Carbon dioxide 5% / Air 95%
Available from a pharmacy with pharmacist advice
Carbon dioxide is a colorless, odorless gas vital to life on Earth.
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2 branded products available
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View all licensed products for Carbon dioxide + Air on the MHRA register
Carbon dioxide 5% / Air 95% cylinders size AV
Carbon dioxide 5% / Air 95% cylinders size L
NHS prescribing volume and spending trends
Guidelines from the National Institute for Health and Care Excellence
NICE clinical guidance(15)
Air pollution: outdoor air quality and health (NG70)
Indoor air quality at home (NG149)
Physical activity: walking and cycling (PH41)
Specialist neonatal respiratory care for babies born preterm (NG124)
Lung volume reduction surgery for advanced emphysema (HTG69)
Endoscopic transluminal pancreatic necrosectomy (HTG421)
Extracorporeal membrane oxygenation for severe acute respiratory failure in adults (HTG260)
Pressurised intraperitoneal aerosol chemotherapy for peritoneal carcinomatosis (HTG558)
Computed tomographic colonography (virtual colonoscopy) (HTG78)
HumiGard for preventing inadvertent perioperative hypothermia (HTG428)
Chronic obstructive pulmonary disease in adults (QS10)
End-tidal Control software for use with Aisys closed circuit anaesthesia systems for automated gas control during general anaesthesia (MIB10)
Obstructive sleep apnoea/hypopnoea syndrome and obesity hypoventilation syndrome in over 16s (NG202)
OxyMask for delivering oxygen therapy (MIB160)
Motor neurone disease: assessment and management (NG42)
Source: National Institute for Health and Care Excellence (NICE). Contains public sector information licensed under the Open Government Licence v3.0.
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Pharmacy links redirect to the retailer's own search and do not represent real-time stock levels. Shortage and safety information sourced from MHRA drug safety updates (gov.uk, Crown Copyright under OGL v3.0).
Codes for healthcare professionals and prescribing systems
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NHS UK identifiers
SNOMED CT and dm+d codes from NHS TRUD (Technology Reference data Update Distribution), licensed under the Open Government Licence v3.0.
Active and completed clinical studies from ClinicalTrials.gov
Source: ClinicalTrials.gov, a database of the U.S. National Library of Medicine (NLM), National Institutes of Health (NIH). Data accessed via ClinicalTrials.gov API v2. Trial information is provided for research purposes and does not constitute medical advice.
Academic studies and reviews for this medicine's active substance
Showing the 50 most relevant studies.
Reviews & meta-analyses: 10 · Randomised trials: 4 · 1985–2026
Showing the 50 most relevant studies, sorted by most relevant.
Feng H, Gu W, Li Q, et al.
2026
Irfan SA, Strobl K, Wariach K, et al.
2026
BackgroundAir pollution has been associated with multisystem health adversities. However, the association between short-term air pollution and hemorrhagic stroke has not been sufficiently evaluated in recent years. Considering that hemorrhagic stroke has a high incidence rate (28.8% of incident strokes) and accounts for almost 7.2 million deaths per year globally, it is important to identify risk factors and use it to guide preventative measures.MethodsA systematic search was conducted on 4 databases (Embase, OVID Medline, Web of Science, PubMed). Studies selected for review included time series, case-crossover, and cohort studies, published in English, from all time periods, and investigated the risk of hemorrhagic stroke after exposure to air pollution (particulate matter ≤ 2.5 μm in diameter [PM2.5], particulate matter ≤ 10 μm in diameter [PM10], nitrogen dioxide [NO2], sulfur dioxide [SO2], ozone [O3], or carbon monoxide [CO]). Data for different risk outcomes (risk ratio, odds ratio) were meta-analyzed using an inverse variance statistical analysis and random effects model.ResultsAmong the 2435 studies identified, 31 were included and deemed eligible for review and meta-analysis. The results illustrated a statistically significant increase in the risk of hemorrhagic stroke per 10 μg/m3 increase in NO2 exposure (risk ratio, 1.0142; 95% confidence interval, 1.0000-1.0286; P = 0.05), and CO exposure (odds ratio, 1.0008; 95% confidence interval, 1.0000-1.0016; P = 0.05).ConclusionsAmong the 6 air pollutants studied, NO2 and CO exposure was associated with a statistically significant increase in the risk of hemorrhagic stroke. This can help guide effective preventative protocols and public health measures in an effort to reduce the burden of cardiovascular and cerebrovascular disease.
Abstract licence: CC BY
Shi H, Li J, Li B, et al.
2026
- Pulmonary Disease, Chronic Obstructive
- Air Pollutants
- Air Pollution
Evidence regarding the short-term effects of ambient air pollution on acute exacerbations of chronic obstructive pulmonary disease (AECOPD) across multiple cities in northern China remains limited. This study aimed to evaluate the associations between major ambient air pollutants and AECOPD hospitalizations, as well as their lagged effects. We conducted an ecological time-series study of 14,786 AECOPD hospitalizations recorded at 49 hospitals in Shijiazhuang, Handan, and Chengde, Hebei Province, from January 1, 2018, to December 31, 2020. City-specific associations between daily concentrations of fine particulate matter (PM2.5), inhalable particulate matter (PM10), sulfur dioxide (SO2), nitrogen dioxide (NO2), carbon monoxide (CO), and 8-hour ozone and AECOPD hospitalizations were estimated using distributed lag nonlinear models, with adjustment for long-term trends, temperature, relative humidity, day of the week, public holidays, and stages of the coronavirus disease 2019 pandemic. Single-day lag effects from lag 0 to lag 5, cumulative lag effects from lag 0-1 to lag 0-5, effects of extreme pollutant concentrations, and associations stratified by age and sex were evaluated. City-specific estimates were subsequently pooled using random-effects multivariate meta-analysis. Associations were expressed as relative risks with 95% confidence intervals. During the 1096-day study period, 14,786 AECOPD hospitalizations were recorded. Compared with the 25th-percentile concentrations, the 75th-percentile concentrations of PM2.5, PM10, SO2, NO2, and CO generally showed stronger cumulative associations with longer lag periods, with the largest estimates usually observed at lag 0-5 days, whereas single-day effects were weak. All 6 pollutants exhibited nonlinear cumulative exposure-response relationships. Compared with median concentrations, the 99th-percentile concentrations of PM2.5, PM10, SO2, NO2, and CO were associated with higher hospitalization risks. High PM2.5 reached its maximum effect at lag 0-5 days (relative risk, 1.391; 95% confidence interval, 1.169-1.658). Higher 8-hour ozone concentrations were generally associated with lower hospitalization risk. Associations were more pronounced among adults aged ≥65 years and males. Short-term exposure to PM2.5, PM10, SO2, NO2, and CO was associated with increased AECOPD hospitalization risk, with nonlinear, lagged, and cumulative effects. Older adults and females may be more susceptible to ambient air pollution.
Abstract licence: CC BY
Yunus, Rossita M., Memon, Breda, Memon, Muhammed A., et al.
Ovid Technologies (Wolters Kluwer Health), 2016
Khawaja SA, Hanna L, Singh A, et al.
2026
- Intracranial Embolism
- Aortic Valve Stenosis
- Embolism, Air
Herbig B, Mayer F, Norrefeldt V, et al.
2026
- Carbon Dioxide
- Air Pollutants
- Cognition
BackgroundIndoor air quality, especially carbon dioxide (CO2) and volatile organic compounds (VOCs), has been linked to cognitive impairment in previous studies, even below guideline levels. Most previous studies employed small cross-over designs and varied only one indoor air factor.ObjectiveThis study aimed to investigate the influence of various combinations of indoor air parameters at typical and elevated levels on cognitive performance.MethodsWe conducted a randomized controlled trial with 398 healthy adults aged 18-69 years. Participants were randomly assigned to 11 groups and exposed to different combinations of pure CO2 (1200, 2750, 4200 ppm), atmospheric pressure (940, 755 hPa), and a VOC mixture of selected compounds at low, medium, and high concentrations. Eight different cognitive domains were assessed with established tests.ResultsParticipants rated air quality as good to very good at the end of exposure in all groups. Analyses of variance with pairwise comparisons showed effects of exposure in 2 out of 8 cognitive domains (concentration and figural working memory). None of the observed differences were systematically aligned with the air quality conditions.ConclusionOur study provides no evidence that short-term exposure to various combinations of CO2 (up to 4200 ppm), TVOCs (up to 2100 μg/m3), and atmospheric pressure up to 8000 ft. elevation had any systematic negative effects on the cognitive abilities of healthy adults. The TVOC results should be viewed with caution, as a specific mixture was used, and other mixtures may occur in other indoor environments. Rigorously designed studies with longer exposure times are recommended.
Abstract licence: CC BY
Schaerli F, Buse S, Farquharson F, et al.
2026
- Asphyxia
- Carbon Dioxide
- Avalanches
IntroductionMortality following complete avalanche burial remains high, primarily due to asphyxiation. Rebreathing-related CO₂ accumulation and oxygen depletion in the air pocket and surrounding snow are considered key mechanisms contributing to asphyxia. Artificial air pocket devices (AAPD) may mitigate this effect by separating exhaled from inhaled air. The present trial aimed to assess this effect in a simulated avalanche burial setting using continuous transcutaneous CO2 monitoring.MethodsIn this randomized, double-blind, crossover trial, 11 healthy participants (3 female) underwent 2 simulated avalanche burials; one with, the other without (sham) a functional AAPD. Continuous measurements included: transcutaneous partial pressure of CO₂ (PtCO2), SpO2, respiratory rate, heart rate and end-tidal CO2/O2. Termination occurred i) per protocol after max. 45 min, ii) when predefined safety criteria were surpassed, iii) per participant request.ResultsDuring burial PtCO2 rose steadily, reaching non-fatal levels. Compared to sham conditions, functional AAPD diminishes CO2-increase per timespan (+0.10 vs. +1.13 mmHg/min). In addition, burial time was markedly prolonged (44.3 vs. 6.4 min), and desaturation was prevented (96% vs. 75%) by the AAPD.ConclusionsIn this simulated avalanche burial trial, use of AAPD resulted in a significant reduction in CO2 accumulation and a substantial increase in tolerated burial time. This study provides evidence that neither low oxygen content within the snow-matrix itself, nor CO2-retention limit burial time. This implies that life-threatening hypoxemia is caused by both: rebreathing-related CO2 accumulation and progressive oxygen depletion of the surrounding snow.
Abstract licence: CC BY
Atkinson, R, H. Ross Anderson, Inga Mills, et al.
Springer Verlag, 2014
D.A. Bossio, K.M. Scow
Microbial Ecology, 1998
Derek H.R. Barton, David Crich, William B. Motherwell
Tetrahedron, 1985
Sources: aggregated from Europe PMC (EMBL-EBI), OpenAlex, Crossref, PubMed and other open scholarly databases. Retracted articles are excluded. Study information is provided for research purposes and does not constitute medical advice.
Pharmacology and chemical data from DrugBank
Key facts
Drug status
Approved
Major interactions
None known
Half-life
Not available
Mechanism
Data not found.
Food interactions
None known
Human targets
None mapped
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
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Half-life
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Pharmacokinetic data: DrugBank · CC BY-NC 4.0
How the body processes this drug — absorption, distribution, metabolism, and elimination
ATC V03AN02
Chemical identifiers
CAS, UNII, InChI Key and database cross-references
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Chemical identifiers
CAS, UNII, InChI Key and database cross-references
DrugBank citations
If you use DrugBank data in your research, please cite:
- DrugBank 6.02024Recommended citationKnox C., Wilson M., Klinger C.M., et alDrugBank 6.0: the DrugBank Knowledgebase for 2024Nucleic Acids Res. 2024 Jan 552(D1):D1265-D1275
- DrugBank 5.02018Wishart D.S., Feunang Y.D., Guo A.C., et alDrugBank 5.0: a major update to the DrugBank database for 2018Nucleic Acids Res. 2017 Nov 846(D1):D1074-D1082
- DrugBank 4.02014Law V., Knox C., Djoumbou Y., et alDrugBank 4.0: shedding new light on drug metabolismNucleic Acids Res. 2014 Jan 142(1):D1091-7
- DrugBank 3.02011Knox C., Law V., Jewison T., et alDrugBank 3.0: a comprehensive resource for 'omics' research on drugsNucleic Acids Res. 2011 Jan39(Database issue):D1035-41
- DrugBank 2.02008Wishart D.S., Knox C., Guo A.C., et alDrugBank: a knowledgebase for drugs, drug actions and drug targets.Nucleic Acids Research2008 Jan36(Database issue):D901-6
- DrugBank 1.02006Wishart D.S., Knox C., Guo A.C., et alDrugBank: a comprehensive resource for in silico drug discovery and exploration.Nucleic Acids Research2006 Jan 134(Database issue):D668-72