|EDGAR, J - Commonwealth Scientific And Industrial Research Organisation (CSIRO)|
|BOPPRE, M - Albert University Of Freiburg|
|MOLYNEUX, R - University Of Hawaii|
Submitted to: Journal of Food Additives & Contaminants
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 12/6/2010
Publication Date: 3/1/2011
Citation: Edgar, J.A., Colegate, S.M., Boppre, M., Molyneux, R.J. 2011. Pyrrolizidine alkaloids in food: A spectrum of potential health consequences. Journal of Food Additives & Contaminants. Part A. 28(3):308-24.
Interpretive Summary: While the immediate toxic effects of large doses of the naturally-occurring dehydropyrrolizidine alkaloids on humans are well known, there is increasing international concern over the potential effects of intermittent or long-term, low-level dietary exposure to these natural toxicants. This report considers the mechanism of action of the dehydropyrrolizidine alkaloids and the published accounts of relevant immediate and slowly developing diseases to rationalize a potential spectrum of adverse health effects due to low-level or intermittent dietary exposure to the dehydropyrrolizidine alkaloids. It is intended that this review will help determine the extent of the health impact of dietary dehydropyrrolizidine alkaloids on humans by alerting the medical community to the possibility of such an etiology in the development of chronic diseases such as liver cirrhosis and pulmonary arterial hypertension.
Technical Abstract: Contamination of grain with 1,2-dehydropyrrolizidine ester alkaloids (dehydroPAs) and their N-oxides is responsible for large incidents of acute and subacute food poisoning, with high morbidity and mortality, in Africa and in central and south Asia. Herbal medicines and teas containing dehydroPAs have also caused fatalities in both developed and developing countries. There is now increasing recognition that some staple and widely consumed foods are sometimes contaminated by dehydroPAs and their N-oxides at levels that, while insufficient to cause acute poisoning, greatly exceed maximum tolerable daily intakes and/or maximum levels determined by a number of independent risk assessment authorities. This suggests that there may have been cases of disease in the past not recognised as resulting from dietary exposure to dehydroPAs. A review of the literature shows that there are a number of reports of liver disease where either exposure to dehydroPAs was suspected but no source was identified or a dehydroPA aetiology was not considered but the symptoms and pathology suggests their involvement. DehydroPAs also cause progressive, chronic diseases such as cancer and pulmonary arterial hypertension but proof of their involvement in human cases of these chronic diseases, including sources of exposure to dehydroPAs, has generally been lacking. Growing recognition of hazardous levels of dehydroPAs in a range of common foods suggests that physicians and clinicians need to be alert to the possibility that these contaminants may, in some cases, be a possible cause of chronic diseases such as cirrhosis, pulmonary hypertension and cancer in humans.