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CO Exposure (co + exposure)
Selected AbstractsHyperbaric Oxygen Does Not Prevent Neurologic Sequelae after Carbon Monoxide PoisoningACADEMIC EMERGENCY MEDICINE, Issue 1 2002Benjamin Gilmer MS Abstract Delayed neurologic sequelae occur in up to 40% of severe carbon monoxide (CO) poisonings. Conflicting clinical data support the efficacy of hyperbaric oxygen (HBO) therapy in the acute treatment of CO poisoning. Objective: To determine whether oxygen therapy reduces neurologic sequelae after CO poisoning in mice. Methods: Male Swiss-Webster mice were exposed to CO at 1,000 ppm for 40 minutes and then 50,000 ppm until loss of consciousness (LOC) (4-9 additional minutes). Total time of both phases of CO exposure was 40-49 minutes. Treatment included HBO with 3 atmospheres (ATA) 100% oxygen, normobaric oxygen (NBO) with 1 ATA 100% oxygen, or ambient air 15 minutes after LOC. All animals underwent passive avoidance training and memory was assessed by measuring step-down latency (SDL) and step-up latency (SUL) seven days following CO exposure. Results: Carbon monoxide poisoning induced significant memory deficits (SDLCO= 156 sec; SULCO= 75%) compared with nonpoisoned (NP) animals (SDLNP= 272 sec; SULNP= 100%). Both HBO and NBO did not prevent these neurologic sequelae. Furthermore, no significant neurobehavioral differences were found between HBO and NBO. Histologic examination of the CA1 layer of the hippocampus for pyknotic cells showed significant damage from CO in the air-treated animals (9.6%) but not in the nonpoisoned animals (3.8%). No significant neuroprotection was seen histologically with NBO and HBO compared with ambient air. Conclusions: These results suggest that HBO is not effective in preventing neurologic sequelae in mice and that there is no benefit of HBO over NBO following severe CO neurotoxicity. [source] Mild carbon monoxide exposure and auditory function in the developing ratJOURNAL OF NEUROSCIENCE RESEARCH, Issue 5 2003Janet E. Stockard-Sullivan Abstract We have examined the influence of chronic mild exposure to carbon monoxide (CO) on cognitive (learning) and auditory function in the developing rat. We have demonstrated that the auditory pathway is compromised at exposures less than 50 ppm, whereas learning was not influenced at 100 ppm. Artificially reared rat pups were exposed to CO during the brain growth spurt and onset of myelination. Spatial learning was assessed using the Morris Water Maze and three tests of auditory function: (1) auditory brainstem conduction times; (2) the amplitude of the eighth nerve's action potential; and (3) otoacoustic emissions carried out on rat pups (age 22, 24 days). The pups were gastrostomy-reared on a rat milk substitute and chronically exposed to CO at discrete concentrations in the range of 12,100 ppm from 6 days of age to post-weaning at 21,23 days of age. We found no difference in auditory brainstem conduction times at all CO concentrations in comparison to non-exposed controls. There was a difference in otoacoustic emissions for test and controls at CO concentrations of 50 ppm but not at lower concentrations. There was a consistent attenuation of the amplitude of the eighth nerve's action potential, even at the lowest CO exposure examined. The attenuation of the amplitude of the action potential of the eighth nerve at 50 ppm carbon monoxide exposure did not completely recover by 73 days of age. We conclude that prolonged mild exposure to carbon monoxide during development causes measurable functional changes at the level of the eighth cranial nerve. © 2003 Wiley-Liss, Inc. [source] Mild carbon monoxide exposure impairs the developing auditory system of the ratJOURNAL OF NEUROSCIENCE RESEARCH, Issue 5 2003Douglas S. Webber Abstract The object of this study was to determine if chronic exposure to mild concentrations of CO in air caused changes in the integrity of the inferior colliculus during the most active period of synaptogenesis/auditory development. We examined all subregions of the inferior colliculus (IC) of rats by immunocytochemical approaches after pups were exposed chronically to CO concentrations of, 0, 12.5, 25, and 50 ppm in air starting at Day 8 through 20,22 days of age. Mother-reared pups were compared to the gastrostomy-reared pups with or without CO exposure for basal neural activity, using c-Fos immunoreactivity as a marker. Half the rats were examined at 27 days of age, 5 days after the end of CO exposure, and the other half were examined 50 days later at 75,77 days of age. In the central nucleus of the IC, the number of cells expressing a basal level of c-Fos was decreased significantly in the CO-exposed animals when compared to controls; however, there was little or no difference in the number of cells expressing c-Fos in the other subregions of the IC. We conclude that the central nucleus of the inferior colliculus is affected selectively by mild CO exposure (0.0012% in air) and that this reduction in neuronal activity persists into adulthood. © 2003 Wiley-Liss, Inc. [source] Relationships between air pollution and preterm birth in CaliforniaPAEDIATRIC & PERINATAL EPIDEMIOLOGY, Issue 6 2006Mary Huynh Summary Air pollution from vehicular emissions and other combustion sources is related to cardiovascular and respiratory outcomes. However, few studies have investigated the relationship between air pollution and preterm birth, a primary cause of infant mortality and morbidity. This analysis examined the effect of fine particulate matter (PM2.5) and carbon monoxide (CO) on preterm birth in a matched case,control study. PM2.5 and CO monitoring data from the California Air Resources Board were linked to California birth certificate data for singletons born in 1999,2000. Each birth was mapped to the closest PM monitor within 5 miles of the home address. County-level CO measures were utilised to increase sample size and maintain a representative population. After exclusion of implausible birthweight,gestation combinations, preterm birth was defined as birth occurring between 24 and 36 weeks' gestation. Each of the 10 673 preterm cases was matched to three controls of term (39,44 weeks) gestation with a similar date of last menstrual period. Based on the case's gestational age, CO and PM2.5 exposures were calculated for total pregnancy, first month of pregnancy, and last 2 weeks of pregnancy. Exposures were divided into quartiles; the lowest quartile was the reference. Because of the matched design, conditional logistic regression was used to adjust for maternal race/ethnicity, age, parity, marital status and education. High total pregnancy PM2.5 exposure was associated with a small effect on preterm birth, after adjustment for maternal factors (adjusted odds ratio [AOR] = 1.15, [95% CI 1.07, 1.24]). The odds ratio did not change after adjustment for CO. Results were similar for PM2.5 exposure during the first month of pregnancy (AOR = 1.21, 95% CI [1.12, 1.30]) and the last 2 weeks of pregnancy (AOR = 1.17, 95% CI [1.09, 1.27]). Conversely, CO exposure at any time during pregnancy was not associated with preterm birth (AORs from 0.95 to 1.00). Maternal exposure to PM2.5, but not CO, is associated with preterm birth. This analysis did not show differences by timing of exposure, although more detailed examination may be needed. [source] Ex vivo Application of Carbon Monoxide in UW Solution Prevents Transplant-Induced Renal Ischemia/Reperfusion Injury in PigsAMERICAN JOURNAL OF TRANSPLANTATION, Issue 4 2010J. Yoshida I/R injury is a major deleterious factor of successful kidney transplantation (KTx). Carbon monoxide (CO) is an endogenous gaseous regulatory molecule, and exogenously delivered CO in low concentrations provides potent cytoprotection. This study evaluated efficacies of CO exposure to excised kidney grafts to inhibit I/R injury in the pig KTx model. Porcine kidneys were stored for 48 h in control UW or UW supplemented with CO (CO-UW) and autotransplanted in a 14-day follow-up study. In the control UW group, animal survival was 80% (4/5) with peak serum creatinine levels of 12.0 ± 5.1 mg/dL. CO-UW showed potent protection, and peak creatinine levels were reduced to 6.9 ± 1.4 mg/dL with 100% (5/5) survival without any noticeable adverse event or abnormal COHb value. Control grafts at 14 days showed significant tubular damages, focal fibrotic changes and numerous infiltrates. The CO-UW group showed significantly less severe histopathological changes with less TGF-, and p-Smad3 expression. Grafts in CO-UW also showed significantly lower early mRNA levels for proinflammatory cytokines and less lipid peroxidation. CO in UW provides significant protection against renal I/R injury in the porcine KTx model. Ex vivo exposure of kidney grafts to CO during cold storage may therefore be a safe strategy to reduce I/R injury. [source] Interaction between maternal smoking and malnutrition in infant risk of gastroschisis,BIRTH DEFECTS RESEARCH, Issue 3 2006Phung K. Lam Abstract BACKGROUND Gastroschisis is a severe birth defect characterized by a tear in the infant's abdominal wall. Young mothers have the highest risk of having an infant with gastroschisis. In an animal model, the defect resulted from exposure of pregnant mice to carbon monoxide (CO) in combination with a low protein and low zinc diet. METHODS We evaluated this model in a study of 55 infants with gastroschisis and 94 age-matched controls that included maternal interview with a food frequency questionnaire. Smoking cigarettes (,1 pack/day) or marijuana (more than once) 3 months prior to pregnancy indicated CO exposure. Low protein or zinc intake and a low body mass index (BMI) indicated maternal malnutrition. RESULTS When assessed separately, high CO, low protein, low zinc, and low BMI were each significantly associated with an increased risk of gastroschisis. Although we observed significant CO-BMI and CO-zinc interactions after adjusting for income, only a combination of high CO exposure and low BMI yielded a synergistic adverse effect. Compared to the low risk of having an infant with gastroschisis for mothers who did not have low BMI and did not smoke, the risk of having an infant with gastroschisis was 16.3 times (95% CI, 2.49,113.4) higher for mothers who did not have low BMI but smoked, and 19.7 times (95% CI, 4.33,89.6) higher for mothers who did not smoke but had low BMI. However, the risk was 26.5 times (95% CI, 7.85,89.4) higher for mothers who had low BMI and smoked. CONCLUSIONS Our results suggest that young mothers are at increased risk of having an infant with gastroschisis if they smoke and are also malnourished. Birth Defects Research (Part A), 2006. © 2006 Wiley-Liss, Inc. [source] | |||||||||||||