Increase In Carbon Monoxide Concentration Research Articles

The influence of canadian forest fires on pollutant concentrations in the united states

High carbon monoxide (CO) concentrations from uncertain origins occurred episodically in the southeastern United States during the summer of 1995. We show that these episodes were caused by large forest fires in Canada. Over a period of 2 weeks, these natural emissions increased CO concentrations in the southeastern United States as well as along the eastern seaboard, a region with one of the world's highest rates of anthropogenic emissions. Within the forest fire plumes, there were also high concentrations of ozone, volatile organic compounds, and aerosols. These results suggest that the impact of boreal forest fire emissions on air quality in the mid-latitudes of the Northern Hemisphere, where anthropogenic pollutant sources have been considered predominant, needs to be reevaluated.

Increased Carbon Monoxide in Exhaled Air of Critically Ill Patients

Heme oxygenase produces carbon monoxide (CO) during breakdown of heme molecules primarily in liver and spleen. Recent data suggest that CO is also produced in the lungs. CO is excreted by exhalation via the lungs. A number of inflammatory agents induce the expression of heme oxygenase, possibly leading to increased CO production. To investigate whether critical illness results in increased CO production we measured the CO concentration in exhaled air in 30 critically ill patients and in healthy controls (n = 6). Critically ill patients showed a significantly higher CO concentration in exhaled air (median 2.4 ppm, 95% CI 1.0–7.0 ppm vs median 1.55 ppm, 95% CI 1.2–1.7 ppm, P = 0.01) as well as total CO production (median 20 ml/min, 95% CI 8 to 90 ml/min vs median 13.5 ml/min, 95% CI 11 to 19 ml/min, P = 0.026) compared to healthy controls. No correlation was found between CO concentration in exhaled air and carboxyhemoglobin concentration in arterial and central venous blood (P > 0.05). The increase of CO concentration in exhaled air in critical illness suggests an induction of inducible heme oxygenase (HO-1) and might reflect the severity of illness.

Humidity Dependence of Carbon Monoxide Oxidation Rate in a Nafion‐Based Electrochemical Cell

In an effort to fabricate cost effective and reliable carbon monoxide sensors, the humidity dependence of the carbon monoxide oxidation rate has been studied. Using a simple electrochemical cell based on the hydrogen form of Nafion® 117 as the electrolyte, the carbon monoxide oxidation rate has been determined to be a linear function of the ambient humidity at room temperature. The oxidation current, or the sensor response has been observed to increase linearly with increasing humidity. The sensor response to carbon monoxide was also found to increase linearly with increasing carbon monoxide concentrations for concentrations less than 200 ppm. The signal to noise ratio was determined to increase from 15.8 to 47.8 with increase in humidity from 12 to 64%.

Inhibition of trichloroethylene oxidation by the transformation intermediate carbon monoxide

Inhibition of trichloroethylene (TCE) oxidation by the transformation intermediate carbon monoxide (CO) was evaluated with the aquifer methanotroph Methylomonas sp. strain MM2. CO was a TCE transformation intermediate. During TCE oxidation, approximately 9 mol% of the TCE was transformed to CO. CO was oxidized by Methylomonas sp. strain MM2, and when formate was provided as an electron donor, the CO oxidation rate doubled. The rate of CO oxidation without formate was 4.6 liter mg (dry weight)-1 day-1, and the rate with formate was 10.2 liter mg (dry weight)-1 day-1. CO inhibited TCE oxidation, both by exerting a demand for reductant and through competitive inhibition. The Ki for CO inhibition of TCE oxidation, 4.2 microM, was much less than the Ki for methane inhibition of TCE oxidation, 116 microM. CO also inhibited methane oxidation, and the degree of inhibition increased with increasing CO concentration. When CO was present, formate amendment was necessary for methane oxidation to occur and both substrates were simultaneously oxidized. CO at a concentration greater than that used in the inhibition studies was not toxic to Methylomonas sp. strain MM2.

Steady-state multiplicity in carbon monoxide oxidation over LaMnO 3

Multiple steady states have been observed during catalytic carbon monoxide oxidation over polycrystalline LaMnO 3. The bistability was noted only at a carbon monoxide partial pressure P co ≥ 46 kPa. The transition to the more reactive state sets in at 220°C. Upon cooling, the activity of the catalyst is sustained at a lower temperature than the ignition point. The width of the hysteresis loop increases with increasing carbon monoxide concentration. An oxidation/reduction mechanism is proposed whereby the high activity state is the surface-reduced form. The apparent activation energy is 16–19 kJ/mol for both steady states of the catalyst, indicating that a similar pathway for carbon monoxide oxidation is followed in the two states.

Carbon monoxide over the Amazon Basin during the wet season

Measurements of carbon monoxide (CO) were made over the Amazon Basin of Brazil during the 1987 wet season as part of the NASA Global Tropospheric Experiment/Amazon Boundary Layer Experiment (ABLE 2B). The distribution of CO over the altitude range sampled (0.15–4.5 km) was influenced by surface emissions from biological sources, long‐range transport of pollutants from northern hemisphere sources, and by transport processes associated with local convective mixing. Surface sources are indicated by a qualitative interpretation of the typical pattern of decreasing concentrations with increasing altitude and increasing concentrations of CO at 0.15‐km altitude during a transect from the Atlantic coast to the central basin. Atmospheric convective activity produced irregular patterns of variability at time scales of less than 1 hour over a localized area. The disruption of mixed layer growth and decay processes has a particularly important influence on CO concentrations in the daytime lower troposphere. Intrusions of northern hemisphere air into the central Amazon resulted in increased CO concentrations in the lower and midtroposphere. The correlation of CO with O3 was positive under conditions interpreted as being influenced by northern hemisphere air, and negative during all other meterological conditions experienced in ABLE 2B.

Development of hypoglycemia is associated with death during carbon monoxide poisoning

A significant fraction of carbon monoxide (CO) poisoning victims die before discovery or rescue. Although survivors usually show normal or elevated blood glucose, data from an animal model now suggest an association between low blood glucose and death during CO poisoning. Hypoglycemia observed during the later stages of CO poisoning in the rat was intensified by increased CO concentration (2,400 ppm, 2,700 ppm, 3,000 ppm) and by the infusion or injection of normal saline, both in survivors and in nonsurvivors, but glucose lowering was especially marked in the latter group. Mortality rate was similarly increased by these two conditions. Based on the change in blood glucose concentration early in CO poisoning, it should be possible to identify survivors and nonsurvivors. Survivors showed a hyperglycemic “rebound” 2 hours after CO. Nonsurvivors tended to maintain a higher body temperature and heart rate, and a relatively smaller decrease in blood pressure during CO exposure, presumably due to a higher metabolic rate. This is possibly a major factor responsible for the rapid lowering of blood glucose concentration. Concurrent administration of ethanol to two to four times the legal intoxication blood level in humans did not alter the severity of CO-induced hypoglycemia in either survivors or nonsurvivors, but did increase survival and exacerbated “rebound” hyperglycemia in survivors. Blood ethanol concentration is elevated by CO poisoning in a dose-dependent manner. The likely mechanisms) underlying CO-induced hypoglycemia, the complicating effect of concurrent ETOH intoxication, and their clinical relevance are discussed.

Heart and lung hypertrophy, changes in blood volume, hematocrit and plasma renin activity in rats chronically exposed to increasing carbon monoxide concentrations.

Changes in blood volume, heart and lung mass and composition and plasma renin activity were examined in two strains of male albino rats inhaling incrementally-increasing concentrations of CO: 250 ppm for 17 days, 500 ppm for 13-14 days, 750 ppm for 10 days, and 1300 ppm for 10 days. Blood volume increased 86% and erythrocyte mass increased 212% at 1300 ppm, while plasma volume was unchanged or decreased slightly. 'Real' hematocrit (hematocrit corrected for plasma trapping) increased from 50% in controls to a peak of 75% at 1300 ppm CO. Wet weight of right ventricle (RV) and combined right and left atria (2A) increased linearly with CO concentration, paralleling changes in blood volume; while real hematocrit increased non-linearly. Left ventricle + interventricular septum (LV + S) wet weight increased less than RV, but more in Sprague-Dawley than in Wistar rats. Plots of RV, LV + S and 2A weight vs real hematocrit showed sharp upward inflections at real hematocrit 65%, suggesting a possible role of increased viscosity in CO cardiomegaly at the higher hematocrit. Assymetric septal hypertrophy was not present. Lung weight increased with CO concentration, but was not due to increased lung blood volume or edema. Hydroxyproline measurements on heart and lung failed to show increased collagen content. Plasma renin activity measured by radioimmunoassay was depressed at 500 ppm, but was normal at 750 and 1300 ppm CO. Neither heart, lung, liver nor plasma renin measurements suggest congestive heart failure, supporting previous studies in the rat with chronic carboxyhemoglobinemia, in spite of enormously increased blood volume, hematocrit and heart weight.

Do older children take in more smoke from their cigarettes? Evidence from carbon monoxide levels.

Expired-air carbon monoxide (CO) concentrations were measured in 125 pupils aged 11-17 years attending a girls' comprehensive school in the South of England who had smoked at least one cigarette on the day of testing. Both number of cigarettes smoked on the day of testing and time since the last cigarette were independently related to CO concentrations. Although there was a positive correlation between age and CO, this disappeared when number of cigarettes smoked on the day of testing and time since the last cigarette were taken into account. Previous reports of increasing CO concentrations with age taking account of cigarette consumption may be due to the use of usual daily cigarette consumption rather than number on the day of testing, which is more relevant given the short half-life of CO in the blood. In this sample, no evidence was found for an increase in smoke inhalation with increasing age.

Soil as a Sink for Atmospheric Carbon Monoxide

The rate of carbon monoxide oxidation by soil increased with increasing carbon monoxide concentration in the gas phase, in line with Michaelis-Menten kinetics. Rates of carbon monoxide oxidation were determined for 20 soils at 0 degrees , 10 degrees , 20 degrees , and 30 degrees C. The observed oxidation rates were used to calculate a global soil uptake rate of atmospheric carbon monoxide of 4.1 x 10(14) grams per year, which is slightly less than the amount of carbon monoxide believed to be produced annually as a result of fossil fuel combustion.

Competitive inhibition of carbon monoxide transport: evidence against a carrier.

The existence of a saturable carbon monoxide (CO) carrier in the lung remains controversial. The carrier hypothesis was invoked to explain data that indicated that pulmonary diffusing capacity for CO (DLCO) decreases with increasing CO concentration. To test this hypothesis, we measured DLCO in 14 normal adult subjects at three alveolar CO concentrations (60, 660, and 2,060 ppm). Each mixture contained a constant amount of labeled C18O (60 ppm) and a balance of unlabeled C16O. If a saturable carrier exists at increasing CO concentrations, the unlabeled CO would compete for most of the sites on the carrier molecule, effectively inhibiting the uptake of the labeled C18O. C18O diffusing capacities (mean +/- SD) for the three levels of CO were 34.9 +/- 5.6, 33.0 +/- 6.0, and 34.7 +/- 7.8. There were no significant differences (P greater than 0.2) among the three levels. In another group of subjects we repeated the study using a gas mixture containing 130 ppm C18O. No significant differences were found. As a result, we find no evidence to support a CO carrier hypothesis.

Correlation between particulate effluent mutagenicity and increased carbon monoxide concentration in a fluidized-bed coal combustor

Correlation between particulate effluent mutagenicity and increased carbon monoxide concentration in a fluidized-bed coal combustor

Carbon monoxide yields of cigarettes and their relation to nicotine yield and type of filter.

Carbon monoxide (CO) yields of 11 popular brands of British cigarette, two types of cigarette containing tobacco-substitute, and one brand of cigar were measured under standardized conditions. Yields of the conventional cigarettes ranged from 5.0 to 20.2 mg per cigarette (1.3 to 4.7% by volume). The cigar yielded 81.7 mg (10.0%) CO and the two semi-synthetic cigarettes 17.2 (4.2%) and 28.2 mg (6.2%) CO. Puff-by-puff analysis showed an increase in CO concentration as a cigarette is smoked. In brands with nicotine yields over 1.0 mg no relationship was apparent between nicotine yield and CO yield, and the filters of cigarettes in this category did not appear to reduce the CO yield. In the low nicotine cigarettes with ventilated filters there appeared to be some correlation between nicotine yield and CO yield, and these filters were highly effective in reducing CO yield, owing mainly to the ventilation. We suggest that official publication of CO yields might motivate manufacturers to produce cigarettes with lower yields.