Keywords

1 Introduction

Ambient air pollution is a major global public health problem which affects both developing and developed countries. Nowadays, energy is derived from natural and inexpensive sources for industrial, commercial, and living purposes in many developing countries. However, technologies to mitigate potential air pollution arising from these energy utilizations are limited. For example, refinery emissions are released from different steps of production line, and a typical oil refinery can emit about 50 different atmospheric air pollutants. In addition, some accidental activities such as spillage, venting, decommissioning, and loading of products are also potential sources of gaseous emissions. According to the World Health Organization (WHO) Ambient Air Pollution database which is collected from 1,600 cities in 91 countries, almost 9 out of 10 individuals living in urban areas are affected by air pollution. The WHO has also estimated that each year ambient (outdoor) air pollution causes 3.7 million premature deaths worldwide (http://www.who.int/), with 40,000-50,000 of which occurring in the United States and 300,000 in China. Most of these deaths are from acute and chronic cardiopulmonary events in clinic. Additionally, it has been demonstrated that exposure to air pollution could worsen existing cardiopulmonary diseases and induce metabolic disorder. In this chapter, the current state of knowledge as to the sources of ambient air pollutants and how air pollution is associated with cardiopulmonary and metabolic diseases are discussed. The chapter will mainly discuss evidence from epidemiologic, controlled human, and animal toxicological studies.

2 Main Ambient Air Pollutants

Current air pollution frequently found in urban areas is a dynamic and complex mixture of pollutants from both human-made (anthropogenic) and natural sources. Five main ambient air pollutants are particulate matter (PM), ozone (O3), sulfur dioxide (SO2), nitrogen oxides (NOx), and carbon monoxide (CO). Unlike coarse particles commonly caused by disturbances of crustal materials (dust), fine particles are mainly formed through industrial processes and from traffic-related sources (gasoline and diesel), coal and oil fuel combustion, farming, and road construction. Fine particulate pollution is particularly prevalent in Asia, where biofuel combustion for heating and cooking produces great amounts of fine PM.

Owing to the complexity of its chemical structure and the temporally changing characteristics of the compounds within ambient air, PM is broadly categorized and regulated by aerodynamic diameter (μm). According to the size, PM is commonly subdivided into three classifications: coarse PM with diameters 2.5-10 μm (PM10), fine particles with diameters less than 2.5 μm (PM2.5), and ultrafine particles with diameters less than 0.1 μm (PM0.1). There are thousands of chemicals and constituents within PM that may solely, or in combination, pose biological hazard. However, the actual “responsible” components remain largely unknown. Nonetheless, it is generally believed that the myriad of compounds that pose intrinsic redox potential (e.g., metals and organic compounds) and/or those capable of activating endogenous sources of oxidative stress within pulmonary tissue (e.g., immune cells) are likely to be the instigators, rather than inert particles (e.g., elemental carbon) [1].

Additionally, with global climate alteration and enlargement of urban centers, it is estimated that ground-level ozone is becoming an even more serious health hazard. Ozone smog forms when NOX and volatile organic compounds from vehicle, power, and other sources mix with sunlight and heat. Other pollutants (CO, NOX, and SO2), mainly produced by fossil fuel combustion and traffic emission, also contribute to air pollution in large urban areas, especially in dense cities in Asia.

Indoor air pollution is also a source of air pollutants, including environmental or second-hand smoke, incomplete combustion of household heating and cooking solid fuels, residential fitment-derived formaldehyde, and volatile organic compounds. Based on the time spent indoors, its contribution to human exposure could be relatively high. In the United States, these primary air contaminants are classified as “criteria” pollutants by the Environmental Protection Agency (EPA), and EPA’s National Ambient Air Quality Standards (NAAQS) have been set for each of these pollutants. Actually, these pollutants are present in other countries at different levels. Since these pollutants are closely associated with adverse human health, an extensive literature review should be updated every 5 years to ensure adequate health protection of the public.

3 Association Between Air Pollution and Pulmonary Health Effects

The human respiratory system develops from in utero to adolescence and more than 80% of new alveoli formed in the first 6 years of life following birth. Due to the immature detoxification and metabolic systems, as well as frequent exposure to outdoor air, children are generally more susceptible to airway toxicants than adults. In the elderly, function of particle clearance is usually less efficient or impaired. Thus, old and young populations are more susceptible to inflammation and respiratory complications induced by air pollution.

It has been demonstrated that environmental exposures adversely affected the development of both immune function, lung mechanics, and lung repairment after injury [2]. In addition, those air pollutants-induced adverse effects in the lung include disruption of airway epithelial barrier and cellular signaling pathways, oxidative stress, impairment of phagocytosis, parenchymal destruction, deregulated cell immunity, inflammatory cell infiltration, epigenetic modifications, and autophagy (Fig. 1) [3,4,5,6,7,8,9,10]. These effects are involved in the following respiratory diseases.

Fig. 1
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Working model of air pollutants in the respiratory tract and cells [10]. Abbreviations: PAH polycyclic aromatic hydrocarbon, IFN interferon, IL interleukin, GM-CSF granulocyte macrophage-colony stimulating factor, TSLP thymic stromal lymphopoietin, VEGF vascular endothelial growth factor

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3.1 Air Pollution and Asthma

Asthma is characterized clinically by intermittent symptoms of wheezing, dyspnea, and cough with some degree of persistent airflow obstruction. Recently, a series of studies demonstrated that air pollution contributed to increased asthma prevalence and symptom onset. Open fires for cooking are still used in many developing countries or regions (e.g., rural China, India, and Malawi), and coal combustion for heating and cooking conferred higher risks of childhood asthma in China [11]. In addition, indoor air pollution, including environmental tobacco smoke and chemical emissions from new furniture was one of the risk factors for asthma, wheeze and daytime breathlessness amongst pupils [12, 13]. According to a large body of epidemiological evidence, exposure to ambient ozone, nitrogen dioxide, PM2.5, and sulphur dioxide was associated with increased asthma exacerbations and hospital admissions [14, 15]. Exposure to PM2.5, PM10, ozone, and NO2 were also found to be associated with a lower forced expiratory volume in the first second (FEV1) and forced vital capacity (FVC) or exacerbated allergic inflammation in children [16,17,18]. Hua et al. suggested that black carbon conferred greater asthma admission risks than PM2.5, with a maximum of a 3-day lag for children in Shanghai, even after stratification by sex, age, and season [19]. These observations were further supported with evidence from mechanism studies and animal experiments. For example, Ozone and SO2 were shown to cause oxidative stress and affect the airway inflammatory and immune responses in laboratory animals [20, 21]. Moreover, although the relationship between air pollution and adult-onset asthma still remains unclear, a large European study conducted in 23,704 adults from eight countries with a 10-year follow-up further suggested that exposure to traffic-related air pollution containing PM2.5 might increase asthma incidence in adults [22].

3.2 Air Pollution and Chronic Obstructive Pulmonary Disease

Air pollution and chornic obstructive pulmonary disease (COPD) is most commonly associated with smoking, but the prevalence of COPD among nonsmokers varies from 1.1% to 40% in different countries [23]. Other risk factors for COPD include occupational exposures and air pollution. Studies demonstrated that indoor/outdoor air pollution and second-hand tobacco smoke contributed to the high incidence of COPD among nonsmokers. In China, development of COPD, especially in rural areas, was attributed to household pollutants, such as coal and wood smoke. The use of improved household stoves in Xuanwei (Yunnan province) resulted in a lower risk of COPD in males (RR 0.58; 95% CI: 0.49-0.70) and females (RR 0.75; 95% CI: (0.62-0.92) than that in lifelong unimproved household stove users [24]. In addition, a longitudinal cohort study also demonstrated that improved ventilation along with clean fuels (biogas instead of biomass) usage was associated with lower OR (0.28) of development of COPD and slower decline in FEV1 when compared with either single improvement of ventilation or changing clean fuels, or neither [25]. Downs et al. demonstrated that decline in PM10 concentration may actually lead to an attenuated impairment in lung function in adult patients [26]. Moreover, data from a global analysis showed that dose–response relationships between air pollutants and COPD mortality were nonlinear and air pollution might induce long-lasting adverse effects on COPD mortality, with mortality risks increasing rapidly at relative lower PM2.5 levels (<100 μg/m3) and reaching a plateau at higher levels (>300 μg/m3) [27].

3.3 Air Pollution and Lung Cancer

Cigarette smoking is a well-known important factor of lung cancer. Recent studies support the role of air pollution in the development of lung cancer. Yu et al. observed somatic genomic mutations in tumor, adjacent normal lung tissues, and peripheral blood samples from 164 non-small cell lung cancer patients from regions with higher levels of air pollutants compared with patients from other regions with lower levels of air pollutants [28]. In addition, air pollution from solid fuel (e.g., coal and wood) combustion predisposes to lung cancer too. An epidemiological study found that a 10 μg/m3 increase in 2-year average level of household PM2.5 derived from coal combustion was correlated with an elevated risk of lung cancer in males (RR: 1.06; 95% CI: 1.04-1.07) and females (1.15; 1.12-1.18) [29]. Smoky coal is used to be a major source of fuel in rural China such as Xuanwei. A study demonstrated that lung cancer mortality is very high in Xuanwei, indicating smoky coal may confer greater risks than non-smoky coal or other fuels [30].

Based on data from human, animal, and mechanistic studies, the International Agency for Research on Cancer declared outdoor air pollution and related PM as a Group I human carcinogen in October 2013. Consistent with it, a recent study conducted in male drivers aged 30-59 years between 1999 and 2011 found professional drivers exposed to diesel engine exhaust had an elevated risk of lung cancer. The authors suggested that the proportionate cancer incidence ratios for lung cancer in professional drivers increased significantly (1.20, 95% CI: 1.13-1.26) during the study period, and that adjustment for the effect of cigarette smoking did not change the associations (1.09, 95% CI: 1.03-1.15). The increased risk was consistent throughout study years and age categories [31]. In addition, a meta-analysis showed that ambient exposure to nitrogen oxides, SO2, and PM2.5 from vehicle emissions significantly increased the risk of lung cancer [32]. Another study indicates that polycyclic aromatic hydrocarbons (PAH) derived from smoky coal burning may also be related with lung cancer [30]. The potential mechanism of lung carcinogenesis remains further study.

4 Association Between Air Pollution and Cardiovascular Disease

The cardiovascular or circulatory system delivers blood to organs and tissues. It consists of the heart, arteries, veins, and capillaries. Cardiovascular disease (CVD) is the number one cause of death in developed nations and is the leading cause of years of life lost due to morbidity and mortality globally [33]. Vascular dysfunction, diabetes, physical inactivity, and smoking have been well described as risk factors for CVDs. Recently, association of air pollution exposure with CVD aroused emerging attention [34]. Two landmark cohort-based mortality studies, the Harvard Six Cities and the ACS (American Cancer Study) studies, reported in the mid-1990s demonstrated that air pollutants (e.g., PM2.5 and sulfate) were associated with increase in all-cause and cardiopulmonary diseases. In both studies, PM air pollution-related mortality was substantially higher for cardiovascular than for pulmonary-related diseases [35, 36]. As air pollution is a modifiable risk factor, elucidation of its adverse cardiovascular effects would provide more evidence for the government to adopt a policy on reducing air pollution levels and providing health care.

4.1 PM and CVD

Due to the small size, PM2.5 and PM0.1 are inhaled deeply into the lungs, followed by depositing in the alveoli and entering the pulmonary and systemic circulation. Thus, the role of PM as a risk factor to CVD has been well established. Scientific studies have linked increases in daily PM2.5 exposure with increased cardiovascular morbidity and mortality. Exposure to ambient air-borne PM2.5 is associated with increased incidences of specific acute CVDs, such as cardiac arrhythmia, atrial fibrillation, ischemic stroke, heart failure, myocardial infarction, as well as peripheral arterial and venous diseases. Multiple studies also have found the significant associations between PM2.5 exposure and elevated blood pressure or decreased heart rate variability (HRV) [37]. However, the relationship between PM10 and CVD is still controversial, for studies demonstrated that after adjustment for PM2.5, there were no statistically significant associations between coarse PM and hospital admissions for CVD or changes in HRV [38, 39]. Table 1 summarizes representative cardiovascular effects of PM in some largest short-term or long-term studies.

Table 1 Summary of representative studies on short-term or long-term cardiovascular effects of PM air pollution
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Potential mechanisms involved in PM-mediated CVD progression include systemic inflammation, oxidative stress, increased blood coagulability, alterations in autonomic balance, and vascular dysfunction [50]. First, pollutants may induce autonomic nervous system (ANS) imbalance favoring sympathetic over parasympathetic tone, which may be prompted by lung irritant sensory receptors and afferent nerve stimulation. Second, air pollution could cause the release of vasculo-active molecules [e.g., histamine or endothelin] or endogenous proinflammatory mediators (e.g., cytokines IL-6 or IL-1) from lung cells and activated immune cells that have been shown to “spill-over” into the systemic circulation, resulting in detrimental vascular effects. Third, some soluble constituents such as metals or nano-sized particles could translocate across the alveolar membrane and gain access to the bloodstream and directly influence the vascular endothelium. The relevance of each pathway may vary depending upon susceptibility of the individuals and pollutants characteristics, and these pathways are likely to overlap to some degree in their adverse actions. In sum, air pollution can induce cardiovascular detriment in a biphasic manner consisting of an initial response within minutes-to-hours (due to acute ANS imbalance) and a subsequent arterial vasoconstrictor responsiveness via endothelial dysfunction, oxidative stress, and inflammation [50].

4.2 O3 and Cardiovascular Diseases

O3 is the primary oxidant of concern in photochemical smog due to its inherent bioreactivity. It is a bluish, explosive, irritating, and highly toxic gas. So far, effects of ground-level O3 on the CVD are still controversial. Although no associations were observed in studies conducted in Tucson, Arizona, London, the United Kingdom, Edinburgh, and Scotland, a positive association between O3 and ischemic heart disease was observed in Helsinki, Finland [51,52,53]. O3 has a high oxidizing power by reacting with biomolecules to form ozonides and free radicals. This process triggers an inflammatory response in the body, which induces adverse effects in both pulmonary and cardiovascular systems. According to Srebot et al., pulmonary oxidant stress mediated by PM and/or O3 exposure resulted in downstream perturbations in the cardiovasculature, as the pulmonary and cardiovascular systems were intricately associated [54]. Mechanisms by which ground-level O3 exposure induced cardiotoxicity have been explored, which include modification of endothelial function, vascular angiotasis, alterations in autonomic control of cardiac frequency, activation of systemic inflammatory response mediated by cytokines, and increase of oxidative stress. In a randomized, double-blind, crossover chamber study by Brook et al., O3 caused acute arterial vasoconstriction in healthy adults with altered macrovascular diameter and tone [55]. Ambient levels of O3 pollution may lead to short-term autonomic imbalance, as evidenced by reduced high-frequency component of HRV, with patients in hypertension being particularly susceptible to this effect [53]. In addition, stimulation of peripheral human blood mononuclear cells with O3 induces increase in lipid peroxidation and protein thiol group content.

4.3 NO2 and CVD

NO2 is a gaseous chemical and a member of nitrogen oxides. The harmful health effects of NO2 may potentially result from NO2 itself or its reaction products such as O3. Previous studies have reported that exposure to higher concentration of NO2 was associated with daily hospital emergency for ischemic heart diseases, as well as for subsequent cardiac insufficiency and arrhythmia. For instance, Mar et al. has reported that an interquartile range increase in NO2 was associated with an increase of 6.1% of cardiovascular mortality [56]. The cardiovascular effects of NO2 were mainly observed in patients with CVDs aged 65 years or older who had high risks of atherogenesis [57]. Additionally, Takano et al. found that daily exposure to ambient level (0.16 ppm) of NO2 could enhance atherogenic lipid metabolisms primarily in the Otsuka Long-Evans Tokushima Fatty (OLETF) rats, but less in the Long-Evans Tokushima Otsuka (LETO) rats, which suggested that ambient NO2 air pollution was an atherogenic risk primarily in obese subjects [58].

4.4 SO2 and CVD

SO2 is a colorless, highly soluble, and chemical irritant. Interestingly, SO2 is a two-edged sword. In one hand, SO2 is an endogenous gaseous signaling molecule involved in the regulation of cardiovascular functions [59]. In the other hand, SO2 is considered to be toxic and detrimental to human health. For example, previous study has suggested that daily exposure to SO2 pollution might play an independent role in triggering ischemic cardiac events in Europe [60]. Blood viscosity is a risk factor of CVD. A positive association of CVD incidence with increased levels of ambient total suspended particles and SO2 was observed as well [61].

4.5 CO and CVD

CO is an odorless gas that causes thousands of deaths each year in North America. Evidence from human studies has shown that CO typically affects oxygenation of tissue by production of carboxyhemoglobin (COHb), which subsequently results in adverse cardiovascular effects, such as exacerbating the ischemic heart disease. The harmful effects of CO are more profound in the myocardium than in peripheral tissues due to the high oxygen extraction by the myocardium at rest [62]. In addition, exposure to CO has been implicated in the process of atherosclerosis.

5 Other Air Pollutants and CVD

Other air pollutants, including cigarette smoke, biomass smoke, and lead pollution were also reported to contribute to the development of CVD. As a well-established risk factor for CVD, cigarette smoking is associated with a number of clinical atherosclerotic syndromes, including sudden death, acute coronary syndromes, stable angina, and stroke. Smokers who inhale deeply are more likely to have an increased risk of both abdominal aortic aneurysm and symptomatic peripheral arterial disease. Household burning of solid fuels releases several pollutants including inhalable PM, PAHs, heavy metals, and many other organic pollutants, which have been linked to CVDs [63]. The cardiovascular effects of lead exposure include elevation of blood pressure, hypertension, coronary heart disease, stroke, and peripheral arterial disease, as well as other cardiovascular function abnormalities including left ventricular hypertrophy and alterations in cardiac rhythm [64].

6 Association Between Air Pollution and Metabolic Diseases

6.1 Air Pollution and Diabetes Mellitus (DM)

Type 2 diabetes mellitus (T2DM) affects approximately 9% of the global population and accounts for 2.7% of global deaths (WHO, 2012), and the number is expected to increase to 592 million by 2035 [65], with the sharp increases occurring in low- and middle-income countries. Epidemiologic studies have uncovered a number of factors for the risk of metabolic disorders, including changes in lifestyle factors due to urbanization, such as reduced physical activity, overnutrition, lack of sleep, and alterations in light cycle. Recently, there is cumulative evidence of the association between air pollution exposure and T2DM. PM2.5 and other air pollutants exaggerate insulin resistance and the development of T2DM. Table 2 summarizes a number of representative studies concerning a positive association between long-term ambient air pollution exposure and increased risk of T2DM.

Table 2 Epidemiological associations among air pollutants, diabetes, and diabetes-associated mortality
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  • Gestational diabetes

Women who experience gestational diabetes are at a higher risk for subsequent T2DM. Previous studies have demonstrated that air pollutants might have the potential to affect gestational diabetes development too. A large retrospective cohort including 219,952 singleton deliveries showed exposure to higher levels of NOx and SO2 during the 3 months preconception was related to higher relative risks for gestational diabetes in women [76]. The results were consistent when considering only air pollution exposures that occurred during the first trimester. Consistent with it, a dose–response relationship was also found in a Swedish study linking registry data from 81,110 pregnancies with individual NOx exposure [77]. However, a study conducted in Taiwan demonstrated that exposure to O3 might lead to more preterm births in women with gestational diabetes [78]. With O3 air pollution getting more serious, further exploring the effects of O3 exposure on maternal metabolism and offspring are necessary.

  • Precursors of T2DM

Exposure to ambient air pollution is also associated with predisposing conditions for diabetes. In 9,102 newly diagnosed T2DM patients in Germany, higher regional levels of PM10 were associated with higher HbA1c concentrations, a biomarker of the average blood glucose levels in an individual during the initial 30-120 days [79]. Adverse effects of several pollutants on HbA1c and fasting glucose concentrations were also observed in an elderly population in Taiwan [80]. Insulin resistance is another potential precursor of T2DM, which could lead to elevated fasting glucose accompanied by elevated insulin levels due to impaired insulin action. Previous study conducted among 560 elderly individuals in Korea showed that short-term exposure to NO2 was associated with elevated homeostatic model assessment of insulin resistance (HOMA-IR) in participants without a history of diabetes. For participants with diabetes, especially for those carrying risk genotypes in the oxidative stress-related human glutathione S-transferase genes (GSTM1, GSTT1, and GSTP1), PM10, NO2, and O3 were all associated with increased HOMA-IR [81]. In addition, long-term exposure to NO2 and PM10 or short-term exposure to PM10 and CO were associated with elevated HOMA-IR in healthy children aged from 10 to 18 years [82], with increased inflammation and oxidized low-density lipoprotein.

6.2 Air Pollution and Obesity

Obesity is becoming a major global public health problem and consumes substantial social resources. The prevalence of obesity more than doubled among the American adults from 1976-1980 to 2013-2014. The global obesity prevalence is expected to exceed 21% in women and reach 18% in men by 2025 [83].

Interestingly, several mechanisms may link unhealthy body weight to air pollution, which is likely to be highly complex and differ across subpopulation (e.g., adults versus children), severity, and type of pollution. Air pollution could increase oxidative stress and adipose tissue inflammation, induce hepatic lipid accumulation, and decrease glucose utilization in skeletal muscle, which may result in metabolic dysfunction [84, 85]. In addition, air pollution may indirectly prevent people from engaging in regular physical activity by inducing cardiovascular and respiratory symptoms (e.g., decreased lung function and elevated blood pressure) and impairing exercise performance. Emerging evidence demonstrates that air pollution level is negatively associated with physical activity and/or positively associated with leisure-time physical inactivity. A unit (μg/m3) increase in ambient PM2.5 concentration was associated with an increase in the odds of physical inactivity by 1.1% among the U.S. adults [86]. Participants, in particular those with respiratory diseases, self-reported a reduction in outdoor activities to mitigate the detrimental impact of air pollution. Indeed, smog appearance could also discourage people from engaging in outdoor activities [87].

6.3 Mechanistic Insights into Air Pollution and Diabetes

A number of mechanisms have been proposed for extrapulmonary effects of inhaled pollutants. On the basis of experimental studies examining the metabolic effects of ambient PM in mouse models, studies suggested that systemic inflammation, oxidative stress, ER stress, and neuronal mechanisms might be involved in insulin-sensitive organs [88, 89].

In the visceral adipose tissue, PM2.5 exposure might induce shift of adipose tissue macrophages to a pro-inflammatory phenotype (M1) characterized by increase in TNF-a and IL-6, and decrease in IL-10 gene expression [90]. In the same study, a transgenic model of yellow-fluorescent protein expression restricted to monocytes (c-fmsYFP) rendered insulin resistant with high-fat diet, and exposure to PM2.5 could result in doubling in the number of endothelial adherent YFP+ cells in mesenteric fat with a sixfold increase in monocytes within adipose [90]. Thus, PM mediates migration and adhesion of YFP+ cells in visceral fat depots. In another study, a CCR2 KO model was exposed to PM2.5, increased number of immune cells [F4/80+ (macrophage) or F4/80+/CD11c+ (M1 macrophage)] in visceral adipose tissue in response to PM2.5 exposure was ablated by CCR2 deficiency, suggesting a dependence of PM2.5 on CCR2 in recruitment of innate immune cells [85].

The central nervous system (CNS) plays a critical role in energy balance with multiple environmental and internal signals serving as cues to trigger the requisite behavioral and physiological response to maintain energy homeostasis. Interestingly, PM2.5 exposure could induce hyperglycemia and insulin resistance, which is accompanied by increased hypothalamic IL-6, IKKβ, and TNFα mRNA expression and microglial/astrocyte reactivity. Targeting the NF-κB pathway with intra-cerebroventricular administration of an IKKβ inhibitor improved insulin sensitivity, glucose tolerance, reduced peripheral inflammation, and rectified energy homeostasis in response to PM2.5 [91]. Intra-cerebroventricular administration of IMD-0354 (an IKKβ inhibitor) inhibited the expression of the enzymes for gluconeogenesis and lipogenesis in the liver [92]. Thus, hypothalamic inflammation plays a key role in PM2.5 exposure-mediated peripheral inflammation, exaggeration of type II diabetes, hepatic glucose, and lipid metabolism disorder.

How may air pollutants induce CNS inflammation and secondarily lead to systemic metabolic disorder? For the most widely studied air pollutants, evidence supports the hypothesis that exposure to PM components of air pollution, ozone, or other gas upon inhalation can oxidatively modify surfactant lining and cellular components. Such exposure can also induce stress response to injury through direct sympathetic stimulation, activation of hypothalamus–pituitary–adrenal axis, and subsequently releasing of hormones from the adrenal cortex. These processes may trigger a release of free fatty acids, glucose, and branched-chain amino acids into the circulation (Fig. 2). A variety of systemic inflammatory and homeostatic metabolic mechanisms might be involved in neurohormone regulation, and these factors are involved in insulin resistance, dyslipidemia, and glycemia.

Fig. 2
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Potential mechanisms involved in air pollution-induced insulin resistance and diabetes [89]

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7 Targets for Intervention

Instead of a local or regional problem, air pollution now is recognized as a global issue with potential long-distance atmospheric transportation and rendering health implications. Most importantly, there is no threshold for exposure to particulate air pollution below which exposure is safe. It indicates that individuals are always at risk for adverse events, whether they reside in polluted areas or communities in compliance with EPA’s NAAQS. Therefore, apart from strengthening efforts to guarantee air quality compliance with the NAAQS, we might take effective interventions to mitigate the adverse health outcomes of exposure to air pollution for susceptible populations living in areas with high pollution. For instance, personal indoor PM exposure can be minimized by using particulate air filters, air conditioning, avoiding use of indoor combustion for heating and cooking, and smoking cessation. Susceptible groups may benefit from limiting their outdoor exercise during poor air quality days. Since air pollution remains a complex mixture of anthropogenic pollutants and natural sources, it is essential that local, national, and global efforts are undertaken by government, enterprises, and individuals to lessen the burden of air pollution and provide better health protection. Effective measures to reduce exposure to air pollution, both at organizational and personal level (Table 3), could lead to substantial healthy benefit.

Table 3 Personal- and organizational-level interventions to reduce exposures or susceptibility to air pollution
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8 Conclusion

Growing bodies of evidence have demonstrated modest increase in risk of cardiopulmonary and metabolic diseases associated with exposure to major air pollutants. The increase in the relative risk for these adverse health outcomes due to air pollution for an individual is relatively small compared with other established risk factors, such as diet, physical activity, and behavior. Given the ubiquitous nature of air pollution and the economic costs of cardiopulmonary and obesity/DM-related diseases, even conservative risk estimates would still translate into a substantial increase in the population attributable fraction of public health problem related to air pollutants. Additional research is therefore needed to confirm the currently available evidence and to explore the impact of air-borne pollutants in populous cities of developing countries. Further investigations on effective interventions that improve air quality and attenuate the adverse effects are therefore warranted.