THE HIDDEN HEALTH EFFECTS OF POLLUTION IN URBAN ENVIRONMENTS: Evaluating the biological pathways between how urban air pollution may cause mental health and psychiatric disorders

Editie: 30 - Shifts in the Real Estate Industry

Published on: 23 mei 2023

On the 15th of November 2022, the global population reached 8 billion. This figure is estimated to grow to 9 billion within the next 15 years in 2037 (United Nations, 2023). Today approximately 56% of the world’s inhabitants live within urban environments, which is expected to increase to 70% by 2050 (World Bank Group, 2022). This population increase implies further exasperating the climate crisis related to cities, such as a rise in air pollution. Air pollution is the leading environmental cause of disease, accounting for more than 16% of global deaths annually (Landrigan et al., 2018). Most notable air pollution comprises particulate matter with diameters of less than 10μm (PM10), 2.5μm (PM2.5), ultrafine particles >0.1μm (UFP); nitrogen oxides (NOx) and Carbon monoxide (CO) and is assumed to derive from cars and transportation predominately. However, 40% of air pollution and particulate matter is related to the built environment (Weiser et al., 2021), such as the heating and cooling of homes and commercial buildings and building-related construction.   


In addition to the climate crisis facing the future of cities, there is a significant and growing risk of urban-related poor health (Okkels et al., 2018). Exposure to air pollution is a well-established determinant of poor physical health and disease (Hahad et al., 2019), with mounting research linking air pollution to psychiatric disorders and mental illness (Zeng et al., 2019). For example, a recent epidemiology study highlighted that the risk of suffering from a range of mental health, neurodegenerative and psychiatric disorders, such as depression, Alzheimer’s, and schizophrenia, is materially increased if you live within a city (Ventriglio et al., 2021). In addition, similar global studies identify a linear relationship between levels of urbanity and mental health (Allender et al., 2010) suggesting the closer you live to a city, the higher your chances of mental illness; one of the strongest indicators for a link between urbanism and poor mental health.  


Wider literature attributes some of this link to air quality and pollution, suggesting that as our cities become more polluted, we may run the risk of further exasperating an already growing urban mental health crisis (Arantes et al., 2019). Therefore, the race to reduce pollution in our cities not only represents an opportunity to improve planetary health, but also human health.  


However, the underlying mechanisms linking air pollution and mental health outcomes remain inconclusive. It is critical to be able to establish these pathways so that the medical profession can adequately treat the effects of air pollution on mental health and more importantly, so that the built environment can start to repurpose, redevelop and design our cities in a way to minimise air pollution and subsequent negative effects on human health.  


Recent research has suggested three potential pathways where air pollution can dysregulate neurobiology and cause mental health issues; indirect inflammation; the crossing the blood-brain barrier (BBB), and confounding influences, such as noise (Hahad et al., 2019). This paper explores how air pollution may impact mental health through the three proposed biological pathways, providing both the medical and built environment sectors with useful insights into how to treat and remediate the effects of our cities on human health.   



Whilst inflammation is a natural healing process (Miller & Raison, 2016), clinical and animal models demonstrate that exposure to air pollution can result in damage to the nasal epithelium (cells lining the inside of the nostrils) (Hahad et al., 2019), resulting in local inflammation in the lungs (Ogino et al., 2017) and respiratory system (Saveleva et al., 2022). Whilst damage to these body systems from inhaling polluted air are well documented and acknowledged by the building environment industries, the effect of general inflammation on mental health is not as well understood. Inflammation is a core feature of several psychiatric disorders (Bauer & Teixeira., 2019). A recent study using a mouse model demonstrated a causal link between exposure to traffic-related particulate matter, inflammation of body systems related to smelling (the olfactory system) and behavioral abnormalities that are consistent with autism (Nephew et al., 2020). However, this study fails to define what particulate matter makes up ‘traffic-related’ particulate matter and therefore it is not possible to assess which particulate matter most mediates inflammation. A recent meta-analysis and systematic review found that short-term exposure to PM2.5 PM10, NO2, and CO increased the risk of depression, but there was no link between O3 and depression (Zeng et al., 2019), highlighting that different particulate matter compounds may cause differing inflammatory effects, which in turn may lead to different psychiatric pathologies.  


A clinical study of young Dutch adults did define air pollution exposure to PM2.5, and found prolonged exposure was associated with elevated levels of endothelial microparticles (indicators of inflammation), olfactory-based inflammation and raised pro-inflammatory cytokines such as, interleukin-6 (IL-6) (Pope et al., 2016), demonstrating a pathway between PM 2.5 commonly emitted in by cars, transport and domestic woodburning (Cyrys et al., 2015) and inflammation in humans. The presence of IL-6 is associated with down-stream, subsequent systematic inflammation which has been shown to be a core feature in the maintenance and promotion of depression (Bauer & Teixeira., 2019). Elevated levels of IL-6 in fetuses and young children have also been shown in clinical studies to impair and stunt brain development (Jiang et al., 2014), causing smaller hippocampal volume, which is a common feature of depression (Barch et al., 2019), also visible in small children exposed to high air pollution (Chiu et al., 2016). Whilst there may be other sources of inflammation during pregnancy or early childhood years (Sawyer, 2021), such as maternal depression or infection which may also account for the inflammation, the mounting evidence linking air quality and shared inflammation physiology with mental health disorders provides a strong indication that exposure to increased air pollution in cities may not only be effecting our health today, but the potential health and neurocognitive performance of children yet to be born. These findings when taken together suggest that air pollution in urban environments may be influencing or creating inflammation within the body, which has either a shared of causal effect on mental health or psychiatric disorders. Further research is required to substantiate this causal effect, but ,managers of the built environment should start to evaluate how to reduce pollution-related inflammation within the urban environment.  



Until recently, neuroscientists believed that the blood-brain-barrier (BBB) was impermeable to external molecules such as air pollution (Spinder & Hsu, 2012), providing protection to neurotoxicity from the outside world. However, in recent studies air pollution particulate matter has been shown to cross the BBB and cause neuroinflammation-based behavioural abnormalities in both mouse (Xuan Tan et al., 2021) and clinical models (Calderón-Garcidueñas et al., 2008). The implication of this is we have begun to demonstrate that whatever we breathe not only effects our health through the respiratory system, but that it may cause direct neurological changes within the brain itself, leading to mental health disorders.  


In a study of young urbanites living in Mexico City, researchers found iron-rich ultra-fine-particles within neurons, glia, and several neurovascular organelles, versus no ultra-fine-particles found in matched clean air controls (González-Maciel et al., 2017). Further, participants within this study displayed increased short-term memory deficits, and accumulation of amyloid β-42, often associated with Alzheimer’s (Xuan Tan et al., 2021); suggesting a direct link between air pollution particulate matter crossing into the BBB and dementia. However, several studies have shown that the presence of amyloid β-42 is not always synonymous with dementia, sometimes present within healthy populations (Sturchio et al., 2021) so we cannot conclusively say that dementia is caused by exposure to air pollution. Further recent studies of dementia have begun to dispel the amyloid-theory of dementia, providing further example of how hard it is for urban designers to understand the health impact of urban factors on mental health when must of the biological basis of mental health is still unknown.  


However, a 2017 epidemiological review of the rates of dementia for adults aged 55−85 years living close to road traffic found a significant and positive correlation between participants living less than 50m to road traffic, who never moved home and the onset of dementia (Chen et al., 2017). These findings suggest that the proximity to road traffic, duration of air pollution exposure and subsequent amyloid plaque development may mediate or even cause dementia. Further supporting evidence for air pollution particulate matter crossing the BBB can be found in studies demonstrating trace elements of toxic metals within brain and central nervous system (CNS) organelles. Air pollution particulate matter has been shown to allow for the transmission of air-borne toxic metals, such as copper and lead (Gilani et al., 2015), which have been linked in small children with a range of mental health issues later in life (Potter et al., 2021). As these metals are exogenous and not naturally found within the body, we can conclude that they must have entered the brain through the olfactory or alternative pathway. In addition, studies of gastrointestinal transmission have also been shown to transmit particulate matter into the central nervous system (Costa et al., 2020) which may also account for the presence of toxic metals within the body. Therefore, further research is required to establish whether the presence of toxic metals is more likely entering the body enter through air pollution inhalation through the olfactory system or through eating and digesting food with trace metals.  Either way, the growing presence of unnatural metal compounds and particulate matter that are being found within the body and which are associated with increases in a host of mental health disorders and conditions, provides further evidence to reduce air pollution within urban environments.  



Whilst this paper has demonstrated a significant body of evidence biologically linking air pollution and mental health, the final potential pathway linking these two dynamics is a pathway of association. Higher levels of noise frequently accompany air pollution within city environments, as they typically share common sources, such as car traffic and industrial activity (Markevych et al., 2017). The influence of noise may therefore contribute to, or confound, the impact of air pollution on mental health, especially when noise is not accounted for in studies evaluating the link between sir pollution and mental health.  


Noise has been linked with a wide range of poor mental health outcomes and sleep disturbance (Hegewald et al., 2020). In a multilevel analysis of perceived noise pollution and mental health in China, researchers found perceived higher noise-pollution exposure is significantly associated with worse mental health (Ma et al., 2018). A study of night-time noise and sleep quality also found that noise-related sleep disturbance increased the production of adrenaline and cortisol, as well as elevated heart rate and blood pressure (Halperin, 2014); all of which have been shown to also initiate a similar inflammation process compared to air pollution (Corcoran et al., 2001) and associated with poor mental and physical health. A 2020 study found evidence of elevated IL-6 levels in a clinical model of noise pollution (Daiber et al., 2020), suggesting that unless noise pollution is accounted for in models of air pollution, any subsequent inflammation response may be generated from noise, air pollution or a combined effect of the two.  

However conflicting research exists correlating noise and other aspects of environmental pollution to specific mental health disorders (Li et al., 2022). In a Dutch cross-sectional study of 387,195 adults, air pollution was positively associated with general poor mental health; however, road-traffic noise was only positively associated with anxiety, and rail-traffic noise was only positively associated with self-reported psychological distress (Klompmaker et al., 2019). This suggests that different noises may produce differing impacts on mental health, or it could suggest specific air pollution particulate matter generated from different modes of transportation, such as PM2.5 from cars (Talaiekhozani et al., 2017) and PM10 from trains, have differing effects on different mental health effects (Jaffe et al., 2014). This finding clearly represents the complexity of understanding the link between urban environments and mental health.  


However, a limitation of Klompmaker et al. (2019) study, and many others, is that proxies are used to assess assumed exposure to air pollution or mental health outcomes. For example, Klompmaker et al. (2019) assumed the average air quality rating across a city as a proxy for exposure to air pollution and general prescribing rates of antidepressants for rates of mental health at a city level. Without controlling for actual, individual environmental exposure and health outcomes, it is not possible to assess whether participants were actually exposed to particulate matter or noise pollution, as studies may not control for time spent inside or travelling outside of the ascribed area, which has been shown to significantly change exposure measurements (Weisskopf & Webster, 2017). Further, prescribing of antidepressants and consumption of antidepressants are two different things, with some studies reporting that as much as 50% of antidepression medication prescribed, is not adhered to and taken as intended (Sansone & Sansone, 2012). Without accurate assessment of actual noise and air pollution exposure, it is not possible to validate the specific influence of air pollution or noise individually, jointly and their causative effects on mental health outcomes. However, current research heavily suggests that there is a strong mechanistic link between noise, air pollution and mental health, which warrants further investigation.  



Whilst limitations within the current research exist, there is clear and plausible evidence of mechanistic links between air pollution, indirect inflammation of the olfactory system, subsequent weakening and crossing the BBB and associated mental health disorders. These findings add further justification and motivation to reduce air pollution within urban environments, not just to improve planetary health, but also human health.  


Urban environments are associated with disproportionately negative human health outcomes and should therefore be considered in more detail by built environment industries. As our understanding of neurobiology and mental health disorders increases, it is likely that we will find more evidence of the way in which urban environments and buildings may affect human health on a molecular and biological level. Therefore, built environment industries should shift from focussing on the correlation between purely planetary health and air pollution to increasingly collaborate and work with biomedical, mental health and related professions to further elucidate the way in which our urban world may impact human health and subsequent quality of life.   





Allender, S., Lacey, B., Webster, P., Rayner, M., Deepa, M., Scarborough, P., Arambepola, C., Datta, M., & Mohan, V. (2010). Level of urbanization and noncommunicable disease risk factors in Tamil Nadu, India. Bulletin of the World Health Organization, 88(4), 297–304. 


Arantes, B. L., Mauad, T., & Filho, D. F. D. S. (2019). Urban forests, air quality and health: A systematic review. International Forestry Review, 21(2), 167–181. 


Barch, Deanna M., et al. “Early Childhood Depression, Emotion Regulation, Episodic Memory, and Hippocampal Development.” Journal of Abnormal Psychology, vol. 128, no. 1, Jan. 2019, pp. 81–95. (Crossref), 


Bauer, Moisés E., and Antonio L. Teixeira. “Inflammation in Psychiatric Disorders: What Comes First?: Inflammation in Psychiatric Disorders.” Annals of the New York Academy of Sciences, vol. 1437, no. 1, Feb. 2019, pp. 57–67. (Crossref), 


Bové, Hannelore, et al. “Ambient Black Carbon Particles Reach the Fetal Side of Human Placenta.” Nature Communications, vol. 10, no. 1, Dec. 2019, p. 3866. (Crossref), 


Calderón-Garcidueñas, Lilian, et al. “Long-Term Air Pollution Exposure Is Associated with Neuroinflammation, an Altered Innate Immune Response, Disruption of the Blood-Brain Barrier, Ultrafine Particulate Deposition, and Accumulation of Amyloid β-42 and α-Synuclein in Children and Young Adults.” Toxicologic Pathology, vol. 36, no. 2, Feb. 2008, pp. 289–310. (Crossref), 


Chen, Hong, et al. “Living near Major Roads and the Incidence of Dementia, Parkinson’s Disease, and Multiple Sclerosis: A Population-Based Cohort Study.” The Lancet, vol. 389, no. 10070, Feb. 2017, pp. 718–26. (Crossref), 


Chiu, Yueh-Hsiu Mathilda, et al. “Prenatal Particulate Air Pollution and Neurodevelopment in Urban Children: Examining Sensitive Windows and Sex-Specific Associations.” Environment International, vol. 87, Feb. 2016, pp. 56–65. (Crossref), 


Corcoran, Cheryl, et al. “The Neurobiology of the Stress Cascade and Its Potential Relevance for Schizophrenia:” Journal of Psychiatric Practice, vol. 7, no. 1, Jan. 2001, pp. 3–14. (Crossref), 


Costa, Lucio G., et al. “Effects of Air Pollution on the Nervous System and Its Possible Role in Neurodevelopmental and Neurodegenerative Disorders.” Pharmacology & Therapeutics, vol. 210, June 2020, p. 107523. (Crossref), 


Daiber, Andreas, et al. “Oxidative Stress and Inflammation Contribute to Traffic Noise-Induced Vascular and Cerebral Dysfunction via Uncoupling of Nitric Oxide Synthases.” Redox Biology, vol. 34, July 2020, p. 101506. (Crossref), 


Giebel, Clarissa M., et al. “Depressive Symptomatology in Severe Dementia in a European Sample: Prevalence, Associated Factors and Prescription Rate of Antidepressants.” International Psychogeriatrics, vol. 27, no. 4, Apr. 2015, pp. 657–67. (Crossref), 


Gilani, S. R., Zaidi, S. R., Batool, M., Bhatti, A. A., Durrani, A. I., & Mahmood, Z. (2015). Report: Central nervous system (CNS) toxicity caused by metal poisoning: Brain as a target organ. Pakistan journal of pharmaceutical sciences, 28(4), 1417–1423. 


González-Maciel, Angélica, et al. “Combustion-Derived Nanoparticles in Key Brain Target Cells and Organelles in Young Urbanites: Culprit Hidden in Plain Sight in Alzheimer’s Disease Development.” Journal of Alzheimer’s Disease, vol. 59, no. 1, July 2017, pp. 189–208. (Crossref), 


Gurgueira, Sonia A., et al. “Rapid Increases in the Steady-State Concentration of Reactive Oxygen Species in the Lungs and Heart after Particulate Air Pollution Inhalation.” Environmental Health Perspectives, vol. 110, no. 8, Aug. 2002, pp. 749–55. (Crossref), 


Hahad, Omar, et al. “Environmental Noise-Induced Effects on Stress Hormones, Oxidative Stress, and Vascular Dysfunction: Key Factors in the Relationship between Cerebrocardiovascular and Psychological Disorders.” Oxidative Medicine and Cellular Longevity, vol. 2019, Nov. 2019, pp. 1–13. (Crossref), 


Halperin, Demian. “Environmental Noise and Sleep Disturbances: A Threat to Health?” Sleep Science, vol. 7, no. 4, Dec. 2014, pp. 209–12. (Crossref), 


Hegewald, Janice, et al. “Traffic Noise and Mental Health: A Systematic Review and Meta-Analysis.” International Journal of Environmental Research and Public Health, vol. 17, no. 17, Aug. 2020, p. 6175. (Crossref), 


Jaffe, Daniel A., et al. “Diesel Particulate Matter Emission Factors and Air Quality Implications from in–Service Rail in Washington State, USA.” Atmospheric Pollution Research, vol. 5, no. 2, Apr. 2014, pp. 344–51. (Crossref), pollution R.2014.040. 


Jayaraj, Richard L., et al. “Outdoor Ambient Air Pollution and Neurodegenerative Diseases: The Neuroinflammation Hypothesis.” Current Environmental Health Reports, vol. 4, no. 2, June 2017, pp. 166–79. (Crossref), 


Jiang, Nona M., et al. “Febrile Illness and Pro-Inflammatory Cytokines Are Associated with Lower Neurodevelopmental Scores in Bangladeshi Infants Living in Poverty.” BMC Pediatrics, vol. 14, no. 1, Dec. 2014, p. 50. (Crossref), 


Klompmaker, Jochem O., et al. “Associations of Combined Exposures to Surrounding Green, Air Pollution and Traffic Noise on Mental Health.” Environment International, vol. 129, Aug. 2019, pp. 525–37. (Crossref), 


Landrigan, Philip J., et al. “The Lancet Commission on Pollution and Health.” The Lancet, vol. 391, no. 10119, Feb. 2018, pp. 462–512. (Crossref), 


Li, Huan, et al. “Short-Term Effects of Air Pollution on Cause-Specific Mental Disorders in Three Subtropical Chinese Cities.” Environmental Research, vol. 191, Dec. 2020, p. 110214. (Crossref), 


Li, Ping, et al. “In Situ Visualization of Ozone in the Brains of Mice with Depression Phenotypes by Using a New near-Infrared Fluorescence Probe.” Chemical Science, vol. 10, no. 9, 2019, pp. 2805–10. (Crossref), 


Ma, Jing, et al. “A Multilevel Analysis of Perceived Noise Pollution, Geographic Contexts and Mental Health in Beijing.” International Journal of Environmental Research and Public Health, vol. 15, no. 7, July 2018, p. 1479. (Crossref), 


Maleki, K., & Hosseini, S. M. (2011). Investigation of the Effect of Leaves, Branches and Canopies of Trees on Noise Pollution Reduction. Annals of Environmental Science, 5. Retrieved from  


Markevych, Iana, et al. “Exploring Pathways Linking Greenspace to Health: Theoretical and Methodological Guidance.” Environmental Research, vol. 158, Oct. 2017, pp. 301–17. (Crossref), 


Miller, Andrew H., and Charles L. Raison. “The Role of Inflammation in Depression: From Evolutionary Imperative to Modern Treatment Target.” Nature Reviews Immunology, vol. 16, no. 1, Jan. 2016, pp. 22–34. (Crossref), 


Mittal, Manish, et al. “Reactive Oxygen Species in Inflammation and Tissue Injury.” Antioxidants & Redox Signaling, vol. 20, no. 7, Mar. 2014, pp. 1126–67. (Crossref), 


Nephew, Benjamin C., et al. “Traffic-Related Particulate Matter Affects Behavior, Inflammation, and Neural Integrity in a Developmental Rodent Model.” Environmental Research, vol. 183, Apr. 2020, p. 109242. (Crossref), 


Ogino, Keiki, et al. “Involvement of PM2.5-Bound Protein and Metals in PM2.5-Induced Allergic Airway Inflammation in Mice.” Inhalation Toxicology, vol. 30, no. 13–14, Dec. 2018, pp. 498–508. (Crossref), 


Okkels, N., Kristiansen, C. B., Munk-Jørgensen, P., & Sartorius, N. (2018). Urban mental health: Challenges and perspectives. Current Opinion in Psychiatry, 31(3), 258–264. 


Palacios, Natalia. “Air Pollution and Parkinson’s Disease – Evidence and Future Directions.” Reviews on Environmental Health, vol. 32, no. 4, Dec. 2017. (Crossref), 


Pope, C. Arden, et al. “Exposure to Fine Particulate Air Pollution Is Associated With Endothelial Injury and Systemic Inflammation.” Circulation Research, vol. 119, no. 11, Nov. 2016, pp. 1204–14. (Crossref), 


Popa-Wagner, Aurel, et al. “ROS and Brain Diseases: The Good, the Bad, and the Ugly.” Oxidative Medicine and Cellular Longevity, vol. 2013, 2013, pp. 1–14. (Crossref), 


Potter, Nicole A., et al. “Particulate Matter and Associated Metals: A Link with Neurotoxicity and Mental Health.” Atmosphere, vol. 12, no. 4, Mar. 2021, p. 425. (Crossref), 


Prüss-Üstün, Annette, et al. Preventing Disease through Healthy Environments: A Global Assessment of the Burden of Disease from Environmental Risks. World Health Organization, 2016. WHO IRIS, 


Pujol, Jesus, et al. “Traffic Pollution Exposure Is Associated with Altered Brain Connectivity in School Children.” NeuroImage, vol. 129, Apr. 2016, pp. 175–84. (Crossref), 


Rudolph, Kara E., et al. “Environmental Noise and Sleep and Mental Health Outcomes in a Nationally Representative Sample of Urban US Adolescents.” Environmental Epidemiology, vol. 3, no. 4, Aug. 2019, p. e056. (Crossref), 


Salvi, Ankita, et al. “Involvement of Oxidative Stress and Mitochondrial Mechanisms in Air Pollution-Related Neurobiological Impairments.” Neurobiology of Stress, vol. 12, May 2020, p. 100205. (Crossref), 


Sansone, R. A., & Sansone, L. A. (2012). Antidepressant adherence: Are patients taking their medications? Innovations in Clinical Neuroscience, 9(5–6), 41–46. 


Saveleva, Liudmila, et al. “Subacute Inhalation of Ultrafine Particulate Matter Triggers Inflammation without Altering Amyloid Beta Load in 5xFAD Mice.” NeuroToxicology, vol. 89, Mar. 2022, pp. 55–66. (Crossref), 


Sawyer, Kristi M. “The Role of Inflammation in the Pathogenesis of Perinatal Depression and Offspring Outcomes.” Brain, Behavior, & Immunity – Health, vol. 18, Dec. 2021, p. 100390. (Crossref), 


Spindler, K. R., & Hsu, T.-H. (2012). Viral disruption of the blood–brain barrier. Trends in Microbiology, 20(6), 282–290. 


Sturchio, Andrea, et al. “High Cerebrospinal Amyloid-β 42 Is Associated with Normal Cognition in Individuals with Brain Amyloidosis.” EClinicalMedicine, vol. 38, Aug. 2021, p. 100988. (Crossref), 


Talaiekhozani, Amirreza & Ghaffarpasand, Omid & Talaie khozani, Mohammad Reza & Neshat, Neda & Eydivandi, Behnam. (2017). Evaluation of emission inventory of air pollutants from railroad and air transportation in Isfahan metropolitan in 2016. Journal of Air Pollution and Health. 2. 1-18. 


Tan, Zi-Xuan, et al. “The Beneficial Role of Exercise on Treating Alzheimer’s Disease by Inhibiting β-Amyloid Peptide.” Molecular Neurobiology, vol. 58, no. 11, Nov. 2021, pp. 5890–906. (Crossref), 


United Nations. Day of 8 Billion. United Nations. Geraadpleegd 16 maart 2023, van 


Ventriglio, A., Torales, J., Castaldelli-Maia, J. M., De Berardis, D., & Bhugra, D. (2021). Urbanization and emerging mental health issues. CNS Spectrums, 26(1), 43–50. 


Weisskopf, Marc G., and Thomas F. Webster. “Trade-Offs of Personal Versus More Proxy Exposure Measures in Environmental Epidemiology:” Epidemiology, vol. 28, no. 5, Sept. 2017, pp. 635–43. (Crossref), 


Wentworth, Paul, et al. “Evidence for Ozone Formation in Human Atherosclerotic Arteries.” Science, vol. 302, no. 5647, Nov. 2003, pp. 1053–56. (Crossref), 


Wieser, A. A., Scherz, M., Passer, A., & Kreiner, H. (2021). Challenges of a healthy built environment: Air pollution in construction industry. Sustainability, 13(18), 10469. 


World Bank. Geraadpleegd 16 maart 2023, van 


Zeng, Ying, et al. “Ambient Air Pollution Exposure and Risk of Depression: A Systematic Review and Meta-Analysis of Observational Studies.” Psychiatry Research, vol. 276, June 2019, pp. 69–78. (Crossref), 



Over de auteur: Sophie Schuller


Sophie Schuller is a neuroarchitectural researcher and EMEA Head of Living Lab and Scientific Research for Cushman & Wakefield. Sophie has over 18 years’ experience advising some of the world’s largest organisations on how workplace design and the built environment impacts employee health, wellbeing and organisational performance. In addition, Sophie is currently studying for her PhD at the Technical University of Eindhoven (TU/e) in the Netherlands. Her area of research focusses on how commercial architecture (offices) may influence our neurophysiology and how this may impact human health and cognition. Sophie is a frequent author, speaker and presenter on this subject.


Mail the editors