FOOD SAFETY – A 21^ST CENTURY ISSUE

 Ian Shaw – Institute of Environmental Science and Research, Christchurch.

New Zealand Science Review Vol. 58(2) 2001 p38-46.

 Throughout history people have accepted risk associated with eating.  Prehistoric humans risked death to capture and collect their food.  But the risk was worth it because without sustenance they would perish.  In the Dark Ages food-related illness was rife.  The seasonality of food was a key issue and necessitated preservation techniques (e.g., salting) to provide for the long winter months when little grew and animals did not breed.  Meat was often so foul when eaten in the depths of winter that complex mixtures of spices and herbs were necessary to hide its terrible putrid taste.   The bacterial composition of these foods was complex and presumable pathogenic.  Indeed, the diseases associated with food were far worse than most of those that we are familiar with today.  As the ages passed people became aware that certain activities might taint their food and cause illness.  At this point in history it was likely that consumers would become ill both due to the microbes contaminating their food and because of dietary deficiencies (e.g., Scurvy; vitamin C deficiency) due to lack of specific nutrients or vitamin-containing foods at particular times of the year (e.g., fresh fruit in winter).  By Victorian times, as the first Europeans were setting foot in New Zealand, there was a very much better understanding of food safety.  Food was chilled to keep it fresh using ice produced by wetting clay pots and encouraging evaporation to reduce the temperature and so freeze water.  Jams and preserves were made to keep fruit fresh for the winter and canning was introduced to keep meats, fish and vegetables fresh for many years.

At the beginning of the 20^th Century there was a healthy philosophy relating to food.  It was understood that a balanced diet was essential to avoid diseases associated with dietary deficiencies and there was a developing understanding of food-related illness.  By the 1920s the associated between food contamination and illness was well understood.  McFarland (1924) pointed out that if human excrement is used to fertilise crops, dangers might ‘lurk in green vegetables’ harvested from the land, whereas fruits from trees and bushes are likely to be safe.  He also emphasised the importance of milk as a vector of tuberculosis from cows to people.

 As we move into the new millennium we have moved away from an acceptance of risk associated with food towards a paranoia about food-related disease.  At first this might seem healthy but we have gone far beyond sensibility.   We now consider risk in a vacuum and are unwilling to set it in the context of the risks of daily life.  For example, the risk of death travelling to a shop to buy food is far greater than the risk of death from eating the food that has been purchased (Shaw, 1999).   Most people blindly accept the former while bemoaning the latter.  In the UK consumers are so worried about contracting new variant Creutzfeldt Jacob disease (nvCJD) from BSE-contaminated beef that beef consumption has plummeted.  Since the first case of BSE was identified in the UK in 1986 (Wells et al, 1987) there have been approximately 80 deaths from nvCJD.  In the same time period there were approximately 49,000 deaths on the roads.  Clearly cars pose a greater risk than BSE.

 The knock-on effect that the BSE saga has had around the world is astounding.  Most developed countries will no longer import UK beef or beef products.  But perhaps the most interesting outcome is that the Peoples Republic of China recently (January 2001) banned UK meat and bone products to eliminate a risk from nvCJD that pales into insignificance when the myriad of other food-related risks are considered.

Estimating the dietary intakes of Xenoestrogens

 First it is important to set a level playing field.  To do this the estorgenic activities of the various xenoestrogens are expressed relative to the most potent estrogen
(17b- estradiol) utilising data from the E Screen assay (Muller et al., 1995) (Table 4).

 Using food intake data (in this case for the UK from Gregory et al., 1990) and known residues or levels of xenoestrogens in food (from UK government surveillance data; pesticides, MAFF (1998); plasticisers, MAFF (1996, 1997); phytoestrogens, Price and Fenwick (1985)) daily intakes can be calculated. 

 The pharmacological impact of xenoestrogens is dependent on the plasma level attained relative to normal levels of endogenous estrogens.  In the human male the plasma concentration of 17b- estradiol = 20 ng/l (De Coster et al 1985; Ongphiphadhanakul and Rajatanavi, 1998).  Therefore if a plasma concentration of exogenous estrogen could be attained that is either a significant proportion of, or greater than, the endogenous estrogen concentration, it is likely that a pharmacological effect will result.

 Assuming an average human blood volume of 4 1 and total absorbtion of dietary estrogens and that the body represents a single compartment pharmacokinetic model (which of course it is not!), the human estrogenic pesticide concentration based on dietary intake = 0.005 ng/l E. eq.  This is only 0.025% of the normal male estrogen concentration and therefore is unlikely to have a pharmacological effect.

 Similar calculations can be carried out for the other groups of dietary xenoestrogens as a means of assessing their potential impact on human males (Table 5). 

 From Table 5 it is clear that the total plasma concentration of bisphenol-A and the phthalates (ie, 0.1 ng/l E. eq.) is a very small proportion (ie, 0.67%) of the normal endogenous estrogen concentration in human male blood and therefore that they are extremely unlikely to have a pharmacological effect. 

 Therefore the dietary intakes of estrogenic plasticisers and pesticides are likely to be too low to cause effects (eg. reduced sperm count) in human males.  However, the intakes of phytoestrogens are likely to be high enough to result in significant pharmacological effects and provided their intake was reasonable constant and prolonged, they are a possible cause of the human effects attributed to xenoestrogens.

 The most likely source of phytoestrogens are legumes, particularly Soya.  It is therefore interesting to speculate that the human sperm count decrease over the past five decades might relate to the introduction of Soya into the western diet and the increasing popularity of vegetarianism – a sting in the tail for apparently healthy eating!

 Dietary estrogens are an excellent example of chronic food residue toxins.  According to the calculations presented here they will have a pharmacological impact on the consumer.  It is interesting that it is the natural phytoestrogens that are the potential problem rather than the man-made contaminants.  Their importance is now being realised by governments around the world.  The USA has recently investigated selected dietary estrogens with a view to taking action to reduce their levels in food.  The time is right to assess their potential impact upon New Zealanders.