Individual-level PM2 Research Articles

Integrating Time-Activity and Air Sensors into Smartphone-based PM2.5 and Ozone Exposure Model for Epidemiologic Studies

BACKGROUND AND AIM: Epidemiologic studies of fine particulate matter (PM2.5) and ozone (O3) often use outdoor concentrations as exposure surrogates, which can induce measurement error. The goal of this study was to improve PM2.5 and O3 exposure assessments for a repeated measurement study with 20 individuals in Philadelphia, Pennsylvania by applying a smartphone-based exposure model called TracMyAir. METHODS: We developed TracMyAir, which is a smartphone (iPhone, Android) application that determines multiple tiers of individual-level exposure metrics in real-time for ambient and non-ambient PM2.5 and O3 using outdoor concentrations, home building characteristics, weather, time-locations, and time-activities. In this study, we extended TracMyAir by including (1) outdoor concentrations from an air quality model (CMAQ), (2) indoor and outdoor PM2.5 concentrations from low-cost air sensors (PurpleAir) and a building infiltration model, (3) a microenvironment model (MicroTrac) based on time-resolved smartphone geolocations, and (4) inhaled ventilation models based on physical activity data from smartphone and smartwatch accelerometers and heart rate sensors. The five tiers of exposure metrics with increasing information needs and model complexity include: residential air exchange rates (AER, Tier 1), infiltration factors (Finf_home, Tier 2), indoor concentrations (Cin_home, Tier 3), exposures (E, Tier 4), and inhaled doses (D, Tier 5). We applied TracMyAir to determine hourly PM2.5 and O3 exposure metrics for three consecutive days for 20 participants consisting of two age groups (18-30 years old, n=10; 55-75 years old, n=10). RESULTS: The TracMyAir predictions showed considerable temporal and house-to-house variability of AER, Finf_home, and Cin_home (Tiers 1-3), and person-to-person variability of E and D (Tiers 4-5). CONCLUSIONS: Our study demonstrates the capability of extending TracMyAir with air pollutant and time-activity sensors and models to estimate individual-level PM2.5 and O3 exposure metrics for an epidemiologic study, in support of improving risk estimation.

Individual exposure to ambient PM2.5 and hospital admissions for COPD in 110 hospitals: a case-crossover study in Guangzhou, China

Few studies have evaluated the short-term association between hospital admissions and individual exposure to ambient particulate matter (PM2.5). Particularly, no studies focused on hospital admissions for chronic obstructive pulmonary disease (COPD) at the individual level. We assessed the short-term effects of PM2.5 on hospitalization admissions for COPD in Guangzhou, China, during 2014–2015, based on satellite-derived estimates of ambient PM2.5 concentrations at a 1-km resolution near the residential address as individual-level exposure for each patient. Around 40,002 patients with COPD admitted to 110 hospitals were included in this study. A time-stratified case-crossover design with conditional logistic regression models was applied to assess the effects of PM2.5 based on a 1-km grid data of aerosol optical depth provided by the National Aeronautics and Space Administration on hospital admissions for COPD. Further, we performed stratified analyses by individual demographic characteristics and season of hospital admission. Around 10 μg/m3 increase in individual-level PM2.5 was associated with an increase of 1.6% (95% confidence interval [CI]: 0.6%, 2.7%) in hospitalization for COPD at a lag of 0–5 days. The impact of PM2.5 on hospitalization for COPD was greater significantly in males and patients admitted in summer. Our study strengthened the evidence for the adverse effect of PM2.5 based on satellite-based individual-level exposure data.

Short-term and Intermediate-term Fine Particulate Air Pollution are Synergistically Associated with Habitual Sleep Variability in Adolescents

BACKGROUND AND AIM: While both fine particulate (PM2.5) exposure and high sleep variability are potential risk factors for cardiovascular diseases (CVD), the association between PM2.5 and sleep variability remains unclear. Our study aimed at investigating the association between PM2.5 exposure and habitual sleep variability (HSV) in a population-based sample of U.S. adolescents. METHODS: Data obtained from 421 adolescents, who participated in the Penn State Child Cohort follow-up examination, were analyzed. For each participant, we collected 24-hour (i.e. short-term) individual-level PM2.5 exposure by using a personal nephelometer. We further estimated their residential-level PM2.5, during the 60-day period prior to the examination (i.e. intermediate-term), by utilizing a GIS-based kriging approach. Actigraphy was used to collect participants’ total sleep time (TST) for 7 consecutive nights. HSV was calculated as the standard deviation (SD) of the 7-night TST. Multivariable-adjusted linear regression was used to assess the association between PM2.5 exposures and HSV. An interaction between the short- and intermediate-term PM2.5 was created to test their potential synergistic impact on HSV. RESULTS:Both short-term and intermediate-term PM2.5 exposure were significantly (both p0.01) associated with HSV. There was a marginally significant (p=0.08) synergistic interaction between short-term and intermediate-term PM2.5. Specifically, the association between intermediate-term PM2.5 and HSV became stronger as short-term PM2.5 increased, and vice versa. For example, the regression coefficients (SE) between 1 SD (2.2 µg/m3) increase in intermediate-term PM2.5 and HSV were 3.5 (2.7, p=0.21), 5.1 (2.3, p=0.03), and 10.5 (3.4, p0.01) minutes, when short-term PM2.5 were at its 10th percentile (1.7 µg/m3), median (9.7 µg/m3), and 90th percentile (35.3 µg/m3), respectively. CONCLUSIONS:Both short-term and intermediate-term PM2.5 exposure were associated with higher sleep variability among adolescents. More importantly, short-term and intermediate-term PM2.5 exposure may impact sleep variability in a synergistic manner, which highlighted the importance of PM2.5 reduction in the early prevention of CVD. KEYWORDS: Particulate Matter, Sleep Variability, Adolescents

Abstract MP70: Short-term Fine Particulate Air Pollution Is Associated With Shorter Sleep Duration And Higher Sleep Variability In Adolescents

Introduction: Sleep deprivation and large sleep variability are potential risk factors for obesity and cardiovascular diseases. While it is plausible that particulate air pollution may contribute to these unfavorable sleep patterns, very few studies have been conducted to assess the association between fine particulate (PM 2.5 ) air pollution and objectively measured sleep duration and its variability in an adolescent U.S. population. Hypothesis: We tested the hypothesis that higher individual-level short-term PM 2.5 exposure is associated with shorter sleep duration and higher sleep variability among adolescents. Methods: We analyzed the available data collected from 421 adolescents who participated in the follow-up examination of the population-based Penn State Child Cohort (PSCC) study. To estimate individual-level short-term PM 2.5 exposure, a personal nephelometer (Thermo pDR-1200) was used to measure real-time PM 2.5 concentration for 24 hours from the study participants. The 24-hour mean PM 2.5 concentration was used to quantify the short-term PM 2.5 exposure. To obtain objectively-measured habitual sleep duration (HSD) and habitual sleep variability (HSV), an actigraphy (GT3X+) was used to collect sleep data for 7 consecutive nights, including 1 night in parallel with the PM 2.5 monitoring and 6 nights thereafter. HSD and HSV were calculated as the intra-individual mean and standard deviation (SD) of the 7-night sleep duration, respectively. Participants with < 5 nights (70% of 7 nights) of data were excluded from the analyses. The associations between the individual-level PM 2.5 exposure and HSD/HSV were evaluated by using multi-variable adjusted linear regression models, controlling for age, race, sex, BMI percentile, environmental temperature, and relative humidity. Results: The mean (SD) age of the study population was 16.9 (2.2) years. The study sample consisted of 54% males and 78% whites. The 24-hour mean (SD) of PM 2.5 concentration was 16.9 (26.8) μg/m 3 , while the average HSD and HSV were 7.0 (0.9) hours and 1.2 (0.6) hours, respectively. We observed that a 10 μg/m 3 increase in the 24-hour mean PM 2.5 was associated with significantly lower HSD [β (SE): -0.06 (0.03) hours, p=0.02] and larger HSV [β (SE): 0.04 (0.02) hours, p=0.04]. The effect sizes were approximately 7% of their respective SDs. Conclusion: Individual-level short-term PM 2.5 exposure is associated with objective-measured shorter sleep duration and higher night-to-night sleep variability among U.S. adolescents. These observed associations suggest that particulate air pollution exposure in early life may impact habitual sleep pattern, which may in turn be associated with the risks of obesity and cardiovascular diseases in later life.

The acute response profile of inflammatory and oxidative stress biomarkers in welders

Objectives: Welding fume is an occupational hazard that can cause a variety of health effects. We aimed to investigate inflammatory response profile and oxidative stress level after acute welding fume exposure. Methods: In 87 US adult boilermakers, we took measurements repeatedly immediately before and after a welding shift, as well as at two matched time points on non-welding days, following a self-controlled design. The measured plasma inflammatory biomarkers include IL-1β, IL-2, IL-6, IL-8, IL-10, TNF-α, VEGF, CRP, SAA, sICAM-1, and sVCAM-1; while urinary 8-isoprostane and 8-OHdG were measured as oxidative stress and DNA damage biomarkers, respectively. Individual level PM2.5 exposure were measured during the welding task, as well as non-welding days. Results: The average PM2.5 level was significantly higher during welding shifts, compared to baseline measured on non-welding days (0.42 vs. 0.12 mg/m3, p<0.01). The log(u-8-isoprostane) increased 0.21 unit (p<0.01) after welding shift, but did not change (p=0.91) during the matched period on non-welding days, adjusted for covariates. In a balanced subset, we observed the same but insignificant trend. Log(u-8-OHdG) was 0.07 unit higher (p=0.04) on welding days, at both time points. Also, log(IL-6) had opposite trends between welding shift and self-control (pinteraction=0.03). We found u-8-isoprostane and u-8-OHdG to be higher among smokers, and non-smokers were more sensitive to the effect of welding fume exposure. Conclusions: We studied the controlled health effect of welding fume exposure, and captured indicative signals, but it subjected to insufficient power. The result could promote understanding about pathogenesis of occupational diseases.

The factors associated with distress following exposure to smoke from an extended coal mine fire

In February 2014, the coalmine adjacent to the Hazelwood Power Station in the Latrobe Valley of Victoria, Australia, caught fire, with residents from the nearby town of Morwell and the wider area exposed to smoke for six weeks. Although there was evidence linking the mine-fire event with psychological distress, no studies have evaluated the degree of distress in relation to the level of smoke exposure. We aimed to investigate the exposure-response relationship between particulate matter 2.5 μm or less in diameter (PM2.5) released during the Hazelwood mine fire event and long-term symptoms of posttraumatic distress in the affected community, including the consideration of other key factors. A total of 3096 Morwell residents, and 960 residents from the largely unexposed comparison community of Sale, were assessed for symptoms of posttraumatic distress 2.5 years after the Hazelwood incident using the Impact of Events Scale-Revised (IES-R). Individual-level PM2.5 exposure was estimated by mapping participants’ self-reported location data on modelled PM2.5 concentrations related to the mine fire. Multivariate linear regression was used to evaluate the exposure-response relationship. Both mean and peak exposure to mine fire-related PM2.5 were found to be associated with participant IES-R scores with an interaction effect between age and mean PM2.5 exposure also identified. Each 10 μg/m3 increase in mean PM2.5 exposure corresponded to a 0.98 increase in IES-R score (95% CI: 0.36 to 1.61), and each 100 μg/m3 increase in peak PM2.5 exposure corresponded to a 0.36 increase (95% CI: 0.06 to 0.67). An age-effect was observed, with the exposure-response association found to be stronger for younger adults. The results suggest that increased exposure to PM2.5 emissions from the Hazelwood mine fire event was associated with higher levels of psychological distress associated with the mine fire and the most pronounced effect was on younger adults living in the affected community.

Air pollution and child obesity: Assessing the feasibility of measuring personal PM2.5 exposures and behaviours related to BMI in preschool-aged children in China

BackgroundAccumulating evidence suggests that air pollutant exposures affect multiple metabolic functions which may place populations at a higher risk for obesity. A pilot study was conducted to assess the feasibility of measuring personal exposures to fine particulate matter (PM2.5) and tobacco smoke, to assess the influence of these exposures on the risk of obesity in children in Kunming, a rapidly developing city in China. MethodsWe recruited 52 children ages 4–5 years from three preschools in Kunming. Individual-level PM2.5 exposures were assessed using real-time personal monitors. Tobacco smoke exposures were assessed by a parent-reported questionnaire. ResultsSubjects' daily mean PM2.5 exposure (n = 52) was 32.8 (SD = 13.4) μg m−3 and daily tobacco exposure was 14.4 (SD = 21.1) cigarettes day−1. Our subjects’ daily mean exposure to PM2.5 was 31% higher than the level set by the WHO daily ambient concentration guidelines. ConclusionWe found personal PM2.5 monitoring to be a feasible method for measuring exposure to PM2.5 in young children. Future studies with larger sample sizes are warranted to explore the relationship between air pollution exposure and risk of obesity in China.

Long-term exposure to fine particulate matter and incidence of disability in activities of daily living

PDS 72: Environmental health issues in LMIC, Exhibition Hall (PDS), Ground floor, August 28, 2019, 10:30 AM - 12:00 PM Background/Aim: Currently the Chinese government has adopted WHO guideline air quality interim target values as the national ambient air quality standards values for fine particulate matter (PM2.5), while population-based evidence was insufficient. The study was to evaluate the association of individual-level PM2.5 exposure and incidence of disability in activities of daily living (ADL) among the oldest old. Methods: A total of 15,453 participants aged 80+ (mean age, 92.3 ± 7.3 years) with independent ADL at baseline were included. Annual average residential PM2.5 exposure with 1 km*1 km spatial resolution was estimated from satellite observations. Katz index of independence in ADL was used to assess disability from 2002 to 2014. Penalized splines were constructed to fit Cox proportional hazards models to survival data. Competing risk models were constructed to estimate risk of disability in ADL for each 10 μg/m3 increase in PM2.5 adjusted for confounders. Results: Over a follow-up of 71,396 person-years, 3,373 (21.8%) cases of incident disability in ADL occurred. After adjusting for potential confounders, a J-shaped association existed between PM2.5 exposure with a threshold concentration of 33 μg/m3, and incident disability in ADL. Above this threshold, the risk magnitude significantly increased along with PM2.5 concentrations; compared to 33 μg/m3, the hazard ratio ranged from 1.02 (1.00-1.05) at 40 μg/m3 to 2.26 (1.55-3.29) at 110 μg/m3. The risk magnitude was not significantly changed blow this threshold. Each 10 μg/m3 increase in PM2.5 exposure corresponded to a 7.6% increase in the risk of disability in ADL (hazard ratio 1.076, 95% CI 1.050-1.103). Conclusions: The study provided limited population-based evidence for the oldest old and detected a threshold of 33 μg/m3, which was basically consistent with current WHO air quality guidelines and values of Chinese national ambient air quality standards. Keywords: PM2.5, incidence, disability, activities of daily living, oldest old, cohort study.

Long-term exposure to ambient fine particulate matter and incidence of diabetes in China: A cohort study

BackgroundDiabetes caused substantial economic and health burden worldwide. However, the associations between air pollution and diabetes incidence were rarely reported in the developing countries, especially in China with relatively high PM2.5 concentrations. ObjectivesA cohort-based study was conducted to assess the diabetes incidence associated with long-term exposure to ambient PM2.5. MethodsWe collected individual health data and risk factors from the project of Prediction for Atherosclerotic Cardiovascular Disease Risk in China (China-PAR Project) from 15 provinces over China. Diabetes was defined as fasting glucose levels ≥7.0 mmol/L at the follow-ups and/or the use of insulin or oral hypoglycemic agents and/or diagnosed medical history of diabetes during 2004 to 2015. Individual-level PM2.5 exposures were estimated from satellite-based PM2.5 concentrations (10 km spatial resolution) during the study period. Cox proportional hazards models with random intercepts of each cohort and region were employed to estimate the diabetes incidence attributable to PM2.5, after the adjustment for age, gender, body mass index, smoking status, education, work-related physical activity level, hypertension, urbanicity, county-level averaged years of education, and long-term levels of temperature and relative humidity. ResultsA total of 88,397 subjects were analyzed with 580,928 person-years of follow-up after 2004, among which 6439 new cases of diabetes were observed. The mean age of the subjects was 51.7 years at baseline. For an increase of 10 μg/m3 in long-term PM2.5 exposure, the multivariable-adjusted percent increase in the diabetes incidence was estimated to be 15.66% (95% confidence interval: 6.42%, 25.70%). The adverse effects of PM2.5 were larger among females, rural subjects, non-smokers, normotensives, subjects younger than 65 years and subjects with body mass index <25 kg/m2. ConclusionsOur findings provided evidence for the association of long-term exposure to PM2.5 with diabetes incidence in China. A sustained improvement of air quality will benefit the reduction for diabetes epidemic in China.

Ambient PM2.5 air pollutionexposure and hepatocellular carcinoma incidence in the United States.

To conduct the first epidemiologic study prospectively examining the association between particulate matter air pollution < 2.5µm in diameter (PM2.5) exposure and hepatocellular carcinoma (HCC) risk in the U.S. Surveillance, Epidemiology, and End Results (SEER) provided information on HCC cases diagnosed between 2000 and 2014 from 16 population-based cancer registries across the U.S. Ambient PM2.5 exposure was estimated by linking the SEER county with a spatial PM2.5 model using a geographic information system. Poisson regression with robust variance estimation was used to calculate incidence rate ratios and 95% confidence intervals (CIs) for the association between ambient PM2.5 exposure per 10µg/m3 increase and HCC risk adjusting for individual-level age at diagnosis, sex, race, year of diagnosis, SEER registry, and county-level information on health conditions, lifestyle, demographic, socioeconomic, and environmental factors. Higher levels of ambient PM2.5 exposure were associated with a statistically significant increased risk for HCC (n = 56,245 cases; adjusted IRR per 10µg/m3 increase = 1.26, 95% CI 1.08, 1.47; p < 0.01). If confirmed in studies with individual-level PM2.5 exposure and risk factor information, these results suggest that ambient PM2.5 exposure may be a risk factor for HCC in the U.S.

Association of individual-level concentrations and human respiratory tract deposited doses of fine particulate matter with alternation in blood pressure

Fine particulate matter (PM2.5) contributes to the risk of cardiovascular events, partially owing to its deposition in the human respiratory tract. To investigate short-term effects of ambient PM2.5 exposure on alternation of blood pressure (BP), this study was conducted during the winter-summer period between 2014 and 2015. The study included 106 community residents in Wuhan city, China. We repeatedly monitored the household and outdoor PM2.5 concentrations as well as individual-level PM2.5 in each season, and then assessed personal PM2.5 exposure (including deposited doses of PM2.5 in the human respiratory tract) by using different methodology (such as using a dosimetry model). All participants took part in the physical examination, including the inflammatory indicators, BP and lung function parameters measurements. Subsequently, we assessed the health damage of exposure to PM2.5 using generalized additive models. We observed increased BP at 2-day lag for an interquartile range increase in ambient fixed-site, households, individual-level PM2.5 exposure and the corresponding lung deposited doses of each exposure concentration (p < 0.05), decreased BP at 3-day lag for an interquartile range increase in ambient fixed-site, households PM2.5 and the corresponding lung deposited doses of each exposure concentration (p < 0.05). The estimated deposited doses of PM2.5 by the deposition fractions in this study and the referenced deposition fractions by previous reported method were equivalent associated with alternation in BP. In conclusion, lung deposited dose of PM2.5 as a quantitative indicator may be used to assess adverse cardiovascular effects following the systemic inflammation. However, we require careful assessment of acute adverse cardiovascular effects using ambient fixed-site PM2.5 after short-term PM2.5 exposure.

Preliminary study to explore gene-PM2.5 interactive effects on respiratory system in traffic policemen.

Traffic-related particulate matter (PM) is one of the major sources of air pollution in metropolitan areas. This study is to observe the interactive effects of gene and fine particles (particles smaller than 2.5 μm - PM2.5) on the respiratory system and explore the mechanisms linking PM2.5 and pulmonary injury. The participants include 110 traffic policemen and 101 common populations in Shanghai, China. Continuous 24 h individual-level PM2.5 is detected and the pulmonary function, high-sensitivity C-reactive protein (hs-CRP), Clara cell protein 16 (CC16) and the polymorphism in CXCL3, NME7 and C5 genes are determined. The multiple linear regression method is used to analyze the association between PM2.5 and health effects. Meanwhile, the interactive effects of gene and PM2.5 on lung function are analyzed. The individual PM2.5 exposure for traffic policemen was higher than that in the common population whereas the forced expiratory volume in 1 s (FEV1), the ratio of FEV1 to forced vital capacity (FEV1/FVC) and lymphocytes are lower. In contrast, the hs-CRP level is higher. In the adjusted analysis, PM2.5 exposure was associated with the decrease in lymphocytes and the increase in hs-CRP. The allele frequencies for NME7 and C5 have significant differences between FEV1/FVC ≤ 70% and FEV1/FVC > 70% participants. The results didn't find the interaction effects of gene and PM2.5 on FEV1/FVC in all the 3 genes. The results indicated that traffic exposure to high levels of PM2.5 was associated with systemic inflammatory response and respiratory injury. Traffic policemen represent a high risk group suffering from the respiratory injury.

The biological effects of individual-level PM2.5 exposure on systemic immunity and inflammatory response in traffic policemen

BackgroundAmbient fine-particle particulate matter (PM2.5) exposure is associated with the decline in pulmonary function, prevalence of coronary heart disease and incidence of myocardial infarction. The study is to observe the...

Individual-level PM2.5 exposure and the time course of impaired heart rate variability: the APACR Study

In 106 community-dwelling middle-aged non-smokers we examined the time-course and the acute effects of fine particles (PM₂.₅) on heart rate variability (HRV), which measures cardiac autonomic modulation (CAM). Twenty-four hours beat-to-beat ECG data were visually examined. Artifacts and arrhythmic beats were removed. Normal beat-to-beat RR data were used to calculate HRV indices. Personal PM₂.₅ nephelometry was used to estimate 24-h individual-level real-time PM₂.₅ exposures. We use linear mixed-effects models to assess autocorrelation- and other major confounder-adjusted regression coefficients between 1-6 h moving averages of PM₂.₅ and HRV indices. The increases in preceding 1-6 h moving averages of PM₂.₅ was significantly associated with lower HF, LF, and SDNN, with the largest effect size at 4-6 h moving averages and smallest effects size at 1 h moving average. For example, a 10 μg/m³ increase in 1 and 6-h moving averages was associated with 0.027 and 0.068 ms² decrease in log-HF, respectively, and with 0.024 and 0.071 ms² decrease in log-LF, respectively, and with 0.81 and 1.75 ms decrease in SDNN, respectively (all P-values <0.05). PM₂.₅ exposures are associated with immediate impairment of CAM. With a time-course of within 6 h after elevated PM₂.₅ exposure, with the largest effects around 4-6 h.

Sensitivity of Regional Health Effect Estimates to Different Approaches to Estimating Long-Term PM2.5 Exposure

ISEE-0838 Background and Objective: Estimation of long-term individual-level PM2.5 exposure in health effects studies has made use of prediction approaches such as nearest monitor and kriging. A recent simulation study indicated that health effect estimates using these two approaches differed more in regions where pollutant concentrations were less spatially correlated. This simulation study extends this finding by examining whether nearest-monitor and kriged PM2.5 exposure estimates produce different health effect estimates in 6 U.S. regions with different spatial correlation structures of PM2.5. Methods: Six US study regions (Mid-Atlantic, Northeast, Southeast, Midwest, Northern and Southern California) were defined by overlapping 200 kilometer buffers from the centroids of 24 Women’s Health Initiative Observational Study (WHI-OS) cities. Using year 2000 annual average PM2.5 at EPA monitoring sites, we estimated geostatistical parameters and characterized the spatial correlation structure as the range divided by square root partial sill for each region. Then, we simulated PM2.5 using estimated parameters and survival time to cardiovascular events based on previous findings from the WHI-OS (an incidence rate of 0.032 and relative risk (RR) of 1.24 per 10 μg/m3 increase in PM2.5) in each region. Given the simulated PM2.5 concentration at monitoring locations, we predicted exposure to PM2.5 at hypothesized subject locations using nearest-monitor and kriging approaches. RRs of cardiovascular events were estimated separately given the two prediction approaches in each region. Differences in RR from the two methods were then compared across regions. Result: Long-term PM2.5 spatial correlation was higher in the Midwest and lower in California. Differences in RRs for cardiovascular events from two predicted PM2.5 were higher in the regions with lower PM2.5 spatial correlation. Conclusion: Health effect estimates of long-term PM2.5 exposure are more sensitive to the approach to estimating individual exposure in regions where PM2.5 is less spatially correlated.

Interactions Between Environmental Health and Pediatric Obesity

Accumulating evidence suggests that air pollutant exposures affect multiple metabolic functions which may place populations at a higher risk for obesity. A pilot study was conducted to assess the feasibility of measuring personal exposures to fine particulate matter (PM2.5) and tobacco smoke, to assess the influence of these exposures on the risk of obesity in children in Kunming, a rapidly developing city in China.We recruited 52 children ages 4–5 years from three preschools in Kunming. Individual-level PM2.5 exposures were assessed using real-time personal monitors. Tobacco smoke exposures were assessed by a parent-reported questionnaire.Subjects' daily mean PM2.5 exposure (n = 52) was 32.8 (SD = 13.4) μg m−3 and daily tobacco exposure was 14.4 (SD = 21.1) cigarettes day−1. Our subjects’ daily mean exposure to PM2.5 was 31% higher than the level set by the WHO daily ambient concentration guidelines.We found personal PM2.5 monitoring to be a feasible method for measuring exposure to PM2.5 in young children. Future studies with larger sample sizes are warranted to explore the relationship between air pollution exposure and risk of obesity in China.

04/01556 Energy and environmental conservation in Slovakia and institutional support: Rousek, J. International Journal of Risk Assessment and Management, 2003, 4, (2/3), 158–166

Fine particulate matter (PM2.5) contributes to the risk of cardiovascular events, partially owing to its deposition in the human respiratory tract. To investigate short-term effects of ambient PM2.5 exposure on alternation of blood pressure (BP), this study was conducted during the winter-summer period between 2014 and 2015. The study included 106 community residents in Wuhan city, China. We repeatedly monitored the household and outdoor PM2.5 concentrations as well as individual-level PM2.5 in each season, and then assessed personal PM2.5 exposure (including deposited doses of PM2.5 in the human respiratory tract) by using different methodology (such as using a dosimetry model). All participants took part in the physical examination, including the inflammatory indicators, BP and lung function parameters measurements. Subsequently, we assessed the health damage of exposure to PM2.5 using generalized additive models. We observed increased BP at 2-day lag for an interquartile range increase in ambient fixed-site, households, individual-level PM2.5 exposure and the corresponding lung deposited doses of each exposure concentration (p < 0.05), decreased BP at 3-day lag for an interquartile range increase in ambient fixed-site, households PM2.5 and the corresponding lung deposited doses of each exposure concentration (p < 0.05). The estimated deposited doses of PM2.5 by the deposition fractions in this study and the referenced deposition fractions by previous reported method were equivalent associated with alternation in BP. In conclusion, lung deposited dose of PM2.5 as a quantitative indicator may be used to assess adverse cardiovascular effects following the systemic inflammation. However, we require careful assessment of acute adverse cardiovascular effects using ambient fixed-site PM2.5 after short-term PM2.5 exposure.