Talking Points to accompany presentation by Barbara Petersen


In the past 11 months the scientific and regulatory community has responded rapidly and in concert to follow-up on findings from research in Sweden – money has been spent in industry, academia and by government to understand mechanisms, to estimate exposure and to identify additional research that is needed. Today I will try to highlight the state of the information about the formation, exposure and possible approaches to lowering overall exposure to acrylamide. I am drawing on presentations and information that has been presented at numerous meetings and workshops including the FAO/WHO meeting, workshop organized by JIFSAN and by presenters at the US FDA Food Advisory Committee meetings. I hope that I have accurately summarized their findings but I have also noted the location of the information for you to return to the original sources.


One meeting organized by the Joint Institute for Food Safety and Nutrition but funded by the participants focused on identifying the gaps in our knowledge and on designing research to fill those gaps.


That workshop divided the task into five broad research areas.


The summary of that workshop as well as other materials are available on the JIFSAN homepage


Consumer exposure to acrylamide has been estimated for many different populations. The first international meeting on acrylamide was held last June and at that meeting exposures were estimated for consumers around the world. The data were preliminary but ranges of exposure were estimated.



The WHO/FAO meeting concluded that exposures were likely to be in the range of 0.3-0.8 ug/kg bw/day but acknowledged that only a small number of foods had been evaluated for acrylamide. The meeting also recommended further evaluations of food levels and associated exposures.



The Swiss government conducted a duplicated diet study. The estimated exposure in that study was within the range estimated by the FAO/WHO meeting. The Swiss study also estimated exposure by meals. Coffee was estimated separately.


In February 2003, the US FDA presented several estimates of exposure using the available data on acrylamide levels in food and different food consumption surveys. Today I’ll present results based on the USDA’s Continuing Survey of Food Intake by Individuals that was conducted in 1994-96 and in 1998 for children. FDA estimated levels in a number of different foods but noted that for many categories there were only a very few observations and that more data are required. Simple estimate of mean exposure were presented along with estimated that used monte carlo modeling to estimate the distribution of exposure in the population.


This slide is difficult to read, but all data that were publicly available on various websites in Feb 2003 are summarized. Want to make the points that:

1. Widespread across many different food types – clearly not a "potato issue" only

2. Measured amounts vary greatly within and across food categories

3. This is only what we know so far- as additional foods are examined the list will surely grow longer.

4. Any interventions we can contemplate to address this question will have widespread effects.


It is often necessary to use factors to match food consumption data to the acrylamide sampling data. These are examples of the factors used in the US analysis.


The estimated mean intake of the US population under a typical scenario is 0.37 ug/kg body weight/day. The following slide presents a graphical display of the distribution of exposure.


There is a distribution of exposure. The mean as we noted previously is .37 ug/kg bw/day of acrylamide. The high end of the exposure is displayed; the 90th percentile consumer is estimated to consume .81 ug/kg bw day of acrylamide. However, it is important to note that these estimates were prepared using short term estimates of food consumption and are somewhat lower over time;

Slide 13

FDA also determined the contribution of different food categories. The estimated mean contribution is listed for a number of foods on this and the following slide along with a cumulative percentile. That is, the third column first identified the contribution of french fries and then adds to the coffee, etc. to determine the summed contribution of all foods. There are two types of french fries listed – the first are fries prepared by restaurants (including fast food) and labeled as (RF) on the slide; the latter are french fries prepared and subsequently "cooked" by oven baking (OB). It is not clear how this corresponds to consumer preparation preferences and does not consider consumer home oven thermostat variations, etc.  Toast is based on 5 samples and not clear how the toasting done at FDA analytical lab corresponds to consumer preparation preferences.  Cookies - based on 7 samples.  The limited data for products like toast and cookies and preparation preferences introduces significant uncertainty in the exposure assessment for these categories.  Uncertainty in levels in foods categories will be reduced with more data.  However, FDA does not believe the mean population exposure will change a large amount. 

Slide 14

This slide continues identifying the contribution of various food groups to overall intake of acrylamide. It further demonstrates the wide number of categories that have been shown to contain some acrylamide. It also notes the likely importance of home food preparation on overall acrylamide exposure.


FDA also conducted a series of analyses to determine the impact of removing acrylamide in selected food categories.


It is clear from these analyses that reducing the exposure to acrylamide will be complicated and will have to be applied broadly.


The foods that have been reported to contain acrylamide also contribute significant sources of most nutrients; therefore it is extremely important than any control measures evaluate the potential impact on nutrition


FDA’s research is consistent with those that had been conducted previously, including those presented at the June 2002 FAO/WHO meeting. The levels of acrylamide and the amount of the food consumed (quantity and frequency) are important. FDA has noted that some commonly consumed foods – including soft breads and cereals contribute to overall exposure as a result of frequent consumption.

FDA was particularly concerned that the changes could have significant impacts on the nutritional quality of the diet.


Various mechanisms for the formation of acrylamide have been studied. It now appears that acrylamide is most likely formed in foods through a reaction that requires the presence of asparagine and reducing sugars, such as glucose under the proper conditions.


These data suggest that asparagine is a critical factor in acrylamide formation. And that other possible mechanisms such as starch and oil oxidation products (acrolein and/or acrylic acid) are not a factor.


Next researchers looked at acrylamide formation with a fixed asparagine concentration and increasing dextrose (10g asparagine is equivalent to 1.25% in the system). As you can see, there is a linear response to dextrose up to a 1:1 ratio with asparagine. Thus, controlling both asparagine and dextrose (reducing sugars) will affect acrylamide formation. There are several different reducing sugars that are expected to allow this reaction to proceed.


A number of groups have now concluded that Asparagine is the major source of acrylamide formation in foods and that a carbonyl source, usually in the form of a reducing sugar such as glucose or fructose, is required in the reaction.


•This slide was kindly supplied by Don Mottram, and shows some data from the UK.

•The finding that two different varieties of potato, prepared similarly, have vastly different acrylamide levels is an important clue to what may be going on, and leads to some potential intervention strategies.

•Clearly the starting material has some impact.


•There is a wide range of asparagine within and across crops.


It is now also known that the browning of foods is a factor in the formation of acrylamide.


Likewise temperature is an important variable


It is most likely a combination of time at the temperature that determines the levels of acrylamide that are formed; a typical potato chip frying temperature is noted by the red arrow.


pH also has an effect


Numerous researchers are currently looking for ways to inhibit the reaction. Overall this is the general approach to inhibiting the formation of acrylamide. Easy to summarize – very hard to implement. I am going to go quickly in the next slides to a few possible approaches – these are really all in the early research stage and may not be useful in the context of changing foods that are prepared either commercially or by the consumer in their kitchens. Some suggestions have been the use of another enzyme, cysteine to inhibit the reaction. The purpose n presenting them is to perhaps stimulate additional thinking and research to a very difficult problem.


It may be possible to reduce levels of acrylamide by reducing levels of the required precursors. For example, different varieties of potato may have lower levels of either asparagine or reducing sugars or possibly both. It is important to remember, however, that the precursors may b e present in such large quantities that they are not the limiting factor.


Any change that results in the removal of substrates must take into account the kinetics of formation of acrylamide along with importance of other constituents of the food. Changing acrylamide by lowering temperatures will require development of new cooking methods. Some foods will be impossible to cook at low temperature

No universal solutions have been found. Addition of substances may work for some products but with variable efficacy and potentially major changes in foods.

There is no precedent for an intervention into the food supply on this scale. There is a significant potential to alter nutritional and/or safety aspects of food.


These samples were highly cooked in order to maximize acrylamide formation and this is shown in the level of acrylamide in the control sample which produced 20,500 ppb acrylamide; however, the asparaginase treated sample produced only 164 ppb acrylamide – a 99% reduction. Since asparagine was removed during this experiment, these data suggest that asparagine is the major source of acrylamide formation in potato products.


This is an example of research conducted by a US company: Potatoes, purchased from the local grocery store, were washed and then boiled for 1 hour. The flesh was blended with distilled water in a 1:3 ratio (potato:water). The sample was split – one aliquot was treated with asparaginase and the other was untreated. This treatment was carried out with stirring for 45 min at room temperature. Next, the samples were microwaved at 2-min intervals for a total of 10 min. Both samples were of similar brown color and fairly dry following the microwaving step. These products were highly cooked in order to maximize acrylamide formation.


By treating with asparaginase there was a 99% reduction in the levels of acrylamide in the potato mixture following the use of the microwave

It is important to note that this is an artificial system that would be extremely difficult to implement in food production and impossible to apply under home food preparation methods


the concerted research and actions by government, industry and academia have resulted in rapid progress towards understanding the mechanisms of formation in food

The notion of "carcinogens" in food is not new (cooked meat, US National Academy of Sciences Report1), research by Lois Gold & Bruce Ames and in numerous research articles

Humans have eaten these foods for millennia


Any change that results in the removal of substrates must take into account the kinetics of formation of acrylamide along with importance of other constituents of the food. Changing acrylamide by lowering temperatures will require development of new cooking methods. Some foods will be impossible to cook at low temperature

No universal solutions have been found. Addition of substances may work for some products but with variable efficacy and potentially major changes in foods.

There is no precedent for an intervention into the food supply on this scale. There is a significant potential to alter nutritional and/or safety aspects of food.


The issue affects a large portion of the food supply. Lowering acrylamide in one or a few foods has little effect on long-term intakes- many foods would need to be altered.

Food cooked at home and in restaurants represent significant source of acrylamide exposure and would be less amenable to intervention strategies.


Before any interventions are proposed, we need to fully understand two things:

The nature of the low dose hazard to humans, and

The impact of any proposed interventions. Are there any unintended consequences to public health?

Copies of the presentation and or the original references/presentations can be provided on request