Sodium nitrite is a preservative, and ingestion of foods containing excessive amounts of sodium nitrite can also result in acute poisoning or death. Clinical studies have reported that intentional overdose of Sodium nitrite can cause methemoglobinemia, hypotension, lead to systemic hypoxia, metabolic acidosis, dyspnea and tachycardia. If left untreated it may result in death.

The mechanism of toxicity of sodium nitrite may be related to the fact that sodium nitrite causes an increase in the concentration of methemoglobin (MHb), which normally accounts for only 1-2% of total circulating hemoglobin. Haemoglobin is a tetrameric metalloprotein with four subunits, each of which is bound to a haemoglobin moiety capable of binding Fe2+/Fe3+ ions. Normally, haemoglobin binds to ferrous iron (Fe2+), which is able to transport oxygen molecules so that they can be released into the tissues. Sometimes, for example in the presence of sodium nitrite, ferrous iron is oxidised to elemental iron (Fe3+), which loses its ability to bind oxygen, resulting in an increased affinity for oxygen of the remaining Fe2+ haemoglobin moiety in the same haemoglobin structure. As a result, haemoglobin is converted to MHb, which has a lower capacity to transport oxygen and release it into the tissues. Indeed, the heterogeneous modification of MHb, in addition to allowing binding to a smaller number of oxygen molecules, leads to the establishment of stronger binding, which is responsible for the difficulty in releasing oxygen into the tissues; therefore, in clinical practice, the percentage of residual oxygenated haemoglobin constitutes only the theoretical oxygen transport capacity, since the effective peripheral release capacity has to be taken into account.The systemic hypoxia induced by MHb leads to a decrease in aerobic cellular metabolism, which leading to a variety of different conditions ranging from metabolic acidosis to cyanosis and death.  

References:

[1] Sodium-nitrite[J]. Reactions Weekly, 2023. DOI:10.1007/s40278-023-51709-1.