Beyond Residential Ambient Concentrations: Quantifying Exposure Error and Advancing Personal PM2.5 Prediction with a Scalable Modeling Framework.

BackgroundAir pollution is associated with poor asthma outcomes in children. However, most studies focus on ambient or indoor monitor pollution levels. Few studies evaluate breathing zone exposures, which may be more consequential for asthma outcomes.MethodsWe measured personal exposures to NO2, O3, PM10 and PM10 constituents, including black carbon (BC), brown carbon (BrC), environmental tobacco smoke (ETS), endotoxins, and \U0001d6fd-glucan, in a cohort of children with exacerbation-prone asthma for 72 h using wearable monitors. Personal exposures were compared to concentrations from in-home monitors in the child’s bedroom and ambient EPA air quality monitoring using correlation analyses. Personal exposures were tested for association with lung function and compared between participants with and without well-controlled asthma and signs of exacerbation in the prior 60 days using censored regression with robust standard errors.Results81 children completed 219 monitoring sessions. Personal NO2, O3, and PM10 exposures ranged from < 2 to 99.1 parts per billion (ppb), < 1.5 to 23.3 ppb, and < 1 to 141.9 \U0001d707g/m3, respectively. Personal endotoxin ranged from 0.04 to 101.3 EU/m3, \U0001d6fd-glucan from 18.5 to 1,162 pg/m3, BC from < 0.3 to 46.9 \U0001d707g/m3, BrC from < 0.3 to 6.1 \U0001d707g/m3, and ETS from < 0.3 to 56.6 \U0001d707g/m3. Correlations between personal and ambient PM10, NO2, and O3 concentrations were poor, whereas personal PM10 and NO2 correlated with in-home concentrations. In-home monitoring less frequently detected BrC (Personal:79% > lower limit of detection, Home:36.8%) and ETS (Personal:83.7%, Home:4.1%) than personal exposures, and detected BC in participants without personal exposure (Personal: 26.5%, Home: 96%). Personal exposures were not significantly associated with lung function or daily asthma control. Children requiring corticosteroid treatment for asthma exacerbation within 60 days of exposure monitoring had 1.98, 2.21 and 2.04 times higher personal exposures to BrC (p < 0.001; 95% CI: 1.43–2.37), ETS (p = 0.007; 95% CI: 1.25–3.91), and endotoxin (p = 0.012; 95% CI: 1.14–3.68), respectively.ConclusionsAlthough in-home monitoring was correlated with personal exposure to PM10 and NO2, in-home detection of ETS and BrC was not associated with personal exposures. Personal PM10 exposures in general, as well as BrC, ETS, and endotoxin levels were associated with recent childhood asthma exacerbations.Clinical trial numberNot applicable.

Ambient Gas Concentrations and Personal Particulate Matter Exposures

Particle Exposure Assessment for Community Elderly (PEACE) in Tianjin, China: Mass concentration relationships

BACKGROUND AND AIM: Errors in air pollution exposure assessment are often considered a major limitation in epidemiologic studies. However, it is difficult to obtain accurate personal level exposure on cohort populations due to the often prohibitively expensive costs. Personal exposure estimation models are used in lieu of personal exposures, but still suffer from the issues of availability and accuracy. We aim to establish a personal PM2.5 exposure assessment model for a cohort population, and assess its performance by applying our model on cohort subjects. METHODS: We analyzed data from representative sites selected from the Sub-Clinical Outcomes of Polluted Air in China (SCOPA-China) cohort study, and established a random forest model to estimate PM2.5 personal exposure. Parameters obtained from questionnaires and outdoor and meteorological monitoring sites were pre-screened using the Boruta algorism, and parameter contributions were evaluated using the rank of variable importance. We also applied the model among subjects recruited in the above project within the same area and study period to estimate the reliability of the model. RESULTS:The established model showed good fit with an R2 of 0.81. Ambient PM2.5 contributed the most to personal exposure concentrations, and indoor passive smoking, meteorological parameters, and durations in different microenvironments also ranked high in feature importance. The model application results showed similar patterns with empirically measured data, supporting the performance of our established model. CONCLUSIONS:Our pilot study provided a validated and feasible modeling approach to assess personal PM2.5 exposure for large cohort populations, and the preliminary application among cohort subjects proved satisfactory. The promising model framework can improve PM2.5 exposure assessment accuracy for future environmental health studies of large populations. KEYWORDS: Particulate matter, Exposure assessment, Methodological study design, Modeling

Exposure chain of urban air PM 2.5—associations between ambient fixed site, residential outdoor, indoor, workplace and personal exposures in four European cities in the EXPOLIS-study

In the framework of the EXPOLIS study in Milan, Italy, 48-h carbon monoxide (CO) exposures of 50 office workers were monitored over a 1-year period. In this work, the exposures were assessed for different averaging times and were compared with simultaneous ambient fixed-site concentrations. The effect of gas cooking and smoking and different methods of commuting on the microenvironment and exposure levels of CO were investigated. During the sampling the subjects completed a time-microenvironment-activity diary differentiating 11 microenvironments and three exposure influencing activities: gas cooking, smoking and commuting. After sampling, all exposure and time allocation data were stored in a relational database that is used in data analyses. Ambient 48-h and maximum 8-h distributions were similar compared to the respective personal exposures. The maximum 1-h personal exposures were much higher than the maximum 8-h exposures. The maximum 1-h exposures were as well higher than the corresponding ambient distribution. These findings indicate that high short-term exposures were not reflected in ambient monitoring data nor by long-term exposures. When gas cooking or smoking was present, the indoor levels at "home-" and in "other indoor" microenvironments were higher than without their presence. Compared with ambient data, the latter source was the most affective to increase the indoor levels. Exposure during commuting was higher than in all other microenvironments; the highest daily exposure contribution was found during "car/taxi" driving. Most of the CO exposure is acquired in indoor microenvironments. For the indoor microenvironments, ambient CO was the weakest predictor for "home indoor" concentrations, where the subjects spent most of their time, and the strongest for "other indoor" concentrations, where the smallest fraction of the time was spent. Of the main indoor sources, gas cooking, on average, significantly raised the indoor exposure concentrations for 45 min and tobacco smoking for 30 min. The highest exposure levels were experienced in street commuting. Personal exposures were well predicted, but 1-h maximum personal exposures were poorly predicted, by respective ambient air quality data. By the use of time-activity diaries, ETS exposure at the workplaces were probably misclassified due to differences in awareness to tobacco smoke between smokers and nonsmokers.

Personal PM10 exposure in asthmatic adults in Padova, Italy: seasonal variability and factors affecting individual concentrations of particulate matter

Ambient particulate air pollution assessed as outdoor concentrations of particulate matter less than or equal to 2.5 micro m in diameter (PM(2.5)) in urban background has been associated with cardiovascular diseases at the population level. However, the significance of individual exposure and the involved mechanisms remain uncertain. We measured personal PM(2.5) and carbon black exposure in 50 students four times in 1 year and analyzed blood samples for markers of protein and lipid oxidation, for red blood cell (RBC) and platelet counts, and for concentrations of hemoglobin and fibrinogen. We analyzed protein oxidation in terms of gamma-glutamyl semialdehyde in hemoglobin (HBGGS) and 2-aminoadipic semialdehyde in hemoglobin (HBAAS) and plasma proteins (PLAAS), and lipid peroxidation was measured as malondialdehyde (MDA) in plasma. Median exposures were 16.1 micro g/m(3) for personal PM(2.5) exposure, 9.2 micro g/m(3) for background PM(2.5) concentration, and 8.1 X 10(-6)/m for personal carbon black exposure. Personal carbon black exposure and PLAAS concentration were positively associated (p < 0.01), whereas an association between personal PM(2.5) exposure and PLAAS was only of borderline significance (p = 0.061). A 3.7% increase in MDA concentrations per 10 micro g/m(3) increase in personal PM(2.5) exposure was found for women (p < 0.05), whereas there was no significant relationship for the men. Similarly, positive associations between personal PM(2.5)exposure and both RBC and hemoglobin concentrations were found only in women (p < 0.01). There were no significant relationships between background PM(2.5) concentration and any of the biomarkers. This suggests that exposure to particles in moderate concentrations can induce oxidative stress and increase RBCs in peripheral blood. Personal exposure appears more closely related to these biomarkers potentially related to cardiovascular disease than is ambient PM(2.5) background concentrations.

Ambient particulate air pollution assessed as outdoor concentrations of particulate matter less than or equal to 2.5 micro m in diameter (PM(2.5)) in urban background has been associated with cardiovascular diseases at the population level. However, the significance of individual exposure and the involved mechanisms remain uncertain. We measured personal PM(2.5) and carbon black exposure in 50 students four times in 1 year and analyzed blood samples for markers of protein and lipid oxidation, for red blood cell (RBC) and platelet counts, and for concentrations of hemoglobin and fibrinogen. We analyzed protein oxidation in terms of gamma-glutamyl semialdehyde in hemoglobin (HBGGS) and 2-aminoadipic semialdehyde in hemoglobin (HBAAS) and plasma proteins (PLAAS), and lipid peroxidation was measured as malondialdehyde (MDA) in plasma. Median exposures were 16.1 micro g/m(3) for personal PM(2.5) exposure, 9.2 micro g/m(3) for background PM(2.5) concentration, and 8.1 X 10(-6)/m for personal carbon black exposure. Personal carbon black exposure and PLAAS concentration were positively associated (p < 0.01), whereas an association between personal PM(2.5) exposure and PLAAS was only of borderline significance (p = 0.061). A 3.7% increase in MDA concentrations per 10 micro g/m(3) increase in personal PM(2.5) exposure was found for women (p < 0.05), whereas there was no significant relationship for the men. Similarly, positive associations between personal PM(2.5)exposure and both RBC and hemoglobin concentrations were found only in women (p < 0.01). There were no significant relationships between background PM(2.5) concentration and any of the biomarkers. This suggests that exposure to particles in moderate concentrations can induce oxidative stress and increase RBCs in peripheral blood. Personal exposure appears more closely related to these biomarkers potentially related to cardiovascular disease than is ambient PM(2.5) background concentrations.

A study to characterize 1-hr multi-pollutant exposures was performed in Baltimore, MD, during the summer of 1998 and the winter of 1999, and was conducted over a 15-day period in each of the two seasons. Personal exposures were measured by a trained field technician, who wore a newly developed Roll-Around System (RAS) to measure 1-hr PM2 5 and gaseous (CO, O3, NO2, SO2, volatile organic compounds [VOCs]) exposures. One-hour O3, NO2, and SO2 personal exposures were measured using samplers developed in our laboratory, while short-term PM2.5, CO, and VOCs exposures were measured using currently available monitors. All 1-hr multi-pollutant exposures were measured while the technician performed pre-determined activities, beginning at 7:00 a.m. and ending at 7:00 p.m. of the same day. Activities were scripted to simulate activities performed by older adults (65+ years of age). Corresponding 1-hr ambient pollutant concentrations were obtained from federal or state monitoring networks. In this paper, we discuss the results from our study and present our descriptive analysis of the 1-hr personal particulate and gaseous exposure data. Personal PM2.5, O3, CO, and VOCs exposures showed substantial variability over the 12-hr sampling periods. Multiple pairwise comparison tests showed that 1-hr personal O3 exposures were significantly lower in indoor microenvironments as compared with outdoor microenvironments. One-hour personal CO exposures measured in vehicles were significantly higher than those measured in other microenvironments. The associations between 1-hr personal exposures and corresponding ambient concentrations differed by pollutant and by microenvironment. For example, the correlation between personal PM2.5 exposures and ambient concentrations was lowest (rs = 0.36, p < 0.05) in the winter for indoor non-residential microenvironments, and was highest (rs = 0.90, p < 0.05) in the winter for in-vehicle microenvi-ronments. For O3, the correlation between personal exposures and ambient levels was weakest in the winter for residential microenvironments (rs = 0.05, p > 0.05), and was strongest in the summer for outdoor near-roadway microenvironments (rs = 0.91, p < 0.05).

Characteristics and determinants of personal exposure to PM2.5 mass and components in adult subjects in the megacity of Guangzhou, China

Personal monitoring can estimate individuals' exposures to environmental pollutants; however, accuracy depends on consistent monitor wearing, which is under evaluated. To study the association between device wearing and personal air pollution exposure. Using personal device accelerometry data collected in the context of a randomized cooking intervention in Ghana with three study arms (control, improved biomass, and liquified petroleum gas (LPG) arms; N = 1414), we account for device wearing to infer parameters of PM2.5 and CO exposure. Device wearing was positively associated with exposure in the control and improved biomass arms, but weakly in the LPG arm. Inferred community-level air pollution was similar across study arms (~45 μg/m3). The estimated direct contribution of individuals' cooking to PM2.5 exposure was 64 μg/m3 for the control arm, 74 μg/m3 for improved biomass, and 6 μg/m3 for LPG. Arm-specific average PM2.5 exposure at near-maximum wearing was significantly lower in the LPG arm as compared to the improved biomass and control arms. Analysis of personal CO exposure mirrored PM2.5 results. Personal monitor wearing was positively associated with average air pollution exposure, emphasizing the importance of high device wearing during monitoring periods and directly assessing device wearing for each deployment. We demonstrate that personal monitor wearing data can be used to refine exposure estimates and infer unobserved parameters related to the timing and source of environmental exposures. In a cookstove trial among pregnant women, time-resolved personal air pollution device wearing data were used to refine exposure estimates and infer unobserved exposure parameters, including community-level air pollution, the direct contribution of cooking to personal exposure, and the effect of clean cooking interventions on personal exposure. For example, in the control arm, while average 48 h personal PM2.5 exposure was 77 μg/m3, average predicted exposure at near-maximum daytime device wearing was 108 μg/m3 and 48 μg/m3 at zero daytime device wearing. Wearing-corrected average 48 h personal PM2.5 exposures were 50% lower in the LPG arm than the control and improved biomass and inferred direct cooking contributions to personal PM2.5 from LPG were 90% lower than the other arms. Our recommendation is that studies assessing personal exposures should examine the direct association between device wearing and estimated mean personal exposure.

BackgroundEndotoxin exposure has been associated with asthma exacerbations and increased asthma prevalence. However, there is little data regarding personal exposure to endotoxin in children at risk, or the relation of personal endotoxin exposure to residential or ambient airborne endotoxin. The relation between personal endotoxin and personal air pollution exposures is also unknown.MethodsWe characterized personal endotoxin exposures in 45 school children with asthma ages 9-18 years using 376 repeated measurements from a PM2.5 active personal exposure monitor. We also assayed endotoxin in PM2.5 samples collected from ambient regional sites (N = 97 days) and from a subset of 12 indoor and outdoor subject home sites (N = 109 and 111 days, respectively) in Riverside and Whittier, California. Endotoxin was measured using the Limulus Amoebocyte Lysate kinetic chromogenic assay. At the same time, we measured personal, home and ambient exposure to PM2.5 mass, elemental carbon (EC), and organic carbon (OC). To assess exposure relations we used both rank correlations and mixed linear regression models, adjusted for personal temperature and relative humidity.ResultsWe found small positive correlations of personal endotoxin with personal PM2.5 EC and OC, but not personal PM2.5 mass or stationary site air pollutant measurements. Outdoor home, indoor home and ambient endotoxin were moderately to strongly correlated with each other. However, in mixed models, personal endotoxin was not associated with indoor home or outdoor home endotoxin, but was associated with ambient endotoxin. Dog and cat ownership were significantly associated with increased personal but not indoor endotoxin.ConclusionsDaily fixed site measurements of endotoxin in the home environment may not predict daily personal exposure, although a larger sample size may be needed to assess this. This conclusion is relevant to short-term exposures involved in the acute exacerbation of asthma.

Health Risk of Air Pollution Exposure to the Elderly in China

Personal exposures to particulate matter among children with asthma in Detroit, Michigan