Effects Of Short-term Exposure Research Articles

The Effect of Short-Term Exposure to Lower Body Positive Pressure on Motor Signal Processing, Reaction Times, and Cardiovascular Parameters in Healthy Volunteers Using Medical Anti-shock Trousers

The Effect of Short-Term Exposure to Lower Body Positive Pressure on Motor Signal Processing, Reaction Times, and Cardiovascular Parameters in Healthy Volunteers Using Medical Anti-shock Trousers

Short-term associations between ambient PM1, PM2.5, and PM10 and hospital admissions, length of hospital stays, and hospital expenses for patients with cardiovascular diseases in rural areas of Fuyang, East China

ABSTRACT Evidence on the impacts of PM1, PM2.5, and PM10 on the hospital admissions, length of hospital stays (LOS), and hospital expenses among patients with cardiovascular disease (CVD) is still limited in China, especially in rural areas. This study was performed in eight counties of Fuyang from 1 January 2015 to 30 June 2017. We use a three-stage time-series analysis to explore the effects of short-term exposure to PM1, PM2.5, and PM10 on hospital admissions, LOS, and hospital expenses for CVDs. An increment of 10 ug/m3 in PM1, PM2.5, and PM10 corresponded to an increment of 1.82% (95% CI: 1.34, 2.30), 0.96% (95% CI: 0.44, 1.48), and 0.79% (95% CI: 0.63%, 0.95%) in CVD hospital admissions, respectively. We observed that daily concentrations of PMs were associated with an increase in hospital admissions, LOS, and expenses for CVDs. Sustained endeavors are required to reduce air pollution so as to attenuate disease burdens from CVDs.

Joint Effect of Short-Term Exposure to Fine Particulate Matter and Ozone on Mortality: A Time Series Study in 272 Chinese Cities.

Short-term exposure to PM2.5 or O3 can increase mortality risk; however, limited studies have evaluated their interaction. A multicity time series study was conducted to investigate the synergistic effect of PM2.5 and O3 on mortality in China, using mortality data and high-resolution pollutant predictions from 272 cities in 2013-2015. Generalized additive models were applied to estimate associations of PM2.5 and O3 with mortality. Modification and interaction effects were explored by stratified analyses and synergistic indexes. Deaths attributable to PM2.5 and O3 were evaluated with or without modification of the other pollutant. The risk of total nonaccidental mortality increased by 0.70% for each 10 μg/m3 increase in PM2.5 when O3 levels were high, compared to 0.12% at low O3 levels. The effect of O3 on total nonaccidental mortality at high PM2.5 levels (1.26%) was also significantly higher than that at low PM2.5 levels (0.59%). Similar patterns were observed for cardiovascular or respiratory diseases. The relative excess risk of interaction and synergy index of PM2.5 and O3 on nonaccidental mortality were 0.69% and 1.31 with statistical significance, respectively. Nonaccidental deaths attributable to short-term exposure of PM2.5 or O3 when considering modification of the other pollutant were 28% and 31% higher than those without considering modification, respectively. Our results found synergistic effects of short-term coexposure to PM2.5 and O3 on mortality and suggested underestimations of attributable risks without considering their synergistic effects.

Long-term exposure to wildland fire smoke PM2.5 and mortality in the contiguous United States.

The area burned by wildland fire has greatly increased in the U.S. in recent decades. Short-term exposure to smoke pollutants emitted by wildland fires, particularly PM 2.5 , is associated with numerous adverse health effects. However, the impacts of long-term exposure to wildland fire smoke PM 2.5 on health and specifically mortality remain unclear. Utilizing wildland fire smoke PM 2.5 and mortality data in the contiguous U.S. during 2007-2020, we found positive associations between long-term smoke PM 2.5 exposure and increased non-accidental, cardiovascular, ischemic heart disease, digestive, endocrine, diabetes, mental, and chronic kidney disease mortality rates. Each year, in addition to the well-recognized mortality burden from non-smoke PM 2.5 , smoke PM 2.5 contributed to an estimated over 10 thousand non-accidental deaths in the U.S. This study demonstrates the detrimental effects of wildland fire smoke PM 2.5 on a wide range of health outcomes, and calls for more effective public health actions and communications that span the health risks of both short- and long-term exposure.

Histological, biochemical and immunohistochemical assessments of Roundup®, atrazine, and 2,4-D mixtures on tissue architecture, body fluid conditions, nitrotyrosine protein and Na+/K+-ATPase expressions in the American oyster, Crassostera virginica

Pesticides are widely used to control weeds and pests in agricultural settings but harm non-target aquatic organisms. In this study, our objective was to evaluate the effect of short-term exposure (one week) to environmentally relevant concentrations of pesticides mixture (low concentration: 0.4 μg/l atrazine, 0.5 μg/l Roundup®, and 0.5 μg/l 2,4-D; high concentration: 0.8 μg/l atrazine, 1 μg/l Roundup®, and 1 μg/l 2,4-D) on tissue architecture, body fluid conditions, and 3-nitrotyrosine protein (NTP) and Na+/K+-ATPase, expressions in tissues of American oyster (Crassostrea virginica) under controlled laboratory conditions. Histological analysis demonstrated the atrophy in the gills and digestive glands of oysters exposed to pesticides mixture. Periodic acid-Schiff (PAS) staining showed the number of hemocytes in connective tissue increased in low- and high-concentration pesticides exposure groups. However, pesticides treatment significantly (P < 0.05) decreased the amount of mucous secretion in the gills and digestive glands of oysters. The extrapallial fluid (i.e., body fluid) protein concentrations and glucose levels were dropped significantly (P < 0.05) in oysters exposed to high-concentration pesticides exposure groups. Moreover, immunohistochemical analysis showed significant upregulations of NTP and Na+/K+-ATPase expressions in the gills and digestive glands in pesticides exposure groups. Our results suggest that exposure to environmentally relevant pesticides mixture causes morphological changes in tissues and alters body fluid conditions and NTP and Na+/K+-ATPase expressions in tissues, which may lead to impaired physiological functions in oysters.

High sugar consumption for seven days in adult mice increased blood glucose variability, induced an anxiolytic effect and triggered oxidative stress in cerebral cortex.

Brain function is highly altered by glucose toxicity related to diabetes. High consumption of sugar in normal conditions is suspected to affect as well brain integrity. The present study investigates the possible effects of short-term exposure to high sugar diet on brain redox homeostasis in healthy mice. Male adult healthy mice were divided into two groups: control (CG) and sugar-exposed group (SG), that was exposed continually to 10% of glucose in drinking water for 7 days and 20% sucrose pellets food. Behavior, blood glucose variability and cerebral cortex oxidative stress biomarkers were measured at the end of exposure. Animals exposed to the high sugar diet expressed a significant increase in blood glucose levels and high glucose variability compared to control. These animals expressed as well anxiolytic behavior as revealed by the plus maze test. Exposure to the sugar diet altered redox homeostasis in the brain cortex as revealed by an increase in lipid peroxidation and the activity of antioxidant enzymes superoxide dismutase (SOD) and glutathione-s-transferase (GST). On the other hand, catalase (CAT) activity was decreased, and reduced glutathione (GSH) level was not altered compared to control. Further studies are required to understand the mechanisms trigging oxidative stress (OS) in the brain in response to short term exposure to high sugar diet and glucose fluctuations.

Air pollution mixture associated with oxidative stress exacerbation and symptoms deterioration in allergic rhinitis patients: Evidence from a panel study

With allergic rhinitis (AR) on the rise globally, there has been a growing focus on the role of environmental pollutants in the onset of AR. However, the potential mechanisms by how and which these pollutants exacerbate AR conditions remain unknown. This panel study of 49 patients diagnosed with AR over one year aimed to assess the individual and combined effects of short-term exposure to multiple ambient pollutants on oxidative stress, symptoms, and quality of life among patients with AR. All participants underwent four repeated assessments of health conditions and personal environmental exposures (PM2.5, O3, SO2, and NO2) over warm and cold seasons during 2017–2018. We evaluated two oxidative stress biomarkers (malondialdehyde [MDA], and superoxide dismutase [SOD]) via nasal lavage. We collected information on self-reported symptoms and quality of life using the Rhinitis Symptom Scale (SRS), the Visual Analog Scale (VAS), and the Rhinoconjunctivitis Quality of Life Questionnaire (RQLQ) through in-person interviews. Bayesian kernel machine regression (BKMR) was used to evaluate the joint effects of pollutant mixture and identify key contributors. The results revealed a significant association of the pollutant mixture when all four pollutants were at or above their median levels, with increased oxidative stress. This was evidenced by elevated MDA and reduced SOD. We found a joint detrimental effect of the pollutant mixture on AR symptoms with a strong association with increased SRS scores, but a non-significant positive association with VAS and RQLQ scores. PM2.5, O3, and SO2 presented as the potentially primary contributors to the adverse health effects associated with the pollutant mixture in Taiyuan city. Patients with AR exposed to short-term air pollutant mixture are more likely to have greater nasal symptoms and worse quality of life from increased oxidative stress and reduced antioxidant capacity. Further research is warranted to better elucidate the underlying mechanisms.

Effects of short-term exposure to red or near-infrared light on axial length in young human subjects.

To determine whether visible light is needed to elicit axial eye shortening by exposure to long wavelength light. Incoherent narrow-band red (620 ± 10 nm) or near-infrared (NIR, 875 ± 30 nm) light was generated by an array of light-emitting diodes (LEDs) and projected monocularly in 17 myopic and 13 non-myopic subjects for 10 min. The fellow eye was occluded. Light sources were positioned 50 cm from the eye in a dark room. Axial length (AL) was measured before and after the exposure using low-coherence interferometry. Non-myopic subjects responded to red light with significant eye shortening, while NIR light induced minor axial elongation (-13.3 ± 17.3 μm vs. +6.5 ± 11.6 μm, respectively, p = 0.005). Only 41% of the myopic subjects responded to red light exposure with a decrease in AL and changes were therefore, on average, not significantly different from those observed with NIR light (+0.2 ± 12.1 μm vs. +1.1 ± 11.2 μm, respectively, p = 0.83). Interestingly, there was a significant correlation between refractive error and induced changes in AL after exposure to NIR light in myopic eyes (r(15) = -0.52, p = 0.03) and induced changes in AL after exposure to red light in non-myopic eyes (r(11) = 0.62, p = 0.02), with more induced axial elongation with increasing refractive error. Incoherent narrow-band red light at 620 nm induced axial shortening in 77% of non-myopic and 41% of myopic eyes. NIR light did not induce any significant changes in AL in either refractive group, suggesting that the beneficial effect of red laser light therapy on myopia progression requires visible stimulation and not simply thermal energy.

Exploring neonicotinoid effects on Drosophila: insights into olfactory memory, neurotransmission, and synaptic connectivity.

Neonicotinoid insecticides, the fastest-growing class in recent decades, interfere with cholinergic neurotransmission by binding to the nicotinic acetylcholine receptor. This disruption affects both targeted and non-targeted insects, impairing cognitive functions such as olfaction and related behaviors, with a particular emphasis on olfactory memory due to its ecological impact. Despite the persistent presence of these chemicals in the environment, significant research gaps remain in understanding the intricate interplay between cognitive function, development, neuronal activity, and neonicotinoid-induced toxicity. This study focuses on the fruit fly Drosophila melanogaster, chosen for its genetic tractability, well-characterized neural circuitry, and remarkable parallels with bees in neurotransmitter systems and brain structures. Our aim is to establish the fruit fly as a valuable model organism for studying the effects of neonicotinoids on behavior and neuronal circuitry, with particular attention to olfactory memory and associated brain circuitries. To achieve this aim, we conducted experiments to investigate the effects of short-term exposure to sublethal doses of the neonicotinoid imidacloprid, mimicking realistic environmental insecticide exposure, on the formation of odor memories. Additionally, we evaluated synaptic contacts and cholinergic neurotransmission within the mushroom body, the primary memory network of insects. Our results showed significant impairments in odor memory formation in flies exposed to imidacloprid, with exposure during the adult stage showing more pronounced effects than exposure during the larval stage. Additionally, functional studies revealed a decrease in synaptic contacts within the intrinsic olfactory projection neurons and the mushroom body. Furthermore, another experiment showed an odor-dependent reduction in cholinergic neurotransmission within this network. In summary, employing Drosophila as a model organism provides a robust framework for investigating neonicotinoid effects and understanding their diverse impacts on insect physiology and behavior. Our study initiates the establishment of the fruit fly as a pivotal model for exploring neonicotinoid influences, shedding light on their effects on olfactory memory, neuronal integrity, and synaptic transmission.

Short-term effects of ambient gaseous air pollution on blood platelet mitochondrial DNA methylation and myocardial ischemia

BackgroundThe potential effects of short-term exposure to major ambient gaseous pollutants (ozone: O3, carbon monoxide: CO, and sulfur dioxide: SO2) on platelet mitochondrial DNA (mtDNA) methylation have been uncertain and no studies have examined whether platelet mtDNA methylation levels could modify the associations between ambient gaseous pollutants and the risks of ST-segment depression (STDE) and T-wave inversion events (TIE), two indicators of myocardial ischemia. MethodsThis study used data from a randomized, double-blind, placebo-controlled intervention study with a standardized 24-hour exposure protocol among 110 participants in Beijing. Absolute changes in platelet mtDNA methylation (ACmtDNAm) levels were determined by two repeated measurements on platelet mtDNA methylation levels in blood samples collected before and after the 24-hour exposure period. A multivariable linear regression model and a generalized linear model with a Poisson link function were used to investigate the associations of ambient gaseous pollutants with platelet mtDNA methylation levels, STDE, and TIE, respectively. ResultsShort-term O3 exposure was significantly associated with decreased ACmtDNAm at ATP6_P1 but increased ACmtDNAm at mt12sRNA, MT-COX1, and MT-COX1_P2; short-term CO and SO2 exposures were significantly associated with decreased ACmtDNAm at D-loop, MT-COX3- and ATP-related genes. Moreover, short-term O3 exposure was significantly associated with increased risks of STDE and TIE, and ACmtDNAm at MT-COX1 and MT-COX1_P2 modified the association between short-term O3 exposure and STDE events. L-Arg supplementation attenuated the effects of ambient gaseous pollutants, particularly O3, on ACmtDNAm and STDE. ConclusionsPlatelet mtDNA methylation levels are promising biomarkers of short-term exposure to ambient gaseous air pollution, and are likely implicated in the mechanism behind the association of ambient O3 pollution with adverse cardiovascular effects. L-Arg supplementation showed the potential to mitigate the adverse effects of ambient O3 pollution.

Effect of Honey and Aqueous Garlic Extracts against Short-Term Exposure of Cigarette Tobacco Smoking in Mice: Histopathological and Biochemical Investigations.

It is well known that cigarette smoking adversely affects human health and induces oxidative stress in most vital organs. This study aims to assess the biochemical, histological, and ultrastructural values of honey and garlic extracts in ameliorating the effects of short-term exposure to cigarette smoke in mice. Forty-eight mice were randomly divided into six equal groups: group I was exposed to fresh air only, group II was exposed to cigarette smoke, group III was given 0.2 ml of honey extract, group IV was exposed to cigarette smoke and was given 0.2 ml of honey extract, group V was given 0.2 ml of garlic extract, and group VI was exposed to cigarette smoke and was given 0.2 ml of aqueous garlic extract. These exposures were repeated daily for 21 consecutive days among the treated groups. By the end of the third week, the animals were euthanized by physical cervical dislocation. Blood was taken for biochemical study, and the selected organs of the liver, kidney, and jejunum were processed for histological and ultrastructural studies. The biochemical results showed that short-term exposure of experimental mice to cigarette smoking did not alter the liver function tests except for decreasing the albumin level. Moreover, cigarette smoking elevates the concentration of carbonyl protein content and cystatin C. Histologically, the use of honey and garlic showed good protection to the liver, kidney, and jejunum, which was proved by transmission electron microscopy, in addition to lowering the oxidative stress biomarkers. In conclusion, using honey and/or garlic helps protect the liver, kidney, and jejunum against the hazardous effects of cigarette smoke.

Effect of short-term exposure to high-altitude hypoxic climate on feed-intake, blood glucose level and physiological responses of native and non-native goat.

The exposure to high altitude and cold stress poses challenges in maintaining normal physiological standards and body homeostasis in non-native animals. To enhance our understanding of the physiology of native and non-native goats in high-altitude environments, we conducted a comparative study to examine the impact of natural hypoxic and cold stress conditions on their feed intake (FIT) and associated changes in physiological responses, including plasma glucose concentration (PGC). The study took place at an altitude of 3505.2m above mean sea level and involved twenty-two healthy females from two different breeds of goats. This study was conducted over a period of 56days after the arrival of non-native Black Bengal goats (BBN) and compared with native Changthangi (CHAN) goats. Both groups were extensively reared in a natural high-altitude and cold-stress environment in Leh, India, and were subjected to defined housing and management practices. The parameters evaluated included FIT, PGC, respiration rate, heart rate, pulse rate, and rectal temperature. High altitudes had a significant (p < 0.05) impact on FIT, PGC, respiration rate, heart rate, pulse rate, and rectal temperature in BBN, whereas these parameters remained stable in CHAN throughout the study period. Additionally, the detrimental effects of high-altitude stress were more pronounced in non-native goats compared to native goats. These findings suggest that physiological responses in non-native goats tend to stabilize after an initial period of adverse effects in high-altitude environments. Based on the physiological responses and glucose concentration, it is recommended to pay special attention to the nutrition of non-native goats for up to the third week (21days) after their arrival in high-altitude areas.

The mediation effect of asprosin on the association between ambient air pollution and diabetes mellitus in the elderly population in Taiyuan, China.

Evidence around the relationship between air pollution and the development of diabetes mellitus (DM) remains limited and inconsistent. To investigate the potential mediation effect of asprosin on the association between fine particulate matter (PM2.5), tropospheric ozone (O3) and blood glucose homeostasis. A case-control study was conducted on a total of 320 individuals aged over 60years, including both diabetic and non-diabetic individuals, from six communities in Taiyuan, China, from July to September 2021. Generalized linear models (GLMs) suggested that short-term exposure to PM2.5 was associated with elevated fasting blood glucose (FBG), insulin resistance index (HOMA-IR), as well as reduced pancreatic β-cell function index (HOMA-β), and short-term exposure to O3 was associated with increased FBG and decreased HOMA-β in the total population and elderly diabetic patients. Mediation analysis showed that asprosin played a mediating role in the relationship of PM2.5 and O3 with FBG, with mediating ratios of 10.2% and 18.4%, respectively. Our study provides emerging evidence supporting that asprosin mediates the short-term effects of exposure to PM2.5 and O3 on elevated FBG levels in an elderly population. Additionally, the elderly who are diabetic, over 70years, and BMI over 24kg/m2 are more vulnerable to air pollutants and need additional protection to reduce their exposure to air pollution.

Effect of short-term exposure to air pollution on hospital admission for cardiovascular disease: A time-series study in Xiangyang, China

BackgroundData on the relationship between short-term exposure to air pollution and cardiovascular diseases (CVDs) and the potential modifying factors are limited and inconsistent. ObjectiveTo explore the relationship between short-term exposure to air pollution and CVD risk, and potential modification effect factors. MethodA time series study was conducted on 52,991 hospital admissions for CVD from 2015 to 2019 in Xiangyang City, China. Air pollution data from four national fixed monitoring stations were collected to estimate exposure level in Xiangyang City. A quasi-Poisson generalized additive model incorporating a distributed lag nonlinear model was applied to evaluate the association between air pollution and CVD risk. The potential modification effect of sex, age, and season on the above associations was also evaluated. ResultsCVD risk was positively associated with air pollution. Peak associations in single lag day structures were observed for particulate matter ≤10 μm in aerodynamic (PM10; RR: 1.040, 95 % CI: 0.996–1.087), PM2.5 (1.025, 1.004–1.045), nitrogen dioxide (NO2; 1.074, 1.039–1.111), and sulfur dioxide (SO2; 1.079, 1.019–1.141) at Lag 0 and ozone (O3; 1.018, 1.004–1.031) at Lag 4. In cumulative lag day structures, the highest RRs were 1.225 (1.079,1.392) for PM10 at Lag 06, 1.054 (1.013, 1.098) for PM2.5 at Lag 03, 1.200 (1.119, 1.287) for NO2 at Lag 04, and 1.135 (1.025, 1.257) for SO2 at Lag 02. Moreover, the association between air pollution and CVD risk was modified by sex and age (P < 0.05). Females and individuals aged ≤65 years were more vulnerable to NO2 and had a higher CVD risk. ConclusionShort-term exposure to air pollution was positively associated with CVD risk. Moreover, sex and age could modify the effect of air pollution on CVD risk. Females and individuals aged ≤65 years had a higher NO2 exposure-induced CVD risk.

Investigating the Impact of Carbon Nanotube Nanoparticle Exposure on Testicular Oxidative Stress and Histopathological Changes in Swiss albino Mice.

Carbon nanotubes (CNTs) possess remarkable properties that make them valuable for various industrial applications. However, concerns have arisen regarding their potential adverse health effects, particularly in occupational settings. The main aim of this research was to examine the effects of short-term exposure to multiwalled carbon nanotube nanoparticles (MWCNT-NPs) on testicular oxidative stress in Swiss albino mice, taking into account various factors such as dosage, duration of exposure, and particle size of MWCNT-NP. In this study, 20 mice were used and placed into six different groups randomly. Four of these groups comprised four repetitions each, while the two groups served as the vehicle control with two repetitions each. The experimental groups received MWCNT-NP treatment, whereas the control group remained untreated. The mice in the experimental groups were exposed to MWCNT-NP for either 7 days or 14 days. Through oral administration, the MWCNT-NP solution was introduced at two distinct dosages: 0.45 and 0.90 μg, whereas the control group was subjected to distilled water rather than the MWCNT-NP solution. The investigation evaluated primary oxidative balance indicators-glutathione (GSH) and glutathione disulfide (GSSG)-in response to MWCNT-NP exposure. Significantly, a noticeable reduction in GSH levels and a concurrent increase in GSSG concentrations were observed in comparison to the control group. To better understand and explore the assessment of the redox status, the Nernst equation was used to calculate the redox potential. Intriguingly, the calculated redox potential exhibited a negative value, signifying an imbalance in the oxidative state in the testes. These findings suggest that short-term exposure to MWCNT-NP can lead to the initiation of testicular oxidative stress and may disrupt the male reproductive system. This is evident from the alterations observed in the levels of GSH and GSSG, as well as the negative redox potential. The research offers significant insights into the reproductive effects of exposure to MWCNTs and emphasizes the necessity of assessing oxidative stress in nanomaterial toxicity studies.

Association of short-term PM2.5 exposure with airway innate immune response, microbiota and metabolism alterations in human airways

Exposure to fine particulate matter (PM2.5) has been associated with impaired airway innate immunity, leading to diverse lung disorders. However, the mechanisms of the adverse effects of PM2.5 on the airway innate immune system has not been adequately elucidated. This study aimed to investigate the association between short-term exposure to ambient PM2.5 and airway innate immune responses. A panel study of 53 undergraduate students was conducted in November 2020 and April 2021. Levels of airway innate immune biomarkers including interleukin-1β (IL-1β), IL-4, IL-6, IL-8, IL-17, interferon-γ (IFN-γ), tumor necrosis factor-α (TNF-α), myeloperoxidase (MPO), and matrix metalloproteinase-9 (MMP-9) in induced sputum were measured, and airway microbiota and metabolites examined. Linear mixed-effect model was used to evaluate the effects of short-term exposure to PM2.5 on the above-listed airway immune biomarkers. The results indicated that for every 10 μg/m3 increase in PM2.5 concentration (at lag3), was associated with an increase of 21.3 % (5.4 %–37.1 %), 26.2 % (0.30 %–52.1 %), 22.4 % (0.70 %–44.2 %), 27.4 % (6.6 %–48.3 %), 18.3 % (4.6 %–31.9 %), 3.9 % (0.20 %–7.6 %) or 2.4 % (0.10 %–4.7 %) in IL-6, TNF-α, IL-17, IL-4, IFN-γ, MPO, or MMP-9 levels, respectively. Meanwhile, exposure to higher levels of ambient PM2.5 was found to significantly modulate airway microbiota and metabolite profile. Specifically, Prevotella and Fusobacterium, as well as 96 different metabolites were associated with PM2.5 levels. The metabolic pathways associated with these metabolites mainly included amino acid biosynthesis and metabolism. Notably, PM2.5 exposure-induced alterations of some airway microbiota were significantly correlated with specific airway metabolic change. Taken together, these results demonstrated that short-term exposure to PM2.5 was associated with alterations of airway immune response, microbial dysbiosis and changes of metabolites. This study provided insights into the mechanisms underlying PM2.5-induced airway innate immune responses.

Modification of heat-related effects on mortality by air pollution concentration, at small-area level, in the Attica prefecture, Greece

BackgroundThe independent effects of short-term exposure to increased air temperature and air pollution on mortality are well-documented. There is some evidence indicating that elevated concentrations of air pollutants may lead to increased heat-related mortality, but this evidence is not consistent. Most of these effects have been documented through time-series studies using city-wide data, rather than at a finer spatial level. In our study, we examined the possible modification of the heat effects on total and cause-specific mortality by air pollution at municipality level in the Attica region, Greece, during the warm period of the years 2000 to 2016.MethodsA municipality-specific over-dispersed Poisson regression model during the warm season (May–September) was used to investigate the heat effects on mortality and their modification by air pollution. We used the two-day average of the daily mean temperature and daily mean PM10, NO2 and 8 hour-max ozone (O3), derived from models, in each municipality as exposures. A bivariate tensor smoother was applied for temperature and each pollutant alternatively, by municipality. Α random-effects meta-analysis was used to obtain pooled estimates of the heat effects at different pollution levels. Heterogeneity of the between-levels differences of the heat effects was evaluated with a Q-test.ResultsA rise in mean temperature from the 75th to the 99th percentile of the municipality-specific temperature distribution resulted in an increase in total mortality of 12.4% (95% Confidence Interval (CI):7.76–17.24) on low PM10 days, and 21.25% (95% CI: 17.83–24.76) on high PM10 days. The increase on mortality was 10.09% (95% CI: − 5.62- 28.41) on low ozone days, and 14.95% (95% CI: 10.79–19.27) on high ozone days. For cause-specific mortality an increasing trend of the heat effects with increasing PM10 and ozone levels was also observed. An inconsistent pattern was observed for the modification of the heat effects by NO2, with higher heat effects estimated in the lower level of the pollutant.ConclusionsOur results support the evidence of elevated heat effects on mortality at higher levels of PM10 and 8 h max O3. Under climate change, any policy targeted at lowering air pollution levels will yield significant public health benefits.

Short-term effects of exposure to cold spells on blood pressure among adults in Nanjing, China

Short-term effects of exposure to cold spells on blood pressure among adults in Nanjing, China

Association between Ambient Particulate Air Pollution and Soluble Biomarkers of Endothelial Function: A Meta-Analysis.

The burden of cardiovascular diseases caused by ambient particulate air pollution is universal. An increasing number of studies have investigated the potential effects of exposure to particulate air pollution on endothelial function, which is one of the important mechanisms for the onset and development of cardiovascular disease. However, no previous study has conducted a summary analysis of the potential effects of particulate air pollution on endothelial function. To summarize the evidence for the potential effects of short-term exposure to ambient particulate air pollution on endothelial function based on existing studies. A systematic literature search on the relationship between ambient particulate air pollution and biomarkers of endothelial function including endothelin-1 (ET-1), E-selectin, intercellular cell adhesion molecule-1 (ICAM-1), and vascular cell adhesion molecule-1 (VCAM-1) was conducted in PubMed, Scopus, EMBASE, and Web of Science up to 20 May 2023. Subsequently, a meta-analysis was conducted using a random effects model. A total of 18 studies were included in this meta-analysis. A 10 μg/m3 increase in short-term exposure to ambient PM2.5 was associated with a 1.55% (95% CI: 0.89%, 2.22%) increase in ICAM-1 and a 1.97% (95% CI: 0.86%, 3.08%) increase in VCAM-1. The associations of ET-1 (0.22%, 95% CI: -4.94%, 5.65%) and E-selectin (3.21%, 95% CI: -0.90% 7.49%) with short-term exposure to ambient PM2.5 were statistically insignificant. Short-term exposure to ambient PM2.5 pollution may significantly increase the levels of typical markers of endothelial function, including ICAM-1 and VCAM-1, suggesting potential endothelial dysfunction following ambient air pollution exposure.

Effect of short-term exposure to Raag Bilawal of North Indian classical music on young Indian adults: a high-density electroencephalogram microstate study

Effect of short-term exposure to Raag Bilawal of North Indian classical music on young Indian adults: a high-density electroencephalogram microstate study