tetano
Editor, Senior Moderator
Environ Health Perspect
. 2021 Nov;129(11):117003.
doi: 10.1289/EHP9726. Epub 2021 Nov 17.
Ambient Air Pollution in Relation to SARS-CoV-2 Infection, Antibody Response, and COVID-19 Disease: A Cohort Study in Catalonia, Spain (COVICAT Study)
Manolis Kogevinas[SUP] 1 2 3 4 [/SUP], Gemma Castaño-Vinyals[SUP] 1 2 3 4 [/SUP], Marianna Karachaliou[SUP] 1 [/SUP], Ana Espinosa[SUP] 1 2 3 4 [/SUP], Rafael de Cid[SUP] 5 [/SUP], Judith Garcia-Aymerich[SUP] 1 2 3 [/SUP], Anna Carreras[SUP] 5 [/SUP], Beatriz Cortés[SUP] 5 [/SUP], Vanessa Pleguezuelos[SUP] 6 [/SUP], Alfons Jiménez[SUP] 1 [/SUP], Marta Vidal[SUP] 1 [/SUP], Cristina O'Callaghan-Gordo[SUP] 1 2 3 7 [/SUP], Marta Cirach[SUP] 1 [/SUP], Rebeca Santano[SUP] 1 [/SUP], Diana Barrios[SUP] 1 [/SUP], Laura Puyol[SUP] 1 [/SUP], Rocío Rubio[SUP] 1 [/SUP], Luis Izquierdo[SUP] 1 [/SUP], Mark Nieuwenhuijsen[SUP] 1 2 3 [/SUP], Payam Dadvand[SUP] 1 2 3 [/SUP], Ruth Aguilar[SUP] 1 [/SUP], Gemma Moncunill[SUP] 1 [/SUP], Carlota Dobaño[SUP] 1 [/SUP], Cathryn Tonne[SUP] 1 2 3 [/SUP]
Affiliations
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 ≤2.5μm
(PM2.5)], nitrogen dioxide (NO2), black carbon (BC), and ozone (O3
) 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 NO2
, 1.04 (95% CI: 0.94, 1.14) for PM2.5, 1.00 (95% CI: 0.92, 1.09) for BC, and 0.97 (95% CI: 0.89, 1.06) for O3. Among infected participants, exposure to NO2 and PM2.5 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 RRs=1.14 (95% CI: 1.00, 1.29) for NO2 and 1.17 (95% CI: 1.03, 1.32) for PM2.5. Exposure to O3 was associated with a slightly decreased risk (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 RRs=1.26 (95% CI: 0.89, 1.79) for NO2 and 1.51 (95% CI: 1.06, 2.16) for PM2.5
.
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.
. 2021 Nov;129(11):117003.
doi: 10.1289/EHP9726. Epub 2021 Nov 17.
Ambient Air Pollution in Relation to SARS-CoV-2 Infection, Antibody Response, and COVID-19 Disease: A Cohort Study in Catalonia, Spain (COVICAT Study)
Manolis Kogevinas[SUP] 1 2 3 4 [/SUP], Gemma Castaño-Vinyals[SUP] 1 2 3 4 [/SUP], Marianna Karachaliou[SUP] 1 [/SUP], Ana Espinosa[SUP] 1 2 3 4 [/SUP], Rafael de Cid[SUP] 5 [/SUP], Judith Garcia-Aymerich[SUP] 1 2 3 [/SUP], Anna Carreras[SUP] 5 [/SUP], Beatriz Cortés[SUP] 5 [/SUP], Vanessa Pleguezuelos[SUP] 6 [/SUP], Alfons Jiménez[SUP] 1 [/SUP], Marta Vidal[SUP] 1 [/SUP], Cristina O'Callaghan-Gordo[SUP] 1 2 3 7 [/SUP], Marta Cirach[SUP] 1 [/SUP], Rebeca Santano[SUP] 1 [/SUP], Diana Barrios[SUP] 1 [/SUP], Laura Puyol[SUP] 1 [/SUP], Rocío Rubio[SUP] 1 [/SUP], Luis Izquierdo[SUP] 1 [/SUP], Mark Nieuwenhuijsen[SUP] 1 2 3 [/SUP], Payam Dadvand[SUP] 1 2 3 [/SUP], Ruth Aguilar[SUP] 1 [/SUP], Gemma Moncunill[SUP] 1 [/SUP], Carlota Dobaño[SUP] 1 [/SUP], Cathryn Tonne[SUP] 1 2 3 [/SUP]
Affiliations
- PMID: 34787480
- DOI: 10.1289/EHP9726
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 ≤2.5μm
(PM2.5)], nitrogen dioxide (NO2), black carbon (BC), and ozone (O3
) 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 NO2
, 1.04 (95% CI: 0.94, 1.14) for PM2.5, 1.00 (95% CI: 0.92, 1.09) for BC, and 0.97 (95% CI: 0.89, 1.06) for O3. Among infected participants, exposure to NO2 and PM2.5 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 RRs=1.14 (95% CI: 1.00, 1.29) for NO2 and 1.17 (95% CI: 1.03, 1.32) for PM2.5. Exposure to O3 was associated with a slightly decreased risk (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 RRs=1.26 (95% CI: 0.89, 1.79) for NO2 and 1.51 (95% CI: 1.06, 2.16) for PM2.5
.
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.