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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.

An understanding of the physiology of acute carbon monoxide (CO) poisoning remains incomplete. This study describes a novel approach—considering a CO cycle driven by CO inhalation which includes: alveolar CO uptake → the transport to peripheral tissues → an increase in the PCO and [COHb] in peripheral capillary blood → and a return of COHb to the lungs. Unlike earlier models, this model allows evaluation of how [COHb] changes will affect physiological events at different sites in this cycle. We calculated increases in the PCO and the [COHb] at these sites during constant breathing of different CO concentrations, using an approach that emphasizes the importance of the rate of the replacement reaction (CO + oxyhemoglobin (O2Hb) ↔ COHb + oxygen (O2)) in the physiology of CO poisoning. Key findings include: (i) how interactions between inhaled CO, COHb recirculating back to alveolar capillaries, and alveolar capillary PCO back‐pressure regulate pulmonary CO uptake; (ii) how a decrease in the arterial [O2Hb] evokes an amplification of the PCO in blood entering peripheral tissues; (iii) that hemoglobin's R‐to‐T allosteric shifts influence CO delivery to peripheral tissues; and (iv) a clearer characterization of how tissue PCO is increased during CO exposures.

Abstract 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 (CO) poisoning is a common health problem among people in many countries, primarily because of its severe clinical effects and high toxicological morbidity and mortality. Acute brain injury and delayed encephalopathy after acute carbon monoxide poisoning (DEACMP) are the most common neurological complications. This study was performed to assess the efficacy of N-butylphthalide (NBP) and dexamethasone (DXM) combined with hyperbaric oxygen (HBO) in patients with DEACMP. A total of 171 patients with DEACMP were recruited and assigned to the combined therapy group (receiving NBP and DXM 5 mg/day plus HBO therapy) or the control group (HBO therapy as monotherapy). Conventional treatments were provided for all patients. The cognition and movement changes in patients were evaluated by the Mini-Mental State Examination (MMSE), the Montreal Cognitive Assessment (MoCA) scale and the Barthel index of activities of daily living (ADL) before and after the treatment at 1 month, 3 months, and 1 year, respectively. At 1 month, 3 months, and 1 year after the treatment, the MMSE, MoCA and ADL scores were all significantly higher in the combined therapy group than those in the control group. There were no significant alterations in blood glucose, blood lipids, or liver and kidney function during the whole treatment session. Some patients experienced loss of appetite, mild headache and minor skin irritations. However, these patients recovered by themselves and needed no additional medications or special treatment. These results indicated that NBP and DXM combined with HBO for the treatment of DEACMP can significantly improve the cognitive and motor functions of patients and is very safe.

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.

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.

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.

The 2023 Canadian forest fires have been extreme in scale and intensity with more than seven times the average annual area burned compared to the previous four decades 1 . Here, we quantify the carbon emissions from these fires from May to September 2023 on the basis of inverse modelling of satellite carbon monoxide observations. We find that the magnitude of the carbon emissions is 647 TgC (570–727 TgC), comparable to the annual fossil fuel emissions of large nations, with only India, China and the USA releasing more carbon per year 2 . We find that widespread hot–dry weather was a principal driver of fire spread, with 2023 being the warmest and driest year since at least 1980 3 . Although temperatures were extreme relative to the historical record, climate projections indicate that these temperatures are likely to be typical during the 2050s, even under a moderate climate mitigation scenario (shared socioeconomic pathway, SSP 2–4.5) 4 . Such conditions are likely to drive increased fire activity and suppress carbon uptake by Canadian forests, adding to concerns about the long-term durability of these forests as a carbon sink 5 – 8 . Satellite carbon monoxide observations show that carbon emissions from the 2023 Canadian forest fires are comparable to the annual fossil fuel emissions of large nations.

In this study, we analyzed the factors influencing the development of delayed encephalopathy in patients with acute carbon monoxide poisoning (ACOP) (DEACMP) following conventional treatment such as hyperbaric oxygen therapy (HBOT). Between January 2012 and January 2022, we retrospectively analyzed 775 patients with ACOP, who were admitted to the Second Department of Rehabilitation Medicine and received HBOT in the Second Hospital of Hebei Medical University. These patients were divided into the non-DEACMP and DEACMP groups based on their follow-up; we then compared the general data, clinical characteristics, admission examination, and treatment between the two groups to identify risk factors for the development of DEACMP. The DEACMP group comprised of 168 cases, while the non-DEACMP group consisted of 607 cases. Univariate analysis showed that there were 20 possible prognostic factors in the non-DEACMP and DEACMP groups. The results of multivariable regression analyses suggested that the occurrence of DEACMP was significantly correlated with advanced age, the combination of multiple medical histories, the duration of CO exposure, the duration of coma, poisoning degree, the Interval between ACOP and the first HBOT, the total number of HBOTs, and the combination with rehabilitation treatment. DEACMP patients who are older, have more comorbidities, prolonged CO exposure, prolonged coma, severe intoxication, long intervals between ACOP and the first HBOT, fewer HBOT treatments, and who are not treated with a combination of rehabilitative therapies have a poor prognosis.