FOOD SAFETY – A 21ST 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 20th 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.
Table
4: Estrogenic potency of xenoestrogens relative to 17b-
estradiol (data from Muller et al. (1995).
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).
Table 5: Theoretical blood
levels of phytoestrogens and selected estrogenic plasticisers resulting
from dietary intake in the UK. Phytoestrogen data from Price and
Fenwick (1985); plasticiser data from MAFF (1996, 1997).
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.
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