By Taylor Riedley, Biology, ‘20
Author’s Note: I wrote this paper for my UWP 102B class with Dr. Brenda Rinard in Winter Quarter 2019. For the preliminary stage of an assignment, I reviewed primary research on metal phosphide poisoning and wrote a formal paper geared towards a medical audience. For the final stage, I translated my formal paper into this one, intending it for a curious though not necessarily scientific audience. I chose this topic because I am considering an occupation in forensic pathology, and while I searched for articles about pathological findings, I came across an autopsy of a victim of metal phosphide poisoning. I was struck by the discrepancy between the general outward symptoms and the lethal organ damage of phosphide patients. I was further appalled when I learned that metal phosphides are within ready reach of children. I viewed this paper as an opportunity to draw attention to the need for more research on metal phosphides, and especially in this more accessible incarnation, to encourage readers to advocate for those who are not given the information necessary to stay safe.
Purpose: The goal of this article is to raise awareness about metal phosphide poisoning. Metal phosphides, although highly toxic, are used in commercial goods in Turkey, Ecuador, and India. Doctors are unable to properly diagnose and treat intoxicated patients due to a lack of understanding about metal phosphides’ biochemical effects on the human body. This culminates in the illness and death of thousands of patients every year, mostly young children or individuals with mental health issues.
Only six years ago, a four-year-old girl with common flu symptoms visited Ïnönü University’s Faculty of Medicine in Malayta, Turkey. Doctors would have given her fever reducers and a quick dismissal had the girl’s parents not mentioned finding a firecracker in her mouth. The girl did not have a flu; she was experiencing acute liver failure (ALF). She promptly died of secondary cardiac arrest while the doctors were preparing her for a liver transplant (1).
The firecracker that killed the girl was of the Çatapat brand, which contains yellow phosphorus (YP), an explosive that is lethal in a ratio of 1 mg YP to 1 kg (2.2 lbs) body weight (2). In other words, an 18 mg dose of YP — the size of an allergy pill — can kill a four-year-old. YP derives its potency from its placement within a volatile group of compounds called metal phosphides. Metal phosphides release large quantities of heat and light if they come into contact with any acid, even water molecules floating in the air, so labs that experiment with metal phosphides must store them in oil. The phosphide reaction produces a phosphine gas, which is commonly used as a fumigant pesticide. When the reaction occurs inside patients, the gas escapes their bodies and can affect other individuals, as if they were a toxic diffuser. There have been cases of pet owners falling ill after driving their phosphide-intoxicated pet to the vet and of doctors experiencing symptoms after treating a patient with phosphide poisoning (3).
In spite of the threat metal phosphide poses to the human body, the Çatapat firecracker market remains successful. This is partially due to the lenient warning label laws in Turkey; Çatapat is not forced to include the potential dangers of its product on its packaging or advertisements. This lulls parents into a false sense of security, so they leave their children unsupervised with these seemingly harmless toys.
Another metal phosphide called white phosphorus (WP) is a hazard in Ecuadorian firecrackers and matches. A common method of suicide among adults, especially adolescent women with undiagnosed psychiatric illnesses such as depression, anxiety, or PTSD from sexual assault, involves ingesting firecrackers called diablillos (“little devils”). The diablillos cost only $0.25 and are popular during winter festivities, but contain so much WP that ingesting just one can cause serious illness. (WP’s toxicity should come as no surprise. Its use in chemical warfare remains controversial because it effectively obliterates enemies — and civilians.) Ecuadorian firecracker manufacturers continue to use WP instead of safer, albeit pricier, combusting agents to profit from low-income households. Likewise, incidents involving Ecuadorian matches are seen as “phossy jaw,” or phosphorus-induced cell death, in match factory workers (4). WP is continuously responsible for employee illness, but match companies refuse to use safer flame-inducers that are more expensive.
Another issue involving the metal phosphide YP is the consumption of pesticides such as Ratol rat poison in India. Ratol is easily accessed in agricultural communities for crop protection. It can be accidentally eaten by children, but it is a common means of suicide among adults, especially adolescents from lower socioeconomic backgrounds (3-8). Similar pesticides containing metal phosphides have been common in Romania and Iran for over one hundred years and bring unintentional death to both farm animals and humans (3).
Metal phosphides pose an obvious danger if they are not handled with care, so we should have established a procedure for identifying and treating metal phosphide poisoning. Surprisingly, this is not the case. Doctors acknowledge the havoc metal phosphides wreak upon the body, but there is little research that identifies the biochemistry behind it (2). Even though we can see the damage done by metal phosphides during an autopsy, we do not know how the damage is done. Without this critical information, it is impossible to engineer a specific cure.
Most patients with metal phosphide poisoning, including the four-year-old from Turkey, outwardly appear to have a flu. There are a few non-flu symptoms, including jaundice, liver palpability (when the liver is so swollen that one can feel it pushing up against the surface of the patient’s abdomen), blood cell deficiency, delayed blood clotting, low blood pressure, and irregular or elevated heart rates, but most of these are also general and are not always present (2, 4-5). An even rarer symptom is cholestasis, when the liver stops producing bile. It is a sign of liver damage and can be clinically identified from skin that itches so persistently that patients create sores from excessive scratching. Even though this points directly to the liver, it is usually unhelpful in identifying metal phosphide poisoning due to its rarity and late exhibition (6). All of these symptoms present themselves in varying combinations and last until the patient either recovers or dies; death can occur anytime between eight hours to seventeen days after metal phosphide consumption (7). If doctors are not informed that a patient consumed metal phosphides, they may be unaware of the accumulating internal damage until it is too late.
Dr. Emine Türkmen Şamdanci, a professor of pathology at Ïnönü University, performed an autopsy on the four-year-old and discovered severe organ destruction, especially in the girl’s liver and kidneys. The girl’s levels of liver enzymes were twenty times the normal value, which means her liver was working overtime to clean the metal phosphide out of her blood. The liver was also yellowed and had fatty buildup, which were indications of severe cell damage. In the kidneys, the tubular lining degraded upon contact with the metal phosphide. With the two major blood-cleansing organs out of operation, the YP spread through the bloodstream and infiltrated the girl’s other organs. Congestion was discovered in the girl’s brain, lungs, and kidneys. Finally, the heart, the capitol of the bloodstream, succumbed to this lethal destroyer (1).
Additional internal signs have been recorded in other autopsies. Some signs, such as bleeding, interstitial fluid, loss of cell nuclei, and cell death, can be shared by the liver, heart, brain, and lungs. Other signs are centralized. In the liver, these include inflammation, crumbling, and high white blood cell counts. In the heart, there can be congestion and loss of normal muscle definition. The digestive tract distinctively suffers from congestion in the mucous lining, peeling, phosphine gas, erosion, and acid buildup (2-3, 6-7). Unfortunately, these symptoms, which are more specific to metal phosphide poisoning, are only observable after a patient has deceased.
Although there are no exact protocols for metal phosphide poisoning, doctors have multiple options to address the diverse symptoms of individual patients (7). The most common treatments aim to reduce acidity in the digestive tract to decrease the amount of metal phosphide that turns into phosphine gas. Such treatments include stomach pumping, ranitidine (an antacid and antihistamine), sodium bicarbonate (commonly known as baking soda, a relatively safe base used to neutralize acids), and activated charcoal. Other treatments support the body as it cleans the metal phosphide from the blood. These include IV fluids and electrolytes, dopamine (to improve blood flow), noradrenaline (a kidney hormone), piperacillin/tazobactam (antibiotics), and sertraline (a calming drug) (2, 4-5, 8). If a patient additionally exhibits cholestasis, ursodeoxycholic (bile) acid and skin moisturizer are commonly given (6). The most preferable treatment is a liver transplant, since the damage to the liver is often irreparable, but the procedure is extremely expensive. Given the demographics of metal phosphide victims, most patients are unable to obtain the surgery even if ALF is identified soon enough (2, 4, 8).
With such little research about metal phosphide poisoning, some treatments are still up for debate. One of these is the use of N-Acetyl Cysteine (NAC), a drug used in instances of acetaminophen overdose to prevent ALF. Dr. Smitha Bhat, a professor at the Father Muller Medical College in Mangalore, India, found that patients treated with NAC had a lower death rate, so she argued that NAC would be a noteworthy substitute for patients who cannot afford a liver transplant. Unfortunately, there were far fewer patients in the NAC group than in the non-NAC group, so when the statistical calculations were conducted, the NAC group had both the lowest death rate and the lowest survival rate (8). Other studies that included NAC did not herald it as an antidote, and some even resulted in patient death (4-5).
In summary, more research is needed to effectively diagnose and treat metal phosphide patients. Clinicians must collaborate with laboratory scientists so they can study the biochemical effects of metal phosphide gas. Doctors cannot effectively cure metal phosphide poisoning without more knowledge about how the phosphide and its derivatives chemically impact the body. Since most of the specific symptoms are internal, doctors can easily mistake clinical symptoms of metal phosphide intoxication for influenza or a multitude of other tamer illnesses. They would benefit from additional chemical tests, such as those analyzing blood content, that could help identify metal phosphide intoxication. Unfortunately, considering the demographics of patients, the communities that suffer most from metal phosphide poisoning lack the resources to find an antidote.
Furthermore, individuals with financial difficulties are at a greater risk of metal phosphide poisoning. In India, those who cannot pay for mental therapy are at a greater risk of using Ratol to commit suicide. Women are especially impacted because their marginalization prevents them from receiving treatment for depression and PTSD. Instead, the availability of Ratol poses a persistent, more affordable temptation. Metal phosphides are also cheaper than safer firecracker oxidants, so companies left to their own devices stoop below the line of morality to profit from low-income customers. Countries like the United States can successfully produce firecrackers that are less toxic and cost upwards of $2 a piece, while the Turkish YP-based firecracker sells successfully because it markets for as little as $0.25 and withholds information from the public. In the absence of protective legislation, Turkish firecracker manufacturers avoid responsibility for the casualties they cause.
- Türkmen Şamdanci E., Çakir E., Şahín N. et. al. 2013. Clinical and pathological findings on intoxication by yellow phosphorus after ingesting firework cracker: A rare case of autopsy. Turk Patoloji Dergisi.
- Taskesen M. and Adıguzel S. 2012. A rare cause of poisoning in childhood: yellow phosphorus. J of Emergency Medicine. pp 1-3.
- Nagy A., Bolfa P., Mihaiu M., et. al. 2015. Intentional fatal metallic phosphide poisoning in a dog — a case report. BMC Veterinary Research.
- González-Andrade F. and López-Pulles R. 2011. White phosphorus poisoning by oral ingestion of firecrackers or little devils: Current experience in Ecuador. Clinical Toxicology, 49: 29-33.
- Kumar K., Kumar M., Sankuru D., et. al. 2018. Fatal yellow phosphorus poisoning in a child. Sri Lanka Journal of Child Health, 47: 273-275.
- Lakshimi C. P., Goel A., and Basu D. 2016. Cholestatic presentation of yellow phosphorus poisoning. J of Pharmacology and Pharmacotherapeutics, Vol. 5, Issue 1.
- Das S., Reddy U., Hamide A. et. al., Sept. 20, 2018. Histopathological profile in fatal yellow phosphorus poisoning. J Forensic Sci.
- Bhat S., Kenchetty K. Jan 2015. N-Acetyl Cysteine in the management of rodenticide consumption — life saving?. J of Clinical and Diagnostic Research, Vol 9.