Food Safety in Europe: A Dive Down a Particular Rabbit Hole
Turns out 'the Science™' is hard at-work in 'our' regulatory agencies whose primary function is…what exactly?
A few days ago, I published a little ‘foodnote’ about strange ingredients in regular (sic) cheese. Specifically, I complained about the use of ‘potato flour’ in ‘cheese’ without the specific declaration of said potato flour as an anticaking agent.
Here’s a bit more background: earlier this year, we planted some cabbage in our vegetable garden, and while they are growing nicely (they are huge these days), it’s also the time of the year to ponder how to keep them from turning bad before too long.
Hence, we began pickling; while we did all the relevant preparatory steps (esp. cleaning the pickling jars in boiling water), we used the salt from the kitchen drawer, which we assumed, wrongly, as it turned out, to be ‘regular’ salt.
Sadly, that was not the case. I’ve long since discarded the cardboard box, but while at the supermarket, I checked the brand I (think I) bought many months ago. And, almost ‘as a matter of course’, I now read that the ‘salt’ was ‘special’ as it ‘contains less’ of whatever renders salt ‘bad™’ for you. Shame on me.
In the spirit of ‘fool me once…’, I began looking for salt without any additives (that also incl. iodine), which, as it turns out, isn’t that easy. I finally found one (!) brand of sea salt that, according to its label, is ‘pure’, or ‘without any additives’, such as anticaking agents or the like. (We’ll return to the pickling business later today, so I’ll keep you informed if that salt actually works.)
So, I bought a big bag of larger salt crystals for pickling, and I also bought a small container of said sea salt from the same brand for regular use. Silly as I was, I didn’t read the label and presumed that, since it’s the same product from the same manufacturer, it would be, well, the same sea salt without additives.
Little did I know, for that smaller container of sea salt, presumably because it was ground into smaller bits, actually contained an anticaking agent as I ‘learned’ upon returning home: E 535.
Thus began yet another journey down a rabbit hole, this time into the vast domain of food additives used in salt, which, believe it or not, also leads back to ‘the Science™’.
All emphases, if not mentioned otherwise, are mine. As are the ‘sighs’. Sigh.
What, then, is E 535?
What seems like a simple question that should be easily answered by a simple online search—quickly turned into something very much different.
It began with my standard search engine—DuckDuckGo—suggesting ‘E 536’ instead of ‘E 535’. While annoying, this obstacle was easy to overcome. What I learned next, well, is something else.
I quickly landed on the Wikipedia site with the title ‘Sodium ferrocyanide’, which is (references omitted)
known as yellow prussiate of soda…Despite the presence of the cyanide ligands, sodium ferrocyanide has low toxicity (acceptable daily intake 0-0.025 mg/kg body weight). The ferrocyanides are less toxic than many salts of cyanide [how reassuring], because they tend not to release free cyanide. However, like all ferrocyanide salt solutions, addition of an acid or exposure to UV light can result in the production of hydrogen cyanide gas, which is extremely toxic.
So, being a historian with a curious mind, I recalled that hydrogen cyanide is highly toxic and forms the basis for gases, such as Zyklon B, or Prussic Blue. Moving on to ‘uses’, I was quite surprised, at first, to learn the following (from the former Wikipedia link):
In the EU, ferrocyanides (E 535–538) were, as of 2018, solely authorized as additives in salt and salt substitutes, where they serve as anticaking agents. The kidneys are the organ susceptible to ferrocyanide toxicity, but according to the EFSA, ferrocyanides are of no safety concern at the levels at which they are used.
That short paragraph is adorned with endnote 7, which leads to a study (sic) by Aggett et al., ‘Re-evaluation of sodium ferrocyanide (E 535), potassium ferrocyanide (E 536) and calcium ferrocyanide (E 538) as food additives’, EFSA Journal. 16 (7): 5374.
What is ‘the EFSA’, we might briefly enquire about? Well, it’s the European Food Safety Authority. Based in Parma, Italy, its primary function is that of a supreme, supra-national food safety and licensing agency in the European Union.
So, the above study is about as official as it gets, and we’ll now check it out.
Speaking about ‘official’ information, well, it’ll perhaps interest you that the EFSA Journal is, according to their website, the EFSA’s own online journal, which
publishes the scientific advice of the European Food Safety Authority which underpins the policies and measures taken to protect European consumers and the environment. The articles published in EFSA Supporting Publications inform the Authority’s scientific assessments or report on scientific events that are organised in the context of its scientific mandate.
So, it’s an in-house journal whose contents ‘inform the Authority’s scientific assessments’. In other words: it’s articles are therefore neither refereed in the conventional sense of the term ‘peer-review’ nor free from undue influence of those who order said assessments and/or pay for it.
With that being said, here’s what Aggett and colleagues have to say.
‘Re-evaluation of ferrocyanides…as food additives’
From the abstract:
The Panel on Food Additives and Nutrient Sources added to Food (ANS) provided a scientific opinion re-evaluating the safety of sodium ferrocyanide (E 535), potassium ferrocyanide (E 536), and evaluating the safety of calcium ferrocyanide (E 538) as food additives. The Panel considered that adequate exposure and toxicity data were available. Ferrocyanides (E 535–538) are solely authorised in two food categories as salt substitutes. To assess the dietary exposure to ferrocyanides (E 535–538) from their use as food additives, the exposure was calculated based on regulatory maximum level exposure assessment scenario (maximum permitted level (MPL)) and the refined exposure assessment scenario [so much data available, they didn’t even use it to assess it]. Dietary exposure to ferrocyanides was calculated based on mean and high levels consumption of salts in both the regulatory maximum level and the refined scenario [same shit, different smell]. In the MPL scenario, the exposure to ferrocyanides (E 535–538) from their use as a food additive was up to 0.009 mg/kg body weight (bw) per day in children and adolescents. In the refined estimated exposure scenario, the exposure was up to 0.003 mg/kg bw per day in children and adolescents. Absorption of ferrocyanides is low and there is no accumulation in human. There is no concern with respect to genotoxicity and carcinogenicity [oh, look, ‘no concerns’, ‘the Science™’ says]. Reproductive studies were not available [what does it matter, eh?], but a no observed adverse effect level (NOAEL) of 1,000 mg sodium ferrocyanide/kg bw per day (highest dose tested) was identified from a prenatal developmental toxicity study. The kidney appeared to be the target organ for ferrocyanides toxicity and 4.4 mg sodium ferrocyanide/kg bw per day was identified as the NOAEL for the renal effects in a chronic (2-year) study in rats. Assuming that the toxicity of this compound is due to the ferrocyanide ion only, the Panel established a group acceptable daily intake (ADI) for sodium, potassium and calcium ferrocyanide of 0.03 mg/kg bw per day expressed as ferrocyanide ion. The Panel concluded that ferrocyanides (E 535–538) are of no safety concern at the current authorised use and use levels.
So much for whatever ‘the Science™’ knows. Note, in passing, that the above ‘re-evaluation’ was published in 2018, i.e., before the WHO-declared, so-called ‘Pandemic™’.
Let’s read on, shall we? From the ‘summary’:
In the EU, sodium and potassium ferrocyanide, used as food additives, were previously evaluated by the Scientific Committee on Food (SCF) in 1990. In that evaluation, the SCF agreed with the acceptable daily intake (ADI) of 0.025 mg/kg body weight (bw) per day (calculated as sodium ferrocyanide) established by the Joint FAO/WHO Expert Committee on Food Additives (JECFA) for sodium and potassium ferrocyanide…
The Scientific Committee for Animal Nutrition (SCAN) evaluated the safety for the target animals, the users, the workers, the consumers and the environment of sodium and potassium ferrocyanide used as anticaking agents. It was concluded that sodium and potassium ferrocyanide in salt for feed use (20, 80 and 100 mg/kg in salt for man, poultry and livestock, respectively) is acceptable in regard to the safety for target animals and human consumers. Sodium, potassium and calcium ferrocyanide were evaluated by a working group established by the Nordic Council of Ministers in 2000. Sodium, potassium and calcium ferrocyanide were not considered to cause a safety problem due to the very small quantities consumed [are you re-assured yet?].
And this is the study design:
To assess the dietary exposure to ferrocyanides (E 535–538) from their use as food additives, the exposure was calculated based on (1) maximum permitted level (MPL) in FC 12.1.1 ‘Salt’ set out in the EU legislation (defined as the regulatory maximum level exposure assessment scenario) and (2) the mean reported use levels of salt (defined as the refined exposure assessment scenario).
The Panel decided to use salt intake data from urinary excretion studies for the assessment of exposure to ferrocyanides (E 535–538) instead of the food consumption data from the EFSA Comprehensive European Food Consumption Database as dietary surveys are commonly not considered as a good source of information in the estimation of salt intake while a more accurate way of estimation of the salt intake is a calculation from the urinary excretion of sodium [makes sense, so to speak].
Dietary exposure to ferrocyanides was calculated based on mean and high levels consumption of salts in both the regulatory maximum level and the refined scenario [so, a bunch of calculations came out of this re-evaluation].
In the MPL scenario, the exposure to ferrocyanides (E 535–538) from their use as a food additive was up to 0.009 mg/kg bw per day in children and adolescents. In the refined estimated exposure scenario, the exposure was up to 0.004 mg/kg bw per day in children and adolescents. Considering that the majority of the use levels in salt reported by Industry were for sodium ferrocyanide (E 535), these exposures would correspond approximately to 0.003 mg ferrocyanide ion/kg bw per day in children and adolescents in the refined exposure scenario…
And this is what the panel concluded:
Considering that:
in the refined exposure scenario estimated exposure to ferrocyanides (E 535–538) would correspond approximately to 0.003 mg ferrocyanide ion/kg bw per day in children and adolescents;
absorption of ferrocyanides from the gastrointestinal tract was low [i.e., not ‘ineistent], and there is no accumulation in human;
ferrocyanides are of low acute toxicity and not mutagenic or carcinogenic;
reproductive studies were not available, but a NOAEL of 1,000 mg sodium ferrocyanide/kg bw per day (highest dose tested) was identified from a prenatal developmental toxicity study;
the kidney is the target organ for ferrocyanides toxicity as characterised by the high number of cells excreted in the urine in rats;
4.4 mg sodium ferrocyanide/kg bw per day was identified as the NOAEL for this effect in a chronic (2-year) study in rats;
assuming that the toxicity of this compound is due to the ferrocyanide ion only, the Panel established a ADI for ferrocyanide ion of 0.03 mg/kg bw per day;
ferrocyanides (E 535–538) are only permitted as food additives in two food categories.
The Panel concluded that ferrocyanides (E 535–538) are of no safety concern in these current authorised use and use levels.
The Panel further concluded that the available data give reason to revise the ADI of 0.025 mg sodium ferrocyanide/kg bw per day (equivalent approximately to 0.02 mg ferrocyanide ion/kg bw per day).
See, ‘no safety concern’, but the Panel ‘further concluded…to revise the ADI’ downwards by 20%—because?
About the Toxicity of E535-E538
I’ll skip over much of the opinion, because we’re mostly interested in the toxicity profiles of these additives; this is on pp. 17-21.
No toxicological information was submitted for the re-evaluation of sodium, potassium and calcium ferrocyanide following an EFSA public call for data, prior to the start of this re-evaluation…
Potassium ferrocyanide was absorbed to a limited extent from the gastrointestinal tract following oral administration to rats (unpublished data from Gage (1950), cited in JECFA (1975); Nielsen et al., 1990a). The majority was excreted unchanged in the faeces (approximately 95% of the dose). Ferrocyanide was detected in liver, spleen, kidney, heart and lungs. Free iron was detected in erythrocytes and free cyanide [yep, that’s the supremely toxic stuff, and this was known since around 1950—now: why would the EU allow ferrocyanides as additives?] was detected in urine and expired air. The exposure to free cyanide was estimated to be less than 0.06 mg/kg bw after oral administration to rats of 10 mg 59 Fe- and 14 C-labelled potassium ferrocyanide per animal (Nielsen et al., 1990a). In humans, absorption was 0.25–0.42% (Nielsen et al., 1990b).
There follow a few paragraphs summarising further evidence from rats (10 animals/sex, for a total of 20 rats; hey, this is more than the 8 mice the Omicron modRNA junk was ‘tested’ on) and dogs (4 beagles/sex, for a total of 8 dogs—now we’re getting into ‘the Science™’ territory).
The dog data is from the 1970s, specifically ‘unpublished data from
Morgaridge (1970), cited in JECFA (1975)’, i.e., an indirect sourcing (note: in the Humanities, this is frowned upon; jus’ sayin’).
No treatment-related effects were observed in appearance, behaviour, body weight change, physical condition, urinary pathology, haematology, biochemical parameters, or gross and histopathology.
Overall, treatment-related effects were observed in kidneys (higher organ weight, tubular damage and granular and calcified deposits) in rats given 0.5% and 5% sodium ferrocyanide (450 and 4,500 mg/kg bw per day) in the diet for 13 weeks ([look, yet another] unpublished study by Oser (1959), cited in JECFA (1975)). No treatment-related effects were observed in dogs given dietary sodium ferrocyanide up to 1,000 mg/kg (25 mg/kg bw per day) for 13 weeks ([another one] Unpublished data from Morgaridge (1970), cited in JECFA (1975) [and another indirect citation].
On genotoxicity, the ‘re-evaluation’ holds:
No data were submitted to EFSA following a public call for data. Additional data were identified in the literature search and are summarised below. Neither the SCF (1991) nor JECFA (1970a, 1974a, 1975) have described any data on genotoxicity of sodium, potassium or calcium ferrocyanide.
Translation: we don’t know, but at least we asked; too bad we didn’t receive any data (which is why, I’d argue, that there’s no mention of genotoxicity in the ‘summary’ cited above).
Potassium ferrocyanide was actually tested in E. coli (Olivier and Marzin, 1987).
Sodium and potassium ferrocyanide were tested for genotoxicity in human lymphocyte cells in an in vitro Comet assay (Basu et al., 2013)…The tail DNA (%) (± SEM) was increased after treatment with potassium ferrocyanide…Sodium ferrocyanide did not induce DNA damage. Potassium ferrocyanide significantly reduced cell viability at all tested concentrations for about 20% [why bother reporting that in the ‘summary’] compared to control, whereas sodium ferrocyanide [E 535] significantly reduced cell viability for approximately 17% at the highest tested concentration only [phew]…
Overall, the Panel considered that the use of ferrocyanides as food additives is not of genotoxic concern.
On chronic toxicity and carcinogenicity, it was noted that
Neither the SCF (1991) nor JECFA (1970a, 1974a, 1975) have described any data on chronic toxicity and carcinogenicity of sodium, potassium or calcium ferrocyanide [call me surprised *not*]
And this is where we get to the meaty parts:
In a study carried out at BIBRA (British Industrial Biological Research Association) between 1974 and 1976, Wistar rats (48 animals/sex per group, initial body weight 40–60 g [this is how the Science used to roll back in the 1970s, by the way]) were given 0, 50, 500 or 5,000 mg/kg sodium ferrocyanide decahydrate in the diet (equal to 0, 4.4, 45 and 450.7 mg/kg bw per day for males and 0, 6.2, 62.5 and 630.1 mg/kg bw per day for females) for 2 years (COT, 1994b) [this is the above-mentioned study with the 4.4 mp/kg as the ‘no observed adverse effect level’, but somehow the sex difference was ‘lost’ in the 2018 re-evaluation]…
The Panel noted that no analyses were carried out to verify the concentrations of ferrocyanide in the various diets [so, we don’t know the intake]. The Panel further noted that it was a pre-GLP study, but that the BIBRA GLP Unit audited the study to ensure that the results accurately reflects the raw data generated during the study. There are some further inadequacies in the 2-year study as compared by current standards. No clinical biochemistry parameters were measured and several organs were missing for histopathological examination [we therefore also don’t know much]. However, The Panel considered none of the inadequacies large enough to invalidate the study [well, if it’s all we’ve got and we don’t want to know ‘more’, there we go, I s’ppose].
Rats were observed on a daily basis for abnormalities of appearance and behaviour or signs of ill-health and weighed regularly…Food and water intake were recorded…Blood was sampled…[and] was analysed…The average daily intakes of sodium ferrocyanide were estimated to be equal to 0, 4.4, 45 or 450.7 mg/kg bw per day for males and 0, 6.2, 62.5 or 630.1 mg/kg bw per day for females given 0, 50, 500 or 5,000 mg/kg sodium ferrocyanide in the diet…
Except for a higher number of cells excreted in 2-h urine samples from treated animals (all levels of treatment…)…no treatment-related adverse effects were observed in the urine analysis (COT 1994b).
In a study performed concurrently with the 2-year study, rats (12 animals/sex per group) were given 0, 50, 500 or 5,000 mg/kg sodium ferrocyanide decahydrate in the diet for 49 weeks (COT, 1994b)…There was a statistically significant increase in the mean number of cells excreted per hour in 2-h urine samples of treated animals (both sexes) from the 500 and 5,000 mg/kg groups compared with controls…
No carcinogenic effect was seen in these studies and neither were there any non-neoplastic findings observed considered to be of toxicological relevance. In particular, no treatment-related effects were observed in kidneys of rats given 0, 4.5, 45 or 450 mg sodium ferrocyanide/kg bw per day, for either 49 weeks or 2 years (COT, 1994b). However, in the 2-year study, mid- and high dose animals frequently showed a higher cell excretion rate in 2-h urine samples than did controls…An increased cell excretion rate compared to controls was also seen at the low-dose group but only on three occasions. No adverse renal effects were seen at histopathological examination, other than a slight increase in incidence and severity of glomerulonephrosis in males in the first interim study. Nevertheless, since the kidneys are known to be the target organ for ferrocyanide toxicity, the Panel considered the increased cell excretion rate indicative for occasional, transient kidney toxicity and a NOAEL of 50 mg/kg diet (equal to an intake of 4.4 mg/kg bw per day in male rats and 6.2 mg/kg bw per day in females) was identified.
There are no reproductive toxicity studies available. There are also no data available on hypersensitivity, allergenicity, and food intolerance, to say nothing about cross-reactivity with any of the other food additives.
From the discussion:
Based on the available data, the Panel considered that the use of ferrocyanides as food additives is not of genotoxic concern [remember: they just reduced viability of cells by 17-20%].
No carcinogenic effects were observed in rats given 0, 50, 500 or 5,000 mg/kg sodium ferrocyanide in the diet for either 49 weeks or 2 years (ot, 1994b) [i.e., there’s no long-term safety data, and the sex difference in Cot 1994b has somehow ‘disappeared’ from the Panel’s conclusions]…
There were no reproductive toxicity studies available [we’re flying blind here]…
The Panel considered the excretion of a high number of cells in the urine of mid- and high-dose rats in the 2-year study as pivotal effect. Based on the lowest NOAEL for this effect of 4.4 mg sodium ferrocyanide/kg bw per day for male rats, the Panel derived an ADI of 0.044 mg sodium ferrocyanide/kg bw per day…
Information from the Mintel’s GNPD showed that from the salt products of subcategory ‘Seasonings’ only 13% was labelled with ferrocyanides (E 535–538) while in the exposure assessment it was assumed that 100% of the salt consumed contains the additive [i.e., it’s everywhere, and you perhaps never thought about it (neither did I until earlier last week)]…
Exposure estimates are based on information provided on the reported level of use of ferrocyanides (E 535–538) [i.e., they’re trusting the manufacturer, which, at least as far as food labels are concerned, don’t divulge the share of these additives to any quantity of the product]. If [muahahaha] actual practice changes this refined estimates may no longer be representative and should be updated [told you, we’re flying very blind here].
I’ve also tried to locate some more information about the amounts, or shares, of (sodium) ferrocyanides in our food supply, which you can check here. Ferrocyanides are found, according to Appendix B, in .8% of 221,103 products spread out across a variety of foodstuffs, but they are much more widely used in seasonings, coffee, and ‘meal kits’ (data intake between 2013-18), hence it’s certainly higher now.
Final Frontiers: Livestock Food
As of 2024, ferrocyanides are now fed to virtually all livestock, as another ‘scientific opinion’ with the title ‘Safety and efficacy of a feed additive consisting of sodium ferrocyanide and potassium ferrocyanide for all animal species (Eusalt a.i.s.b.l.)’, published by the same EFSA Journal in June 2024, shows.
I’m not going through the opinion in the same way as above, mainly because the application to use ferrocyanides in feedstock is currently under review (the applicant failed to submit all relevant data), hence I’m merely quoting from the abstract:
Following a request from the European Commission, EFSA was asked to deliver a scientific opinion on the safety and efficacy of sodium ferrocyanide and potassium ferrocyanide as technological feed additives for all animal species. In its previous opinion on the safety and efficacy of the additives, the FEEDAP Panel concluded that the use of sodium ferrocyanide and potassium ferrocyanide is safe, when added to sodium chloride at a maximum content of 80 mg ferrocyanide anions (anhydrous)/kg for turkeys for fattening and laying hens and other laying/breeding birds, all porcine species and categories, all ruminant species and categories, rabbits, horses, salmonids and other minor fin fish, dogs and cats. However, the Panel could not conclude on the safety of the additives for chickens for fattening and other poultry species for fattening or reared for laying/breeding other than turkeys, and for all species/categories other than the above listed. In the current assessment, the applicant is proposing a maximum content of 60 mg ferrocyanide anions (anhydrous)/kg sodium chloride for chickens for fattening and other poultry species (except turkeys) for fattening or reared for laying/breeding and for all species/categories other than the listed above. The FEEDAP Panel concluded that sodium ferrocyanide and potassium ferrocyanide are safe at a maximum content of 80 mg ferrocyanide anions (anhydrous)/kg sodium chloride for: turkeys for fattening and reared for breeding, laying hens and other laying/breeding birds, all porcine species, all ruminant species, rabbits, equines, salmonids and minor fin fish, dogs and cats. The Panel concluded also that a maximum content of 60 mg ferrocyanide anions (anhydrous)/kg sodium chloride is safe for chickens for fattening and minor poultry species for fattening or reared for laying/breeding and all other animal species.
So, we note that ferrocyanides are now everywhere, fed to virtually all livestock, and, on top of it, we’re also ingesting it as food additive in salt. There’s little new data available on its effects, in particular in terms of toxicity. ‘The Science™’ at its best, well before Covid.
Bottom Lines: Know Your Food Labels
Do we really need to look at every detail, however irrelevant it seems?
Given the experiences with ‘the Science™’ during the past 4.5 years, it is necessary, esp. since the terms and authorities that are telling ‘us’ to simply ‘trust’ (all of) ‘them’ are virtually identical to the individuals and institutions that ran amok during the WHO-declared, so-called ‘Pandemic™’.
Sure, but what’s the fuss about anticaking agents, the reader might object. Well, if you wish to preserve foodstuffs you’ve grown yourself without taking recourse to a freezer, there’s not many alternatives to salt (depending on the food item in question, of course).
Then, there’s the notion of what else is in what looks like ‘food™’, incl. other additives, such as E 282, or Calcium propanoate or calcium propionate. It, too, is ‘used as a preservative in a wide variety of products, including: bread, other baked goods, processed meat, whey, and other dairy products’, according to Wikipedia.
What is Calcium propionate, you might ask? It’s a mould inhibitor. Why it’s there, well, here’s Wikipedia (references omitted):
A few decades ago, Bacillus mesentericus (rope), was a serious problem, but today’s improved sanitary practices in the bakery, combined with rapid turnover of the finished product, have virtually eliminated this form of spoilage.
We therefore see it’s practically unnecessary, yet I challenge you to check a few labels for E 282 next time you’re at the grocery store.
Why? Well, here’s what Wikipedia also says about E 282 (ref’s omitted):
Children were challenged with calcium propionate or placebo through daily bread in a double‐blind placebo‐controlled crossover trial. Although there was no significant difference by two measures, a statistically significant difference was found in the proportion of children whose behaviours ‘worsened’ with challenge (52%), compared to the proportion whose behaviour ‘improved’ with challenge (19%). When propanoic acid was infused directly into rodents’ brains, it produced reversible behavior changes (e.g. hyperactivity, dystonia, social impairment, perseveration) and brain changes (e.g. innate neuroinflammation, glutathione depletion) partially mimicking human autism.
Here’s a few choice excerpts from the EFSA’s ‘scientific opinion’ (2014):
As regards the above-mentioned cross-over study with children, ‘the Panel noted that the evidence for an effect of calcium propionate on the behaviour of children is limited because of shortcomings of the study design (cross over) and that the results have not been confirmed when using appropriate statistical testing. The Panel also noted that there is not a plausible
biological explanation for such an effect.’
We’ll briefly mention, albeit it passing, that this study was done in 2002. It is the one and only human study mentioned.
Animal studies (rats, dogs) contain a litany of issues, most of which are like the ones discussed at length above, i.e., unpublished industry studies from 50+ years ago, small sample sizes, etc.
Propionic acid has a local effect at the first site of contact with the body. In repeated doses toxicity studies, propionic acid did show lesions in the forestomach of rats with NOAELs of 558 mg/kg bw/day (90-day study) and 900 mg/kg bw/day (28-day study). From a 90-day study in dogs, the Panel identified a NOAEL of 210 mg/kg bw/day based on epithelial hyperplasia in the oesophagus [i.e., excessive cell growth, a first step on the way to cancer, or neoplasms].
Remember: it’s a very common food additive, which tells you a lot about ‘repeat doses’. Let’s not forget that E 282 is no longer necessary.
Moreover, there are genotoxicity studies both in vitro and in vivo covering several pages. Despite the length of this section, the Panel held ‘there was no concern with respect to genotoxicity for propionic acid, calcium propionate and sodium propionate’.
As regasds carcinogenicity risks, it was concluded that ‘most of the studies did not report any effects apart from reactions observed in the forestomach
of rats’. How re-assuring, eh?
Like with E 535-E 538, there are ‘no Reproductive toxicity studies…available’, and concluded ‘that the few human data available do not indicate that propionic acid and its salts used as food additives may represent a concern as regards hypersensitivity, allergenicity and intolerance’.
Overall, taking into account of all these considerations including the natural occurrence in food, the Panel concluded that for food as consumed, there would not be a safety concern from the maximum concentrations of propionic acid - propionates [propionic acid (E 280), sodium propionate (E 281), calcium propionate (E 282) and potassium propionate (E 283)] at their currently authorised uses and use levels as food additives.
Basically, the ‘scientific opinion’ on E 280-E 283 is way more detailed in terms of possible harms, existing studies, etc. compared to E 535-E 538. Both are assessed at essentially the same level of (minuscule) risk, but then again, since there’s so much ‘missing’ in terms of data and studies, we don’t really know.
It would be ‘nice’ to learn, at least from the EFSA, that E 282 was, at one point, banned as an additive in West Germany, albeit for political shadow-boxing reasons. I’ll let Udo Pollmer (source; my translation) do the explaining here:
Propionic acid is a natural trace substance in blue cheese. In higher concentrations, it exudes a pungent odour and corrodes the mucous membranes. In rats, it causes changes (hyperplasia) in the forestomach, which are interpreted as a precursor to cancer. In the opinion of the former Federal Health Office, this is of no significance for humans, as they do not have a forestomach.
However, when it became clear that the EU would allow propionic acid in Europe as part of the harmonisation process, German politicians took up the issue and quickly issued a ban, citing the supposedly high level of consumer protection in Germany. The EU’s plans were loudly attacked as anti-consumer.
However, this had virtually no consequences for manufacturers, as shortly after the German ban, the EU reauthorised the tried and tested propionic acid for sliced bread and bread for ready-baked products. This meant that everything was back to normal and the consumer protection politicians’ propaganda coup was a success.
In addition to its use in the bakery, propionic acid is also used to preserve animal feed and cosmetics.
Assessment: Not the ideal additive for bread, but tolerable. Completely okay in pig feed.
As regards E 535, Udo Pollmer wrote the following in 2017:
Yellow blood lye salt. It improves the pourability of table salt. Ferrocyanic potash (E 536) in particular is authorised for refining wine. The hydrocyanic acid bound in the additives can only be released by strong acids. Stomach acid or pickles are too weak for this.
Assessment: A harmless additive that is only consumed in minimal quantities.
Well, that was in 2017; now, with the addition of E 535-E 538 to virtually all livestock feed, ‘secondary’ intake must be considered.
While I personally doubt these things are particularly dangerous (esp. relative to all the other crap we breath, ingest, swim in, etc.), increasing food label literacy is a good thing, in particular as some of these additives do have quite negative effects, such as on the first batch of out pickled cabbage (which turned bad pretty fast, presumably due to whatever crap was added to the salt we used).
So, read up, and be on the look-out for ‘new’ E’s and stuff, esp. as manufacturers are adding ‘insects’ to the food. And, if possible, grow as much yourself as you can.
The trick of looking for excretion in the blood is an old one. That’s how they hide the danger of mercury and aluminum in meds and vx’s. It accumulates in the brain and other organs and doesn’t show up in the blood so they say that ”it’s eliminated quickly from the body” and so is safe