The effects of ambient particulate matter air pollution on platelets and hemostasis.

Introduction: Elevated ambient pollution exposure is potentially linked to thromboembolism. However, the mechanisms by which particulate matter (PM) interferes with the balance of hemostatic system remain unclear. This study investigates PM-mediated hemostatic changes in individuals across unique seasonal variations of ambient pollution. Methods: This prospective study was conducted between February and July 2020 during alterations in ambient pollution in Chiang Mai, Thailand. Blood tests from 30 healthy subjects were assessed at four-week intervals, four times in total. Various coagulation tests, including prothrombin time (PT), activated partial thromboplastin time (aPTT), von Willebrand factor (vWF), platelet count, and platelet functions, were evaluated. A mixed-effects model was used to analyze the impact of high PM2.5 and PM10 on hemostatic parameters. Results: Thirty male subjects with mean age of 38.9 ± 8.2 years, were included. High levels of PM2.5 and PM10 were significantly associated with PT shortening, with no such effect observed in aPTT. PM2.5 and PM10 values also positively correlated with vWF function, while vWF antigen levels remained unchanged. Soluble P-selectin showed a strong positive association with PM2.5 and PM10 levels. Platelet function analysis revealed no correlation with PM values. Conclusion: Short-term exposure to elevated PM2.5 and PM10 concentrations was linked to shortened PT and enhanced vWF function in healthy individuals. Exploring the impact of these changes on clinically relevant thrombosis is crucial. Additional studies on the pathogenesis of pollution-related thrombosis are warranted for maintaining good health.

Short-term associations of PM10 attributed to biomass burning with respiratory and cardiovascular hospital admissions in Peninsular Malaysia.

BACKGROUND: Biomass burning (BB) is a major source of air pollution and particulate matter (PM) in Southeast Asia. However, the health effects of PM smaller than 10 µm (PM10) originating from BB may differ from those of other sources. This study aimed to estimate the short-term association of PM10 from BB with respiratory and cardiovascular hospital admissions in Peninsular Malaysia, a region often exposed to BB events. METHODS: We obtained and analyzed daily data on hospital admissions, PM10 levels and BB days from five districts from 2005 to 2015. We identified BB days by evaluating the BB hotspots and backward wind trajectories. We estimated PM10 attributable to BB from the excess of the moving average of PM10 during days without BB hotspots. We fitted time-series quasi-Poisson regression models for each district and pooled them using meta-analyses. We adjusted for potential confounders and examined the lagged effects up to 3 days, and potential effect modification by age and sex. RESULTS: We analyzed 210 960 respiratory and 178 952 cardiovascular admissions. Almost 50% of days were identified as BB days, with a mean PM10 level of 53.1 µg/m3 during BB days and 40.1 µg/m3 during normal days. A 10 µg/m3 increment in PM10 from BB was associated with a 0.44% (95% CI: 0.06, 0.82%) increase in respiratory admissions at lag 0-1, with a stronger association in adults aged 15-64 years and females. We did not see any significant associations for cardiovascular admissions. CONCLUSIONS: Our findings suggest that short-term exposure to PM10 from BB increased the risk of respiratory hospitalizations in Peninsular Malaysia.

Estimating the short-term effect of PM2.5 on the mortality of cardiovascular diseases based on instrumental variables.

BACKGROUND: PM2.5 can induce and aggravate the occurrence and development of cardiovascular diseases (CVDs). The objective of our study is to estimate the causal effect of PM2.5 on mortality rates associated with CVDs using the instrumental variables (IVs) method. METHODS: We extracted daily meteorological, PM2.5 and CVDs death data from 2016 to 2020 in Binzhou. Subsequently, we employed the general additive model (GAM), two-stage predictor substitution (2SPS), and control function (CFN) to analyze the association between PM2.5 and daily CVDs mortality. RESULTS: The 2SPS estimated the association between PM2.5 and daily CVDs mortality as 1.14% (95% CI: 1.04%, 1.14%) for every 10 µg/m3 increase in PM2.5. Meanwhile, the CFN estimated this association to be 1.05% (95% CI: 1.02%, 1.10%). The GAM estimated it as 0.85% (95% CI: 0.77%, 1.05%). PM2.5 also exhibited a statistically significant effect on the mortality rate of patients with ischaemic heart disease, myocardial infarction, or cerebrovascular accidents (P < 0.05). However, no significant association was observed between PM2.5 and hypertension. CONCLUSION: PM2.5 was significantly associated with daily CVDs deaths (excluding hypertension). The estimates from the IVs method were slightly higher than those from the GAM. Previous studies based on GAM may have underestimated the impact of PM2.5 on CVDs.

Forecasting rheumatoid arthritis patient arrivals by including meteorological factors and air pollutants.

The burden of rheumatoid arthritis (RA) has gradually elevated, increasing the need for medical resource redistribution. Forecasting RA patient arrivals can be helpful in managing medical resources. However, no relevant studies have been conducted yet. This study aims to construct a long short-term memory (LSTM) model, a deep learning model recently developed for novel data processing, to forecast RA patient arrivals considering meteorological factors and air pollutants and compares this model with traditional methods. Data on RA patients, meteorological factors and air pollutants from 2015 to 2022 were collected and normalized to construct moving average (MA)- and autoregressive (AR)-based and LSTM models. After data normalization, the root mean square error (RMSE) was adopted to evaluate models' forecast ability. A total of 2422 individuals were enrolled. Not using the environmental data, the RMSEs of the MA- and AR-based models' test sets are 0.131, 0.132, and 0.117 when the training set: test set ratio is 2:1, 3:1, and 7:1, while they are 0.110, 0.130, and 0.112 for the univariate LSTM models. Considering meteorological factors and air pollutants, the RMSEs of the MA- and AR-based model test sets were 0.142, 0.303, and 0.164 when the training set: test set ratio is 2:1, 3:1, and 7:1, while they were 0.108, 0.119, and 0.109 for the multivariable LSTM models. Our study demonstrated that LSTM models can forecast RA patient arrivals more accurately than MA- and AR-based models for datasets of all three sizes. Considering the meteorological factors and air pollutants can further improve the forecasting ability of the LSTM models. This novel method provides valuable information for medical management, the optimization of medical resource redistribution, and the alleviation of resource shortages.

Adverse effects of meteorological factors and air pollutants on dry eye disease: a hospital-based retrospective cohort study.

Although previous studies have suggested that meteorological factors and air pollutants can cause dry eye disease (DED), few clinical cohort studies have determined the individual and combined effects of these factors on DED. We investigated the effects of meteorological factors (humidity and temperature) and air pollutants [particles with a diameter ≤ 2.5 µ m (PM2.5), ozone (O3), nitrogen dioxide (NO2), and carbon monoxide (CO)] on DED. A retrospective cohort study was conducted on 53 DED patients. DED was evaluated by Symptom Assessment in Dry Eye (SANDE), tear secretion, tear film break-up time (TBUT), ocular staining score (OSS), and tear osmolarity. To explore the individual, non-linear, and joint associations between meteorological factors, air pollutants, and DED parameters, we used generalized linear mixed model (GLMM) and Bayesian kernel machine regression (BKMR). After adjusting for all covariates, lower relative humidity or temperature was associated with a higher SANDE (p < 0.05). Higher PM2.5, O3, and NO2 levels were associated with higher SANDE and tear osmolarity (p < 0.05). Higher O3 levels were associated with lower tear secretion and TBUT, whereas higher NO2 levels were associated with higher OSS (p < 0.05). BKMR analyses indicated that a mixture of meteorological factors and air pollutants was significantly associated with increased SANDE, OSS, tear osmolarity, and decreased tear secretion.

Boletim mensal VigiAR: 02/2024: volume 66

O Programa em Saúde Ambiental relacionado a populações expostas à poluição do ar do Município de São Paulo (VIGIAR) tem por objetivo desenvolver ações de vigilância em saúde ambiental, para populações expostas aos poluentes atmosféricos, de forma a orientar medidas de prevenção, promoção da saúde e de atenção integral, conforme preconizado pelo Sistema Único de Saúde (SUS).

Exposure to ambient fine particulate matter components during pregnancy and early childhood and its association with asthma, allergies, and sensitization in school-age children.

BACKGROUND: Exposure to fine particulate matter (PM2.5) has been associated with allergic diseases, including asthma. However, information about the effects of specific PM2.5 components is limited. This study aimed to investigate the relationship of exposure to chemical components of PM2.5 during pregnancy and early childhood with the development of asthma, allergies, and sensitization in school-age children. METHODS: This study included 2,408 children in the second grade of elementary school. Questionnaire surveys of respiratory/allergic symptoms and measurements of serum total IgE and specific IgE levels to house dust mite (HDM) and animal proteins were conducted. Exposures to ambient PM2.5 mass, sulfate (SO42-), nitrate (NO3-), ammonium (NH4+), elemental carbon (EC), and organic carbon (OC) of PM2.5 in participants' residences from conception to age six were estimated using predictive models. Multiple logistic regression analysis was used to analyze the association of respiratory/allergic symptoms and allergen sensitization with estimated exposure concentrations, after adjustment for survey year, sex, season of birth, feeding method during infancy, presence of siblings, history of lower respiratory tract infection, use of childcare facilities, passive smoking, presence of pets, mother's age, history of allergic diseases, smoking during pregnancy, and annual household income. RESULTS: No significant association was found between PM2.5 and its component concentrations and asthma. However, wheezing significantly increased with mean NO3- concentrations during pregnancy (odds ratio of 1.64 [95% confidence interval: 1.10, 2.47] for an interquartile range increase). Significant associations were also found between EC in the second trimester of pregnancy and PM2.5, NO3-, EC, and OC concentrations in early childhood. Higher PM2.5, SO4-, and NH4+ concentrations during the second trimester increased the risk of rhinitis. Sensitizations to HDM and animal proteins were significantly associated with exposure to components such as SO42- and NH4+ during pregnancy but not with postnatal exposure. CONCLUSIONS: Exposures to NO3-, EC, and OC during pregnancy and early childhood were associated with wheezing. SO42- and NH4+ exposures during pregnancy were associated with sensitization to HDM and animal proteins. Asthma was not associated with exposure to PM2.5 and its main components at any period.

Impact of climate change on paediatric respiratory health: pollutants and aeroallergens.

Paediatric populations are particularly vulnerable to respiratory diseases caused and exacerbated by aeroallergens, pollutants and infectious agents. Worsening climate change is expected to increase the prevalence of pollutants and aeroallergens while amplifying disease severity and causing disproportionate effects in under-resourced areas. The purpose of this narrative review is to summarise the role of anthropogenic climate change in the literature examining the future impact of aeroallergens, pollutants and infectious agents on paediatric respiratory diseases with a focus on equitable disease mitigation. The aeroallergens selected for discussion include pollen, dust mites and mould as these are prevalent triggers of paediatric asthma worldwide. Human rhinovirus and respiratory syncytial virus are key viruses interacting with climate change and pollution and are primary causal agents of viral respiratory disease. Within this review, we present the propensity for aeroallergens, climate change and pollution to synergistically exacerbate paediatric respiratory disease and outline measures that can ameliorate the expected increase in morbidity and severity of disease through a health equity lens. We support shifting from fossil fuels to renewable energy worldwide, across sectors, as a primary means of reducing increases in morbidity.

Microplastic and plastic pollution: impact on respiratory disease and health.

Throughout their lifecycle, from production to use and upon disposal, plastics release chemicals and particles known as micro- and nanoplastics (MNPs) that can accumulate in the environment. MNPs have been detected in different locations of the human body, including in our lungs. This is likely a consequence of MNP exposure through the air we breathe. Yet, we still lack a comprehensive understanding of the impact that MNP exposure may have on respiratory disease and health. In this review, we have collated the current body of evidence on the implications of MNP inhalation on human lung health from in vitro, in vivo and occupational exposure studies. We focused on interactions between MNP pollution and different specific lung-resident cells and respiratory diseases. We conclude that it is evident that MNPs possess the capacity to affect lung tissue in disease and health. Yet, it remains unclear to which extent this occurs upon exposure to ambient levels of MNPs, emphasising the need for a more comprehensive evaluation of environmental MNP exposure levels in everyday life.

Prenatal exposure to air pollutants and the risk of congenital heart disease: a Korean national health insurance database-based study.

Air pollution and heavy metal exposure are emerging public health concerns. Prenatal exposure to air pollutants and heavy metals has been implicated in the development of congenital heart disease (CHD). However, the relationship between exposure to airborne heavy metals and CHD has not yet been investigated. Therefore, in this large population-based study, we investigated the association between air pollutants, including airborne heavy metals, and the risk of CHD using national health insurance claims data from South Korea. Data regarding 1,129,442 newborns and their mothers were matched with air pollutant levels during the first 8 weeks of gestation. In the five-air pollutant model, we found significant positive correlations between prenatal exposure to sulfur dioxide (SO2; odds ratio [OR] 6.843, 95% confidence interval [CI] 5.746-8.149) and cadmium (Cd; OR 1.513, 95% CI 1.187-1.930) and the risk of ventricular septal defects in newborns. This study highlights the association between prenatal exposure to air pollutants, including airborne heavy metals, and an elevated CHD risk. Further research is essential to validate and expand these findings, with the ultimate goal of enhancing public health outcomes.

Prenatal exposure to PM2.5 and childhood body mass index growth trajectories from birth to 6 years old.

This study aimed to determine the relationships between prenatal PM2.5 exposure and childhood growth trajectories during the first 6 years of life. A total of 47,625 pairs of mothers and children were recruited from a prospective birth cohort conducted between 2011 and 2013 in Wuhan, China, and followed for 6 years. We used the group-based trajectory models to classify the population into three trajectory groups: slow growth (n = 13,671, 28.7%), normal growth (n = 29,736, 62.4%), and rapid growth (n = 4218, 8.9%). Multinomial logistic regression models were used to determine the associations of prenatal PM2.5 exposure and childhood growth trajectories. Compared to normal growth trajectory, increased PM2.5 exposure in trimester 1, trimester 2 and the entire pregnancy showed significant associations with an increased risk of the slow growth trajectory but reduced the risk for the rapid growth trajectory, significant association of prenatal PM2.5 exposure with rapid growth trajectory was only observed in the trimester 3. Stratified analyses displayed relatively stronger associations among those mothers with maternal age over 35 years, pre-pregnancy BMI ≥ 25 kg/m2, and previous delivery experience. Prenatal exposure to PM2.5, particularly during the midpoint period of pregnancy, was more likely to have a slow growth trajectory and a lower risk of rapid growth trajectory. Maternal age, pre-pregnancy BMI, and previous delivery experience might modify these associations.

[Spatiotemporal Trends and Driving Factors of PM2.5-related Health Burden in Gansu Province, China from 2013 to 2020].

To evaluate the spatiotemporal trends and drivers of PM2.5-related health effects in Gansu Province since the implementation of the Air Pollution Prevention and Control Action Plan, the latest global exposure mortality model （GEMM） was adopted to estimate the health burden attributable to PM2.5 in Gansu Province from 2013 to 2020. The factor decomposition method was used to further quantify the main causes of the long-term changes in deaths attributable to PM2.5 pollution. The results showed that from 2013 to 2020, the population-weighted PM2.5 concentration in Gansu Province decreased by 34.57%, and the proportion of people exposed to areas with an annual average PM2.5 concentration exceeding 35 µg·m-3 decreased significantly from 72.89% to 11.61%. Moreover, the number of attributable deaths in Gansu Province declined from 12 826 （95%CI： 7 840-17 408） in 2 013 to 9 814 （95%CI： 6 407-13 036） in 2020, indicating a decrease of 23.48%. Attributable deaths from stroke, chronic obstructive pulmonary disease, lung cancer, and lower respiratory infection declined, whereas deaths from ischemic heart disease increased by 12.11%. Notably, individuals aged 60 years and older accounted for more than 80% of all age-related deaths. The number of deaths attributable to PM2.5 in central and eastern Gansu Province was significantly higher than that in the Hexi region, and most regions showed a downward trend. The contribution of the total population, age structure, baseline mortality rate, and PM2.5 concentration to the change in PM2.5-related deaths was -1.26%, 16.16%, -9.84%, and -28.55%, respectively. Overall, population aging and a decrease in PM2.5 concentration were the main factors contributing to the increase and decrease in PM2.5-related deaths, respectively. The active clean air policies in Gansu Province have reduced the health burden caused by PM2.5 pollution, but with the trend of population aging, a significant reduction in PM2.5 concentration will be needed in the future to avoid more attributable deaths.

Particulate Matter and Its Impact on Macrophages: Unraveling the Cellular Response for Environmental Health.

Particulate matter (PM) imposes a significant impact to environmental health with deleterious effects on the human pulmonary and cardiovascular systems. Macrophages (Mφ), key immune cells in lung tissues, have a prominent role in responding to inhaled cells, accommodating inflammation, and influencing tissue repair processes. Elucidating the critical cellular responses of Mφ to PM exposure is essential to understand the mechanisms underlying PM-induced health effects. The present review aims to give a glimpse on literature about the PM interaction with Mφ, triggering the cellular events causing the inflammation, oxidative stress (OS) and tissue damage. The present paper reviews the different pathways involved in Mφ activation upon PM exposure, including phagocytosis, intracellular signaling cascades, and the release of pro-inflammatory mediators. Potential therapeutic strategies targeting Mφ-mediated responses to reduce PM-induced health effects are also discussed. Overall, unraveling the complex interplay between PM and Mφ sheds light on new avenues for environmental health research and promises to develop targeted interventions to reduce the burden of PM-related diseases on global health.

Effects of major air pollutants on angina hospitalizations: a correlation study.

BACKGROUND: Angina is a crucial risk signal for cardiovascular disease. However, few studies have evaluated the effects of ambient air pollution exposure on angina. OBJECTIVE: We aimed to explore the short-term effects of air pollution on hospitalization for angina and its lag effects. METHODS: We collected data on air pollutant concentrations and angina hospitalizations from 2013 to 2020. Distributed lag nonlinear model (DLNM) was used to evaluate the short-term effects of air pollutants on angina hospitalization under different lag structures. Stratified analysis by sex, age and season was obtained. RESULTS: A total of 39,110 cases of angina hospitalization were included in the study. The results showed a significant positive correlation between PM2.5, SO2, NO2, and CO and angina hospitalization. Their maximum harmful effects were observed at lag0-7 (RR = 1.042; 95% CI: 1.017, 1.068), lag0-3 (RR = 1.067; 95% CI: 1.005, 1.133), lag0-6 (RR = 1.078; 95% CI: 1.041, 1.117), and lag0-6 (RR = 1.244; 95% CI: 1.109, 1.397), respectively. PM10 did not have an overall risk effect on angina hospitalization, but it did have a risk effect on women and the elderly. O3 was significantly negatively correlated with angina hospitalization, with the most pronounced effect observed at lag0-6 (RR = 0.960; 95% CI: 0.940, 0.982). Stratified analysis results showed that women and the elderly were more susceptible to pollutants, and the adverse effects of pollutants were stronger in the cold season. CONCLUSION: Short-term exposure to PM2.5, SO2, NO2, and CO increases the risk of hospitalization for angina.

Impact of secondhand smoke on air quality in partially enclosed outdoor hospitality venues: a review.

BACKGROUND: Smoking is a leading cause of premature mortality and morbidity globally. The pollutants generated from smoke are not only harmful to smokers, but also to those exposed to secondhand smoke. As a result of increasingly restrictive indoor smoke-free policies in many countries, there is a tendency for tobacco smoking to move outdoors into partially enclosed settings in hospitality venues. The aim of this systematic review was to evaluate the impact of secondhand smoke on air quality in outdoor hospitality venues. METHODS: Two electronic databases PubMed and Scopus were searched from 1 January 2010 to 30 June 2022 for studies of air quality impacts from tobacco smoking in outdoor hospitality venues. A total of 625 studies were screened and 13 studies were included in this review. RESULTS: The majority (9 studies) of reviewed studies monitored PM2.5 concentration as an indicator of secondhand smoke. PM2.5 was reported from 10.9 µg/m3 to 91.0 µg/m3 in outdoor smoking areas, compared to 4.0 µg/m3 to 20.4 µg/m3 in outdoor control sites unaffected by smoking. Secondhand smoke can also drift into adjacent outdoor areas or infiltrate into indoor environments thus affecting air quality in spaces where smoking is not permitted. CONCLUSIONS: The reviewed studies indicated that air quality within outdoor hospitality venues where smoking is permitted is unlikely to meet current World Health Organization (WHO) ambient air quality guidelines for PM2.5. Customers and staff in outdoor hospitality venues with active smoking, and in adjacent outdoor and indoor non-smoking areas, are potentially exposed to secondhand smoke at levels exceeding WHO guidelines. Stronger smoking control policies are recommended for outdoor hospitality venues to protect the health of customers and staff from harmful secondhand smoke exposure. PROSPERO REGISTRATION: CRD42022342417.

From Inhalation to Neurodegeneration: Air Pollution as a Modifiable Risk Factor for Alzheimer's Disease.

Air pollution, a growing concern for public health, has been linked to various respiratory and cardiovascular diseases. Emerging evidence also suggests a link between exposure to air pollutants and neurodegenerative diseases, particularly Alzheimer's disease (AD). This review explores the composition and sources of air pollutants, including particulate matter, gases, persistent organic pollutants, and heavy metals. The pathophysiology of AD is briefly discussed, highlighting the role of beta-amyloid plaques, neurofibrillary tangles, and genetic factors. This article also examines how air pollutants reach the brain and exert their detrimental effects, delving into the neurotoxicity of air pollutants. The molecular mechanisms linking air pollution to neurodegeneration are explored in detail, focusing on oxidative stress, neuroinflammation, and protein aggregation. Preclinical studies, including in vitro experiments and animal models, provide evidence for the direct effects of pollutants on neuronal cells, glial cells, and the blood-brain barrier. Epidemiological studies have reported associations between exposure to air pollution and an increased risk of AD and cognitive decline. The growing body of evidence supporting air pollution as a modifiable risk factor for AD underscores the importance of considering environmental factors in the etiology and progression of neurodegenerative diseases, in the face of worsening global air quality.

[Research progress on the association between prenatal exposure to air pollutants and hypospadias in the offspring].

Recent epidemiological studies have increasingly found that pregnant women who are exposed to air pollutants (for example airborne particulate matter, nitrogen oxides, ozone, and sulfur dioxide) increase the risk of various birth defects in their offspring, such as congenital heart disease, neural tube defects, cleft lip and palate, and hypospadias. Hypospadias not only impairs the sexual function of infants but also causes major social and psychological problems during their growth period, therefore, the prevention and treatment of hypospadias infant carry substantial public health importance. However, the association between prenatal exposure to air pollution and hypospadias remains controversial. The study reviews the epidemiological research progress and potential biological mechanisms of prenatal maternal exposure to air pollutants such as particulate matter, nitrogen oxides, ozone, sulfur dioxide, and the risk of hypospadias in offspring. The study also summarizes the limitations of previous research and looks forward to future research directions, to provide scientific evidence for creating a healthy living environment for pregnant women, and reducing the risk of hypospadias in offspring.

Long-term effects of air quality on hospital readmission for heart failure in patients with acute myocardial infarction.

BACKGROUND: Cardiovascular disease (CVD) is the leading cause of death worldwide, with air pollution posing significant risks to cardiovascular health. The effect of air quality on heart failure (HF) readmission in acute myocardial infarction (AMI) patients is unclear.The aim of this study was to evaluate the role of a single measure of air pollution exposure collected on the day of first hospitalization. METHODS: We retrospectively analyzed data from 12,857 acute coronary syndrome (ACS) patients (January 2015-March 2023). After multiple screenings, 4023 AMI patients were included. The air pollution data is updated by the automatic monitoring data of the national urban air quality monitoring stations in real time and synchronized to the China Environmental Monitoring Station. Cox proportional hazards regression assessed the impact of air quality indicators on admission and outcomes in 4013 AMI patients. A decision tree model identified the most susceptible groups. RESULTS: After adjusting for confounders, NO2 (HR 1.009, 95% CI 1.004-1.015, P = 0.00066) and PM10 (HR 1.006, 95% CI 1.002-1.011, P = 0.00751) increased the risk of HF readmission in ST-segment elevation myocardial infarction (STEMI) patients. No significant effect was observed in non-STEMI (NSTEMI) patients (P > 0.05). STEMI patients had a 2.8-fold higher risk of HF readmission with NO2 > 13 µg/m3 (HR 2.857, 95% CI 1.439-5.670, P = 0.00269) and a 1.65-fold higher risk with PM10 > 55 µg/m3 (HR 1.654, 95% CI 1.124-2.434, P = 0.01064). CONCLUSION: NO2 and PM10 are linked to increased HF readmission risk in STEMI patients, particularly when NO2 exceeds 13 µg/m3 and PM10 exceeds 55 µg/m3. Younger, less symptomatic male STEMI patients with fewer underlying conditions are more vulnerable to these pollutants.