Understanding the Cardiovascular and Metabolic Health Effects of Air Pollution in the Context of Cumulative Exposomic Impacts.

Poor air quality accounts for more than 9 million deaths a year globally according to recent estimates. A large portion of these deaths are attributable to cardiovascular causes, with evidence indicating that air pollution may also play an important role in the genesis of key cardiometabolic risk factors. Air pollution is not experienced in isolation but is part of a complex system, influenced by a host of other external environmental exposures, and interacting with intrinsic biologic factors and susceptibility to ultimately determine cardiovascular and metabolic outcomes. Given that the same fossil fuel emission sources that cause climate change also result in air pollution, there is a need for robust approaches that can not only limit climate change but also eliminate air pollution health effects, with an emphasis of protecting the most susceptible but also targeting interventions at the most vulnerable populations. In this review, we summarize the current state of epidemiologic and mechanistic evidence underpinning the association of air pollution with cardiometabolic disease and how complex interactions with other exposures and individual characteristics may modify these associations. We identify gaps in the current literature and suggest emerging approaches for policy makers to holistically approach cardiometabolic health risk and impact assessment.

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.

Environmental Interventions for Preventing Atopic Diseases.

PURPOSE OF REVIEW: In this review, we detail the exposome (consisting of environmental factors such as diet, microbial colonization, allergens, pollutants, and stressors), mechanistic and clinical research supporting its influence on atopic disease, and potentiation from climate change. We highlight contemporary environmental interventions and available evidence substantiating their roles in atopic disease prevention, from observational cohorts to randomized controlled trials, when available. RECENT FINDINGS: Early introduction to allergenic foods is an effective primary prevention strategy to reduce food allergy. Diverse dietary intake also appears to be a promising strategy for allergic disease prevention, but additional study is necessary. Air pollution and tobacco smoke are highly associated with allergic disease, among other medical comorbidities, paving the way for campaigns and legislation to reduce these exposures. There is no clear evidence that oral vitamin D supplementation, prebiotic or probiotic supplementation, daily emollient application, and antiviral prophylaxis are effective in preventing atopic disease, but these interventions require further study. While some environmental interventions have a well-defined role in the prevention of atopic disease, additional study of many remaining interventions is necessary to enhance our understanding of their role in disease prevention. Alignment of research findings from randomized controlled trials with public policy is essential to develop meaningful public health outcomes and prevent allergic disease on the population level.

[Allergies in the light of global environmental changes]. / Allergien im Lichte globaler Umweltveränderungen.

BACKGROUND: The increase in allergies began worldwide with the onset of the Great Acceleration. Environmental pollution and climate change now threaten to cancel out decades of success in health research. OBJECTIVE: A summary of environmental influences is provided, which not only shows the significant increase in the prevalence of allergies worldwide but also that of noncommunicable diseases. The effects of the climate crisis on allergies and the multifactorial and interfunctional relationships with other environmental changes are described in detail. MATERIAL AND METHODS: In order to obtain an overview of the possible effects of global environmental changes on allergies, a wide range of literature was evaluated and the study results were prepared and summarized. RESULTS: A large number of allergens are influencing the human exposome on a daily basis. These allergens are triggered by environmental changes, such as air pollution in the ambient air and indoors, chemicals in everyday objects or residues in food. People are sensitized by the interaction of allergens and pollutants. CONCLUSION: The prevalence of allergies is stagnating in industrialized countries. This is probably just the calm before the storm. The accelerating effects of global warming could make pollen and air pollutants even more aggressive in the future. Urgent action is therefore needed to minimize environmental pollution and mitigate climate change.

The Role of Climate Change in Asthma.

Human activity and increased use of fossil fuels have led to climate change. These changes are adversely affecting human health, including increasing the risk of developing asthma. Global temperatures are predicted to increase in the future. In 2019, asthma affected an estimated 262 million people and caused 455,000 deaths. These rates are expected to increase. Climate change by intensifying climate events such as drought, flooding, wildfires, sand storms, and thunderstorms has led to increases in air pollution, pollen season length, pollen and mold concentration, and allergenicity of pollen. These effects bear implications for the onset, exacerbation, and management of childhood asthma and are increasing health inequities. Global efforts to mitigate the effects of climate change are urgently needed with the goal of limiting global warming to between 1.5 and 2.0 °C of preindustrial times as per the 2015 Paris Agreement. Clinicians need to take an active role in these efforts in order to prevent further increases in asthma prevalence. There is a role for clinician advocacy in both the clinical setting as well as in local, regional, and national settings to install measures to control and curb the escalating disease burden of childhood asthma in the setting of climate change.

Air Pollution and Diet: Potential Interacting Exposures in Asthma.

PURPOSE OF REVIEW: To provide a review of emerging literature describing the impact of diet on the respiratory response to air pollution in asthma. RECENT FINDINGS: Asthma phenotyping (observable characteristics) and endotyping (mechanistic pathways) have increased the specificity of diagnostic and treatment pathways and opened the doors to the identification of subphenotypes with enhanced susceptibility to exposures and interventions. Mechanisms underlying the airway immune response to air pollution are still being defined but include oxidative stress, inflammation, and activation of adaptive and innate immune responses, with genetic susceptibility highlighted. Of these, neutrophil recruitment and activation appear prominent; however, understanding neutrophil function in response to pollutant exposures is a research gap. Diet may play a role in asthma pathogenesis and morbidity; therefore, diet modification is a potential target opportunity to protect against pollutant-induced lung injury. In particular, in vivo and in vitro data suggest the potential for diet to modify the inflammatory response in the airways, including impacts on neutrophil recruitment and function. Murine models provide compelling results in regard to the potential for dietary components (including fiber, antioxidants, and omega-3 fatty acids) to buffer against the inflammatory response to air pollution in the lung. Precision lifestyle approaches to asthma management and respiratory protection in the context of air pollution exposures may evolve to include diet, pending the results of further epidemiologic and causal investigation and with neutrophil recruitment and activation as a candidate mechanism.

Impact of environmental nitrogen pollution on pollen allergy: A scoping review.

The current rise in the prevalence of allergies to aeroallergens is incompletely understood and attributed to interactions with environmental changes and lifestyle changes. Environmental nitrogen pollution might be a potential driver of this increasing prevalence. While the ecological impact of excessive nitrogen pollution has been widely studied and is relatively well understood, its indirect effect on human allergies is not well documented. Nitrogen pollution can affect the environment in various ways, including air, soil, and water. We aim to provide a literature overview of the nitrogen-driven impact on plant communities, plant productivity, and pollen properties and how they lead to changes in allergy burden. We included original articles investigating the associations between nitrogen pollution, pollen, and allergy, published in international peer-reviewed journals between 2001 and 2022. Our scoping review found that the majority of studies focus on atmospheric nitrogen pollution and its impact on pollen and pollen allergens, causing allergy symptoms. These studies often examine the impact of multiple atmospheric pollutants and not just nitrogen, making it difficult to determine the specific impact of nitrogen pollution. There is some evidence that atmospheric nitrogen pollution affects pollen allergy by increasing atmospheric pollen levels, altering pollen structure, altering allergen structure and release, and causing increased allergenic reactivity. Limited research has been conducted on the impact of soil and aqueous nitrogen pollution on pollen allergenic reactivity. Further research is needed to fill the current knowledge gap about the impact of nitrogen pollution on pollen and their related allergic disease burden.

Examining individual-level tri-exposure to greenspace and air/noise pollution using individual-level GPS-based real-time sensing data.

OBJECTIVE: Although exposure to air/noise pollution and greenspace has been found to significantly affect people's physical and mental health outcomes, there is still a lack of knowledge on what built-environment and socioeconomic factors are significantly associated with people's tri-exposure to air/noise pollution and greenspace. This study analyzes the associations between built-environment and socioeconomic factors and the tri-exposure to greenspace and air/noise pollution in Hong Kong. METHOD: Based on individual-level activity data, real-time GPS trajectories, and exposure data collected by portable sensors as well as remote sensing satellite imagery, we employ multinomial logistic regression to determine the socioeconomic and built-environment factors that are significantly associated with the type of participants' tri-exposure at the grid cell level. RESULTS: The results show that higher transit nodal accessibility, building density, building height and land-use mix are significantly associated with a higher likelihood of being disadvantaged in terms of tri-exposure to air/noise pollution and greenspace. While more advantageous tri-exposures are significantly related to higher median monthly household income and sky view factor. CONCLUSION: Old high-rise high-density neighborhoods are more likely to be triply disadvantaged with low greenspace exposure but high air pollution and noise pollution exposure. The findings provide policymakers with critical reference in terms of addressing the inequalities in the tri-exposure outcomes.

Traffic-related air pollution and supplemental folic acid intake in relation to DNA methylation in granulosa cells.

BACKGROUND: Higher exposure to traffic-related air pollution (TRAP) is related to lower fertility, with specific adverse effects on the ovary. Folic acid may attenuate these effects. Our goal was to explore the relation of TRAP exposure and supplemental folic acid intake with epigenetic aging and CpG-specific DNA methylation (DNAm) in granulosa cells (GC). Our study included 61 women undergoing ovarian stimulation at a fertility center (2005-2015). DNAm levels were profiled in GC using the Infinium MethylationEPIC BeadChip. TRAP was defined using a spatiotemporal model to estimate residence-based nitrogen dioxide (NO2) exposure. Supplemental folic acid intake was measured with a validated food frequency questionnaire. We used linear regression to evaluate whether NO2 or supplemental folic acid was associated with epigenetic age acceleration according to the Pan-tissue, mural GC, and GrimAge clocks or DNAm across the genome adjusting for potential confounders and accounting for multiple testing with a false discovery rate < 0.1. RESULTS: There were no associations between NO2 or supplemental folic acid intake and epigenetic age acceleration of GC. NO2 and supplemental folic acid were associated with 9 and 11 differentially methylated CpG sites. Among these CpGs, only cg07287107 exhibited a significant interaction (p-value = 0.037). In women with low supplemental folic acid, high NO2 exposure was associated with 1.7% higher DNAm. There was no association between NO2 and DNAm in women with high supplemental folic acid. The genes annotated to the top 250 NO2-associated CpGs were enriched for carbohydrate and protein metabolism, postsynaptic potential and dendrite development, and membrane components and exocytosis. The genes annotated to the top 250 supplemental folic acid-associated CpGs were enriched for estrous cycle, learning, cognition, synaptic organization and transmission, and size and composition of neuronal cell bodies. CONCLUSIONS: We found no associations between NO2, supplemental folic acid, and DNAm age acceleration of GC. However, there were 20 differentially methylated CpGs and multiple enriched GO terms associated with both exposures suggesting that differences in GC DNAm could be a plausible mechanism underlying the effects of TRAP and supplemental folic acid on ovarian function.

[Exposome: from definition to future challenges.] / Esposoma: dalla definizione alle sfide future.

The exposome concept arises from the need to integrate different disciplines of public health and environmental sciences, mainly including environmental epidemiology, exposure science, and toxicology. The role of the exposome is to understand how the totality of an individual's exposures throughout the lifetime can impact human health. The etiology of a health condition is rarely explained by a single exposure. Therefore, examining the human exposome as a whole becomes relevant to simultaneously consider multiple risk factors and more accurately estimate concurrent causes of different health outcomes. Generally, the exposome is explained through three domains: general external exposome, specific external exposome, and internal exposome. The general external exposome includes measurable population-level exposures such as air pollution or meteorological factors. The specific external exposome includes information on individual exposures, such as lifestyle factors, typically obtained from questionnaires. Meanwhile, the internal exposome encompasses multiple biological responses to external factors, detected through molecular and omics analyses. Additionally, in recent decades, the socio-exposome theory has emerged, where all exposures are studied as a phenomenon dependent on the interaction between socioeconomic factors that vary depending on the context, allowing the identification of mechanisms that lead to health inequalities. The considerable production of data in exposome studies has led researchers to face new methodological and statistical challenges, introducing various approaches to estimate the effect of the exposome on health. Among the most common are regression models (Exposome-Wide Association Study - ExWAS), dimensionality reduction and exposure grouping techniques, and machine learning methods. The significant conceptual and methodological innovation of the exposome for a more holistic evaluation of the risks associated with human health is continuously expanding and will require further investigations related to the application of information obtained from studies into prevention and public health policies.

Eicosapentaenoic acid (EPA) reduces pulmonary endothelial dysfunction and inflammation due to changes in protein expression during exposure to particulate matter air pollution.

AIMS: Inhalation of air pollution small particle matter (PM) is a leading cause of cardiovascular (CV) disease. Exposure to PMs causes endothelial cell (EC) dysfunction as evidenced by nitric oxide (NO) synthase uncoupling, vasoconstriction and inflammation. Eicosapentaenoic acid (EPA) has been shown to mitigate PM-induced adverse cardiac changes in patients receiving omega-3 fatty acid supplementation. We set out to determine the pro-inflammatory effects of multiple PMs (urban and fine) on pulmonary EC NO bioavailability and protein expression, and whether EPA restores EC function under these conditions. METHODS AND RESULTS: We pretreated pulmonary ECs with EPA and then exposed them to urban or fine air pollution PMs. LC/MS-based proteomic analysis to assess relative expression levels. Expression of adhesion molecules was measured by immunochemistry. The ratio of NO to peroxynitrite (ONOO-) release, an indication of eNOS coupling, was measured using porphyrinic nanosensors following calcium stimulation. Urban/fine PMs also modulated 9/12 and 13/36 proteins, respectively, linked to platelet and neutrophil degranulation pathways and caused > 50% (p < 0.001) decrease in the stimulated NO/ONOO- release ratio. EPA treatment altered expression of proteins involved in these inflammatory pathways, including a decrease in peroxiredoxin-5 and an increase in superoxide dismutase-1. EPA also increased expression of heme oxygenase-1 (HMOX1), a cytoprotective protein, by 2.1-fold (p = 0.024). EPA reduced elevations in sICAM-1 levels by 22% (p < 0.01) and improved the NO/ONOO- release ratio by > 35% (p < 0.05). CONCLUSION: These cellular changes may contribute to anti-inflammatory, cytoprotective and lipid changes associated with EPA treatment during air pollution exposure.

Effects of Pear Extracts on Microbiome and Immunocytokines to Alleviate Air Pollution-Related Respiratory Hypersensitivity.

Pears are ancient functional foods for modern times. Particularly, Korean pears (Pyrus pyrifolia cv.) have been used as folk medicine for respiratory diseases and have strong potential for the treatment of hazardous aerosol-related diseases. Thus, the effects of pear ethanol extracts on air pollution-related respiratory hypersensitivity were studied by toxicokinetics, pro-inflammatory cytokines, and microbiomics in preclinical and randomized double-blind clinical studies. The mild-asthma subjects, who lived in the same city, Seoul, Korea, were separated into the placebo and the treatment (pear extracts, as brix 55; arbutin 5.01 mg and chlorogenic acid 0.18 mg/3 mL per day) groups for 4 weeks (n = 20). As results, there were positive associations between urinary 2-naphthol (NT) or 1-hydroxypyrene (OHP), exposure biomarkers for polyaromatic hydrocarbons in PM2.5, and pro-inflammatory cytokines, interleukin (IL)-4 or IgE, respectively, in the human subjects. The pear extracts somewhat reduced 2-NT and 1-OHP levels. The proportions of fiber-degrading bacteria that stimulate growth of beneficial microflora for immune defense, that is, Bifidobacterium and Eubacterium, were significantly higher in the pear consuming group than in the placebo group. Moreover, pro-inflammatory cytokines, including IgE, IL-4, IL-5, and IL-13, were significantly suppressed by the pear extracts in the preclinical tests of the ovalbumin-induced asthma mice. Thus, we suggest that air pollution-related respiratory hypersensitivity can be alleviated by Korean pear extracts by modulation of microbiome and immunocytokines.

Fine particulate matter exposure and pediatric mental health outcomes: An integrative review.

INTRODUCTION: Climate change is expected to worsen air pollution globally, which contributes to a multitude of negative health outcomes in humans. AIM: The purpose of this integrative review is to examine the relationship between exposure to fine particulate matter (PM2.5 ) and mental health outcomes in children and adolescents. METHODS: This review utilized Whittemore and Knafl's methodology for conducting an integrative review. After a thorough search of the literature, 17 articles were selected for this review and evaluated utilizing the Johns Hopkins Evidence Based Practice Appraisal Tool. RESULTS: Of the 17 articles, all were quantitative observational study designs. The studies were then synthesized into four outcome themes. These themes included emergent and general psychiatric outcomes, neurodevelopmental disorders, stress and anxiety, and depression. DISCUSSION: The strongest evidence supports a possible correlation between PM2.5 exposure and adolescent mental health outcomes, although there were some studies that contradicted these associations. While research on this topic is in its early stages, more needs to be conducted to determine causality with any of the associations presented to improve generalizability of the findings. IMPLICATIONS FOR PRACTICE: Nurses must be aware of and part of the solution to address climate change and resulting air pollution, as it is a potentially significant threat to children's mental health in the 21st century.

Association of Long-term Exposure to Particulate Air Pollution With Cardiovascular Events in California.

Importance: Long-term exposure to fine particulate air pollution (PM2.5) is a known risk factor for cardiovascular events, but controversy remains as to whether the current National Ambient Air Quality Standard (12 µg/m3 for 1-year mean PM2.5) is sufficiently protective. Objective: To evaluate the associations between long-term fine particulate air pollution and cardiovascular events using electronic health record and geocoded address data. Design, Setting, and Participants: This retrospective cohort study included adults in the Kaiser Permanente Northern California integrated health care system during 2007 to 2016 and followed for up to 10 years. Study participants had no prior stroke or acute myocardial infarction (AMI), and lived in Northern California for at least 1 year. Analyses were conducted January 2020 to December 2022. Exposure: Long-term exposure to PM2.5. Individual-level time-varying 1-year mean PM2.5 exposures for every study participant were updated monthly from baseline through the end of follow-up, accounting for address changes. Main Outcomes and Measures: Incident AMI, ischemic heart disease (IHD) mortality, and cardiovascular disease (CVD) mortality. Cox proportional hazards models were fit with age as time scale, adjusted for sex, race and ethnicity, socioeconomic status, smoking, body mass index, baseline comorbidities, and baseline medication use. Associations below the current regulation limit were also examined. Results: The study cohort included 3.7 million adults (mean [SD] age: 41.1 [17.2] years; 1 992 058 [52.5%] female, 20 205 [0.5%] American Indian or Alaskan Native, 714 043 [18.8%] Asian, 287 980 [7.6%] Black, 696 796 [18.4%] Hispanic, 174 261 [4.6%] multiracial, 1 904 793 [50.2%] White). There was a 12% (95% CI, 7%-18%) increased risk of incident AMI, a 21% (95% CI, 13%-30%) increased risk of IHD mortality, and an 8% (95% CI, 3%-13%) increased risk of CVD mortality associated with a 10 µg/m3 increase in 1-year mean PM2.5. PM2.5 exposure at moderate concentrations (10.0 to 11.9 µg/m3) was associated with increased risks of incident AMI (6% [95% CI, 3%-10%]) and IHD mortality (7% [95% CI, 2%-12%]) compared with low concentrations (less than 8 µg/m3). Conclusions and Relevance: In this study, long-term PM2.5 exposure at moderate concentrations was associated with increased risks of incident AMI, IHD mortality, and CVD mortality. This study's findings add to the evidence that the current regulatory standard is not sufficiently protective.

Interventions of Unani medicine for maintenance of health with special reference to air quality: an evidence-based review.

OBJECTIVES: This article aims to discuss the impact of air quality on human health, measures to achieve the goal of good indoor air quality and proposed benefits of interventions of Unani Medicine with an evidence-based approach. CONTENT: The significance of air quality on the health of the community cannot be denied. Recent evidences from WHO illustrated data on severe air pollutants and their impacts on human health ranges from minor upper respiratory irritation to chronic respiratory ailments including lung carcinoma and heart disease associated with premature mortality and reduced life expectancy. In Unani Medicine, air has been included in the list of factors, which are six in number and play the central role in prevention of diseases and maintenance of health. Air is considered as the medium of most of the extrinsic factors such as chemical and biological pollutants affecting health and their exposure results in short and long-term health issues. The literature of Unani Medicine proposes many simple and effective measures, which help to improve indoor and outdoor air quality. The goal of outdoor clean air is achieved through implementation of measures to tackle the source of pollution, while indoor clean air is attained through various means e.g., fumigation with herbal drugs. Hence, an extensive literature survey on Unani reserve was conducted to collect information about the concept of air discussed under the heading of six essential factors and its implication in prevention of diseases and maintenance of health. Further, research databases such as Pub Med, Google Scholar, and Science-Direct were broadly searched for evidence on the efficacy of herbals mentioned in Unani literature for the indoor air purification and subsequent air quality improvement. SUMMARY AND OUTLOOK: Recent studies showed good air quality leads to decrease in mortality, particularly of respiratory and cardiovascular deaths whereas poor air quality results in a variety of diseases. Unani scholars prescribed several regimens such as Bukhoor (Fumigation), Sa'oot (Nasal instillation) and use of Abeer (Perfumes) and Nadd (Incense) for the improvement of air quality. Likewise various herbal fumigants and sprays containing drugs like mi'a sa'ila (Liquidambar orientalis Mill.), mastagi (Pistacia lentiscus L.), mushk (Moschus moschiferus L.), loban (Styrax benzoides W. G. Craib), abnoos (Diospyros ebenum J. Koenig ex Retz), za'fran (Crocus sativus L.) and sirka (vinegar) etc. has been well explained and used exclusively for air purification and improvement of AQI. Therefore, in the present scenario of altered air quality, we forward certain measures described in Unani system of medicine for health promotion and protection. Scientific evidence on several drugs reveal the presence of a number of pharmacologically active substances, which may provide a new approach into the purification of air.

Mechanistic insights into the health benefits of fish-oil supplementation against fine particulate matter air pollution: a randomized controlled trial.

BACKGROUND: Dietary fish-oil supplementation might attenuate the associations between fine particulate matter (PM2.5) and subclinical biomarkers. However, the molecular mechanisms remain to be elucidated. This study aimed to explore the molecular mechanisms of fish-oil supplementation against the PM2.5-induced health effects. METHODS: We conducted a randomized, double-blinded, and placebo-controlled trial among healthy college students in Shanghai, China, from September 2017 to January 2018. A total of 70 participants from the Fenglin campus of Fudan University were included. We randomly assigned participants to either supplementation of 2.5-gram fish oil (n = 35) or sunflower-seed oil (placebo) (n = 35) per day and conducted four rounds of health measurements in the last two months of the trial. As a post hoc exploratory study, the present untargeted metabolomics analysis used remaining blood samples collected in the previous trial and applied a Metabolome-Wide Association Study framework to compare the effects of PM2.5 on the metabolic profile between the sunflower-seed oil and fish oil groups. RESULTS: A total of 65 participants completed the trial (34 of the fish oil group and 31 of the sunflower-seed oil group). On average, ambient PM2.5 concentration on the day of health measurements was 34.9 µg/m3 in the sunflower-seed oil group and 34.5 µg/m3 in the fish oil group, respectively. A total of 3833 metabolites were significantly associated with PM2.5 in the sunflower-seed oil group and 1757 in the fish oil group. Of these, 1752 metabolites showed significant between-group differences. The identified differential metabolites included arachidonic acid derivatives, omega-3 fatty acids, omega-6 fatty acids, and omega-9 fatty acids that were related to unsaturated fatty acid metabolism, which plays a role in the inflammatory responses. CONCLUSION: This trial suggests fish-oil supplementation could mitigate the PM2.5-induced inflammatory responses via modulating fatty acid metabolism, providing biological plausibility for the health benefits of fish-oil supplementation against PM2.5 exposure. TRIAL REGISTRATION: This study is registered at ClinicalTrails.gov (NCT03255187).

Climate Change Factors and the Aerobiology Effect.

There is clear evidence that climate change is occurring as there has been an acceleration of global temperatures since the mid-nineteenth century along with rising atmospheric carbon dioxide levels. It has been proposed that one of the most significant consequences of climate change on human health could be the impact on aeroallergens. Evidence from around globe has pointed to longer and more abundant pollen season associated with global warming. Additional studies have also suggested increased pollen allergenicity due to air pollution.

Biologic Pollution Due to Ambrosia (Ragweed) Pollen in Urban Environment of Bucharest.

Ragweed pollen is an important component of biological pollution in the urban environment, responsible for increasing respiratory allergies and significant contribution to the health impact of air pollution in the Bucharest area. The aim of this paper is to present the eight-year ragweed pollen monitoring data from Bucharest, to place them in the context of local air pollution, public health regulations and available data on the health impact of ragweed pollen in the urban environment. Our pollen data were correlated with major air pollutant concentrations and with meteorological factors in a recently published local paper and the clinical data of patients with ragweed-induced respiratory symptoms were collected and published in 2019. The ragweed pollen monitoring data, correlated with field data reported by patients and plant specialists confirm the rapid spread of Ambrosia in the Bucharest city area, in addition to some stringent environmental local problems due to air pollution. The number of patients addressed to allergists almost doubled from one year to another, confirming the real alarming health impact of this environmental hazard. Our study confirms the need for more coherent strategies to control ragweed spread, based on application of existing local and international regulations, air pollution control and evaluation of consequences on human health.

The Role of Neighborhood Air Pollution Exposure on Somatic Non-Small Cell Lung Cancer Mutations in the Los Angeles Basin (2013-2018).

Limited previous work has identified a relationship between exposure to ambient air pollution and aggressive somatic lung tumor mutations. More work is needed to confirm this relationship, especially using spatially resolved air pollution. We aimed to quantify the association between different air pollution metrics and aggressive tumor biology. Among patients treated at City of Hope Comprehensive Cancer Center in Duarte, CA (2013-2018), three non-small cell lung cancer somatic tumor mutations, TP53, KRAS, and KRAS G12C/V, were documented. PM2.5 exposure was assessed using state-of-the art ensemble models five and ten years before lung cancer diagnosis. We also explored the role of NO2 using inverse-distance-weighting approaches. We fitted logistic regression models to estimate odds ratio (OR) and their 95% confidence intervals (CIs). Among 435 participants (median age: 67, female: 51%), an IQR increase in NO2 exposure (3.5 µg/m3) five years before cancer diagnosis was associated with an increased risk in TP53 mutation (OR, 95% CI: 1.30, 0.99-1.71). We found an association between highly-exposed participants to PM2.5 (>12 µg/m3) five and ten years before cancer diagnosis and TP53 mutation (OR, 95% CI: 1.61, 0.95-2.73; 1.57, 0.93-2.64, respectively). Future studies are needed to confirm this association and better understand how air pollution impacts somatic profiles and the molecular mechanisms through which they operate.

The Impact of Air Pollution on the Protection of World Cultural Heritage in China.

The damage of air pollution to cultural heritage is widely known. However, the quantitative effects still need to be explored at a holistic level. Different from existing research which focuses on the "model calculation" methods, this paper uses an econometric approach to assess the overall impact of air pollution on the sustainable protection of world cultural heritage in China. Based on the data of the annual monitoring report from 2014 to 2020 released by the China World Cultural Heritage Monitoring Platform, this paper uses the thermal inversion as an instrument variable of air pollution to estimate the overall effects of air pollution on all world cultural heritage sites in China. The results indicate that almost all the air pollutants (except for CO) have significantly negative effects on heritage. The damaging effects of gaseous pollutants including SO2, NO2 and O3 is greater than that of particulate pollutants such as PM2.5 and PM10. Rainfall can exacerbate the worsening effects of gaseous pollutants, but will mitigate the negative effects of particulate pollutants; the windy weather may weaken the negative impact. In addition, environmental regulations from the local government can also alleviate the negative influence of air pollution on heritage protection. This research can provide a more comprehensive environmental prevention policy reference for the protection of world cultural heritage.