Ambient Air Pollution in Relation to SARS-CoV-2 Infection, Antibody Response, and COVID-19 Disease: A Cohort Study in Catalonia, Spain (COVICAT Study)

Abstract

Background: Emerging evidence links ambient air pollution with coronavirus 2019 (COVID-19) disease, an association that is methodologically challenging to investigate.

Objectives: We examined the association between long-term exposure to air pollution with SARS-CoV-2 infection measured through antibody response, level of antibody response among those infected, and COVID-19 disease.

Methods: We contacted 9,605 adult participants from a population-based cohort study in Catalonia between June and November 2020; most participants were between 40 and 65 years of age. We drew blood samples from 4,103 participants and measured immunoglobulin M (IgM), IgA, and IgG antibodies against five viral target antigens to establish infection to the virus and levels of antibody response among those infected. We defined COVID-19 disease using self-reported hospital admission, prior positive diagnostic test, or more than three self-reported COVID-19 symptoms after contact with a COVID-19 case. We estimated prepandemic (2018-2019) exposure to fine particulate matter [PM with an aerodynamic diameter of $\le 2.5\mu m$ (${\mathrm{PM}}_{2.5}$)], nitrogen dioxide (${\mathrm{NO}}_2$), black carbon (BC), and ozone ($O_3$) at the residential address using hybrid land-use regression models. We calculated log-binomial risk ratios (RRs), adjusting for individual- and area-level covariates.

Results: Among those tested for SARS-CoV-2 antibodies, 743 (18.1%) were seropositive. Air pollution levels were not statistically significantly associated with SARS-CoV-2 infection: Adjusted RRs per interquartile range were 1.07 (95% CI: 0.97, 1.18) for ${\mathrm{NO}}_2$, 1.04 (95% CI: 0.94, 1.14) for ${\mathrm{PM}}_{2.5}$, 1.00 (95% CI: 0.92, 1.09) for BC, and 0.97 (95% CI: 0.89, 1.06) for $O_3$. Among infected participants, exposure to ${\mathrm{NO}}_2$ and ${\mathrm{PM}}_{2.5}$ were positively associated with IgG levels for all viral target antigens. Among all participants, 481 (5.0%) had COVID-19 disease. Air pollution levels were associated with COVID-19 disease: adjusted $\text{RRs}=1.14$ (95% CI: 1.00, 1.29) for ${\mathrm{NO}}_2$ and 1.17 (95% CI: 1.03, 1.32) for ${\mathrm{PM}}_{2.5}$. Exposure to $O_3$ was associated with a slightly decreased risk ($\text{RR}=0.92$; 95% CI: 0.83, 1.03). Associations of air pollution with COVID-19 disease were more pronounced for severe COVID-19, with $\text{RRs}=1.26$ (95% CI: 0.89, 1.79) for ${\mathrm{NO}}_2$ and 1.51 (95% CI: 1.06, 2.16) for ${\mathrm{PM}}_{2.5}$.

Discussion: Exposure to air pollution was associated with a higher risk of COVID-19 disease and level of antibody response among infected but not with SARS-CoV-2 infection. https://doi.org/10.1289/EHP9726.

Figure 1.

Association of air pollutants—(A) ${\mathrm{NO}}_2$, (B) ${\mathrm{PM}}_{2.5}$, (C) BC, and (D) ${\mathrm{O}}_3$)—with levels of IgM, IgA, and IgG against five viral target antigens among participants of the COVICAT study who were seropositive ($n=743$). Linear regression beta coefficients and 95% CIs were adjusted for potential confounders. The model was adjusted for age, sex, education (less than primary/primary/secondary/university), deprivation index (quintiles), population density, type of survey (online/telephone), and batch. Precise numerical values are shown in Table S6. Note: BC, black carbon; CI, confidence interval; COVICAT, COVID-19 cohort in Catalonia study; IgA, immunoglobulin A; IgG, immunoglobulin G; IgM, immunoglobulin M; NCt), nucleocapsid C-terminal region; NFL, nucleocapsid full protein; ${\mathrm{NO}}_2$, nitrogen dioxide; ${\mathrm{O}}_3$, ozone; ${\mathrm{PM}}_{2.5}$, fine particulate matter; RBD, receptor-binding domain; S, spike full protein; S2, S2 fragment.