2025 Volume 30 Pages 7
Under the background of climate change, the escalating air pollution and extreme weather events have been identified as risk factors for chronic respiratory diseases (CRD), causing serious public health burden worldwide. This review aims to summarize the effects of changed atmospheric environment caused by climate change on CRD. Results indicated an increased risk of CRD (mainly COPD, asthma) associated with environmental factors, such as air pollutants, adverse meteorological conditions, extreme temperatures, sandstorms, wildfire, and atmospheric allergens. Furthermore, this association can be modified by factors such as socioeconomic status, adaptability, individual behavior, medical services. Potential pathophysiological mechanisms linking climate change and increased risk of CRD involved pulmonary inflammation, immune disorders, oxidative stress. Notably, the elderly, children, impoverished groups and people in regions with limited adaptability are more sensitive to respiratory health risks caused by climate change. This review provides a reference for understanding risk factors of CRD in the context of climate change, and calls for the necessity of adaptive strategies. Further interdisciplinary research and global collaboration are needed in the future to enhance adaptability and address climate health inequality.
Climate change refers to long-term shifts or alterations in weather conditions and patterns of extreme weather events (EWEs), such as temperature, precipitation, wind patterns, and other aspects of the earth’s climate system [1]. Adverse outcome caused by climate change includes intensified air pollution, rising temperatures, and increased frequency of EWEs [2]. Overall, climate change arises from two main factors: anthropogenic activities, such as greenhouse gas (GHGs) emissions, fossil fuel combustion, agriculture, deforestation and natural processes, including solar radiation fluctuations and volcanic eruptions [3, 4]. Global warming, a key component of climate change, is marked by the rise in earth’s average surface temperature, primarily driven by increased atmospheric concentrations of carbon dioxide (CO2) and other GHGs, which enhance the greenhouse effect and trap heat [5]. Besides, continued emission of GHGs will cause further warming and long-lasting changes in the climate system, such as precipitation patterns, more frequent and intense EWEs, and shifts in seasonal temperatures [6]. Notably, climate change can exert detrimental impacts on public health and wellbeing, specifically causing significant damage to the respiratory system [7, 8].
Climate change has significantly intensified air pollution concerns. Air pollution consists of particulate matter (PM) and gases such as nitrogen oxides (NOx), sulfur dioxide (SO2), and ozone (O3) in the air [9]. When the amount of these pollutants released into the atmosphere exceeds its self-purification capacity, leading to an increase in pollutant concentrations, it results in direct, indirect, or potential adverse effects on human health and the ecological environment [9]. Elevated temperatures contribute to a surge in heatwaves and degrade air quality further. For example, higher temperatures and more intense sunlight can accelerate the production of ground-level O3 [10]. Moreover, climate change is contributing to more frequent and severe wildfires, which produce harmful smoke and particulates [11]. It is estimated that under a 2 °C warming scenario, wildfire frequency is projected to increase significantly in many regions [12]. By altering temperature, precipitation, and wind patterns, as well as increasing the likelihood of EWEs, climate change creates conditions that are more conducive to wildfire occurrence, spread, and intensity [13, 14]. Specifically, higher temperatures and prolonged droughts dry out vegetation, making it more flammable, while changing precipitation patterns can affect the availability and condition of burnable material. Furthermore, shifting wind patterns can facilitate the rapid spread of fires [15, 16].
The World Health Organization identifies chronic respiratory diseases (CRD) as one of the four principal chronic conditions, responsible for an estimated 7.5 million fatalities annually, which is about 14% of global deaths each year [17], causing tremendous economic and human burden. Data from the 2017 Global Burden of Diseases, Injuries, and Risk Factors Study (GBD) indicates that chronic respiratory conditions continue to be a predominant source of mortality and impairment globally [18]. Chronic obstructive pulmonary disease (COPD) and asthma are among the most frequently diagnosed chronic respiratory diseases [19]. The occurrence and progression of CRD are influenced by multiple factors, among which environmental factors play a significant role [20].
Although previous studies have summarized the association and mechanism of action between air pollution and CRD, there is still a lack of systematic review about the impact of climate change on respiratory health from the perspective of combined exposure to the atmospheric environment, which refers to the physical and chemical characteristics of the atmosphere on which organisms depend, including air pollutants, adverse meteorological conditions and atmospheric allergens. This review summarizes the respiratory health effects associated with climate change, including potential pathophysiological mechanisms, influencing factors, and health inequalities, etc. The purpose of this study aims to provide reference for understanding the risk factors of chronic respiratory diseases in the context of climate change, and calls for the necessity of adaptive strategies.
The methodology for this literature review is structured to systematically identify recent studies and conduct a comprehensive evaluation. The CRD included in this study primarily consist of COPD (ICD-10, J44) and asthma (ICD-10, J45–J46). Searches were conducted between January, 1 and April, 30 2024 using PubMed and Web of Science, with a combination of the following search terms: “climate change”, “air pollution”, “global warming”, “extreme weather events”, “sandstorms”, “thunderstorm”, “heatwave”, “respiratory health”, “respiratory diseases”, “asthma”, “chronic obstructive pulmonary disease”, “particulate matters (PM)”, “ozone (O3)”, “nitrogen dioxide (NO2)”, “sulfur dioxide (SO2)”, as well as disease-specific keywords for the conditions discussed in this review. Publications from 2000 to 2024 were considered for inclusion, with particular emphasis on those published within the last five years. Articles were excluded if they were not peer-reviewed, not available in English, or did not address the effects of climate change on at least one of the chronic respiratory diseases covered in this review. Meeting abstracts, letters, news articles, and comments were not included in the review.
Air pollution and climate change are intricately connected, with their origins, impacts, and mitigation strategies deeply interwoven [21]. From a causative standpoint, air pollution and climate change are generally driven by similar sources, particularly the combustion of fossil fuels [22]. This process primarily releases CO2, methane (CH4), and nitrous oxide (N2O), which are potent greenhouse gases contributing to global warming [23]. Additionally, it emits SO2, NOx, PM, and volatile organic compounds (VOCs), which contribute to air pollution and can form secondary pollutants such as ground-level O3 and smog [24]. Notably, certain air pollutants, particularly black carbon, serves as both an air pollutant and a potent short-term climate forcer by absorbing solar radiation, thereby accelerating local and global warming [25, 26]. Climate change can also exacerbate air pollution by intensifying EWEs like droughts, heatwaves, and wildfires, which contribute to higher pollutant concentrations [12]. Therefore, air pollution control policies and climate change mitigation strategies are often synergistic, offering dual benefits when implemented together.
Table 1 summarized the air pollution issues and countermeasures in major countries during different historical periods. It is worth noting that different countries or regions have adopted targeted control strategies for major air pollutants. For example, the photochemical smog issue in Los Angeles was primarily addressed through the reduction of vehicle emissions and industrial emission controls, targeting the reduction of NOx, VOCs and O3 [27]. In contrast, the haze events in China were primarily mitigated by the transition to cleaner energy sources (with a focus on reducing coal usage) and the implementation of stricter vehicle emissions standards alongside the promotion of electric vehicles in order to address particulate matter pollution [28].
Region/Country | Period | Major pollutants | Related health issues | Strategies implemented |
---|---|---|---|---|
Los Angeles, U.S. |
1940s to 1960s | O3; NOx; VOCs; Particulate matter |
Respiratory diseases (e.g., asthma, bronchitis); Eye irritation; Sore throat, coughing; Reduced cardiopulmonary function |
Implementation of the Clean Air Act (1970) to strengthen air quality standards; Reduction of vehicle emissions (e.g., catalytic converters); Promotion of public transportation and industrial emission controls; Air quality monitoring, and smog control and warning mechanisms |
London, UK | 1950s | SO2; Particulate matter; Coal smoke |
Respiratory problems (e.g., bronchitis, pneumonia); Heart failure; Eye irritation; Premature deaths |
Implementation of the Clean Air Act (1956) to restrict coal burning in urban areas; Promotion of cleaner energy sources; Improved air quality monitoring; Control industrial emissions |
Japan | 1960s to 1970s | SO2; NOx; Particulate matter |
Yokkaichi Asthma; Respiratory diseases caused by SO2 and PM, including bronchitis and asthma; Increased rates of respiratory infections and heart disease |
Enactment of laws like the Basic Law for Environmental Pollution Control (1967) and Air Pollution Control Act (1968); Establishment of Environment Agency in 1971 to oversee pollution control; Stricter regulations on industrial emissions and waste management |
Belgium | 1930s | SOx; Particulate matter; NOx |
Respiratory problems, such as severe bronchitis and asthma attacks; Cardiovascular complications, including heart failure due to dyspnea; Eye and throat irritation |
Increased monitoring of air pollution in industrial areas; Awareness of public health risks from industrial emissions; Enhanced enforcement of air pollution prevention laws. |
China | Early 2000s, with severe episodes in 2013 and 2015 | Particulate matter (PM2.5 and PM10); SO2; NOx; O3 |
Increased cases of respiratory diseases, such as asthma and chronic bronchitis; Higher incidence of cardiovascular diseases; Increased hospital admissions, especially among vulnerable populations (elderly, children, those with pre-existing conditions) |
Implementation of Air Pollution Prevention and Control Action Plan (2013) to reduce PM levels by tightening emissions standards; Transition to cleaner energy sources (reducing coal usage); Stricter vehicle emissions standards and the promotion of electric vehicles; Strengthened monitoring and enforcement of pollution controls; Public awareness campaigns and encouragement of individual actions to reduce pollution (e.g., limiting vehicle use). |
Abbreviations: PM2.5, particulate matter ≤2.5 µm in aerodynamic diameter; PM10, particulate matter ≤10 µm in aerodynamic diameter; NOx, nitrogen oxides; VOCs, volatile organic compounds; O3, ozone; SO2, sulfur dioxide; SOx, sulfur oxides; CO, carbon monoxide.
Table 2 summarized the major pollutants and key contributing factors in countries or regions where air pollution remains severe. It has been reported that air pollution significantly impacts human health in Africa, one of the world’s most affected regions. In 2019, a study utilizing WHO Global Health Observatory and GBD data estimated that Africa, severely affected by air pollution, accounted for 1.1 million premature deaths or 16.3% of the worldwide total [29]. Outdoor air pollution in Africa arises from various sources including dust storms, waste incineration, biomass burning, industrial emissions, etc. Notably, dust storms significantly exacerbate air pollution in Africa, impacting air quality and human health [30]. In addition, other countries such as India, Pakistan, and Bangladesh are also confronting significant challenges related to air pollution within the context of climate change, with their efforts to implement efficacious strategies to mitigate these issues proving deficient [31–33].
Region/Country | Main pollutants | Key factors contributing to air pollution |
---|---|---|
Africa | Particulate matter (PM2.5 and PM10); SO2; NOx; CO; VOCs |
Dust storms; Biomass burning; Waste incineration; Agricultural burning; Industrial emissions |
India | Particulate matter (PM2.5 and PM10); SO2; NOx |
Industrial emissions; Vehicular exhaust; Biomass burning; Fossil fuel combustion |
Pakistan | Particulate matter (PM2.5 and PM10); NOx; SO2; VOCs; O3 |
Industrial emissions; Agricultural burning; Construction dust; Fossil fuel combustion |
Bangladesh | Particulate matter (PM2.5 and PM10); SO2; NOx; CO; VOCs |
Vehicular exhaust; Burning of biomass and agricultural waste; Industrial emissions; Construction activities; Wood and coal burning |
Abbreviations: PM2.5, particulate matter ≤2.5 µm in aerodynamic diameter; PM10, particulate matter ≤10 µm in aerodynamic diameter; NOx, nitrogen oxides; VOCs, volatile organic compounds; SO2, sulfur dioxide; CO, carbon monoxide.
Climate change can affect the transport and chemical reactions of air pollutants. For example, rising temperatures can lead to an increase in ground-level O3 concentrations by accelerating the chemical reactions between VOCs and NOx in the presence of sunlight [34, 35]. Especially in the troposphere O3 is considered a pollutant, which means global warming may exacerbate the O3 pollution in the ground layer [36]. On the other hand, climate change can indirectly affect O3 levels through its impact on atmospheric circulation patterns [37]. Changes in wind patterns and temperature gradients can alter the transport of O3 between different layers of the atmosphere, potentially impacting stratospheric O3 concentrations [38]. Furthermore, climate change can also impact stratospheric O3 through water vapour cycle. As climate change progresses, the cooling of the polar stratosphere may slow the recovery of the O3 layer [39]. Notably, climate change can exacerbate EWEs, which could further affect the stability of the O3 layer. A reduction in stratospheric O3 results in increased ultraviolet (UV) radiation reaching the earth’s surface, heightening the risk of health concerns and also negatively affecting ecosystems [40, 41].
3.2 Climate change elevates the levels of particulate matters and other pollutantsClimate change can exacerbate air pollution by influencing the distribution and concentration of particulate matters and other air pollutants [42]. Particulate matter plays a significant role in the air quality deterioration resulting from a range of both natural and human-induced actions [43]. According to the aerodynamic diameter of particulate matters, it can be categorized as PM10 (aerodynamic diameter <10 µm), PM2.5 (aerodynamic diameter <2.5 µm), and ultrafine particles (aerodynamic diameter <100 nm) [44]. In the context of climate change, the frequency of EWEs, such as wildfires and dust storms has increased, which can lead to large amounts of PM release into the atmosphere, and then be carried over long distances [45]. Besides, higher temperatures enhance the formation of secondary PM from atmospheric pollutants like NOx and VOCs, while altered weather patterns can reduce pollutant dispersion, further raising PM levels. Climate change can also directly influence local and regional air quality by altering chemical reaction rates, boundary layer heights that impact the vertical mixing of pollutants, and synoptic airflow patterns that control pollutant transport [46]. Therefore, the exacerbation of air pollution caused by climate change is global, which means increased levels of PM can happened in regions that are not directly affected by EWEs. Additionally, climate change can also affect the sources and emissions of other air pollutants, e.g. NO2, carbon monoxide (CO), SO2 and VOCs [45].
3.3 Climate change affects atmospheric allergen levelsClimate change significantly impacts both the release and distribution of allergens. For example, it can alter the timing, duration, and intensity of pollen seasons, leading to prolonged plant growth seasons and thereby promoting pollen release. Besides, elevated atmospheric CO2 levels have been shown to enhance plant photosynthesis and reproductive processes, resulting in increased pollen production. Consequently, this exacerbates the exposure to allergens and intensifies allergic reactions [47]. Notably, climate change may also lead to changes in the region of plants, resulting in an expansion or alteration of the distribution range of allergens [48]. In particular, pollen sufferers may face more types of allergens as new plant species enter their regions. Additionally, high humidity and air pollutants induced by climate change can exacerbate effects of atmospheric allergens by irritating the respiratory system, making individuals more susceptible to allergic reactions.
As a result of climate change, patterns of air pollution are shifting in many urban regions globally, exerting a considerable impact on respiratory health, both as a standalone factor and in combination with meteorological conditions [49]. Furthermore, EWEs such as sandstorms, wildfires, thunderstorms, along with adverse meteorological conditions, including temperature variability and high humidity environments, also exert adverse impact on respiratory health [50–52].
4.1 The impact of air pollution on CRDResults from a systematic review and meta-analysis which included 436 studies globally indicated that per 10 µg/m3 increase in PM2.5 levels correlates with a higher incidence of COPD, with a pooled hazard ratio (HR) of 1.18 (95% CI: 1.13, 1.23) [53]. According to the WHO Global Air Quality Guidelines, the maximum 8-h O3 concentration standard is 100 µg/m3 [54]. Findings from a meta-analysis revealed that an increase of 10 µg/m3 in maximum 8-h O3 concentration correlated with a 0.84% (95% CI: 0.09%, 1.59%) rise in hospital admissions for COPD [55]. Additionally, several epidemiological studies have indicated that patients with asthma were particularly vulnerable to rises in ground-level O3 [56, 57]. Fang X et al. found that male and older asthma patients may be more vulnerable to O3 especially in the warm season [57].
PM2.5 from wildfire was also positively correlated to adverse respiratory health outcomes. For example, results from Alman, BL et al. showed positive relationships between PM2.5 and COPD (OR = 1.05, 95%CI: 1.02, 1.08 per 5 µg/m3) and asthma (OR = 1.04, 95% CI: 1.02, 1.06 per 5 µg/m3) [58]. Furthermore, particulate matter in outdoor air pollution was identified as Group I carcinogen by the International Agency for Research on Cancer (IARC) [59]. Prolonged exposure to elevated levels of particulate matter can elevate the risk of numerous health problems, with CRD being particularly prominent. Although the wildfire usually maintains relatively short duration, the released smoke and PM will persist in the atmosphere for a long time, thereby affecting a potential large population. In addition, temperature rise can also increase the release of VOCs, which can stimulate respiratory mucosa, cause respiratory diseases and allergic reactions.
4.2 The effects of extreme weather events on CRDClimate change exacerbates the frequency and intensity of drought and extreme high temperatures, while also affecting precipitation patterns and amounts, thereby increasing the risk of forest fires. A systematic review and meta-analysis revealed that a rise in EWEs elevated the risk ratios of asthma occurrences to 1.19 (95% CI: 1.08, 1.32) in children and 1.29 (95% CI: 0.98, 1.69) in female, respectively [60]. Previous evidence indicated that particulate matter levels typically exceeded the standard pollution levels of the area during wildfire incidents [61]. In summer 2010, a prolonged heatwave occurred in the Russian, accompanied by catastrophic wildfires. Compared to the same period, a rise in respiratory disease-related deaths, amounting to 339, was observed in Moscow (RR = 2.05, 95% CI: 1.80–2.39), which demonstrated a combined impact of heat and air pollution on mortality [62]. Meanwhile, changes in overall climate patterns have led to soil drying and water depletion in some areas, increasing the frequency and intensity of sandstorms. Long-term exposure to sandstorm environments may lead to the development and aggravation of COPD, etc. [52, 63].
Climate change is closely related to extreme precipitation events such as heavy rainfall, flood and hurricane [64]. Patients with CRD (such as COPD, asthma, etc.) already suffered from chronic inflammation of the respiratory tract, and are easily affected by moisture and humid environments. Heavy rainfall also increases the growth of indoor fungi, leading to aggravated allergic reactions and respiratory infections in CRD patients. For example, Hayes D Jr et al. found a strong correlation between mold sensitization and asthma, with humidity identified as a worsening factor for patients suffering from allergic asthma [65]. In addition, while humidity is not a direct cause for interstitial pneumonia, it facilitates the growth of mold and microorganisms, which upon inhalation, may exacerbate inflammation or lead to secondary infections. In hypersensitivity pneumonitis, elevated humidity accelerates mold and fungal spore proliferation, with exposure to these allergens frequently inducing symptoms such as coughing and dyspnea [66]. High humidity can also promote the growth of bacteria and viruses, thereby increasing the risk of respiratory tract infections.
It is predicted that atmospheric alterations related to thunderstorms are likely to become more intense in face of climate change [67]. Thunderstorm-induced asthma refers to the onset of sudden asthma attacks that happen immediately following a thunderstorm, often referred to as “thunderstorm asthma” [68]. During thunderstorms, high winds and electrical activity can cause pollen grains to rupture into smaller particles, which can be inhaled and penetrate deeper into the airway. Pollen allergens can trigger the release of pro-inflammatory and immunomodulatory mediators, thereby accelerating the onset of IgE-mediated sensitization and allergic reactions [47]. This process can precipitate early asthmatic reactions, following the inhalation of elevated concentrations of aeroallergens [69]. Additionally, the increased humidity and cooler air associated with the thunderstorm may exacerbate airway sensitivity, leading to bronchoconstriction and asthma symptoms, especially in individuals with preexisting allergies or asthma [70]. Except for asthma, Eric Zou et al. found that emergency department visits for COPD also significantly increased during thunderstorms period. The primary mechanism underlying thunderstorm-related acute respiratory disease except for asthma may be the preceding increases in the concentration of particulate matter and temperature variation [67].
4.3 The impact of adverse meteorological conditions on CRDSudden changes in temperature and humidity are also linked to increased emergency department (ED) visits for patients suffering from chronic respiratory disease [71]. Previous evidence showed that a 1 °C rise in maximum temperature variability elevates the risk of asthma by 5.0% globally, with this effect being particularly pronounced among individuals residing in high-latitude regions or those aged between 50 and 70 years [50]. Tran HM et al. found that following adjustments for annual PM2.5 levels, socio-demographic index level, smoking prevalence, and geographical regions, a 0.26% rise in deviance percentage of temperature corresponded to reductions in the log of age-standardized mortality rates (LASMR) of COPD by 0.016, 0.017, and 0.014 per 100,000 individuals and in the LASMR of asthma by 0.042, 0.046, and 0.040 per 100,000 individuals across both genders, males, and females, respectively [72]. Besides, for CRD patients, when the barometric pressure decreases suddenly, the pressure of the gas in the lungs also decreases, which may lead to dyspnea and worsen symptoms [73]. Excessive humidity may also pose negative impact on the respiratory system. In high humidity environments, moisture in the air can easily trigger the growth of fungi and mold, such as Aspergillus, Cladosporium, Penicillium and Stachybotrys, which may lead to respiratory allergic reactions and infections, thereby exacerbating symptoms of allergic respiratory diseases [74, 75]. For example, Aspergillus can trigger allergic reactions like asthma, allergic bronchopulmonary aspergillosis, sinusitis and invasive aspergillosis [76, 77]. Cladosporium may result in hay fever-like symptoms, asthma, and allergic rhinitis, with rare cases of lung infections in immunocompromised individuals [78, 79]. Penicillium exposure can cause respiratory symptoms such as asthma, nasal congestion, sinus inflammation and penicilliosis, a lung-focused fungal infection [80].
The augmentation in air pollution attributable to climate change could potentially intensify the inflammatory response within the pulmonary system. PM2.5 could potentially facilitate the progression of COPD by damaging pulmonary function and aggravating lung injury, with potential underlying mechanisms associated with inflammation [81]. Research from Zhao C et al. found that the soluble extract of PM2.5 could trigger an increase in pro-inflammatory factor expression by stimulating the nuclear factor kappa B (NF-κB) and mitogen-activated protein kinase (MAPK) signalling pathways. This was coupled with a decrease in airway barrier functionality, contributing to the aggravated progression of asthma [82]. Wang L et al. also found that PM2.5 could aggravate airway inflammation in asthmatic mice by activating NF-κB via myeloid differentiation primary response 88 (MyD88) signaling pathway [83]. Acute O3 exposure could also induce airway hyperreactivity and neutrophilic inflammation [84]. Besides, air pollution can directly affect the recruitment of inflammatory cells. For instance, a classic research identified that increased levels of O3 can stimulate an amplified inflammatory response, characterized by a rise in the proportion of neutrophils and total protein concentrations in bronchoalveolar lavage in asthmatic patients compared to non-asthmatic ones [85].
5.2 Immune disordersAir pollution leads to not only the recruitment of granulocytes in the airway, but also the influx of immune-modulatory cells exhibiting altered cell surface phenotypes associated with antigen presentation [86]. For instance, exposure to O3 not only results in an increased presence of dendritic cells and monocytes exhibiting elevated levels of CD14, CD86, human leukocyte antigen-DR isotype (HLA-DR), but also notably escalates the count of neutrophils and myeloperoxidase levels in airway lavages [85, 87]. Exposure to PM2.5 can lead to a decrease in the expression of programmed death-ligand 1 (PD-L1) in the lungs, consequently disrupting the establishment of immune tolerance and ultimately leading to allergic airway inflammation [88]. PM2.5 can alco exacerbate effects of asthma by regulating transient receptor potential ankyrin 1 (TRPA1), transient receptor potential vanilloid 1 (TRPV1) and the relevant inflammation mediators, such as interleukin (IL)-13, prostaglandin D2 (PGD2) [89]. Animal study showed that exposure to SO2 can alter the inflammatory and immune responses in the airways of asthmatic rats by enhancing the expression of pro-inflammatory cytokines and disrupting the Th1/Th2 balance, potentially contributing to an elevated risk of asthma [90].
5.3 Oxidative stressAir pollutants can induce potent oxidative stress responses, which not only leads to cellular damage through the production of reactive oxygen species (ROS), but also disrupts the body’s antioxidant defense mechanisms. Prolonged exposure to air pollutants can trigger the activation of oxidative pathways, leading to cellular death and persistent inflammation in the airways, culminating in emphysema [91]. For example, PM2.5 exposure can activate nuclear factor erythroid 2-related factor 2 (Nrf2) related signaling pathways and facilitate lung injury [92]. Xia R et al. found that PM2.5 could promote apoptosis of alveolar epithelial cells via targeting ROS/P38 signaling pathway and thus lead to emphysema in mice [93]. Li N et al. found that PM2.5 could contribute to pulmonary epithelial senescence and ferroptosis by regulating USP3-SIRT3-P53 axis [94]. Results from Havet A et al. indicated a direct positive correlation between O3 exposure and persistent asthma (OR = 1.68, 95%CI: 0.57, 7.25), further elucidating the role of oxidative stress in the relationship between air pollution and chronic asthma [95].
Overall, considerable previous research attention has been devoted to elucidating the pathophysiological mechanisms linked to the intensification of air pollution with CRD. However, investigations into the potential biological pathways of EWEs and unfavorable meteorological conditions remain relatively limited, which highlights the need for more comprehensive studies to clarify the systematic adverse outcome pathway of respiratory health impacts associated with changing climate.
Individual behavior can pose substantial effects on reducing exposure to air pollution [96]. For example, personal adaptive behavioral such as avoiding cooking with solid fuels, ensuring proper ventilation and separation of cooking areas, and utilizing air purifiers equipped with high-efficiency particulate air filters, can significantly mitigate the respiratory health hazards associated with air pollution under climate change (Fig. 1) [97]. Conversely, smoking related airway inflammation can exacerbate the impact of O3 exposure on blood oxygen saturation in COPD patients [98]. It is predicted that outdoor physical activities in areas with high air pollution can expose individuals to harmful pollutants, potentially leading to respiratory health issues. Research conducted by Tikkakoski, AP et al. demonstrated a significant correlation between exercise-induced bronchoconstriction and particulate matter as well as air humidity in preschool-aged children [99]. However, Chen, L et al. indicated that regular physical activity could lower the risk of COPD, and such protective benefits were not influenced by exposure to ambient PM2.5 [100]. Therefore, the interaction between physical activity and air pollution on the incidence of CRD still needs further exploration.
Potential risk and influencing factors linking climate change and chronic respiratory diseases
Limited by the level of economic development in some developing countries or regions, the ability to adapt to climate change is relatively poor in vulnerable areas [101]. Lack of adaptation measures and coping abilities can more easily lead to respiratory health problems [102]. Specifically, factors such as industrialization, traffic congestion, energy consumption and domestic pollution can also exacerbate the impact on respiratory health [103].
6.3 Medical services and health examinationsIt is difficult for people with limited medical resources and physical examination to detect early symptoms of chronic respiratory diseases, making them more susceptible to the impact of climate change [104]. The fair allocation and comprehensive coverage of health resources are crucial for ensuring health equity and addressing the health impacts of climate change [105]. Therefore, it is necessary to increase investment in medical resources, strengthen health education, and improve climate change adaptation capabilities.
Climate change has exacerbated health inequality, making vulnerable populations (such as the elderly, children and impoverished individuals) more susceptible to the negative impacts of climate change [106–109]. For example, EWEs such as heatwaves, wildfires and sandstorms can lead to increased health risks for children’s respiratory system [110]. Besides, the impact of climate change on respiratory health is more significant in patients with underlying cardiovascular and pulmonary diseases [111, 112]. People living in regions lacking the ability to respond to EWEs and provide health infrastructure, such as well-equipped sanitation facilities and medical services, are also facing health inequality associated with climate change [113]. Previous studies have shown that the health effects related to heat exposure vary greatly due to geographical regions and socio-economic status [114]. For example, desert regions in Africa face challenges such as fragile ecosystems, lagging economic development, weak sanitation facilities, and limited risk resistance [115]. Climate change has further exacerbated these issues. The increased concentration of particulate matter and other pollutants caused by drought and desertification can directly harm the respiratory system, making the impact on respiratory health particularly more prominent [116].
As climate change progressively intensifies, it is crucial to address these interconnected issues of air pollution and climate change to protect both global environment and public health. Firstly, it is necessary to adopt policies that focus on simultaneous pollution reduction and carbon mitigation, such as promoting renewable energy to replace fossil fuels, which not only reduces carbon dioxide emissions but also decreases air pollutants. The introduction of carbon pricing strategies, including carbon taxes or cap-and-trade mechanisms, could offer financial motivations for companies to decrease carbon emissions and invest in more environmentally friendly technologies. Secondly, it is of vital importance to raise public awareness of the association between climate change and respiratory health through health education and publicity, and further guide them to adopt positive health behaviors and individual protective measures [117]. Finally, in order to address the issues of respiratory health inequality, the international community should strengthen cooperation and take comprehensive measures, such as increasing climate change adaptation capacity, providing health services and infrastructure support, promoting sustainable development and fair and just health rights [118].
This review provided epidemiological evidence, potential influencing factors and pathophysiological mechanisms underlying the increased risk of chronic respiratory diseases associated with climate change, and calls for the necessity of adaptive strategies. In the future, it is necessary to strengthen interdisciplinary research in the fields of climate change and respiratory health, in order to protect vulnerable populations and improve climate change response capabilities, thereby promoting the climate health equity.
All authors are in agreement that the work is prepared for submission to the journal, accept full responsibility for the manuscript’s contents, and confirm that there are no conflicts of interest associated with this article. This systematic review does not involve ethics approval.
Consent for publicationNot applicable.
Availability of data and materialNo data was used for the research described in the article.
Competing interestsThe authors declare that they have no competing interests.
FundingThis work was supported by the 34th Batch of Jinan Science and Technology Innovation Development Plan (Clinical Medicine Science and Technology Innovation Plan) Projects (grant number 202134008), the Foundation of Jinan Municipal Health Commission Big Data Technology Program (grant number 2022-BD-04), the Postdoctoral Fellowship Program of CPSF under Grant Number GZC20240798, and the China Postdoctoral Science Foundation (Certificate Number: 2024M751734).
Authors’ contributionsJX: Conceptualization, Investigation, Methodology, Writing – original draft, review and editing, Funding acquisition. ZS: Investigation, Project administration. CL: Investigation, Writing – original draft. YN: Investigation, Writing – review & editing. LC: Conceptualization, Funding acquisition, Writing – review & editing. All authors have read and approved the final version of the manuscript for publication.
AcknowledgementsJiayu Xu appreciate the Shuimu Tsinghua Scholar Program of Tsinghua University.