PAPER
PATHOLOGY/BIOLOGY; TOXICOLOGY
Riza Yilmaz,
1M.D.; Eyy
€up Yilmaz,
2M.D.; Veli Ozdemir,
2M.D.; Muhammet Can,
3M.D.;
Isil Pakis,
4M.D.; Ibrahim E. Piskin,
5M.D.; Halis Dokgoz,
6M.D.; Erdal Ozer,
7M.D.;
and Kemal V. Numanoglu,
8M.D.
An Evaluation of Childhood Deaths in Turkey
Due to Yellow Phosphorus in Firecrackers
ABSTRACT:Yellow phosphorus (YP) is a powerful protoplasmic poison used in the manufacturing of matches, pest poisons, firecrackers, firework cracker, lights for watches, military ammunition, and agriculture fertilizer. YP is extremely flammable and toxic and easily absorbed from the gastrointestinal tract. In this study, we examined childhood deaths from 1997 to 2012 resulting from the ingestion of firecrackers. The patients ranged from 2 to 15 years of age and were admitted to the hospital with a variety of symptoms. Those that presented with nausea, vomiting, and hypotension rapidly deteriorated and entered a coma. An autopsy was performed in all but one of the 16 cases reviewed. Macro-scopically, the livers had a yellowish discoloration with petechial bleeding. Histopathologic examination revealed acute toxic hepatitis. In con-clusion, these firecrackers are found in corner shops throughout Turkey, may cause death in children with little warning, and should be banned to prevent further deaths.
KEYWORDS:forensic science, yellow phosphorus, intoxication, firecracker, childhood deaths, autopsy, toxic hepatitis
Elemental phosphorus exists in red and yellow forms. Red phosphorus is nonvolatile, insoluble, and unabsorbable and, therefore, nontoxic when ingested. Yellow phosphorus (YP), also known as white phosphorus, is an inorganic substance that does not naturally occur in the environment. YP is waxy, transparent, and combustible, as it reacts rapidly with oxygen. YP easily catches fire at room temperature, although it is stable in water, which is used for its transportation and storage (1–3).
YP is a powerful protoplasmic poison used in the manufactur-ing of matches, pest poisons, firecrackers, firework cracker, lights for watches, military ammunition, and agriculture fertilizer. YP is extremely flammable and toxic, easily absorbed from the gastrointestinal tract. The estimated lethal dose of yellow phos-phorus is 1 mg/kg. YP poisoning produces serious pathologic effects in almost all organ systems, particularly the liver, heart,
kidney, spleen, and brain, and may result in significant mortality (3–5).
Poisoning or death resulting from ingestion of firecracker is rarely seen. However, in Turkey, these firecrackers (Fig. 1) are used as toys by children, who occasionally chew explosive firecrackers as if they were chocolate bars (6,7), leading to a serious risk of toxic exposure. The aim of this study was to examine childhood deaths attributed to firecracker poisoning in Turkey.
Materials and Methods
In Turkey, autopsies are performed in compliance with Article 86–89 of the Turkish Code of Criminal Procedures by a forensic specialist and a pathologist or any other medical specialist or two practitioners. The identity of the deceased is determined ini-tially, and visible external characteristic evidence on his/her body is noted. The necroptic examination is then performed to determine and assess the cause and time of death. All findings are formulated in the form of a report (8). Biologic specimens can be obtained from the corpse for histopathological, toxicolog-ical, and biological examinations and/or criminal investigations if the case warrants. The specimens obtained are further exam-ined by the authorities in the Council of Forensic Medicine.
The Council of Forensic Medicine is the official organ of the Turkish Ministry of Justice, which is the only official expert authority in Turkey. The duties and responsibilities of the Coun-cil of Forensic Medicine are defined by law. Each year, approxi-mately 85,000 reports are written on scientific and technical subjects related to forensic sciences based on requests from the courts and the district attorneys. The Council of Forensic
Medi-1The Department of Forensic Medicine, Medical Faculty, Bulent Ecevit
University, Zonguldak, Turkey.
2The Council of Forensic Medicine, Istanbul, Turkey. 3
The Department of Forensic Medicine, Medical Faculty, Balikesir Univer-sity, Balikesir, Turkey.
4
The Department of Forensic Medicine, Medical Faculty, Acibadem Uni-versity, Istanbul, Turkey.
5
The Department of Pediatrics, Medical Faculty, Bulent Ecevit University, Zonguldak, Turkey.
6The Department of Forensic Medicine, Medical Faculty, Mersin
Univer-sity, Mersin, Turkey.
7The Department of Forensic Medicine, Medical Faculty, Gaziosmanpasa
University, Tokat, Turkey.
8The Department of Pediatric Surgery, Medical Faculty, Bulent Ecevit
University, Zonguldak, Turkey.
Received 4 Jan. 2014; and in revised form 1 April 2014; accepted 17 April 2014.
648 © 2015 American Academy of Forensic Sciences
cine incorporates specialized departments, such as those perform-ing autopsies and toxicological analyses, and prepares medical and legal records. The main department employs a general surgeon, cardiovascular surgeon, neurosurgeon, gynecologist, internist, cardiologist, hematologist, immunologist, pathologist, and forensic specialists.
The Council of Forensic Medicine collectively evaluates testi-monies and statements of the intimates of the deceased, event scene investigation evidence, medical records (if any), necroptic findings, and reported results of histopathological examinations. However, public prosecutors can request further evaluation from the Forensic Medicine Departments of University hospitals.
In this study, we retrospectively reviewed all cases evaluated by the Council of Forensic Medicine for oral firecracker ing in Turkey from 1997 to 2009, as well as firecracker poison-ing cases referred to the emergency services of hospitals, where the patients died despite resuscitation efforts, from 2009 to 2012. We also evaluated documents from autopsied cases available from the relevant authorities.
Nineteen death cases were identified and were reportedly linked to ingestion of firecrackers. We excluded three cases without any relevant toxicological evidence or necroptic examin-ations. The remaining 16 cases were evaluated based on age, gender, hospital records if present, and macroscopic, micro-scopic, and chemical evidence gathered during autopsy.
Results
We evaluated all cases assessed by the Turkish Council of Forensic Medicine for firecracker ingestion from 1997 to 2009, as well as 16 cases with claims of firework poisoning referred to the hospital emergency services or autopsied from 2009 to 2012. A total of 16 cases (six females, 37.5%, and 10 males, 63.5%) with a median age of 4.06 years were evaluated. The ages of the youngest and the oldest were two and fifteen years, respectively. The cases who died were aged 15 (n= 1), 9 (n = 1), 4 (n = 5), 3 (n= 6), and 2 (n = 3) years. After excluding a deceased 15 year old with mental retardation, the median age of the cases was 3.33 years. The deceased died within 24–72 h (n = 11) or >72 h (n = 5) after the incident.
Age, gender, incident location, date of firecracker ingestion (event date), survival period after the incident, and the poorest laboratory test results of the inpatients are shown in Table 1.
TABLE 1–– Demog raph ics, poorest clinical laboratory findin gs, and survival time in the included cases of firecracker ingestion Ca se N umber Age Sex pH pC O2 pO 2 HC O3 Na mEq/L K mEq/L Ca mg/dL CL mEq/L AL T IU/mL AS T IU/mL CK IU/mL LDH mg/d L Total Bilirubin mg/dL Gluco se mg/dL PT sec aP TT sec Sur vival after the Incident (days) 14 M 411 527 29,4 42,3 2 2 3 F 6.3 376 406 28,4 35,8 2 33 M 1706 5580 11 43 M 668 492 5,7 155, 3 3 54 M 692 488 27,6 46,5 3 6 1 5 F 127. 79 2.98 7.22 1531 1527 288. 78 10 7 3 F 136 6.2 6.7 113 466 630 13.9 2 8 4 M 134 5.5 7.43 386 432 1.5 145 29,6 37,4 4 9 2 M 7.16 16 10.9 136 3.2 413 435 306. 70 2 10 3 M 122 3.1 9.67 85 395 427 2 11 4 M 672 496 29,8 42,6 2 12 4 F 6.97 2 13.6 103.4 3.66 529 986 1612 3 13 4 F 7.16 1 32.5 48.7 12.2 140. 3 2.97 9.88 104. 6 646 545 1.14 129 3 14 2 M 7.61 0 2 1 184 129 2.5 7.1 96 771 547 2335 2646 13.6 176 11 15 3 M 7.75 9 16.2 42.6 24.1 115 2.1 5.8 87 342 1024 3670 2114 8.3 195 8 16 4 F 7.4 314 325 258 1.2 2 pC O2, carbon dioxi de part ial pre ssure; pO 2, oxyg en part ial pre ssure; ALT, alanine amin otransferase; AST, aspartate amin otransferase; CK, creatine kina se; LDH, lac tate deh ydroge nase; PT, p rothrombin time; and aPT T, activated partial thro mboplastin time.
FIG. 1––Appearance of a firecracker.
The cases who died had been living in different geographic regions of Turkey, including Southeast Anatolia (n= 7), Mar-mara (n = 6), Central Anatolia (n = 1), the Aegean (n = 1), and the Mediterranean (n = 1).
The medical histories of the deceased indicated that in three cases, one of the parents noticed that the child had been eating fire-crackers and tried to remove the remnants from their mouth; in four cases, a sibling informed a family member that the child had been seen eating firecrackers; three children were caught while eating firecrackers; and one child told the mother that they had eaten firecrackers. Postmortem statements indicated that in four cases, the children had eaten firecrackers without the family’s knowledge. In 12 cases, the parents had their children ingest yoghurt or milk.
Children were referred to the hospital for symptoms including pallor, fatigue, nausea, vomiting, and abdominal pain. Three patients with elevated liver enzyme levels were sent home from the hospital after physical examination with the recommendation to ingest milk or yoghurt and/or a drug prescription, while assuring the family that the child had nothing serious. These children returned to the hospital with complaints of increasing severity.
In children referred to the hospital with extremely severe symptoms, the physical examinations revealed a moderately or severely deteriorated general health state, acidotic respiration, hyperventilation, tachycardia, hypoactive deep tendon reflexes, and icteric appearance of the face, whole body, and cyanotic lips. Medical records revealed that the patients had been hospi-talized with initial diagnoses of foreign substance intake, intoxi-cation, hepatic coma, or Reye’s syndrome. After vascular access, these severely affected patients were treated by repeated gastric lavage. The Drug and Poison Information Center was consulted for potential development of complications, and information about treatment alternatives weas obtained. This Center indicated possible development of electrocardiographic (ECG) abnormali-ties, hypotension, tachypnea, apnea, pulmonary edema, convul-sion, coma, and eventually death.
The available documents indicated that these cases were pre-emptively transferred to the intensive care units of tertiary care hospitals. A stepwise approach was implemented to establish vascular access, provide appropriate fluids and electrolyte replacements, and prevent and/or manage hypotension, metabolic acidosis, tachypnea, hyperglycemia, agitation, convulsion, ECG abnormalities, and ventricular extrasystoles. The hospital stay after onset of firework poisoning ranged from 28 h to 11 days.
Various laboratory tests were performed in the patients. These included extremely increased levels of alanine aminotransferase (ALT) to 1706 (10–44) U/L, aspartate aminotransferase (AST) to 5580 (10–50) U/L, and total bilirubin to 13.9 (0.2–1.0) mg/dL. The cases also had glucose levels of 306.70 (70–105) mg/dL, direct bilirubin of 9.3 (0.0–0.3) mg/dL, Na+ of 115 (130– 150) mEq/L, K+ of 2.1 and 6.2 (3.5–5.5) mEq/L, Ca2+ of 5.8 (8.5–10.5) mg/dL, Cl-of 85 (95–110) mEq/L, creatinine kinase of
3670 (male, 39–308; female, 26–192) U/L, and lactic dehydroge-nase of 2646 (60–130 mg/dL). In children surviving a few days after the incident, their pH and oxygen partial pressure (pO2)
lev-els rose above normal levlev-els, but decreased to below normal levlev-els near the time of death. However, the pCO2 values did not
corre-spond to these values.
An autopsy was performed on 15 of the 16 cases. Macroscopi-cally, a yellowish color was detected on the body surface of the corpses because of increased blood bilirubin levels. Surgical exploration of the brains revealed cerebral edema, and serous fluid
collection (130–965 cc) within the thoracic cavity was drained. Lungs were heavier (458–732 g) than normal. No macroscopic abnormal gross findings were detected in the heart, kidney, and spleen.
Macroscopic examination of the livers of four cases treated for 7–10 days prior to death revealed a yellowish discoloration with petechial bleeding on the surface and coconut appearance on the cut surfaces. Gallbladders were hemorrhagic with increased bile salt density. Liver specimens of the other 11 cases who died immediately after swallowing firecrackers contained occasional areas of subcapsular bleeding with the stomachs con-taining digested blood and gastric contents covered with a coal-like substance.
Histopathological examination of the livers of four cases trea-ted for 7–10 days prior to death revealed acute toxic hepatitis with massive necrosis around the portal region, cells of acute inflammation, macrophages, bile ductal proliferation with pseudoglandular formation, and widespread cholestasis with nor-mal hepatocytes. In the remaining 11 cases, widespread microve-sicular fatty degeneration of hepatocytes, blood stagnation within the hepatic vasculature, and an increased number of round cells in the portal regions were detected during histopathological examination of liver specimens. During diagnostic workup, parenchymal destruction was characterized by intensification of bridging and anastomizing necrotic areas (Fig. 2). Pneumonia and renal tubular degeneration were detected in histopathological examinations of four inpatients who had been treated for 7–10 days, while no gross abnormality was found in other visceral organs.
During necroptic examination, no evidence of toxicity was revealed in toxicological analyses of blood samples in the four cases hospitalized for 7–10 days. In 11 cases, methemoglobine-mia (2.4–70%) was noted, while trace amounts of barbituric acid were found in blood samples of eight cases secondary to medical therapy.
FIG. 2––Massive necrosis around the portal region, acute inflammatory cells, macrophages, and bile ductal proliferation with pseudoglandular for-mation in the liver (hematoxylin & eosin,9200).
Discussion
Firecrackers, as a source of amusement, explode and produce a big noise when they are pressed under the foot or rubbed on a hard surface. Adults describe their recollections about firecracker online as follows:“Firecrackers are children’s toys which consist of two brown colored spheres stuck on a slip of paper. They produce loud noises which make the children cry joyfully. When they were gently rubbed against the ground, a“click” sound was heard, and they burned with a spark. However, if we placed them on a hard surface and hit them with a stone, they would explode with a cracking noise. This method of exploding fire-crackers meant shorter entertainment. It took a longer time to rub them against a wall. Firecracker spheres on paper bands measured nearly 1 cm (9)”; “Firecrackers were the most enjoy-able toys of the children under 5 years of age, what we called ‘ape age’. They had small brown colored spheres on a paper band resembling a wound plaster, which were blown out by impatient me with a big stone. When they were soaked in water, and then rubbed on our hands, phosphorescent green color was produced, which made our hands shine in the dark like an elec-tric lamp. For that reason, my brother and I used to wet them by saliva. Then we used to spit them on our palms and spread all over our hands” (10).
Firecracker is primarily composed of YP (10%), silica, potas-sium chlorate, iron oxide, and magnepotas-sium carbonate (1–4). YP poisoning may result from industrial accidents in developed countries, but it also occurs in adults attempting suicide and by accidental oral intake in children, particularly on festival days, in developing countries (3–5,11–13). Although the youngest child suicide case was reported in an 8 year old in Turkey (14), fire-cracker ingestion-related deaths are commonly reported on those between 2 and 4 years of age, except in mental retardation cases and in some of cases in which children ate firecrackers as if they were chocolate, which can accidently occur on festival days.
YP is a general protoplasmic and poison causing cardiac, hepatic, renal, and multiorgan failure. YP intoxication has three stages (3,4,13). The first stage is characterized by nausea, vomit-ing, diarrhea, and abdominal pain, which occur within the first 24 h after ingestion. Laboratory tests are near normal during this period, although sudden death may occur for an unknown reason (15). In the three cases we excluded in this study, the causes of deaths could not be determined due to lack of medical evidence, even though it was likely these cases died due to firecracker ingestion. Ingestion of a large amount of firecrackers can result directly in cardiovascular arrhythmia and collapse within the first 24 h. Cardiac collapse may also occur because of fluid and elec-trolyte loss due to vomiting or diarrhea, in addition to heart tox-icity. Repeated electrocardiograms may demonstrate myocardial damage with dysrhythmias, widened QRS complexes, or depres-sion of ST segments, and early death is generally due to cardiac dysrhythmias secondary to electrolyte abnormalities such as hypocalcemia and hyperkalemia (3,4,16). However, in our cases, we could not document dysrhythmias or electrolyte disturbances. The second stage of YP intoxication occurs between 24 and 72 h after ingestion. It is essentially an asymptomatic period, but liver enzyme levels become elevated and toxic hepatitis begins to spread. Eleven cases in our review died in the hospital during this period. However, during this period, some patients may be discharged prematurely, which may have occurred in three of the cases reviewed in this study. These children did not have medical treatment and/or liver transplantation as an option. Thus, the primary care physicians or pediatricians who examine
chil-dren in the emergency units should be trained about firecracker, their toxic effects, and the corresponding treatments.
The third stage of YP intoxication will result in death due to multiorgan failure because of the systemic effects of high-dose phosphorus after absorption. Liver transplantation is the only treatment during this stage, and death is inevitable when it is not performed. In our case review, five patients in this stage sur-vived 3–11 days, and none of them received a liver transplant.
There is no specific medical test for the diagnosis of YP poi-soning. The diagnosis depends primarily on the history provided by the children or their parents. If the history is unclear, a gar-licky odor and luminescence in the vomitus or stool may be helpful. Faint fumes emanating from the stool are called smok-ing stool syndrome (17,18). Because our cases had been hospi-talized with initial diagnoses of foreign substance intake, intoxication, hepatic coma, or Reye’s syndrome, ingested fire-crackers were not reported in the hospital. These may be due to lack of knowledge by the family or miscommunication between medical personnel and the family.
No antidote or specific medical treatment is available for patients who have ingested firecracker containing YP (3,13,18,19). Biochemical tests can indicate metabolic acidosis, hypohyperglycemia, hyperbilirubinemia, and increased AST and ALT levels. Haematological abnormalities include elevations of the international normalized ratio (INR), the partial thrombo-plastin time, and leukopenia. An electrocardiogram may demon-strate inverted T waves and changes in the QRS complex, arrhythmias, and atrial fibrillation. All these findings can be observed easily during the third stage (3–5,16) and were reported in some of our cases in Table 1.
YP intoxication treatment during the first and second stages should include the removal of phosphorus and general support-ive measures (1–3). It is known that yogurt and ayran, a cold yogurt beverage mixed with salt, are used to treat patients with diarrhea as a traditional alternative medical method in Turkey. It is common for patients in rural areas to consume these before arriving at the hospital (20), and they were administered by fam-ilies or advised by medical personnel in some of our cases.
The utility of liver transplantation for managing acute liver failure due to the ingestion of firecrackers containing YP has been recommended since 2009. If yellow phosphorus affects the brain and the heart, in addition to the liver, the mortality rate is high despite liver transplantation (13,21,22). In our case review, macroscopic and microscopic pathologic findings were deter-mined in the livers of four cases that survived 3–11 days. Although these patients were candidates for liver transplantation, they died without any intervention.
On autopsy, macroscopic nonspecific findings, such as wide-spread hyperemia, pulmonary edema, hepatocellular necrosis, tubular degeneration, and gastrointestinal bleeding, may be seen. Together with clinical findings, these nonspecific changes may contribute to a diagnosis of YP intoxication. A yellow appear-ance accompanied by petechial hemorrhage and hemorrhagic gallbladders was found upon macroscopic evaluation of the liv-ers in four patients who were treated for 7–11 days. In the other 11 cases, macroscopic examination of the livers revealed subcap-sular hemorrhagic areas and digested blood in the stomachs. In the cases treated for an extended period in the hospital, hepato-cellular necrosis could be diagnosed both macroscopically and microscopically. In the cases that died quickly after ingestion, hepatic changes could not be detected precisely.
Limited information is available in the literature about the effect of yellow phosphorus on health; some case reports and a
few experimental animal studies have shown that it causes acute hepatic failure (23). Sßamdancı et al. (24) showed macrovesicular and microvesicular vacuolization in almost all hepatocytes of hepatic sections. Another study of liver histopathology due to yellow phosphorus poisoning obtained from postmortem or transplanted livers showed features of toxic hepatitis with exten-sive necrosis, ballooning degeneration, and steatosis (15). In our cases, liver histopathology revealed acute hepatitis (toxic hepati-tis) showing massive necrosis in the portal region, bile ductal proliferation with pseudoglandular formation, and widespread cholestasis (Fig. 2).
Delayed hospital referral in these patients is caused by the presence of common clinical symptoms, such as nausea and vomiting, low educational and economic status of the family, and inadequate parental guidance due to a large number of chil-dren. Only four of our cases were brought to the hospital imme-diately after the symptoms had started, and these patients survived 7–11 days. The others died a short time after the onset of symptoms.
In 1987, the Council of Ministers in Turkey enacted a statute regulating the production, storage, sale, use, and supervision of firecracker. However, it was not used effectively in practice, and children continue to die due to ingestion of firecrackers (15,22,25–27). As YP poisoning is a significant health problem with a high mortality rate, it should be considered a potential toxic hazard and should no longer be sold as an explosive device, and measures should be taken to decrease its use (26). In Turkey, firecrackers are used by children as a toy on festival days. These firecrackers are found in corner shops throughout Turkey, may cause death in children with little warning, and should be banned to prevent further deaths.
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Additional information and reprint requests: RizaYilmaz, M.D.
The Department of Forensic Medicine, Medical Faculty Bulent Ecevit University, Esenkoy-kozlu
67600, Zonguldak Turkey
