Fine Particulate Matter Exposure Research Articles

Physical activity, long‐term fine particulate matter exposure and type 2 diabetes incidence: A prospective cohort study

Physical activity, long‐term fine particulate matter exposure and type 2 diabetes incidence: A prospective cohort study

Effect of fine particulate matter exposure on gestational diabetes mellitus risk: a retrospective cohort study.

The literature on the association between fine particulate matter (PM2.5) exposure and gestational diabetes mellitus (GDM) risk has focused mainly on exposure during the first and second trimesters, and the research results are inconsistent. Therefore, this study aimed to investigate the associations between PM2.5 exposure during preconception, the first trimester and second trimester and GDM risk in pregnant women in Guangzhou. A retrospective cohort study of 26 354 pregnant women was conducted, estimating PM2.5, particulate matter with a diameter >10 µm (PM10), sulphur dioxide (SO2), carbon monoxide (CO) and ozone (O3) exposure during preconception and the first and second trimesters. Analyses were performed using Cox proportional hazards models and nonlinear distributed lag models. The study found that exposure to PM2.5 or a combination of two pollutants (PM2.5+PM10, PM2.5+SO2, PM2.5+CO and PM2.5+O3) was found to be significantly associated with GDM risk (P < 0.05). In the second trimester, with significant interactions found for occupation and anaemia between PM2.5 and GDM. When the PM2.5 concentrations were ≥19.56, ≥25.69 and ≥23.87 μg/m3 during preconception and the first and second trimesters, respectively, the hazard ratio for GDM started to increase. The critical window for PM2.5 exposure was identified to be from 9 to 11 weeks before conception. Our study results suggest that PM2.5 exposure during preconception and the first and second trimesters increases the risk of GDM, with the preconception period appearing to be the critical window for PM2.5 exposure.

The association of short-term increases in ambient PM2.5 and temperature exposures with stillbirth: racial/ethnic disparities among Medicaid recipients.

Racial/ethnic disparities in the association between short-term (e.g. days, weeks) ambient fine particulate matter (PM2.5) and temperature exposures and stillbirth in the US have been understudied. A time-stratified, case-crossover design using a distributed lag non-linear model (0 to 6-day lag) estimated stillbirth odds due to short-term increases in average daily PM2.5 and temperature exposures among 118,632 Medicaid recipients from 2000-2014. Disparities by maternal race/ethnicity (Black, White, Hispanic, Asian, American Indian) and zip-code level socioeconomic status (SES) were assessed. In the temperature-adjusted model, a 10 μg/m3 increase in PM2.5 concentration was marginally associated with increased stillbirth odds at lag 1 (0.68% 95%CI:[-0.04,1.40]) and lag 2 (0.52% 95%CI:[-0.03,1.06]), but not lag 0-6 (2.80% 95%CI:[-0.81,6.45]). An association between daily PM2.5 concentrations and stillbirth odds was found among Black individuals at the cumulative lag (0-6 days: 9.26% 95%CI:[3.12,15.77]), but not among other races/ethnicities. A stronger association between PM2.5 concentrations and stillbirth odds existed among Black individuals living in zip codes with the lowest median household income (lag0-6:14.13% 95%CI:[4.64,25.79]). Short-term temperature increases were not associated with stillbirth risk among any race/ethnicity. Black Medicaid enrollees, and especially those living in lower SES areas, may be more vulnerable to stillbirth due to short-term increases in PM2.5 exposure.

Fine particulate matter exposure and systemic inflammation: A potential mediating role of bioactive lipids

Inflammation is a key mechanism underlying the adverse health effects of exposure to fine particulate matter (PM2.5). Bioactive lipids in the arachidonic acid (ARA) pathway are important in the regulation of inflammation and are reportedly altered by PM2.5 exposure. Ceramide-1-phosphate (C1P), a class of sphingolipids, is required to initiate ARA metabolism. We examined the role of C1P in the alteration of ARA metabolism after PM2.5 exposure and explored whether changes in the ARA pathway promoted systemic inflammation based on a panel study involving 112 older adults in Beijing, China. Ambient PM2.5 levels were continuously monitored at a fixed station from 2013 to 2015. Serum cytokine levels were measured to assess systemic inflammation. Multiple bioactive lipids in the ARA pathway and three subtypes of C1P were quantified in blood samples. Mediation analyses were performed to test the hypotheses. We observed that PM2.5 exposure was positively associated with inflammatory cytokines and the three subtypes of C1P. Mediation analyses showed that C1P significantly mediated the associations of ARA and 5, 6-dihydroxyeicosatrienoic acid (5, 6-DHET), an ARA metabolite, with PM2.5 exposure. ARA, 5, 6-DHET, and leukotriene B4 mediated systemic inflammatory response to PM2.5 exposure. For example, C1P C16:0 (a subtype of C1P) mediated a 12.9 % (95 % confidence interval: 3.7 %, 32.5 %) increase in ARA associated with 3-day moving average PM2.5 exposure, and ARA mediated a 27.1 % (7.8 %, 61.2 %) change in interleukin-8 associated with 7-day moving average PM2.5 exposure. Our study indicates that bioactive lipids in the ARA and sphingolipid metabolic pathways may mediate systemic inflammation after PM2.5 exposure.

Continued Rise in Health Burden from Ambient PM2.5 in India under SSP Scenarios Until 2100 despite Decreasing Concentrations.

Forecasting alterations in ambient air pollution and the consequent health implications is crucial for safeguarding public health, advancing environmental sustainability, informing economic decision making, and promoting appropriate policy and regulatory action. However, predicting such changes poses a substantial challenge, requiring accurate data, sophisticated modeling methodologies, and a meticulous evaluation of multiple drivers. In this study, we calculate premature deaths due to ambient fine particulate matter (PM2.5) exposure in India from the 2020s (2016-2020) to the 2100s (2095-2100) under four different socioeconomic and climate scenarios (SSPs) based on four CMIP6 models. PM2.5 concentrations decreased in all SSP scenarios except for SSP3-7.0, with the lowest concentration observed in SSP1-2.6. The results indicate an upward trend in the five-year average number of deaths across all scenarios, ranging from 1.01 million in the 2020s to 4.12-5.44 million in the 2100s. Further analysis revealed that the benefits of reducing PM2.5 concentrations under all scenarios are largely mitigated by population aging and growth. These findings underscore the importance of proactive measures and an integrated approach in India to improve atmospheric quality and reduce vulnerability to aging under changing climate conditions.

Spatially differentiated health impacts and costs of fine particulate matter exposure from agriculture waste management in Thailand

The agricultural sector in Thailand contributes to air pollution, due to the practice of open burning of agricultural wastes. An in depth-analysis of regionalized health impacts and related damage costs of fine particulate matter (PM2.5) exposure were computed for the 77 provinces of Thailand by parameterizing PM2.5 characterization model. The characterization factors for PM2.5 showed a wide variation for the various provinces ranging between 2 and 130 h of healthy population lifetime loss per kg PM2.5 emitted. The factors were applied to compare the agricultural waste management of major crops (rice, sugarcane, maize, cassava, and oil palm) in Thailand between the business-as-usual scenario representing current management practices and five alternative scenarios of agricultural waste utilization or open burning. The total health impacts and damage costs of the business-as-usual scenario were 732,065 DALYs and 425 billion Thai Baht (THB), respectively. The open burning alternative scenario yielded additional damage of 524 billion THB. The alternative scenarios of management via animal feed, fertilizer, residues left in the field, and electricity generation provided economic benefits (431, 427, 422, and 399 billion THB, respectively). In this study, using the global average factor to assess the overall health impacts of PM2.5 emissions in Thailand resulted in an underestimation of health impacts as compared to province-specific factors. While substituting province-specific factors with country average factor yields similar overall results at the country level, using province-specific factors are important to capture the large variability of impacts across individual provinces. In addition to developing a tool to quantify the PM2.5 related health impacts of various agricultural wastes in Thailand, recommendations on the implementation of the alternative scenarios have also been outlined in the study.

Association between Fine Particulate Matter Exposure and Cerebrospinal Fluid Biomarkers of Alzheimer's Disease among a Cognitively Healthy Population-Based Cohort.

Epidemiological evidence suggests air pollution adversely affects cognition and increases the risk of Alzheimer's disease (AD), but little is known about the biological effects of fine particulate matter (, particulate matter with aerodynamic diameter ) on early predictors of future disease risk. We investigated the association between 1-, 3-, and 5-y exposure to ambient and traffic-related and cerebrospinal fluid (CSF) biomarkers of AD. We conducted a cross-sectional analysis using data from 1,113 cognitively healthy adults (45-75 y of age) from the Emory Healthy Brain Study in Georgia in the United States. CSF biomarker concentrations of , tTau, and pTau, were collected at enrollment (2016-2020) and analyzed with the Roche Elecsys system. Annual ambient and traffic-related residential concentrations were estimated at a and resolution, respectively, and computed for each participant's geocoded address, using three exposure time periods based on specimen collection date. Associations between and CSF biomarker concentrations, considering continuous and dichotomous (dichotomized at clinical cutoffs) outcomes, were estimated with multiple linear/logistic regression, respectively, controlling for potential confounders (age, gender, race, ethnicity, body mass index, and neighborhood socioeconomic status). Interquartile range (IQR; ) increases in 1-y [; 95% confidence interval (CI): , ] and 3-y (; 95% CI: , ) ambient exposures were negatively associated with CSF concentrations. Associations between ambient and were similar for 5-y estimates (; 95% CI: , 0.005). Dichotomized CSF variables revealed similar associations between ambient and . Associations with traffic-related were similar but not significant. Associations between exposures and tTau, pTau , or levels were mainly null. In our study, consistent trends were found between 1-y exposure and decreased CSF , which suggests an accumulation of amyloid plaques in the brain and an increased risk of developing AD. https://doi.org/10.1289/EHP13503.

Dietary intake changes the associations between long-term exposure to fine particulate matter and the surrogate indicators of insulin resistance

The relationship of fine particulate matter (PM2.5) exposure and insulin resistance remains inclusive. Our study aimed to investigate this association in the project of Prediction for Atherosclerotic Cardiovascular Disease Risk in China (China-PAR). Specifically, we examined the associations between long-term PM2.5 exposure and three surrogate indicators of insulin resistance: the triglyceride-glucose index (TyG), TyG with waist circumference (TyG-WC) and metabolic score for insulin resistance (METS-IR). Additionally, we explored potential effect modification of dietary intake and components. Generalized estimating equations were used to evaluate the associations between PM2.5 and the indicators with an unbalanced repeated measurement design. Our analysis incorporated a total of 162,060 observations from 99,329 participants. Each 10 μg/m3 increment of PM2.5 was associated with an increase of 0.22 % [95 % confidence interval (CI): 0.20 %, 0.25 %], 1.60 % (95 % CI: 1.53 %, 1.67 %), and 2.05 % (95 % CI: 1.96 %, 2.14 %) in TyG, TyG-WC, and METS-IR, respectively. These associations were attenuated among participants with a healthy diet, particularly those with sufficient intake of fruit and vegetable, fish or tea (pinteraction < 0.0028). For instance, among participants with a healthy diet, TyG increased by 0.11 % (95 % CI: 0.08 %, 0.15 %) per 10 μg/m3 PM2.5 increment, significantly lower than the association observed in those with an unhealthy diet. The findings of this study emphasize the potential of a healthy diet to mitigate these associations, highlighting the urgency for improving air quality and implementing dietary interventions among susceptible populations in China.

Abstract 841: Fine particulate matter exposure during breast cancer treatment among older women associated with increased mortality

Abstract Background: Fine Particulate Matter (PM2.5) is associated with higher mortality among people with chronic conditions. Breast cancer (BC) survivors may be particularly vulnerable during cancer treatment. We assessed the association between PM2.5 during 9-months following BC diagnosis and all-cause and BC-mortality using policy relevant PM2.5 cut-offs. Methods: Using SEER-Medicare linked with a high-resolution model-based PM2.5 by residential zipcode (2007-2016), we assembled a cohort of women ≥66 years with incident stage I-IV BC. We assessed PM2.5 exposure, categorized as &amp;lt;8 µg/m3 (low), 8-12 µg/m3 (moderate) and &amp;gt;12 µg/m3 (high—above air quality standard), and types of cancer treatments (surgery [SX], chemotherapy [CTX], radiation therapy [RTX]) during a 9-month landmark period. We identified all-cause and BC death within 5 years of diagnosis. We fit multivariable Cox proportional hazard models to assess associations with PM2.5 exposure adjusting for individual-level characteristics (demographics, tumor characteristics, comorbidities), neighborhood SES, SEER state, and long-term PM2.5 exposure. We also evaluated the association between PM2.5 exposure and mortality by treatment types (SX, SX + RTX, SX + CTX, SX + RTX + CTX, and RTX and/or CTX). We used multiple imputation to account for missing variables (race, ER status, HER2 status, grade). Results: Among 72,798 women (mean age 75 years, 83% white, 56% stage I, 32% II, 9.2% III, 2.9% IV), 41%, 32%, 13%, 8.4%, and 5.1% received SX + RTX, SX only, SX + Chemo + RTX, SX + Chemo, and CTX and/or RTX. The mean PM2.5 level was 8.8 µg/m3 [36%, 52% and 11% were exposed to &amp;lt;8, 8-12, and &amp;gt;12, respectively]. We observed 12,163 all-cause and 4,729 BC deaths during follow-up. Compared to those exposed to low levels, higher levels of PM2.5 exposure were associated with increased all-cause mortality for both moderate PM2.5 [HR 1.03 (95%CI:1.00-1.05)] and high PM2.5 [HR 1.09 (95%CI: 1.06-1.14)] but not BC-specific mortality. Among treatment subgroups, PM2.5 was associated with higher all-cause mortality in SX+RTX for moderate [HR 1.24 (95%CI:1.18-1.32)] and high PM2.5 [HR 1.36 (95%CI: 1.25-1.48)] and SX+RTX+CTX for high PM2.5 [HR 1.33 (95%CI: 1.17-1.51)]. There were no association between moderate/high PM2.5 with all-cause mortality in SX only and SX+CTX. Among the SX+RTX subgroup, BC-specific mortality was elevated for both moderate [HR 1.50 (95%CI:1.35-1.66)] and high PM2.5 [HR 1.81 (95%CI: 1.55-2.12)]. Conclusion: Even below EPA regulatory thresholds (PM2.5 &amp;lt;12 µg/m3), we observed increased risk of death in BC survivors who had high PM2.5 exposure during treatment period. The elevated mortality primarily occurred among women who received RTX and was present for all-cause and BC-specific mortality. The potential interaction between RTX and PM2.5 exposure, even after adjusting for tumor subtype and stage, warrants further evaluation. Citation Format: Benjamin Bates, Rachel Nethery, Melanie Rua, Hari Iyer, Elisa Bandera, Soko Setoguchi. Fine particulate matter exposure during breast cancer treatment among older women associated with increased mortality [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2024; Part 1 (Regular Abstracts); 2024 Apr 5-10; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2024;84(6_Suppl):Abstract nr 841.

Abstract 3456: The role of particulate matter exposure in racial differences in colorectal cancer mortality in metropolitan Detroit

Abstract Colorectal cancer (CRC) is the third most diagnosed cancer in the United States and the third leading cause of cancer-related deaths. Non-Hispanic Black (NHB) individuals have the highest rates of CRC incidence and mortality in the United States. These disparities are highly influenced by social determinants of health (SDOH). Neighborhood quality, a well-established SDOH, has been shown to influence cancer outcomes, oftentimes more heavily in minorities. Additionally, neighborhood quality is known to influence an individual’s risk of exposure to harmful environmental contaminants including ambient air pollution as a result of systemic racism such as segregation and historic redlining, leading to environmental injustices. Fine particulate matter (PM2.5) exposure has been shown to increase the risk of CRC mortality, however, its effects by race have not yet been examined. We sought to understand whether higher rates of exposure to PM2.5 played a role in racial differences in CRC survival in metropolitan Detroit. Patient data including census tract at diagnosis, demographics, and clinical features were obtained from the metropolitan Detroit cancer surveillance system registry. Ambient PM2.5 concentration data at the census tract were obtained from the Environmental Protection Agency (EPA) Remote Sensing Information Gateway (RSIG) and converted to annual averages to use in an interval-censored Cox proportional hazards regression model. We found that PM2.5 exposure partly attenuated the effect of race on overall mortality in all patients (NHB vs NHW: Hazard Ratio (HR) = 1.24, 95% Confidence Interval (CI) 1.20 - 1.27, p &amp;lt; 0.0001, NHB vs NHW after accounting for PM2.5: HR = 1.19, 95% CI = 1.16 - 1.23 p &amp;lt; 0.0001) and the effect was stronger among patients under 50 than over 50, though still significant in both models. Additionally, the effect of PM2.5 on mortality was much stronger among NHB patients than NHW patients (NHB HR = 1.30, 95% CI = 1.17 - 1.45, p &amp;lt; 0.0001; NHW HR = 1.06, 95% CI = 1.02 - 1.11 p = 0.008) and especially strong among NHB patients under 50 (HR = 2.51, 95% CI = 2.38 - 3.38, p &amp;lt; 0.0001) compared to any other group. We conclude that ambient air pollution, particularly PM2.5, disproportionately affects mortality risk in NHB CRC patients. These results highlight the importance of environmental justice research in biomedical research, and the need for a better understanding of environmental impact on tumor biology to prevent tumor progression and mortality among all patients. Citation Format: Natalie Gail Snider, Theresa Hastert, Gregory Dyson, Carina Gronlund, Elena M. Stoffel, Ed Peters, Laura Rozek, Ann Schwartz, Kristen Purrington. The role of particulate matter exposure in racial differences in colorectal cancer mortality in metropolitan Detroit [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2024; Part 1 (Regular Abstracts); 2024 Apr 5-10; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2024;84(6_Suppl):Abstract nr 3456.

Commercial real estate and air pollution

AbstractWe analyze the causal effect of air pollution (acute fine particulate matter) exposure on the commercial real estate (CRE) market. We instrument for air pollution using changes in local wind direction to find that an increase in fine particulate matter exposure leads to a contemporaneous decrease in CRE market values and (net) income as well as an increase in capital expenditures. Heterogeneous treatment analysis within a building‐level fixed effects framework uncovers that the negative effect on market values is concentrated in the office sector, consistent with the notion that air pollution‐induced decreases in CRE values are driven by a reduction in CRE assets’ productive capacity. Additionally, we document that the negative impact on (net) income is concentrated in the apartment sector, which is consistent with a broad set of local disamenity mechanisms identified in previous residential real estate literature.

Lycium barbarum polysaccharide's protective effects against PM2.5-induced cellular senescence in HUVECs

Fine particulate matter (PM2.5) exposure is strongly associated with vascular endothelial senescence, a process implicated in cardiovascular diseases. While there is existing knowledge on the impact of Lycium barbarum polysaccharide (LBP) on vascular endothelial damage, the protective mechanism of LBP against PM2.5-induced vascular endothelial senescence remains unclear. In this study, we investigated the impact of PM2.5 exposure on vascular endothelial senescence and explored the intervention effects of LBP in human umbilical vein endothelial cells (HUVECs). We found that PM2.5 exposure dose-dependently reduced cell viability and proliferation in HUVECs while increasing the production of reactive oxygen species (ROS), malondialdehyde (MDA), and hydrogen peroxide (H2O2). Additionally, PM2.5 exposure inhibited the activity of superoxide dismutase (SOD). Notably, PM2.5 exposure induced autophagy impairments and cellular senescence. However, LBP mitigated PM2.5-induced cell damage. Further studies demonstrated that correcting autophagy impairment in HUVECs reduced the expression of the senescence markers P16 and P21 induced by PM2.5. This suggests the regulatory role of autophagy in cellular senescence and the potential of LBP in improving HUVECs senescence. These findings provide novel insights into the mechanisms underlying PM2.5-induced cardiovascular toxicity and highlight the potential of LBP as a therapeutic agent for improving vascular endothelial health.

Wildfire-related PM2.5 and cardiovascular mortality: A difference-in-differences analysis in Brazil

Brazil has experienced unprecedented wildfires recently. We aimed to investigate the association of wildfire-related fine particulate matter (PM2.5) with cause-specific cardiovascular mortality, and to estimate the attributable mortality burden. Exposure to wildfire-related PM2.5 was defined as exposure to annual mean wildfire-related PM2.5 concentrations in the 1-year prior to death. The variant difference-in-differences method was employed to explore the wildfire-related PM2.5-cardiovascular mortality association. We found that, in Brazil, compared with the population in the first quartile (Q1: ≤1.82 μg/m3) of wildfire-related PM2.5 exposure, those in the fourth quartile (Q4: 4.22–17.12 μg/m3) of wildfire-related PM2.5 exposure had a 2.2% (RR: 1.022, 95% CI: 1.013–1.032) higher risk for total cardiovascular mortality, 3.1% (RR: 1.031, 95% CI: 1.014–1.048) for ischaemic heart disease mortality, and 2.0% (RR: 1.020, 95% CI: 1.002–1.038) for stroke mortality. From 2010 to 2018, an estimation of 35,847 (95% CI: 22,424–49,177) cardiovascular deaths, representing 17.77 (95% CI: 11.12–24.38) per 100,000 population, were attributable to wildfire-related PM2.5 exposure. Targeted health promotion strategies should be developed for local governments to protect the public from the risk of wildfire-related cardiovascular premature deaths.

Nasopharyngeal microbiota in children is associated with severe asthma exacerbations

BackgroundThe respiratory microbiome has been associated with the etiology and disease course of asthma. ObjectiveThis study assessed the nasopharyngeal microbiota in children with a severe asthma exacerbation and their associations with medication, air quality and viral infection. MethodsA cross-sectional study was performed among children aged 2-18 years admitted to the medium (MCU; n=84) or intensive care (ICU; n=78) with an asthma exacerbation. For case-control analyses, we matched all cases aged 2-6 years (n=87) to controls in a 1:2 ratio. Controls were participants of either a prospective case-control study or a longitudinal birth cohort (n=182). The nasopharyngeal microbiome was characterized by 16S-rRNA-gene sequencing. ResultsCases showed higher Shannon diversity (ICU and MCU combined; p=0.002) and a distinct microbial community composition when compared to controls (PERMANOVA R2=1.9%, p<0.001). We observed significantly higher abundance of Staphylococcus and ‘oral’ taxa, including Neisseria, Veillonella and Streptococcus spp. and lower abundance of Dolosigranulum pigrum, Corynebacterium and Moraxella spp. (MaAsLin2, q<0.25) in cases versus controls. Furthermore, Neisseria abundance was associated with more severe disease (ICU vs MCU MaAslin2 p=0.03, q=0.30). Neisseria spp. abundance was also related with fine particulate matter exposure, whereas Haemophilus and Streptoccocus abundance was related with recent inhalation corticosteroid use. We observed no correlations with viral infection. ConclusionOur results demonstrate that children admitted with asthma exacerbations harbor a microbiome characterized by overgrowth of Staphylococcus and ‘oral’ microbes, and an underrepresentation of beneficial niche-appropriate commensals. Several of these associations may be explained by (environmental or medical) exposures, although cause-consequence relationships remain unclear and requires further investigations.

Atmospheric fine particulate matter (PM2.5) induces pulmonary fibrosis by regulating different cell fates via autophagy

The presence of respiratory diseases demonstrates a positive correlation with atmospheric fine particulate matter (PM2.5) exposure. The respiratory system is the main target organ affected by PM2.5, and exposure to PM2.5 elevates the likelihood of developing pulmonary fibrosis (PF). In this study, lung epithelial cell (BEAS-2B) and fibroblast (NIH-3T3) were used as in vitro exposure models to explore the mechanisms of PF. PM2.5 exposure caused mitochondrial damage in BEAS-2B cells and increased a fibrotic phenotype in NIH-3T3 cells. Epithelial cells and fibroblasts have different fates after PM2.5 exposure due to their different sensitivities to trigger autophagy. Exposure to PM2.5 inhibits mitophagy in BEAS-2B cells, which hinders the removal of damaged mitochondria and triggers cell death. In this process, the nuclear retention of the mitophagy-related protein Parkin prevents it from being recruited to mitochondria, resulting in mitophagy inhibition. In contrast, fibroblasts exhibit increased levels of autophagy, which may isolate PM2.5 and cause abnormal fibroblast proliferation and migration. Fibrotic phenotypes such as collagen deposition and increased α-actin also appear in fibroblasts. Our results identify PM2.5 as a trigger of PF and delineate the molecular mechanism of autophagy in PM2.5 induced PF, which provides new insights into the pulmonary injury.

Gestational exposure to PM2.5 disrupts fetal development by suppressing placental trophoblast syncytialization via progranulin/mTOR signaling

Recent epidemiological and animal studies have indicated that ambient fine particulate matter (PM2.5) exposure during pregnancy is closely associated with intrauterine growth restriction (IUGR). However, the underlying mechanisms remain to be revealed. In this study, we found that gestational exposure to PM2.5 significantly decreased fetal weight and crown-rump length in mice, accompanied by insufficient placental trophoblast syncytialization and increased expression of progranulin (PGRN) in mice placenta. Administering PGRN neutralizing antibody to pregnant mice alleviated growth restriction and insufficient placental trophoblast syncytialization caused by PM2.5, accompanied with suppressed activation of the mTOR signaling pathway. Furthermore, in vitro experiments using human placental BeWo cells showed that 10 μg·mL−1 PM2.5 activated PGRN/mTOR signaling and suppressed forskolin-induced cell fusion, which was blocked by knockdown of PGRN. Taken together, our results demonstrated that PM2.5 exposure during pregnancy inhibited placental trophoblast syncytialization by activating PGRN/mTOR signaling, leading to abnormal placental development and IUGR. This study reveals a novel mechanism underlying the developmental toxicity of PM2.5 exposure during pregnancy.

Association of PM2.5 Exposure and Alzheimer Disease Pathology in Brain Bank Donors-Effect Modification by APOE Genotype.

Fine particulate matter (PM2.5) exposure has been found to be associated with Alzheimer disease (AD) and is hypothesized to cause inflammation and oxidative stress in the brain, contributing to neuropathology. The APOE gene, a major genetic risk factor of AD, has been hypothesized to modify the association between PM2.5 and AD. However, little prior research exists to support these hypotheses. This study investigates the association between traffic-related PM2.5 and AD hallmark pathology, including effect modification by APOE genotype, in an autopsy cohort. A cross-sectional study was conducted using brain tissue donors enrolled in the Emory Goizueta AD Research Center who died before 2020 (n = 224). Donors were assessed for AD pathology including the Braak stage, Consortium to Establish a Registry for AD (CERAD) score, and combined AD neuropathologic change (ABC) score. Traffic-related PM2.5 concentrations were modeled for the metro-Atlanta area during 2002-2019 with a spatial resolution of 200-250 m. One-year, 3-year, and 5-year average PM2.5 concentrations before death were matched to participants' home address. We assessed the association between traffic-related PM2.5 and AD hallmark pathology and effect modification by APOE genotype, using adjusted ordinal logistic regression models. Among the 224 participants, the mean age of death was 76 years, and 57% had at least 1 APOE ε4 copy. Traffic-related PM2.5 was significantly associated with the CERAD score for the 1-year exposure window (odds ratio [OR] 1.92; 95% CI 1.12-3.30) and the 3-year exposure window (OR 1.87; 95% CI 1.01-3.17). PM2.5 was also associated with higher Braak stage and ABC score albeit nonsignificantly. The strongest associations between PM2.5 and neuropathology markers were among those without APOE ε4 alleles (e.g., for the CERAD score and 1-year exposure window, OR 2.31; 95% CI 1.36-3.94), though interaction between PM2.5 and APOE genotype was not statistically significant. Our study found traffic-related PM2.5 exposure was associated with the CERAD score in an autopsy cohort, contributing to epidemiologic evidence that PM2.5 affects β-amyloid deposition in the brain. This association was particularly strong among donors without APOE ε4 alleles. Future studies should further investigate the biological mechanisms behind this association.

Fine particulate matter exposure and incident atopic dermatitis: A birth cohort study

Fine particulate matter exposure and incident atopic dermatitis: A birth cohort study

Association between prenatal and childhood PM2.5 exposure and preadolescent anxiety and depressive symptoms.

Fine particulate matter (PM2.5) exposure has been linked to anxiety and depression in adults; however, there is limited research in the younger populations, in which symptoms often first arise. We examined the association between early-life PM2.5 exposure and symptoms of anxiety and depression in a cohort of 8-11-year-olds in Mexico City. Anxiety and depressive symptoms were assessed using the Spanish versions of the Revised Children's Manifest Anxiety Scale and Children's Depression Inventory. Daily PM2.5 was estimated using a satellite-based exposure model and averaged over several early and recent exposure windows. Linear and logistic regression models were used to estimate the change in symptoms with each 5-µg/m3 increase in PM2.5. Models were adjusted for child's age, child's sex, maternal age, maternal socioeconomic status, season of conception, and temperature. Average anxiety and depressive symptom T-scores were 51.0 (range 33-73) and 53.4 (range 44-90), respectively. We observed consistent findings for exposures around the fourth year of life, as this was present for both continuous and dichotomized anxiety symptoms, in both independent exposure models and distributed lag modeling approaches. This window was also observed for elevated depressive symptoms. An additional consistent finding was for PM2.5 exposure during early pregnancy in relation to both clinically elevated anxiety and depressive symptoms, this was seen in both traditional and distributed lag modeling approaches. Both early life and recent PM2.5 exposure were associated with higher mental health symptoms in the child highlighting the role of PM2.5 in the etiology of these conditions.

The impact of ambient PM2.5 air pollution on student performance: Evidence from finnish matriculation examinations

We examine the impact of fine particulate matter pollution on upper secondary school matriculation exams in Finland. Considering the subject-specific abilities of exam takers, we observe that fine particulate matter exposure influences performance in mathematical but not in verbal subjects.