Ambient Air Pollution in Relation to SARS-CoV-2 Infection, Antibody Response, and COVID-19 Disease: A Cohort Study in Catalonia, Spain (COVICAT Study).
Ambient Air Pollution in Relation to SARS-CoV-2 Infection, Antibody Response, and COVID-19 Disease: A Cohort Study in Catalonia, Spain (COVICAT Study).
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DOI：
10.1289/ehp9726
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发表时间：
2021-11
影响因子：
10.4
通讯作者：
Tonne C
中科院分区：
文献类型：
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作者：
Kogevinas M;Castaño-Vinyals G;Karachaliou M;Espinosa A;de Cid R;Garcia-Aymerich J;Carreras A;Cortés B;Pleguezuelos V;Jiménez A;Vidal M;O'Callaghan-Gordo C;Cirach M;Santano R;Barrios D;Puyol L;Rubio R;Izquierdo L;Nieuwenhuijsen M;Dadvand P;Aguilar R;Moncunill G;Dobaño C;Tonne C
新出现的证据将环境空气污染与2019冠状病毒（COVID-19）疾病联系起来，这种联系在方法上具有挑战性。我们研究了长期暴露于空气污染与SARS-CoV-2感染之间的关联，通过抗体反应，感染者的抗体反应水平和COVID-19疾病来测量。我们联系了2020年6月至11月期间在加泰罗尼亚进行的一项基于人群的队列研究中的9，605名成年参与者;大多数参与者的年龄在40至65岁之间。我们从4，103名参与者中抽取血液样本，并测量针对五种病毒靶抗原的免疫球蛋白M（IgM），伊加和IgG抗体，以确定病毒感染和感染者的抗体反应水平。我们使用自我报告的住院、既往诊断检测阳性或接触COVID-19病例后自我报告的三种以上COVID-19症状来定义COVID-19疾病。我们使用混合土地利用回归模型估计了大流行前（2018-2019年）居住地址的细颗粒物[空气动力学直径为（）的PM]、二氧化氮（）、黑碳（BC）和臭氧（）暴露量。我们计算了对数二项风险比（RR），调整了个体和地区水平的协变量。在SARS-CoV-2抗体检测中，743例（18.1%）血清学阳性。空气污染水平与SARS-CoV-2感染无统计学显著相关：每个四分位数范围调整后的RR为1.07（95% CI：0.97，1.18），1.04（95% CI：0.94，1.14），1.00（95% CI：0.92，1.09），BC和0.97（95% CI：0.89，1.06）。在受感染的参与者中，暴露于和与所有病毒靶抗原的IgG水平呈正相关。在所有参与者中，481人（5.0%）患有COVID-19疾病。空气污染水平与COVID-19疾病相关：调整后（95% CI：1.00，1.29）为1.17（95% CI：1.03，1.32）。暴露与风险略微降低相关（; 95% CI：0.83，1.03）。对于严重的COVID-19，空气污染与COVID-19疾病的相关性更明显，分别为（95% CI：0.89，1.79）和1.51（95% CI：1.06，2.16）。暴露于空气污染与感染者的COVID-19疾病风险和抗体反应水平相关，但与SARS-CoV-2感染无关。https://doi.org/10.1289/EHP9726
Emerging evidence links ambient air pollution with coronavirus 2019 (COVID-19) disease, an association that is methodologically challenging to investigate. 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. 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 ()], nitrogen dioxide (), black carbon (BC), and ozone () at the residential address using hybrid land-use regression models. We calculated log-binomial risk ratios (RRs), adjusting for individual- and area-level covariates. 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 , 1.04 (95% CI: 0.94, 1.14) for , 1.00 (95% CI: 0.92, 1.09) for BC, and 0.97 (95% CI: 0.89, 1.06) for . Among infected participants, exposure to and 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 (95% CI: 1.00, 1.29) for and 1.17 (95% CI: 1.03, 1.32) for . Exposure to was associated with a slightly decreased risk (; 95% CI: 0.83, 1.03). Associations of air pollution with COVID-19 disease were more pronounced for severe COVID-19, with (95% CI: 0.89, 1.79) for and 1.51 (95% CI: 1.06, 2.16) for . 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