Nasal oxidative stress mediating the effects of colder temperature exposure on pediatric asthma symptoms.

BACKGROUND: Colder temperature exposure is a known trigger for pediatric asthma exacerbation. The induction of oxidative stress is a known pathophysiologic pathway for asthma exacerbation. However, the role of oxidative stress in linking colder temperature exposure and worsened pediatric asthma symptoms is poorly understood. METHODS: In a panel study involving 43 children with asthma, aged 5-13 years old, each child was visited 4 times with a 2-week interval. At each visit, nasal fluid, urine, and saliva samples were obtained and measured for biomarkers of oxidative stress in the nasal cavity (nasal malondialdehyde [MDA]), the circulatory system (urinary MDA), and the oral cavity (salivary MDA). Childhood Asthma-Control Test (CACT) was used to assess asthma symptoms. RESULTS: When ambient daily-average temperature ranged from 7 to 18 °C, a 2 °C decrement in personal temperature exposures were significantly associated with higher nasal MDA and urinary MDA concentrations by 47-77% and 6-14%, respectively. We estimated that, of the decrease in child-reported CACT scores (indicating worsened asthma symptoms and asthma control) associated with colder temperature exposure, 14-57% were mediated by nasal MDA. CONCLUSION: These results suggest a plausible pathway that colder temperature exposure worsens pediatric asthma symptoms partly via inducing nasal oxidative stress. IMPACT: The role of oxidative stress in linking colder temperature exposure and worsened asthma symptoms is still poorly understood. Lower temperature exposure in a colder season was associated with higher nasal and systemic oxidative stress in children with asthma. Nasal MDA, a biomarker of nasal oxidative stress, mediated the associations between colder temperature exposures and pediatric asthma symptoms. The results firstly suggest a plausible pathway that colder temperature exposure worsens pediatric asthma symptoms partly via inducing oxidative stress in the nasal cavity.

Oral cavity response to air pollutant exposure and association with pulmonary inflammation and symptoms in asthmatic children.

Exposure to fine particulate matter (PM2.5) and ozone (O3) may lead to inflammation and oxidative damage in the oral cavity, which is hypothesized to contribute to the worsening of airway inflammation and asthma symptoms. In this panel study of 43 asthmatic children aged 5-13 years old, each child had 4 clinic visits with a 2-week interval between two consecutive visits. At each visit, saliva samples were collected and subsequently analyzed for interleukin 6 (IL-6) and eosinophil cationic protein (ECP) as biomarkers of inflammation and malondialdehyde (MDA) as a biomarker of oxidative stress in the oral cavity. At each visit, children were measured for fractional exhaled nitric oxide (FeNO) as a marker of pulmonary inflammation. Asthma symptoms of these children were measured using the Childhood Asthma Control Test (C-ACT). We found that an interquartile range (IQR) increase in 24-h average personal exposure to PM2.5 measured 1 and 2 days prior was associated with increased salivary IL-6 concentration by 3.0% (95%CI: 0.2%-6.0%) and 4.2% (0.7%-8.0%), respectively. However, we did not find a clear association between personal O3 exposure and any of the salivary biomarkers, except for a negative association between salivary MDA and O3 exposure measured 1 day prior. An IQR increase in salivary IL-6 concentration was associated with significantly increased FeNO by 28.8% (4.3%-53.4%). In addition, we found that increasing salivary IL-6 concentrations were associated with decreased individual and total C-ACT scores, indicating the worsening of asthma symptoms. We estimated that 13.2%-22.2% of the associations of PM2.5 exposure measured 1 day prior with FeNO and C-ACT scores were mediated by salivary IL-6. These findings suggest that the induction of inflammation in the oral cavity may have played a role in linking air pollution exposure with the worsening of airway inflammation and asthma symptoms.

Personal Exposure to PM2.5 Oxidative Potential in Association with Pulmonary Pathophysiologic Outcomes in Children with Asthma.

Fine particulate matter (PM2.5) with a higher oxidative potential has been thought to be more detrimental to pulmonary health. We aim to investigate the associations between personal exposure to PM2.5 oxidative potential and pulmonary outcomes in asthmatic children. We measured each of the 43 asthmatic children 4 times for airway mechanics, lung function, airway inflammation, and asthma symptom scores. Coupling measured indoor and outdoor concentrations of PM2.5 mass, constituents, and oxidative potential with individual time-activity data, we calculated 24 h average personal exposures 0-3 days prior to a health outcome measurement. We found that increases in daily personal exposure to PM2.5 oxidative potential were significantly associated with increased small, large, and total airway resistance, increased airway impedance, decreased lung function, and worsened scores of individual asthma symptoms and the total symptom score. Among the PM2.5 constituents, organic matters largely of indoor origin contributed the greatest to PM2.5 oxidative potential. Given that the variability in PM2.5 oxidative potential was a stronger driver than PM2.5 mass for the variability in the respiratory health outcomes, it is suggested to reduce PM2.5 oxidative potential, particularly by reducing the organic matter constituent of indoor PM2.5, as a targeted source control strategy in asthma management.

Chemical exposures from upholstered furniture with various flame retardant technologies.

Upholstered furniture is often manufactured with polyurethane foam (PUF) containing flame retardants (FRs) to prevent the risk of a fire and/or to meet flammability regulations, however, exposure to certain FRs and other chemicals have been linked to adverse health effects. This study developed a new methodology for evaluating volatile organic compound (VOC) and FR exposures to users of upholstered furniture by simulating use of a chair in a controlled exposure chamber and assessing the health significance of measured chemical exposure. Chairs with different fire-resistant technologies were evaluated for VOC and FR exposures via inhalation, ingestion, and dermal contact exposure routes. Data show that VOC exposure levels are lower than threshold levels defined by the US and global indoor air criteria. Brominated FRs were not detected from the studied chairs. The organophosphate FRs added to PUF were released into the surrounding air (0.4 ng/m3 ) and as dust (16 ng/m2 ). Exposure modeling showed that adults are exposed to FRs released from upholstered furniture mostly by dermal contact and children are exposed via dermal and ingestion exposure. Children are most susceptible to FR exposure/dose (2 times higher average daily dose than adults) due to their frequent hand to mouth contact.

Real-time measurements of PM2.5 and ozone to assess the effectiveness of residential indoor air filtration in Shanghai homes.

Portable air cleaners are increasingly used in polluted areas in an attempt to reduce human exposure; however, there has been limited work characterizing their effectiveness at reducing exposure. With this in mind, we recruited forty-three children with asthma from suburban Shanghai and deployed air cleaners (with HEPA and activated carbon filters) in their bedrooms. During both 2-week filtration and non-filtration periods, low-cost PM2.5 and O3 air monitors were used to measure pollutants indoors, outdoors, and for personal exposure. Indoor PM2.5 concentrations were reduced substantially with the use of air cleaners, from 34 ± 17 to 10 ± 8 µg/m3 , with roughly 80% of indoor PM2.5 estimated to come from outdoor sources. Personal exposure to PM2.5 was reduced from 40 ± 17 to 25 ± 14 µg/m3 . The more modest reductions in personal exposure and high contribution of outdoor PM2.5 to indoor concentrations highlight the need to reduce outdoor PM2.5 and/or to clean indoor air in multiple locations. Indoor O3 concentrations were generally low (mean = 8±4 ppb), and no significant difference was seen by filtration status. The concentrations of pollutants and the air cleaner effectiveness were highly variable over time and across homes, highlighting the usefulness of real-time air monitors for understanding individual exposure reduction strategies.

Malondialdehyde in Nasal Fluid: A Biomarker for Monitoring Asthma Control in Relation to Air Pollution Exposure.

Fine particulate matter (PM2.5) and ozone (O3) may exert oxidative damage in the nose, which is hypothesized to be associated with worsened asthma symptoms. This study, hence, is to explore whether an oxidative stress biomarker, malondialdehyde (MDA) in the nasal fluid, has the potential to aid personalized asthma control. In a panel study of 43 asthmatic children, 5-13 years old, each child was measured 4 times with a 2-week interval between consecutive clinic visits. At each visit, nasal fluid and urine samples were collected, and fractional exhaled nitric oxide (FeNO) was measured as a biomarker of pulmonary inflammation. In addition to nasal MDA, urinary MDA and 8-hydroxy-2'-deoxyguanosine (8-OHdG) were measured as biomarkers of systemic oxidative stress. We also assessed asthma symptoms using the Childhood Asthma-Control Test (C-ACT). We found that interquartile range (IQR) increases in 24 h average personal PM2.5 exposure (22.2-33.5 µg/m3), estimated 0 to 5 days prior to a clinic visit, were associated with increased nasal MDA concentrations by 38.6-54.9%. Similarly, IQR increases in 24 h average personal O3 exposure (7.7-8.2 ppb) estimated 2 to 4 days prior were associated with increased nasal MDA by 22.1-69.4%. Only increased PM2.5 exposure was associated with increased FeNO. Increased nasal MDA concentration was associated with decreased total and individual C-ACT scores, indicating worsening of asthma symptoms. However, no significant associations were observed between urinary MDA or 8-OHdG and C-ACT scores. The results confirm that oxidative stress plays an important role in linking air pollution exposure and adverse respiratory health effects. These findings support that MDA in the nasal fluid may serve as a useful biomarker for monitoring asthma status, especially in relation to PM2.5 and O3 exposures, two known risk factors of asthma exacerbation.

The impact of household air cleaners on the oxidative potential of PM2.5 and the role of metals and sources associated with indoor and outdoor exposure.

The health effects associated with human exposure to airborne fine particulate matter (PM2.5) have been linked to the ability of PM2.5 to facilitate the production of excess cellular reactive oxygen species (oxidative potential). Concern about the adverse human health impacts of PM2.5 has led to the increased use of indoor air cleaners to improve indoor air quality, which can be an important environment for PM2.5 exposure. However, the degree to which the oxidative potential of indoor and personal PM2.5 can be influenced by an indoor air cleaner remains unclear. In this study we enrolled 43 children with physician diagnosed asthma in suburban Shanghai, China and collected two paired-sets of 48-h indoor, outdoor, and personal PM2.5 exposure samples. One set of samples was collected under "real filtration" during which a functioning air cleaner was installed in the child's bedroom, and the other ("false filtration") with an air cleaner without internal filters. The PM2.5 samples were characterized by inductively coupled plasma mass spectroscopy for elements, and by an alveolar macrophage assay for oxidative potential. The sources of metals contributing to our samples were determined by the EPA Positive Matrix Factorization model. The oxidative potential was lower under real filtration compared to sham for indoor (median real/sham ratio: 0.260) and personal exposure (0.813) samples. Additionally, the sources of elements in PM2.5 that were reduced indoors and personal exposure samples by the air cleaner (e.g. regional aerosol and roadway emissions) were found by univariate multiple regression models to be among those contributing to the oxidative potential of the samples. An IQR increase in the regional aerosol and roadway emissions sources was associated with a 107% (95% CI: 80.1-138%) and 38.1% (17.6-62.1%) increase in measured oxidative potential respectively. Our results indicate that indoor air cleaners can reduce the oxidative potential of indoor and personal exposure to PM2.5, which may lead to improved human health.

Chemical Composition and Toxicity of Particles Emitted from a Consumer-Level 3D Printer Using Various Materials.

Consumer-level 3D printers emit ultrafine and fine particles, though little is known about their chemical composition or potential toxicity. We report chemical characteristics of the particles in comparison to raw filaments and assessments of particle toxicity. Particles emitted from polylactic acid (PLA) appeared to be largely composed of the bulk filament material with mass spectra similar to the PLA monomer spectra. Acrylonitrile butadiene styrene (ABS), extruded at a higher temperature than PLA, emitted vastly more particles and their composition differed from that of the bulk filament, suggesting that trace additives may control particle formation. In vitro cellular assays and in vivo mice exposure all showed toxic responses when exposed to PLA and ABS-emitted particles, where PLA-emitted particles elicited higher response levels than ABS-emitted particles at comparable mass doses. A chemical assay widely used in ambient air-quality studies showed that particles from various filament materials had comparable particle oxidative potentials, slightly lower than those of ambient particulate matter (PM2.5). However, particle emissions from ABS filaments are likely more detrimental when considering overall exposure due to much higher emissions. Our results suggest that 3D printer particle emissions are not benign and exposures should be minimized.

Real-Time Exposure to 3D-Printing Emissions Elicits Metabolic and Pro-Inflammatory Responses in Human Airway Epithelial Cells.

Three-dimensional (3D) printer usage in household and school settings has raised health concerns regarding chemical and particle emission exposures during operation. Although the composition of 3D printer emissions varies depending on printer settings and materials, little is known about the impact that emissions from different filament types may have on respiratory health and underlying cellular mechanisms. In this study, we used an in vitro exposure chamber system to deliver emissions from two popular 3D-printing filament types, acrylonitrile butadiene styrene (ABS) and polylactic acid (PLA), directly to human small airway epithelial cells (SAEC) cultured in an air-liquid interface during 3D printer operation. Using a scanning mobility particle sizer (SMPS) and an optical particle sizer (OPS), we monitored 3D printer particulate matter (PM) emissions in terms of their particle size distribution, concentrations, and calculated deposited doses. Elemental composition of ABS and PLA emissions was assessed using scanning electron microscopy coupled with energy dispersive X-ray spectroscopy (SEM-EDX). Finally, we compared the effects of emission exposure on cell viability, inflammation, and metabolism in SAEC. Our results reveal that, although ABS filaments emitted a higher total concentration of particles and PLA filaments emitted a higher concentration of smaller particles, SAEC were exposed to similar deposited doses of particles for each filament type. Conversely, ABS and PLA emissions had distinct elemental compositions, which were likely responsible for differential effects on SAEC viability, oxidative stress, release of inflammatory mediators, and changes in cellular metabolism. Specifically, while ABS- and PLA-emitted particles both reduced cellular viability and total glutathione levels in SAEC, ABS emissions had a significantly greater effect on glutathione relative to PLA emissions. Additionally, pro-inflammatory cytokines including IL-1ß, MMP-9, and RANTES were significantly increased due to ABS emissions exposure. While IL-6 and IL-8 were stimulated in both exposure scenarios, VEGF was exclusively increased due to PLA emissions exposures. Notably, ABS emissions induced metabolic perturbation on amino acids and energy metabolism, as well as redox-regulated pathways including arginine, methionine, cysteine, and vitamin B3 metabolism, whereas PLA emissions exposures caused fatty acid and carnitine dysregulation. Taken together, these results advance our mechanistic understanding of 3D-printer-emissions-induced respiratory toxicity and highlight the role that filament emission properties may play in mediating different respiratory outcomes.

Exposure hazards of particles and volatile organic compounds emitted from material extrusion 3D printing: Consolidation of chamber study data.

Ultrafine particles and volatile organic compounds (VOCs) have been detected from material extrusion 3D printing, which is widely used in non-industrial environments. This study consolidates data of 447 particle emission and 58 VOC emission evaluations from a chamber study using a standardized testing method with various 3D printing scenarios. The interquartile ranges of the observed emission rates were 109-1011 #/h for particles and 0.2-1.0 mg/h for total VOC. Print material contributed largely to the variations of particle and total VOC emissions and determined the most abundantly emitted VOCs. Printing conditions and filament specifications, included printer brand, print temperature and speed, build plate heating setup, filament brand, color and composite, also affected emissions and resulted in large variations observed in emission profiles. Multiple regression showed that particle emissions were more impacted by various print conditions than VOC emissions. According to indoor exposure modeling, personal and residential exposure scenarios were more likely to result in high exposure levels, often exceeding recommended exposure limits. Hazardous VOCs commonly emitted from 3D printing included aromatics, aldehydes, alcohols, ketones, esters and siloxanes, among which were various carcinogens, irritants and developmental and reproductive toxins. Therefore, 3D printing emits a complex mixture of ultrafine particles and various hazardous chemicals, exposure to which may exceed recommended exposure limits and potentially induce acute, chronic, or developmental health effects for users depending on exposure scenarios.

Characterization of an Electronic Nicotine Delivery System (ENDS) Aerosol Generation Platform to Determine Exposure Risks.

Evaluating vaping parameters that influence electronic nicotine delivery system (ENDS) emission profiles and potentially hazardous exposure levels is essential to protecting human health. We developed an automated multi-channel ENDS aerosol generation system (EAGS) for characterizing size-resolved particle emissions across pod- and mod-type devices using real-time monitoring instruments, an exposure chamber, and vaping parameters including different ventilation rates, device type and age, e-liquid formulation, and atomizer setup. Results show the ENDS device type, e-liquid flavoring, and nicotine content can affect particle emissions. In general, pod-type devices have unimodal particle size distributions and higher number emissions, while mod-type devices have bimodal size distributions and higher mass emissions. For pod-type devices, later puff fractions emit lower aerosols, which is potentially associated with the change of coil resistance and power during ageing. For a mod-type device, an atomizer with a lower resistance coil and higher power generates larger particle emissions than an atomizer with a greater resistance coil and lower power. The unventilated scenario produces higher particle emission factors, except for particle mass emission from pod-type devices. The data provided herein indicate the EAGS can produce realistic and reproducible puff profiles of pod- and mod-type ENDS devices and therefore is a suitable platform for characterizing ENDS-associated exposure risks.

Toxicological Assessment of Particulate and Metal Hazards Associated with Vaping Frequency and Device Age.

Electronic nicotine delivery systems (ENDS) aerosols are complex mixtures of chemicals, metals, and particles that may present inhalation hazards and adverse respiratory health risks. Despite being considered a safer alternative to tobacco cigarettes, metal exposure levels and respiratory effects associated with device aging and vaping frequency have not been fully characterized. In this study, we utilize an automated multi-channel ENDS aerosol generation system (EAGS) to generate aerosols from JUUL pod-type ENDS using tobacco-flavored e-liquid. Aerosol puff fractions (1-50) and (101-150) are monitored and sampled using various collection media. Extracted aerosols are prepared for metal and toxicological analysis using human primary small airway epithelial cells (SAEC). ENDS aerosol-mediated cellular responses, including reactive oxygen species (ROS), oxidative stress, cell viability, and DNA damage, are evaluated after 24 h and 7-day exposures. Our results show higher particle concentrations in later puff fractions (0.135 mg/m3) than in initial puff fractions (0.00212 mg/m3). Later puff fraction aerosols contain higher toxic metal concentrations, including chromium, copper, and lead, which elicit increased levels of ROS followed by significant declines in total glutathione and cell viability. Notably, a 30% increase in DNA damage was observed after 7 days because of later puff fraction exposures. This work is consistent with ENDS aerosols becoming more hazardous across the use of pre-filled pod devices, which may threaten respiratory health.

Metal compositions of particle emissions from material extrusion 3D printing: Emission sources and indoor exposure modeling.

Material extrusion 3D printing has been widely used in industrial, educational and residential environments, while its exposure health impacts have not been well understood. High levels of ultrafine particles are found being emitted from 3D printing and could pose a hazard when inhaled. However, metals that potentially transfer from filament additives to emitted particles could also add to the exposure hazard, which have not been well characterized for their emissions. This study analyzed metal (and metalloid) compositions of raw filaments and in the emitted particles during printing; studied filaments included pure polymer filaments with metal additives and composite filaments with and without metal powder. Our chamber study found that crustal metals tended to have higher partitioning factors from filaments to emitted particles; silicon was the most abundant element in emitted particles and had the highest yield per filament mass. However, bronze and stainless-steel powder added in composite filaments were less likely to transfer from filament to particle. For some cases, boron, arsenic, manganese, and lead were only detected in particles, which indicated external sources, such as the printers themselves. Heavy metals with health concerns were also detected in emitted particles, while their estimated exposure concentrations in indoor air were below air quality standards and occupational regulations. However, total particle exposure concentrations estimated for indoor environments could exceed ambient air fine particulate standards.

Association between Childhood Asthma Control Test scores and lung pathophysiologic indicators in longitudinal measurements.

Background: Childhood Asthma Control Test (C-ACT) is a well-validated questionnaire for asthma controls among 4-11 years old children. This study aims to examine if longitudinal C-ACT score changes could also reflect lung pathophysiologic changes. Methods: Thirty-seven children (43% female) aged 5 to 10 years old with mild or moderate asthma were followed up for 6 weeks with bi-weekly assessments of C-ACT, airway mechanics, lung function and respiratory inflammation. Associations of longitudinal changes in C-ACT score with lung pathophysiologic indicators were evaluated using linear mixed-effects models. Results: A two-point worsening of total C-ACT score (sum of child and caregiver-reported) was associated with significant decreases in forced expiratory volume during the 1st second (FEV1) by 1.7% (P=0.04) and forced vital capacity (FVC) by 1.6% (P=0.01) and increased total airway resistance [airway resistance at 5 Hz (R5)] by 3.8% (P=0.05). A two-point worsening in child-reported score was significantly associated with 3.1% and 2.5% reductions in FEV1 and FVC, respectively, and with increases in R5 by 6.5% and large airway resistance [airway resistance at 20 Hz (R20)] by 5.5%. In contrast, a two-point worsening of caregiver-reported score was associated with none of the concurrent lung pathophysiologic measurements. Worsening of total C-ACT score was significantly associated with increased respiratory inflammation [fractional exhaled nitric oxide (FeNO)] in a subset (n=23) of children without eosinophilic airway inflammation. C-ACT scores were associated with none of the small airway measures. Conclusions: In children with mild or moderate asthma, longitudinal C-ACT score changes could reflect acute changes in large airway resistance and lung function. Measures of small airway physiology would provide valuable complementary information for asthma control. Asthma phenotype may affect whether C-ACT score could reflect respiratory inflammation.

Associations between personal apparent temperature exposures and asthma symptoms in children with asthma.

Ambient temperature and relative humidity can affect asthma symptoms. Apparent temperature is a measure of temperature perceived by humans that takes into account the effect of humidity. However, the potential link between personal exposures to apparent temperature and asthma symptoms has not been investigated. We conducted a panel study of 37 asthmatic children, aged 5-11 years, during an early spring season (average daily ambient temperature: 14°C, range: 7-18°C). Asthma symptoms were measured 4 times for each participant with a 2-week interval between consecutive measurements using the Childhood Asthma-Control Test (C-ACT). Average, minimum, and maximum personal apparent temperature exposures, apparent temperature exposure variability (TV), and average ambient temperature were calculated for the 12 hours, 24 hours, week, and 2 weeks prior to each visit. We found that a 10°C lower in 1-week and 2-week average & minimum personal apparent temperature exposures, TV, and average ambient temperature exposures were significantly associated with lower total C-ACT scores by up to 2.2, 1.4, 3.3, and 1.4 points, respectively, indicating worsened asthma symptoms. Our results support that personal apparent temperature exposure is potentially a stronger driver than ambient temperature exposures for the variability in asthma symptom scores. Maintaining a proper personal apparent temperature exposure could be an effective strategy for personalized asthma management.

Role of endogenous melatonin in pathophysiologic and oxidative stress responses to personal air pollutant exposures in asthmatic children.

BACKGROUND: Heightening oxidative stress and inflammation is an important pathophysiological mechanism underlying air pollution health effects in people with asthma. Melatonin can suppress oxidative stress and inflammation in pulmonary and circulatory systems. However, the role of melatonin in the oxidative stress and physiological responses to air pollution exposure has not been examined in children with asthma. METHODS: In this panel study of 43 asthmatic children (5-13 years old), each child had 4 clinic visits with a 2-week interval between two consecutive visits. At each visit, urine samples were collected and subsequently analyzed for 6-sulfatoxymelatonin (aMT6s) as a surrogate of circulating melatonin and for malondialdehyde (MDA) and 8-hydroxy-2'-deoxyguanosine (8-OHdG) as two biomarkers of systemic oxidative stress. At each clinic visit, children were measured for pulmonary function and fractional exhaled nitric oxide (FeNO, a marker of pulmonary inflammation). None of the children reported to have taking melatonin supplementation. Concentrations of indoor and ambient PM2.5 and ozone (O3) were combined with individual time-activity data to calculate personal air pollutant exposures. RESULTS: We found that interquartile range increases in urinary MDA and 8-OHdG concentrations were associated with significantly increased urinary aMT6s concentrations by 73.4% (95% CI: 52.6% to 97.0%) and 41.7% (22.8% to 63.4%), respectively. Increases in daily personal exposure to O3 and to PM2.5 were each associated with increased urinary aMT6s concentrations. Increasing urinary aMT6s concentrations were associated with decreased FeNO and resonant frequency, indicating improved airway inflammation and lung elasticity, respectively. CONCLUSION: The results suggest that systemic oxidative stress heightened by air pollution exposure may stimulate melatonin excretion as a defense mechanism to alleviate the adverse effects.

Children's microenvironmental exposure to PM2.5 and ozone and the impact of indoor air filtration.

BACKGROUND: In highly polluted urban areas, personal exposure to PM2.5 and O3 occur daily in various microenvironments. Identifying which microenvironments contribute most to exposure can pinpoint effective exposure reduction strategies and mitigate adverse health impacts. METHODS: This work uses real-time sensors to assess the exposures of children with asthma (N = 39) in Shanghai, quantifying microenvironmental exposure to PM2.5 and O3. An air cleaner was deployed in participants' bedrooms where we hypothesized exposure could be most efficiently reduced. Monitoring occurred for two 48-h periods: one with bedroom filtration (portable air cleaner with HEPA and activated carbon filters) and the other without. RESULTS: Children spent 91% of their time indoors with the majority spent in their bedroom (47%). Without filtration, the bedroom and classroom environments were the largest contributors to PM2.5 exposure. With filtration, bedroom PM2.5 exposure was reduced by 75% (45% of total exposure). Although filtration status did not impact O3, the largest contribution of O3 exposure also came from the bedroom. CONCLUSIONS: Actions taken to reduce bedroom PM2.5 and O3 concentrations can most efficiently reduce total exposure. As real-time pollutant monitors become more accessible, similar analyses can be used to evaluate new interventions and optimize exposure reductions for a variety of populations.

Associations of personal exposure to air pollutants with airway mechanics in children with asthma.

BACKGROUND: The importance of airway mechanics has been increasingly recognized in pediatric asthma. However, no studies have examined responses of airway mechanics to air pollution exposure in asthmatic children. METHODS: In this panel study involving indoor air filtration manipulation that created a large gradient of personal exposure to PM2.5, the airway mechanics and lung function of 43 asthmatic children 5-13 years old in a suburb of Shanghai were measured four times within 3 consecutive months. Concentrations of indoor and outdoor PM2.5 and ozone were coupled with individual time-activity data to calculate personal exposures. Linear mixed effects models were used to examine the relationships of personal exposure with indicators of airway mechanics and lung function, respectively. RESULTS: An interquartile range (IQR) increase in 24-hour average PM2.5 personal exposure (30.3 µg/m3) in the prior day was associated with significant increases in small airway resistance (R5-R20) of 15.8%, total airway resistance (R5) of 6.3%, and airway inflammation (FeNO) of 9.6%. These associations were stronger in children with lower blood eosinophil counts (<450/µL). No significant associations were found between personal PM2.5 exposure and lung function. Low-level ozone exposure (daily maximum 8-hour exposure range 1.1-56.4 ppb) was not significantly associated with any of the outcomes. CONCLUSION: Changes in personal PM2.5 exposure, partly enhanced by air filtration, were associated with significant changes in airway resistance and inflammation in children with asthma. These findings suggest the importance of reducing PM2.5 exposure, via personal air quality management, in improving airflow limitation in the airways, especially the small airways.