewed if iron was the only substance listed as responsible for the clinical presentation. The total number of exposures to CVI iron products was determined manually from the American Association of Poison Control Centers’ (AAPCC) Annual Report of the TESS (1,6 –19). Data on cases involving AIP were extracted from the same AAPCC Annual Reports for comparison purposes. Poison centers participating in the TESS program are required by the AAPCC to provide a completed “death verification form” [included in the AAPCC Data Collection Manual (20)] with an abstract or description of the death for all fatal poisoning cases reported to the center. Each death report is reviewed and signed by the corresponding medical director of the poison center from which it is submitted, and reviewed by a physician toxicologist at the AAPCC headquarters in Washington, DC. Many death abstracts are published in the AAPCC TESS Annual Report (1,6 –19). Results were compared using chi squared analysis. Data and cases submitted to the AAPCC are reported by number only, and results published by TESS are devoid of any identifying characteristics, thus ensuring complete anonymity of results.
RESULTS From 1983 through 1998, a total of 195,780 exposures to CVI were reported to the TESS. During the same study period, there were 147,079 total exposures to AIP reported to the TESS. Of these total exposures, children accounted for 107,029 (73%) of the AIP ingestions, and 176,971 (90%) of the CVI ingestions. There were no deaths recorded from exposures to CVI in our data. By contrast, there were 60 total deaths reported from exposures to AIP, 44 children and 16 adults, showing a statistically significant difference (p ⬍ 0.0001) between the two groups (Table 1).
DISCUSSION We failed to find any fatalities reported in the TESS resulting from ingestions of CVI during a 15-year period. A possible explanation for our findings may be that the amount of iron that needs to be absorbed to produce systemic toxicity and the potential for fatal iron poison-
Table 1. Numbers of Fatal Exposures Per Year of Children’s Iron Products Compared to Adult Iron Products Children’s Chewable Iron Products
Adult Iron Products
Year
Exposures
Deaths
Exposures
Deaths
1983 1984 1985 1986 1987 1988 1989 1990 1991 1992 1993 1994 1995 1996 1997 1998 Total
2,707 8,595 8,352 11,676 10,013 10,475 11,003 11,558 11,524 12,461 13,696 15,195 16,687 17,453 16,758 17,627 195,780
0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0*
1,622 3,593 4,330 5,674 7,132 9,201 10,587 10,610 12,077 12,690 10,901 11,267 11,352 11,640 12,502 11,895 147,079
3 2 1 1 2 6 3 5 14 7 5 3 3 2 2 1 60*
* p ⬍ 0.0001 children’s chewable vs adult iron product exposures resulting in death, 2 analysis.
ing is greater than the total amount of iron found in containers of CVI. Typically, containers of children’s chewable vitamin products have 60 to 100 tablets. If each tablet contains 5 to 18 mg of elemental iron, a 15 kg child would need to eat 50 or more of the highest concentration CVI tablets to approach a severe toxicity threshold for iron of 60 mg/kg. The mannitol or sorbitol content of each chewable tablet may limit the quantity a person can tolerate before gastrointestinal symptoms occur. By contrast, AIP are usually not chewable forms, contain two or three times more elemental iron in each tablet, and usually do not contain sorbitol or mannitol. The vast majority of pediatric fatalities from exposures to adult forms of iron have involved the ingestion of very large quantities of tablets (more than 50). Iron absorption is thought to occur as an active process mainly in the upper part of the small intestine. The exact mechanisms involved in mucosal iron uptake are still not completely understood. It appears that select active transport proteins (mucins, mobiliferrin, integrins) are required for dietary iron absorption (21). These proteins control the amount of iron absorbed to prevent oxidative damage to cells from free iron. Large ingestions of iron preparations produce corrosive effects on gastric and intestinal mucosa (22,23). This corrosive effect may leave areas of denuded tissue in the gastrointestinal tract, possibly facilitating simple diffusion of free iron from the gut lumen into the systemic circulation. With a lower concentration of elemental iron available per tablet, children’s iron products may not be as
Please Supply Running Head
257
irritating to the gastrointestinal (GI) mucosa when ingested. A swine model of iron poisoning has recently suggested that there may be differences in GI epithelial damage when similar amounts of elemental iron in CVI and AIP are ingested. (23) Without prospective data, basing treatment considerations regarding exposures to AIP and CVI on our retrospective findings is premature. However, our findings have caused us to reconsider our treatment recommendations in these cases. Considerable nausea, vomiting, and diarrhea, leading to dehydration, may occur from large ingestions of CVI, and some victims may still require intravenous hydration and supportive care after ingestions of either of these preparations even in the absence of other systemic findings. Until a prospective evaluation is performed comparing outcomes and management of different iron preparations, therapeutic recommendations still should be based on the clinical presentation of the patient. Several potential limitations of this study must be remembered. These include the use of retrospective data, and a large sub-population of patients whose cases were not followed to a known outcome either because the ingestion was judged to be sub-toxic, their symptoms were judged to be unrelated to any iron product ingested, or because they were lost to follow-up. However, the
proportion of patients not followed to known outcome was similar for the adult iron product exposures and for the exposures to children’s iron preparations (32.6% vs. 33.0%, respectively). In addition, the usual “tip of the iceberg” limitation applies as in all poison center studies that may exclude data (such as co-ingestants) or cases not reported by health care providers. Nevertheless, our findings are interesting, and together with other recent literature suggest the need for a prospective evaluation.
CONCLUSION Our study reviewed the TESS for cases of death following exposures to children’s vitamin products containing iron and adult iron preparations. We failed to find any fatal outcomes resulting from ingestions of children’s vitamins containing iron. A prospective study should be undertaken to further evaluate possible divergence in the clinical presentations and outcomes of different iron preparations.
Acknowledgments—The authors wish to thank the American Association of Poison Control Centers for providing the funding for data analysis of the TESS.
REFERENCES 1. Litovitz TL, Holm KA, Bailey KM, Schmitz BF. 1991 Annual report of the American Association of Poison Control Centers National Data Collection System. Am J Emerg Med 1992;10:452– 505. 2. Westlin WF. Deferoxamine in the treatment of acute iron poisoning. Clin Pediatr 1966;5:531–5. 3. Henriksson P, Nilsson L, Nilsson IM, Stenberg P. Fatal iron intoxication with multiple coagulation defects and degradation of factor VIII and factor XIII. Scand J Haematol 1979;22:235– 40 . 4. Weiss B, Alkon E, Weindlar F, Kelter A, Delacruz P. Toddler deaths resulting from ingestion of iron supplements—Los Angeles, 1992–1993. MMWR 1993;42:111–3. 5. Dean BS, Krenzelok EP. Multiple vitamins and vitamins with iron: accidental poisoning in children. Vet Hum Toxicol 1988;30:23–5. 6. Veltri JC, Litovitz TL. 1983 Annual report of the American Association of Poison Control Centers National Data Collection System. Am J Emerg Med 1984;2:420 – 43. 7. Litovitz TL, Veltri JC. 1984 Annual report of the American Association of Poison Control Centers National Data Collection System. Am J Emerg Med 1985;3:423–50. 8. Litovitz TL, Normann SA, Veltri JC. 1985 Annual report of the American Association of Poison Control Centers National Data Collection System. Am J Emerg Med 1986;4:427–58. 9. Litovitz TL, Martin TG, Schmitz B. 1986 Annual report of the American Association of Poison Control Centers National Data Collection System. Am J Emerg Med 1987;5:405– 45. 10. Litovitz TL, Schmitz BF, Matyunas N, Martin TG. 1987 Annual report of the American Association of Poison Control Centers National Data Collection System. Am J Emerg Med 1988;6:479 – 515. 11. Litovitz TL, Schmitz BF, Holm KA. 1988 Annual report of the
12.
13.
14.
15.
16.
17.
18.
19.
American Association of Poison Control Centers National Data Collection System. Am J Emerg Med 1989;7:495–545. Litovitz TL, Schmitz BF, Bailey KM. 1989 Annual report of the American Association of Poison Control Centers National Data Collection System. Am J Emerg Med 1990;8:394 – 442. Litovitz TL, Bailey KM, Schmitz BF, Holm KC, Klein-Schwartz W. 1990 Annual report of the American Association of Poison Control Centers National Data Collection System. Am J Emerg Med 1991;9:461–509. Litovitz TL, Holm KA, Clancy C, Schmitz BF, Clark LA, Oderda GM. 1992 Annual report of the American Association of Poison Control Centers National Data Collection System. Am J Emerg Med 1993;11:494 –555. Litovitz TL, Clark LR, Soloway RA. 1993 Annual report of the American Association of Poison Control Centers National Data Collection System. Am J Emerg Med 1994;12:546 – 84. Litovitz TL, Felberg L, Soloway RA, Ford M, Geller R. 1994 Annual report of the American Association of Poison Control Centers National Data Collection System. Am J Emerg Med 1995; 13:551–97. Litovitz TL, Felberg L, White S, Klein-Schwartz W. 1995 Annual report of the American Association of Poison Control Centers National Data Collection System. Am J Emerg Med 1996;14:487– 537. Litovitz TL, Smilkstein M, Fleberg L, Klein–Schwartz W, Berlin R, Morgan JL. 1996 Annual report of the American Association of Poison Control Centers National Data Collection System. Am J Emerg Med 1997;15:447–500. Litovitz TL, Klein-Schwartz W, Dyer KS, Shannon M, Lee S, Powers M. 1997 Annual report of the American Association of Poison Control Centers National Data Collection System. Am J Emerg Med 1998;16:443–97.
258 20. Instructions for the American Association of Poison Control Centers National Data Collection System. Washington, DC: 1985:29 –30. 21. Conrad ME, Umbreit JN. A concise review: iron absorption—the mucin-mobiliform-integrin pathway. Am J Hematol 1993;42:67–73. 22. Gandhi RK, Robarts FH. Hour-glass stricture of the stomach and
B. D. Anderson et al. pyloric stenosis due to ferrous sulphate poisoning. Br J Surg 1962;49:613–7. 23. Nordt SP, Williams SR, Behling C, Richter P, Manoguerra AS, Clark RF. Comparison of the toxicities of two iron formulations in a swine model. Acad Emerg Med 1999;6:1104 – 8.
PII S0736-4679(00)00234-7
Selected Topics: Toxicology RETROSPECTIVE ANALYSIS OF INGESTIONS OF IRON CONTAINING PRODUCTS IN THE UNITED STATES: ARE THERE DIFFERENCES BETWEEN CHEWABLE VITAMINS AND ADULT PREPARATIONS? Bruce D. Anderson,* Steven G. Turchen,‡,§ Anthony S. Manoguerra,†,‡,§ and Richard F. Clark†,§ *Maryland Poison Center, University of Maryland, School of Pharmacy, Baltimore, Maryland; †San Diego Division of the California Poison Control System, San Diego, California; ‡University of California School of Pharmacy, San Francisco, California; and §Division of Medical Toxicology, Department of Emergency Medicine, UCSD Medical Center, San Diego, California Reprint Address: Richard F. Clark, MD, Department of Emergency Medicine, UCSD Medical Center, 200 W. Arbor Dr., San Diego, CA 92103-8676
e Abstract—Iron is the one of the leading causes of pediatric poisoning deaths in the United States. Most cases of serious iron overdose reported in the medical literature have resulted from adult formulations of iron. To begin evaluating the possibility that differences in toxicity exist between iron preparations, we performed a retrospective evaluation of all exposures to pediatric and adult iron products reported to the American Association of Poison Control Centers’ (AAPCC) Toxic Exposure Surveillance System (TESS) from 1983 to 1998. We attempted to determine the incidence of fatal iron poisoning for each group. A total of 195,780 ingestions of children’s vitamins containing iron were reported to the TESS between 1983 and 1998 with no resulting fatalities. During the same twelve-year study period, 147,079 exposures to adult forms of iron were reported with 60 fatalities (p < 0.0001). A prospective study is required to assess whether differences may exist in the toxicity of these two iron preparations. © 2000 Elsevier Science Inc.
numerous case series and reports of serious or fatal iron overdose cited in the medical literature, including five toddler deaths in Los Angeles county during 7 months in 1992 (1– 4). Most of this literature involves ingestions of adult preparations of iron, and we were unable to find any reported deaths from ingestion of children’s vitamins containing iron (CVI). One retrospective review of ingestions involving CVI describes no serious toxicity in 113 exposures (5). Most textbooks consider the possibility of systemic iron poisoning based on the quantity of elemental iron ingested. CVI are known to contain less iron than adult preparations, and possibly require more pills to cause systemic toxicity. Unfortunately, no prospective human studies have been performed to date comparing clinical findings in poisonings from these two preparations. Therefore, to begin studying these two forms of iron, we conducted a retrospective review of poison center records to examine outcome after exposures to CVI and adult iron products (AIP).
e Keywords—iron; poisoning; overdose; absorption
INTRODUCTION
MATERIALS AND METHODS
Acute iron poisoning is one of the leading causes of pediatric poisoning death in the United States. (1) There are
All exposures to CVI and AIP reported to the American Association of Poison Control Centers’ Toxic Exposure Surveillance System (TESS) from 1983 through 1998 were retrospectively reviewed. The CVI group included any type of pediatric multivitamin containing iron, such
Presented in part at the International Congress of Clinical Toxicology, Sep 13, 1993; New York, New York.
Selected Topics: Toxicology is coordinated by Kenneth Kulig,
RECEIVED: 4 October 1999; FINAL ACCEPTED: 5 April 2000
SUBMISSION RECEIVED:
MD,
3 April 2000; 255
of Denver, Colorado
256
B. D. Anderson et al.
as Flintstones® Brand. The AIP group would include compounds such as ferrous sulfate and ferrous gluconate, as well as standard generic prenatal vitamins. The data elements of TESS were searched to identify all exposures to these products with an outcome coded as “death.” Cases were only reviewed if iron was the only substance listed as responsible for the clinical presentation. The total number of exposures to CVI iron products was determined manually from the American Association of Poison Control Centers’ (AAPCC) Annual Report of the TESS (1,6 –19). Data on cases involving AIP were extracted from the same AAPCC Annual Reports for comparison purposes. Poison centers participating in the TESS program are required by the AAPCC to provide a completed “death verification form” [included in the AAPCC Data Collection Manual (20)] with an abstract or description of the death for all fatal poisoning cases reported to the center. Each death report is reviewed and signed by the corresponding medical director of the poison center from which it is submitted, and reviewed by a physician toxicologist at the AAPCC headquarters in Washington, DC. Many death abstracts are published in the AAPCC TESS Annual Report (1,6 –19). Results were compared using chi squared analysis. Data and cases submitted to the AAPCC are reported by number only, and results published by TESS are devoid of any identifying characteristics, thus ensuring complete anonymity of results.
RESULTS From 1983 through 1998, a total of 195,780 exposures to CVI were reported to the TESS. During the same study period, there were 147,079 total exposures to AIP reported to the TESS. Of these total exposures, children accounted for 107,029 (73%) of the AIP ingestions, and 176,971 (90%) of the CVI ingestions. There were no deaths recorded from exposures to CVI in our data. By contrast, there were 60 total deaths reported from exposures to AIP, 44 children and 16 adults, showing a statistically significant difference (p ⬍ 0.0001) between the two groups (Table 1).
DISCUSSION We failed to find any fatalities reported in the TESS resulting from ingestions of CVI during a 15-year period. A possible explanation for our findings may be that the amount of iron that needs to be absorbed to produce systemic toxicity and the potential for fatal iron poison-
Table 1. Numbers of Fatal Exposures Per Year of Children’s Iron Products Compared to Adult Iron Products Children’s Chewable Iron Products
Adult Iron Products
Year
Exposures
Deaths
Exposures
Deaths
1983 1984 1985 1986 1987 1988 1989 1990 1991 1992 1993 1994 1995 1996 1997 1998 Total
2,707 8,595 8,352 11,676 10,013 10,475 11,003 11,558 11,524 12,461 13,696 15,195 16,687 17,453 16,758 17,627 195,780
0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0*
1,622 3,593 4,330 5,674 7,132 9,201 10,587 10,610 12,077 12,690 10,901 11,267 11,352 11,640 12,502 11,895 147,079
3 2 1 1 2 6 3 5 14 7 5 3 3 2 2 1 60*
* p ⬍ 0.0001 children’s chewable vs adult iron product exposures resulting in death, 2 analysis.
ing is greater than the total amount of iron found in containers of CVI. Typically, containers of children’s chewable vitamin products have 60 to 100 tablets. If each tablet contains 5 to 18 mg of elemental iron, a 15 kg child would need to eat 50 or more of the highest concentration CVI tablets to approach a severe toxicity threshold for iron of 60 mg/kg. The mannitol or sorbitol content of each chewable tablet may limit the quantity a person can tolerate before gastrointestinal symptoms occur. By contrast, AIP are usually not chewable forms, contain two or three times more elemental iron in each tablet, and usually do not contain sorbitol or mannitol. The vast majority of pediatric fatalities from exposures to adult forms of iron have involved the ingestion of very large quantities of tablets (more than 50). Iron absorption is thought to occur as an active process mainly in the upper part of the small intestine. The exact mechanisms involved in mucosal iron uptake are still not completely understood. It appears that select active transport proteins (mucins, mobiliferrin, integrins) are required for dietary iron absorption (21). These proteins control the amount of iron absorbed to prevent oxidative damage to cells from free iron. Large ingestions of iron preparations produce corrosive effects on gastric and intestinal mucosa (22,23). This corrosive effect may leave areas of denuded tissue in the gastrointestinal tract, possibly facilitating simple diffusion of free iron from the gut lumen into the systemic circulation. With a lower concentration of elemental iron available per tablet, children’s iron products may not be as
Please Supply Running Head
257
irritating to the gastrointestinal (GI) mucosa when ingested. A swine model of iron poisoning has recently suggested that there may be differences in GI epithelial damage when similar amounts of elemental iron in CVI and AIP are ingested. (23) Without prospective data, basing treatment considerations regarding exposures to AIP and CVI on our retrospective findings is premature. However, our findings have caused us to reconsider our treatment recommendations in these cases. Considerable nausea, vomiting, and diarrhea, leading to dehydration, may occur from large ingestions of CVI, and some victims may still require intravenous hydration and supportive care after ingestions of either of these preparations even in the absence of other systemic findings. Until a prospective evaluation is performed comparing outcomes and management of different iron preparations, therapeutic recommendations still should be based on the clinical presentation of the patient. Several potential limitations of this study must be remembered. These include the use of retrospective data, and a large sub-population of patients whose cases were not followed to a known outcome either because the ingestion was judged to be sub-toxic, their symptoms were judged to be unrelated to any iron product ingested, or because they were lost to follow-up. However, the
proportion of patients not followed to known outcome was similar for the adult iron product exposures and for the exposures to children’s iron preparations (32.6% vs. 33.0%, respectively). In addition, the usual “tip of the iceberg” limitation applies as in all poison center studies that may exclude data (such as co-ingestants) or cases not reported by health care providers. Nevertheless, our findings are interesting, and together with other recent literature suggest the need for a prospective evaluation.
CONCLUSION Our study reviewed the TESS for cases of death following exposures to children’s vitamin products containing iron and adult iron preparations. We failed to find any fatal outcomes resulting from ingestions of children’s vitamins containing iron. A prospective study should be undertaken to further evaluate possible divergence in the clinical presentations and outcomes of different iron preparations.
Acknowledgments—The authors wish to thank the American Association of Poison Control Centers for providing the funding for data analysis of the TESS.
REFERENCES 1. Litovitz TL, Holm KA, Bailey KM, Schmitz BF. 1991 Annual report of the American Association of Poison Control Centers National Data Collection System. Am J Emerg Med 1992;10:452– 505. 2. Westlin WF. Deferoxamine in the treatment of acute iron poisoning. Clin Pediatr 1966;5:531–5. 3. Henriksson P, Nilsson L, Nilsson IM, Stenberg P. Fatal iron intoxication with multiple coagulation defects and degradation of factor VIII and factor XIII. Scand J Haematol 1979;22:235– 40 . 4. Weiss B, Alkon E, Weindlar F, Kelter A, Delacruz P. Toddler deaths resulting from ingestion of iron supplements—Los Angeles, 1992–1993. MMWR 1993;42:111–3. 5. Dean BS, Krenzelok EP. Multiple vitamins and vitamins with iron: accidental poisoning in children. Vet Hum Toxicol 1988;30:23–5. 6. Veltri JC, Litovitz TL. 1983 Annual report of the American Association of Poison Control Centers National Data Collection System. Am J Emerg Med 1984;2:420 – 43. 7. Litovitz TL, Veltri JC. 1984 Annual report of the American Association of Poison Control Centers National Data Collection System. Am J Emerg Med 1985;3:423–50. 8. Litovitz TL, Normann SA, Veltri JC. 1985 Annual report of the American Association of Poison Control Centers National Data Collection System. Am J Emerg Med 1986;4:427–58. 9. Litovitz TL, Martin TG, Schmitz B. 1986 Annual report of the American Association of Poison Control Centers National Data Collection System. Am J Emerg Med 1987;5:405– 45. 10. Litovitz TL, Schmitz BF, Matyunas N, Martin TG. 1987 Annual report of the American Association of Poison Control Centers National Data Collection System. Am J Emerg Med 1988;6:479 – 515. 11. Litovitz TL, Schmitz BF, Holm KA. 1988 Annual report of the
12.
13.
14.
15.
16.
17.
18.
19.
American Association of Poison Control Centers National Data Collection System. Am J Emerg Med 1989;7:495–545. Litovitz TL, Schmitz BF, Bailey KM. 1989 Annual report of the American Association of Poison Control Centers National Data Collection System. Am J Emerg Med 1990;8:394 – 442. Litovitz TL, Bailey KM, Schmitz BF, Holm KC, Klein-Schwartz W. 1990 Annual report of the American Association of Poison Control Centers National Data Collection System. Am J Emerg Med 1991;9:461–509. Litovitz TL, Holm KA, Clancy C, Schmitz BF, Clark LA, Oderda GM. 1992 Annual report of the American Association of Poison Control Centers National Data Collection System. Am J Emerg Med 1993;11:494 –555. Litovitz TL, Clark LR, Soloway RA. 1993 Annual report of the American Association of Poison Control Centers National Data Collection System. Am J Emerg Med 1994;12:546 – 84. Litovitz TL, Felberg L, Soloway RA, Ford M, Geller R. 1994 Annual report of the American Association of Poison Control Centers National Data Collection System. Am J Emerg Med 1995; 13:551–97. Litovitz TL, Felberg L, White S, Klein-Schwartz W. 1995 Annual report of the American Association of Poison Control Centers National Data Collection System. Am J Emerg Med 1996;14:487– 537. Litovitz TL, Smilkstein M, Fleberg L, Klein–Schwartz W, Berlin R, Morgan JL. 1996 Annual report of the American Association of Poison Control Centers National Data Collection System. Am J Emerg Med 1997;15:447–500. Litovitz TL, Klein-Schwartz W, Dyer KS, Shannon M, Lee S, Powers M. 1997 Annual report of the American Association of Poison Control Centers National Data Collection System. Am J Emerg Med 1998;16:443–97.
258 20. Instructions for the American Association of Poison Control Centers National Data Collection System. Washington, DC: 1985:29 –30. 21. Conrad ME, Umbreit JN. A concise review: iron absorption—the mucin-mobiliform-integrin pathway. Am J Hematol 1993;42:67–73. 22. Gandhi RK, Robarts FH. Hour-glass stricture of the stomach and
B. D. Anderson et al. pyloric stenosis due to ferrous sulphate poisoning. Br J Surg 1962;49:613–7. 23. Nordt SP, Williams SR, Behling C, Richter P, Manoguerra AS, Clark RF. Comparison of the toxicities of two iron formulations in a swine model. Acad Emerg Med 1999;6:1104 – 8.