Effect of carbon monoxide on exercise performance in chronic obstructive pulmonary disease

doi:10.1016/0002-9343(77)90544-7

The American Journal of Medicine

Volume 63, Issue 6, December 1977, Pages 904-908

https://doi.org/10.1016/0002-9343(77)90544-7 Get rights and content

Abstract

We evaluated the effect of breathing 100 ppm of carbon monoxide versus compressed, purified air for 1 hour on exercise performance in 10 patients with chronic obstructive pulmonary disease in a double-blind, randomized, crossover study. The mean arterial carboxyhemoglobin was 1.48 per cent in the carbon monoxide control period and increased from 1.43 to 4.08 per cent after breathing carbon monoxide (P < 0.001). The mean arterial carboxyhemoglobin level was 1.52 per cent in the air control period and decreased from 1.47 to 1.34 per cent after purified air (P < 0.001). The mean exercise time until marked dyspnea decreased from 218.5 seconds in the carbon monoxide control period to 146.6 seconds after breathing carbon monoxide (P < 0.001). The mean exercise time was 219.9 seconds in the air control period and 221.3 seconds after purified air (P not significant). Breathing 100 ppm of carbon monoxide for 1 hour caused a significant reduction in exercise performance in patients with chronic obstructive pulmonary disease.

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Effects of Traffic-Related Air Pollution on Exercise Endurance, Dyspnea, and Cardiorespiratory Responses in Health and COPD: A Randomized, Placebo-Controlled, Crossover Trial
2022, Chest
Citation Excerpt :
Our finding of reduced exercise tolerance in healthy participants is in agreement with some studies,17,18 but not others.19-21 One previous study in participants with COPD22 showed that exposure to carbon monoxide pollution negatively impacted exercise duration. Unfortunately, comparing our findings with the work of others is difficult because of the heterogeneity in the type, concentration, and size of the pollutant used for exposures; effective dose, duration, and timing of exposure; washout periods; exercise protocols; and participant characteristics, among other factors.
Individuals with COPD have increased sensitivity to traffic-related air pollution (TRAP) such as diesel exhaust (DE), but little is known about the acute effects of TRAP on exercise responses in COPD.
Does exposure before exercise to TRAP (DE titrated to 300 μg/m³ particulate matter < 2.5 μm in diameter [DE₃₀₀]) show greater adverse effects on exercise endurance, exertional dyspnea, and cardiorespiratory responses to exercise in participants with mild to moderate COPD compared with former smokers with normal spirometry and healthy control participants?
In this double-blind, randomized, placebo-controlled, crossover study, 11 healthy control participants, nine former smokers without COPD, and nine former smokers with COPD were separately exposed to filtered air (FA) and DE₃₀₀ for 2 h separated by a minimum of 4 weeks. Participants performed symptom-limited constant load cycling tests within 2.5 h of exposure with detailed cardiorespiratory and exertional symptom measurements.
A significant negative effect of TRAP on exercise endurance time was found in healthy control participants (DE₃₀₀ vs FA, 10.2 ± 8.2 min vs 12.9 ± 9.5 min, respectively; P = .03), but not in former smokers without COPD (10.1 ± 6.9 min vs 12.2 ± 8.0 min, respectively; P = .57) or former smokers with COPD (9.8 ± 6.4 min vs 8.4 ± 6.6 min, respectively; P = .31). Furthermore, significant increases in inspiratory duty cycle and absolute end-expiratory and end-inspiratory lung volumes were observed, and dyspnea ratings were elevated at select submaximal measurement times only in healthy control participants.
Contrary to our hypothesis, it was the healthy control participants, rather than the former smokers with and without COPD, who were negatively impacted by TRAP during exercise.
ClinicalTrials.gov; No.: NCT02236039; URL: www.clinicaltrials.gov
A quantitative risk assessment method based on population and exposure distributions using australian air quality data
1999, Environment International
This paper develops a practical probabilistic method for assessing aggregate population health risks from different types of population exposures. The method consists of calculating the product of two functions: a population-weighted distribution of concentrations and a concentration-response distribution. This operation yields the corresponding aggregated health-risk distribution function. The method can use alternative exposure-response distributions and populations-specific exposure patterns, depending on the context of the assessment. A deterministic sensitivity analysis is included in the methodological aspects of this research. The distributions of concentrations are generated by combining area-specific population densities with atmospheric concentrations for each of the areas where exposure to air pollutants occurs. The exposure-response functions are developed from the literature. The method is exemplified using alternative exposure probabilities to carbon monoxide, nitrogen dioxide, particulate matter (PM₁₀), and exposure-response models developed specifically for these pollutants for assessing health risks, and applied to data from a number of Australian cities. The results, which hold when the functions are monotonic, show single maximum per pollutant, regardless of the choice of exposure and exposure-response distribution. Although those maxima are often below the Australian Air Pollution Standards, there are instances when this is not the case.
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1999, Current Anaesthesia and Critical Care
Carbon Monoxide (CO) is a product of the incomplete combustion of organic materials. It is also produced endogenously in animals by haemoxygenase enzymes. Inducable haemoxygenase is involved in the breakdown of haeme to biliverdin. Constitutive haemoxygenase produces CO at a cellular level, where it acts as a neurotransmitter. It has a role in hyperpolarizing excitable membranes, and appears to be important in the formation and maintenance of memory.
CO intoxication is not uncommon, and may result in a thousand deaths per year in Britain. Most cases are due to deliberate self poisoning or to faulty domestic heating appliances. Two iatrogenic sources have been investigated. Intraperitoneal diathermy in a carbon dioxide atmosphere has not been found to cause dangerous intoxication. Excessive dehydration of carbon dioxide absorbing salts in anaesthetic circuits has been shown to be dangerous.
CO displaces oxygen from oxyhaemaglobin causing tissue asphyxia. In addition, dissolved CO is delivered to tissues where it acts as a cellular poison by binding to cytochrome a3 and blocking the electron transfer of aerobic respiration. Victims of CO poisoning may show an initial recovery, followed by delayed-onset neurological damage. Controversy continues as to whether CO intoxication should be treated by normobaric or hyperbaric oxygen therapy. A body of evidence is accumulating, which suggests that hyperbaric oxygen therapy is more effective, particularly in preventing delayed neurological deterioration.
The effect of nicotine and carbon monoxide on exercise performance in normal subjects
1993, Respiratory Medicine
In a partially blind randomized control study, nine healthy adult men performed progressive sub-maximal exercise tests, either after chewing nicotine chewing gum (4 mg) or breathing carbon monoxide (320 p.p.m.). Neither agent significantly affected exercise performance, despite a mean rise in blood nicotine to 17·0 ng ml⁻¹ during nicotine administration and a COHb rise to 6·9% whilst breathing carbon monoxide. There was a significant rise in heart rate and blood pressure (P <0·01) after nicotine administration.
The reasons for absence of significant effect on cardiovascular or respiratory performance are discussed.
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1990, Journal of Clinical Anesthesia
Carboxyhemoglobin and methemoglobin levels in 312 units of banked blood and their relationship to the duration of storage were determined. The carboxyhemoglobin level decreased as the storage time increased, and its mean was 1.4% ± 2.0% (SD) with a range from 0% to 9.6%. Methemoglobin increased during storage, showing a mean level of 1.6% ± 0.4% and a range from 0.5% to 4.2%. In a separate study, blood drawn, from six volunteers who had smoked two cigarettes each was stored as banked blood for 21 days. The mean initial level of carboxyhemoglobin was 4.4% ± 1.6%, and the mean half-life of carboxyhemoglobin was approximately 47 days. Methemoglobin increased from an initial 1.3% ± 0.2% to 2.4% ± 0.6% at the end of storage. The use of banked blood containing high levels of these abnormal hemoglobins could be a potential risk in critically ill patients.
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1985, Addictive Behaviors
Unobtrusive observations of smoking behavior at four hospital areas designated as no-smoking and two designated as smoking revealed almost total compliance to a revised and stringent smoking control policy. The smoking control policy was a radical departure from the traditional, liberal practices. Of particular importance was the relative absence of complaints from patients and employees following the initiation of the smoking control program. The implications of practical, cost-effective smoking control procedures existing for hospitals are discussed in reference to their liability to protect patients from controllable hazards.

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¹: From the Cardiovascular and Pulmonary Sections, Long Beach Veterans Administration Hospital, and the University of California, Irvine, California.

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Clinical studyEffect of carbon monoxide on exercise performance in chronic obstructive pulmonary disease

Abstract

Circulation

J Biol Chem

Prog Cardiovasc Dis

Prog Cardiovasc Dis

Am J Med

Carboxyhemoglobin caused by smoking non-nicotine cigarettes: effects in angina pectoris

Circulation

Effect of freeway travel on angina pectoris

Ann Intern Med

Effects of low concentrations of carbon monoxide. Myocardial and systemic responses to carboxyhemoglobin

Ann NY Acad Sci

Effect of cigarette smoking and breathing carbon monoxide on cardiovascular hemodynamics in anginal patients

Circulation

Effect of low-level carbon monoxide exposure on onset and duration of angina pectoris. A study of ten patients with ischemic heart disease

Ann Intern Med

Carbon monoxide effect on exercise-induced angina pectoris

Ann Intern Med

Clinical study
Effect of carbon monoxide on exercise performance in chronic obstructive pulmonary disease