Fatal aluminium phosphide poisoning

Aluminium phosphide (AlP) is a cheap solid fumigant and a highly toxic pesticide which is commonly used for grain preservation. AlP has currently aroused interest with a rising number of cases in the past four decades due to increased use for agricultural and non-agricultural purposes. Its easy availability in the markets has increased also its misuse for committing suicide. Phosphine inhibits cellular oxygen utilization and can induce lipid peroxidation. Poisoning with AlP has often occurred in attempts to commit suicide, and that more often in adults than in teenagers. This is a case of suicidal consumption of aluminium phosphide by a 32-year-old young medical anesthetist. Toxicological analyses detected aluminium phosphide. We believe that free access of celphos tablets in grain markets should be prohibited by law.


Introduction
Aluminium phosphide (AlP) is a solid fumigant which has been extensively used since the 1940s. In India it is marketed as a tablet of celphos, alphos, quick phos, phostoxin, etc. (Chopra et al., 1986). In Iran it is known as the rice tablet (Mehrpour et al., 2010) that can be purchased in local shops.
This highly toxic chemical is cheap and usually formulated in tablets or pellets, granules and as powder. Upon contact with moisture, aluminium phosphide liberates phosphine, which is the active pesticidal component (Sudakin, 2005). Human toxicity, which is usually acute, occurs due to the toxic effects of phosphine released in the stomach after ingestion of aluminium phosphide. Phosphine is widely absorbed from the gastrointestinal tract. It emerges as a poison of suicidal deaths as this pesticide has no effective antidote, is cheap, freely available, and is a 'sure agent of death' (Nagar, 1985, Singh et al., 2003. In India, this poisoning was not known before 1980. The first case in India was reported in 1981 from M.G.M. Medical College, Indore (Kabra et al., 1988). The incidence of the poisoning has been increasing steadily and is now the commonest mode of suicide in the agricultural community in northern India (Ranga et.al, 2004). Overall smell of phosphine gas was present. All the internal organs were congested with petechial hemorrhages. The lungs were congested and edematous with rupture of alveoli, gastrointestinal mucosal congestion (Figure 1), and petechial hemorrhages on the surface of the liver and brain. On toxicological analysis, aluminium phosphide was detected.

Discussion
Aluminium phosphide is marketed in India as tablets of Celphos, Quickphos, etc. It is available in small and large packs containing grayish-white tablets weighing about 3 g each, containing 56% aluminium phosphide and 44% aluminium carbonate, capable of releasing 1 g of phosphine.
Following oral ingestion, AlP reacts with water and stomach acid to produce phosphine gas, which may account in large part for its observed toxicity. Phosphine generated in the gastrointestinal tract is readily absorbed into the blood stream. Phosphine may denature or reduce oxyhemoglobin in addition to enzymes important for respiration and metabolism and may also affect cellular membranes. The exact mechanism of action of phosphine is still not clear. Some authors have claimed it to be an inhibitor of cytochrome oxidase in animals (Chefurka et al., 1976), while others showed reduction in catalase activity leading to free-radical toxicity in animals (Bolter et al., 1989) and humans (Chugh et al., 1996).
Symptoms of severe toxicity by AlP ingestion include diarrhea, cyanosis, breathing difficulty, pulmonary edema, respiratory failure, tachycardia, hypotension, dizziness, and death. The most common abnormality seen in the serum of 42% of poisoned patients was hypoxemia with severe metabolic acidosis (Khosla et al., 1992).
Phosphides, like phosphine, are toxic to the central nervous system, which is excited and then depressed. Arora et al. in 1995 reported that histopathological changes revealed varying degrees of congestion, similar to those produced by hypoxic injury. Phosphine was detected in tissues of the brain, liver, and kidneys.
The results of postmortem examinations of victims of phosphine poisoning generally indicate hypoxia with evidence of local trauma in the gastrointestinal tract, liver, kidneys, and central nervous system. The fatal dose of aluminium phosphide was stated to be in the range of 150-500 mg/70 kg by Chugh et al. in 1988. The mortality rate in clinical reports is stated to vary between 37-100% by different authors (Chopra et al., 1986;Kabra et al., 1988;Sepaha et al., 1985;Saraswat et al., 1985;Ram et al., 1985;Khosla et al., 1986;Mishra et al., 1989;Chugh et al., 1991Chugh et al., , 1992Chugh et al., , 1995. The manner of death was reported to be suicidal in 87% of the cases by Dalbir et al. in 1985, 76% in a study by Chugh et al. and 100% in Jain et al. (2005) with all the cases being suicidal. Garry et al. reported in 1993 an accidental death related to phosphine exposure from stored grain fumigated with AlP pellets. The aluminium blood concentration was 713 pg/L, whereas normal laboratory values range from 2 to 42 pg/L. Ten control blood samples from various autopsies showed Al values between 9 and 15 μg/L using emission spectrometry, whereas blood in the deceased contained 100 times more. Similarly to the phosphine results, aluminium concentrations were found to be higher in the brain, adrenals, and liver. In urine and the kidneys, no difference from the usual published values was found, probably because death occurred shortly after ingestion.
Suicide was the most common mode of poisoning deaths, with overall mortality varying between 70-100%. Mortality is higher in those who consume more than two tablets and none of the patients survived who had ingested more than 3 tablets (Siwach et al., 1988;Singh et al., 1985;Raman et al. 1985). According to Karamjit et al. (2003) the pattern of poisoning varied in urban and rural areas, with a higher incidence of poisoning deaths in rural (64%) than in urban areas (36%). Aluminium phosphide was the most common poison consumed, being responsible for 50% of deaths, followed by insecticides 24% (Gupta et al., 2006). Poisoning deaths increased from 19% in 1996 to 24% in 2005. The age group most commonly affected was 16-25 years (49%). The male to female ratio was 1.9:1.0 and the rural to urban ratio was 1.5:1.0 (Gupta et al., 2006).

Conclusion
Exposure to phosphine gas released from ALP fumigants increases risks of major morbidity and mortality. People handling this fumigant must be aware of its lethal aspects. An important preventive measure lies in better regulated supply of ALP, which otherwise is an excellent and safe fumigant as it leaves little residue on grain. Legislative and administrative measures have been suggested to restrict and modify its supply in India. Unfortunately there has been a failure in their implementation. Except the largest producer of it in India, it has been marketed as granulated