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BACKGROUND: Epidemiological evidence regarding the association between air pollutants and cardiopulmonary disease, mortality in individuals with preserved ratio impaired spirometry (PRISm), and their combined effects remains unclear. METHODS: We followed 36,149 participants with PRISm in the UK Biobank study. Annual concentrations of PM2.5, PM10, NO2, NOx, and SO2 at residential addresses were determined using a bilinear interpolation method, accounting for address changes. A multistate model assessed the dynamic associations between air pollutants and cardiopulmonary diseases and mortality in PRISm. Quantile g-computation was used to investigate the joint effects of air pollutants. RESULTS: Long-term exposure to PM2.5, PM10, NO2, NOx, and SO2 was significantly associated with the risk of cardiopulmonary disease in PRISm. The corresponding hazard ratios (HRs) [95 % confidence intervals (95 % CIs)] per interquartile range (IQR) were 1.49 (1.43, 1.54), 1.52 (1.46, 1.57), 1.34 (1.30, 1.39), 1.30 (1.26, 1.34), and 1.44 (1.41, 1.48), respectively. For mortality, the corresponding HRs (95 % CIs) per IQR were 1.36 (1.25, 1.47), 1.35 (1.24, 1.46), 1.27 (1.18, 1.36), 1.23 (1.15, 1.31), and 1.29 (1.20, 1.39), respectively. In PRISm, quantile g-computation analysis demonstrated that a quartile increase in exposure to a mixture of all air pollutants was positively associated with the risk of cardiopulmonary disease and mortality, with HRs (95 % CIs) of 1.84 (1.76, 3.84) and 1.45 (1.32, 1.57), respectively. CONCLUSION: Long-term individual and joint exposure to air pollutants (PM2.5, PM10, NO2, NOx, and SO2) might be an important risk factor for cardiopulmonary disease and mortality in high-risk populations with PRISm.
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Individuals with cardiovascular disease (CVD) are particularly vulnerable to dementia, but it remains unclear whether air pollution exposure links with higher risk of dementia among those with CVD. The data were derived from the UK Biobank study (UKB). Dementia-free participants with CVD at baseline were included. Air pollution exposure was assessed through land use regression models, including particulate matter (PM2.5, PM2.5-10, and PM10), nitrogen dioxide (NO2), and nitrogen oxides (NOX). A Cox proportional hazards model was used to investigate the associations between air pollution exposure and incident dementia among individuals with CVD. Air pollution was associated with dementia among individuals with CVD, and the hazard ratios of dementia associated with each interquartile range (IQR) µg/m3 increase in air pollution were 1.07 (95% CI: 1.02, 1.12) for PM2.5, 1.10 (95% CI: 1.04, 1.15) for PM10, 1.08 (95% CI: 1.03, 1.14) for NO2 and 1.05 (95% CI: 1.00, 1.09) for NOx. Associations between air pollution and all-cause dementia were found to be significant among individuals with hypertension. Adverse effects of air pollution were also observed for Alzheimer's dementia (AD) and vascular dementia (VaD), with a higher effect for AD. Observed associations remained similar in subgroups of APOE ε4 carriers and noncarriers, although there was a higher risk difference across different air pollution concentration among these individuals carrying APOE ε4. Air pollution emerges as a critical risk factor for dementia among individuals with CVD, regardless of genetic susceptibility indicated by the APOE genotype. Notably, individuals with hypertension might be susceptible to the adverse effects of air pollution, leading to a higher incidence of dementia. Understanding these impacts on dementia among individuals with CVD may promote better targeted prevention and clinical management strategies.
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Contaminantes Atmosféricos , Contaminación del Aire , Enfermedad de Alzheimer , Enfermedades Cardiovasculares , Hipertensión , Humanos , Enfermedades Cardiovasculares/epidemiología , Enfermedades Cardiovasculares/genética , Enfermedades Cardiovasculares/inducido químicamente , Contaminantes Atmosféricos/análisis , Dióxido de Nitrógeno/análisis , Estudios Longitudinales , Apolipoproteína E4 , Exposición a Riesgos Ambientales/efectos adversos , Exposición a Riesgos Ambientales/análisis , Contaminación del Aire/efectos adversos , Contaminación del Aire/análisis , Material Particulado/análisis , Hipertensión/inducido químicamente , GenotipoRESUMEN
BACKGROUND: Although the indoor environment has been proposed to be associated with childhood sleep health, to our knowledge no study has investigated the association between home renovation and childhood sleep problems. METHODS: The study included 186,470 children aged 6-18 years from the National Chinese Children Health Study (2012-2018). We measured childhood sleeping problems via the Chinese version of the Sleep Disturbance Scale for Children (C-SDSC). Information on home renovation exposure within the recent 2 years was collected via parent report. We estimated associations between home renovation and various sleeping problems, defined using both continuous and categorized (binary) C-SDSC t-scores, using generalized mixed models. We fitted models with city as a random effect variable, and other covariates as fixed effects. RESULTS: Out of the overall participants, 89,732 (48%) were exposed to recent home renovations. Compared to the unexposed group, children exposed to home renovations had higher odds of total sleep disorder (odd ratios [OR] = 1.3; 95% confidence interval [CI] = 1.2, 1.4). Associations varied when we considered different types of home renovation materials. Children exposed to multiple types of home renovation had higher odds of sleeping problems. We observed similar findings when considering continuous C-SDSC t-scores. Additionally, sex and age of children modified the associations of home renovation exposure with some of the sleeping problem subtypes. CONCLUSIONS: We found that home renovation was associated with higher odds of having sleeping problems and that they varied when considering the type of renovation, cumulative exposure, sex, and age differences.
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Convulsiones , Trastornos del Sueño-Vigilia , Niño , Humanos , Encuestas y Cuestionarios , Ciudades , China/epidemiología , Trastornos del Sueño-Vigilia/epidemiologíaRESUMEN
Limited evidence is available regarding the association between acute exposure to ambient air pollutants and the risk of urticaria, even though the skin is an organ with direct contact with the external environment. This study utilized generalized additive models to investigate the association between particulate matter with an aerodynamic diameter smaller than 10 µm (PM10) and 2.5 µm (PM2.5), nitrogen dioxide (NO2) and sulfur dioxide (SO2), and daily outpatient visits for urticaria in Guangzhou, China from 2013 to 2017. We also estimated the attributable fraction of urticaria outpatient visits due to air pollution. A total of 216,648 outpatient visits due to urticaria occurred during the study period. All air pollutants were significantly associated with an increased excess risk of urticaria. Each 10 µg/m3 increase in PM2.5, PM10, NO2, and SO2 was associated with an increase of 1.23% (95% CI: 0.42%, 2.06%), 0.88% (95% CI: 0.28%, 1.49%), 3.09% (95% CI: 2.16%, 4.03%), and 2.82% (95% CI: 0.93%, 4.74%) in hospital visits for urticaria at lag05, respectively. It was estimated that 3.77% (95% CI: 1.26%, 6.38%), 1.91% (95% CI: 0.60%, 3.26%), 6.36% (95% CI: 4.38%, 8.41%), and 0.08% (95% CI: 0.03%, 0.14%) of urticaria outpatient visits were attributable to PM2.5, PM10, NO2, and SO2 using the World Health Organization's air quality guideline as the reference. Relatively stronger associations were observed during the cold season. This study indicates that short-term air pollution may play a significant role in outpatient visits for urticaria, and that such relationships could be modified by season.
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BACKGROUND: The association between air pollution and mental disorders has been widely documented in the general population. However, the evidence among susceptible populations, such as individuals with prediabetes or diabetes, is still insufficient. METHODS: We analyzed data from 48,515 participants with prediabetes and 24,393 participants with diabetes from the UK Biobank. Annual pollution data were collected for fine particulate matter (PM2.5), inhalable particulate matter (PM10), nitrogen dioxide (NO2), and nitrogen dioxides (NOx) during 2006-2021. The exposure to air pollution and temperature for each participant were estimated by the bilinear interpolation approach and time-weighted method based on their geocoded home addresses and time spent at each address. We employed the generalized propensity score model based on the generalized estimating equation and the time-varying covariates Cox model to assess the effects of air pollution. RESULTS: We observed causal links between air pollutants and mental disorders among both prediabetic and diabetic participants, with stronger effects among those with diabetes than prediabetes. The hazard ratios were 1.18 (1.12, 1.24), 1.15 (1.10, 1.20), 1.18 (1.13, 1.23), and 1.15 (1.11, 1.19) in patients with prediabetes, and 1.21 (1.13, 1.29), 1.17 (1.11, 1.24), 1.19 (1.13, 1.25), and 1.17 (1.12, 1.23) in patients with diabetes per interquartile range elevation in PM2.5, PM10, NO2, and NOx. Furthermore, the effects were more pronounced among people who were older, alcohol drinkers, and living in urban areas. CONCLUSIONS: Our study indicates the potential causal links between long-term exposure to air pollution and incident mental disorders among those with prediabetes and diabetes. Reducing air pollution levels would significantly benefit this vulnerable population by reducing the incidence of mental disorders.
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Contaminantes Atmosféricos , Contaminación del Aire , Diabetes Mellitus , Trastornos Mentales , Estado Prediabético , Humanos , Estado Prediabético/epidemiología , Dióxido de Nitrógeno/análisis , Estudios Prospectivos , Exposición a Riesgos Ambientales/análisis , Contaminación del Aire/análisis , Contaminantes Atmosféricos/efectos adversos , Contaminantes Atmosféricos/análisis , Material Particulado/efectos adversos , Material Particulado/análisis , Diabetes Mellitus/epidemiología , Trastornos Mentales/epidemiologíaRESUMEN
Objectives The relationship between prenatal physical activity (PA) and adverse birth outcomes is still inconclusive. We aimed to investigate the association between PA during pregnancy and adverse birth outcomes by using data from the Guangxi Zhuang birth cohort (GZBC) in China.Study Design A total of 11,292 mother-infant pairs were included from GZBC in China. The information on PA status, intensity, adequacy, and volume and birth outcomes were collected. Multivariable linear and logistic regression models were applied to analyze the effects of PA during pregnancy on birth weight z-scores (BW z-scores) and gestational age and risk of small-for-gestational age (SGA) and preterm birth (PTB), respectively. Cubic spline analysis was conducted to detect a nonlinear dose-response of total weekly activity metabolic equivalents (MET) and birth outcomes.Results Compared to no regular PA during pregnancy, moderate and high-intensity PA (MVPA) was associated with increase BW z-scores (ß = 0.08, 95%CI: 0.002, 0.15, p = .044) and associated with a marginal significant decrease in risk of PTB (OR = 0.73, 95%CI: 0.51, 1.05, p = .093). However, PA had no relationship with gestational age and risk of SGA, and Nonlinear relationships were not observed between total weekly activity MET and risk of SGA and PTB.Conclusion These finding shows that PA during pregnancy may increase the BW z-score and reduce risk of PTB, supporting the guidelines that pregnant women should be encouraged to engage in appropriate physical activity during pregnancy in China.
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Nacimiento Prematuro , Embarazo , Recién Nacido , Humanos , Femenino , Nacimiento Prematuro/epidemiología , Estudios Prospectivos , China/epidemiología , Recién Nacido Pequeño para la Edad Gestacional , Peso al Nacer , Parto , Retardo del Crecimiento Fetal , Ejercicio Físico , Resultado del Embarazo/epidemiologíaRESUMEN
OBJECTIVES: Epidemiological evidence suggests associations between ambient air pollution and cardiovascular disease (CVD), while circadian rhythm dysregulation, presented by circadian syndrome (CircS), is emerging as a new proxy to cardiovascular disorder that could provide a bridge between them. The present study aims to clarify the effect of high levels ambient air pollution exposure on CircS and CVD in China. METHODS: From the China Health and Retirement Longitudinal Study, we recruited 9116 Chinese participants in 2011 and followed them to 2015. A spatiotemporal model was applied to estimate exposure to particles with diameters ≤2.5 µm (PM2.5). The variable CircS was defined based on 7 components, including the 5 components used to define metabolic syndrome as well as other two components, lack of sleep and depression. The associations between PM2.5 exposure and prevalent CircS as well as incident CVD were modeled via logistic regression analysis displaying odds ratios (ORs) and 95 % CIs (confidence intervals). A mediation analysis was undertaken to identify the potential mediating role of CircS between PM2.5 exposure and CVD. RESULTS: The mean age (standard deviation) was 59 (9) and 48.22 % were male. The OR (95 % CI) between the highest (Q4) and the lowest (Q1) quartile of PM2.5 exposure for CircS was 1.13 (1.01-1.28) in 2011 and 1.44 (1.22-1.72) in 2015. The cumulative effect of the components of CircS became more obvious with the increase of the PM2.5 quartile exposure. For the Q4 versus Q1 of PM2.5 increment, the multivariate-adjusted OR (95 % CI) was 1.66 (1.20-2.29) for CVD incidence. CircS partially mediated the association between PM2.5 exposure and CVD. CONCLUSIONS: Exposure to PM2.5 is a risk factor for CircS and CVD, and the effect of PM2.5 on CVD may be explained by CircS. Improving air quality would have high value in preventing CircS as well as CVD in public health.
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Contaminantes Atmosféricos , Contaminación del Aire , Enfermedades Cardiovasculares , Humanos , Masculino , Femenino , Material Particulado/análisis , Estudios Longitudinales , Enfermedades Cardiovasculares/epidemiología , Contaminación del Aire/análisis , China/epidemiología , Contaminantes Atmosféricos/análisis , Exposición a Riesgos Ambientales/análisisRESUMEN
BACKGROUND: Long-term exposure to air pollution has been associated with the onset and progression of kidney diseases, but the association between short-term exposure to air pollution and mortality of kidney diseases has not yet been reported. METHODS: A nationally representative sample of 101,919 deaths from kidney diseases was collected from the Chinese Center for Disease Control and Prevention from 2015 to 2019. A time-stratified case-crossover study was applied to determine the associations. Satellite-based estimates of air pollution were assigned to each case and control day using a bilinear interpolation approach and geo-coded residential addresses. Conditional logistic regression models were constructed to estimate the associations adjusting for nonlinear splines of temperature and relative humidity. RESULTS: Each 10 µg/m3 increment in lag 0-1 mean concentrations of air pollutants was associated with a percent increase in death from kidney disease: 1.33% (95% confidence interval [CI]: 0.57% to 2.1%) for PM1, 0.49% (95% CI: 0.10% to 0.88%) for PM2.5, 0.32% (95% CI: 0.08% to 0.57%) for PM10, 1.26% (95% CI: 0.29% to 2.24%) for NO2, and 2.9% (95% CI: 1.68% to 4.15%) for SO2. CONCLUSIONS: Our study suggests that short-term exposure to ambient PM1, PM2.5, PM10, NO2, and SO2 might be important environmental risk factors for death due to kidney diseases in China.
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Contaminantes Atmosféricos , Contaminación del Aire , Enfermedades Renales , Humanos , Contaminantes Atmosféricos/efectos adversos , Contaminantes Atmosféricos/análisis , Contaminación del Aire/efectos adversos , China/epidemiología , Estudios Cruzados , Enfermedades Renales/mortalidad , Dióxido de Nitrógeno/efectos adversos , Dióxido de Nitrógeno/análisis , Material Particulado/efectos adversosRESUMEN
BACKGROUND AND OBJECTIVES: Studies on the effects of airborne particulates of diameter ≤ 1 µm (PM1), airborne particulates of diameter ≤ 2.5 µm (PM2.5) and airborne particulates of diameter ranges from 1 to 2.5 µm (PM1-2.5) on incidence of hyperuricemia are limited. We aimed to investigate the associations between PM1, PM2.5, and PM1-2.5 and hyperuricemia among male traffic officers. METHODS: We conducted a prospective cohort study of 1460 traffic officers without hyperuricemia in Guangzhou, China from 2009 to 2016. Exposures of PM1 and PM2.5 were estimated with a spatiotemporal model. PM1-2.5 concentrations were calculated by subtracting PM1 from PM2.5 concentrations. Cox's proportional hazards regressions models were used to examine the association between PM1, PM2.5, and PM1-2.5 and hyperuricemia, adjusted for potential confounders. Associations between PM1, PM2.5, and PM1-2.5 and serum uric acid (SUA) levels were evaluated with multiple linear regression models. RESULTS: Hazard ratios (HRs) and 95% confidence intervals (CIs) of hyperuricemia associated with 10 µg/m3 increment in PM1, PM2.5, and PM1-2.5 were 1.67 (95% CI:1.30-2.36), 1.49 (95% CI: 1.27-1.75), and 2.18 (95% CI: 1.58-3.02), respectively. The SUA concentrations increased by 12.23 µmol/L (95% CI: 5.91-18.56), 6.93 µmol/L (95% CI: 3.02-10.84), and 8.72 µmol/L (95% CI: 0.76-16.68) per 10 µg/m3 increase in PM1, PM2.5, and PM1-2.5, respectively. Stratified analyses indicated the positive associations of PM2.5 and PM1-2.5 with SUA levels were stronger in non-smokers, and PM1, PM2.5, and PM1-2.5 with SUA levels were stronger in non-drinkers. CONCLUSION: Long-term PM1, PM2.5, and PM1-2.5 exposures may increase the risk of hyperuricemia and elevate SUA levels among male traffic officers, especially in non-smokers and non-drinkers.
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Contaminantes Atmosféricos , Contaminación del Aire , Hiperuricemia , Humanos , Masculino , Material Particulado/toxicidad , Material Particulado/análisis , Contaminantes Atmosféricos/análisis , Hiperuricemia/epidemiología , Estudios Prospectivos , Ácido Úrico/análisis , Exposición a Riesgos Ambientales/efectos adversos , Exposición a Riesgos Ambientales/análisis , China/epidemiología , Contaminación del Aire/análisisRESUMEN
BACKGROUND: Previous studies have revealed the relationship between cold spells and morbidity and mortality due to respiratory diseases, while the detrimental effects of cold spells on the length of hospital stay and hospitalization expenses remain largely unknown. METHODS: We collected hospitalization data for respiratory diseases in 11 cities of Shanxi, China during 2017-2019. In each case, exposure to meteorological variables and air pollution was estimated by the bilinear interpolation approach and inverse distance weighting method, respectively, and then averaged at the city level. Cold spells were defined as the daily mean temperature below the 10th, 7.5th, or 5th percentiles for at least 2 to 5 consecutive days. We applied distributed lag non-linear models combined with generalized additive models to assess cumulative effects and harvesting effects. RESULTS: There were significant associations between cold spells and hospital admissions, length of hospital stay, and hospital expenses for respiratory diseases. Compared with the non-cold spell period, the overall (lag 0-21) cumulative risk of hospitalization for total respiratory diseases was 1.232 (95 % CI: 1.090, 1.394) on cold spell days, and the increased length of hospital stay and hospitalization expenses were 112.793 (95 % CI: 10.755, 214.830) days and 127.568 (95 % CI: 40.513, 214.624) thousand Chinese yuan. The overall cumulative risks of cold spells on total respiratory diseases and pneumonia were statistically significant. We further observed harvesting effects in the associations between cold spells and hospital admission, length of hospital stay, and hospitalization expenses for respiratory diseases. CONCLUSIONS: Cumulative cold-spell exposure for up to three weeks is associated with hospitalization, length of hospital stay, and hospital expenses for respiratory diseases. The observed harmful effects of cold spells on respiratory diseases can be partly attributable to harvesting effects.
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Contaminación del Aire , Trastornos Respiratorios , Enfermedades Respiratorias , Humanos , Tiempo de Internación , Frío , Hospitalización , Enfermedades Respiratorias/epidemiología , China/epidemiología , HospitalesRESUMEN
BACKGROUND: To estimate the associations between ambient particulate matter (PM) pollution of different sizes (PM1, PM2.5, and PM10) and risk of rehospitalization among stroke patients, as well as the attributable burden in China. METHODS: We built a cohort of 1,066,752 participants with an index stroke hospitalization in Sichuan, China from 2017 to 2019. Seven-day and annual average exposures to PM pollution prior to the date of the index hospitalization were linked with residential address using a bilinear interpolation approach. Cox proportional hazard models were constructed to assess the association between ambient PM and the risk of rehospitalization. The burden of stroke rehospitalization was estimated using a counterfactual approach. RESULTS: 245,457 (23.0 %) participants experienced rehospitalization during a mean of 1.15 years (SD: 0.90 years) of follow-up. Seven-day average concentrations of PM were associated with increased risk of rehospitalization: the hazard ratios (HRs) per 10 µg/m3 were 1.034 (95 % confidence interval [CI]: 1.029-1.038) for PM1, 1.033 (1.031-1.036) for PM2.5, and 1.030 (1.028-1.031) for PM10; the hazard ratios were larger for annual average concentrations: 1.082 (1.074-1.090) for PM1, 1.109 (1.104-1.114) for PM2.5, and 1.103 (1.099-1.106) for PM10. The associations were stronger in participants who were female, of minority ethnicity (non-Han Chinese), who suffered from an ischemic stroke, and those admitted under normal conditions. Population attributable fractions for stroke rehospitalization ranged from 4.66 % (95 % CI: 1.69 % to 7.63 %) for the 7-day average of PM1 to 17.05 % (14.27 % to 19.83 %) for the annual average of PM10; the reducible average cost of rehospitalization per participant attributable to PM ranged from 492.09 (178.19 to 806) RMB for the 7-day average of PM1 to 1801.65 (1507.89 to 2095.41) RMB for the annual average of PM10. CONCLUSIONS: Ambient PM pollution may increase the risk of rehospitalization in stroke patients and is responsible for a significant burden of stroke rehospitalization.
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Contaminantes Atmosféricos , Contaminación del Aire , Accidente Cerebrovascular , Humanos , Femenino , Masculino , Material Particulado/análisis , Contaminantes Atmosféricos/análisis , Estudios de Cohortes , Contaminación del Aire/análisis , Accidente Cerebrovascular/epidemiología , Accidente Cerebrovascular/inducido químicamente , Exposición a Riesgos Ambientales/análisis , Hospitalización , China/epidemiologíaRESUMEN
BACKGROUND: Although ozone exposure has neurological toxicity, it remains unclear whether it was associated with an increased risk of attention-deficit/hyperactivity disorders (ADHD) among childhood. METHODS: We matched the four-year average ozone concentration with questionnaire data for 35,103 children aged 3-12 years from seven cities in Liaoning, China, 2012-2013. Using mixed-effect logistic regression models, we assessed the association of ozone concentration with multiple ADHD indicators using the Conners Abbreviated Symptom Questionnaire (C-ASQ), including explicit attention-deficit/hyperactivity symptoms (ADHD; score ≥15), attention-deficit/hyperactivity disorder tendencies (ADHD-T; 11 ≤ score ≤14), and attention-deficit/hyperactivity problems (ADHP; score ≥11). Results were also stratified by sociodemongraphics. RESULTS: After adjusting for covariates, we found that each interquartile range (IQR) increase in ozone concentration was associated with an increased risk of ADHD, ADHD-T, and ADHP (P < 0.001) with an odds ratio of 1.12 (95% confidence interval, 1.04-1.21), 1.08 (1.03-1.13), and 1.09 (1.05-1.14), respectively. Additionally, we found greater effect estimates in children who reported longer exercise time (vs those with limited exercise time) with odds ratio of 1.18 (1.07-1.31) vs 1.06 (0.96-1.17) for ADHD, 1.13 (1.06-1.21) vs 1.03 (0.96-1.10) for ADHD-T, and 1.15 (1.08-1.21) vs 1.04 (0.98-1.10) for ADHP. Non-breastfed children were also shown to be more vulnerable to ADHD with an odds ratio of 1.22 (1.09-1.36) compared with 1.06 (0.96-1.16) among the rest. CONCLUSIONS: Long-term ozone exposure may be associated with increased ADHD among children. Additional studies are needed to validate our findings and support policies and interventions to address this growing public health concern.
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Trastorno por Déficit de Atención con Hiperactividad , Ozono , Niño , Humanos , Trastorno por Déficit de Atención con Hiperactividad/inducido químicamente , Trastorno por Déficit de Atención con Hiperactividad/epidemiología , Oportunidad Relativa , Encuestas y Cuestionarios , Atención , Ozono/toxicidadRESUMEN
BACKGROUND: Fine particulate matter (PM2.5), smoking, and genetic factors are associated with lung cancer. However, the relationship between PM2.5, smoking and subtypes of lung cancer remains unclear. Moreover, it is unclear whether genetic risk modifies the impact of PM2.5 and smoking on incident lung cancer. METHODS: A total of 298,069 participants from the UK Biobank study without lung cancer at baseline were included in this study. Hazard ratios (HRs) with 95 % confidence intervals (CIs) were estimated using multivariable Cox proportional models for the association of lung cancer and its subtypes with PM2.5, smoking, and genetic risk. Potential gene-smoking or gene-PM2.5 interactions were also estimated. We further estimated population attributable fractions for incident lung cancer. RESULTS: During 10.4 years of follow-up, 1683 incident lung cancer cases were identified. Our analysis found that genetic variants, smoking, and PM2.5 were significantly associated with incident lung cancer. For different histological types of lung cancer, the HRs for squamous cell lung carcinoma associated with PM2.5 (per 5 µg/m3 increment) and current smoking were 2.76 (95 % CI: 1.72, 4.42, p < 0.001) and 48.64 (95 % CI: 27.96, 84.61, p < 0.001), while the HRs for lung adenocarcinoma were 1.59 (95 % CI: 1.13, 2.23, p < 0.001) and 9.89 (95 % CI: 7.91, 12.36, p < 0.001), respectively. We further found that participants with high levels of PM2.5 pollution and high genetic risk had the highest risk of incident lung cancer (HR = 1.81, 95 % CI: 1.39, 2.35, p < 0.001), while the interaction between PM2.5 and genetic risk was not statistically significant. We observed that the population attributable fractions of lung cancer attributable to current smoking and high PM2.5 exposure were estimated to be 67.45 % and 17.59 %. CONCLUSION: Genetic susceptibility, smoking, and PM2.5 are important risk factors for lung cancer. Both smoking and PM2.5 are more closely associated with an elevated risk of squamous cell lung cancer.
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Contaminantes Atmosféricos , Contaminación del Aire , Neoplasias Pulmonares , Humanos , Contaminantes Atmosféricos/análisis , Predisposición Genética a la Enfermedad , Material Particulado/análisis , Neoplasias Pulmonares/etiología , Neoplasias Pulmonares/genética , Fumar/efectos adversos , Fumar/epidemiología , Polvo/análisis , Exposición a Riesgos Ambientales/análisis , Contaminación del Aire/efectos adversos , Contaminación del Aire/análisisRESUMEN
BACKGROUND: Though the association between air pollution and incident type 2 diabetes (T2D) has been well documented, evidence on the association with development of subsequent diabetes complications and post-diabetes mortality is scarce. We investigate whether air pollution is associated with different progressions and outcomes of T2D. METHODS: Based on the UK Biobank, 398,993 participants free of diabetes and diabetes-related events at recruitment were included in this analysis. Exposures to particulate matter with a diameter ≤ 10 µm (PM10), PM2.5, nitrogen oxides (NOx), and NO2 for each transition stage were estimated at each participant's residential addresses using data from the UK's Department for Environment, Food and Rural Affairs. The outcomes were incident T2D, diabetes complications (diabetic kidney disease, diabetic eye disease, diabetic neuropathy disease, peripheral vascular disease, cardiovascular events, and metabolic events), all-cause mortality, and cause-specific mortality. Multi-state model was used to analyze the impact of air pollution on different progressions of T2D. Cumulative transition probabilities of different stages of T2D under different air pollution levels were estimated. RESULTS: During the 12-year follow-up, 13,393 incident T2D patients were identified, of whom, 3791 developed diabetes complications and 1335 died. We observed that air pollution was associated with different progression stages of T2D with different magnitudes. In a multivariate model, the hazard ratios [95% confidence interval (CI)] per interquartile range elevation in PM2.5 were 1.63 (1.59, 1.67) and 1.08 (1.03, 1.13) for transitions from healthy to T2D and from T2D to complications, and 1.50 (1.47, 1.53), 1.49 (1.36, 1.64), and 1.54 (1.35, 1.76) for mortality risk from baseline, T2D, and diabetes complications, respectively. Generally, we observed stronger estimates of four air pollutants on transition from baseline to incident T2D than those on other transitions. Moreover, we found significant associations between four air pollutants and mortality risk due to cancer and cardiovascular diseases from T2D or diabetes complications. The cumulative transition probability was generally higher among those with higher levels of air pollution exposure. CONCLUSIONS: This study indicates that ambient air pollution exposure may contribute to increased risk of incidence and progressions of T2D, but to diverse extents for different progressions.
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Contaminantes Atmosféricos , Contaminación del Aire , Diabetes Mellitus Tipo 2 , Humanos , Incidencia , Diabetes Mellitus Tipo 2/epidemiología , Exposición a Riesgos Ambientales/efectos adversos , Exposición a Riesgos Ambientales/análisis , Contaminación del Aire/efectos adversos , Material Particulado/efectos adversos , Contaminantes Atmosféricos/efectos adversos , Contaminantes Atmosféricos/análisisRESUMEN
INTRODUCTION: It remains unknown whether higher dietary intake of antioxidant vitamins could reduce the harmful effects of air pollution on incident diabetes mellitus. METHODS: A total of 156,490 participants free of diabetes mellitus in the UK Biobank data were included in this analysis. Antioxidant vitamin intake was measured using a 24-h food intake questionnaire, and results were categorized as sufficient or insufficient according to the British Recommended Nutrient Intake. Exposure to fine particles (PM2.5), thoracic particles (PM10), nitrogen dioxide (NO2), and nitrogen oxide (NOx) was estimated using land use regression models at participants' residences. Incident diabetes mellitus was identified using health administrative datasets. Cox regression models were used to assess the associations. RESULTS: A total of 4271 incident diabetes mellitus cases were identified during a median follow-up of 11.7 years. Compared with participants with insufficient intake of antioxidant vitamins, those with sufficient consumption had a weaker association between air pollution (PM2.5, PM10 and NO2) and diabetes mellitus [sufficient vs. insufficient: HR = 1.12 (95 % CI: 0.87, 1.45) vs. 1.69 (95 % CI: 1.42, 2.02) for PM2.5, 1.00 (95 % CI: 0.88, 1.14) vs. 1.21 (95 % CI: 1.10, 1.34) for PM10, and 1.01 (95 % CI: 0.98, 1.04) vs. 1.05 (95 % CI: 1.03, 1.07) for NO2 (all p for comparison < 0.05)]. Among different antioxidant vitamins, we observed stronger effects for vitamin C and E. CONCLUSION: Our study suggests that ambient air pollution is one important risk factor of diabetes mellitus, and sufficient intake of antioxidant vitamins may reduce such adverse effects of air pollution on diabetes mellitus.
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Contaminantes Atmosféricos , Contaminación del Aire , Diabetes Mellitus , Humanos , Dióxido de Nitrógeno/toxicidad , Antioxidantes , Estudios de Cohortes , Material Particulado/toxicidad , Contaminantes Atmosféricos/análisis , Vitaminas , Exposición a Riesgos Ambientales , Contaminación del Aire/efectos adversos , Contaminación del Aire/análisis , Diabetes Mellitus/epidemiología , Vitamina A , Vitamina K , Ingestión de AlimentosRESUMEN
BACKGROUND AND OBJECTIVE: Ambient air pollution has been widely linked with morbidity and mortality of stroke. However, its effects on dynamic progression trajectory of stroke remain unknown.We investigated the effects of ambient air pollution on progression trajectory from healthy status to incident stroke, poststroke cardiovascular diseases, and subsequent death. METHODS: We retrieved 318,752 participants from the UK Biobank. The annual concentrations of air pollution [particulate matter (PM2.5, PMcoarse, PM10 and PM2.5 absorbance), nitrogen dioxide (NO2), and nitrogen oxides (NOx)] were estimated through land use regressions. A multistate regression model was used to investigate the effects of air pollution on each stage of the progression of stroke. RESULTS: During 3,765,630 person-years of follow-up, we identified 5,967 incident stroke patients, 2,985 poststroke cardiovascular patients, and 1,020 deaths afterward. Each 5 µg/m3 increase in PM2.5, NO2, and NOx was associated with the transition from healthy status to incident stroke [hazard ratios (HRs) (95% confidence intervals (CI)) = 1.24 (1.10, 1.40); 1.02 (1.00, 1.03); 1.01 (1.00, 1.02)] and transitions from healthy status to death directly [1.30 (1.21, 1.40); 1.03 (1.02, 1.04); and 1.02 (1.01, 1.02)]. We also observed positive associations for poststroke CVDs, especially for NO2 [1.04 (95% CI: 1.02, 1.06)], but these effects gradually declined for mortality outcome. DISCUSSION: This study provides the first evidence that ambient air pollution is one important factor associated with the progression of stroke, and the effects differed across different clinical stages. A better understanding of the differential effects of air pollutants on different stroke transition stages could provide valuable insight toward targets for health management and clinical prevention.
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Contaminantes Atmosféricos , Contaminación del Aire , Enfermedades Cardiovasculares , Accidente Cerebrovascular , Humanos , Dióxido de Nitrógeno/efectos adversos , Dióxido de Nitrógeno/análisis , Estudios Prospectivos , Exposición a Riesgos Ambientales/efectos adversos , Incidencia , Contaminación del Aire/efectos adversos , Material Particulado/efectos adversos , Contaminantes Atmosféricos/efectos adversos , Accidente Cerebrovascular/epidemiologíaRESUMEN
INTRODUCTION: Epidemiological evidence suggests associations between long-term exposure to air pollution and accelerated cognitive decline. China implemented a strict clean air action plan in 2013; however, it is unclear whether the improvement of air quality has alleviated cognitive impairment in the population. METHODS: From the China Health and Retirement Longitudinal Study, 8536 Chinese adults were enrolled in 2011 and followed up in 2015. Satellite-based spatiotemporal models were used to estimate exposure to air pollutants (including particles with diameters ≤1.0 µm [PM1], ≤2.5 µm [PM2.5], ≤10 µm [PM10], nitrogen dioxide [NO2], and ozone [O3]). Cognitive function was evaluated using a structured questionnaire in three dimensions: episodic memory, orientation and attention, and visuoconstruction. The associations between changes in the levels of air pollutants and cognitive function were elucidated by a logistic model. The Bayesian Kernel Machine Regression (BKMR) model was applied to evaluate the cumulative effect of air pollutants. RESULTS: The mean (standard deviation) age of all participants was 58.6 (8.7) years. The odds ratio (95% confidence interval) between the highest and the lowest quartile of PM1 exposure reduction for cognitive impairment was 0.46 (0.41, 0.53) after adjusting for confounders. Similar protective effects of cognitive function were observed with the decrease in the level of PM2.5 (0.34 [0.30, 0.39]), PM10 (0.54 [0.48, 0.62]), and NO2 (0.59 [0.51, 0.67]), while the reduction in O3 appeared to be less related to changes in cognitive function (OR: 0.97 [0.85, 1.10]). The protective association of PM1 reduction was stronger in males than in females. Decreased in PM2.5 dominate the cognitive function benefit relative to PM1, PM10, NO2. CONCLUSIONS: The implementation of the clean air action plan led to a significant reduction in PM1, PM2.5, PM10, and NO2, which could slow the decline of cognitive function, while a reduction in O3 may not.
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Contaminantes Atmosféricos , Contaminación del Aire , Adulto , Contaminantes Atmosféricos/análisis , Contaminantes Atmosféricos/toxicidad , Contaminación del Aire/análisis , Contaminación del Aire/prevención & control , Teorema de Bayes , China/epidemiología , Cognición , Exposición a Riesgos Ambientales/análisis , Femenino , Humanos , Estudios Longitudinales , Masculino , Persona de Mediana Edad , Dióxido de Nitrógeno/análisis , Material Particulado/análisis , Mejoramiento de la CalidadRESUMEN
BACKGROUND: Currently, there is no evidence of fine particulate matter pollution (PM2.5) altering the relationship between physical activity (PA) and the risk of conjunctivitis. METHODS: Based on the UK Biobank study, we included 308,507 participants aged 40-69 years at baseline (2006 to 2010) and prospectively followed up for conjunctivitis diagnosis till 2020. Annual concentrations of PM2.5 in 2010 were estimated for each participant using Land Use Regression models. PA levels during work and leisure time were reported via the International Physical Activity Questionnaire at baseline. We used Cox proportional hazards models to examine the associations of PM2.5 and PA with incident conjunctivitis, as well as their interaction at both multiplicative and additive scales. RESULTS: During the 11.6 years of follow up, we identified 4002 incident conjunctivitis cases. High-PA (≥3000 metabolic equivalent of task [MET]-mins/week) was associated with lower risk of conjunctivitis (hazard ratio [HR]: 0.79, 95% confidence interval [CI]: 0.73-0.86) compared to low-PA (0 to <600 MET-mins/week), while every 1 µg/m3 increment in PM2.5 was associated with a 16% higher risk of conjunctivitis (HR = 1.16, 95% CI: 1.09-1.23). We did not observe statistically significant interactions between PM2.5 and PA on their associations with conjunctivitis. CONCLUSION: Habitual PA and PM2.5 exposure were oppositely related to incident conjunctivitis. The benefits of PA remain in people irrespective of exposure to air pollution.
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Contaminantes Atmosféricos , Contaminación del Aire , Conjuntivitis , Contaminantes Atmosféricos/análisis , Contaminación del Aire/análisis , Conjuntivitis/epidemiología , Exposición a Riesgos Ambientales , Ejercicio Físico , Humanos , Material Particulado/análisis , Estudios ProspectivosRESUMEN
BACKGROUND: Studies on the obesogenic effect of air pollution on children have been mixed and sparse. Moreover, due to insufficient air monitoring, few studies have investigated the role of more tiny but unregulated particles (ambient particles with a diameter of 0.1 µm or less, ultrafine particles). OBJECTIVE: We sought to explore the associations between long-term exposure to ambient ultrafine particles (UFPs) and childhood obesity in Chinese children. METHODS: In this cross-sectional study, we randomly recruited 47,990 children, aged 6-18 years, from seven cities in Northeastern China between 2012 and 2013. Child age- and sex-specific z-scores for body mass index (BMI Z-score) and weight status were generated using the World Health Organization growth reference. Four-year average concentrations of UFPs and airborne particulates of diameter ≤ 1 µm (PM1), ≤2.5 µm (PM2.5), and ≤10 µm (PM10) were estimated at home, using neural network simulated WRF-Chem model and spatiotemporal model, respectively. Confounder-adjusted generalized linear mixed models examined the associations between air pollution and BMI Z-score and the prevalence of childhood obesity. RESULT: We found that UFPs exposure was associated with greater childhood BMI Z-score and a higher likelihood of obesity. Compared with the lowest quartile, higher quartiles of UFPs were associated with greater odds for obesity prevalence in children (i.e., the adjusted OR was 1.25; 95 % CI, 1.12-1.39; 1.43; 95 % CI, 1.27-1.61; and 1.41; 95 % CI, 1.25-1.58 for the second, third, and fourth quartile, respectively). Similar associations were observed for PM1, PM2.5, and PM10, and were greater in boys and children living close to roadways. CONCLUSIONS: Long-term UFPs exposure was associated with a greater likelihood of childhood obesity, and stronger associations on BMI Z-score were observed in boys and children living close to roadways. This study indicates that more attention should be paid to the health effects of UFPs, and routinely monitoring of UFPs should be considered.
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Contaminantes Atmosféricos , Contaminación del Aire , Obesidad Infantil , Contaminantes Atmosféricos/análisis , Contaminación del Aire/análisis , Niño , China/epidemiología , Ciudades , Estudios Transversales , Exposición a Riesgos Ambientales/análisis , Femenino , Humanos , Masculino , Material Particulado/análisis , Obesidad Infantil/epidemiologíaRESUMEN
OBJECTIVE: To characterize the association of ambient particulate matter (PM) pollution of different sizes (particulate matter ≤1 µm in aerodynamic diameter [PM1], PM2.5, and PM10) with in-hospital case fatality among stroke patients in China. METHODS: We collected hospitalizations due to stroke in four provinces in China from 2013 to 2019. Seven-day and annual averages of PM prior to hospitalization were estimated using bilinear interpolation and residential addresses. Associations with in-hospital case fatality were estimated using random-effects logistic regression models. Potential reducible fraction and the number of fatalities attributed to PM were estimated using a counterfactual approach. RESULTS: Among 3,109,634 stroke hospitalizations (mean age 67.23 [standard deviation 12.22]; 1,765,644 [56.78%] male), we identified 32,140 in-hospital stroke fatalities (case fatality rate 1.03%). Each 10 µg/m3 increase in 7-day average (short-term) exposure to PM was associated with increased in-hospital case fatality: odds ratios (ORs) were 1.058 (95% confidence interval [CI]: 1.047-1.068) for PM1, 1.037 (95% CI: 1.031-1.043) for PM2.5, and 1.025 (95% CI: 1.021-1.029) for PM10. Similar but larger ORs were observed for annual averages (long-term): 1.240 (95% CI: 1.217-1.265) for PM1, 1.105 (95% CI: 1.094-1.116) for PM2.5, and 1.090 (95% CI: 1.082-1.099) for PM10. In counterfactual analyses, PM10 was associated with the largest potential reducible fraction in in-hospital case fatality (10% [95% CI: 8.3%-11.7%] for short-term exposure and 21.1% [19.1%-23%] for long-term exposure), followed by PM1 and PM2.5. CONCLUSION: PM pollution is a risk factor for in-hospital stroke-related deaths. Strategies that target reducing PM pollution may improve the health outcomes of stroke patients.