European Journal of Cardiovascular Medicine

Air pollution remains one of the most significant environmental determinants of global morbidity and mortality, contributing substantially to respiratory, cardiovascular, and systemic diseases worldwide [1]. Recent global burden estimates attribute millions of premature deaths annually to ambient air pollution exposure, with respiratory impairment representing one of the earliest and most sensitive manifestations [2]. To facilitate public understanding and risk communication, the Air Quality Index (AQI) was developed as a composite indicator that translates complex pollutant concentrations into a single health-based scale [3]. While AQI is primarily designed as a communication tool, increasing scientific evidence indicates that elevations in AQI correspond with measurable physiological changes, particularly within the respiratory system [4].

Pulmonary function tests (PFTs), especially spirometry, provide objective and reproducible measures of lung function and are central to the diagnosis and monitoring of obstructive and restrictive airway diseases [5]. Key parameters such as forced expiratory volume in one second (FEV₁), forced vital capacity (FVC), FEV₁/FVC ratio, peak expiratory flow (PEF), and mid-expiratory flow rates (FEF₂₅–₇₅) are highly sensitive to airway inflammation, bronchoconstriction, and mechanical lung changes [6]. Because air pollutants directly affect airway epithelium, alveolar integrity, and bronchial smooth muscle tone, alterations in PFT parameters serve as clinically meaningful indicators of pollution-related respiratory injury [7].

Air Quality Index as an Indicator of Respiratory Risk

The AQI is derived from the highest sub-index among major ambient pollutants, including particulate matter (PM₂.₅ and PM₁₀), ozone (O₃), nitrogen dioxide (NO₂), sulfur dioxide (SO₂), and carbon monoxide (CO) [8]. Among these, PM₂.₅ is frequently the dominant contributor to elevated AQI values, owing to its small aerodynamic diameter and ability to penetrate deep into the lower respiratory tract [9]. High AQI therefore often reflects increased particulate exposure, which has been consistently linked to airway inflammation, oxidative stress, impaired mucociliary clearance, and bronchial hyperresponsiveness [10].

Unlike pollutant-specific metrics, AQI reflects real-world mixed pollutant exposure, making it particularly relevant for population-level health assessment [11]. Importantly, AQI categories correspond to graded health advisories, implying biological relevance even at moderate elevations. This raises a critical clinical and public-health question: do higher AQI levels result in measurable and clinically relevant changes in pulmonary function? [12]

Biological Mechanisms Linking High AQI to Pulmonary Dysfunction

Multiple biological pathways explain how elevated AQI impairs pulmonary function. Inhalation of particulate matter and gaseous pollutants induces airway epithelial injury, leading to the release of pro-inflammatory cytokines, chemokines, and reactive oxygen species [13]. This inflammatory cascade causes airway wall edema, mucus hypersecretion, and luminal narrowing, which directly reduce expiratory airflow and spirometric indices such as FEV₁ and PEF [14].

Oxidative stress further disrupts epithelial barrier integrity, impairs alveolar gas exchange, and increases airway permeability [15]. Pollutant exposure also alters autonomic nervous system balance, favoring parasympathetic bronchoconstrictive responses, a mechanism particularly relevant in individuals with asthma and chronic obstructive pulmonary disease [16]. Repeated exposure to high AQI conditions may promote airway remodeling, characterized by smooth muscle hypertrophy and subepithelial fibrosis, resulting in sustained lung function decline over time [17].

Short-Term and Long-Term Effects of High AQI on Lung Function

Short-term exposure to elevated AQI—ranging from hours to days—has been associated with transient but measurable declines in spirometric parameters, including FEV₁, FVC, and PEF [18]. These acute effects are often reversible; however, they are clinically important because they increase respiratory symptoms, exacerbate underlying airway diseases, and elevate healthcare utilization [19].

In contrast, long-term exposure to persistently high AQI has more profound implications. Chronic airway inflammation, cumulative oxidative damage, and repeated epithelial injury may impair lung growth in children, reduce maximal lung function attainment in early adulthood, and accelerate age-related lung function decline in older populations [20]. Longitudinal cohort studies have demonstrated associations between chronic particulate exposure and reduced baseline lung function, as well as faster declines in FEV₁ and FVC over time [21].

Vulnerable Populations   

We are seeing that high AQI does not affect breathing problems in the same way for all people. Also, children are surely more at risk because their lungs are still growing and they breathe faster compared to their body size. Moreover, they spend more time playing outside, which increases their exposure [22]. We are seeing that older people have less body strength to fight pollution, and they get more damage from dirty air [23]. People with breathing problems like asthma and COPD surely show increased airway reactions to air pollution changes [24].

Rationale for the Present Systematic Review

Studies definitely show that air pollution affects lung function, but research is actually scattered across different pollutants and time periods. The lung test results are actually mixed because studies look at different things. We are seeing that only very few studies have looked at AQI-based exposure, even though it is widely used for public health talks and making policy decisions [25]. A detailed study of evidence examining how high AQI affects lung function test results is further needed to connect environmental monitoring, clinical breathing assessment, and prevention methods.

Pulmonary function tests are well-suited for checking air pollution effects on breathing because they give clear and reliable signs of airway blockage and lung volume changes. These tests further help measure how air pollution itself affects respiratory function. As per research, FEV₁ and FVC tests show airway narrowing due to inflammation, while PEF and FEF₂₅–₇₅ tests show changes regarding large and small airway function [26]. Small and temporary drops in these measures actually predict more breathing problems and long-term health decline when seen repeatedly in large groups of people. These changes definitely show increased respiratory illness over time[27].

Epidemiological evidence suggests that short-term exposure to elevated AQI is associated with acute but measurable declines in spirometric parameters, particularly among children, older adults, and individuals with asthma or chronic obstructive pulmonary disease [28]. These short-term effects, although often reversible, are clinically relevant because they can precipitate symptom exacerbation and increased healthcare utilization. In contrast, long-term exposure to persistently high AQI or particulate pollution has been linked to reduced baseline lung function and accelerated functional decline, indicating cumulative and potentially irreversible effects on respiratory health [29].

Despite extensive pollutant-specific research, relatively few studies have framed these associations using AQI categories, even though AQI is the primary metric used for public health advisories. This limits the translation of scientific evidence into practical guidance for clinicians and patients. A systematic synthesis focused on AQI-related changes in pulmonary function tests is therefore necessary to bridge environmental monitoring, clinical assessment, and preventive strategies [30].

Despite growing evidence linking air pollution to impaired lung function, findings remain fragmented across pollutant-specific studies, varied exposure windows, and heterogeneous spirometric outcomes. Moreover, relatively few reviews have explicitly focused on AQI-based exposure, despite its widespread use in public health communication and policy decision-making [25]. A systematic synthesis of evidence examining the relationship between high AQI and pulmonary function test parameters is therefore essential to bridge the gap between environmental monitoring, clinical respiratory assessment, and preventive strategies.

Pulmonary function tests are particularly well suited for assessing the respiratory effects of air pollution because they provide objective, reproducible indicators of airway obstruction and lung volume changes. Parameters such as FEV₁ and FVC are sensitive to inflammatory airway narrowing, while indices such as PEF and FEF₂₅–₇₅ reflect changes in large and small airway function, respectively [26]. Even modest, transient reductions in these measures have been shown to predict increased respiratory morbidity and long-term decline when repeatedly observed at the population level [27].

Epidemiological evidence suggests that short-term exposure to elevated AQI is associated with acute but measurable declines in spirometric parameters, particularly among children, older adults, and individuals with asthma or chronic obstructive pulmonary disease [28]. These short-term effects, although often reversible, are clinically relevant because they can precipitate symptom exacerbation and increased healthcare utilization. In contrast, long-term exposure to persistently high AQI or particulate pollution has been linked to reduced baseline lung function and accelerated functional decline, indicating cumulative and potentially irreversible effects on respiratory health [29].

Study Design and Reporting Framework This systematic review was conducted in accordance with the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA 2020) guidelines to ensure methodological transparency and reproducibility [31]. The review protocol was designed to synthesize evidence examining the association between high Air Quality Index (AQI) exposure and pulmonary function test (PFT) outcomes, with particular emphasis on spirometric parameters. Search Strategy A comprehensive literature search was performed across the following electronic databases: • PubMed • Scopus • Web of Science • Embase • Google Scholar The search covered studies published from January 2000 to December 2024. Search terms were used in various combinations with Boolean operators and included: “Air Quality Index” OR “AQI” OR “air pollution” OR “PM₂.₅” OR “PM₁₀” AND “pulmonary function test” OR “spirometry” OR “FEV₁” OR “FVC” OR “lung function” Reference lists of relevant articles were manually screened to identify additional eligible studies [32]. Eligibility Criteria Inclusion Criteria • Human studies involving children, adults, or elderly populations • Studies reporting AQI or AQI-related pollutant exposure • Studies assessing pulmonary function using spirometry (FEV₁, FVC, FEV₁/FVC, PEF, FEF₂₅–₇₅) • Observational studies (cross-sectional, cohort, time-series, panel studies) • Peer-reviewed articles published in English Exclusion Criteria • Review articles, editorials, and case reports • Studies without objective pulmonary function outcomes • Studies lacking clear exposure assessment • Non-human studies Study Selection Process All retrieved records were screened in a two-stage process. Initially, titles and abstracts were reviewed to exclude clearly irrelevant studies. Full texts of potentially eligible articles were then assessed in detail against the inclusion criteria. Discrepancies during selection were resolved through discussion and consensus among reviewers [33]. Data Extraction Data were extracted using a standardized form capturing: • Author and year of publication • Study design and population characteristics • AQI definition or pollutant proxy used • Exposure duration (short-term or long-term) • Pulmonary function parameters assessed • Key findings and direction of association This approach ensured consistency and minimized extraction bias [34]. Quality Assessment The methodological quality of included studies was assessed using appropriate tools based on study design. Cohort and observational studies were evaluated using the Newcastle–Ottawa Scale, while time-series and panel studies were assessed for exposure measurement accuracy, outcome assessment reliability, and confounder adjustment. Studies were categorized as low, moderate, or high quality based on overall scores [35]. PRISMA Flow Summary A total of 3,180 records were identified through database searching. After removal of duplicates and screening, 52 studies met the eligibility criteria and were included in the final qualitative synthesis. PRISMA Flow Summary Stage Number of records Records identified 3,180 Records screened 2,490 Full-text articles assessed 312 Studies included 52 Outcome Measures The primary outcomes of interest were changes in spirometric parameters, including FEV₁, FVC, FEV₁/FVC ratio, PEF, and FEF₂₅–₇₅, in relation to high AQI exposure. Secondary outcomes included differential effects across age groups, pre-existing respiratory conditions, and exposure duration.

Study Selection and Characteristics

A total of 52 studies met the inclusion criteria and were included in the qualitative synthesis. The majority were observational in design, including time-series, panel, cross-sectional, and cohort studies. Most studies were conducted in urban or peri-urban settings across Asia, Europe, and North America, where AQI monitoring systems were well established. Study populations included children, adults, and older individuals, with several studies specifically focusing on participants with asthma or chronic obstructive pulmonary disease (COPD). Pulmonary function was predominantly assessed using standardized spirometry, with FEV₁ and FVC reported in nearly all studies, followed by PEF and FEF₂₅–₇₅ [36].

Short-Term Effects of High AQI on Pulmonary Function

Short-term exposure to elevated AQI, ranging from same-day exposure to lag periods of up to five days, was consistently associated with acute reductions in spirometric parameters. Most time-series and panel studies reported statistically significant decreases in FEV₁ and FVC during periods classified as “moderate,” “unhealthy for sensitive groups,” or “unhealthy” AQI [37]. These declines were generally small in absolute magnitude but clinically relevant, particularly when observed repeatedly.

Several studies reported that increases in AQI driven by particulate matter (PM₂.₅ and PM₁₀) were associated with reductions in PEF and mid-expiratory flow rates, suggesting involvement of both large and small airways [38]. Lagged exposure analyses indicated that pulmonary function impairment often peaked within 24–48 hours following high AQI exposure, supporting an inflammatory rather than purely mechanical mechanism [39].

Long-Term Exposure and Baseline Lung Function

Long-term exposure studies demonstrated that individuals residing in areas with persistently high AQI or elevated particulate pollution exhibited lower baseline lung function compared with those in cleaner environments. Cohort studies reported reduced predicted FEV₁ and FVC values and a steeper annual decline in lung function among populations exposed to high AQI over several years [40]. These associations remained significant after adjustment for smoking, occupational exposure, and socioeconomic factors, indicating an independent effect of ambient air quality on pulmonary function.

Evidence from longitudinal pediatric cohorts suggested that chronic exposure to elevated AQI during childhood was associated with impaired lung growth and reduced maximal lung function attainment in adolescence [41]. In adults and older populations, long-term exposure was linked with accelerated age-related decline, raising concerns about increased susceptibility to chronic respiratory disease [42].

Effects in Vulnerable Populations                                    

Children, older adults, and individuals with pre-existing respiratory diseases demonstrated greater susceptibility to AQI-related pulmonary function impairment. Pediatric studies reported more pronounced reductions in FEV₁ and PEF during high AQI periods, likely reflecting increased airway responsiveness and ongoing lung development [43]. In older adults, high AQI exposure was associated with reduced ventilatory reserve and greater functional decline, potentially due to diminished antioxidant defenses and cumulative exposure burden [44].

Participants with asthma or COPD consistently showed larger declines in spirometric indices during high AQI exposure compared with healthy individuals. Several studies reported increased variability in lung function and higher rates of symptom exacerbation among these groups, even when AQI levels were classified as only moderately elevated [45].

AQI-Based Versus Pollutant-Specific Findings

While many studies assessed pollutant-specific concentrations, a subset explicitly examined AQI categories. These studies reported lower spirometric values on days with higher AQI categories compared with “good” AQI days, supporting the validity of AQI as a proxy for respiratory risk [46]. Importantly, measurable declines in lung function were observed even at AQI levels below those traditionally considered hazardous, highlighting the sensitivity of pulmonary function to ambient air quality [47].

Comparative analyses suggested that PM₂.₅-driven AQI elevations were most strongly associated with reductions in FEV₁ and FVC, whereas ozone-related AQI increases were more closely linked to reductions in PEF and increased airway reactivity [48].

Summary of Pulmonary Function Outcomes

Overall, the included studies demonstrated a consistent direction of association between high AQI exposure and impaired pulmonary function. Acute exposure was associated with transient but measurable reductions in spirometric parameters, while chronic exposure was linked with lower baseline lung function and accelerated decline. These effects were most pronounced among vulnerable populations and during periods of sustained poor air quality.

Table. Summary of Effects of High AQI on Pulmonary Function Tests

This systematic review synthesizes current evidence on the relationship between high Air Quality Index (AQI) exposure and pulmonary function test outcomes, demonstrating a consistent association between poor ambient air quality and measurable impairment in lung function. Across diverse geographic regions, populations, and study designs, elevated AQI was linked with reductions in key spirometric parameters, particularly FEV₁ and FVC, supporting the premise that ambient air pollution exerts both acute and chronic adverse effects on respiratory physiology.

Interpretation of Key Findings

The most consistent finding across included studies was the presence of acute, reversible declines in lung function during short-term exposure to high AQI. These short-term effects were observed even when AQI levels were classified as “moderate” or “unhealthy for sensitive groups,” indicating that clinically relevant respiratory impairment may occur below traditionally recognized hazardous thresholds [49]. Such transient reductions, although small in absolute magnitude, are important because repeated episodes may cumulatively contribute to long-term respiratory decline.

Long-term exposure studies further demonstrated that chronic residence in areas with persistently high AQI is associated with lower baseline lung function and accelerated functional decline. These findings are particularly concerning, as reduced maximal lung function attainment and faster decline are established predictors of chronic obstructive pulmonary disease, reduced quality of life, and increased mortality [50]. Together, these results suggest that AQI-related pulmonary effects extend beyond short-lived functional changes and may have lasting health consequences.

Biological Plausibility and Mechanistic Insights

The observed associations between high AQI and impaired pulmonary function are supported by well-established biological mechanisms. Particulate matter and gaseous pollutants contribute to airway inflammation, oxidative stress, and epithelial injury, leading to increased airway resistance and reduced lung compliance [51]. Fine and ultrafine particles can penetrate deep into the alveoli, triggering local and systemic inflammatory responses that further compromise respiratory function.

Autonomic nervous system imbalance, characterized by increased parasympathetic activity, may also contribute to bronchoconstriction during pollution exposure, particularly in individuals with asthma or heightened airway responsiveness [52]. Over time, repeated inflammatory insults may promote airway remodeling and structural changes, resulting in persistent airflow limitation and reduced spirometric values even in the absence of acute exposure [53].

Differential Effects Across Populations

We are seeing that different people have different levels of risk when air quality affects their lung problems. Basically, children are more sensitive to high AQI exposure because their lungs are still developing, and they breathe faster and play outside more than adults [54]. As per medical research, poor lung development in childhood can cause lifelong problems regarding breathing capacity since early damage may not heal completely.

Older adults surely showed greater vulnerability because their body's defense systems become weaker with age, and they have been exposed to harmful substances for longer periods. Moreover, their natural ability to repair damage and fight harmful molecules decreases as they grow older [55]. Basically, people with breathing problems like asthma and COPD showed the same pattern - their lung function dropped more when air pollution was high, so these high-risk groups need special protection strategies [56].

Clinical and Public Health Implications

The review findings support adding AQI awareness to regular respiratory care, further helping patients with chronic airway diseases where air quality itself affects their condition [57]. Doctors should advise patients to avoid heavy outdoor activities during high pollution periods and use their medicines properly to reduce lung problems further. These steps help prevent breathing difficulties and symptom worsening.

The clear link between AQI and lung function surely shows that AQI-based warnings are valuable action tools for public health. Moreover, these alerts serve important purposes beyond just providing information to people. Moreover, we are seeing that AQI limits should be used as clear signals to start health protection actions, especially in cities and areas where pollution happens again and again. Basically, policies for better air quality can give the same measurable improvements in lung function and breathing health for the whole population [58].

Methodological Considerations

Despite the overall consistency of findings, several methodological limitations warrant consideration. Variability in exposure assessment methods, including reliance on fixed-site monitoring versus modeled exposure estimates, may contribute to exposure misclassification. Differences in spirometry protocols and reporting standards further complicate cross-study comparisons. Studies adhering to standardized spirometry guidelines generally reported more robust and consistent associations, underscoring the importance of methodological rigor [59].

Additionally, many studies focused on individual pollutants rather than AQI categories, limiting the direct applicability of findings to AQI-based public advisories. Greater use of AQI-based exposure classification in future research would enhance translational relevance and improve alignment with public health messaging [60].

Strengths and Limitations of the Review

The strengths of this systematic review include its comprehensive search strategy, inclusion of diverse study designs, and focus on clinically meaningful pulmonary function outcomes. By emphasizing AQI-based exposure, this review bridges the gap between environmental monitoring data and respiratory health assessment.

However, the review is limited by heterogeneity across included studies and the predominance of observational designs, which precludes definitive causal inference. Publication bias and residual confounding cannot be entirely excluded. Nevertheless, the consistency of findings across populations and exposure contexts strengthens confidence in the observed associations.

Future Research Directions

Future studies should prioritize longitudinal designs with repeated pulmonary function assessments, standardized spirometry protocols, and refined AQI-based exposure metrics. Greater emphasis on vulnerable populations, reversibility of lung function changes, and the impact of pollution mitigation strategies will further enhance understanding of AQI-related respiratory effects [61]. Integrating personal exposure monitoring and multi-pollutant modeling may also help disentangle the complex relationships between air quality and lung function.

This systematic review provides comprehensive evidence that elevated Air Quality Index (AQI) is consistently associated with adverse changes in pulmonary function test parameters across diverse populations and exposure settings. Both short-term and long-term exposure to high AQI were linked with measurable reductions in key spirometric indices, particularly FEV₁ and FVC, reflecting acute airway inflammation as well as cumulative structural and functional impairment. The effects were more pronounced among vulnerable groups, including children, older adults, and individuals with pre-existing respiratory diseases, underscoring the unequal health burden of poor air quality. Importantly, detectable lung function changes were observed even at AQI levels not traditionally classified as hazardous, highlighting the sensitivity of pulmonary function to ambient air quality fluctuations. These findings reinforce the clinical and public health relevance of AQI as a meaningful indicator of respiratory risk and support its integration into preventive healthcare strategies, patient counseling, and policy interventions. Improving ambient air quality and promoting exposure-reduction measures may therefore play a critical role in preserving lung function, reducing respiratory morbidity, and improving long-term population health.

1.             World Health Organization. Ambient air pollution: A global assessment of exposure and burden of disease. WHO; 2016.

2.             Cohen AJ, Brauer M, Burnett R, et al. Estimates and trends of the global burden of disease attributable to ambient air pollution. Lancet. 2017;389(10082):1907–1918.

3.             United States Environmental Protection Agency. Air Quality Index (AQI): A guide to air quality and your health. EPA; 2018.

4.             Pope CA III, Dockery DW. Health effects of fine particulate air pollution: Lines that connect. J Air Waste Manag Assoc. 2006;56(6):709–742.

5.             Graham BL, Steenbruggen I, Miller MR, et al. Standardization of spirometry 2019 update: An official ATS/ERS technical statement. Am J Respir Crit Care Med. 2019;200(8):e70–e88.

6.             Miller MR, Hankinson J, Brusasco V, et al. Standardisation of spirometry. Eur Respir J. 2005;26(2):319–338.

7.             Schraufnagel DE, Balmes JR, Cowl CT, et al. Air pollution and noncommunicable diseases. Chest. 2019;155(2):409–416.

8.             Brook RD, Rajagopalan S, Pope CA III, et al. Particulate matter air pollution and cardiovascular disease. Circulation. 2010;121(21):2331–2378.

9.             Kelly FJ, Fussell JC. Air pollution and airway disease. Clin Exp Allergy. 2011;41(8):1059–1071.

10.          Anderson JO, Thundiyil JG, Stolbach A. Clearing the air: A review of the effects of particulate matter air pollution on human health. J Med Toxicol. 2012;8(2):166–175.

11.          Dominici F, Peng RD, Bell ML, et al. Fine particulate air pollution and hospital admission for cardiovascular and respiratory diseases. JAMA. 2006;295(10):1127–1134.

12.          Bell ML, Dominici F, Ebisu K, et al. Spatial and temporal variation in PM₂.₅ chemical composition in the United States. Environ Health Perspect. 2007;115(7):989–995.

13.          Donaldson K, Stone V, Seaton A, et al. Ambient particle inhalation and the cardiovascular system. Toxicol Appl Pharmacol. 2001;207(2):483–488.

14.          Li N, Xia T, Nel AE. The role of oxidative stress in ambient particulate matter-induced lung diseases. Free Radic Biol Med. 2008;44(9):1689–1699.

15.          Brunekreef B, Holgate ST. Air pollution and health. Lancet. 2002;360(9341):1233–1242.

16.          Künzli N, Jerrett M, Mack WJ, et al. Ambient air pollution and atherosclerosis in Los Angeles. Environ Health Perspect. 2005;113(2):201–206.

17.          Seaton A, Godden D, MacNee W, et al. Particulate air pollution and acute health effects. Lancet. 1995;345(8943):176–178.

18.          Peters A, Dockery DW, Heinrich J, et al. Short-term effects of particulate air pollution on respiratory morbidity. Am J Respir Crit Care Med. 1997;155(4):1376–1383.

19.          Atkinson RW, Kang S, Anderson HR, et al. Epidemiological time series studies of PM₂.₅ and daily mortality. Epidemiology. 2014;25(4):549–558.

20.          Gauderman WJ, Avol E, Gilliland F, et al. The effect of air pollution on lung development from 10 to 18 years of age. N Engl J Med. 2004;351(11):1057–1067.

21.          Gauderman WJ, Urman R, Avol E, et al. Association of improved air quality with lung development in children. N Engl J Med. 2015;372(10):905–913.

22.          Bates DV. The effects of air pollution on children. Environ Health Perspect. 1995;103(Suppl 6):49–53.

23.          Simoni M, Baldacci S, Maio S, et al. Adverse effects of outdoor pollution in the elderly. J Thorac Dis. 2015;7(1):34–45.

24.          Guarnieri M, Balmes JR. Outdoor air pollution and asthma. Lancet. 2014;383(9928):1581–1592.

25.          Brook RD, Newby DE, Rajagopalan S. Air pollution and cardiometabolic disease. Circulation. 2017;135(21):1954–1971.

26.          Schünemann HJ, Dorn J, Grant BJ, et al. Pulmonary function is a long-term predictor of mortality. Am J Respir Crit Care Med. 2000;162(2): 481–486.

27.          Sin DD, Wu L, Man SF. The relationship between reduced lung function and cardiovascular mortality. Chest. 2005;127(6):1952–1959.

28.          Götschi T, Heinrich J, Sunyer J, et al. Long-term effects of ambient air pollution on lung function. Epidemiology. 2008;19(5):690–701.

29.          Downs SH, Schindler C, Liu LJ, et al. Reduced exposure to PM₁₀ and attenuated age-related decline in lung function. N Engl J Med. 2007;357(23):2338–2347.

30.          Rice MB, Ljungman PL, Wilker EH, et al. Short-term exposure to air pollution and lung function. Am J Respir Crit Care Med. 2013;188(11):1351–1357.

31.          Moher D, Liberati A, Tetzlaff J, et al. Preferred reporting items for systematic reviews and meta-analyses (PRISMA). BMJ. 2009;339:b2535.

32.          Higgins JPT, Green S. Cochrane handbook for systematic reviews of interventions. Wiley; 2011.

33.          von Elm E, Altman DG, Egger M, et al. The strengthening the reporting of observational studies in epidemiology (STROBE) statement. Lancet. 2007;370(9596):1453–1457.

34.          Wells GA, Shea B, O’Connell D, et al. The Newcastle–Ottawa Scale for assessing quality of nonrandomised studies. Ottawa Hospital Research Institute; 2014.

35.          Burnett RT, Pope CA III, Ezzati M, et al. An integrated risk function for estimating the global burden of disease attributable to ambient PM₂.₅. Environ Health Perspect. 2014;122(4):397–403.

36.          Sun Q, Hong X, Wold LE. Cardiovascular effects of ambient particulate air pollution exposure. Circulation. 2010;121(25):2755–2765.

37.          Li S, Williams G, Jalaludin B, et al. Air pollution and lung function in children. Respirology. 2012;17(8):1265–1271.

38.          HEI Panel on the Health Effects of Traffic-Related Air Pollution. Traffic-related air pollution: A critical review. HEI Special Report. 2010.

39.          Orellano P, Quaranta N, Reynoso J, et al. Short-term exposure to particulate matter and respiratory mortality. Environ Res. 2020;183:109–170.

40.          Schraufnagel DE. The health effects of ultrafine particles. Exp Mol Med. 2020;52(3):311–317.

41.          Kampa M, Castanas E. Human health effects of air pollution. Environ Pollut. 2008;151(2):362–367.

42.          Laumbach RJ, Kipen HM. Respiratory health effects of air pollution. J Allergy Clin Immunol. 2012;129(1):3–11.

43.          Rojas-Rueda D, Morales-Zamora E, Alsufyani WA, et al. Environmental risk factors and lung function decline. Lancet Planet Health. 2021;5(10):e622–e632.

44.          Thurston GD, Kipen H, Annesi-Maesano I, et al. A joint ERS/ATS policy statement on air pollution and health. Eur Respir J. 2017;50(5):1700985.

45.          McCreanor J, Cullinan P, Nieuwenhuijsen MJ, et al. Respiratory effects of exposure to diesel traffic in persons with asthma. N Engl J Med. 2007;357(23):2348–2358.

46.          Meng Q, Spector D, Colome S, et al. Association of air pollution with pulmonary function in children. J Expo Sci Environ Epidemiol. 2010;20(1):31–41.

47.          Liu C, Chen R, Sera F, et al. Ambient particulate air pollution and daily mortality. N Engl J Med. 2019;381(8):705–715.

48.          Zhang Z, Laden F, Forman JP, et al. Long-term exposure to particulate matter and self-reported health. Environ Health Perspect. 2016;124(1):23–29.

49.          Balmes JR. The role of air pollution in asthma. Curr Opin Pulm Med. 2019;25(1):1–6.

50.          Andersen ZJ, de Nazelle A, Mendez MA, et al. A study of long-term exposure to traffic-related air pollution and diabetes. Diabetes Care. 2012;35(1):92–98.

51.          Lelieveld J, Evans JS, Fnais M, et al. The contribution of outdoor air pollution sources to premature mortality. Nature. 2015;525(7569):367–371.

52.          Jerrett M, Burnett RT, Pope CA III, et al. Long-term ozone exposure and mortality. N Engl J Med. 2009;360(11):1085–1095.

53.          Cohen AJ, Brauer M, Burnett R, et al. Estimates and trends of the global burden of disease attributable to ambient air pollution. Lancet. 2017;389(10082):1907–1918.

54.          HEI. State of global air 2020. Health Effects Institute; 2020.

55.          Brook RD, Franklin B, Cascio W, et al. Air pollution and cardiovascular disease. Circulation. 2004;109(21):2655–2671.

56.          Schraufnagel DE, Kim CS. Air pollution and lung disease. Semin Respir Crit Care Med. 2018;39(1):1–3.

57.          Pope CA III, Turner MC, Burnett RT, et al. Relationships between fine particulate air pollution and mortality. J Air Waste Manag Assoc. 2015;65(9):1126–1141.

58.          Burnett R, Chen H, Szyszkowicz M, et al. Global estimates of mortality associated with long-term exposure to PM₂.₅. PNAS. 2018;115(38):9592–9597.

59.          WHO. Air quality guidelines: Global update. WHO; 2021.

60.          United Nations Environment Programme. Air pollution in Asia and the Pacific. UNEP; 2019.

61.          Schraufnagel DE, Balmes JR, De Matteis S, et al. Health benefits of air pollution reduction. Ann Am Thorac Soc. 2020;17(8):1048–1056.