National unintentional carbon monoxide poisoning estimates using hospitalization and emergency department data

Utilizing Syndromic Surveillance for Hurricane Irma-Related CO Poisonings in Florida

Carbon monoxide (CO) poisoning is a leading cause of morbidity and mortality during natural disasters. On January 26-27, 2009, a severe ice storm occurred in Kentucky, causing widespread, extended power outages and disrupting transportation and communications. After the storm, CO poisonings were reported throughout the state. The objectives of this investigation were to determine the extent of the problem, identify sources of CO poisoning, characterize cases, make recommendations to reduce morbidity and mortality, and develop prevention strategies. We obtained data from the Kentucky Regional Poison Center (KRPC), hyperbaric oxygen treatment (HBOT) facilities, and coroners. Additionally, the Kentucky Department for Public Health provided statewide emergency department (ED) and hospitalization data. During the two weeks after the storm, KRPC identified 144 cases of CO poisoning; exposure sources included kerosene heaters, generators, and propane heaters. Hospitals reported 202 ED visits and 26 admissions. Twenty-eight people received HBOT. Ten deaths were attributed to CO poisoning, eight of which were related to inappropriate generator location. Higher rates of CO poisoning were reported in areas with the most ice accumulation. Although CO poisonings are preventable, they continue to occur in postdisaster situations. Recommendations include encouraging use of CO alarms, exploring use of engineering controls on generators to decrease CO exposure, providing specific information regarding safe use and placement of CO-producing devices, and using multiple communication methods to reach people without electricity.

Cost of accidental carbon monoxide poisoning: A preventable expense

Hospital burden of unintentional carbon monoxide poisoning in the United States, 2007

TPS 683: Short-term health effects of air pollutants 2, Exhibition Hall, Ground floor, August 28, 2019, 3:00 PM - 4:30 PM Background: CDC’s National Environmental Public Health Tracking Program (Tracking Program) aims to provide information from a nationwide network of integrated unintentional carbon monoxide (CO) poisoning data that could inform relevant public health action and prevention. Methods: The Tracking Program has developed dynamic environmental health surveillance system that includes standard visualization tools such as charts, interactive maps, and tables, and displays a variety of measures of morbidity and mortality (e.g., crude, and age-adjusted rates per 100,000) for unintentional CO poisoning. Users also can explore these measures by cause (i.e., fire, non-fire, unknown intent or mechanism). The hospitalization and emergency department (ED) data are obtained by the Tracking Program from funded state recipients (26 states); mortality data are from the National Vital Statistics System. We pooled the CO poisoning data from 2010-2014, and examined the proportion of unintentional non-fire CO poisonings, and compared state-specific age-adjusted rates during the same period. Results: During 2010-2014, there were more than 4,500 unintentional CO poisoning deaths with an average of 916 deaths annually. Deaths and hospitalizations categorized as non-fire comprised of 41.4%, and 55.4% of cases respectively. During the same period, states that had the two highest annual age-adjusted rate of ED visits for unintentional CO poisoning were Connecticut (AR: 21.4 in 2011) and Vermont (AR=15.7 in 2013), and the highest hospitalization rate were observed in New Mexico (AR: 2.1 in 2011) and Maryland (AR=1.8 in 2009). Conclusions: The Tracking Program demonstrates the opportunity to visualize environmental and health data on one data platform. This allows users to examine temporal and spatial trends and to identify communities at greater risk for CO poisoning. The Tracking Program’s CO poisoning data can be used to drive public health policy and actions that ultimately will reduce the burden of mortality and morbidity for CO poisoning.

Unintentional, non-fire-related (UNFR) carbon monoxide (CO) poisoning is a leading cause of poisoning in the United States. A comprehensive national CO poisoning surveillance framework is needed to obtain accurate estimates of CO poisoning burden and guide prevention efforts. This article describes the current national CO poisoning surveillance framework and reports the most recent national estimates. We analyzed mortality data from the National Vital Statistics System multiple cause-of-death file, emergency department (ED) and hospitalization data from the Healthcare Cost and Utilization Project's Nationwide Emergency Department Sample and Nationwide Inpatient Sample, hyperbaric oxygen treatment (HBOT) data from HBOT facilities, exposure data from the National Poison Data System, and CO alarm prevalence data from the American Housing Survey and the National Health Interview Survey. In the United States, 2,631 UNFR CO deaths occurred from 1999 to 2004, an average of 439 deaths annually. In 2007, there were 21,304 (71 per one million population) ED visits and 2,302 (eight per one million population) hospitalizations for confirmed cases of CO poisoning. In 2009, 552 patients received HBOT, and from 2000 to 2009, 68,316 UNFR CO exposures were reported to poison centers. Most nonfatal poisonings were among children (<18 years of age) and females; hospitalizations and deaths occurred more frequently among males and elderly people (>65 years of age). More poisonings occurred during winter months and in the Midwest and Northeast. UNFR CO poisoning poses a significant public health burden. Systematic evaluation of data sources coupled with modification and expansion of the surveillance framework might assist in developing effective prevention strategies.

&lt;div class="htmlview paragraph"&gt;The cause of accidental carbon monoxide (CO) poisonings often involves an interaction of poor vehicular design, flimsy vehicular construction, poor vehicular maintenance, faulty repair work, and careless use of the vehicle. An approach to the reduction of these accidents must therefore concentrate on practical ways to prevent, detect, and eliminate vehicular defects leading to the introduction of exhaust gases into passenger compartments.&lt;/div&gt; &lt;div class="htmlview paragraph"&gt;Examples of such methods include redesign of exhaust systems, implementation of sturdier construction materials, more comprehensive motor vehicle inspection systems, and the education of vehicle owners and vehicle repairmen on the prevention and detection of defects in vehicular exhaust systems and components of vehicle bodies adjacent to the exhaust system.&lt;/div&gt; &lt;div class="htmlview paragraph"&gt;Case studies are presented representing common modes of CO poisoning in vehicular settings, and for each case a cause is determined and discussed in terms of preventive action needed. Suggestions for familiarizing all persons involved in the operation and repair of motor vehicles with practical means by which to determine the integrity of the exhaust system and vehicle body are proposed as a step toward reducing the human errors which result in accidental CO poisonings.&lt;/div&gt;

Age as a predisposing factor of respiratory alkalosis in accidental carbon monoxide poisoning

Currently, there is no known optimal therapy for carbon monoxide (CO) poisoning and CO-associated delayed neurological sequelae. Hyperbaric oxygen therapy (HBOT) is a well-known treatment method, but its use for CO poisoning patients is controversial to use due to lack of evidences regarding its efficacy. Thus, it is unlikely that HBOT alone will be accepted as the standard treatment method. In this article, current and potential treatment methods of CO poisoning are presented as well as the tentative multi-factorial pathophysiology. A series of treatments are suggested for use as a bundle therapy, with targeted temperature management as the base treatment method. Such a therapy holds a great potential, especially for the cases where HBOT is not readily available. We suggest further investigations for elucidating the effects of these suggested treatments and their roles in terms of the complex pathophysiology of CO poisoning. Future acceptance of this therapy based on the improved scientific and clinical knowledge may result in injury prevention and minimization of the signs and the symptoms in CO poisoning.

Each year in the United States, approximately 500 persons die from unintentional carbon monoxide (CO) poisoning, often during electric power outages caused by severe storms. Use of residential CO alarms has been recommended to reduce the incidence of CO poisoning. In September 2000, Mecklenburg County, North Carolina (2002 population: 722,367), adopted a public health ordinance requiring a CO alarm in the majority of residences; all-electric residences without attached garages (35.4% of all homes) were exempt. The ordinance also permitted use of alarms without battery back-up. On December 4, 2002, an ice storm caused 78.9% of county households to lose power. During the next 9 days, 124 cases of symptomatic CO poisoning were reported. To characterize these poisonings and the effectiveness of the CO alarm ordinance, local emergency physicians, fire department authorities, and CDC conducted an investigation. This report summarizes the results of that investigation, which determined that 96.2% of the severe poisonings occurred in homes with no reported functioning CO alarm. As a result of these findings, on October 8, 2003, Mecklenburg County officials amended the ordinance to require alarms with battery back-ups in all residences. Officials in other communities should consider enacting such alarm ordinances to prevent CO poisonings.

On December 13, 2014, the emergency management system in Lake Delton, Wisconsin, was notified when a male hockey player aged 20 years lost consciousness after participation in an indoor hockey tournament that included approximately 50 hockey players and 100 other attendees. Elevated levels of carbon monoxide (CO) (range = 45 ppm-165 ppm) were detected by the fire department inside the arena. The emergency management system encouraged all players and attendees to seek medical evaluation for possible CO poisoning. The Wisconsin Department of Health Services (WDHS) conducted an epidemiologic investigation to determine what caused the exposure and to recommend preventive strategies. Investigators abstracted medical records from area emergency departments (EDs) for patients who sought care for CO exposure during December 13-14, 2014, conducted a follow-up survey of ED patients approximately 2 months after the event, and conducted informant interviews. Ninety-two persons sought ED evaluation for possible CO exposure, all of whom were tested for CO poisoning. Seventy-four (80%) patients had blood carboxyhemoglobin (COHb) levels consistent with CO poisoning; 32 (43%) CO poisoning cases were among hockey players. On December 15, the CO emissions from the propane-fueled ice resurfacer were demonstrated to be 4.8% of total emissions when actively resurfacing and 2.3% when idling, both above the optimal range of 0.5%-1.0%. Incomplete fuel combustion by the ice resurfacer was the most likely source of elevated CO. CO poisonings in ice arenas can be prevented through regular maintenance of ice resurfacers, installation of CO detectors, and provision of adequate ventilation.

Objective To explore the mechanism of ultrastructural and functional impairment of mitochondria and the protective effect of sulforaphane (SFP) at different dosages on hippocampus neurons in rats after acute carbon monoxide(CO)poisoning. Methods One hundred and fifty adult healthy SD rats were randomly divided into the normal control group, the CO poisoning group and the SFP treatment group. The rat model of CO poisoning was established through exposure to CO in a hyperbaric chamber. The uhrastructural changes of mitochondria in nerve cells of the brain tissue were observed by transmission electron microscopy (TEM). Mitochondrial membrane potential (MFI) was detected with JC-1 fluorescent probe, and the expressions of Nrf-2 and Trx-1 proteins and mRNA were evaluated by immunohistochemistry and quantitative RT-PCR before and after intervention. Results CO poisoning could induce impairment of mitochondria ultrastructure in neurocytes in the brain tissue. SFP could obviously alleviate the damage of mitochondria ultrastructure. The MFI level in the brain tissue was obviously reduced in rats after CO exposure. Though MFI level was decreased 3 to 7 days after SFP administration, its level was significantly higher than that of the CO poisoning group at the same time point (P<0.05). As compared with those in the normal control group, the expression levels of Nrf-2 and Trx-1 proteins as well as their mRNA in the CO poisoning group were slightly increased (P<0.05). After treatment with SFP, the expressions of both the proteins and mRNA were obviously increased, and there was significant difference when compared with that of the CO poisoning group at the same time point (P<0.05). Conclusion Early administration of either moderate or high dose SFP could efficiently improve mitochondrial structure and function, enhance anti-oxidative stress of cells, thus exerting a positive effect against brain damage induced by acute CO poisoning. Key words: CO poisoning; Sulforaphane; Mitochondrial ultrastructure; Mitochondrial membrane potential; Nrf-2; Trx-1

Introduction and Overview of the Field D. G. Penney Exposure to Ambient and Microenvironmental Concentrations of Carbon Monoxide P. G. Flachsbart Carbon Monoxide Build-Up in Houses and Small Volume Enclosures R.E. Engberg Formation and Movement of Carbon Monoxide into Mobile Homes, Trailers, and Other Enclosures R. E. Schreter Carbon Monoxide Emissions from Gas Ranges And The Development of a Field Protocol for Measuring Co Emissions R. J. Karg Investigating Carbon Monoxide-Related Accidents Involving Gas-Burning Appliances M. Hanzlick Carbon Monoxide Dangers in the Marine Environment J. McCammon Application of warnings and Labels for Carbon Monoxide Protection G. Hutter Public Health Surveillance for Carbon Monoxide In The United States: A Review of National Data M. E. King and J. A. Mott Carbon Monoxide Sensors and Systems K. Galatsis and W. B. Wlodarski Marketing of Carbon Monoxide Information and Alarms In Europe and Beyond: Use of the World Wide Web in Saving Lives R. Aiers Investigating Carbon Monoxide Poisonings T. M. Dydek Carbon Monoxide Detectors as Preventive Medicine J.s W. Rhee and J. B. Leikin Misconceptions about Carbon Monoxide D.G. Penney A Survey Study of Public Perceptions about Carbon Monoxide D. G. Penney The Case for the Use of Hyperbaric Oxygen Therapy In Carbon Monoxide Poisoning C. Tomaszewski Hyperbaric Oxygen for Acute Carbon Monoxide Poisoning: Useful Therapy or Unfulfilled Promise? C. D. Scheinkestel and I. L. Millar A Challenge to The Healthcare Community: The Misdiagnosis Of Carbon Monoxide Poisoning D.G. Penney Neuroimaging after Carbon Monoxide Exposure G. Heuser Recent Advances in Brain Spect Imaging after Carbon Monoxide Poisoning S. G. Hipskind Neurocognitive and Affective Sequelae of Carbon Monoxide Poisoning R. O. Hopkins Neurocognitive and Neurobehavioral Sequelae of Chronic Carbon Monoxide Poisoning: A Retrospective Study and Case Presentation D. A. Helffenstein Chronic Carbon Monoxide Poisoning: A Case Series D. G. Penney Functional and Developmental Effects of Carbon Monoxide Toxicity in Children C. L. Armstrong and J. L. Cunningham Issues in Rehabilitation and Life Care Planning For Patients With Carbon Monoxide Poisoning J.M. Gracey Treatment of Carbon Monoxide Poisoning With Yoked Prism Lenses J. F. Georgis Firefighters and Carbon Monoxide K.J. Reilly Jr., F. Ricci, and D. Cone The Purpose and the Process of Litigation In A Carbon Monoxide Poisoning Case S.P. Willison Offering Expert Opinions in A Carbon Monoxide Case S. P. Willison Injury Caused By Carbon Monoxide Poisoning: Defining Monetary Damages S. Collard My Carbon Monoxide Poisoning: A Victim's Story J. A. Cramer Noninvasive Measurement of Blood Carboxyhemoglobin With Pulse Co-Oximetry N. B. Hampson Chronic Carbon Monoxide Exposure: How much do we know About It?-An Update A.W.M. Hay Essential Reference Tables, Graphs, and Other Data

Accuracy of Noninvasive Multiwave Pulse Oximetry Compared With Carboxyhemoglobin From Blood Gas Analysis in Unselected Emergency Department Patients

Background and Objectives: Carbon Monoxide (CO) poisoning is a leading cause of injury and death due to poisoning in many parts of the world. Among numerous sources of CO, the gas water heater can be a potential under looked source causing an accidental Carbon monoxide poisoning. In the perspective of Kathmandu valley, where there are houses with small bathrooms, inadequate ventilation and absent CO detectors, gas water heaters can be extremely dangerous even if it liberates small amount of CO gas. Herein, we present a case of CO poisoning to increase awareness about the gas water heater use and the possible risk of CO poisoning in our community.Presentation of Case: A 34 years old healthy female from Patan, presented with the history of loss of consciousness for 15 minute while taking bath on a gas water heater. There was no spontaneous respiration, no cardiac activity and her body temperature was below normal.Discussion: CO is toxic to all aerobic forms to life. CO binds to hemoglobin 230 times faster than oxygen causing cellular hypoxic damage and death. CO poisoning is not uncommon in our society and many such cases are misdiagnosed for some other illness.Conclusion: Use of the gas water heaters and likelihood of CO poisoning should be notified as a public concern. People need to be aware of these hazards to prevent fatal events and likely death due to exploitation of gas water heaters. Janaki Medical College Journal of Medical Sciences (2017) Vol. 5(2): 56-59