Air pollution is a known environmental health hazard. Epidemiologic studies have demonstrated associations between burden of cardiovascular, respiratory, as well as other organs, various types of cancer, and mortality attributed to air pollution. Air pollution appears to be associated with a higher risk of cognitive defects and neurodegenerative disorders. Despite substantial effects of air pollution on human health, economy and environment, it has been neglected for comprehensive health research and certain policy implications and instructions, especially in low- and middle- income countries. There remains a need for future research on air pollution, exposure methods, short-term and long-term side effects of air pollution, limiting its sources, biomarkers assay, and prepare guidelines of reasonable conditions to participate in exercise and work at air pollution. The study objective is to investigate the impact of air pollution on disease and need for more strict policies to reduce it. 

Epidemiological studies demonstrated an association between increased levels of ambient air pollution particles and human morbidity and mortality. Oxidative stress following particulate matter (PM) exposure initiates a series of cellular reactions that includes activation of kinase cascades and transcription factors and release of inflammatory mediators, which ultimately lead to cell injury or apoptosis. Consequently, oxidative stress in cells and tissues is a central mechanism by which PM exposure leads to injury, disease, and mortality [1].

In a systematic review of epidemiological studies conducted in Europe, North America (Canada and USA only), Australia and New Zealand on the association between outdoor and indoor exposure to solid fuel (biomass and coal) combustion and respiratory outcomes in adults, consisted of 34 articles: A significant association was found between indoor solid fuel exposure and COPD risk. The available epidemiological evidence between outdoor exposure to residential coal burning and respiratory outcomes suggests an increased risk of adverse respiratory effects. The identified epidemiological studies have several limitations [2]. 

Indoor air contributes significantly to overall exposure, particularly for rural Chinese who often use solid fuels for cooking and/or heating. Unfortunately, overlooked rural indoor air leads to a critical knowledge gap. Simultaneous measurements in the kitchen, living room, and immediately outside of houses using six-channel particle counters were carried out in 18 biomass-burning rural and 3 non-biomass-burning urban households (as a comparison) in winter to characterize dynamic change patterns indoor air pollution and indoor-outdoor relationship. The rural households mainly used wood or crop residues for cooking and heating, while the urban households used pipelined natural gas for cooking and air conditioners for heating. In rural households with significant solid-fuel burning internal sources, the highest concentration was found in the kitchen, with comparable levels in the living room and low levels in outdoor air [3]. 

A study conducted a time-stratified case-crossover to investigate if individual and contextual socioeconomic status (SES) modified the relationship between short-term exposure to ozone (O3), nitrogen dioxide (NO2), and particulate matter with aerodynamic diameter less than 10 µm (PM10) on cardiovascular, respiratory, and all nonaccidental mortality. Analyses were based on information on 280,685 deaths from 2011 to 2015 in the city of São Paulo. According to this study, exposure to air pollutants increases the chance of dying by nonaccidental, cardiovascular, and respiratory causes. 

Lower educational levels and living on lower contextual SES increased the risk of mortality associated with air pollution exposure [4].

Air pollutants

Particulate matter (PM) is a complex mixture of solid and liquid particles suspended in air that is released into the atmosphere when coal, gasoline, diesel fuels and wood are burned. It is also produced by chemical reactions of nitrogen oxides and organic compounds that occur in the environment. Vegetation and livestock are also sources of PM. In big cities, production of PM is attributed to cars, trucks and coal-fired power plants (5). PM > 10 µm in diameter (coarse particles) is deposited in the extra thoracic region, PM with a diameter between 5 and 10 µm is deposited in the tracheobronchial alveolar region (5,6). It has been suggested that particles ≤0.1 µm in diameter (ultrafine particles) are more toxic than larger particles as they may cover a greater area of the alveolus. One host defense mechanism is phagocytosis of ultrafine particles by alveolar macrophages. However, due to their small size, ultrafine particles overwhelm macrophage phagocytosis, resulting in increased penetration, which causes deleterious effects in other organs (e.g., brain, heart, bone marrow, etc.) (5,7,8). Ozone (O3) is mainly formed by the interaction of ultraviolet light with both nitrogen oxides and organic compounds. O3 exhibits potent anti-oxidant properties and induces alterations in the airways that depend on concentration and the duration of exposure [5].

In the ambient atmosphere, the major sources of NO2 are the combustion of fossil fuels and motor-vehicle emissions. Indoor sources include such appliances as gas stoves, water heaters, and kerosene space heaters. In the workplace, exposures to NO2 have been reported in such occupations as electroplating, acetylene welding, agriculture, space exploration, detonation of explosives, certain military activities, and burning of nitrogen-containing propellants [9].

According to the Sao Paulo Official Monitoring Agency, in 2014, 296.34 thousand tons of pollutants (carbon monoxide, hydrocarbons, nitrogen oxides, particulate matter and sulfur oxides) were discharged into the atmosphere of the Sao Paulo Metropolitan Region, of which 259.98 tons were from vehicular emissions [10]. Elements derived from vehicular traffic that accumulated in tree barks were determined using energy-dispersive X-ray fluorescence spectrometry (EDXRF). The genotoxic effects caused by air pollution were tested through a pollen abortion bioassay. The elements aluminum (Al), sulfur(S), iron(Fe), manganese(Mn), copper(Cu), and zinc(Zn) showed a strong correlation with mortality rates (R2 > 0.87) and pollen abortion rates (R2 > 0.82). The results demonstrated that tree barks and pollen abortion rates allow for correlations between vehicular traffic emissions and associated outcomes such as genotoxic effects and mortality data [10].

-Respiratory effects

A study utilized a distributed lag nonlinear model (DLNM) to investigate the short-term effects of changes in air pollutant concentrations during peak traffic hours on respiratory diseases (RD) hospitalization in Lanzhou, China. Between 2014 and 2019, a total of 109,419 RD patients were hospitalized across seven hospitals in Lanzhou, China (11). Except for ozone (O3), fine particulate matter (PM2.5), inhalable particulate matter (PM10), sulfur dioxide (SO2), nitrogen dioxide (NO2) and carbon monoxide (CO), which increased by 10 µg/m3 (1 mg/m3 for CO), the relative risk (RR) values of hospitalization for RD were 1.0211, 1.0026, 1.0615, 1.0650 and 1.1229, respectively. PM2.5, PM10, NO2, and CO had a greater impact on individuals aged less than 15 years, while SO2 had a more pronounced effect on those aged ≥ 65 years [11].

Currently, the mechanisms related to the effects of air pollutants on RD are not well defined. The dominant potential mechanisms are oxidative stress, inflammatory responses, and phagocyte dysfunction [11,12]. PM2.5 increases lung oxidants, like malondialdehyde, while decreasing antioxidants, such as superoxide dismutase, resulting in cellular damage in the lungs [11,13]. Additionally, PM2.5 exposure elevates inflammation biomarkers like Th1 and Th17 cytokines, further exacerbating systemic inflammation [11,14,15]. NO2 can enter the bronchioles and alveoli, leading to edema and impairing small airway function [10,15,16]. Air pollutants reduce the ability to recognize pathogens by regulating phagocyte receptor expression, impair phagocyte motility and phagocytosis, and increase cytokine and chemokine production [11,17]. 

A study performed analyses at enrollment and after 1 year of follow-up in the IPF-PRO (Idiopathic Pulmonary Fibrosis Prospective Outcomes) Registry, a prospective observational registry that enrolled individuals with IPF at 46 U.S. sites from 2014 to 2018. According to that study, long-term exposure to PM2.5 was associated with worse quality of life and lung function at enrollment, but not with short-term disease progression or mortality [18].

The analysis of 20 studies showed significant associations between exposure to these pollutants and increased asthma incidence and prevalence, particularly in children. Specifically, pollutants such as elemental carbon (EC), benzene, NO2, PM10, and sulfur dioxide (SO2) were found to be significantly associated with asthma development in children, while NO2 and PM2.5 were linked to asthma exacerbations in both children and adults. Additionally, hospitalizations and emergency room visits were positively correlated with exposure to PM2.5 and O3 in both children and adults, and the elderly showed significant associations with O3 exposure. These findings highlight the importance of reducing exposure to outdoor air pollutants to mitigate asthma risk and improve public health outcomes, particularly in vulnerable populations like children and the elderly [19].

The current evidence suggests that 13% of pediatric asthma cases worldwide may be attributable to traffic-related air pollutants (TRAPs), and that air pollution has a negative impact on asthma outcomes in both adult and pediatric patients [20,21].

Several epidemiological studies have shown that air pollutants exacerbate airway diseases such as allergic rhinitis (AR), asthma, bronchitis, and chronic obstructive pulmonary disease (COPD). Pollutants such as TRAPs also have negative effects on other upper airway diseases such as AR and non-AR, sinusitis, and otitis media. Increasing evidence suggests that PM, photochemical pollutants, and ozone are also linked to the development of upper airway diseases [20,22]. 

In the UK, an estimated 15% of asthma patients have concurrent COPD, yet the underlying causes and mechanisms remain largely unexplored. In a study, 46 832 participants with asthma were recruited from the UK Biobank during the baseline period (2006-2010). Particulate matter with a diameter of 2.5 μm (PM2.5) and nitrogen dioxide (NO2) were estimated at baseline address using land-use regression models. Over a median follow-up of 10.84 years, 3759 participants with asthma at baseline developed COPD. Ambient air pollution is strongly associated with progression from asthma to comorbidity COPD, particularly among individuals with high genetic risk [23].

-Cardiovascular effects

Airborne particulate matter (PM), in particular, has been associated with a wide range of detrimental cardiovascular effects, including impaired vascular function, raised blood pressure, alterations in cardiac rhythm, blood clotting disorders, coronary artery disease, and stroke [24]. 

A study included 432 530 participants free of heart failure (HF), atrial fibrillation, or coronary heart disease in the UK Biobank study. All participants were enrolled from 2006 to 2010 and followed up to 2018. The information on particulate matter (PM) with diameters ≤2.5 µm (PM2.5), ≤10 µm (PM10), and between 2.5 and 10 µm (PM2.5-10) as well as nitrogen oxides (NO2 and NOx) was collected. During a median of 10.1 years (4 346 642 person-years) of follow-up, they documented 4201 incident HF. The hazard ratios (HRs) [95% confidence interval (CI)] of HF for a 10 µg/m3 increase in PM2.5, PM10, PM2.5-10, NO2, and NOx were 1.85, 1.61, 1.13, 1.10, and 1.04, respectively. They found that the air pollution score was associated with an increased risk of incident HF in a dose-response fashion [25]. 

There is a strong correlation of acute and chronic air pollutant exposure and the incidence of atrial fibrillation. Acute increases in air pollution increase the risk of emergency room visits and hospital admissions for atrial fibrillation and the risk of stroke and mortality in patients with atrial fibrillation. Similarly, there is a strong correlation of increases of air pollutants and the risk of ventricular arrhythmias, out-of-hospital cardiac arrest, and sudden cardiac death [26].

A study cohort included 28,349 patients, of whom 17,448 (61.6%) had pacemakers and 9079 (32%) had defibrillators. They limited it to the 8687 patients living in Western US Fire States (California, Oregon, Washington, Arizona, Utah, Nevada, New Mexico, and Colorado). There was a strong association between PM2.5 and premature ventricular contraction burden, with an odds ratio of 7.72 for PM2.5 ≥ 13.7. In a large cohort of patients with cardiac implantable electronic devices (CIEDs), Air Quality Index (AQI) and PM2.5 had significant associations with premature ventricular contraction burden, physical activity, and heart rate [27]. 

In a study, starting from a population at risk of 1,719,475 subjects aged 30 years or above, a total of 14,629 incident cases known as peripheral artery disease (PAD) in the Rome Longitudinal Study (RLS) during 2011-2019 were identified. An interquartile range (IQR)IQR (1.13 μg/m3) increase in PM2.5 was positively associated with a hazard ratio (HR) of 1.011. Positive associations were also obtained for NO2 ([IQR 7.86 μg/m3] HR: 1.022 and black carbon ([IQR 0.39 x10-5/m] HR: 1.020. According to this study, long-term exposure to PM2.5, NO2 and BC is associated with an increased incidence of PAD, and male subjects and individuals aged between 55-69 years were at greater risk [28].

-Cancer risk

Air pollution is an under-recognized global health threat linked to an increased risk of cancers and is due primarily to the burning of fossil fuels. Outdoor air pollutants are largely due to the burning of fossil fuels from human activities, although there is growing data implicating outdoor pollution from wildfire smoke. Indoor air pollution is primarily caused by burning solid fuel sources such as wood, coal and charcoal for household cooking and heating. The strongest evidence is seen on the positive association of air pollution, particularly particulate matter 2.5 with lung cancer. Emerging data implicate exposure to pollutants in the development of breast, gastrointestinal and other cancers. The mechanisms underlying these associations include oxidative stress, inflammation and direct DNA damage facilitated by pollutant absorption and distribution in the body. Despite the mounting evidence, air pollution is often overlooked in predictive cancer risk models and public health intervention [29]. Outdoor air pollution Exposure to air pollution is estimated to be responsible for 8.9 million deaths in 2015 [29,30].

Major components of air pollution are primary air pollutants that are directly emitted into the atmosphere from identifiable sources, such as the burning of fossil fuels in combustion engines, factories, healthcare, agriculture and electricity generation. These include PM, especially those with diameter less than 10 µm and less than 2.5 µm (PM)2.5, sulfur oxides (SOx), nitrogen oxides (NOx), carbon monoxide (CO) and volatile organic compounds (VOCs). VOCs are a group of organic chemicals that play a significant role in air pollution. Formaldehyde is a VOC that is emitted from vehicle exhaust, industrial processes and wood-burning, and is a known carcinogen [29,31]. It is one of the most important hazardous air pollutants (HAPs) that is associated with health risks, accounting for over 50% of the total HAPs- related cancer risks in the USA [29,32].

PM2.5 is composed of inorganic ions, organic compounds, toxic metals and mineral dust particles; as mentioned above, it is difficult to single out one component of PM2.5 as being solely responsible for the observed cancer risks. Secondary air pollutants include gaseous ozone, a major component of photochemical smog, and PM2.5, which are formed in the atmosphere from primary pollutants. Indoor air pollution is primarily caused by burning solid fuel sources such as wood, crop waste, coal, charcoal and dung for household cooking and heating. Wood smoke is a complex mixture consisting of PM, various gases and chemicals [29]. The International Agency for Research on Cancer (IARC) has classified PM, diesel exhaust and outdoor air pollution overall as Group 1 carcinogens [29,33].

Burning of fossil fuels results in submicron combustion- related PM containing numerous toxic compounds including acids and heavy metals and can penetrate deeper into the lung than the larger PM. PM induces oxidative stress in epithelial cells, generating reactive oxygen species that may damage DNA, proteins and lipids [29,34].

Long- term exposure to air pollution causes lung cancer even in people who have never smoked. One study found lung cancer mortality was adversely associated with increases in PM2.5, in both the overall population studied as well as in a cohort of over 340 000 never smokers. The risk of all cancer mortality was adversely associated with a 19% increase per 10 µg/m3 increase in PM 2.5 in never- smokers [29,35].

Epidemiological studies in low- and middle- income countries (LMICs) have found an association between household wood combustion and lung cancer. The Sister Study (29,36) found that increased frequency of using wood- burning in indoor fireplace and stove was associated with incident lung cancer even in never smokers, which was related to their use (1–29 days/year (HR adj=1.64; 95% CI, 0.87 to 3.10) and≥30 days/year (HR adj=1.99; 95% CI, 1.02 to 3.89).

Air pollution has been considered a hazard to human health. Future research should aim at establishing a cleared picture of the cytotoxic and carcinogenic mechanisms of PM in the lungs, as well as mechanisms of formation during internal engine combustion processes and other sources of airborne fine particles of air pollution [37].

In a systematic search conducted for studies that were published up to February 2020 and performed a meta-analysis of all available epidemiologic studies evaluating the associations between long-term exposure to NO2 with all-cause, cardiovascular, and respiratory mortality. The search initially retrieved 1349 unique studies, of which 34 studies met the inclusion criteria. The pooled hazard ratio (HR) for all-cause mortality was 1.06 per 10 ppb increase in annual NO2 concentrations. They provide robust epidemiological evidence that long-term exposure to NO2, a proxy for traffic-sourced air pollutants, is associated with a higher risk of all-cause, cardiovascular, and respiratory mortality that might be independent of other common air pollutants [38].

In a study of 10,532 adults in the China Health and Retirement Longitudinal Study (2011–2018), over 43,181 person-years, 141 incident lung-cancer cases were recorded (3.3 per 1,000 person-years). Independently, high PM₂․₅ (HR 1.82, 95% CI 1.29–2.57) and high sedentary time (HR 2.10, 95% CI 1.55–2.84) increased risk. Participants simultaneously exposed to high PM₂․₅, high warm-season heat, and ≥8 h sitting exhibited a nearly five-fold hazard (HR 4.95, 95% CI 2.24 10.95) versus the dual-low reference [39].

-Neurology effects

This observational cohort study included 307 304 British participants from the United Kingdom Biobank, who were stroke-free and possessed comprehensive baseline data on genetics, air pollutant exposure, alcohol consumption, and dietary habits.  Over a median follow-up duration of 13.67 years, a total of 2476 initial ischemic stroke (IS) events were detected. The hazard ratios (95% CI) of IS for per 10 µg/m3 increase in particulate matter with diameters equal to or less than 2.5 µm, ranging from 2.5 to 10 µm, equal to or less than 10 µm, nitrogen dioxide, and nitrogen oxide were 1.73 (1.33-2.14), 1.24 (0.88-1.70), 1.13 (0.89-1.33), 1.03 (0.98-1.08), and 1.04 (1.02-1.07), respectively. Furthermore, individuals in the highest quintile of the air pollution score exhibited a 29% to 66% higher risk of IS compared with those in the lowest quintile. Their findings suggested that prolonged joint exposure to air pollutants may contribute to an increased risk of IS, particularly among individuals with elevated genetic susceptibility to IS [40].

Stroke is a leading cause of disability and the second most common cause of death worldwide. Increasing evidence suggests that air pollution is an emerging risk factor for stroke. Over the past decades, air pollution levels have continuously increased and are now estimated to be responsible for 14% of all stroke-associated deaths. The risk for ischemic stroke is increased after short-term or long-term exposure to air pollution. Short-term exposure to air pollution increases the risk of intracerebral hemorrhage, a subtype of hemorrhagic stroke, whereas the effects of long-term exposure are less clear [41]. 

In a study, PubMed was queried from 2000 to 2023 to identify clinical and epidemiological studies examining the association between PM exposure and stroke subtypes (ischemic and hemorrhagic stroke). A total of 50 articles were included in this review. Overall, PM exposure increases ischemic stroke risk in both lightly and heavily polluted countries. The association between PM exposure and hemorrhagic stroke is variable and may be influenced by a country's ambient air pollution levels. A stronger association between PM exposure and stroke is demonstrated in older individuals and those with pre-existing diabetes [42]. 

In a study, data were extracted from the Korean Health Insurance Review and Assessment Service database, which contains health claims information of the entire South Korean population. Variables of interest included the number of patients diagnosed with benign paroxysmal positional vertigo (BPPV) in Seoul, South Korea, patients' clinical and demographic characteristics, and osteopenia status. Seoul's daily air pollution indicators, including SO2, CO, O3, NO2, PM10, and PM2.5, were obtained from the Korea Environment Corporation website. Air levels of NO2 were associated with increased incidence of benign paroxysmal positional vertigo (BPPV) in the present study [43].

 More recently, various studies have also shown that the central nervous system is also attacked by air pollution. Air pollution appears to be strongly associated with a higher risk of cognitive defects, neurodevelopmental (e.g., schizophrenia) and neurodegenerative (e.g., Alzheimer's disease) disorders. Results from epidemiological studies suggest potential associations, but are still insufficient to confirm causality [44]. 

To evaluate associations between traffic-related air pollution exposures ultrafine particles (UFP, ≤100 nm), black carbon [BC], and nitrogen dioxide [NO2]) and late-life dementia incidence, in the Seattle-based Adult Changes in Thought (ACT) prospective cohort study (beginning in 1994) and assessed ten-year average TRAP exposures for each participant based on prediction models derived from an extensive mobile monitoring campaign. The study did not find evidence of a greater hazard of late-life dementia risk with elevated long-term traffic-related air pollution exposures in this population-based prospective cohort study [45].

Psychology effects

In a systematic review the link between air pollution and poor mental health may relate to neurostructural and neurofunctional changes was studied.  Air pollution was consistently associated (95% of articles reported significant findings) with neurostructural and neurofunctional effects (e.g., increased inflammation and oxidative stress, changes to neurotransmitters and neuromodulators and their metabolites) within multiple brain regions (24% of articles), or within the hippocampus (66%), prefrontal cortex (7%), and amygdala (1%). The extant literature suggests that air pollution is associated with increased depressive and anxiety symptoms and behaviors, and alterations in brain regions implicated in risk of psychopathology [46]. 

To reveal the impact of air pollution on psychiatric disorders (autism spectrum disorders [ASD, n = 46,351], attention-deficit/hyperactivity disorder [ADHD, n = 55,374], anxiety disorders [ANX, n = 17,310], schizophrenia [SCZ, n = 127,906], and major depressive disorder [MDD, n = 500,199]), the Mendelian Randomization (MR) analysis was conducted. The mediating effects of brain imaging phenotypes were also accessed (n = 8428). According to that study, they observed that the significant relationship between PM2.5 absorbance and ADHD, also they discovered that NO2 or PM2.5 absorbance increased the risk of ASD. In addition, there were associations between NO2 and SCZ as well as PM2.5 and ANX. The findings revealed genetic causal relationships between air pollution and psychiatric disorders, mediated or masked by brain imaging phenotypes [47]. 

In a study of 24,387 deaths due to suicide and 10,767 deaths due to homicide in California, risk of suicide and homicide mortality increases with increasing daily ambient temperatures. Findings have public health relevance given anticipated increases in temperatures due to global climate change. No air pollutant associations were statistically significant [48].

In a study the relationship between wildfire smoke exposure and suicide risk in the United States in 2007 to 2019 using data on all deaths by suicide and satellite-based measures of wildfire smoke and ambient fine particulate matter (PM2.5) concentrations was evaluated. In rural counties, an additional day of smoke increases monthly mean PM2.5 by 0.41 μg/m3 and suicide deaths by 0.11 per million residents, such that a 1-μg/m3 (13%) increase in monthly wildfire-derived fine particulate matter leads to 0.27 additional suicide deaths per million residents (a 2.0% increase). By contrast, they find no evidence that smoke pollution increases suicide risk among any urban demographic group [49]. 

-Renal effects

A study included 419,835 UK Biobank participants who did not have kidney stone disease (KSD) at baseline. During a follow-up period of 12.7 years, 4503 cases of KSD were diagnosed. Significant associations were found between KSD risk and air pollution score (HR: 1.08, 95% CI: 1.03-1.13), PM2.5 (1.06, 1.02-1.11), PM10 (1.04, 1.01-1.07), nitrogen dioxide (NO2) (1.09, 1.02-1.16), nitrogen oxides (NOx) (1.08, 1.02-1.11), greenspace buffered at 300 m (0.95, 0.91-0.99), and greenspace buffered at 1000 m (0.92, 0.86-0.98) increase per interquartile range (IQR). PM2.5 and NO2 reductions may be a key mechanism for the protective impact of residential greenspace on KSD (P for indirect path less than 0.05). Prolonged exposure to air pollution was correlated with a higher risk of KSD, while residential greenspace exhibits an inverse association with KSD risk, partially mediated by the reduction in air pollutants concentrations [50].

In a large multicenter population-based European cohort of 289564 persons, the link between air pollution and cause-specific mortality, its relation to chronic kidney disease (CKD)-associated mortality was studied.  Over a mean follow-up time of 20.4 years, 313 of 289,564 persons died from CKD. Associations were positive for PM2.5 hazard ratio (HR) with 95% confidence interval (CI) of 1.31 (1.03-1.66) per 5 μg/m3, BC (1.26 (1.03-1.53) per 0.5 × 10- 5/m), NO2 (1.13 (0.93-1.38) per 10 μg/m3) and inverse for O3 (0.71 (0.54-0.93) per 10 μg/m3). Among the elemental constituents, copper (Cu), iron (Fe), potassium(K), nickel (Ni), sulfur(S) and zinc (Zn), representing different sources including traffic, biomass and oil burning and secondary pollutants, were associated with CKD-related mortality. In conclusion, the results suggest an association between air pollution from different sources and CKD-related mortality [51].

-Insulin resistance

A study aimed to determine the relationships between mixed exposure to six air pollutants, namely:PM2.5, PM10, sulfur dioxide (SO2), nitrogen dioxide (NO2), cobalt (CO) and ozone (O3), and insulin resistance (IR) indices in a total of 2,219 middle-aged and older populations from China Health and Retirement Longitudinal Study (CHARLS), who are followed from 2011 to 2015. Fully adjusted linear models revealed that increases in the levels of the six air pollutants (in μg/m3) were associated with higher triglyceride–glucose–body mass index (TyG-BMI; Beta = 0.027–0.128), triglyceride–glucose–waist circumference (TyG-WC; Beta = 0.155–0.674), and metabolic score for insulin resistance (METS-IR; Beta = 0.001–0.029) values during the four-year follow-up period. Among the pollutants, NO2 and O3 were identified as the primary contributor to the cumulative effect [52].

-Mortality

In a study, they address the health effects at low air pollution levels by performing new analyses within selected cohorts of the ESCAPE study (European Study of Cohorts for Air Pollution Effects; Beelen et al. 2014a) and within seven very large European administrative cohorts. Long-term exposure to PM2.5, NO2, and black carbon (BC) was positively associated with natural-cause and cause-specific mortality in the pooled cohort and the administrative cohorts. In the mortality analysis of the pooled cohort, significant negative associations with ozone(O3) remained in two-pollutant models. Long-term exposure to PM2.5, NO2, and BC was also positively associated with morbidity outcomes in the pooled cohort. For stroke, asthma, and COPD, positive associations were found for PM2.5, NO2, and BC. For acute coronary heart disease, an increased hazard ratio (HR) was observed for NO2. For lung cancer, an increased HR was found only for PM2.5 [53].

A review identified 2068 studies of which 95 were subject to full-text review with 45 meeting the inclusion criteria. An update in September 2018 identified 159 studies with 1 meeting the inclusion criteria. Of the 46 included studies, 41 reported results for NO2 and 20 for O3. The majority of studies were from the USA and Europe with the remainder from Canada, China and Japan. Forty-two studies reported results for all-cause mortality and 22 for respiratory mortality. Associations for NO2 and mortality were positive; random-effects summary relative risks (RR) were 1.02, 1.03, 1.03, and 1.06 per 10 μg/m3 for all-cause (24 cohorts), respiratory (15 cohorts), COPD (9 cohorts) and ALRI (5 cohorts) mortality respectively. Certainty of evidence assessments were moderate or low for both NO2 and O3 for all causes of mortality except for NO2 and COPD mortality where the certainty of the evidence was judged as high [54].

A study investigated the trend of death attributed to household air pollution and associate factors in East Africa from 2010 to 2019 and projection up to 2030. This study analyzed mortality attributed to household air pollution in East Africa from 2010 to 2019 using data from the World Health Organization (WHO) Global Health Estimates. Bayesian generalized Poisson regression and autoregressive integrated moving average (ARIMA) modeling were employed to examine the associated factors and project future mortality rates up to 2030 respectively. In 2019, these rates peaked at around 134,709 deaths. Projections indicate that, if current trends persist, East Africa may experience approximately 134,709 premature deaths each year. Acute lower respiratory infections accounted for around 21% of these deaths, while chronic obstructive pulmonary disease was responsible for about 19%. The analysis identified significant disparities in mortality rates based on sex, geographic location, underlying health conditions and year. This study highlights the significant burden of mortality attributed to household air pollution from 2010 to 2019 with a concerning upward trend in deaths, particularly from 2014 to 2019 with disproportionately affect vulnerable populations. The projections indicate that the mortality burden may continue if current trend continuous [55]. In a study all residents aged ≥ 30 years (3,083,227) in Denmark from 2000 until December 2017 were followed. According to this study, long-term exposure to PM2.5, NO2, and/or BC in Denmark were associated with mortality beyond cardiorespiratory diseases, including diabetes, dementia, psychiatric disorders, asthma, and acute lower respiratory infection (ALRI) [56].

Air pollution and Physical exercise 

As air pollution is often accompanied by slower air velocity and higher concentrations of a particulate matter, people may unconsciously inhale more the deposited particulate matter and other harmful substances when they exercise in an air-polluted environment [57]. A recent study in young and healthy males has also found that exposure to ambient air pollution during short-term submaximal exercise is associated with a decrease in airflow (FEV1/FVC) and goes one step further to state that the decrease is more apparent when the exercise takes place under particularly high exposure conditions [57,58].

Particulate matter (PM) contains a variety of carcinogenic or cancer-promoting components, including polycyclic aromatic hydrocarbons, cadmium, and mercury. One epidemiological research also supported the associations between PM and cancer, indicating that the mortality of lung cancer increased by 8% for every 10 pg/m−3 increase in PM concentration [57,59].

According to a systematic review, endurance exercise in environments with high air pollution can have significant negative impacts on cardiopulmonary health. These include increased levels of inflammation and oxidative stress, as well as decreased respiratory function. Although physical exercise has general benefits, exposure to vehicular traffic pollutants such as fine particulate matter and gases may negate these positive effects, especially in urban areas. In other instances, exercising in places with high air pollution could impair cardiopulmonary health via various mechanisms, and air pollution affects cardiovascular health through multiple interconnected mechanisms. The inhalation of PM2.5, NO2, O3, and CO generates oxidative stress, increasing the level of reactive oxygen species (ROS) and reducing the level of antioxidants, which damages endothelial cells and promotes systemic inflammation through the release of Interleukin 6 (IL-6), tumor necrosis factor-α (TNF-α), and IL-1β. This causes endothelial dysfunction, decreases nitric oxide (NO), and promotes vasoconstriction. In addition, activation of the sympathetic nervous system increases blood pressure and alters heart rate variability, increasing the risk of arrhythmias. Chronic exposure also induces a pro coagulant state, increasing platelet aggregation and thrombus formation, which can lead to hypertension, atherosclerosis, heart attack, and stroke. These effects, in addition to increasing cardiovascular mortality, compromise the body’s ability to benefit from aerobic exercise in polluted environments [60].

Active travel (walking or cycling for transport) is considered the most sustainable form of per sonal transport. Yet its net effects on mobility-related CO2 emissions are complex and under- researched. According to a collected travel activity data in seven European cities and derived life cycle CO2 emissions across modes: daily mobility-related life cycle CO2 emissions were 3.2 kgCO2 per person, with car travel contributing 70% and cycling 1% [61].

It remains a need for detailed and evidence-driven guidelines on air pollution for those participating in sports. Limited evidence supports reducing exposure time and proximity, transition to indoor activity, pre-competition acclimation, monitoring air quality when choosing location, and the use of masks and supplements. In addition, special considerations should be made for the unique exposures and challenges faced by populations, such as warfighters, para-athletes, or those living in disadvantaged communities [62]. 

Potential adverse consequences of exposure to air pollutants during exercise include decreased lung function, and exacerbation of asthma and exercise-induced bronchoconstriction.  The availability of high time-resolved exposure data in the stadiums opens up the possibility to calculate doses of specific pollutants for individual athletes in future athletics events, to understand the impact of environmental factors on athletic performance [63].

The case for action to reduce air pollution is overwhelming and this action can take many forms. Some of these include urban planning, technological developments (e.g. the design of new vehicles that produce less pollution), and at the government level, the introduction of new laws. It has been estimated that reducing both black carbon and O3 levels would prevent over 3 million premature deaths and increase crop yields by around 50 million tons annually. Improvements to cooking stoves would also decrease demand for firewood and reduce deforestation in the developing world [5]. Similarly, improved brick kilns that are used in parts of Latin America and Asia use 50% of the fuel used by traditional kilns [5,64]. If air pollution levels in heavy traffic areas were reduced, the incidence of asthma and other respiratory diseases would be significantly reduced [5,65]. While it is generally accepted that efforts to reduce air pollution will prevent further environmental changes, they will not reverse existing warming [5]. Totally different model schemes are needed to quantitatively address indoor air pollution and inhalation exposure [3].

Policy analyses and decisions draw on the evidence integration and findings and may incorporate risk and cost assessments to determine the optimal policy action. Surveillance studies assess the policy impact (e.g., change in air pollution levels or reduction of adverse health outcomes) and provide guidance on what additional research is needed to make the policy action more effective [66]. A study, urge priority for advancing research and technical capacity in this context, emphasizing the foundation of monitoring air quality and health data systems and building a cadre of researchers, informed and empowered citizens, and policy-makers who will work together towards cleaner air for all [66]. 

Another study recommended research on the most effective policies to promote switching from biomass burning to cleaner home-heating systems, supplementing existing routine network data with additional chemical speciation to facilitate identification of source contributions, and on consumer products that emit volatile organic compounds, and quantifying the potential health benefits of switching from cooking with natural gas to cleaner cooking methods (e.g., induction stoves) [67]. 

It is crucial to consider air quality as a key element in optimizing the positive effects of exercise and reducing potential health hazards. Policymakers should enforce stricter vehicle emission regulations, and expand real-time air quality monitoring networks to provide accurate pollution data for residents. From a healthcare perspective, professionals should incorporate air quality considerations into exercise recommendations, particularly for vulnerable populations, including individuals with pre-existing cardiovascular or respiratory conditions [60]. 

Taking dietary supplements or medications with antioxidant or anti-inflammatory properties has the potential to provide at least partial protection against air pollution-induced adverse health effects in those individuals who are known to be most susceptible, namely those with pre-existing respiratory and cardiovascular diseases [68]. 

Also, to design research on other products for possible benefit such as Sirtuin1 (SIRT1), a Chinese herbal medicine has many biological activities, exerting anti-inflammatory, anti-oxidation, anti-tumor, and immune regulatory effects relate to lung aging, such as genomic instability, lung stem cell exhaustion, mitochondrial dysfunction, telomere shortening, and immune senescence [69], or other pharmacologic intervention. Better conducted epidemiological studies is necessary to establish adverse outcomes of indoors and outdoors exposure methods, outcome detection to consider implementing strategies for integrated intervention for pollution production restrictions and introduce the safe level of air quality for physical activity. Measures as high-efficiency particulate air (HEPA) filtration, increase greenspace areas, healthier travel options, and education of people for regarding public health and safety preservation of environment are warranted.