Smoke in the water
because of their ability to bind (via other reactive molecules) to cellular macromolecules such as DNA, and therefore disrupting or damaging the cell structure. This damage is replicated and exacerbated when the cells subsequently reproduce, potentially causing tumours and mutagenic diseases.
As confirmation, recent experiments have detected enhanced levels of the P53 protein in the blood of people who have just ingested PAHs – P53 is also known as the tumour suppressor gene and indicates that the body is trying to limit DNA damage caused by eating PAHs by spurring an increase of P53 proteins.
Smoking via smoke
Coming back to the subject, it would be reasonable to assume that smoke compounds get into meats and food by the simple process of allowing food substances to comingle with and absorb the smoke vapours arising from heated woods in a smoker or covered BBQ.
To some extent, this is correct though it has to be mentioned that not all woods are suitable for smoking food. Harder woods like oak and hickory are best for meats and lighter woods such as those from fruit trees such as apple or cherry are better for fish and poultry – it is also possible to mix different woods for smoking, which is what some specialist restaurants do for their unique flavours.
Some woods, such as pine, cedar, sycamore, eucalyptus, and et cetera, should never be used for smoking food due to their high resin content or toxic compounds in the sap which render the smoke poisonous.
Smoking via water
What is also true but much less wellknown is that the majority of modern smoked foods have never seen the inside of a smoker or barbecue. These smoked foods are given their smoky flavour by the application of liquid smoke – which is very probably the substance I find problematic.
Liquid smoke was originally known as wood vinegar, later as pyroligneous acid, and is derived quite simply by extracting the vaporised compounds from the pyrolysis of certain woods via condensation.
Water is then added to the condensate to separate it out into three distinct sections. The top section is where the lighter waxes and phytosterols (plant oils) are contained, while the bottom section is a dense, often pungent goo known as wood tar. Only the middle section is used for food smoking, being a watersuspension blend of PAHs, carboxylic acid, aldehyde, and phenols.
The reason why liquid smoke is probably the cause of my negative reaction is because unlike actual smoke in a smoker, practically all of the PAHs are collected in the condensate solution – whereas wood smoked foods will accumulate only some of the PAHs, usually mainly on thet surface of the foodd frofrom the light ter compounds in ththe smoking vapou urs swirlinrling around.
In short,hort liquid smoke contains more PAHs and in denser concentrations – and this is exactly what commercial food producers want.
The use of liquid smoke reduces the natural wastage caused by the dry, heated environment in food smokers, where meats and fish can lose a significant degree of moisture – thus reducing the saleable weight of the smoked product.
It also requires more time and labour to load and unload the food items for smoke treatment.
With liquid smoke, there is no loss of moisture or weight and it delivers very little difference in taste to undiscerning consumers – resulting in more profits, simplified processing and time savings for the producers.
A couple of questions
The fact that smoked foods decay slower than ordinary cooked foods indicates additional chemical processes are happening in smoked foods – so a valid question might be: is it a problem if we ingest smoked foods?
The historical evidence suggests that humans tolerate foods smoked with real wood pretty well, otherwise we would not be around enjoying BBQs. So a better question might be: is it a problem if we ingest modern smoked foods which are treated with liquid smoke?
The answer is somewhat complicated and is related to the extra twist mentioned earlier about the maximum recommended quantities of PAHs allowed in food.
But the easy part is that if you ingest an excessive amount of PAHs, then your chances of developing cancers and mutagenic diseases will increase pretty significantly, based on numerous tests on mammals.
Food treated with PAHs, including both real smoke and liquid smoke, are rated as Group 1 carcinogens by the WHO. As you might know from earlier articles, Group 1 carcinogens include mustard gas, asbestos and plutonium though the death rates from PAHs are not nearly as high as for those other agents – mainly because it is usually difficult to eat so much PAHs on a frequently consistent basis.
Statistically, eating commercial smoked foods in “normal” amounts can raise the risk of bowel cancer from 6% to 7% – however, if safety limits are exceeded, then in test mammals, the risks increases rapidly, possibly even exponentially for certain types of PAHs.
How to measure PAHs
And this is the problem. PAHs are a diverse group of several hundred compounds so to derive a standard for measuring PAH food safety, it is impossible to assay individually every PAH in, for example, a piece of smoked salmon. The industry solution was to develop a series of “PAH profiles” to assess the levels of PAHs in food, in the atmosphere, in soils, et cetera.
The technique is rather simplistic. For each PAH analysis situation, a select number of PAHs are picked to indicate the overall level of contamination.
So for air pollution in Western Europe, the PAH most usually measured is benzo[a]pyrene (BaP) along with around 30 other PAHs, usually linked to vehicular and industrial pollution. This makes up the PAH profile for air quality monitoring, even though there are often hundreds of other PAH pollutants in the air.
Breaches in any of the limits assigned to the PAHs in the air profile are reported. It is like having a country represented by a government. The actions of an administration won’t always reflect the wishes of the citizens, but other countries will judge the nation by its government.
For smoked food in Western Europe, BaP is also among the 16 PAHs out of hundreds tested for food safety – the rationale for this profile selection is the higher carcinogenic propensity of these 16 PAHs.
As for air monitoring, a breach of any of the monitored PAH levels in the PAH food profile has to be reported – but there is yet another twist to this somewhat general methodology.
Research has shown that some PAHs need to combine and interact with other PAHs and compounds before becoming more severe health issues – and these combinations are not monitored.
For example, PAHs which have passed through the digestive system are turned into PAH metabolites – and certain PAH metabolites such as bay-region diol epoxides have been cited as significant health dangers.
Another downside is that other PAHs are not checked, so a severe spike in an unmonitored PAH can go undetected, even if it reached dangerous levels.
Furthermore, studies in mammals have indicated that individual genetic differences also play a significant role in carcinogenicity and mutagenicity – so there are many varied and complex factors to consider before an authoritative objective assessment of PAH safety is feasible.
But for the moment, what is currently in place is about the best that can be achieved given the level of knowledge and resources.
For my personal situation, gastrointestinal irritation is the main symptom after ingestion of one or more problematic PAHs. And based on current regulations and data, there is no way to find out which PAH or combination of PAHs is the culprit – PAHs are not even listed as food ingredients.
All I am reasonably certain of is that it has something to do with liquid smoke, for wood-smoked foods and BBQs are always fine. It is irritatingly similar to a scatty witness of a car accident – the only recollection is that the cars hit each other at about the same time.