Carbon Monoxide Poisoning | Tobacco, Air Quality, and Heart Attacks | Interpreting the Pollutant Standards Index | Effects of Pollutants on Lungs & Cardiovascular System
CARBON MONOXIDE POISONING

The Premier Neurotoxicant

By Allan D. Lieberman, M.D.
Center for Occupational and Environmental Medicine, Charleston, SC

Goal: Increase awareness that Carbon Monoxide (CO) poisoning is the single greatest cause of poisoning in America.

Objectives:
1.   Recognize the chemical patterns of injury
2.   Recognize the underlying tissue pathology
3.   To not underestimate the impairments and disability that can come from CO poisoning

In the course of practicing occupational and environmental medicine, physicians see a host of workers and patients who are exposed to neurotoxic substances.

My experience over 29 years of practice in Environmental Medicine reveals a failure of most physicians to recognize neurotoxicity and to deny truly impaired and disabled workers their right to fair compensation for a work related injury.

This presentation recognizes three of the most common causes of neurotoxic injury - solvents, pesticides, and carbon monoxide. Many of the other speakers will present papers on solvents.

An appreciation of the extensive pathological changes seen at autopsy in CO poisoned people explains clearly the clinical features which follow CO poisoning.

In acute CO poisoning with early death, all the viscera, muscles, and the brain show a pink color, marked congestion, and petecheal or massive hemorrhages. In the brain of patients dying after a delay of weeks, the changes typical of anoxia or ischemia are seen and consist of focal or laminar necrosis of the second and third cortical layers and often of the superficial white matter. Lesions of the Purkinje cells of the cerebellum and Ammon's horn are common and consist of ischemic, homogenizing degeneration with glial proliferation and loss of nerve cells. Autopsy studies of those who survive and die years later for other reasons show varying degrees of total, laminar or disseminated focal atrophy. Occasional ischemic necrosis is found in other organs including the heart, skeletal muscles, and kidneys.

Localized damage or hemorrhage into the anterior part of globus pallidus has been considered a characteristic of CO poisoning and attributed to a primary vascular lesion rather than to an effect produced by anoxia. Demyelination of the white matter is more frequently found in those surviving the early stages and is then accompanied by diffuse gliosis and cereberal atropy.1

The acute and chronic effects of CO can mimic virtually any neurologic or psychiatric illness with symptoms resembling:
1.   MS
2.   Parkinsonism
3.   Korsakoffs Amnestic Syndrome
4.   Bipolar Disorder
5.   Schizophrenia
6.   Hysterical conversion reaction
All have been reported.

Insults to the basal ganglia cause:
1.   Tremor
2.   Decreases in motor speed
3.   Slowed reaction time
4.   Poor manual dexterity
5.   Decreased eye hand coordination, and
6.   Poor sequencing of complex motor movements.2

Characteristic of CO poisoning is an induced delayed neuropsychiatric syndrome, consisting of :
1.   A pseudorecovery period (of up to several weeks)
2.   Followed by an abrupt onset of neurologic and psychiatric deterioration (reported to range from 2-30%)
3.   Manifestations include gross neurologic impairment as:
· Parkinsonism
· Apraxia
· Intellectual deterioration
· Memory impairment
· Personality changes
4. Long term sequelae of CO poisoning is:
· Depression
· Anxiety
· Agitation

Case Reports were given
Conclusion:
COHb level correlates poorly, if at all, with loss of consciousness, eventual neurological defect and mortality. Duration of exposure usually provides a better correlation. Longer exposures to low levels may have more dangerous consequences than higher-level, shorter exposures.
If exposed to CO seek immediate medical attention if you experience:
1.   Severe headache
2.   Dizziness
3.   Nausea and vomiting

References
1.   Garland H, Pierce J. Neurological complications of CO poisoning. Quarterly J Med 1967;144:445-455.
2.   Sullivan and Krieger. Hazardous materials toxicology. page 1162.
3.   Bogusz et al. A comparison of two types of acute CO poisoning. Arch Toxicol 1975; 33:141-149.
4.   Sokal & Kralkowska. CO poisoning. Arch Toxicol 1985;57;196-199.
5.   Lasater SR. CO posioning. Can Med Asso J 1986;134:991-92.
6.   Penney DG, White SR. The neural and behavioral effects of carbon monoxide. In Jemsen KF, ed. The vulnerable brain and environmental risks, volume 3: toxins in air and water. New York: Plenum Press, 1994.
 

Disclaimer:
All material provided on the Center for Occupational & Environmental Medicine web site is for educational purposes only. Access to the web site does not create a doctor-patient relationship nor should the information contained on the web site be considered specific medical advice for any person, patient and/or medical condition. Consult a physician regarding the application of any opinions or recommendations from this website, for any symptom or medical condition. Dr. Lieberman specifically disclaims any liability, loss or risk, personal or otherwise, that is or may be incurred as a consequence, directly or indirectly, resulting from use or application pertaining to any of the information provided on the web site.