Particulate Air Pollution Research Articles

Cardiotoxicity Induced by Intratracheal Instillation of Diesel Exhaust Particles in Mice, and the Protective Effects of Carnosol: Suppression of Inflammation and Oxidative and Nitrosative Stress via Modulation of NF-κb/MAPKs Signaling Pathways.

Inhaled particulate air pollution is associated with cardiotoxicity with underlying mechanisms including oxidative stress and inflammation. Carnosol, commonly found in rosemary and sage, is known to possess a broad range of therapeutic properties such as antioxidant, anti-inflammatory and antiapoptotic. However, its cardioprotective effects on diesel exhaust particles (DEPs)-induced toxicity have not been studied yet. Hence, we evaluated the potential ameliorative effects of carnosol on DEPs-induced heart toxicity in mice, and the underlying mechanisms involved. Mice were intratracheally instilled with DEPs (1 mg/kg) or saline, and 1 hour prior to instillation they were given intraperitoneally either carnosol (20 mg/kg) or saline. Twenty-four hours after the DEPs instillation, multiple parameters were evaluated in the heart by enzyme-linked immunosorbent assay, colorimetric assay, Comet assay and Western blot technique. Carnosol has significantly reduced the elevation in the plasma levels of lactate hydrogenase and brain natriuretic peptide induced by DEPs. Likewise, the augmented cardiac levels of proinflammatory cytokines, lipid peroxidation, and total nitric oxide in DEPs-treated groups were significantly normalized with the treatment of carnosol. Moreover, carnosol has markedly reduced the heart mitochondrial dysfunction, as well as DNA damage and apoptosis of mice treated with DEPs. Similarly, carnosol significantly reduced the elevated expressions of phosphorylated nuclear factor-кB (NF-кB) and mitogen-activated protein kinases (MAPKs) in the hearts. Furthermore, the treatment with carnosol has restored the decrease in the expression of sirtuin-1 in the hearts of mice exposed to DEPs. Carnosol significantly attenuated DEP-induced cardiotoxicity in mice by suppressing inflammation, oxidative stress, DNA damage, and apoptosis, at least partly via mechanisms involving sirtuin-1 activation and the inhibition of NF-кB and MAPKs activation.

Causal analysis of air pollution mixtures: estimands, positivity, and extrapolation.

Causal inference for air pollution mixtures is an increasingly important issue with appreciable challenges. When the exposure is a multivariate mixture, there are many exposure contrasts that may be of nominal interest for causal effect estimation, but the complex joint mixture distribution often renders observed data extremely limited in their ability to inform estimates of many commonly defined causal effects. We use potential outcomes to (1) define causal effects of air pollution mixtures, (2) formalize the key assumption of mixture positivity required for estimation, and (3) offer diagnostic metrics for positivity violations in the mixture setting that allow researchers to assess the extent to which data can actually support estimation of mixture effects of interest. For settings where there is limited empirical support, we redefine causal estimands that apportion causal effects according to whether they can be directly informed by observed data versus rely entirely on model extrapolation, isolating key sources of information on the causal effect of an air pollution mixture. The ideas are deployed to assess the ability of a national US data set on the chemical components of ambient particulate matter air pollution to support estimation of a variety of causal mixture effects. This article is part of a Special Collection on Environmental Epidemiology.

Climate Change and Cardiovascular Health

Climate change may increase the risk of adverse cardiovascular outcomes by causing direct physiologic changes, psychological distress, and disruption of health-related infrastructure. Yet, the association between numerous climate change-related environmental stressors and the incidence of adverse cardiovascular events has not been systematically reviewed. To review the current evidence on the association between climate change-related environmental stressors and adverse cardiovascular outcomes. PubMed, Embase, Web of Science, and Cochrane Library were searched to identify peer-reviewed publications from January 1, 1970, through November 15, 2023, that evaluated associations between environmental exposures and cardiovascular mortality, acute cardiovascular events, and related health care utilization. Studies that examined only nonwildfire-sourced particulate air pollution were excluded. Two investigators independently screened 20 798 articles and selected 2564 for full-text review. Study quality was assessed using the Navigation Guide framework. Findings were qualitatively synthesized as substantial differences in study design precluded quantitative meta-analysis. Of 492 observational studies that met inclusion criteria, 182 examined extreme temperature, 210 ground-level ozone, 45 wildfire smoke, and 63 extreme weather events, such as hurricanes, dust storms, and droughts. These studies presented findings from 30 high-income countries, 17 middle-income countries, and 1 low-income country. The strength of evidence was rated as sufficient for extreme temperature; ground-level ozone; tropical storms, hurricanes, and cyclones; and dust storms. Evidence was limited for wildfire smoke and inadequate for drought and mudslides. Exposure to extreme temperature was associated with increased cardiovascular mortality and morbidity, but the magnitude varied with temperature and duration of exposure. Ground-level ozone amplified the risk associated with higher temperatures and vice versa. Extreme weather events, such as hurricanes, were associated with increased cardiovascular risk that persisted for many months after the initial event. Some studies noted a small increase in cardiovascular mortality, out-of-hospital cardiac arrests, and hospitalizations for ischemic heart disease after exposure to wildfire smoke, while others found no association. Older adults, racial and ethnic minoritized populations, and lower-wealth communities were disproportionately affected. Several environmental stressors that are predicted to increase in frequency and intensity with climate change are associated with increased cardiovascular risk, but data on outcomes in low-income countries are lacking. Urgent action is needed to mitigate climate change-associated cardiovascular risk, particularly in vulnerable populations.

Greenspace and risk of obesity-related cancer in the UK Biobank cohort: An analysis of private residential gardens and other greenspace types

BackgroundCohort studies linking greenspace exposure to a lower risk of obesity-related cancer (ORC) are scarce. Existing evidence on site-specific cancers has predominantly relied on non-specific greenspace measures, including vegetation indices. We examined the associations of total greenspace, private residential gardens, and other greenspace types with the risk of being diagnosed with overall and site-specific ORC. MethodsWe used data from the participants in the UK Biobank recruited between 2006 and 2010 and censored until December 31, 2016. We defined greenspace variables using Ordnance Survey MasterMap™ greenspace categories. The incidence of ORC was ascertained through data linkage to cancer registries. Hazard ratios (HRs) and 95 % confidence intervals (CIs) were estimated using Cox proportional hazard models and adjusted for covariates. We conducted mediation and modification analysis by physical activity, serum 25-hydroxyvitamin D [25(OH)D], and particulate matter air pollution with an aerodynamic diameter ≤ 2.5 (PM2.5) and nitrogen dioxide (NO2), as well as subgroup analysis by covariates. ResultsAmong 279,326 participants, 9550 developed ORC over a median follow-up period of 7.82 years. An increase in private residential gardens within a 100 m buffer was associated with a decreased risk of overall ORC (HR:0.92; 95 % CI: 0.88, 0.96), breast cancer (HR: 0.91; 95 % CI: 0.84, 0.98), and uterine cancer (HR:0.80; 95 % CI: 0.67, 0.96). There was no association between other greenspace types and ORC, except for uterine cancer. The association for ORC was partly mediated by NO2 and modified by physical activity levels, 25(OH)D, PM2.5, and NO2, and sociodemographic factors, including sex and neighbourhood socioeconomic status. ConclusionIncreased exposure to private residential gardens may lower the risk of being diagnosed with obesity-related cancer, particularly breast and uterine cancer. Future studies might move beyond considering greenspace quantity to explore functional types of greenspace exposure that should be prioritized for targeted health intervention and cancer prevention.

Light painting photography makes particulate matter air pollution visible

The World Health Organization estimates that air pollution causes approximately seven million premature deaths worldwide each year. Solutions to air pollution are well known, yet this rarely equates to easily actionable. Here we demonstrate how art science collaboration can successfully highlight the issue of air pollution and create wider civic discourse around its amelioration. We document a light painting photographic technique that uses data from calibrated low-cost particulate matter sensors to measure and depict air pollution. We also use a postcard technique to grasp individuals’ sentiments regarding air pollution. The photographs from three countries, Ethiopia, India and United Kingdom, visually highlight the importance of location and occupation upon human exposure. The photographs are used as a proxy to communicate and create dialogues, spaces and places about air pollution. The sentiment analysis shows how this approach can foster awareness and create agency for stakeholders to take actions to tackle air pollution.

Particulate contamination of human placenta: Plastic and non-plastic

Recent evidence indicates that the human womb is contaminated with a variety of particulate contaminants. Microplastics (MPs, tiny plastic particles, 0.1 – 5000 µm) generated by the breakdown of larger plastic products in the environment) accumulation in human placenta has recently been described. In addition, recent evidence has correlated the number of air pollution particulates in term placentas to the loading of these particles in dust from the gestational parent home. The current study sought to characterize the accumulation of plastic and non-plastic particles (NPP) within the term human placenta. Placenta tissues were collected from healthy, singleton pregnancies following vaginal (n = 5) and caesarean section (n = 5) deliveries at a tertiary care centre located in an urban Canadian city (Ottawa, ON), with particles detected and characterized by Raman micro-spectroscopy. Both plastic and non-plastic particles were identified in all placentas examined, with an average of 1 ± 1.2 MPs /g and 4 ± 2.9 NPP /g of tissue. Similar tissue concentrations of MPs and NNP were identified in all regions of the placenta (basal plate, chorionic villous, chorionic plate), and did not differ according to mode of delivery. MPs ranged in size (2 – 60 μm), with the most abundant MPs being polyethylene (PE), polypropylene (PP), polystyrene (PS) and polyvinyl chloride (PVC). The most abundantly identified NPP were carbon, graphite, and lead oxide. Collectively, these results demonstrate the accumulation of foreign particles, including MPs, throughout the human placenta. Given the vital functions of the placenta in supporting fetal growth and development, and a potential for MPs to induce toxicity, further investigations into the potential harmful effects of these environmental toxicants on maternal and fetal health is warranted.

Assessment of the Effect of Meteorological Conditions on the Concentration of Suspended PM2.5 Particulate Matter in Central Europe

The purpose of this study was to use principal component analysis to determine the effect of meteorological elements on the concentration of PM2.5 particulate matter in Krakow, the capital of the Lesser Poland Voivodeship in southern Poland. Daily values for selected meteorological elements measured in spring, summer, autumn, and winter over a 10-year period, obtained from the Institute of Meteorology and Water Management—National Research Institute, were adopted as variables explaining PM2.5 concentrations. Data on particulate air pollution were obtained from the air monitoring station in Krakow. In spring, autumn, and winter, the first factor significantly influencing the PM2.5 concentration was the maximum, minimum, and average temperature. In summer, the average and maximum temperatures were significant. The second factor in spring was precipitation and wind speed, and the third was relative humidity. In summer, the second factor was atmospheric pressure, and the third was relative humidity. The second factor in autumn was atmospheric pressure and precipitation, and the third was relative humidity. In winter, the second factor was wind speed, and the third was precipitation and relative humidity. Throughout the study, the annual mean PM2.5 concentrations exceeded acceptable and target levels defined by the Regulation of the Minister of the Environment, and even further exceeded the level recommended by the WHO.

Fine particulate matter air pollution and health implications for Nairobi, Kenya

Background: Continuous ambient air quality monitoring in Kenya has been limited, resulting in a sparse data base on the health impacts of air pollution for the country. We have operated a centrally located monitor in Nairobi for measuring fine particulate matter (PM2.5), the pollutant that has demonstrated impact on health. Here, we describe the temporal levels and trends in PM2.5 data for Nairobi and evaluate associated health implications. Methods: We used a centrally located reference sensor, the beta attenuation monitor (BAM-1022), to measure hourly PM2.5 concentrations over a 3-year period (21 August 2019 to 20 August 2022). We used, at minimum, 75% of the daily hourly concentration to represent the 24-hour concentrations for a given calendar day. To estimate the deaths attributable to air pollution, we used the World Health Organization (WHO) AirQ+ tool with input as PM2.5 concentration data, local mortality statistics, and population sizes. Results: The daily (24-hour) mean (±SEM) PM2.5 concentration was 19. 2 ± 0.6 (µg/m3). Pollutant levels were lowest at 03:00 and, peaked at 20:00. Sundays had the lowest daily concentrations, which increased on Mondays and remained high through Saturdays. By season, the pollutant concentrations were lowest in April and highest in August. The mean annual concentration was 18.4 ± 7.1 (µg/m3), which was estimated to lead to between 400 and 1,400 premature deaths of the city’s population in 2021 hence contributing 5%–8% of the 17,432 adult deaths excluding accidents when referenced to WHO recommended 2021 air quality guideline for annual thresholds of 5 µg/m3. Conclusion: Fine particulate matter air pollution in Nairobi showed daily, day-of-week, and seasonal fluctuations consistent with the anthropogenic source mix, particularly from motor vehicles. The long-term population exposure to PM2.5 was 3.7 times higher than the WHO annual guideline of 5 µg/m3 and estimated to lead to a substantial burden of attributable deaths. An updated regulation targeting measures to reduce vehicular emissions is recommended.

Gene-environment interactions between clonal hematopoiesis of indeterminate potential and air pollution in non-small cell lung cancer among non-smokers.

10514 Background: Small particulate matter air pollution (≤ 2.5µm diameter; PM2.5) is a recognized driver of non-small cell lung cancer (NSCLC) among non-smokers. PM2.5 recruits pro-inflammatory macrophages to the lungs, which facilitate the clonal expansion of mutated epithelial cells and eventual transformation to NSCLC. Clonal hematopoiesis of indeterminate potential (CHIP) is a common age-related condition caused by the acquisition of somatic mutations in hematopoietic stem cells. CHIP and its accompanying pro-inflammatory phenotype have been linked with various age-related diseases, including incident NSCLC; however, the mechanisms underlying this relationship are unknown. In this study, we aimed to explore the interaction between CHIP and exposure to PM2.5 in the development of incident NSCLC. Methods: This study was conducted using data from participants in the UK Biobank (n = 451,095). CHIP status was determined from peripheral blood whole exome sequencing data, and defined as the presence of a somatic driver mutation in the blood at variant allele frequency (VAF) ≥2% (PMID: 36652671). Incident NSCLC was determined from UK cancer registry data, and PM2.5 exposure was determined based on ambient regional measures from 2010. Cox proportional hazard models were used to evaluate associations between CHIP, PM2.5, and NSCLC. Proteomics data was measured using OLINK proteomics in a subset of UK Biobank participants (n = 44,625). Results: CHIP was prevalent in 3.4% of UK Biobank participants (n = 15,633; never smokers: 3.0%, n = 6,916/227,133). There were 1983 incident cases of NSCLC (never smokers: n = 307). CHIP status was associated with incident NSCLC when adjusting for smoking status (HR = 1.73, 95% CI: 1.48–2.02) and analyzing exclusively non-smokers (HR = 2.01, 95% CI: 1.34-3.00). PM2.5 levels were not associated with NSCLC in non-smokers (HR = 1.00, 95% CI: 0.89–1.12 per µg/m3 increase in PM2.5); however, there was a significant interaction between PM2.5 and CHIP (HR = 1.46, 95% CI: 1.02–2.11, pint = 0.04), suggesting that it is the interplay between the two that drives incident NSCLC risk. We found no association between PM2.5 levels and increased CHIP prevalence or CHIP VAF. PM2.5 and CHIP were also found to interact to increase systemic inflammatory markers C-reactive peptide (pint = 0.01) and IL-6 (pint = 0.002). Conclusions: PM2.5 and CHIP act as a novel gene x environment interaction pair that play a key role in NSCLC etiology among non-smokers. Rather than acting in isolation to increase risk of NSCLC, PM2.5 intensifies the relationship between CHIP and NSCLC, presumably by exacerbating systemic inflammation and the hyper-inflammatory lung microenvironment. With PM2.5 levels in the UK among the lowest in the world, we posit that the CHIP x PM2.5 interaction contributes substantially to the global burden of NSCLC in non-smokers.

Palliative effects of carnosol on lung-deposited pollutant particles-induced thrombogenicity and vascular injury in mice.

The toxicity of inhaled particulate air pollution perseveres even at lower concentrations than those of the existing air quality limit. Therefore, the identification of safe and effective measures against pollutant particles-induced vascular toxicity is warranted. Carnosol is a bioactive phenolic diterpene found in rosemary herb, with anti-inflammatory and antioxidant actions. However, its possible protective effect on the thrombotic and vascular injury induced by diesel exhaust particles (DEP) has not been studied before. We assessed here the potential alleviating effect of carnosol (20 mg/kg) administered intraperitoneally 1 h before intratracheal (i.t.) instillation of DEP (20 μg/mouse). Twenty-four hours after the administration of DEP, various parameters were assessed. Carnosol administration prevented the increase in the plasma concentrations of C-reactive protein, fibrinogen, and tissue factor induced by DEP exposure. Carnosol inhibited DEP-induced prothrombotic effects in pial microvessels invivo and platelet aggregation invitro. The shortening of activated partial thromboplastin time and prothrombin time induced by DEP was abated by carnosol administration. Carnosol inhibited the increase in pro-inflammatory cytokines (interleukin-6 and tumor necrosis factor α) and adhesion molecules (intercellular adhesion molecule-1, vascular cell adhesion molecule-1, E-selectin, and P-selectin) in aortic tissue. Moreover, it averted the effects of DEP-induced increase of thiobarbituric acid reactive substances, depletion of antioxidants and DNA damage in the aortic tissue. Likewise, carnosol prevented the decrease in the expression of nuclear factor erythroid 2-related factor 2 (Nrf2) and heme oxygenase-1 (HO-1) caused by DEP. We conclude that carnosol alleviates DEP-induced thrombogenicity and vascular inflammation, oxidative damage, and DNA injury through Nrf2 and HO-1 activation.

Successful cultivation of edible fungi on textile waste offers a new avenue for bioremediation and potential food production

Textile waste contains both natural fibres such as cotton and bamboo viscose, and synthetic fibres such as elastane and polyester. As a complex mixture, textiles present a challenging pollution issue as breakdown in landfill results in microplastics entering water and soil environments, and incineration results in particulate air pollution. Here the use of edible fungi as bioremediation agents of waste textiles is described for the first time. Three species of filamentous fungi were shown to colonise and grow on mixed fibre textile waste (underpants made from 28% cotton: 68% bamboo viscose: 4% elastane). All three fungi were able to metabolise the common textile dye Reactive Black 5 to some extent. The metabolome was captured to elucidate the dye remediation pathway utilized and to characterise the volatiles released during bioremediation with a view to assessing the safety profile of this process for future industrial applications. The results suggest that edible fungi may be cultivated on textiles, and that some interesting and useful compounds may be produced in the process. This has great biotechnological potential. No mushrooms were produced in this study, suggesting that further work will be needed to optimise conditions for crop production from waste textiles.

The pressure drop of fibrous surface filters for gas Filtration: Modeling and experimental studies

Surface filters are extensively utilized for the control of particulate matter and air pollution, and predicting the pressure drop can offer theoretical guidance in the selection of operational parameters for fibrous surface filters. However, there is presently a dearth of efficient and user-friendly methods for predicting the pressure drop. This paper focuses on the accurate and convenient prediction of the pressure drop of fibrous surface filters for gas filtration. Firstly, an analytical model for pressure drop, including the blocked fiber layer and the dust cake, was developed by considering the characteristics of the filter media, dust properties, and loading conditions. The model was validated through laboratory experiments, and the relative error between the model values and experimental data remains within a 15% error. Furthermore, based on the model, the quantitative analysis of the relationship between the pressure drop of the fiber layer and the pressure drop of the dust cake, and the filtration parameter importance were conducted. The influence of filtration parameters on the pressure drop follows the order of filtration velocity, dust concentration, and dust particle size, which provides guidance for choosing the gas filtration operating conditions in the efficient and low-resistance operation of surface filters. Additionally, the model was validated through field test data collected with large-scale cartridge filters in bulk grain loading. The predicted values fit well with the field test results. Overall, this study provides a promising tool for predicting the pressure drop of fibrous surface filters.

Measuring global monetary damages from particulate matter and carbon dioxide emissions to track sustainable growth

An integrated framework that tracks global stocks and flows of natural capital is needed to assess sustainable economic growth. Here, we develop a set of globally comprehensive monetary damages from particulate matter air pollution and greenhouse gas emissions in 165 countries from 1998 to 2018. Our results show that pollution intensity began to rise after a decade during which the global economy became less pollution-intensive from the late 1990s until the Great Recession. Larger economic production shares and higher pollution intensity in China and India drove this change. Deducting pollution damage from output from the late 1990s until the Great Recession yields higher growth estimates. After the Great Recession, this adjustment for pollution damage attenuated growth. We show that modeling monetary damages instead of physical measures of environmental quality affects inferences about sustainable development. Further, the monetary damages from exposure to particulate emissions peak earlier in the development path than damages due to carbon dioxide emissions. Monetary damages peak later than physical measures of both pollutants. For carbon dioxide, per capita emissions maximize at just over 60,000 dollars while monetary damages peak at nearly 80,000 dollars. In 2018, all but two countries were below this income level. Our results suggest that the global economy is likely to exhibit rising damages from particulates and carbon dioxide emissions in the years to come as nations grow and develop.

Does socioeconomic and environmental burden affect vulnerability to extreme air pollution and heat? A case-crossover study of mortality in California.

Extreme heat and air pollution is associated with increased mortality. Recent evidence suggests the combined effects of both is greater than the effects of each individual exposure. Low neighborhood socioeconomic status ("socioeconomic burden") has also been associated with increased exposure and vulnerability to both heat and air pollution. We investigated if neighborhood socioeconomic burden or the combination of socioeconomic and environmental exposures ("socioenvironmental burden") modified the effect of combined exposure to extreme heat and particulate air pollution on mortality in California. We used a time-stratified case-crossover design to assess the impact of daily exposure to extreme particulate matter <2.5 μm (PM2.5) and heat on cardiovascular, respiratory, and all-cause mortality in California 2014-2019. Daily average PM2.5 and maximum temperatures based on decedent's residential census tract were dichotomized as extreme or not. Census tract-level socioenvironmental and socioeconomic burden was assessed with the CalEnviroScreen (CES) score and a social deprivation index (SDI), and individual educational attainment was derived from death certificates. Conditional logistic regression was used to estimate associations of heat and PM2.5 with mortality with a product term used to evaluate effect measure modification. During the study period 1,514,292 all-cause deaths could be assigned residential exposures. Extreme heat and air pollution alone and combined were associated with increased mortality, matching prior reports. Decedents in census tracts with higher socioenvironmental and socioeconomic burden experienced more days with extreme PM2.5 exposure. However, we found no consistent effect measure modification by CES or SDI on combined or separate extreme heat and PM2.5 exposure on odds of total, cardiovascular or respiratory mortality. No effect measure modification was observed for individual education attainment. We did not find evidence that neighborhood socioenvironmental- or socioeconomic burden significantly influenced the individual or combined impact of extreme exposures to heat and PM2.5 on mortality in California. We investigated the effect measure modification by socioeconomic and socioenvironmental of the co-occurrence of heat and PM2.5, which adds support to the limited previous literature on effect measure modification by socioeconomic and socioenvironmental burden of heat alone and PM2.5 alone. We found no consistent effect measure modification by neighborhood socioenvironmental and socioeconomic burden or individual level SES of the mortality association with extreme heat and PM2.5 co-exposure. However, we did find increased number of days with extreme PM2.5 exposure in neighborhoods with high socioenvironmental and socioeconomic burden. We evaluated multiple area-level and an individual-level SES and socioenvironmental burden metrics, each estimating socioenvironmental factors differently, making our conclusion more robust.

Differential associations of fine and coarse particulate air pollution with cause-specific pneumonia mortality: A nationwide, individual-level, case-crossover study

BackgroundThe connections between fine particulate matter (PM2.5) and coarse particulate matter (PM2.5-10) and daily mortality of viral pneumonia and bacterial pneumonia were unclear. ObjectivesTo distinguish the connections between PM2.5 and PM2.5-10 and daily mortality due to viral pneumonia and bacterial pneumonia. MethodsUsing a comprehensive national death registry encompassing all areas of mainland China, we conducted a case-crossover investigation from 2013 to 2019 at an individual level. Residential daily particle concentrations were evaluated using satellite-based models with a spatial resolution of 1 km. To analyze the data, we employed the conditional logistic regression model in conjunction with polynomial distributed lag models. ResultsWe included 221,507 pneumonia deaths in China. Every interquartile range (IQR) elevation in concentrations of PM2.5 (lag 0–2 d, 37.6 μg/m3) was associated with higher magnitude of mortality for viral pneumonia (3.03%) than bacterial pneumonia (2.14%), whereas the difference was not significant (p-value for difference = 0.38). An IQR increase in concentrations of PM2.5-10 (lag 0–2 d, 28.4 μg/m3) was also linked to higher magnitude of mortality from viral pneumonia (3.06%) compared to bacterial pneumonia (2.31%), whereas the difference was not significant (p-value for difference = 0.52). After controlling for gaseous pollutants, their effects were all stable; however, with mutual adjustment, the associations of PM2.5 remained, and those of PM2.5-10 were no longer statistically significant. Greater magnitude of associations was noted in individuals aged 75 years and above, as well as during the cold season. ConclusionThis nationwide study presents compelling evidence that both PM2.5 and PM2.5-10 exposures could increase pneumonia mortality of viral and bacterial causes, highlighting the more robust effects of PM2.5 and somewhat higher sensitivity of viral pneumonia.

Dust Storm Effects on Air Quality and Particulate Matter Pollution in Babylon Governorate, Iraq

Dust, a major pollutant in urban air, is a recent weather phenomenon in specific areas. Dust particles with diameters ranging from 100 to 1000 microns can injure crops and clog streams, polluting them with heavy metals and other pollutants. The province of Babylon, located in central Iraq, was the focus of this study. Three stations (A1, A2, A3) were selected within a governorate to measure the concentration of pollutants during dust storms. 26 samples were collected for three months during the summer of 2022. Our finding revealed that the average of CO2, SO2, and NO2, compared with National Ambiment Air Quality and World Health Organization, show that these averages were lower than the limits at the study area. The mean Partuclate Matter, PM 2.5 concentration in the study region was 85.14µg/m3, which was contrasted with National Ambiment Air Quality and the findings showed that the PM concentrations were above the limit. The existence of several petrol stations, in addition to stations for producing power, in addition to the plastics industrial facilities along with other industries and car maintenance shops, is the cause for this increase, particularly in station A3. The Air Quality Index for the study region in three stations occurred within the Yellow color range, indicating that there are few or none impact on the general population's health.

Lung function benefits of traditional Chinese medicine Qiju granules against fine particulate air pollution exposure: a randomized controlled trial.

Multiple targets are considered as the causes of ambient fine particulate matter [aerodynamic diameters of < 2.5 μm (PM2.5)] induced lung function injury. Qiju granules are derived from the traditional Chinese medicine (TCM) formula known as Qi-Ju-Di-Huang-Wan (Lycium, Chrysanthemum, and Rehmannia Formula, QJDHW), which has been traditionally used to treat symptoms such as cough with phlegm, dry mouth and throat, and liver heat. This treatment approach involves attenuating inflammation, oxidative stress, and fibrosis response. This study investigated the effects of Qiju granules on protecting lung function against PM2.5 exposure in a clinical trial. A randomized, double-blinded, and placebo-controlled trial was performed among 47 healthy college students in Hangzhou, Zhejiang Province in China. The participants were randomly assigned to the Qiju granules group or the control group based on gender. Clinical follow-ups were conducted once every 2 weeks during a total of 4 weeks of intervention. Real-time monitoring of PM2.5 concentrations in the individually exposed participants was carried out. Data on individual characteristics, heart rate (HR), blood pressure (BP), and lung function at baseline and during the follow-ups were collected. The effects of PM2.5 exposure on lung function were assessed within each group using linear mixed-effect models. In total, 40 eligible participants completed the scheduled follow-ups. The average PM2.5 level was found to be 64.72 μg/m3 during the study period. A significant negative correlation of lung function with PM2.5 exposure concentrations was observed, and a 1-week lag effect was observed. Forced expiratory volume in one second (FEV1), peak expiratory flow (PEF), maximal mid-expiratory flow (MMEF), forced expiratory flow at 75% of forced vital capacity (FVC) (FEF75), forced expiratory flow at 50% of FVC (FEF50), and forced expiratory flow at 25% of FVC (FEF25) were significantly decreased due to PM2.5 exposure in the control group. Small airway function was impaired more seriously than large airway function when PM2.5 exposure concentrations were increased. In the Qiju granules group, the associations between lung function and PM2.5 exposure were much weaker, and no statistical significance was observed. The results of the study showed that PM2.5 exposure was associated with reduced lung function. Qiju granules could potentially be effective in protecting lung functions from the adverse effects of PM2.5 exposure. identifier: ChiCTR1900021235.

Molecular-Level Insights into the Relationship between Volatility of Organic Aerosol Constituents and PM2.5 Air Pollution Levels: A Study with Ultrahigh-Resolution Mass Spectrometry.

Volatility of organic aerosols (OAs) significantly influences new particle formation and the occurrence of particulate air pollution. However, the relationship between the volatility of OA and the level of particulate air pollution (i.e., particulate matter concentration) is not well understood. In this study, we compared the chemical composition (identified by an ultrahigh-resolution Orbitrap mass spectrometer) and volatility (estimated based on a predeveloped parametrization method) of OAs in urban PM2.5 (particulate matter with aerodynamic diameter ≤ 2.5 μm) samples from seven German and Chinese cities, where the PM2.5 concentration ranged from a light (14 μg m-3) to heavy (319 μg m-3) pollution level. A large fraction (71-98%) of compounds in PM2.5 samples were attributable to intermediate-volatility organic compounds (IVOCs) and semivolatile organic compounds (SVOCs). The fraction of low-volatility organic compounds (LVOCs) and extremely low-volatility organic compounds (ELVOCs) decreased from clean (28%) to heavily polluted urban regions (2%), while that of IVOCs increased from 34 to 62%. We found that the average peak area-weighted volatility of organic compounds in different cities showed a logarithmic correlation with the average PM2.5 concentration, indicating that the volatility of urban OAs increases with the increase of air pollution level. Our results provide new insights into the relationship between OA volatility and PM pollution levels and deepen the understanding of urban air pollutant evolution.

Association between particulate air pollution and hypertensive disorders in pregnancy: A retrospective cohort study.

Epidemiological findings regarding the association of particulate matter ≤2.5 μm (PM2.5) exposure with hypertensive disorders in pregnancy (HDP) are inconsistent; evidence for HDP risk related to PM2.5 components, mixture effects, and windows of susceptibility is limited. We aimed to investigate the relationships between HDP and exposure to PM2.5 during pregnancy. A large retrospective cohort study was conducted among mothers with singleton pregnancies in Kaiser Permanente Southern California from 2008 to 2017. HDP were defined by International Classification of Diseases-9/10 (ICD-9/10) diagnostic codes and were classified into 2 subcategories based on the severity of HDP: gestational hypertension (GH) and preeclampsia and eclampsia (PE-E). Monthly averages of PM2.5 total mass and its constituents (i.e., sulfate, nitrate, ammonium, organic matter, and black carbon) were estimated using outputs from a fine-resolution geoscience-derived model. Multilevel Cox proportional hazard models were used to fit single-pollutant models; quantile g-computation approach was applied to estimate the joint effect of PM2.5 constituents. The distributed lag model was applied to estimate the association between monthly PM2.5 exposure and HDP risk. This study included 386,361 participants (30.3 ± 6.1 years) with 4.8% (17,977/373,905) GH and 5.0% (19,381/386,361) PE-E cases, respectively. In single-pollutant models, we observed increased relative risks for PE-E associated with exposures to PM2.5 total mass [adjusted hazard ratio (HR) per interquartile range: 1.07, 95% confidence interval (CI) [1.04, 1.10] p < 0.001], black carbon [HR = 1.12 (95% CI [1.08, 1.16] p < 0.001)] and organic matter [HR = 1.06 (95% CI [1.03, 1.09] p < 0.001)], but not for GH. The population attributable fraction for PE-E corresponding to the standards of the US Environmental Protection Agency (9 μg/m3) was 6.37%. In multi-pollutant models, the PM2.5 mixture was associated with an increased relative risk of PE-E ([HR = 1.05 (95% CI [1.03, 1.07] p < 0.001)], simultaneous increase in PM2.5 constituents of interest by a quartile) and PM2.5 black carbon gave the greatest contribution of the overall mixture effects (71%) among all individual constituents. The susceptible window is the late first trimester and second trimester. Furthermore, the risks of PE-E associated with PM2.5 exposure were significantly higher among Hispanic and African American mothers and mothers who live in low- to middle-income neighborhoods (p < 0.05 for Cochran's Q test). Study limitations include potential exposure misclassification solely based on residential outdoor air pollution, misclassification of disease status defined by ICD codes, the date of diagnosis not reflecting the actual time of onset, and lack of information on potential covariates and unmeasured factors for HDP. Our findings add to the literature on associations between air pollution exposure and HDP. To our knowledge, this is the first study reporting that specific air pollution components, mixture effects, and susceptible windows of PM2.5 may affect GH and PE-E differently.

Personal Strategies to Reduce the Cardiovascular Impacts of Environmental Exposures.

Ubiquitous environmental exposures increase cardiovascular disease risk via diverse mechanisms. This review examines personal strategies to minimize this risk. With regard to fine particulate air pollution exposure, evidence exists to recommend the use of portable air cleaners and avoidance of outdoor activity during periods of poor air quality. Other evidence may support physical activity, dietary modification, omega-3 fatty acid supplementation, and indoor and in-vehicle air conditioning as viable strategies to minimize adverse health effects. There is currently insufficient data to recommend specific personal approaches to reduce the adverse cardiovascular effects of noise pollution. Public health advisories for periods of extreme heat or cold should be observed, with limited evidence supporting a warm ambient home temperature and physical activity as strategies to limit the cardiovascular harms of temperature extremes. Perfluoroalkyl and polyfluoroalkyl substance exposure can be reduced by avoiding contact with perfluoroalkyl and polyfluoroalkyl substance-containing materials; blood or plasma donation and cholestyramine may reduce total body stores of perfluoroalkyl and polyfluoroalkyl substances. However, the cardiovascular impact of these interventions has not been examined. Limited utilization of pesticides and safe handling during use should be encouraged. Finally, vasculotoxic metal exposure can be decreased by using portable air cleaners, home water filtration, and awareness of potential contaminants in ground spices. Chelation therapy reduces physiological stores of vasculotoxic metals and may be effective for the secondary prevention of cardiovascular disease.