The Impact of Environmental Pollution and Climate Change on Allergic Rhinitis and Lung Diseases

ABSTRACT

Environmental pollution and climate change seriously affect human health, leading to the onset and exacerbation of chronic respiratory diseases, such as allergic rhinitis and lung diseases. Over the past several decades, increasing air pollution and environmental exposure owing to global urbanization, industrialization, and rapid economic growth have led to an increase in the prevalence of allergic and respiratory diseases. Allergic rhinitis and lung diseases are global health problems affecting people of all ages. This article summarizes the effects of environmental pollution and accompanying climate change on allergic rhinitis and lung diseases and discusses the interactions between the pathogenesis of allergic rhinitis and lung diseases and environmental pollution. The molecular mechanisms of allergic rhinitis and lung diseases and their common features are discussed. The prevention and control measures of allergic rhinitis and lung diseases caused by air pollution and climate change are described. Given that climate change could bring about numerous unforeseen and enduring impacts on allergic respiratory conditions, healthcare practitioners ought to champion efficient measures for mitigation and adaptation to curtail its adverse effects on respiratory health.

1. Introduction

Owing to the rise in global industrialization, the primary cause of urban air pollution is the discharge of waste gases from factories and particles released by motor vehicles. These particles combine with gaseous elements in the atmosphere, which can cause significant harm to the respiratory, cardiovascular, and immune systems of people [1]. Over the past few decades, the increased air pollution and environmental exposure associated with global urbanization, industrialization, and rapid economic growth have resulted in an increasing incidence of allergic respiratory diseases [2, 3].

Allergic rhinitis is a chronic noninfectious inflammatory disease of the nasal mucosa that is mainly mediated by allergen‐specific immunoglobulin E (IgE) and involves a variety of immune cells and cytokines in atopic individuals after exposure to allergens [4]. A growing body of evidence suggests that air pollution contributes to the increased incidence of allergic rhinitis as well as the onset and worsening of symptoms in individuals sensitized to airborne pollen [5, 6, 7].

Respiratory system diseases are common and frequently occurring diseases that seriously affect human health. Many factors affect death from respiratory diseases, including tobacco exposure (active or passive exposure to secondhand smoke), occupational exposure (dust, smoke, or chemicals), air pollution, and severe respiratory infections. The combination of these factors can lead to worsening symptoms or death in patients with respiratory disease [8, 9].

2. Air Pollutants

Air pollutants include both indoor and outdoor pollutants, as shown in Figure 1. Indoor pollutants include mainly fine dust particles, microorganisms, and chemical substances, while outdoor pollutants include solid and gaseous substances. Solid pollutants are particle‐like matter divided into inhalable particulate matter (PM10) and fine particulate matter (PM2.5) according to their diameter [10].

Figure 1.

Classification of air pollutants.

2.1. Indoor Air Pollutants

Various factors affect the composition of indoor air, including outdoor pollutants, ventilation quality and quantity, indoor allergens, and activities such as smoking, heating, and cooking [11].

2.1.1. Environmental Tobacco Smoke

Environmental tobacco smoke, also known as passive or second‐hand smoke, is the main indoor air pollutant and results mainly from nonsmokers being exposed to tobacco combustion products emitted by others. Tobacco smoke comprises at least 4500 toxic chemical compounds, including particulate matter, oxidative gases, heavy metals, and 50 carcinogens [12]. Nonsmokers exposed to tobacco smoke face considerable health risks in different microenvironments, such as households or workplaces. Recently, pyrosynthesis and cigarette combustion associated with indoor smoking have been identified as significant factors contributing to elevated levels of particulate matter and toxic chemical agents within households [13]. In poorly ventilated homes of smokers, PM2.5 concentrations may be 10 times greater than those in nonsmoking homes [14, 15], and approximately 40% of children and one‐third of adults worldwide are exposed to long‐term environmental tobacco smoke [16]. Epidemiological studies have shown that tobacco smoke is significantly associated with the incidence of allergic rhinitis [17, 18, 19]. Active and passive smoking are negatively correlated with lung function in adults, with smoking being a risk factor for reduced lung function [20].

Grillo et al. [21] reported that tobacco exposure can lead to an increase in interleukin‐33 (IL‐33) levels, which can promote the activation of inflammatory cells and indirectly drive immune regulation, resulting in inflammation and an immune response, leading to an increase in eosinophils, collagen production, and airway remodeling [22]. Tobacco smoke can cause changes in Toll‐like receptor levels, increase the susceptibility of T‐helper 2 (Th2) cells in the complement system, and cause allergic rhinitis [17]. Environmental tobacco smoke can reduce the activity of natural killer (NK) cells and Th1 cytokines, and a decrease in Th1 function may lead to a decrease in respiratory anti‐infection ability, which may be related to cancer incidence [23], as described in Figure 2. A 2020 study of college students and faculty members revealed that tobacco smoke increases nasal resistance and exacerbates the inflammatory response in people with allergic rhinitis and that exposure to tobacco smoke may also increase airborne allergen sensitization and worsen the symptoms of allergic rhinitis [24]. Tobacco smoke can reduce the oscillation frequency of ciliary cells in the human respiratory tract and weaken its self‐purification ability [25]. Smoking contributes to increased platelet viscosity, reduced levels of high‐density lipoprotein cholesterol, diminished distensibility and compliance of large arteries, and other pathological and biochemical changes that can adversely affect pulmonary gas exchange [26]. Both lung function impairment and lung cancer are associated with genetic backgrounds with genetic variants that regulate tobacco dependence [27]. Smoking is the most significant exogenous factor known to affect the level of genomic DNA methylation [28]. As a “bridge” connecting genes, environment, and disease, epigenetics has great potential in explaining the common pathogenesis of COPD and lung cancer. The abnormal genomic DNA methylation patterns caused by smoking may be the biological basis of the occurrence of diseases [29]. In recent years, the CpG sites reported in the EWAS studies of lung function levels and lung cancer have been found to be associated with smoking. Imboden's group performed EWAS analysis of lung function levels and their changes using a two‐stage discovery (2043 adults) and validation (3327 adults and 420 children) population‐based study design, and found and validated 57 DNA methylation sites significantly associated with lung function in adults. We found that these lung function‐related DNA methylation sites were closely associated with smoking, and the aryl hydrocarbon receptor inhibitor methylation level was significantly associated with reduced lung function [30].

Figure 2.

Tobacco exposure can lead to an increase in interleukin‐33 (IL‐33), which can promote the activation of inflammatory cells, indirectly drive immune regulation, cause inflammation and an immune response, and can lead to an increase in eosinophils, collagen production, and airway remodeling. Tobacco smoke can cause changes in Toll‐like receptor expression, increase the susceptibility of T helper 2 (Th2) cells in the complement system, and cause allergic rhinitis. Tobacco smoke can reduce the activities of natural killer (NK) cells and Th1 cytokines, and decreased Th1 function can lead to decreased resistance to respiratory infection.

2.1.2. Volatile Organic Compounds

Indoor pollutants, such as nitrogen dioxide (NO₂), carbon monoxide (CO), and certain volatile organic compounds (VOCs), such as formaldehyde, are also significant contaminants [31]. Indoor environmental pollutants include VOCs commonly found in paint, fabric, wood, cleaning products, cosmetics, air fresheners, furniture, and flooring. These compounds can be released into indoor environments as the temperature increases, with formaldehyde, acetaldehyde, polycyclic aromatic hydrocarbons, and benzene being the most prevalent substances [32].

Previous studies have shown that exposure to VOCs is associated with the development of allergic rhinitis and can worsen allergic rhinitis symptoms [33, 34]. In America, the incidence of allergic asthma in children exposed to VOCs was 2.6 times greater than that in unexposed families [35]. In France, 20 different VOCs were examined in main residential areas and more than 1000 long‐term residents were surveyed using a standardized questionnaire. The results revealed a positive correlation between VOC scores and the incidence of allergic rhinitis and asthma [36]. Wang et al. showed that polyethylene exposure could increase the secretion of inflammatory mediators such as IL‐4 and γ‐interferon in mice, increase the level of total IgE and sIgE in the serum, and aggravate respiratory allergic reactions [37]. VOCs can bind with endogenous proteins, such as haptens, to induce immune responses, and some volatile gases can also produce immune adjuvants, which increase the body's responsiveness to allergens and aggravate the symptoms of allergic reactions [38]. Bonisch et al. [39] reported that exposure to VOCs could enhance allergic reactions by disrupting the function of dendritic cells and inducing oxidative stress. This type of exposure is also a risk factor for allergic diseases. The expression of cell adhesion molecule‐1 and vascular intercellular adhesion molecule‐1 can be increased by exposure to formaldehyde. Vascular intercellular adhesion molecule‐1 and vascular intercellular adhesion molecule‐1 contribute to the activation and aggregation of eosinophils, resulting in the aggravation of allergic symptoms [40]. The association between VOC and COPD might be mediated by oxidative damage or systemic inflammation. A previous study suggested that increased C‐reactive protein, a marker of systemic inflammation, significantly mediated 5.39% and 5.87% of the N‐ace‐S‐(N‐methlcarbamoyl)‐l‐cys (AMCC)‐associated forced vital capacity and forced expiratory volume in 1 s declines, respectively [41]. Other studies have also demonstrated that the decline in lung function due to single VOC metabolite is partly mediated by oxidative DNA damage, inflammation, and pulmonary epithelial injury [42]. The primary sources of indoor NO₂ are gas‐powered heating and cooking equipment [43]. The use of solid fuels, such as coal, for cooking and heating continues to persist as a significant source of indoor pollution in developing countries. Surprisingly, this practice remains prevalent, even in numerous Western households, as a means of residential heating. The inhalation of smoke produced by biomass burning has been associated with various respiratory ailments in both children and adults [44]. Pryor et al. [45] showed that NO₂ reacts with unsaturated fatty acids to produce free radicals, destroys unsaturated fatty acids in biofilms, and generates lipid peroxidation products. NO₂ dramatically increases oxygen consumption by activated inflammatory cells, strengthens oxidative metabolism, and generates a large number of free oxygen radicals, resulting in a vicious cycle. The fatty acid chain is broken, resulting in reduced membrane fluidity and increased permeability. Membrane function is impaired by the inactivation of membrane receptors and their related enzymes. Lipid peroxidation products can also react with proteins, sugars, and other substances, affecting the activity of a variety of enzymes and resulting in tissue damage. These products can also increase the synthesis of arachidonic acid metabolites, such as thromboxin, prostaglandin E, and leukotriene C4, which participate in the inflammatory process, promote inflammatory cells to release inflammatory mediators, form a vicious cycle, and aggravate the occurrence of allergic diseases [46].

2.1.3. Indoor Allergens

Indoor air quality is also affected by indoor allergens originating from furry pets, molds, and house dust mites (HDMs) [33]. Indoor allergens elicit more severe forms of airway allergies than outdoor seasonal allergens [47, 48].

HDMs primarily inhabit household dust as well as surfaces such as mattresses, pillows, sheets, carpets, upholstered furniture, and other similar locations [34]. Globally, 1%–2% of the population is sensitive to HDMs [49]. HDMs are recognized as the primary triggers of airway allergies, with sensitization to HDMs occurring in as many as 50% of individuals with asthma [50]. A questionnaire survey was conducted among 600 students, and the findings indicated a significant association between the presence of dust mites and other allergens and between the occurrence of asthma and allergic rhinitis [51]. Newly available information suggests that wheezing in children is associated with sensitization to HDMs, which is associated with heightened bronchial inflammation and decreased lung function [52]. A study conducted across multiple centers in Germany revealed a greater occurrence of allergic rhinitis in newborns nwho were exposed to HDMs during their first 3 years of life [49]. Approximately 10%–15% of households experience dampness, which can result in the colonization of molds or cockroaches and subsequently lead to allergic sensitization among occupants [53, 54]. In addition to allergic mechanisms, molds can induce inflammation in both the upper and lower airways through various metabolites such as glucans or mycotoxins [55]. Jaakkola et al. [56] reported that exposure to humidity and mold at home increases the incidence of allergic rhinitis and other types of rhinitis. A separate study conducted as part of the Health Effects of School Environment project examined the impact of fungi and reported that in 33% of the classrooms surveyed, the concentration of viable molds in the indoor air exceeded the maximum standard of 300 cfu/m [3, 57]. These findings aligned with those reported in a recent study conducted in southern Italy [58]. Allergic reactions to animal‐derived allergens are a prevalent cause of airborne allergies and can trigger allergic rhinitis. More than 15% of the global population are allergic fur‐bearing animals, and there is a high incidence of cross‐reactivity among different species [59]. Factors associated with the allergen itself can affect pet allergens, such as the level of activity exhibited by the organism and the timing, variability, and intensity of exposure. Similarly, Dunlop et al. [60] reported that exposure to household pets with fur, such as dogs and cats, at an early age might lower the risk of developing sensitization and allergic diseases. Therefore, early allergen exposure may protect against allergic diseases. For example, Shargorodsk et al. [61] reported that American children exposed to cat and dog dander had a lower incidence of allergic rhinitis. In contrast, adults exposed to dog and cat dander exhibit higher rates of allergic rhinitis. These findings seem to contradict studies showing that early neonatal exposure to dust mites leads to a greater incidence of allergic rhinitis.

2.1.4. Interactions Between Indoor Pollutants

There is evidence suggesting that the impact of air pollutants on health goes beyond the cumulative effect of the different pollutants. Although still not completely characterized, the interactions between chemical and biological pollutants, including allergens, may be in some cases synergistic [62]. Studies have shown that some pollutants can affect the interaction between allergens and human immune system, acting as adjuvants [63]. In a French epidemiological study, formaldehyde in houses showed a significant synergistic effect with the dog allergen Can f1 [64]. In addition, co‐exposure to VOCs and allergens has shown peculiar effects on airway surfactant protein D, myeloperossidase, and Clara cell secretory protein 16 [58]. Finally, the analysis of the influence of NO₂ and Der p 1 (major allergen of the HDM) on human nasal epithelial cells evidenced that NO₂ has a pro‐inflammatory effect determining an increased release of IL‐6 and IL‐8 [65].

2.2. Outdoor Air Pollutants

Airborne pollutants from outdoor sources primarily consist of particulate matter and gas pollution stemming from traffic, including O₃, NO₂, and SO₂. Exposure to these pollutants can exacerbate allergic rhinitis symptoms and contribute to disease progression. Furthermore, air pollution exacerbates global warming and intensifies the allergenicity of certain plant allergens, thereby affecting human health [66].

2.2.1. Particulate Matter

The particulate matter in air pollutants mainly arise from the incomplete combustion of coal and petroleum fuel, among which PM2.5 can be inhaled into the bronchioles and alveoli. The surfaces of the lung tissue easily attach to various harmful substances, such as inorganic heavy metals, sulfates, nitrates, organic polycyclic aromatic hydrocarbons, ethanol, benzene, SO_2, and other harmful gases. Various pathogenic microorganisms [67] can damage all the organs of the body through blood circulation. Nitropolycyclic aromatic hydrocarbons (NPAHs), the organic components of PM2.5, have been widely studied because of their mutagenicity and carcinogenicity [68].

Mechanistic studies have shown that subchronic exposure to PM2.5 causes inflammatory injury in rats and impairs the phagocytic function of alveolar macrophages [41]. In addition, PM2.5 has been shown to increase the phagocytic capacity of macrophages in COPD mice, thereby increasing oxidative stress [69]. The study showed that for every 10 µg/m³ increase in PM2.5 exposure, the incidence of cough symptoms in COPD patients increased by 33%, the incidence of expectoration symptoms increased by 23%, and the daily change rate of peak expiratory flow decreased [70]. In population‐based cohort studies, long‐term exposure to PM2.5 reduces forced expiratory volume and forced vital capacity in 1 s and accelerates the decline in lung function in healthy adults [71]. According to a meta‐analysis conducted by Zou et al. [72], exposure to particulate matter can result in oxidative stress, airway hyperreactivity, and airway remodeling. Several studies have confirmed that PM2.5 can increase the incidence of respiratory allergic rhinitis and allergic asthma [73]. Excessive concentrations of metal cations and polycyclic aromatic hydrocarbons present in particulate matter can exacerbate Th2‐driven allergic inflammation in mice with allergic rhinitis, resulting in an imbalance in oxidation–reduction, detachment of nasal epithelial cells, and infiltration of eosinophils [74]. Inhalable particulate matter can transport significant quantities of toxic pollutants, including organic and transition metals. These pollutants can activate reactive oxygen species, leading to pro‐inflammatory responses [75]. Numerous in vivo experimental studies and epidemiological investigations have demonstrated that exposure to pollutants can lead to an elevated production of total IgE in individuals without allergies. Moreover, it induces an increase in both total and specific IgE production in patients with allergic rhinitis. There are two potential mechanisms by which pollutants enhance IgE production. First, pollutants directly activate B cells, thereby promoting IgE synthesis. Second, coexposure to pollutants and allergens can alter the gene methylation status of helper T cells and elevate IL‐14 levels, consequently amplifying IgE production [76]. PM2.5 can also induce IgE production by B cells, promote the differentiation of Th cells into Th2 cells, and activate eosinophils. Exposure to pollutants increases the levels of IL‐5, an eosinophilic growth factor. Exposure to pollutants increases the level of granulocyte–macrophage colony‐stimulating factor in nasal epithelial cells, which can prolong the survival of eosinophils and macrophages [77]. Ouyang et al. [78] demonstrated in vivo and in vitro that PM2.5 exposure induced the activation of the intracellular pattern recognition receptor Nod1 and stimulated the immune response by activating the NF‐κB signaling pathway. Research indicates that PM2.5 can prompt alveolar epithelial cells to release cytokines and inflammatory factors, such as IL‐6, IL‐8, tumor necrosis factor‐α, and histamine. When inhaled and subsequently circulated in the bloodstream, PM2.5 can exacerbate the inflammatory response [79]. Following exposure to air pollutants, endotoxins present in bacteria and microorganisms activate Toll‐like receptors. This activation triggers the release of cytokines and chemokines and initiates antigen‐specific adaptive immune responses. Consequently, it serves as a crucial link between innate and specific immunity and plays a significant role in the development of allergic rhinitis [80]. PM2.5 can increase mucosal oxidative stress. Oxidative stress refers to the excessive production of highly reactive molecules, such as reactive oxygen free radicals and reactive nitrogen free radicals, when the body is subjected to various harmful stimuli, and an imbalance between the oxidative and antioxidant systems leads to tissue damage. Excessive inhalation of PM2.5 can result in an imbalance between the oxidative and antioxidant systems of nasal mucosal epithelial cells. This can lead to excessive production of reactive oxygen and nitrogen species, consequently impairing clearance mechanisms [80]. Reactive oxygen species, such as superoxide, hydrogen peroxide, and hydroxyl radicals, are highly reactive and can react with intracellular proteins, lipids, and DNA, causing direct cytotoxic effects and ultimately resulting in damage to alveolar epithelial cells [81]. Certain inorganic substances, including sodium, magnesium, aluminum, iron, and copper, which are adsorbed by PM2.5, have been found to induce the Fenton reaction of hydrogen peroxide in human alveolar epithelial cells. This reaction leads to the oxidation of organic substances within cells, ultimately causing cellular damage [82]. Many experiments have proved that PM2.5 exposure increases the risk of respiratory infections. In addition, long‐term exposure to PM2.5 is associated with increased morbidity and mortality from lung diseases such as chronic obstructive pulmonary disease and asthma [71]. Numerous studies have shown that PM2.5 exposure produces excessive ROS, which reduces antioxidant enzyme activity and consequently leads to cellular oxidative stress [83].

2.2.2. Gaseous Pollutants

O₃, also known as ozone, is the primary constituent of atmospheric oxidants. It is generated mainly through the reaction of sunlight with precursors, such as nitrogen oxides, hydrocarbons, VOCs, and carbon monoxide, present in exhaust emissions. Most O₃ is located in the stratosphere 10–50 km above the ground, and can block ultraviolet rays and protect humans. However, O₃ in the lower troposphere is harmful to human health. Extensive research has provided substantial evidence that ambient O₃ levels are linked to allergic rhinitis, asthma, and atopic dermatitis [84]. A study conducted in 59,754 children in China revealed that prolonged exposure to ambient O₃ significantly increased the risk of allergic rhinitis and bronchial symptoms in children [85]. In the presence of O₃, the secretion of IL‐8 and hyaluronic acid by epithelial cells and macrophages cultured using the Bauer method was greater than that by cells cultured without O₃. In addition, the immunophenotype of macrophages is altered [86]. O₃ can directly affect respiratory epithelial cells by acting on epidermal growth factor receptor (EGFR), tumor necrosis factor receptor, and the IL‐1 receptor. This interaction occurs through various signal transduction pathways, predominantly through the mitogen‐activated protein kinase (MAPK) pathway. O₃ triggers the expression of ERK1/2, P65, and P50/P52. These actions can stimulate the production of Th2 cytokines or induce cellular stress responses. Furthermore, it can regulate the expression of inflammation‐related target genes through intracellular kinase or EGFR through the MKK4–P38 pathway and MEK–ERK pathway, respectively. These effects can significantly affect respiratory responses to allergens [87]. O₃ indirectly reduced mucociliary clearance and free radical production. In addition, O₃ contributes to increased pollen production and sensitization [34]. In Germany, Beck et al. [88] further demonstrated that birch trees exposed to high concentrations of O₃ exhibited elevated production of pollen allergens and pollen‐related lipid mediators. Moreover, sensitized extracts derived from trees exposed to high O₃ concentrations resulted in larger wheal diameters during skin‐prick tests conducted on patients with allergic rhinitis who were specifically allergic to birch pollen. An in vivo study revealed that when healthy individuals were exposed to continuous inhalation of 0.3 PPM O₃ for 2 h, the number of eosinophils in nasal secretions increased. Furthermore, O₃ exacerbates damage to bronchial brush cells and leads to an increase in the expression of the IL‐8 and COX‐2 genes in bronchoalveolar lavage fluid [89]. O₃ triggers alterations in the expression of inflammatory factors, leading to an amplified inflammatory response. This includes the heightened secretion of various cytokines associated with inflammation, such as IL‐1β, IL‐6, IL‐8, and TNF‐α, which can exacerbate allergic symptoms. O₃ enhances the expression of the cytokines CCL2, HMOX1, AMD, and COX‐2 both in vitro and in vivo in human bronchial epithelial basal cells [90].

SO₂ is a well‐known noxious air pollutant classified as one of the three major global public hazards and poses a threat to both human life and the living environment. The unique characteristics of SO₂ include its colorless appearance, pungent and irritating odor, and density that exceeds that of air. According to the data, 70% of atmospheric SO₂ originates from anthropogenic emissions, such as the combustion of sulfur‐containing substances (such as coal), oil, and natural gas. Additionally, SO₂ is produced during the smelting and roasting of sulfur‐containing ores. SO₂, a prominent constituent of air pollutants, poses a significant risk to human health, animal well‐being, and plant life. High exposure to SO₂ can lead to respiratory irritation and impairment. In particular, in children residing in close proximity to industrial pollution sources, the release of SO₂ from petroleum sources is linked to acute respiratory symptoms [34]. An investigation conducted among primary school students in Korea revealed that SO₂, an indicator of industrialization, was a significant risk factor for allergic rhinitis in this age group [91]. Tomic‐Spiric et al. [92] further demonstrated that brief exposure to SO₂ increased the likelihood of hospital visits due to allergic respiratory ailments, particularly asthma accompanied by allergic rhinitis. When the average concentration of SO₂ was 0.013–0.929 mg/m³, with increasing ambient air SO₂ concentration, the changes in lung function indices (FVC and FEV1) were negatively correlated with SO₂ concentration, and the decline in lung function in girls was significantly greater than that in boys [93]. SO₂ also has a significant impact on the hospitalization rate of chronic obstructive pulmonary disease patients [94]. After the inhalation of SO₂, the phagocytic function of alveolar macrophages in guinea pigs in the exercised state is significantly weakened [95]. SO₂ can upregulate the expression of pro‐inflammatory cytokines in the lungs of asthmatic rats, causing a Th1/Th2 imbalance, leading to an abnormal immune response, aggravating the pneumonia response, and enhancing the sensitivity of asthmatic rats to foreign stimuli [96]. Other studies have shown that SO₂ is associated with the risk of lung cancer in northern China [97].

2.2.3. Traffic‐Related Air Pollution

Air pollution caused by the release of harmful gases and soot from vehicles, such as motor vehicles, trains, and aircrafts that burn coal or oil, is known as traffic‐related air pollution. Primary emissions can result in the formation of secondary pollutants such as nitrate, organic aerosols, and O₃. The prevalence of allergic diseases is exacerbated by traffic pollution both in China and globally. Young et al. [98] investigated the impact of traffic pollution on asthma incidence among 5443 primary school students in 10 cities in the Republic of Korea. The results revealed a negative association between proximity to the main road (within 200 m) and the risk of asthma in children. Additionally, a positive correlation was observed between the size of the main road and the volume of traffic within a 75‐m radius from the main road. In wheezing or allergic rhinitis, the main role of traffic‐related air pollution is similar to that of sensitizing agents, which cooperate with allergens to increase the probability of sensitization [99].

3. Climate Change

Climate change refers to the extended change in weather patterns that arise owing to changes in precipitation, temperature, wind speed, and the occurrence of extreme weather events. Climate change is a primary contributor to worldwide health crises, significantly affects human health, and adversely affects respiratory allergies [100]. According to mathematical simulation studies conducted by Kurganskiy et al. [101], climate change can potentially amplify the severity of allergic rhinitis by up to 60%. The influence of climate change on respiratory allergies is a multifaceted process involving the interaction of various factors, including the impact of climate change on airborne allergens, shifting environmental pollution, and changes in meteorological variables [34]. A strong correlation exists between climate change and air pollution. Currently, a significant portion of the world's energy relies on burning fossil fuels, which results in the release of CO₂, methane, black carbon, nitrogen oxides, and sulfate aerosols into the environment [66]. Greenhouse gases play a crucial role in maintaining the Earth's warmth by absorbing solar energy and reflecting it back to the surface [100]. However, excessive gas emissions lead to an imbalance, trapping excessive heat in the atmosphere, and causing global warming. Consequently, global warming induces changes in local vegetation patterns, accelerates plant growth rates and phenology, increases airborne pollen concentrations, and modifies the geographical distribution of plants [33]. Anderegg et al. [102] reported that earlier spring resulted in earlier and longer release of tree pollen. Multiple studies conducted in North America and Europe have shown a correlation between climate change and a prolonged ragweed pollen season [103, 104]. A continuous increase in atmospheric CO₂, which serves as the primary carbon source for photosynthesis, results in an increased energy supply for the production of pollen, including ragweed. Additionally, plant growth contributes to greater availability of nutrients for molds. Changes in atmospheric humidity and precipitation further influence the proliferation and distribution of fungi [105]. Furthermore, climate change amplifies the occurrence of extreme weather events such as heavy rainfall and flooding. These events have detrimental effects on indoor air quality because they promote moisture and mildew. In addition, intense rainfall and thunderstorms contribute to increased concentrations of allergenic particles in the atmosphere, exacerbating airway inflammation. Consequently, climate change disrupts pollination patterns and changes the distribution of allergenic microorganisms, such as molds and fungi, which in turn worsens symptoms and prolongs the onset of allergic rhinitis and asthma [106]. Moreover, increased air pollution resulting from weather events exacerbates respiratory diseases triggered by allergens [107]. These changes subsequently lead to intensified symptoms and an increased need for medication among affected individuals [34]. Plant pollen and mold spores as allergens can trigger the release of pro‐inflammatory factors and immunomodulatory mediators, thereby accelerating IgE‐mediated sensitization and allergic reactions. Studies have shown that, in response to high levels of CO₂ in the atmosphere, plants increase their photosynthetic and reproductive functions, resulting in more pollen production [63]. Wayne et al. [108] observed that the doubling of the atmospheric concentration of CO₂ potentiated the production of pollen from ragweed by 61% more per plant. Mold is a major culprit in severe asthma, and it proliferates more significantly during floods and heavy rains. There is also evidence that increased atmospheric mold spore concentrations may play a role in thunderstorm asthma with increase in asthma hospital emergency visits following this natural phenomenon. A Canadian study concludes that fungal spore counts doubled and pediatric asthma emergency admissions increased by more than 15% on days with thunderstorms while no increases were found in the concentration of pollens [109].

4. Pathophysiology and Mechanisms

4.1. Allergic Rhinitis

Allergic rhinitis is a persistent, noninfectious inflammation of the nasal mucosa that occurs in individuals with atopic tendencies following exposure to allergens. Inflammation is mainly triggered by allergen‐specific IgE, although non‐IgE‐mediated mechanisms and neurological immune dysregulation also play roles in its development [110].

4.1.1. Epidemiology

The prevalence of allergic rhinitis continues to increase worldwide, with more than 400 million people suffering from allergic rhinitis worldwide [111]. In China, more than 200 million people are affected, and epidemiological studies show that the incidence of allergic rhinitis increased from 11.1% in 2005 to 17.6% in 2011 [112]. Considering allergic rhinitis's adverse impacts, the increasing evidence for the possible epidemiological exacerbating factors associated with allergic rhinitis has been studied in recent years [33, 113]. Specially, it has been postulated that air pollution is a major risk factor for the increased risk of allergic rhinitis [114].

4.1.2. IgE‐Mediated Allergic Rhinitis

The nasal mucosa serves as the foremost air regulator in the respiratory tract and acts as an initial barrier against airborne infectious pathogens. The nasal mucosa plays a crucial role in preserving and restoring epithelial integrity and initiating immune responses. When mucosal integrity is compromised by certain conditions or factors, signaling factors are released by epithelial cells that activate repair mechanisms and induce protective inflammation [115]. In allergic rhinitis, allergens can directly damage the epithelial barrier or activate pattern recognition receptors, causing epithelial cells to release IL‐33, thymic stromal lymphopoietin, or IL‐25 to initiate an innate immune response [116, 117]. In turn, these cytokines activate type 2 innate lymphocytes and rapidly produce type 2 cytokines, such as IL‐4, IL‐5, and IL‐13, which play key roles in initiating and maintaining Type 2 adaptive immune responses and can lead to IgE class switching and mucosal inflammation [115]. Following the inhalation of allergens, individuals with atopic tendencies enter the sensitization stage. During this stage, allergen‐specific IgE is generated in the lymph nodes and nasal cavity. Specific IgE then attaches to high‐affinity IgE receptors present on the surface of mast cells and basophils, leading to sensitization of the nasal mucosa. In the sensitized state, when the body is re‐exposed to the same allergen, IgE binds to mast cells and basophils within the nasal mucosa. This triggers the activation of these cells, leading to the release of pre‐existing and newly synthesized mediators such as histamine, leukotrienes, and prostaglandins. The specific flow chart is shown in Figure 3. Consequently, nasal sensory nerve endings and blood vessels are stimulated along with parasympathetic nerves. These processes result in acute symptoms of allergic rhinitis, including nasal itching, sneezing, and clear watery discharge, often accompanied by dilation of blood vessels in the nasal mucosa and increased glandular secretion [118]. Environmental pollutants play key roles in stimulating the nasal mucosa and causing allergic reactions.

Figure 3.

IgE‐mediated allergic reactions.

4.1.3. Non‐IgE‐Mediated Inflammation in Allergic Rhinitis

Although IgE‐mediated Type I allergy is the core mechanism of allergic rhinitis, non‐IgE‐mediated inflammation is also involved in the occurrence and development of allergic rhinitis. Once aeroallergens enter the host, they first encounter the nasal epithelium. Allergens can disrupt the function of the epithelial barrier through various mechanisms, including proteolytic action, lipid‐binding activity, interactions with polysaccharides, and molecular recognition systems. This disruption may enable allergens to penetrate surrounding tissues, leading to the continuation of chronic and persistent inflammatory processes [119, 120]. This can occur with aeroallergens and irritants such as chlorine and air pollution. These irritants can disrupt the function of the epithelial barrier, allowing the irritants to penetrate surrounding tissues and perpetuate ongoing inflammatory processes [121].

4.1.4. Neural Mechanisms

Sensory neurons, axonal reflexes, and neurotransmitters significantly affect the pathophysiology of allergic rhinitis, by shaping the underlying mechanisms and processes associated with allergic rhinitis [122]. Inflammatory mediators, such as bradykinin, histamine, acetylcholine, and capsaicin, activate sensory neurons in the trigeminal nerve. This activation occurs primarily via TRP ion channels [123, 124]. With repeated depolarization, lasting changes occur in TRP channels, specifically TRPV1 and TRPA1, which belong to the TRP cation channel subfamily. These changes result in the hyperexcitability of neurons in patients with allergic rhinitis by modifying the stimulation threshold and membrane potentials [125]. The depolarization of nociceptive channels on sensory nerves results in the release of neuropeptides such as substance P, CGRP, and neurokinin‐A [126]. Substance P receptors are found in various nasal structures, including the nasal epithelium, glands, arterial and venous vessels, and sinusoidal vessels. This activation leads to increased glandular secretion, enhanced vessel permeability, edema formation, vasodilation, and further activation of inflammatory cells [127].

4.2. Lung Diseases

The most common respiratory system diseases include chronic obstructive pulmonary disease, respiratory tract infections, asthma, and lung cancer. Coughing, chest pain, and respiratory obstruction are the primary manifestations of this mild disease. Severe patients present with respiratory distress and hypoxia and may die from respiratory failure [128]. The lung is the target organ of most environmental pollutants [129]. It has been shown that genotoxicity of environmental pollutants is not only related to oxidative stress and DNA damage caused by chemicals, but also to increased metabolic enzyme activity [130]. The occurrence of lung diseases is often accompanied by a variety of regulatory mechanisms, including inflammation, oxidative stress, and DNA damage.

4.2.1. Epidemiology

According to the Global Burden of Disease Study, in 2017, an estimated 544.9 million people were living with chronic lung diseases globally [128]. In 2022, a global epidemiological survey data collected 260 study sites in 65 countries showed that the global prevalence of chronic obstructive pulmonary disease was 10.3%, about 399 million people [131]. There are about 300 million asthma patients in the world [132]. The epidemiological survey results of asthma in various countries show that the prevalence of asthma in children is 3.3%–29.5%, and the prevalence of asthma in adults is 1.2%–25.5% [133].

4.2.2. Mechanisms of Inflammation

Inflammation is the immune response of the body to external stimuli (such as various injuries and irritants), and its occurrence is often accompanied by other pathological reactions [134]. Normally, a moderate inflammatory stimulus causes the body to produce an immune response for protection. Excessive inflammatory stimulation can cause the body to experience various levels of damage, including weakening and decline of organ function [135]. The signaling pathways associated with inflammation, known as MAPKs, include extracellular signal‐regulated kinase (ERK) 1/2, p38 MAP kinase, c‐Jun N‐terminal kinase, and TLR4. In addition to the TLR4 pathway, PM2.5 can activate three other pathways, thereby initiating inflammatory responses [136]. PM2.5 can stimulate the TGF‐β1/Smad pathway, subsequently enhancing the expression of NF‐κB, inducing an inflammatory response, and leading to lung injury [137]. Numerous studies have provided compelling evidence linking PM2.5‐induced respiratory system damage to inflammatory responses. Cui et al. showed that neutrophil infiltration worsened the lung injury caused by PM2.5 [138]. Similarly, Yang et al. discovered that exposure to PM2.5 in an underground garage led to lung injury in mice, as evidenced by significantly elevated levels of inflammatory factors in the lung tissue [139]. In the context of PM2.5‐induced inflammatory injury to the respiratory system, the inflammasome NLRP3 is activated [140]. Animal studies have demonstrated that the NLRP3/caspase‐1 pathway plays a crucial role in pathological changes associated with pulmonary inflammation triggered by ambient PM2.5 exposure [141]. Furthermore, cellular studies have provided evidence that exposure to PM2.5 induces inflammatory responses in pulmonary vascular endothelial cells [142]. Epidemiological investigations have revealed that following human exposure to PM2.5, which is rich in metals, the mRNA expression of inflammation‐related markers increases in alveolar macrophages. Additionally, the mRNA levels of these inflammatory factors were markedly increased in bronchial epithelial cells. Furthermore, PM2.5 exposure can induce the expression of specific microRNAs, resulting in abnormal regulation of inflammatory genes and ultimately leading to lung injury [143]. Research has demonstrated that the metallic constituents present in PM2.5 can prompt the release of inflammatory mediators from human lung epithelial cells. This in turn stimulates inflammatory cell aggregation and cytokine secretion, ultimately exacerbating inflammation [144]. Consequently, inflammatory factors play pivotal roles in respiratory system injuries caused by PM2.5.

4.2.3. Oxidative Stress

In addition to inflammatory mechanisms, the regulatory processes underlying lung diseases involve oxidative stress. Oxidative stress is characterized by an imbalance in the oxidation–antioxidant system, wherein cells exposed to internal or external stimuli experience an excess of prooxidants compared with antioxidants. This process is accompanied by the overproduction of intracellular reactive oxygen species or reactive nitrogen species. Various airborne components can trigger oxidative stress, with PM2.5 being a prominent contributor owing to its complex composition. Both soluble and insoluble components of PM2.5, albeit to varying extents, can induce cells to generate reactive oxygen species. Soluble components can produce higher levels of hydrogen peroxide than their insoluble counterparts [145]. Polycyclic aromatic hydrocarbons (PAHs) are crucial organic components of PM2.5 and are significant atmospheric pollutants. Exposure to PAHs can increase the production of reactive oxygen species, leading to autophagy [146]. The inhalation of SO₂ has been shown to affect the antioxidant system in multiple organs, including the brain, lungs, heart, liver, kidney, and spleen, in mice. SO₂ acts as a systemic toxin, and its toxicity intensifies as the concentration of inhaled SO₂ increases. This effect is accompanied by a decrease in antioxidant defense capacity and an exacerbation of oxidative stress.

4.2.4. DNA Damage

Genomic instability, which encompasses DNA damage and errors in DNA replication, plays a significant role in the initiation and progression of tumors. Certain cancer syndromes, such as xeroderma pigmentosum, which results from impaired DNA damage repair, commonly lead to tumor development before the age of 20 years in most affected individuals [147]. Hence, DNA damage and cancer onset are closely associated. Animals rely on DNA, which is stable, as their primary genetic material. However, when exposed to external factors, such as ultraviolet radiation, strong acids and bases, endogenous reactive oxygen species, or DNA replication errors, DNA damage can occur. There are multiple types of DNA damage, including DNA base damage, DNA strand breakage, DNA oxidative damage, and the formation of DNA adducts. Following DNA damage, the body triggers its own DNA repair response. Apoptosis can occur in cases of severe damage, and cell apoptosis may occur [148]. Research has revealed that exposure to PM2.5 can inflict DNA damage on several cell types, such as alveolar epithelial type II cells and lymphocytes [149]. PM2.5 can interfere with the development of healthy fetal tissues and organs by triggering DNA damage, ultimately leading to negative pregnancy outcomes [150].

5. Allergic Rhinitis and Lung Diseases

Allergic rhinitis may share the molecular mechanisms of some lung diseases, especially asthma. Asher et al. [151] showed that allergic rhinitis and asthma are closely related, and put forward the view of “united airway” and “one airway one disease.” Oxidative injury leads to increased lipid peroxidation, increased airway reactivity and secretions, production of chemoattractant molecules, and increased vascular permeability, which collectively lead to an augmentation of the existing inflammation that is a hallmark of asthma [152]. Moon et al. [153] showed that the expression of NADPH oxidase 1 and NADPH oxidase 4, as well as superoxide anions, was increased in the nasal mucosa of patients with allergic rhinitis compared to healthy individuals. Profita et al. [154] reported higher FENO and IL‐5 levels and lower pH in nasal and oral EBC from children with allergic rhinitis and asthma. Finally, Gratziou et al. [155] showed that nitrate/nitrite and exhaled NO levels were elevated in patients with asthma and allergic rhinitis compared to patients with allergic rhinitis only. Alternatively, It is likely that in a disease setting such as allergic rhinitis and asthma airway threats will use similar B‐cell activation pathways to evoke host defense and enhance immunity. Such Th2 cells will now rapidly produce IL‐4 and IL‐13. Activated B cells rapidly up‐regulate IL‐4Rα receptor expression [156]. The current evidence showed that NLRP3 inflammasome promoted the development of allergic airway diseases. NLRP3 inflammasome has been identified as the inflammasome responsible for allergen activation of innate immunity and driving type 2 immune responses. Studies have shown that the content of NLRP3 and caspase‐1 in nasal mucosa of AR patients is increased compared with healthy controls, leading to the overexpression of inflammatory factor IL‐1β and aggravation of allergic airway response [157, 158].

6. Conclusions

This review comprehensively describes the direct and indirect effects of environmental pollution and climate change on allergic rhinitis and lung diseases, and elaborates the pathogenesis of allergic rhinitis and lung diseases, as well as the common pathogenesis between them. An increasing number of studies have shown that environmental factors, such as air pollution and climate change, play important roles in the pathogenesis of allergic rhinitis and lung diseases. Environmental pollutants can affect human health through a variety of physical, chemical, and biological effects and can induce or aggravate respiratory allergic and inflammatory responses. Studying the effects of pollutants on the respiratory system can provide a theoretical basis for treating allergic rhinitis and lung diseases in the future. However, the mechanisms underlying the effects of environmental factors, such as air pollution and climate change, on allergic rhinitis and lung diseases still need to be further studied to clarify their pathogenesis, lay a foundation for formulating more effective prevention and control measures, and provide patients with more accurate diagnosis, treatment, and prevention. Simultaneously, attention should also be given to the impact of air pollution and meteorological factors on different populations to develop targeted personal protection and air pollution control measures to optimize the allocation of medical resources. Children exhibit a higher incidence of asthma compared to adults and are more susceptible to environmental influences. The importance of early intervention and safeguarding children cannot be overstated. Healthcare experts must engage with policymakers to promote the reduction of greenhouse gases, air pollution, and allergens. Urban planning and the design of public roads should aim to minimize exposure to these pollutants and allergens, thereby preventing synergistic effects and safeguarding the health of urban dwellers. To mitigate air pollution, it is advisable to establish a buffer zone of 200–300 m between high‐traffic areas and spaces where people reside, work, and study, as this can substantially lower exposure to harmful substances. In addressing aeroallergens, the “Allergy Safe Tree Decalogue” model offers practical measures, such as incorporating nonallergenic plants in green spaces, trimming hedges before flowering or pollen release, and referring to pollen level maps when scheduling public events [159]. Health professionals ought to take a pivotal role in advocating for effective strategies to address the health impacts of global environmental changes by conducting research on the relationship between climate change and respiratory health and utilizing these findings for the prevention and control of diseases.

Author Contributions

Xin‐Yan Liu conceptualized and wrote the manuscript. Dong‐Dong Zhu reviewed the manuscript. Rui‐Ming Han and Yong‐Tai Wang performed the literature searches and prepared the images. Cui‐Da Meng supervised the manuscript and provided critical review. All the authors have read and agreed to the published version of the manuscript.

Ethics Statement

The authors have nothing to report.

Conflicts of Interest

Professor Dong‐Dong Zhu is a member of World Journal of Otorhinolaryngology – Head & Neck Surgery (WJOHNS) editorial board and is not involved in the peer review process of this article.

Data Availability Statement

All data pertaining to this systematic review are available from the corresponding author upon reasonable request.