Short-term Air Pollution Exposure Research Articles

Direct current cardioversion and the impact of short-term exposure to air pollution: a report from the nationwide EP-PARTICLES study

Abstract Background Air pollution and atrial fibrillation (AF) represent significant public health challenges, impacting global health considerably. Numerous studies have focused on areas with high or very high air pollution concentrations, our study examines a unique area in Poland characterized by low to moderate air pollution levels. Our research also addresses a commonly overlooked in research type of pollution - Polish smog. Due to its composition rich in particulate matter and the conditions in which it is formed - is characterized by extremely adverse health effects. Aim To explore the correlation between short-term air pollution exposure and the incidence of acute direct current cardioversion (DCC) for AF treatment. Methods The study area encompassed three voivodeships from Eastern Poland at the NUTS-2 level, with a population of 5,429,378 individuals. Data on hospitalizations from 2011 to 2020 were obtained from the National Health Fund. We combined air pollution and weather condition data from both ground monitoring stations and satellite observations. Emergency visits for AF and DCC were identified using ICD-9 and ICD-10 codes. For a national perspective, we applied meta-analytical strategies to the municipality-specific outcomes. The results are presented as percentage increases in admissions (% IR) with 95% confidence intervals (95%CI). Results Over the decade, 190,454 hospitalizations for AF were reported with a standardized hospitalization rate (SHR) of 358 per 100,000/year (SD=113) and 30,291 DCC admissions (SHR=56.9 [SD]=26). The mean age for AF vs. DCC cohort was 69.6 (SD=11.2) vs. 68.7 (SD=10.4) years, with females representing 56.1% (N=106,822) of AF cases vs. 46.1% (N=13,953) of DCC admissions (P<0.001). Each 10 µg/m3 increase in PM2.5, PM10, and NO2 concentration on the exposure day led to 1.6% (1.1%–2.1%), 1% (0.8%–1.6%), and 1.8% (1.1%–2.6%) increases in acute AF admissions, respectively, with effects lasting up to 6 days. Women and older individuals were more vulnerable to AF episodes induced by air pollution (P<0.001). A 10 µg/m3 increase in PM2.5 on the day of admission increased DCC admissions by 1.5% (0.1%–2.9%, P=0.04), with effects persisting for up to 3 days. The impact of PM10 was time-delayed: 1.3% (0.2%–2.4%, P=0.02) for LAG1 (i.e. one day after exposure), and 1.1% (0.1%–2.2%, P=0.4) for LAG2. No significant effects of gaseous pollutants on DCC (SO2, NO2, and BaP) were observed, nor any differences in the effects by age or sex. Exposure-response functions show steeper slopes of the PM2.5 associations in the lower ranges of exposures, far below air quality norms set by the World Health Organization. Conclusions Air pollution acts as a triggering factor for acute AF hospitalizations and DCC. The differential impact of air pollution on AF events between groups highlights that women and older individuals are particularly vulnerable. Air pollution exposure should be considered into AF management and prevention strategies.Pooled exposure–response function: % inc

Ambient air pollution exposure is associated with liver fat and stiffness in Latino youth with a more pronounced effect in those with PNPLA3 genotype and more advanced liver disease

BackgroundExposure to ambient air pollutants has emerged as a risk for metabolic-dysfunction associated steatotic liver disease (MASLD). ObjectivesWe sought to examine associations between short-term (prior month) and long-term (prior year) ambient air pollution exposure with hepatic fat fraction (HFF) and liver stiffness in Latino youth with obesity. A secondary aim was to investigate effect modification by patatin-like phospholipase domain-containing protein 3 (PNPLA3) genotype and liver disease severity. MethodsData was analyzed from 113 Latino youth (age 11–19) with obesity in Southern California. Individual exposure to particulate matter with aerodynamic diameter ≤ 2.5μm (PM2.5), ≤ 10μm (PM10), nitrogen dioxide (NO2), 8-hour maximum ozone (8hrMax-O3), 24-hr O3, and redox-weighted oxidative capacity (Oxwt) were estimated using residential address histories and United States Environmental Protection Agency air quality observations. HFF and liver stiffness were measured using magnetic resonance imaging. Linear models were used to determine associations between short-term and long-term exposure to air pollutants with HFF and liver stiffness. Modification by PNPLA3 and liver disease severity was then examined. ResultsShort-term exposure to 8hrMax-O3 was positively associated with HFF. Relationships between air pollution exposure and HFF were not impacted by PNPLA3 genotype or liver disease severity. Long-term exposure to 8hrMax-O3 and Oxwt were positively associated with liver stiffness. Associations between air pollution exposure and liver stiffness depended on PNPLA3 genotype, such that individuals with GG genotypes exhibited stronger, more positive relationships between short-term exposure to PM10, 8hrMax-O3, 24-hr O3, and Oxwt and liver stiffness than individuals with CC/CG genotypes. In addition, relationships between short-term exposure to NO2 and liver stiffness were stronger in those with severe liver disease. DiscussionAir pollution exposure may be a risk factor for liver disease among Latino youth with obesity, particularly in those with other preexisting risks for liver damage.

Criteria air pollutants and HIV-related mortality: Insights from a nationwide case-crossover investigation

The heightened vulnerability of individuals with HIV to environmental stressors is well-recognized, yet the role of air pollution in exacerbating HIV-related mortality remains underexplored. In this nationwide, individual-level case-crossover study conducted from 2013 to 2019, we investigated the association between short-term exposure to criteria air pollutants and HIV-related mortality. Our analysis of 38,510 HIV-related deaths revealed significant associations between exposure to PM2.5, PM10, NO2, and CO and increased mortality risk. The effects of PM2.5 and PM10 persisted for two days, whereas NO2 and CO had immediate, same-day impacts. Vulnerability was heightened in individuals under 65 years, males, those with lower educational attainment, and unmarried individuals. Among causes of death, HIV-related malignant neoplasms exhibited the highest sensitivity to particulate matter. Our findings provide novel insights into the relationship between short-term air pollution exposure and HIV-related mortality, emphasizing the increased susceptibility of this immunocompromised population. The results underscore the need for targeted public health interventions to reduce pollution exposure, particularly for the most at-risk demographic groups. This study contributes to a deeper understanding of environmental health risks faced by individuals living with HIV and informs evidence-based policy recommendations.

Short-term exposure to ambient air pollution and severe COVID-19: mortality and hospital admission to COVID-19 in the Netherlands from february to december 2020

This study aimed to examine acute effects of exposure to ambient air pollution on COVID-19 hospital admissions and mortality in the Netherlands. We hypothesized that exposure to increased air pollution in the preceding week might trigger an exacerbation of health of infected individuals.Associations between daily concentrations of particulate matter with an aerodynamic diameter ≤2.5 µm (PM2.5) and ≤10 µm (PM10), nitrogen dioxide (NO2), ozone (O3) and risk of hospital admissions and mortality due to COVID-19 from February to December 2020 was analyzed across all 352 Dutch municipalities grouped into 12 provinces. Time-series models were used to fit province-specific estimates, followed by meta-analyses to produce national estimates. Analyses were based on daily averages of PM2.5, PM10, NO2, and maximum 8-hour running average of O3 on a 1×1 km grid and averaged on municipality level by population weight. Models were adjusted for spatiotemporal confounders, including government policies in response to the number of COVID-19 infections. Since there were only few COVID-19 cases during the summertime when O3 levels were highest, associations between O3 and COVID-19 health outcomes were not further explored.We found associations between exposure to air pollution in the preceding week (average of lag 0-7 days) and COVID-19 hospital admissions and mortality. On a national level, an interquartile range increase in PM2.5, PM10 and NO2 exposure was associated with 11-12% increased mortality risk; the risk for hospital admissions was higher: 19-25%. Observed associations were more robust for PM than NO2 in two-pollutant models.Our results suggest that short-term exposure to PM2.5 and PM10 may increase the risk of COVID-19 mortality and hospital admission. This indicates that, consistent with previous studies on air pollution and respiratory infections, the population at risk of being hospitalized or dying of COVID-19 is extra vulnerable to the adverse effects of short-term air pollution exposure.

The temporal trend and disparity in short-term health impacts of fine particulate matter in California (2006–2019)

Most epidemiological studies assume that the relationship between short-term air pollution exposure and health outcomes is constant over time, which ignores potential changes in population composition and particulate matter emission sources. Limited studies have assessed changes in the relationship between fine particulate matter (PM2.5) and adverse health outcomes over time, with mixed results. Additionally, there is a need to identify which subgroups are disproportionately impacted over time by PM2.5-related health consequences. Therefore, we aimed to examine whether temporal trends exist in the relationships between daily PM2.5 exposure and circulatory and respiratory acute care utilization in California from 2006 to 2019. We further assessed whether certain subpopulations are more susceptible to PM2.5 exposure by demographic characteristics and extreme wildfire frequency. Daily PM2.5 concentrations estimated from a stacked ensemble model and daily cause-specific acute care utilization and demographic data from the California Department of Health Care Access and Information. We analyzed this relationship using modified two-stage Bayesian hierarchical models, where we first did not consider temporal trends, then stratified by two periods, and finally flexibly considered non-linear changes over time. Increases in circulatory (0.56 %; 95 % credible interval (CI): 0.17 %, 0.96 %) and respiratory acute care utilization risk (2.61 %; 95%CI: 2.29 %, 2.94 %) were found with every 10 μg/m3 increase in PM2.5 on the same day and previous two days. These risks were found to increase over time, where 0.13 % (95%CI: 0.02 %, 0.22 %) and 1.40 % (95%CI: 1.24 %, 1.54 %) increases were identified for circulatory and respiratory acute care utilizations, respectively, from the first (2006–2012) to second period (2013–2019). Differences by age, sex, race/ethnicity, and extreme wildfire frequency were noted. These findings confirm that air pollution guidelines should consider the dynamic nature of epidemiological dose-response and can provide insight for targeted air pollution control and adaptation policies designed to reduce PM2.5 exposure, particularly for the most susceptible subpopulations.

Assessment of short-term effects of ambient air pollution exposure on osteoarthritis outpatient visits

The association of short-term ambient air pollution exposure with osteoarthritis (OA) outpatient visits has been unclear and no study has assessed the modifying roles of district-level characteristics in the association between ambient air pollution exposure and OA outpatient visits. We investigated the cumulative associations of ambient air pollution exposure with daily OA outpatient visits and vulnerable factors influencing the associations using data from 16 districts of Beijing, China during 2013–2019. A total of 18,351,795 OA outpatient visits were included in the analyses. An increase of 10 μg/m3 in fine particulate matter (PM2.5), inhalable particulate matter (PM10), nitrogen dioxide (NO2), sulfur dioxide (SO2), maximum 8-hour moving-average ozone (8 h-O3), and 0.1 mg/m3 in carbon monoxide (CO) at representative lag days were associated with significant increases of 0.31 %, 0.06 %, 0.77 %, 0.87 %, 0.30 %, and 0.48 % in daily OA outpatient visits, respectively. Considerable OA outpatient visits were attributable to short-term ambient air pollution exposure. In addition, low temperature and high humidity aggravated ambient air pollution associated OA outpatient visits. District-level characteristics, such as population density, green coverage rate, and urbanization rate modified the risk of OA outpatient visits associated with air pollution exposure. These findings highlight the significance of controlling ambient air pollution during the urbanization process, which is useful in policy formation and implementation.

Short Term Air Pollution Exposure is Associated with Hospital Admissions and Emergency Department Visits for Individuals with Sickle Cell Disease

Short Term Air Pollution Exposure is Associated with Hospital Admissions and Emergency Department Visits for Individuals with Sickle Cell Disease

Short term air pollution exposure during pregnancy and associations with maternal immune markers

BackgroundAir pollution exposure during pregnancy has been associated with numerous adverse pregnancy, birth, and child health outcomes. One proposed mechanism underlying these associations is maternal immune activation and dysregulation. We examined associations between PM2.5 and NO2 exposure during pregnancy and immune markers within immune function groups (TH1, TH2, TH17, Innate/Early Activation, Regulatory, Homeostatic, and Proinflammatory), and examined whether those associations changed across pregnancy. MethodsIn a pregnancy cohort study (n = 290) in Rochester, New York, we measured immune markers (using Luminex) in maternal plasma up to 3 times during pregnancy. We estimated ambient PM2.5 and NO2 concentrations at participants’ home addresses using a spatial-temporal model. Using mixed effects models, we estimated changes in immune marker concentrations associated with interquartile range increases in PM2.5 (2.88 μg/m3) and NO2 (7.82 ppb) 0–6 days before blood collection, and assessed whether associations were different in early, mid, and late pregnancy. ResultsIncreased NO2 concentrations were associated with higher maternal immune markers, with associations observed across TH1, TH2, TH17, Regulatory, and Homeostatic groups of immune markers. Furthermore, the largest increases in immune markers associated with each 7.82 ppb increase in NO2 concentration were in late pregnancy (e.g., IL-23 = 0.26 pg/ml, 95% CI = 0.07, 0.46) compared to early pregnancy (e.g., IL-23 = 0.08 pg/ml, 95% CI = −0.11, 0.26). ConclusionsResults were suggestive of NO2-related immune activation. Increases in effect sizes from early to mid to late pregnancy may be due to changes in immune function over the course of pregnancy. These findings provide a basis for immune activation as a mechanism for previously observed associations between air pollution exposure during pregnancy and reduced birthweight, fetal growth restriction, and pregnancy complications.

Air pollution and acute kidney injury with comorbid disease: A nationwide case-crossover study in South Korea

Emerging evidence suggests that air pollution is a significant contributor to the global burden of kidney disease. Although acute kidney injury (AKI) is a common secondary event in ill patients, evidence regarding the association between air pollution and AKI accompanied by specific comorbidities is limited. This study aimed to estimate the association between short-term exposure to air pollution (fine particulate matter ≤2.5 μm [PM2.5] and ozone [O3]) and incident AKI by comorbid diseases using the Korea National Health Information Database (NHID). Total of 160,390 incident AKI cases, defined as an emergency department (ED) visit due to AKI, were observed within the period 2015–2021 in inland South Korea. A time-stratified case-crossover design was applied for PM2.5 and O3 individually, using a conditional logistic regression model within each case and its own control (three or four days of the same day of the week in the same month) to estimate the association between short-term air pollution exposure and ED visits due to AKI. Short-term exposure to PM2.5 and O3 was associated with ED visits due to AKI with ORs of 1.008 (95% confidence interval [CI]: 0.999, 1.017) and 1.019 (95% CI: 1.005, 1.033) for an interquartile range (IQR) increase in lag 0–1 day PM2.5 and O3 respectively, although OR for PM2.5 was marginally significant. The odds of incident AKI associated with PM2.5 was evident in conjunction with ischemic heart disease, cerebrovascular disease, gastrointestinal bleeding, and pneumonia. For O3, the estimated odds was prominent for AKI with ischemic heart disease. In addition, the comorbid disease-specific odds of AKI attributed to air pollution varied by sex and age. Our findings provide epidemiological evidence of a plausible mechanism between air pollution and incident AKI and suggest the need for personalized AKI prevention strategies attributed to air pollution.

P1105 Short-term exposure to environmental air pollution and inflammatory bowel disease flares: a time-stratified case cross-over study

Abstract Background Some epidemiological studies suggest that long-term exposure to environmental air pollutants, such as particulate matter (PM), could have a role in inflammatory bowel disease (IBD) incidence and pathogenesis. However, less is known about the potential effect of short-term air pollution exposure. The aim of this study is to investigate whether short-term exposure to environmental air pollution is associated with the occurrence of IBD flares. Methods Anonymized hospital discharge records (HDR) with ICD-9-CM codes 555 (Crohn’s disease) and 556 (ulcerative colitis) for years 2002-2009 from all hospitals of the Lombardy region were collected. All HDR of adult patients (18-75 years) resident in Milan were included, except for recurrent hospitalizations within 6 months. Each record was assigned daily PM ≤10 µm (PM10) concentrations at municipality level by averaging PM10 levels of the day of admission with the levels of the day before (lag01) and of each preceding day up to six days before (lag06). To evaluate the association between PM10 and IBD-related hospitalizations, a time-stratified case-crossover study design was applied. Conditional logistic regression models, calculating Odds Ratios (OR) and 95% Confidence Intervals (95%CI) per increments of 10 µg/m3 of PM10, were performed. Results Overall, 2,176 hospital admissions (males=1,137, Crohn’s disease=1,264, ulcerative colitis=912) were included. In the entire population no clear association between PM10 and IBD-related hospitalization was identified, notwithstanding a small risk increase for males (OR: 1.03; 95%CI: 0.99-1.08 at lag04). When further stratifying for ICD code, an increased risk of hospitalization for "left-sided ulcerative colitis" (ICD code: 556.5) was found in males only, for exposures in all days preceding hospitalization up to lag04 (1.28; 1.05-1.28; 59 cases, 207 controls) (Figure 1). In females, the association was weaker, although positive (1.14; 0.91-1.42; 49 cases, 164 controls). No relevant findings emerged when looking at other ICD codes. Conclusion We observed an increased risk of IBD-related hospitalization in male patients with left-sided ulcerative colitis per increasing levels of air pollution in the days preceding hospital admission. Although preliminary, our findings suggest the possible role of sex as an effect modifier of the influence that air pollution might exert on IBD flares. Further studies are needed to better comprehend the complex framework characterizing the interplay between environmental and individual factors contributing to IBD.

Emerging Stroke Risk Factors: A Focus on Infectious and Environmental Determinants.

This review focuses on emerging risk factors for stroke, including air pollution and climate change, gut microbiota, high altitude, and systemic infection. Up to 14% of all stroke-associated mortality is attributed to air pollution and is more pronounced in developing countries. Fine particulate matter and other air pollutants contribute to an increased stroke risk, and this risk appears to increase with higher levels and duration of exposure. Short term air pollution exposure has also been reported to increase the stroke risk. The gut microbiota is a complex ecosystem of bacteria and other microorganisms that reside in the digestive system and affect multiple body systems. Disruptions in the gut microbiota may contribute to stroke development, possibly by promoting inflammation and atherosclerosis. High altitudes have been associated with erythrocytosis and cerebrovascular sinus thrombosis, but several studies have reported an increased risk of thrombosis and ischemic stroke at high altitudes, typically above 3000 m. Systemic infection, particularly infections caused by viruses and bacteria, can also increase the risk of stroke. The risk seems to be greatest in the days to weeks following the infection, and the pathophysiology is complex. All these emerging risk factors are modifiable, and interventions to address them could potentially reduce stroke incidence.

Metabolic profiles associated with exposure to ambient particulate air pollution: findings from the Betula cohort.

Air pollution is a significant contributor to morbidity and mortality globally and has been linked to an increased risk of dementia. Previous studies within the Betula cohort in Northern Sweden have demonstrated associations between air pollution and dementia, as well as distinctive metabolomic profiles in dementia patients compared to controls. This study aimed to investigate whether air pollution is associated with quantitative changes in metabolite levels within this cohort, and whether future dementia status would modify this association. Both short-term and long-term exposure to air pollution were evaluated using high spatial resolution models and measured data. Air pollution from vehicle exhaust and woodsmoke were analyzed separately. Metabolomic profiling was conducted on 321 participants, including 58 serum samples from dementia patients and a control group matched for age, sex, and education level, using nuclear magnetic resonance spectroscopy. No statistically significant associations were found between any metabolites and any measures of short-term or long-term exposure to air pollution. However, there were trends potentially suggesting associations between both long-term and short-term exposure to air pollution with lactate and glucose metabolites. Notably, these associations were observed despite the lack of correlation between long-term and short-term air pollution exposure in this cohort. There were also tendencies for associations between air pollution from woodsmoke to be more pronounced in participants that would later develop dementia, suggesting a potential effect depending on urban/rural factors. While no significant associations were found, the trends observed in the data suggest potential links between air pollution exposure and changes in lactate and glucose metabolites. These findings provide some new insights into the link between air pollution and metabolic markers in a low-exposure setting. However, addressing existing limitations is crucial to improve the robustness and applicability of future research in this area. The pronounced associations in participants who later developed dementia may indicate an influence of urban/rural factors, warranting further investigation.

Short-term exposure to ambient air pollution and injuries due to external causes according to intentions and mechanisms

Although injuries are a leading cause of death and affect the life expectancy of individuals who live with disabilities globally, the potential role of air pollution exposure on injuries due to external causes has received little scientific attention, especially compared with that given to the association of air pollution and non-external causes of morbidity and mortality. We investigated the association between emergency department visits for externally caused injuries and short-term exposure to major ambient air pollutants, with focus on the intentions and mechanisms of injuries. We identified 2,049,855 injured patients in Seoul, South Korea between 2008 and 2016 using the National Emergency Database. Daily short-term exposure to air pollution including particles <10 μm (PM10) and <2.5 μm (PM2.5), nitrogen dioxide (NO2), sulfur dioxide (SO2), carbon monoxide (CO), and ozone (O3) was estimated based on hourly concentrations. We employed a time-stratified case-crossover study design using a conditional Poisson regression model adjusted for meteorological variables, influenza epidemics, and holidays. Immediate exposure (lag 0) to most pollutants significantly increased the risk of total injuries (PM2.5, 0.42 %; NO2, 0.68 %; SO2, 1.05 %; CO, 0.57 %; O3, 1.86 % per interquartile range increment), and the associations differed according to the intention and mechanism of injury. Unintentional and assault injuries were significantly associated with air pollution exposure, whereas self-harm injuries showed no association. In mechanism-specific analyses, injuries caused by falls, blunt objects, penetration, traffic accidents, machinery, and slips were associated with specific air pollutants, even in the co-pollutant models. The associations were stronger in injured patients aged <15 years, and in males than in their counterparts. Our results suggest that short-term air pollution exposure might play a role in the risk of externally caused injuries and the association may differ depending on the intention and mechanism of injury, which provide important evidence for injury prevention and air quality strategies.

Air pollution and cerebrovascular diseases

Amongst the primary environmental issues affecting global health, air pollution is considered the leading cause of concern. Globally, around 800,000 deaths were attributed to air pollution according to WHO. Evidence suggests that there has been strong association of air pollution with stroke. Approximately, 25% of the stroke mortality was due to air pollution according to a study in 2013. The aim of this review is to analyze association of stroke and air pollution and its burden globally with a special focus on South Asia along with its association with COVID 19 pandemic. There is currently a lot of research that links air pollution to cardiovascular disorders including stroke. Short term and long-term air pollution exposure has been shown to increase the stroke incidence in epidemiological data. It was concluded that air pollution, both gaseous and particle, show a strong and tight temporal relationship with stroke hospitalizations and death. Even though air pollution poses a significant threat to human health, the great number of countries still fail to achieve internationally agreed air quality standards. Air pollution should be recognized amongst the most significant controllable risk factors for cardiovascular and cerebrovascular disease prevention and treatment. Nonetheless, during the last decade, global knowledge of the health implications of air pollution has increased significantly, and the desire for global initiatives to combat air pollution has begun with optimism.

Increased Risk for Hospitalization Associated with Short Term Particle Air Pollution Exposure for California Residents with Sickle Cell Disease

Background: Air pollution is associated with numerous adverse health outcomes in the general population such as asthma exacerbations, pneumonia, myocardial infarction, and stroke. There is a strong association between air pollution and mechanistic processes associated with oxidative stress, vasoconstriction, and inflammation, suggesting a high risk of exposure for those with sickle cell disease (SCD). A small number of published studies have explored this relationship, primarily focusing on children. Only two studies have examined air pollution in the US, both with outcomes among urban area hospitals in Atlanta, GA. None have taken place in California, which has the worst air quality, including the four most polluted cities in year-round particle pollution in the nation. Additionally, all published studies have overlooked more rural exposure areas. Recent advances in environmental exposure assessment have enabled high-resolution predictions of ambient air pollution concentrations in the whole US, making it possible to cover unmonitored suburban and rural areas that were unrepresented in the past. In addition, these high-resolution predictions are more precise surrogates of the personal exposure measures than monitored data. Particulate matter with a diameter of 2.5 microns or less (PM 2.5) is the most harmful pollutant based on current research findings. We hypothesized that short term increases in PM 2.5 exposure were associated with an increased risk for hospitalization among individuals with SCD in California. Methods: We designed a time-stratified case-crossover study to estimate the percent change in risk for hospitalization for SCD complications associated with each 1mg/m 3 increase in PM 2.5 exposure. The zip code of residence was used to spatially link each hospital admission with PM 2.5 exposure using a novel hybrid exposure model allowing for estimated exposure in areas without direct remote sensing. We used conditional logistic regressions to examine the PM 2.5 exposures at 7-day moving average and single lag days (from lag 0 to 6 days) before admission, adjusting for nonlinear confounding effects of air temperature and humidity at the same exposure window. We examined risk for all hospitalizations and specifically for vaso-occlusive pain (VOC) and acute chest syndrome (ACS). Results: From 2000-2016, among 5,835 California residents with SCD, there were 107,450 admissions for sickle cell disease complications with VOC being the most common indication (71.1%). PM 2.5 air pollution data was examined among 2,634 zip codes throughout the state. Residents with SCD were noted to be living among 1,180 zip codes. The daily burden of PM 2.5 was higher in zip codes with residents with SCD (mean 11.5 mg/m 3, standard deviation [SD] 9.0) when compared to zip codes without residents known to have SCD (mean 9.2 mg/m 3, SD 8.6, p&amp;lt;0.001) ( Table 1). Overall, the mean daily burden of PM 2.5 declined in the period of 2010-2016 when compared to that from 2000-2009. However, the daily mean PM 2.5 concentration remained higher in zip codes with individuals with SCD. No significant association was seen in examining the week-long exposure to PM 2.5 and increase risk in hospitalizations for any indication over the entire study period (2000-2016). However, when examining the more contemporary period of 2010-2016, we identified that each 1mg/m 3 increase in PM 2.5 was associated with 0.22% increased risk for SCD hospitalization (Confidence Interval [CI] 0.02-0.42, p=0.03) 3 days prior to admission. We observed a 0.26% increased risk for hospitalization for VOC with each 1 mg/m 3 increase in PM 2.5 exposure (CI 0.02-0.49, p=0.03) at lag day 3 (Figure 1). No effect was seen with PM 2.5 on hospitalizations for ACS during any time period. Discussion: Our study suggests that short term air pollution exposure may be a trigger for hospitalization for individuals with SCD. In particular this effect is seen in the more recent years with a lower daily average PM 2.5 burden overall, suggesting attention may be needed well below Environmental Protection Agency (EPA) thresholds. Consistent with previous studies, lag day 3 PM 2.5 exposure is associated with an increased risk for hospitalization for VOC. These results may have important implications in understanding risk factors for hospitalization for children and adults with SCD.

Association between short-term air pollution exposure and perturbation in thyrotropin levels in 1.38 million Chinese women: A national longitudinal analysis, 2014–2019

Prevalence of subclinical hypothyroidism substantially increased during the last decade in China, which has been commonly/clinically diagnosed as elevation in thyrotropin (thyroid-stimulating hormone [TSH]). Tobacco smoke containing toxic substances has been linked to thyroid dysfunction; however, data on perturbation of TSH following air pollution exposure in human has not been assessed at nationwide population level. We investigated the longitudinal impact of daily ambient air pollution estimated at residential level on serum TSH in 1.38 million women from China’s 29 mainland provinces between 2014 and 2019. We observed that particulate matter with aerodynamic diameter ≤ 10 and ≤ 2.5 µm (PM10, PM2.5) and nitrogen dioxide (NO2) at cumulative lag 0–7 days of exposure were associated with percent elevations in TSH (0.88% [95% CI: 0.71, 1.05] per [interquartile range, IQR: 54.8 μg/m3] of PM10; 0.89% [95% CI, 0.71, 1.07] per IQR [40.3 μg/m3] of PM2.5; 2.01% [95% CI: 1.81, 2.22] per IQR [27.4 μg/m3] of NO2). Greater associations were observed in participants living in areas with ≥adequate iodine intake and those with low BMI levels and high inflammation status. Our results suggest that increased concentrations of recent ambient air pollutants at exposure ranges commonly encountered in Asia were associated with increases in TSH, supporting disturbing role of short-term air pollution exposure on the regulation of thyroid hormone homeostasis.

Short-term air pollution exposure and mechanisms of plaque instability in acute coronary syndromes: An optical coherence tomography study

Background and aimsAir pollution is emerging as an important risk factor for acute coronary syndrome (ACS). In this study, we investigated the association between short-term air pollution exposure and mechanisms of coronary plaque instability evaluated by optical coherence tomography (OCT) imaging in ACS patients. MethodsPatients with ACS undergoing OCT imaging were retrospectively selected. Mechanism of culprit lesion instability was classified as plaque rupture (PR) or intact fibrous cap (IFC) by OCT. Based on each case's home address, the mean daily exposures to several pollutants, including particulate matter 2.5 (PM2.5), on the same day of ACS and in the immediate days (up to 6 days) prior to the index ACS, were collected. Results139 ACS patients were included [69 (49.6%) had PR and 70 (50.4%) IFC]. Patients with PR, compared to those with IFC, had higher PM2.5 exposure levels on the same day of ACS, without differences in the immediate 6 days before index ACS. At multivariate analysis, PM2.5 exposure on the same day of ACS was the only independent predictor of PR [OR = 1.912 per SD (8.6 μg/m3), CI95 % (1.087–3.364), p = 0.025]. Patients with PR presented a steady increase in PM2.5 daily exposure levels in the days preceding the occurrence of ACS, with a peak the day of ACS (p for trend = 0.042) ConclusionsThis study demonstrates for the first time that a higher short-term PM2.5 exposure, on the same day of ACS, is associated with an increased risk of PR as a pathobiological mechanism of coronary plaque instability.

Effect of ambient air pollution on hospital admission for respiratory diseases in Hanoi children during 2007–2019

Air pollution poses a threat to children's respiratory health. This study aims to quantify the association between short-term air pollution exposure and respiratory hospital admissions among children in Hanoi, Vietnam, and estimate the population-attributable burden using local data. A case-crossover analysis was conducted based on the individual records where each case is their own control. The health data was obtained from 13 hospitals in Hanoi and air pollution data was collected from four monitoring stations from 2007 to 2019. We used conditional logistic regression to estimate Percentage Change (PC) and 95% Confidence Interval (CI) in odd of hospital admissions per 10 μg/m3 increase in daily average particulate matter (e.g. PM1, PM2.5, PM10), Sulfur Dioxide (SO2), Nitrogen Dioxide (NO2), 8-h maximum Ozone and per 1000 μg/m3 increase in daily mean of Carbon Monoxide (CO). We also calculated the number and fraction of admissions attributed to air pollution in Hanoi by using the coefficient at lag 0. A 10 μg/m3 increase in the concentration of PM10, PM2.5, PM1, SO2, NO2, O3 8-h maximum and 1000 μg/m3 increase in CO concentration was associated with 0.6%, 1.2%, 1.4%, 0.8%, 1.6%, 0.3%, and 1.7% increase in odd of admission for all respiratory diseases among children under 16 years at lag 0–2. All PM metrics and NO2 are associated with childhood admission for pneumonia and bronchitis. Admissions due to asthma and upper respiratory diseases are related to increments in NO2 and CO. For attributable cases, PM2.5 concentrations in Hanoi exceeding the World Health Organization Air Quality Guidelines accounted for 1619 respiratory hospital admissions in Hanoi children in 2019. Our findings show that air pollution has a detrimental impact on the respiratory health of Hanoi children and there will be important health benefits from improved air quality management planning to reduce air pollution in Vietnam.

The modification effect of fasting blood glucose level on the associations between short-term ambient air pollution and blood lipids

ABSTRACT The association between short-term ambient air pollution (AAP) exposure and blood lipids is inconsistent across populations. This study aimed to investigate the modifying effects of fasting blood glucose (FBG) levels on the associations between short-term AAP exposure and blood lipids in 110,637 male participants from Beijing, China. The results showed that FBG modified the association between short-term AAP exposure and blood lipids, especially low-density lipoprotein cholesterol (LDL-C). In the hyperglycemia group, a 10-μg/m3 increase in particles with diameters ≤ 2.5 μm (PM2.5), particles with diameters ≤ 10 μm (PM10), sulfur dioxide (SO2), nitrogen dioxide (NO2), or a 1-mg/m3 increase in carbon monoxide (CO) was associated with a 0.454%, 0.305%, 1.507%, 0.872%, or 3.961% increase in LDL-C, respectively. In the nonhyperglycemic group, short-term increases in air pollutants were even associated with small decreases in LDL-C. The findings demonstrate that lipids in hyperglycemic individuals are more vulnerable to short-term AAP exposure than those in normal populations.

Abstract 14863: Omega-3 Fatty Acids Intake and Oxylipins Production in Response to Short-Term Ambient Air Pollution Exposure in Healthy Adults

Rationale: Exposure to air pollution is associated with adverse health effects through systemic inflammation and oxidative stress. One mechanism of beneficial effects of omega-3 polyunsaturated fatty acids (n-3 FA) is mediated via their inflammation resolution process by generating bioactive lipid mediators known as oxylipins. Objective: This study examined the association between n-3 FA-derived bioactive oxylipins and short-term exposure to ambient air pollution in healthy adults. Methods: Fifteen healthy adults were enrolled into either high or low n-3 groups based on n-3 FA intake and the participants underwent 4-5 blood collections for lipidomic profile of 55 oxylipins. Associations between ambient ozone, nitrogen dioxide (NO 2 ), and fine particulate matter (PM 2.5 ) levels and plasma oxylipins were assessed using mixed-effects models stratified by fatty acids levels. Results: Average concentrations of ozone (40.8±11.1 ppb), NO 2 (5.3±3.8 ppb), and PM 2.5 (10.2±4.1 μg/m 3 ) were below national ambient air quality standards during the study period. Compared to the low n-3 group exposed to ozone and PM 2.5 , high n-3 group had significant reduction in arachidonic acids (AA) derived pro-inflammatory oxylipins produced by lipoxygenase (LOX). For instance, 12 HETE was negatively associated with ozone levels [for an IQR increase in ozone, -58.1% (95% CI:-96.8, -19.4) vs. 14.5% (95% CI:-33, 62)] and PM 2.5 concentrations [for an IQR increase in PM 2.5 , -29.6% (95% CI:-49.1, -10.1) vs. 28.5% (95% CI:-3.8, 60.9)] at lag4 in the high n-3 group while the association was null in the low n-3 group. In contrast, high n-3 group exposed to ozone and PM 2.5 had significant increases in EPA and DHA derived pro-resolving oxylipins produced by LOX and cytochrome p450 (CYP) and soluble epoxide hydrolase (sEH) compared to the low n-3 group. Conclusions: We observed negative associations between short-term ambient air pollutants and pro-inflammatory oxylipins in the high n-3 groups, while the associations between short-term ambient air pollutants and pro-resolving oxylipins were positive in the high n-3 groups, suggesting that n-3 derived lipid mediators may mediate the inflammation resolution process in response to low levels of ambient air pollution in healthy adults.