ReviewCarbon monoxide poisoning — a public health perspective
Introduction
Carbon monoxide (CO) is one of many ubiquitous contaminants of our environment that requires prevention and control measures to insure adequate protection of public health. A primary focus of air pollution control by industrialized societies has been the regulation of CO in ambient air and occupational settings. The term ambient air is interpreted to mean outdoor air available to the general public. The recommended multi-hour ambient air-quality standard of 9 ppm (10 mg/m3) CO for 8 h (Federal Register, 1994, World Health Organization, 1999a, World Health Organization, 1999b) is intended to protect susceptible population groups from adverse effects resulting from CO exposures in the outdoor environment. The recommended limits for occupational exposure, which range from 25 to 50 ppm (30–60 mg/m3) CO worldwide (Cook, 1987, Commission of the European Communities, 1993), are intended to protect healthy workers from the adverse effects of CO during a typical 8-h working day. Average monitored exposures from the controlled outdoor and occupational environments, however, represent only part of the total human exposure to CO. Potential exposures that exceed the existing standards may be of greater concern to public health because they increase the total body burden for CO (US Environmental Protection Agency, 1999). For example, the ambient standard outdoors is exceeded as a result of CO emissions from transportation sources, primarily motor vehicles, and from stationary sources producing industrial combustion gases at times or locations that may not be measured. Transient concentrations of CO also can be high in tunnels and parking garages because of the accumulation of engine exhaust fumes; but these locations are not considered to be part of the regulated ambient environment. In addition, the results of time activity/pattern analyses in the United States and other developed countries have indicated that a majority of the public spends most of its time indoors, where exposures to CO emitted from industrial processes, tobacco smoke (see Appendix A), and other combustion sources (such as gas, coal, and wood stoves and fireplaces; and kerosene or other fossil-fuel-burning heaters and appliances) may present problems. Although voluntary standard performance requirements exist for many individual combustion appliances to minimize CO emissions, maintaining healthful CO levels inside homes can present difficulties, especially if multiple combustion sources are located in the same enclosed environment.
Carbon monoxide is impossible to detect by an exposed person because it is colorless, tasteless, odorless, and nonirritating. When inhaled, CO is readily absorbed from the lungs into the bloodstream, where it forms a tight but slowly reversible complex with hemoglobin (Hb) known as carboxyhemoglobin (COHb). The presence of COHb in the blood decreases the oxygen carrying capacity, reducing the availability of oxygen to body tissues and resulting in tissue hypoxia. A reduction in oxygen delivery because of the elevated COHb level, exacerbated by impaired perfusion resulting from hypoxic cardiac dysfunction, potentially will impair cellular oxidative metabolism. This occurs because hypoxia and reductions in blood flow may allow CO to bind to cytochrome c oxidase, which inhibits aerobic adenosine triphosphate synthesis (Brown and Piantadosi, 1990). The disturbance in mitochondrial electron transport also causes generation of oxidative stress, measured as an increase in the hydroxyl-like radical fraction, and causes generation of hydroxyl-like radicals (Chance et al., 1970, Brown and Piantadosi, 1992, Piantadosi et al., 1997). Energy production and mitochondrial function are restored slowly after COHb levels decrease because of continued inhibition of respiration (Brown and Piantadosi, 1992).
A proposed pathological mechanism of CO, which may be independent of hypoxic stress, is related to an elevation in the steady-state concentration of the free radical, nitric oxide (NO). This phenomenon has been documented in vitro with human and rat platelets, and bovine lung endothelial cells, and in vivo in both lung and brain of experimental animals (Thom et al., 1997, Thom et al., 1999a, Thom et al., 1999b). The elevation of NO can occur with exposures as little as 22 nM CO, which is the concentration expected with an interstitial CO partial pressure of about 20 ppm and a COHb level of 7% (Thom and Ischiropoulos, 1997, Thom et al., 1997). The mechanism for enhanced NO release appears to be based on competition between CO and NO for intracellular hemoprotein binding sites, rather than on a net increase in enzymatic production of NO (Thom et al., 1994, Thom and Ischiropoulos, 1997, Thom et al., 1997). Vascular oxidative stress from NO can cause leakage of high-molecular-weight substances into organ parenchyma and trigger leukocyte adherence/activation (Ischiropoulos et al., 1996, Thom et al., 1999a, Thom et al., 1999b).
The health risks associated with CO vary with its concentration and duration of exposure. Effects range from subtle cardiovascular and neurobehavioral effects at low concentrations to unconsciousness and death after prolonged exposures or after acute exposures to high concentrations of CO. Risks associated with the relatively low ambient concentrations found in the environment and in contaminated work places have been reviewed in several excellent reports (US Environmental Protection Agency, 1991, Kleinman, 1992, Bascom et al., 1996, Penney, 1996, US Environmental Protection Agency, 1999).
Section snippets
History
Carbon monoxide poisoning is a major public health problem and mat be responsible for a significant percentage of all poisoning deaths. In fact, CO may be responsible for more than one-half of all fatal poisonings that are reported worldwide each year (National Safety Council, 1982, Cobb and Etzel, 1991, Mathieu et al., 1996). The frequency of health problems associated with sublethal levels of CO is difficult to quantify. Certain indoor and outdoor environments exist where the risk of exposure
Health effects
The symptoms, signs, and prognosis of acute CO poisoning correlate poorly with the level of COHb measured at the time of arrival at the hospital (Garland and Pearce, 1967, Winter and Miller, 1976, Okeda et al., 1982, Choi, 1983, Klees et al., 1985a, Klees et al., 1985b, Myers et al., 1985, Meredith and Vale, 1988, Thom et al., 1995). This observation has created two concerns. The first is that investigators must be extremely careful when attempting to study patient populations because
Treatment and prognosis
Management of CO-poisoned patients first consists of removing the patient from exposure to the toxic atmosphere and supplying pure oxygen to accelerate the elimination of CO and improve tissue oxygenation. Respiratory and circulatory conditions are assessed rapidly, and resuscitative measures are performed, if needed. Evaluation includes the neurological status of conscious level, motor response and reflectivity, and a complete physical examination looking for complications, associated trauma
Prevention
One way to avoid dangerous CO exposures is to prevent high concentrations of CO from occurring in residences and other indoor environments. This can be accomplished by: (1) frequent inspection and routine maintenance of vented combustion appliances and fireplaces; (2) not allowing automobiles to idle in closed or open garages; (3) not using unvented combustion sources indoors, such as space heaters, cooking devices (e.g., charcoal grills and hibachis), and tobacco products, or not misusing
Summary
Carbon monoxide is responsible for a large percentage of the accidental poisonings and deaths reported throughout the world each year. Certain conditions exist both in the indoor and outdoor environments that cause a small percentage of the population to become exposed to dangerous levels of CO. Outdoors, concentrations of CO are highest near street intersections, in congested traffic, near exhaust gases from internal combustion engines and industrial sources, and in poorly ventilated areas
Disclaimer
The technical discussion in this paper is based on a review of the scientific literature and the best professional judgement of the authors. It does not necessarily represent official policy of the US Environmental Protection Agency or any other governmental health agency.
Acknowledgements
The authors gratefully acknowledge the contributions to this review of CO poisoning by Dr Claude Piantadosi of Duke University Medical Center, and Dr Sandra Inkster of the US Consumer Products Safety Commission. The authors also wish to thank Dr Vernon Benignus and Dr David Mage of the US Environmental Protection Agency, Dr James McGrath of Texas Tech University for their helpful review comments, and the production staff of OAO Corporation for their help in preparation of this manuscript.
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