“…The initial literature search of Medline, Embase and the WHO COVID-19 database yielded 1,442 studies, which was reduced to 18 after screening. One study was excluded even though it met the inclusion criteria because it reported only statistically significant results rather than all results regardless of significance (20). A full list of screened studies along with reasons for exclusion is available in our public repository (9).…”
Background and objective Ecological studies indicate ambient particulate matter ≤2.5mm (PM2.5) air pollution is associated with poorer COVID-19 outcomes. However, these studies cannot account for individual heterogeneity and often have imprecise estimates of PM2.5 exposure. We review evidence from studies using individual-level data to determine whether PM2.5 increases risk of COVID-19 infection, severe disease, and death. Methods Systematic review of case-control and cohort studies, searching Medline, Embase, and WHO COVID-19 up to 30 June 2022. Study quality was evaluated using the Newcastle-Ottawa Scale. Results were pooled with a random effects meta-analysis, with Egger′s regression, funnel plots, and leave-one-out and trim-and-fill analyses to adjust for publication bias. Results N=18 studies met inclusion criteria. A 10μg/m3 increase in PM2.5 exposure was associated with 66% (95% CI: 1.31-2.11) greater odds of COVID-19 infection (N=7) and 127% (95% CI: 1.41-3.66) increase in severe illness (hospitalisation or worse) (N=6). Pooled mortality results (N=5) were positive but non-significant (OR 1.40; 0.94 to 2.10). Most studies were rated "good" quality (14/18 studies), though there were numerous methodological issues; few used individual-level data to adjust for confounders like socioeconomic status (4/18 studies), instead using area-based indicators (12/18 studies) or not adjusting for it (3/18 studies). Most severity (9/10 studies) and mortality studies (5/6 studies) were based on people already diagnosed COVID-19, potentially introducing collider bias. Conclusion There is strong evidence that ambient PM2.5 increases the risk of COVID-19 infection, and weaker evidence of increases in severe disease and mortality.
“…The initial literature search of Medline, Embase and the WHO COVID-19 database yielded 1,442 studies, which was reduced to 18 after screening. One study was excluded even though it met the inclusion criteria because it reported only statistically significant results rather than all results regardless of significance (20). A full list of screened studies along with reasons for exclusion is available in our public repository (9).…”
Background and objective Ecological studies indicate ambient particulate matter ≤2.5mm (PM2.5) air pollution is associated with poorer COVID-19 outcomes. However, these studies cannot account for individual heterogeneity and often have imprecise estimates of PM2.5 exposure. We review evidence from studies using individual-level data to determine whether PM2.5 increases risk of COVID-19 infection, severe disease, and death. Methods Systematic review of case-control and cohort studies, searching Medline, Embase, and WHO COVID-19 up to 30 June 2022. Study quality was evaluated using the Newcastle-Ottawa Scale. Results were pooled with a random effects meta-analysis, with Egger′s regression, funnel plots, and leave-one-out and trim-and-fill analyses to adjust for publication bias. Results N=18 studies met inclusion criteria. A 10μg/m3 increase in PM2.5 exposure was associated with 66% (95% CI: 1.31-2.11) greater odds of COVID-19 infection (N=7) and 127% (95% CI: 1.41-3.66) increase in severe illness (hospitalisation or worse) (N=6). Pooled mortality results (N=5) were positive but non-significant (OR 1.40; 0.94 to 2.10). Most studies were rated "good" quality (14/18 studies), though there were numerous methodological issues; few used individual-level data to adjust for confounders like socioeconomic status (4/18 studies), instead using area-based indicators (12/18 studies) or not adjusting for it (3/18 studies). Most severity (9/10 studies) and mortality studies (5/6 studies) were based on people already diagnosed COVID-19, potentially introducing collider bias. Conclusion There is strong evidence that ambient PM2.5 increases the risk of COVID-19 infection, and weaker evidence of increases in severe disease and mortality.
“…We also did not perform viral sequencing for the hospitalized patients, but instead separated different pandemic periods based on reliable genomic sequence surveillance data deposited in the GISAID. Moreover, rates of death due to COVID-19 may, to some extent, be influenced by additional variables, such as changes in healthcare system capacity or environmental factors (e.g., air quality) [ 55 , 56 ]. Since our analysis involved hospitalized patients, and thus the vast majority of symptomatic individuals, its results cannot be translated to the entire infected population in subsequent waves of the pandemic.…”
The COVID-19 pandemic proceeds in waves, with variable characteristics of the clinical picture resulting from the evolution of the SARS-CoV-2 virus. This study aimed to compare the epidemiological characteristics, symptomatology, and outcomes of the disease in patients hospitalized for COVID-19 during periods of different variants dominance. Comparing the periods of dominance of variants preceding the Delta variant, the Delta period was characterized by a higher share of hospitalized females, less frequent comorbidities among patients, and a different age distribution. The lowest need for oxygen therapy and mechanical ventilation was observed under Omicron dominance. The triad of classic COVID-19 symptoms, cough, fever, dyspnoea, and fatigue, were most prevalent during the Delta period, and significantly less common under the Omicron dominance. During the Omicron period, nearly twice as many patients as in the previous periods could be discharged from the hospital within 7 days; the overall 28-day mortality was significantly lower compared to that of the Delta period. It also did not differ between periods that were dominated by the BA.1 and BA.2 subvariants. The study indicates that the Omicron SARS-CoV-2 variant that dominated between January and June 2022 caused a disease which resembled the common cold, and was caused by seasonal alpha and beta-coronaviruses with a low pathogenicity for humans. However, one should note that this effect may not only have been related to biological features of the Omicron lineage, but may additionally have been driven by the increased levels of immunization through natural infections and vaccinations, for which we could not account for due to a lack of sufficient data.
“…The strength of our research is the use of individualized exposure levels preceding hospitalization reflecting a time of transition of SARS‐CoV‐2 infection from incubation phase to symptoms onset, instead of using long‐term air quality monitoring or data generalized for the population of a particular region as conducted by numerous other studies 13–16,33,36,52,66–69 . Moreover, we have also included data for B(a)P, for which an association with the clinical course of COVID‐19 was only a subject of a few previous investigations during the pandemic 12,44 . Although the pandemic waves included in the present study, dominated by Delta and Omicron SARS‐CoV‐2 variants, encompassed different periods of the year, each of them also included months characterized by increased emission of PM and B(a)P in Poland, that is, autumn‐early winter during the Delta wave and late winter‐early spring during Omicron wave 64,70 .…”
Section: Discussionmentioning
confidence: 99%
“…The period of the week preceding hospitalization was chosen as it most likely represented a time of transition of infection from the incubation phase to the symptomatic stage, a time window during which the innate response constitutes a substantial line of the antiviral defense. 12,[44][45][46][47] In turn, its alterations can lead to hyperinflammation, resulting in a more severe clinical course of COVID-19 and a worse prognosis. [48][49][50][51] Air pollutants such as PM and B(a)P were shown to reveal proinflammatory action and adversely influence innate immune responses, also following short-term exposures.…”
Air pollution may affect the clinical course of respiratory diseases, including This study aimed to evaluate the relationship between exposure of adult patients to mean 24 h levels of particulate matter sized <10 μm (PM 10 ) and <2.5 μm (PM 2.5 ) and benzo(a)pyrene (B(a)P) during a week before their hospitalization due to SARS-CoV-2 infection and symptomatology, hyperinflammation, coagulopathy, the clinical course of disease, and outcome. The analyses were conducted during two pandemic waves: (i) dominated by highly pathogenic Delta variant (n = 1440) and (ii) clinically less-severe Omicron (n = 785), while the analyzed associations were adjusted for patient's age, BMI, gender, and comorbidities. The exposure to mean 24 h B(a)P exceeding the limits was associated with increased odds of fever and fatigue as early COVID-19 symptoms, hyperinflammation due to serum C-reactive protein >200 mg/L and interleukin-6 >100 pg/mL, coagulopathy due to D-dimer >2 mg/L and fatal outcome. Elevated PM 10 and PM 2.5 levels were associated with higher odds of respiratory symptoms, procalcitonin >0.25 ng/mL and interleukin >100 pg/mL, lower oxygen saturation, need for oxygen support, and death. The significant relationships between exposure to air pollutants and the course and outcomes of COVID-19 were observed during both
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