Effects Of Personal Exposure Research Articles

Continuous Markov Models for Analyzing the Effect of Environmental Personal Exposure on Multiple Sclerosis Progression.

Multiple sclerosis (MS) is an inflammatory autoimmune demyelinating disorder of the central nervous system, leading to progressive functional impairments. Predicting disease progression with a probabilistic and time-dependent approach might help suggest interventions for a better management of the disease. Recently, there has been increasing focus on the impact of air pollutants as environmental factors influencing disease progression. This study employs a Continuous-Time Markov Model (CMM) to explore the impact of air pollution measurements on MS progression using longitudinal data from MS patients in Italy between 2013 and 2022. Preliminary findings indicate a relationship between air pollution and MS progression, with pollutants like Particulate Matter with a diameter of 10 micrometers (PM10) or 2.5 micrometers (PM2.5), Nitrogen Dioxide (NO2), and Carbon Monoxide (CO) showing potential effects on disease activity.

Effects of personal noise exposure, sleep quality, and burnout on quality of life: An online participation cohort study in Taiwan

Chronic noise exposure in daily life not only causes physical and mental illness but also reduces quality of life. However, collecting objective data on sound exposure and subjective acoustic comfort through a traditional one-shot survey is difficult. This study applied online chatbots in social media to explore the effects of daily sound exposure, personal characteristics, noise sensitivity, burnout status, and sleep quality on quality of life using a short-term participatory cohort design. During the two-month survey in 2022, 207 participants completed at least 15 days of collection of data on sound exposure and perception, as well as periodic structural questionnaires during the follow-ups. Linear regression and generalized linear models were applied to explore the factors influencing personal burnout, the Pittsburgh Sleep Quality Index, and quality of life. A chain mediation model was applied to explore the direct and indirect effects of noise exposure on quality of life. The results showed a better quality of life among respondents who rated their home environment better, were in good health, had better daily acoustic comfort, and were less exposed to noise during the week. In contrast, respondents with lower daily acoustic comfort and a higher frequency of noise-induced sleep disturbances and mood disorders were more likely to have poorer sleep quality. A higher personal burnout was associated with poorer health, longer exposure to noise during the week, a higher frequency of noise-induced illnesses, and neurotic traits. In the mediation analyses, noise-induced sleep disturbance and better daily acoustic comfort also had important direct influences on quality of life compared to the indirect pathway through sleep quality and personal burnout. In conclusion, noise exposure in daily life not only exacerbated poor sleep quality and personal burnout but also reduced quality of life.

Effects of in-utero personal exposure to PM2.5 sources and components on birthweight

In-utero exposure to fine particulate matter (PM2.5) and specific sources and components of PM2.5 have been linked with lower birthweight. However, previous results have been mixed, likely due to heterogeneity in sources impacting PM2.5 and due to measurement error from using ambient data. Therefore, we investigated the effect of PM2.5 sources and their high-loading components on birthweight using data from 198 women in the 3rd trimester from the MADRES cohort 48-h personal PM2.5 exposure monitoring sub-study. The mass contributions of six major sources of personal PM2.5 exposure were estimated for 198 pregnant women in the 3rd trimester using the EPA Positive Matrix Factorization v5.0 model, along with their 17 high-loading chemical components using optical carbon and X-ray fluorescence approaches. Single- and multi-pollutant linear regressions evaluated the association between personal PM2.5 sources/components and birthweight, adjusting for gestational age, maternal age, race, infant sex, parity, diabetes status, temperature, maternal education, and smoking history. Participants were predominately Hispanic (81%), with a mean (SD) gestational age of 39.1 (1.5) weeks and age of 28.2 (6.0) years. Mean birthweight was 3295.8 g (484.1) and mean PM2.5 exposure was 21.3 (14.4) µg/m3. A 1 SD increase in the mass contribution of the fresh sea salt source was associated with a 99.2 g decrease in birthweight (95% CI − 197.7, − 0.6), and aged sea salt was associated with a 70.1 g decrease in birthweight (95% CI − 141.7, 1.4). Magnesium, sodium, and chlorine were associated with lower birthweight, which remained after adjusting for PM2.5 mass. This study found evidence that major sources of personal PM2.5 including fresh and aged sea salt were negatively associated with birthweight, with the strongest effect on birthweight from Na and Mg. The effect of crustal and fuel oil sources differed by infant sex with negative associations seen in boys compared to positive associations in girls.

Effects of personal exposure to the oxidative potential of PM2.5 on oxidative stress biomarkers in pregnant women

Oxidative stress is a prominent pathway for the health effects associated with fine particulate matter (PM2.5) exposure. Oxidative potential (OP) of PM has been associated to several health endpoints, but studies on its impact on biomarkers of oxidative stress remains insufficient. 300 pregnant women from the SEPAGES cohort (France) carried personal PM2.5 samplers for a week and OP was measured using ascorbic acid (AA) and dithiothreitol (DTT) assays, and normalized by 1) PM2.5 mass (OPm) and 2) sampled air volume (OPv). A pool of three urine spots collected on the 7th day of PM sampling was analyzed for biomarkers, namely 8-hydroxy-2-deoxyguanosine (8-OHdG), malondialdehyde (MDA) and 8-isoprostaglandin-F2α (8-isoPGF2α). Associations were investigated using adjusted multiple linear regressions. OP effects were additionally investigated by stratifying by median PM2.5 concentration (14 μg m−3). In the main models, no association was observed with 8-isoPGF2α, nor MDA. An interquartile range (IQR) increase in OPmAA exposure was associated with increased 8-OHdG (percent change: 6.2 %; 95 % CI: 0.2 % to 12.6 %). In the stratified analysis, exposure to OPmAA was associated with 8-OHdG for participants exposed to low levels of PM2.5 (percent change: 11.4 %; 95 % CI: 3.3 % to 20.1 %), but not for those exposed to high levels (percent change: −1.0 %; 95 % CI: −10.6 % to 9.6 %). Associations for OPmDTT also followed a similar pattern (p-values for OPmAA-PM and OPmDTT-PM interaction terms were 0.12 and 0.11, respectively). Overall, our findings suggest that OPmAA may be associated with increased DNA oxidative damage. This association was not observed with PM2.5 mass concentration exposure. The effects of OPmAA in 8-OHdG tended to be stronger at lower (below median) vs. higher concentrations of PM2.5. Further epidemiological, toxicological and aerosol research are needed to further investigate the OPmAA effects on 8-OHdG and the potential modifying effect of PM mass concentration on this association.

Effects of short-term air pollution exposure on symptoms development in the course of idiopathic pulmonary fibrosis

ABSTRACT Background Lately a potential detrimental effect of air pollution to idiopathic pulmonary fibrosis emerged. We aimed to assess the effects of short-term air pollution exposure to the clinical course of IPF. Research design and methods IPF patients were followed intensively for four nonconsecutive study periods between 13 July 2020 and 5 September 2021. Short-term exposure to O3, NO2 and PM10 concentrations was estimated using spatio-temporal land use regression models. Associations among symptoms, lung function, oxygen saturation, and short-term personal air pollutant exposure were assessed through multiple mixed effects logistic regression models. Results Data for up to 24 IPF patients (mean age: 72.2 ± 7.6 years) were analyzed. We detected positive significant associations between cough and a 10 μg/m3 increase in same day mean level of NO2 (OR = 1.59, 95%CI: 1.00–2.53), PM10 (OR = 2.42, 95%CI: 1.54–3.79), and O3 (OR = 1.63, 95%CI: 1.14–2.32). A 10 μg/m3 increase in same day mean level of NO2 was also associated with the risk of appearance of wheezing (OR = 3.01, 95%CI: 1.00–9.04), while exposure to O3 was associated with common cold (OR = 6.30, 95%CI: 3.59–11.07). No significant associations were detected between short-term exposure to air pollutants and forced vital capacity or saturation of oxygen. Conclusions Short-term exposure to increased concentrations of air pollutants is an independent risk factor for IPF symptoms' aggravation.

Personal exposure to fine particulate matter (PM2.5) and self-reported asthma-related health

PM2.5 (fine particulate matter ≤2.5 μm in diameter) is a key pollutant that can produce acute asthma exacerbations and longer-term deterioration of respiratory health. Individual exposure to PM2.5 is unique and varies across microenvironments. Low-cost sensors (LCS) can collect data at a spatiotemporal resolution previously unattainable, allowing the study of exposures across microenvironments. The aim of this study is to investigate the acute effects of personal exposure to PM2.5 on self-reported asthma-related health.Twenty-eight non-smoking adults with asthma living in Scotland collected PM2.5 personal exposure data using LCS. Measurements were made at a 2-min time resolution for a period of 7 days as participants conducted their typical daily routines. Concurrently, participants were asked to keep a detailed time-activity diary, logging their activities and microenvironments, along with hourly information on their respiratory health and medication use. Health outcomes were modelled as a function of hourly PM2.5 concentration (plus 1- and 2-h lag) using generalized mixed-effects models adjusted for temperature and relative humidity.Personal exposures to PM2.5 varied across microenvironments, with the largest average microenvironmental exposure observed in private residences (11.5 ± 48.6 μg/m3) and lowest in the work microenvironment (2.9 ± 11.3 μg/m3). The most frequently reported asthma symptoms, wheezing, chest tightness and cough, were reported on 3.4%, 1.6% and 1.6% of participant-hours, respectively. The odds of reporting asthma symptoms increased per interquartile range (IQR) in PM2.5 exposure (odds ratio (OR) 1.29, 95% CI 1.07–1.54) for same-hour exposure. Despite this, no association was observed between reliever inhaler use (non-routine, non-exercise related) and PM2.5 exposure (OR 1.02, 95% CI 0.71–1.48).Current air quality monitoring practices are inadequate to detect acute asthma symptom prevalence resulting from PM2.5 exposure; to detect these requires high-resolution air quality data and health information collected in situ. Personal exposure monitoring could have significant implications for asthma self-management and clinical practice.

Effect and microbial mechanism of pharmaceutical and personal care product exposure on partial nitrification process and nitrous oxide emission

This study focused on the short- and long-term exposure of pharmaceutical and personal care products (PPCPs) to the partial nitrification process and nitrous oxide emission. The corresponding microbial mechanisms were also explored. The results revealed a concentration-dose effect on the partial nitrification process. Moreover, the PPCP concentration of ≥2 μg/L featured inhibitory effects on the process. The solo effect of PPCP on the partial nitrification process was analyzed through microcosmic experiments, and the results revealed significant variations in PN. A dose-effect relationship existed between the PPCP concentration and N2O emission intensity. After exposure to PPCPs, the N2O emission released during the partial nitrification process was significantly reduced. Different PPCPs featured various effects in mitigating N2O emissions. Low PPCP concentrations led to a reduction in the richness and diversity of microbes, but their community structure remained significantly unchanged. High PPCP concentrations (≥5 μg/L) resulted in increased species richness and diversity, but their microbial community composition was significantly affected. The function prediction and nitrogen metabolic pathway analysis indicated that PPCP exposure led to the inhibition of the ammonia oxidation process. However, all genes encoding denitrification enzymes were upregulated. The microorganisms in the microbial community featured modular structural properties and wide synergistic relationships between genera. This study provides valuable insights into the effect of PPCP exposure on the particle nitrification process and corresponding changes in the microbial community.

Exploring the relationship between exposure to COVID-19 and donations during the COVID-19 pandemic: The mediating roles of emotions and risk perception.

Public emergency events like the COVID-19 pandemic are special occasions that need immediate massive funding from public donations. Thus, understanding the determinants of donation behaviors under public emergencies is important for both researchers and practitioners. This study investigated the effect of personal and local exposure to incidences of COVID-19 on donation behaviors. Specifically, we examined the mediating effects of risk perception and emotions on the relationship between exposure to COVID-19 and donation behaviors. The data were from a survey distributed in China between March 20 and 30th, 2020. Participants' donation choice at the end of the survey was used to measure their donation behaviors. Participants' emotions, risk perception, and personal exposure were assessed in the questionnaire. Local exposure was the 30-day confirmed cases obtained from the National Health Commission of the People's Republic of China. A total of 8,720 participants (Mean age = 28.91, 43.6% females) completed the online survey. Based on the results from the mediation analysis, we found that people with stronger positive and negative emotions, higher risk perception, and more personal exposure to COVID-19 were more likely to donate. Furthermore, the effects of both personal and local exposure on donations are mediated by risk perception and negative emotion. Both higher personal and local exposure led to stronger negative emotions and higher risk perception, which in turn led to more donation behaviors. This study extends our knowledge of donation behaviors during public emergencies. Our results suggest that policymakers and charity organizations should elicit stronger emotions and risk perception by exposing the severity of the disaster in advertisements to promote donations.

The role of systemic inflammation and oxidative stress in the association of particulate air pollution metal content and early cardiovascular damage: A panel study in healthy college students

Exposure to fine particulate matter (PM2.5) has been associated with adverse cardiovascular outcomes. However, the effects of toxic metals in PM2.5 on cardiovascular health remain unknown. To investigate the early cardiovascular effects of specific PM2.5 metal constituents at the personal level, we conducted a panel study on 45 healthy college students in Caofeidian, China. Personal exposure concentrations and cardiovascular effect markers were monitored simultaneously within one year in four study periods. Four linear mixed-effects models were used to analyze the relationship between personal exposure to PM2.5 and 15 metal fractions (Al, V, Cr, Mn, Fe, Co, Ni, Cu, Zn, As, Se, Mo, Cd, Sb, and Pb) with soluble CD36 (sCD36), C-reactive protein (CRP), and oxidized low-density lipoprotein (OX-LDL) levels, heart rate, and blood pressure. The concentrations of most individual metals (Mn, Cu, Zn, As, Se, Mo, Cd, Sb and Pb) were the highest in winter. Meanwhile, there were significant differences in inflammatory (sCD36 and CRP) and oxidative stress (OX-LDL) markers in the serum of participants over the four seasons. In particular, the estimated effects of personal metal exposure (such as V, As, Se, Cd, and Pb) on sCD36 and pulse pressure (PP) levels were consistently significant across the four LME models. A significant mediating role of sCD36 was also found in the relationship between personal exposure to Zn and Cr and changes in PP levels. Our findings provide clues and potential mechanisms regarding the cardiovascular effects of specific toxic constituents of PM2.5 in healthy young adults.

Short-term effects of personal exposure to temperature variability on cardiorespiratory health based on subclinical non-invasive biomarkers

Growing literatures have explored the cardiorespiratory health effects of the daily temperature, but such effects of temperature variability remain unclear. We investigated the acute associations of personal levels of temperature variability with cardiorespiratory biomarkers. This is a panel study with four repeated measurements among forty eligible college students in Hefei, Anhui Province, China. We collected personal-level temperature data using temperature/humidity data loggers. Temperature variability parameters included diurnal temperature range (DTR), the standard-deviation of temperature (SDT) and temperature variability (TV). Cardiorespiratory health indicators included three BP parameters [systolic BP (SBP), diastolic BP (DBP) and mean article pressure (MAP)], fractional exhaled nitric oxide (FeNO), and four saliva biomarkers [C-reactive protein (CRP), cortisol, alpha-amylase and lysozyme]. Linear mixed-effect models were then used to assess the associations of temperature variability with these cardiorespiratory biomarkers. We found that short-term exposure to the three temperature variability parameters was associated with these cardiorespiratory biomarkers. The magnitude, direction and significance of these associations varied by temperature variability parameters, by biomarkers and by lags of exposure. Specifically, temperature variability parameters were inversely associated with BP and saliva lysozyme; positively associated with airway inflammation biomarkers (FeNO and saliva CRP) and stress response biomarkers (saliva cortisol and alpha-amylase). The results were robust to further control for air pollutants, and these associations were more prominent in females and in subjects with abnormal body mass index. Our findings suggested that acute exposure to temperature variability could significantly alter cardiorespiratory biomarker profiles among healthy young adults in China.

Short-Term Effects of Personal Exposure to Temperature Variability on Cardiorespiratory Health Based on Subclinical Non-Invasive Biomarkers

Short-Term Effects of Personal Exposure to Temperature Variability on Cardiorespiratory Health Based on Subclinical Non-Invasive Biomarkers

Comparing types of exposure metrics for identifying the effects of air pollution: an application in a panel of COPD patients

BACKGROUND AND AIM: Measured or modelled concentrations used in epidemiological studies can differ from true exposures, a difference known as measurement error. To account for this, personal exposure measurements can be regarded as the “gold-standard” method but do not differentiate between the effects of indoor- and outdoor-generated pollution. We apply a statistical apportionment method to identify and separate the effects of personal exposure to air pollution from indoor and outdoor sources on chronic obstructive pulmonary disease (COPD) patients in London. METHODS: A panel of 130 patients was followed up for an average period of 128 days during which each patient carried sensors measuring PM2.5, PM10, NO2, NO, CO and O3 at one-minute resolution. Total personal exposures (PExT) were separated into those from indoor- (PExI) and outdoor-generated pollution (PExO) using GPS data and matching ambient concentrations from the London reference ambient air quality monitoring network. Each patient recorded daily respiratory symptoms, peak expiratory flow (PEF) and exacerbation of symptoms. The associations of these outcomes with PExT, PExI, PExO and ambient pollution were assessed with mixed-effects models. RESULTS:Preliminary results for PM2.5 have shown that while total personal exposure was not associated with any outcome, a unit increase in PExO was found to increase the odds of exacerbation, cough and sputum by approximately 1.0%. Using ambient concentrations, which is the equivalent error-prone proxy to PExO, these odds were decreased to 0.6-0.7% for exacerbation and cough, while for sputum the finding was not statistically significant. PEF was negatively associated only with PExI. Work is ongoing for the other pollutants. CONCLUSIONS:Our findings suggest that the exposure metric used in identifying the health effects of air pollution is important in epidemiological studies. Using proxies can introduce measurement error bias. For decision-making, it is important to separate the effects of indoor- and outdoor-generated pollution as different policies apply to each. KEYWORDS: Air pollution, Respiratory outcomes, Methodological study design, Exposure assessment, Measurement error

Does real-time and perceived environmental exposure to air pollution and noise affect travel satisfaction? evidence from Beijing, China

Poor air quality and noise pollution have become major environmental risks in urban China. However, the effect of personal exposure to air pollution and noise in various traffic microenvironments on individuals’ daily travel satisfaction has rarely been investigated. Drawing upon real-time data collected using portable sensors and GPS tracking devices in Beijing from December 2017 to February 2018, this paper explores the variations in the co-exposure to real-time air pollution and noise among various transportation modes. It then employs structural equation models to investigate whether and how the objectively measured and subjectively perceived exposure to air pollution and noise in different traffic microenvironments influences individuals’ daily travel satisfaction. Findings show that travel satisfaction and co-exposure to real-time air pollution and noise vary greatly among different transportation modes. People travelling by public transport experience high personal noise exposure and tend to have lower levels of travel satisfaction. While perceived air pollution and noise have significant direct effects on travel experiences, the pathways between objective pollution and travel satisfaction differ for air pollution and noise. Objective air pollution negatively affects travel satisfaction indirectly by influencing perceived air pollution, whereas objective noise has a positive and direct effect on travel satisfaction. Moreover, people with different socio-economic backgrounds tend to bear unequal burdens of air pollution and noise during their daily travels. These findings indicate that more research should be conducted to enhance our understanding of the relationships between personal micro-environmental exposures and subjective wellbeing.

Effects of short-term personal exposure to air pollution on platelet mitochondrial DNA methylation levels and the potential mitigation by L-arginine supplementation

The potential effect of short-term exposure to air pollution on mitochondrial DNA (mtDNA) methylation remains to be explored. This study adopted an experimental exposure protocol nested with an intervention study on L-arginine (L-Arg) supplementation among 118 participants. Participants walked along a traffic road for 2 hours in the last day of a 14-day intervention to investigate the effects of short-term personal exposure to air pollution on platelet mtDNA methylation and the possible modifying effects of L-Arg supplementation. Results showed that short-term personal exposure to air pollutants was associated with hypomethylation in platelet mtDNA in 110 participants who completed the study protocol. Specifically, 2-h fine particulate matter (PM2.5) exposure during the outdoor walk was significantly associated with hypomethylation in mt12sRNA; 24-h PM2.5 and black carbon (BC) exposures from the start of the walk till next morning were both significantly associated with hypomethylation in the D-loop region; 24-h BC exposure was also significantly associated with hypomethylation in ATP8_P1. Supplementation with L-Arg could mitigate the air pollution effects on platelet mtDNA methylation, especially the D-loop region. These findings suggest that platelet mtDNA methylation may be sensitive effect biomarker for short-term exposure to air pollution and may help deepen the understanding of the epigenetic mechanisms of adverse cardiovascular effects of air pollution.

Adverse effects of short-term personal exposure to fine particulate matter on the lung function of patients with chronic obstructive pulmonary disease and asthma: a longitudinal panel study in Beijing, China.

Fine particulate matter (PM2.5) is an important environmental factor affecting human health. However, most studies on PM2.5 and health have used data from fixed monitoring sites to assess PM2.5 exposure, which may have introduced misleading information on the exposure-response relationship. We aimed to assess the effect of short-term personal PM2.5 exposure on lung function in patients with chronic obstructive pulmonary disease (COPD) and asthma. To achieve this, we conducted a longitudinal panel study among 37 COPD patients and 45 asthma patients from Beijing, China. The COPD group and the asthma group completed 148 and 180 lung function tests, respectively. We found that in COPD patients, for every 10-μg/m3 increase in PM2.5 exposure at lag2, the FEV1, FVC and DLco decreased by -0.014 L (95% CI -0.025, -0.003), -0.025 L (95% CI -0.050, -0.003) and -0.089 mmol/min/kPa (95% CI -0.156, -0.023), respectively. There was also a decrease of -0.023 L/s (95% CI -0.042, -0.003) and -0.017 L/s (95% CI -0.032, -0.002) in MMEF at lag3 and lag03, respectively. In the asthma group, every 10-μg/m3 increase in PM2.5 exposure led to a reduction of -0.012 L (95% CI -0.023, -0.001), -0.042 L (95% CI -0.081, -0.003) and -0.061 L/s (95% CI -0.116, -0.004) in the FEV1, FVC and PEF at lag3, respectively. Our findings suggest that PM2.5 exposure may primarily affect both airway function and lung diffusion function in COPD patients, and airway function in asthma patients.

Acute effects of personal exposure to fine particulate matter on salivary and urinary biomarkers of inflammation and oxidative stress in healthy adults

Non-invasive bio-samples, such as saliva and urine, are promising tools for assessment of inflammation and oxidative stress biomarkers. Few studies have investigated potential responses of those biomarkers towards short-term PM2.5 exposure. We conducted a longitudinal study with 4 repeated examinations among 40 healthy, nonsmoking adults in Shanghai, China. Personal samplings were performed for PM2.5 exposure assessment. Then, five biomarkers, including C-reactive protein (CRP), tumor necrosis factor-α (TNF-α), alpha-1 antitrypsin (A1AT) in saliva and 8-Iso-Prostaglanding F2α (8-iso-PGF2α), total antioxidant capacity (TAC) in urine, were measured. We fitted linear mixed-effect models to evaluate short-term effect of personal PM2.5 exposure on salivary and urinary biomarkers, adjusting for potential confounders of meteorology, sociodemographic characteristics and biomarker detection. We also explored sensitive time windows of exposure for different biomarkers. We found robust associations of salivary CRP, TNF-α, and urinary 8-iso-PGF2α with PM2.5 exposure, and responses of salivary inflammatory markers occurred more acutely than urinary oxidative stress markers. For instance, a 10 μg/m3 increase in PM2.5 was associated with an elevation of 5.49% (95% CI: 1.17%, 9.99%) in CRP and 7.05% (95% CI: 1.29%, 13.13%) in TNF-α both at lag 12 h, and 6.97% (95% CI: 1.33%, 12.92%) in 8-iso-PGF2α at lag 01 d. Based on non-invasive samples, this study provided evidence on effect of PM2.5 exposure on responses of systematic inflammation and oxidative stress. Sub-daily (6–12 h) and daily (≥24 h) period after PM2.5 exposure might be sensitive time window to detect the responses of salivary (i.e. CRP, TNF) and urinary biomarkers (i.e. 8-iso-PGF2α), respectively.

Toxicological effects of personal exposure to fine particles in adult residents of Hong Kong.

Toxicological studies have demonstrated the associations between fine particle (PM2.5) components and various cytotoxic endpoints. However, few studies have investigated the toxicological effects of source-specific PM2.5 at the individual level. To investigate the potential impact of source-specific PM2.5 on cytotoxic effects, we performed repeated personal PM2.5 monitoring of 48 adult participants in Hong Kong during the winter and summer of 2014-2015. Quartz filters were analyzed for carbonaceous aerosols and water-soluble ions in PM2.5. Teflon filters were collected to determine personal PM2.5 mass and metal concentrations. The toxicological effects of personal PM2.5 exposure-including cytotoxicity, inflammatory response, and reactive oxygen species (ROS) production-were measured using A549cells invitro. Personal PM2.5 samples collected in winter were more effective than those collected in summer at inducing cytotoxicity and the expression of proinflammation cytokine IL-6. By contrast, summer personal PM2.5 samples induced high ROS production. We performed a series of statistical analyses, Spearman correlation and a source apportionment approach with a multiple linear regression (MLR) model, to explore the sources contributing most significantly to personal PM2.5 bioreactivity. Secondary inorganic species and transition metals were discovered to be weak-to-moderately associated with cytotoxicity (rs: 0.26-0.55; p<0.01) and inflammatory response (rs: 0.26-0.44; p<0.05), respectively. Carbonaceous aerosols (i.e., organic and elemental carbon; rs: 0.23-0.27; p<0.05) and crustal material (Mg and Ca) was positively associated with ROS generation. The PMF-MLR models revealed that tailpipe exhaust and secondary sulfate contributed to ROS generation, whereas secondary nitrate was the major contributor to PM2.5 cytotoxicity and inflammation. These results improve and variate the arguments for practical policies designed to mitigate the risks posed by air pollution sources and to protect public health.

Acute Effects of Personal Ozone Exposure on Biomarkers of Inflammation, Oxidative Stress, and Mitochondrial Oxidative Damage - Shanghai Municipality, China, May-October 2016.

What is already known on this topic?It remains inconclusive whether short-term ozone exposure can cause an inflammatory response and oxidative damage in the circulatory system, particularly at low concentrations.What is added by this report?This study made an accurate exposure assessment by conducting personal ozone monitoring, thus minimizing the exposure misclassification commonly found in previous environmental epidemiological studies. Our study found that even short-term exposure to low concentrations of ozone was associated with inflammation, lipid peroxidation, and mitochondrial oxidative damage.What are the implications for public health practice?Short-term exposure to low concentrations of ozone can still lead to subclinical cardiovascular effects, suggesting the current air quality standards for ozone need to be further tightened in China.

Effects of personal air pollution exposure on inflammatory responses: potential mediation by endogenous melatonin

Background/Aim: Melatonin is a free radical scavenger and an anti-inflammatory molecule. Air pollution exposure has been associated with increased inflammatory responses. We hypothesize that endogenous melatonin plays a role in inflammatory responses to air pollution exposure. Methods: We tested this hypothesis in a cohort of 53 healthy adults (22-52 years old, 16 women), none of whom were on melatonin supplementation. Early morning urine and blood were collected from each participant for up to three times. We analyzed urinary 6-sulfatoxymelatonin (aMT6s), as a surrogate of circulating melatonin, and pro- and anti-inflammatory cytokines in plasma. Indoor and outdoor air pollutants were measured and combined with participants' time-activity pattern to calculate personal exposure to O3, PM2.5, NO2, and SO2 averaged over 12-hour, 24-hour, 1-week, and 2-week prior to biospecimen collection, respectively. Linear mixed effects models were used to examine the relationships of urinary aMT6s with personal pollution exposure and plasma cytokines controlling for covariates including temperature, humidity, sex, age, and respiratory infection &amp; smoking status. Mediation analysis was conducted to test whether aMT6s is a mediator for the relationships between pollution exposure and inflammatory cytokines. Results: A one interquartile range (4.2 ppb) increase in 2-week O3 exposure was associated with a -29.4% (95% CI: -50.0%, -0.50%) decrease in aMT6s, while the relationships of aMT6s with other pollutant exposures were nonsignificant. Within the range of endogenous aMT6s concentration (0.5-53.0 ng/ng creatinine), increasing aMT6s level was associated with decreasing levels of pro-inflammatory cytokines, including IL-1β, IL-6, IL-8, IL-17A, IFN-γ, and TNF-α. The mediation analysis showed that 5.2%, 7.7%, 8.2%, 10.5%, 16.1%, and 8.3% of the total effects of 2-week O3 exposure on IL-1β, IL-6, IL-8, IL-17A, IFN-γ, and TNF-α were mediated by urinary aMT6s, respectively. Conclusions: Our findings suggest that air pollution exposure may decrease endogenous melatonin, which may further contribute to enhanced pro-inflammatory responses.

Effects of Personal Exposure to Fine Particulate Matter Air Pollutionon Gut microbiotain elderly: The China BAPE study

Background: In recent years, it is confirmed that human gut microbiota is critical for human health. Animal studies suggest that air pollutants may alter the composition of the gut microbiota, which may negatively impact health through changes in the composition or function of the gut microbiome.However, Research on the effects of personal exposure to fine particulate matter on gut microbiota is lacking in developing countries, especially in highly polluted areas.Methods:Participants (60-69 years, n=76) were enrolled between Sep 10th 2018 and Jan 19th 2019 with a month interval.MicroPEMTM real-time personal measurements was used to monitor the subject's personal PM2.5 exposure. Faecal samples from 76 healthy elderly were sequenced using 16S rDNA amplification to assess microbial diversity, richness and relative taxa abundance. Operational Units were clustered with 97% similarity cutoff and chimeric sequences were identified and removed. A linear mixed-effect model was applied to estimate the associations of exposure to Fine Particulate Matter with alpha diversity indices and relative abundance of the gut microbiota. Results:A total of 516 genus level microbiota were identified in this study.The five most abundant bacteria in the fecal flora of the participants were Bacteroides, Prevotella, Pachyphyte, Faecalibacterium and Roseburia.Exposure to fine particulate matter was associated with the alterations in gut microbiota diversity and relative abundance of 20 genus level microbiota. By analyzing the abundance composition of the KEGG pathway of the intestinal flora of the Participants,the pathways enriched by the intestinal flora mainly include transport, DNA repair and recombinant proteins, ribosomes, and purine metabolism. Involves environmental information processing, genetic information processing, and metabolic mechanisms.Conclusions: Exposure to fine particulate matter may alter the relative abundance, and decrease the diversity of the gut microbiota.These findings can extend our understanding of the mechanism of air pollution inducing diseases.