PM2.5 and its respiratory tract depositions on blood pressure, anxiety, depression and health risk assessment: A mechanistic study based on urinary metabolome.

Effects of fine particulate matter (PM2.5) and regional respiratory tract depositions on blood pressure (BP), anxiety, depression, health risk and the underlying mechanisms need further investigations. A repeated-measures panel investigation among 40 healthy young adults in Hefei, China was performed to explore the acute impacts of PM2.5 exposure and its deposition doses in 3 regions of respiratory tract over diverse lag times on BP, anxiety, depression, health risk, and the potential mechanisms. We collected PM2.5 concentrations, its deposition doses, BP, the Self-Rating Anxiety Scale (SAS) score and the Self-Rating Depression Scale (SDS) score. An untargeted metabolomics approach was used to detect significant urine metabolites, and the health risk assessment model was used to evaluate the non-carcinogenic risks associated with PM2.5. We applied linear mixed-effects models to assess the relationships of PM2.5 with the aforementioned health indicators We further evaluate the non-carcinogenic risks associated with PM2.5. We found deposited PM2.5 dose in the head accounted for a large proportion. PM2.5 and its three depositions exposures at a specific lag day was significantly related to increased BP levels and higher SAS and SDS scores. Metabolomics analysis showed significant alterations in urinary metabolites (i.e., glucoses, lipids and amino acids) after PM2.5 exposure, simultaneously accompanied by activation of the cAMP signaling pathway. Health risk assessment presented that the risk values for the residents in Hefei were greater than the lower limits of non-cancer risk guidelines. This real-world investigation suggested that acute PM2.5 and its depositions exposures may increase health risks by elevating BP, inducing anxiety and depression, and altering urinary metabolomic profile via activating the cAMP signaling pathway. And the further health risk assessment indicated that there are potential non-carcinogenic risks of PM2.5 via the inhalation route in this area.

Acute cardiorespiratory response to air quality index in healthy young adults.

BACKGROUND: Little is known about the acute health impacts of air quality index (AQI) on cardiorespiratory risk factors. OBJECTIVES: To assess the short-term links of AQI with cardiorespiratory risk factors in young healthy adults. METHODS: We performed a longitudinal panel study with 4 repeated visits in 40 healthy young adults in Hefei, Anhui Province, China from August to October 2021. Cardiorespiratory factors included systolic blood pressure (BP), diastolic BP (DBP), mean arterial pressure (MAP) and fractional exhaled nitric oxide (FeNO). We collected hourly AQI data from a nearby air quality monitoring site. Linear mixed-effects model was applied to assess the effects of AQI on BP and FeNO. RESULTS: The study participants (75.0% females) provided 160 pairs of valid health measurements with average age of 24 years. The mean AQI level was 44.43 during the study period. There were significant positive associations of AQI with three BP parameters and FeNO at different lag periods. For example, an interquartile range increase in AQI (26.54 unit) over lag 0-24 h was associated with increments of 6.69 mmHg (95%CI: 2.95-10.44), 5.71 mmHg (95%CI: 3.30-8.13), 6.04 mmHg (95%CI: 3.46-8.62) and 5.67% (95%CI: 1.05%-16.05%) in SBP, DBP, MAP and FeNO, respectively. The results were robust after controlling for PM1. We did not find effect modifications by gender, BMI, physical activity, or AQI category level on the associations. CONCLUSIONS: The current findings on associations of AQI with cardiorespiratory factors might add evidence of the acute adverse cardiorespiratory consequences following air pollution.

Short-term ambient air pollution exposure and adult primary insomnia outpatient visits in Chongqing, China: A time-series analysis.

Growing evidence suggest that air pollutants can be associated with sleep disorders. However, no study has explored the association of short-term air pollution exposure with primary insomnia, a specific type of sleep disorders. To evaluate the correlation of short-term air pollution exposure with adult primary insomnia outpatient visits in Chongqing, China, we collected data of adult primary insomnia outpatient visits and air pollutants' concentrations between 2013 and 2019 and the associations were estimated with single-day lags as well as moving average lags using a generalized additive model. Totally, 23,919 outpatient visits for adult primary insomnia were identified. The daily data of adult insomnia outpatient visits, air pollutants (NO2, CO, SO2, O3, PM10 and PM2.5) and meteorological conditions (daily mean temperature and relative humidity) were gathered. Short-term exposure to multiple air pollutants, especially NO2 and SO2, was associated with adult primary insomnia visits. A 10 µg/m3 increase in NO2 and SO2 at lag 05 corresponded to increased primary insomnia outpatient visits 3.87% (95% CI: 1.50%-6.24%) and 7.22% (95% CI: 2.10%-12.35%), respectively. Moreover, stronger links were presented in females and cool seasons for NO2 while in the elderly for SO2. Collectively, this time-series study suggested that short-term exposure to air pollutants, especially to NO2 and SO2, was associated with higher risk of adult primary insomnia outpatient visits, and such association could to be sex-, age-, and season-modified.

Mechanistic insights into the health benefits of fish-oil supplementation against fine particulate matter air pollution: a randomized controlled trial.

BACKGROUND: Dietary fish-oil supplementation might attenuate the associations between fine particulate matter (PM2.5) and subclinical biomarkers. However, the molecular mechanisms remain to be elucidated. This study aimed to explore the molecular mechanisms of fish-oil supplementation against the PM2.5-induced health effects. METHODS: We conducted a randomized, double-blinded, and placebo-controlled trial among healthy college students in Shanghai, China, from September 2017 to January 2018. A total of 70 participants from the Fenglin campus of Fudan University were included. We randomly assigned participants to either supplementation of 2.5-gram fish oil (n = 35) or sunflower-seed oil (placebo) (n = 35) per day and conducted four rounds of health measurements in the last two months of the trial. As a post hoc exploratory study, the present untargeted metabolomics analysis used remaining blood samples collected in the previous trial and applied a Metabolome-Wide Association Study framework to compare the effects of PM2.5 on the metabolic profile between the sunflower-seed oil and fish oil groups. RESULTS: A total of 65 participants completed the trial (34 of the fish oil group and 31 of the sunflower-seed oil group). On average, ambient PM2.5 concentration on the day of health measurements was 34.9 µg/m3 in the sunflower-seed oil group and 34.5 µg/m3 in the fish oil group, respectively. A total of 3833 metabolites were significantly associated with PM2.5 in the sunflower-seed oil group and 1757 in the fish oil group. Of these, 1752 metabolites showed significant between-group differences. The identified differential metabolites included arachidonic acid derivatives, omega-3 fatty acids, omega-6 fatty acids, and omega-9 fatty acids that were related to unsaturated fatty acid metabolism, which plays a role in the inflammatory responses. CONCLUSION: This trial suggests fish-oil supplementation could mitigate the PM2.5-induced inflammatory responses via modulating fatty acid metabolism, providing biological plausibility for the health benefits of fish-oil supplementation against PM2.5 exposure. TRIAL REGISTRATION: This study is registered at ClinicalTrails.gov (NCT03255187).

Combined oxidant capacity, redox-weighted oxidant capacity and elevated blood pressure: A panel study.

BACKGROUND: Evidence is limited on the potential health effects of Ox (sum value) and Oxwt(weighted value), the two surrogates for ozone (O3) and nitrogen dioxides (NO2). OBJECTIVES: To investigate the impacts of Ox and redox-weighted oxidant capacity (Oxwt) on blood pressure (BP). METHODS: A panel study was conducted with four repeated follow-up visits among 40 healthy college students in Hefei, Anhui Province, China from August to October, 2021. We measured BP by using an automated sphygmomanometer and obtained hourly data of air pollutants at a nearby site. The sum of O3 and NO2 (Ox) and their weighted average (Oxwt) were obtained as exposure variables. We applied linear mixed-effect models to evaluate the effects of Ox and Oxwton systolic BP (SBP), diastolic BP (DBP), mean arterial pressure (MAP) and pulse pressure (PP). RESULTS: Totally, 160 pairs of valid BP values were obtained. The 24-h mean levels of Ox and Oxwt were 64.38 µg/m3 and 110.28 µg/m3, respectively. Overall, both Ox and Oxwt were significantly linked with SBP, DBP and MAP at most lag periods, whereas non-significant with PP. A 10-µg/m3 increase in Oxwt at lag 0-24 h was linked to increases of 2.43 mmHg (95% CI: 0.96, 3.91) in SBP, 2.31 mmHg (95% CI: 1.37, 3.26) in DBP and 2.35 mmHg (95% CI: 1.35, 3.36) in MAP, while the corresponding effect estimates for Ox were 1.51 mmHg (95%CI: 0.60, 2.43), 1.43 mmHg (95% CI: 0.85, 2.02) and 1.46 mmHg (95%CI: 0.83, 2.09). In two-pollutant models, our results were almost unchanged after controlling for simultaneous exposure to other pollutants. The effects were more pronounced among males and those with physical activity. CONCLUSIONS: The findings provide first-hand evidence that short-term exposure to Ox and Oxwt was associated with BP increases in young adults.

Effects of filtered fresh air ventilation on classroom indoor air and biomarkers in saliva and nasal samples: A randomized crossover intervention study in preschool children.

To evaluate the short-term effects of filtered fresh air ventilation system on classroom indoor air and biomarkers in saliva and nasal samples in preschool children, a randomized crossover study was conducted in a kindergarten in Shanghai, China in 2016. Two classrooms at the same grade (n = 43) were selected and fresh air ventilation systems (FAVS) with high efficiency particulate air filter (HEPA) were installed. In the first week, FAVS-HEPA was run in one classroom for 2 continuous school days and the other classroom was remained as usual with no use of FAVS-HEPA. After one week of wash-out, the ventilation modes exchanged between two classrooms and another 2 days of intervention were repeated. Real-time indoor and outdoor air pollution and climate factors (PM2.5, Temp and relative humidity (R.H.)) were measured. Saliva and nasal internal mucosa samples were collected immediately at the end of each intervention scenario. Linear mixed-effect regression model was applied to evaluate the effects of intervention on children's health indicators controlling for age, gender, height, BMI and temperature. The results showed, with FAVS-HEPA, the classroom indoor fine particulate matter (PM2.5)(29.1 ±â€¯17.9 µg/m3) was on average significantly lower than that without FAVS-HEPA (85.7 ±â€¯43.2 µg/m3). By regression analysis, each 10 µg/m3 decrease of indoor PM2.5 during the 8 school hours in the first intervention day was associated with an average of 1.76% (95% confidence interval (CI) 0.43-3.08%) increase in saliva lysozyme. This percentage increased to 2.41% (95%CI 0.52-4.26%) if related to the PM2.5 level in 16 school hours over 2 days of intervention. A total of 19 nasal bacterial taxa were lower in subjects exposed to FAVS-HEPA, compared to that with no use of FAVS-HEPA, despite the general bacteria diversity levels in nasal samples were not statistically different. Among others, Providencia species showed significant effects in mediating the associations between higher PM2.5 and lower lysozyme. In conclusion, using FAVS-HEPA was effective in decreasing the classroom indoor PM2.5. Saliva lysozyme, as a non-specific immune biomarker, was significantly inversely associated with indoor PM2.5. Certain nasal bacteria might play key roles in mediating PM2.5 exposure and children's lysozyme levels.

Effects of personal nitrogen dioxide exposure on airway inflammation and lung function.

BACKGROUND: Few epidemiological studies have evaluated the respiratory effects of personal exposure to nitrogen dioxide (NO2), a major traffic-related air pollutant. The biological pathway for these effects remains unknown. OBJECTIVES: To evaluate the short-term effects of personal NO2 exposure on lung function, fractional exhaled nitric oxide (FeNO) and DNA methylation of genes involved. METHODS: We conducted a longitudinal panel study among 40 college students with four repeated measurements in Shanghai from May to October in 2016. We measured DNA methylation of the key encoding genes of inducible nitric oxide synthase (NOS2A) and arginase (ARG2). We applied linear mixed-effect models to assess the effects of NO2 on respiratory outcomes. RESULTS: Personal exposure to NO2 was 27.39 ±â€¯23.20 ppb on average. In response to a 10-ppb increase in NO2 exposure, NOS2A methylation (%5 mC) decreased 0.19 at lag 0 d, ARG2 methylation (%5 mC) increased 0.21 and FeNO levels increased 2.82% at lag 1 d; and at lag 2 d the percentage of forced vital capacity, forced expiratory volume in 1 s and peak expiratory flow in predicted values decreased 0.12, 0.37 and 0.67, respectively. The model performance was better compared with those estimated using fixed-site measurements. These effects were robust to the adjustment for co-pollutants and weather conditions. CONCLUSIONS: Our study suggests that short-term personal exposure to NO2 is associated with NOS2A hypomethylation, ARG2 hypermethylation, respiratory inflammation and lung function impairment. The use of personal measurements may better predict the respiratory effects of NO2.

Household renovation before and during pregnancy in relation to preterm birth and low birthweight in China.

From October 2010 to April 2012, we conducted a cross-sectional study of associations between household environments and childhood health among preschool children in eight Chinese cities. Here, we analyze associations of early household renovation with preterm birth (PTB), low birthweight (LBW), term low birthweight (Term-LBW), and small for gestational age (SGA). Parents responded to questions about household renovation and their children's gestational age and birthweight. In the multivariate logistic regression analyses, household renovation in the year before pregnancy was significantly associated with LBW (sample size: N = 25 813; adjusted odds ratio (OR) with 95% confidence intervals (CIs): 1.23, 1.01-1.50) and Term-LBW (N = 24 823; 1.29, 1.01-1.67). Household renovation during pregnancy was significantly associated with PTB (N = 25 202; 1.28, 1.01-1.69). These significant associations were also found in the two-level (city-child) logistic regression analyses and in the sensitivity analyses among 21 009 children with complete data in all studied variates. Stronger associations were found in certain subgroups. Our findings indicate that household renovation within one year before pregnancy might be a risk factor for LBW and Term-LBW, while household renovation during pregnancy could be a risk factor for PTB.

Alleviated systemic oxidative stress effects of combined atmospheric oxidant capacity by fish oil supplementation: A randomized, double-blinded, placebo-controlled trial.

BACKGROUND: Combined atmospheric oxidant capacity (Ox), represented by the sum of nitrogen dioxide (NO2) and ozone (O3), is an important hazardous property of outdoor air pollution mixture. It remains unknown whether its adverse effects can be ameliorated by dietary fish-oil supplementation. OBJECTIVE: To assess the effects of fish-oil supplementation against oxidative stress induced by acute Ox exposure. METHODS: We conducted a randomized, double-blinded and placebo-controlled study among 65 young adults in Shanghai, China between September 2017 and January 2018. We randomly assigned participants to receive either 2.5 g/day of fish oil or placebo, and conducted four repeated physical examinations during the last two months of treatments. Ox concentrations were calculated as the sum of hourly measurements of NO2 and O3. We measured six biomarkers on systemic oxidative stress and antioxidant activity. Linear mixed-effect models were used to assess the short-term effects of Ox on biomarkers in each group. RESULTS: During our study period, the 72-h average Ox concentration was 93.6 µg/m3. Short-term exposure to Ox led to weaker changes in all biomarkers in the fish oil group than in the placebo group. Compared with the placebo group, for a 10-µg/m3 increase in Ox, there were smaller decrements in myeloperoxidase (MPO, difference = 5.92%, lag = 0-2 d, p = 0.03) and malondialdehyde (MDA, difference = 5.00%, lag = 1 d, p = 0.04) in the fish-oil group; there were also larger increments in total antioxidant capacity (TAC, difference = 16.33%, lag = 2 d, p = 0.02) and in glutathione peroxidase (GSH-Px, difference = 8.89%, lag = 0-2 d, p = 0.03) in the fish-oil group. The estimated differences for MPO were robust to adjustment for all co-pollutants and the differences for other biomarkers remained for some co-pollutants. CONCLUSIONS: This trial provides first-hand evidence that dietary fish-oil supplementation may alleviate the systemic oxidative stress induced by Ox.

Possible Mediation by Methylation in Acute Inflammation Following Personal Exposure to Fine Particulate Air Pollution.

Air pollution may increase cardiovascular and respiratory risk through inflammatory pathways, but evidence for acute effects has been weak and indirect. Between December 2014 and July 2015, we enrolled 36 healthy, nonsmoking college students for a panel study in Shanghai, China, a city with highly variable levels of air pollution. We measured personal exposure to particulate matter with an aerodynamic diameter less than or equal to 2.5 µm (PM2.5) continuously for 72 hours preceding each of 4 clinical visits that included phlebotomy. We measured 4 inflammation proteins and DNA methylation at nearby regulatory cytosine-phosphate-guanine (CpG) loci. We applied linear mixed-effect models to examine associations over various lag times. When results suggested mediation, we evaluated methylation as mediator. Increased PM2.5 concentration was positively associated with all 4 inflammation proteins and negatively associated with DNA methylation at regulatory loci for tumor necrosis factor alpha (TNF-α) and soluble intercellular adhesion molecule-1. A 10-µg/m3 increase in average PM2.5 during the 24 hours preceding blood draw corresponded to a 4.4% increase in TNF-α and a statistically significant decrease in methylation at one of the two studied candidate CpG loci for TNF-α. Epigenetics may play an important role in mediating effects of PM2.5 on inflammatory pathways.

Associations Between Ambient Nitrogen Dioxide and Daily Cause-specific Mortality: Evidence from 272 Chinese Cities.

BACKGROUND: There has been a long history of debate regarding whether ambient nitrogen dioxide (NO2) directly affects human health. METHODS: We conducted a nationwide time-series analysis in 272 major Chinese cities (2013-2015) to evaluate the associations between short-term exposure to NO2 and cause-specific mortality. We used the overdispersed generalized linear model together with the Bayesian hierarchical model to estimate the associations between NO2 and mortality at the national and regional levels. We examined two-pollutant models with adjustment of fine particles, sulfur dioxide, carbon monoxide, and ozone to evaluate robustness for the effects of NO2. RESULTS: At the national-average level, we observed linear and positive associations between NO2 and mortality from all causes and main cardiorespiratory diseases. A 10 µg/m increase in 2-day average concentrations of NO2 would lead to increments of 0.9% (95% posterial interval [PI], 0.7%, 1.1%) in mortality from total nonaccidental causes, 0.9% (95% PI, 0.7%, 1.2%) from total cardiovascular disease, 1.4% (95% PI, 0.8%, 2.0%) from hypertension, 0.9% (95% PI, 0.6%, 1.2%) from coronary heart disease, 0.9% (95% PI, 0.5%, 1.2%) from stroke, 1.2% (95% PI, 0.9%, 1.5%) from total respiratory diseases, and 1.6% (95% PI, 1.1%, 2.0%) from chronic obstructive pulmonary disease. There were no appreciable differences in estimates from single-pollutant and two-pollutant models. The associations were stronger in the south of China, in the elderly, and in females. CONCLUSIONS: The present study provided robust epidemiologic evidence of associations between day-to-day NO2 and mortality from total natural causes and main cardiorespiratory diseases that might be independent of other criteria air pollutants.

Personal Ozone Exposure and Respiratory Inflammatory Response: The Role of DNA Methylation in the Arginase-Nitric Oxide Synthase Pathway.

Little is known regarding the molecular mechanisms behind respiratory inflammatory response induced by ozone. We performed a longitudinal panel study with four repeated measurements among 43 young adults in Shanghai, China from May to October in 2016. We collected buccal samples and measured the fractional exhaled nitric oxide (FeNO) after 3-day personal ozone monitoring. In buccal samples, we measured concentrations of inducible nitric oxide synthase (iNOS) and arginase (ARG), and DNA methylation of NOS2A and ARG2. We used linear mixed-effect models to analyze the effects of ozone on FeNO, two enzymes and their DNA methylation. A 10 ppb increase in ozone (lag 0-8 h) was significantly associated with a 3.89% increase in FeNO, a 36.33% increase in iNOS, and a decrease of 0.36 in the average methylation (%5mC) of NOS2A. Ozone was associated with decreased ARG and elevated ARG2 methylation, but the associations were not significant. These effects were more pronounced among allergic subjects than healthy subjects. The effects were much stronger when using personal exposure monitoring than fixed-site measurements. Our study demonstrated that personal short-term exposure to ozone may result in acute respiratory inflammation, which may be mainly modulated by NOS2A hypomethylation in the arginase-nitric oxide synthase pathway.

Effects of Personal Short-Term Exposure to Ambient Ozone on Blood Pressure and Vascular Endothelial Function: A Mechanistic Study Based on DNA Methylation and Metabolomics.

Short-term exposure to ambient ozone is associated with adverse cardiovascular effects, with inconsistent evidence on the molecular mechanisms. We conducted a longitudinal panel study among 43 college students in Shanghai to explore the effects of personal ozone exposure on blood pressure (BP), vascular endothelial function, and the potential molecular mechanisms. We measured real-time personal ozone exposure levels, serum angiotensin-converting enzyme (ACE) and endothelin-1 (ET-1), and locus-specific DNA methylation of ACE and EDN1 (coding ET-1). We used an untargeted metabolomic approach to explore potentially important metabolites. We applied linear mixed-effect models to examine the effects of ozone on the above biomarkers. An increase in 2 h-average ozone exposure was significantly associated with elevated levels of BP, ACE, and ET-1. ACE and EDN1 methylation decreased with ozone exposure, but the magnitude differed by genomic loci. Metabolomics analysis showed significant changes in serum lipid metabolites following ozone exposure that are involved in maintaining vascular endothelial function. Our findings suggested that acute exposure to ambient ozone can elevate serum levels of ACE and ET-1, decrease their DNA methylation, and alter the lipid metabolism, which may be partly responsible for the effects of ozone on BP and vascular endothelial function.

Associations between ambient temperature and daily hospital admissions for rheumatic heart disease in Shanghai, China.

Rheumatic heart disease (RHD) remains a serious public health burden in developing countries. We conducted a time-series study to explore the association between ambient temperature and daily hospital admissions for RHD in Shanghai, China. We collected data on daily hospital admissions for RHD from 2013 to 2015 from the database of Shanghai Health Insurance System. We applied the generalized additive models together with the distributed lag nonlinear model to estimate the association between temperature and RHD hospital admissions after controlling for relative humidity, time trend, day of the week, and holidays. Stratification analyses by age and gender were performed to evaluate their potential effect modification. A total of 4178 cases of RHD hospitalizations were identified over the study period. There were almost linear, positive, and significant associations between daily mean temperature and RHD hospital admissions with higher risks at hotter days. Compared to reference temperature (0 °C), the cumulative risks of moderate heat (the 90th percentile of temperature, 28.0 °C) and extreme heat (the 99th percentile of temperature, 33.5 °C) over lags 0-5 days were 2.55 (95% confidence interval 1.14, 5.73) and 3.22 (95% confidence interval 1.36, 7.61), respectively. These associations were significantly stronger in older people than in younger people. This study indicated larger risks of RHD hospital admissions associated with higher temperature, especially in older people. Our findings provided first-hand epidemiological evidence regarding the effects of ambient temperature on RHD incidence.

Fine particulate matter constituents and blood pressure in patients with chronic obstructive pulmonary disease: A panel study in Shanghai, China.

OBJECTIVE: The evidence is limited about the potentially different health effects of various chemical constituents of fine particulate matter (PM2.5). We thus assessed the acute effects of various chemical constituents of PM2.5 on blood pressure (BP). METHODS: We performed a longitudinal panel study with six repeated visits in 28 urban residents with chronic obstructive pulmonary disease in Shanghai, China from May to July, 2014. Twelve (43%) of them took antihypertensive medications. We measured resting BP by using a mercury sphygmomanometer and monitored real-time concentrations of PM2.5 constituents at a nearby site. Based on the linear mixed-effects model, we evaluated the effects of 10 major constituents in PM2.5 on BP, using a single-constituent model and a constituent-residual model after accounting for the multicollinearity. RESULTS: We obtained a total of 168 pairs of effective BP measurements during the study period. There are moderate or high correlations among various PM2.5 constituents. An interquartile range increase of PM2.5 (19.1µg/m3) was associated with increments of 1.90mmHg [95% confidence interval (CI): 0.66, 3.13] in systolic BP, 0.68mmHg (95%CI: -0.02, 1.37) in diastolic BP and 1.23mmHg (95%CI: 0.19, 2.29) in pulse pressure. Some constituents of PM2.5, including organic carbon, elemental carbon, nitrate and ammonium, were robustly associated with elevated BP after controlling for total PM2.5 mass and accounting for multi-collinearity. Two constituents (magnesium and calcium) were associated with decreased BP. CONCLUSIONS: Organic carbon, elemental carbon, nitrate and ammonium may be mainly responsible for elevated BP from a short-term exposure to PM2.5.

Association between fine particulate matter chemical constituents and airway inflammation: A panel study among healthy adults in China.

BACKGROUND: Ambient fine particulate matter (PM2.5) air pollution has been associated with increased airway inflammation, but the roles of various PM2.5 constituents remain to be determined. OBJECTIVES: To investigate the acute effects of PM2.5 constituents on fractional exhaled nitric oxide (FeNO), a well-established biomarker of respiratory inflammation. METHODS: A longitudinal panel study was performed among 32 healthy young adults in Shanghai, China from January 12th to February 6th, 2015. FeNO was repeatedly measured, 6-8 times per subject. Real-time mass concentration of ambient PM2.5 and chemical constituents were obtained from a nearby monitoring station. Linear mixed-effect models were applied to evaluate the association between FeNO and PM2.5 constituents, with the adjustment of age, gender, body mass index, temperature, relative humidity and day of week. The robustness of constituents' effects was also evaluated. RESULTS: A total of 234 effective measurements of FeNO were obtained with a geometric mean of 13.1 ppb. The PM2.5-FeNO associations were strongest at lags of 0-6h and diminished at lags longer than 12h. An interquartile range increase in PM2.5 constituents (NH4(+), NO3(-), K(+), SO4(2-) and elemental carbon) at lags of 0-6h were significantly associated with increments in FeNO by 12.3%, 11.3%, 11.1%, 9.6% and 10.7%, respectively. After controlling for PM2.5 total mass and the colinearity, only elemental carbon remained significant. CONCLUSION: Several chemical constituents of PM2.5 may impact FeNO following acute exposure. Elemental carbon in particular may be the primary component responsible for increased airway inflammation.

Size-fractionated particulate air pollution and circulating biomarkers of inflammation, coagulation, and vasoconstriction in a panel of young adults.

BACKGROUND: Short-term associations between size-fractionated particulate air pollution and circulating biomarkers are not well established, especially in developing countries with high levels of particulate matter (PM). METHODS: We designed a panel study involving 34 healthy young adults to evaluate acute effects of size-fractionated PM on 13 circulating biomarkers of inflammation, coagulation, and vasoconstriction. We measured real-time, size-fractionated number concentrations of PM (aerodynamic diameters from 0.25 to 10 µm, mass concentrations of PM < 10 µm) over four follow-up measurements. The short-term associations between size-fractionated PM and biomarkers were assessed using linear mixed effect models. RESULTS: We found positive associations between short-term exposure to PM and 10 biomarkers. PM with smaller size had stronger associations. The size fractions with the strongest associations were 0.25-0.40 µm for number concentrations and <1 µm for mass concentrations. For example, an interquartile range increase in 24-hour-average number concentrations of PM0.25-0.40 was associated with a 7%-32% increase in biomarkers of inflammation, 34%-68% of blood coagulation, and 45% of vasoconstriction. Similar estimates were found for mass concentrations of PM1. Furthermore, our results demonstrated an apparent acute effect on circulating biomarkers, even 2 hours after exposure. The effects were strongest within the first 12-24 hours, and effects on inflammation occurred more quickly than on coagulation and vasoconstriction. CONCLUSIONS: Our results provided potentially vital insights into the size and temporal characteristics of PM that could modify subclinical cardiovascular effects. These findings may have implications on disease prevention and environmental regulation in China.

The long non-coding RNA PANDAR regulates cell proliferation and epithelial-to-mesenchymal transition in glioma.

Glioma is one of the most aggressive intracranial tumors in the central nervous system. The long non-coding RNA P21 associated ncRNA DNA damage activated (PANDAR) has been reported to be an oncogene or tumor suppressor in several cancers. However, the prognostic value and biological function of PANDAR in glioma have not been described. Here, we report that expression of PANDAR is significantly up-regulated in glioma tissues and cell lines. PANDAR expression was correlated with tumor size (p=0.044) and World Health Organization (WHO) grades (p=0.005), as shown by chi-squared test. Moreover, significant upregulation of PANDAR was found to correlate with poor prognosis in glioma, as shown using Kaplan-Meier method and Cox multivariate survival analysis. Furthermore, PANDAR knockdown suppressed cell proliferation, G1/S transition, migration and invasion, and promoted apoptosis in glioma cell lines (U251 and U87). PANDAR knockdown decreased expression of CDK4, Bcl-2, N-cadherin and Vimentin, but increased E-cadherin expression in glioma cells. In conclusion, our data suggest PANDAR as a potential prognostic biomarker and therapeutic candidate for glioma.

Association between short-term exposure to ambient air pollution and number of outpatient Helicobacter pylori infection visits.

Helicobacter pylori infection (HPI) is an important risk factor of gastrointestinal diseases, but factors leading to it are still not fully understood. To investigate the association between short-term exposure to air pollution and HPI during outpatient visits, we collected daily data for HPI outpatient visits and air pollutant concentrations during 2014-2021 in Hefei, Anhui Province, China. A time-stratified case-crossover design was performed to analyze the acute impacts of air pollution on HPI outpatient visits. We also explored potential effect modifiers. A total of 9072 outpatient visits were recorded. We found positive and statistically significant associations of acute exposure to nitrogen dioxide (NO2), sulfur dioxide (SO2), and carbon monoxide (CO) with HPI outpatient visits. Threshold concentrations of the three pollutants with same-day exposure (lag 0 day) for outpatient visits were 37 µg/m3 for NO2, 8 µg/m3 for SO2, and 0.8 mg/m3 for CO. The odds ratios for HPI outpatient visits at the 95th percentile of NO2, SO2, and CO against the thresholds were 1.207 (1.120-1.302), 1.175 (1.052-1.312), and 1.110 (1.019-1.209), respectively. The associations were more evident in patients older than 45 years, females, with health insurance, and in cold seasons. Null associations of exposure to either ozone (O3) or particulate matter (PM) were observed. In summary, short-term exposure to NO2, SO2, and CO above certain concentrations, but not PM or O3, may trigger the increased risk of outpatient visits due to HP infection in Chinese population.