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Toxicology Notes and Literature

Carbon Monoxide Notes

Alcohol, DWI, DUI, DramShop

HSDB

  • symptoms include headache, dizziness, weakness, nausea, confusion, disorientation and visual disturbances; also exertional dyspnea, increases in pulse and respiratory rates
  • symptoms: headache, irritability, emotional instability, impaired judgement, defective memory, rapid fatigue (20-30% COHb)
  • delayed development of neuropsychiatric impairment, esp in children

PROGRESSION OF SYMPTOMS

  • 0-10% COHb - no SOB during vigorous exercise
  • 10-20% - mild headache, breathlessness on moderate exercise
  • 20-30% - throbbing headache, irritability, emotional instability, impaired judgement, defective memory, rapid fatigue
  • 40-50% - increasing confusion, sometime hallucinations, severe ataxia, accelerated respirations
  • 50-60% - syncope or coma with intermittent convulsions, tachycardia with a weak pulse, pallor or cyanosis
  • 60-70% - increased depth of coma with incontinence of urine and feces
  • 70-80% - profound coma with depressed or absent reflexes, weak thready pulse, shallow and irregular respirations and complete quiesence
  • above 80% - rapid death from respiratory arrest

MISCELLANEOUS SYMPTOMS

  • atypical:-  skin lesions, sweating, hepatomegaly hyperrexia, albuminuria, oliguria, anginal pain and congestive heart failure; during convalescence: bronchopneumonia may develop because of aspiration of saliva or vomitus; myocardial infarction with or without coronary thrombosis may appear at any time up to a week post exposure; after convalescence -
  • signs of nerve and brain injury may appear at any time within three weeks of exposure;
  • peripheral neuropathy reported infrequently and only after severe acute exposures; symmetrical distal motor weakness and numbness; some impairment of perceptual discrimination has been associated with long term exposure to low levels of carbon monoxide
  • Neurologic sequelae include visual loss, dementia, retardation, constructional apraxia, temporospacial disorientation, memory loss, dysphagia, personality changes, concentration deficits, and frank psychoses; Parkinson’s disease does occur after acute intoxication; after initial recovery patients may develop neurologic symptoms including apathy, mutism, amnesia, urinary incontinence, headaches, irritability, personality changes, confusion, memory loss, visual changes within 2-4 wks of exposure; hearing loss may occur
  • hemolytic anemia, thrombocytopenic purpura with respiratory dysfunction; rhabdomyolysis, acute renal failure and peripheral neuropathies(ulnar palsy) occur rarely
  • among permanent sequelae are neuropathies, various motor and mental defects some of which mimic multiple sclerosis or parkinsonism; and death

SMOKING

  • heavy cigarette smokers may have COHb levels as high as 15-17%
  • cigarette smoke concentration of CO reaching lungs is about 400ppm

HEART DISEASE


  • persons with hx of coronary heart disease, anemia, pumonary heart disease, cerebrovascular disease, thyrotoxicosis and smokers would be expected to be at greater risk for CO poisoning

EXPOSURE LEVELS

  • 35ppm 6-8 hrs light work produces COHb of about 5%
  • 200ppm for 15mins of heavy work produces COHb of about 5%
  • biological half life in blood of sedentary adults is about 2-5hrs; the lower the level, the slower the elim
  • hemoglobin has a 210-300x more affinity for CO than for oxygen
  • PEL TWA 50ppm(55mg/m3); ceiling limit of 200ppm(229mg/m3) is still enforced in some states
  • TLV(TWA) 25ppm; 75ppm for no more than 30 minutes during a work day
  • NIOSH recommends 10hr TWA of 35ppm(40mg/m3) with ceiling of 200ppm
  • Emergency Response Planning Guidelines(ERPG) (1) 200ppm( no more than mild, transient effects) for up to 1 hour exposure; ERPG(2) - 350ppm without serious side effects for up to 1 hour; ERPG(3) - 500ppm (not life threatening) for one hour exposure

INTEGRATED SCIENCE ASSESSMENT FOR CARBON MONOXIDE - March 2009;
US EPA EPA/600/R-09/019

  • Modeling produces estimates of exposure to 35ppm for 1 hour results in an increase of 0.6% COHb over baseline and exposure to 9ppm CO for 8h results in an increase of 0.8% COHb over baseline; 24 hour exposure to 3ppm CO results in an increase of 0.4% over baseline which can also be obtained following 1 hour exposure to 30ppm CO
  • p4-7 - COHb resulting from 35ppm for 1 hour (0.56%) is approximately equivalent to 6ppm for 8 hours(0.55%) or 4ppm for 24 hours(0.57%)
  • National Air Quality Standard for 1 hour exposure is 35ppm; 8 hr TWA is 9ppm
  • sufficient evidence to conclude a causal relationship is like to exist between relevant short term CO exposures and cardiovascular morbidity
  • those with cardiovascular detriments are at increased risk of health effects from CO
  • suggestive evidence of a causal relationship between relevant short and long-term CO exposures and CNS EFFECTS
  • Exposure to high levels of CO has long been known to produce CNS related symptoms including headache, dizziness, cognitive difficulties, disorientation and coma; the relationship between ambient levels of CO and neurological function is less clear
  • no studies of CNS effects in those exposed at ambient levels probably no effects owing to adaptive mechanisms including increased cardiac output and cerebral blood flow but those with impaired cardiovascular function may be susceptible
  • see page 2-13 for effects of CO on individuals with stable angina in controlled studies
  • see pg 3-60 for table showing home exposures averaging about 1.8ppm CO another study 1.4ppm
  • p5-14 Epi studies; p5-45 controlled human studies; p5-54 Human studies(CNS); Epi studies with long term exposure to CO on p5-132; Annex C summary of epi studies
  • suggestive of a causal relatinship between relevant short term and long term CO exposures and CNS effects

CARDIOVASCULAR EFFECTS


  • sufficient evidence to conclude that a causal relationship is likely to exist between relevant short term CO exposures and cardiovascular morbidity;
  • evidence suggests that those with CAD may be subject to the hypoxic aspects of CO exposure but also through a non-hypoxic mechanism involving disruption of cell signaling;
  • those with CAD already have a compromised oxygen delivery system;; normal individuals can vasodilate to accomodate COHb concentrations but individuals unable to vasodilate may show evidence of ischemia at low concentrtions of COHb;
  • Anderson et al(1973) studied 10 adult males with stable angin and exposed them to 50 and 100ppm for 4 hours resulting in average COHb concentrations of 2.9% and 4.5%; both exposures significantly decreased the time of onset of exercise induced angina relative to control room air(1.6% COHb); (similar study by Allred et al, 1989)

EXPOSURE SCENARIOS

  • p3-58 shows distribution of time spent indoors in residence vs at other places;
  • p3-61 shows average exposures in home, work and other; ave home 1.8ppm CO
  • Chemical affinity for CO binding to Hb is 218 times greater than oxygen

EPIDEMIOLOGICAL STUDIES WITH LONG TERM EXPOSURE

  • Roselund et al(2006) - 2246 cases and 3206 controls in Sweden - increased CO associated with out of hospital MI (OR=1.81ss) per 0.5ppm increase in the 30yr ave conc of CO
  • Allred et al(1989, 1991) studied the effects of CO on exercise induced angina in men with stable angina; relative to clean air exposure (COHb = 0.6%), exposures resulting in COHB of 2.4% and 4.7% were shown to increase the time required to induce the ST-segment changes by 5.1 and 12.1%(ss); these changes correlated with exercise induced angina; see other studies p 5-46; section concludes that COHb levels between 3 and 6% will consistently produced myocardial ischemia in those with CAD
  •  a causal relationship is likely to exist between relevant short term CO exposure and cardiovascular morbidity;

TOXICOLOGICAL STUDIES

  • p5-48: chronic CO exposure in animals have been reported to result in atherosclerosis development(refs)
  • non-hypoxic mechanisms of CO toxicity are discsussed in some detail; severe CO poisoning can lead to release of NO* from platelets with subsequent neutrophil activation and vascular injury
  • heart is a known target for CO toxicity because of its high oxygen consumption; cardiac hypertrophy demonstrated in rats;

CENTRAL NERVOUS SYSTEM EFFECTS p5-54

  • In controlled human studies, decreases in visual tracking as well as visual and auditory vigilance noted from CO exposures resulting in COHb levels between 5 and 20%(see refs)
  • one study reported similar behavioral effects(time discrimination) among a group of healthy volunteers with COHb levels <3%(ref) but these studies could not be duplicated
  • Other studies have demonstrated decreases in reaction time as well as decrements in cognitive function and fine motor skills following controlled exposure to CO; however - not blinded(Benignus, 1993)

  • in utero or perinatal exposure of animals to 25-750ppm CO has resulted in changes in behavior, memory, learning, locomotor ability, PNS myelination, auditory decrements, and neurotransmitter changes;
  • high exposures to CO known to induce headaches, dizziness, congnitive difficulties, disorientation and coma; lower level exposure effects unclear;
  • multiple studies in rodents in utero have shown impairment of multiple behavioral outcomes such as avoidance behavior at 150ppm; non-spatial memory at 75 and 150ppm, etc etc
  • multiple studies in rodents involving in utero CO exposure have demonstrated that CO exposure affects glutaminergic, cholinergic, catecholaminergic, dopaminergic neurotransmitters levels; perinatal exposures target the middle ear;
  • “the evidence is suggestive of a causal relationship between relevant short and long term CO exposures and central nervous system effects”

Table 2-1. Causal determinations for health effects outcomes.
Outcome Category Exposure Period Causality Determination
Cardiovascular morbidity Short-term Likely to be a causal relationship
Central nervous system effects Short- and long-term Suggestive of a causal relationship
Birth outcomes and Developmental effects Long-term Suggestive of a causal relationship;            Short-term Suggestive of a causal relationship
Respiratory morbidity: Long-term Inadequate to infer a causal relationship; Short-term Suggestive of a causal relationship
Mortality:       Long-term Suggestive of no causal relationship

Table 4-1a. CO concentration in pmol/100 g ww tissue – human. p4-8
Exposure                              Blood                                     % COHb
Background                           165 ± 143        1.5 ± 1.2
Fire                                                                  286 ± 127        3.8 ± 3.2
Fire + CO                                3623 ± 1975   40.7 ± 28.8
CO asphyxiation                                            5196 ± 2625 5                         6.4 ± 28.9
Source: Vreman et al. (2006)

Selected References

D Neslihan and S Nurten, Arch Environ Occup Heath, vol 65 no 1, 49-53(2010) - carbon monoxide aan increased blood viscosities have been associated with cardiovascular disease; here study effect of low level exposure to CO on blood viscosity(Hct, plasma viscosity and other factors); 10men exposed at work to CO for at least 6 mo vs controls; plasma fibrinogens higher in exposed group; concludes low level CO exposure = increased risk of cardiovascular disease
·                    

V Davutoglu et al, Tohoku J Exp Med, vol 219, no 3, 201-206(2009) - here look at association of chronic CO expsoure with atherosclerosis based on 40 healthy indoor barbeque workers, non smokers with control group; CoHb, C-reactive protein, and carotid intima-media thickness all correlated with CoHb concentration; these factors suggest an increased risk of atherosclerotic cardiovascular events
·                    

J Tellez et al, Rev Salud Publica (Bogata), vol 8 no 1, 108-117(2006) - abstr:- low levels of exposure to CO can result in cardiovascular or neuropsychological effects at CO levels of less than 25ppm and CoHb levels of less than 10%; main cardiac effects include arrhythmias and ECG signs of ischemia; also signs  include lack of memory, attention, concentration problems; Parkinson-type movements and neuropsyc changes particularly at low CO exposures


·                     JA Raub et al, Toxicology vol 145 no 1, 1-14(2000) - symptoms of CO intoxication range from subtle cardiovascular and neurobehavioural effects at low concs to unconsciousness and death at high doses; acute symptoms correlate poorly with CoHb levels; early symptoms include headache, dizziness, weakness, nausea, confusion, disorientation and visual disturbances
·                     I S San Lorenzo et al, Cardiologia vol 34 no 5, 439-46(1989) -abstr - effect of carbon monoxide on cardiac tissue; hypoxia; found cardiac rate increased during CO exposure and atrial fibrillation and tachycardia
·                     MC Dolan, CMAJ, vol 133 no 5, 392-399(1985) - low levels of CO aggravate chronic cardiopulmonary problems and high levels are associated with cardiac arrhythmias and cerebral edema; delayed neurologic sequelae in those who survive acute poisoning
·                     Anon “Revised Evaluation of Health Effects Associated with Carbon Monoxide Exposure: An addendum to the 1979 EPA Air Quality Criteria Document for Carbon Monoxide” USEPA Office of Environmental Assessment, Washington, DC; EPA-600/8-83-033F; August 1984;(I HAVE THIS) cites studies suggesting that aggravation of angina  and other cardiovascular diseases may occur at CoHb levels as low as 2.7 to 2.9%;
·                     C-T Wu et al, “Acute carbon monoxide poisoning with severe cardiopulmonary compromise: a case report”, Cases Journal, vol 2 no 52. 1-3(2009) (I HAVE THIS) Paper describes 15yo boy who suffered severe cardiopulmonary compromise without overt neuropsychiatric sequelae as a result of a home heater

NEUROPSYCHIATRIC SYMPTOMS

  • Anon “Nonfatal, Unintentional, Non-Fire-Related Carbon Monoxide Exposures - United States, 2004-2006", MMWR vol 57, no 33, 896-899(2008) - health effects from exposure to CO can range from viral-like symptoms(ie fatigue, dizziness, headache, confusion, nausea) to more severe conditions (disorientatin, unconsciousness, long-term neurologic disabilities, coma, cardiopulmonary failure and death; primary source of CO exposures was home heating systems; (I HAVE THIS)
  • Anon “Carbon Monoxide - Related  Deaths - United States, 1999-2004", MMWR vol 56 no 50, 1309-1312(2007) - symptoms include headache, nausea, dizziness or confusion); estimated 500 unintentional deaths per year in the US(I HAVE THIS)
  • T Beppu et al, Neuroradiology vol 52, no 8, 735-743(2010) - chronic neurpsychiatric symptoms after CO poisoning are caused by demyelination of cerebral white matter fibers; study of 13 adult patients biochemical measurements confirm some demyelination in the CNS of patients representing damage to white matter fibers
  • T Tapeantong N Poungvarinn,  J Med Assoc Thai, vol 92, no 10, 1374-1379(2009) - serious delayed encephalopathy and cognitive sequelae follow acute CO intox; here MRI of brain shows abnormal white matter change of cerebral hemispheres bilaterally with abnormal signal intensity at both patumens and caudate nuclei;
  • EG Birkenhager-Gillesse, MF van der Poel, Tijdschr Psychiatr, vol  50, no 4, 235-239(2008) - 81yo woman with chronic CO exposure showing symptoms resembling someone with depression

  • J Tellez et al, Rev Salud Publica (Bogata), vol 8 no 1, 108-117(2006) - abstr:- low levels of exposure to CO can result in cardiovascular or neuropsychological effects at CO levels of less than 25ppm and CoHb levels of less than 10%; main cardiac effects include arrhythmias and ECG signs of ischemia; also signs  include lack of memory, attention, concentration problems; Parkinson-type movements and neuropsyc changes particularly at low CO exposures
  • LD Prockop, J Neuroimaging vol 15, no 2, 144-149(2005) - CO is a common cause of toxic brain damage MRI findings include global pallidus and white matter lesions; here transient moderate level of CO exposure resulting in intellectual impairment without MRI changes; intellectual impairment and a Parkinsonism syndrome has been noted
  • LW Kao, KA Nanagas, Emer Med Clin North Amm, vol 22 no 4, 985-1018(2004) - CO signs of poisoning may be subtle and easily missdiagnosed; headache, flu-like symptoms, mentions controversy relating to hyperbaric treatments; not much here
  • JA Raub, VA Benignus, Neurosci Biobehav Rev, vol 26, no 8, 925-940(2002); symptoms of CO intox include headache, dizziness, weakness,  nausea, vomiting, disorientation, confusion, collapse and coma at high concentrations; at low concentrations CNS effects include  reduction in visual perception, manual dexterity, learning, driving performance, attention level, there is some literature that suggests that 5% COHb  would  be sufficient to produce visual sensitivity reduction and various neurobehavioral performance deficits; however, a crit lit review suggests that COHb would have to rise to 15-20% to produce a 10% reduction in any neurobehavioral parameters;
  • SA Devine et al, Environ Health Perspect vo 110 no 10, 1051-55(2002): - 45yo woman with long term chronic exposure to CO in a restaurant kitchen where she was a cook; pt believed to have been exposed to CO for about a year; initially flu-like symptoms; her persistent complaints included difficulty reading, writing, speaking and word retrieval; test results consistent with secondary frontal lobe dysfunction associated  with subcortical disorder MRI performed 15mo after exposure showed multiple bilateral lesions of the basal ganglia which were consistent with chronic CO exposure;
  • F Roohi et al, Clin Neurol Neurosurg vol 103 no 2, 92-95(2001) - residual effects of severe CO intoxication showing symptoms 29 years after the exposure
  • BM Ares et al, Rev Neurol vol 32 no 4, 339-341(2001) abstr - chronic intox with CO can result in serious neurological sequelae - an extrapyramidal syndrome dementia or a vegetative state; the diagnosis is made when CoHb is >10%; early hyperbaric treatment can help to avoid serious neurological sequelae; case report showing headache and episodes of migraine; diagn of CO intox is based on finding CoHb blood levels of >10%; early treatment avoids lesions of the globus pallidus and irreversible extrapyramidal sequelae
  • JA Raub et al, Toxicology vol 145 no 1, 1-14(2000) - symptoms of CO intoxication range from subtle cardiovascular and neurobehavioural effects at low concs to unconsciousness and death at high doses; acute symptoms correlate poorly with CoHb levels; early symptoms include headache, dizziness, weakness, nausea, confusion, disorientation and visual disturbances

  • L Knobeloch and R Jackson, WMJ vol 98, no 6, 26-29(1999) (Western Medical Journal??) - chronic exposure to low levels of CO can cause vague symptoms that are easily mistaken for other common illnesses; chronic fatigue syndrome, depression, influenza are dx frequently made in cases of chronic CO intox; pattern of chronic CO intox include the following: headache, fatigue, dizziness, nausea, mental confusion especially in winter
  • N Pavese et al, Ital J Neurol Sci, vol 20, no 3, 171-178(1999) - long term flup study in 30pts after 3 years; 22 acutely exposed and 8 chronically exposed: only 1  of 8 chronically exposed showed a neurological sequelae; those with acute exposures showed MRI abnormalities
  • RA Myers et al, J Clin Psychol, vol 54, no 5, 555-567(1998) - chronic exposure to CO produces a clinical syndrome with a range of presentations; objective symptomatology is presented
  • BA Wilson, Brain Inj vol 10, no 12, 863-874(1996) - survivors of cerebral hypoxia 567pts some with CO intox; greatest number of pts showed memory deficits and deficits in executive functioning
  • EW Ely et al, Am J Med vol 98 no 2, 145-155(1995) - this is study of warehouse workers exposed to CO; 30 workers; workers experienced difficulty concentrating, confusion;
  • AW Deckel Brain Inj vol 8 no 4, 345-356(1994) - two pts experienced CO intox together; both showed deficits in frontal lobe/executive functioning along with mild memory disturbances and visual-spatial information processing; lit says frontal lobe deficits are common following CO poisoning along with memory deficits
  • SM Candura et al, G Ital Med Lav vol 115, nos 1-4, 67-70(1993) - abstr - exposure to low levels of CO in homes; here couple, non-smokers exposed in home; suffered cephalea, nausea, neurobeh disturbs during period of about one year; non-lethal levels of CO from malfunctioning flue in bed chamber; levels of CoHb were low 4-5%
  • CM Ryan, Arch Clin Neuropsychol vol 5 no 1, 59-67(1990) - neuropsychiatric sequelae are common feature of CO intox; here chronic 3yr low level exposure to CO produced deficits in concentration and memory
  • JN Kirkpatrick, West J Med, vol 146 no 1, 52-56(1987) - a syndrome of headache, fatigue, dizziness, paresthesias, chest pain, palpitations and visual disturbances was assocaited with chronic occult carbon monoxide exposure in 26 pts causal relationship established by finding elevated levels of CO in a pts home, workplace or vehicle; high CoHb in 11 of 14pts and source removed;
  • Anon “Revised Evaluation of Health Effects Associated with Carbon Monoxide Exposure: An addendum to the 1979 EPA Air Quality Criteria Document for Carbon Monoxide” USEPA Office of Environmental Assessment, Washington, DC; EPA-600/8-83-033F; August 1984; (I HAVE THIS); talks about COHb levels in the 3.0-7.6% range that result in significant decrements in vigilance performance; also that inhalation of CO results in decrements in vigilance, visual perception, manual dexterity, learning ability and performance of sensorimotor tasks such as driving

 


DAMAGE TO WHITE MATTER

  • T Beppu et al, Neuroradiology vol 52, no 8, 735-743(2010) - chronic neurpsychiatric symptoms after CO poisoning are caused by demyelination of cerebral white matter fibers; study of 13 adult patients biochemical measurements confirm some demyelination in the CNS of patients representing damage to white matter fibers
  • T Tapeantong N Poungvarinn,  J Med Assoc Thai, vol 92, no 10, 1374-1379(2009) - serious delayed encephalopathy and cognitive sequelae follow acute CO intox; here MRI of brain shows abnormal white matter change of cerebral hemispheres bilaterally with abnormal signal intensity at both patumens and caudate nuclei;
  • O Mahmoud et al, Encephale vol 35, no 3, 281-285(2009) - CO still major cause of brain damage as a result of hypoxia; here CT scan revealed bilateral hippocampus low density in the central white and grey matter; results correlate with several series of CT scans in CO intox showin low density lesions in the cerebral white matter in some specific brain stuctures such as the global pallidus, and the hippocampus
  • D Kondziella et al, J Neurol vol 256 no 6, 970-979(2009) - here study of seven pts with CO poisoning; concludes taht the (1)H magnetic resonance spectroscopy (MRS)  showed abnormal grey and white matter scans; not much here - no effect from chronic exposure
  • CA Haaxma et al, Ned Tijdschr Geneeskd, vol 151 no 15, 868-73, (2007) - 40yo expoed to chronic low level of CO in his home resulting in coordination disorder and intermittent paresthesias; CT scan of brain revealed calcification of leftt caudate nucleus and putamen, cerebral MRI showed basal ganglial lesions and extensive periventricular white matter lesions.
  • AC Durak et al, Acta Radiol vol 46, no 3, 322-327(2005) use of MRI to define chronic phase of CO intox: most common finding was bilateral symmetrical hyperintensity of the white matter; cerebral cortical atrophy seen in 10pts; mild atrophy of cerebellar hemispheres noted in 8 pts; persistent cerebral changes noted
  • LD Prockop, J Neuroimaging vol 15, no 2, 144-149(2005) - CO is a common cause of toxic brain damage MRI findings include global pallidus and white matter lesions; here transient moderate level of CO exposure resulting in intellectual impairment without MRI changes; intellectual impairment and a Parkinsonism syndrome has been noted
  • JH Kim et al, AJNR Am J Neuroadiol, vol 24 no 8, 1592-7(2003) - CO intox has delayed effects on cerebral white matter characterized by bilateral confluent lesions that reflect the diffusion characteristics of these lesions; 5pts with delayed encephalopathy examined by MRI;

  • SA Devine et al, Environ Health Perspect vo 110 no 10, 1051-55(2002): - 45yo woman with long term chronic exposure to CO in a restaurant kitchen where she was a cook; pt believed to have been exposed to CO for about a year; initially flu-like symptoms; her persistent complaints included difficulty reading, writing, speaking and word retrieval; test results consistent with secondary frontal lobe dysfunction associated  with subcortical disorder MRI performed 15mo after exposure showed multiple bilateral lesions of the basal ganglia which were consistent with chronic CO exposure;
  • N Pavese et al, Ital J Neurol Sci, vol 20, no 3, 171-178(1999) - long term flup study in 30pts after 3 years; 22 acutely exposed and 8 chronically exposed: only 1  of 8 chronically exposed showed a neurological sequelae; those with acute exposures showed MRI abnormalities; 
  • A Uchino et al, Neuroradiology vol 36 no 5, 399-401(1994) - examined 13ptss with CO poisoning by MRI; symmetrical lesions of the globus pallidus observed as was degeneration of the withe matter with fical cortical atrophy; the temporal, parietal and occipital lobes were usually affected; those with white matter degen 7 had definite asymmetricl cortical and subcortical lesions;
  • M Lou et al, “Delayed substantia nigra damage and leukoencephalopathy after hypoxic-ischemic injury”, J Neurol Sci, vol 277, nos 1-2, 147-9(2009); post-anoxic encephalopathy associated with carbon monoxide poisoning; delayed neurological decline; MRI revealed early globus pallidus necrosis following by delayed substantia nigra damage and leukencephalopathy
  • Y Umazaki and A Yamada, “Delayed Encephalopathy after Carbon Monoxide Intoxication”, Inter Med vol 47, 1071-1072(2008) - 34yo man showing disorientation and abnormal behavior from carbon monoxide exposure; diagn of delayed encephalopathy after CO inhalation was made; T-2 weighted MRI showed reversible in the splenium of the corpus callosum and periventricular white matter
  • Lo, C_P et al, “Brain Injury after Acute Carbon Monoxide Poisoning: Early and Late Complications”, AJR vol 189, W205-W211(2007) - brain injury in  CO exposed pts arises mainly from hypoxia; usually focused on cerebral cortex; CTs usually show symmetric hypodensity; MRI show the medial portions of the globus pallidus appear as bilateral areas of low signal intensity on T1 weighted images; caudate nucleaus, putamen and thalamus occasionally involved in CO changes;white matter demyelination is believed to be responsible for delayed neuropsyc syndrome

SOURCES

  • CK Chong et al, “Carbon monoxide poisoning from gas water heater and operated in the bathroom”, Med. J Malaysia, vol 52, no 2, 169-171(1997) - gas water heater found to produce 1200ppm CO in bathroom; victims found dead in bathroom
  • JL Thompsen and T Kardel, “Intoxication at home due to carbon monoxide production from gas water heaters”, Forensic Sci Int, vol 36 no 1-2, 69-72(1988) - cites a number of fatalities due to the production of carbon monoxide from gas water heaters; symptoms are insidious;
  • Anon, J Toxicol Clin Toxicol vol 26 no 7, 419-441(1988) - registry of Co poisonings in NYC; mean half life of CO was 2.1hrs

 
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