Short-term Air Pollution Exposure Research Articles

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.

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.

Effects of short-term air pollution exposure on symptoms development in the course of idiopathic pulmonary fibrosis

ABSTRACT Background Lately a potential detrimental effect of air pollution to idiopathic pulmonary fibrosis emerged. We aimed to assess the effects of short-term air pollution exposure to the clinical course of IPF. Research design and methods IPF patients were followed intensively for four nonconsecutive study periods between 13 July 2020 and 5 September 2021. Short-term exposure to O3, NO2 and PM10 concentrations was estimated using spatio-temporal land use regression models. Associations among symptoms, lung function, oxygen saturation, and short-term personal air pollutant exposure were assessed through multiple mixed effects logistic regression models. Results Data for up to 24 IPF patients (mean age: 72.2 ± 7.6 years) were analyzed. We detected positive significant associations between cough and a 10 μg/m3 increase in same day mean level of NO2 (OR = 1.59, 95%CI: 1.00–2.53), PM10 (OR = 2.42, 95%CI: 1.54–3.79), and O3 (OR = 1.63, 95%CI: 1.14–2.32). A 10 μg/m3 increase in same day mean level of NO2 was also associated with the risk of appearance of wheezing (OR = 3.01, 95%CI: 1.00–9.04), while exposure to O3 was associated with common cold (OR = 6.30, 95%CI: 3.59–11.07). No significant associations were detected between short-term exposure to air pollutants and forced vital capacity or saturation of oxygen. Conclusions Short-term exposure to increased concentrations of air pollutants is an independent risk factor for IPF symptoms' aggravation.

The influence of PM2.5 exposure duration and concentration on outpatient visits of urban hospital in a typical heavy industrial city.

To explain the duration and dose effects of pollutant exposure on public health and provide scientific data for air pollution prevention and control and disease prevention by examining the influence of PM2.5 concentration and exposure duration on daily outpatient visits among patients with cardiovascular, cerebrovascular, and respiratory diseases in a typical heavy industrial city in China. Daily outpatient data on cardiovascular, cerebrovascular, and respiratory diseases and regional PM2.5 exposure duration and concentration were collected from a provincial hospital in Taiyuan, China, from 2016 to 2021. The correlations of numeric variables were analyzed using the Pearson correlation method. A generalized additive model (GAMs) was also established to investigate the effects of PM2.5 concentration and exposure duration on outpatient visits. Correlation analysis showed that the outpatient visits in Taiyuan was significantly correlated with the PM2.5 concentration and exposure duration. The longer the exposure time of PM2.5 pollution, the stronger the correlation of PM2.5 with outpatient visits showed. Cardiovascular outpatient visits were extremely significant related with medium to long-term exposure of PM2.5 (exposure with more than 30days) (p < 0.001). In addition, outpatient visits of cerebrovascular and respiratory disease were extremely significant correlated with PM2.5 (exposures within 0-360days) (p < 0.001). The results of GAMs showed the linear or the nonlinear relationships between outpatient visits and exposure of PM2.5. Among the linear relationships, when average concentration of PM2.5 (exposure within less than 15days) increased by 1mg/m3, the cardiovascular outpatient visits increased most dramatically (by about 440 people). For nonlinear relationships, when the average PM2.5 concentration (exposure with over 30days or more) increased by 1mg/m3, the most dramatic increase occurred in cardiovascular outpatient visits (with a maximum increase of 7000), followed by cerebrovascular outpatient visits (with a maximum increase of 1200), and respiratory outpatient visits (with a maximum increase of 250). The GAMs also revealed a dose effect in the relationship between outpatient visits and PM2.5 exposure. In moderately polluted air (based on air quality standards of China, GB3095-2012), when the average concentration of PM2.5 increased by 1mg/m3, the cardiovascular outpatient visits increased the most (by 1200 people), followed by cerebrovascular outpatient visits (by 200 people) and respiratory outpatient visits (by 20 people). We concluded that outpatient visits in cardiovascular, cerebrovascular, and respiratory disease are closely correlated with the concentration and exposure duration of air pollution. There is a linear relationship between short-term air pollution exposure (exposure within less than 15days) and outpatient visits. As PM2.5 concentration increases, cardiovascular outpatient visits increase gradually, with its growth trend exceeding that of cerebrovascular and respiratory disease. There is a nonlinear relationship between medium and long-term air pollution exposure (exposure with more than 30days) and outpatient visits, with cardiovascular and cerebrovascular outpatient visits showed a nonlinear but overall upward trend when the atmosphere is moderately polluted.

Short-term air pollution exposure and mortality in Brazil: Investigating the susceptible population groups

This is the first study to examine the association between ambient air pollution (PM2.5, O3, and NO2) and mortality (in different population groups by sex and age) based on a nationwide death record across Brazil over a 15-year period (2003–2017). We used a time-series analytic approach with a distributed lag model. Our study population includes 2,872,084 records of deaths in Brazil between 2003 and 2017. Men accounted for a higher proportion of deaths, with 58% for all-cause mortality, 54% for respiratory mortality, and 52% for circulatory mortality. Most individuals were over 65 years of age. Our results suggest an association between air pollution and mortality in Brazil. The direction, statistical significance, and effect size of these associations varied considerably by type of air pollutant, region, and population group (sex and age group). In particular, the older population group (>65 years) was most affected. The national meta-analysis for the entire data set (without stratification by sex and age) showed that for every 10 μg/m3 increase in PM2.5 concentration, the risk of death from respiratory diseases increased by 2.93% (95%CI: 1.42; 4.43). For every 10 ppb increase in O3, there is a 2.21% (95%CI: 0.59; 3.83) increase in the risk of all-cause mortality for the group of all people between 46 and 65 years old, and a 3.53% (95%CI: 0.34; 6.72) increase in the risk of circulatory mortality for the group of women, all ages. For every 10 ppb increase in NO2, the risk of respiratory mortality increases by 17.56% (95%CI: 4.44; 30.64) and the risk of all-cause mortality by 5.63% (95%CI: 1.83; 9.44). The results of our study provide epidemiological evidence that air pollution is associated with a higher risk of cardiorespiratory mortality in Brazil. Given the lack of nationwide studies on air pollution in Brazil, our research is an important contribution to the local and international literature that can provide better support to policymakers to improve air quality and public health.

Short-Term Ambient Air Pollution Exposure and Risk of Out-of-Hospital Cardiac Arrest in Sweden: A Nationwide Case-Crossover Study.

Background Air pollution is one of the main risk factors for cardiovascular disease globally, but its association with out-of-hospital cardiac arrest at low air pollution levels is unclear. This nationwide study in Sweden aims to investigate if air pollution is associated with a higher risk of out-of-hospital cardiac arrest in an area with relatively low air pollution levels. Methods and Results This study was a nationwide time-stratified case-crossover study investigating the association between short-term air pollution exposures and out-of-hospital cardiac arrest using data from the SRCR (Swedish Registry for Cardiopulmonary Resuscitation) between 2009 and 2019. Daily air pollution levels were estimated in 1×1-km grids for all of Sweden using a satellite-based machine learning model. The association between daily air pollutant levels and out-of-hospital cardiac arrest was quantified using conditional logistic regression adjusted for daily air temperature. Particulate matter <2.5 μm exposure was associated with a higher risk of out-of-hospital cardiac arrest among a total of 29 604 cases. In a multipollutant model, the association was most pronounced for intermediate daily lags, with an increased relative risk of 6.2% (95% CI, 1.0-11.8) per 10 μg/m3 increase of particulate matter <2.5 μm 4 days before the event. A similar pattern of association was observed for particulate matter <10 μm. No clear association was observed for O3 and NO2. Conclusions Short-term exposure to air pollution was associated with higher risk of out-of-hospital cardiac arrest. The findings add to the evidence of an adverse effect of particulate matter on out-of-hospital cardiac arrest, even at very low levels below current regulatory standards.

Short-term effects of air pollution on hospitalization of children with acute upper respiratory infections: A time series analysis in Lanzhou, China.

Short-term air pollution exposure is correlated with childhood acute upper respiratory infections (AURI) hospitalizations. We surveyed the relationship between AURI hospitalizations and air pollutant concentrations in children aged 0-14 years from 1 January 2014 to 31 December 2019 in Lanzhou City. We collected both data on air pollutant concentrations and children's AURI hospitalizations during the study period. Distributional lagged nonlinear models were adopted to assess the short-term effects of air pollutants on children's AURI hospitalizations. We also performed subgroup analysis and sensitivity analysis. A total of 15,881 children were hospitalized for AURI during the study period. The results showed that for each 10 µg/m3 increase in PM2.5 , SO2 , and NO2 concentrations at lag0-6, the relative risk (RR) values for children hospitalized for AURI were RR = 1.0247 (95% CI: 1.0092,1.0405), RR = 1.0928 (95% CI: 1.0562, 1.1308), and RR = 1.0715 (95% CI: 1.0495, 1.0940), respectively. PM10 was significantly associated with AURI hospitalization in children only at lag0, RR = 1.0028 (95% CI: 1.0000, 1.0056). Short-term exposures to PM2.5 , PM10 , SO2 , and NO2 all increase the risk of AURI hospitalization in children variously.

An update on the association between ambient short-term air pollution exposure and daily outpatient visits for conjunctivitis: a time-series study in Hangzhou, China.

Air pollution is a major public health problem that can lead to conjunctivitis. This study aimed to explore the associations between air pollutants and outpatient visits for conjunctivitis in Hangzhou, China. This study collected data on 50,772 patients with conjunctivitis and the concentrations of six air pollutants from February 1, 2014, to August 31, 2018. A time series analysis using a generalized additive model (GAM) was conducted. We found that the risk of conjunctivitis was related to the air pollutants PM2.5, PM10, SO2, NO2, and O3, which had concentration hysteresis effects. The risk of conjunctivitis increased by 1.009 (95% confidence interval (CI): 1.003, 1.014), 1.011 (95% CI: 1.008, 1.015), 1.238 (95% CI: 1.186, 1.292), 1.028 (95% CI: 1.019, 1.038), and 1.013 (95% CI: 1.008, 1.017) for every 10µg/m3 increase in PM2.5, PM10, SO2, NO2, and O3 concentrations, respectively. The lag effects of SO2 and NO2 were stronger than those of particulate matter. Females exposed to PM10, PM2.5, SO2, and O3 had a higher risk of conjunctivitis than males, while males exposed to NO2 had a nearly identical risk of conjunctivitis as females. People aged 19-59 were more likely to suffer from conjunctivitis. The risk of conjunctivitis caused by PM10, SO2, and O3 was highest in the transitional season, while the risk caused by NO2 was highest in the winter season. In conclusion, females and middle-aged adults were at higher risk of conjunctivitis. People were more susceptible to conjunctivitis during the transitional season. These findings highlight the importance of atmospheric pollution governance and reference for public health measures.

Criteria air pollutants and diabetes mortality classified by different subtypes and complications: A nationwide, case-crossover study

The associations between air pollution and diabetes mortality of different subtypes and complications were largely unclear. We performed an individual-level, time-stratified case-crossover study among over 0.9 million diabetes deaths from all administrative regions of Chinese mainland during 2013–2019. Daily concentrations of fine particles (PM2.5), coarse particles (PM2.5–10), nitrogen dioxide (NO2) and ozone (O3) were obtained for each decedent using high-resolution prediction models. Conditional logistic regression models were utilized to analyze the data. Each interquartile range increment in PM2.5, PM2.5–10, NO2 and O3 concentrations on lag 0–2 d increased the risks of overall diabetes mortality by 2.81 %, 1.92 %, 3.96 % and 2.15 %, respectively. Type 2 diabetes had stronger associations with air pollution than type 1 diabetes. Air pollutants were associated with diabetic ketoacidosis and diabetic nephropathy, but not other complications. The exposure-response curves were approximately linear with a plateau at higher concentrations of PM2.5, PM2.5–10, and NO2, while the associations for O3 appear to be statistically significant beyond 60 μg/m3. This nationwide study reinforces the evidence of higher risks of acute diabetic events following short-term air pollution exposure. We identified differential effects of air pollutants on various subtypes and complications of diabetes, which require further mechanistic investigations.

Effect of short-term ambient air pollution exposure on early miscarriage and pregnancy hormones with critical window identification

BackgroundPregnancy hormones are particularly important in early miscarriage, and some evidence suggests that exposure to air pollution is associated with pregnancy hormones and miscarriage. However, the effects of air pollution on pregnancy hormone-mediated miscarriages have not yet been investigated. MethodsWe collected air pollution exposure measurements and pregnancy hormone tests from the participants. Logistic regression models were used to investigate the association between air pollution and early miscarriages. A distributed lag nonlinear model (DLNM) was used to investigate non-linear and delayed associations and identify the crucial window. We performed mediation analysis to estimate the potential association that may exist between pregnancy hormone levels and early miscarriage. ResultsShort-term exposure to CO and SO2 was associated with early miscarriage. Lag 22–28 days of exposure to both CO and SO2 and lag 15–21 days of exposure to CO were significantly positively associated with early miscarriage, with an obvious exposure dose response. Serum progesterone concentration explained 36.79 % of the association between lag 15–28 days of CO exposure and early miscarriage. ConclusionThis study provides evidence for the association between short-term exposure to air pollution and early miscarriage, and provides clues for further exploration of biological mechanisms.

Pro-inflammation and pro-atherosclerotic responses to short-term air pollution exposure associated with alterations in sphingolipid ceramides and neutrophil extracellular traps

Air pollution has been associated with the development of atherosclerosis; however, the pathophysiological mechanisms underlying pro-atherosclerotic effects of air pollution exposure remain unclear. We conducted a prospective panel study in Beijing and recruited 152 participants with four monthly visits from September 2019 to January 2020. Linear mixed-effect models were applied to estimate the associations linking short-term air pollution exposure to biomarkers relevant to ceramide metabolism, pro-inflammation (neutrophil extracellular traps formation and systemic inflammation) and pro-atherosclerotic responses (endothelial stimulation, plaque instability, coagulation activation, and elevated blood pressure). We further explored whether ceramides and inflammatory indicators could mediate the alterations in the profiles of pro-atherosclerotic responses. We found that significant increases in levels of circulating ceramides of 9.7% (95% CIs: 0.7, 19.5) to 96.9% (95% CIs: 23.1, 214.9) were associated with interquartile range increases in moving averages of ambient air pollutant metrics, including fine particulate matter (PM2.5), black carbon, particles in size fractions of 100–560 nm, nitrogen dioxide, carbon monoxide and sulfur dioxide at prior up to 7 days. Higher air pollution levels were also associated with activated neutrophils (increases in citrullinated histone H3, neutrophil elastase, double-stranded DNA, and myeloperoxidase) and exacerbation of pro-atherosclerotic responses (e.g., increases in vascular endothelial growth factor, lipoprotein-associated phospholipase A2, matrix metalloproteinase-8, P-selectin, and blood pressure). Mediation analyses further showed that dysregulated ceramide metabolism and potentiated inflammation could mediate PM2.5-associated pro-atherosclerotic responses. Our findings extend the understanding on potential mechanisms of air pollution-associated atherosclerosis, and suggest the significance of reducing air pollution as priority in urban environments.

Exploring Associations Between Short-Term Air Pollution and Daily Outpatient Visits for Allergic Rhinitis.

Many studies have reported that exposure to air pollution increases the likelihood of acquiring allergic rhinitis (AR). This study investigated associations between short-term air pollution exposure and AR outpatient visits. The Department of Otorhinolaryngology, Affiliated Hospital of Hangzhou Normal University provided AR outpatient data from January 1, 2019 to December 31, 2021. Daily air quality information for that period was gathered from the Hangzhou Air Quality Inspection Station. We used the Poisson's generalized additive model (GAM) to investigate relationships between daily outpatient AR visits and air pollution, and investigated lag-exposure relationships across days. Subgroup analyses were performed by age (adult (>18 years) and non-adult (<18 years)) and sex (male and female). We recorded 20,653 instances of AR during the study period. Each 10 g/m3 increase in fine particulate matter (PM10 and PM2.5) and carbon monoxide (CO) concentrations was associated with significant increases in AR outpatient Visits. The relative risks (RR) were: 1.007 (95% confidence interval (CI): 1.001-1.013), 1.026 (95% CI: 1.008-1.413), and 1.019 (95% CI: 1.008-1.047). AR visits were more likely due to elevated PM2.5, PM10, and CO levels. Additionally, children were more affected than adults. To better understand the possible effects of air pollution on AR, short-term exposure to ambient air pollution (PM2.5, PM10, and CO) may be linked to increased daily outpatient AR visits.