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.

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

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.

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

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.

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.

Context. On October 29, 2012, Hurricane Sandy made landfall and devastated New York's metropolitan area, causing widespread damage to homes and the utility infrastructure. Eight days later, snow and freezing temperatures from a nor'easter storm delayed utility restoration. Objective. To examine carbon monoxide (CO) exposures in the 2 weeks following Hurricane Sandy. Methods. This was a retrospective review of prospectively collected, standardized, and de-identified data sets. CO exposures and poisonings identified from two electronic surveillance systems, the New York City Poison Control Center (NYCPCC) and New York City's Syndromic Surveillance Unit, were compared with CO exposures from identical dates in 2008–2011. Data collected from the poison center included exposure type, CO source, poisoning type, treatment, and outcomes. Data collected from the Syndromic Surveillance Unit cases, which were identified by CO-related chief complaints presenting to NYC hospitals, included visit date and time, and patient demographics. Results. Four hundred thirty-seven CO exposures were reported to the NYCPCC, 355 from NYC callers, and the remainder from surrounding counties, which represented a significant increase when compared with CO exposures from identical dates in the preceding 4 years (p < 0.001). The total cases that were reported to the NYCPCC in 2008, 2009, 2010, and 2011 were 18, 13, 24, and 61, respectively. Excluding a single apartment fire that occurred (n = 311), the more common sources of CO were grilling indoors (26.2%) and generators (17.5%). Syndromic surveillance captured 70 cases; 6 cases were captured by both data sets. Conclusions. CO exposures following weather-related disasters are a significant public health concern, and the use of fuel-burning equipment is a clear source of storm-related morbidity and mortality. Multiple real-time epidemiologic surveillance tools are useful in estimating the prevalence of CO exposure and poisoning and are necessary to assist public health efforts to prevent CO poisoning during and after disasters.

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

Surveillance for Carbon Monoxide Poisoning using a National Media Clipping Service

Background Carbon monoxide (CO) is a colorless, odorless, nonirritating gas that is produced through the incomplete combustion of carbon-containing substances. CO poisoning is a leading cause of unintentional poisoning deaths in the United States. The Centers for Disease Control and Prevention (CDC) routinely collects surveillance data from different sources to better understand unintentional CO exposures and identify potential environmental risk factors. Methods We used four different data sources to track unintentional CO-related exposures and CO poisoning: exposures called to poison control centers (PCCs), emergency department (ED) visits, hospitalizations, and mortality for 2005-2016. We conducted descriptive analyses by cause (fire, non-fire, unknown), month, age, region, and medical outcome (no effect, minor effect, moderate effect, major effect, and death). Results Over the 12-year study period, we observed 141,762 PCCS calls (national), 92,390 ED visits (16 states), 14,816 hospitalizations (25 states), and 12,478 deaths (national) due to unintentional CO poisoning. Non-fire unintentional cases comprised more than 70% of all hospitalizations and ED visits and 48% of all deaths compared to other unintentional cases. Across all data sources, CO exposures and poisonings were most commonly reported in January and December. Adults aged 50-59 years were the highest proportions for hospitalizations (19.7%) and deaths (17.0%). For PCC data, CO exposures were most frequently reported among children aged 0-9 years (21.1%) and in Northeastern states (>70 per 100,000 population). Medical outcomes were most often reported as none or minor effect (n=146,067, 72.2%) in PCC data. Conclusions This surveillance report provides the most comprehensive review of unintentional CO poisonings in the US. Unintentional CO poisoning remains a public health concern. More standardized and continued public health surveillance of unintentional CO poisoning will be necessary to monitor the public health burden, identify novel exposure pathways, and assess the effectiveness of targeted prevention strategies.

Prevention methods for carbon monoxide (CO) poisoning in Wisconsin address occupational and nonoccupational exposures together, but differences between the settings could inform new approaches to preventing occupational CO poisonings. We described occupational CO poisonings in Wisconsin from July 1, 2018, through July 1, 2021, using surveillance data from the Wisconsin Electronic Disease Surveillance System and Wisconsin Poison Center. We identified cases of CO poisoning from the Wisconsin Electronic Disease Surveillance System and Wisconsin Poison Center. Occupational CO poisonings were records where "workplace" was recorded as the location of exposure. We excluded records classified as suspect/not a case, those missing laboratory results or information on exposure source/location, and intentional poisonings. We compared characteristics between occupational and nonoccupational settings using odds ratios (ORs), and we estimated crude incidence rates of occupational exposures by occupation. We identified 614 cases of CO poisoning, of which 168 (27.4%) were occupational exposures. When compared with patients with nonoccupational exposures, patients with occupational exposures were more likely to be male (OR = 3.8; 95% CI, 2.4-6.1), Hispanic (OR = 2.4; 95% CI, 1.4-4.2), and younger (mean difference [SD] = 6.6 [20.9]). Several CO sources were significantly associated with occupational poisonings: forklifts (OR = 58.4; 95% CI, 13.9-246.1; P < .001), pressure sprayers (OR = 2.4; 95% CI, 1.3-4.4; P = .003), and other gasoline-powered tools (OR = 3.8; 95% CI, 2.3-6.3; P < .001). The natural resources, construction, and maintenance occupation group had the highest crude incidence rate-45.0 poisonings per 100 000 full-time equivalent employees. Incorporating data from the Wisconsin Poison Center improved data quality, but surveillance is limited by underreporting. Creating strategies to increase reporting would allow for a more comprehensive understanding of occupational CO 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.

Hurricanes Katrina and Rita struck the U.S. Gulf Coast on August 29, 2005, and September 24, 2005, respectively, causing widespread damage and leaving approximately 4 million households without electrical power. Despite public health measures to prevent carbon monoxide (CO) poisonings after major power outages, multiple CO poisonings were reported in Gulf Coast states in the wake of these hurricanes. The Alabama Department of Public Health and Texas Department of State Health Services asked CDC to assist in investigating the extent and causes of these hurricane-related CO poisonings. The investigation identified 27 incidents of CO poisoning resulting in 78 nonfatal cases and 10 deaths in hurricane-affected counties in Alabama and Texas, nearly all of which were caused by gasoline-powered generators. Most of the generators involved were placed outside but close to the home to power window air conditioners (ACs) or connect to central electric panels. Few homes had functioning CO detectors. CDC continues to recommend that generators be placed far from homes, away from window ACs, and that CO detectors be used by all households operating gasoline-powered appliances (e.g., generators and gas furnaces), with batteries replaced yearly. Although the risk for CO poisoning likely decreases as generators are placed further from the home, additional studies are needed to establish a safe distance for generator placement.

Objective o investigate the prophylactic and therapeutic effects of montelukast, a cysteinyl leukotriene receptor-1 (CysLT1R) antagonist, on the delayed neuropsychological sequelae (DNS) in rat model of carbon monoxide (CO) poisoning and to explore the possible underlying mechanism. Methods A total of 90 rats were acclimated for one week prior to screening rat by Morris water maze test. Ten rats were randomly assigned to control group (Con group), and the remaining 80 rats were subjected to modified method of intraperitoneal injection of CO gas to establish animal model of acute CO poisoning, Thereafter, the survival rats randomized into CO poisoning group (Mod group), low-dose montelukast group (ML group), medium-dose montelukast group (MM group), high-dose montelukast group (MH group) (n=10 each). Montelukast was accordingly administered via intragastric tube at different intervals (30 min, 4 h and 12 h) after CO poisoning, and then montelukast was administered every 12 hours for 7 consecutive days. The rats of control group and Mod group received equal volume of normal saline instead at given intervals. Twenty-one days after CO exposure, the average escape latency was measured by Morris water maze test to screen DNS rats followed by H-E staining to observe the pathological changes of cortex and hippocampal CA1 region and TUNEL was used to assess the apoptosis of neurons in cortex and hippocampal CA1 region after rats sacrificed. Results All CO-exposed rats exhibited cognition function lowered, and the escape latency (seconds) in Mod group (43.3 ± 15.5), ML group (31.5 ± 13.2) and MH groups (30.1 ± 12.2) was significantly prolonged compared with Con group (12.1 ± 3.0) (P 0.05). Compared with Mod group, the escape latency in montelukast treatment groups was shortened, whereas the significant difference in escape latency only found between Mod group and MM group (P < 0.05). Except for Con group, DNS was evident in CO-exposed groups, and the numbers of DNS rats in Mod, ML, MM and MH groups were 8, 5, 1, 4, respectively, which made statistically significant differences to Con group (P< 0.05) except MM group. The DNS incidence in MM group was lower than that in Mod group (P < 0.05). Mod group exhibited severe histopathological injury to the brain, with evident apoptosis of neural cells, whereas in the groups with montelukast treatment, histopathological damage to the brain was mitigated and the number of apoptotic neuronal cells was diminished noticeably in MM group. Conclusion Montelukast can ameliorate the cognitive function of rats, decrease the incidence of DNS and reduce the apoptosis of neural cells as well as attenuate neuronal cell injury, thus exerting neuroprotection against DNS in rats with CO poisoning. Key words: Montelukast; Cysteinyl leukotriene receptor-1; Rat; Carbon monoxide poisoning; Delayed neuropsychologic sequelae; Morris water maze; Escape latency; Neuronal apoptosis