Carbon monoxide: Human health tier II assessment

04 July 2014

CAS Number: 630-08-0

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This assessment was carried out by staff of the National Industrial Chemicals Notification and Assessment Scheme (NICNAS) using the Inventory Multi-tiered Assessment and Prioritisation (IMAP) framework.

The IMAP framework addresses the human health and environmental impacts of previously unassessed industrial chemicals listed on the Australian Inventory of Chemical Substances (the Inventory).

The framework was developed with significant input from stakeholders and provides a more rapid, flexible and transparent approach for the assessment of chemicals listed on the Inventory.

Stage One of the implementation of this framework, which lasted four years from 1 July 2012, examined 3000 chemicals meeting characteristics identified by stakeholders as needing priority assessment. This included chemicals for which NICNAS already held exposure information, chemicals identified as a concern or for which regulatory action had been taken overseas, and chemicals detected in international studies analysing chemicals present in babies’ umbilical cord blood.

Stage Two of IMAP began in July 2016. We are continuing to assess chemicals on the Inventory, including chemicals identified as a concern for which action has been taken overseas and chemicals that can be rapidly identified and assessed by using Stage One information. We are also continuing to publish information for chemicals on the Inventory that pose a low risk to human health or the environment or both. This work provides efficiencies and enables us to identify higher risk chemicals requiring assessment.

The IMAP framework is a science and risk-based model designed to align the assessment effort with the human health and environmental impacts of chemicals. It has three tiers of assessment, with the assessment effort increasing with each tier. The Tier I assessment is a high throughput approach using tabulated electronic data. The Tier II assessment is an evaluation of risk on a substance-by-substance or chemical category-by-category basis. Tier III assessments are conducted to address specific concerns that could not be resolved during the Tier II assessment.

These assessments are carried out by staff employed by the Australian Government Department of Health and the Australian Government Department of the Environment and Energy. The human health and environment risk assessments are conducted and published separately, using information available at the time, and may be undertaken at different tiers.

This chemical or group of chemicals are being assessed at Tier II because the Tier I assessment indicated that it needed further investigation.

For more detail on this program please


NICNAS has made every effort to assure the quality of information available in this report. However, before relying on it for a specific purpose, users should obtain advice relevant to their particular circumstances. This report has been prepared by NICNAS using a range of sources, including information from databases maintained by third parties, which include data supplied by industry. NICNAS has not verified and cannot guarantee the correctness of all information obtained from those databases. Reproduction or further distribution of this information may be subject to copyright protection. Use of this information without obtaining the permission from the owner(s) of the respective information might violate the rights of the owner. NICNAS does not take any responsibility whatsoever for any copyright or other infringements that may be caused by using this information.

Acronyms & Abbreviations

Chemical Identity

Synonyms Carbon oxide
Carbonic oxide
Flue gas
Structural Formula Structural formula of Carbon monoxide
Molecular Formula CO
Molecular Weight (g/mol) 28.01
Appearance and Odour (where available) A colourless and tasteless gas.
SMILES C{-}#O{+}


The following Australian industrial uses were reported under previous mandatory and/or voluntary calls for information:

The chemical carbon monoxide (CO) has reported site-limited use including in chemical manufacturing processes and as a laboratory agent.

The total volume introduced into Australia, reported under previous mandatory and/or voluntary calls for information, was less than 10 tonnes.

The National Pollutant Inventory (NPI) holds data for all sources of emissions of the chemical in Australia.



The following international uses have been identified through European Union Registration, Evaluation and Authorisation of Chemicals (EU REACH) dossiers; the Organisation for Economic Cooperation and Development Screening information data set International Assessment Report (OECD SIAR); Galleria Chemica; Substances and Preparations in the Nordic countries (SPIN) database; the European Commission Cosmetic Ingredients and Substances (CosIng) database;  and eChemPortal: OECD High Production Volume chemical program—OECD HPV, and the US Environmental Protection Agency's Aggregated Computer Toxicology Resource—ACToR.

The chemical has reported commercial and site-limited uses including in the petrochemical industry and in the manufacturing of metal carbonyls and polymer. The chemical is also used as a reagent in laboratories and a reducing agent in metal refineries.

The chemical is produced during the incomplete combustion of fossil fuels and biomass. It is naturally and anthropogenically produced, but the majority of the CO emitted into the atmosphere arises from gasoline-powered automobile usage, and tobacco smoke is a major contributor to indoor air levels.


No known restrictions have been identified.


The chemical is listed on the following (Galleria Chemica):

EU Cosmetics Regulation 1223/2009 Annex II—List of substances prohibited in cosmetic products; and

New Zealand Cosmetic Products Group Standard—Schedule 4: Components cosmetic products must not contain.

Existing Work Health and Safety Controls

Hazard Classification

The chemical is classified as hazardous, with the following risk phrases for human health in the Hazardous Substances Information System (HSIS) (Safe Work Australia):

Repr. Cat 1: R61 T;  May cause harm to the unborn child

R23 Toxic by inhalation

R48/23 Toxic; Danger of serious damage to health by prolonged exposure through inhalation.


The chemical has an exposure standard of 34 mg/m³ (30 ppm) time weighted average (TWA).


The following exposure standards are identified (Galleria Chemica):

An exposure limit (time weighted average) of:

    •  3 mg/m³ or 5 ppm threshold limit value (TLV)  in Lithuania;
    • 20 mg/m³ in China and Latvia;
    • 20 mg/m³ in Russia;
    • 23 mg/m³ in Ireland and Poland;
    • 25 ppm in Colombia;
    • 29 mg/m³ or 25 ppm in Belgium, Canada (all provinces except Yukon), Denmark, Iceland, Netherlands, Hong Kong, Italy, Malaysia, Nicaragua, Norway, Peru, Portugal, United Arab Emirates, Indonesia, Singapore,  Spain, USA (CA), Venezuela and Indonesia;
    • 30 mg/m³ in Czech Republic;
    • 33 mg/m³ or 30 ppm in Austria, Hungary and Croatia;  
    • 35 mg/m³ or 30 ppm in Finland, South Korea, Germany, Slovak Republic, South Africa, Switzerland, United Kingdom;
    • 40 mg/m³ in Taiwan, Bulgaria, Sweden, USA;
    • 43 mg/m³ or 39 ppm in Brazil;
    • 46 mg/m³ or 40 ppm in Chile;
    • 55 mg/m³ or 50 ppm in Argentina, Thailand, United Kingdom, Philippines, Mexico, Egypt, France, Greece, USA (ID, OR, WY), India and Canada (Yukon); and
    • 57 mg/m³ or 50 ppm in Japan.

The workplace exposure standard (WES) in New Zealand is 25 ppm and the short-term exposure limit (STEL) in Slovak Republic is 35 mg/m³ or 30 ppm. The American Conference of Governmental Industrial Hygienists (ACGIH) recommends a TLV of 25 ppm (29 mg/m³) TWA. This value is intended to maintain blood carboxyhaemoglobin (COHb) levels below 3.5 %, to minimise potential for adverse neurobehavioural changes, and to maintain cardiovascular work and exercise capabilities (ACGIH, 2011).

Due to the gaseous nature of the chemical under normal exposure conditions, data on exposure routes other than inhalation are scarce and unlikely to relate to actual conditions of human exposure.


Upon inhalation, CO is rapidly absorbed through the lungs and extensively distributed throughout the body through the bloodstream. In the blood, CO forms a tight but reversible complex with haemoglobin (Hb) known as carboxyhaemoglobin (COHb) and in muscles, it exists as a complex with myoglobin (COMb). The amount of CO absorbed largely depends on the concentration of environmental CO, minute ventilation and duration of exposure.

The binding affinity of CO for haemoglobin (Hb) is over 200 times greater than that of oxygen. The presence of CO in the blood competes with oxygen at the haem binding sites; thus, reducing its oxygen carrying capacity. As a consequence, the release of oxygen from the bloodstream is impaired, which leads to tissue hypoxia (lack of oxygen). This gives rise to CO-induced toxicity which largely affects the metabolic activity of the cell through hypoxic and to some extent, non-hypoxic modes of action.

Considering that COHb is fully dissociable, the absorbed CO does not accumulate in the body. It is eliminated from the system predominantly by exhaling and to a lesser extent, by oxidative metabolism. The elimination half time of CO is influenced by several factors including age and sex. In sedentary adults, the biological half-life of CO is between two to five hours. For individuals aged two to 20 years, the elimination half-life is increased. It is also 6 % longer in males than in females. During pregnancy, the concentration of COHb in the foetal blood is higher than in maternal blood. The elimination kinetics of COHb are slower in the foetal blood than in the maternal blood (ATSDR 2012; EPA, 2010; EHC; REACH; Raub et al., 2000; Weaver, 2009).


No data are available.


No data are available.


The chemical is classified as hazardous with the risk phrase ‘Toxic by inhalation’ (T; R23) in HSIS (Safe Work Australia). The data available support this classification with reported median lethal concentrations (LC50s) in rats of between 1.4 and 2 mg/L/4hr. Reported signs of toxicity include loss of consciousness, unsteady gait, irregular breathing and pink/red extremities (REACH). Similar effects were observed in mice and guinea pigs although the mortality in guinea pigs was lower than in mice, suggesting that mice are more susceptible to CO-induced toxicity. The LC50 for this study was reported to be 2.8 mg/L/4hr  for mice and 6.5 mg/L/4hr for guinea pigs (REACH).

Observation in humans

The toxic effects of CO from acute inhalation exposure are well-documented in humans. The extent of adverse effects depends upon the concentration and duration of exposure and the underlying health status of the exposed individual. Findings from clinical reports indicated that acute inhalation exposure to CO can lead to pathological damage, most notably to the cardiovascular system (CVS) and central nervous system (CNS) (see Neurotoxicity). CO inhalation can be fatal at high concentrations. The CNS and the CVS are the most metabolically active and the largest consumers of oxygen and are primary targets of CO poisoning. Acute CO posioning during pregnancy has been associated with developmental effects (see Reproductive and developmental toxicity).

CO-induced effects in the CVS, occuring from minutes to hours after exposure, include the lowering of the blood pressure and blood disorder (methaemoglobinaemia), chest pains and myocardial infarction (ASTDR 2012, Marius-Nunez, 1990). Effects of severe CO poisoning may be life-threatening and include cardiac arrhythmias, myocardial ischaemia, cardiac arrest, hypotension, respiratory arrest and noncardiogenic pulmonary oedema (ASTDR, 2012). Results of controlled clinical studies in patients with coronary artery disease showed that acute-duration exposure to CO at levels producing blood COHb levels between 2.4 % and 5.9 % exacerbates underlying cardiovascular conditions, including increased myocardial ischaemia and cardiac arrhythmias (ASTDR, 2012).

Skin Irritation

No data are available.

Eye Irritation

No data are available.

Skin Sensitisation

No data are available.


No data are available.


No data are available.


The chemical is classified as hazardous with the risk phrase ‘Toxic: danger of serious damage to health by prolonged exposure through inhalation’ (T; R48/23) in HSIS (Safe Work Australia). The data available support this classification. The primary targets for toxicity are the heart and cardiovascular system, the central nervous system (see Neurotoxicity), and the foetus and neonate (see Reproductive and developmental toxicity). Adverse effects in the respiratory tract have been observed in human clinical studies and in animal studies at higher exposures than those associated with effects on the cardiovascular and central nervous systems and on development (ASTDR, 2012).

In a 72-week repeat dose inhalation toxicity study in male and female Sprague Dawley rats, the lowest observed adverse effect concentration (LOAEC) for the chemical was reported to be 229 mg/m³ (200 ppm). Exposure to 229 mg/m³ CO (comparable to tobacco smoking) for 20 hours a day, five days a week for 72 weeks resulted in the enlargement of the heart. Other parameters such as incidence of tumour development, organ weights and alteration in pulmonary and systemic arteries were also evaluated in this study; however, no other significant pathologies were observed (Sorhaug et al., 2006).

The effects of chronic CO exposure in the cardiovascular system at various doses were also reported. Exposure of male Wistar rats to 30 -100 ppm (34.5 - 115 mg/m³) CO for four weeks resulted in significant myocardial abnormalities, including  arrhythmia and impairment of ventricular myocyte functions (Myer et al., 2009). In a similar study, Mirza and colleagues reported that exposure of male Wistar rats to 500 ppm (573 mg/m³) CO induced cardiac hypertrophy and elevated expression of heme oxygenase-1, a marker for stress in the myocardium. The ensuing damage was worst in rats suffering from pre-existing myocardial condition. These findings also support previous reports that chronic CO inhalation can exacerbate heart failure in those with pre-existing conditions (Myer et al., 2009). In rabbits, exposure to 180 ppm (206 mg/m³) CO for two weeks resulted in extensive structural damage of the myofibrillar elements and mitochrondria of the heart (Kjeldsen et al., 1974). Similarly, exposure to 500 ppm (573 mg/m³) of CO for three to four weeks caused cardiac abnormalities (Bugaisky and Penney 1976).

Observation in humans

Clinical findings have established that chronic exposure to CO induces reversible and irreversible damage in humans. In particular, the heart and the brain are more susceptible to CO-induced toxicity due to the high metabolic demands of these tissues. Mild or moderate levels of the CO exposure leads to myocardial injuries, fatigue, memory loss, sleep disturbance, vertigo, hearing loss, bilateral cataracts and brain lesions in humans; while exposure to high levels is fatal (Kasbekar and Gonzalez-Martin 2011; Henry et al., 2006; Mehrparvar et al., 2013; Weaver, 2009; Townsend and Maynard 2002).

Whilst the heart and the brain are expected to be more susceptible to CO-induced toxicity due to their high metabolic demand, epidemiological evidence of the effects of long-term CO exposure in the CVS and CNS is limited. In addition, the causal association between long-term exposure to CO and respiratory effects is uncertain (ASTDR, 2012, US EPA 2010).


Limited data are available.

It was reported that exposure to CO inhibited DNA synthesis in an in vitro bacterial replication assay in Escherichia coli, although the lack of data reporting limits the interpretation of this study (ASTDR, 2012).

Increases in micronuclei and sister chromatid exchanges in maternal bone marrow and foetal blood were observed in pregnant mice exposed either to 0, 1, 500, 2500, or 3500 ppm CO for 10 minutes on gestational days 5, 11, or 15 or to 0 or 500 ppm CO for one hour on gestational days 0–6, 7–13, or 14–20 (ASTDR, 2012).


No data are available.

The chemical is classified as hazardous—Category 1 substance toxic to reproduction—with the risk phrase ‘May cause harm to the unborn child’ (T; R61) in HSIS (Safe Work Australia). The available data support this classification.

Numerous animal studies are available which show adverse developmental effects of gestational and early postnatal CO exposure (ASTDR 2012; US EPA 2010; Margulies, 1986; Caravati et al., 1989; Clubb et al., 1989; Webber et al., 2003). Effects include:

  •  increased mortality;
  •  decreased birth weight and prenatal growth;
  •  adverse central nervous system development such as behavioural changes, learning/memory deficits and locomotor effects;
  •  cardiac effects including transient cardiomegaly and delayed myocardial electrophysiological maturation; and
  • changes in the auditory system.

The lowest LOAEC value for developmental effects was reported in a study evaluating effects of CO exposure on the auditory system. In this study, newly-born rat pups were chronically exposed to mild doses of CO at 0, 12.5, 25 and 50 ppm (0, 14.3, 28.6, 57.3 mg/m3) from postnatal day (PND) 8 to 20-22. The CO-induced effects were evaluated at PND27, five days after the cessation of exposure and at PND75-77 (50 days after exposure). The results showed that, following exposure to 12.5 – 25 ppm of CO, marked changes in the brain activity and anomalies in the development of the auditory system occured (ASTDR 2012; US EPA, 2010).

Furthermore, there is limited epidemiological evidence of developmental effects in humans, including pre-term birth, cardiac defects and reduced foetal growth as a result of CO exposure (ASTDR, 2012; US EPA, 2010).


Acute or chronic exposures to mild or high levels of CO are neurotoxic in both humans and animals. Several studies have suggested that COHb levels between five to 20 % in the blood cause neurological abnormalities. Because it is a tasteless and an odourless gas, CO poisoning is difficult to detect and the symptoms can be vague and non-specific. Immediate clinical manifestations in patients with acute CO poisoning include neurotoxic effects such as dizziness, nausea, lethargy, headache, drowsiness, weakness, vomiting, cognitive deficits, confusion, visual disturbances, convulsions and coma. Following CO poisoning, patients continue to suffer from several neurological disorders including motor disturbances, hearing loss, peripheral neuropathy, delayed neuropsychiatric impairment and other neurobehavioural abnormalities. These observed clinical and pathological effects were also reported in several experimental studies in animal models for this condition, strongly indicating the neurotoxicity of CO (Raub et al., 2000; Mehrparvar et al., 2013; Bateman 2007; Blumenthal 2001; Lopez et al., 2009; Prockop et al., 2007; ATSDR 2012; Devine et al., 2001; Penny et al., 1989).

In utero CO exposure has been shown to cause neurodevelopmental effects (see Reproductive and developmental toxicity).

Critical Health Effects

The critical health effects for risk characterisation include systemic long-term effects (developmental and cardiovascular toxicity) and systemic acute effects by inhalation. The heart and cardiovascular system, the central nervous system and the developing foetus are sensitive to the chemical. Individuals diagnosed with existing cardiovascular and/or respiratory disease are particularly susceptible.

Endogenously produced CO is not associated with toxicity.

Public Risk Characterisation

Given the uses identified for the chemical, it is unlikely that the public will be exposed through use of consumer products other than through combustion (e.g. cigarettes, motor vehicles and gas heaters). Exposures from industrial sources are expected to be much lower than ambient exposures from cigarette smoke and petrol fumes. Thus, the chemical is not considered to pose an unreasonable risk to public health from industrial uses of CO.

Occupational Risk Characterisation

During industrial use, inhalation exposure to CO is expected to be highly controlled because of its well known acute toxicity. In the absence of adequate control measures, particularly for inhalation exposure, the chemical may pose an unreasonable risk.

The chemical should be appropriately classified and labelled to ensure that a person conducting a business or undertaking (PCBU) at a workplace (such an employer) has adequate information to determine appropriate controls. As individuals with existing cardiovascular and/or respiratory disease or pregnant workers may be particularly susceptible to the effects of CO, the airborne concentration of the chemical should be kept as low as practically possible and within the exposure standards (see Exposure standards) to minimise risk.

Based on the available data, the hazard classification in HSIS is considered appropriate.

The chemical is also expected to be a constituent of a number of UVCB chemicals within the petroleum industry, for which the exposures should be controlled. The risks from exposure to CO as a constituent of UVCB chemicals will be further considered as part of any IMAP assessment of these chemicals.  

NICNAS Recommendation

Current risk management measures are considered adequate to protect public and workers’ health and safety, provided that all requirements are met under workplace health and safety and poisons legislation as adopted by the relevant state or territory. No further assessment is required.

Work Health and Safety

The chemical is recommended for classification and labelling under the current approved criteria and adopted GHS as below. This assessment does not consider classification of physical hazards and environmental hazards.

Hazard Approved Criteria (HSIS)a GHS Classification (HCIS)b
Acute Toxicity Toxic by inhalation (T; R23)* Toxic if inhaled - Cat. 3 (H331)
Repeat Dose Toxicity Toxic: danger of serious damage to health by prolonged exposure through inhalation (T; R48/23)* Causes damage to organs through prolonged or repeated exposure through inhalation - Cat. 1 (H372)
Reproductive and Developmental Toxicity Repro. Cat 1 - May cause harm to the unborn child (T; R61)* May damage fertility or the unborn child - Cat. 1A (H360)

a Approved Criteria for Classifying Hazardous Substances [NOHSC:1008(2004)].

b Globally Harmonized System of Classification and Labelling of Chemicals (GHS) United Nations, 2009. Third Edition.

* Existing Hazard Classification. No change recommended to this classification

Advice for industry

Control measures

Control measures to minimise the risk from inhalation exposure to the chemical should be implemented in accordance with the hierarchy of controls. Approaches to minimise risk include substitution, isolation and engineering controls. Measures required to eliminate or minimise risk arising from storing, handling and using a hazardous chemical depend on the physical form and the manner in which the chemical is used. Examples of control measures which may minimise the risk include, but are not limited to:

  • using closed systems or isolating operations;
  • using local exhaust ventilation to prevent the chemical from entering the breathing zone of any worker;
  • health monitoring for any worker who is at risk of exposure to the chemical if valid techniques are available to monitor the effect on the worker’s health;  
  • air monitoring to ensure control measures in place are working effectively and continue to do so;
  • minimising manual processes and work tasks through automating processes;
  • work procedures that minimise splashes and spills;
  • regularly cleaning equipment and work areas; and
  • using protective equipment that is designed, constructed, and operated to ensure that the worker does not come into contact with the chemical.

Guidance on managing risks from hazardous chemicals are provided in the Managing Risks of Hazardous Chemicals in the Workplace—Code of Practice  available on the Safe Work Australia website.

Personal protective equipment should not solely be relied upon to control risk and should only be used when all other reasonably practicable control measures do not eliminate or sufficiently minimise risk. Guidance in selecting personal protective equipment can be obtained from Australian, Australian/New Zealand or other approved standards.

Obligations under workplace health and safety legislation

Information in this report should be taken into account to assist with meeting obligations under workplace health and safety legislation as adopted by the relevant state or territory.  This includes, but is not limited to:

  • ensuring that hazardous chemicals are correctly classified and labelled;
  • ensuring that (material) safety data sheets ((m)SDS) containing accurate information about the hazards (relating to both health hazards and physicochemical (physical) hazards) of the chemical are prepared; and
  • managing risks arising from storing, handling and using a hazardous chemical.

Your work health and safety regulator should be contacted for information on the work health and safety laws in your jurisdiction.

Information on how to prepare an (m)SDS and how to label containers of hazardous chemicals are provided in relevant codes of practice such as the Preparation of Safety Data Sheets for Hazardous Chemicals— Code of Practice and Labelling of Workplace Hazardous Chemicals—Code of Practice, respectively. These codes of practice are available from the Safe Work Australia website.

A review of the physical hazards of the chemical has not been undertaken as part of this assessment.


ACGIH (American Conference of Governmental Industrial Hygienists).  Documentation of the Threshold Limit Values for Chemical Substances, ACGIH Signature Publications, 7th Edition,  2011.

Agency for Toxic Substances and Disease Registry (ATSDR) 2012. Toxicological profile for Carbon monoxide. Accessed December 2013.

Bateman DN 2007. Carbon Monoxide. Medicine 35 (11) pp. 604

Blumenthal I 2001. Carbon monoxide poisoning. Journal of the Royal Society of Medicine 94 pp. 270-272

Bugaisky L, Penney D 1976. Chronic carbon monoxide poisoning: effects on performance of the isolated right ventricle. Journal of Applied Physiology 40 (3) pp. 324-328

Caravati EM, Adams C, Joyce S, Schafer N 1988. Fetal toxicity associated with maternal carbon monoxide poisoning. Annals of Emergency Medicine 7 (17) pp 105-108

ChemIDPlus Advanced. Accessed December 2013 at

Clubb JF, Penney DG, Bishop SP 1989. Cardiomegaly in neonatal rats exposed to 500 ppm carbon monoxide. Journal of Molecular and Cellular Cardiology 21 pp. 945-955

Devine S, Kirkley S, Palumbo C, White R 2002. MRI and neuropsychological correlates of carbon monoxide exposure: A case report. Grand Rounds in Environmental Medicine 110 (10) pp. 1051-1055

Environmental Health Criteria (EHC, 213) for carbon monoxide (second edition). Accessed December 2013.

Environmental Protection Agency (2010). Quantitative Risk and Exposure Assessment of Carbon Monoxide - Amended. Accessed December 2013.

Galleria Chemica. Accessed December 2013.

Henry CR, Satran D, Lindgren B, Adkinson C, Nicholson CI, Henry TD 2006. Myocardial injury and long-term mortality following moderate to severe carbon monoxide poisoning. The Journal of the American Medical Association 295 (4) pp. 398-402

Kasbekar S, Gonzalez JA 2011. Chronic carbon monoxide poisoning resulting in bilateral cataracts and a cystic globus pallidus lesion. BMJ Case Reports 10 pp. 3985

Kjeldsen K, Thomsen HK, Astrup P 1974. Effects of carbon monoxide on myocardium: ultrastructural changes in rabbits after moderate, chronic exposure. Circulation Research 34 pp. 339-348

Lopez I, Acuna D, Beltran-Parraza L, Lopez I, Amarnani A, Cortes M, Edmond J 2009. Evidence for oxidative stress in the developing cerebellum of the rat after chronic mild carbon monoxide exposure (0.0025%). BMC Neuroscience doi: 10.1186/1471-2202-10-53 (

Margulies, JL. 1986. Acute carbon monoxide poisoning during pregnancy. The American Journal of Emergency Medicine 4 (6) pp. 518-519

Marius-Nunez AL 1990. Myocardial infarction with normal coronary arteries after acute exposure to carbon monoxide. Chest 97(2) pp. 491-494

Mehrparvar A, Davari M, Mollasadeghi A, Vahidi M, Mostaghaci M, Bahaloo M, Shokouh P 2013. Hearing loss due to carbon monoxide poisoning. Case Reports in Otolaryngology 1155 (10) pp. 1-3

Myer G, Andre L, Tanguy S, Boissiere J, Farah C, Lopez-Lauri F, Gayrard S, Richard S, Boucher F, Cazorla O, Obert P, Reboul C 2010. Simulated urban carbon monoxide air pollution exacerbates rat heart ischemia-reperfusion injury. American Journal of Physiology Heart and Circulatory Physiology  298(5) pp. 1445-1453

National Pollutant Inventory (NPI). Accessed December 2013 at

Penney DG, Verma K, Hull JA 1989. Cardiovascular, metabolic and neurologic effects of acute carbon monoxide poisoning in the rat. Toxicology Letters 45 (2-3) pp. 207-2013

Prockop L and Chichkova R 2007. Carbon monoxide intoxication: an updated review. Neurological Sciences 262 pp. 122-130

Raub J, Mathieu-Nolf M, Hampson N, Thom S 2000. Carbon monoxide poisoning – a public health perspective. Toxicology 145 pp. 1-14

REACH Dossier. Carbon monoxide ( 680-08-0) Accessed December 2013 at

Safe Work Australia (SWA). Hazardous Substances Information System (HSIS). Accessed December 2013,

Sorhaug S, Steinshamn S, Nilsen O, Waldum H 2006. Chronic inhalation of carbon monoxide: Effects on the respiratory and cardiovascular system at doses corresponding to tobacco smoking. Toxicology 228 pp 280-290

Townsend C, Maynard R 2002. Effects on health of prolonged exposure to low concentrations of carbon monoxide. Occupational and Environmental Medicine 59 pp. 708-711

US Environmental Protection Agency (2010). Integrated Science Assessment for Carbon Monoxide. Accessed December 2013 at

Weaver L 2009. Carbon monoxide poisoning. The New England Journal of Medicine 360 (12) pp.1217-1225

Webber D, Korsak R, Sininger L, Sampogna S, Edmond J 2003. Mild carbon monoxide exposures impairs the developing auditory system of the rat. Journal of Neuroscience Research 74 (5) pp. 655-665

Last update 04 July 2014