NITROSAMINE CONTAMINATION OF SOME NIGERIAN BEVERAGES

Abstract

N-Nitrosamines are amongst the most potent and versatile experimental carcinogens ever tested on laboratory animals. As a result, their presence and that of their precursors in food meant for human consumption is a possible environmental factor in the causation of human cancers. Consequently, the distribution of 2 nitrosamines, which have been consequently reported in food, and nitrosamine precursors in some popular Nigerian beverages (palm-wine, nono, pito, burukutu and ogogoro) that hawked for sale ready for consumption: the possible role of microorganisms in nitrosamine formation in palmwine, and comparative nitrosamine poisoning in 6 animal species (including a subhuman primate) and chick embryo, have been studied. Nitrosamines were assayed by colorimetric, thin-layer (TLC) - and gas-liquid (GLC) chromatographic methods using synthesized compounds as standards, and presence of nitrosamines confirmed by mass spectrometry. Nitrosamine precursors were assayed by colorimetric methods. 86% of all beverages sampled, in the Kwara and Benue States, contained detectable amounts of dimethyl-and/or diethylnitrosamine, and individual nitrogen levels ranged between 0.6 and 22 ug/l. 80% of all samples contained nitrates, 100% dimethylamine while 68% contained nitrite. Detection limits of nitrosamine by TLC and GLC were 2 ug and 2 ng respectively and 0.2 and 2 ug N/ml respectively for nitrite and dimethylamine. A single oral necrotizing dose for rats (50 mg dimethylnitrosamine/kg body weight) was more acutely hepatotoxic to cat by 30 hours than to a guinea pig, rat and monkey in that order but was not toxic to a lizard or a duck. A similar dosage of 220 mg diethylnitrosamine/kg body weight was not toxic to a monkey. A daily oral dose of 5mg dimethylnitrosamine/kg body weight was comparable as toxic to a rat and guinea pig in extremis, as the single dose but produced severer toxicity in a cat and a monkey. A similar dosage of 1 mg dimethylnitrosamine/kg body weight was toxic to a cat and a lizard mainly, by 1 month; but 3mg diethylnitrosamine/kg body weight given similarly produce no toxicity at all. Pathological lesions in liver were histologically similar in affected species and differed only in severity. No kidney lesions were detected. Death induction, reduction in the body weight gains and liver-/body weight ratio, elevation of serum enzymes, hyperhilirubinaemia and histopathological lesions were toxicity indices. Cat liver slices and microsome + soluble fractions were most active and those of duck least active in demethylatinc dimethylnitrosamine in vitro. LD50 studies revealed strain differences in chick embryo susceptibility to nitrosamine poisoning. Metabolism of nitrosamine precursors added to palm sap in various combinations and concentrations of organic and inorganic nitrogen, progressed fairly rapidly with fermentation time and was paralleled either by an overall increase in rats of dimethynitrosamine formation or an initial increase followed by a decrease due to in situ degradation of formed nitrosamine. Cell suspensions and/or intracellular supernatant extracts of some palmwine microorganisms were active in the formation of nitrosamine in vitro from added precursors. These findings and their implication on public health are discussed.