Epidemiological and experimental studies have revealed connections between air pollution exposure and respiratory viral infections. The H1N1 flu is a subtype of influenza A, and was first detected in the spring of 2009 in the USA; it then spread rapidly throughout the world. The H1N1 virus includes a novel mix of influenza genes that have not been detected before in either animals or humans. It was named the influenza A (H1N1) pdm09 virus because it was very distinct from the viruses that were circulating throughout the pandemic [185]. This virus, which caused a global flu pandemic in 2009–2010, was popularly known as “swine flu.” Despite the large number of studies that have been conducted to analyze the many parameters that influence susceptibility to viral infections, the processes by which inhaled oxidants might change viral pathogenesis are extremely complicated. It has been demonstrated that oxidative stress worsens the severity of viral infections. One of the most common air contaminants in cities is ozone, an elemental form of oxygen. It is a strong inducer of oxidative stress, which can lead to airway inflammation and increased respiratory morbidity [186,187]. Environmentally persistent free radicals (EPFRs) were found in PM samples taken from several cities in the United States [188]. In this regard, Lee et al. found that EPFRs associated with combustion-derived PM were crucial in increasing the severity and mortality of respiratory tract viral infections [189]. A study by Hirota et al. found that in vitro scratch injury and H1N1 influenza A exposure boosted IL-1 production in human airway epithelial cells. Several studies have been conducted with the goal of documenting the worldwide mortality effect of influenza A (H1N1) pdm09 and finding variables that explain mortality variances reported across populations [190]. Some research has concentrated on risk factors such as environmental exposure. In Brisbane, Australia, Xu et al. (2013) discovered substantial interaction impacts of PM and mean temperature on pediatric influenza [191]. When searching for possible explanations as to why some countries were harder hit by the H1N1 virus pandemic in 2009, Morales et al. (2017) highlighted the importance of monitoring environmental exposure to air pollution, which is a burden on the respiratory system and immune-compromising chronic infections [192].

In an ecologic study on air pollution conducted in China, Cui et al. (2003) discovered that patients with SARS from locations with an intermediate air pollution index (API) exhibited higher mortality compared to those with a lower API [193]. Kan et al. (2005) found similar results when they evaluated the relationship between air pollution and daily SARS mortality in the Beijing (China) population. They discovered that each 10 g/m³ rise in PM₁₀, SO₂, and NO₂ levels over a 5-day moving average was associated with a relative risk of daily SARS death of 1.06, 0.74, and 1.22, respectively [194]. Cai et al. (2007) conducted ecological research in mainland China to examine the possible link between the SARS outbreak and climatic conditions and air pollution [195]. In contrast to the findings of Cui et al. (2003), they found no link between air pollution and the SARS outbreak. Although air pollution should not influence SARS-CoV survival in vitro, it may exert an effect by altering the host’s local resistance. The authors suggested that more research should be conducted on this subject [193,195].

Coronavirus disease 2019 (COVID-19) is caused by a coronavirus that causes severe acute respiratory illness (SARS-CoV-2). Although a unique coronavirus illness epidemic was detected in Wuhan (China) in December 2019, the outbreak was formally confirmed as a pandemic only on 11 February 2020 [196]. A significant number of studies on SARS-CoV-2 and COVID-19 have been published in recent weeks/months. The connection between severe viral respiratory illnesses, which afflict 10–20% of the population, and air pollution is widely known [197]. Pollutants in the air, such as PM_2.5, PM₁₀, sulfur dioxide, nitrogen dioxide, carbon monoxide, and ozone, can alter airways upon inhalation, increasing susceptibility to respiratory viral infections and the severity of these illnesses [198]. In this regard, Frontera et al. (2020) recently hypothesized that an atmosphere with a high concentration of air pollutants, together with meteorological circumstances, would promote the persistence of virus particles in the air for a longer period of time, favoring indirect transmission of SARS-CoV-2 in addition to direct transmission from person to person [199]. Martelletti and Martelletti (2020) discovered that the northern regions of Italy most impacted by COVID-19 also have the greatest concentrations of PM₁₀ and PM_2.5 [200]. According to these authors, SARS-CoV-2 might find appropriate transporters in air pollution particles. Furthermore, in a linear connection, the viruses would live longer and grow more aggressive in an immune system already weakened by air pollution [200]. Individuals who live in areas with high concentrations of air pollution are more likely to acquire respiratory disorders and are more susceptible to viral infections [201,202]. Pollution wreaks havoc on the upper airway’s first line of defense, the cilia. Based on this, Conticini et al. (2020) explored whether communities living in polluted areas, such as Lombardy and Emilia Romagna, were more likely to die of COVID-19 because of their poorer previous health state induced by air pollution. The normally high concentrations of air pollution in Northern Italy have been determined to be an additional co-factor of the high level of lethality documented in that location [203]. Zhu et al. (2020) studied the connection between six air pollutant concentrations (PM_2.5, PM₁₀, CO, NO₂, and O₃) and daily verified COVID-19 cases in 120 Chinese cities. These contaminants were shown to have significant positive relationships with COVID-19-verified cases. However, SO₂ levels were shown to be inversely related to the number of daily confirmed cases. Nevertheless, the findings of this study support the notion that air pollution may play a role in SARS-CoV-2 infections [204]. The findings of this study, which has been replicated in Italy (Conticini et al., 2020) and in the United States (Wu et al., 2020), suggest that PM_2.5 leads to a large increase in COVID death rate, suggesting that persistent exposure to air pollution hinders recovery and leads to more severe and deadly types of illness [203,205]. Coccia (2020) investigated the mechanisms of COVID-19 transmission dynamics in the environment to determine a feasible approach for dealing with future epidemics comparable to coronavirus infections. Their research focused on a case study of Italy, which has one of the highest rates of mortality in the world. The findings demonstrated that increased COVID-19 transmission dynamics in certain situations were caused by two mechanisms: air pollution-to-human transmission and human-to-human transmission in a context of high population density. The two main findings were as follows: (1) the acceleration of COVID-19 transmission dynamics in North Italy was highly associated with city air pollution, and (2) cities with more than 100 days of air pollution (exceeding the limits set for PM₁₀, PM_2.5) had a very high average number of infected individuals (about 3340 infected individuals), whereas cities with less than 100 days of air pollution had a lower average number of infected individuals (about 1450 infected individuals) on April 2020 [206]. Finally, as a scientific curiosity, it is worth noting that, given the significant reduction in air pollution following the quarantine, the COVID-19 pandemic may have paradoxically reduced the total number of deaths during this period by drastically reducing the number of deaths caused by air pollution [207].