Fine particle air pollution and lung cancer risk: Extending the long list of health risks.

Exposures to fine particulate matter (PM2.5) concentrations above the WHO guidelines affect 99% of the world population. In a recent issue of Nature, Hill et al. dissect the tumor promotion paradigm orchestrated by PM2.5 inhalation exposures in lung carcinogenesis, supporting the hypothesis that PM2.5 can increase your risk of lung carcinoma without ever smoking.

PM2.5 exposure contributes to anxiety and depression-like behaviors via phenyl-containing compounds interfering with dopamine receptor.

As a global problem, fine particulate matter (PM2.5) really needs local fixes. Considering the increasing epidemiological relevance to anxiety and depression but inconsistent toxicological results, the most important question is to clarify whether and how PM2.5 causally contributes to these mental disorders and which components are the most dangerous for crucial mitigation in a particular place. In the present study, we chronically subjected male mice to a real-world PM2.5 exposure system throughout the winter heating period in a coal combustion area and revealed that PM2.5 caused anxiety and depression-like behaviors in adults such as restricted activity, diminished exploratory interest, enhanced repetitive stereotypy, and elevated acquired immobility, through behavioral tests including open field, elevated plus maze, marble-burying, and forced swimming tests. Importantly, we found that dopamine signaling was perturbed using mRNA transcriptional profile and bioinformatics analysis, with Drd1 as a potential target. Subsequently, we developed the Drd1 expression-directed multifraction isolating and nontarget identifying framework and identified a total of 209 compounds in PM2.5 organic extracts capable of reducing Drd1 expression. Furthermore, by applying hierarchical characteristic fragment analysis and molecular docking and dynamics simulation, we clarified that phenyl-containing compounds competitively bound to DRD1 and interfered with dopamine signaling, thereby contributing to mental disorders. Taken together, this work provides experimental evidence for researchers and clinicians to identify hazardous factors in PM2.5 and prevent adverse health outcomes and for local governments and municipalities to control source emissions for diminishing specific disease burdens.

Air Pollution-Related Neurotoxicity Across the Life Span.

Air pollution is a complex mixture of gases and particulate matter, with adsorbed organic and inorganic contaminants, to which exposure is lifelong. Epidemiological studies increasingly associate air pollution with multiple neurodevelopmental disorders and neurodegenerative diseases, findings supported by experimental animal models. This breadth of neurotoxicity across these central nervous system diseases and disorders likely reflects shared vulnerability of their inflammatory and oxidative stress-based mechanisms and a corresponding ability to produce brain metal dyshomeo-stasis. Future research to define the responsible contaminants of air pollution underlying this neurotoxicity is critical to understanding mechanisms of these diseases and disorders and protecting public health.

Quantifying fire-specific smoke exposure and health impacts.

Rapidly changing wildfire regimes across the Western United States have driven more frequent and severe wildfires, resulting in wide-ranging societal threats from wildfires and wildfire-generated smoke. However, common measures of fire severity focus on what is burned, disregarding the societal impacts of smoke generated from each fire. We combine satellite-derived fire scars, air parcel trajectories from individual fires, and predicted smoke PM2.5 to link source fires to resulting smoke PM2.5 and health impacts experienced by populations in the contiguous United States from April 2006 to 2020. We quantify fire-specific accumulated smoke exposure based on the cumulative population exposed to smoke PM2.5 over the duration of a fire and estimate excess asthma-related emergency department (ED) visits as a result of this exposure. We find that excess asthma visits attributable to each fire are only moderately correlated with common measures of wildfire severity, including burned area, structures destroyed, and suppression cost. Additionally, while recent California fires contributed nearly half of the country's smoke-related excess asthma ED visits during our study period, the most severe individual fire was the 2007 Bugaboo fire in the Southeast. We estimate that a majority of smoke PM2.5 comes from sources outside the local jurisdictions where the smoke is experienced, with 87% coming from fires in other counties and 60% from fires in other states. Our approach could enable broad-scale assessment of whether specific fire characteristics affect smoke toxicity or impact, inform cost-effectiveness assessments for allocation of suppression resources, and help clarify the growing transboundary nature of local air quality.

Exposure to urban particulate matter (UPM) impairs mitochondrial dynamics in BV2 cells, triggering a mitochondrial biogenesis response.

World Health Organisation data suggest that up to 99% of the global population are exposed to air pollutants above recommended levels. Impacts to health range from increased risk of stroke and cardiovascular disease to chronic respiratory conditions, and air pollution may contribute to over 7 million premature deaths a year. Additionally, mounting evidence suggests that in utero or early life exposure to particulate matter (PM) in ambient air pollution increases the risk of neurodevelopmental impairment with obvious lifelong consequences. Identifying brain-specific cellular targets of PM is vital for determining its long-term consequences. We previously established that microglial-like BV2 cells were particularly sensitive to urban (U)PM-induced damage including reactive oxygen species production, which was abrogated by a mitochondrially targeted antioxidant. Here we extend those studies to find that UPM treatment causes a rapid impairment of mitochondrial function and increased mitochondrial fragmentation. However, there is a subsequent restoration of mitochondrial and therefore cell health occurring concomitantly with upregulated measures of mitochondrial biogenesis and mitochondrial load. Our data highlight that protecting mitochondrial function may represent a valuable mechanism to offset the effects of UPM exposure in the neonatal brain. KEY POINTS: Air pollution represents a growing risk to long-term health especially in early life, and the CNS is emerging a target for airborne particulate matter (PM). We previously showed that microglial-like BV2 cells were vulnerable to urban (U)PM exposure, which impaired cell survival and promoted reactive oxygen species production. Here we find that, following UPM exposure, BV2 mitochondrial membrane potential is rapidly reduced, concomitant with decreased cellular bioenergetics and increased mitochondrial fission. However, markers of mitochondrial biogenesis and mitochondrial mass are subsequently induced, which may represent a cellular mitigation strategy. As mitochondria are more vulnerable in the developing brain, exposure to air pollution may represent a greater risk to lifelong health in this cohort; conversely, promoting mitochondrial integrity may offset these risks.

Cardiovascular Effects of Particulate Air Pollution.

Inhalation of fine particulate matter (PM2.5), produced by the combustion of fossil fuels, is an important risk factor for cardiovascular disease. Exposure to PM2.5 has been linked to increases in blood pressure, thrombosis, and insulin resistance. It also induces vascular injury and accelerates atherogenesis. Results from animal models corroborate epidemiological evidence and suggest that the cardiovascular effects of PM2.5 may be attributable, in part, to oxidative stress, inflammation, and the activation of the autonomic nervous system. Although the underlying mechanisms remain unclear, there is robust evidence that long-term exposure to PM2.5 is associated with premature mortality due to heart failure, stoke, and ischemic heart disease.

Redox-activity and in vitro effects of regional atmospheric aerosol pollution: Seasonal differences and correlation between oxidative potential and in vitro toxicity of PM1.

Particulate Matter (PM) is a complex and heterogeneous mixture of atmospheric particles recognized as a threat to human health. Oxidative Potential (OP) measurement is a promising and integrative method for estimating PM-induced health impacts since it is recognized as more closely associated with adverse health effects than ordinarily used PM mass concentrations. OP measurements could be introduced in the air quality monitoring, along with the parameters currently evaluated. PM deposition in the lungs induces oxidative stress, inflammation, and DNA damage. The study aimed to compare the OP measurements with toxicological effects on BEAS-2B and THP-1 cells of winter and summer PM1 collected in the Po Valley (Italy) during 2021. PM1 was extracted in deionized water by mechanical agitation and tested for OP and, in parallel, used to treat cells. Cytotoxicity, genotoxicity, oxidative stress, and inflammatory responses were assessed by MTT test, DCFH-DA assay, micronucleus, γ-H2AX, comet assay modified with endonucleases, ELISA, and Real-Time PCR. The evaluation of OP was performed by applying three different assays: dithiothreitol (OPDTT), ascorbic acid (OPAA), and 2',7'-dichlorofluorescein (OPDCFH), in addition, the reducing potential was also analysed (RPDPPH). Seasonal differences were detected in all the parameters investigated. The amount of DNA damage detected with the Comet assay and ROS formation highlights the presence of oxidative damage both in winter and in summer samples, while DNA damage (micronucleus) and genes regulation were mainly detected in winter samples. A positive correlation with OPDCFH (Spearman's analysis, p < 0.05) was detected for IL-8 secretion and γ-H2AX. These results provide a biological support to the implementation in air quality monitoring of OP measurements as a useful proxy to estimate PM-induced cellular toxicological responses. In addition, these results provide new insights for the assessment of the ability of secondary aerosol in the background atmosphere to induce oxidative stress and health effects.

RGS2 attenuates alveolar macrophage damage by inhibiting the Gq/11-Ca2+ pathway during cowshed PM2.5 exposure, and aberrant RGS2 expression is associated with TLR2/4 activation.

Staff and animals in livestock buildings are constantly exposed to fine particulate matter (PM2.5), which affects their respiratory health. However, its exact pathogenic mechanism remains unclear. Regulator of G-protein signaling 2 (RGS2) has been reported to play a regulatory role in pneumonia. The aim of this study was to explore the therapeutic potential of RGS2 in cowshed PM2.5-induced respiratory damage. PM2.5 was collected from a cattle farm, and the alveolar macrophages (NR8383) of the model animal rat were stimulated with different treatment conditions of cowshed PM2.5. The RGS2 overexpression vector was constructed and transfected it into cells. Compared with the control group, cowshed PM2.5 significantly induced a decrease in cell viability and increased the levels of apoptosis and proinflammatory factor expression. Overexpression of RGS2 ameliorated the above-mentioned cellular changes induced by cowshed PM2.5. In addition, PM2.5 has significantly induced intracellular Ca2+ dysregulation. Affinity inhibition of Gq/11 by RGS2 attenuated the cytosolic calcium signaling pathway mediated by PLCß/IP3R. To further investigate the causes and mechanisms of action of differential RGS2 expression, the possible effects of oxidative stress and TLR2/4 activation were investigated. The results have shown that RGS2 expression was not only regulated by oxidative stress-induced nitric oxide during cowshed PM2.5 cells stimulation but the activation of TLR2/4 had also an important inhibitory effect on its protein expression. The present study demonstrates the intracellular Ca2+ regulatory role of RGS2 during cellular injury, which could be a potential target for the prevention and treatment of PM2.5-induced respiratory injury.

Fine particulate matter (PM2.5) promotes chemoresistance and aggressive phenotype of A549 lung cancer cells.

Lung cancer is one of the most aggressive malignancies with a high mortality rate. In large cities, particulate matter (PM) is a common air pollutant. High PM levels with aerodynamic size ≤2.5 µm (PM2.5) associates with lung cancer incidence and mortality. In this work, we explored PM2.5 effects on the behavior of lung cancer cells. To this, we chronically exposed A549 cells to increasing PM2.5 concentrations collected in México City, then evaluating cell proliferation, chemoresponse, migration, invasion, spheroid formation, and P-glycoprotein and N-cadherin expression. Chronic PM2.5 exposure from 1 µg/cm2 stimulated A549 cell proliferation, migration, and chemoresistance and upregulated P-glycoprotein and N-cadherin expression. PM2.5 also induced larger multicellular tumor spheroids (MCTS) and less disintegration compared with control cells. Therefore, these results indicate lung cancer patients exposed to airborne PM2.5 as urban pollutant could develop more aggressive tumor phenotypes, with increased cell proliferation, migration, and chemoresistance.

Fine particulate matter contributes to COPD-like pathophysiology: experimental evidence from rats exposed to diesel exhaust particles.

BACKGROUND: Ambient fine particulate matter (PM2.5) is considered a plausible contributor to the onset of chronic obstructive pulmonary disease (COPD). Mechanistic studies are needed to augment the causality of epidemiologic findings. In this study, we aimed to test the hypothesis that repeated exposure to diesel exhaust particles (DEP), a model PM2.5, causes COPD-like pathophysiologic alterations, consequently leading to the development of specific disease phenotypes. Sprague Dawley rats, representing healthy lungs, were randomly assigned to inhale filtered clean air or DEP at a steady-state concentration of 1.03 mg/m3 (mass concentration), 4 h per day, consecutively for 2, 4, and 8 weeks, respectively. Pulmonary inflammation, morphologies and function were examined. RESULTS: Black carbon (a component of DEP) loading in bronchoalveolar lavage macrophages demonstrated a dose-dependent increase in rats following DEP exposures of different durations, indicating that DEP deposited and accumulated in the peripheral lung. Total wall areas (WAt) of small airways, but not of large airways, were significantly increased following DEP exposures, compared to those following filtered air exposures. Consistently, the expression of α-smooth muscle actin (α-SMA) in peripheral lung was elevated following DEP exposures. Fibrosis areas surrounding the small airways and content of hydroxyproline in lung tissue increased significantly following 4-week and 8-week DEP exposure as compared to the filtered air controls. In addition, goblet cell hyperplasia and mucus hypersecretions were evident in small airways following 4-week and 8-week DEP exposures. Lung resistance and total lung capacity were significantly increased following DEP exposures. Serum levels of two oxidative stress biomarkers (MDA and 8-OHdG) were significantly increased. A dramatical recruitment of eosinophils (14.0-fold increase over the control) and macrophages (3.2-fold increase) to the submucosa area of small airways was observed following DEP exposures. CONCLUSIONS: DEP exposures over the courses of 2 to 8 weeks induced COPD-like pathophysiology in rats, with characteristic small airway remodeling, mucus hypersecretion, and eosinophilic inflammation. The results provide insights on the pathophysiologic mechanisms by which PM2.5 exposures cause COPD especially the eosinophilic phenotype.

The cross-linking between DNA damage, oxidative stress and epidermal barrier in keratinocytes after exposure to particulate matters and carbon black.

As the largest organ, the skin provides the first line of defence against environmental pollutants. Different pollutants have varied damage to the skin due to their own physical-chemical properties. A previous epidemiological study by our team revealed that eczema was positively correlated with different air pollutants. However, the mechanism of action from different pollutants on the skin is less known. In this work, the differences among the genotoxicity, intracellular reactive oxygen species, and barrier-related parameters caused by two kinds of air pollutants, that is, S1650b and carbon black (CB) were investigated by Western blot, TUNEL, comet assay and RNA-sequences. The results indicated that both S1650b and CB caused DNA damage of keratinocytes. With the content of lipophilic polycyclic aromatic hydrocarbons (PAH), S1650b leaked into the keratinocytes easily, which activated the aromatic hydrocarbon receptor (AhR) in keratinocytes, leading to worse damage to barrier-related proteins than CB. And CB-induced higher intracellular ROS than S1650b due to the smaller size which make it enter the keratinocytes easier. RNA-sequencing results revealed that S1650b and CB both caused DNA damage of keratinocytes, and the intervention of S1650b significantly upregulated AhR, cytochrome oxidase A1 and B1 (CYP1A1 and CYP1B1) genes, while the results showed oppositely after CB intervention. The mechanism of keratinocyte damage caused by different air particle pollutants in this study will help to expand our understanding on the air pollutant-associated skin disease at cell levels.

Road-traffic-related air pollution contributes to skin barrier alteration and growth defect of sensory neurons.

The effects of air pollution on health are gaining increasing research interest with limited data on skin alterations available. It was suggested that air pollution is a trigger factor for sensitive skin (SS). However, this data was based on surveys with a lack of experimental data. SS is related to altered skin nerve endings and cutaneous neurogenic inflammation. TTe present study was to assess the in vitro effect of particulate matter (PM) on epidermis and nerve ending homeostasis. PM samples were collected according to a validated protocol. Reconstructed human epidermis (RHE, Episkin®) was exposed to PM and subsequently the supernatants were transferred to a culture of PC12 cells differentiated into sensory neurons (SN). Cell viability, axonal growth and neuropeptide-release were measured. The modulation of the expression of different inflammatory, keratinocytes differentiation and neurites growth markers was assessed. PM samples contained a high proportion of particles with a size below 1 µm and a complex chemical composition. Transcriptomic and immunohistochemical analyses revealed that PM altered keratinocytes terminal differentiation and induced an inflammatory response. While viability and functionality of the SN were not modified, their outgrowth was significantly decreased after incubation with PM-exposed Episkin® supernatants. This was closely related to the modification of nerve growth factor/semaphorin 3A balance. This study showed that air pollutants have negative effects on keratinocytes and sensory nerve endings including inflammatory responses. These effects are probably involved in the SS pathophysiology and might be involved in inflammatory skin disorders.

Secondary Organic Aerosol Generated from Biomass Burning Emitted Phenolic Compounds: Oxidative Potential, Reactive Oxygen Species, and Cytotoxicity.

Phenolic compounds are largely emitted from biomass burning (BB) and have a significant potential to form SOA (Phc-SOA). However, the toxicological properties of Phc-SOA remain unclear. In this study, phenol and guaiacol were chosen as two representative phenolic gases in BB plumes, and the toxicological properties of water-soluble components of their SOA generated under different photochemical ages and NOx levels were investigated. Phenolic compounds contribute greatly to the oxidative potential (OP) of biomass-burning SOA. OH-adducts of guaiacol (e.g., 2-methoxyhydroquinone) were identified as components of guaiacol SOA (GSOA) with high OP. The addition of nitro groups to 2,5-dimethyl-1,4-benzoquinone, a surrogate quinone compound in Phc-SOA, increased its OP. The toxicity of both phenol SOA (PSOA) and GSOA in vitro in human alveolar epithelial cells decreased with aging in terms of both cell death and cellular reactive oxygen species (ROS), possibly due to more ring-opening products with relatively low toxicity. The influence of NOx was consistent between cell death and cellular ROS for GSOA but not for PSOA, indicating that cellular ROS production does not necessarily represent all processes contributing to cell death caused by PSOA. Combining different acellular and cellular assays can provide a comprehensive understanding of aerosol toxicological properties.

Exposure to Airborne PM2.5 Water-Soluble Inorganic Ions Induces a Wide Array of Reproductive Toxicity.

Water-soluble inorganic ions (WSIIs, primarily NH4+, SO42-, and NO3-) are major components in ambient PM2.5, but their reproductive toxicity remains largely unknown. An animal study was conducted where parental mice were exposed to PM2.5 WSIIs or clean air during preconception and the gestational period. After delivery, all maternal and offspring mice lived in a clean air environment. We assessed reproductive organs, gestation outcome, birth weight, and growth trajectory of the offspring mice. In parallel, we collected birth weight and placenta transcriptome data from 150 mother-infant pairs from the Rhode Island Child Health Study. We found that PM2.5 WSIIs induced a broad range of adverse reproductive outcomes in mice. PM2.5 NH4+, SO42-, and NO3- exposure reduced ovary weight by 24.22% (p = 0.005), 14.45% (p = 0.048), and 16.64% (p = 0.022) relative to the clean air controls. PM2.5 SO42- exposure reduced the weight of testicle by 5.24% (p = 0.025); further, mice in the PM2.5 SO42- exposure group had 1.81 (p = 0.027) fewer offspring than the control group. PM2.5 NH4+, SO42-, and NO3- exposure all led to lower birth than controls. In mice, 557 placenta genes were perturbed by exposure. Integrative analysis of mouse and human data suggested hypoxia response in placenta as an etiological mechanism underlying PM2.5 WSII exposure's reproductive toxicity.

Toxic Potencies of Particulate Matter from Typical Industrial Plants Mediated with Acidity via Metal Dissolution.

Acidity is an important property of particulate matter (PM) in the atmosphere, but its association with PM toxicity remains unclear. Here, this study quantitively reports the effect of the acidity level on PM toxicity via pH-control experiments and cellular analysis. Oxidative stress and cytotoxicity potencies of acidified PM samples at pH of 1-2 were up to 2.8-5.2 and 2.1-13.2 times higher than those at pH of 8-11, respectively. The toxic potencies of PM samples from real-world smoke plumes at the pH of 2.3 were 9.1-18.2 times greater than those at the pH of 5.6, demonstrating a trend similar to that of acidified PM samples. Furthermore, the impact of acidity on PM toxicity was manifested by promoting metal dissolution. The dramatic increase by 2-3 orders of magnitude in water-soluble metal content dominated the variation in PM toxicity. The significant correlation between sulfate, the pH value, water-soluble Fe, IC20, and EC1.5 (p < 0.05) suggested that acidic sulfate could enhance toxic potencies by dissolving insoluble metals. The findings uncover the superficial association between sulfate and adverse health outcomes in epidemiological research and highlight the control of wet smoke plume emissions to mitigate the toxicity effects of acidity.

Ozone risk assessment with free-air controlled exposure (FACE) experiments: A critical revisit.

Since risk assessments of tropospheric ozone (O3) are crucial for agricultural and forestry sectors, there is a growing body for realistic assessments by a stomatal flux-based approach in Free-Air Controlled Exposure (FACE) facilities. Ozone risks are normally described as relative risks (RRs), which are calculated by assuming the biomass or yield at zero O3 dose as "reference". However, the estimation of the reference biomass or yield is challenging due to a lack of O3-clean-air treatment at the FACEs and the extrapolation without data in a low O3 range increases the bias for estimating the reference values. Here, we reviewed a current methodology for the risk assessment at FACEs and presented a simple and effective way ("modified Paoletti's approach") of defining RRs just using biomass or yield data with a range of expected impacts under the FACE conditions hypothesizing three possible scenarios based on prediction limits using 95% credible intervals (CI) (1. Best fit using the intercept as reference, 2. Optimistic scenario using a lower CI and 3. Worst scenario using an upper CI). As a result, O3-sensitive species show a relatively narrow effect range (optimistic vs. worst scenario) whereas a wide range of response may be possibly taken in resistant species. Showing a possible effect range allows for a comprehensive understanding of the potential risks and its uncertainties related to a species sensitivity to O3. As a supporting approach, we also recommend to use scientifically relevant tools (i.e., ethylenediurea treatments; mechanistic plant models) for strengthening the obtained results for the RRs against O3. Interestingly, the moderately sensitive or resistant species showed non-linear rather than linear dose-response relationships, suggesting a need for the flexible functional form for the risk assessment to properly describe the complex plant response such as hormesis, which depends on their plasticity to O3 stress.

Evaluating the adverse effects and mechanisms of nanomaterial exposure on longevity of C. elegans: A literature meta-analysis and bioinformatics analysis of multi-transcriptome data.

Exposure to large-size particulate air pollution (PM2.5 or PM10) has been reported to increase risks of aging-related diseases and human death, indicating the potential pro-aging effects of airborne nanomaterials with ultra-fine particle size (which have been widely applied in various fields). However, this hypothesis remains inconclusive. Here, a meta-analysis of 99 published literatures collected from electronic databases (PubMed, EMBASE and Cochrane Library; from inception to June 2023) was performed to confirm the effects of nanomaterial exposure on aging-related indicators and molecular mechanisms in model animal C. elegans. The pooled analysis by Stata software showed that compared with the control, nanomaterial exposure significantly shortened the mean lifespan [standardized mean difference (SMD) = -2.30], reduced the survival rate (SMD = -4.57) and increased the death risk (hazard ratio = 1.36) accompanied by upregulation of ced-3, ced-4 and cep-1, while downregulation of ctl-2, ape-1, aak-2 and pmk-1. Furthermore, multi-transcriptome data associated with nanomaterial exposure were retrieved from Gene Expression Omnibus (GSE32521, GSE41486, GSE24847, GSE59470, GSE70509, GSE14932, GSE93187, GSE114881, and GSE122728) and bioinformatics analyses showed that pseudogene prg-2, mRNAs of abu, car-1, gipc-1, gsp-3, kat-1, pod-2, acdh-8, hsp-60 and egrh-2 were downregulated, while R04A9.7 was upregulated after exposure to at least two types of nanomaterials. Resveratrol (abu, hsp-60, pod-2, egrh-2, acdh-8, gsp-3, car-1, kat-1, gipc-1), naringenin (kat-1, egrh-2), coumestrol (egrh-2) or swainsonine/niacin/ferulic acid (R04A9.7) exerted therapeutic effects by reversing the expression levels of target genes. In conclusion, our study demonstrates the necessity to use phytomedicines that target hub genes to delay aging for populations with nanomaterial exposure.

Childhood exposure to outdoor air pollution in different microenvironments and cognitive and fine motor function in children from six European cohorts.

BACKGROUND: Exposure to air pollution during childhood has been linked with adverse effects on cognitive development and motor function. However, limited research has been done on the associations of air pollution exposure in different microenvironments such as home, school, or while commuting with these outcomes. OBJECTIVE: To analyze the association between childhood air pollution exposure in different microenvironments and cognitive and fine motor function from six European birth cohorts. METHODS: We included 1301 children from six European birth cohorts aged 6-11 years from the HELIX project. Average outdoor air pollutants concentrations (NO2, PM2.5) were estimated using land use regression models for different microenvironments (home, school, and commute), for 1-year before the outcome assessment. Attentional function, cognitive flexibility, non-verbal intelligence, and fine motor function were assessed using the Attention Network Test, Trail Making Test A and B, Raven Colored Progressive Matrices test, and the Finger Tapping test, respectively. Adjusted linear regressions models were run to determine the association between each air pollutant from each microenvironment on each outcome. RESULTS: In pooled analysis we observed high correlation (rs = 0.9) between air pollution exposures levels at home and school. However, the cohort-by-cohort analysis revealed correlations ranging from low to moderate. Air pollution exposure levels while commuting were higher than at home or school. Exposure to air pollution in the different microenvironments was not associated with working memory, attentional function, non-verbal intelligence, and fine motor function. Results remained consistently null in random-effects meta-analysis. CONCLUSIONS: No association was observed between outdoor air pollution exposure in different microenvironments (home, school, commute) and cognitive and fine motor function in children from six European birth cohorts. Future research should include a more detailed exposure assessment, considering personal measurements and time spent in different microenvironments.

Epigenome-wide association study on ambient PM2.5 exposure in Han Chinese, the NSPT study.

Ambient PM2.5 exposure has been recognized as a major health risk and related to aging, cardiovascular, respiratory and neurologic diseases, and cancer. However, underlying mechanism of epigenetic alteration and regulated pathways still remained unclear. The study on methylome effect of PM2.5 exposure was quite limited in Chinese population, and cohort-based study was absent. The study included blood-derived DNA methylation for 3365 Chinese participants from the NSPT cohort. We estimated individual PM2.5 exposure level of short-medium-, medium- and long-term, based on a validated prediction model. We preformed epigenome-wide association studies to estimate the links between PM2.5 exposure and DNA methylation change, as well as stratification and sensitive analysis to examined the robustness of the association models. A systematic review was conducted to obtain the previously published CpGs and examined for replication. We also conducted comparison on the DNA methylation variation corresponding to different time windows. We further conducted gene function analysis and pathway enrichment analysis to reveal related biological response. We identified a total of 177 CpGs and 107 DMRs associated with short-medium-term PM2.5 exposure, at a strict genome-wide significance (P < 5 × 10-8). The effect sizes on most CpGs tended to cease with the exposure of extended time scale. Associated markers and aligned genes were related to aging, immunity, inflammation and carcinogenesis. Enriched pathways were mostly involved in cell cycle and cell division, signal transduction, inflammatory pathway. Our study is the first EWAS on PM2.5 exposure conducted in large-scale Han Chinese cohort and identified associated DNA methylation change on CpGs and regions, as well as related gene functions and pathways.

Associations of low levels of air pollution with cardiometabolic outcomes and the role of diet quality in individuals with obesity.

BACKGROUND: Exposure to air pollution is associated with adverse cardiometabolic health effects and increased mortality, even at low concentrations. Some of the biological mechanisms through which air pollution can affect cardiometabolic health overlap with health outcomes associated with diet quality and changes in diet. OBJECTIVE: The objective of this study is to investigate associations of air pollutants at average concentrations below the World Health Organization, 2021 air quality guidelines with cardiometabolic outcomes. Furthermore, potential interaction between air pollutants and diet quality will be assessed. METHODS: 82 individuals with obesity participated in a combined weight loss and weight loss maintenance study for a total of 33 weeks. A secondary analysis was conducted incorporating air pollution measurements. Data were analysed with linear mixed-effects models. RESULTS: A total of 17 significant associations were observed for single pollutants with 10 cardiometabolic outcomes, predominantly related to blood lipids, hormones, and glucose regulation. Diet quality, as measured by the Baltic Sea Diet score, did not appear to mediate the association of air pollution with cardiometabolic outcomes, however, diet quality was observed to significantly modify the association of PM2.5 with total cholesterol, and the associations of NO and O3 with ghrelin. DISCUSSION: These findings suggest that exposure to ambient air pollutants, especially particulate matter, at levels below World Health Organization, 2021 air quality guidelines, were associated with changes in cardiometabolic risk factors. Diet may be a personal-level approach for individuals to modify the impact of exposure to air pollution on cardiometabolic health.