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Direct evidence on the impact of air pollution on preterm birth (PTB) among advanced maternal age (AMA) primiparas is limited. This study examined the association between air pollution and PTB among 6,295 AMA primiparas in rural Henan Province. Logistic regression and distributed lag nonlinear models showed that prenatal exposure to carbon monoxide (CO), sulfur dioxide (SO2), nitrogen dioxide (NO2), and fine particulate matter (PM2.5) was associated with an increased PTB risk among AMA primiparas, while ozone (O3) exposure was inversely related to PTB risk (all P < 0.05). Moreover, the vulnerable periods were identified as gestational weeks 1–6 and 22–28. The education level, smoking status, and season of conception significantly modified the association between PTB and air pollution (P interaction < 0.10) among AMA primiparas. These findings emphasize the impact of air pollution on PTB risk in AMA primiparas, highlighting the need for targeted interventions in vulnerable populations. [ABSTRACT FROM AUTHOR]

Acute carbon monoxide (CO) poisoning may cause liver damage and liver dysfunction. Therefore, in this study, we aimed to compare the efficiency of normobaric oxygen (NBO) and high-flow nasal cannula oxygen (HFNCO) treatments on liver injury. For that purpose, 28 male Wistar albino rats were divided into four groups (Control, CO, CO + NBO, and CO + HFNCO). The control group was allowed to breath room air for 30 min. Acute CO poisoning in CO, CO + NBO, CO + HFNCO was induced by CO exposure for 30 min. Thereafter, NBO group received 100% NBO with reservoir mask for 30 min. HFNCO group received high-flow oxygen through nasal cannula for 30 min. At the end of the experiment, all animals were sacrificed by cardiac puncture under anesthesia. Serum liver function tests were measured. Liver tissue total antioxidant status (TAS), total oxidant status (TOS), and oxidative stress index (OSI) levels, tissue histomorphology and immunoexpression levels of Bax, Caspase 3, TNF-α, IL-1β, and NF-κB were also examined. Our observations indicated that acute CO poisoning caused significant increases in blood COHb, serum aminotransferase (AST), alanine aminotransferase (ALT0, alkaline phosphatase (ALP), total protein, albumin, and globulin levels but a decrease in albumin to globulin ratio (all, p < 0.05). Furthermore, acute CO poisoning significantly increased the OSI value, and the immunoexpresssion of Bax, Caspase 3, TNF-α, IL-1β, and NF-κB in liver tissue (all, p < 0.05). These pathological changes in serum and liver tissue were alleviated through both of the treatment methods. In conclusion, both the NBO and HFNCO treatments were beneficial to alleviate the acute CO poisoning associated with liver injury and dysfunction. Twenty-eight rats were divided into four groups (control, CO, CO + NBO, and CO + HFNCO) and the animals in CO, CO + NBO, CO + HFNCO were exposed to CO poisoning in a closed box (1), CO + NBO group received 100% normobaric oxygen with a reservoir mask at a flow rate 15 L/min (2), CO + HFNCO group received high-flow oxygen through nasal cannula at a flow rate of 60 L/min (3). All rats were sacrificed by cardiac puncture under anesthesia (4), blood and liver tissues were received (5) for the laboratory examinations (6). Our observations indicated that CO poisoning (7) caused significant increases in blood COHb, serum AST, ALT, ALP, total protein, albumin, globulin levels but a decrease in albumin to globulin ratio as well as the upregulation of tissue oxidative stress, and inflammatory cytokine levels (8). The upregulated oxidative stress and inflammation possibly led to increases in apoptotic protein expressions of Bax (9), Caspase 3, and NF-κB (10). The elevated NF-κB potentially increased the pro-inflammatory cytokine levels (11). However, both O2 treatments alleviated the pathological alterations in both serum and liver tissue (12). [ABSTRACT FROM AUTHOR]

Delayed neuropsychiatric sequelae (DNS) are critical complications following acute carbon monoxide (CO) poisoning that can substantially affect the patient's life. Identifying high-risk patients for developing DNS may improve the quality of follow-up care. To date, the predictive DNS determinants are still controversial. Consequently, this study aimed to construct a practical nomogram for predicting DNS in acute CO-poisoned patients. This retrospective study was conducted on patients with acute CO poisoning admitted to the Tanta University Poison Control Center (TUPCC) from December 2018 to December 2022. Demographic, toxicological, and initial clinical characteristics data, as well as laboratory investigation results, were recorded for the included patients. After acute recovery, patients were followed up for six months and categorized into patients with and without DNS. Out of 174 enrolled patients, 38 (21.8%) developed DNS. The initial Glasgow Coma Scale (GCS), carboxyhemoglobin (COHb) level, CO exposure duration, oxygen saturation, PaCO2, and pulse rate were significantly associated with DNS development by univariate analysis. However, the constructed nomogram based on the multivariable regression analysis included three parameters: duration of CO exposure, COHb level, and GCS with adjusted odd ratios of 1.453 (95% CI: 1.116–1.892), 1.262 (95% CI: 1.126–1.415), and 0.619 (95% CI: 0.486–0.787), respectively. The internal validation of the nomogram exhibited excellent discrimination (area under the curve [AUC] = 0.962), good calibration, and satisfactory decision curve analysis for predicting the DNS probability. The proposed nomogram could be considered a simple, precise, and applicable tool to predict DNS development in acute CO-poisoned patients. [ABSTRACT FROM AUTHOR]

No definitive prognostic biomarkers for carbon monoxide (CO) poisoning have been proposed. The aim of this study is to investigate, through a systematic literature review and pooled analysis, whether red blood cell distribution width (RDW) can predict disease severity in CO-poisoned patients. We performed an electronic search in Scopus and PubMed using the keywords: 'red blood cell distribution width' OR 'RDW' AND 'carbon monoxide' AND 'poisoning,' with no time or language restrictions (i.e. through August 2023) to find clinical studies that examined the value of RDW in patients with varying severity of CO poisoning. The analysis was performed according to the PRISMA (Preferred Reporting Items for Systematic Reviews and Meta-Analyses) 2020 reporting checklist. We identified 29 articles, seven of which were included in our analysis, with a total of 1979 CO-poisoned patients, 25.9% of whom were severely ill. In all but one of the studies, the RWD mean or median value was higher in CO-poisoned patients with severe disease. The weighted mean difference (WMD) of RDW was 0.36 (95% confidence interval (CI), 0.26–0.47)%. In the three articles in which the severity of illness in CO-poisoned patients was defined as cardiac injury, the WMD of the RDW was 1.26 (95%CI, 1.02–1.50)%. These results suggest that monitoring RDW in CO-poisoned patients may help to determine the severity of disease, particularly cardiac injury. [ABSTRACT FROM AUTHOR]

Duplicate measure of hemoglobin mass by carbon monoxide (CO)-rebreathing is a logistical challenge as recommendations prompt several hours between measures to minimize CO-accumulation. This study investigated the feasibility and reliability of performing duplicate CO-rebreathing procedures immediately following one another. Additionally, it was evaluated whether the obtained hemoglobin mass from three different CO-rebreathing devices is comparable. Fifty-five healthy participants (22 males, 23 females) performed 222 duplicate CO-rebreathing procedures in total. Additionally, in a randomized cross-over design 10 participants completed three experimental trials, each including three CO-rebreathing procedures, with the first and second separated by 24 h and the second and third separated by 5–10 min. Each trial was separated by >48 h and conducted using either a glass-spirometer, a semi-automated electromechanical device, or a standard three-way plastic valve designed for pulmonary measurements. Hemoglobin mass was 3 ± 22 g lower (p < 0.05) at the second measure when performed immediately after the first with a typical error of 1.1%. Carboxyhemoglobin levels reached 10.9 ± 1.3%. In the randomized trial, hemoglobin mass was similar between the glass-spirometer and three-way valve, but ∼6% (∼50 g) higher for the semi-automated device. Notably, differences in hemoglobin mass were up to ∼13% (∼100 g) when device-specific recommendations for correction of CO loss to myoglobin and exhalation was followed. In conclusion, it is feasible and reliable to perform two immediate CO-rebreathing procedures. Hemoglobin mass is comparable between the glass-spirometer and the three-way plastic valve, but higher for the semi-automated device. The differences are amplified if the device-specific recommendations of CO-loss corrections are followed. [ABSTRACT FROM AUTHOR]

An indispensable precondition for the determination of hemoglobin mass (Hbmass) and blood volume by CO rebreathing is complete mixing of CO in the blood. The aim of this study was to demonstrate the kinetics of CO in capillary and venous blood in different body positions and during moderate exercise. Six young subjects (4 male, 2 female) performed three 2-min CO rebreathing tests in seated (SEA) & supine (SUP) positions as well as during moderate exercise (EX) on a bicycle ergometer. Before, during, and until 15 min after CO rebreathing cubital venous and capillary blood samples were collected simultaneously and COHb% was determined. COHb% kinetics were significantly slower in SEA than in SUP or EX. Identical COHb% in capillary and venous blood were reached in SEA after 5.0 ± 2.3 min, in SUP after 3.2 ± 1.3 min and in EX after 1.9 ± 1.2 min (EX vs. SEA p <.01, SUP vs. SEA p <.05). After 7th min, Hbmass did not differ between the resting positions (capillary: SEA 766 ± 217 g, SUP 761 ± 227 g; venous: SEA 759 ± 224 g, SUP 744 ± 207 g). Under exercise, however, a higher Hbmass (p <.05) was determined (capillary: 823 ± 221 g, venous: 804 ± 226 g). In blood, the CO mixing time in the supine position is significantly shorter than in the seated position. By the 6th minute complete mixing is achieved in either position giving similar Hbmass determinations. CO-rebreathing under exercise conditions, however, leads to ∼7% higher Hbmass values. [ABSTRACT FROM AUTHOR]

Many reports in the literature have suggested the therapeutic value of carbon monoxide-releasing molecules (CORMs) against various diseases. However, to date, little is known about their possible influence on periodontal disease. This study was performed to investigate the influence of CORM-401 on the generation of nitric oxide (NO) in murine macrophage cells activated with lipopolysaccharide (LPS) derived from Prevotella intermedia, a pathogen associated with periodontal disease. LPS was isolated by the hot phenol-water method. Culture supernatants were analyzed for NO. Real-time PCR and immunoblotting were conducted to quantify mRNA and protein expression, respectively. NF-κB-dependent SEAP levels were estimated by reporter assay. DNA-binding of NF-κB was also analyzed. CORM-401 caused an apparent suppression of NO production through inhibition of iNOS at both the mRNA and protein levels in RAW264.7 cells stimulated with P. intermedia LPS. CORM-401 upregulated the expression of both the HO-1 gene and its protein in LPS-activated cells, and treatment with the HO-1 inhibitor significantly reversed the attenuating influence of CORM-401 against LPS-induced generation of NO. CORM-401 caused an apparent attenuation of NF-κB-dependent SEAP release induced by LPS. IκB-α degradation and nuclear translocation of NF-κB p50 subunit induced by LPS were significantly reduced by CORM-401. Additionally, CORM-401 significantly attenuated DNA-binding of p65 and p50 induced by LPS. CORM-401 attenuated NO generation induced by P. intermedia LPS independently of PPAR-γ, JNK, p38 and STAT1/3. The modulation of host inflammatory response by CORM-401 might be of help in the therapy of periodontal disease. [ABSTRACT FROM AUTHOR]

Incidence of carbon monoxide (CO) poisoning in Nepal has not been studied. The objective of this study was to evaluate baseline carboxyhemoglobin (COHb) concentrations, population risk factors, and incidence of CO poisoning at a single hospital in Nepal. This was a prospective, observational study of patients presenting to Patan Hospital Emergency Department from April 2019 to March 2020. Demographics, risk factors for CO poisoning, symptoms, and clinical pretest probability of CO poisoning was documented. COHb concentration was obtained using a noninvasive co-oximeter. Significant CO exposure was defined as COHb concentration > 10%. CO poisoning was defined as COHb > 10% coupled with symptoms. Of 1,040 patients, 745 patients had a recordable COHb concentration. Median age was 40 years (IQR 33) with 407 (55%) females. Average COHb was 7.2%. Warm months were associated with higher COHb concentrations (8.1% vs 6.0%, p < 0.05). Firewood use had higher COHb concentrations compared to gas heating (8.6% vs 7.0%, p < 0.05). Overall, 228 (31%) patients had a COHb concentration > 10% indicating significant CO exposure. Sixteen patients had CO poisoning. We found a significant baseline incidence of COHb > 10% (31%) in patients presenting to a hospital in Nepal. Risk factors for higher baseline COHb concentrations included warm months and cooking with firewood. [ABSTRACT FROM AUTHOR]

Carbon monoxide (CO) is a toxic gas that causes neuropathy. However, CO is endogenously produced in small amounts showing various beneficial effects. We hypothesized that CO-bound haemoglobin-vesicle (HbV) administration would reduce cerebral ischaemia–reperfusion injury without causing neuropathy. Three experiments were conducted. First, rats were exposed to CO inhalation to create a CO-poisoning group, and they were sacrificed on 0, 7, 14, and 21 days after CO exposure. Histopathologically, hippocampal damage was prominent at 14 days. Second, the rats were administered with CO-HbV equivalent to 50 or 25% of circulating blood volume (CO-HbV50 or CO-HbV25 group). Rats were sacrificed 14 days after administration. Third, rats put into haemorrhagic shock by 50% of circulating blood withdrawal were resuscitated using saline, autologous blood, and CO-HbV. They were sacrificed 14 days after resuscitation. Hippocampal damage assessment clarified that almost no necrotic cells were observed in the CO-HbV50 group. Necrotic cells in the CO-HbV25 group were comparable to those found for the control group. In rats resuscitated from haemorrhagic shock, the hippocampal damage in the group using CO-HbV was the mildest. Administration of CO-HbV did not lead to marked hippocampal damage. Furthermore, CO-HbV was effective at preventing cerebral ischaemia-reperfusion injury after haemorrhagic shock. [ABSTRACT FROM AUTHOR]

Cyanide is a prevalent, lethal chemical. Possible sources of exposure include products of combustion, plant material, industry, chemical warfare and terrorism. Retrospective review of UK Poisons Information Database of telephone enquiries to the National Poisons Information Service between 1st January 2008 and 31st December 2019 where cyanide poisoning was considered a possibility. Data extracted included demographics, exposure source, clinical features, Poisoning Severity Score, lactate concentration and antidotes given. A total of 1,252 cases of suspected cyanide poisoning were identified, 239 (19%) involved children under 10 years. The commonest sources of exposure were ingestion of plant material (437 cases; 35%) and smoke inhalation (399; 32%). Smoke inhalation caused the majority of severe and fatal cases (139; 71%). Clinical features associated with fatal outcomes were cardiac arrest (OR 36.4; 95% CI 14.4–92.2), hypotension (15.8; 7.0–35.9), coma (10.8; 5.6–21.0) and lactic acidosis (7.8; 4.1–14.8). 110 patients (9%) were given an antidote and 40 patients (3%) died. Lactate concentrations correlate with Poisoning Severity Score category (r = 0.6, p < 0.0001). Serum lactate <2.0 mmol/L was associated with Poisoning Severity Score None or Minor (sensitivity 76%; specificity 86%) and >11.0 mmol/L was associated with fatal outcome (sensitivity 74%; specificity 80%). 61 cases (5%) had severe carboxyhaemoglobin toxicity (COHb >30%). This was associated with a fatal outcome (OR 7.0; 95% CI 1.5-33.7) and there was positive correlation between carboxyhaemoglobin and Poisoning Severity Score, r = 0.57, p < 0.0001. Most cases of ingestion of plant material involved children under five years and resulted in no or mild symptoms. In adults smoke inhalation was associated with the most severe poisoning. The lactate cut-off values associated with each severity score calculated in this study are lower than the values used by NPIS on TOXBASE. Analytical conformation of cyanide exposure was unavailable in the majority of case, limiting the strength of these conclusions. [ABSTRACT FROM AUTHOR]

Historically, the first step in treating cyanide (CN-) toxicity utilized antidotes to induce methemoglobinemia. This is concerning in patients who are already hypoxemic or have elevated carboxyhemoglobin. Hydroxocobalamin (OHCbl) is now the first-line antidote for CN- toxicity and is not known to induce methemoglobinemia. We observed elevated methemoglobin (MetHb) levels in several patients treated with OHCbl and sought to investigate the incidence of MetHb formation following administration of OHCbl. Chart review: A single-center, retrospective case series of patients who received 5 or 10 g of hydroxocobalamin from 01/01/2011 through 04/30/2019. Data was analyzed using descriptive statistics. In-vitro study: Discarded blood was separated into whole blood and plasma samples. OHCbl and normal saline was added to reach 0×, 1×, 2×, and 4× peak therapeutic concentrations and analyzed at times 0, 2, and 4 h after administration. Chart review: Twenty-seven cases of OHCbl administration were identified. The median age was 53 years (IQR 38 − 64) and 20 (74.1%) were male. Exposure to a house fire or smoke inhalation was the reason for OHCbl administration in 21 (77.8%) patients. Five (18.5%) patients received 10 g of OHCbl while the rest received 5 g. Six (22.2%) patients developed methemoglobinemia, all after 5 g OHCbl administration; four had been exposed to fire and smoke, two received the medication for severe acidosis of unknown etiology not related to fire or smoke. The median peak level was 7.1% (IQR 2.2 − 16.4%) at a median time of 11.4 h post-administration. Two patients received methylene blue (MB), neither responded. Death occurred in 17 (63%) cases. In-vitro study: We observed a dose dependent elevation in total hemoglobin but did not detect any increase in MetHb. We observed a noteworthy temporal association between the formation of methemoglobinemia and the administration of hydroxocobalamin. This does not appear to be an artifact of the CO-oximeters. This could have profound implications for patients who are already hypoxemic or have impaired oxygen carrying capacity from carboxyhemoglobin. [ABSTRACT FROM AUTHOR]

Freshwater fish Pangasius sutchi was used in this study as a vertebrate model. We evaluated the induction of certain antioxidant enzymes in various vital organs. The radioprotective efficacy of Gymnema sylvestre leaves extract (GS) [25 mg/kg Body Weight (B.W)] and its bioactive compound Gymnemagenin (GG) [0.3 mg/kg B.W] was compared with Amifostine (Ami), the only radioprotector clinically approved by the US-FDA [Ami- 83.3 mg/kg B.W] against different doses of gamma radiation – 60Co (Lethal Dose: LD30-9.2 Gy, LD50-10.2 Gy and LD70-11.4 Gy). This study was done via stress marker enzymes, cell cycle analysis (CCA) and DNA damage assay prediction with molecular docking, which are reported here for the first time. The results indicate an elevated LPO level and decreased level of CAT, SOD and GSH due to oxidative stress initiation by 60Co Ionizing Radiation (IR) on 4th day and slightly reduced on 32nd day while the reverse observed when the fishes were pretreated with Ami, GS and GG. Similarly, CCA and dead/live cells counts were conducted with pretreatment of Ami, GS and GG against 60Co IR dose (LD50-10.2 Gy). In CCA, G0/G1 phase was observed to be the highest in Ami and lowest in GG, against 60Co IR doses 10.2 Gy which was 51.76 ± 7.55. The dead cells range observed in pretreated group of Ami, GS and GG was lowest in Ami and highest in GG and live cells (highest in Ami and lowest in GG) as compared to 60Co IR group (86.43 ± 3.42 and 8.77 ± 5.95). Thus, antioxidant profile improvement by oxidative stress reduction and gradual progression of different phases of cell cycle except the apoptotic phase along with the live cells counts indicates that the radio-protective efficacy of GS is similar to Ami. Predictive assessment was carried out by docking of Ami, various components of GS with p53, NF-κβ cells and Rad51 proteins structures responsible for CCA, apoptosis and repair mechanism. These structural proteins were docked with other structural proteins like USP7, TNF-α and partner and localizer of BRCA2 associated (PALB2/BRCA2) complex which made us perform these systemic efforts to find the functional activity of these known radio-protectants. [ABSTRACT FROM AUTHOR]

Carbon monoxide (CO) poisoning causes cardiotoxicity and so far, no definite antidote has been proposed to overcome CO-induced adverse outcomes. Hesperidin, a citrus flavonoid, has shown cardio-protective effects in cardiac ischemia/reperfusion models. This study investigated the protective effects of hesperidin against CO-induced cardiac injury. To induce CO poisoning, rats were exposed to CO at 3000 ppm for 60 min. On the exposure day and the four following days, hesperidin (at three different doses of 25, 50, and 100 mg/kg/day) was administered intraperitoneally. A group of animals received normal saline and served as the control group. The electrocardiogram (ECG) was recorded and evaluated with special focus on S–T segment changes (depression or elevation), T-wave alterations, AV block and ventricular and supraventricular arrhythmias. On day 6 (i.e., the day after the last injection day), the animals were sacrificed and the hearts were harvested and evaluated for necrosis using hematoxylin and eosin staining. In addition, Akt protein expression levels and BAX/BCL2 ratio were determined by western blotting. Our results showed that hesperidin decreased cardiac necrosis. In animals treated with hesperidin 100 mg/kg, Akt protein expression was increased, while the BAX/BCL2 ratio was significantly decreased. ECG changes were reversed in all groups 2 h following CO exposure, regardless of hesperidin administration. Overall, hesperidin decreased the deleterious cardiac effects of CO poisoning in rats. [ABSTRACT FROM AUTHOR]

Background and purpose: Low-dose of carbon monoxide delivered by CO-releasing molecule-2 (CORM-2) had been confirmed having anti-inflammatory efficacy in some inflammatory diseases. Herein, we assessed the usefulness of CORM-2 in correcting intracerebral hemorrhage (ICH)-mediated inflammation. Methods: Healthy male Sprague Dawley (SD) rats randomly entered into four groups: sham-ICH, ICH, ICH+CORM-2, and ICH+ inactive carbon monoxide releasing molecule 2 (iCORM-2). ICH was induced by 50 μl of autologous arterial blood injected in situ in the rat brain. Neuro-functions of the ICH rats were evaluated with Garcia 18 scores at the 6th, 24th , 48th hou, and the fifthh day post-ICH. And brain tissues surrounding the hematoma area were collected from all ICH rats and assayed with Western blot and immunofluoresence analysis. Results: Neuro-dysfunctions in ICH rats were very severe than those in ICH +CORM-2 rats. Compared to sham group, the levels of HO-1, IKKβ, NF-κB, and TNF-α in ICH group began to elevate at the 6th hour, and reached to peak at the 48th hour post-ICH, all p < 0.05. While in ICH +CORM-2 group, the expressions of IKKβ, NF-κB, and TNF-α were very weaker than that in ICH group at every time points mentioned above; however, this phenomenon was not reproduced in ICH + iCORM-2 group. HO-1 in ICH+CORM-2 group highlighted in perihematomal area with many activated microglia (Iba-1-positive cells) and co-expressed with TNF-α, all of which were diminished at the fifth day post-ICH. Conclusion: CORM-2 may attenuate ICH-mediated inflammation by inhibiting microglial activation, which may involve the IKK/NF-κB pathway. AbbreviationsICH: intracerebral hemorrhage; CO: carbon monoxide; CORM-2: carbon monoxide releasing molecule-2; iCORM-2: inactive carbon monoxide releasing molecule-2; HO-1: heme oxygenase 1; IKKβ: inhibitor of IκB kinases β; NF-κB: nuclear factor-κB; TNF-α: tumor necrosis factor-α; Iba-1: ionized calcium binding adaptor molecule-1; IκB: inhibitor of NF-κB; iNOS: inducible nitric oxide synthase; Keap1: Kelch-like ECH-associated protein 1; Nrf2: NF-E2-related factor 2; DMSO: dimethylsulfoxide [ABSTRACT FROM AUTHOR]

The purpose of this study is the development of a porcine model of carbon monoxide (CO) poisoning to investigate alterations in brain and heart mitochondrial function. Two group large animal model of CO poisoning. Laboratory. Ten swine were divided into two groups: Control (n = 4) and CO (n = 6). Administration of a low dose of CO at 200 ppm to the CO group over 90 min followed by 30 min of re-oxygenation at room air. The Control group received room air for 120 min. Non-invasive optical monitoring was used to measure cerebral blood flow and oxygenation. Cerebral microdialysis was performed to obtain semi real time measurements of cerebral metabolic status. At the end of the exposure, both fresh brain (cortical and hippocampal tissue) and heart (apical tissue) were immediately harvested to measure mitochondrial respiration and reactive oxygen species (ROS) generation and blood was collected to assess plasma cytokine concentrations. Animals in the CO group showed significantly decreased Complex IV-linked mitochondrial respiration in hippocampal and apical heart tissue but not cortical tissue. There also was a significant increase in mitochondrial ROS generation across all measured tissue types. The CO group showed a significantly higher cerebral lactate-to-pyruvate ratio. Both IL-8 and TNFα were significantly increased in the CO group compared with the Control group obtained from plasma. While not significant there was a trend to an increase in optically measured cerebral blood flow and hemoglobin concentration in the CO group. Low-dose CO poisoning is associated with early mitochondrial disruption prior to an observable phenotype highlighting the important role of mitochondrial function in the pathology of CO poisoning. This may represent an important intervenable pathway for therapy and intervention. [ABSTRACT FROM AUTHOR]

Gasotransmitters are small molecules of gases, including nitric oxide (NO), hydrogen sulfide (H2S), and carbon monoxide (CO). These three gasotransmitters can be endogenously produced and regulate a wide range of pathophysiological processes by interacting with specific targets upon diffusion in the biological media. By redox and epigenetic regulation of various physiological functions, NO, H2S, and CO are critical for the maintenance of intracellular energy homeostasis. Accumulated evidence has shown that these three gasotransmitters control ATP generation, mitochondrial biogenesis, glucose metabolism, insulin sensitivity, lipid metabolism, and thermogenesis, etc. Abnormal generation and metabolism of NO, H2S, and/or CO are involved in various abnormal metabolic diseases, including obesity, diabetes, and dyslipidemia. In this review, we summarized the roles of NO, H2S, and CO in the regulation of energy homeostasis as well as their involvements in the metabolism of dysfunction-related diseases. Understanding the interaction among these gasotransmitters and their specific molecular targets are very important for therapeutic applications. [ABSTRACT FROM AUTHOR]

Introduction: Carbon monoxide exposure is a relatively unknown risk of smoking hookah. Dozens of cases of hookah-associated carbon monoxide toxicity have been described over the past decades, but smoking hookah is generally perceived as safe. Only recently have larger series of hookah-associated carbon monoxide toxicity been published. This study evaluates the incidence of hookah-associated carbon monoxide toxicity over 4 years, and compares the exposures from hookah against other carbon monoxide sources. Methods: This is a retrospective cohort study of all patients with carbon monoxide toxicity referred for hyperbaric oxygen therapy at an urban hyperbaric oxygen referral center from January 2015 through December 2018. Cases of hookah-associated carbon monoxide toxicity were compared to patients exposed to other carbon monoxide sources, with an analysis of patient comorbidities, symptomatology, and laboratory evaluation. Results: Over a 48-month period, 376 patients underwent hyperbaric oxygen therapy for carbon monoxide exposure. After exclusions, 265 patients with carbon monoxide toxicity from various sources were analyzed. There were 58 patients with hookah-associated carbon monoxide toxicity (22%). The proportion of hookah-associated carbon monoxide cases increased markedly in the latter years: 2015: 9.5%, 2016: 8.6%, 2017: 24.1%, 2018 41.6%. In the final 2 years analyzed, hookah smoking was the most frequent source of carbon monoxide toxicity referred for therapy. Hookah-associated carbon monoxide patients were younger (28.1 vs. 45.0 years, mean difference 16.8 years, 95% confidence interval: 11.5, 22.1 years, p < 0.001) and more likely to be female (60% vs. 46.6%, p = 0.06) than patients exposed to other carbon monoxide sources. The mean difference in carboxyhemoglobin concentration between hookah associated and those exposed to other carbon monoxide sources was 4.6% (mean 20.1% vs. 24.6%, 95%CI: 1.7, 7.5, p = 0.002). Conclusion: A substantial portion of patients with severe carbon monoxide toxicity was exposed through smoking hookah. The incidence of hookah-related carbon monoxide toxicity appears to be increasing. [ABSTRACT FROM AUTHOR]

Objectives: The early identification of patients with a high risk of developing delayed neurological sequelae (DNS) can improve the quality of care in carbon monoxide (CO) poisoning cases. The aim of this study is to investigate whether the serum netrin-1 levels measured at presentation to the emergency department (ED) predicted the development of DNS after acute CO intoxication. Methods: This prospective observational study was conducted between 1 August 2018 and 31 July 2019 in a single tertiary hospital. The patients with acute CO intoxication and serum netrin-1 levels measured at the time of ED presentation were included in the study. All patients were followed up for six weeks regarding the development of DNS. The patients were divided into two groups, including those who developed DNS (DNS group) and those who did not (non-DNS group). Results: A total of 183 patients were included in the study, and 54 (29.5%) developed DNS. The median serum netrin-1 level at ED presentation was significantly lower in the DNS group (391.5 pg/mL [263.0–550.5]) than in the non-DNS group (626.0 pg/mL [505.9–755.6]) (p <.001). Multivariate analysis revealed that a low serum netrin-1 level (adjusted odds ratio [AOR]: 8.02, 95% CI: 2.45–26.20), low Glasgow coma scale (GCS) score at ED presentation (AOR: 0.81, 95% CI: 0.68–0.97), long CO exposure time (AOR: 1.96, 95% CI: 1.49–2.56), and the presence of acute brain lesions (AOR: 8.24, 95% CI: 2.37–28.58) on diffusion-weighted imaging were independent predictors of DNS. Serum netrin-1 levels less than 432 pg/mL predicted the development of DNS with a sensitivity of 68.5% (95% CI: 54.4%-80.5%) and a specificity of 86.0% (95% CI: 78.8%-91.5%). Conclusions: Low serum netrin-1 levels were significantly associated with the development of DNS. Therefore, serum netrin-1 at ED presentation can help identify patients at risk of developing DNS following discharge. [ABSTRACT FROM AUTHOR]

Objective: Preterm infants are prone to increased bilirubin burden and display adverse outcomes if left unmonitored; therefore, predicting an increased bilirubin production is of paramount importance.Methods: We aimed to evaluate carboxyhemoglobin (COHb) levels in moderate (GA: 320/7-336/7) and late preterm (GA: 340/7-366/7) infants to assess whether this molecule could be used as an early predictor of phototherapy requirement.Results: A total of 221 infants were enrolled in the study. On admission, carboxyhemoglobin levels of infants who received phototherapy were significantly higher than that of infants who did not require this treatment, and this difference persisted in the consecutive hours (median (min-max): 1.2% (0.3-1.7) versus 0.8% (0.4-1.1); p < .001). The initial and consecutive COHb levels showed positive correlation (r = 0.77, p < .001). In the post-hoc analysis, direct antiglobulin test positivity significantly affected phototherapy requirement (p < .001). Receiver operating characteristics analysis showed that a COHb level of ≥0.95% was found to have a sensitivity of 90% and a specificity of 88%. Multinomial logistic regression analysis demonstrated that high COHb levels on admission significantly increased the likelihood of phototherapy requirement when adjusted for covariants (adjusted odds ratio: 2.2; 95% confidence interval: 1.4-3.5; p < .001).Conclusion: Carboxyhemoglobin measurement can be simply used to predict preterm infants who will require phototherapy. [ABSTRACT FROM AUTHOR]

Objective: This study aimed at assessing the serial carboxyhemoglobin (COHb) levels in preterm infants during the first week of life and their variation with late-onset sepsis (LOS). Study Design: Infants with <37 gestational weeks were categorized into two groups according to the presence of culture proven LOS. Serial COHb levels were obtained during the first week of life, at the onset of the LOS episode, and upon blood culture negativity with response to antibiotics. Result: Overall 207 infants were enrolled. A LOS episode resulted in a significant increase in COHb levels (p < 0.001), which decreased to normal levels when the blood cultures were sterile (p < 0.001). At a cut of level of 1.35% COHb had a sensitivity of 56% and a specificity of 90% to confirm LOS (p < 0.001). Conclusion: In this study, we demonstrated an increase in COHb levels at the onset of LOS and a decrease with response to antibiotherapy. [ABSTRACT FROM AUTHOR]

Aims: We investigated the relationship between total serum bilirubin (TSB) and carboxyhemoglobin (COHb) in term neonates with detected and treated hemolysis within a particular time frame with the aim of augmenting the case for early diagnosis and prevention of morbidity in hemolysis. Materials and Methods: The study group comprised term newborns who were above the 95th percentile for TSB, underwent intravenous immunoglobulin (IVIG) or applied total exchange transfusion due to hemolysis. Newborns without hemolysis who were above the 95th TSB percentile and required phototherapy comprised the control group. Results: At a cutoff COHb value of 2.2%, 80.8% sensitivity, 95.5% specificity, 18.1 likelihood ratio, positive predictive value of 94.7%, and negative predictive value of 83.2% were identified. Conclusion: We found that COHb is a sensitive and specific method for detecting hemolysis, and it can be used in the early diagnosis of hemolytic diseases causing early and severe hyperbilirubinemia. [ABSTRACT FROM AUTHOR]

The effect of CO2 gas-stunning methods (G1: 30% CO2 15 sec, 55% CO2 40 sec, 70% CO2 45 sec; G2: 30% CO2 15 sec, 80% CO2 85 sec) on the efficacy of stunning, blood stress indicators and meat quality of turkeys were assessed. A total of 375 turkeys (125 heavy males, 125 light males, and 125 light females) were used. After stunning, clinical parameters (posture-loss, wing-flapping, breathing, response to toe-pinching, eye movements, and palpebral, corneal and pupillary reflexes) and glucose, lactate and cortisol levels were assessed. The G2 method showed a higher percentage of correctly stunned birds (81.3 vs. 70.7%) and lower cortisol levels (0.44 vs. 1.22 g/dL). The weight and sex had a significant influence on the behavioral and physiological responses after stunning. The G2 method was found to be acceptable for animal welfare during stunning, based on both the percentage of animals correctly stunned and dead (92% to 100%) and the blood cortisol level after stunning. [ABSTRACT FROM AUTHOR]

Objective/Background: Sleep disturbances are considered among the negative consequences of smoking. However, the relationship between sleep quality and smoking among young adults, a population in which the prevalence of smoking is highest, has scarcely been examined. The current study aimed at examining differences in sleep indices, assessed by both subjective and objective (actigraphy) measures, between smokers and nonsmokers, and whether such differences are associated with levels of nicotine dependence. Participants: Eighty-six young (19–28 years old) volunteers, of them 46 nonsmokers (69.6% women) and 40 regular smokers (70.0% women) smoking at least 10 cigarettes a day. Methods: The participants completed the State-Trait Anxiety Inventory, Beck Depression Inventory, Brief Questionnaire on Smoking Urges, the Fagerstrom Test for Nicotine Dependence, and the Pittsburgh Sleep Quality Index. Their sleep was monitored objectively for one week using an actigraph. Results: Smokers' self-reported sleep quality was similar to that of nonsmokers. However, actigraphy data pointed to lower sleep continuity in smokers compared to nonsmokers as reflected by increased wake time after sleep onset (Mean ± SD: 18.56 ± 15.29 vs. 11.21 ± 11.19, p <.01) and decreased sleep efficiency (Mean ± SD: 95.63 ± 3.53 vs. 97.23 ± 2.62, p <.012). Total sleep time and sleep onset latency did not differ between the groups. Notably, severity of nicotine dependence was negatively associated with sleep efficiency (β = −.32; p <.05). Conclusion: Young adult smokers have lower sleep continuity without necessarily subjectively experiencing their sleep as poor. Nevertheless, their lower sleep continuity is related to their level of nicotine dependence. [ABSTRACT FROM AUTHOR]

The aim of this study was to identify whether or not the dual users of conventional cigarettes and e-cigs were naturally reducing the amount of their cigarette smoking while they were using e-cigs, and whether their urine cotinine level became similar or less compared to conventional cigarette-only smokers. We used data from the Korean National Health and Nutrition Examination Survey (KNHANES), a nationally representative sample collected in 2014-2016. We selected 2,442 participants who were over 19 years old and were current users of conventional cigarettes and e-cigs. Among the total sample, 12.8% were dual users of e-cigs and conventional cigarettes. Conventional cigarette-only users smoked 14.26 (±23.19) cigarettes a day, while dual users of electronic and conventional cigarettes smoked 14.46 (±7.88) cigarettes a day (p < .001). Means of urine cotinine level in conventional cigarette-only users and dual users were 1250.35 ng/mL (±832.75) and 1364.95 ng/mL (±827.96), respectively (p < .001). The result of a multiple linear regression analysis identified that dual users' cotinine level was 136.80 ng/mL higher, compared to conventional cigarette smokers' one (p = .011). Unlike the argument that e-cigs can be used as a smoking cessation aid, we found that using e-cigs might be less likely to support quitting smoking or reducing cigarette consumption. [ABSTRACT FROM AUTHOR]

Carbon monoxide (CO) exposure levels encountered by wildland firefighters (WLFs) throughout their work shift can change considerably within a few minutes due to the varied tasks that are performed and the changing environmental and fire conditions encountered throughout the day. In a U.S. Forest Service study during the 2009–2012 fire seasons, WLFs from 57 different fires across the U.S. were monitored for CO using CO data-logging detectors while an observer recorded worker tasks, fire characteristics, and environmental conditions at scheduled intervals. Exposures to CO for 735 WLF's work shifts were analyzed to assess the effect of variations among work tasks, fire characteristics, and environmental conditions. Geometric mean full shift time-weighted averages were low at 2.4 parts per million (ppm) and average length of work shift was 11 hr and 15 min. The task with the highest mean CO exposure was sawyer/swamper at 6.8 ppm; workers performing that task had an estimated 9 times higher odds of a having a 1-min CO measurement exceeding 25 ppm than the referent pump task (OR = 8.89, 95% CI = 1.97, 40.24). After adjusting CO exposure limits for shift length, elevation, and work level, 2% and 4% of the WLF's work shifts exceeded the National Institute for Occupational Safety and Health's recommended exposure level and the American Conference of Governmental Industrial Hygienist's threshold limit value, respectively. In regression modeling, variables that were significantly associated with elevated levels of CO exposure included: task, fuel model, wind orientation, crew type, relative humidity, type of attack, and wind speed. In the absence of instruments such as CO detectors that can determine and alert WLFs to elevated CO levels, recognition of the conditions that lead to elevated levels of CO exposure can assist WLFs to effectively use administrative controls, such as work rotations, to minimize exposures. [ABSTRACT FROM AUTHOR]

Hypoxia drives sickle cell disease (SCD) by inducing sickle cell haemoglobin to polymerize and deform red blood cells (RBC) into the sickle shape. A novel carboxyhaemoglobin-based oxygen carrier (PEG-COHb; PP-007) promotes unsickling in vitro by relieving RBC hypoxia. An in vivo rat model of vaso-occlusive crisis (VOC) capable of accommodating a suite of physiological and microcirculatory measurements was used to compare treatment with PEG-COHb to a non-oxygen carrying control solution (lactated ringer's [LRS]). Male Sprague-Dawley rats were anesthetized and surgically prepared to monitor microvascular interstitial oxygenation (PISFO2), cardiovascular parameters and blood chemistry. Human homozygous SCD RBCs were isolated and exchange transfused into the rats until the distal microcirculation of the exteriorized spinotrapezius muscle was hypoxic and RBC aggregates were visualized. VOC was left untreated (Sham) or treated 15 min later with PEG-COHb or LRS and observed for up to 4 h. Treatment with PEG-COHb showed better improvement of PISFO2, end-point lactate, mean arterial pressure and survival duration compared to Sham and LRS. Restoring PISFO2 was associated with relieving the RBC aggregates driving VOC, which then affected other study metrics. Compared to LRS, PEG-COHb's oxygen-carrying properties were key to improved outcomes. [ABSTRACT FROM AUTHOR]

Introduction: Cannabis smoking can result in elevation of heart rate and blood pressure immediately after use, possibly from sympathetic nervous system stimulation and parasympathetic nervous system inhibition. Vascular inflammation, platelet activation, and carboxyhemoglobin generation have also been proposed as potential side effects of cannabis smoking. As such, an association between cannabis use and acute coronary syndrome has been postulated. Objective: The objective of our study was to analyze systematically the medical literature pertaining to this putative association. Methods: PubMed, Google Scholar, and OpenGrey were queried using a unique search string. All human trials, case series, or case reports of cannabis use and acute coronary syndrome in any language were considered in the literature search. The definition of acute coronary syndrome represented a penumbra that included chest pain, angina pectoris, unstable angina, myocardial infarction, myocardial ischemia, and cardiac arrest. Preferred Reporting Items for Systematic Reviews and Meta-analyses (PRISMA) guidelines were followed. Our final search strategy included free-text words (TW): ("cannabis"[TW] OR "marijuana"[TW]) AND ("acute coronary syndrome"[TW] OR "myocardial" OR "ischemia"[TW] OR "infarction"[TW] OR "chest pain"[TW] OR "cardiac arrest"[TW] OR "angina"[TW]). To remain consistent over a span of five decades, we specifically did not include any publications with non-phytogenic, non-smoked cannabis as the sole etiology, as these are relatively recent and may possess additional pharmacologic characteristics compared to phytogenic cannabinoids. Therefore, for the purpose of this review, the term "cannabis" refers to the smoked phytogenic form. The search resulted in 325 articles. References in each selected publication were carefully hand-searched for any additional reports having relevance, and a total of 12 publications were identified in this manner. Following comparison and discussion amongst the co-authors, duplicate and non-relevant publications were removed, and a total of 85 publications involving 541,518 human subjects were selected for inclusion. Results were synthesized and reviewed by the authors for relevance. Clinical trials, observational studies, retrospective studies, case series, and case reports were graded using Oxford Centre for Evidence-based Medicine guidelines. Results: There were no Level I randomized blinded controlled studies specifically addressing the cannabis/acute coronary syndrome association. However, there were five Level I systematic reviews, 14 Level II studies with 83,961 subjects, and 14 Level III studies with 457,495 subjects. Conclusions from 28 of these 33 studies highlighted an increased risk of both acute coronary syndrome and chronic cardiovascular disease from cannabis use. The systematic reviews were wide-ranging in topic and scale, and none specifically focused on the association between cannabis use and acute coronary syndrome. The dissenting studies included two systematic reviews, one concluding there was limited and weak evidence for association of cardiovascular disease and acute coronary syndromes with cannabis use, and another citing the evidence was inconclusive. The other dissenting articles were two longitudinal prospective studies and a retrospective review concluding cannabis users had lower post-myocardial infarction mortality. There were 51 case series (Level IV) and case reports (Level V) with 62 subjects. Six cases were female (10%). Average age was 31 ± 12 years, reported maximum heart rate was 88 ± 21 bpm, systolic blood pressure was 125 ± 32 mmHg, and diastolic blood pressure was 80 ± 17 mmHg. ST-segment elevation was documented on 37 (60%) electrocardiograms, and the most common angiographic finding was left anterior descending coronary arterial occlusion and/or stenosis in 22 (35%) patients. Concomitant cardiomyopathy was described in 21 (34%) cases. There were 14 (23%) deaths attributed to acute coronary syndrome associated with cannabis use. Conclusion: There were five Level I systematic reviews, 14 Level II studies with 83,961 subjects, and 14 Level III studies with 457,495 subjects. All but five Level I–III publications highlighted an increased risk of both acute coronary syndrome and chronic cardiovascular disease associated with cannabis use. [ABSTRACT FROM AUTHOR]

Purpose: Nonconventional vapor products (NVP), designed to reduce exposure to cigarette smoke toxicants (CSTs), could cause changes in biomarkers of potential harm (BoPH). Although, NVPs reduced CSTs exposure compared to conventional cigarettes (CC), the changes in the BoPH values varied among the studies. Hence, further information on BoPH using NVPs is needed. Material and methods: The data of two similarly designed studies using a kind of NVP, a noncombustion and nonheating inhaler type of smokeless tobacco product (NCIT) used under 31-day confinement, were pooled, and the differences in 15 BoPH between smokers and nonsmokers at baseline and between the 1 mg tar CC (CC1) group and NCIT group at Day 28/29 were analyzed. Results: At baseline, the levels of eight BoPH (red blood cells, white blood cells, 8-epi-prostaglandin F2α, 8-hydroxy-2′-deoxyguanosine, malondialdehyde, 11-dehydrothromboxane B2, total cholesterol and glucose) were significantly different between smokers and nonsmokers. At Day 28/29, the levels of six BoPH were significantly different between NCIT and CC1 (8-epi-prostaglandin F2α, malondialdehyde, 11-dehydrothromboxane B2: CC1 > NCIT, total bilirubin, low-density lipoprotein cholesterol and total cholesterol: CC1 < NCIT). Conclusions: Reduced exposure to CSTs has favorable effects on BoPH associated with oxidative stress, antioxidant capacity and platelet activation/coagulation but not in lipid metabolism. [ABSTRACT FROM AUTHOR]

Background: Acute carbon monoxide poisoning is a common environmental emergency worldwide. Treatment options are limited to normobaric oxygen therapy with a nonrebreather face mask or endotracheal tube and hyperbaric oxygen. The aim of this study is to determine the half-life of carboxyhemoglobin (COHb) in adult patients admitted to the emergency department with acute carbon monoxide poisoning receiving high flow nasal cannula (HFNC) oxygen. Device tolerability and patient comfort with the high flow nasal cannula were also evaluated. Methods: This study was conducted between January 2017 and February 2018 in two academic emergency departments. Venous blood samples were obtained at 10 minute intervals to determine the rate of elimination of COHb. Patient comfort was evaluated by a verbal numeric rating scale. The primary outcome was the determination of the half-life of COHb. The secondary outcome was device tolerability and patient comfort with the high flow nasal cannula oxygen delivery system. Results: A total of 33 patients were enrolled in the study. The mean baseline COHb level of the patients was 22.5% (SD 8%). The mean half-life of carboxyhemoglobin was determined as 36.8 minutes (SD 9.26 min) with high flow nasal cannula oxygen. COHb levels were halved during the first 40 minutes in 22 (67%) of the study patients. Twenty of the patients receiving HFNC oxygen did not report intolerance or discomfort. Among the 11 patients who requested a change in the flow rate, the median verbal numeric rating score was 7. After decreasing the flow rate, the median verbal numeric rating score was 9. Conclusion: High flow nasal cannula oxygen is an easy, safe, comfortable and effective method to reduce COHb. HFNC may be a promising alternative method if it is validated as effective in future studies with clinical outcomes. [ABSTRACT FROM AUTHOR]

Objective:Waterpipe smoking may increasingly account for unintentional carbon monoxide poisoning, a serious health hazard with high morbidity and mortality. We aimed at identifying waterpipe smoking as a cause for carbon monoxide poisoning in a large critical care database of a specialty care referral center. Methods:This retrospective cohort study included patients with a history of exposure to waterpipe smoking and carbon monoxide blood gas levels >10% or presence of clinical symptoms compatible with CO poisoning admitted between January 2013 and December 2016. Patients’ initial symptoms and carbon monoxide blood levels were retrieved from records and neurologic status was assessed before and after hyperbaric oxygen treatment. Results:Sixty-one subjects with carbon monoxide poisoning were included [41 males, 20 females; mean age 23 (SD ± 6) years; range 13–45] with an initial mean carboxyhemoglobin of 26.93% (SD ± 9.72). Most common symptoms included syncope, dizziness, headache, and nausea; 75% had temporary syncope. Symptoms were not closely associated with blood COHb levels. Conclusion:CO poisoning after waterpipe smoking may present in young adults with a wide variability of symptoms from none to unconsciousness. Therefore diagnosis should be suspected even in the absence of symptoms. [ABSTRACT FROM PUBLISHER]

Heme oxygenase (HO) is an essential, rate-limiting protein which catalyses the breakdown of heme to iron, carbon monoxide (CO), and biliverdin. The alpha methene bridge of the heme is eliminated as CO which can be measured as blood carboxyhaemoglobin (COHb). Using blood concentrations of COHb as a measure reflecting HO activity, we tested the postulate that the activity of HO changes with exercise. Ten healthy, nonsmoking volunteers (5 females and 5 males with a mean age ± standard deviation of 25.7 ± 3.2 years), lifetime nonsmokers with no history of respiratory diseases and not taking any medication, were included in the study. Subjects were exposed to filtered air for 2 hrs while alternating exercise for 15 minutes on a cycle ergometer with rest for 15 minutes. Workload was adjusted so that subjects breathed at a ventilatory rate, normalised for body surface area, of 25 L/m2/minute. Immediately before, immediately after, and the day following exercise, blood was drawn by standard venipuncture technique. COHb was determined using the interleukin (IL) 682 Co-Oximeter (Instrumentation Laboratory, Bedford, MA). COHb increased in each participant during the exercise session with the mean value (± standard deviation) almost doubling (1.1 ± 1.6 to 2.1 ± 1.6%) and returned to baseline by the following day (1.3 ± 1.3%). We conclude that exercise increases HO activity. [ABSTRACT FROM AUTHOR]

Introduction:Installation of ventilated cookstoves has been shown to improve 24-h carbon monoxide (CO) and particulate exposure in the Guatemalan highlands. However, a survey of villagers around San Lucas Tolimán found much higher than expected CO levels. Our purpose is to evaluate the effects of improved cookstoves on CO levels in these villagers.Methods:This is cross sectional observational study in six rural communities. Blood carboxyhemoglobin (SpCO) was measured at three different times during the day. Stove type and location, as well as any respiratory, eye, or general symptoms reported were recorded.Results:122 patients were included. CO levels were much higher than would be expected in a non-smoking population, with an average level of 4.6 ± 2.3 percent. There was no significant correlation in CO level and stove type or in CO level and time of day. Reported frequency of respiratory and eye symptoms (dyspnea,p = 0.03; cough,p = 0.01; burning eyes,p = 0.001; and excessive tearing,p = 0.001) did vary significantly between improved and unimproved stove groups.Conclusion:This study found high average SpCO levels in all villagers. This suggests that some contributor other than cookstoves may be an additional driver of individual CO exposure in this area. [ABSTRACT FROM PUBLISHER]

Carbon monoxide (CO) increases middle cerebral artery mean flow velocity (MCAVmean), but the effect of CO on the near-infrared spectroscopy (NIRS) determined cerebral oxygenation (ScO2) is not detailed. In our study, 11 non-smoking subjects breathed 100% O2through a closed circuit. A CO2scrubber with CO (1.5 mL kg−1) was added to the circuit. Two NIRS systems (NIRO-200NX and INVOS-5100) assessed ScO2as the ratio of oxygenated to deoxygenated hemoglobin, while venous blood samples were analyzed for carboxyhemoglobin (COHb). After CO/O2rebreathing COHb increased to 8.7% (IQR; 7.9–9.4;p = .004) vs. normoxia, but MCAVmeanremained stable (55.6 cm s−1; 53.1–69.7) compared to inhalation of O2(54.6 cm s−1; 48.4–62.9;p = .178) and normoxia (54.1 cm s−1; 44.5–66.9;p = .055). Also, INVOS-5100 determined ScO2increased during CO/O2(74.4 ± 7.5%) and O2inhalation (73.1 ± 7.2%) compared to normoxia (68.9 ± 6.9%;p < .001). In contrast, NIRO-200NX determined ScO2remained unchanged during CO/O2and O2inhalations but oxygenated and deoxygenated hemoglobin decreased (by 19.7 μM (median; IQR 2.8–34.8;p = .016) and 37.3 μM (30.8–46.6;p = .004), respectively) during inhalation of CO/O2compared to inhalation of O2. Therefore, NIRO-200NX determined ‘total’ hemoglobin (sum of O2Hb and HHb) decreased (by 62.1 μM; 44.5–78.2;p = .001). In conclusion, exposure to CO did not increase MCAVmean, and neither NIRO-200NX nor INVOS-5100 detected a change in ScO2when CO was added to inhalation of oxygen. Unaffected ScO2after exposure to CO reflected a similar decrease in oxygenated and deoxygenated hemoglobin suggesting that detection of exposure to CO by NIRS should focus on ‘total’ hemoglobin rather than on ScO2. [ABSTRACT FROM PUBLISHER]

To describe predictors for severe carbon monoxide (CO) poisoning in children due to coal stove. Patients (n = 176) were divided into two groups retrospectively: severe and mild-moderate clinical presentation. Forty-two patients received hyperbaric oxygen (HBO) therapy. No patient died. pH < 7.30 (p = 0.030; OR:1.0211), carboxyhemoglobin (COHb) (p= 0.002; OR:1.0558), and mean platelet volume (MPV) (p = 0.004; OR:1.4695) were significantly different between the groups. COHb > 20%, (AUC: 0.691) was comparable to those for pH (AUC: 0.536) and MPV (AUC: 0.639) (p > 0.05) in ROC analysis. Although COHb, pH and MPV were poor predictors for severe manifestations, performance of MPV was similar to the COHb and pH levels. [ABSTRACT FROM AUTHOR]

Purpose: This study aimed to investigate whether increased carboxyhemoglobin (COHB) levels and ECG changes, which associated with fatal ventricular dysrhythmias, including increased QT, P-wave and T peak (Tp)-Tend (Te) dispersion, can be detected after smoking narghile, which is a traditional method of smoking tobacco that is smoked from hookah device. Materials and methods: After local ethics committee approval, this prospective study was conducted using healthy volunteer subjects at a “narghile café,” which is used by people smoking narghile in an open area. Before beginning to smoke narghile, all subjects’ 12-lead electrocardiographs (ECG), measurements of COHB levels, and vital signs were recorded. After smoking narghile for 30 min, the recording of the 12-lead ECGs and the measurements of COHB level and all vital signs were repeated. Results: The mean age of subjects was 26.8 ± 6.2 years (min-max: 18–40), and 28 subjects (84.8%) were male. Before smoking narghile, the median value of subjects’ COHB levels was 1.3% (min-max: 0–6), whereas after smoking, the median value of COHB was 23.7% (min-max: 6–44), a statistically significant increase (p < 0.001). Analysis of the subjects’ ECG changes after smoking narghile showed that dispersions of QT, QTc, P-wave and Tp-Te were increased, and all changes were statistically significant (p < 0.001 for all parameters). Conclusion: Although, especially among young people, it is commonly thought that smoking narghile has less harmful or toxic effects than other tobacco products. The results of this study and past studies clearly demonstrated that smoking narghile can cause several ECG changes - including increased QT, P-wave and Tp-Te dispersion - which can be associated with ventricular dysrhythmias. [ABSTRACT FROM AUTHOR]

Context: The inhalation of carbon monoxide produced by the incomplete combustion of carbon remains a popular method of suicide. A much less common method of producing carbon monoxide for suicide is by mixing formic and sulfuric acids. Case details: We describe a patient who attempted suicide by mixing formic and sulfuric acids. He presented with a depressed level of consciousness, chemical burns of his airway and skin, and respiratory distress. He was found to have a metabolic acidosis, a carboxyhemoglobin of 36.8%, hyperkalemia, and rhabdomyolysis. His hospital course was notable for copious pulmonary secretions and hypoxia, but he ultimately recovered with supportive care. Discussion: The case highlights the potential toxicity, particularly from inhaled carbon monoxide and formic acid, with this method of suicide. [ABSTRACT FROM AUTHOR]

In August 2013, the North Carolina Division of Public Health investigated a carbon monoxide (CO) exposure on a farm. Two employees were overcome by CO and lost consciousness while using a propane-powered forklift to load produce into a refrigerated trailer backed up to a warehouse. One employee died, and the second employee was admitted to the hospital for hyperbaric oxygen treatment. Eighteen people, ranging in age from 18 to 69 years, were potentially exposed to CO, including the two employees, a family member who discovered the employees, two bystanders who stopped to offer assistance, and 13 first responders. Thirteen people who assisted in the emergency response experienced symptoms such as headache and dizziness, and all 16 who assisted were evaluated in a local hospital emergency department and released after receiving 100% oxygen. Blood tests showed five people (the two employees, family member, and two bystanders) had elevated blood carboxyhemoglobin levels, but all first responders had levels within normal range. Firefighters measured a peak CO concentration of 2214 parts per million in the warehouse. The North Carolina Division of Occupational Safety and Health investigated and determined that the forklift, operated inside the trailer with no ventilation, was the source of the CO. Public health investigation activities included interviewing responders, obtaining ambient CO concentration measurements from the fire department, advising the local health director, reviewing medical records, and developing a line listing of exposed persons. To prevent CO poisoning, employers should consider replacing gas-powered equipment with electric equipment, which does not produce CO. [ABSTRACT FROM AUTHOR]

Objectives: To evaluate carboxyhemoglobin (COHb) values measured with a CO-oximeter (Roche-cobas b 221) in jaundiced newborns with or without hemolysis and healthy controls in order to assess whether COHb measurement determined with a CO-oximeter could be used as an indicator of hemolysis in newborns with ABO alloimmunization.Methods: A total of 86 term newborn infants were prospectively studied. The study cohort consisted of three subgroups: 18 infants with ABO HDN, 21 infants with hyperbilirubinemia without hemolytic disease who required phototherapy, and 47 healthy controls. The COHb, bilirubin, and Hb levels were measured.Results: The three subgroups did not differ significantly with respect to birth weight, gestational age, gender, Apgar score, or mode of delivery. The ABO HDN infants had significantly higher COHb values than the healthy controls (median 2.4% versus 1.3%, p < 0.0005) and the group with hyperbilirubinemia without hemolytic disease (median 2.4% versus 1.3%, p < 0.0005), although the infants with hyperbilirubinemia without hemolytic disease did not have significantly higher COHb values compared with the healthy controls. The cut-off value of 1.7% COHb had 72% sensitivity and 97% specificity for confirming hemolysis in ABO alloimmunization.Conclusions: Our data show that COHb values determined with CO-oximeters are higher in newborns with hemolysis than in those without hemolysis. COHb measured with CO-oximeters could be used to confirm hemolysis in infants with ABO alloimmunization. [ABSTRACT FROM AUTHOR]

The levels of the inactive hemoglobin (Hb) pigments [such as methemoglobin (metHb), carboxyhemoglobin (HbCO) and sulfohemoglobin (SHb)] and the active Hb [in the oxyhemoglobin (oxyHb) form] as well as the blood Hb concentration in healthy non pregnant female volunteers were determined using a newly developed multi-component spectrophotometric method. The results of this method revealed values of SHb% in the range (0.0727–0.370%), metHb% (0.43–1.0%), HbCO% (0.4–1.52%) and oxyHb% (97.06–98.62%). Furthermore, the results of this method revealed values of blood Hb concentration in the range (12.608–15.777 g/dL). The method is highly sensitive, accurate and reproducible. [ABSTRACT FROM AUTHOR]

As has been known for over a century, oxygen binding onto hemoglobin is influenced by the activity of hydrogen ions (H+), as well as the concentration of carbon dioxide (CO2). As is also known, the binding of both CO2 and H+ on terminal valine-1 residues is competitive. One-parametric situations of these hemoglobin equilibria at specific levels of H+, O2 or CO2 are also well described. However, we think interpolating or extrapolating this knowledge into an 'empirical' function of three independent variables has not yet been completely satisfactory. We present a model that integrates three orthogonal views of hemoglobin oxygenation, titration, and carbamination at different temperatures. The model is based only on chemical principles, Adair's oxygenation steps and Van't Hoff equation of temperature dependences. Our model fits the measurements of the Haldane coefficient and CO2 hemoglobin saturation. It also fits the oxygen dissociation curve influenced by simultaneous changes in H+, CO2 and O2, which makes it a strong candidate for integration into more complex models of blood acid-base with gas transport, where any combination of mentioned substances can appear. [ABSTRACT FROM AUTHOR]

Despite the lack of evidence, many reports exist which have implied that smokers inhale low-yield cigarette smoke more deeply than that of high-yield cigarettes. The objective of this study was to investigate the effect of short-term switching between smoker's own brand and test cigarettes with different smoke yields on puffing topography, respiratory parameters and biomarkers of exposure. Participants were randomly assigned to smoke either a Test Cigarette-High Tar (TCH), for two days, and then switched to a Test Cigarette-Low Tar (TCL), for two days or the reverse order ( n = 10 each sequence). Puffing topography (CReSS microdevice), respiratory parameters (inductive plethysmography) and biomarkers of exposure (BOE, urinary nicotine equivalents - NE and blood carboxyhemoglobin - COHb) were measured at baseline and on days 2 and 4. The average puffs per cigarette, puff volume and puff durations were statistically significantly lower, and inter-puff interval was significantly longer for the TCH compared to the TCL groups. Respiratory parameters were not statistically significantly different between the TCH and TCL groups. Post-baseline NE and COHb were statistically significantly lower in the TCL compared to the TCH groups. Under the conditions of this study, we found no indication of changes in respiratory parameters, particularly inhalation time and volume, between study participants smoking lower versus higher yield cigarettes. Likewise, the BOE provides no indication of deeper inhalation when smoking low- versus high-yield cigarettes. These findings are consistent with the published literature indicating smoking low-yield cigarettes does not increase the depth of inhalation. [ABSTRACT FROM AUTHOR]

Context: Carbon monoxide (CO) poisoning is the most common form of accidental lethal poisoning and is associated with a risk of brain damage in survivors. Objective: The goal of this study was to examine whether Tau protein or S100B protein may be used as a biomarker for acute brain dysfunction. Materials and methods: The determination of Tau and S100B proteins was performed in serum samples collected from 27 CO-poisoned patients and 12 healthy volunteers. Results: The level of Tau protein in the serum of patients (444±227ng L-1) differed significantly compared with those in the healthy controls (240 ±61 ng L-1) and correlated with the level of carboxyhemoglobin. A higher concentration of Tau protein was found in patients who had lost consciousness during CO exposure. The concentration of S100B in the serum of CO-poisoned subjects (0.08 ± 0.03 µg L-1) was not statistically different from values obtained for the controls (0.07± 0.02 µg L-1). Conclusion: CO poisoning appears to be associated with an elevated level of Tau and S100B proteins in the serum of patients who had suffered a loss of consciousness. The study has shown that Tau protein is a more sensitive biomarker than SI OOB protein for the earlier stage of neurotoxic effects of CO intoxication. [ABSTRACT FROM AUTHOR]

Context. Pre-hospital administration of hydroxocobalamin (B12a) is used for empiric treatment of cyanide poisoning because cyanide poisoning is difficult to identify and requires immediate treatment. B12a interferes with the accuracy of several blood laboratory tests. This study aimed to explore how B12a affects carboxyhemoglobin (COHb) measurements in human blood at both physiologic and pathologic COHb levels. Methods. Several clinically relevant concentrations of B12a were added to human blood samples containing physiologic (∼ 3%) and pathologic (30% and 50%) COHb levels. We then measured the COHb levels of the samples using two different co-oximeters, the Radiometer ABL 700 and the Rapidpoint 500, and compared to their actual baseline COHb levels. Results. B12a had minimal effects on the COHb measured at both physiologic and pathologic levels when measured on the Radiometer. In contrast, the Rapidpoint B12a caused a dose-dependent decrease in the COHb measured, especially of pathologic COHb levels (∼ 30 and 50%). Conclusion. The magnitude of B12a interference on measured COHb is dependent upon the specific co-oximeter used, the actual COHb level and the serum B12a concentration. These errors may potentially influence clinical decision making and thus affect patient outcomes. Our findings emphasize the importance of measuring COHb levels on blood samples collected prior to B12a administration. [ABSTRACT FROM AUTHOR]

Fire victims often suffer from burn injury and concomitant inhalation trauma, the latter significantly contributing to the morbidity and mortality in these patients. Measurement of blood carboxyhemoglobin levels has been proposed as a diagnostic marker to verify and, perhaps, quantify the degree of lung injury following inhalation trauma. However, this correlation has not yet been sufficiently validated. A total of 77 chronically instrumented sheep received sham injury, smoke inhalation injury, or combined burn and inhalation trauma following an established protocol. Arterial carboxyhemoglobin concentrations were determined directly after injury and correlated to several clinical and histopathological determinants of lung injury that were detected 48 hours post-injury. The injury induced severe impairment of pulmonary gas exchange and increases in transvascular fluid flux, lung water content, and airway obstruction scores. No significant correlations were detected between initial carboxyhemoglobin levels and all measured clinical and histopathological determinants of lung injury. In conclusion, the amount of arterial carboxyhemoglobin concentration cannot predict the degree of lung injury at 48 hours after ovine burn and smoke inhalation trauma. [ABSTRACT FROM AUTHOR]

Indoor smoke exposure is responsible for two million deaths per year and has been studied globally, but the impacts of exposure have not yet been evaluated in Haiti, the Western hemisphere's poorest nation. This study measures the disproportionate impact of indoor smoke exposure on the women and children of Haiti. We studied 2296 clinic patients in four Haitian villages to determine the extent of carbon monoxide (CO) exposure, using carboxyhemoglobin saturation in the blood as a proxy for overall smoke exposure. We predicted CO levels to be higher in women, who traditionally perform the majority of cooking duties, and in children who accompany their mothers. CO levels averaged 4.9% in women and 3.4% in men. Women of child-bearing age carried a minimum relative risk (RR) for CO exposure of 1.22, relative to all males and younger females. Older females carried no significant difference in risk. Children averaged the lowest CO exposure among all cohorts. These findings demonstrate the burden of indoor smoke exposure that falls disproportionately on women in these regions of Haiti. Global efforts to mitigate indoor exposure have demonstrated the health, economic, environmental and social improvements that are possible by tackling this problem. [ABSTRACT FROM AUTHOR]

Background. Hydrogen cyanide (HCN) is one of the most toxic components of fire smoke, but insufficient attention is paid to its potential role as a cause of injury or death in victims (alive or dead) of enclosed-space fires. Objective. To analyse the prevalence of toxic HCN exposure in fire victims and factors that may influence its toxicity, particularly the co-presence of carbon monoxide (CO) and ethanol. Materials and methods. Blood samples from fire victims and persons rescued from fires were analysed. Results. A positive result for HCN (mean concentration 16.83 mg/l) was detected in blood samples from 169 of 285 fire-related deaths (59%). Ethanol was present in 91 (65%) of 139 samples with coincident presence of HCN and carboxyhaemoglobin (COHb). HCN (mean 4.0 mg/l) was also detected in 20 of 40 (50%) fire survivors. Discussion. The high prevalence of coincident CO and HCN in enclosed-space, fire-related deaths should alert clinicians to suspect toxic HCN exposure in all persons rescued from fire with signs and symptoms of respiratory distress. Conclusions. Medical procedures in persons rescued from enclosed-space fires, especially in the pre-hospital setting, should be augmented to cover the possibility of toxic HCN exposure, particularly in individuals who do not respond to standard supportive therapy. Likewise, post-mortem investigations should routinely include assays for HCN when determining probable cause of death. [ABSTRACT FROM AUTHOR]

Between 60 and 80% of all deaths related to fire are attributed to toxic fumes. Carbon monoxide (CO) is commonly thought to be the major cause. However, hydrogen cyanide (HCN) is also formed. Still, the exact contribution of HCN to fire-related fatalities is unknown. The aim of the study was to investigate the impact of HCN in relation to CO as a cause of death in fire victims. Data on carboxyhemoglobin (COHb) and blood cyanide from deceased fire victims in the period 1992-2009 were collected from two Swedish nationwide forensic databases (ToxBase and RättsBase). The databases contain data on COHb and/or cyanide from 2303 fire victims, whereof 816 on both COHb and cyanide. Nonparametric statistical tests were used. Seventeen percent of the victims had lethal or life-threatening blood cyanide levels (>1 µg/g) and 32% had lethal COHb levels (>50% COHb). Over 31% had cyanide levels above 0.5 µg/g, an indication of significant HCN exposure. The percentages may be underestimates, as cyanide is quickly eliminated in blood also after death. Our results support the notion that HCN contributes more to the cause of death among fire victims than previously thought. [ABSTRACT FROM AUTHOR]

Total haemoglobin mass (Hbmass) can be assessed with low measurement error using carbon monoxide (CO) rebreathing. However, variability in measurement error of Hbmass has been reported across laboratories and it has previously been suggested that CO leaks contribute to this variability. As a result of employing a standardized leak monitoring procedure using two CO detectors, we were able to retrospectively examine the impact of CO leaks on Hbmass values from past test-retest studies in our laboratory using the optimized CO rebreathing method. Test-retest data were collected to determine measurement error, with subjects tested twice within 5 days. Test-retest data were placed into separate categories based on magnitude and duration of CO leak observed during one of the two tests. The No Leak category contained test-retest data in which no leak occurred during either test. The Minor Leak category contained test-retest data in which one of the tests had a CO leak of magnitude less than 30 ppm and less than 5 seconds duration, whereas the Major Leak category included test-retest data in which a leak greater than this magnitude or duration occurred. Measurement error was lowest in the No Leak category (1.9%; 95%CI: 1.6-2.3%; n == 56), approximately doubled in the Minor Leaks category (3.6%; 95%CI: 2.6-6.1%; n == 13), and dramatically increased in the Major Leaks category (9.3%; 95%CI: 6.3-17.6%; n == 10). We recommend careful monitoring of potential CO leaks using multiple detectors. To minimize measurement error, tests in which any CO leak is detected should be excluded. [ABSTRACT FROM AUTHOR]