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EC number: 211-128-3
CAS number: 630-08-0
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
Migrated from Short description of key information:
Skin sensitisation - waiver
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
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.
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
EHC, 1999. Environmental Health Criteria,
213, International Programme for Chemical Safety, WHO.
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
EPA, 2010 Integrated Science Assessment for
Carbon Monoxide. EPA/600/R-09/019F. January 2010.
Assessment of respiratory sensitisation from reviews of published literature
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.
Information on Registered Substances comes from registration dossiers which have been assigned a registration number. The assignment of a registration number does however not guarantee that the information in the dossier is correct or that the dossier is compliant with Regulation (EC) No 1907/2006 (the REACH Regulation). This information has not been reviewed or verified by the Agency or any other authority. The content is subject to change without prior notice.Reproduction or further distribution of this information may be subject to copyright protection. Use of the information without obtaining the permission from the owner(s) of the respective information might violate the rights of the owner.
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