Long-term Air Pollution Exposure Research Articles

Multiple myeloma risk in relation to long-term air pollution exposure - A pooled analysis of four European cohorts

BackgroundAir pollution is a growing concern worldwide, with significant impacts on human health. Multiple myeloma is a type of blood cancer with increasing incidence. Studies have linked air pollution exposure to various types of cancer, including leukemia and lymphoma, however, the relationship with multiple myeloma incidence has not been extensively investigated. MethodsWe pooled four European cohorts (N = 234,803) and assessed the association between residential exposure to nitrogen dioxide (NO2), fine particles (PM2.5), black carbon (BC), and ozone (O3) and multiple myeloma. We applied Cox proportional hazards models adjusting for potential confounders at the individual and area-level. ResultsDuring 4,415,817 person-years of follow-up (average 18.8 years), we observed 404 cases of multiple myeloma. The results of the fully adjusted linear analyses showed hazard ratios (95% confidence interval) of 0.99 (0.84, 1.16) per 10 μg/m³ NO2, 1.04 (0.82, 1.33) per 5 μg/m³ PM2.5, 0.99 (0.84, 1.18) per 0.5 10−5 m−1 BCE, and 1.11 (0.87, 1.41) per 10 μg/m³ O3. ConclusionsWe did not observe an association between long-term ambient air pollution exposure and incidence of multiple myeloma.

Long-term air pollution exposure, habitual physical activity, and incident chronic kidney disease

Both air pollution and physical inactivity contribute to the increased risk of incident chronic kidney disease (CKD). However, the detrimental effects of air pollution exposure could be augmented by an elevated intake of air pollutants during exercise. In the present study, we analyzed 367,978 participants who were CKD-free at baseline (2006–2010) based on the UK Biobank. Air pollutants included fine particulate matter (PM2.5 and PM10), nitrogen dioxide (NO2), and nitrogen oxides (NOX). Physical activity (PA) was obtained by the self-reported questionnaire. Using Cox proportional hazards models, hazard ratios (HRs) for incident CKD related to air pollution, PA, and incident CKD were evaluated. During a median of 12.4 years of follow-up, 14,191 incident CKD events were documented. High PM2.5, PM10, NO2, and NOX increased CKD risks by 11 %, 15 %, 14 %, and 12 %, respectively, while moderate and high PA reduced CKD risks by 18 % and 22 %, respectively. Participants with high PA and low air pollution exposure had 29 %, 31 %, 30 %, and 30 % risks of incident CKD than those with low PA and high air pollution exposure for the four air pollutants, with multivariable-adjusted HRs of 0.71 (95 % confidence intervals [CI]: 0.65–0.76) for PM2.5, 0.69 (95 % CI: 0.64–0.75) for PM10, 0.70 (95 % CI: 0.64–0.75) for NO2, and 0.70 (95 % CI: 0.64–0.75) for NOX. No clear interactions were observed between each air pollutant exposure and PA (all P for interaction > 0.05). The findings that reducing air pollution exposure and increasing PA were both independently correlated with a diminished risk of incident CKD suggest that PA could be targeted to prevent CKD generally regardless of air pollution levels. Further research is needed in areas polluted moderately and severely to examine our findings.

The association of long-term exposure to criteria air pollutants, fine particulate matter components, and airborne trace metals with late-life brain amyloid burden in the Atherosclerosis Risk in Communities (ARIC) study

BackgroundStudies suggest associations between long-term ambient air pollution exposure and outcomes related to Alzheimer’s disease (AD). Whether a link exists between pollutants and brain amyloid accumulation, a biomarker of AD, is unclear. We assessed whether long-term air pollutant exposures are associated with late-life brain amyloid deposition in Atherosclerosis Risk in Communities (ARIC) study participants. MethodsWe used a chemical transport model with data fusion to estimate ambient concentrations of PM2.5 and its components, NO2, NOx, O3 (24-hour and 8-hour), CO, and airborne trace metals. We linked concentrations to geocoded participant addresses and calculated 10-year mean exposures (2002 to 2011). Brain amyloid deposition was measured using florbetapir amyloid positron emission tomography (PET) scans in 346 participants without dementia in 2012–2014, and we defined amyloid positivity as a global cortical standardized uptake value ratio ≥ the sample median of 1.2. We used logistic regression models to quantify the association between amyloid positivity and each air pollutant, adjusting for putative confounders. In sensitivity analyses, we considered whether use of alternate air pollution estimation approaches impacted findings for PM2.5, NO2, NOx, and 24-hour O3. ResultsAt PET imaging, eligible participants (N = 318) had a mean age of 78 years, 56% were female, 43% were Black, and 27% had mild cognitive impairment. We did not find evidence of associations between long-term exposure to any pollutant and brain amyloid positivity in adjusted models. Findings were materially unchanged in sensitivity analyses using alternate air pollution estimation approaches for PM2.5, NO2, NOx, and 24-hour O3. ConclusionsAir pollution may impact cognition and dementia independent of amyloid accumulation, though whether air pollution influences AD pathogenesis later in the disease course or at higher exposure levels deserves further consideration.

Long-term air pollution exposure and tumors of the central nervous system - a pooled analysis of six European cohorts

Long-term air pollution exposure and tumors of the central nervous system - a pooled analysis of six European cohorts

Interaction between long-term air pollution exposure and neighbourhood unemployment on cognitive functions in Central-European aging population

Interaction between long-term air pollution exposure and neighbourhood unemployment on cognitive functions in Central-European aging population

Investigating links between long-term air pollution exposure and SARS-CoV-2 infection, hospitalisation and mortality:a meta-analysis of cohort studies

Investigating links between long-term air pollution exposure and SARS-CoV-2 infection, hospitalisation and mortality:a meta-analysis of cohort studies

ZnO Intercalated PVA-PEDOT:PSS Composite Nanofiber for Detection of Ammonia Gases

Keywords: Ammonia, Electrospinning, and Zinc OxideThe matter of air pollution has dramatically risen the worldwide concern on detecting of hazardous gases present in the atmosphere because they are highly detrimental to human health [4,5]. Additionally, the detection and monitoring of such harmful gases is necessary for process control in the industry as well as the general safety of the environment. Zinc oxide (ZnO) is an n-type semiconductor with a wide direct bandgap width (3.37 eV), high excitation binding energy (60meV), high electron mobility, thermal stability, and excellent electrical properties [1]. Other promising materials for gas-sensing applications encompass single elements, silicon and tellurium-based materials and organic semiconductors. The sensing materials that are of intense research interest are conducting polymers such as polyaniline (PANI), polypyrrole (PPy) and poly(3,4-thylenedioxythiophene) (PEDOT) used in the fabrication of polymer-based gas sensors [2]. Its capability to work at low operating temperatures while maintaining high sensitivity leads to the synergistic effect when in combination with metal oxides to produce high-performance gas sensors. They are very appealing in terms of energy saving as they do not need an additional source of heat, consequently reducing the operating cost, simplifying the fabrication process, and extending the lifespan of the device [3]. In this work, ZnO intercalated PVA-PEDOT:PSS composite nanofiber as a sensing layer was prepared by electrospinning method. This material was characterized both morphologically and structurally by X-ray diffraction analysis, scanning electron microscopy (SEM), transmission electron microscopy (TEM), Fourier-transform infrared spectroscopy and thermogravimetric analysis. The results from TEM and SEM show well distribution of ZnO particles in the polymer matrix. The gas measurement results reveal that the fabricated ZnO loaded PVA-PEDOT:PSS composite sensor exhibits excellent gas response (63%) to ammonia gas in 100 ppm gas concentration at 120 °C. Acknowledgment This research was supported by the research grant 021220CRP0122 “Development of highly sensitive MOS based nano-film gas sensors” from Nazarbayev University. References S. Bhati, M. Hojamberdiev, and M. Kumar, “Enhanced sensing performance of ZnO nanostructures-based gas sensors: A Review,” Energy Reports, vol. 6, pp. 46–62, 2020.Yan, Y. et al. (2020) “Conducting polymer-inorganic nanocomposite-based Gas Sensors: A Review,” Science and Technology of Advanced Materials, 21(1), pp. 768–786.Zhang, J. et al. (2015) “Nanostructured materials for room-temperature gas sensors,” Advanced Materials, 28(5), pp. 795–831.C. Eze, E. Schaffner, E. Fischer, T. Schikowski, M. Adam, M. Imboden, M. Tsai, D. Carballo, A. von Eckardstein, N. Künzli, C. Schindler, and N. Probst-Hensch, “Long-term air pollution exposure and diabetes in a population-based Swiss cohort,” Environment International, vol. 70, pp. 95–105, 2014.C. Shim, J. Han, D. K. Henze, M. W. Shephard, L. Zhu, N. Moon, S. K. Kharol, E. Dammers, and K. Cady-Pereira, “Impact of NH3 emissions on particulate matter pollution in South Korea: A case study of the seoul metropolitan area,” Atmosphere, vol. 13, no. 8, p. 1227, 2022. Figure 1

Potential causal links of long-term air pollution with lung cancer incidence: From the perspectives of mortality and hospital admission in a large cohort study in southern China.

Evidence on the potential causal links of long-term air pollution exposure with lung cancer incidence (reflected by mortality and hospital admission) was limited, especially based on large cohorts. We examined the relationship between lung cancer and long-term exposure to particulate matter (PM, including PM2.5 , PM10 and PM10-2.5 ) and nitrogen dioxide (NO2 ) among a large cohort of general Chinese adults using causal inference approaches. The study included 575 592 participants who were followed up for an average of 8.2 years. The yearly exposure of PM and NO2 was estimated through satellite-based random forest approaches and the ordinary kriging method, respectively. Marginal structural Cox models were used to examine hazard ratios (HRs) of mortality and hospital admission due to lung cancer following air pollution exposure, adjusting for potential confounders. The HRs of mortality due to lung cancer were 1.042 (95% confidence interval [CI]: 1.033-1.052), 1.032 (95% CI:1.024-1.041) and 1.052 (95% CI:1.041-1.063) for each 1 μg/m3 increase in PM2.5 , PM10 and NO2 , respectively. In addition, we observed statistically significant effects of PMs on hospital admission due to lung cancer. The HRs (95%CI) were 1.110 (1.027-1.201), 1.067 (1.020-1.115) and 1.079 (1.010-1.153) for every 1 μg/m3 increase in PM2.5 , PM10 , PM10-2.5 , respectively. Furthermore, we found larger effect estimates among the elderly and those who exercised more frequently. We provided the most comprehensive evidence of the potential causal links between two outcomes of lung cancer and long-term air pollution exposure. Relevant policies should be developed, with special attention to protecting the vulnerable groups of the population.

Ambient air pollution associated with incident asthma, subsequent cardiovascular disease and death: A trajectory analysis of a national cohort

No previous study has examined the impact of air pollution on the cardiovascular disease (CVD) trajectory, especially among asthmatic subjects. Based on the UK Biobank cohort, we retrieved 292,227 adults free of asthma and CVD aged 37–73 years at recruitment (2006–2010). Annual mean concentrations of particulate matter (PM10 and PM2.5) and nitrogen oxides (NO2 and NOx) were assessed at each individual’s addresses. We used multi-state models to estimate the associations of air pollution with the trajectory from healthy to incident asthma, subsequent CVD, and death. During a median follow-up of 11.7 years, a total of 6338 (2.2%) participants developed asthma, among which, 638 (10.1%) subsequently proceeded to CVD. We observed significant impacts of various air pollutants on the CVD dynamic transitions, with a more substantial effect of particulate matter pollutants than gaseous air pollutants. For example, the hazard ratios (95% confidence intervals) for per interquartile range increase in PM2.5 and PM10 were 1.28 (1.13, 1.44) and 1.27 (1.13, 1.43) for transitions from incident asthma to subsequent CVD. In conclusion, long-term air pollution exposure could affect the CVD trajectory. Distinguishing the effect of air pollutants on CVD transition stages has great significance for CVD health management and clinical prevention, especially among asthma patients.

Long-term air pollution exposure accelerates ageing-associated degradation of lung function

Several longitudinal studies have associated ambient air pollution exposure with lung function, while cohort evidence was extremely sparse in low- and middle-income countries (LMICs) experiencing heavy air pollution. In this study, we sought to establish the concentration-response association between long-term exposures to fine particulate matter (PM2.5) and gaseous air pollutants (e.g., nitrogen dioxide [NO2] and ozone [O3]) and lung function in Chinese middle-aged and older adults. We conceived a nationwide longitudinal study from 2011 through 2015, by enrolling 13,614 participants aged 45 and above from 28 provincial regions across mainland of China. Lung function in each survey wave was measured as peak expiratory flow (PEF) repeatedly by well-trained interviewers using standardized devices. We assigned the exposures to ambient air pollutants (PM2.5, NO2 and O3) of participants according to their residential cities at baseline, via deriving monthly estimates from well-validated spatiotemporal datasets developed by machine learning methods. Possible exposure biases were examined through Monte Carlo simulation approach with 1000 random simulations of the residential addresses for each participant. The associations of long-term air pollution exposure with PEF and PEF z-score were assessed using mixed-effects linear models. We compared estimated effects of each pollutant with the effect of aging on lung function to elevate interpretability of the association magnitude. Subgroup analyses were conducted to identify potential effect modifiers. We evaluated totally 34,196 repeated measurements of lung function from 13,614 adults. Mean of age at survey was 60.8 years (standard deviation 9.4 years). An increase of 10-μg/m3 in annual PM2.5, NO2 and O3 exposure was respectively associated with a decline in PEF of 14.6 (95% confidence interval: 13.1–16.2) L/min, 21.7 (19.6–23.8) L/min, and 25.5 (20.6–30.4) L/min, which were equivalent to the effects of aging by 3.9–7.3 years and percent declines of 4.9–8.5%. We observed approximately linear relationships between PEF and PM2.5 and O3, while a reversely J-shaped NO2-PEF relation was identified with steeper drops below 30 μg/m3. Stratified analyses suggested significantly greater lung function impairment associated with ambient air pollutants in men, younger (<65), and less-educated adults. Our primary findings were robust to the sensitivity analyses based on Monte Carlo simulation approach with 1000 simulations, as well as adjustments for co-pollutant analyses. This study provided national evidence that long-term exposure to ambient PM2.5, NO2 and O3 may be independently associated with reduced lung function in Chinese middle-aged and older adults. Improvement of air quality may substantially offset the deterioration of lung function due to ageing in LMICs.

Exposure to ambient air pollutants is associated with an increased incidence of hyperuricemia: A longitudinal cohort study among Chinese government employees

BackgroundIt is widely recognized that ambient air pollution can induce various detrimental health outcomes. However, evidence linking ambient air pollutants and hyperuricemia incidence is scarce. ObjectivesTo assess the association between long-term air pollution exposure and the risk of hyperuricemia. MethodsIn this study, a total of 5854 government employees without hyperuricemia were recruited and followed up from January 2018 to June 2021 in Hunan Province, China. Hyperuricemia was defined as serum uric acid (SUA) level of >420 μmol/L for men and >360 μmol/L for women or use of SUA-lowering medication or diagnosed as hyperuricemia during follow-up. Data from local air quality monitoring stations were used to calculate individual exposure levels of PM10, PM2.5, SO2 and NO2 by inverse distance weightingn (IDW) method. Cox proportional hazard model was applied to evaluate the causal relationships between air pollutant exposures and the risk of hyperuricemia occurrence after adjustment for potential confounders and meanwhile, restricted cubic spline was used to explore the dose-response relationships. ResultsThe results indicated that exposures to PM10 (hazard ratio, HR = 1.042, 95% conficence interal, 95% CI: 1.028, 1.057), PM2.5 (HR = 1.204, 95% CI: 1.141, 1.271) and NO2 (HR = 1.178, 95% CI: 1.125,1.233) were associated with an increased HR of hyperuricemia. In addition, a nonlinear dose-response relationship was found between PM10 exposure level and the HR of hyperuricemia (p for nonlinearity = 0.158) with a potential threshold of 50.11 μg/m3. Subgroup analysis demonstrated that participants usually waking up at night and using natural ventilation were more vulnerable to the exposures of PM10, PM2.5, NO2, and SO2. ConclusionLong-term exposures to ambient PM10, PM2.5 and NO2 are associated with an increased incidence of hyperuricemia among Chinese government employees.

Long-term air pollution exposure and malignant intracranial tumours of the central nervous system: a pooled analysis of six European cohorts.

Risk factors for malignant tumours of the central nervous system (CNS) are largely unknown. We pooled six European cohorts (N = 302,493) and assessed the association between residential exposure to nitrogen dioxide (NO2), fine particles (PM2.5), black carbon (BC), ozone (O3) and eight elemental components of PM2.5 (copper, iron, potassium, nickel, sulfur, silicon, vanadium, and zinc) and malignant intracranial CNS tumours defined according to the International Classification of Diseases ICD-9/ICD-10 codes 192.1/C70.0, 191.0-191.9/C71.0-C71.9, 192.0/C72.2-C72.5. We applied Cox proportional hazards models adjusting for potential confounders at the individual and area-level. During 5,497,514 person-years of follow-up (average 18.2 years), we observed 623 malignant CNS tumours. The results of the fully adjusted linear analyses showed a hazard ratio (95% confidence interval) of 1.07 (0.95, 1.21) per 10 μg/m³ NO2, 1.17 (0.96, 1.41) per 5 μg/m³ PM2.5, 1.10 (0.97, 1.25) per 0.5 10-5m-1 BC, and 0.99 (0.84, 1.17) per 10 μg/m³ O3. We observed indications of an association between exposure to NO2, PM2.5, and BC and tumours of the CNS. The PM elements were not consistently associated with CNS tumour incidence.

Low-level ambient sulfur dioxide exposure and genetic susceptibility associated with incidence of idiopathic pulmonary fibrosis: A national prospective cohort study

BackgroundThe association between long-term air pollution exposure and the development of idiopathic pulmonary fibrosis (IPF) has been established, but the evidence regarding the effect of low levels of air pollution, especially ambient sulfur dioxide (SO2), is limited. Besides, the combined effect and interaction between genetic susceptibility and ambient SO2 on IPF remain uncertain. MethodsThis study retrieved data from 402,042 participants who were free of IPF at baseline in the UK Biobank. The annual mean concentration of ambient SO2 was estimated for each participant based on their residential addresses using a bilinear interpolation method. Cox proportional hazard models were used to examine the relationship between ambient SO2 and incident IPF. We further generated a polygenic risk score (PRS) for IPF and estimated the combined effects of genetic susceptibility and ambient SO2 on incident IPF. ResultsAfter a median follow-up of 11.78 years, 2562 cases of IPF were identified. The results indicated that each 1 μg/m3 increase in ambient SO2 was associated with a hazard ratio (HR) (95% confidence interval [CI]) of 1.67 (1.58, 1.76) for incident IPF. The study found statistically significant synergistic additive interaction between genetic susceptibility and ambient SO2. Individuals with high genetic risk and high ambient SO2 exposure had a higher risk of developing IPF (HR = 7.48, 95% CI:5.66, 9.90). ConclusionThe study suggests that long-term exposure to ambient SO2, even at concentrations lower than current air quality guidelines set by the Word Health Organization and European Union, may be an important risk factor for IPF. This risk is more pronounced among people with a high genetic risk. Therefore, these findings emphasize the need to consider the potential health effects of SO2 exposure and the necessity for stricter air quality standards.

Effect of Air Pollution on Heart Failure: Systematic Review and Meta-Analysis.

Heart failure (HF) poses a significant global disease burden. The current evidence on the impact of air pollution on HF remains inconsistent. We aimed to conduct a systematic review of the literature and meta-analysis to provide a more comprehensive and multiperspective assessment of the associations between short- and long-term air pollution exposure and HF from epidemiological evidences. Three databases were searched up to 31 August 2022 for studies investigating the association between air pollutants (, , , , CO, ) and HF hospitalization, incidence, or mortality. A random effects model was used to derive the risk estimations. Subgroup analysis was conducted by geographical location, age of participants, outcome, study design, covered area, the methods of exposure assessment, and the length of exposure window. Sensitivity analysis and adjustment for publication bias were performed to test the robustness of the results. Of 100 studies covering 20 countries worldwide, 81 were for short-term and 19 were for long-term exposure. Almost all air pollutants were adversely associated with the risk of HF in both short- and long-term exposure studies. For short-term exposures, we found the risk of HF increased by 1.8% [relative risk , 95% confidence interval (CI): 1.011, 1.025] and 1.6% (, 95% CI: 1.011, 1.020) per increment of and , respectively. HF was also significantly associated with , , and CO, but not . Positive associations were stronger when exposure was considered over the previous 2 d (lag 0-1) rather than on the day of exposure only (lag 0). For long-term exposures, there were significant associations between several air pollutants and HF with RR (95% CI) of 1.748 (1.112, 2.747) per increment in , 1.212 (1.010, 1.454) per increment in , and 1.204 (1.069, 1.356) per increment in , respectively. The adverse associations of most pollutants with HF were greater in low- and middle-income countries than in high-income countries. Sensitivity analysis demonstrated the robustness of our results. Available evidence highlighted adverse associations between air pollution and HF regardless of short- and long-term exposure. Air pollution is still a prevalent public health issue globally and sustained policies and actions are called for to reduce the burden of HF. https://doi.org/10.1289/EHP11506.

Long-term exposure to air pollution and cognitive function in older adults: a systematic review and meta-analysis

BackgroundNow more than ever before, air pollution and cognitive decline are global concerns. Credible links are now emerging between exposure to specific pollutants and cognitive decline. However, the role of specific pollutants on different cognitive domains in adults are inconclusive as the pathways to cognitive decline remain poorly understood.ObjectiveTo systematically review and meta-analyse the evidence for the association between long-term air pollution exposure and cognitive function in adults.Data sourcesWeb of Science, PubMed, Embase searched up to February 2021 with no language restrictions. Individual studies were identified from similar review articles.Eligibility criteriaStudies investigating the long-term (&amp;gt;3 years) associations between airborne pollutants and cognitive function in older adults (&amp;gt;50 years old).ResultsFrom 1996 records, 26 satisfied the inclusion criteria. The total sample size included over 2.4 million (53.8% female) subjects with ages ranging from 45 to 100 years (estimated mean age 70 years). Only 18/26 publications included both male and female subjects. Pollutants reported included particulate matter ≤2.5 µm (PM2.5); particulate matter ≤10 µm (PM10); nitrogen dioxide (NO2); nitrogen oxide species (NOx) and ozone (O3). Papers showed great variance in their study characteristics, air pollution modelling methodology and assessment of cognitive domain. Long-term exposure to increased levels of PM2.5 and NO2 were most strongly associated with increased risk of dementia. Decline in cognitive function, executive function, memory and language were most strongly associated with greater exposure to PM2.5, PM10 and NO2 to varying degrees.ConclusionAn increasing number of studies are supporting the hypothesis that greater exposure to air pollutants is associated with decline in cognitive functions.

Associations of air pollutant concentrations with longitudinal kidney function changes in patients with chronic kidney disease

This longitudinal cohort study investigated the associations of air pollutant exposures, including CO, NO, NO2, NOx, O3, PM10, PM2.5, and SO2, with long-term kidney function changes in patients with chronic kidney disease (CKD). We enrolled 447 CKD patients who took part in a universal hospital pre-ESRD care program during 2011–2015. The daily average air pollutant exposures and temperature were estimated for each patient, with different levels of air pollutant concentrations defined by 5-knot and restricted cubic spline function. Predicted annual estimated glomerular filtration (eGFR) slope values by one mixed model were considered as the study outcome. The average age of the study population was 77.1 ± 12.6 years, and the median annual eGFR decreased by 2.1 ml/min/1.73 m2 per year from 30 ml/min/1.73 m2 at baseline during a mean follow-up time of 3.4 years. The univariable and multivariable analyses revealed no significant linear and non-linear associations between 5-knot air pollutant concentrations and annual eGFR slope. In addition, the visualized spline effect plots show insignificant variation patterns in annual eGFR slope values with increased air pollutant concentrations. These results encourage more extensive studies to clarify the causal relationships and mechanisms of long-term specific air pollutant exposures and longitudinal kidney function change, especially in CKD populations.

Association between long-term exposure to ambient air pollutants and the risk of tuberculosis: A time-series study in Nantong, China

BackgroundIncreasing evidence has shown that the risk of tuberculosis (TB) might be related to the exposure to air pollutants; however, the findings are inconsistent and studies on long-term air pollutant exposure and TB risk are scarce. This study aime to assess the relationship between monthly exposure to air pollution and TB risk in Nantong, China. MethodsWe collected the time series data on the number of TB cases, as well as environmental and socioeconomic covariates from January 2005 to December 2020. The impact of air pollutant exposure on TB risk was evaluated using the distributed lag nonlinear model (DLNM). Stratified analyses were conducted to examine the effect modifications of sex and age on the association between air pollutants and TB risk. Sensitivity analyses were applied to test the stability of the model. ResultsThere were a total of 54,096 cases of TB in Nantong during the study period. In the single-pollutant model, for each 10 μg/m3 increase in concentration, the pooled relative risks (RRs) of TB reached the maximum to 1.10 (95% confidence interval (CI): 1.04–1.16, lag 10 months) for particulate matter with aerodynamic diameter less than 2.5 μm (PM2.5), 1.05 (95% CI: 1.01–1.10, lag 9 months) for particulate matter with aerodynamic diameter less than 10 μm (PM10), and 1.11 (95%CI: 1.04–1.19, lag 10 months) for nitrogen dioxide (NO2). Ozone (O3) did not show significant effect on TB risk. Effect modifications of sex and age on the association between air pollutants and TB risk were not observed. The multi-pollutant model results showed no significant variation compared with the single-pollutant model. ConclusionsOur study suggests that air pollutants pose a substantial threat to the TB risk. Reducing air pollution might be crucial for TB prevention and control.

Association of SO2/CO exposure and greenness with high blood pressure in children and adolescents: A longitudinal study in China.

We aimed to investigate the association between greenness around schools, long-term gaseous air pollution exposure (SO2 and CO), and blood pressure in children and adolescents. From 2006 to 2018, a total of 219,956 Chinese children and adolescents aged 7-17 years in Beijing and Zhongshan were included in this longitudinal study. Annual average concentrations of SO2 and CO and the mean values of normalized difference vegetation index around schools were calculated. We used the generalized estimation equation model, restricted cubic spline model, and Cox model to analyze the health effects. Among all the subjects, 52,515 had the first onset of HBP. During the follow-up, HBP's cumulative incidence and incidence density were 23.88% and 7.72 per 100 person-year respectively. Exposures to SO2 and CO were significantly associated with SBP [β = 1.30, 95% CI: (1.26, 1.34) and 0.78 (0.75, 0.81)], DBP [β = 0.81 (0.79, 0.84) and 0.46 (0.44, 0.48)] and HBP [HR = 1.58 (1.57, 1.60) and 1.42 (1.41, 1.43)]. The risks of HBP attributed to SO2 and CO pollution would be higher in school-aged children in the low greenness group: the attributable fractions (AFs) were 26.31% and 20.04%, but only 13.90% and 17.81% in the higher greenness group. The AFs were also higher for normal-BMI children and adolescents in the low greenness group (AFs = 30.90% and 22.64%, but 14.41% and 18.65% in the high greenness group), while the AFs were not as high as expected for obese children in the low greenness group (AFs = 10.64% and 8.61%), nor was it significantly lower in the high greenness group (AFs = 9.60% and 10.72%). Greenness could alleviate the damage effects of SO2/CO exposure on the risks of HBP among children and adolescents, and the benefit is BMI sensitivity. It might offer insights for policymakers in making effective official interventions to prevent and control the prevalence of childhood HBP and the future disease burden caused by air pollution.

Association of long-term air pollution and ambient noise with cognitive decline in the Heinz Nixdorf Recall study

Little is known about the impact of long-term ambient air pollution (AP) and noise exposure on change in cognitive function over years in the elderly. In this study, we wanted to examine the association between long-term exposure to AP and noise with the rate of cognitive decline in a population aged 50 and older and susceptible groups with mild cognitive impairment or at a genetically higher risk of Alzheimer's disease (Apolipoprotein E ε4 positive). Participants in the German population-based Heinz Nixdorf Recall study carried out five neuropsychological tests. Individual tests scores at the first (T1 = 2006–2008) and second (T2 = 2011–2015) follow-up for each test were used as outcomes after standardization using predicted means adjusted for age and education. Global cognitive score (GCS) was defined as sum of five standardized scores of individual tests. Long-term exposures to particulate matter (PM2.5, PM10, PM2.5 absorbance), accumulation mode particle number (PNacc), a proxy of ultrafine particles, and nitrogen dioxide were estimated by the land-use regression and chemistry transport models. Noise exposures were assessed as outdoor weighted nighttime road traffic noise (Lnight) means. We performed linear regression analyses adjusted for sex, age, individual and neighborhood socio-economic status, and lifestyle variables. Effect modification in vulnerable groups was estimated using multiplicative interaction terms between exposure and a modifier. Overall, 2554 participants (49.5% men, median age is 63 (IQR = 12)) were included. We found weak associations between higher exposure to PM10 and PM2.5 with faster decline in the immediate verbal memory test. Adjustment for potential confounders and for co-exposures did not change the results. We saw no effects on GCS, and no effect of noise exposure. In susceptible groups, higher AP and noise exposure were tended to be associated with faster decline in GCS. Our results suggest that AP exposure may accelerate cognitive decline in older ages, particularly in susceptible groups.

Combined effects of ambient air pollution and PM2.5 components on renal function and the potential mediation effects of metabolic risk factors in China

Growing evidence links long-term air pollution exposure with renal function. However, little research has been conducted on the combined effects of air pollutant mixture on renal function and multiple mediation effects of metabolic risk factors. This study enrolled 8996 adults without chronic kidney disease (CKD) at baseline from the CHCN-BTH cohort study. Three-year exposure to air pollutants [particulate matter ≤ 2.5 µm (PM2.5), PM10, PM1, ozone (O3), nitrogen dioxide (NO2), sulfur dioxide (SO2) and carbon monoxide (CO)] and PM2.5 components [black carbon (BC), ammonium (NH4+), nitrate (NO3-), sulfate (SO42-) and organic matter (OM)] were assessed using well-validated machine learning methods. Linear mixed models were applied to investigate the associations between air pollutants and estimated glomerular filtration rate (eGFR). Quantile G-computation was used to assess the combined effects of pollutant mixtures. Causal mediation analysis and Bayesian mediation analysis were employed to estimate the mediation effects of metabolic risk factors. An interquartile range increases in BC (−0.256, 95 %CI: −0.331, −0.180) and OM (−0.603, 95 %CI: −0.810, −0.397) were significantly associated with eGFR decline; while O3 (1.151, 95 %CI: 0.813, 1.489), PM10 (0.721, 95 %CI: 0.309, 1.133), NH4+ (0.990, 95 %CI: 0.638, 1.342), and NO3- (0.610, 95 %CI: 0.405, 0.815) were associated with higher eGFR. The combined effect of the PM2.5 component mixture was found to be associated with lower eGFR (−1.147, 95 % CI: −1.456, −0.839), with OM contributing 72.4 % of the negative effect. Univariate mediation analyses showed that high-density lipoprotein (HDL) mediated 7.1 %, 6.9 %, and 6.1 % effects of O3, BC, and OM, respectively. However, these mediation effects were not significant in Bayesian mediation analysis. These findings suggest the effect of the PM2.5 component mixture on eGFR decline and the strong contribution of OM. Metabolic risk factors may not mediate the effects of air pollutants. Further study is warranted to clarify the potential mechanisms involved.