Interquartile Range Increase Research Articles

Risk of heavy metal(loid) compositions in fine particulate matter on acute cardiovascular mortality: a poisson analysis in Anyang, China.

Fine particulate matter (PM2.5) is a risk factor of cardiovascular disease. Associations between PM2.5 compositions and cardiovascular disease are a point of special interest but inconsistent. This study aimed to explore the cardiovascular effects of heavy metal(loid) compositions in PM2.5. Data for mortality, air pollutants and meteorological factors in Anyang, China from 2017 to 2021 were collected. Heavy metal(loid) in PM2.5 were monitored and examined monthly. A Case-crossover design was applied to the estimated data set. The interquartile range increase in cadmium (Cd), antimony (Sb) and arsenic (As) at lag 1 was associated with increment of 8.1% (95% CI: 3.3, 13.2), 4.8% (95% CI: 0.2, 9.5) and 3.5% (95% CI: 1.1, 6.0) cardiovascular mortality. Selenium in lag 2 was inversely associated with cerebrovascular mortality (RR = 0.920 95% CI: 0.862, 0.983). Current-day exposure of aluminum was positively associated with mortality from ischemic heart disease (RR = 1.083 95% CI: 1.001, 1.172). Stratified analysis indicated sex, age and season modified the cardiovascular effects of As (P < 0.05). Our study reveals that heavy metal(loid) play key roles in adverse effects of PM2.5. Cd, Sb and As were significant risk factors of cardiovascular mortality. These findings have potential implications for accurate air pollutants control and management to improve public health benefits.

Differentiated impacts of short-term exposure to fine particulate constituents on infectious diseases in 507 cities of Chinese children and adolescents: A nationwide time-stratified case-crossover study from 2008 to 2021

This study assesses the association of short-term exposure to PM2.5 (particles ≤2.5 μm) on infectious diseases among Chinese children and adolescents. Analyzing data from 507 cities (2008–2021) on 42 diseases, it focuses on PM2.5 components (black carbon (BC), ammonium (NH4+), inorganic nitrate (NO3−), organic matter (OM), and sulfate (SO42−)). PM2.5 constituents significantly associated with incidence. Sulfate showed the most substantial effect, increasing all-cause infectious disease risk by 2.72 % per interquartile range (IQR) increase. It was followed by BC (2.04 % increase), OM (1.70 %), NO3− (1.67 %), and NH4+ (0.79 %). Specifically, sulfate and BC had pronounced impacts on respiratory diseases, with sulfate linked to a 10.73 % increase in seasonal influenza risk and NO3− to a 16.39 % rise in tuberculosis. Exposure to PM2.5 also marginally increased risks for gastrointestinal, enterovirus, and vectorborne diseases like dengue (7.46 % increase with SO42−). Sexually transmitted and bloodborne diseases saw an approximate 6.26 % increase in incidence, with specific constituents linked to diseases like hepatitis C and syphilis. The study concludes that managing PM2.5 levels could substantially reduce infectious disease incidence, particularly in China's middle-northern regions. It highlights the necessity of stringent air quality standards and targeted disease prevention, aligning PM2.5 management with international guidelines for public health protection.

Long-term exposure to ambient air pollution and risk of microvascular complications among patients with type 2 diabetes: a prospective study.

Patients with type 2 diabetes (T2D) may disproportionately suffer the adverse cardiovascular effects of air pollution, but relevant evidence on microvascular outcome is lacking. We aimed to examine the association between air pollution exposure and the risk of microvascular complications among patients with T2D. This prospective study included 17 995 participants with T2D who were free of macro- and micro-vascular complications at baseline from the UK Biobank. Annual average concentrations of particulate matter (PM) with diameters <2.5 μm (PM2.5), <10 μm (PM10), nitrogen dioxide (NO2) and nitrogen oxides (NOx) were assessed using land use regression models. Cox proportional hazards regression was used to estimate the associations of air pollution exposure with incident diabetic microvascular complications. The joint effects of the air pollutant mixture were examined using quantile-based g-computation in a survival setting. In single-pollutant models, the adjusted hazard ratios (95% confidence intervals) for composite diabetic microvascular complications per interquartile range increase in PM2.5, PM10, NO2 and NOx were 1.09 (1.04-1.14), 1.06 (1.01-1.11), 1.07 (1.02-1.12) and 1.04 (1.00-1.08), respectively. Similar significant results were found for diabetic nephropathy and diabetic neuropathy, but not for diabetic retinopathy. The associations of certain air pollutants with composite microvascular complications and diabetic nephropathy were present even at concentrations below the World Health Organization limit values. Multi-pollutant analyses demonstrated that PM2.5 contributed most to the elevated risk associated with the air pollutant mixture. In addition, we found no interactions between air pollution and metabolic risk factor control on the risk of diabetic microvascular complications. Long-term individual and joint exposure to PM2.5, PM10, NO2 and NOx, even at low levels, was associated with an increased risk of diabetic microvascular complications, with PM2.5 potentially being the main contributor.

Association of ambient air pollution with hemoglobin levels and anemia in the general population of Korean adults

BackgroundEmerging evidence has suggested significant associations between ambient air pollution and changes in hemoglobin levels or anemia in specific vulnerable groups, but few studies have assessed this relationship in the general population. This study aimed to evaluate the association between long-term exposure to air pollution and hemoglobin concentrations or anemia in general adults in South Korea.MethodsA total of 69,830 Korean adults from a large-scale nationwide survey were selected for our final analysis. Air pollutants included particulate matter with an aerodynamic diameter less than or equal to 10 micrometers (PM10), particulate matter with an aerodynamic diameter less than or equal to 2.5 micrometers, nitrogen dioxide, sulfur dioxide (SO2), and carbon monoxide (CO). We measured the serum hemoglobin concentration to assess anemia for each participant.ResultsIn the fully adjusted model, exposure levels to PM10, SO2, and CO for one and two years were significantly associated with decreased hemoglobin concentrations (all p < 0.05), with effects ranging from 0.15 to 0.62% per increase in interquartile range (IQR) for each air pollutant. We also showed a significant association of annual exposure to PM10 with anemia (p = 0.0426); the odds ratio (OR) [95% confidence interval (CI)] for anemia per each increase in IQR in PM10 was estimated to be 1.039 (1.001–1.079). This association was also found in the 2-year duration of exposure (OR = 1.046; 95% CI = 1.009–1.083; adjusted Model 2). In addition, CO exposure during two years was closely related to anemia (OR = 1.046; 95% CI = 1.004–1.091; adjusted Model 2).ConclusionsThis study provides the first evidence that long-term exposure to air pollution, especially PM10, is significantly associated with reduced hemoglobin levels and anemia in the general adult population.

Exposure to outdoor ambient air toxics and risk of breast cancer: The multiethnic cohort

BackgroundA growing literature has reported associations between traffic-related air pollution and breast cancer, however there are fewer investigations into specific ambient agents and any putative risk of breast cancer development, particularly studies occurring in populations residing in higher pollution areas such as Los Angeles. ObjectivesTo estimate breast cancer risks related to ambient air toxics exposure at residential addresses. MethodsWe examined the relationships between ambient air toxics and breast cancer risk in the Multiethnic Cohort among 48,665 California female participants followed for cancer from 2003 through 2013. We obtained exposure data on chemicals acting as endocrine disruptors or mammary gland carcinogens from the National-Scale Air Toxics Assessment. Cox proportional hazards models were used to estimate breast cancer risk per one interquartile range (IQR) increase in air toxics exposure lagged by 5-years. Stratified analyses were conducted by race, ethnicity, and hormone receptor types. ResultsAmong all women, increased risks of invasive breast cancer were observed with toxicants related to industries [1,1,2,2-tetrachloroethane (hazard ratio [HR] = 4.22, 95% confidence interval [95% CI] 3.18–5.60), ethylene dichloride (HR = 2.81, 95% CI 2.20–3.59), and vinyl chloride (HR = 2.27, 95% CI 1.81, 2.85); these 3 agents were correlated (r2 = 0.45–0.77)]. Agents related to gasoline production or combustion were related to increased breast cancer risk [benzene (HR = 1.32, 95% CI 1.24, 1.41), ethylbenzene (HR = 1.20, 95% CI 1.13–1.28), toluene (HR = 1.29, 95% CI 1.20–1.38), naphthalene (HR = 1.11, 95% CI 1.02–2.22), acrolein (HR = 2.26, 95% CI 1.92, 2.65)]. Higher hazard ratios were observed in African Americans and Whites compared to other racial and ethnic groups (p-heterogeneity <0.05 for traffic-related air toxics, acrolein, and vinyl acetate). ConclusionsOur findings suggest that specific toxic air pollutants may be associated with increase breast cancer risk.

Per- and polyfluoroalkyl substances and bone mineral content in early adolescence: Modification by diet and physical activity

BackgroundPer- and polyfluoroalkyl substance (PFAS) exposures may negatively impact bone mineral accrual, but little is known about potential mitigators of this relation. We assessed whether associations of PFAS and their mixture with bone mineral content (BMC) in adolescence were modified by diet and physical activity. MethodsWe included 197 adolescents enrolled in a prospective pregnancy and birth cohort in Cincinnati, Ohio (2003–2006). At age 12 years, we collected serum for PFAS measurements and used dual-energy x-ray absorptiometry to measure BMC. We calculated dietary calcium intake and Health Eating Index (HEI) scores from repeated 24-h dietary recalls, physical activity scores using the Physical Activity Questionnaire for Older Children (PAQ-C), and average moderate to vigorous physical activity (MVPA) based on accelerometry. We estimated covariate-adjusted differences in BMC z-scores per interquartile range (IQR) increase of individual PFAS concentrations using linear regression and per simultaneous IQR increase in all four PFAS using g-computation. We evaluated effect measure modification (EMM) using interaction terms between each modifier and PFAS. ResultsHigher serum perfluorooctanoic acid, perfluorooctanesulfonic acid, and perfluorononanoic acid concentrations and the PFAS mixture were associated with lower BMC z-scores. An IQR increase in all PFAS was associated with a 0.27 (−0.54, 0.01) lower distal radius BMC z-score. Associations with lower BMC were generally stronger among adolescents classified as < median for calcium intake, HEI scores, or MVPA compared to those ≥ median. The difference in distal radius BMC z-score per IQR increase in all PFAS was −0.38 (−0.72, −0.04) for those with <median calcium intake versus −0.03 (−0.48, 0.35) for ≥ median (EMM p-value = 0.16); the corresponding differences by MVPA were −0.42 (−0.76, −0.07) for < median and −0.05 (−0.42, 0.32) for ≥ median (EMM p-value = 0.13). ConclusionHealthy, calcium-rich diets and higher intensity physical activity may mitigate the adverse impact of PFAS on adolescent bone health.

Is short-term exposure to primary gaseous air pollutants associated with AIDS-related deaths? Evidence from a time-stratified case-crossover study.

Primary gaseous air pollutants have been associated with death from multiple causes, however, it remains unknown if they play a role in premature mortality among individuals living with HIV/AIDS. Data on HIV/AIDS patients were collected from the Hubei Provincial Center for Disease Control and Prevention, with a total of 1,467 AIDS-related deaths (ARD) between 2013 and 2020. Daily mean sulfur dioxide (SO2), nitrogen dioxide (NO2), and carbon monoxide (CO) were generated by artificial intelligence algorithms combined with big data. We employed a time-stratified case-crossover approach and conditional logistical regression models to investigate the acute effects of primary gaseous air pollutants on ARD. Per interquartile range increase in the concentrations of SO2 was significantly linked with ARD, with a corresponding odds ratio (OR) of 1.17 [95% confidence intervals (CIs): 1.01, 1.35] at lag 4day. Furthermore, our findings indicated that males exhibited a heightened vulnerability to the adverse effects of SO2 and NO2, for example, the ORs were 1.24 (95% CIs: 1.05, 1.47) and 1.16 (95% CIs: 1.01, 1.34), respectively. Moreover, individuals aged over 65years were more susceptible to SO2 and CO. Additionally, we identified the warm season as a sensitive period for mortality associated with SO2 and NO2. Our study furnished fresh evidence regarding the detrimental effects of primary gaseous air pollutants on ARD.

Multiple dietary patterns and the association between long-term air pollution exposure with type 2 diabetes risk: Findings from UK Biobank cohort study

BackgroundEvidence of modifying effect of various dietary patterns (DPs) on risk of type 2 diabetes (T2D) induced by long-term exposure to air pollution (AP) is still rather lacking, which therefore we aimed to explore in this study. MethodsWe included 78,230 UK Biobank participants aged 40–70 years with at least 2 typical 24-hour dietary assessments and without baseline diabetes. The annual average concentration of particulate matter with diameter micrometers ≤2.5 (PM2.5) and ≤10 (PM10), nitrogen dioxide (NO2), and nitrogen oxides (NOX) estimated by land use regression model was the alternative proxy of long-term AP exposure. Three well-known prior DPs such as Mediterranean diet (MED), dietary approaches to stop hypertension diet (DASH), and empirical dietary inflammatory pattern (EDIP), as well as three posterior DPs derived by the rank reduced regression model were used to capture participants’ dietary habits. Cox regression models were used to estimate AP-T2D and DP-T2D associations. Modifying effect of DPs on AP-T2D association was assessed using stratified analysis and heterogeneity test. ResultsDuring a median follow-up 12.19 years, 1,693 participants developed T2D. PM2.5, PM10, NO2, and NOX significantly increased the T2D risk (P <0.05), with hazard ratio (HR) and 95% confidence interval (95% CI) for per interquartile range increase being 1.09 (1.02,1.15), 1.04 (1.00, 1.09), 1.11 (1.04, 1.18), and 1.08 (1.03, 1.14), respectively. Comparing high with low adherence, healthy DPs were associated with a 14–41% lower T2D risk. Participants with high adherence to MED, DASH, and anti-EDIP, alongside the posterior anti-oxidative dietary pattern (AODP) had attenuated and statistically non-significant NO2-T2D and NOX-T2D associations (Pmodify <0.05). ConclusionsMultiple forms of healthy DPs help reduce the T2D risk associated with long-term exposure to NO2 and NOX. Our findings indicate that adherence to healthy DPs is a feasible T2D prevention strategy for people long-term suffering from NO2 and NOX pollution.

Outdoor Light at Night, Air Pollution, and Risk of Cerebrovascular Disease: A Cohort Study in China.

We sought to explore the associations of outdoor light at night (LAN) and air pollution with the risk of cerebrovascular disease (CeVD). We included a total of 28 302 participants enrolled in Ningbo, China from 2015 to 2018. Outdoor LAN and air pollution were assessed by Satellite-derived images and land-use regression models. CeVD cases were confirmed by medical records and death certificates and further subdivided into ischemic and hemorrhagic stroke. Cox proportional hazard models were used to estimate hazard ratios and 95% CIs. A total of 1278 CeVD cases (including 777 ischemic and 133 hemorrhagic stroke cases) were identified during 127 877 person-years of follow-up. In the single-exposure models, the hazard ratios for CeVD were 1.17 (95% CI, 1.06-1.29) for outdoor LAN, 1.25 (1.12-1.39) for particulate matter with an aerodynamic diameter ≤2.5 µm, 1.14 (1.06-1.22) for particulate matter with aerodynamic diameter ≤10 μm, and 1.21 (1.06-1.38) for NO2 in every interquartile range increase. The results were similar for ischemic stroke, whereas no association was observed for hemorrhagic stroke. In the multiple-exposure models, the associations of outdoor LAN and PM with CeVD persisted but not for ischemic stroke. Furthermore, no interaction was observed between outdoor LAN and air pollution. Levels of exposure to outdoor LAN and air pollution were positively associated with the risk of CeVD. Furthermore, the detrimental effects of outdoor LAN and air pollution might be mutually independent.

Considering the Size Distribution of Elements in Particle Matter and Oxidation Potential: Association before and after Respiratory Exposure

Oxidation potential (OP), reflecting the redox activities of particle matter (PM), is considered an optimal measure to explain the biological effects of PM exposure. However, the size resolution of the relationship between OP and chemical composition in PM, especially how the relationship changes after respiratory exposure, has not been well investigated. In this study, size-resolved indoor PM10 samples were collected from a waste recycling plant from November to December 2021 using an Anderson eight-stage cascade impactor. OP, measured by a dithiothreitol (DTT) assay (defined as OPDTT), and elements, determined by inductively coupled plasma–mass spectrometry (ICP-MS) in size-resolved PM, were determined to check their relationships and the related human exposure risk. The results indicated that compared with PM0.4 and PM0.4–2.1, PM2.1–10 contributed the most to total OPDTT and its bound elements contributed the most to potential health risks, both before and after respiratory exposure. The association between OPDTT and the elements varied with PM size. Pearson correlation analysis showed that the PM0.4- and PM0.4–2.1-bound elements were moderate-to-strongly positively correlated with OPvDTT (r: 0.60–0.90). No significant correlation or dose–response relationship was found in PM2.1–10. After respiratory exposure, several PM0.4- and PM0.4–2.1-bound elements had a moderate-to-strongly positive correlation with deposition fluxes of OP (defined as OPFlux) (0.69–0.90). A generalized linear model analysis showed that the interquartile range (IQR) increase in the PM-bound elements (ng h−1) was associated with a 41.7–58.1% increase in OPFlux. Our study is a special case that enriches the knowledge of the association between OPDTT and the chemical composition of PM of different sizes, especially after respiratory exposure, but the generalizability of the findings to other settings or types of PM may be limited. The associations among OPDTT, other chemical compositions of PM, and human exposure risk merit further research.

Association between Ambient Volatile Organic Compounds Exposome and Emergency Hospital Admissions for Cardiovascular Disease.

The limited research on volatile organic compounds (VOCs) has not taken into account the interactions between constituents. We used the weighted quantile sum (WQS) model and generalized linear model (GLM) to quantify the joint effects of ambient VOCs exposome and identify the substances that play key roles. For a 0 day lag, a quartile increase of WQS index for n-alkanes, iso/anti-alkanes, aromatic, halogenated aromatic hydrocarbons, halogenated saturated chain hydrocarbons, and halogenated unsaturated chain hydrocarbons were associated with 1.09% (95% CI: 0.13, 2.06%), 0.98% (95% CI: 0.22, 1.74%), 0.92% (95% CI: 0.14, 1.69%), 1.03% (95% CI: 0.14, 1.93%), 1.69% (95% CI: 0.48, 2.91%), and 1.85% (95% CI: 0.93, 2.79%) increase in cardiovascular disease (CVD) emergency hospital admissions, respectively. Independent effects of key substances on CVD-related emergency hospital admissions were also reported. In particular, an interquartile range increase in 1,1,1-trichloroethane, methylene chloride, styrene, and methylcyclohexane is associated with a greater risk of CVD-associated emergency hospital admissions [3.30% (95% CI: 1.93, 4.69%), 3.84% (95% CI: 1.21, 6.53%), 5.62% (95% CI: 1.35, 10.06%), 8.68% (95% CI: 3.74, 13.86%), respectively]. We found that even if ambient VOCs are present at a considerably low concentration, they can cause cardiovascular damage. This should prompt governments to establish and improve concentration standards for VOCs and their sources. At the same time, policies should be introduced to limit VOCs emission to protect public health.

Short-Term Effects of Primary and Secondary Particulate Matter on Ceramide Metabolism, Pro-Inflammatory Response, and Blood Coagulation.

Evidence of the precise biological pathway responsible for acute cardiovascular events triggered by particulate matter (PM) exposure from anthropogenic emissions is sparse. We investigated the associations of biomarkers relevant to the pathophysiology of atherothrombosis (ceramide metabolism, pro-inflammatory response, and blood coagulation) with primary and secondary components in particulate matter with aerodynamic diameters less than 2.5 μm (PM2.5). A total of 152 healthy participants were followed with four repeated clinical visits between September 2019 and January 2020 in Beijing. Exposure to ambient inorganic aerosols (sulfate, nitrate, ammonium, and chloride), as well as organic aerosols (OA) in PM2.5, was measured by a real-time aerosol chemical speciation monitor, and sources of OA were performed by positive matrix factorization. We found significant increases of 101.9-397.9% in ceramide indicators associated with interquartile-range increases in inorganic aerosols and OA prior to 72 h of exposure. Higher levels of organic and inorganic aerosols in PM2.5 were associated with increases of 3.1-6.0% in normal T cells regulated upon activation and expressed and secreted relevant to the pro-inflammatory response; increases of 276.9-541.5% were observed in D-dimers relevant to coagulation. Detrimental effects were further observed following OA exposure from fossil fuel combustion. Mediation analyses indicated that ceramide metabolism could mediate the associations of PM2.5 components with pro-inflammatory responses. Our findings expand upon the current understanding of potential pathophysiological pathways of cardiovascular events posed by ambient particulates and highlight the importance of reducing primary and secondary PM from anthropogenic combustions.

Air pollution and bronchiolitis: a case-control study in Antwerp, Belgium.

This case-control study aimed to investigate the association between short-term (1 to 5days) and medium-term (31days) exposure to air pollutants (PM2.5, PM10, BC, NO2) at home/daycare and the risk of 'severe bronchiolitis' (defined as 'requiring hospitalization for bronchiolitis') in children under 2years in Antwerp, Belgium. We included 118 cases and 79 controls admitted to three general hospitals from October 2020 to June 2021. Exposure levels were predicted using an interpolation model based on fixed measuring stations. We used unconditional logistic regression analysis to assess associations, with adjustment for potential confounders. There were hardly any significant differences in the day-to-day air pollution values between cases and controls. Medium-term (31days) exposure to PM2.5, PM10, and NO2 was however significantly higher in cases than controls in univariate analysis. Logistic regression revealed an association between severe bronchiolitis and interquartile range (IQR) increases of PM2.5 and PM10 at home and in daycare, as well asIQR increases of NO2 in daycare. Controls were however overrepresented in low pollution periods. Time-adjustment reduced the odds ratios significantly at home for PM2.5 and PM10 (aOR 1.54, 95%CI 0.51-4.65; and 2.69, 95%CI 0.94-7.69 respectively), and in daycare for. PM2.5 (aOR 2.43, 95%CI 0.58-10.1). However, the association between severe bronchiolitis and medium-term air pollution was retained in daycare for IQR increases of PM10 (aOR 5.13, 95%CI 1.24-21.28) and NO2 (aOR 3.88, 95%CI 1.56-9.61) in the time-adjusted model. Conclusion: This study suggests a possible link between severe bronchiolitis and medium-term (31days) air pollution exposure (PM10 and NO2), particularly in daycare. Larger studies are warranted to confirm these findings. What is Known: • Bronchiolitis is a leading cause of hospitalization in infants globally and causes a yearly seasonal wave of admissions in paediatric departments worldwide. • Existing studies, mainly from the USA, show heterogeneous outcomes regarding the association between air pollution and bronchiolitis. What is New: • There is a possible link between severe bronchiolitis and medium-term (31 days) air pollution exposure (PM10 and NO2), particularly in daycare. • Larger studies are needed to validate these trends.

Long-term associations of PM1 versus PM2.5 and PM10 with asthma and asthma-related respiratory symptoms in the middle-aged and elderly population.

Few studies have compared the associations between long-term exposures to particulate matters (aerodynamic diameter ≤1, ≤2.5 and ≤10 µm: PM1, PM2.5 and PM10, respectively) and asthma and asthma-related respiratory symptoms. The objective of the present study was to compare the strength of the aforementioned associations in middle-aged and elderly adults. We calculated the mean 722-day personal exposure estimates of PM1, PM2.5 and PM10 at 1 km×1 km spatial resolution between 2013 and 2019 at individual levels from China High Air Pollutants (CHAP) datasets. Using logistic regression models, we presented the associations as odds ratios and 95% confidence intervals, for each interquartile range (IQR) increase in PM1/PM2.5/PM10 concentration. Asthma denoted a self-reported history of physician-diagnosed asthma or wheezing in the preceding 12 months. We included 7371 participants in COPD surveillance from Guangdong, China. Each IQR increase in PM1, PM2.5 and PM10 was associated with a greater odds (OR (95% CI)) of asthma (PM1: 1.22 (1.02-1.45); PM2.5: 1.24 (1.04-1.48); PM10: 1.30 (1.07-1.57)), wheeze (PM1: 1.27 (1.11-1.44); PM2.5: 1.30 (1.14-1.48); PM10: 1.34 (1.17-1.55)), persistent cough (PM1: 1.33 (1.06-1.66); PM2.5: 1.36 (1.09-1.71); PM10: 1.31 (1.02-1.68)) and dyspnoea (PM1: 2.10 (1.84-2.41); PM2.5: 2.17 (1.90-2.48); PM10: 2.29 (1.96-2.66)). Sensitivity analysis results were robust after excluding individuals with a family history of allergy. Associations of PM1, PM2.5 and PM10 with asthma and asthma-related respiratory symptoms were slightly stronger in males. Long-term exposure to PM is associated with increased risks of asthma and asthma-related respiratory symptoms.

Low-level ambient ozone exposure associated with neutrophil extracellular traps and pro-atherothrombotic biomarkers in healthy adults

Background and aimsUncertainty of the causality determinations for ambient ozone (O3) on cardiovascular events is heightened by the limited understanding of the mechanisms involved in humans. We aimed to examine the pro-atherothrombotic impacts of O3 exposure and to explore the potential mediating roles of dysfunctional neutrophils, focusing on neutrophil extracellular traps (NETs). MethodsA longitudinal panel study of 152 healthy adults was conducted in the cool to cold months with relatively low levels of O3 between September 2019 and January 2020 in Beijing, China. Four repeated measurements of indicators reflecting atherothrombotic balance and NETs were performed for each participant. ResultsDaily average exposure levels of ambient O3 were 16.6 μg/m3 throughout the study period. Per interquartile range increase in average concentrations of O3 exposure at prior up to 7 days, we observed elevations of 200.1–276.3% in D-dimer, 27.2–36.8% in thrombin-antithrombin complex, 10.8–60.3% in plasminogen activator inhibitor 1, 13.9–21.8% in soluble P-selectin, 16.5–45.1% in matrix metalloproteinase-8, and 2.4–12.4% in lipoprotein-associated phospholipase A2. These pro-atherothrombotic changes were accompanied by endothelial activation, lung injury, and immune inflammation. O3 exposure was also positively associated with circulating NETs indicators, including citrullinated histone H3, neutrophil elastase, myeloperoxidase, and double-stranded DNA. Mediation analyses indicated that NETs could mediate O3-associated pro-atherothrombotic responses. The observational associations remained significant and robust after controlling for other pollutants, and were generally greater in participants with low levels of physical activity. ConclusionsAmbient O3 exposure was associated with significant increases in NETs and pro-atherothrombotic potential, even at exposure levels well below current air quality guidelines of the World Health Organization.

Reduction in Placental Metal and Metalloid in Preeclampsia: A Case-Control Study.

Preeclampsia is a primary placental disorder, with impaired placental vascularization leading to uteroplacental hypoperfusion. We aimed to investigate differences in metal and metalloid content between the placentas of women with preeclampsia and healthy controls. This was a case-control study in 63 women with preeclampsia and 113 healthy women. Clinical data were obtained from medical records. Inductively coupled plasma mass spectrometry (ICP-MS) was used to measure the placental metals and metalloids content. Compared with healthy control subjects, preeclampsia was associated with a significantly lower concentration of essential elements (magnesium, calcium, iron, copper, zinc, and selenium) in the placental tissue. After multivariable adjustment, an interquartile range (IQR) increase in selenium concentration was associated with a reduced risk of preeclampsia with an OR of 0.50 (95% CI: 0.33-0.77). The joint effects of multiple selected metals and metalloids were associated with a reduced risk of preeclampsia. The lower placental magnesium, chromium, iron, zinc, and selenium concentrations of preeclampsia cases indicate a potential link to its pathogenesis. It also provides an intriguing avenue for future research in revealing the underlying mechanisms and potential intervention strategies for preeclampsia.

Ultrafine Particles and Hospital Visits for Chronic Lower Respiratory Diseases in New York State.

Rationale: Exposure to particulate matter is associated with various adverse health outcomes. Ultrafine particles (UFPs; diameter <0.1 μm) are a unique public health challenge because of their size. However, limited studies have examined their impacts on human health, especially across seasons and demographic characteristics. Objectives: To evaluate the effect of UFP exposure on the risk of visiting the emergency department (ED) for a chronic lower respiratory disease (CLRD) in New York State in 2013-2018. Methods: We used a case-crossover design and conditional logistic regression to estimate how UFP exposure led to CLRD-related ED visits. GEOS-Chem Advanced Particle Microphysics, a state-of-the-art chemical transport model with a size-resolved particle microphysics model, generated air pollution simulation data. We then matched UFP exposure estimates to geocoded health records for asthma, bronchiectasis, chronic bronchitis, emphysema, unspecified bronchitis, and other chronic airway obstructions in New York State from 2013 through 2018. In addition, we assessed interactions with age, ethnicity, race, sex, meteorological factors, and season. Results: Each 1-(interquartile range [IQR]) increase in UFP exposure led to a 0.37% increased risk of a respiratory-related ED visit on lag 0-0, or the day of the ED visits, (95% confidence interval [CI], 0.23-0.52%) and a 1.81% increase on lag 0-6, or 6 days before the ED visit, (95% CI, 1.58-2.03%). The highest risk was in the emphysema subtype (lag 0-5, 4.18%; 95% CI, 0.16-8.37%), followed by asthma (lag 0-6, 2.00%), chronic bronchitis (lag 0-6, 1.78%), other chronic airway obstructions (lag 0-6, 1.60%), and unspecified bronchitis (lag 0-6, 1.49%). We also found significant interactions between UFP health impacts and season (Fall, 3.29%), temperature (<90th percentile, 2.27%), relative humidity (>90th percentile, 4.63%), age (children aged <18 yr, 3.19%), and sex (men, 2.06%) on lag 0-6. Conclusions: In this study, UFP exposure increased CLRD-related ED visits across all seasons and demographic characteristics, yet these associations varied according to various factors, which requires more research.

Greenness, Genetic Predisposition, and Tinnitus.

This study aimed to investigate the association between residential greenness and tinnitus and the potential interaction between greenness and genetic predisposition to tinnitus. The normalized difference vegetation index (NDVI) is used to measure residential greenness. The tinnitus is defined based on self-reported. In the cross-sectional analyses, logistic regression models are used for the baseline sample of the United Kingdom Biobank cohort. In the secondary analysis, a Cox proportional hazard model is used for a subsample of participants who completed the tinnitus questionnaire at follow-up. In the cross-sectional analysis including 106471 participants, higher residential greenness is associated with lower odds of tinnitus for each interquartile range increase in continuous NDVI, with an adjusted odds ratio of 0.97 (95% confidence interval: 0.95 to 0.99) for tinnitus. A similar association is observed in the longitudinal analysis, with an adjusted hazard ratio of 0.92 (95% confidence interval: 0.86 to 0.98) for the association of NDVI increased per interquartile range with incident tinnitus. Moreover, there is a significant interaction between greenness and genetic predisposition to tinnitus (P < 0.05). This study suggested that residential greenness is negatively associated with tinnitus. Greenness and genetic predisposition to tinnitus are found to have a significant interaction.

Abstract PR-009: Associations between PM2.5, vegetation density and childhood brain tumors: a case-control registry-based study from Texas 1995-2011

Abstract Background: Air pollution has been reported to be associated with some childhood cancers, namely leukemias. Less is known about air pollution and childhood brain tumor risk. In adult cancers, increasing vegetation density, or greenness, has been inversely associated with cancer incidence and survival. The interplay between air pollution and greenness, which co-occur, in childhood cancer etiology is unclear. Therefore, we sought to estimate the association between prenatal and early life exposure to air pollution, greenness, and childhood cancer in Texas (1995-2011). Materials and Methods: We included 1,316 individuals with a childhood brain tumor diagnosed &amp;lt;17 years of age and 109,762 age- and sex-matched controls. We linked birth certificate residential address to census tract annual average particulate matter 2.5 µg/m³ (PM2.5) and Normalized Difference Vegetation Index (NDVI) to approximate prenatal and early life exposure to greenness and air pollution. We estimated odds ratios (OR) and 95% confidence intervals (95% CI) as the measure of association between PM2.5 and NDVI interquartile range (IQR) increases and brain tumors. Models were adjusted for birth year, sex, maternal race/ethnicity, and area-level socioeconomic status (Yost index). Results: The following brain tumor types were included: ependymoma (n=136), astrocytoma (n=619), medulloblastoma (n=187), PNET (n=57), ATRT (n=54), and other gliomas (n=263). Average birth year PM2.5 and NDVI exposure levels were similar in cases and controls, 11 µg/m³ and 0.4, respectively. Each IQR increase (2.6 µg/m³) in PM2.5 was associated with ependymoma (OR: 1.27, 95% CI: 1.01-1.60) when adjusting for control-derived quartiles of NDVI. Conversely, after adjusting for PM2.5 quartiles, each IQR increase in NDVI (0.13) was inversely associated with ependymoma in those diagnosed at 0-4 years of age (OR: 0.75, 95% CI: 0.56-0.97) and with medulloblastoma in those aged 0-16 years at diagnosis (OR: 0.75, 95% CI: 0.62-0.91). There was no evidence of statistical interaction between NDVI and PM2.5 (all Likelihood Ratio Test p-values&amp;gt;0.05) for any brain tumors. Conclusions: Increasing residential air pollution during prenatal and early life increased the risk of childhood ependymoma in Texas independent of greenness. Conversely, increasing greenness exposure in prenatal and early life decreased the risk of ependymoma and medulloblastoma independent of PM2.5. These findings highlight the complex relationship between air pollution and greenness in childhood cancer etiology. Citation Format: Lindsay Williams, David Haynes, Jeannette Sample, Laura McGuinn, Thanh Hoang, Philip Lupo, Michael Scheurer. Associations between PM2.5, vegetation density and childhood brain tumors: a case-control registry-based study from Texas 1995-2011 [abstract]. In: Proceedings of the AACR Special Conference on Brain Cancer; 2023 Oct 19-22; Minneapolis, Minnesota. Philadelphia (PA): AACR; Cancer Res 2024;84(5 Suppl_1):Abstract nr PR-009.

Exposure to green spaces, cardiovascular risk biomarkers and incident cardiovascular disease in older adults: The Seniors-Enrica II cohort

IntroductionThe impact of residential green spaces on cardiovascular health in older adults remains uncertain. MethodsCohort study involving 2114 adults aged ≥ 65 years without cardiovascular disease (CVD), residing in five dense municipalities (Prince et al., 2015) of the Madrid region and with detailed characterization of their socioeconomic background, health behaviors, CVD biological risk factors, and mental, physical, and cognitive health. Greenness exposure was measured using the Normalized Difference Vegetation Index (NDVI) at varying distances from participants' homes. Traffic exposure, neighborhood environment, neighborhood walkability, and socioeconomic deprivation at the census level were also assessed. Serum N-terminal pro-B-type natriuretic peptide (NT-ProBNP), high-sensitivity troponin T (hs-TnT), interleukin 6 (IL-6), and Growth Differentiation Factor 15 (GDF‐15) were measured at baseline, and incident CVD events identified through electronic medical records (International Classification of Primary Care-2 codes K74, K75, K77, K90, and K92). ResultsAfter adjusting for sex, age, educational attainment, financial hardship and socioeconomic deprivation at the census level, an interquartile range (IQR) increase in NDVI at 250, 500, 750, and 1000 m around participants' homes was associated with mean differences in ProBNP of −5.56 % (95 %CI: −9.77; −1.35), −5.05 % (-9.58; −0.53), −4.24 % (-8.19, −0.19), and −4.16 % (-7.59; −0.74), respectively; and mean differences in hs-TnT among diabetic participants of −8.03 % (95 %CI: −13.30; −2.77), −9.52 % (-16.08; −2.96), −8.05 % (-13.94, −2.16) and −5.56 % (-10.75; −0.54), respectively. Of similar magnitude, although only statistically significant at 250 and 500 m, were the observed lower IL-6 levels with increasing greenness. GDF-15 levels were independent of NDVI. In prospective analyses (median follow-up 6.29 years), an IQR increase in residential greenness at 500, 750, and 1000 m was associated with a lower risk of incident CVD. The variables that contributed most to the apparent beneficial effects of greenness on CVD were lower exposure to traffic, improved cardiovascular risk factors, and enhanced physical performance. Additionally, neighborhood walkability and increased physical activity were notable contributors among individuals with diabetes. ConclusionIncreased exposure to residential green space was associated with a moderate reduction in CVD risk in older adults residing in densely populated areas.