IAQ relationship to human health
Clean air is a vital requirement for human life and health, yet the air we breathe inside our homes, schools, offices, and care facilities often contains a silent mixture of chemical, physical, and biological contaminants.[1] Modern Europeans spend roughly 90% of their day indoors, with around 70% of that time spent at home.[2][3] Globally, household air pollution caused an estimated loss of 86 million healthy life years (Disability-Adjusted Life Years, or DALYs) in 2019, falling most heavily on vulnerable women and children.[4] Over 3.2 million premature deaths worldwide are linked each year to pollutants from household combustion, cooking, and heating, including more than 237,000 children under the age of five.[4]
Across the European Union, ambient and indoor air pollution represents the single largest environmental health risk, contributing to approximately 400,000 premature deaths annually.[5][6] Poor indoor air quality (IAQ) alone is responsible for losing an estimated 2 million healthy life years across the EU every year.[5][7] Impaired indoor air does not merely cause temporary stuffiness: it directly drives chronic illnesses, including asthma, chronic obstructive pulmonary disease (COPD), cardiovascular disease, stroke, cognitive decline, and lung cancer.[8][9][2]
How Indoor Air Pollution Affects Occupants
Think of the respiratory system as a building ventilation intake: coarse airborne debris is trapped by upper filters (the nose and throat), while ultra-fine chemical fumes and microscopic dust pass directly into the deeper mechanical cores (the lung air sacs) and enter the circulatory system.
Short-Term vs. Long-Term Exposure
How indoor air affects the body depends on the duration and intensity of exposure:
- Short-term (acute) exposure: Immediate physical reactions occur when nerve endings in the eyes, nose, and throat are irritated by airborne chemicals, smoke, or gases.[10] Common signs include headaches, watery eyes, sneezing, throat dryness, dizziness, and sudden fatigue. In sensitive individuals or people with asthma, sudden exposure can cause bronchial spasms and acute asthma attacks.[1][2]
- Long-term (chronic) exposure: Sustained inhalation of fine particles, combustion by-products, and volatile chemicals over months or years leads to persistent tissue inflammation and cellular oxidative stress.[11] Over time, chronic exposure causes cellular DNA damage, impairs local immune defences, stiffens blood vessels, and increases the lifetime risk of cardiovascular degeneration, chronic lung damage, and cancer.[2][12][13]
Susceptibility: Who is Most at Risk?
Indoor air pollution affects occupants unevenly. Vulnerability depends on individual biology, pre-existing illnesses, daily habits, and housing conditions.[10][2]
Children

Children represent an exceptionally vulnerable group due to distinct physiological, anatomical, and behavioural factors:
- Higher breathing rate: Relative to their body weight, children breathe faster and inhale significantly greater volumes of air (and contaminants) than adults.[14][15]
- Developing organs: Because their lungs, immune systems, and brains are actively growing, cellular injury from airborne toxins leads to permanent structural or functional impairment.[14]
- Floor-level microenvironment: Toddlers and young children play close to carpets and floors, where heavy dust, settled particulates, and semi-volatile chemicals concentrate.[13]
- Environmental and traffic vulnerability: Clinical and epidemiological studies demonstrate that children exhibit marked susceptibility to environmental tobacco smoke, traffic-derived particulate matter, nitrogen dioxide, and indoor allergens.[10][16]
EDIAQI project research underscores clear dose-response patterns in children: for every 10 µg/m³ rise in indoor coarse particles (PM2.5 to PM10), children experience a 6% increase in symptom days involving coughing, wheezing, or chest tightness.[2] Each 10 µg/m³ increase in fine particles (PM2.5) leads to a 7% increase in days with severe wheezing and a 4% increase in days requiring emergency rescue medication.[2] Globally, nearly half of all fatal lower respiratory infections in children under five stem from inhaling combustion and household dust particles.[4]
Women and Maternal Health
In many households, women face high daily exposures to cooking fumes, cleaning chemicals, and unvented domestic heating.[4] Exposure to fine particulate matter and combustion gases during pregnancy is linked to adverse birth outcomes, including low infant birth weight, intrauterine growth retardation, preterm birth, and abnormal fetal lung development.[17][4][2]
Older Adults
Ageing involves a gradual decline in physiological defences, including reduced mucociliary clearance of inhaled particles from the bronchial tree and slower metabolic clearance of absorbed chemicals.[10] Chronic inhalation of fine particulate matter, secondary ozone, and combustion gases accelerates vascular stiffness, impairs cardiac function, aggravates chronic obstructive pulmonary disease, and accelerates cognitive impairment.[18][5]
Individuals with Pre-Existing Conditions
Individuals with asthma, chronic bronchitis, COPD, or cardiovascular disease possess reduced physiological reserves.[19] In people with asthma, low concentrations of nitrogen dioxide (NO2) from unvented gas cookers, volatile organic compounds, or formaldehyde trigger bronchial hyperreactivity and airway remodeling.[1][20] In cardiac patients, fine particulate exposure promotes systemic inflammation and plaque instability, increasing the immediate risk of myocardial infarction and stroke.[21][22]
Socioeconomically Disadvantaged Households
Socioeconomic status strongly modulates indoor air exposure across Europe.[23][24] Lower-income families frequently face fuel poverty and occupy older housing with structural dampness, inadequate thermal insulation, and persistent mould.[5] These homes often lack mechanical ventilation systems, rely on unvented kerosene or solid-fuel space heaters, and are located closer to heavy traffic corridors, creating pronounced health inequities across the European building stock.[5][13]
Health Effects by Physiological System
Indoor contaminants affect multiple organs and biological systems throughout the body:
Sensory Irritation and Sick Building Syndrome (SBS)
Airborne chemical irritants directly stimulate trigeminal and olfactory nerve endings in the mucous membranes of the eyes, nose, and upper airways.[25] Common manifestations include burning sensations in the eyes, nasal congestion, sinus irritation, dry throat, hoarseness, and odor annoyance.[10] These symptoms are primary indicators of Sick Building Syndrome (SBS), typically resulting from insufficient outdoor air supply, high total volatile organic compounds (TVOCs) from cleaning agents, and formaldehyde outgassing from furnishings and adhesives.[26][3]
Cognitive Function and Mental Focus
Elevated indoor air pollutants directly impair central nervous system function, executive decision-making, and academic performance in schools and offices:
- Carbon dioxide (CO2): Serving as a proxy for inadequate ventilation and occupant bioeffluents, elevated CO2 levels (exceeding 1,000 to 1,200 ppm) correlate with drowsiness, reduced concentration, and slower decision-making speeds.[27][28]
- Combustion gases and fine dust: Exposure to indoor nitric oxide (NO), nitrogen dioxide (NO2), and fine particulate matter is linked to measurable reductions in attention span and verbal ability.[10][27]
- Neurodegenerative risks: In older adults, long-term inhalation of traffic-derived particles infiltrating indoors accelerates cognitive decline and increases the risk of neurodegenerative conditions such as Alzheimer's disease.[18][5]
Acute and Allergic Respiratory Reactions
Short-term exposures induce acute illness and exacerbate chronic allergic diseases:
- Asthma exacerbation: Fine particles (PM2.5), nitrogen dioxide from unvented gas cookers, and environmental tobacco smoke aggravate asthma symptoms and drive emergency hospital admissions.[20][29] Second-hand tobacco smoke shifts the balance of regulatory T cells (Treg) toward an inflammatory Th17 profile, characteristic of severe, steroid-resistant asthma.[2]
- Moisture and biological agents: Indoor dampness and mould proliferation increase the risk of respiratory infections, allergic rhinitis, and wheezing by 30% to 50%.[30] Dust mite allergens (Der p 1 and Der f 1) concentrated in mattresses and carpets cause chronic mucosal inflammation.[2][31]
- Carbon monoxide (CO) toxicity: Malfunctioning combustion heating appliances emit colourless, odourless CO gas, which binds to haemoglobin to form carboxyhaemoglobin, starving vital organs of oxygen and causing headaches, neurological damage, or fatal poisoning.[1]
The Indoor Microbiome and Immune Development
Human beings co-exist with complex communities of microbes present in domestic dust.[32][33] Research in the EDIAQI project examining child birth cohorts shows that early-life microbial exposure shapes long-term immune function:
- High microbial diversity in early-life environments (such as homes with pets, siblings, or contact with farms) trains the child immune system, protecting against childhood asthma and atopic sensitization.[2][33]
- Fungal richness in infant bedding dust at six months of age is associated with a significantly lower risk of developing asthma and allergic rhinitis by age six.[34][2]
- Bed-dust samples displaying a rural-type microbial composition provide protective immune benefits compared to sterile or urbanised domestic dust.[34]
Chronic Systemic and Cardiovascular Effects
Microscopic airborne pollutants pass through the lungs into the systemic bloodstream, damaging vascular networks:
- Vascular and ischemic damage: Globally, 32% of premature deaths from household combustion pollutants stem from ischaemic heart disease, and 23% result from stroke.[4] Inhaled fine particles (PM2.5) trigger vascular endothelial inflammation, oxidative stress, and platelet activation.[4][2]
- Ozone exposure: Even below regulatory guideline thresholds, short-term exposure to indoor and infiltrating ambient ozone activates platelets, elevates arterial blood pressure, and increases clotting markers in healthy adults.[9][35]
- Metabolic disorders: Longitudinal cohort analyses demonstrate that chronic exposure to combustion-derived fine particles and nitrogen oxides disrupts metabolic pathways, elevating biomarkers associated with type 2 diabetes mellitus and metabolic syndrome.[36][5]
Carcinogenic Substances in Indoor Air
Several common indoor contaminants are classified as Group 1 known human carcinogens by the International Agency for Research on Cancer (IARC):[37]
- Radon (222Rn): A naturally occurring radioactive gas seeping from bedrock and soil into basements and ground floors. Its solid decay progeny deposit deep in the tracheobronchial tree, emitting alpha radiation that damages cellular DNA. Radon is the second leading cause of lung cancer after tobacco smoking in Europe, prompting EU Council Directive 2013/59/EURATOM to establish a national reference level not exceeding 300 Bq/m³.[38][39]
- Polycyclic Aromatic Hydrocarbons (PAHs): Emitted by incomplete combustion during cooking, open fireplaces, wood stoves, and candle use. High molecular weight PAHs, particularly benzo[a]pyrene (BaP), bind tightly to fine and ultrafine particles.[40][13] EDIAQI source apportionment and incremental lifetime cancer risk assessments confirm that long-term exposure to particle-bound BaP equivalents in poorly ventilated or biomass-heated spaces creates elevated carcinogenic risks.[40][13]
- Volatile chemicals (Formaldehyde and Benzene): Formaldehyde emits continuously from composite wood resins, furniture varnishes, and adhesives, while benzene originates from tobacco smoke, attached garages, and solvent products. Chronic inhalation elevates the lifetime risk of nasopharyngeal cancer and leukemia.[1][13]
Emerging Contaminants of Concern
EDIAQI is actively investigating unmonitored indoor pollutants whose physical and toxicological profiles are currently under-regulated:
- Ultrafine Particles (UFPs, <100 nm): Emitted during frying, baking, candle burning, and heating, UFPs possess tiny mass but enormous surface-area-to-mass ratios.[41][40] They bypass upper airway clearance, reach deep alveolar sacs, and translocate directly across the air-blood barrier into the vascular system and secondary organs.[41][2]
- Black Carbon (BC): A combustion-derived graphitic soot particle carrying toxic, mutagenic surface chemicals deep into alveolar tissue, amplifying localized oxidative stress and vascular toxicity.[2][42]
- Indoor Microplastics: Synthetic textiles, soft furnishings, and worn polymer flooring shed airborne synthetic fibres (<5 mm). Inhaled microplastics lodge deep in lung tissue, releasing chemical plasticizers, flame retardants, and persistent additives directly to epithelial cells.[43][2]
[+] Click here to view technical details: Cellular toxicological mechanisms and laboratory assays
The EDIAQI project investigates the biological mechanisms of action (MoA) connecting indoor exposures to clinical endpoints using human biomonitoring, in vitro (2D and 3D cell models), and in vivo models in accordance with 3R principles (Replace, Reduce, Refine):[2][32]
- Primary DNA Damage: Assessed via the alkaline comet assay, measuring single-strand and double-strand DNA breaks in human alveolar epithelial cells (A549), hepatic spheroids (HepG2), and peripheral blood lymphocytes (PBLs).[2]
- Genomic Instability: Evaluated via the cytokinesis-block micronucleus (CBMN) assay in peripheral blood lymphocytes and non-invasive exfoliated buccal cells of children, detecting chromosomal breakage, whole chromosome loss, nucleoplasmic bridges, and nuclear buds.[44][2]
- Histone Phosphorylation (γ-H2AX): Utilizing automated microscopy to identify DNA double-strand break response markers in cellular matrices exposed to complex chemical mixtures.[45][2]
- Epigenetic Reprogramming: Investigating genome-wide DNA methylation changes that alter immune regulatory gene expression in young children exposed to indoor pollutants.[2]
Premature Mortality
At its most extreme, indoor air pollution leads to premature mortality. According to the World Health Organization, annual global deaths attributable to household air pollution are distributed across major pathologies:[4]
- 32% result from ischaemic heart disease.[4]
- 23% result from stroke.[4]
- 21% result from acute lower respiratory infections.[4]
- 19% result from chronic obstructive pulmonary disease.[4]
- 6% result from tracheal, bronchus, and lung cancer.[4]
In the European region alone, exposure to particulate matter in indoor settings shortens the statistical life expectancy of European citizens by nearly one full year on average.[2][5]
Action Framework: Identifying Issues and Mitigating Health Risks
Protecting occupants from indoor environmental health risks follows the practical stages of the EDIAQI Decision Tree:
| Decision Stage | Key Observations & Indicators | Practical Mitigation Actions |
|---|---|---|
| Why Measure? | Headaches, persistent fatigue, stuffy classrooms, morning congestion, worsening asthma, or musty smells. | Establish baseline air quality indicators; verify whether rooms exceed recommended comfort and health guidelines (CO2 above 1,000 ppm, elevated PM2.5). |
| How to Measure? | Deploy verified multi-sensor monitors or low-cost sensor units. | Place monitors at breathing height (1.0 to 1.5 m from the floor). Keep devices away from open windows, unsealed exterior doors, direct radiator heat, and chemical storage cupboards. |
| What is the Issue? |
|
Compare indoor readings with outdoor ambient levels to verify whether pollutants are generated indoors or entering from the outside. |
| What Now? | Actionable solutions for occupants, school administrators, and property managers. |
|
References
- ↑ 1.0 1.1 1.2 1.3 1.4 World Health Organization. (2010). WHO guidelines for indoor air quality: selected pollutants.
- ↑ 2.00 2.01 2.02 2.03 2.04 2.05 2.06 2.07 2.08 2.09 2.10 2.11 2.12 2.13 2.14 2.15 2.16 2.17 2.18 2.19 2.20 2.21 Lovrić, M., et al. (2024). A transdisciplinary approach for investigating indoor air quality and health in vulnerable European populations: The EDIAQI project. BioFactors, 50, 1-18.
- ↑ 3.0 3.1 Halios, C. H., Landeg-Cox, C., Lowther, S. D., Middleton, A., Marczylo, T., & Dimitroulopoulou, S. (2022). Chemicals in European residences–Part I: A review of emissions, concentrations and health effects of volatile organic compounds (VOCs). Science of the Total Environment, 839, 156201.
- ↑ 4.00 4.01 4.02 4.03 4.04 4.05 4.06 4.07 4.08 4.09 4.10 4.11 4.12 World Health Organization. (2023, September 26). Household air pollution and health (Fact sheet).
- ↑ 5.0 5.1 5.2 5.3 5.4 5.5 5.6 5.7 European Environment Agency. (2019). Healthy environment, healthy lives: how the environment influences health and well-being in Europe. (Report)
- ↑
- ↑ Asikainen, A., Carrer, P., Kephalopoulos, S., de Oliveira Fernandes, E., Wargocki, P., & Hänninen, O. (2016). Reducing burden of disease from residential indoor air exposures in Europe (HEALTHVENT project). Environmental Health, 15(S1), 61-72.
- ↑ European Commission. EU clean air policy.
- ↑ 9.0 9.1 World Health Organization. (2021). WHO global air quality guidelines: particulate matter (PM2.5 and PM10), ozone, nitrogen dioxide, sulfur dioxide and carbon monoxide.
- ↑ 10.0 10.1 10.2 10.3 10.4 10.5 Scientific Committee on Health and Environmental Risks (SCHER). (2008). Opinion on risk assessment on indoor air quality. European Commission, Directorate-General for Health and Consumer Protection, Brussels.
- ↑ González-Caballero, M. C., et al. (2023). Pollution, Indoor Air. In Reference Module in Biomedical Sciences. Elsevier.
- ↑ Stading, R., et al. (2021). Molecular mechanisms of pulmonary carcinogenesis by polycyclic aromatic hydrocarbons (PAHs): Implications for human lung cancer. Seminars in Cancer Biology, 76, 3-16.
- ↑ 13.0 13.1 13.2 13.3 13.4 13.5 Račić, N., et al. (2025). Indoor volatile organic compounds and polycyclic aromatic hydrocarbons in European environments: Sources, concentrations, and health risks. Indoor Air, 2025, 5945455.
- ↑ 14.0 14.1 14.2 European Environment Agency. (2023). Air pollution and children's health. (Briefing no. 07/2023)
- ↑ Bennett, W. D., & Zeman, K. L. (1998). Deposition of fine particles in children spontaneously breathing at rest. Inhalation Toxicology, 10(9), 831-842.
- ↑ Janssen, N. A. H., et al. (2003). The relationship between air pollution from heavy traffic and allergic sensitization, bronchial hyperresponsiveness, and respiratory symptoms in Dutch schoolchildren. Environmental Health Perspectives, 111(12), 1512-1518.
- ↑ Šrám, R. J., et al. (2005). Ambient air pollution and pregnancy outcomes: a review of the literature. Environmental Health Perspectives, 113(4), 375-382.
- ↑ 18.0 18.1 Ranft, U., et al. (2009). Long-term exposure to traffic-related particulate matter impairs cognitive function in the elderly. Environmental Research, 109(8), 1004-1011.
- ↑ Cincinelli, A., & Martellini, T. (2017). Indoor air quality and health. International Journal of Environmental Research and Public Health, 14(11), 1286.
- ↑ 20.0 20.1 Tiotiu, A. I., et al. (2020). Impact of air pollution on asthma outcomes. International Journal of Environmental Research and Public Health, 17(17), 6212.
- ↑ Lelieveld, J., et al. (2019). Cardiovascular disease burden from ambient air pollution in Europe reassessed using novel hazard ratio functions. European Heart Journal, 40(20), 1590-1596.
- ↑ Mustafić, H., et al. (2012). Main air pollutants and myocardial infarction: a systematic review and meta-analysis. JAMA, 307(7), 713-721.
- ↑ Laurent, É. (2022). Air (ine) quality in the European Union. Current Environmental Health Reports, 9(2), 123-129.
- ↑ WHO Regional Office for Europe. (2019). Environmental health inequalities in Europe: Second assessment report. Copenhagen: WHO Regional Office for Europe.
- ↑ Wolkoff, P. (2008). "Healthy" eye in office-like environments. Environment International, 34(8), 1204-1214.
- ↑ Jafari, M. J., et al. (2015). Association of sick building syndrome with indoor air parameters. Tanaffos, 14(1), 55-62.
- ↑ 27.0 27.1 Sadrizadeh, S., Yao, R., Yuan, F., Awbi, H., Bahnfleth, W., Bi, Y., ... & Li, B. (2022). Indoor air quality and health in schools: A critical review for developing the roadmap for the future school environment. Journal of Building Engineering, 57, 104908.
- ↑ Mendell, M. J., & Heath, G. A. (2005). Do indoor pollutants and thermal conditions in schools influence student performance? A critical review of the literature. Indoor Air, 15(1), 27-52.
- ↑ Wang, Z., et al. (2015). Effects of secondhand smoke exposure on asthma morbidity and health care utilization in children: A systematic review and meta-analysis. Annals of Allergy, Asthma & Immunology, 115(5), 396-401.
- ↑ World Health Organization. (2009). WHO guidelines for indoor air quality: dampness and mould.
- ↑ Gaffin, J. M., & Phipatanakul, W. (2009). The role of indoor allergens in the development of asthma. Current Opinion in Allergy and Clinical Immunology, 9(2), 128-135.
- ↑ 32.0 32.1
- ↑ 33.0 33.1 Gupta, S., et al. (2020). Environmental shaping of the bacterial and fungal community in infant bed dust and correlations with the airway microbiota. Microbiome, 8, 115.
- ↑ 34.0 34.1 Lehtimäki, J., et al. (2021). Urbanized microbiota in infants, immune constitution, and later risk of atopic diseases. Journal of Allergy and Clinical Immunology, 148(1), 234-243.
- ↑ Day, D. B., et al. (2017). Association of ozone exposure with cardiorespiratory pathophysiologic features in healthy adults. JAMA Internal Medicine, 177(9), 1344-1353.
- ↑ Nassan, F. L., et al. (2021). Ambient PM2.5 species and ultrafine particle exposure and their differential metabolomic signatures. Environment International, 151, 106447.
- ↑ International Agency for Research on Cancer (IARC). (2013). Outdoor air pollution. IARC Monographs on the Evaluation of Carcinogenic Risks to Humans, Vol. 109. Lyon, France.
- ↑ Darby, S., et al. (2005). Radon in homes and risk of lung cancer: collaborative analysis of individual data from 13 European case-control studies. BMJ, 330, 223.
- ↑ Council of the European Union. (2013, December 5). Council Directive 2013/59/Euratom of 5 December 2013 laying down basic safety standards for protection against the dangers arising from exposure to ionising radiation. Official Journal of the European Union, L 13, 1-73.
- ↑ 40.0 40.1 40.2 Lovrić, M., Račić, N., Pehnec, G., Horvat, T., Lovrić Štefiček, M. J., & Jakovljević, I. (2024). Indoor Polycyclic Aromatic Hydrocarbons: Relationship to Ambient Air, Risk Estimation, and Source Apportionment Based on Household Measurements. Atmosphere, 15(12), 1525.
- ↑ 41.0 41.1 Manigrasso, M., Vitali, M., Protano, C., & Avino, P. (2018). Ultrafine particles in domestic environments: Regional doses deposited in the human respiratory system. Environment International, 118, 134-145.
- ↑ Zhao, Y., et al. (2020). Measurement of ultrafine particles and black carbon in indoor residential environments. Atmospheric Environment, 228, 117428.
- ↑ Carreira, L., et al. (2023). Inhalation of indoor microplastics and potential respiratory health hazards. Environmental Pollution, 318, 120890.
- ↑ Bonassi, S., et al. (2021). The micronucleus assay in human lymphocytes as a biomarker of genotoxic risk. Scientific Reports, 11, 16793.
- ↑ Štampar, M., Tomc, J., Filipič, M., & Žegura, B. (2019). Hepatocyte spheroids as an advanced 3D in vitro model for genotoxicity testing. Archives of Toxicology, 93, 3321-3333.