The commonest agent of poisoning in rural India is aluminium phosphide (AlP), as compared to organophosphorus compounds in other areas (Singh & Kaur 2012). It is easily available in India and sold under trade names like celphos, quickphos, etc. as tablets or pellets. A tablet weighs 3 g containing 56% of AlP and 44% of ammonium carbonate to reduce self-ignition (Aggrawal 2006). Phosphine gas is produced from this on reaction with moisture or acid. It acts as a mitochondrial poison by inhibiting cytochrome C oxidase and leads to reduced oxidative phosphorylation, ATP depletion and cell death (Pal et al. 2011; Singh et al. 2014; Soltani et al. 2013). It has toxic effects on all the systems and induces acid–base disturbances (Soltani et al. 2013). Moreover, phosphides and phosphine have a corrosive action (Pal et al. 2011). The type of acid, quantity, physical structure, pH, concentration and its affinity for hydroxyl ions are responsible for the severity of tissue injury from an acid (Pillay 2013; Contini & Scarpignato 2013). The primary mechanism of action of mineral acid is the coagulation necrosis of tissues. Battery acid contains about 30% of sulfuric acid (Fig. 3), which produces local effect and on systemic absorption there can be metabolic acidosis, haemolysis and acute renal failure (Pillay 2013; Wormald & Wilson 1993). The deceased being a mechanic in an automobile shop had easy access to battery acid while rodenticides are available at a cheap rate in the market. These could be a facilitator for a method of suicide in this case. Fatal poisoning by a combination of these two compounds has not been reported in medical literature.
According to Singh Y et al. (Singh et al. 2014) AlP poisoning showed features of vomiting, abdominal pain, acidosis, marked hypotension, palpitation, acute renal failure, acute liver failure, disseminated intravascular coagulation (DIC) clinically. Phosphine gas causes injury to the alveolar capillary membrane and acute lung injury (Gurjar et al. 2011). This gas on absorption to blood stream damages the blood vessel and RBC cell membrane causing intravascular haemolysis (Pal et al. 2011). It may be the possible reason for reduced haemoglobin level in the present case. He was non-diabetic but had hyperglycaemia and the level of which is one of the prognostic sign of mortality (Mehrpour et al. 2008). Moreover, he had features of abdominal pain, vomiting, acute renal and liver failure, diffuse alveolar damage and DIC suggestive of phosphide poisoning. The effusion in the pleural cavity and peritoneum could be due to liver and kidney failure.
Sulfuric acid has a great affinity for water and produces a severe rise in temperature on reaction with it to cause eschar. Ingestion of this acid causes burning pain from oral cavity to stomach, hematemesis (coffee coloured vomiting), excessive salivation, dysphagia, dysphonia and dyspnoea. (Pillay 2013) It causes more coagulative necrosis of columnar mucosa of the stomach than to the stratified squamous epithelium of the oesophagus (Arévalo-Silva et al. 2006). But as per one study, oesophageal corrosions were observed in 55% of battery acid ingestion cases (Wormald & Wilson 1993). He had coffee coloured hematemesis which is one of the presenting features of an acid poisoning. Abdominal pain, dyspnoea and vomiting are common to both poisons, and we also observed in the instant case.
The autopsy revealed features of acid poisoning more distinctively. The stomach mucosa showed blackish brown discolouration and thinning of the wall; suggestive of damages caused by sulfuric acid. In a death due to acid ingestion; autopsy showed distal third oesophagus perforation, stomach corrosion, pulmonary and cerebral oedema (Amadasi et al. 2016). We also, observed similar autopsy findings.
Atypical findings noticed in our case may be the result of two poisonous chemical substances which reacted with each other both inside and outside the body. The combination has a unique peculiarity that, when AlP comes in contact with acid there will be more extraction of phosphine gas as given by equation below (Chan et al. 1983; Proudfoot 2009; De 2007).
$$ 2\ \mathrm{A}\mathrm{l}\mathrm{P} + 3\ {\mathrm{H}}_2{\mathrm{SO}}_4\to {\mathrm{Al}}_2{\left({\mathrm{SO}}_4\right)}_3 + 2\ {\mathrm{PH}}_3 $$
It could be the probable reason for not finding any typical features of sulfuric acid ingestion inside the oral cavity or larynx. The same principle used for the enhanced detection of phosphine gas from post-mortem samples (Chan et al. 1983). Phosphine will rapidly get absorbed through the airway tract or gastrointestinal mucosa. The remaining Aluminium sulphate [Al2 (SO4) 3] may react with water to produce sulfuric acid inside our body (Munim).
$$ {\mathrm{Al}}_2{\left({\mathrm{SO}}_4\right)}_3 + 6\ {\mathrm{H}}_2\mathrm{O}\to 2\mathrm{A}\mathrm{l}{\left(\mathrm{OH}\right)}_3 + 3{\mathrm{H}}_2{\mathrm{SO}}_4 $$
It could be the likely reason for the reappearance of sulfuric acid like corrosion in oesophagus and stomach.
Histopathological changes in the gastrointestinal tract in acid poisoning ranges from simple hyperaemia/erosions to diffuse transmural necrosis (Contini & Scarpignato 2013). But in a case of phosphide poisoning, almost all vital organs are involved. Microscopic changes in phosphine poisoning in the liver are fatty change, necrosis and sinusoidal congestion (Aggrawal 2006). Kidney microscopy showed glomerulus congestion, intra-parenchymal congestion and tubular degeneration in phosphide poisoning (Mehrpour et al. 2008). We also observed diffuse acute tubular necrosis of kidney, sinusoidal congestion of the liver, and transmural necrosis of stomach wall on microscopy.
In case of metal phosphide poisoning, a forensic scientist generally carries out a phosphide/phosphine gas test for the detection and identification of phosphide in the viscera (Bhadkambekar et al. 2008). Silver nitrate test is used for the detection of phosphine after acid hydrolysis by sulfuric acid on metal phosphide. But this test will answer only for unutilized phosphides and not for absorbed phosphine. So there is no role in testing the blood for phosphine (Balali-Mood M. Phosphine. Simple Qualitative Test(s). Available at http://www.inchem.org/documents/pims/chemical/pim865.htm#DivisionTitle:8.2.1.1. Accessed 6 Nov 2015). If this test is positive, the presence of zinc or aluminium in the viscera at high levels could provide the information about the specific metallic phosphides. But, the human body also contains trace amount of these elements, within certain ranges, which can be differentiated from their quantities. Hence, it is ideal to detect and quantify these metals along with phosphide determination to be able to frame a definitive opinion (Bhadkambekar et al. 2008). But in developing countries like India, because of high case load and procedural cost, quantitative analysis is not routinely performed. To detect the aluminium, we should add ammonium chloride and ammonium hydroxide to the sample solution which will form a gelatinous white precipitate, and will turn into red lakes on addition of alcoholic alizarin (Vogel 1979a).
Dilute sulfuric acid is absorbed as hydrogen and sulphate ion through the mucous membrane. About 85–90% of inorganic sulphate is excreted as salts with sodium, potassium, calcium or ammonia (Biologic effects of exposure). Sulphate ion can be detected by the addition of 1% barium chloride and concentrated nitric acid to the sample solution, and a positive result will be indicated by formation of a white precipitate which will persist on heating or dilution (Vogel 1979b). From our history, clinical, laboratory and autopsy findings, the forensic scientist approached the case. But here, already he survived for 5 days and there may be a scant quantity of non-metabolized form of phosphine left. This could be the reason why phosphine or phosphide was not detected from any post-mortem samples.
Tha case history, clinical features, laboratory and autopsy findings, histopathology and chemical analysis reports were analysed to opine the cause of death as combined effect of pulmonary oedema and acute tubular necrosis of kidney as a result of aluminium phosphide and sulfuric acid poisoning.