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Review

Effects of Indoor Air Quality on Human Physiological Impact: A Review

by
Tong Nie
1,
Guofu Zhang
2,*,
Yinan Sun
1,
Wenhao Wang
1,
Tianai Wang
1 and
Haoyan Duan
1
1
College of Architecture and Urban Planning, Qingdao University of Technology, Qingdao 266033, China
2
Weifang Product Quality Inspection Research Institute (Weifang Fiber Inspection Institute), Weifang 261036, China
*
Author to whom correspondence should be addressed.
Buildings 2025, 15(8), 1296; https://doi.org/10.3390/buildings15081296
Submission received: 25 February 2025 / Revised: 30 March 2025 / Accepted: 8 April 2025 / Published: 15 April 2025
(This article belongs to the Section Building Energy, Physics, Environment, and Systems)
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Abstract

:
As urbanization accelerates, indoor air quality has emerged as a critical determinant of population health. To systematically evaluate the relationship between indoor air quality (IAQ) and human physiological responses, we conducted a comprehensive review of 63 experimental studies retrieved from three major databases (ScienceDirect, Google Scholar, Web of Science) spanning the years 2000–2023. This systematic review synthesizes evidence from experimental studies examining the physiological impacts of indoor air contaminants, including gaseous pollutants, particulate matter (PM), and volatile organic compounds (VOCs). Through an analysis of cardiovascular biomarkers (heart rate variability, blood pressure), respiratory parameters, and neurological indicators (electroencephalogram patterns), we identify the mechanisms linking air quality degradation to impaired physiological functioning. Our findings demonstrate that optimized ventilation systems and high-efficiency particulate filtration can mitigate exposure risks, potentially enhancing cardiovascular efficiency, pulmonary capacity, and cognitive performance. The evidence further suggests that sustained improvements for indoor environments may decrease incidence rates of respiratory pathologies and neurological disorders.

1. Introduction

In recent years, air pollution has placed an enormous burden on global public health [1]. Globally, fewer than 1% of low-income and middle-income countries have urban air quality that meets the thresholds recommended by the World Health Organization (WHO). Data from the most recent Global Air Quality Guidelines released by the WHO show that about 7 million people die each year globally from ambient air pollution, accounting for about 11.6% of all deaths worldwide. Nearly 3.8 million of these premature deaths are due to indoor air pollution [2]. Studies have found that pollutant levels for indoor air are sometimes even higher than for outdoor air [3,4]. Individuals who spend extended periods indoors may experience health problems due to poorer indoor air quality (IAQ) [5]. Therefore, there is an urgent need to improve IAQ.
Indoor air pollutants are heterogeneous mixtures of particulate matter (PM), gases, and liquids, including CO2, O3, PM2.5, PM10, and substances such as formaldehyde and benzene. Indoor air pollution triggers physiological problems in the human body caused by either a single factor or a combination of factors, involving various response mechanisms. Many experimental studies have confirmed the existence of an effect of IAQ on human mental and psychological states, primarily in terms of subjective comfort and work efficiency [6]. It has been found that, as the IAQ decreases, children’s academic performance [7] as well as adults’ performance in the office [3,7] decreases, along with an increase in fatigue. More than 20% of the exposed population experiences exacerbated symptoms of sick building syndrome (SBS). Poor IAQ negatively impacts the human psyche and can lead to irreversible physiological health problems, especially in the cardiovascular and respiratory systems [8]. Many studies have found that elderly, obese, or sick individuals are more susceptible to the effects of air pollutants than healthy people [9,10,11,12,13].
This review systematically evaluates five cardiorespiratory and neurological biomarkers: arterial blood pressure, heart rate (HR), heart rate variability (HRV), forced vital capacity (FVC), and electroencephalogram (EEG). These parameters quantitatively assess autonomic regulation, pulmonary function, and cortical activation patterns in response to IAQ fluctuations, providing the multisystem physiological profiling of environmental exposure impacts. Numerous studies have shown that, in terms of cardiovascular indicators, elevated levels of pollutants, such as CO2, PM2.5, and VOCs for indoor air, lead to an increased HR [8,14,15,16], blood pressure [17,18,19], and a decrease in the HRV index [20,21]. Respiratory studies demonstrate dose-dependent CO2 effects, with hypercapnic exposure reducing forced vital capacity (FVC) [22], and elevating minute ventilation rates [23]. Neurophysiological investigations reveal CO2-mediated cortical oscillation alterations, specifically α-band (8–13 Hz) suppression with concomitant β-band (14–30 Hz) and θ-band (4–7 Hz) amplification [24,25]. Current reviews exhibit limited scope in addressing IAQ biomarker interactions, predominantly focusing on singular pollutants like formaldehyde and CO2 [26,27]. Therefore, this paper provides a comprehensive and objective review of the relevant literature, summarizes the effects of indoor air quality on human physiological indicators, and answers the following questions:
  • How do distinct categories of indoor air pollutants (e.g., gaseous pollutants, particulate matter, VOCs) differentially impact cardiovascular, respiratory, and neurological physiological indicators?
  • What synergistic effects emerge from combined exposure to multiple pollutants, and how do these interactions modulate health risks?
  • To what extent can current intervention strategies (e.g., ventilation optimization, air filtration) mitigate pollutant-induced physiological disturbances across diverse populations?
It also identifies research trends and their status, outlines optimization strategies, and provides an outlook for future research.

2. Materials and Methods

To investigate recent developments in the IAQ’s physiological impacts and assess pollutant-exposure relationships, we systematically reviewed the literature from three multidisciplinary databases (ScienceDirect, Google Scholar, Web of Science). This methodology enables comprehensive tracking of emerging trends while establishing mechanistic links between indoor air contaminants and measurable physiological responses. Searching terms included IAQ or air pollutants (e.g., “carbon dioxide”, “particulate matter”, “ozone”, or “volatile organic compounds”) and physiological indicators (e.g., “blood pressure”, “electroencephalogram”, “heart rate variability”, or “oximetry”). The keywords used in this study are shown in Table 1. The inclusion criteria for this study are as follows: (1) only studies with authentic or quasi-experimental designs were reviewed in this study; (2) studies on the effects of inhalation of indoor air pollutants on human physiological indices were excluded, with a focus on individual-level, maskless, IAQ intervention studies; and (3) experimental studies in which subjects engaged in physical activity were excluded. The testing state was dominated by a sedentary state to ensure the smooth breathing of the subjects. This study systematically reviewed the nearly 20 years of research literature on IAQ, with 63 articles retained for review according to inclusion and exclusion criteria. Figure 1 illustrates the literature on the effects of IAQ on human physiological indices and the number and type of publications per year since 2000, with the majority of the studies occurring after 2010 (N = 43). The search process is shown in Figure 2.
The journals to which the papers included in the review belonged were analyzed and the results are shown in Table 2. The papers were primarily published in Japan, China, and South Korea, in East Asia; Denmark and the United Kingdom, in Europe, as well as the United States and Canada, in North America. The cited studies are primarily from these seven countries for to the following reasons: East Asia’s industrialization drives air pollution research, with Japan/South Korea excelling in IAQ tech, and China prioritizing smog control. In Europe, Denmark leads in green building standards, while the UK emphasizes pollution epidemiology. North America leverages interdisciplinary approaches and diverse demographics. Shared drivers include strong funding, policy–science synergy, and global academic networks. The relevant journal articles that did not involve the experimental locations or data measurement locations were standardized according to the regions to which the authors belonged.

3. Effects of Gaseous Pollutants on Human Physiological Indicators

3.1. Effect of CO2 Content on Human Physiological Indicators

Carbon dioxide is one of the more common gaseous pollutants affecting IAQ and has a significant effect on human physiological indicators. Table A1 shows some of the studies on the effects of CO2 on human physiological indicators. Elevated CO2 levels influence cardiovascular functioning through blood pressure regulation, heart rate (HR), and heart rate variability (HRV). Research documents dose-dependent SBP reductions (4.8–7.3 mmHg/1000 ppm CO2 decrease) [28], concurrent with improved IAQ assessments [29], suggesting systemic cardiovascular–environment interactions. The diastolic blood pressure (DBP) of the human body significantly increased after the CO2 concentration reached 3000 ppm [19] or 5000 ppm [23] when subjects completed the task test. Regarding HR, Zhang et al. [30] found that HR remained unchanged when subjects completed the task test at a CO2 concentration of 5000 ppm by adding CO2. Several studies have documented modest HR reductions occurring at specific CO2 concentration thresholds [19,23]. Emerging evidence demonstrates a dose-dependent elevation in HR under elevated CO2 exposure. Controlled experiments by Chen and Hsiao [16] revealed a 7.2% HR increase in hypercapnic conditions (>1000 ppm) compared to normocapnic environments (<800 ppm), while Snow et al. [14] documented acute 2.4 bpm HR surges during rapid CO2 escalation (830–2700 ppm). This compensatory mechanism enhances cardiac output to accelerate pulmonary perfusion, optimizing gas exchange efficiency for blood oxygen saturation maintenance. The experimental evidence demonstrates bidirectional cardiovascular responses to CO2 exposure, with paradoxical heart rate modulation observed across concentration gradients. Elevated CO2 levels consistently compromise HRV, indicating autonomic nervous system dysregulation. Kajtár and Herczeg [23] documented dose-dependent autonomic responses, with mid-frequency (MF) power and MF/HF ratio reductions (≤4000 ppm CO2) coinciding with high-frequency (HF) power elevation at 5000 ppm, suggesting coordinated sympathetic activation with parasympathetic withdrawal. These patterns reflect impaired autonomic regulation that elevates cardiovascular morbidity risks [8,13,31,32]. Conversely, investigations under acute hypercapnic exposure (unventilated environments) revealed paradoxical increases in time-domain HRV indices—SDNN [33] and pNN50 [25]. This paradoxical response potentially reflects compensatory autonomic modulation [34] to optimize metabolic efficiency during CO2 challenges.
High indoor CO2 concentrations can negatively affect the human respiratory system. Mechanistically, an increase in CO2 concentration results in insufficient alveolar ventilation, leading to CO2 retention in the human body. The blood’s CO2 concentration increases, and SpO2 decreases accordingly [16]. This situation elevates the partial pressure of CO2 (PCO2) delivered to the lungs, resulting in hypercapnia. Hypercapnia falls under the classification of type II respiratory failure. Additionally, an increased CO2 concentration causes a reduction in forced vital capacity (FVC) [22] and an elevation in respiratory volume [23] among subjects. Notably, respiratory rate [23,26,35] and end-tidal CO2 (ETCO2) [22] remain statistically unaffected under acute hypercapnic conditions.
Increased CO2 concentrations affect human brain activity. It was found that subjects exposed to low levels of CO2 concentration (1244 ± 70 ppm) exhibited effects on EEG signals when completing a task test. Both alpha and theta wave relative power increased, indicating decreased attention and increased drowsiness, respectively [35]. Subjects exposed to high levels of CO2 concentration (5087 ± 318 ppm) demonstrated an increase in beta wave relative power [25]. Individuals exposed to ultra-high CO2 concentrations (40,000 ppm) exhibited a decrease in alpha waves and an increase in theta waves [24]. However, this finding contrasts with the conclusion of Shan et al. [35], who observed an increase in the relative power of theta waves, as mentioned above. This difference may be attributed to variations in experimental procedures, both with and without the task test setup, leading to differing levels of psychological stress among subjects, which consequently affects the EEG signal. Furthermore, individuals with inadequate sleep are more susceptible to the effects of CO2 in an enclosed space [14]. The correlation between EEG and CO2 concentration was notably linked to the hours of sleep the subjects had the previous night.
In addition, CO2 concentrations have an effect on other physiological indicators in the human body. For example, exposure to medium-to-high CO2 concentrations of 1000 ppm, 3000 ppm, and 5000 ppm increased the concentration of α-amylase in human saliva [19,30]. However, no significant changes in salivary cortisol were observed when exposed to high CO2 concentrations of 5000 ppm [30]. Chen and Hsiao [16] noted that facial temperature was positively correlated with CO2 concentration. Zhang et al. [25] concluded no significant changes in urinary pH after subjects slept at high CO2 levels. All the above experiments were conducted under thermo-neutral conditions. However, under high-temperature conditions with increasing CO2 concentration, there was no substantial change in physiological indices, such as tympanic membrane temperature of the right ear, skin temperature, heart rate (HR), blood pressure (BP), arterial oxygen saturation, etc. [36]. Kang et al. [37] studied the effects of differences in carbon dioxide concentrations on sleep quality. The study found that sleep quality was significantly reduced at ventilation rates of 1000 ppm and 1300 ppm CO2 compared to ventilation with an average CO2 concentration of 750 ppm [37].
In summary, elevated CO2 exposure adversely impacts multiple physiological systems. Cardiovascular effects include increased blood pressure, reduced HRV, elevated HR, and heightened cardiovascular disease risk. Respiratory consequences involve increased respiratory volume, decreased FVC, and hypercapnia, disrupting acid-base balance and cellular metabolism [27]. Neurophysiological studies report altered EEG patterns with reduced alpha waves and increased beta/theta wave activity. Current guidelines recommend maintaining indoor CO2 ≤ 1000 ppm for acceptable IAQ [38]. This is in line with the results of Kim et al. that indoor CO2 levels should be maintained below 1000 ppm to safeguard human physiological health [28]. However, recent ASHRAE guidelines emphasize CO2 as an indicator of ventilation effectiveness rather than a direct health-based limit [39]. As Persily notes, the previous 1000 ppm benchmark was often misinterpreted as a safety threshold, whereas contemporary standards prioritize context-specific ventilation rates [39]. The main summary of the study is shown in Figure 3.

3.2. Effect of O3 Content on Human Physiological Indicators

Table A2 shows some of the studies on the effects of O3 on human physiological indicators. Current research consensus standardizes indoor ozone exposure at 120 ppb, demonstrating the null effects on cardiovascular parameters (SBP, MAP, HR) [40] and vascular endothelial markers (FMD, NMD) [41]. Hoffmann et al. [42] quantified marginal blood pressure reductions (SBP: −4.0%, DBP: −2.0%, MAP: −2.8%) per IQR increase in ozone exposure, though statistically non-significant. Contrasting evidence from Urch et al. [43] identified significant brachial artery diameter constriction (−0.09 mm BAD) at this exposure level [41], revealing potential exposure–response divergences across vascular metrics.
Environmental studies demonstrate synergistic interactions between ozone (O3) and PM2.5 through atmospheric multipollutant mechanisms [44,45,46]. For example, in two randomized double-blind crossover trials, Brook et al. [46] demonstrated that DBP increased by 2.9 mmHg under PM2.5-only exposure and 3.6 mmHg during combined PM2.5–O3 exposure. This effect might be attributed to O3 reducing vagal tone, subsequently leading to autonomic nervous system changes. In the crossover design experiment conducted by Fakhri et al. [44], which included ten mild asthmatics, it was observed that DBP increased by 2.0 mmHg, and the SDNN intervals increased in the subjects following the combined effect of PM2.5 and O3. Notably, no heterogeneity in asthma status was identified.
In summary, a single O3 concentration does not significantly affect cardiovascular function. However, a more substantial synergistic effect may be induced when older groups or vulnerable individuals with cardiovascular and respiratory diseases are exposed to both PM2.5 and O3. These individual differences need to be addressed in future studies.

3.3. Effects of Other Gaseous Pollutant Contents on Human Physiological Indicators

Beyond CO2 and O3, indoor air quality analysis must consider carbon monoxide (CO) and oxygen (O2) dynamics. Ambient CO concentrations demonstrate null cardiovascular effects, with preserved heart rate stability during controlled exposures [47]. Covariance analysis reveals no HRV–CO correlations at subthreshold concentrations [48], though elevated CO (>2.7 ppm) induces autonomic modulation evidenced by increased r-MSSD metrics [47]. Regarding oxygen homeostasis, Wang et al. [49] observed negligible EEG signal variation in hypercapnic subjects under hyperoxic (150 mmHg) and hypoxic (50 mmHg) challenges, suggesting neural adaptation mechanisms. In summary, fewer studies exist on the effects of gaseous pollutants other than CO2 and O3 for indoor air on human physiological indices. Only a few studies have focused on CO and O2, and they do not significantly affect human physiological indices, such as HR and EEG, at low concentration levels.

4. Effects of Particulate Matter on Human Physiological Indicators

Indoor air contains a significant amount of atomized PM with individual particle sizes ranging from a few nanometers to 10 microns. This PM primarily originates from direct emissions from various indoor sources, but can also result from the infiltration of PM from outdoor air. In this paper, the primary PM studied for indoor air is dominated by PM2.5, while also encompassing submicron particles, PM1, PM5, PM10, and so forth. The main summary of the study is shown in Figure 3.

4.1. Effects of PM2.5 on Human Physiological Indicators

Table A3 shows some of the studies on the effects of PM2.5 on human physiological indicators. It was found that short-term indoor exposure to PM2.5 decreased the frequency domain indexes HF [21,45,50] and LF [50] of HRV and SDNN of time domain indexes [45,50,51]. Additionally, emerging evidence demonstrates CO2-induced cardiovascular activation, triggering significant elevations in heart rate [8,17] and blood pressure [18,40,52,53]. These effects are not conducive to the relaxation of the autonomic nervous system. Moreover, PM2.5 exposure heightens the risk of infection or inflammation in the body, as evidenced by elevated malondialdehyde concentrations in plasma [54], and indirectly through increased ultrasensitive C-reactive protein and 8-hydroxydeoxyguanosine levels in the blood [53].
Currently, most studies on the effects of PM2.5 for indoor air on human physiological indicators primarily focus on the human cardiovascular system. It has been found that exposure to indoor PM2.5 in healthy populations leads to an increase in blood pressure [18]. Moreover, for each increase in the interquartile range (IQR) of PM2.5, the HR of subjects increases by an average of 4–6 bpm [8]. Studies investigating the effects on specific sensitive groups, such as the elderly, overweight individuals, and mildly or critically ill patients with heart or lung diseases, have been intensified. The morbidity and mortality of cardiovascular diseases associated with acute PM2.5 exposure are higher in sensitive populations than in healthy populations. Pan et al. recruited 43 patients with physician-diagnosed stable COPD and measured their 24-h HRV and HR [21]. They observed that HF decreased by only 2.01% in COPD patients with normal body weight after exposure to PM2.5, whereas it decreased by as much as 34.85% in overweight COPD patients. The effect on parasympathetic activity associated with indoor particulate matter was more pronounced. Hoffmann et al. [42] conducted a panel study of 70 subjects with T2DM, with blood pressure measured every 2 weeks by automated oscillometric sphygmomanometer and pulse wave analysis, and hourly central site measurements of fine particulate matter, ozone, and meteorology. They noted that indoor PM2.5 raised arterial blood pressure in patients with type 2 diabetes. Regarding age, the elderly are more sensitive to PM2.5 than the young [44,55]. Jia et al. [56] found that a five-minute exposure to PM2.5 increased HF and LF by 1.30% and 1.34%, respectively, in healthy elderly subjects. Baumgartner et al. [18] reported that a 1-log µg/m3 increase in PM2.5 concentration elevated blood pressure in adult females, with middle-aged and older females above 50 years of age showing a stronger correlation with increased blood pressure. Furthermore, pronounced sex differences have been noted in changes in hematological parameters and protein oxidation products induced by PM2.5 exposure. Physiological responses generally appear weaker in men than in women. Sørensen et al. [54] discovered that, for every 10 µg/m3 increase in indoor PM2.5 concentrations, plasma proteins increased by an average of 1.6% in both sexes, and malondialdehyde concentrations increased by 3.7% in females. However, there was no significant change observed for males.
In recent years, with the increasing awareness of health protection, people are increasingly focusing on purifying indoor air from PM2.5. This is typically achieved through air conditioning filtration [48]. Studies have demonstrated that, when individuals are exposed to unfiltered indoor air, the SBP, DBP, and HR of student subjects increase by 4.11 mmHg, 2.78 mmHg, and 3.11 bpm per IQR, respectively, averaged over 4 h [57]. After the filter is activated, the subjects’ BP and HR do not change significantly with rising PM2.5 levels [57]. However, microvascular functioning experiences a significant enhancement after the second day [58]. Zhou et al. [59] assessed the relationship between short-term exposure to indoor PM2.5 in the workplace and cognitive ability in adults. Even during short-term indoor exposure, elevated concentrations of PM2.5 can have adverse effects on cognitive ability [59]. Furthermore, air conditioning filtration does not improve lung function, systemic inflammation, nor does it significantly reduce monocyte activation or lung cell damage in the elderly [58], which suggests that the ameliorative effect of air conditioning filtration is limited. The effects of other filtration methods exhibit similar variability.
Liu et al. [60] utilized active filtration (with activated carbon filters) in their experiments. Their study demonstrated that each 10 µg/m3 increment in the 8-h moving average PM2.5 concentration during sham filtration (without filter) correlated with a statistically significant 1.34% reduction in SDNN. By contrast, active filtration attenuated this effect, resulting in a non-significant 0.81% decrease in SDNN. Additionally, Liu et al. [61] used an ionization air purifier to reduce PM2.5 levels indoors, which enhanced the six major pathways of HRV in children (1. galactose metabolism is upregulated, 2. downregulation of purine metabolism, 3. upregulation of vitamin B metabolism, 4. lysine degradation upregulation, 5. improved β-oxidation of fatty acids, And 6. upregulation of progesterone biosynthesis), leading to increased energy production and improved anti-inflammatory capacity. However, the NAI produced worsened effects on the five major pathways of HRV (1. UTP synthesis down-regulation, 2. TCA cycle down, 3. dysregulation of tyrosine and phenylalanine metabolism, 4. reduced antioxidant scavenging activity, And 5. histidine degradation increased), decreased energy production, and inhibited antioxidant capacity.
Moreover, studies have been conducted using indoor plants to reduce and purify PM2.5 for indoor air. Chen et al. [15] conducted six 24-h home visits with each elderly subject and measured PM2.5, TVOCs, HR, and BP consecutively at each home visit. They discovered that placing plants indoors resulted in a reduction of about 9.1 µg/m3 of PM2.5 in the air, along with corresponding reductions in SBP (without plants: 128.4 mmHg vs. with plants: 114.1 mmHg) and HR (without plants: 76.4 bpm vs. with plants: 70.3 bpm) [15]. However, the precise mechanisms underlying the observed reductions in SBP and HR remain unresolved. These effects may arise from BVOC emissions by indoor plants, their psychophysiological stress-reducing properties, or interactions with PM2.5 attenuation dynamics. Future investigations should delineate the relative contributions of phytochemical, perceptual, and particulate-modulating pathways to indoor plant-mediated physiological adaptations.
In summary, PM2.5 for indoor air causes subjects to experience increased sympathetic activation, decreased parasympathetic tone, or both, which reduces the level of autonomic control over the human heart [58,62], resulting in acute health damage to the cardiovascular system [50]. Notably, studies have shown that the degree of harm caused by PM2.5 is likely to be correlated with the carbon level in PM2.5 [40], leading to arterial constriction and subsequently increasing blood pressure [43]. Therefore, in future studies, further consideration should be given to the physiological effects of the elemental composition and levels of particulate matter. The main summary of the study is shown in Figure 4.

4.2. Effects of Other Diameters of PM on Human Physiological Indicators

Current research on the physiological effects of particulate matter beyond PM2.5 remains focused on cardiovascular outcomes, including blood pressure elevation [8] and reduced HRV indices (SDNN, r-MSSD) [48]. These alterations are associated with autonomic dysfunction, contributing to cardiac conditions (e.g., myocardial infarction, hypertension) and non-cardiac disorders (e.g., diabetes mellitus, COPD). Smaller particulate fractions exhibit stronger associations with HRV suppression and heart rate elevation [21,50], particularly posing risks for myocardial ischemia or arrhythmia in high-risk cardiovascular populations [63]. Chuang et al. [62] observed that PM0.3–1.0 exposure specifically reduced HRV in patients with hypertension and coronary heart disease, whereas larger particulates (PM0.3–1.0) showed no significant effects.
In summary, there is a correlation between particle size and physiological indicators, such as HRV. The pathophysiological impact of particulate matter intensifies inversely with aerodynamic diameter, demonstrating heightened cardiopulmonary toxicity at smaller particle sizes. Consequently, indoor air purification systems should prioritize size-selective filtration strategies targeting ultrafine particulate fractions to optimize particulate removal efficacy and mitigate cardiopulmonary health risks.

5. Effects of VOCs on Human Physiological Indicators

Volatile Organic Compounds represent a class of ubiquitous chemical contaminants that significantly compromise IAQ. This group encompasses formaldehyde, benzene, toluene, xylene, ethylbenzene, styrene, trichloroethylene, and chlorinated derivatives including p-dichlorobenzene and perchloroethylene—all classified as established neurotoxicants. Current research indicates a knowledge gap regarding their systematic toxicological classification, with limited experimental data elucidating exposure–response relationships. Notably, formaldehyde has emerged as a prototypical VOC in IAQ research, serving as the primary subject of focused investigation in controlled IAQ studies. Table A4 shows some of the studies on the effects of VOCs on human physiological indicators. The main summary of the study is shown in Figure 5.
VOCs can affect the human cardiovascular system [53], especially for the physiological health of individuals with poorer or compromised health. Studies have shown that HR and SBP significantly increase in the elderly as the concentration of VOCs for indoor air rises [15]. Overweight or obese subjects exhibit higher SBP levels compared to normal-weight subjects [17]. Fifty percent of chemically sensitized patients exhibit significantly lower HF and suppressed parasympathetic activity in humans [20]. The mid-expiratory flow rate (FEF50), an indicator of human lung function, is affected in SBS patients compared to healthy adults, indicating reduced respiratory function. Skin measurements of sebum and perspiration are only responsive in SBS patients [64]. Changes in the concentration of VOCs themselves can have varying effects on the same physiological indicators. Mizukoshi et al. [65] measured seven healthy subjects for 24 h under usual daily living conditions. They found that, when the VOCs, primarily toluene and xylene, increased, the HF of HRV in subjects was negatively correlated with them and positively correlated with LF/HF [65]. The opposite result was found when the VOCs decreased.
VOCs affect human brain activity. Chen et al. [66] found that, at a formaldehyde concentration of 0.05 mg/m3, an EEG showed that human brain waves began to show abnormalities. Nakayama et al. [67] found that an EEG showed a significantly greater percentage of increases/decreases in α/β values of the brainwaves in subjects at higher levels of 79 VOCs. However, subjects did not experience changes in cerebral blood flow [68], but they exerted more effort when performing tasks at maximum speed. Subjectively, they reported increased fatigue during exposure.
VOCs can affect the human respiratory system. Formaldehyde amplifies lung damage, causing small airways to function abnormally and increasing the resistance to lung ventilation [58,69,70], which is not conducive to physiological relaxation. VOCs also affect the metabolic rate of the human body in the working conditions of office workers. For example, Bakó-Biró et al. [71] found a significant decrease in the CO2 production rate of about 5% for subjects in the office environment, which could be caused by a change in breathing pattern (shallow breathing) or a slower work rate, leading to a decrease in metabolic rate. However, Wargocki et al. [72] reported that subjects exposed to 41 VOCs, mainly acetone and acetic acid, had a metabolic rate in the office state of 1.3, much higher than the relaxed sedentary normal value of 1.2. This is due to the unconscious tension of the muscles during mental labor.
In addition, formaldehyde in VOCs readily reacts with the biological tissues of the body, especially the mucous tissues of the respiratory tract and eyes [73], causing the potential for inflammation [64]. Formaldehyde-exposed women have an increased risk of spontaneous abortion and adverse pregnancy outcomes, including chromosome and DNA damage (genotoxicity), oxidative stress, altered levels and/or function of biological enzymes, hormones and proteins, and DNA methylation [74]. Most importantly, exposure to airborne formaldehyde dramatically increases non-carcinogenic health risks and carcinogenic risks in various human systems [26]. Kim et al. [75] noted that chronic exposure to formaldehyde reduces the number of human leukocytes and may lower platelet and hemoglobin counts [64,69], which can lead to cancers of the lymphopoietic system in humans [76], and can increase the risk of acute myeloid leukemia (AML) and other blood cancers [77]. Shim et al. [78] objectively measured indoor concentrations of aldehydes and VOCs in 128 stores in 10 underground commercial areas in Korea. The results showed that, on the environmental side, eye irritation symptoms were related to n-butanol, n-heptane, and xylene; respiratory symptoms were related to n-heptane; and systemic symptoms were related to benzene, n-heptane, and decanal concentrations [78].
In summary, exposure to VOCs can have a more serious negative impact on human physiological health. This effect is even more severe than exposure to some gaseous pollutants or particulate matter. However, it was found that the concentration of VOCs for indoor air could be effectively reduced by opening windows, ventilation, or air conditioning filtration. Therefore, in future research, the consideration of purification methods for VOCs for indoor air should be strengthened to provide methods with universal applicability to enhance the comfort and health of building occupants.

6. Effects of Other IAQ Factors on Human Physiological Indicators

In addition to indoor air pollutants, such as gaseous pollutants, particulate matter, and VOCs, some studies have investigated the effects of environmental tobacco smoke (ETS) and carbon black (BC) on human physiological health. ETS is a class of substances produced by people smoking tobacco products indoors, containing more than 7000 compounds including nicotine and tar. By measuring vascular tone and function and blood pressure in 65 nonsmoking subjects, Brook et al. [52] found that, for every 10 µg/m3 increase in the average daily concentration of ETS, the SBP of ETS-exposed subjects increased by 3.94 mmHg and 6.57 mmHg on lagged days 1 and 2 after exposure, respectively. Pope et al. [69] noted that ETS exposure was negatively correlated with all HRV indices. Among them, SDNN decreased by about 12%, independent of mean HR and oxygen saturation. The effects of BC were similar, even more pronounced for overweight individuals [50], and the changes in parasympathetic activity were more noticeable [21]. For every 1 µg/m3 increase in BC concentration for indoor air in the experiments by Liu et al. [60], SBP was not significantly reduced by 1.09% after active filtration, and the SBP was not significantly reduced after control for pseudo filtration. The SBP after control for sham filtration was significantly increased by 2.41%. This indicates that activated charcoal filtration is very effective in the absorption of BC, thus significantly reducing the SBP of the subjects and inducing physiological relaxation. Taken together, both ETS and BC are capable of affecting the autonomic function of the human heart, which in severe cases can lead to acute health damage to the cardiovascular system.

7. Conclusions

This comprehensive review examines the physiological impacts of indoor air pollutants on human health through systematic analysis of IAQ research. We evaluate current evidence linking IAQ variations to measurable changes in cardiovascular and respiratory biomarkers, focusing on blood pressure, HR, HRV, and EEG as critical physiological indicators. Epidemiological data confirm that compromised IAQ under low ventilation conditions adversely affects systemic physiological regulation. Dose-dependent IAQ alterations correlate linearly with cardiovascular stress, respiratory compensation, and autonomic dysfunction. Also, in response to the article, the following conclusions were drawn:
  • Gaseous pollutants for indoor air have a wide range of effects on human physiological indicators. The effects of CO2 on the human body cover indicators of the cardiovascular system, the respiratory system, and brain activity, while studies of O3 have focused on the effects on indicators of the human cardiovascular system. Since elevated aerosol concentrations for indoor air are often accompanied by the accumulation of other types of indoor pollutants, the simultaneous exposure of subjects to O3 and PM2.5 may cause synergistic effects in terms of changes in physiological indicators. Therefore, potential interactions between multiple indoor air pollutant exposures deserve further exploration in future studies.
  • PM for indoor environments predominantly impacts the cardiovascular system, with adverse effects intensifying as particle size decreases and carbon content increases. Empirical evidence indicates that air filtration systems and ionization technologies can mitigate these effects by improving cardiovascular and respiratory biomarker profiles in settings with suboptimal IAQ. Future research should prioritize evaluating the efficacy of particulate purification devices across PM size fractions and compositional variations, while exploring integrated applications of IoT-based monitoring and AI-driven environmental control systems for enhanced indoor air management. Improvements in the performance of purification devices, IoT, and AI should be considered as a future challenge, which will improve the IAQ and promote the physiological health of people.
  • VOCs for indoor air can also affect physiological indicators in a number of human systems. If the trend of VOCs for indoor air changes in the opposite direction, the effect on human physiological indicators may also have the opposite effect. The negative effects of VOCs on IAQ are more severe than those of other factors that affect IAQ. However, current research on indoor VOCs lacks standardized classification frameworks for specific chemical subgroups. Addressing these knowledge gaps requires large-scale controlled intervention trials employing longitudinal study designs to identify dominant VOC species and characterize their temporal concentration patterns. Such methodological refinements will enable comprehensive assessment of public health risks associated with targeted indoor air remediation strategies.

Author Contributions

Conceptualization, T.N. and G.Z.; methodology, T.N.; software, T.N.; validation, T.N., G.Z. and Y.S.; formal analysis, W.W.; investigation, T.W. and Y.S.; resources, H.D.; data curation, W.W.; writing—original draft preparation, T.N.; writing—review and editing, T.N.; visualization, T.N.; supervision, T.N.; project administration, T.N.; funding acquisition, H.D. All authors have read and agreed to the published version of the manuscript.

Funding

This study was funded by the Natural Science Foundation of Qingdao Municipality (23-2-1-96-zyyd-jch).

Data Availability Statement

The data presented in this study are available on request from the corresponding author.

Conflicts of Interest

The authors declare no conflicts of interest.

Appendix A

Table A1. The effect of CO2 concentration for indoor air on human physiology.
Table A1. The effect of CO2 concentration for indoor air on human physiology.
AuthorParticipantsAgesRangeTaskInterventionPhysiological IndexEffect
Zhang et al. (2021) [25]Adults
N = 4 (4 males)		24.20 ± 2.481626 ± 306 ppm, 3562 ± 259 ppm, 5087 ± 318 ppm√—HRV, EEGDecreased SDNN standard deviation and increased PNN50 for HRV (1500 ppm: 8% vs. 3500 ppm: 9.6%); Increase in β relative power of EEG.
Kim et al.
(2020) [29]		Adults
N = 22 (16 males, 6 females)		27.57 ± 0.091000–2000 ppm——Blood pressureSBP increased (2000 ppm: 126.388 mmHg vs. 1000 ppm: 122.337 mmHg).
Zhang et al.
(2017) [19]		University students
N = 25 (10 males, 15 females)		23 ± 2500 ppm, 1000 ppm, 3000 ppm√—Respiration rate, HR, α-amylase, DBPNo change in respiration rate; HR reduced; significant increase in α-amylase concentration; DBP increased significantly.
Zhang et al. (2016) [30]University students
N = 10 (5 males, 5 females)		25 ± 2500 ppm, 5000 ppm√—Respiration rate, HR, α-amylase, cortisolRespiratory rate, HR unchanged; α-amylase concentration increased; no difference in cortisol.
Snow et al. (2019) [14]Employees or
Students of the University
N = 31		22.5 ± 4.8830 ppm, 2700ppm√—EEG, HR, skin temperature, respiratory rateEEG unchanged; HR increased.
Chen and Hsiao (2014) [16]Youngster
N = 10 (6 males, 4 females)		26 ± 5More than 800 ppm,
800–1000 ppm,
More than 1000 ppm		——HR, SpO2, facial temperatureIncreased HR; increased facial temperature; decreased SpO2.
Mishra et al.
(2021) [22]		Adults
N = 15 (8 males, 7 females)		21~55900 ppm, 1450ppm√—Respiration rate, ETCO2, FVCRespiratory rate, ETCO2 unchanged; lung volume FVC decreased.
Shan et al.
(2022) [35]		University students
N = 25 (15 males, 15 females)		—1244 ± 70 ppm,
618 ± 45 ppm		√—EEGThe relative power of both alpha and theta waves of EEG increased.
Jin et al.
(2022) [24]		Adults
N = 15 (8 males, 7 females)		26.6 ± 3.44000 ppm, 40,000 ppm——EEGEEG was affected.
Liu et al.
(2017) [36]		University students
N = 12 (6 males, 6 females)		24.8 ± 2.6380 ppm, 3000 ppm——Right ear tympanic membrane temperature, skin temperature, heart rate, blood pressure, SpO2, ETCO2All unchanged.
Kang et al.
(2023) [37]		Adults
N = 36 (16 males,16 females)		23.7 ± 3.60–9999 ppm√√Wrist skin temperature, blood pressure and pulse, oxygen saturation of blood, salivary biomarkerThere was no significant difference.
Table A2. Effects of O3 concentration for indoor air on human physiology.
Table A2. Effects of O3 concentration for indoor air on human physiology.
AuthorParticipantsAgesRangeTaskInterventionPhysiological IndexEffect
Urch et al. [40]Healthy adults
N = 23 (13 males, 10 females)		32 ± 10121 ± 3 ppb——DBP, HRDBP increased from 1 mmHg to 6 mmHg when exposed in combination with PM2.5.
Brook et al.
(2002) [41]		Healthy adults
N = 25 (15 males, 10 females)		34.9 ± 10120 ppb——Blood pressure, FMD, NMD, BADBAD (−0.09 ± 0.15 mm vs. 0.01 ± 0.18 mm) was significantly lower, and there were no significant differences in FMD (0.29 ± 4.11% vs. −0.03 ± 6.63%), NMD (3.87 ± 5.43% vs. 3.46 ± 7.92%), and blood pressure.
Hoffmann et al.
(2012) [42]		Diabetes mellitus type 2 (T2DM)
N = 70 (53 males, 37 females)		Mean 64.413.3 ppb——Blood pressureFor each additional interquartile spacing, SBP, DBP, and central mean arterial blood pressure decreased by 4.0%, 2.0%, and 2.8%, respectively.
Urch et al.
(2004) [43]		Healthy adults
N = 24 (14 males, 10 females)		35 ± 10120 ppb——BADBAD reduced by 0.09 mm. Unable to assess.
Brook et al. (2009) [46]Healthy adults
N = 50 (19 males, 31 females)		27 ± 8120 ppb——DBPThere was little impact on DBP.
Fakhri et al.
(2009) [44]		Adults
N = 50 (24 males, 26 females)		27.08 ± 7.13113.9 ± 6.6 ppb——HRV, blood pressure, respiratory rate, HRIn synergistic exposure with O3
DBP increased by 2 mmHg and SDNN increased.
Power et al. (2008) [45]Asthmatic
N = 5 (1 males, 4 females)		Mean 37200 ppb—FiltrationHRVCombined particle and ozone exposure reduces SDNN in asthmatics.
Table A3. Effects of PM2.5 concentration for indoor air on human physiology.
Table A3. Effects of PM2.5 concentration for indoor air on human physiology.
AuthorParticipantsAgesRangeTaskInterventionPhysiological IndexEffect
Dong et al.
(2018) [50]		Older people
N = 29 (29 females)		Mean 68.255.7 ± 55.4 μg/m3——HRVHRV’s HF, LF, and SDNN declined.
Lu et al.
(2018) [21]		COPD patients
N = 43 (40 males, 3 females)		71.49 ± 6.4058.01 ± 52.82 μg/m3——HRV, HRHF decreased by 34.85% in overweight patients compared to 2.01% in normal weight patients.
Power et al.
(2008) [45]		Asthmatic
N = 5 (1 males, 4 females)		Mean 37313 ± 19.5 μg/m3—FiltrationHRVThe SDNN standard deviation of HRV was significantly lower when exposed synergistically with O3; there was no significant change in HRV when exposed to particles only.
Jung et al.
(2016) [17]		Office staff
N = 115 (83 males, 32 females)		34.2 ± 5.740.7 ± 29.1 μg/m3——Blood pressure, HRHR increased.
Rumchev et al. (2018) [8]Adults
N = 63 (28 males, 35 females)		Mean 6118.74 μg/m3——Blood pressure, HRFor each IQR increase in PM2.5, heart rate increases by 4–6 bpm.
Brook et al.
(2015) [52]		Adults
N = 65 (50 males, 15 females)		Mean 44.611.6 ± 8.5 μg/m3——Blood pressure, HR, BAD and FMDA 10 μg/m3 increase in PM2.5 was associated with a 1.41 mmHg increase in SBP after 1 day.
Fakhri et al.
(2009) [44]		Adults
N = 50 (24 males, 26 females)		27.08 ± 7.13121.6 ± 48.0 μg/m3——HRV, blood pressure, respiratory rate, HRDBP does not have a significant effect and SDNN increases when younger subjects are exposed only to PM2.5.
Jia et al.
(2012) [56]		Healthy older people
N = 30 (12 males, 18 females)		57.9 ± 5.445.58 μg/m3——HRVHF and LF increased by 1.30% and 1.34%, respectively.
Lin et al.
(2011) [57]		Healthy students
N = 60 (30 males, 30 females)		Median age 25.023.65 ± 12.6 μg/m3
18.05 ± 8.45 μg/m3		—FiltrationBlood pressure, HRWithout filter, SBP, DBP, and HR increased by 4.11 mmHg, 2.78 mmHg, and 3.11 bpm, respectively; after filtering the air, BP, and HR did not change significantly with the rise of PM2.5.
Karottki et al.
(2013) [58]		Older people
N = 48 (22 males, 26 females)		67 ± 6.54 μg/m3
8 μg/m3		—FiltrationBlood pressure, microvascular function, pulmonary functionThere was no improvement in microvascular, functional lung function, and no significant reduction in systemic inflammation, monocyte activation, or lung cell injury.
Liu et al.
(2018) [60]		Healthy older people, COPD patients
N = 35 (20 males, 15 females)		66.26 ± 7.7158.24 μg/m3
37.99 μg/m3		—Activated carbon filtrationBlood pressure, HRVFor every 10 μg/m3 increase in PM2.5, there was a significant reduction of 1.34% for sham-filtered SDNN and a non-significant reduction of 0.81% for activated carbon filtration.
Liao et al.
(1999) [70]		Older people
N = 26 (7 males, 19 females)		Mean 819.8 ± 3.7 μg/m3——HRVHRV decreased.
Zhou et al.
(2023) [59]		Adults
N = 66		18–650–30 μg/m3; ±3 μg/m3. 30–1000 μg/m3; ± 10%——electrodermal activity, EDA and heart rate variability, HRVReducing significantly indoor elevated PM2.5 levels can improve some cognitive abilities in office workers.
Table A4. Effects of VOCs concentration for indoor air on human physiology.
Table A4. Effects of VOCs concentration for indoor air on human physiology.
AuthorParticipantsAgesRangeTaskInterventionPhysiological IndexEffect
Kjærgaard et al. (1991) [64]Adults
N = 35 (15 males, 20 females)		Mean 41.2525,000 µg/m3√—PML, sebaceous sweat, mid-expiratory flowPML increased; skin indicators regarding sebum and sweat, and mid-expiratory flow (FEF50) responded only in the SBS group.
Chuang et al.
(2017) [53]		Healthy adults
N = 200 (100 males, 100 females)		Mean 43.40.98 ± 0.56 ppm,
0.43 ± 0.21 ppm,
1.22 ± 0.81 ppm		—RefrigerationBlood pressure, Hs-CRP, 8-OHdGBP, Hs-CRP, and 8-OHdG increased.
Chen et al.
(2019) [15]		Older people
N = 100 (50 males, 50 females)		Mean 67.3347.5 ± 78.2 ppb,
748.4 ± 163.4 ppb		——Blood pressure, HRSBP and HR increased.
Mizukoshi et al.
(2015) [20]		Chemically sensitized patients
N = 8 (3 males, 5 females)		44 ± 11306 ± 148 µg/m3——HRVHF was significantly negatively correlated with it.
Jung et al.
(2016) [17]		Office staff
N = 115 (83 males, 32 females)		34.2 ± 5.7528.7 ± 315.4 μg/m3——Blood pressure, HRSBP levels were higher in overweight or obese subjects.
Mizukoshi et al.
(2010) [65]		Adults
N = 7 (4 males, 3 females)		32 ± 1363–1447 µg/m3——HRVΔTVOC is negatively correlated with HF and positively correlated with LF/HF.
Bakó-Biró et al.
(2005) [71]		Adults
N = 60 (60 females)		Not mentionedNot mentioned√—CO2 exhalation rateThe CO2 exhalation rate was significantly reduced by approximately 5%.
Wargocki et al.
(1999) [72]		Healthy adults
N = 30 (30 females)		Mean 24165 ± 50 µg/m3,
195 ± 10 µg/m3,
220 ± 20 µg/m3		√—CO2 exhalation rateThe metabolic rate was 1.3, much higher than the relaxed sedentary normal of 1.2.
Nakayama et al.
(2021) [67]		Healthy adults
N = 168		20~50s3629 µg/m3,
55 µg/m3		√—EEGThe rate of increase/decrease in α/β values was significantly higher in the group with higher levels of VOCs than in the group with lower concentrations.
Lin et al.
(2013) [48]		Healthy adults
N = 300 (136 males, 164 females)		Mean 43.277.2 ± 27.3 ppb,
68.6 ± 23.1 ppb,
52.3 ± 20.4 ppb		—Air conditionerHRV, Hs-CRP, 8-OHdG, plasma fibrinogenHs-CRP, 8-OHdG and plasma fibrinogen were elevated.
Shim et al.
(2023) [78]		Underground stores
N = 454		Over 20Not mentioned——eye irritation, respiratory, general symptomsThe concentrations of n-butanol, n-heptane, and xylene were associated with eye irritation symptoms, while those of n-heptane were associated with respiratory symptoms, and those of benzene, n-heptane, and decanal were associated with general symptoms.

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Buildings 15 01296 g001
Figure 1. Number and typology of published papers on IAQ.
Figure 1. Number and typology of published papers on IAQ.
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Figure 2. Search process.
Figure 2. Search process.
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Figure 3. Effect of CO2 content on human physiological indicators.
Figure 3. Effect of CO2 content on human physiological indicators.
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Figure 4. Effect of PM2.5 on human physiological indicators.
Figure 4. Effect of PM2.5 on human physiological indicators.
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Figure 5. Effect of VOCs on human physiological indicators.
Figure 5. Effect of VOCs on human physiological indicators.
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Table 1. Keywords used in this study.
Table 1. Keywords used in this study.
CategoryKeywords
Pollutants“Indoor air quality”, “carbon dioxide”, “particulate matter”, “ozone”, or “volatile organic compounds”
Physiological Indicators“Blood pressure”, “electroencephalogram”, “heart rate variability”, or “oximetry”
Exposure Scenarios“Controlled experiment”, “human subjects”, “residential buildings”, or “office”
Table 2. Journals belonging to the 63 papers included in the review.
Table 2. Journals belonging to the 63 papers included in the review.
Journal TitleNumber of Citations
Building and Environment12
Environmental Health Perspectives11
Indoor Air8
International Journal of Environmental Research and Public Health4
Science of The Total Environment3
Atmospheric Environment3
Environment International3
Environmental Research2
Other (1 each of 21 journals)21
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Nie, T.; Zhang, G.; Sun, Y.; Wang, W.; Wang, T.; Duan, H. Effects of Indoor Air Quality on Human Physiological Impact: A Review. Buildings 2025, 15, 1296. https://doi.org/10.3390/buildings15081296

AMA Style

Nie T, Zhang G, Sun Y, Wang W, Wang T, Duan H. Effects of Indoor Air Quality on Human Physiological Impact: A Review. Buildings. 2025; 15(8):1296. https://doi.org/10.3390/buildings15081296

Chicago/Turabian Style

Nie, Tong, Guofu Zhang, Yinan Sun, Wenhao Wang, Tianai Wang, and Haoyan Duan. 2025. "Effects of Indoor Air Quality on Human Physiological Impact: A Review" Buildings 15, no. 8: 1296. https://doi.org/10.3390/buildings15081296

APA Style

Nie, T., Zhang, G., Sun, Y., Wang, W., Wang, T., & Duan, H. (2025). Effects of Indoor Air Quality on Human Physiological Impact: A Review. Buildings, 15(8), 1296. https://doi.org/10.3390/buildings15081296

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