Climate change is perhaps the greatest threat humans face today, with far-reaching implications for food supply chains, migration patterns, shifting habitats, extreme weather events, and human health. The average global surface temperature in July 2022 was the sixth warmest for July since 1880 when record keeping began,1 and global temperatures are expected to continue rising over the next several decades.2 As of 2016, global atmospheric CO2 concentrations have permanently crossed above 400 ppm, an important threshold with implications for further rising global temperatures and other climate impacts. According to the World Health Organization, climate change has both direct and indirect effects on health and disproportionately impacts vulnerable groups like children, the elderly, racial and ethnic minority groups, low-income populations, and citizens of developing nations.3 Some of the many climate-sensitive health risks include injury or death from extreme weather events, heat-related illnesses, increase in waterborne and vector-borne diseases, malnutrition, and respiratory illnesses. Similar effects of rising global temperatures on survival have been described in animals.4

Earth’s changing climate is primarily the result of human activity, namely the production of greenhouse gases due to our reliance on burning of fossil fuels for energy.5 Toxic pollutants like black carbon, sulfur dioxide (SO2), nitrogen oxides (NOx), volatile organic compounds (VOC), particulate matter (PM), and polyaromatic hydrocarbons emitted as a result of burning of fossil fuels worsen air quality and increase absorption of solar radiation that further increases temperatures.6 Higher temperatures accelerate formation of ground-level ozone (O3) from NOx and VOC precursors that increase risk of cardiopulmonary morbidity and mortality. Drought conditions leading to wildland fires and desertification effects increase air particulates that exacerbate respiratory conditions like asthma and COPD and increase the risk for emergency department (ED) visits and hospitalizations.7

Viral respiratory tract infections are most common illnesses in humans,8,9 with estimated 17 billion incident cases globally in 201910. Common viruses causing respiratory tract infection include influenza, respiratory syncytial virus (RSV), rhinovirus (RV), and SARS-CoV-2. Viral respiratory infection imposes a substantial burden on populations and health systems.11 Non-influenza viral respiratory infections were estimated to cost the US economy $40 billion annually.11 Viruses are also the primary trigger for acute asthma exacerbations12 and a major cause of COPD exacerbations.13 While most viral respiratory infections are mild and self-limited,11 they can lead to severe complications in susceptible patients, including pneumonia and even respiratory failure.14,15 The SARS-CoV-2 pandemic in particular has contributed to over 3 million deaths worldwide.16

More than 90% of the world's population is exposed to polluted air.17 Convincing epidemiologic data has linked air pollution exposure with increased incidence of viral respiratory infections like upper respiratory tract (URI) infections,18,19 bronchitis,20 and lower respiratory tract infections (LTRI)21,22 such as pneumonia23,24 and bronchiolitis.25,26 Similarly, temperature,27,28 humidity,29 and extreme weather events30–32 have also been directly and indirectly associated with respiratory infections.

Climate change, air pollution, and viral respiratory infection are highly interconnected, and without interventions to halt global warming, we can expect the burden of viral respiratory disease to increase worldwide. This review will summarize the epidemiologic and experimental evidence for a relationship between climate change/air pollution and susceptibility to viral respiratory disease as well as future research priorities (Table 1).

Table 1 Summary Points and Knowledge Gaps


We conducted a search for peer-reviewed studies pertinent to climate change, air pollution, and viral respiratory infection using PubMed and Google Scholar databases. We applied the keywords: climate change, air pollution, particulate matter (PM), nitrogen dioxide (NO2), O3, RSV, RV, influenza, SARS-CoV-2, COVID-19, asthma, COPD, viral respiratory infection. Studies were included if they were 1) relevant to the aims of this review, 2) published in peer-reviewed journals, and 3) written in English.

Climate Change and Respiratory Viral Infection

Temperature, humidity, and extreme weather events are linked with respiratory infection incidence (reviewed by33). In temperate climates, lower temperature was usually associated with higher infection incidence. A study conducted in Sweden observed that lower temperature and larger weekly drop in temperature were associated with higher influenza incidence the following week.34 Lower temperature was associated with higher incidence of influenza A, respiratory syncytial virus (RSV), human metapneumovirus, bocavirus, and adenovirus, while no association with temperature was observed for human rhinovirus and enterovirus infection incidence.34 A US study found that warmer winters were associated with more severe epidemics of influenza A and B during the following winter season.27 Specifically, a mild winter was followed by a more severe than average influenza epidemic 72% of the time, and this epidemic had a growth rate 40% higher and peaking 11 days earlier than average.27 A study of RSV seasons over 8 years in the Netherlands reported a negative correlation between minimum temperature and RSV incidence (r=−0.338),28 with others reporting similar findings.35 For RSV specifically, some experts have proposed that climate change and resulting warmer winters may be beneficial in terms of shortening RSV seasons.36 In contrast, Zoran et al observed a positive correlation between COVID-19 cases and air temperature (r=0.67), indicating high transmission during warmer temperatures, which may partially explain continued high levels of transmission of the SARS-CoV-2 virus observed even during the summer months.37

In tropical climates, increased temperature was associated with higher rates of respiratory infections. Phung et al reported that among urban children <5 years of age in the Mekong Delta region of Vietnam, rates of hospital admissions for respiratory infections increased by 3.8% (95% CI 0.4, 7.2) for every 1°C increase in 2-day moving average temperature.38 Temperature variability was also linked to viral respiratory infection incidence. Greater temperature variability, day-to-day and within the same day, was positively associated with greater frequency of healthcare visits for acute bronchitis39 and pneumonia in children.40,41 However, most analyses did not account for air pollution, socioeconomic status, or behavior factors, which could have influenced infection frequency.

The relationship of humidity to viral respiratory disease incidence is inconsistent and may vary depending on the specific respiratory virus. Chowell et al reported a strong negative correlation (r=−0.70) between relative humidity and peak incidence of H1N1 influenza during the 2009 pandemic.29 Similarly, an inverse relationship was observed between COVID-19 cases and relative humidity levels in the Lombardy region of Italy during early 2020 (r=−0.47), suggesting that dry air favors virus transmission.37 In contrast, RSV incidence was positively correlated with relative humidity,28,35 suggesting that higher humidity was associated with higher RSV activity.

Extreme weather events such as wildfires, heavy rainfall with flooding, and heat waves have been linked with respiratory infection risk as well. In addition to direct effects, these events can also have indirect effects on risk of respiratory infections, such as displacement of large groups of people from their homes, indoor crowding and increased time spent indoors, and inadequate food supply with malnutrition that enhance susceptibility to and transmission of disease. Increased time spent indoors may also increase exposure to indoor pollution sources such as burning biomass that contribute to respiratory symptoms.

A systematic review of air pollution exposure during natural disasters including wildland fires and volcanic eruptions concluded that PM generated by these events was associated with increased rates of acute respiratory infection, pneumonia, bronchitis, and bronchiolitis.30 A consistent association across multiple studies was observed between exposure to wildfire-related particulate matter less than 2.5 µm in diameter (PM2.5) and increased ED visits and hospitalizations for acute respiratory infection.31,42–47 Delfino et al found that during wildfires in Southern California, the number of hospital admissions for pneumonia increased by 1.3x (95% CI 1.17, 1.48) and admissions for acute bronchitis/bronchiolitis increased by 1.6x (95% CI 1.09, 2.29) among area residents.46 Rappold et al reported similar findings following wildfires in North Carolina, with residents from exposed counties experiencing an increased risk of ED visits for bronchitis and pneumonia (cRR 1.59, 95% CI 1.07, 2.34).43

Extreme rainfall and flooding were linked with acute respiratory infections as well. Phung et al reported a significant relationship between extreme river water levels in the Mekong Delta region and daily pediatric hospitalizations for respiratory infection (cRR 1.66, 95% CI 1.57, 1.74).32 A retrospective study from the Netherlands reported that exposure to floodwater and performing clean-up after flooding were associated with higher odds of acute respiratory infection (aOR 3.3, 95% CI 2.0, 5.4).48

Heat waves may also contribute to increased respiratory infections. In California, more ED visits for respiratory infections were observed among all age groups during the July–August 2006 heat wave compared to reference periods immediately before and after the heat wave.49 Similarly, a time-stratified case–crossover study conducted in China over a 2-year period observed that heatwaves increased the risk of outpatient visits for respiratory infection among all ages (RR 1.31, 95% CI 1.18, 1.45), with children (1.74, 95% CI 1.52, 1.99) and the elderly (1.41, 95% CI 1.11, 1.79) at particularly elevated risk.50 The contribution of unmeasured factors such as increased time spent indoors during periods of extreme heat is unknown. A mechanism by which extreme heat may directly contribute to increased risk of infection is unclear, though heat stress has been shown to impair airway innate immune responses in animal studies.51 Chronic heat stress in mice was associated with a reduced production of inflammatory cytokines IL-6 and IFN-β, increased viral load and increased mortality rate following avian influenza H5N1 infection.

Air Pollution and Respiratory Infection: Epidemiologic Evidence

Short- and long-term exposure to air pollution has been extensively linked with increased susceptibility to respiratory infection. Short-term exposure to increased PM was associated with increased susceptibility to respiratory infections including influenza24,52 and influenza-like illness,53–55 RSV bronchiolitis,25,26,56 and acute lower respiratory tract infections (LTRI)22 including pneumonia.23,24,57 Chen et al observed that across 47 Chinese cities, a 10 μg/m3 increase in PM2,5 was associated with an increased risk of influenza (RR 1.020, 95% CI 1.006, 1.034) at lag days 2–3, after controlling for seasonality and weather conditions.52 Croft et al examined data from 500,000 ED visits and hospitalizations from New York state and found that IQR increases in PM2.5 during the prior week were significantly associated with higher rates of ED visits for influenza (3.9%, 95% CI 2.105.6%; at 7 days) and culture-negative pneumonia (2.5%, 95% CI 1.4–3.6%; at 6 days).24 Similarly, in two studies in Italy, RSV infection incidence and risk of hospitalization for RSV bronchiolitis in infants were positively associated with concentrations of PM less than 10 µm in diameter (PM10) during the prior 1–2 weeks.25,26 Using both single and multipollutant exposure models to estimate the association between air pollutants and respiratory infection in preschool-aged children, Zhang et al observed a significant association between PM2.5 levels and respiratory infections in children 6 months of age and under (single pollutant model: OR 1.012, 95% CI 1.008–1.018) (multipollutant model: 1.019, 95 CI 1.012–1.026).58 Similar associations with viral respiratory infections were seen with O3 (1.025, 95% CI 1.018–1.033) in children ≤6 months of age, with smaller but significant associations in 7–12 month old and 1–3-year-old children. PM10 levels were associated with viral respiratory infections as well (1.025, 95% CI 1.008–1.042) but only among 3-6-year-old children.

NO2 exposure was also implicated to increase susceptibility to viral respiratory infections. Elevated NO2 concentrations were associated with increased hospital admissions for acute respiratory infections,19 including croup20,59 and viral infection-induced asthma exacerbation,60 pneumonia,21 and influenza.21 Exposure to increased O3 was also associated with hospital admission for pneumonia21,61 and influenza21 infection.

Further, in a systematic review and meta-analysis of ambient air pollution and pneumonia in children, Nhung et al reported an overall positive association between pediatric hospitalization for pneumonia and exposure to air pollutants, including PM2.5, PM10, SO2, O3, and NO2. The largest association observed was for SO2, with ER visits increasing by 2.9% (95% CI 0.4–5.3%) per 10 ppb increase. The authors noted significant effect modification by study location, with stronger associations observed in low- and middle-income countries compared to high-income countries.23 The same authors later reported that higher O3 and PM10 concentrations were associated with an increased length of hospital stay among children 5 years and under admitted for lower respiratory infection, with no relationship between PM2.5, SO2, or NOx and length of stay.62 Specifically, per IQR increase in O3, there was a 5% (95% CI 2–8%) decrease in odds of hospital discharge, and for PM10, there was a 6% decrease in odds of hospital discharge in the 2–5-year-old group only.

There is also convincing evidence suggesting that long-term exposure to air pollutants predisposes to respiratory infection, though it is unclear whether this susceptibility is a function of exposure during the prenatal period, postnatal period, or both. Within the Prevention and Incidence of Asthma and Mite Allergy (PIAMA) birth cohort, Brauer et al observed that long-term exposure to traffic-related pollutants (PM2.5, NO2, soot) was associated with higher odds of ear, nose, and throat infections at 2 years of age63 as well as influenza and serious cold infections at 4 years of age.64 A meta-analysis of over 16,000 children from 10 birth cohorts from the ESCAPE project found that physician-diagnosed pneumonia during the first 2 years of life was significantly associated with annual average air pollution levels of PM10 (OR 1.76, 95% CI 1.00, 3.09 per 10 μg/m3) and NO2 (1.30, 95% CI 1.02, 1.65 per 10 μg/m3), but not PM2.5 (2.58, 95% CI 0.91, 7.27).65

Air Pollution and SARS-CoV-2

Many have hypothesized that air pollution contributed to the initial spread of SARS-CoV-2 during the early days of the pandemic66–68 and may also increase the risk of mortality.69,70 Air particulates from indoor71 and outdoor samples were shown to contain SARS-CoV-2 viral particles.72,73 In addition to having high levels of air pollution, densely populated urban centers like Wuhan and New York City were also hot spots for SARS-CoV-2 transmission and COVID-19-related mortality. Concentrations of PM2.5, PM10, NO2, and O3 in the prior 2 weeks were significantly associated with daily confirmed COVID-19 cases in an analysis of data from 120 cities in China between January and February 2020, with the largest association observed with per 10 μg/m3 increase in NO2 (6.94%, 95% CI 2.38%, 11.51%).74 Higher SO2 concentrations were associated with a decrease in new COVID-19 cases. Moderate correlations were observed between air pollutants and COVID-19 cases (Pearson’s r ranging from 0.41 for PM10 to 0.58 for PM2.5) in hard-hit regions of Italy.75 In China’s Hubei province, a significant correlation was observed between NO2 levels and SARS-CoV-2 transmission rate in 11 cities (r > 0.5), indicating that SARS-CoV-2 transmission was higher in regions with higher NO2 exposure.76 The same group reported a significant association between higher COVID-19 case fatality rates and higher levels of PM2.5 and PM10 in Wuhan, China.77 Ogen observed that over 80% of COVID-19-related fatalities in Europe during the first 2 months of the SARS-CoV-2 pandemic occurred in places with the highest NO2 concentrations, particularly the Lombardy region of Italy.69 In the majority of studies, potentially confounding health variables such as age and pre-existing disease could not be accounted for, limiting the ability to accurately estimate the impact of pollutant exposure on outcomes. Another uncertainty is the effect of length of exposure and whether short- or long-term exposure is more important in terms of risk of contracting SARS-CoV-2 infection, disease severity, and mortality risk. A recently published prospective study of residents in Varese, Italy, found that long-term exposure to airborne pollutants PM2.5, PM10, NO2, and NO increased the incidence of COVID-19.78 The largest effect was seen in single and bi-pollutant models of PM2.5, which was associated with a 5% increase in COVID-19 incidence (95% CI 2.7%, 7.5%). Further studies are needed to answer remaining questions about the relationship between air pollution and SARS-CoV-2 infection.

Summary of Epidemiologic Studies

The totality of the epidemiological evidence supports a link between air pollution exposure and increased susceptibility to viral respiratory infection. However, our review of the literature has several limitations. Population-level studies are limited in their ability to accurately estimate an individual’s pollutant exposure. Additionally, under real-world conditions, populations are exposed to a mixture of air pollutants. Differences in study outcomes were influenced by differences in study design, exposure assessment, and adjustment for potential confounders. Further work is needed to address important research questions about the causal pathway between air pollution exposure and viral respiratory infection, particularly for SARS-CoV-2 virus. It is currently unclear whether air pollutants predominantly influence transmission and susceptibility to viral infection or if they significantly impact disease severity and mortality risk. The impact of short- versus long-term exposure to pollutants on infection risk is another poorly understood area in need of high-quality research.

Air Pollution and Increased Susceptibility to Viral Respiratory Infection: Mechanistic Evidence

Since it is not possible to separate out the health effects of individual pollutants in epidemiologic studies, in vitro studies, animal model studies, and human controlled exposure studies have been performed to help establish the mechanisms of the apparent synergistic relationships between exposure to air pollutants and viral respiratory infection (Figure 1).

Figure 1 Proposed mechanisms by which air pollutants contribute to viral respiratory infection susceptibility and severity.

Altered Immune Response to Viral Infection

Exposure to air pollutants augments airway inflammatory responses to viral infection, through exaggeration or impairment of the innate and adaptive immune responses and/or skewing of the response from predominantly antiviral to an allergic, Th2-predominant response. In human bronchial epithelial cells exposed to urban PM, enhanced activation of the NLRP3 inflammasome was observed with increased production of interleukin (IL)-1β following influenza A infection, but not RSV infection, suggesting an exaggerated inflammatory response.79 Similar to PM, DEP exposure was associated with enhanced susceptibility and inflammatory response to influenza infection in primary human bronchial epithelial cells80,81 and mouse models.82

Primary human nasal epithelial cells infected with RV and exposed to NO2 or O3 showed enhanced release of the inflammatory cytokine IL-8 compared to RV infection alone or pollutant exposure alone, suggesting that epithelial-derived inflammation from viral respiratory infection is enhanced by exposure to air pollutants.83 However, other groups observed a reduction in virus-induced lung injury84 and mortality85 when mice were exposed to O3 during influenza infection, potentially owing to dampening of the immune response to infection.84 Similarly, alveolar macrophages exposed to O3 showed diminished cytokine production after infection with RSV.86 The effects of O3 exposure on respiratory viral infection may be virus-specific.

Mice exposed to ultrafine carbon black prior to RSV infection showed skewing of the immune response away from an antiviral Th1 milieu (IFN-gamma, IL-12, and IP-10) towards an allergic, Th2-predominant inflammatory milieu (RANTES, eotaxin, MCP-1, MIP-1a, MIP-1b, and IL-13).87,88 Ultrafine PM exposure in neonatal mice resulted in increased amounts of immunosuppressive T-regulatory (Treg) cells and IL-10 following influenza infection and showed decreased influenza-specific T-cell responses.89 Exposure to carbon black particles was associated with increased morbidity from RSV in these mice, including increased airway hyperresponsiveness.90 Similar Th2 skewed airway inflammation was observed after exposure of primary respiratory epithelial cells to diesel exhaust particles (DEP), a type of PM,80 which may increase susceptibility to viral infection. Chronic exposure to DEP was associated with decreased interferon production in response to influenza infection in mice; infection-specific antibody titers were also reduced compared to controls.91

Altered Epithelial Barrier Function

The epithelial barrier represents the first line of defense against inhaled pathogens. Integrity of epithelial junctions, mucociliary clearance, and antioxidant and antimicrobial protein composition of airway lining fluid are key defenses. Exposure to O3,92,93 NO2,94,95 and PM96 has been shown to alter airway epithelial permeability.66 Rats exposed to O3 and injected with an IV tracer showed increased presence of tracer in bronchoalveolar lavage fluid (BAL) compared to rats exposed to clean air, suggesting disruption of the airway epithelium induced by O3.93 Short-term exposure of hamsters to NO2 showed significant but transient disruption of bronchiole tight junctions (TJ) with as little as 6 hours of exposure.97 Experiments testing the effect of long-term NO2 exposure in hamsters showed significant, non-reversible TJ disruption.94 Liu et al showed that PM exposure of primary human bronchial epithelial cells infected with Pseudomonas aeruginosa resulted in oxidative injury with degradation of TJs and increased intracellular bacteria.96 PM was also shown to impair airway mucociliary clearance,98 and increase production of the pathogenic glycoprotein mucin MUC5AC.99 Exposure to O3100 in vivo and NO2101 ex vivo were associated with depletion of antioxidant proteins from lung lining fluid. Epithelial cell-derived defense proteins like surfactants SP-A and SP-D are important in the defense against respiratory viral infection.102,103 Ciencewicki et al observed that DEP exposure of mice increased susceptibility to infection with influenza virus by reducing expression of SP-A and SP-D.82 Interestingly, SP-D was previously shown to bind SARS-CoV-1 spike protein, which could suggest a defensive role against SARS-CoV-2.66,104

Altered Cell Surface Receptor Expression and Viral Entry

Pollutants may enhance susceptibility to viral infection by altering viral entry into respiratory epithelial cells. Exposure of rat lung epithelial cells to DEP resulted in upregulated expression of intercellular adhesion molecule 1 (ICAM-1), the receptor used by RV to gain entry into the cell, in a concentration-dependent manner, increasing opportunities for viral entry;105 similar effects were observed with NO2 exposure in vitro.83 Human nasal and bronchial epithelial cells exposed to DEP showed increased influenza virus attachment to epithelial cells and increased numbers of influenza-infected cells 24 hours after application of virus.80 Similarly, mice exposed to DEP had more severe influenza infection assessed by the presence of lung consolidation, increased viral replication and decreased antiviral interferon production compared to controls.91 Mice exposed to PM2.5 showed upregulation of ACE2 expression in the lungs,106 and it was suggested that PM-induced overexpression of ACE2 may impact susceptibility to SARS-CoV-2 infection and infection severity.107 The effects of O3 exposure on viral respiratory infection are less consistent. O3 exposure of human nasal epithelial cells resulted in increased expression of proteases that cleave influenza HA surface protein, an essential step in viral entry into the cell, thus promoting viral entry and enhancing viral replication.108 However, primary human bronchial epithelial cells exposed to O3 prior to RSV infection showed decreased viral production.109 Mice exposed to O3 and infected with influenza showed reduced severity of lung injury and reduced immune response to infection with fewer T and B cells recovered from the lungs and reduced influenza-specific antibody titers in serum.84

Impaired Cytotoxicity

Pollutant exposure may impact the ability of immune cells to engulf and/or kill viral-infected cells.110–112 Rose et al found that mice exposed to NO2 required 100-fold lower amounts of murine cytomegalovirus to become infected compared to mice exposed to clean air, and NO2-exposed mice also showed signs of decreased clearance of the virus by macrophages.112 Alveolar macrophages exposed to PM10 infected with RSV showed reduced activation, cytokine production, and uptake of viral particles, suggesting impairment of the antiviral response.110 Guinea pig alveolar macrophages exposed to PM10 and infected with RSV showed markedly reduced viral replication and infection-induced inflammatory cytokine production.111 Using a macrophage cell line, Renwick et al observed that exposure to ultrafine particulates significantly impaired phagocytic activity.113 Natural killer (NK) cells stimulated with polyinosinic:polycytidylic acid (pI:C) to simulate viral infection and DEP showed reduced production of IL-1β, IL-8 and TNFα and reduced expression of granzyme B and perforin. Cell-mediated cytotoxicity functional assay showed a significant reduction in cytotoxic activity with pI:C+DEP compared to pI:C alone.114 BAL fluid cells from volunteers with repeated exposure to NO2 showed reduced quantities of cytotoxic T cells and NK cells but intact phagocytic activity of alveolar macrophages.115

Direct Viral Transmission

In addition to increasing susceptibility to viral respiratory infection, PM may serve as a carrier for viral particles. Hsiao et al detected influenza virus within samples of PM2.5 and suggested that this could be a mode of direct transmission of virus to the airway epithelium.116 Multiple research groups have identified SARS-CoV-2 virus within PM2.5 from air samples supporting this conclusion, with the caveat that temperature, humidity, and other weather conditions can also affect the efficiency of viral transmission.71,73,117 However, the World Health Organization (WHO) has concluded based on properties of the virus that ambient air pollution is not likely to contribute to SARS-CoV-2 transmission.118


There is substantial evidence supporting the relationship between natural and anthropogenic sources of climate change, namely air pollution, and increased susceptibility to respiratory infections through several proposed mechanisms. Conversely, it is possible that climate change could have some positive effects on respiratory viral infection due to shorter, warmer winters, particularly in the case of RSV. However, this comes at the expense of increased exposure to toxic air pollutants and susceptibility to respiratory viruses whose transmission is not impaired by warmer temperatures (as appears to be the case with SARS-CoV-2, for example). Another important consideration is that climate change also alters animal migration patterns and shifts habitats such that humans and domesticated animals are in closer proximity to wild animals.119 These changes can be the catalyst for the emergence of new zoonotic viruses with potential to cause future pandemics. The need has never been greater for aggressive interventions to reduce emissions of greenhouse gases and toxic pollutants to mitigate the effects of climate change. The initial rapid fall in air pollutants around the world during the initial COVID-19 lockdowns showed us what is possible, though at a significant economic price. A report from a joint workshop between the WHO, the European Respiratory Society, and several other scientific societies noted that the COVID-19 pandemic has brought to light the vast interconnectedness between climate change and infectious disease.118 Without significant long-term strategies for phasing out fossil fuel use in favor of green energy, we will likely see an increase in the burden of respiratory viruses in human populations, particularly in vulnerable groups such as children, the elderly, and those with chronic respiratory disease.


The author has no conflicts of interest in this study to disclose.


1. National Oceanic and Atmospheric Administration. Selected significant climate anomalies and events: July 2022; 2022. Available from: Accessed September 8, 2022.

2. Intergovernmental Panel on Climate Change. Global Warming of 1.5°C; 2018. Available from: Accessed September 8, 2022.

3. World Health Organization. Climate change and health; 2021. Available from: Accessed September 9, 2022.

4. Paital B, Panda SK, Hati AK, et al. Longevity of animals under reactive oxygen species stress and disease susceptibility due to global warming. World J Biol Chem. 2016;7(1):110–127. doi:10.4331/wjbc.v7.i1.110

5. Climate science special report: fourth national climate assessment, Volume I. Washington, DC, USA (U.S. Global Change Research Program); 2017. Accessed September 9, 2022.

6. Jacob DJ, Winner DA. Effect of climate change on air quality. Atmos Environ. 2009;43(1):51–63. doi:10.1016/j.atmosenv.2008.09.051

7. Takaro TK, Knowlton K, Balmes JR. Climate change and respiratory health: current evidence and knowledge gaps. Expert Rev Respir Med. 2013;7(4):349–361. doi:10.1586/17476348.2013.814367

8. Hasegawa K, Tsugawa Y, Cohen A, Camargo CA. Infectious Disease-related Emergency Department Visits Among Children in the US. Pediatr Infect Dis J. 2015;34(7):681–685. doi:10.1097/INF.0000000000000704

9. Witek TJ, Ramsey DL, Carr AN, Riker DK. The natural history of community-acquired common colds symptoms assessed over 4-years. Rhinology. 2015;53(1):81–88. doi:10.4193/Rhino14.149

10. Jin X, Ren J, Li R, et al. Global burden of upper respiratory infections in 204 countries and territories, from 1990 to 2019. EClinicalMedicine. 2021;37:100986. doi:10.1016/j.eclinm.2021.100986

11. Fendrick AM, Monto AS, Nightengale B, Sarnes M. The economic burden of non-influenza-related viral respiratory tract infection in the United States. Arch Intern Med. 2003;163(4):487–494. doi:10.1001/archinte.163.4.487

12. Castillo JR, Peters SP, Busse WW. Asthma exacerbations: pathogenesis, prevention, and treatment. J Allergy Clin Immunol Pract. 2017;5(4):918–927. doi:10.1016/j.jaip.2017.05.001

13. Ko FW, Chan KP, Hui DS, et al. Acute exacerbation of COPD. Respirology. 2016;21(7):1152–1165. doi:10.1111/resp.12780

14. Nicholson KG, Kent J, Hammersley V, Cancio E. Acute viral infections of upper respiratory tract in elderly people living in the community: comparative, prospective, population based study of disease burden. BMJ. 1997;315(7115):1060–1064. doi:10.1136/bmj.315.7115.1060

15. Arroll B. Common cold. BMJ Clin Evid. 2008;2008:1510.

16. Lavine JS, Bjornstad ON, Antia R. Immunological characteristics govern the transition of COVID-19 to endemicity. Science. 2021;371(6530):741–745. doi:10.1126/science.abe6522

17. Burnett R, Chen H, Szyszkowicz M, et al. Global estimates of mortality associated with long-term exposure to outdoor fine particulate matter. Proc Natl Acad Sci U S A. 2018;115(38):9592–9597. doi:10.1073/pnas.1803222115

18. Jaakkola JJ, Paunio M, Virtanen M, Heinonen OP. Low-level air pollution and upper respiratory infections in children. Am J Public Health. 1991;81(8):1060–1063. doi:10.2105/AJPH.81.8.1060

19. Fusco D, Forastiere F, Michelozzi P, et al. Air pollution and hospital admissions for respiratory conditions in Rome, Italy. Eur Respir J. 2001;17(6):1143–1150. doi:10.1183/09031936.01.00005501

20. Dockery DW, Speizer FE, Stram DO, Ware JH, Spengler JD, Ferris BG. Effects of inhalable particles on respiratory health of children. Am Rev Respir Dis. 1989;139(3):587–594. doi:10.1164/ajrccm/139.3.587

21. Wong TW, Lau TS, Yu TS, et al. Air pollution and hospital admissions for respiratory and cardiovascular diseases in Hong Kong. Occup Environ Med. 1999;56(10):679–683. doi:10.1136/oem.56.10.679

22. Horne BD, Joy EA, Hofmann MG, et al. Short-term elevation of fine particulate matter air pollution and acute lower respiratory infection. Am J Respir Crit Care Med. 2018;198(6):759–766. doi:10.1164/rccm.201709-1883OC

23. Nhung NTT, Amini H, Schindler C, et al. Short-term association between ambient air pollution and pneumonia in children: a systematic review and meta-analysis of time-series and case-crossover studies. Environ Pollut. 2017;230:1000–1008. doi:10.1016/j.envpol.2017.07.063

24. Croft DP, Zhang W, Lin S, et al. The association between respiratory infection and air pollution in the setting of air quality policy and economic change. Ann Am Thorac Soc. 2019;16(3):321–330. doi:10.1513/AnnalsATS.201810-691OC

25. Vandini S, Corvaglia L, Alessandroni R, et al. Respiratory syncytial virus infection in infants and correlation with meteorological factors and air pollutants. Ital J Pediatr. 2013;39(1):1. doi:10.1186/1824-7288-39-1

26. Carugno M, Dentali F, Mathieu G, et al. PM10 exposure is associated with increased hospitalizations for respiratory syncytial virus bronchiolitis among infants in Lombardy, Italy. Environ Res. 2018;166:452–457. doi:10.1016/j.envres.2018.06.016

27. Towers S, Chowell G, Hameed R, et al. Climate change and influenza: the likelihood of early and severe influenza seasons following warmer than average winters. PLoS Curr. 2013;5. doi:10.1371/currents.flu.3679b56a3a5313dc7c043fb944c6f138

28. Meerhoff TJ, Paget JW, Kimpen JL, Schellevis F. Variation of respiratory syncytial virus and the relation with meteorological factors in different winter seasons. Pediatr Infect Dis J. 2009;28(10):860–866. doi:10.1097/INF.0b013e3181a3e949

29. Chowell G, Towers S, Viboud C, et al. The influence of climatic conditions on the transmission dynamics of the 2009 A/H1N1 influenza pandemic in Chile. BMC Infect Dis. 2012;12:298. doi:10.1186/1471-2334-12-298

30. Burhan EMU, Mukminin U. A systematic review of respiratory infection due to air pollution during natural disasters. Med J Indones. 2020;29(1):11–18. doi:10.13181/mji.oa.204390

31. Sheldon TL, Sankaran C. The Impact of Indonesian forest fires on Singaporean pollution and health. Am Econ Rev. 2017;107(5):526–529. doi:10.1257/aer.p20171134

32. Phung D, Huang C, Rutherford S, Chu C, Wang X, Nguyen M. Association between annual river flood pulse and paediatric hospital admissions in the Mekong Delta area. Environ Res. 2014;135:212–220. doi:10.1016/j.envres.2014.08.035

33. Di Cicco ME, Ferrante G, Amato D, et al. Climate change and childhood respiratory health: a call to action for paediatricians. Int J Environ Res Public Health. 2020;17(15):5344. doi:10.3390/ijerph17155344

34. Sundell N, Andersson LM, Brittain-Long R, Lindh M, Westin J. A four year seasonal survey of the relationship between outdoor climate and epidemiology of viral respiratory tract infections in a temperate climate. J Clin Virol. 2016;84:59–63. doi:10.1016/j.jcv.2016.10.005

35. Nenna R, Evangelisti M, Frassanito A, et al. Respiratory syncytial virus bronchiolitis, weather conditions and air pollution in an Italian urban area: an observational study. Environ Res. 2017;158:188–193. doi:10.1016/j.envres.2017.06.014

36. Donaldson GC. Climate change and the end of the respiratory syncytial virus season. Clin Infect Dis. 2006;42(5):677–679. doi:10.1086/500208

37. Zoran MA, Savastru RS, Savastru DM, Tautan MN. Assessing the relationship between ground levels of ozone (O3) and nitrogen dioxide (NO2) with coronavirus (COVID-19) in Milan, Italy. Sci Total Environ. 2020;740:140005. doi:10.1016/j.scitotenv.2020.140005

38. Phung D, Rutherford S, Chu C, et al. Temperature as a risk factor for hospitalisations among young children in the Mekong Delta area, Vietnam. Occup Environ Med. 2015;72(7):529–535. doi:10.1136/oemed-2014-102629

39. Xie MY, Ni H, Zhao DS, et al. Effect of diurnal temperature range on the outpatient visits for acute bronchitis in children: a time-series study in Hefei, China. Public Health. 2017;144:103–108. doi:10.1016/j.puhe.2016.12.016

40. Xu Z, Hu W, Tong S. Temperature variability and childhood pneumonia: an ecological study. Environ Health. 2014;13(1):51. doi:10.1186/1476-069X-13-51

41. Sohn S, Cho W, Kim JA, Altaluoni A, Hong K, Chun BC. ‘Pneumonia Weather’: short-term effects of meteorological factors on emergency room visits due to pneumonia in Seoul, Korea. J Prev Med Public Health. 2019;52(2):82–91. doi:10.3961/jpmph.18.232

42. Duclos P, Sanderson LM, Lipsett M. The 1987 forest fire disaster in California: assessment of emergency room visits. Arch Environ Health. 1990;45(1):53–58. doi:10.1080/00039896.1990.9935925

43. Rappold AG, Stone SL, Cascio WE, et al. Peat bog wildfire smoke exposure in rural North Carolina is associated with cardiopulmonary emergency department visits assessed through syndromic surveillance. Environ Health Perspect. 2011;119(10):1415–1420. doi:10.1289/ehp.1003206

44. Martin KL, Hanigan IC, Morgan GG, Henderson SB, Johnston FH. Air pollution from bushfires and their association with hospital admissions in Sydney, Newcastle and Wollongong, Australia 1994–2007. Aust N Z J Public Health. 2013;37(3):238–243. doi:10.1111/1753-6405.12065

45. Morgan G, Sheppeard V, Khalaj B, et al. Effects of bushfire smoke on daily mortality and hospital admissions in Sydney, Australia. Epidemiology. 2010;21(1):47–55. doi:10.1097/EDE.0b013e3181c15d5a

46. Delfino RJ, Brummel S, Wu J, et al. The relationship of respiratory and cardiovascular hospital admissions to the southern California wildfires of 2003. Occup Environ Med. 2009;66(3):189–197. doi:10.1136/oem.2008.041376

47. Alman BL, Pfister G, Hao H, et al. The association of wildfire smoke with respiratory and cardiovascular emergency department visits in Colorado in 2012: a case crossover study. Environ Health. 2016;15(1):64. doi:10.1186/s12940-016-0146-8

48. Mulder AC, Pijnacker R, de Man H, et al. ”Sickenin’ in the rain” - increased risk of gastrointestinal and respiratory infections after urban pluvial flooding in a population-based cross-sectional study in the Netherlands. BMC Infect Dis. 2019;19(1):377. doi:10.1186/s12879-019-3984-5

49. Knowlton K, Rotkin-Ellman M, King G, et al. The 2006 California heat wave: impacts on hospitalizations and emergency department visits. Environ Health Perspect. 2009;117(1):61–67. doi:10.1289/ehp.11594

50. Zhang A, Hu W, Li J, Wei R, Lin J, Ma W. Impact of heatwaves on daily outpatient visits of respiratory disease: a time-stratified case-crossover study. Environ Res. 2019;169:196–205. doi:10.1016/j.envres.2018.10.034

51. Jin Y, Hu Y, Han D, Wang M. Chronic heat stress weakened the innate immunity and increased the virulence of highly pathogenic avian influenza virus H5N1 in mice. J Biomed Biotechnol. 2011;2011:367846. doi:10.1155/2011/367846

52. Chen G, Zhang W, Li S, et al. The impact of ambient fine particles on influenza transmission and the modification effects of temperature in China: a multi-city study. Environ Int. 2017;98:82–88. doi:10.1016/j.envint.2016.10.004

53. Su W, Wu X, Geng X, Zhao X, Liu Q, Liu T. The short-term effects of air pollutants on influenza-like illness in Jinan, China. BMC Public Health. 2019;19(1):1319. doi:10.1186/s12889-019-7607-2

54. Feng C, Li J, Sun W, Zhang Y, Wang Q. Impact of ambient fine particulate matter (PM2.5) exposure on the risk of influenza-like-illness: a time-series analysis in Beijing, China. Environ Health. 2016;15:17. doi:10.1186/s12940-016-0115-2

55. Tang S, Yan Q, Shi W, et al. Measuring the impact of air pollution on respiratory infection risk in China. Environ Pollut. 2018;232:477–486. doi:10.1016/j.envpol.2017.09.071

56. Ye Q, Fu JF, Mao JH, Shang SQ. Haze is a risk factor contributing to the rapid spread of respiratory syncytial virus in children. Environ Sci Pollut Res Int. 2016;23(20):20178–20185. doi:10.1007/s11356-016-7228-6

57. He M, Zhong Y, Chen Y, Zhong N, Lai K. Association of short-term exposure to air pollution with emergency visits for respiratory diseases in children. iScience. 2022;25(9):104879. doi:10.1016/j.isci.2022.104879

58. Zhang D, Li Y, Chen Q, et al. The relationship between air quality and respiratory pathogens among children in Suzhou City. Ital J Pediatr. 2019;45(1):123. doi:10.1186/s13052-019-0702-2

59. Schwartz J, Spix C, Wichmann HE, Malin E. Air pollution and acute respiratory illness in five German communities. Environ Res. 1991;56(1):1–14. doi:10.1016/S0013-9351(05)80104-5

60. Chauhan AJ, Inskip HM, Linaker CH, et al. Personal exposure to nitrogen dioxide (NO2) and the severity of virus-induced asthma in children. Lancet. 2003;361(9373):1939–1944. doi:10.1016/S0140-6736(03)13582-9

61. Schwartz J. Air pollution and hospital admissions for the elderly in Detroit, Michigan. Am J Respir Crit Care Med. 1994;150(3):648–655. doi:10.1164/ajrccm.150.3.8087333

62. Nhung NTT, Schindler C, Dien TM, Probst-Hensch N, Kunzli N. Association of ambient air pollution with lengths of hospital stay for Hanoi children with acute lower-respiratory infection, 2007–2016. Environ Pollut. 2019;247:752–762. doi:10.1016/j.envpol.2019.01.115

63. Brauer M, Hoek G, Van Vliet P, et al. Air pollution from traffic and the development of respiratory infections and asthmatic and allergic symptoms in children. Am J Respir Crit Care Med. 2002;166(8):1092–1098. doi:10.1164/rccm.200108-007OC

64. Brauer M, Hoek G, Smit HA, et al. Air pollution and development of asthma, allergy and infections in a birth cohort. Eur Respir J. 2007;29(5):879–888. doi:10.1183/09031936.00083406

65. MacIntyre EA, Gehring U, Molter A, et al. Air pollution and respiratory infections during early childhood: an analysis of 10 European birth cohorts within the ESCAPE Project. Environ Health Perspect. 2014;122(1):107–113. doi:10.1289/ehp.1306755

66. Woodby B, Arnold MM, Valacchi G. SARS-CoV-2 infection, COVID-19 pathogenesis, and exposure to air pollution: what is the connection? Ann N Y Acad Sci. 2021;1486(1):15–38. doi:10.1111/nyas.14512

67. Brandt EB, Beck AF, Mersha TB. Air pollution, racial disparities, and COVID-19 mortality. J Allergy Clin Immunol. 2020;146(1):61–63. doi:10.1016/j.jaci.2020.04.035

68. Maleki M, Anvari E, Hopke PK, Noorimotlagh Z, Mirzaee SA. An updated systematic review on the association between atmospheric particulate matter pollution and prevalence of SARS-CoV-2. Environ Res. 2021;195:110898. doi:10.1016/j.envres.2021.110898

69. Ogen Y. Assessing nitrogen dioxide (NO2) levels as a contributing factor to coronavirus (COVID-19) fatality. Sci Total Environ. 2020;726:138605. doi:10.1016/j.scitotenv.2020.138605

70. Zoran MA, Savastru RS, Savastru DM, Tautan MN. Impacts of exposure to air pollution, radon and climate drivers on the COVID-19 pandemic in Bucharest, Romania: a time series study. Environ Res. 2022;212(Pt D):113437. doi:10.1016/j.envres.2022.113437

71. Nor NSM, Yip CW, Ibrahim N, et al. Particulate matter (PM2.5) as a potential SARS-CoV-2 carrier. Sci Rep. 2021;11(1):2508. doi:10.1038/s41598-021-81935-9

72. Tao Y, Zhang X, Qiu G, Spillmann M, Ji Z, Wang J. SARS-CoV-2 and other airborne respiratory viruses in outdoor aerosols in three Swiss cities before and during the first wave of the COVID-19 pandemic. Environ Int. 2022;164:107266. doi:10.1016/j.envint.2022.107266

73. Setti L, Passarini F, De Gennaro G, et al. SARS-Cov-2RNA found on particulate matter of Bergamo in Northern Italy: first evidence. Environ Res. 2020;188:109754. doi:10.1016/j.envres.2020.109754

74. Zhu Y, Xie J, Huang F, Cao L. Association between short-term exposure to air pollution and COVID-19 infection: evidence from China. Sci Total Environ. 2020;727:138704. doi:10.1016/j.scitotenv.2020.138704

75. Fattorini D, Regoli F. Role of the chronic air pollution levels in the Covid-19 outbreak risk in Italy. Environ Pollut. 2020;264:114732. doi:10.1016/j.envpol.2020.114732

76. Yao Y, Pan J, Liu Z, et al. Ambient nitrogen dioxide pollution and spreadability of COVID-19 in Chinese cities. Ecotoxicol Environ Saf. 2021;208:111421. doi:10.1016/j.ecoenv.2020.111421

77. Yao Y, Pan J, Liu Z, et al. Temporal association between particulate matter pollution and case fatality rate of COVID-19 in Wuhan. Environ Res. 2020;189:109941. doi:10.1016/j.envres.2020.109941

78. Veronesi G, De Matteis S, Calori G, Pepe N, Ferrario MM. Long-term exposure to air pollution and COVID-19 incidence: a prospective study of residents in the city of Varese, Northern Italy. Occup Environ Med. 2022;79(3):192–199. doi:10.1136/oemed-2021-107833

79. Hirota JA, Marchant DJ, Singhera GK, et al. Urban particulate matter increases human airway epithelial cell IL-1beta secretion following scratch wounding and H1N1 influenza A exposure in vitro. Exp Lung Res. 2015;41(6):353–362. doi:10.3109/01902148.2015.1040528

80. Jaspers I, Ciencewicki JM, Zhang W, et al. Diesel exhaust enhances influenza virus infections in respiratory epithelial cells. Toxicol Sci. 2005;85(2):990–1002. doi:10.1093/toxsci/kfi141

81. Ciencewicki J, Brighton L, Wu WD, Madden M, Jaspers I. Diesel exhaust enhances virus- and poly(I:C)-induced Toll-like receptor 3 expression and signaling in respiratory epithelial cells. Am J Physiol Lung Cell Mol Physiol. 2006;290(6):L1154–1163. doi:10.1152/ajplung.00318.2005

82. Ciencewicki J, Gowdy K, Krantz QT, et al. Diesel exhaust enhanced susceptibility to influenza infection is associated with decreased surfactant protein expression. Inhal Toxicol. 2007;19(14):1121–1133. doi:10.1080/08958370701665426

83. Spannhake EW, Reddy SP, Jacoby DB, Yu XY, Saatian B, Tian J. Synergism between rhinovirus infection and oxidant pollutant exposure enhances airway epithelial cell cytokine production. Environ Health Perspect. 2002;110(7):665–670. doi:10.1289/ehp.02110665

84. Jakab GJ, Hmieleski RR. Reduction of influenza virus pathogenesis by exposure to 0.5 ppm ozone. J Toxicol Environ Health. 1988;23(4):455–472. doi:10.1080/15287398809531128

85. Wolcott JA, Zee YC, Osebold JW. Exposure to ozone reduces influenza disease severity and alters distribution of influenza viral antigens in murine lungs. Appl Environ Microbiol. 1982;44(3):723–731. doi:10.1128/aem.44.3.723-731.1982

86. Soukup J, Koren HS, Becker S. Ozone effect on respiratory syncytial virus infectivity and cytokine production by human alveolar macrophages. Environ Res. 1993;60(2):178–186. doi:10.1006/enrs.1993.1025

87. Lambert AL, Trasti FS, Mangum JB, Everitt JI. Effect of preexposure to ultrafine carbon black on respiratory syncytial virus infection in mice. Toxicol Sci. 2003;72(2):331–338. doi:10.1093/toxsci/kfg031

88. Li N, Harkema JR, Lewandowski RP, et al. Ambient ultrafine particles provide a strong adjuvant effect in the secondary immune response: implication for traffic-related asthma flares. Am J Physiol Lung Cell Mol Physiol. 2010;299(3):L374–383. doi:10.1152/ajplung.00115.2010

89. Jaligama S, Saravia J, You D, et al. Regulatory T cells and IL10 suppress pulmonary host defense during early-life exposure to radical containing combustion derived ultrafine particulate matter. Respir Res. 2017;18(1):15. doi:10.1186/s12931-016-0487-4

90. Lambert AL, Mangum JB, DeLorme MP, Everitt JI. Ultrafine carbon black particles enhance respiratory syncytial virus-induced airway reactivity, pulmonary inflammation, and chemokine expression. Toxicol Sci. 2003;72(2):339–346. doi:10.1093/toxsci/kfg032

91. Hahon N, Booth JA, Green F, Lewis TR. Influenza virus infection in mice after exposure to coal dust and diesel engine emissions. Environ Res. 1985;37(1):44–60. doi:10.1016/0013-9351(85)90048-9

92. Mudway IS, Kelly FJ. An investigation of inhaled ozone dose and the magnitude of airway inflammation in healthy adults. Am J Respir Crit Care Med. 2004;169(10):1089–1095. doi:10.1164/rccm.200309-1325PP

93. Bhalla DK, Crocker TT. Pulmonary epithelial permeability in rats exposed to O3. J Toxicol Environ Health. 1987;21(1–2):73–87. doi:10.1080/15287398709531003

94. Gordon RE, Solano D, Kleinerman J. Tight junction alterations of respiratory epithelium following long-term NO2 exposure and recovery. Exp Lung Res. 1986;11(3):179–193. doi:10.3109/01902148609064295

95. Robison TW, Kim KJ. Dual effect of nitrogen dioxide on barrier properties of Guinea pig tracheobronchial epithelial monolayers cultured in an air interface. J Toxicol Environ Health. 1995;44(1):57–71. doi:10.1080/15287399509531943

96. Liu J, Chen X, Dou M, et al. Particulate matter disrupts airway epithelial barrier via oxidative stress to promote Pseudomonas aeruginosa infection. J Thorac Dis. 2019;11(6):2617–2627. doi:10.21037/jtd.2019.05.77

97. Case BW, Gordon RE, Kleinerman J. Acute bronchiolar injury following nitrogen dioxide exposure: a freeze fracture study. Environ Res. 1982;29(2):399–413. doi:10.1016/0013-9351(82)90041-X

98. Ferreira-Ceccato AD, Ramos EM, de Carvalho LC, et al. Short-term effects of air pollution from biomass burning in mucociliary clearance of Brazilian sugarcane cutters. Respir Med. 2011;105(11):1766–1768. doi:10.1016/j.rmed.2011.08.003

99. Val S, Belade E, George I, Boczkowski J, Baeza-Squiban A. Fine PM induce airway MUC5AC expression through the autocrine effect of amphiregulin. Arch Toxicol. 2012;86(12):1851–1859. doi:10.1007/s00204-012-0903-6

100. Behndig AF, Blomberg A, Helleday R, Duggan ST, Kelly FJ, Mudway IS. Antioxidant responses to acute ozone challenge in the healthy human airway. Inhal Toxicol. 2009;21(11):933–942. doi:10.1080/08958370802603789

101. Kelly FJ, Tetley TD. Nitrogen dioxide depletes uric acid and ascorbic acid but not glutathione from lung lining fluid. Biochem J. 1997;325(Pt 1):95–99. doi:10.1042/bj3250095

102. Harrod KS, Trapnell BC, Otake K, Korfhagen TR, Whitsett JA. SP-A enhances viral clearance and inhibits inflammation after pulmonary adenoviral infection. Am J Physiol. 1999;277(3):L580–588. doi:10.1152/ajplung.1999.277.3.L580

103. LeVine AM, Hartshorn K, Elliott J, Whitsett J, Korfhagen T. Absence of SP-A modulates innate and adaptive defense responses to pulmonary influenza infection. Am J Physiol Lung Cell Mol Physiol. 2002;282(3):L563–572. doi:10.1152/ajplung.00280.2001

104. Leth-Larsen R, Zhong F, Chow VT, Holmskov U, The LJ. SARS coronavirus spike glycoprotein is selectively recognized by lung surfactant protein D and activates macrophages. Immunobiology. 2007;212(3):201–211. doi:10.1016/j.imbio.2006.12.001

105. The Great Migration. A&E television networks; 2021. Available from: Accessed September 10, 2021.

106. Lin CI, Tsai CH, Sun YL, et al. Instillation of particulate matter 2.5 induced acute lung injury and attenuated the injury recovery in ACE2 knockout mice. Int J Biol Sci. 2018;14(3):253–265. doi:10.7150/ijbs.23489

107. Paital B, Agrawal PK. Air pollution by NO2 and PM2.5 explains COVID-19 infection severity by overexpression of angiotensin-converting enzyme 2 in respiratory cells: a review. Environ Chem Lett. 2021;19(1):25–42. doi:10.1007/s10311-020-01091-w

108. Kesic MJ, Meyer M, Bauer R, Jaspers I, Pekosz A. Exposure to ozone modulates human airway protease/antiprotease balance contributing to increased influenza A infection. PLoS One. 2012;7(4):e35108. doi:10.1371/journal.pone.0035108

109. Becker S, Soukup JM, Reed W, Carson J, Devlin RB, Noah TL. Effect of ozone on susceptibility to respiratory viral infection and virus-induced cytokine secretion. Environ Toxicol Pharmacol. 1998;6(4):257–265. doi:10.1016/S1382-6689(98)00043-X

110. Becker S, Soukup JM. Exposure to urban air particulates alters the macrophage-mediated inflammatory response to respiratory viral infection. J Toxicol Environ Health A. 1999;57(7):445–457. doi:10.1080/009841099157539

111. Kaan PM, Hegele RG. Interaction between respiratory syncytial virus and particulate matter in Guinea pig alveolar macrophages. Am J Respir Cell Mol Biol. 2003;28(6):697–704. doi:10.1165/rcmb.2002-0115OC

112. Rose RM, Fuglestad JM, Skornik WA, et al. The pathophysiology of enhanced susceptibility to murine cytomegalovirus respiratory infection during short-term exposure to 5 ppm nitrogen dioxide. Am Rev Respir Dis. 1988;137(4):912–917. doi:10.1164/ajrccm/137.4.912

113. Renwick LC, Donaldson K, Clouter A. Impairment of alveolar macrophage phagocytosis by ultrafine particles. Toxicol Appl Pharmacol. 2001;172(2):119–127. doi:10.1006/taap.2001.9128

114. Muller L, Chehrazi CV, Henderson MW, Noah TL, Jaspers I. Diesel exhaust particles modify natural killer cell function and cytokine release. Part Fibre Toxicol. 2013;10:16. doi:10.1186/1743-8977-10-16

115. Sandstrom T, Ledin MC, Thomasson L, Helleday R, Stjernberg N. Reductions in lymphocyte subpopulations after repeated exposure to 1.5 ppm nitrogen dioxide. Br J Ind Med. 1992;49(12):850–854. doi:10.1136/oem.49.12.850

116. Hsiao TC, Cheng PC, Chi KH, et al. Interactions of chemical components in ambient PM2.5 with influenza viruses. J Hazard Mater. 2022;423(PtB):127243. doi:10.1016/j.jhazmat.2021.127243

117. Santurtun A, Colom ML, Fdez-Arroyabe P, Real AD, Fernandez-Olmo I, Zarrabeitia MT. Exposure to particulate matter: direct and indirect role in the COVID-19 pandemic. Environ Res. 2022;206:112261. doi:10.1016/j.envres.2021.112261

118. Andersen ZJ, Hoffmann B, Morawska L, et al. Air pollution and COVID-19: clearing the air and charting a post-pandemic course: a joint workshop report of ERS, ISEE, HEI and WHO. Eur Respir J. 2021;58(2). doi:10.1183/13993003.01063-2021

119. Gilbert M, Slingenbergh J, Xiao X. Climate change and avian influenza. Rev Sci Tech. 2008;27(2):459–466. doi:10.20506/rst.27.2.1821

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