Nitrogen dioxide

CAS RN:10102-44-0

Toxicity Summary

IDENTIFICATION: Nitric oxide is a colorless, odorless gas that is only slightly soluble in water. The main sources of nitrogen oxides (including nitric oxide) emissions are combustion processes. Fossil fuel power stations, motor vehicles and domestic combustion appliances emit nitrogen oxides, mostly in the form of nitric oxide. Nitric oxide can be present at significant concentrations in ambient air and in indoor air. HUMAN EXPOSURE: Human exposure to nitrogen oxides varies from indoors to outdoors, from cities to the countryside, and with the time of day and season. Nitric oxide is readily oxidized to nitrogen dioxide and peroxidation then occurs. Because of the concurrent exposure to some nitrogen dioxide in nitric oxide exposures, it is difficult to discriminate nitric oxide effects from nitrogen dioxide. Nitric oxide functions as an intracellular second messenger modulating a wide variety of essential enzymes, and it inhibits its own production (e.g., negative feedback). Nitric oxide activates guanylate cyclase which in turn increases intracellular cGMP levels. Nitric oxide is acknowledged as an important endogenous second messenger within several organ systems. At certain levels, inhaled nitric oxide concentrations can cause vasodilation in the pulmonary circulation without affecting the systemic circulation. The lowest effective concentration is not established. Information on pulmonary function and lung host defenses consequent to nitric oxide exposure are too limited for any conclusions to be drawn. Relatively high concentrations have been used in clinical applications for brief periods without reported adverse effects. ANIMAL STUDIES: The toxicological database for nitric oxide is small, relative to nitrogen dioxide. It is often difficult to obtain pure nitric oxide in air without some contamination with nitrogen dioxide. Endogenous nitric oxide synthesis occurs by nitric oxide formation from physiological substrate in cells of many of the organ systems such as nerve tissue, blood vessels and the immune system. Nitric oxide may be more potent than nitrogen dioxide in introducing certain changes in lung morphology. In a study examining the effects of nitric oxide on bacterial defenses, there were no statistically significant effects for either sex at any of the time points studied. In vitro data indicate that nitric oxide stimulates guanylate cyclase and leads to smooth muscle relaxation and vasodilation and functional effects on the nervous system. These effects are probably responsible for vasodilation in the pulmonary circulation and an acute bronchodilator effect of inhaled nitric oxide. Nitric oxide has an affinity for heme-bound iron which is two times higher than that of carbon monoxide. This affinity leads to the formation of methemoglobin and the stimulation of guanylate cyclase. Furthermore, nitric oxide reacts with thiol-associated iron in enzymes and eventually displaces the iron. This is a possible mechanism for the cytotoxic effects of nitric oxide. Nitric oxide can deaminate DNA, evoke DNA chain breaks, and inhibit DNA polymerase and ribonucleotide reductase. It might be antimitogenic and inhibit T cell proliferation in rat spleen cells.
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