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Associations of air pollution with COVID-19 positivity, hospitalisations, and mortality: Observational evidence from UK Biobank.

ABSTRACT: Individual-level studies with adjustment for important COVID-19 risk factors suggest positive associations of long-term air pollution exposure (particulate matter and nitrogen dioxide) with COVID-19 infection, hospitalisations and mortality. The evidence, however, remains limited and mechanisms unclear. We aimed to investigate these associations within UK Biobank, and to examine the role of underlying chronic disease as a potential mechanism. UK Biobank COVID-19 positive laboratory test results were ascertained via Public Health England and general practitioner record linkage, COVID-19 hospitalisations via Hospital Episode Statistics, and COVID-19 mortality via Office for National Statistics mortality records from March-December 2020. We used annual average outdoor air pollution modelled at 2010 residential addresses of UK Biobank participants who resided in England (n = 424,721). We obtained important COVID-19 risk factors from baseline UK Biobank questionnaire responses (2006-2010) and general practitioner record linkage. We used logistic regression models to assess associations of air pollution with COVID-19 outcomes, adjusted for relevant confounders, and conducted sensitivity analyses. We found positive associations of fine particulate matter (PM_2.5) and nitrogen dioxide (NO₂) with COVID-19 positive test result after adjustment for confounders and COVID-19 risk factors, with odds ratios of 1.05 (95% confidence intervals (CI) = 1.02, 1.08), and 1.05 (95% CI = 1.01, 1.08), respectively. PM 2.5 and NO 2 were positively associated with COVID-19 hospitalisations and deaths in minimally adjusted models, but not in fully adjusted models. No associations for PM₁₀ were found. In analyses with additional adjustment for pre-existing chronic disease, effect estimates were not substantially attenuated, indicating that underlying chronic disease may not fully explain associations. We found some evidence that long-term exposure to PM_2.5 and NO₂ was associated with a COVID-19 positive test result in UK Biobank, though not with COVID-19 hospitalisations or deaths.

SUBMITTER: Sheridan C

PROVIDER: S-EPMC9243647 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:BackgroundLong-term exposure to air pollution concentrations is known to be adversely associated with a broad range of single non-communicable diseases, but its role in multimorbidity has not been investigated in the UK. We aimed to assess associations between long-term air pollution exposure and multimorbidity status, severity, and patterns using the UK Biobank cohort.MethodsMultimorbidity status was calculated based on 41 physical and mental conditions. We assessed cross-sectional associations between annual modeled particulate matter (PM)2.5, PMcoarse, PM10, and nitrogen dioxide (NO2) concentrations (μg/m3-modeled to residential address) and multimorbidity status at the baseline assessment (2006-2010) in 364,144 people (mean age: 52.2 ± 8.1 years, 52.6% female). Air pollutants were categorized into quartiles to assess dose-response associations. Among those with multimorbidity (≥2 conditions; n = 156,395) we assessed associations between air pollutant exposure levels and multimorbidity severity and multimorbidity patterns, which were identified using exploratory factor analysis. Associations were explored using generalized linear models adjusted for sociodemographic, behavioral, and environmental indicators.ResultsHigher exposures to PM2.5, and NO2 were associated with multimorbidity status in a dose-dependent manner. These associations were strongest when we compared the highest air pollution quartile (quartile 4: Q4) with the lowest quartile (Q1) [PM2.5: adjusted odds ratio (adjOR) = 1.21 (95% CI = 1.18, 1.24); NO2: adjOR = 1.19 (95 % CI = 1.16, 1.23)]. We also observed dose-response associations between air pollutant exposures and multimorbidity severity scores. We identified 11 multimorbidity patterns. Air pollution was associated with several multimorbidity patterns with strongest associations (Q4 vs. Q1) observed for neurological (stroke, epilepsy, alcohol/substance dependency) [PM2.5: adjOR = 1.31 (95% CI = 1.14, 1.51); NO2: adjOR = 1.33 (95% CI = 1.11, 1.60)] and respiratory patterns (COPD, asthma) [PM2.5: adjOR = 1.24 (95% CI = 1.16, 1.33); NO2: adjOR = 1.26 (95% CI = 1.15, 1.38)].ConclusionsThis cross-sectional study provides evidence that exposure to air pollution might be associated with having multimorbid, multi-organ conditions. Longitudinal studies are needed to further explore these associations.

Project description:BackgroundRecent studies suggest potential interactions of air pollutants with dietary factors and genetic susceptibility on mortality risk; however, evidence from prospective studies is still lacking. We aimed to assess the association between air pollution and mortality, and investigate the modification effects of a healthy diet and genetic susceptibility.MethodsA total of 386 937 participants were enrolled from 2006 to 2010 and followed up to 2018 in the UK Biobank study. The annual average air pollutant concentrations of particulate matter (PM) with diameters ≤2.5 (PM2.5), ≤10 (PM10) and between 2.5 and 10 µm (PM2.5-10) and nitrogen oxides (NO2 and NOx) were calculated and linked to participants' residential addresses. Healthy dietary patterns were evaluated by a healthy diet score (HDS) based on intakes of vegetables, fruit, fish, unprocessed red meat and processed meat. We also calculated genetic risk score (GRS) of the lifespan. We examined potential interactions by setting variable cross-product terms of air pollutants with diets or GRS in the models.ResultsWe identified 11 881 deaths [2426 from cardiovascular diseases (CVD), 1211 from coronary heart disease (CHD) and 466 from stroke] during a median follow-up of 8.9 years. We found that PM2.5 [hazard ratio (HR), 1.27; 95% CI, 1.05-1.55], PM10 (HR, 1.18; 95% CI, 1.04-1.34), NO2 (HR, 1.05; 95% CI, 1.01-1.08), and NOx (HR, 1.02; 95% CI, 1.01-1.03) were associated with all-cause mortality. PM2.5 was also associated with increased risks of CVD mortality (HR, 1.68; 95% CI, 1.10-2.56) and CHD mortality (HR, 2.08; 95% CI, 1.16-3.75). In addition, we found that adherence to healthy dietary patterns modified associations of PM2.5, NO2 and NOx with all-cause mortality (P-interaction = 0.006, 0.006 and 0.02, respectively). Among the individual dietary components, vegetable intakes showed interactions with PM2.5, NO2 and NOx (P-interaction = 0.007, 0.004 and 0.02, respectively). The associations between air pollutants and increased risks of all-cause mortality were attenuated among participants with higher vegetable intakes. We did not observe interactions between air pollutants and HDS on CVD, CHD or stroke mortality (P-interaction > 0.05). Besides, we did not find interactions between air pollutants and genetic risk for lifespan on mortality risk.ConclusionThis study provides evidence linking long-term exposure to various air pollutants to the risk of all-cause, CVD and CHD mortality, and the potential attenuation of a healthy diet, especially high vegetable intakes, on such relations. Our findings highlight the importance of adherence to a healthy diet in lowering ambient air-pollution-related mortality risk.

Project description:BackgroundExtensive evidence indicates that both lifestyle factors and air pollution are strongly associated with all-cause mortality. However, little studies in this field have integrated these two factors in order to examine their relationship with mortality and explore potential interactions.MethodsA cohort of 271,075 participants from the UK Biobank underwent analysis. Lifestyles in terms of five modifiable factors, namely smoking, alcohol consumption, physical activity, diet, and sleep quality, were classified as unhealthy (0-1 score), general (2-3 score), and healthy (4-5 score). Air pollution, including particle matter with a diameter ≤ 2.5 μm (PM2.5), particulate matter with a diameter ≤ 10 μm (PM10), particulate matter with a diameter 2.5-10 μm (PM2.5-10), nitrogen dioxide (NO2), and nitrogen oxides (NOx), was divided into three levels (high, moderate, and low) using Latent Profile Analysis (LPA). Cox proportional hazard regression analysis was performed to examine the links between lifestyle, air pollution, and all-cause mortality before and after adjustment for potential confounders. Restricted cubic spline curves featuring three knots were incorporated to determine nonlinear relationships. The robustness of the findings was assessed via subgroup and sensitivity analyses.ResultsWith unhealthy lifestyles have a significantly enhanced risk of death compared to people with general lifestyles (HR = 1.315, 95% CI, 1.277-1.355), while people with healthy lifestyles have a significantly lower risk of death (HR = 0.821, 95% CI, 0.785-0.858). Notably, the difference in risk between moderate air pollution and mortality risk remained insignificant (HR = 0.993, 95% CI, 0.945-1.044). High air pollution, on the other hand, was independently linked to increased mortality risk as compared to low air pollution (HR = 1.162, 95% CI, 1.124-1.201). The relationship between NOx, PM10, and PM2.5-10 and all-cause mortality was found to be nonlinear (p for nonlinearity < 0.05). Furthermore, no significant interaction was identified between lifestyle and air pollution with respect to all-cause mortality.ConclusionsExposure to ambient air pollution elevated the likelihood of mortality from any cause, which was impacted by individual lifestyles. To alleviate this hazard, it is crucial for authorities to escalate environmental interventions, while individuals should proactively embrace and sustain healthy lifestyles.

Project description:BackgroundAir pollution may cause inflammatory and oxidative stress damage to the brain, leading to neurodegenerative disease. The association between air pollution and dementia, and modification by apolipoprotein E genotype 4 (APOE-ε4) has yet to be fully investigated.ObjectivesTo examine associations of air pollution with three types of incident dementias (Alzheimer's disease (AD), frontotemporal dementia (FTD), and vascular dementia (VAD)), and their potential modification by APOE-ε4 genotype.MethodsThe UK Biobank enrolled >500,000 participants (2006-2010) with ongoing follow-up. We used annual averages of air pollution (PM2.5, PM10, PM2.5-10, PM2.5absorbance, NO2, NOX) for 2010 scaled to interquartile ranges (IQR). We included individuals aged ≥60 years, with no dementia diagnosis prior to January 1, 2010. Time to incident dementia and follow-up time were reported from baseline (January 01, 2010) to last censor event (death, last hospitalization, or loss to follow-up). Cox proportional hazard ratios (HR) and 95% confidence intervals (95% CI) were calculated to estimate the association of air pollutants and incident dementia, and modification of these associations by APOE-ε4.ResultsOur sample included 187,194 individuals (including N = 680 AD, N = 377 VAD, N = 63 FTD) with a mean follow-up of 7.04 years. We observed consistent associations of PM2.5 with greater risk of all-cause dementia (HR = 1.17, 95% CI: 1.10, 1.24) and AD (HR = 1.17, 95% CI: 1.06, 1.29). NO2 was also associated with greater risk of any incident dementia (HR = 1.18, 95% CI: 1.10, 1.25), AD (HR = 1.15, 95% CI: 1.04, 1.28) and VAD (HR = 1.18, 95% CI: 1.03, 1.35). APOE-ε4 did not modify the association between any air pollutants and dementia.DiscussionPM2.5 and NO2 levels were associated with several types of dementia, and these associations were not modified by APOE-ε4. Findings from the UK Biobank support and extend to other epidemiological evidence for the potential association of air pollutants with detrimental brain health during aging.

Project description:Air pollution has consistently been associated with cardiometabolic outcomes, although associations with obesity have only been recently reported. Studies of air pollution and adiposity have mostly relied on body mass index (BMI) rather than body fat percentage (BF%), and most have not accounted for noise as a possible confounder. Additionally, it is unknown whether genetic predisposition for obesity increases susceptibility to the obesogenic effects of air pollution. To help fill these gaps, we used the UK Biobank, a large, prospective cohort study in the United Kingdom, to explore the relationship between air pollution and adiposity, and modification by a polygenic risk score for BMI. We used 2010 annual averages of air pollution estimates from land use regression (NO2, NOX, PM2.5, PM2.5absorbance, PM2.5-10, PM10), traffic intensity (TI), inverse distance to road (IDTR), along with examiner-measured BMI, waist-hip-ratio (WHR), and impedance measures of BF%, which were collected at enrollment (2006-2010, n = 473,026) and at follow-up (2012-2013, n = 19,518). We estimated associations of air pollution with BMI, WHR, and BF% at enrollment and follow-up, and with obesity, abdominal obesity, and BF%-obesity at enrollment and follow-up. We used linear and logistic regression and controlled for noise and other covariates. We also assessed interactions of air pollution with a polygenic risk score for BMI. On average, participants at enrollment were 56 years of age, 54% were female, and 32% had completed college or a higher degree. Almost all participants (~95%) were white. All air pollution measures except IDTR were positively associated with at least one continuous measure of adiposity at enrollment. However, NO2 was negatively associated with BMI but positively associated with WHR at enrollment, and IDTR was also negatively associated with BMI. At follow-up (controlling for enrollment adiposity), we observed positive associations for PM2.5-10 with BMI, PM10 with BF%, and TI with BF% and BMI. Associations were similar for binary measures of adiposity, with minor differences for some pollutants. Associations of NOX, NO2, PM2.5absorbance, PM2.5 and PM10, with BMI at enrollment, but not at follow-up, were stronger among individuals with higher BMI polygenic risk scores (interaction p <0.05). In this large, prospective cohort, air pollution was associated with several measures of adiposity at enrollment and follow-up, and associations with adiposity at enrollment were modified by a polygenic risk score for obesity.

Project description:Later chronotype (i.e. evening preference) and later timing of sleep have been associated with greater morbidity, including higher rates of metabolic dysfunction and cardiovascular disease (CVD). However, no one has examined whether chronotype is associated with mortality risk to date. Our objective was to test the hypothesis that being an evening type is associated with increased mortality in a large cohort study, the UK Biobank. Our analysis included 433 268 adults aged 38-73 at the time of enrolment and an average 6.5-year follow-up. The primary exposure was chronotype, as assessed through a single self-reported question-defining participants as definite morning types, moderate morning types, moderate evening types or definite evening types. The primary outcomes were all-cause mortality and mortality due to CVD. Prevalent disease was also compared among the chronotype groups. Analyses were adjusted for age, sex, ethnicity, smoking, body mass index, sleep duration, socioeconomic status and comorbidities. Greater eveningness, particularly being a definite evening type, was significantly associated with a higher prevalence of all comorbidities. Comparing definite evening type to definite morning type, the associations were strongest for psychological disorders (OR 1.94, 95% CI 1.86-2.02, p = < 0.001), followed by diabetes (OR 1.30, 95% CI 1.24-1.36, p = < 0.001), neurological disorders (OR 1.25, 95% CI 1.20-1.30, p = < 0.001), gastrointestinal/abdominal disorders (OR 1.23, 95% CI 1.19-1.27, p = < 0.001) and respiratory disorders (OR 1.22, 95% CI 1.18-1.26, p = < 0.001). The total number of deaths was 10 534, out of which 2127 were due to CVD. Greater eveningness, based on chronotype as an ordinal variable, was associated with a small increased risk of all-cause mortality (HR 1.02, 95% CI 1.004-1.05, p = 0.017) and CVD mortality (HR 1.04, 95% CI 1.00-1.09, p = 0.06). Compared to definite morning types, definite evening types had significantly increased risk of all-cause mortality (HR 1.10, 95% CI 1.02-1.18, p = 0.012). This first report of increased mortality in evening types is consistent with previous reports of increased levels of cardiometabolic risk factors in this group. Mortality risk in evening types may be due to behavioural, psychological and physiological risk factors, many of which may be attributable to chronic misalignment between internal physiological timing and externally imposed timing of work and social activities. These findings suggest the need for researching possible interventions aimed at either modifying circadian rhythms in individuals or at allowing evening types greater working hour flexibility.

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Associations of air pollution with COVID-19 positivity, hospitalisations, and mortality: Observational evidence from UK Biobank.

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