Introduction

doi:10.1002/9780470385081.ch1

Cited by 2 publications

(3 citation statements)

References 10 publications

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“…This means that chloride ions accelerate colour development in cured meat. Nitrous acid can also react with the sulfhydryl groups in meat proteins to release nitric oxide in an oxidation-reduction reaction that results in a disulfide according to the following reaction (Pegg and Shahidi, 2004):…”

Section: Stability Of the Substance And Reaction And Fate In Foodmentioning

confidence: 99%

“…Ascorbate is more reactive than ascorbic acid. The reactivity of ascorbic acid/ascorbate as a reductant increases with increasing pH (Pegg and Shahidi, 2004). So, the conversion of nitrite into NO, which can react with other meat ingredients, is accelerated in the presence of ascorbate, which can also sequester oxygen and retard the oxidation of NO to NO 2 and thus reduce the generation of nitrate (Pegg and Honikel, 2015).…”

Section: Stability Of the Substance And Reaction And Fate In Foodmentioning

confidence: 99%

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Re‐evaluation of potassium nitrite (E 249) and sodium nitrite (E 250) as food additives

Mortensen¹,

Aguilar²,

Crebelli³

et al. 2017

EFS2

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The Panel on Food Additives and Nutrient Sources added to Food (ANS) provided a scientific opinion re-evaluating the safety of potassium nitrite (E 249) and sodium nitrite (E 250) when used as food additives. The ADIs established by the SCF (1997) and by JECFA (2002) for nitrite were 0-0.06 and 0-0.07 mg/kg bw per day, respectively. The available information did not indicate in vivo genotoxic potential for sodium and potassium nitrite. Overall, an ADI for nitrite per se could be derived from the available repeated dose toxicity studies in animals, also considering the negative carcinogenicity results. The Panel concluded that an increased methaemoglobin level, observed in human and animals, was a relevant effect for the derivation of the ADI. The Panel, using a BMD approach, derived an ADI of 0.07 mg nitrite ion/kg bw per day. The exposure to nitrite resulting from its use as food additive did not exceed this ADI for the general population, except for a slight exceedance in children at the highest percentile. The Panel assessed the endogenous formation of nitrosamines from nitrites based on the theoretical calculation of the NDMA produced upon ingestion of nitrites at the ADI and estimated a MoE > 10,000. The Panel estimated the MoE to exogenous nitrosamines in meat products to be < 10,000 in all age groups at high level exposure. Based on the results of a systematic review, it was not possible to clearly discern nitrosamines produced from the nitrite added at the authorised levels, from those found in the food matrix without addition of external nitrite. In epidemiological studies there was some evidence to link (i) dietary nitrite and gastric cancers and (ii) the combination of nitrite plus nitrate from processed meat and colorectal cancers. There was evidence to link preformed NDMA and colorectal cancers.

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Section: Stability Of the Substance And Reaction And Fate In Foodmentioning

confidence: 99%

Section: Stability Of the Substance And Reaction And Fate In Foodmentioning

confidence: 99%

Re‐evaluation of potassium nitrite (E 249) and sodium nitrite (E 250) as food additives

Mortensen¹,

Aguilar²,

Crebelli³

et al. 2017

EFS2

View full text Add to dashboard Cite

show abstract

“…Nitrous acid can also react with sulfhydryl groups of meat proteins to release nitric oxide an oxidation-reduction reaction that results in a disulfide according to the following reaction (Pegg and Shahidi, 2004):…”

mentioning

confidence: 99%

Re‐evaluation of sodium nitrate (E 251) and potassium nitrate (E 252) as food additives

Mortensen¹,

Aguilar²,

Crebelli³

et al. 2017

EFS2

View full text Add to dashboard Cite

The Panel on Food Additives and Nutrient Sources added to Food (ANS) provided a scientific opinion re‐evaluating the safety of sodium nitrate (E 251) and potassium nitrate (E 252) when used as food additives. The current acceptable daily intakes (ADIs) for nitrate of 3.7 mg/kg body weight (bw) per day were established by the SCF (1997) and JECFA (2002). The available data did not indicate genotoxic potential for sodium and potassium nitrate. The carcinogenicity studies in mice and rats were negative. The Panel considered the derivation of an ADI for nitrate based on the formation of methaemoglobin, following the conversion of nitrate, excreted in the saliva, to nitrite. However, there were large variations in the data on the nitrate‐to‐nitrite conversion in the saliva in humans. Therefore, the Panel considered that it was not possible to derive a single value of the ADI from the available data. The Panel noticed that even using the highest nitrate‐to‐nitrite conversion factor the methaemoglobin levels produced due to nitrite obtained from this conversion would not be clinically significant and would result to a theoretically estimated endogenous N‐nitroso compounds (ENOC) production at levels which would be of low concern. Hence, and despite the uncertainty associated with the ADI established by the SCF, the Panel concluded that currently there was insufficient evidence to withdraw this ADI. The exposure to nitrate solely from its use as a food additive was estimated to be less than 5% of the overall exposure to nitrate in food based on a refined estimated exposure scenario. This exposure did not exceed the current ADI (SCF, 1997). However, if all sources of exposure to dietary nitrate are considered (food additive, natural presence and contamination), the ADI would be exceeded for all age groups at the mean and the highest exposure.

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Introduction

Cited by 2 publications

References 10 publications

Re‐evaluation of potassium nitrite (E 249) and sodium nitrite (E 250) as food additives

Re‐evaluation of potassium nitrite (E 249) and sodium nitrite (E 250) as food additives

Re‐evaluation of sodium nitrate (E 251) and potassium nitrate (E 252) as food additives

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