Effects Of Particulate Matter Exposure Research Articles

How long-term PM exposure may affect all-site cancer mortality: Evidence from a large cohort in southern China

BackgroundEvidence of a potential causal link between long-term exposure to particulate matter (PM) and all-site cancer mortality from large population cohorts remained limited and suffered from residual confounding issues with traditional statistical methods. AimsWe aimed to examine the potential causal relationship between long-term PM exposure and all-site cancer mortality in South China using causal inference methods. MethodsWe used a cohort in southern China that recruited 580,757 participants from 2009 through 2015 and tracked until 2020. Annual averages of PM1, PM2.5, and PM10 concentrations were generated with validated spatiotemporal models. We employed a causal inference approach, the Marginal Structural Cox model, based on observational data to evaluate the association between long-term exposure to PM and all-site cancer mortality. ResultsWith an increase of 1 µg/m³ in PM1, PM2.5, and PM10, the hazard ratios (HRs) and 95% confidence interval (CI) for all-site cancer were 1.033 (95% CI: 1.025–1.041), 1.032 (95% CI: 1.027–1.038), and 1.020 (95% CI: 1.016–1.025), respectively. The HRs (95% CI) for digestive system and respiratory system cancer mortality associated with each 1 µg/m³ increase in PM1 were 1.022 (1.009–1.035) and 1.053 (1.038–1.068), respectively. In addition, inactive participants, who never smoked, or who lived in areas of low surrounding greenness were more susceptible to the effects of PM exposure, the HRs (95% CI) for all-site cancer mortality were 1.042 (1.031–1.053), 1.041 (1.032–1.050), and 1.0473 (1.025–1.070) for every 1 µg/m³ increase in PM1, respectively. The effect of PM1 tended to be more pronounced in the low-exposure group than in the general population, and multiple sensitivity analyses confirmed the robustness of the results. ConclusionThis study provided evidence that long-term exposure to PM may elevate the risk of all-site cancer mortality, emphasizing the potential health benefits of improving air quality for cancer prevention.

Effect modification of diabetic status on the association between exposure to particulate matter and cardiac arrhythmias in a general population: A systematic review and meta-analysis.

Particulate matter (PM) has various health effects, including cardiovascular diseases. Exposure to PM and a diagnosis of diabetes mellitus (DM) have been associated with an increased risk of cardiac arrhythmias. However, no comprehensive synthesis has been conducted to examine the modifying effect of DM on the association between PM and arrhythmia events. Thus, the objectives of this review were to investigate whether the association of PM is linked to cardiac arrhythmias and whether DM status modifies its effect in the general population. The search was conducted on PubMed/MEDLINE and Embase until January 18, 2023. We included cohort and case-crossover studies reporting the effect of PM exposure on cardiac arrhythmias and examining the role of diabetes as an effect modifier. We used the DerSimonian and Laird random-effects model to calculate the pooled estimates. A total of 217 studies were found and subsequently screened. Nine studies met the inclusion criteria, and five of them were included in the meta-analysis. The participants numbered 4,431,452, with 2,556 having DM. Exposure to PM of any size showed a significant effect on arrhythmias in the overall population (OR 1.10, 95% CI 1.04-1.16). However, the effect modification of DM was not significant (OR 1.18 (95% CI 1.01-1.38) for DM; OR 1.08 (95% CI 1.02-1.14) for non-DM; p-value of subgroup difference = 0.304). Exposure to higher PM concentrations significantly increases cardiac arrhythmias requiring hospital or emergency visits. Although the impact on diabetic individuals is not significant, diabetic patients should still be considered at risk. Further studies with larger sample sizes and low bias are needed.

Effects of particulate matter exposure on the expression of the SARS-CoV-2 ACE2 receptor in ocular surface tissues and cells.

Particulate matter (PM) has been reported to be one of the risk factor for COVID-19 caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). However, although the ocular surface is deeply affected by both PM exposure and SARS-COV-2 infection, no studies have investigated the effects of PM exposure on the ocular route of SARS-COV-2 infection. To this end, we explored the effects of PM on the expression of SARS-COV-2-associated receptors and proteins in ocular surface. Herein, short- and long-term PM-exposed rat models were established by topically administering PM for 3 and 10days, respectively. Immortalized human corneal epithelial cells (HCECs) and human conjunctival epithelial cells (HCjECs) were exposed to PM. ACE2, TMPRSS2, CD147, and ADAM17 expression levels were measured by western blot analysis. Our results show that short-term PM exposure had little effect on the expressions of ACE2, TMPRSS2, and CD147 in ocular surface tissues. However, long-term PM exposure decreased the ACE2 expression in conjunctival tissues and increased the CD147 expression in corneal or conjunctival tissues. PM exposure reduced the ACE2 expression by increasing the ADAM17 expression and ACE2 shedding level in HCECs and HCjECs. Our findings suggest that long-term PM exposure down-regulate the expression of the SARS-CoV-2 receptor ACE2 in conjunctival tissues through ADAM17-dependent ACE2 shedding. However, long-term PM exposure up-regulates the expression of another SARS-CoV-2 receptor CD147 in ocular surface tissues, accompanied by ocular surface damage and cytotoxicity. This study provides a new insight into uncovering potential risk factors for infection with SARS-CoV-2 via the ocular route.

The short-term effect of ambient particulate matter on suicide death

BackgroundAir pollution can cause various respiratory and neurological diseases and continuous exposure can lead to death. Previous studies have reported that particulate matter (PM) exposure increases the risk of depression, suicidal thoughts, and suicidal death; however, the results are inconsistent and limited. This study aimed to examine the relationship between short-term PM exposure and suicide deaths, as well as investigate the short-term effects of PM on suicide death within vulnerable groups based on factors such as sex, age group, suicide-related information (note, method, and cause), psychiatric disorders, and physical diseases.MethodsData on a total of 28,670 suicide deaths from 2013 to 2017, provided by the Korea Foundation for Suicide Prevention, were analyzed. The study design employed a time-series analysis with a two-stage approach. In the first step, a generalized additive model combined with a distributed lag nonlinear model was used to estimate the short-term effect of PM exposure on suicide risk specific to each city. In the second step, the estimated results from each city were pooled through a meta-analysis to derive the overall effect. We determined the effects of single lag, cumulative lag, and moving average PM concentrations from days 0–7 before suicide.ResultsWe confirmed an association between exposure to PM10 (≤ 10 μm in diameter) and deaths due to suicide. In particular, among individuals with psychiatric disorders and those who employed non-violent suicide methods, increased exposure to PM10 was associated with a higher risk of death by suicide, with percentage changes of 5.92 (95% confidence interval [CI]: 3.95–7.92) and 11.47 (95% CI: 7.95–15.11), respectively. Furthermore, in the group with psychiatric disorders, there was an observed tendency of increasing suicide risk as PM10 levels increased up to 120 µg/m3, whereas in the group with non-violent suicide deaths, there was a pronounced trend of rapid increase in suicide risk with an increase in PM10 up to 100 µg/m3.ConclusionsThese results show an association between short-term exposure to PM and suicide. Our study adds evidence for the benefits of reducing PM in preventing diseases and improving mental health.

Particulate matter 10 induces oxidative stress and apoptosis in rhesus macaques skin fibroblast.

Particulate matter (PM) is a major air pollutant that affects human health worldwide. PM can pass through the skin barrier, thus causing skin diseases such as heat rash, allergic reaction, infection, or inflammation. However, only a few studies have been conducted on the cytotoxic effects of PM exposure on large-scale animals. Therefore, herein, we investigated whether and how PM affects rhesus macaque skin fibroblasts. Rhesus macaque skin fibroblasts were treated with various concentrations of PM10 (1, 5, 10, 50, and 100 μg/mL) and incubated for 24, 48, and 72 h. Then, cell viability assay, TUNEL assay, and qRT-PCR were performed on the treated cells. Further, the reactive oxygen species, glutathione, and cathepsin B levels were determined. The MTT assay revealed that PM10 (>50 μg/mL) proportionately reduced the cell proliferation rate. PM10 treatment increased TUNEL-positive cell numbers, following the pro-apoptosis-associated genes (CASP3 and BAX) and tumor suppressor gene TP53 were significantly upregulated. PM10 treatment induced reactive oxidative stress. Cathepsin B intensity was increased, whereas GSH intensity was decreased. The mRNA expression levels of antioxidant enzyme-related genes (CAT, GPX1 and GPX3) were significantly upregulated. Furthermore, PM10 reduced the mitochondrial membrane potential. The mRNA expression of mitochondrial complex genes, such as NDUFA1, NDUFA2, NDUFAC2, NDUFS4, and ATP5H were also significantly upregulated. In conclusion, these results showed that PM10 triggers apoptosis and mitochondrial damage, thus inducing ROS accumulation. These findings provide potential information on the cytotoxic effects of PM10 treatment and help to understand the mechanism of air pollution-induced skin diseases.

Ambient particulate matter and renal function decline in people with HIV/AIDS.

We aimed to explore the effect of particulate matter exposure on renal function in people with HIV/AIDS (PWHA). A total of 37 739 repeated measurements were conducted on eGFR levels, serum creatinine (Scr), and the triglyceride-glucose (TyG) index in 6958 PWHAs. The relationship between 1 and 28 day moving averages of particulate matter concentrations with Scr and eGFR was assessed using linear mixed-effects models. Modified Poisson regression models were employed to assess the associations of cumulative particulate matter exposure with the incidence of chronic kidney disease (CKD). Mediation analyses were used to examine the role of TyG index. Short-term exposure to particulate matter was related to reduced renal function. The strongest associations between exposure to particulate matter (PM) 1 , PM 2.5 , and PM 10 and percentage changes in eGFR were observed at 7-day moving average exposure windows, with a respective decrease of 0.697% (-1.008%, -0.386%), 0.429% (-0.637%, -0.220%), and 0.373% (-0.581%, -0.164%) per IQR increment. Long-term exposure to PM 1 , PM 2.5 , and PM 10 was positively linked with the incidence of CKD, with each IQR increment corresponding to fully adjusted RRs (95% CIs) of 1.631 (1.446-1.839), 1.599 (1.431-1.787), and 1.903 (1.665-2.175), respectively. TyG index-mediated 8.87, 8.88, and 7.58% of the relationship between cumulative exposure to PM 1 , PM 2.5 , and PM 10 and increased risk of CKD, respectively. Exposure to particulate matter among PWHAs is linked to reduced renal function, potentially contributing to increased CKD incidence, where the TyG index might serve as a partial mediator.

Impact of Particulate Matter Exposure and Aerobic Exercise on Circulating Biomarkers of Oxidative Stress, Antioxidant Status, and Inflammation in Young and Aged Mice.

Exposure to particulate matter (PM) and exercise training can have antagonistic effects on inflammatory responses and the balance between pro-oxidants and antioxidants in the body. However, the underlying mechanisms of these effects remain unclear. This study aimed to investigate the effects of PM exposure and aerobic exercise training on oxidative stress, antioxidant status, and inflammation in mice of different ages. Two groups of male C57BL/6 mice, comprising forty 1-month-old and forty 12-month-old mice, were exposed to either PM or exercise training or both for 8 weeks. PM exposure led to significantly higher 8-hydroxydeoxyguanosine (8-OHdG), malondialdehyde (MDA), interleukin-1β (IL-1β), interleukin-6 (IL-6), and tumor necrosis factor α (TNF-α) levels (p < 0.05) and significantly lower superoxide dismutase (SOD) and catalase (CAT) activities (p < 0.05) in both age groups exposed to PM compared to the control groups. Conversely, aerobic exercise training led to significantly lower 8-OHdG, MDA, IL-1β, IL-6, and TNF-α levels (p < 0.05) and significantly higher SOD and CAT activities (p < 0.05) in both age groups receiving exercise training, compared to those exposed to PM. Moreover, young mice in the exercise training and PM group showed significantly lower 8-OHdG, MDA, and IL-1β levels (p < 0.05) and significantly higher SOD and CAT activities (p < 0.05) than young mice in the PM exposure group. However, these levels did not vary significantly between the group of old mice that either received exercise training or exposure to PM. Our results suggest that while PM exposure could cause pro-oxidant/antioxidant imbalances and inflammatory responses, regular aerobic exercise could ameliorate these negative effects, although these vary with age. Nevertheless, the antioxidant and anti-inflammatory effects of exercise were countered by PM exposure, especially in older mice.

Maternal particulate matter exposure and gestational diabetes mellitus: a population–based cohort study

Gestational diabetes mellitus (GDM) prevalence is steadily increasing worldwide, posing a significant threat to the short- and long-term health of both mother and offspring. As particulate matter (PM) air pollution has been reported to affect glucose metabolism, it was suggested that maternal PM exposure may be associated with the development of GDM; however, evidence is limited and inconsistent. To study the association between maternal exposure to PM2.5 and PM10 and the risk of GDM, to identify critical windows of susceptibility and to evaluate effect modification by ethnicity. A retrospective cohort study was conducted including pregnancies of women who delivered at a large tertiary medical center in Israel between the years 2003 and 2015. Residential PM levels were estimated by a hybrid spatiotemporally resolved satellite-based model at 1-km spatial resolution. Multivariable logistic analyses were applied to study the association between maternal PM exposure in different pregnancy periods and GDM risk, while adjusting for background, obstetrical and pregnancy characteristics. Analyses were also stratified by ethnicity (Jewish / Bedouin). The study included 89,150 pregnancies, 3,245 (3.6%) were diagnosed with GDM. First trimester exposure to both PM2.5 (adj. OR per 5 μg/m3 = 1.09; 95%CI: 1.02, 1.17) and PM10 (adj. OR per 10 μg/m3 = 1.11; 95%CI: 1.06, 1.17) was significantly associated with increased risk for GDM. In the stratified analyses, the association with first trimester PM10 exposure was consistent among pregnancies of both Jewish and Bedouin women, while the association with first trimester PM2.5 exposure was significant among pregnancies of Jewish women only (adj. OR per 5 μg/m3 = 1.09; 95%CI: 1.00, 1.19), as well as association with preconception PM10 exposure (adj. OR per 10 μg/m3 = 1.07; 95%CI: 1.01, 1.14). No association was found between second trimester PM exposure and GDM risk. Maternal exposure to both PM2.5 and PM10 during the first trimester of pregnancy is associated with GDM, suggesting the first trimester as a particular window of susceptibility to the effect of PM exposure on GDM risk. The effects found in this study differed by ethnic group, emphasizing the importance of addressing ethnic disparities when assessing environmental impacts on health.

Biomarkers of particulate matter exposure in patients with chronic obstructive pulmonary disease: a systematic review.

In recent years, ambient particulate matter (PM) exposure has been strongly linked with health effects. Elevated levels of PM in polluted air have been correlated with the onset and development of chronic obstructive pulmonary disease (COPD). This systematic review was conducted to evaluate biomarkers that could reflect the effects of PM exposure in patients with COPD. We performed a systematic review of studies published on biomarkers associated with PM exposure in patients with COPD between January 01, 2012 and June 30, 2022 in PubMed/MEDLINE, EMBASE, and Cochrane databases. Studies that included data on biomarkers with COPD exposed PM were eligible for inclusion. Biomarkers were classified into 4 groups according to their mechanisms. Of the 105 studies identified, 22 were included in this study. Nearly 50 biomarkers have been proposed in the studies included in this review, and the most studied in relation to PM are several interleukins. Various mechanisms have been reported by which PM induces and aggravates COPD. Six studies related to oxidative stress, one related to direct effect of innate and adaptive immune systems, 16 associated with genetic regulation of inflammation, and two related to epigenetic regulation of physiology and susceptibility were found. Biomarkers related to these mechanisms were detected in serum, sputum, urine, exhaled breath concentration (EBC), and showed various correlations with PM in COPD. Various biomarkers have shown potential in predicting the extent of PM exposure in COPD patients. Future studies are needed to establish recommendations for regulation to reduce airborne PM, which could be used to develop strategies for prevention and management of environmental respiratory diseases.

Risk of type 2 diabetes after diagnosed gestational diabetes is enhanced by exposure to PM2.5.

Air pollution and gestational diabetes mellitus (GDM) are both associated with increased diabetes mellitus (DM) occurrence. However, whether air pollutants modify the effects of GDM on the occurrence of DM has been unknown. This study aims to determine whether the effect of GDM on DM development can be modified by exposure to ambient air pollutants. Women with one singleton birth delivery during 2004-14 according to the Taiwan Birth Certificate Database (TBCD) were included as the study cohort. Those newly diagnosed as having DM 1 year or later after childbirth were identified as DM cases. Controls were selected among women without DM diagnosis during follow-up. Personal residence was geocoded and linked with interpolated concentrations of air pollutants into township levels. Conditional logistic regression was used to determine the odds ratio (OR) of pollutant exposure and GDM, adjusting for age, smoking and meteorological variables. There were 9846 women who were newly diagnosed as having DM over a mean follow-up period of 10.2 years. We involved them and the 10-fold matching controls involved in our final analysis. The OR (odds ratio) (95% confidence interval, 95% CI) of DM occurrence per interquartile range increased in particulate matter (PM) smaller than or equal to 2.5 µm (PM2.5) and ozone (O3) was 1.31 (1.22-1.41) and 1.20 (1.16-1.25), respectively. The effects of PM exposure on DM development were significantly higher in the GDM group (OR: 2.46, 95% CI: 1.84-3.30) than in the non-GDM group (OR: 1.30, 95% CI: 1.21-1.40). Exposure to high levels of PM2.5 and O3 elevates the risk of DM. GDM acted synergistically in DM development with exposure to PM2.5 but not with that to O3.

Effects of Particulate Matter Exposure on the Eustachian Tube and Middle Ear Mucosa of Rats.

Particulate matter (PM) is a risk factor for various diseases. Recent studies have established an association between otitis media (OM) and PM exposure. To confirm this relationship, we developed a novel exposure model designed to control the concentration of PM, and we observed the effects of PM exposure on the Eustachian tube (ET) and middle ear mucosa of rats. Forty healthy, 10-week-old, male Sprague-Dawley rats were divided into 3-day, 7-day, 14-day exposure, and control groups (each, n=10). The rats were exposed to incense smoke as the PM source for 3 hours per day. After exposure, bilateral ETs and mastoid bullae were harvested, and histopathological findings were compared using microscopy and transmission electron microscopy (TEM). The expression levels of interleukin (IL)-1β, IL-6, tumor necrosis factor-α, and vascular endothelial growth factor (VEGF) in the middle ear mucosa of each group were compared using real-time reverse transcription polymerase chain reaction (RT-PCR). In the ET mucosa of the exposure group, the goblet cell count significantly increased after PM exposure (P=0.032). In the middle ear mucosa, subepithelial space thickening, increased angio-capillary tissue, and inflammatory cell infiltration were observed. Moreover, the thickness of the middle ear mucosa in the exposure groups increased compared to the control group (P<0.01). The TEM findings showed PM particles on the surface of the ET and middle ear mucosa, and RT-PCR revealed that messenger RNA (mRNA) expression of IL-1β significantly increased in the 3-day and 7-day exposure groups compared to the control group (P=0.035). VEGF expression significantly increased in the 7-day exposure group compared to the control and 3-day exposure groups (P<0.01). The ET and middle ear mucosa of rats showed histopathologic changes after acute exposure to PM that directly reached the ET and middle ear mucosa. Therefore, acute exposure to PM may play a role in the development of OM.

Co-exposure to particulate matter and humidity increases blood pressure in hypertensive mice via the TRPV4-cPLA2-COX2 pathway

Epidemiological studies have demonstrated that particulate matter (PM) can induce or exacerbate hypertension. High relative humidity has been associated with elevated blood pressure in certain regions. However, the coupling effect of humidity and PM on elevated blood pressure and the underlying mechanisms remain unknown. Herein, we aimed to explore the effects of exposure to PM and/or high relative humidity on hypertension, as well as elucidate underlying mechanisms. Male C57/BL6 mice were intraperitoneally administered NG-nitro-L-arginine methyl ester (L-NAME) to establish a hypertensive mouse model. The hypertensive mice were exposed to PM (0.15 mg/kg/day) and/or different relative humidities (45/90%) for eight weeks. Histopathological changes, systolic blood pressure (SBP), endothelial-derived contracting factors (thromboxane B2 [TXB2], Prostaglandin F2α [PGF2α], endothelin-1 [ET-1], and angiotensin II [Ang II]), and relaxing factors (prostaglandin I2 [PGI2] and nitric oxide [NO]) were measured to assess the effects of PM exposure and humidity on hypertension in mice. Levels of transient receptor potential vanilloid 4 (TRPV4), cytosolic phospholipase A2 (cPLA2), and cyclooxygenase 2 (COX2) were measured to explore their potential mechanisms. Herein, exposure to 90% relative humidity or PM alone had a slight but insignificant effect on hypertension. However, pathological changes and elevated blood pressure were markedly exacerbated following exposure to PM and 90% relative humidity. Levels of PGF2α, TXB2, and ET-1 were significantly increased, whereas the PGI2 level was substantially decreased. HC-067047-mediated blockade of TRPV4 suppressed TRPV4, cPLA2, and COX2 expression and effectively alleviated the increased blood pressure induced by exposure to PM and 90% relative humidity. These results indicate that 90% relative humidity and PM can activate the TRPV4-cPLA2-COX2 ion channel in the aorta, altering the endothelial-derived contracting and relaxing factors and enhancing blood pressure in hypertensive mice.

The possible role of particulate matter on the respiratory microbiome: evidence from in vivo to clinical studies.

Environmental pollution, which contains ambient particulate matter, has been shown to have a significant impact on human health and longevity over the past 30 years. Recent studies clearly showed that exposure to particulate matter directly caused adverse effects on the respiratory system via various mechanisms including the accumulation of free radical peroxidation, the imbalance of intercellular calcium regulation, and inflammation, resulting in respiratory diseases. Recent evidence showed the importance of the role of the respiratory microbiome on lung immunity and lung development. In addition, previous studies have confirmed that several chronic respiratory diseases were associated with an alteration in the respiratory microbiome. However, there is still a lack of knowledge with regard to the changes in the respiratory microbiome with regard to the role of particulate matter exposure in respiratory diseases. Therefore, this review aims to summarize and discuss all the in vivo to clinical evidence which investigated the effect of particulate matter exposure on the respiratory microbiome and respiratory diseases. Any contradictory findings are incorporated and discussed. A summary of all these pieces of evidence may offer an insight into a therapeutic approach for the respiratory diseases related to particulate matter exposure and respiratory microbiome.

Associations of Particulate Matter Exposures With Brain Gray Matter Thickness and White Matter Hyperintensities: Effect Modification by Low-Grade Chronic Inflammation.

Numerous studies have shown the effect of particulate matter exposure on brain imaging markers. However, little evidence exists about whether the effect differs by the level of low-grade chronic systemic inflammation. We investigated whether the level of c-reactive protein (CRP, a marker of systemic inflammation) modifies the associations of particulate matter exposures with brain cortical gray matter thickness and white matter hyperintensities (WMH). We conducted a cross-sectional study of baseline data from a prospective cohort study including adults with no dementia or stroke. Long-term concentrations of particulate matter ≤ 10 µm in diameter (PM10) and ≤ 2.5 µm (PM2.5) at each participant's home address were estimated. Global cortical thickness (n = 874) and WMH volumes (n = 397) were estimated from brain magnetic resonance images. We built linear and logistic regression models for cortical thickness and WMH volumes (higher versus lower than median), respectively. Significance of difference in the association between the CRP group (higher versus lower than median) was expressed as P for interaction. Particulate matter exposures were significantly associated with a reduced global cortical thickness only in the higher CRP group among men (P for interaction = 0.015 for PM10 and 0.006 for PM2.5). A 10 μg/m3 increase in PM10 was associated with the higher volumes of total WMH (odds ratio, 1.78; 95% confidence interval, 1.07-2.97) and periventricular WMH (2.00; 1.20-3.33). A 1 μg/m3 increase in PM2.5 was associated with the higher volume of periventricular WMH (odds ratio, 1.66; 95% confidence interval, 1.08-2.56). These associations did not significantly differ by the level of high sensitivity CRP. Particulate matter exposures were associated with a reduced global cortical thickness in men with a high level of chronic inflammation. Men with a high level of chronic inflammation may be susceptible to cortical atrophy attributable to particulate matter exposures.

Extracellular vesicles and their miRNA contents counterbalance the pro-inflammatory effect of air pollution during physiological pregnancy: A focus on Syncytin-1 positive vesicles.

The impact of exposure to respirable particulate matter (PM) during pregnancy is a growing concern, as several studies have associated increased risks of adverse pregnancy and birth outcomes, and impaired intrauterine growth with air pollution. The molecular mechanisms responsible for such effects are still under debate. Extracellular vesicles (EVs), which travel in body fluids and transfer microRNAs (miRNAs) between tissues (e.g., pulmonary environment and placenta), might play an important role in PM-induced risk. We sought to determine whether the levels of PM with aerodynamic diameters of ≤10µm (PM10) and ≤2.5µm (PM2.5) are associated with changes in plasmatic EV release and EV-miRNA content by investigating 518 women enrolled in the INSIDE study during the first trimester of pregnancy. In all models, we included both the 90-day averages of PM (long-term effects) and the differences between the daily estimate of PM and the 90-day average (short-term effects). Short-term PM10 and PM2.5 were associated with increased concentrations of all seven EV types that we assayed (positive for human antigen leukocyte G (HLA-G), Syncytin-1 (Sync-1), CD14, CD105, CD62e, CD61, or CD25 determinants), while long-term PM10 showed a trend towards decreased EV concentrations. Increased Sync-1+EV levels were associated with the plasmatic decrease of sVCAM-1, but not of sICAM-1, which are circulating biomarkers of endothelial dysfunction. Thirteen EV-miRNAs were downregulated in response to long-term PM10 and PM2.5 variations, while seven were upregulated (p-value<0.05, false discovery rate p-value (qFDR)<0.1). Only one EV-miRNA (hsa-miR-221-3p) was downregulated after short-term variations. The identified PM-modulated EV-miRNAs exhibited putative roles in inflammation, gestational hypertension, and pre-eclampsia, as highlighted by miRNA target analysis. Our findings strongly support the hypothesis that EVs have an important role in modulating PM exposure effects during pregnancy, possibly through their miRNA cargo.

Particulate matter exposure exacerbates cellular damage by increasing stress granule formation in respiratory syncytial virus-infected human lung organoids

Exposure to atmospheric particulate matter (PM) increases morbidity and mortality in respiratory diseases by causing various adverse health effects; however, the effects of PM exposure on cellular stress under virus-infected conditions remain unclear. The effects of PM under 10 μm (PM10) and diesel PM (DPM) on respiratory syncytial virus (RSV) infection were investigated in human two-dimensional lung epithelial cells and human three-dimensional lung organoids mimicking the lung tissue. We evaluated the formation of stress granules, which are important in cellular adaptation to various stress conditions. Furthermore, we investigated the effects of repeated exposure to PM10 and DPM on DNA damage and cell death during viral infection. PM10 and DPM did not cause stress granule formation in the absence of RSV infection but drastically increased stress granule formation and signal transduction during RSV infection in human lung epithelial cells and human lung organoids. Further, repeated exposure to PM10 and DPM caused cell death by severely damaging DNA under RSV infection conditions. Thus, PM10 and DPM induce severe lung toxicity under stress conditions, such as viral infection, suggesting that the effects of PMs under various stressful conditions should be examined to accurately predict the lung toxicity of PM.

Associations of particulate matter exposures with brain cortical thickness and white matter hyperintensities: effect modification by c-reactive protein

Background and aim: Numerous studies have shown the effect of particulate matter exposure on brain imaging markers. However, little evidence exists about whether the effect differs by the level of systemic inflammation, a mechanism of neurotoxicity of particulate matter. We investigated whether the level of c-reactive protein (CRP; a marker of systemic inflammation) modifies the associations of particulate matter exposures with brain cortical thickness and white matter hyperintensities (WMH). Methods: Adults with no dementia or stroke were recruited. Concentrations of particulate matter &amp;#x2264;10 µm in diameter (PM10) and &amp;#x2264;2.5 µm (PM2.5) at each participant’s home address were estimated. Mean cortical thickness (n=874) and WMH volumes (n=397) were estimated from brain magnetic resonance images. We built generalized linear and logistic regression models for mean cortical thickness and WMH volumes (higher versus lower than median), respectively. Significance of the CRP group (higher versus lower than median) difference in the association was expressed as p for interaction. Results: Particulate matter exposures were significantly associated with a reduced mean cortical thickness only in the higher CRP group among men (p for interaction=0.012 for PM10 and 0.006 for PM2.5). A 10 &amp;#x3bc;g/m3 increase in PM10 was associated with having higher volumes of total WMH (odds ratio, 1.67; 95% confidence interval, 1.01–2.76) and periventricular WMH (1.81; 1.10–2.98). A 1 &amp;#x3bc;g/m3 increase in PM2.5 was associated with having a higher volume of periventricular WMH (odds ratio, 1.53; 95% confidence interval, 1.01–2.33). These associations did not significantly differ by the level of CRP. Conclusions: Particulate matter exposures were associated with a reduced mean cortical thickness in men with a high level of systemic inflammation. Particulate matter exposures were associated with having a high volume of WMH, with no evidence of effect modification by the level of systemic inflammation. Keywords: air pollution; neuroimaging; inflammation

Long-term exposure to ambient air pollution and greenness in relation to pulmonary tuberculosis in China: A nationwide modelling study

Previous studies have attempted to clarify the relationship between the occurrence of pulmonary tuberculosis (PTB) and exposure to air pollutants. However, evidence from multi-centres, particularly at the national level, is scarce, and no study has examined the modifying effect of greenness on air pollution–TB associations. In this study, we examined the association between long-term exposure to ambient air pollutants (PM10 p.m.2.5, and O3) and monthly PTB or smear-positive pulmonary tuberculosis (SPPTB) incidence to further evaluate whether these associations were affected by greenness in mainland China using a two-stage analytic procedure. PM2.5 was positively associated with both PTB and SPPTB incidence, with relative risk (RR) of 1.12 (95% confidence interval [CI]: 1.03, 1.22) and 1.08 (95% CI: 1.02, 1.10) per 10 μg/m3 increase, respectively. Furthermore, PM10 was positively associated with PTB incidence, with RR of 1.07 (95% CI: 1.01, 1.13). However, O3 was not associated with the monthly incidence of PTB or SPPTB. The normalized difference vegetation index (NDVI) exhibited a modifying effect on the association between PM2.5 exposure and SPPTB incidence in northern areas, with RR of 1.16 (95% CI: 1.03, 1.31) in lower mean annual NDVI areas than in the higher areas (RR = 0.98, 95% CI: 0.87, 1.09). This nationwide analysis indicated that NDVI could reduce the effect of air pollutants on TB incidence particularly in the northern areas. Long-term exposure to particulate matter (PM) may increase the occurrence of PTB or SPPTB in China, and further studies involving larger numbers of SPPTB cases are required to confirm the effects of PM exposure on SPPTB incidence in the future.

The Effect of Particulate Matter Exposure During Pregnancy on Pregnancy and Child Health Outcomes in South Asia: Protocol for an Instrumental Variable Analysis.

BackgroundDetermining the longer-term health effects of air pollution has been difficult owing to the multitude of potential confounding variables in the relationship between air pollution and health. Air pollution in many areas of South Asia is seasonal, with large spikes in particulate matter (PM) concentration occurring in the winter months. This study exploits this seasonal variation in PM concentration through a natural experiment.ObjectiveThis project aims to determine the causal effect of PM exposure during pregnancy on pregnancy and child health outcomes.MethodsWe will use an instrumental variable (IV) design whereby the estimated month of conception is our instrument for exposure to PM with a diameter less than 2.5 μm (PM2.5) during pregnancy. We will assess the plausibility of our assumption that timing of conception is exogenous with regard to our outcomes of interest and will adjust for date of monsoon onset to control for confounding variables related to harvest timing. Our outcomes are 1) birth weight, 2) pregnancy termination resulting in miscarriage, abortion, or still birth, 3) neonatal death, 4) infant death, and 5) child death. We will use data from the Demographic and Health Surveys (DHS) conducted in relevant regions of Bangladesh, India, Nepal, and Pakistan, along with monthly gridded data on PM2.5 concentration (0.1°×0.1° spatial resolution), precipitation data (0.5°×0.5° resolution), temperature data (0.5°×0.5°), and agricultural land use data (0.1°×0.1° resolution).ResultsData access to relevant DHSs was granted on June 6, 2021 for India, Nepal, Bangladesh, August 24, 2021 for Pakistan, and June 19 2022 for the latest DHS from India.ConclusionsIf the assumptions for a causal interpretation of our instrumental variable analysis are met, this analysis will provide important causal evidence on the maternal and child health effects of PM2.5 exposure during pregnancy. This evidence is important to inform personal behavior and interventions, such as the adoption of indoor air filtration during pregnancy as well as environmental and health policy.International Registered Report Identifier (IRRID)DERR1-10.2196/35249

Particulate Matter Exposure after a Cancer Diagnosis and All-Cause Mortality in a Regional Cancer Registry-Based Cohort in South Korea.

Although particulate matter (PM) is a Group 1 carcinogen, few studies have evaluated the effect of PM exposure after a cancer diagnosis on survival. Herein, we evaluated the effect of exposure to ambient PM10 after a cancer diagnosis on survival using data from the Regional Cancer Registry cohort in Chungbuk Province, Korea. A total of 44,432 patients with cancer who survived for >1 year after being diagnosed between 2005 and 2018 were followed until 31 December 2019; there were 32,734 survivors (73.7%) and 11,698 deceased (26.3%). The average follow-up period was 67.7 months, and the cumulative average concentration of PM10 exposure of patients with cancer after a diagnosis was 49.0 µg/m3. When PM10 concentration increased by 1 standard deviation (5.2 µg/m3), the all-cause mortality risk increased 2.06-fold (95% CI: 2.02–2.11). This trend was most pronounced in the younger patient group and in patients with local-stage cancer. This study demonstrates that exposure to PM10 after cancer diagnosis might influence the survival of patients with cancer, requiring environmental preventive measures such as lower pollutant exposure.