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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.

To undertake a scoping review to identify methods and diagnostic levels used in determining unintentional, non-fire related carbon monoxide exposure. Online databases and grey literature were searched from 1946 to 2023 identifying 80 papers where carbon monoxide levels were reported. 80 papers were included; 71 research studies and 9 clinical guidelines. Four methods were described: blood carboxyhaemoglobin (arterial or venous blood analysis), carbon monoxide oximetry (SpO2), expired carbon monoxide, and ambient carbon monoxide sampling. Blood analysis methods predominated (60.0% of the papers). Multiple methods of measurement were used in 26 (32.5%) of the papers. Diagnostic levels for carboxyhaemoglobin were described in 54 (67.5%) papers, ranging between 2% and 15%. 26 (32.5%) papers reported diagnostic levels that were adjusted for the smoking status of the patient. Four methods were found for use in different settings. Variability in diagnostic thresholds impairs diagnostic accuracy. Agreement on standardised diagnostic levels is required to enable consistent diagnosis of unintentional, non-fire related carbon monoxide exposure.

Delayed encephalopathy after carbon monoxide poisoning (DEACMP) is the most severe and prevalent neurological sequela associated with carbon monoxide exposure. This study aims to investigate the time-varying characteristics of dynamic brain networks and their topological properties in DEACMP patients using resting-state functional magnetic resonance imaging (rs-fMRI). We conducted Functional MRI scans and clinical assessments for 25 DEACMP patients and 25 healthy controls (HCs). To capture the variability patterns of dynamic functional connectivity (dFC) between the two groups, we employed a sliding time window analysis method. Additionally, theoretical graph analysis was utilized to examine the variations in the topological properties of whole-brain functional networks. We found that DEACMP patients have two dFC states characterized by different connection patterns, State 1 and State2, and there were multiple inter-network and intra-network dynamic interactions in State2.Next, Abnormal dFC indicators were related to the MoCA scores. Finally, the dynamic brain network topological properties were variable. These findings may provide valuable insights into the disruptions in local information transmission and processing functions within the brain’s functional networks in individuals with DEACMP.

Carbon monoxide (CO) poisoning is common in modern society, resulting in significant morbidity and mortality in the United States annually. Over the past two decades, sufficient information has been published about carbon monoxide poisoning in the medical literature to draw firm conclusions about many aspects of the pathophysiology, diagnosis, and clinical management of the syndrome, along with evidence-based recommendations for optimal clinical practice. This article provides clinical practice guidance to the pulmonary and critical care community regarding the diagnosis, management, and prevention of acute CO poisoning. The article represents the consensus opinion of four recognized content experts in the field. Supporting data were drawn from the published, peer-reviewed literature on CO poisoning, placing emphasis on selecting studies that most closely mirror clinical practice.

Carbon monoxide dehydrogenase/acetyl-CoA synthase (CODH/ACS) is a five-subunit enzyme complex responsible for the carbonyl branch of the Wood–Ljungdahl (WL) pathway, considered one of the most ancient metabolisms for anaerobic carbon fixation, but its origin and evolutionary history have been unclear. While traditionally associated with methanogens and acetogens, the presence of CODH/ACS homologs has been reported in a large number of uncultured anaerobic lineages. Here, we have carried out an exhaustive phylogenomic study of CODH/ACS in over 6,400 archaeal and bacterial genomes. The identification of complete and likely functional CODH/ACS complexes in these genomes significantly expands its distribution in microbial lineages. The CODH/ACS complex displays astounding conservation and vertical inheritance over geological times. Rare intradomain and interdomain transfer events might tie into important functional transitions, including the acquisition of CODH/ACS in some archaeal methanogens not known to fix carbon, the tinkering of the complex in a clade of model bacterial acetogens, or emergence of archaeal–bacterial hybrid complexes. Once these transfers were clearly identified, our results allowed us to infer the presence of a CODH/ACS complex with at least four subunits in the last universal common ancestor (LUCA). Different scenarios on the possible role of ancestral CODH/ACS are discussed. Despite common assumptions, all are equally compatible with an autotrophic, mixotrophic, or heterotrophic LUCA. Functional characterization of CODH/ACS from a larger spectrum of bacterial and archaeal lineages and detailed evolutionary analysis of the WL methyl branch will help resolve this issue.

Purpose: To investigate whether altered functional activity, functional connectivity (FC), and structural connectivity (SC) following acute carbon monoxide (CO) poisoning contribute to delayed neurological sequelae (DNS) occurrence. Methods: Binary degree centrality (DC) and seed-based FC were investigated in 18 patients with DNS, 26 patients without DNS, and 30 healthy controls. Duration of CO exposure and coma severity indices-related fibers was detected by connectometry analysis and the identified fiber tracts were tracked and their SC alteration was quantify by fractional anisotropy (FA). Results: Acute CO exposure induced DC change in the prefrontal cortex (PFC), visual cortex, primary sensory cortex, and anterior cerebellum, and FC alteration between the right fusiform gyrus (seed) and bilateral PFC and left inferior occipital gyrus (Gaussian random field corrected, P  < 0.05). Poisoning severity indices-related WM fibers consisted of corpus callosum and some association and projection fibers (false discovery rate corrected, P  < 0.05). Only altered DC in the right fusiform gyrus and right postcentral gyrus and reduced FC of the PFC could identify DNS occurrence ( P  < 0.05). Conclusions: The functional abnormalities in the visual- and sensory- cortex and PFC subsequent to acute CO poisoning represent one of the potential neural mechanisms underlying the occurrence of DNS.

Key Points For more than a century, carbon monoxide (CO) has been primarily studied as a toxic substance that interferes with oxygen delivery to tissue beds. This dogma has changed in recent years, whereby low concentrations of CO displays remarkably protective effects against disease pathology. CO is now being viewed as a protective homeostatic molecule that is being developed for therapy as an inhaled gas and as CO-releasing molecules (CO-RMs). This concept stemmed from the extensive studies of haem oxygenase, which is a cytoprotective enzyme that is thought to impart benefit through its ability to generate CO. There is a large amount of broad preclinical evidence of the benefits of CO in large and small animal models. Importantly, CO is effective both as a prophylactic and as a therapeutic in diverse models, such as malaria, organ transplantation and pulmonary hypertension. Inhaled CO and CO-RMs are in development as therapeutics; inhaled CO is being tested in Phase II clinical trials for kidney transplantation and various CO-RMs are under preclinical evaluation. The precise molecular targets for CO remain unclear with a wide range of evidence for both haem and non-haem targets. A commonality revolves around the contributions of the mitochondria and alterations in cellular bioenergetics. Inhaled CO delivery can be accomplished with an innovative delivery device. In addition strong medicinal chemistry is driving CO-RM development with efforts towards tissue specificity and the appropriate pharmacokinetic and pharmacodynamic profiling. Carbon monoxide (CO) is increasingly being accepted as a cytoprotective and homeostatic molecule. Here, the authors review the physiology of CO, summarize the effects of CO gas and CO-releasing molecules in preclinical animal models of cardiovascular disease, inflammatory disorders and organ transplantation, and discuss the therapeutic development of this gaseous molecule. Carbon monoxide (CO) is increasingly being accepted as a cytoprotective and homeostatic molecule with important signalling capabilities in physiological and pathophysiological situations. The endogenous production of CO occurs through the activity of constitutive (haem oxygenase 2) and inducible (haem oxygenase 1) haem oxygenases, enzymes that are responsible for the catabolism of haem. Through the generation of its products, which in addition to CO includes the bile pigments biliverdin, bilirubin and ferrous iron, the haem oxygenase 1 system also has an obligatory role in the regulation of the stress response and in cell adaptation to injury. This Review provides an overview of the physiology of CO, summarizes the effects of CO gas and CO-releasing molecules in preclinical animal models of cardiovascular disease, inflammatory disorders and organ transplantation, and discusses the development and therapeutic options for the exploitation of this simple gaseous molecule.

Unintentional non-fire-related (UNFR) carbon monoxide (CO) poisoning has been among the leading causes of poisoning in the United States. Current estimation of its economic burden is important for an optimal allocation of resources for UNFR CO poisoning prevention. This study was to estimate the morbidity costs of UNFR CO poisoning. We also compared the costs and benefits of installing CO detectors in residences. We used 2010–2014 charges and cost data from Healthcare Cost and Utilization Project (HCUP), and Truven© Health MarketScan Commercial Claims and Encounters and Medicare Supplemental data. We directly measured the morbidity cost as the summation of costs for different healthcare services. Benefit of installing CO detector was estimated by summing up the avoidable morbidity cost and mortality cost (value of life). Cost of CO detectors was calculated using the average market price of CO detectors. We also calculated the benefit-to-cost ratio by dividing the benefit by its cost. All expenditures were converted into 2013 U.S. dollars. For UNFR CO poisoning, total annual medical cost ranged from $33.6 to $37.7 million. Annual non-health-sector costs varied from $3.7 to almost $4.4 million. The benefit-to-cost ratio can be as high as 7.2 to 1. UNFR CO poisoning causes substantial economic burden in the U.S. The benefit of using CO detectors in homes to prevent UNFR CO poisoning can considerably exceed the cost of installation. Public health programs could use these findings to promote broad installation of CO detectors in homes.

Carbon monoxide (CO) results from incomplete combustion of carbon-based materials, causing symptoms such as headaches, dizziness, nausea, chest pain, confusion, and, in severe cases, unconsciousness. Normobaric oxygen therapy (NBOT) is the standard therapy, whereas hyperbaric oxygen therapy (HBOT) is recommended in severe cases of organ damage. This study examined the early and late adverse outcomes in patients with severe CO poisoning. This study analyzed severe cases of CO poisoning among patients admitted to the emergency department between January 2020 and May 2022. The demographic, clinical, and laboratory data of symptomatic individuals and those requiring HBOT were examined. The study recorded early outcomes, such as intubation and in-hospital mortality, and late outcomes, such as delayed neurological sequelae and 1-year mortality. Chi-square tests, Spearman's rho correlation tests, and logistic regression analyses were performed to identify factors affecting these outcomes. Patients who received HBOT showed a significant difference in delayed neurological sequelae (DNS) compared to those who received NBOT (p = 0.037). Significant differences were observed in the need for intubation, in-hospital mortality, and 1-year mortality between patients based on COHb levels, but no significant differences were found in DNS. The 1-year mortality probability was significantly influenced by COHb level (odds ratio = 1.159, 95% CI [1.056-1.273]). Patients receiving NBOT had a higher odds ratio for DNS risk than those receiving HBOT (odds ratio = 8.464, 95% [1.755-40.817], p = 0.008). The study showed no differences in intubation, in-hospital mortality, and 1-year mortality rates between the HBOT and NBOT groups. However, significant differences in DNS suggest that treatment modalities have different effects on neurological outcomes. High COHb levels are associated with an increased risk of intubation, and mortality underscores the significance of monitoring COHb levels in clinical evaluations.

In this study, we aimed to quantify carbon monoxide (CO) in human brain tissue to better understand the toxic mechanisms of CO poisoning. Currently, conventional CO measurement methods are limited; however, the hemoCD assay has proven to be a simple and rapid method for quantifying CO in human tissues. Using this method, CO concentrations were measured in various brain regions, revealing significantly higher CO concentrations in the CO-exposed group (approximately 30–50 pmol/mg) compared to the non-exposed group (approximately 20–30 pmol/mg). However, the absence of region-specific elevation suggests that CO inhalation is not selectively associated with brain areas with high CO affinity or those that typically show abnormal MRI signals during CO intoxication. The observed difference of 10–20 pmol/mg between the CO-exposed and non-exposed groups suggests that an additional 10–20 pmol/mg of external CO may represent a lethal dose, potentially causing death. The results of this study are expected to contribute to the elucidation of the pathogenesis of CO poisoning and ultimately aid in the development of effective treatment strategies.