RÉSUMÉ
BACKGROUND: PM2.5 can induce and aggravate the occurrence and development of cardiovascular diseases (CVDs). The objective of our study is to estimate the causal effect of PM2.5 on mortality rates associated with CVDs using the instrumental variables (IVs) method. METHODS: We extracted daily meteorological, PM2.5 and CVDs death data from 2016 to 2020 in Binzhou. Subsequently, we employed the general additive model (GAM), two-stage predictor substitution (2SPS), and control function (CFN) to analyze the association between PM2.5 and daily CVDs mortality. RESULTS: The 2SPS estimated the association between PM2.5 and daily CVDs mortality as 1.14% (95% CI: 1.04%, 1.14%) for every 10 µg/m3 increase in PM2.5. Meanwhile, the CFN estimated this association to be 1.05% (95% CI: 1.02%, 1.10%). The GAM estimated it as 0.85% (95% CI: 0.77%, 1.05%). PM2.5 also exhibited a statistically significant effect on the mortality rate of patients with ischaemic heart disease, myocardial infarction, or cerebrovascular accidents (P < 0.05). However, no significant association was observed between PM2.5 and hypertension. CONCLUSION: PM2.5 was significantly associated with daily CVDs deaths (excluding hypertension). The estimates from the IVs method were slightly higher than those from the GAM. Previous studies based on GAM may have underestimated the impact of PM2.5 on CVDs.
Sujet(s)
Polluants atmosphériques , Maladies cardiovasculaires , Matière particulaire , Humains , Matière particulaire/effets indésirables , Matière particulaire/analyse , Maladies cardiovasculaires/mortalité , Chine/épidémiologie , Polluants atmosphériques/effets indésirables , Polluants atmosphériques/analyse , Exposition environnementale/effets indésirables , Mâle , Femelle , Pollution de l'air/effets indésirables , Adulte d'âge moyenRÉSUMÉ
BACKGROUND: Despite accumulating evidence of an association between air pollution and renal disease, studies on the association between long-term exposure to air pollution and renal function are still contradictory. This study aimed to investigate this association in a large population with relatively low exposure and with improved estimation of renal function as well as renal injury biomarkers. METHODS: We performed a cross-sectional analysis in the middle-aged general population participating in the Swedish CardioPulmonary bioImaging Study (SCAPIS; n = 30 154). Individual 10-year exposure to total and locally emitted fine particulate matter (PM2.5), inhalable particulate matter (PM10), and nitrogen oxides (NOx) were modelled using high-resolution dispersion models. Linear regression models were used to estimate associations between exposures and estimated glomerular filtration rate (eGFR, combined creatinine and cystatin C) and serum levels of renal injury biomarkers (KIM-1, MCP-1, IL-6, IL-18, MMP-2, MMP-7, MMP-9, FGF-23, and uric acid), with consideration of potential confounders. RESULTS: Median long-term PM2.5 exposure was 6.2 µg/m3. Almost all participants had a normal renal function and median eGFR was 99.2 mL/min/1.73 m2. PM2.5 exposure was associated with 1.3% (95% CI 0.6, 2.0) higher eGFR per 2.03 µg/m3 (interquartile range, IQR). PM2.5 exposure was also associated with elevated serum matrix metalloproteinase 2 (MMP-2) concentration, with 7.2% (95% CI 1.9, 12.8) higher MMP-2 per 2.03 µg/m3. There was a tendency towards an association between PM10 and higher levels of uric acid, but no associations were found with the other biomarkers. Associations with other air pollutants were null or inconsistent. CONCLUSION: In this large general population sample at low exposure levels, we found a surprising association between PM2.5 exposure and a higher renal filtration. It seems unlikely that particle function would improve renal function. However, increased filtration is an early sign of renal injury and may be related to the relatively healthy population at comparatively low exposure levels. Furthermore, PM2.5 exposure was associated with higher serum concentrations of MMP-2, an early indicator of renal and cardiovascular pathology.
Sujet(s)
Polluants atmosphériques , Marqueurs biologiques , Exposition environnementale , Débit de filtration glomérulaire , Maladies du rein , Matière particulaire , Humains , Marqueurs biologiques/sang , Adulte d'âge moyen , Mâle , Femelle , Matière particulaire/effets indésirables , Matière particulaire/analyse , Polluants atmosphériques/effets indésirables , Polluants atmosphériques/analyse , Suède/épidémiologie , Études transversales , Exposition environnementale/effets indésirables , Maladies du rein/induit chimiquement , Maladies du rein/épidémiologie , Maladies du rein/sang , Pollution de l'air/effets indésirables , Pollution de l'air/analyse , Sujet âgé , Facteur-23 de croissance des fibroblastes , Rein/physiopathologie , Rein/effets des médicaments et des substances chimiques , Oxydes d'azote/sang , Oxydes d'azote/analyse , Oxydes d'azote/effets indésirables , AdulteRÉSUMÉ
Fine particulate matter (PM2.5) is a major air pollutant affecting human survival, development and health. By predicting the spatial distribution concentration of PM2.5, pollutant sources can be better traced, allowing measures to protect human health to be implemented. Thus, the purpose of this study is to predict and analyze the PM2.5 concentration of stations based on the integrated deep learning of a convolutional neural network long short-term memory (CNN-LSTM) model. To solve the complexity and nonlinear characteristics of PM2.5 time series data problems, we adopted the CNN-LSTM deep learning model. We collected the PM2.5data of Qingdao in 2020 as well as meteorological factors such as temperature, wind speed and air pressure for pre-processing and characteristic analysis. Then, the CNN-LSTM deep learning model was integrated to capture the temporal and spatial features and trends in the data. The CNN layer was used to extract spatial features, while the LSTM layer was used to learn time dependencies. Through comparative experiments and model evaluation, we found that the CNN-LSTM model can achieve excellent PM2.5 prediction performance. The results show that the coefficient of determination (R2) is 0.91, and the root mean square error (RMSE) is 8.216 µg/m3. The CNN-LSTM model achieves better prediction accuracy and generalizability compared with those of the CNN and LSTM models (R2 values of 0.85 and 0.83, respectively, and RMSE values of 11.356 and 14.367, respectively). Finally, we analyzed and explained the predicted results. We also found that some meteorological factors (such as air temperature, pressure, and wind speed) have significant effects on the PM2.5 concentration at ground stations in Qingdao. In summary, by using deep learning methods, we obtained better prediction performance and revealed the association between PM2.5 concentration and meteorological factors. These findings are of great significance for improving the quality of the atmospheric environment and protecting public health.
Sujet(s)
Polluants atmosphériques , , Matière particulaire , Matière particulaire/analyse , Matière particulaire/effets indésirables , Polluants atmosphériques/analyse , Polluants atmosphériques/effets indésirables , Humains , Surveillance de l'environnement/méthodes , Apprentissage profond , Chine , Algorithmes , Pollution de l'air/analyseRÉSUMÉ
Objectives: This research aims to analyze how exposure to fine particulate matter (PM2.5) and ambient heat during pregnancy increases the risk of congenital hydronephrosis (CH) in newborns. Methods: A case-control study was conducted to investigate the relationship between exposure to PM2.5 and ambient heat during pregnancy and the occurrence of CH in newborns. The study, which was conducted from 2015 to 2020, included 409 infants with CH as the case group and 409 infants without any abnormalities as the control group. Using spatial remote sensing technology, the exposure of each pregnant mother to PM2.5 concentration was meticulously mapped. Additionally, data on the ambient temperature of exposure for each participant were also collected. A logistics regression model was used to calculate the influence of exposure to PM2.5 and ambient heat on the occurrence of CH. Stratified analysis and interaction analysis were used to study the interaction between ambient heat exposure and PM2.5 on the occurrence of CH. Results: At the 6th week of gestation, exposure to PM2.5 may increase the risk of CH. For every 10 µg/m3 increase in PM2.5 exposure, the risk of CH increased by 2% (95%CI = 0.98, 1.05) at a p-value of >0.05, indicating that there was no significant relationship between the results. Exposure to intense heat at 6th and 7th weeks of gestation increased the risk of CH. Specifically, for every 1°C increase in heat exposure, the risk of CH in offspring increased by 21% (95%CI = 1.04, 1.41) during the 6th week and 13% during the 7th week (95%CI = 1.02, 1.24). At 5th and 6th weeks of gestation, the relative excess risk due to interaction (RERI) was greater than 0 at the 50th percentile (22.58°C), 75th percentile (27.25°C), and 90th percentile (29.13°C) of daily maximum temperature (Tmax) distribution, indicating that the risk of CH was higher when exposed to both ambient heat and PM2.5 at the same time compared to exposure to a single risk factor. Conclusion: Exposure to higher levels of PM2.5 and ambient heat during pregnancy increases the risk of CH in infants. There was a positive interaction between exposure to intense heat and high concentration of PM2.5 on the occurrence of CH.
Sujet(s)
Température élevée , Hydronéphrose , Exposition maternelle , Matière particulaire , Humains , Femelle , Matière particulaire/effets indésirables , Matière particulaire/analyse , Chine/épidémiologie , Grossesse , Température élevée/effets indésirables , Études cas-témoins , Nouveau-né , Hydronéphrose/étiologie , Exposition maternelle/effets indésirables , Exposition maternelle/statistiques et données numériques , Adulte , Mâle , Facteurs de risque , Polluants atmosphériques/effets indésirables , Polluants atmosphériques/analyseRÉSUMÉ
Background: Previous work reported increased rates of cardiovascular hospitalizations associated with increased source-specific PM2.5 concentrations in New York State, despite decreased PM2.5 concentrations. We also found increased rates of ST elevation myocardial infarction (STEMI) associated with short-term increases in concentrations of ultrafine particles and other traffic-related pollutants in the 2014-2016 period, but not during 2017-2019 in Rochester. Changes in PM2.5 composition and sources resulting from air quality policies (e.g., Tier 3 light-duty vehicles) may explain the differences. Thus, this study aimed to estimate whether rates of STEMI were associated with organic carbon and source-specific PM2.5 concentrations. Methods: Using STEMI patients treated at the University of Rochester Medical Center, compositional and source-apportioned PM2.5 concentrations measured in Rochester, a time-stratified case-crossover design, and conditional logistic regression models, we estimated the rate of STEMI associated with increases in mean primary organic carbon (POC), secondary organic carbon (SOC), and source-specific PM2.5 concentrations on lag days 0, 0-3, and 0-6 during 2014-2019. Results: The associations of an increased rate of STEMI with interquartile range (IQR) increases in spark-ignition emissions (GAS) and diesel (DIE) concentrations in the previous few days were not found from 2014 to 2019. However, IQR increases in GAS concentrations were associated with an increased rate of STEMI on the same day in the 2014-2016 period (Rate ratio [RR] = 1.69; 95% CI = 0.98, 2.94; 1.73 µg/m3). In addition, each IQR increase in mean SOC concentration in the previous 6 days was associated with an increased rate of STEMI, despite imprecision (RR = 1.14; 95% CI = 0.89, 1.45; 0.42 µg/m3). Conclusion: Increased SOC concentrations may be associated with increased rates of STEMI, while there seems to be a declining trend in adverse effects of GAS on triggering of STEMI. These changes could be attributed to changes in PM2.5 composition and sources following the Tier 3 vehicle introduction.
Sujet(s)
Polluants atmosphériques , Carbone , Études croisées , Matière particulaire , Infarctus du myocarde avec sus-décalage du segment ST , Humains , Matière particulaire/analyse , État de New York , Mâle , Adulte d'âge moyen , Femelle , Polluants atmosphériques/analyse , Polluants atmosphériques/effets indésirables , Carbone/analyse , Sujet âgé , Pollution de l'air/effets indésirables , Pollution de l'air/analyse , Emissions des véhicules/analyse , AdulteRÉSUMÉ
Background: Traditional observational studies exploring the association between air pollution and infections have been limited by small sample sizes and potential confounding factors. To address these limitations, we applied Mendelian randomization (MR) to investigate the potential causal relationships between particulate matter (PM2.5, PM2.5-10, and PM10), nitrogen dioxide, and nitrogen oxide and the risks of infections. Methods: Single nucleotide polymorphisms (SNPs) related to air pollution were selected from the genome-wide association study (GWAS) of the UK Biobank. Publicly available summary data for infections were obtained from the FinnGen Biobank and the COVID-19 Host Genetics Initiative. The inverse variance weighted (IVW) meta-analysis was used as the primary method for obtaining the Mendelian randomization (MR) estimates. Complementary analyses were performed using the weighted median method, MR-Egger method, and MR Pleiotropy Residual Sum and Outlier (MR-PRESSO) test. Results: The fixed-effect IVW estimate showed that PM2.5, PM2.5-10 and Nitrogen oxides were suggestively associated with COVID-19 [for PM2.5: IVW (fe): OR 3.573(1.218,5.288), PIVW(fe) = 0.021; for PM2.5-10: IVW (fe): OR 2.940(1.385,6.239), PIVW(fe) = 0.005; for Nitrogen oxides, IVW (fe): OR 1.898(1.318,2.472), PIVW(fe) = 0.010]. PM2.5, PM2.5-10, PM10, and Nitrogen oxides were suggestively associated with bacterial pneumonia [for PM2.5: IVW(fe): OR 1.720 (1.007, 2.937), PIVW(fe) = 0.047; for PM2.5-10: IVW(fe): OR 1.752 (1.111, 2.767), P IVW(fe) = 0.016; for PM10: IVW(fe): OR 2.097 (1.045, 4.208), PIVW(fe) = 0.037; for Nitrogen oxides, IVW(fe): OR 3.907 (1.209, 5.987), PIVW(fe) = 0.023]. Furthermore, Nitrogen dioxide was suggestively associated with the risk of acute upper respiratory infections, while all air pollution were not associated with intestinal infections. Conclusions: Our results support a role of related air pollution in the Corona Virus Disease 2019, bacterial pneumonia and acute upper respiratory infections. More work is need for policy formulation to reduce the air pollution and the emission of toxic and of harmful gas.
Sujet(s)
Pollution de l'air , COVID-19 , Étude d'association pangénomique , Analyse de randomisation mendélienne , Matière particulaire , Polymorphisme de nucléotide simple , Humains , Pollution de l'air/effets indésirables , Matière particulaire/effets indésirables , COVID-19/épidémiologie , Dioxyde d'azote/effets indésirables , SARS-CoV-2/génétique , Oxydes d'azote/effets indésirables , Polluants atmosphériques/effets indésirablesRÉSUMÉ
Background: Little is known about the effect of combined exposure to different air pollutants on mortality in dialysis patients. This study aimed to investigate the association of multiple exposures to air pollutants with all-cause and cause-specific death in dialysis patients. Materials and methods: This registry-based nationwide cohort study included 90,373 adult kidney failure patients initiating maintenance dialysis between 2012 and 2020 identified from the French REIN registry. Estimated mean annual municipality levels of PM2.5, PM10, and NO2 between 2009 and 2020 were combined in different composite air pollution scores to estimate each participant's exposure at the residential place one to 3 years before dialysis initiation. Adjusted cause-specific Cox proportional hazard models were used to estimate hazard ratios (HRs) per interquartile range (IQR) greater air pollution score. Effect measure modification was assessed for age, sex, dialysis care model, and baseline comorbidities. Results: Higher levels of the main air pollution score were associated with a greater rate of all-cause deaths (HR, 1.082 [95% confidence interval (CI), 1.057-1.104] per IQR increase), regardless of the exposure lag. This association was also confirmed in cause-specific analyses, most markedly for infectious mortality (HR, 1.686 [95% CI, 1.470-1.933]). Sensitivity analyses with alternative composite air pollution scores showed consistent findings. Subgroup analyses revealed a significantly stronger association among women and fewer comorbid patients. Discussion: Long-term multiple air pollutant exposure is associated with all-cause and cause-specific mortality among patients receiving maintenance dialysis, suggesting that air pollution may be a significant contributor to the increasing trend of CKD-attributable mortality worldwide.
Sujet(s)
Polluants atmosphériques , Pollution de l'air , Enregistrements , Dialyse rénale , Humains , Femelle , Mâle , France/épidémiologie , Adulte d'âge moyen , Sujet âgé , Dialyse rénale/mortalité , Polluants atmosphériques/effets indésirables , Pollution de l'air/effets indésirables , Exposition environnementale/effets indésirables , Cause de décès , Études de cohortes , Adulte , Modèles des risques proportionnels , Matière particulaire/effets indésirables , Facteurs de risque , Défaillance rénale chronique/mortalité , Défaillance rénale chronique/thérapieRÉSUMÉ
BACKGROUND: Childhood-onset lupus nephritis (cLN) is a severe form of systemic lupus erythematosus (SLE) with high morbidity and mortality. The impact of long-term exposure to fine particulate matter (PM2.5) on adverse outcomes in cLN remains unclear. METHODS: We combined a 19-years cLN cohort from seven provinces in China with high-resolution PM2.5 dataset from 2001 to 2020, investigating the association between long-term exposure to PM2.5 and its constituents (sulfate, nitrate, organic matter, black carbon, ammonium) with the risk of death and kidney failure, analyzed with multiple variables Cox models. We also evaluated the association between 3-year average PM2.5 exposure before study entry and baseline SLE disease activity index (SLEDAI) scores using linear regression models. RESULTS: Each 10 µg/m3 increase in annual average PM2.5 exposure was associated with an increased risk of death and kidney failure (HR = 1.58, 95 % CI: 1.24-2.02). Black carbon showed the strongest association (HR = 2.14, 95 % CI: 1.47-3.12). Higher 3-year average exposures to PM2.5 and its constituents were significantly associated with higher baseline SLEDAI scores. CONCLUSIONS: These findings highlight the significant role of environmental pollutants in cLN progression and emphasize the need for strategies to mitigate exposure to harmful PM2.5 constituents, particularly in vulnerable pediatric populations.
Sujet(s)
Polluants atmosphériques , Glomérulonéphrite lupique , Matière particulaire , Insuffisance rénale , Humains , Glomérulonéphrite lupique/mortalité , Matière particulaire/analyse , Études de cohortes , Chine/épidémiologie , Mâle , Femelle , Insuffisance rénale/épidémiologie , Insuffisance rénale/induit chimiquement , Polluants atmosphériques/analyse , Polluants atmosphériques/effets indésirables , Enfant , Exposition environnementale/statistiques et données numériques , AdolescentRÉSUMÉ
Objectives: To identify the long-term spatiotemporal trend of ozone-related chronic obstructive pulmonary disease (COPD) burden by sex and country and to explore potential drivers. Methods: We retrieved data of ozone-related COPD death and disability adjusted life year (DALY) from the Global Burden of Disease 2019. We used a linear regression of natural logarithms of age-standardized rates (ASRs) with calendar year to examine the trends in ASRs and a panel regression to identify country-level factors associated with the trends. Results: Global ozone-attributable COPD deaths increased from 117,114 to 208,342 among men and from 90,265 to 156,880 among women between 1990 and 2019. Although ASRs of ozone-related COPD death and DALY declined globally, they increased in low and low-middle Socio-demographic Index (SDI) regions, with faster rise in women. Elevated average maximum temperature was associated with higher ozone-attributable COPD burden, while more green space was associated with lower burden. Conclusion: More efforts are needed in low and low-middle SDI regions, particularly for women, to diminish inter-country inequality in ozone-attributable COPD. Global warming may exacerbate the burden. Expanding green space may mitigate the burden.
Sujet(s)
Charge mondiale de morbidité , Santé mondiale , Ozone , Broncho-pneumopathie chronique obstructive , Humains , Broncho-pneumopathie chronique obstructive/épidémiologie , Ozone/effets indésirables , Femelle , Mâle , Analyse spatio-temporelle , Adulte d'âge moyen , Sujet âgé , Espérance de vie corrigée de l'incapacité , Polluants atmosphériques/effets indésirables , Exposition environnementale/effets indésirables , Facteurs sexuels , Pollution de l'air/effets indésirablesRÉSUMÉ
Introduction: Elevated ambient pollution exposure is potentially linked to thromboembolism. However, the mechanisms by which particulate matter (PM) interferes with the balance of hemostatic system remain unclear. This study investigates PM-mediated hemostatic changes in individuals across unique seasonal variations of ambient pollution. Methods: This prospective study was conducted between February and July 2020 during alterations in ambient pollution in Chiang Mai, Thailand. Blood tests from 30 healthy subjects were assessed at four-week intervals, four times in total. Various coagulation tests, including prothrombin time (PT), activated partial thromboplastin time (aPTT), von Willebrand factor (vWF), platelet count, and platelet functions, were evaluated. A mixed-effects model was used to analyze the impact of high PM2.5 and PM10 on hemostatic parameters. Results: Thirty male subjects with mean age of 38.9 ± 8.2 years, were included. High levels of PM2.5 and PM10 were significantly associated with PT shortening, with no such effect observed in aPTT. PM2.5 and PM10 values also positively correlated with vWF function, while vWF antigen levels remained unchanged. Soluble P-selectin showed a strong positive association with PM2.5 and PM10 levels. Platelet function analysis revealed no correlation with PM values. Conclusion: Short-term exposure to elevated PM2.5 and PM10 concentrations was linked to shortened PT and enhanced vWF function in healthy individuals. Exploring the impact of these changes on clinically relevant thrombosis is crucial. Additional studies on the pathogenesis of pollution-related thrombosis are warranted for maintaining good health.
Sujet(s)
Pollution de l'air , Plaquettes , Hémostase , Matière particulaire , Humains , Matière particulaire/effets indésirables , Mâle , Adulte , Hémostase/effets des médicaments et des substances chimiques , Thaïlande , Études prospectives , Pollution de l'air/effets indésirables , Plaquettes/effets des médicaments et des substances chimiques , Polluants atmosphériques/effets indésirables , Adulte d'âge moyen , Facteur de von Willebrand/métabolisme , Facteur de von Willebrand/analyse , Numération des plaquettes , Exposition environnementale/effets indésirables , Saisons , Tests de coagulation sanguineRÉSUMÉ
BACKGROUND: Biomass burning (BB) is a major source of air pollution and particulate matter (PM) in Southeast Asia. However, the health effects of PM smaller than 10 µm (PM10) originating from BB may differ from those of other sources. This study aimed to estimate the short-term association of PM10 from BB with respiratory and cardiovascular hospital admissions in Peninsular Malaysia, a region often exposed to BB events. METHODS: We obtained and analyzed daily data on hospital admissions, PM10 levels and BB days from five districts from 2005 to 2015. We identified BB days by evaluating the BB hotspots and backward wind trajectories. We estimated PM10 attributable to BB from the excess of the moving average of PM10 during days without BB hotspots. We fitted time-series quasi-Poisson regression models for each district and pooled them using meta-analyses. We adjusted for potential confounders and examined the lagged effects up to 3 days, and potential effect modification by age and sex. RESULTS: We analyzed 210 960 respiratory and 178 952 cardiovascular admissions. Almost 50% of days were identified as BB days, with a mean PM10 level of 53.1 µg/m3 during BB days and 40.1 µg/m3 during normal days. A 10 µg/m3 increment in PM10 from BB was associated with a 0.44% (95% CI: 0.06, 0.82%) increase in respiratory admissions at lag 0-1, with a stronger association in adults aged 15-64 years and females. We did not see any significant associations for cardiovascular admissions. CONCLUSIONS: Our findings suggest that short-term exposure to PM10 from BB increased the risk of respiratory hospitalizations in Peninsular Malaysia.
Sujet(s)
Polluants atmosphériques , Pollution de l'air , Biomasse , Maladies cardiovasculaires , Hospitalisation , Matière particulaire , Maladies de l'appareil respiratoire , Humains , Matière particulaire/analyse , Matière particulaire/effets indésirables , Malaisie/épidémiologie , Femelle , Mâle , Adulte , Adulte d'âge moyen , Adolescent , Pollution de l'air/effets indésirables , Pollution de l'air/analyse , Jeune adulte , Hospitalisation/statistiques et données numériques , Maladies cardiovasculaires/épidémiologie , Sujet âgé , Polluants atmosphériques/analyse , Polluants atmosphériques/effets indésirables , Maladies de l'appareil respiratoire/épidémiologie , Enfant , Enfant d'âge préscolaire , Nourrisson , Exposition environnementale/effets indésirables , Exposition environnementale/statistiques et données numériques , Nouveau-néRÉSUMÉ
Accumulating research suggested that long-term exposure to fine particulate matter (PM2.5) is related to cardiovascular disease (CVD). However, evidence regarding the relationship between PM2.5 and CVD risk factors remains inconsistent. We hypothesized that this association may be partially modified by socioeconomic status (SES). To investigate the relationships and to test the modifying effect of SES, we included baseline data for 21,018 adults from September 2017 to May 2018. PM2.5 concentrations were determined by employing an amalgamation of linear measurements obtained from monitoring stations located near the participants' residential and workplace addresses. We assessed SES across several domains, including income, education, and occupation levels, as well as through a composite SES index. The results indicated that for every 10 µg/m3 increase in PM2.5 exposure, the risk of hypercholesterolemia, hyperbetalipoproteinemia, diabetes, and hyperhomocysteinemia (HHcy) increased by 7.7% [Odds ratio (OR) = 1.077, 95% Confidence Interval (CI) = 1.011, 1.146], 19.6% (OR = 1.196, 95% CI = 1.091, 1.312), 4.2% (OR = 1.042, 95% CI = 1.002, 1.084), and 17.1% (OR = 1.171, 95% CI = 1.133, 1.209), respectively. Compared to the high SES group, those with low SES are more prone to hypercholesterolemia, hyperbetalipoproteinemia, diabetes, and HHcy. Notably, the disparities in SES appear significant in the relationship between PM2.5 exposure and hypercholesterolemia as well as hyperbetalipoproteinemia. But for diabetes and HHcy, the modification effect of SES on PM2.5 shows an inconsistent pattern. In conclusion, the results confirm the association between PM2.5 and cardiovascular risk factors and low SES significantly amplified the adverse PM2.5 effect on dyslipidemia. It is crucial to emphasize a need to improve the socioeconomic inequality among adults in Beijing and contribute to the understanding of the urgency in protecting the health of vulnerable groups.
Sujet(s)
Maladies cardiovasculaires , Exposition environnementale , Facteurs de risque de maladie cardiaque , Matière particulaire , Classe sociale , Humains , Matière particulaire/analyse , Mâle , Femelle , Études transversales , Pékin/épidémiologie , Adulte d'âge moyen , Maladies cardiovasculaires/épidémiologie , Exposition environnementale/effets indésirables , Exposition environnementale/statistiques et données numériques , Adulte , Sujet âgé , Polluants atmosphériques/analyse , Polluants atmosphériques/effets indésirables , Facteurs de risque , Pollution de l'air/effets indésirablesRÉSUMÉ
BACKGROUND: Recent studies have reported the burden of attention deficit hyperactivity disorder [ADHD], autism spectrum disorder [ASD], and depressive disorder. Also, there is mounting evidence on the effects of environmental factors, such as ambient air pollution, on these disorders among children and adolescents. However, few studies have evaluated the burden of mental disorders attributable to air pollution exposure in children and adolescents. METHODS: We estimated the risk ratios of major mental disorders (ADHD, ASD, and depressive disorder) associated with air pollutants among children and adolescents using time-series data (2011-2019) obtained from a nationwide air pollution monitoring network and healthcare utilization claims data in the Republic of Korea. Based on the estimated risk ratios, we determined the population attributable fraction (PAF) and calculated the medical costs of major mental disorders attributable to air pollution. RESULTS: A total of 33,598 patients were diagnosed with major mental disorders during 9 years. The PAFs for all the major mental disorders were estimated at 6.9% (particulate matter < 10 µm [PM10]), 3.7% (PM2.5), and 2.2% (sulfur dioxide [SO2]). The PAF of PM10 was highest for depressive disorder (9.2%), followed by ASD (8.4%) and ADHD (5.2%). The direct medical costs of all major mental disorders attributable to PM10 and SO2 decreased during the study period. CONCLUSION: This study assessed the burden of major mental disorders attributable to air pollution exposure in children and adolescents. We found that PM10, PM2.5, and SO2 attributed 7%, 4%, and 2% respectively, to the risk of major mental disorders among children and adolescents.
Sujet(s)
Pollution de l'air , Trouble déficitaire de l'attention avec hyperactivité , Matière particulaire , Humains , Enfant , Adolescent , République de Corée/épidémiologie , Pollution de l'air/effets indésirables , Matière particulaire/effets indésirables , Matière particulaire/analyse , Mâle , Femelle , Trouble déficitaire de l'attention avec hyperactivité/épidémiologie , Trouble déficitaire de l'attention avec hyperactivité/étiologie , Exposition environnementale/effets indésirables , Troubles mentaux/épidémiologie , Troubles mentaux/étiologie , Trouble du spectre autistique/épidémiologie , Trouble du spectre autistique/étiologie , Polluants atmosphériques/effets indésirables , Polluants atmosphériques/analyse , Dioxyde de soufre/effets indésirables , Dioxyde de soufre/analyse , Enfant d'âge préscolaire , Facteurs de risque , Coûts des soins de santéRÉSUMÉ
Background: Prior research has linked exposure to particulate matter with an aerodynamic diameter of ≤2.5 µm (PM2.5) with preterm birth (PTB). However, the modulating effect of preconception thyroid stimulating hormone (TSH) levels on the relationship between PM2.5 exposure and PTB has not been investigated. Objective: This study aimed to assess whether preconception TSH levels modulate the impact of PM2.5 exposure on PTB. Methods: This cohort study was conducted in Guangdong, China, as a part of the National Free Pre-Pregnancy Checkups Project. PM2.5 exposure was estimated by using the inverse distance weighting method. To investigate the moderating effects of TSH levels on trimester-specific PM2.5 exposure and PTB, we used the Cox proportional hazards model. Additionally, to identify the susceptible exposure windows for weekly specific PM2.5 exposure and PTB, we built distributed lag models incorporating Cox proportional hazards models. Results: A total of 633,516 women who delivered between January 1, 2014, to December 31, 2019, were included. In total, 34,081 (5.4%) of them had abnormal preconception TSH levels. During the entire pregnancy, each 10-µg/m3 increase in PM2.5 was linked to elevated risks of PTB (hazard ratio [HR] 1.559, 95% CI 1.390-1.748), early PTB (HR 1.559, 95% CI 1.227-1.980), and late PTB (HR 1.571, 95% CI 1.379-1.791) among women with abnormal TSH levels. For women with normal preconception TSH levels, PM2.5 exposure during the entire pregnancy was positively associated with the risk of PTB (HR 1.345, 95% CI 1.307-1.385), early PTB (HR 1.203, 95% CI 1.126-1.285), and late PTB (HR 1.386, 95% CI 1.342-1432). The critical susceptible exposure windows were the 3rd-13th and 28th-35th gestational weeks for women with abnormal preconception TSH levels, compared to the 1st-13th and 21st-35th gestational weeks for those with normal preconception TSH levels. Conclusions: PM2.5 exposure was linked with a higher PTB risk, particularly in women with abnormal preconception TSH levels. PM2.5 exposure appears to have a greater effect on pregnant women who are in the early or late stages of pregnancy.
Sujet(s)
Matière particulaire , Naissance prématurée , Thyréostimuline , Humains , Femelle , Matière particulaire/analyse , Matière particulaire/effets indésirables , Naissance prématurée/épidémiologie , Thyréostimuline/sang , Adulte , Grossesse , Chine/épidémiologie , Études de cohortes , Modèles des risques proportionnels , Exposition maternelle/effets indésirables , Exposition maternelle/statistiques et données numériques , Polluants atmosphériques/analyse , Polluants atmosphériques/effets indésirables , Exposition environnementale/effets indésirables , Exposition environnementale/statistiques et données numériques , Jeune adulteRÉSUMÉ
Objective: To investigate the association between exposure to atmospheric pollutants and preterm birth in a river valley-type city and its critical exposure windows. Methods: A retrospective cohort study was used to collect data from the medical records of preterm and full-term deliveries in two hospitals in urban areas of a typical river valley-type city from January 2018 to December 2019. A total of 7,288 cases were included in the study with general information such as pregnancy times, the number of cesarean sections, occupation, season of conception and regularity of the menstrual cycle. And confounding factors affecting preterm birth were inferred using the chi-square test. The effects of exposure to each pollutant, including particulate matter 2.5 (PM2.5), particulate matter 10 (PM10), nitrogen dioxide (NO2), sulfur dioxide (SO2), carbon monoxide (CO) and ozone (O3), during pregnancy on preterm birth and the main exposure windows were explored by establishing a logistic regression model with pollutants introduced as continuous variables. Results: Maternal age, pregnancy times, number of births, number of cesarean sections, season of conception, complications diseases, comorbidities diseases, hypertension disorder of pregnancy and neonatal low birth weight of the newborn were significantly different between preterm and term pregnant women. Logistic regression analysis after adjusting for the above confounders showed that the risk of preterm birth increases by 0.9, 0.6, 2.4% in T2 and by 1.0, 0.9, 2.5% in T3 for each 10 µg/m3 increase in PM2.5, PM10, NO2 concentrations, respectively. The risk of preterm birth increases by 4.3% in T2 for each 10 µg/m3 increase in SO2 concentrations. The risk of preterm birth increases by 123.5% in T2 and increases by 188.5% in T3 for each 10 mg/m3 increase in CO concentrations. Conclusion: Maternal exposure to PM2.5, PM10, NO2, CO was associated with increased risk on preterm birth in mid-pregnancy (T2) and late pregnancy (T3), SO2 exposure was associated with increased risk on preterm birth in mid-pregnancy (T2).
Sujet(s)
Polluants atmosphériques , Matière particulaire , Naissance prématurée , Humains , Femelle , Naissance prématurée/épidémiologie , Études rétrospectives , Grossesse , Polluants atmosphériques/effets indésirables , Polluants atmosphériques/analyse , Adulte , Matière particulaire/effets indésirables , Matière particulaire/analyse , Nouveau-né , Exposition maternelle/effets indésirables , Exposition maternelle/statistiques et données numériques , Chine/épidémiologie , Dioxyde de soufre/analyse , Dioxyde de soufre/effets indésirables , Dioxyde d'azote/analyse , Dioxyde d'azote/effets indésirables , Monoxyde de carbone/analyse , Monoxyde de carbone/effets indésirables , Pollution de l'air/effets indésirables , Pollution de l'air/statistiques et données numériques , Facteurs de risque , VillesRÉSUMÉ
The burden of rheumatoid arthritis (RA) has gradually elevated, increasing the need for medical resource redistribution. Forecasting RA patient arrivals can be helpful in managing medical resources. However, no relevant studies have been conducted yet. This study aims to construct a long short-term memory (LSTM) model, a deep learning model recently developed for novel data processing, to forecast RA patient arrivals considering meteorological factors and air pollutants and compares this model with traditional methods. Data on RA patients, meteorological factors and air pollutants from 2015 to 2022 were collected and normalized to construct moving average (MA)- and autoregressive (AR)-based and LSTM models. After data normalization, the root mean square error (RMSE) was adopted to evaluate models' forecast ability. A total of 2422 individuals were enrolled. Not using the environmental data, the RMSEs of the MA- and AR-based models' test sets are 0.131, 0.132, and 0.117 when the training set: test set ratio is 2:1, 3:1, and 7:1, while they are 0.110, 0.130, and 0.112 for the univariate LSTM models. Considering meteorological factors and air pollutants, the RMSEs of the MA- and AR-based model test sets were 0.142, 0.303, and 0.164 when the training set: test set ratio is 2:1, 3:1, and 7:1, while they were 0.108, 0.119, and 0.109 for the multivariable LSTM models. Our study demonstrated that LSTM models can forecast RA patient arrivals more accurately than MA- and AR-based models for datasets of all three sizes. Considering the meteorological factors and air pollutants can further improve the forecasting ability of the LSTM models. This novel method provides valuable information for medical management, the optimization of medical resource redistribution, and the alleviation of resource shortages.
Sujet(s)
Polluants atmosphériques , Polyarthrite rhumatoïde , Prévision , Concepts météorologiques , Humains , Polyarthrite rhumatoïde/épidémiologie , Polyarthrite rhumatoïde/étiologie , Prévision/méthodes , Polluants atmosphériques/analyse , Polluants atmosphériques/effets indésirables , Femelle , Mâle , Adulte d'âge moyen , Apprentissage profond , Pollution de l'air/effets indésirables , Pollution de l'air/analyseRÉSUMÉ
Although previous studies have suggested that meteorological factors and air pollutants can cause dry eye disease (DED), few clinical cohort studies have determined the individual and combined effects of these factors on DED. We investigated the effects of meteorological factors (humidity and temperature) and air pollutants [particles with a diameter ≤ 2.5 µ m (PM2.5), ozone (O3), nitrogen dioxide (NO2), and carbon monoxide (CO)] on DED. A retrospective cohort study was conducted on 53 DED patients. DED was evaluated by Symptom Assessment in Dry Eye (SANDE), tear secretion, tear film break-up time (TBUT), ocular staining score (OSS), and tear osmolarity. To explore the individual, non-linear, and joint associations between meteorological factors, air pollutants, and DED parameters, we used generalized linear mixed model (GLMM) and Bayesian kernel machine regression (BKMR). After adjusting for all covariates, lower relative humidity or temperature was associated with a higher SANDE (p < 0.05). Higher PM2.5, O3, and NO2 levels were associated with higher SANDE and tear osmolarity (p < 0.05). Higher O3 levels were associated with lower tear secretion and TBUT, whereas higher NO2 levels were associated with higher OSS (p < 0.05). BKMR analyses indicated that a mixture of meteorological factors and air pollutants was significantly associated with increased SANDE, OSS, tear osmolarity, and decreased tear secretion.
Sujet(s)
Polluants atmosphériques , Syndromes de l'oeil sec , Humains , Études rétrospectives , Mâle , Femelle , Syndromes de l'oeil sec/étiologie , Syndromes de l'oeil sec/épidémiologie , Adulte d'âge moyen , Polluants atmosphériques/effets indésirables , Polluants atmosphériques/analyse , Sujet âgé , Matière particulaire/effets indésirables , Matière particulaire/analyse , Adulte , Larmes/métabolisme , Dioxyde d'azote/analyse , Dioxyde d'azote/effets indésirables , Humidité/effets indésirables , Concepts météorologiques , Ozone/effets indésirables , Ozone/analyse , TempératureRÉSUMÉ
Allergic rhinitis ï¼ARï¼ is a nasal hypersensitivity disease that is influenced by environmental factors, genetic factors, and various inflammatory factors. The role and mechanisms of ozone, as a component of air pollution, in the pathogenesis of AR are not yet fully understood. This article provides a review of the impact of ozone on the epidemiology and pathology of AR, as well as its possible mechanisms, to provide new insights into the prevention and treatment of AR.
Sujet(s)
Ozone , Rhinite allergique , Humains , Ozone/effets indésirables , Rhinite allergique/étiologie , Rhinite allergique/épidémiologie , Pollution de l'air/effets indésirables , Polluants atmosphériques/effets indésirablesRÉSUMÉ
O Programa em Saúde Ambiental relacionado a populações expostas à poluição do ar do Município de São Paulo (VIGIAR) tem por objetivo desenvolver ações de vigilância em saúde ambiental, para populações expostas aos poluentes atmosféricos, de forma a orientar medidas de prevenção, promoção da saúde e de atenção integral, conforme preconizado pelo Sistema Único de Saúde (SUS).