Increased Air Pollution Exposure Research Articles

The association between outdoor air pollution and body mass index, central obesity, and visceral adiposity index among middle-aged and elderly adults: a nationwide study in China.

Previous animal studies have suggested that air pollution (AP) exposure may be a potential risk factor for obesity; however, there is limited epidemiological evidence available to describe the association of obesity with AP exposure. A retrospective cross-sectional study was conducted on 11,766 participants across mainland China in 2015. Obesity was assessed using body mass index (BMI), waist circumference (WC), and visceral adiposity index (VAI). The space-time extremely randomized tree (STET) model was used to estimate the concentration of air pollutants, including SO2, NO2, O3, PM1, PM2.5, and PM10, matched to participants' residential addresses. Logistic regression models were employed to estimate the associations of obesity with outdoor AP exposure. Further stratified analysis was conducted to evaluate whether sociodemographics or lifestyles modified the effects. Increased AP exposure was statistically associated with increased odds of obesity. The odds ratio (ORs) and 95% confidence interval (CI) of BMI-defined obesity were 1.21 (1.17, 1.26) for SO2, 1.33 (1.26, 1.40) for NO2, 1.15 (1.10, 1.21) for O3, 1.38 (1.29, 1.48) for PM1, 1.19 (1.15, 1.22) for PM2.5, and 1.11 (1.09, 1.13) for PM10 per 10 μg/m3 increase in concentration. Similar results were found for central obesity. Stratified analyses suggested that elderly participants experienced more adverse effects from all 6 air pollutants than middle-aged participants. Furthermore, notable multiplicative interactions were found between O3 exposure and females as well as second-hand smokers in BMI-defined obesity. This study suggested that outdoor AP exposure had a significant association with the risk of obesity in the middle-aged and elderly Chinese population. Elderly individuals and women may be more vulnerable to AP exposure.

The Impact of Social Determinants and Air Pollution on Healthcare Disparities in Chronic Rhinosinusitis With Nasal Polyps.

Multiple factors affect healthcare disparities in chronic rhinosinusitis (CRS) with and without nasal polyps. These factors include access to care, economic burdens to treatment, and differences in air pollution and air quality. In this paper, we will discuss how socioeconomic status, race, and air pollution burden influence healthcare disparities in the diagnosis and treatment outcomes of chronic rhinosinusitis with nasal polyps (CRSwNP). A literature search was performed via PubMed for articles related to CRSwNP, healthcare disparities, race, socioeconomic status, and air pollution in September 2022. Original studies from 2016 to 2022, landmark articles, and systematic reviews were included. We summarized these articles to cohesively discuss factors contributing to healthcare disparities in CRSwNP. Literary search produced 35 articles. Individual factors such as socioeconomic status, race, and air pollution influence CRSwNP severity and treatment outcomes. Correlations were noted with socioeconomic status, race, and air pollution exposure and CRS severity and post-surgical outcomes. Air pollution exposure was also associated with histopathologic changes in CRSwNP. Lack of access to care was a notable contributor to healthcare disparities in CRS. Healthcare disparities in the diagnosis and treatment of CRSwNP differentially affect racial minorities and individuals of lower socioeconomic status. Increased air pollution exposure in areas of lower socioeconomic status is a compounding factor. Clinician advocacy for greater healthcare access and reductions in environmental exposures for patients, among other societal changes, may help improve disparities.

Air Pollution, Oxidative Stress, and the Risk of Development of Type 1 Diabetes.

Despite multiple studies focusing on environmental factors conducive to the development of type 1 diabetes mellitus (T1DM), knowledge about the involvement of long-term exposure to air pollution seems insufficient. The main focus of epidemiological studies is placed on the relationship between exposure to various concentrations of particulate matter (PM): PM1, PM2.5, PM10, and sulfur dioxide (SO2), nitrogen dioxide (NO2), carbon monoxide (O3), versus the risk of T1DM development. Although the specific molecular mechanism(s) behind the link between increased air pollution exposure and a higher risk of diabetes and metabolic dysfunction is yet unknown, available data indicate air pollution-induced inflammation and oxidative stress as a significant pathway. The purpose of this paper is to assess recent research examining the association between inhalation exposure to PM and associated metals and the increasing rates of T1DM worldwide. The development of modern and more adequate methods for air quality monitoring is also introduced. A particular emphasis on microsensors, mobile and autonomous measuring platforms, satellites, and innovative approaches of IoT, 5G connections, and Block chain technologies are also presented. Reputable databases, including PubMed, Scopus, and Web of Science, were used to search for relevant literature. Eligibility criteria involved recent publication years, particularly publications within the last five years (except for papers presenting a certain novelty or mechanism for the first time). Population, toxicological and epidemiological studies that focused particularly on fine and ultra-fine PM and associated ambient metals, were preferred, as well as full-text publications.

Associations between wildfire air pollution and online search interest for skin diseases and symptoms

To the Editor: Wildfires are becoming more frequent and severe, causing increased air pollution exposure.1 Wildfire smoke has been associated with increased rates of clinic visits for atopic dermatitis (AD) and itch.1 We hypothesized that exposure to local wildfire air pollution would increase interest in skin-related topics, as detected by online search trends. They reflect shifts in population-level information-seeking behaviors related to short-term events that could indicate environmental impacts on skin health.

Perturbation of amino acid metabolism mediates air pollution associated vascular dysfunction in healthy adults

The molecular mechanisms of air pollution-associated adverse cardiovascular effects remain largely unknown. In the present study, we investigated the impacts of ambient air pollution on vascular function and the potential mediation effects of amino acids in a longitudinal follow-up of 73 healthy adults living in Beijing, China, between 2014 and 2016. We estimated associations between air pollutants and serum soluble intercellular adhesion molecule 1 (sICAM-1) and plasma levels of amino acids using linear mixed-effects models, and elucidated the biological pathways involved using mediation analyses. Higher air pollutant levels were significantly associated with increases in sICAM-1 levels. Metabolomics analysis showed that altered metabolites following short-term air pollution exposure were mainly involved in amino acid metabolism. Significant reductions in levels of plasma alanine, threonine and glutamic acid of 2.1 μM [95% confidence interval (CI): −3.8, −0.3] to 62.0 μM (95% CI: −76.1, −47.9) were associated with interquartile range increases in moving averages of PM2.5, BC, CO and SO2 in 1–7 days prior to clinical visits. Mediation analysis also showed that amino acids can mediate up to 48% of the changes in sICAM-1 associated with increased air pollution exposure. Our results indicated that air pollution may prompt vascular dysfunction through perturbing amino acid metabolism.

Association of long-term exposure to ambient air pollutants with blood lipids in Chinese adults: The China Multi-Ethnic Cohort study

BackgroundDyslipidemia is a crucial risk factor for cardiovascular diseases. Previous studies have suggested that air pollution is associated with blood lipids. However, little evidence exists in low- and middle-income regions. We aimed to investigate the association between air pollution and blood lipids in southwestern China. MethodsWe included 67,305 participants aged 30–79 years from the baseline data of the China Multi-Ethnic Cohort (CMEC) study. Three-year average concentrations of particles with diameters ≤1 μm (PM1), particles with diameters ≤ 2.5 μm (PM2.5), particles with diameters ≤ 10 μm (PM10), nitrogen dioxide (NO2), and ozone (O3) were estimated using satellite-based spatiotemporal models. Individual serum lipids, including cholesterol (TC), triglycerides (TG), low-density lipoprotein cholesterol (LDL-C), and high-density lipoprotein cholesterol (HDL-C), were measured. Linear, logistic, and quantile regression models were used to evaluate the association between ambient air pollution and blood lipids. ResultsAll five air pollutants in our study were associated with lipid levels. Increased air pollution exposure was associated with a high risk of dyslipidemia. Each 10 μg/m3 increase in PM2.5 was associated with 0.92% (95% confidence interval (CI): 0.64%, 1.20%), 2.23% (95% CI: 1.44%, 3.02%), and 3.04% (95% CI: 2.61%, 3.47%) increases in TC, TG, and LDL-C levels, respectively, and a 2.03% (95% CI: 1.69%, 2.37%) decrease in HDL-C levels, and high risks of dyslipidemia (OR = 1.14, 95% CI: 1.10, 1.18). Stronger associations of air pollution with blood lipids were found in participants with high lipid levels than in those with low lipid levels. ConclusionLong-term exposure to air pollutants was associated with blood lipid levels and the risk of dyslipidemia. People with high lipid levels were more susceptible to air pollution. Therefore, air pollution prevention and control may help reduce the incidence of dyslipidemia and the burden of CVDs.

Native American Ancestry and Air Pollution Interact to Impact Bronchodilator Response in Puerto Rican Children with Asthma.

Asthma is the most common chronic disease in children. Short-acting bronchodilator medications are the most commonly prescribed asthma treatment worldwide, regardless of disease severity. Puerto Rican children display the highest asthma morbidity and mortality of any US population. Alarmingly, Puerto Rican children with asthma display poor bronchodilator drug response (BDR). Reduced BDR may explain, in part, the increased asthma morbidity and mortality observed in Puerto Rican children with asthma. Gene-environment interactions may explain a portion of the heritability of BDR. We aimed to identify gene-environment interactions associated with BDR in Puerto Rican children with asthma. Genetic, environmental, and psycho-social data from the Genes-environments and Admixture in Latino Americans (GALA II) case-control study. Our discovery dataset consisted of 658 Puerto Rican children with asthma; our replication dataset consisted of 514 Mexican American children with asthma. We assessed the association of pairwise interaction models with BDR using ViSEN (Visualization of Statistical Epistasis Networks). We identified a non-linear interaction between Native American genetic ancestry and air pollution significantly associated with BDR in Puerto Rican children with asthma. This interaction was robust to adjustment for age and sex but was not significantly associated with BDR in our replication population. Decreased Native American ancestry coupled with increased air pollution exposure was associated with increased BDR in Puerto Rican children with asthma. Our study acknowledges BDR's phenotypic complexity, and emphasizes the importance of integrating social, environmental, and biological data to further our understanding of complex disease.

Increased air pollution exposure among the Chinese population during the national quarantine in 2020.

The COVID-19 quarantine in China is thought to have reduced ambient air pollution. The overall exposure of the population also depends, however, on indoor air quality and human mobility and activities. Here, by integrating real-time mobility data and a questionnaire survey on time-activity patterns during the pandemic, we show that despite a decrease in ambient PM2.5 during the quarantine, the total population-weighted exposure to PM2.5 considering both indoor and outdoor environments increased by 5.7 μg m-3 (95% confidence interval, 1.2-11.0 μg m-3). The increase in population-weighted exposure was mainly driven by a nationwide urban-to-rural population migration before the Spring Festival coupled with the freezing of the migration backward due to the quarantine, which increased household energy consumption and the fraction of people exposed to rural household air pollution indoors. Our analysis reveals an increased inequality of air pollution exposure during the quarantine and highlights the importance of household air pollution for population health in China.

Adverse Birth Outcomes Related to NO2 and PM Exposure: European Systematic Review and Meta-Analysis.

There is a growing number of international studies on the association between ambient air pollution and adverse pregnancy outcomes, and this systematic review and meta-analysis has been conducted focusing on European countries, to assess the crucial public health issue of this suspected association on this geographical area. A systematic literature search (based on Preferred Reporting Items for Systematic reviews and Meta-Analyses, PRISMA, guidelines) has been performed on all European epidemiological studies published up until 1 April 2020, on the association between maternal exposure during pregnancy to nitrogen dioxide (NO2) or particular matter (PM) and the risk of adverse birth outcomes, including: low birth weight (LBW) and preterm birth (PTB). Fourteen articles were included in the systematic review and nine of them were included in the meta-analysis. Our meta-analysis was conducted for 2 combinations of NO2 exposure related to birth weight and PTB. Our systematic review revealed that risk of LBW increases with the increase of air pollution exposure (including PM10, PM2.5 and NO2) during the whole pregnancy. Our meta-analysis found that birth weight decreases with NO2 increase (pooled beta = −13.63, 95% confidence interval (CI) (−28.03, 0.77)) and the risk of PTB increase for 10 µg/m3 increase in NO2 (pooled odds ratio (OR) = 1.07, 95% CI (0.90, 1.28)). However, the results were not statistically significant. Our finding support the main international results, suggesting that increased air pollution exposure during pregnancy might contribute to adverse birth outcomes, especially LBW. This body of evidence has limitations that impede the formulation of firm conclusions. Further studies, well-focused on European countries, are called to resolve the limitations which could affect the strength of association such as: the exposure assessment, the critical windows of exposure during pregnancy, and the definition of adverse birth outcomes. This analysis of limitations of the current body of research could be used as a baseline for further studies and may serve as basis for reflection for research agenda improvements.

Long-term effects of ambient air pollutants to blood lipids and dyslipidemias in a Chinese rural population

Both air pollution and dyslipidemias contributed to large number of deaths and disability-adjusted life lost years. Long-term air pollution exposure was related to changed blood lipids and risk of dyslipidemias. This study was designed to evaluate relationships between air pollutants, blood lipids and prevalence of dyslipidemias in a Chinese rural population exposed to high-level air pollution based on baseline data of The Henan Rural Cohort study. An amount of 39,057 participants from rural areas in China were included. The 3-year average exposure of air pollutants (PM2.5, PM10, NO2) was estimated by a spatiotemporal model. Logistic and linear regression models were employed to explore relationships between air pollutants, blood lipids (TC, TG, HDL-C and LDL-C) and prevalence of dyslipidemias. The three-year concentration of PM2.5, PM10 and NO2 was 72.8 ± 2.3 μg/m3, 131.5 ± 5.7 μg/m3and 39.1 ± 3.1 μg/m3, respectively. Overall, increased air pollution exposure was related to increased TC and LDL-C, while decreased TG and HDL-C. Each 1-μg/m3 increment of PM2.5 was related to 0.10% (0.07%–0.19%) increase in TC, 0.63% (0.50%–0.77%) increase in LDL-C, 2.93% (2.70%–3.16%) decrease in TG, 0.49% (0.38%–0.60%) decrease in HDL-C; and 5.7% (95%CI: 3.7%–7.6%), 4.0% (95%CI: 2.1%–6.0%) and 3.8% (95%CI: 2.5%–5.1%) increase in odds for hypercholesterolemia, hyperbetalipoproteinemia and hypoalphalipoproteinemia, respectively. Stronger associations were found in male and older participants. Findings suggest that air pollutants were associated with changed blood lipid levels and higher risk of dyslipidemias among rural population. Male and elder people should pay more attention to personal safety protection.

Air pollution and resistance to inhaled glucocorticoids: Evidence, mechanisms and gaps to fill.

Substantial evidence indicates that cigarette smoke exposure induces resistance to glucocorticoids, the primary maintenance medication in asthma treatment. Modest evidence also suggests that air pollution may reduce the effectiveness of these critical medications. Cigarette smoke, which has clear parallels with air pollution, has been shown to induce glucocorticoid resistance in asthma and it has been speculated that air pollution may have similar effects. However, the literature on an association of air pollution with glucocorticoid resistance is modest to date. In this review, we detail the evidence for, and against, the effects of air pollution on glucocorticoid effectiveness, focusing on results from epidemiology and controlled human exposure studies. Epidemiological studies indicate a correlation between increased air pollution exposure and worse asthma symptoms. But these studies also show a mix of beneficial and harmful effects of glucocorticoids on spirometry and asthma symptoms, perhaps due to confounding influences, or the induction of glucocorticoid resistance. We describe mechanisms that may contribute to reductions in glucocorticoid responsiveness following air pollution exposure, including changes to phosphorylation or oxidation of the glucocorticoid receptor, repression by cytokines, or inflammatory pathways, and epigenetic effects. Possible interactions between air pollution and respiratory infections are also briefly discussed. Finally, we detail a number of therapies that may boost glucocorticoid effectiveness or reverse resistance in the presence of air pollution, and comment on the beneficial effects of engineering controls, such as air filtration and asthma action plans. We also call attention to the benefits of improved clean air policy on asthma. This review highlights numerous gaps in our knowledge of the interactions between air pollution and glucocorticoids to encourage further research in this area with a view to reducing the harm caused to those with airways disease.

Ambient and Traffic-Related Air Pollution Exposures as Novel Risk Factors for Metabolic Dysfunction and Type 2 Diabetes.

Diabetes mellitus is a top contributor to the global burden of mortality and disability in adults. There has also been a slow, but steady rise in prediabetes and type 2 diabetes in youth. The current review summarizes recent findings regarding the impact of increased exposure to air pollutants on the type 2 diabetes epidemic. Human and animal studies provide strong evidence that exposure to ambient and traffic-related air pollutants such as particulate matter (PM), nitrogen dioxide (NO2), and nitrogen oxides (NOx) play an important role in metabolic dysfunction and type 2 diabetes etiology. This work is supported by recent findings that have observed similar effect sizes for increased exposure to air pollutants on clinical measures of risk for type 2 diabetes in children and adults. Further, studies indicate that these effects may be more pronounced among individuals with existing risk factors, including obesity and prediabetes. Current epidemiological evidence suggests that increased air pollution exposure contributes to alterations in insulin signaling, glucose metabolism, and beta (β)-cell function. Future work is needed to identify the specific detrimental pollutants that alter glucose metabolism. Additionally, advanced tools and new areas of investigation present unique opportunities to study the underlying mechanisms, including intermediate pathways, that link increased air pollution exposure with type 2 diabetes onset.

Variability of Black Carbon and Ultrafine Particle Concentration on Urban Bike Routes in a Mid-Sized City in the Po Valley (Northern Italy)

Cyclists might experience increased air pollution exposure, due to the proximity to traffic, and higher intake, due to their active travel mode and higher ventilation. Several local factors, like meteorology, road and traffic features, and bike lanes features, affect cyclists’ exposure to traffic-related pollutants. This paper investigates the concentration levels and the effect of the features of the bike lanes on cyclists’ exposure to airborne ultrafine particulate matter (UFP) and black carbon (BC) in the mid-sized city of Piacenza, located in the middle of the Po Valley, Northern Italy. Monitoring campaigns were performed by means of portable instruments along different urban bike routes with bike lanes, characterized by different distances from the traffic source (on-road cycle lane, separated cycle lane, green cycle path), during morning (9:00 am–10:00 am) and evening (17:30 pm–18:30 pm) workday rush hours in both cold and warm seasons. The proximity to traffic significantly affected cyclists’ exposure to UFP and BC: exposure concentrations measured for the separated lane and for the green path were 1–2 times and 2–4 times lower than for the on-road lane. Concurrent measurements showed that exposure concentrations to PM10, PM2.5, and PM1 were not influenced by traffic proximity, without any significant variation between on-road cycle lane, separated lane, or green cycle path. Thus, for the location of this study PM mass-based metrics were not able to capture local scale concentration gradients in the urban area as a consequence of the rather high urban and regional background that hides the contribution of local scale sources, such as road traffic. The impact of route choice on cyclists’ exposure to UFPs and BC during commuting trips back and forth from a residential area to the train station has been also estimated through a probabilistic approach through an iterative Monte Carlo technique, based on the measured data. Compared to the best choice, a worst-route choice can result in an increased cumulative exposure up to about 50% for UFPs, without any relevant difference between cold and warm season, and from 20% in the cold season up to 90% in the warm season for equivalent black carbon concentration (EBC).

A42 Transportation, Air pollution and Physical ActivitieS (TAPAS): A comprehensive research programme on active travel

Abstract Background Encouraging walking and cycling as means of transportation may have diverse benefits, such as reduced pollutant emissions and increased physical activity in the population. At the same time, individuals who shift to active travel modes may also experience increased risks of traffic injuries and inhalation of air pollutants. The purpose of the TAPAS research programme ( 2009-2013) was to help decision makers design urban policies that tackle climate change and promote health-related outcomes in Europe, while minimizing potential risks from air pollution and traffic accident. Methods The central approach of the multi-city and multi-disciplinary study was the development of quantitative health impact assessment models to assess overall impacts of active travel policies, complemented by targeted studies to address research gaps on related topics. In particular, we investigated whether increased physical activity and air pollution interacted to increase health risks. Methods included epidemiologic analyses, cross-over real-world exposure-health experiments, activity and air pollution monitoring, travel surveys, and simulation models. Results The health impact assessments indicated that the physical activity-related benefits of active travel were greater than the risks associated with increased air pollution inhalation and traffic injuries in each of the 6 cities investigated (Barcelona, Basel, Copenhagen, Paris, Prague, Warsaw). Epidemiologic analyses from our targeted studies confirmed this finding. Benefits of physical activity were found even when exposed to high pollution, but were greater in areas of low to moderate air pollution (e.g. respiratory mortality and cycling hazard ratio 0.55, 95% confidence interval 0.42, 0.72). No significant interactions were found between air pollution and physical activity in triggering adverse health effects in either epidemiologic or experimental studies. Commute times were shown to contribute significantly to overall air pollution exposure, despite the short exposure periods, and ignoring such information led to bias of health effects estimates. Survey analyses showed some potential for policies such as bike lanes and bike sharing systems to increase active travel, which in turn could increase physical activity in the population. Conclusions Population health benefits can be expected from policies aimed at increasing walking and cycling, despite concerns of increased air pollution exposure while physically active in travel microenvironments. To assess the full extent of such benefits further research is needed to understand the types of policies that are most effective in encouraging active travel, the characteristics of individuals who are most likely to shift to active travel modes, and optimal environmental and personal risk trade-off profiles.

Do Air Pollution Exposure and Food Environment Impact Overweight/Obesity?

Growing evidence suggests environmental factors may contribute to increased prevalence of overweight/obesity. Recent studies link overweight/obesity to increased air pollution exposure, as well as ...