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.

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.

Quercetin alleviates PM2.5-induced chronic lung injury in mice by targeting ferroptosis.

Background: PM2.5 is a well-known harmful air pollutant that can lead to acute exacerbation and aggravation of respiratory diseases. Although ferroptosis is involves in the pathological process of pulmonary disease, the potential mechanism of ferroptosis in PM2.5-caused lung inflammation and fibrosis need to be further clarified. Quercetin is a phenolic compound that can inhibit ferroptosis in various diseases. Hence, this study explores the role of ferroptosis in lung injury induced by PM2.5 in order to further elucidate the beneficial effect of quercetin and its underlying mechanism. Methods: C57BL/6J mice were treated with either saline or PM2.5 by intratracheal instillation 20 times (once every two days). Additionally, PM2.5-treated mice were supplemented with two doses of quercetin. Lung injury, lipid peroxidation, iron content and ferroptosis marker protein expression and the Nrf2 signaling pathway were evaluated. In vitro, cell experiments were applied to verify the mechanisms underlying the links between Nrf2 signaling pathway activation and ferroptosis as well as between ferroptosis and inflammation. Results: In vivo, PM2.5 increased lung inflammation and caused lung fibrosis and increased lipid peroxidation contents, iron contents and ferroptosis markers in lung tissues; these effects were significantly reversed by quercetin. Additionally, quercetin upregulated the nuclear Nrf2 expression and downregulated Keap1 expression in lung tissues of PM2.5-exposed mice. Quercetin decreased lipid peroxidation products, iron contents and ferroptosis levels and increased the nuclear translocation of Nrf2 and the degradation of Keap1 in PM2.5-exposed BEAS-2B cells. Moreover, we found that quercetin and dimethyl fumarate markedly decreased lipid peroxidation production and ferroptosis by activating the Nrf2-Keap1 pathway in PM2.5-exposed cells. Furthermore, quercetin reduced inflammatory cytokines and TGF-ß1 in PM2.5-exposed cells. Conclusion: Our data suggested that Nrf2 is involved in ferroptosis in PM2.5-induced lung injury, and quercetin can alleviate these adverse effects via activating Nrf2-Keap1 signaling pathway.

Liquefied Petroleum Gas or Biomass Cooking and Severe Infant Pneumonia.

BACKGROUND: Exposure to household air pollution is a risk factor for severe pneumonia. The effect of replacing biomass cookstoves with liquefied petroleum gas (LPG) cookstoves on the incidence of severe infant pneumonia is uncertain. METHODS: We conducted a randomized, controlled trial involving pregnant women 18 to 34 years of age and between 9 to less than 20 weeks' gestation in India, Guatemala, Peru, and Rwanda from May 2018 through September 2021. The women were assigned to cook with unvented LPG stoves and fuel (intervention group) or to continue cooking with biomass fuel (control group). In each trial group, we monitored adherence to the use of the assigned cookstove and measured 24-hour personal exposure to fine particulate matter (particles with an aerodynamic diameter of ≤2.5 µm [PM2.5]) in the women and their offspring. The trial had four primary outcomes; the primary outcome for which data are presented in the current report was severe pneumonia in the first year of life, as identified through facility surveillance or on verbal autopsy. RESULTS: Among 3200 pregnant women who had undergone randomization, 3195 remained eligible and gave birth to 3061 infants (1536 in the intervention group and 1525 in the control group). High uptake of the intervention led to a reduction in personal exposure to PM2.5 among the children, with a median exposure of 24.2 µg per cubic meter (interquartile range, 17.8 to 36.4) in the intervention group and 66.0 µg per cubic meter (interquartile range, 35.2 to 132.0) in the control group. A total of 175 episodes of severe pneumonia were identified during the first year of life, with an incidence of 5.67 cases per 100 child-years (95% confidence interval [CI], 4.55 to 7.07) in the intervention group and 6.06 cases per 100 child-years (95% CI, 4.81 to 7.62) in the control group (incidence rate ratio, 0.96; 98.75% CI, 0.64 to 1.44; P = 0.81). No severe adverse events were reported to be associated with the intervention, as determined by the trial investigators. CONCLUSIONS: The incidence of severe pneumonia among infants did not differ significantly between those whose mothers were assigned to cook with LPG stoves and fuel and those whose mothers were assigned to continue cooking with biomass stoves. (Funded by the National Institutes of Health and the Bill and Melinda Gates Foundation; HAPIN ClinicalTrials.gov number, NCT02944682.).

Effects of Cooking with Liquefied Petroleum Gas or Biomass on Stunting in Infants.

BACKGROUND: Household air pollution is associated with stunted growth in infants. Whether the replacement of biomass fuel (e.g., wood, dung, or agricultural crop waste) with liquefied petroleum gas (LPG) for cooking can reduce the risk of stunting is unknown. METHODS: We conducted a randomized trial involving 3200 pregnant women 18 to 34 years of age in four low- and middle-income countries. Women at 9 to less than 20 weeks' gestation were randomly assigned to use a free LPG cookstove with continuous free fuel delivery for 18 months (intervention group) or to continue using a biomass cookstove (control group). The length of each infant was measured at 12 months of age, and personal exposures to fine particulate matter (particles with an aerodynamic diameter of ≤2.5 µm) were monitored starting at pregnancy and continuing until the infants were 1 year of age. The primary outcome for which data are presented in the current report - stunting (defined as a length-for-age z score that was more than two standard deviations below the median of a growth standard) at 12 months of age - was one of four primary outcomes of the trial. Intention-to-treat analyses were performed to estimate the relative risk of stunting. RESULTS: Adherence to the intervention was high, and the intervention resulted in lower prenatal and postnatal 24-hour personal exposures to fine particulate matter than the control (mean prenatal exposure, 35.0 µg per cubic meter vs. 103.3 µg per cubic meter; mean postnatal exposure, 37.9 µg per cubic meter vs. 109.2 µg per cubic meter). Among 3061 live births, 1171 (76.2%) of the 1536 infants born to women in the intervention group and 1186 (77.8%) of the 1525 infants born to women in the control group had a valid length measurement at 12 months of age. Stunting occurred in 321 of the 1171 infants included in the analysis (27.4%) of the infants born to women in the intervention group and in 299 of the 1186 infants included in the analysis (25.2%) of those born to women in the control group (relative risk, 1.10; 98.75% confidence interval, 0.94 to 1.29; P = 0.12). CONCLUSIONS: An intervention strategy starting in pregnancy and aimed at mitigating household air pollution by replacing biomass fuel with LPG for cooking did not reduce the risk of stunting in infants. (Funded by the National Institutes of Health and the Bill and Melinda Gates Foundation; HAPIN ClinicalTrials.gov number, NCT02944682.).

Prediction of PM2.5 concentration based on the CEEMDAN-RLMD-BiLSTM-LEC model.

Air quality has emerged as a critical concern in recent years, with the concentration of PM2.5 recognized as a vital index for assessing it. The accuracy of predicting PM2.5 concentrations holds significant value for effective air quality monitoring and management. In response to this, a combined model comprising CEEMDAN-RLMD-BiLSTM-LEC has been introduced, analyzed, and compared against various other models. The combined decomposition method effectively underlines the fundamental characteristics of the data compared to individual decomposition techniques. Additionally, local error correction (LEC) efficiently addresses the issue of prediction errors induced by excessive disturbances. The empirical results of nine steps indicate that the combined CEEMDAN-RLMD-BiLSTM-LEC model outperforms single prediction models such as RLMD and CEEMDAN, reducing MAE, RMSE, and SAMPE by 36.16%, 28.63%, 45.27% and 16.31%, 6.15%, 37.76%, respectively. Moreover, the inclusion of LEC in the model further diminishes MAE, RMSE, and SMAPE by 20.69%, 7.15%, and 44.65%, respectively, exhibiting commendable performance in generalization experiments. These findings demonstrate that the combined CEEMDAN-RLMD-BiLSTM-LEC model offers high predictive accuracy and robustness, effectively handling noisy data predictions and severe local variations. With its wide applicability, this model emerges as a potent tool for addressing various related challenges in the field.

Reduction of household air pollution through clean fuel intervention and recovery of cellular immune balance.

BACKGROUND: We conducted a clean fuel intervention trial (Bangladesh Global Environmental and Occupational Health (GEOHealth) (NCT02824237) with liquefied petroleum gas (LPG) for 26 months among rural Bangladeshi women chronically exposed to household air pollution (HAP) from biomass fuel (BMF) use. We aimed to evaluate the effect of HAP reduction following LPG intervention on immune response outcome. METHODS: We supplied LPG cook stove and refills in cylinder in 200 households for 26 months. We measured personal exposure to HAP [particulate matter 2.5 (PM2·5), black carbon (BC) and carbon monoxide (CO)] in 200 women (main cook) by personal monitors at pre- and post-intervention. Immune function was assessed before and after intervention, in blood collected within 2 weeks of HAP measurements. Primary endpoints included reduction in HAP, lymphocyte proliferation and oxidative stress response, and alterations in T and B cell proportions. FINDINGS: Exclusive LPG use for 26 months resulted in significant reduction in PM2·5 (43.5%), BC (13%) and CO (48%) exposure in the women. For one unit decrease in BC, Treg cells and memory B cells increased by 7% and 34% respectively, in the peripheral circulation. One unit decrease in CO was significantly associated with increase in early B cells and plasmablasts by 66% and 5% respectively. For one unit decrease in BC, percent-dividing cells, proliferation and expansion indices increased by 2%, 0.4%, and 1%, respectively. INTERPRETATION: Reduced personal exposure to HAP through clean fuel intervention was related to a return towards cellular immune balance.

The impact of particulate matters on apoptosis in various organs: Mechanistic and therapeutic perspectives.

Ecological air contamination is the non-homogenous suspension of insoluble particles into gas or/and liquid fluids known as particulate matter (PM). It has been discovered that exposure to PM can cause serious cellular defects, followed by tissue damage known as cellular stress. Apoptosis is a homeostatic and regulated phenomenon associated with distinguished physiological actions inclusive of organ and tissue generation, aging, and development. Moreover, it has been proposed that the deregulation of apoptotic performs an active role in the occurrence of many disorders, such as autoimmune disease, neurodegenerative, and malignant, in the human population. Recent studies have shown that PMs mainly modulate multiple signaling pathways involved in apoptosis, including MAPK, PI3K/Akt, JAK/STAT, NFκB, Endoplasmic Stress, and ATM/P53, leading to apoptosis dysregulation and apoptosis-related pathological conditions. Here, the recently published data concerning the effect of PM on the apoptosis of various organs, with a particular focus on the importance of apoptosis as a component in PM-induced toxicity and human disease development, is carefully discussed. Moreover, the review also highlighted the various therapeutic approaches, including small molecules, miRNA replacement therapy, vitamins, and PDRN, for treating diseases caused by PM toxicity. Notably, researchers have considered medicinal herbs a potential treatment for PM-induced toxicity due to their fewer side effects. So, in the final section, we analyzed the performance of some natural products for inhibition and intervention of apoptosis arising from PM-induced toxicity.

Long-term exposure to airborne metals and risk of cancer in the French cohort Gazel.

BACKGROUND: The specific compounds that make ambient fine particulate matter (PM2.5) carcinogen remain poorly identified. Some metals contribute to ambient PM2.5 and possibly to its adverse effects. But the challenge of assessing exposure to airborne metals limits epidemiological studies. OBJECTIVE: To analyze the relationships between several airborne metals and risk of cancer in a large population. METHODS: We estimated the individual exposure to 12 airborne metals of âˆ¼ 12,000 semi-urban and rural participants of the French population-based Gazel cohort using moss biomonitoring data from a 20-year national program. We used principal component analyses (PCA) to derive groups of metals, and focused on six single carcinogenic or toxic metals (arsenic, cadmium, chromium, lead, nickel, and vanadium). We used extended Cox models with attained age as time-scale and time-varying weighted average exposures, adjusted for individual and area-level covariables, to analyze the association between each exposure and all-site combined, bladder, lung, breast, and prostate cancer incidence. RESULTS: We identified 2,401 cases of all-site cancer between 2001 and 2015. Over the follow-up, median exposures varied from 0.22 (interquartile range (IQR): 0.18-0.28) to 8.68 (IQR: 6.62-11.79) µg.g-1 of dried moss for cadmium and lead, respectively. The PCA yielded three groups identified as "anthropogenic", "crustal", and "marine". Models yielded positive associations between most single and groups of metal and all-site cancer, with e.g. hazard ratios of 1.08 (95% CI: 1.03, 1.13) for cadmium or 1.06 (95% CI: 1.02,1.10) for lead, per interquartile range increase. These findings were consistent across supplementary analyses, albeit attenuated when accounting for total PM2.5. Regarding specific site cancers, we estimated positive associations mostly for bladder, and generally with large confidence intervals. CONCLUSION: Most single and groups of airborne metals, except vanadium, were associated with risk of cancer. These findings may help identify sources or components of PM2.5 that may be involved in its carcinogenicity.

Dietary polyunsaturated fatty acids intake, air pollution, and the risk of lung cancer: A prospective study in UK biobank.

BACKGROUND: Epidemiological evidence on the association between specific types of polyunsaturated fatty acids (PUFAs) intake and lung cancer risk is limited. However, whether dietary-specific PUFAs intake can modify the association between air pollutants and incident lung cancer remains unknown. METHODS: Cox proportional hazard models and restricted cubic spline regression were used to evaluate the associations of omega-3 PUFAs, omega-6 PUFAs and the ratio of omega-6 PUFAs to omega-3 PUFAs intake with lung cancer risk. Furthermore, we evaluated the associations between air pollutants and incident lung cancer, and whether dietary-specific PUFAs intake would modify the relationship using stratification analyses. RESULTS: This study found significant associations between the risk of lung cancer and omega-3 PUFAs intake (hazard ratio [HR], 0.82; 95 % confidence interval [CI], 0.73-0.93; per 1 g/d), and omega-6 PUFAs intake (HR, 0.98; 95 % CI, 0.96-0.99; per 1 g/d). We did not observe an association between the omega-6 to omega-3 PUFAs intake ratio and incident lung cancer. With regard to air pollution, omega-3 PUFAs intake attenuated the positive relationship between nitrogen oxides (NOx) pollution and lung cancer risk, and an increased incidence of lung cancer was found only in the low omega-3 PUFAs intake group (p < 0.05). Surprisingly, PUFAs intake (regardless of omega-3 PUFAs, omega-6 PUFAs, or in total) reinforced the pro-carcinogenic effects of PM2.5 on lung cancer, and a positive association between PM2.5 pollutants and incident lung cancer was observed only in the high PUFAs groups (p < 0.05). CONCLUSIONS: Higher dietary omega-3 and omega-6 PUFAs intake was associated with a decreased risk of lung cancer in the study population. As omega-3 PUFAs have different modification effects on NOX and PM2.5 air pollution related lung cancer incidence, precautions should be taken when using omega-3 PUFAs as health-promoting dietary supplements, especially in high PM2.5 burden regions.

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.

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.

Spatiotemporal distribution, trend, forecast, and influencing factors of transboundary and local air pollutants in Nagasaki Prefecture, Japan.

The study of PM2.5 and NO2 has been emphasized in recent years due to their adverse effects on public health. To better understand these pollutants, many studies have researched the spatiotemporal distribution, trend, forecast, or influencing factors of these pollutants. However, rarely studies have combined these to generate a more holistic understanding that can be used to assess air pollution and implement more effective strategies. In this study, we analyze the spatiotemporal distribution, trend, forecast, and factors influencing PM2.5 and NO2 in Nagasaki Prefecture by using ordinary kriging, pearson's correlation, random forest, mann-kendall, auto-regressive integrated moving average and error trend and seasonal models. The results indicated that PM2.5, due to its long-range transport properties, has a more substantial spatiotemporal variation and affects larger areas in comparison to NO2, which is a local pollutant. Despite tri-national efforts, local regulations and legislation have been effective in reducing NO2 concentration but less effective in reducing PM2.5. This multi-method approach provides a holistic understanding of PM2.5 and NO2 pollution in Nagasaki prefecture, which can aid in implementing more effective pollution management strategies. It can also be implemented in other regions where studies have only focused on one of the aspects of air pollution and where a holistic understanding of air pollution is lacking.

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).

Correlation of Pollen Concentration and Meteorological Factors with Medical Condition of Allergic Rhinitis in Shenyang Area.

Background: The pathogenesis of allergic rhinitis (AR) was affected by meteorological and environmental factors. This study investigated the association between clinical symptoms of AR patients with pollen dispersal and meteorological conditions. Methods: The clinical features of 10,838 AR patients who were treated in the Department of Otorhinolaryngology, The First Hospital of China Medical University, Shenyang, from March 2021 to October 2021 were retrospectively analyzed. We collected pollen by a pollen collector, read and counted it under a microscope, identified the species of the pollen particles, and recorded meteorological data (average daily temperature, maximum and minimum temperature, average daily wind, average daily precipitation, average daily humidity, average pressure, air quality index, PM2.5, PM10, SO2, NO2, CO, and O3), to analyze the correlation among meteorological conditions, pollen dispersal, and number of AR visits. Finally, pollen allergen-positive and symptoms were scored. Results: Among the AR visits, patients >41 years old accounted for the highest proportion (64.15%). 43.67% of the patients were complicated with bronchial asthma, and the disease incidence peaked in September. During the period of the study, a total of 27,512 pollen grains were collected, and 17 species were identified. The pollens of Compositae and Moraceae were the main allergenic sources leading to the increase in AR visits from August to September. The peak of pollen dispersal was in spring, summer, and autumn. The total amount of pollen was not only related to the average daily minimum temperature, average daily precipitation, and average daily humidity but also had a significant correlation with air quality index and air pollutants (PM2.5 and PM10, SO2, NO2, and CO). In addition, there was a significant correlation between the number of daily pollen allergen-positive patients and the pollen concentration of Compositae and Moraceae as well as air pollution components. The clinical symptoms of pollen allergen-positive patients were mainly nasal congestion, red/itchy eyes, and epiphora. Conclusion: The peak seasons of pollen dispersal in Shenyang were in spring, summer, and autumn, and the allergenic pollens were mainly Compositae and Moraceae. In addition, AR was substantially correlated with pollen concentration and meteorological factors. This study may help provide early warning information and prevention for AR patients.

Liquefied Petroleum Gas or Biomass for Cooking and Effects on Birth Weight.

BACKGROUND: Exposure during pregnancy to household air pollution caused by the burning of solid biomass fuel is associated with adverse health outcomes, including low birth weight. Whether the replacement of a biomass cookstove with a liquefied petroleum gas (LPG) cookstove would result in an increase in birth weight is unclear. METHODS: We performed a randomized, controlled trial involving pregnant women (18 to <35 years of age and at 9 to <20 weeks' gestation as confirmed on ultrasonography) in Guatemala, India, Peru, and Rwanda. The women were assigned in a 1:1 ratio to use a free LPG cookstove and fuel (intervention group) or to continue using a biomass cookstove (control group). Birth weight, one of four prespecified primary outcomes, was the primary outcome for this report; data for the other three outcomes are not yet available. Birth weight was measured within 24 hours after birth. In addition, 24-hour personal exposures to fine particulate matter (particles with a diameter of ≤2.5 µm [PM2.5]), black carbon, and carbon monoxide were measured at baseline and twice during pregnancy. RESULTS: A total of 3200 women underwent randomization; 1593 were assigned to the intervention group, and 1607 to the control group. Uptake of the intervention was nearly complete, with traditional biomass cookstoves being used at a median rate of less than 1 day per month. After randomization, the median 24-hour personal exposure to fine particulate matter was 23.9 µg per cubic meter in the intervention group and 70.7 µg per cubic meter in the control group. Among 3061 live births, a valid birth weight was available for 94.9% of the infants born to women in the intervention group and for 92.7% of infants born to those in the control group. The mean (±SD) birth weight was 2921±474.3 g in the intervention group and 2898±467.9 g in the control group, for an adjusted mean difference of 19.6 g (95% confidence interval, -10.1 to 49.2). CONCLUSIONS: The birth weight of infants did not differ significantly between those born to women who used LPG cookstoves and those born to women who used biomass cookstoves. (Funded by the National Institutes of Health and the Bill and Melinda Gates Foundation; HAPIN ClinicalTrials.gov number, NCT02944682.).

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.

Associations between airborne crude oil chemicals and symptom-based asthma.

RATIONALE: The 2010 Deepwater Horizon (DWH) oil spill response and cleanup (OSRC) workers were exposed to airborne total hydrocarbons (THC), benzene, toluene, ethylbenzene, o-, m-, and p-xylenes and n-hexane (BTEX-H) from crude oil and PM2.5 from burning/flaring oil and natural gas. Little is known about asthma risk among oil spill cleanup workers. OBJECTIVES: We assessed the relationship between asthma and several oil spill-related exposures including job classes, THC, individual BTEX-H chemicals, the BTEX-H mixture, and PM2.5 using data from the Gulf Long-Term Follow-up (GuLF) Study, a prospective cohort of 24,937 cleanup workers and 7,671 nonworkers following the DWH disaster. METHODS: Our analysis largely focused on the 19,018 workers without asthma before the spill who had complete exposure, outcome, and covariate information. We defined incident asthma 1-3 years following exposure using both self-reported wheeze and self-reported physician diagnosis of asthma. THC and BTEX-H were assigned to participants based on measurement data and work histories, while PM2.5 used modeled estimates. We used modified Poisson regression to estimate risk ratios (RR) and 95% confidence intervals (CIs) for associations between spill-related exposures and asthma and a quantile-based g-computation approach to explore the joint effect of the BTEX-H mixture on asthma risk. RESULTS: OSRC workers had greater asthma risk than nonworkers (RR: 1.60, 95% CI: 1.38, 1.85). Higher estimated THC exposure levels were associated with increased risk in an exposure-dependent manner (linear trend test p < 0.0001). Asthma risk also increased with increasing exposure to individual BTEX-H chemicals and the chemical mixture: A simultaneous quartile increase in the BTEX-H mixture was associated with an increased asthma risk of 1.45 (95% CI: 1.35,1.55). With fewer cases, associations were less apparent for physician-diagnosed asthma alone. CONCLUSIONS: THC and BTEX-H were associated with increased asthma risk defined using wheeze symptoms as well as a physician diagnosis.

Birch pollen, air pollution and their interactive effects on airway symptoms and peak expiratory flow in allergic asthma during pollen season - a panel study in Northern and Southern Sweden.

BACKGROUND: Evidence of the role of interactions between air pollution and pollen exposure in subjects with allergic asthma is limited and need further exploration to promote adequate preventive measures. The objective of this study was to assess effects of exposure to ambient air pollution and birch pollen on exacerbation of respiratory symptoms in subjects with asthma and allergy to birch. METHODS: Thirty-seven subjects from two Swedish cities (Gothenburg and Umeå) with large variation in exposure to both birch-pollen and air pollutants, participated in the study. All subjects had confirmed allergy to birch and self-reported physician-diagnosed asthma. The subjects recorded respiratory symptoms such as rhinitis or eye irritation, dry cough, dyspnoea, the use of any asthma or allergy medication and peak respiratory flow (PEF), daily for five consecutive weeks during two separate pollen seasons and a control season without pollen. Nitrogen oxides (NOx), ozone (O3), particulate matter (PM2.5), birch pollen counts, and meteorological data were obtained from an urban background monitoring stations in the study city centres. The data were analysed using linear mixed effects models. RESULTS: During pollen seasons all symptoms and medication use were higher, and PEF was reduced in the subjects. In regression analysis, exposure to pollen at lags 0 to 2 days, and lags 0 to 6 days was associated with increased ORs of symptoms and decreased RRs for PEF. Pollen and air pollution interacted in some cases; during low pollen exposure, there were no associations between air pollution and symptoms, but during high pollen exposure, O3 concentrations were associated with increased OR of rhinitis or eye irritation, and PM2.5 concentrations were associated with increased ORs of rhinitis or eye irritation, dyspnea and increased use of allergy medication. CONCLUSIONS: Pollen and air pollutants interacted to increase the effect of air pollution on respiratory symptoms in allergic asthma. Implementing the results from this study, advisories for individuals with allergic asthma could be improved, minimizing the morbidities associated with the condition.

Effects of a Liquefied Petroleum Gas Stove Intervention on Gestational Blood Pressure: Intention-to-Treat and Exposure-Response Findings From the HAPIN Trial.

BACKGROUND: Approximately 3 to 4 billion people worldwide are exposed to household air pollution, which has been associated with increased blood pressure (BP) in pregnant women in some studies. METHODS: We recruited 3195 pregnant women in Guatemala, India, Peru, and Rwanda and randomly assigned them to intervention or control groups. The intervention group received a gas stove and fuel during pregnancy, while the controls continued cooking with solid fuels. We measured BP and personal exposure to PM2.5, black carbon and carbon monoxide 3× during gestation. We conducted an intention-to-treat and exposure-response analysis to determine if household air pollution exposure was associated with increased gestational BP. RESULTS: Median 24-hour PM2.5 dropped from 84 to 24 µg/m3 after the intervention; black carbon and carbon monoxide decreased similarly. Intention-to-treat analyses showed an increase in systolic BP and diastolic BP in both arms during gestation, as expected, but the increase was greater in intervention group for both systolic BP (0.69 mm Hg [0.03-1.35]; P=0.04) and diastolic BP (0.62 mm Hg [0.05-1.19]; P=0.03). The exposure-response analyses suggested that higher exposures to household air pollution were associated with moderately higher systolic BP and diastolic BP; however, none of these associations reached conventional statistical significance. CONCLUSIONS: In intention-to-treat, we found higher gestational BP in the intervention group compared with controls, contrary to expected. In exposure-response analyses, we found a slight increase in BP with higher exposure, but it was not statistically significant. Overall, an intervention with gas stoves did not markedly affect gestational BP.