Environmental stress, erythrocyte dysfunctions, inflammation, and the metabolic syndrome: adaptations to CO2 increases?

In the Western world, the prevalence of the metabolic syndrome is increasing exponentially. Chronic subacute inflammation characterizes the syndrome, suggesting that inflammation might be a common denominator that links obesity to its pathologic sequelae. Potential mechanisms for the activation of inflammation include current air pollution inhalation and/or excess food intake. Both of these environmental factors have, in fact, been shown to promote oxidation followed by the release of proinflammatory cytokines. Potential sources of systemic inflammation include oxidized erythrocytes. Increased exogenous or endogenous CO2 deoxygenates hemoglobin, thereby increasing the fraction of hemoglobin reacting with nitrite to form methemoglobin together with release of superoxide and nitric oxide. These may form peroxynitrite, which may oxidize erythrocytes. Macrophages may then recognize and engulf these cells, thereby releasing proinflammatory cytokines. Therefore, studies should focus on the red blood cell and its proteins to finely target and appropriately treat a world pandemic ominously related to CO2 increases.