Carbon monoxide poisoning is one of the most common forms of poisoning in the world. Although the primary mode of treatment, oxygen therapy, is highly effective in many cases, there are instances in which it is inadequate or inappropriate. Whereas oxygen therapy relies on high levels of a low-affinity ligand (O2) to displace a high-affinity ligand (CO) from metalloproteins, an antidote strategy relies on introducing a molecule with a higher affinity for CO than native proteins (Kantidote,CO > Kprotein,CO). Based on the fundamental chemistry of CO, such an antidote is most likely required to be an inorganic compound featuring an electron-rich transition metal. A review is provided of the protein-, supramolecular complex-, and small molecule-based CO poisoning antidote platforms that are currently under investigation.

This study aimed to investigate the association between traffic-related air pollution (TRAP) exposure and histone H3 modification among school children in high-traffic (HT) and low-traffic (LT) areas in Malaysia. Respondents' background information and personal exposure to traffic sources were obtained from questionnaires distributed to randomly selected school children. Real-time monitoring instruments were used for 6-h measurements of PM₁₀, PM_2.5, PM₁, NO₂, SO₂, O₃, CO, and total volatile organic compounds (TVOC). Meanwhile, 24-h measurements of PM_2.5-bound black carbon (BC) were performed using air sampling pumps. The salivary histone H3 level was captured using an enzyme-linked immunosorbent assay (ELISA). HT schools had significantly higher PM₁₀, PM_2.5, PM₁, BC, NO₂, SO₂, O₃, CO, and TVOC than LT schools, all at p < 0.001. Children in the HT area were more likely to get higher histone H3 levels (z = -5.13). There were positive weak correlations between histone H3 level and concentrations of NO₂ (r = 0.37), CO (r = 0.36), PM₁ (r = 0.35), PM_2.5 (r = 0.34), SO₂ (r = 0.34), PM₁₀ (r = 0.33), O₃ (r = 0.33), TVOC (r = 0.25), and BC (r = 0.19). Overall, this study proposes the possible role of histone H3 modification in interpreting the effects of TRAP exposure via non-genotoxic mechanisms.

Carbon monoxide (CO) is an inorganic chemical compound that can bind with hemoglobin with highly toxic effects. In living organisms, it is produced endogenously during the degradation of heme by oxygenase, which occurs in three isoforms: HO-1, HO-2 and HO-3. CO can play an important role in the regulation of many physiological functions. Carbon Oxide Releasing Molecules (CORMs) are a novel group of chemical compounds capable of controlled CO release directly in tissues or organs. This release depends on concentration, pH, solvent type and temperature. The biological role and the therapeutic potential of different CORMs is not always well demonstrated. However, this mini review summarizes the various function of these compounds.

Carbon monoxide (CO) poisoning causes between 5,000-6,000 deaths per year in the US alone. The development of small molecule allosteric effectors of CO binding to hemoglobin (Hb) represents an important step toward making effective therapies for CO poisoning. To that end, we have found that the synthetic peptide IRL 2500 enhances CO release from COHb in air, but with concomitant hemolytic activity. We describe herein the design, synthesis, and biological evaluation of analogs of IRL 2500 that enhance the release of CO from COHb without hemolysis. These novel structures show improved aqueous solubility and reduced hemolytic activity and could lead the way to the development of small molecule therapeutics for the treatment of CO poisoning.

Carbon monoxide (CO) poisoning affects 50,000 people a year in the United States. The clinical presentation runs a spectrum, ranging from headache and dizziness to coma and death, with a mortality rate ranging from 1 to 3%. A significant number of patients who survive CO poisoning suffer from long-term neurological and affective sequelae. The neurologic deficits do not necessarily correlate with blood CO levels but likely result from the pleiotropic effects of CO on cellular mitochondrial respiration, cellular energy utilization, inflammation, and free radical generation, especially in the brain and heart. Long-term neurocognitive deficits occur in 15-40% of patients, whereas approximately one-third of moderate to severely poisoned patients exhibit cardiac dysfunction, including arrhythmia, left ventricular systolic dysfunction, and myocardial infarction. Imaging studies reveal cerebral white matter hyperintensities, with delayed posthypoxic leukoencephalopathy or diffuse brain atrophy. Management of these patients requires the identification of accompanying drug ingestions, especially in the setting of intentional poisoning, fire-related toxic gas exposures, and inhalational injuries. Conventional therapy is limited to normobaric and hyperbaric oxygen, with no available antidotal therapy. Although hyperbaric oxygen significantly reduces the permanent neurological and affective effects of CO poisoning, a portion of survivors still have substantial morbidity. There has been some early success in therapies targeting the downstream inflammatory and oxidative effects of CO poisoning. New methods to directly target the toxic effect of CO, such as CO scavenging agents, are currently under development.