Carbon monoxide intoxication continues to be one of the most common causes of morbidity due to poisoning in the United States.1,2 It may be intentional or accidental, and exposure may be lethal. Approximately 600 accidental deaths due to carbon monoxide poisoning are reported annually in the United States,3 and the number of intentional carbon monoxide–related deaths is 5 to 10 times higher.1 The rate of accidental death caused by carbon monoxide from motor vehicles is higher in the northern United States and peaks during the winter months.4 The intentional deaths occur year-round without significant peaks.1 The severe winter of . . .

Carbon Monoxide Poisoning

Glucose-6-phosphate deficiency is the most prevalent enzyme deficiency, with an estimated 400 million people affected worldwide. This inherited deficiency causes neonatal hyperbilirubinemia and chronic hemolytic anemia. Although most affected individuals are asymptomatic, exposure to oxidative stressors such as certain drugs or infection, can elicit acute hemolysis. To characterize the global prevalence of G6PD deficiency, we conducted a systematic review of the G6PD deficiency literature, drawing studies from various databases, including MEDLINE/Pubmed and Biosis. Selected studies included cross-sectional and longitudinal studies published between 1960 and 2008. Additionally, meta-analytic procedures were employed to assess the degree of heterogeneity amongst prevalence estimates and, where appropriate, pool them. The searches yielded a total of 280 prevalence estimates, corresponding to 88 countries. The highest prevalence rates were reported among Sub-Saharan African countries, even after adjusting for assessment method. Meta-analysis revealed a high degree of heterogeneity for regional and global prevalence estimates. This heterogeneity in reported estimates appeared to be due to differences in G6PD deficiency assessment and diagnostic procedures. The magnitude and variation in global, regional, and country-level prevalence rates of G6PD deficiency are of public health import, particularly in planning programs to improve neonatal health and in the distribution of various medications, especially antimalarial drugs, as G6PD deficiency is most prevalent in malaria-endemic areas.

/pdf/the-global-prevalence-of-glucose-6-phosphate-dehydrogenase-ejdrzw5q9l.pdf

The global prevalence of glucose-6-phosphate dehydrogenase deficiency: a systematic review and meta-analysis.

Case reports of sudden death during exertion have not established an association between the sickle-cell trait (hemoglobin AS) and exercise-related death To test this association, all deaths occurring among 2 million enlisted recruits during basic training in the US Armed Forces in 1977 to 1981 were classified from autopsy and clinical records as non-sudden deaths or as sudden deaths explained or unexplained by preexisting disease On the basis of known numbers of entering recruits (according to race, age, and sex) and published prevalence rates for hemoglobin AS (8 percent for black and 008 percent for nonblack recruits), death rates (per 100,000) were 322 for sudden unexplained deaths, 27 for sudden explained deaths, and 0 for non-sudden deaths among black recruits with hemoglobin AS, as compared with 12, 12, and 07 among black recruits without hemoglobin S and 07, 05, and 11 among nonblack recruits without hemoglobin S Among black recruits the relative risk of sudden unexplained death (hemoglobin AS vs non-hemoglobin S) was 276 (95 percent confidence interval, 9 to 100; P less than 0001), whereas among all recruits this risk was 398 (95 percent confidence interval, 17 to 90; P less than 0001) The relative risk of sudden unexplained death among all recruits increased with age (P less than 004), from 13 (ages 17 to 18) to 95 (ages 26 to 30) We conclude that recruits in basic training with the sickle-cell trait have a substantially increased, age-dependent risk of exercise-related sudden death unexplained by any known preexisting cause

https://www.nejm.org/doi/pdf/10.1056/NEJM198709243171301

Sickle-cell trait as a risk factor for sudden death in physical training.

Thirty percent of a cell’s volume is filled with macromolecules, and protein chemistry in a crowded environment is predicted to differ from that in dilute solution. We quantified the effect of crow...

Protein crowding tunes protein stability.

Carbon monoxide (CO) toxicity is the result of a combination of tissue hypoxia and direct CO-mediated damage at a cellular level, since not all the signs and symptoms presented can be explained only by the formation of carboxyhaemoglobin. Mitochondria, specially the electron transport chain, seem to be the target for CO at a subcellular level. However, the direct effect of CO in individual complexes of the human mitochondrial respiratory chain has not been completely elucidated. We here studied the in vitro effect of CO on individual complexes of the mitochondrial respiratory chain of human mitochondria. We obtained muscle tissue from 10 healthy people who underwent orthopaedic surgery for hip replacement. Isolated mitochondria were incubated for 5 min. under CO concentrations of 50, 100 and 500 ppm. Afterwards, enzymatic activities of individual complexes of the mitochondrial respiratory chain were assessed in vitro and compared with those obtained in basal (synthetic air without CO) conditions. Cytochrome c oxidase (complex IV of the mitochondrial respiratory chain) activity showed a decrease from 836+/-439 nmol/min./mg of mitochondrial protein after air incubation to 670+/-401, 483+/-182, and 379+/-131 nmol/min./mg after 50, 100 and 500 ppm of CO incubation, respectively (20%, 42% and 55% decrease in cytochrome c oxidase activity). This gradual decrease in cytochrome c oxidase was found to be statistically significant (P<0.001). Other complex activities showed no any significant variation. Carbon monoxide is toxic for mitochondria in man, altering the mitochondrial respiratory chain at the cytochrome c oxidase level. This inhibition in cytochrome c oxidase may play a role in the development of the symptoms observed in acute CO poisoning, and in some diseases related to smoking.

https://onlinelibrary.wiley.com/doi/pdf/10.1034/j.1600-0773.2003.930306.x

Carbon Monoxide Specifically Inhibits Cytochrome C Oxidase of Human Mitochondrial Respiratory Chain

The relative affinity constants of hemolysates from individuals with hemoglobins A, S, or AS have been measured at 37 and 26 ° C. Observed values of all hemoglobin types were the same at both temperatures, K 37 = 230, K 26 = 296. Control measurements on whole blood containing Hb A gave values of K 37 = 222. The small but significant difference between K 37 values measured in whole blood and in hemolysates may be a result of the greater increase of MetHb in the hemolysates during the in vitro equilibration.

Relative Affinity of Hemoglobin S and Hemoglobin A for Carbon Monoxide and Oxygen

Results of a survey for the incidence of hemoglobin variants occurring in Navy and Marine Corps black male recruits yielded an observed incidence of sickle cell trait as 8.02%. Sickle cell anemia or sickle cell disease was present in 0.2% of the recruits tested. Automated detection of hemoglobin S by the dithionite solubility test yields incidence results identical to those of hemoglobin electrophoresis. Preliminary testing for hemoglobin S alone is considered adequate for the purposes of occupational health safety but not for purposes of genetic counseling concerning hemoglobin variants. The results of this pilot study led to the introduction of testing all recruits for hemoglobin S at all Naval Training Centers and Marine Corps Recruit Depots.

Screening of military recruits for hemoglobin variants.

A survey was conducted to determine the incidence of erythrocyte glucose6-phosphate dehydrogenase (G6PD) deficiency in Navy and Marine Corps black, male recruits. The incidence of G6PD deficiency in 20,810 recruits was 12.6%. The incidence of G6PD deficiency in individuals with hemoglobin AS trait or hemoglobin AC trait was the same as the incidence in persons with hemoglobin A. Automated testing of large numbers of persons for G6PD deficiency is technically feasible.

https://jamanetwork.com/journals/jama/articlepdf/353450/jama_227_12_024.pdf

Glucose-6-Phosphate Dehydrogenase Deficiency in Military Recruits

Automated analyses for glucose-6-phosphate dehydrogenase (EC 1.1.1.49, GPD) and for hemoglobin S have recently been described. We modified these methods to couple them directly to the sample line of the 15-channel Technicon blood-typing analyzer. Rate of analysis is doubled (to 120 per hour) by using the reverse-washout cycle to decrease sample-to-sample interaction. Savings in reagents and technician time are significant.

Coupling of Glucose-6-Phosphate Dehydrogenase and Hemoglobin S Screening to Automated Determinations of Blood Group and Type

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Relative Affinity of Hemoglobin S and Hemoglobin A for Carbon Monoxide and Oxygen

Screening of military recruits for hemoglobin variants.

Glucose-6-Phosphate Dehydrogenase Deficiency in Military Recruits

Coupling of Glucose-6-Phosphate Dehydrogenase and Hemoglobin S Screening to Automated Determinations of Blood Group and Type