Indoor-outdoor levels of nitrogen and sulphur species and their relation to air flow in Antigonish, Nova Scotia.

A study was conducted in Antigonish, Nova Scotia, to determine the extent to which acid rain related pollutants are present in indoor ambient air. The pollutant study included: fine (0 to 2.5 micron) and coarse (2.5 to 10 micron) particulates, sulphates, nitrates, acidity (H2SO4 and HNO3), SO2 and NO2. During the 3 1/2 month study, maximum levels of 173n equivalent/m3 fine sulphate and 55 n equivalent/m3 H2SO4 were recorded for outdoor air within the town site compared to corresponding values of 110 n equivalent/m3 and 13 n equivalent/m3 for indoor air. Based on back trajectory analysis, wind direction, and sulphuric acid content, it was postulated that local or medium range pollution sources are predominant in the winter while long range transport originating from the United States produces the major episodes when SW winds are persistent.

The influence of sulfide and cyanide on axonal function.

The absorption of hydrogen sulfide (H2S) gas by sciatic nerve bundles from Rana pipiens produces an anaesthetic effect of short duration. Subsequent compound action potential (CAP) levels are higher than before exposure while the conduction velocity (CV) shows only small variation. Exposure to hydrogen cyanide (HCN) gas produces declining CAP and CV levels. The effect of H2S on the CAP is faster than that of HCN and the recovery time is shorter, although there is evidence of permanent change. Unlike HCN there is no indication that H2S inhibits the energy metabolism of the nerve cells, except possibly when the nerves are exposed to extremely high sulfide concentrations. A mode of action for H2S is proposed.

The effect of sulfide and cyanide on nerve function.

Sciatic nerve bundles from Rana pipiens were immersed in amphibian Ringer containing sulfide or cyanide. Subsequent examination of the compound action potential (CAP) revealed a distinct difference in the effects of these two anions. Whereas cyanide produced a nerve incapable of repeated firings, sulfide-treated nerves displayed an increased CAP which showed no tendency to diminish over extended stimulation periods.

Nitrite as antidote for acute hydrogen sulfide intoxication?

The detoxification of hydrogen sulfide (H2S) by a heme catalyzed oxidation was examined as part of an on-going study of H2S toxicity. Interlocking O2 absorption and sulfide depletion data indicate that both oxyhemoglobin and methemoglobin are effective catalytic agents. Although the latter is more efficacious, the life time of excess sulfide in the presence of oxygen and either of the above is of the order of minutes. It has also been established that the formation of methemoglobin following nitrite administration occurs preferentially under oxygen poor conditions. Under an atmospheric or oxygen enriched environment, which favors sulfide depletion, the nitrite retards sulfide oxidation. Thus nitrite as an antidote for acute H2S intoxication can only be effective within the first few minutes after the exposure, at which time resuscitation and/or ventilation of the victim is likely to produce conditions in which the nitrite actually slows sulfide removal.