We report an atypical case of salicylate toxicity in a child without a reported exposure to aspirin, who presented with coexisting methemoglobinemia and carboxyhemoglobinemia, and provide mechanistic theories as to the potential pathway by which salicylates can lead to such dyshemoglobinemias. The patient, a 17-month old male, presented to the hospital 10 h after six episodes of vomiting, tachypnea and hyperpnea. Laboratory values showed a mixed respiratory alkalosis and metabolic acidosis; however, the parent's denial of aspirin exposure, coupled with laboratory results indicating carboxyhemoglobinemia, methemoglobinemia and neutrophilic leukocytosis, disguised a toxic salicylate level of 51.1 mg/dL. We searched the PubMed database for sources of salicylate exposure using the terms: "salicylate exposure", "salicylate toxicity", "sources", and an association of salicylates with carboxyhemoglobinemia methemoglobinemia using those three terms. Furthermore, Google Scholar and PubMed were used to search for biochemical literature explaining the association of salicylates with red blood cell oxidation, methemoglobin and carbon monoxide formation. We discovered that the mechanism by which high dose salicylates lead to carboxyhemoglobinemia and methemoglobinemia had not been previously described. We propose that salicylates in high doses can induce a methemoglobinemia through increased vascular release of nitric oxide through induction of IL-1β and carboxyhemoglobinemia via lipid peroxidation, leading to the release of carbon monoxide.