Record Display for the EPA National Library Catalog


OLS Field Name OLS Field Data
Main Title New Look at Physiologic Respiratory Response to H2S Poisoning.
Author Ammann, H. M. ;
CORP Author Environmental Protection Agency, Research Triangle Park, NC. Environmental Criteria and Assessment Office.
Year Published 1987
Report Number EPA/600/D-87/219;
Stock Number PB87-208344
Additional Subjects Hydrogen sulfide ; Lung ; Cells(Biology) ; Cytochrome oxidase ; Enzymes ; Air pollution effects(Humans)
Library Call Number Additional Info Location Last
NTIS  PB87-208344 Most EPA libraries have a fiche copy filed under the call number shown. Check with individual libraries about paper copy. 06/21/1988
Collation 13p
Ever since Heymans elucidated the controlling role of the carotid bodies in the reflex governing ventilation, researchers have puzzled over the seeming paradox presented by the action of hydrogen sulfide on the nervous system. While the dominant effect is a depression of function, manifested as a paralysis of ventilation and loss of the sense of smell, the neural receptors of the carotid and aortic bodies appear stimulated. The immediate effect of sublethal doses of H2S is on these receptors, resulting in hyperpnea. The paper resolves the paradox by examining the described effect in the light of the cellular mechanism of action of H2S. This poison most rapidly affects the intracellular mitochondical enzyme cytochrome oxidase, interfering with the transfer of electrons and hydrogen ions to oxygen, thus blocking oxidative metabolism. The chemosensors associated with ventilatory control are primarily sensitive to partial pressure (pO2) of oxygen in blood flowing through the carotid sinuses and the aortic arch. Normally hyperpnea is instigated with the pO2 falls into the 60-30 mm Hg range. Halting oxidative metabolism through H2S poisoning has the same effect as a decrease in oxygen supply, so that hyperpnea is the initial response of sublethal H2S intoxication.