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Please be aware that this old REACH registration data factsheet is no longer maintained; it remains frozen as of 19th May 2023.

The new ECHA CHEM database has been released by ECHA, and it now contains all REACH registration data. There are more details on the transition of ECHA's published data to ECHA CHEM here.

Diss Factsheets

Toxicological information

Endpoint summary

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Administrative data

Description of key information

Key value for chemical safety assessment

Skin sensitisation

Endpoint conclusion
Additional information:

As carbon monoxide is a gas, sensitisation via skin is not considered relevant. Furthermore, the wealth of available human data on CO does not indicate that the substance is a skin sensitiser.

Migrated from Short description of key information:

Skin sensitisation - waiver

Respiratory sensitisation

Endpoint conclusion
Endpoint conclusion:
no adverse effect observed (not sensitising)
Additional information:


The discussion below regarding respiratory sensitisation of carbon monoxide (CO) is primarily from investigations in humans. The assessment is summarised from authoritative reviews of extensive, relevant and current published literature (EPA, 2010 and EHC, 1999). The citations discussed have been taken from the current published literature. The citations discussed have been taken from the current published literature, with references below documented in full in the published literature.

Markers of respiratory sensitisation are manifest in the form of respiratory reactions including asthma, rhinitis and alveolitis. The studies below used these endpoints by which to assess the effect of CO on the respiratory system.


Respiratory Sensitisation

Hwang et al. (2006) and Lee et al. (2003) both examined the effect of long-term exposure to air pollutants on the prevalence of allergic rhinitis in a population of schoolchildren in Taiwan. Whilst both studies found an association between allergic rhinitis prevalence and CO, they also observed an association with NOX. Consequently it could not be concluded if CO was solely responsible for the effects observed, but rather an effect attributed to the complex mixture of traffic related pollutants. These results were consistent with those presented in a multi-city study that examined the association between short-term exposure to CO and allergic symptoms.

Moon et al. (2009) observed associations between short-term CO exposure and allergic symptoms in children in South Korea. However, allergic symptoms were also associated with other pollutants, including PM10(particulate matter with a nominal mean aerodynamic diameter less than or equal to 10 μm), SO2, and NO2, The study did not present correlation coefficients to allow for further analysis of the results.

Hirsch and colleagues (1999) in a single-city study conducted in Dresden, Germany, observed no associations between annual average concentrations of CO, NO2, SO2, or O3and allergy assessed by skin prick testing or serum IgE measurement in schoolchildren. Furthermore, U.S.-based studies consistently reported no association between long-term exposure to CO and asthma and asthma symptoms.

Human controlled studies provide very little, inconsistent evidence of changes in pulmonary function following exposure to CO. The 2000 CO AQCD (EPA, 2000) reported no evidence of CO-induced changes in exercise ventilation at COHb levels <15% during sub-maximal exercise. Human clinical studies involving exposure to CO (COHb ~10%) found that no significant effect on resting pulmonary ventilation (compared with exposure to clean air under either hypoxic or hyperoxic exposure conditions) was observed.

Recent animal toxicological studies confirm association between increased endogenous CO and the development of allergic rhinitis (Shaoqing et al. (2008)). In this model, guinea pigs which were sensitized and challenged with ovalbumin exhibited high immunoreactivity of HO-1 in the nasal mucosa and a more than doubling of blood COHb levels (measured by gas chromatography). It is not known whether the observed increase in endogenous CO resulting from ovalbumin-mediated inflammation/oxidative stress plays a role in the development of allergic rhinitis but suggests a potential mechanism by which exogenous CO could impact an allergic phenotype.

One older study (Thom et al. (1999)) and two new studies (Carraway et al. (2002); Ghio et al. (2008)) demonstrated effects of 50-100 ppm CO on the lung. Responses included an increase in alveolar capillary permeability, disrupted iron homeostasis, mild pulmonary inflammation, and an exacerbation of pulmonary vascular remodeling elicited by hyobaric hypoxia. These results should be considered in view of the potential for inhaled CO to interact directly with lung epithelial cells and resident macrophages. However, a chronic study involving 200 ppm CO demonstrated no changes in pulmonary morphology (Sorhaug et al. (2006)).



To date, a limited number of studies have examined potential association between long term exposure to CO and respiratory morbidity. Confusion over potential confounders of the CO-respiratory morbidity relationship, especially due to the high correlation between CO and other traffic related pollutants makes it difficult to attribute association observed solely to CO independent of other air pollutants. This is a view also shared by the EPA.

Animal studies suggest that CO may play a role in the development of allergic rhinitis in individuals with already pre-existing respiratory symptoms, EHC (1999) however concludes that it is unlikely that CO has any direct effects on acute pulmonary function / lung tissue except for extremely high concentrations associated with CO poisoning.


EHC, 1999. Environmental Health Criteria, 213, International Programme for Chemical Safety, WHO.

EPA, 2000. Air quality criteria for carbon monoxide. National Center for Environmental Assessment, Office of Research and Development, U.S. Environmental Protection Agency. Research Triangle Park, NC. EPA 600/P-99/001

EPA, 2010 Integrated Science Assessment for Carbon Monoxide. EPA/600/R-09/019F. January 2010.

Migrated from Short description of key information:

Assessment of respiratory sensitisation from reviews of published literature

Justification for classification or non-classification

As carbon monoxide is a gas, skin sensitisation is unlikely to be a relevant endpoint. Whilst no in vivo respiratory sensitisation data exist, human data concludes that carbon monoxide is unlikely to have any direct effects on acute pulmonary function / lung tissue (except at extremely high concentrations associated with CO poisoning). Therefore, carbon monoxide has not been classified as a skin or respiratory sensitiser.