Indian Kanoon - Search engine for Indian Law

(2) No common poisoning could be detected in:

(i) Stomach with contents in liquified form and emitting foul smell;

(ii) Parts of small and large intestine with its contents in liquified form and emitting foul smell;

(iii) Parts of liver, spleen and kidneys in liquified form and emitting foul smell;

(iv) Blood from heart;

(v) Saline preservative; and

(vi) Gastric lavage of the deceased.

On receipt of the report from FSL the same was shown to Dr. S.N. Sharma who initially sought for some clarification from FSL. The FSL responded by saying that viscera/stomach wash etc. of the deceased were screened for the detection of common poisoning only and the same was found to be absent. Nothing could be said about non-common poison being ordinarily inaccessible. After the above said clarification from FSL, on 15.1.1998 the Medical Board consisting of Dr. S.N. Sharma and Dr. Mrs. Alka Vishnoi opined "In view of the Aluminium Phosphide (celphos) detected in two samples, opinion of the casualty Medical Officer case of suspected poisoning and details as per indoor bed head ticket and post mortem report, they were of the opinion that deceased Prakash Devi had died because of Aluminium Phosphide (Celphos) poisoning.

According to Modi symptoms and signs of poisoning by aluminium phosphide are similar to poisoning by zinc phosphide (p.197, ibid). The chief symptoms after the administration of zinc phosphide are a vacant look, frequent vomiting with retching, tremors and drowsiness followed by respiratory distress at death. Zinc phosphide acts as a slow poison and is decomposed by hydrochloric acid in the stomach with the liberation of phosphine which acts as a respiratory poison. Being a very fine powder zinc phosphide adheres firmly to the crypts in the mucous membrane of the stomach, and a very small quantity only in the stomach even after vomiting is sufficient to cause death by slow absorption.

Phosphine released from zinc phosphide (rat poison) and from aluminium phosphide, is mainly used as a fumigant to control insects and rodents in food grains and fields. Liberated from the metal phosphides by the action of water or acids, gaseous phosphine exerts more potent pesticidal action, for it penetrates to all areas otherwise inaccessible for pesticide application. Pathological findings from phosphine inhalation are pulmonary hyperemia and oedema. It causes both fatty degeneration and necrosis of liver. (p.174, ibid) Our attention was invited, as was done in the High Court and the Trial Court, to a paper entitled 'Toxicology Acute Aluminum Phosphide Poisoning in Northern India' written by Dr. Mitra Basu and Prof. S.B. Siwach, Head, Deptt. of Medicine, Post Graduate Institute of Medical Sciences, Rohtak and published in Current Medical Journal, Vol.I, No.5, July 1995. The authenticity of this article has not been doubted by the High Court nor questioned either in the High Court or in this Court. The learned authors have noticed the aluminium phosphide having emerged as a major health problem in northern India when these cases first started coming in 1984 and hardly any literature being available earlier on this malady. In Post- Graduate Institute of Medical Sciences, Rohtak about 2000 cases were reported which were all suicidal.

We have doubts about the genuineness of the samples of vomit said to have been seized from two places i.e. inside the house and outside the house. We have already pointed out the fatal omission on the part of the police in protecting the two places where valuable and clinching evidence as to the cause of death could have been available and the fatal delay in collecting the samples. Though, the house of the accused is situated in a locality inhabited by people and not in a secluded place yet the two witnesses to the seizure memo of the samples are Virender Singh, husband of Smt Beena (PW-3) and brother of the deceased, and one police employee namely Balbir Singh, ASI. It was suggested by the defence, during the cross- examination of Dr. S.N. Sharma, that the samples of vomit would give positive findings regarding aluminium phosphide (celphos) if it was sprinkled over the vomit before lifting the samples. The Trial Court has disbelieved the recovery of vomitus from the two places by the Investigating Officer. In the opinion of the Trial Court the evidence relating to such seizure of vomitus was not trustworthy for two reasons: firstly, it is not mentioned in the FIR or in the statement of Smt. Beena (PW-3) that aluminium phosphide was administered by the accused to the deceased, and secondly, it is also not mentioned either in the FIR or in the police statement of Smt. Beena (PW-3) that the deceased had vomited inside the house. The Trial Court has also commented adversely on the lapse on the part of the Investigating Officer in not promptly seizing the samples of vomitus. The High Court has also doubted the recovery and seizure of vomitus from the room in view of this material fact finding omission in the FIR amongst other relevant factors. Though the High Court was inclined to place reliance on the seizure of vomitus from the place situated outside the house. However that recovery too has its own infirmities. As we have already noticed the vomitus has been seized from place situated at a distance of 150 yards from the house of the accused while according to Smt. Beena the deceased had vomited at a place just about 25 feet from the house. It is difficult to reconcile the two depositions as to the distance. Secondly, in a village it is highly doubtful that vomitus would remain lying untampered and intact for the period of more than 16 hours overnight and on a thoroughfare. From the presence of aluminium phosphide in the sample of vomitus, in the facts and circumstances of the case it is not safe to infer the deceased having been administered aluminium phosphide because a safe link between the vomitus samples and the deceased is not established. Sample of vomitus from the hospital was not taken for whatever reasons.