COVID-19 is a disease caused by the new coronavirus (SARS-CoV-2), which emerged in Wuhan, Hubei Province, China, in December 2019. Initially, the World Health Organization (WHO) was informed by the Chinese government of an outbreak of pneumonia of unknown etiology, and in January, the Chinese National Health Commission already knew it was a pneumonia of viral origin and that from the isolation of the virus in hospitalized patients, the new coronavirus was identified (Wang et al. 2020)(Shereen et al. 2020).
A study developed by Zhu et al. explored the relationship between air pollutants and infection caused by the new coronavirus (Copiello and Grillenzoni 2020). The number of new daily cases, the concentration of pollutants (PM2.5, PM10, SO2, CO, NO2 and O3) and meteorological variables in 120 cities in China were evaluated using a generalized additive linear model. The results showed that there was a positive association of PM2.5, PM10, NO2 and O3 in the last two weeks and the number of new cases. An increase of 10 µg/m3 (lag0-14) in PM2.5, PM10, NO2, and O3 is associated with increases of 2.24% (95% CI: 1.02 to 3.46), 1.76% (95% CI: 0.89 to 2.63), 6.94% (95% CI: 2.38 to 11.51), and 4.76% (95% CI: 1.99 to 7.52) in the daily number of confirmed cases of COVID-19, respectively. For an increase in the same order of SO2, there is a decrease of 7.79% in the number of confirmed cases.
SARS-CoV-2 is an extremely small virus approximately 65–125 nm (nanometers) in diameter. It consists of a simple RNA strand covered by a protein shell (capsid) on which there is an envelope, and it has spikes, which give the appearance of a solar crown; its name coronavirus is derived from its appearance (corona = crown in Latin) (Ciencewicki and Jaspers 2007)(Domingo, Marquès, and Rovira 2020).
In 2017, Ciencewicki and Jaspers conducted an epidemiological study on air pollution and viral respiratory infections. They observed that there is a positive correlation between the levels of particulate matter, cardiovascular mortality and respiratory conditions, suggesting that exposure to PM alters respiratory immunity to viral infections (Ciencewicki and Jaspers 2007).
Another plausible explanation for this association was proposed by Setti and collaborators at the University of Bologna in Italy (Domingo, Marquès, and Rovira 2020). They suggest that air pollution can preserve the viability of the virus, increase its potential for infection and facilitate transmission through interaction with the particulate material present in the air. The particles would act as carriers for the virus, as is already known for other chemical and biological contaminants. Therefore, the particulate material acts as a carrier and substrate for the virus (Weinbauer et al. 2009)(Sedlmaier et al. 2009).
Particulate matter is generated essentially by the incomplete burning of fossil fuels and biomass. It consists of a central core of elemental carbon, and on its surface, other compounds can bond (e.g., heavy metals) (Huffman et al. 2000)(Schlesinger 2007). Its structure also allows the attachment and survival of microorganisms (bacteria, viruses). Studies indicate that biological material comprises a substantial fraction of fine (PM2.5) and coarse (PM10) particles, which may represent 10 to 25% of the mass (Jalava et al. 2015; Samake et al. 2017)(Cardoso et al. 2017).
It is also believed that the biological diversity present in the particulate material is high, with numerous pathogenic and/or nonpathogenic microbial species (viruses, bacteria and fungi) coexisting in the same coarse, fine and ultrafine particles (Acosta-Martínez et al. 2015; Gardner et al. 2012). The pathogenicity and toxicity of these “bioaerosols” will therefore depend on the components of the particulate material, the particle size and the concentration of microorganisms (Samake et al. 2017).
Another study monitoring the presence of pathogenic microorganisms (viruses and bacteria) associated with PM2.5 in Seoul air during the “yellow dust” phenomenon and outside this period showed that there was a presence in the particulate material of viruses that caused respiratory infections such as rhinovirus, norovirus and parechovirus (Chung, n.d.; Han et al. 2018).
Although previous studies have already confirmed and shown effective results in detecting the (Gendron et al. 2010; Han et al. 2018; “A Field Indoor Air Measurement of SARS-CoV-2 in the Patient Rooms of the Largest Hospital in Iran” 2020) of viruses in bioaerosols, the main challenge of monitoring the presence of SARS CoV-2 in the air lies precisely in the probable low concentration of the virus in the particulate matter present in the air (Cao et al. 2014)(Hermann et al. 2006). This study first evaluated two sampling methods (air filtration and liquid collision method AGI-30) over long samplings. Additionally, indoor and outdoor sampling was performed to prove this hypothesis, and we investigated the environmental dispersion of SARS-CoV-2 associated with environmental particles.
In this study, we investigated indoor and outdoor air samples using three different methodologies to detect SARS-CoV-2 and whether environmental factors can predict the presence of SARS-CoV-2 RNA in PM2.5