BACKGROUND AND AIM: Evidence on the associations between long-term exposure to multiple air pollutants and cardiopulmonary mortality is limited, especially for developing regions with higher pollutant level. We aimed to characterize the individual and joint associations of long-term exposure to air pollutants with cardiopulmonary mortality, and to identify air pollutant that primarily contribute to the mortality risk. METHOD: We followed 37,442 participants in four cities in northern China from 1998-2019. Annual PM2.5, PM10, SO2 and NO2 were estimated using daily average values from satellite-derived machine learning models and monitoring stations. Time-varying Cox proportional hazards model was used to evaluate the individual association between air pollutants and mortality from non-accidental causes, cardiovascular diseases (CVDs), non-malignant respiratory diseases (RDs) and lung cancer, accounting for demographic and socioeconomic factors. Effect modifications by age, gender, income and education level were also examined. Quantile-based g-Computation was applied to evaluate the co-effects and the relative weight of contributions. RESULTS: During 785,807 person-years of follow-up, 5,812 (15.5%) died from non-accidental causes, among which 2,932 (7.8%) were from all CVDs, 479 (1.3%) from non-malignant RDs, and 552 (1.4%) from lung cancer. Long-term exposure to PM10 (mean [baseline]: 136.5 µg/m3), PM2.5 (70.2), SO2 (113.0) and NO2 (39.2) were consistently associated with all mortality outcomes. A monotonically increasing curve with linear or supra-linear shape with no evidence of a threshold was observed for the exposure-response relationship of mortality with individual or joint exposure to air pollutants. PM2.5 consistently contributed most to the elevated mortality risks related to air pollutant mixture, followed by SO2 or PM10. CONCLUSIONS: There was a strong and positive association of long-term individual and joint exposure to air pollutants with cardiopulmonary mortality in high-exposure settings, with PM2.5 potentially being the main contributor. The shapes of associations were consistent with a linear or supra-linear exposure-response, with no lower threshold observed.
To investigate the possible effects of meteorological and environmental factors on allergic rhinitis of children.Daily numbers of outpatients consulting general practitioners for AR between Jan 1 2007 and Dec 31 2011 were obtained from the Department of Otolaryngology-Head and Neck Surgery, Shanghai Children Medical Center. Daily maximum, average and minimum temperatures and humidity and wind power for Shanghai of the same 5 years were obtained from the Shanghai Meteorological Office. Air Quality data was provided by the Shanghai Municipal Environmental Protection Monitoring Center on daily SO2, NO2 and PM10, the average of O3 per 8 hours. The data was available as average values derived from the data of 6 state comtrolled monitoring stations distributed across Shanghai. Non-parametric generalized additive model (GAM) was used to analyze the highly non-linear or non-monotonic exposure-response relationship between meteorological and environmental factors and daily outpatient visiting for AR of children.The daily numbers of AR children in outpatients department in this study were highest in the average daily temperature 11°C and 21°C. It showed two peak. But as the humidity increased, daily numbers of outpatients of AR children went down, indicating that the higy humidity has protective effect. Every 10 microg/m3 increase of environmental pollutants O3, SO2 and PM10 was linked to 1.95%, 1.19% and 0.33% increase in the number of visitors, respectively, suggesting the air pollution may increase the risk of onset of AR in children.Meteorological and environmental factors have important effects on AR in children.
In order to investigate associations between air pollution and adverse health effects fine spatial air pollution surfaces are needed to provide cohorts with exposures. In the ELAPSE project we developed hybrid land use regression models for multiple pollutants and linked these to 11 individual and 7 administrative cohorts in 10 countries for a total of 35 million participants.
Methods
Europe-wide hybrid LUR models were developed for 2010 estimating annual mean PM2.5, NO2, O3 and BC (including cold and warm season O3 estimates). Models were developed based on AirBase routine monitoring data (PM2.5, NO2, O3) and ESCAPE monitoring data (BC), incorporating land use and traffic data plus satellite observations and dispersion model estimates as additional predictor variables. Universal kriging was performed on residual spatial variation. Main model was developed using all sites. To evaluate robustness, five more models were developed, each built on 80% of monitoring sites with remaining 20% used for validation. Models were applied to 100 × 100 m grids across Europe to allow for exposure assignment for all ELAPSE cohorts.
Results
Main models explained: NO258%, PM2.5 71% (59% LUR +12% kriging), O362% and BC 51% of spatial variation in measured concentrations. Validation R2 ranged 0.55–0.60 for NO2, 0.63–0.77 for PM2.5, 0.51–0.69 for O3 and 0.43–0.57 for BC. Dispersion model estimates, road density, nature and residential area were predictor variables in NO2 model. PM2.5 model consisted of satellite derived and dispersion model estimates, altitude, road density, nature, ports and residential area. Satellite derived and dispersion model estimates, road density, residential area, urban green and Y-coordinate were predictors in BC model. O3 model included dispersion model estimates, road density, ports, residential area and altitude. Kriging proved an efficient technique to explain part of residual spatial variation.
Conclusion
We were able to develop robust NO2, PM2.5, O3 and BC hybrid LUR models to provide exposure estimates for all cohort participants in the ELAPSE project.
Ambient air pollution is an established risk factor for premature mortality from chronic cardiovascular, respiratory and metabolic diseases, while evidence on neurodegenerative diseases and psychiatric disorders remains limited. We examined the association between long-term exposure to air pollution and mortality from dementia, psychiatric disorders, and suicide in seven European cohorts. Within the multicenter project 'Effects of Low-Level Air Pollution: A Study in Europe' (ELAPSE), we pooled data from seven European cohorts from six countries. Based on the residential addresses, annual mean levels of fine particulate matter (PM2.5), nitrogen dioxide (NO2), black carbon (BC), ozone (O3), and 8 PM2.5 components were estimated using Europe-wide hybrid land-use regression models. We applied stratified Cox proportional hazard models to investigate the associations between air pollution and mortality from dementia, psychiatric disorders, and suicide. Of 271,720 participants, 900 died from dementia, 241 from psychiatric disorders, and 164 from suicide, during a mean follow-up of 19.7 years. In fully adjusted models, we observed positive associations of NO2 (hazard ratio [HR] = 1.38; 95 % confidence interval [CI]: 1.13, 1.70 per 10 µg/m3), PM2.5 (HR = 1.29; 95 % CI: 0.98, 1.71 per 5 µg/m3), and BC (HR = 1.37; 95 % CI: 1.11, 1.69 per 0.5 × 10-5/m) with psychiatric disorders mortality, as well as with suicide (NO2: HR = 1.13 [95 % CI: 0.92, 1.38]; PM2.5: HR = 1.19 [95 % CI: 0.76, 1.87]; BC: HR = 1.08 [95 % CI: 0.87, 1.35]), and no association with dementia mortality. We did not detect any positive associations of O3 and 8 PM2.5 components with any of the three mortality outcomes. Long-term exposure to NO2, PM2.5, and BC may lead to premature mortality from psychiatric disorders and suicide.
Growing epidemiological evidence suggests an adverse relationship between exposure to air pollutants and cognitive health, and this could be related to the effect of air pollution on vascular health.
Objectives: We sought to determine the associations between maternal citizenship and health care access and utilization for US-born Latino youth and to determine whether maternal distress is a moderator of the associations. Methods: Using 2010–2017 Integrated Public Use Microdata Series National Health Interview Survey data, multivariable logistic regressions were run to examine the associations among maternal citizenship and health care access and utilization for US-born Latino youth. Maternal citizenship and distress interactions were tested. Results: Noncitizen mothers had higher odds of reporting uninsurance, lack of transportation for delaying care, and lower odds of health care utilization for their youth than citizen mothers. Compared with no distress, moderate and severe distress were positively associated with uninsurance, delayed medical care due to cost, lack of transportation, and having had an emergency department visit for their youth. Moderate distress was positively associated with youth having had a doctor’s office visit. Noncitizen mothers with moderate distress were less likely to report their youth having had an emergency department visit than citizen mothers with moderate distress. Among severely distressed mothers, noncitizen mothers were more likely to report youth uninsurance and delayed care due to lack of transportation compared with citizen mothers. Conclusions: Health care access and utilization among US-born Latino youth are influenced by maternal citizenship and distress. Maternal distress moderates the associations among maternal citizenship and youth’s health care access and use. Almost one-third of all US-born youth in the United States are Latino and current federal and state noninclusive immigration policies and anti-Latino immigrant rhetoric may exacerbate health care disparities.
BACKGROUND AND AIM: Fine particulate matter (PM₂.₅) is an established risk factor for premature death, but it remains unclear which components and sources are most responsible. We investigated the associations between long-term exposure to PM₂.₅ components and mortality from all-natural causes, cardiovascular disease (CVD), respiratory diseases (RD), lung cancer, diabetes, chronic kidney disease (CKD), dementia, and psychiatric disorders in a Danish nationwide administrative cohort. METHODS: We followed all Danish residents aged ≥30 at January 1, 2000 (3,081,244) until December 31, 2017. Residential annual mean exposure PM₂.₅ components levels (copper, iron, zinc, sulfur, nickel, vanadium, silicon, and potassium) were estimated by Europe-wide land-use regression models at a 100×100m scale, developed within the "Effects of Low-Level Air Pollution: A Study in Europe" project, with two modeling approaches: supervised linear regression (SLR) and random forest (RF). We used Cox proportional hazard models to evaluate the associations between each component and mortality, adjusting for demographic, socioeconomic factors, and PM₂.₅ mass. RESULTS: The cohort accumulated 46,992,890 person-years, and 803,373 died from natural causes. For natural mortality, we observed significant positive associations [hazard ratios (HRs); 95% confidence intervals per interquartile range increase] with SLR-silicon (1.04; 1.03-1.05) and SLR-potassium (1.03; 1.02-1.04) and with RF- iron (1.02; 1.01-1.02), RF-zinc (1.02; 1.01-1.03), RF-nickel (1.01; 1.00-1.02), RF-vanadium (1.02; 1.01-103), RF-silicon (1.01; 1.00-1.02), and RF-potassium (1.06; 1.05-1.07). Potassium and silicon were most strongly associated with all causes of death except CKD and diabetes, respectively, with the highest HRs observed for psychiatric disorders. Furthermore, iron was associated with RD, lung cancer, CKD, and psychiatric disorders, zinc with RD, CKD, and lung cancer, and nickel and vanadium with lung cancer. CONCLUSIONS: We present novel findings that different PM₂.₅ components were relevant to different causes of death. Potassium and silicon seemed most consistently associated with mortality in Denmark. KEYWORDS: Long-term exposure, PM₂.₅ components, mortality
Recent studies have suggested that alternative lengthening of telomeres (ALT) is associated with metastasis and poor survival in pancreatic neuroendocrine tumors (PanNETs). This study evaluated whether this association is applicable to Chinese patients as well as the potential somatic mutations associated with ALT.We assessed the prevalence of ALT by performing telomere-specific fluorescence in situ hybridization and analyzed DAXX/ATRX expression using immunohistochemistry in 112 Chinese patients with PanNETs to evaluate the association between ALT and clinical outcomes. A subset of the noninsulinoma samples (28/60) was subjected to Sanger sequencing and targeted sequencing.The ALT-positive phenotype was identified in 23.2% (26/112) of the samples. The clinicopathologic factors significantly associated with progression in the noninsulinoma (n = 60) cohort were the female sex (p = 0.006), Ki-67 index (p < 0.001), World Health Organization grade (p = 0.031), and ALT positivity (p = 0.013). Patients with ALT-positive PanNETs had significantly shorter progression-free survival than those with ALT-negative PanNETs in the entire cohort (p < 0.001), noninsulinoma subgroup (p = 0.01), and G2 subgroup (p = 0.001). ALT-positive samples frequently harbored somatic mutations in DAXX, ATRX, MEN1, SETBP1, PRKDC, and GNAS.We confirmed that ALT positivity is an effective risk predictor, especially in the noninsulinoma and G2 subgroups. ALT is also related to somatic mutations in MEN1, SETBP1, PRKDC, and GNAS, in addition to DAXX and ATRX.
The link between exposure to ambient air pollution and mortality from cardiorespiratory diseases is well established, while evidence on neurodegenerative disorders including Parkinson's Disease (PD) remains limited.We examined the association between long-term exposure to ambient air pollution and PD mortality in seven European cohorts.Within the project 'Effects of Low-Level Air Pollution: A Study in Europe' (ELAPSE), we pooled data from seven cohorts among six European countries. Annual mean residential concentrations of fine particulate matter (PM2.5), nitrogen dioxide (NO2), black carbon (BC), and ozone (O3), as well as 8 PM2.5 components (copper, iron, potassium, nickel, sulphur, silicon, vanadium, zinc), for 2010 were estimated using Europe-wide hybrid land use regression models. PD mortality was defined as underlying cause of death being either PD, secondary Parkinsonism, or dementia in PD. We applied Cox proportional hazard models to investigate the associations between air pollution and PD mortality, adjusting for potential confounders.Of 271,720 cohort participants, 381 died from PD during 19.7 years of follow-up. In single-pollutant analyses, we observed positive associations between PD mortality and PM2.5 (hazard ratio per 5 µg/m3: 1.25; 95% confidence interval: 1.01-1.55), NO2 (1.13; 0.95-1.34 per 10 µg/m3), and BC (1.12; 0.94-1.34 per 0.5 × 10-5m-1), and a negative association with O3 (0.74; 0.58-0.94 per 10 µg/m3). Associations of PM2.5, NO2, and BC with PD mortality were linear without apparent lower thresholds. In two-pollutant models, associations with PM2.5 remained robust when adjusted for NO2 (1.24; 0.95-1.62) or BC (1.28; 0.96-1.71), whereas associations with NO2 or BC attenuated to null. O3 associations remained negative, but no longer statistically significant in models with PM2.5. We detected suggestive positive associations with the potassium component of PM2.5.Long-term exposure to PM2.5, at levels well below current EU air pollution limit values, may contribute to PD mortality.
'/%3e%3cuse xlink:href='%23a' transform='rotate(23.036 .093 25.536)'/%3e%3cuse xlink:href='%23a' transform='rotate(45.87 1.273 16.18)'/%3e%3cuse xlink:href='%23a' transform='rotate(69.945 .996 12.078)'/%3e%3cuse xlink:href='%23a' transform='rotate(20.66 -19.689 31.932)'/%3e%3c/svg%3e)
