PROJECT REPORT

CARBON MONOXIDE

SUBMITTED TO:

SUBMITTED BY:

DR. AJAY RANGA VARUN

BHARDWAJ

Carbon Monoxide

RO

LL NO.-204/10

SE

MESTER-IX

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INDEX

1) ACKNOWLEDGEMENT…………………………………………………………………………. 2

2) INTRODUCTION…………………………………………………………………………………..

3

3) SOURCES OF CARBON MONOXIDE………………………………………………………….

4

4) DANGERS OF CARBON MONOXIDE………………………………………………………… 5

5) CARBON MONOXIDE POISIONING…………………………………………………………..

6

6) DIAGNOSIS…………………………………………………………………………………………

8

7) DETECTION………………………………………………………………………………………

11

8) CONCLUSION…………………………………………………………………………………… 13

9) BIBLIOGRAPHY………………………………………………………………………………….

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Carbon Monoxide

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Carbon Monoxide

ACKNOWLEDGMENT

I would like to thank our Honorable teacher Dr. Ajay Ranga, for without his valuable

guidance, constant encouragement and detailed approach would not have made it possible for

me to make a proper research for the topic- Objective and Scope of Forensic Science. His

précised examples, detailed descriptions and enthusiastic approach made my efforts to

flourish in a right direction.

The work contained herein is an amalgamation of the remarkable work of various authors

and I am thankful to them for their publications that have helped me prepare this research

paper to the best of my abilities.

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Carbon Monoxide

INTRODUCTION

Carbon monoxide (CO) is a colorless, odorless, and tasteless gas that is slightly less dense

than air. It is toxic to humans and animals when encountered in higher concentrations,

although it is also produced in normal animal metabolism in low quantities, and is thought to

have some normal biological functions. In the atmosphere, it is spatially variable and short

lived, having a role in the formation of ground-level ozone.

Carbon monoxide is produced from the partial oxidation of carbon-containing compounds; it

forms when there is not enough oxygen to produce carbon dioxide(CO2), such as when

operating a stove or an internal combustion engine in an enclosed space. In the presence of

oxygen, including atmospheric concentrations, carbon monoxide burns with a blue flame,

producing carbon dioxide.1 Coal gas, which was widely used before the 1960s for domestic

lighting, cooking, and heating, had carbon monoxide as a significant fuel constituent. Some

processes in modern technology, such as iron smelting, still produce carbon monoxide as a

byproduct.2

1 Thompson, Mike. Carbon Monoxide – Molecule of the Month, Winchester College, UK.2 Ayres, Robert U. and Ayres, Edward H. (2009). Crossing the Energy Divide: Moving from Fossil Fuel Dependence to a Clean-Energy Future. Wharton School Publishing.

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Carbon Monoxide

SOURCES OF CARBON MONOXIDE

Incomplete combustion occurs in all fires and even in the most efficient appliances and

furnaces. All fossil fuels (e.g. coal, fuel oil, kerosene, gasoline, natural gas) contain carbon,

as do other natural fuels (wood and charcoal). When these fuels burn (or oxidize), CO may

be emitted as one of the gaseous by-products. We are usually surrounded by potential

sources, since so many home gas and oil appliances (furnaces, refrigerators, clothes dryers,

ranges, water heaters, space heaters), fireplaces, charcoal grills, and wood burning stoves use

fossil fuels as their source of energy. Fumes from automobiles and gas-powered lawn tools

also contain carbon monoxide. Tobacco smoke produces low levels of CO in the smoker;

however, the long term effects are not clear and are overshadowed by other detrimental

effects associated with smoking.

Additionally, the inhalation of methylene chloride (CH2CI), a popular industrial solvent

found in home products such as paint and varnish strippers, may result in CO poisoning via

its conversion in the liver to carbon monoxide. Contrary to popular belief, the inhalation of

unburned gaseous fuel (e.g. natural gas and propane) cannot produce CO poisoning; the fuel

must first be burned.

Properly adjusted gas burners in residential heating appliances produce little CO, typically

less than 50 parts per million (ppm). incorrectly operating burners can produce CO in

extremely high concentrations, with units in excess of 4,500 ppm found. Reasons for excess

CO production from heating appliance burners may include: insufficient air to burner, rust

and dirt on burners, air blowing across burners, excess gas pressure, and incorrectly adjusted

air shutters. Some sources always produce high concentrations of CO, such as wood burning

in an open fireplace. smoldering embers, charcoal, and most small gasoline engines. Release

of combustion products from any of these sources into enclosed areas is always extremely

dangerous and must be avoided. All gasoline engines, even those with catalytic converters,

produce high concentrations of carbon monoxide when first started. During a cold start,

tailpipe concentrations can exceed 90,000 ppm Catalytic converters, after warm up, reduce

CO concentrations to only a few parts per million.

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Carbon Monoxide

DANGERS OF CARBON MONOXIDE

Carbon monoxide is rapidly absorbed by the lungs and quickly passes to the blood. The

affinity of CO and the red blood cells, hemoglobin, is 2;0 to 270 times greater than the

affinity of oxygen and hemoglobin. Hemoglobin carrying CO (carboxyhemoglobin), is

incapable of releasing oxygen to the tissues. Even small amounts of carbon monoxide in the

air breathed will quickly increase the percentage of carboxyhemoglobin. For instance,

breathing air with 0.0 I % ( 100 ppm)carbon monoxide for two hours has been shown to

increase blood carboxyhemoglobin concentrations to 16.0%, a concentration that can cause

CO poisoning symptoms.

After breathing carbon monoxide three to four hours of breathing fresh air eliminates only

half the CO from the blood (i.e. a three to four hour half-life). Carbon monoxide is an

extremely dangerous poison because it can not be seen. smelled. or tasted. Early symptoms

are similar to the flu. Because CO reduces oxygen delivery to the brain, persons with

elevated levels of CO in their blood do not think; clearly, and might not recognize the

warning signs.

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Carbon Monoxide

CARBON MONOXIDE POISIONING

Carbon monoxide poisoning occurs after enough inhalation of carbon monoxide (CO).

Carbon monoxide is a toxic gas, but, being colorless, odorless, tasteless, and initially non-

irritating, it is very difficult for people to detect. Carbon monoxide is a product of incomplete

combustion of organic matter due to insufficient oxygen supply to enable complete oxidation

to carbon dioxide (CO2). It is often produced in domestic or industrial settings by motor

vehicles that run on gasoline, diesel, propane, methane, or other carbon-based fuels and tools,

heaters, and cooking equipment that are powered by carbon-based fuels. Exposures at

100 ppm or greater can be dangerous to human health.3

Symptoms of mild acute poisoning will include light-headedness,

confusion, headaches, vertigo, and flu-like effects; larger exposures can lead to significant

toxicity of the central nervous system and heart, and even death. Following acute poisoning,

long-term sequelae often occur. Carbon monoxide can also have severe effects on the fetus of

a pregnant woman. Chronic exposure to low levels of carbon monoxide can lead

to depression, confusion, and memory loss. Carbon monoxide mainly causes adverse effects

in humans by combining with hemoglobin to form carboxyhemoglobin (HbCO) in the blood.

This prevents hemoglobin from releasing oxygen in tissues, effectively reducing the oxygen-

carrying capacity of the blood, leading to hypoxia. Additionally, myoglobin and

mitochondrial cytochrome oxidase are thought to be adversely affected. Carboxyhemoglobin

can revert to hemoglobin, but the recovery takes time because the HbCO complex is fairly

stable.

Treatment of poisoning largely consists of administering 100% oxygen or

providing hyperbaric oxygen therapy, although the optimum treatment remains

controversial.4 Oxygen works as an antidote as it increases the removal of carbon monoxide

from hemoglobin, in turn providing the body with normal levels of oxygen. The prevention

of poisoning is a significant public health issue. Domestic carbon monoxide poisoning can be

prevented by early detection with the use of household carbon monoxide detectors. Carbon

monoxide poisoning is the most common type of fatal poisoning in many

countries.5 Historically, it was also commonly used as a method to commit suicide, usually

3 Prockop LD, Chichkova RI (Nov 2007). "Carbon monoxide intoxication: an updated review".Journal of the Neurological Sciences4 Buckley NA, Isbister GK, Stokes B, Juurlink DN (2005). "Hyperbaric oxygen for carbon monoxide poisoning: a systematic review and critical analysis of the evidence".5 Omaye ST (Nov 2002). "Metabolic modulation of carbon monoxide toxicity".

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Carbon Monoxide

by deliberately inhaling the exhaust fumes of a running car engine. Modern automobiles,

even with electronically-controlled combustion and catalytic converters, can still produce

levels of carbon monoxide which will kill if enclosed within a garage or if the tailpipe is

obstructed (for example, by snow) and exhaust gas cannot escape normally. Carbon

monoxide poisoning has also been implicated as the cause of apparent haunted houses;

symptoms such as delirium and hallucinations have led people suffering poisoning to think

they have seen ghosts or to believe their house is haunted.6

6 Albert Donnay. "A True Tale Of A Truly Haunted House"

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Carbon Monoxide

DIAGNOSIS

The most common test for carbon monoxide poisoning is the blood test for

carboxyhemoglobin (COHb) measured at the time of hospital admission.  However, this test

is susceptible to  false negatives.  As with all other neurologic conditions, the soft signs will

point to disability well before the laboratory evidence may indicate it. 

Think of this analogy: early onset of Alzheimer's appears years before disease has progressed

to the point that neuroimaging can see the lesions.  Yet, there is no doubt of a cognitive or

neurobehavioral decline.  The difference is that with Alzheimer's, the laboratory results will

eventually catch up with the symptoms because of the progressive nature of the disease and

the age of the patient makes the diagnosis one which the average practitioner is comfortable

making without so called “scientific proof.” 

Being late on the diagnosis of carbon monoxide is far more serious than being late on

diagnosis of Alzheimer's.  First, in a chronic exposure situation, you may be sending the

patient back into a toxic environment, where the exposure could continue or worsen. 

Second, the Delayed Neurological Sequalae may result in severe disability. 

Other laboratory tests to consider as non-exclusive additions to the diagnostic effort include:

pulse oximetry,

complete blood count,

arterial blood gas monitoring,

electrolytes,

cardiac markers,

blood uera nitrogen,

creatinine,

creatine phosphokinese,

chest radiography

and ECG.

As many symptoms of carbon monoxide poisoning also occur with many other types of poisonings

and infections (such as the flu), the diagnosis is often difficult.7  A history of potential carbon

7 Varon J, Marik PE, Fromm RE Jr, Gueler A (1999). "Carbon monoxide poisoning: a review for clinicians". The Journal of Emergency Medicine

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Carbon Monoxide

monoxide exposure, such as being exposed to a residential fire, may suggest poisoning, but the

diagnosis is confirmed by measuring the levels of carbon monoxide in the blood. This can be

determined by measuring the amount of carboxy hemoglobin compared to the amount of

hemoglobin in the blood.8

As people may continue to experience significant symptoms of CO poisoning long after their blood

carboxyhemoglobin concentration has returned to normal, presenting to examination with a normal

carboxyhemoglobin level (which may happen in late states of poisoning) does not rule out poisoning.9

A CO-oximeter is used to determine carboxyhemoglobin levels.10 Pulse CO-oximeters estimate

carboxyhemoglobin with a non-invasive finger clip similar to apulse oximeter. These devices

function by passing various wavelengths of light through the fingertip and measuring the light

absorption of the different types of hemoglobin in the capillaries.11

The use of a regular pulse oximeter is not effective in the diagnosis of carbon monoxide poisoning as

people suffering from carbon monoxide poisoning may have a normal oxygen saturation level on a

pulse oximeter. This is due to the carboxyhemoglobin being misrepresented as oxyhemoglobin.12

Breath CO monitoring offers a viable alternative to pulse CO-oximetry. Carboxyhemoglobin levels

have been shown to have a strong correlation with breath CO concentration. However, many of these

devices require the user to inhale deeply and hold their breath to allow the CO in the blood to escape

into the lung before the measurement can be made. As this is not possible in a nonresponsive patient,

these devices are not appropriate for use in on-scene emergency care detection of CO poisoning.13

Differential diagnosis

There are many conditions to be considered in the differential diagnosis of carbon monoxide

poisoning. The earliest symptoms, especially from low level exposures, are often non-specific and

readily confused with other illnesses, typically flu-like viral syndromes, depression, chronic fatigue

syndrome, chest pain, andmigraine or other headaches.[79] Carbon monoxide has been called a "great

mimicker" due to the presentation of poisoning being diverse and nonspecific. Other conditions

included in the differential diagnosis include acute respiratory distress syndrome, altitude

8 Lewis Goldfrank; Neal Flomenbaum; Neal Lewin; Mary Ann Howland; Robert Hoffman; Lewis Nelson (2002). "Carbon Monoxide". Goldfrank's toxicologic emergencies (7th ed.). New York: McGraw-Hill. pp. 1689–1704.9 Keleş A, Demircan A, Kurtoğlu G (June 2008). "Carbon monoxide poisoning: how many patients do we miss?". European Journal of Emergency Medicine 15 (3): 154–15710 Rees PJ, Chilvers C, Clark TJ (January 1980)11 Coulange M, Barthelemy A, Hug F, Thierry AL, De Haro L (March 2008)12 Vegfors M, Lennmarken C (May 1991). "Carboxyhaemoglobinaemia and pulse oximetry". British Journal of Anaesthesia13 Jarvis, M. (1986). "Low cost carbon monoxide monitors in smoking assessment". Thorax: 886–887

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Carbon Monoxide

sickness, lactic acidosis, diabetic ketoacidosis, meningitis,methemoglobinemia, or opioid or toxic

alcohol poisoning.14

Detection in biological specimens

Carbon monoxide may be quantitated in blood using spectrophotometric methods or chromatographic

techniques in order to confirm a diagnosis of poisoning in a person or to assist in the forensic

investigation of a case of fatal exposure. Carboxyhemoglobin blood saturations may range up to 8–

10% in heavy smokers or persons extensively exposed to automotive exhaust gases. In symptomatic

poisoned people they are often in the 10–30% range, while persons who succumb may have

postmortem blood levels of 30–90%.15

14 Shochat, Guy N (17 February 2009). "Toxicity, Carbon Monoxide". emedicine15 R. Baselt, Disposition of Toxic Drugs and Chemicals in Man, 8th edition, Biomedical Publications, Foster City, CA, 2008, pp. 237–241

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DETECTION

CO poisoning is known as the great imitator for its ability to present with equivocal signs and

symptoms, many of which closely resemble other diseases. In particular, patients may be

misdiagnosed with viral illness, acute myocardial infarction, and migraine. It is estimated that CO

poisoning misdiagnosis may occur in up to 30-50 percent of CO-exposed patients presenting to

emergency departments.

Regardless of the means of detection used in emergency department care, several factors make

assessing the severity of the CO poisoning difficult. The length of time since CO exposure is one such

factor. The half-life of CO is four to six hours when the patient is breathing room air, and 40–60

minutes when the patient is breathing 100 percent oxygen. If a patient is given oxygen during their

transport to the emergency department, it will be difficult to know when the COHb level peaked.16

In addition, COHb levels may not fully correlate with the clinical condition of CO-poisoned patients

because the COHb level in the blood is not an absolute index of compromised oxygen delivery at the

tissue level. Furthermore, levels may not match up to specific signs and symptoms; patients with

moderate levels will not necessarily appear sicker than patients with lower levels.17

In hospitals, the most common means of measuring CO exposure is through the use of a laboratory

CO-Oximeter. A blood sample, under a physician order, is drawn from either venous or arterial vessel

and injected into a lab CO- Oximeter. The laboratory device measures the invasive blood sample

using a method called spectrophotometric blood gas analysis.18 Because the CO-Oximeter can only

yield a single, discrete reading for each aliquot of blood sampled, the reported value is a

noncontinuous snapshot of the patient’s condition at the particular moment that the sample was

collected. To compound the difficulty of detecting CO exposure, when the laboratory calculates the

patient’s oxygen saturation levels from the oxygen partial pressure (PO2), the arterial SaO2 may

appear normal. The clinical usefulness of CO-Oximetry is inhibited further by the relative deficiency

of devices currently installed in acute care hospitals. One recent study found that fewer than half of

hospitals in the U.S. have the necessary equipment on site to diagnose CO poisoning.19 For those that

did not have the testing equipment, the average time to receive results of a blood sample sent to

16 Wright J. Chronic and occult carbon monoxide poisoning: we don’t know what we’re missing. Emerg Med J.2002;19(5):386-90.17 Abelsohn A, et al. Identifying and managing adverse environmental health effects: 6. Carbon monoxide poisoning. CMAJ. 2002;166(13):1685-9018 Cunnington AJ, Hormbrey P: “Breath analysis to detect recent exposure to carbon monoxide.” Postgraduate Medical Journal. 78(918):233–237, 200219 Hampson NB, Scott KL, Zmaeff JL. Carboxyhemoglobin measurement by hospitals: implications for the diagnosis of carbon monoxide poisoning. J Emerg Med. 2006 Jul;31(1):13-6.

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another facility was over 15 hours. In hospitals that have CO-Oximetry equipment, results may be

returned in an average of 10 minutes.

Unfortunately, standard pulse oximeters are incapable of isolating the carbon monoxide contaminated

hemoglobin from the oxyhemoglobin.20 Thus, pulse oximeters artificially overestimate arterial

oxygen saturation in the presence of elevated blood carbon monoxide. Therefore, the readings will be

falsely high when carbon monoxide is occupying binding sites on the heme molecule.

The latest technology in CO poisoning detection employs a noninvasive and continuous platform. The

Masimo SET® with Rainbow Technology Pulse CO-Oximeter Monitor [Masimo, Irvine, CA] is the

first device that allows clinicians to detect and continuously monitor CO levels in the bloodstream

noninvasively. Using 7+ wavelengths of light to distinguish the various forms of hemoglobin (oxy-,

deoxy-,carboxy- and met-) the device is capable of measuring blood CO saturation (SpCO) levels,

methemoglobin saturation (SpMet) levels, in addition to pulse rate, arterial oxygen saturation, and

perfusion index. The device’s accuracy has been demonstrated accurate to 40 percent SpCO, with a

range of ± 3 percent around the measurement.

Noninvasive monitoring reduces the opportunity for hospital acquired infection and overall patient

discomfort. Needle-free testing means a safer environment for patients and caregivers alike. In

addition, the immediacy of results available at the point-of-care results in less drain on resources

while expediting efficacious treatment and better outcomes. The continuous nature of the noninvasive

Rainbow Pulse CO-Oximeter device enables the ability to trend data over time while conventional

CO-Oximetry requires a new blood sample each time the status of the dyshemoglobins is required.

20 Hampson NB: “Pulse oximetry in severe carbon monoxide poisoning.” Chest.114(4):1036–1041, 1998

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CONCLUSION

The effects of CO poisoning can be reversed if caught in time. Detection and diagnosis of CO

poisoning is currently based upon clinical suspicion and confirmed by invasive blood sampling for

COHb analyzed by CO-Oximetry. While many hospitals have blood gas machines with CO-

Oximetry, many smaller hospitals do not, which makes timely confirmed diagnosis of CO poisoning

in these situations impossible. Organs with a high metabolic requirement for oxygen, such as the

heart and brain, are particularly susceptible to injury from CO. The resulting tissue ischemia can lead

to organ failure, permanent changes in cognition, or death. Those that survive the initial poisoning

may experience serious long-term neurological, cardiac, metabolic, pulmonary and renal impairment

as a result of their CO exposure.

With lives and significant resources at stake, the speed at which suspicion evolves to diagnosis is

critical. A quick noninvasive measurement of COHb using the new Masimo Pulse CO-Oximeter

device may contribute to better informed treatment decisions ending the guessing game.

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BIBLIOGRAPHY

Books

Textbook of Modis Medical Jurisprudence and Toxicology, K. Kannan and K.

Mathiharan, Buttersworths India, 2012

Medical Jurisprudence, R.M. Jhala and K Raju, Eastern Book Company, 1997.

Analytical Toxicology, S.N. Tiwari, Govt of India Publication, New Delhi, 1987.

Websites

http://forensiclaw.uslegal.com

http://lawforensics.org

http://www.annexpublishers.com/journals/journal-of-forensic-science-and-

criminology/aims-and-scope.php

E-Books

Porter, Roy; Lorraine Daston; Katharine Park. The Cambridge History of Science:

Volume 3, Early Modern Science

Madea, Burkhard. Handbook of Forensic Medicine. Sussex: Wiley Blackwell

Lindemann, Mary. Medicine and Society in Early Modern Europe. Cambridge:

University of Cambridge

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