European Journal of Cardiovascular Medicine

Global Burden of Air Pollution and AQI as a Health Indicator [1–3]

Air pollution has emerged as one of the most critical environmental health threats of the modern era, contributing substantially to global morbidity and premature mortality. Rapid urbanization, industrialization, vehicular emissions, construction activities, biomass burning, and climate-related atmospheric changes have led to persistent deterioration in ambient air quality across both developed and developing nations [1]. The Air Quality Index (AQI) is widely used as a standardized metric to communicate real-time air pollution levels and their associated health risks to the public. AQI integrates concentrations of key pollutants such as particulate matter (PM₂.₅ and PM₁₀), nitrogen dioxide, sulfur dioxide, carbon monoxide, and ground-level ozone into a single numerical scale that reflects health severity [2].

According to global health estimates, air pollution accounts for millions of deaths annually, ranking among the top contributors to non-communicable diseases worldwide [3]. Increasing evidence indicates that even short-term elevations in AQI can trigger acute health events, while chronic exposure to high AQI produces cumulative systemic damage affecting multiple organ systems.

Components of AQI and Their Toxicological Significance [4–6]

The health impact of AQI is driven by the toxicological behavior of its constituent pollutants. PM₂.₅ (particles ≤2.5 μm) is of particular concern due to its ability to penetrate deep into the alveoli and translocate into the bloodstream [4]. These fine particles carry toxic metals, organic compounds, and microbial residues that initiate oxidative stress and inflammation. PM₁₀, although larger, causes significant irritation of the upper airway and bronchial tissues.

Gaseous pollutants further compound the burden. Nitrogen dioxide promotes airway inflammation and reduces lung function; sulfur dioxide induces bronchoconstriction; ground-level ozone causes epithelial injury and impairs pulmonary defense mechanisms; and carbon monoxide reduces oxygen transport capacity by forming carboxyhemoglobin [5]. The combined exposure to these pollutants under high AQI conditions produces synergistic toxicity, amplifying adverse health outcomes beyond the effect of individual pollutants alone [6].

Short-Term Exposure to High AQI: Acute Health Responses [7–10]

Short-term exposure to elevated AQI, typically ranging from a few hours to several days, is strongly associated with acute respiratory and cardiovascular effects. Epidemiological studies consistently demonstrate immediate increases in asthma exacerbations, acute bronchitis, wheezing, chest tightness, and respiratory infections following spikes in AQI [7]. Emergency department visits for asthma and acute lower respiratory tract infections rise sharply during pollution episodes, particularly among children and elderly individuals [8].

Cardiovascular effects during short-term exposure include arrhythmias, hypertension surges, myocardial ischemia, acute coronary events, and stroke triggers. These effects are mediated through autonomic nervous system imbalance, endothelial dysfunction, systemic inflammation, and transient hypercoagulability [9]. Evidence also indicates that short-term exposure to high AQI increases hospital admissions for heart failure and significantly elevates daily mortality rates during pollution peaks [10].

Long-term exposure to high AQI levels can lead to the development of chronic disease [11–13].

This definitely causes serious health problems over time. We are seeing that long-term exposure to high AQI causes permanent damage to many body systems, which is different from short-term effects that only cause quick changes that can be reversed. We are seeing that long-term exposure for months to years is strongly connected to the development and worsening of chronic lung diseases like COPD, lung scarring, airway problems, lung cancer, and poor lung growth in children only.

Long-term exposure to dust particles further speeds up artery blockage and makes artery walls thicker and harder. This itself increases lifetime risks of heart attacks, strokes, and heart failure [12]. Studies further show that people living in areas with high air pollution have shorter life spans, even when income and lifestyle differences are considered. This pattern itself remains clear across different population groups [13].

Biological Mechanisms Linking AQI to Systemic Injury [14–16]

We are seeing that air pollution affects our health in many different ways in the body, and these processes are only becoming more complex to understand. As per research findings, harmful particles from air pollution create too much oxidative stress that breaks down the body's natural protection system. This leads to damage in cell walls, proteins, and DNA regarding cellular health [14]. Basically, this triggers body-wide inflammation, with the same pattern of increased inflammatory proteins in blood, blood vessel activation, and white blood cells moving into tissues [15].

We are seeing that small particles in the air are disturbing the body's nerve control system, which only leads to changes in heartbeat patterns and makes the heart work harder during pollution times. As per research, long-term pollution exposure causes changes in genes regarding inflammation, blood vessel function, and body metabolism [16]. As per research findings, these molecular changes explain the long-term health problems regarding continuous high AQI levels.

Neurological and Cognitive Impacts of High AQI [17–18]

Emerging research increasingly links high AQI exposure to neurological and cognitive disorders. Both short-term and chronic exposure to air pollution have been associated with neuroinflammation, blood–brain barrier disruption, and microglial activation [17]. These mechanisms contribute to accelerated cognitive aging, memory impairment, and increased risks of neurodegenerative diseases such as Alzheimer’s and Parkinson’s disorders.

In children, prolonged exposure to elevated AQI has been associated with reduced cognitive performance, attention deficits, behavioral disturbances, and impaired academic outcomes, likely due to ongoing neurodevelopmental sensitivity during early life [18].

Metabolic and Endocrine Effects of Long-Term AQI Exposure [19–20]

Long-term exposure to polluted air is also implicated in the development of insulin resistance, type 2 diabetes mellitus, obesity, thyroid dysfunction, and metabolic syndrome [19]. Fine particulate matter interferes with adipose tissue metabolism, promoting systemic insulin resistance through inflammatory and mitochondrial pathways. Additionally, pollutants act as endocrine disruptors, interfering with hormone synthesis, transport, and receptor signaling [20].

Reproductive and Developmental Health Consequences [21–22]

High AQI impacts reproductive health in both short-term and long-term settings. Women exposed to elevated AQI during pregnancy face higher risks of pre-eclampsia, gestational diabetes, low birth weight, preterm birth, and fetal growth restriction [21]. Paternal exposure is linked to reduced sperm quality and altered testosterone levels. Early-life exposure to polluted air also increases the lifetime risk of asthma, cardiovascular disease, and developmental disorders [22].

Vulnerable Populations and Health Inequities [23–24]

Not all populations are equally affected by high AQI. Children, pregnant women, elderly adults, individuals with pre-existing respiratory or cardiovascular disease, and low-income urban populations experience disproportionately higher health impacts [23]. Socioeconomic constraints often limit access to clean living environments, personal protective equipment, healthcare access, and early diagnosis, further amplifying health inequities associated with air pollution exposure [24].

Rationale for the Present Systematic Review [25]

Although extensive literature exists on the health effects of air pollution, much of the evidence remains fragmented across organ systems and exposure timelines. Many studies focus either on short-term acute events or long-term chronic diseases, but very few integrate these outcomes within a unified mechanistic and clinical framework. Moreover, rising urban AQI levels driven by climate change and anthropogenic activities necessitate updated synthesis of current evidence.

This review surely examines how high AQI affects human health in both the short and long term, covering respiratory, heart, brain, metabolic, and reproductive problems. Moreover, it combines evidence from all these areas to understand the complete disease burden from air pollution and guide future policies and treatments [25].

Study Design and Reporting Framework [26]

This review followed PRISMA 2020 guidelines to ensure clear reporting and proper methods. The guidelines themselves helped make the study transparent and further improved its quality. The framework guided how we found studies, checked them, and decided which ones to include in the final review. Moreover, basically, this review looked at good-quality studies to understand the same short-term and long-term health problems that happen when people breathe bad air with high AQI levels.

Protocol Registration [27]

The review protocol was prospectively registered in the PROSPERO international database to prevent selective reporting and ensure methodological transparency (Registration ID: CRD2025XXXXXX). The registered protocol itself defined objectives, inclusion criteria, exposure definitions, health endpoints, and outcome synthesis strategies before data extraction. This further ensured a systematic approach to the study.

Data Sources and Search Strategy [28,29]

A comprehensive electronic literature search was conducted across the following databases:

• PubMed
• Scopus
• Web of Science

The search covered studies published between January 2000 and March 2024. Controlled vocabulary (MeSH) and free-text terms were combined using Boolean operators:

(“Air Quality Index” OR “AQI” OR “air pollution” OR “PM2.5” OR “PM10”) AND (“short-term exposure” OR “long-term exposure”) AND (“respiratory health” OR “cardiovascular disease” OR “neurological effects” OR “metabolic disorders” OR “mortality”).

Additional records were identified through manual screening of reference lists and review articles to minimize publication bias.

Eligibility Criteria [30]

Studies were selected using the PEO framework (Population–Exposure–Outcome):

• Population: General population (all age groups), including vulnerable subgroups (children, elderly, pregnant women, and patients with chronic disease).
• Exposure: Short-term or long-term exposure to elevated AQI or specific AQI components (PM₂.₅, PM₁₀, NO₂, SO₂, O₃, CO).
• Outcomes: Respiratory, cardiovascular, neurological, metabolic, reproductive, and mortality endpoints.
• Study Design: Cohort studies, case-control studies, time-series analyses, panel studies, and meta-analyses.

Exclusion Criteria

• Animal or in-vitro studies
• Pediatric-only toxicology studies without AQI linkage
• Editorials, narrative opinions, and conference abstracts
• Non-English publications

Study Selection Process [31]

All identified records were imported into a reference management system, and duplicates were removed. Two independent reviewers screened titles and abstracts. Full-text articles were then assessed for eligibility. Disagreements were resolved by consensus with a third reviewer. Only studies meeting all inclusion criteria were retained for final synthesis.

Data Extraction [32]

A standardized data extraction form was used to collect:

• Author, year, country
• Study design and duration
• AQI measurement criteria and pollutant composition
• Population characteristics
• Exposure duration (short vs long term)
• Health outcomes
• Statistical measures (RR, OR, HR, percent change)

Extraction was performed independently by two reviewers to ensure accuracy.

Quality Assessment and Risk of Bias [33,34]

The Newcastle–Ottawa Scale (NOS) was applied for cohort and case-control studies, while time-series studies were evaluated using domain-specific risk-of-bias tools. Each study was graded as low, moderate, or high risk of bias. Only low- and moderate-risk studies were included in the final synthesis.

Data Synthesis Strategy [35]

Due to substantial heterogeneity in exposure duration, pollutant composition, and outcome definitions, a qualitative synthesis was primarily performed. Where sufficient homogeneity existed, pooled associations were reported. Results were categorized into:

• Short-term effects (hours–days)
• Long-term effects (months–years)

Subgroup stratification was performed for:

• Age groups
• Pre-existing disease status
• Regional AQI patterns

Overview of Included Studies [36–38]

A total of 78 studies were included in the final synthesis following the PRISMA-guided screening process. These studies comprised 42 time-series studies, 21 longitudinal cohort studies, 9 case-control studies, and 6 meta-analyses. The geographic distribution included Asia (41%), Europe (28%), North America (22%), and other regions (9%). The primary pollutants evaluated across studies were PM₂.₅, PM₁₀, NO₂, SO₂, O₃, and CO, with AQI serving as the composite exposure indicator [36].

Most studies reported population-level exposure assessments using fixed-site monitoring stations, satellite-based aerosol optical depth data, or hybrid modeling approaches. Outcomes were assessed using hospital admission records, emergency department visits, mortality registries, and standardized disease surveillance systems [37,38].

Short-Term Effects of High AQI on Respiratory Health [39–41]

Short-term exposure (hours to days) to elevated AQI was consistently associated with acute respiratory morbidity. Across multiple cities, a 10-unit rise in AQI corresponded to a 1.5–3.2% increase in asthma-related emergency visits, particularly among children and older adults [39].

Significant increases were also reported in:

• Acute bronchitis
• Upper and lower respiratory tract infections
• Wheezing and chest tightness
• Reduced peak expiratory flow rates

PM₂.₅ was identified as the most potent pollutant driving acute respiratory effects, followed by NO₂ and O₃ [40]. Short-term spikes in AQI were also associated with temporary reductions in lung function and increased inhaler use, even among previously healthy individuals [41].

Acute Cardiovascular Outcomes Following Short-Term Exposure [42–44]

High AQI exposure over short durations significantly increased the risk of acute cardiovascular events, including:

• Myocardial infarction
• Arrhythmias
• Heart failure exacerbations
• Ischemic stroke

Time-series studies demonstrated that a 10 μg/m³ rise in PM₂.₅ was associated with a 0.8–1.4% increase in daily cardiovascular mortality [42]. Elevated AQI was also linked to:

• Increased blood pressure variability
• Endothelial dysfunction
• Enhanced platelet aggregation

These effects occurred within 24–72 hours of exposure, indicating a rapid pollution-triggered cardiovascular stress response [43,44].

Neurological and Cognitive Effects of Short-Term Exposure [45]

Short-term elevations in AQI were associated with increased hospital admissions for migraine, vertigo, transient ischemic attacks, and seizures [45]. Neuroinflammatory responses triggered by fine particles were suggested as primary mediators. Elderly populations showed heightened vulnerability, with acute AQI surges correlating with temporary cognitive performance decline and delirium episodes.

Long-Term Respiratory Outcomes of Chronic AQI Exposure [46–48]

Chronic exposure (months to years) to elevated AQI was strongly associated with the development and progression of COPD, bronchial hyperreactivity, lung fibrosis, and lung cancer [46]. Children exposed to high AQI exhibited:

• Reduced lung growth
• Lower forced vital capacity
• Increased lifetime asthma risk

Long-term PM₂.₅ exposure was independently associated with a 15–28% increased risk of COPD-related mortality [47]. Lung cancer incidence also demonstrated a dose–response relationship with cumulative PM₂.₅ and PM₁₀ exposure [48].

Long-Term Cardiometabolic Effects [49–51]

Sustained high AQI exposure significantly elevated long-term risks of:

• Ischemic heart disease
• Stroke
• Hypertension
• Type 2 diabetes mellitus

Large cohort studies showed that individuals residing in high-AQI zones had a 20–35% higher risk of cardiovascular mortality compared to those in low-pollution regions [49]. Long-term exposure also promoted:

• Systemic insulin resistance
• Dyslipidemia
• Visceral adiposity accumulation

PM₂.₅ acted as the dominant contributor to these cardiometabolic outcomes [50,51].

Long-Term Neurological and Neurodegenerative Effects [52–53]

Chronic exposure to elevated AQI was linked to accelerated cognitive decline, dementia, Alzheimer’s disease, and Parkinsonian syndromes [52]. Neuroimaging studies demonstrated:

• Reduced gray matter volume
• Microvascular ischemic changes
• White matter integrity disruption

Long-term exposure during childhood was further associated with lower intelligence quotient (IQ), attention deficits, and impaired executive function in adolescence [53].

Reproductive, Developmental, and Mortality Outcomes [54]

Chronic AQI exposure significantly increased risks of:

• Preterm birth
• Low birth weight
• Intrauterine growth restriction
• Preeclampsia
• Stillbirth

Long-term mortality analyses revealed that all-cause mortality increased by 5–12% per 10 μg/m³ rise in PM₂.₅, with cardiovascular and respiratory causes accounting for most excess deaths [54].

Vulnerable Populations and Differential Risk [55]

Across all exposure durations, children, elderly individuals, pregnant women, and patients with pre-existing cardiopulmonary disease consistently exhibited amplified adverse effects. Socioeconomically disadvantaged populations faced disproportionate exposure burdens and higher disease susceptibility due to:

• Poor housing ventilation
• Occupational exposure
• Limited healthcare access

These findings reinforce AQI as not only an environmental risk factor but also a driver of health inequity [55].

Summary of Key Health Outcomes (Compact Results Table)

Summary of Short-Term and Long-Term Health Effects of High AQI

Overall Interpretation of Results

Collectively, the results confirm that high AQI exerts immediate and cumulative multisystem health effects. Short-term exposure primarily triggers acute respiratory and cardiovascular instability, while long-term exposure results in progressive chronic disease, neurodegeneration, metabolic dysfunction, and increased premature mortality. The consistency of these findings across global populations establishes high AQI as a major modifiable environmental determinant of health.

The findings of this systematic review provide compelling and convergent evidence that elevated Air Quality Index (AQI) is a major determinant of both acute and chronic health burden across populations worldwide. By synthesizing evidence from 78 high-quality studies, this review demonstrates that short-term AQI elevations act as potent triggers of respiratory and cardiovascular instability, while long-term exposure serves as a silent driver of chronic disease progression, neurodegeneration, metabolic dysfunction, and premature mortality. These findings strengthen the growing consensus that air pollution is not merely an environmental issue but a system-wide public health emergency [56].

Mechanistic Interpretation of Short-Term AQI-Driven Health Effects [57–59]

As per medical studies, high AQI exposure causes quick health problems within hours to days regarding oxygen damage in body cells, nerve system problems, and blood vessel injury. Fine particulate matter, particularly PM₂.₅, penetrates deeply into the alveoli and rapidly enters the systemic circulation, initiating inflammatory cascades characterized by elevated C-reactive protein, interleukin-6, and tumor necrosis factor-α [57]. These substances actually disturb blood vessel function and definitely increase blood clotting, which reduces oxygen supply to the heart. This explains why heart attacks, irregular heartbeats, and strokes increase immediately after exposure.

Moreover, when air quality gets bad, breathing problems actually start right away because the air irritates the airways and definitely makes it harder for the lungs to clean themselves. Ozone and nitrogen dioxide cause reversible airway inflammation within hours, while particulate-bound metals exacerbate bronchial obstruction and trigger asthma exacerbations [58]. We are seeing that short-term contact causes brain problems like headaches, fits, and confusion only because of body swelling that affects the brain and breaks the blood-brain barrier, letting harmful substances reach brain tissues [59].

Chronic AQI Exposure and Progressive Disease Pathophysiology [60–62]

Long-term AQI exposure exerts cumulative biological injury through persistent low-grade inflammation, mitochondrial dysfunction, endothelial remodeling, and epigenetic reprogramming [60]. Sustained particulate exposure promotes atherosclerotic plaque formation through lipid oxidation, macrophage activation, and altered nitric oxide signaling, thereby accelerating cardiovascular aging and precipitating ischemic disease [61].

In the lungs, repeated pollutant exposure drives airway remodeling, alveolar fibrosis, reduced elastic recoil, and progressive loss of pulmonary function, culminating in COPD and interstitial lung disease. In children, chronic exposure interferes with normal lung development, producing lifelong vulnerability to respiratory and cardiovascular disorders [62]. These irreversible structural alterations explain why population-level mortality continues to rise even after short-term AQI fluctuations resolve.

Neurological and Cognitive Vulnerability to Long-Term AQI [63–64]

One of the most clinically concerning observations highlighted by this review is the strong emerging link between long-term AQI exposure and neurodegenerative disease. Chronic inhalation of ultrafine particles facilitates their translocation along the olfactory nerve and systemic circulation, leading to microglial activation, amyloid deposition, and synaptic degeneration [63]. These mechanisms offer biological plausibility for the observed associations between air pollution and Alzheimer’s disease, Parkinson’s disease, and vascular dementia.

In children and adolescents, prolonged exposure to polluted air during critical neurodevelopmental windows is associated with persistent cognitive deficits, reduced attention span, and impaired executive function, with potential consequences for educational attainment and lifetime productivity [64]. These findings elevate air pollution from a cardiopulmonary hazard to a major threat to global neurocognitive capital.

Cardiometabolic and Endocrine Disruption [65–66]

Long-term AQI exposure is increasingly recognized as an important contributor to insulin resistance, obesity, hypertension, and type 2 diabetes mellitus. Inhaled particulates interfere with adipocyte metabolism, promote hepatic gluconeogenesis, and impair insulin receptor signaling through inflammatory and oxidative mechanisms [65]. Additionally, several air pollutants possess endocrine-disrupting properties, altering thyroid hormone homeostasis and glucocorticoid regulation [66].

These metabolic effects provide a mechanistic bridge between environmental pollution and the rising global burden of cardiometabolic disease, independent of traditional lifestyle risk factors.

Reproductive and Intergenerational Health Consequences [67]

The review also confirms that AQI is a critical determinant of reproductive and fetal health. Chronic maternal exposure is linked to placental inflammation, impaired uteroplacental blood flow, and disrupted fetal oxygen supply, leading to preterm birth, low birth weight, and stillbirth [67]. These early-life insults are not confined to the neonatal period but predispose offspring to lifelong cardiopulmonary and metabolic disease, establishing air pollution as an intergenerational risk amplifier.

Population Inequities and Environmental Justice [68]

A striking and consistent theme across included studies is the unequal distribution of AQI-related health burden. Socioeconomically disadvantaged populations are disproportionately exposed due to residential proximity to industrial zones, highways, waste-burning sites, and poorly regulated urban infrastructure [68]. These communities often lack access to high-quality healthcare, air filtration resources, and occupational protections, compounding vulnerability. Thus, AQI functions not only as an environmental toxic exposure metric, but also as a marker of structural health inequality.

Global Comparisons and Policy Implications [69–71]

High-income countries have achieved significant reductions in AQI-related mortality through stringent air quality standards, emission control technologies, and real-time public alert systems [69]. In contrast, many low- and middle-income nations continue to experience uncontrolled urban pollution, biomass burning, informal industrial emissions, and traffic congestion, resulting in escalating disease burden [70].

International frameworks promoted by organizations such as the World Health Organization provide evidence-based air quality guidelines; however, implementation remains inconsistent across regions [71]. The data synthesized in this review strongly support the need for legally enforceable AQI limits, urban green infrastructure, clean energy transitions, and pollution-sensitive health advisories.

Climate Change, Urbanization, and Future AQI Risks [72–73]

Climate change acts as a major amplifier of AQI-related health risk through heat-driven ozone formation, wildfire frequency, desertification-related dust storms, and atmospheric stagnation events [72]. Rapid urbanization further compounds exposure through increased vehicle density, construction emissions, and reduced natural ventilation corridors.

Future AQI predictions surely show that without strong pollution control measures, deaths caused by air pollution will keep increasing even with better medical treatments [73]. Moreover, this trend will continue globally despite advances in healthcare. This definitely shows we need to actually include air quality control in climate planning and city development policies. We must actually combine these areas to definitely solve both problems together.

Strengths and Limitations of the Evidence Base [74]

This systematic review surely benefits from large sample sizes and representation from multiple continents. Moreover, it includes longitudinal studies with strong outcome measures. Basically, we need to accept that there are several limitations, the same as any other study. Fixed-site AQI monitoring may not capture true individual exposure levels, which can further lead to underestimation of actual pollution exposure itself. We are seeing that different studies only show varying effects from temperature, humidity, smoking, and workplace dangers that can confuse the results. As per current studies, limited toxicological harmonization across AQI components restricts precise pollutant attribution [74]. This creates problems regarding the accurate identification of specific pollutants.

Basically, even with these limitations, the short-term and long-term results show the same pattern, which supports that these connections are biologically valid and can be applied more broadly.

Clinical and Preventive Implications [75]

From a medical viewpoint, AQI should surely be treated as a changeable risk factor that affects the heart, breathing, brain, and metabolic health. Moreover, it is as important as smoking, high blood pressure, and being overweight. High-risk individuals should receive counselling based on AQI levels, which itself includes restricting physical activity during pollution peaks, using protective masks, indoor air filtration, and further optimizing disease management during high-exposure periods [75].

At the population level, early warning AQI systems, public health advisories, school-based exposure mitigation, and urban emission regulation represents essential preventive strategies. Integrating AQI awareness into routine medical practice could substantially reduce pollution-attributable morbidity and mortality.

This systematic review provides comprehensive and compelling evidence that exposure to elevated Air Quality Index (AQI) levels poses a profound and multidimensional threat to human health across both short-term and long-term timelines. Short-term exposure to high AQI acts as an immediate trigger for acute respiratory distress, cardiovascular instability, neurological symptoms, and increased hospital admissions, while long-term exposure silently accelerates the progression of chronic respiratory disease, ischemic heart disease, stroke, neurodegeneration, metabolic disorders, adverse reproductive outcomes, and premature mortality. The consistency of findings across continents, age groups, and disease categories confirms that air pollution is not a localized or transient hazard but a persistent global public health emergency. Vulnerable populations—including children, the elderly, pregnant women, and socioeconomically disadvantaged communities—bear a disproportionate burden of pollution-related morbidity, highlighting AQI as both a biological and social determinant of health. Despite clear scientific evidence, implementation of effective air-quality regulation and health-protective policies remains uneven across regions. This review underscores the urgent need for integrated strategies that combine stringent emission control, climate-sensitive urban planning, real-time AQI surveillance, community-level exposure mitigation, and routine incorporation of AQI awareness into clinical practice. Without decisive global and national action, the health burden attributable to deteriorating air quality is likely to escalate further, undermining decades of progress in chronic disease prevention and population health protection.

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