The assaying of haemoglobin using luminol chemiluminescence and its application to the dating of human skeletal remains.

The luminol chemiluminescence reaction has, for some time, been used as a tool for the detection of haemoglobin at crime scenes. More recently, the luminol test has been suggested as a possible tool for estimating the post-mortem interval (PMI) of skeletal remains. The preliminary results from the following study indicate that the chemiluminescent luminol test is a relatively easy and economical method for distinguishing between remains of medico-legal (< or =100 years) and historical (>100 years) interest. The femur was the preferred bone for PMI measurements using the luminol test, due to its robustness and relative resistance to diagenesis. Initial results suggest that bone that was historical in nature, produced a demonstrably weaker reaction than that of medico-legal interest. These results suggest that the luminol test is a promising technique, albeit with some limitations, for the assessment of skeletal material that may be potentially of medico-legal interest.

The forensic use of luminol chemiluminescence to detect traces of blood inside motor vehicles.

The luminol test for blood was carried out on a set of interior fittings and surfaces inside three different makes of modern motor car. The surfaces and fittings provided little interference with the test for blood, although there was some detectable chemiluminescence when the test was applied to blood-free material from a seatbelt, a boot-lining and a gear-knob. The case with which haemoglobin samples could be washed off interior car surfaces was also examined for seat fabrics, carpets, roof-linings and various other plastic interior surfaces. A standard wash with water alone was not very effective and removed only ca. 50% of the haemoglobin. A standard wash with soapy water or with a proprietary multipurpose car cleaner removed ca. 90% of the haemoglobin from the tested surface. The effect of high car interior temperatures on haemoglobin samples that were subsequently used in the luminol test was also examined. It was shown that the sensitivity of the luminol test was not decreased but was increased by the prior heating of a haemoglobin sample. This effect was attributed to the thermal conversion of haemoglobin to the more brighter catalyst for chemiluminescence, methaemoglobin. The enthalpy of this conversion in the solid state was found to be 14.1 kJ/mol.

A comprehensive experimental study of industrial, domestic and environmental interferences with the forensic luminol test for blood.

This paper presents the fi rst comprehensive and quantitative study of substances that interfere with the forensic luminol test for blood. Two hundred and fifty substances have been selected on the basis of modern lifestyles and of contiguity with crime scenes. The intensity of the chemiluminescence produced by each substance has been measured relative to that of haemoglobin and the peak wavelength shift has also been determined. The following is a short list of nine substances that produce chemiluminescence intensities comparable with that of haemoglobin: turnips, parsnips, horseradishes, commercial bleach (NaClO), copper metal, some furniture polishes, some enamel paints, and some interior fabrics in motor vehicles. Care needs to be taken when the luminol test for blood is used in the presence of these substances.

A study of common interferences with the forensic luminol test for blood.

A wide range of domestic and industrial substances that might be mistaken for haemoglobin in the forensic luminol test for blood were examined. The substances studied were in the categories of vegetable or fruit pulps and juices; domestic and commercial oils; cleaning agents; an insecticide; and various glues, paints and varnishes. A significant number of substances in each category gave luminescence intensities that were comparable with the intensities of undiluted haemoglobin, when sprayed with the standard forensic solution containing aqueous alkaline luminol and sodium perborate. In these cases the substance could be easily mistaken for blood when the luminol test is used, but in the remaining cases the luminescence intensity was so weak that it is unlikely that a false-positive test would be obtained. In a few cases the brightly emitting substance could be distinguished from blood by a small but detectable shift of the peak emission wavelength. The results indicated that particular care should be taken to avoid interferences when a crime scene is contaminated with parsnip, turnip or horseradish, and when surfaces coated with enamel paint are involved. To a lesser extent, some care should be taken when surfaces covered with terracotta or ceramic tiles, polyurethane varnishes or jute and sisal matting are involved.

Procainamide-induced agranulocytosis differs serologically and clinically from procainamide-induced lupus.

Agranulocytosis is a well recognized but uncommon complication of procainamide (PA) therapy, whereas a lupus-like syndrome occurs in approximately 20% of patients treated chronically with PA. In order to gain insight into the immunopathogenic relationships among these conditions, we compared the humoral immune abnormalities in these patient groups as well as in asymptomatic PA-treated patients. A relatively uniform profile of IgM but not IgG autoantibody reactivity with a set of chromatin-related antigens was observed in eight elderly men who developed agranulocytosis after treatment with PA. In contrast PA-induced lupus patients had predominant reactivity with [(H2A-H2B)-DNA] in both IgM and IgG classes. Five of eight patients with agranulocytosis had elevated levels of neutrophil-reactive IgG which appeared to be due to immune complexes based on Fc gamma receptor blocking studies. However, 12 of 15 patients with PA-induced lupus, none of whom had neutropenia, had similar levels of neutrophil-reactive IgG, suggesting that this reactivity was not causally related to agranulocytosis. Agranulocytosis developed after less than 3 months treatment with PA in six of eight patients. This time course was similar to that seen in 77 PA-induced agranulocytosis patients reported in the literature plus 127 patients reported to the U.S. Food and Drug Administration in whom 90% developed agranulocytosis within 3 months of starting PA. In contrast, the mode duration of treatment with PA before lupus-like symptoms develop is 10-12 months. These findings, together with the different profiles of autoantibodies and clinical presentations, suggest that agranulocytosis arises from a different mechanism than that underlying PA-induced lupus.