The relative importance of tailpipe and non-tailpipe emissions on the oxidative potential of ambient particles in Los Angeles, CA.

This study examines the associations between the oxidative potential of ambient PM2.5 and PM0.18, measured by means of the dithiothreitol (DTT) assay, and their chemical constituents and modeled sources. Particulate matter (PM) samples were collected from 2012-2013 in Central Los Angeles (LA) and 2013-2014 in Anaheim, California, USA. Detailed chemical analyses of the PM samples, including carbonaceous species, inorganic elements and water-soluble ions, were conducted. Univariate analysis indicated a high correlation (R > 0.60) between the DTT activity and the concentrations of carbonaceous species at both sites. The strongest correlations were observed between DTT and organic tracers of primary vehicle tailpipe emissions including polycyclic aromatic hydrocarbons (PAHs) and hopanes as well as EC, with higher correlations for PM0.18versus PM2.5 components. Moreover, metals and trace elements (e.g., Ba, Cu, Fe, Mn, Pb and Sb) in both size ranges were also associated with DTT activity. Multiple linear regression (MLR) analysis was performed on DTT activity and PM sources identified by a Molecular Marker-Chemical Mass Balance (MM-CMB) model (i.e. major carbonaceous sources: vehicle tailpipe emissions, wood smoke, primary biogenic and secondary organic carbon) together with other typical sources of ambient PM (i.e. crustal material, vehicular abrasion, secondary ions and sea salt). Overall, our findings illustrate the relative importance of different traffic sources on the oxidative potential of ambient PM. Despite major reductions of tailpipe emissions, the lack of similar reductions (and possibly an increase) in non-tailpipe emissions makes them an important source of traffic-related PM in Los Angeles and their increasing role in the overall PM toxicity raises concerns for public health.

Associations of oxidative stress and inflammatory biomarkers with chemically-characterized air pollutant exposures in an elderly cohort.

BACKGROUND: Exposure to air pollution has been associated with cardiorespiratory morbidity and mortality. However, the chemical constituents and pollution sources underlying these associations remain unclear. METHOD: We conducted a cohort panel study involving 97 elderly subjects living in the Los Angeles metropolitan area. Airway and circulating biomarkers of oxidative stress and inflammation were measured weekly over 12 weeks and included, exhaled breath condensate malondialdehyde (EBC MDA), fractional exhaled nitric oxide (FeNO), plasma oxidized low-density lipoprotein (oxLDL), and plasma interleukin-6 (IL-6). Exposures included 7-day personal nitrogen oxides (NOx), daily criteria-pollutant data, five-day average particulate matter (PM) measured in three size-fractions and characterized by chemical components including transition metals, and in vitro PM oxidative potential (dithiothreitol and macrophage reactive oxygen species). Associations between biomarkers and pollutants were assessed using linear mixed effects regression models. RESULTS: We found significant positive associations of airway oxidative stress and inflammation with traffic-related air pollutants, ultrafine particles and transition metals. Positive but nonsignificant associations were observed with PM oxidative potential. The strongest associations were observed among PM variables in the ultrafine range (PM <0.18µm). It was estimated that an interquartile increase in 5-day average ultrafine polycyclic aromatic hydrocarbons was associated with a 6.3% (95% CI: 1.1%, 11.6%) increase in EBC MDA and 6.7% (95% CI: 3.4%, 10.2%) increase in FeNO. In addition, positive but nonsignificant associations were observed between oxLDL and traffic-related pollutants, ultrafine particles and transition metals while plasma IL-6 was positively associated with 1-day average traffic-related pollutants. CONCLUSION: Our results suggest that exposure to pollutants with high oxidative potential (traffic-related pollutants, ultrafine particles, and transition metals) may lead to increased airway oxidative stress and inflammation in elderly adults. This observation was less clear with circulating biomarkers.

Associations between microvascular function and short-term exposure to traffic-related air pollution and particulate matter oxidative potential.

BACKGROUND: Short-term exposure to ambient air pollution has been associated with acute increases in cardiovascular hospitalization and mortality. However, causative chemical components and underlying pathophysiological mechanisms remain to be clarified. We hypothesized that endothelial dysfunction would be associated with mobile-source (traffic) air pollution and that pollutant components with higher oxidative potential to generate reactive oxygen species (ROS) would have stronger associations. METHODS: We carried out a cohort panel study in 93 elderly non-smoking adults living in the Los Angeles metropolitan area, during July 2012-February 2014. Microvascular function, represented by reactive hyperemia index (RHI), was measured weekly for up to 12 weeks (N = 845). Air pollutant data included daily data from regional air-monitoring stations, five-day average PM chemical components and oxidative potential in three PM size-fractions, and weekly personal nitrogen oxides (NOx). Linear mixed-effect models estimated adjusted changes in microvascular function with exposure. RESULTS: RHI was inversely associated with traffic-related pollutants such as ambient PM2.5 black carbon (BC), NOx, and carbon monoxide (CO). An interquartile range change increase (1.06 µg/m(3)) in 5-day average BC was associated with decreased RHI, -0.093 (95 % CI: -0.151, -0.035). RHI was inversely associated with other mobile-source components/tracers (polycyclic aromatic hydrocarbons, elemental carbon, and hopanes), and PM oxidative potential as quantified in two independent assays (dithiothreitol and in vitro macrophage ROS) in accumulation and ultrafine PM, and transition metals. CONCLUSIONS: Our findings suggest that short-term exposures to traffic-related air pollutants with high oxidative potential are major components contributing to microvascular dysfunction.

Relations of exhaled nitric oxide and FEV1 to personal endotoxin exposure in schoolchildren with asthma.

BACKGROUND: Asthma prevalence and acute exacerbations have been associated with endotoxin exposure. However, there are limited data on relations between acute asthma outcomes in children and personal exposure to endotoxin or whether this relation is modified by personal air pollution exposures. METHODS: We made repeated measurements of the fractional concentration of exhaled NO (FeNO), forced expiratory volume in 1 s (FEV1) and personal endotoxin exposures in patients with persistent asthma aged 9-18 years, each of whom was followed for 10 consecutive days in Riverside and Whittier, California. Endotoxin was measured in PM2.5, and simultaneously we measured personal exposure to air pollutants: NO2 and PM2.5 mass, elemental carbon and organic carbon. Endotoxin exposure-response relations and interactions between endotoxin and air pollutants were analysed with mixed models controlling for personal temperature, humidity and the 10-day period. RESULTS: Neither percent-predicted FEV1 nor FeNO was associated with personal endotoxin overall; however, endotoxin was associated with FEV1 among patients with average percent-predicted FEV1<80%. When NO2 was above its median, FeNO increased by 2.2% (95% CI -0.8% to 5.2%) for an interquartile increase in personal endotoxin, whereas FeNO was lower by -1.8% (95% CI -4% to 0.5%) when NO2 was≤its median. However, this is out of 12 interaction tests between personal endotoxin and a binary air pollutant for each outcome (FEV1 and FeNO), and there were no interactions with any continuous-scaled pollutant. CONCLUSIONS: Personal endotoxin exposure was not associated with acute daily changes in FeNO or FEV1 in a cohort panel of schoolchildren with asthma, except for decreased FEV1 among patients with more severe asthma (percent-predicted FEV1<80%). There was limited evidence of effect modification of endotoxin by personal exposure to air pollution.

Asthma morbidity and ambient air pollution: effect modification by residential traffic-related air pollution.

BACKGROUND: Ambient air pollution has been associated with asthma-related hospital admissions and emergency department visits (hospital encounters). We hypothesized that higher individual exposure to residential traffic-related air pollutants would enhance these associations. METHODS: We studied 11,390 asthma-related hospital encounters among 7492 subjects 0-18 years of age living in Orange County, California. Ambient exposures were measured at regional air monitoring stations. Seasonal average traffic-related exposures (PM2.5, ultrafine particles, NOx, and CO) were estimated near subjects' geocoded residences for 6-month warm and cool seasonal periods, using dispersion models based on local traffic within 500 m radii. Associations were tested in case-crossover conditional logistic regression models adjusted for temperature and humidity. We assessed effect modification by seasonal residential traffic-related air pollution exposures above and below median dispersion-modeled exposures. Secondary analyses considered effect modification by traffic exposures within race/ethnicity and insurance group strata. RESULTS: Asthma morbidity was positively associated with daily ambient O3 and PM2.5 in warm seasons and with CO, NOx, and PM2.5 in cool seasons. Associations with CO, NOx, and PM2.5 were stronger among subjects living at residences with above-median traffic-related exposures, especially in cool seasons. Secondary analyses showed no consistent differences in association, and 95% confidence intervals were wide, indicating a lack of precision for estimating these highly stratified associations. CONCLUSIONS: Associations of asthma with ambient air pollution were enhanced among subjects living in homes with high traffic-related air pollution. This may be because of increased susceptibility (greater asthma severity) or increased vulnerability (meteorologic amplification of local vs. correlated ambient exposures).

Modeling the concentrations of on-road air pollutants in southern California.

High concentrations of air pollutants on roadways, relative to ambient concentrations, contribute significantly to total personal exposure. Estimation of these exposures requires measurements or prediction of roadway concentrations. Our study develops, compares, and evaluates linear regression and nonlinear generalized additive models (GAMs) to estimate on-road concentrations of four key air pollutants, particle-bound polycyclic aromatic hydrocarbons (PB-PAH), particle number count (PNC), nitrogen oxides (NOx), and particulate matter with diameter <2.5 µm (PM2.5) using traffic, meteorology, and elevation variables. Critical predictors included wind speed and direction for all the pollutants, traffic-related variables for PB-PAH, PNC, and NOx, and air temperatures and relative humidity for PM2.5. GAMs explained 50%, 55%, 46%, and 71% of the variance for log or square-root transformed concentrations of PB-PAH, PNC, NOx, and PM2.5, respectively, an improvement of 5% to over 15% over the linear models. Accounting for temporal autocorrelation in the GAMs further improved the prediction, explaining 57-89% of the variance. We concluded that traffic and meteorological data are good predictors in estimating on-road traffic-related air pollutant concentrations and GAMs perform better for nonlinear variables, such as meteorological parameters.

Travel patterns during pregnancy: comparison between Global Positioning System (GPS) tracking and questionnaire data.

BACKGROUND: Maternal exposures to traffic-related air pollution have been associated with adverse pregnancy outcomes. Exposures to traffic-related air pollutants are strongly influenced by time spent near traffic. However, little is known about women's travel activities during pregnancy and whether questionnaire-based data can provide reliable information on travel patterns during pregnancy. OBJECTIVES: Examine women's in-vehicle travel behavior during pregnancy and examine the difference in travel data collected by questionnaire and global positioning system (GPS) and their potential for exposure error. METHODS: We measured work-related travel patterns in 56 pregnant women using a questionnaire and one-week GPS tracking three times during pregnancy (<20 weeks, 20-30 weeks, and >30 weeks of gestation). We compared self-reported activities with GPS-derived trip distance and duration, and examined potentially influential factors that may contribute to differences. We also described in-vehicle travel behavior by pregnancy periods and influences of demographic and personal factors on daily travel times. Finally, we estimated personal exposure to particle-bound polycyclic aromatic hydrocarbon (PB-PAH) and examined the magnitude of exposure misclassification using self-reported vs. GPS travel data. RESULTS: Subjects overestimated both trip duration and trip distance compared to the GPS data. We observed moderately high correlations between self-reported and GPS-recorded travel distance (home to work trips: r = 0.88; work to home trips: r = 0.80). Better agreement was observed between the GPS and the self-reported travel time for home to work trips (r = 0.77) than work to home trips (r = 0.64). The subjects on average spent 69 and 93 minutes traveling in vehicles daily based on the GPS and self-reported data, respectively. Longer daily travel time was observed among participants in early pregnancy, and during certain pregnancy periods in women with higher education attainment, higher income, and no children. When comparing self-reported vs. GPS data, we found that estimated personal exposure to PB-PAH did not differ remarkably at the population level, but the difference was large at an individual level. CONCLUSION: Self-reported home-to-work data overestimated both trip duration and trip distance compared to GPS data. Significant differences in PAH exposure estimates were observed at individual level using self-reported vs. GPS data, which has important implications in air pollution epidemiological studies.

Glutathione peroxidase inhibitory assay for electrophilic pollutants in diesel exhaust and tobacco smoke.

We developed a rapid kinetic bioassay demonstrating the inhibition of glutathione peroxidase 1 (GPx-1) by organic electrophilic pollutants, such as acrolein, crotonaldehyde, and p-benzoquinone, that are frequently found as components of tobacco smoke, diesel exhaust, and other combustion sources. In a complementary approach, we applied a high-resolution proton-transfer reaction time-of-flight mass spectrometer to monitor in real-time the generation of electrophilic volatile carbonyls in cigarette smoke. The new bioassay uses the important antioxidant selenoenzyme GPx-1, immobilized to 96-well microtiter plates, as a probe. The selenocysteine bearing subunits of the enzyme's catalytic site are viewed as cysteine analogues and are vulnerable to electrophilic attack by compounds with conjugated carbonyl systems. The immobilization of GPx-1 to microtiter plate wells enabled facile removal of excess reactive inhibitory compounds after incubation with electrophilic chemicals or aqueous extracts of air samples derived from different sources. The inhibitory response of cigarette smoke and diesel exhaust particle extracts were compared with chemical standards of a group of electrophilic carbonyls and the arylating p-benzoquinone. GPx-1 activity was directly inactivated by millimolar concentrations of highly reactive electrophilic chemicals (including acrolein, glyoxal, methylglyoxal, and p-benzoquinone) and extracts of diesel and cigarette smoke. We conclude that the potential of air pollutant components to generate oxidative stress may be, in part, a result of electrophile-derived covalent modifications of enzymes involved in the cytosolic antioxidant defense.

Modeling personal particle-bound polycyclic aromatic hydrocarbon (pb-pah) exposure in human subjects in Southern California.

BACKGROUND: Exposure to polycyclic aromatic hydrocarbon (PAH) has been linked to various adverse health outcomes. Personal PAH exposures are usually measured by personal monitoring or biomarkers, which are costly and impractical for a large population. Modeling is a cost-effective alternative to characterize personal PAH exposure although challenges exist because the PAH exposure can be highly variable between locations and individuals in non-occupational settings. In this study we developed models to estimate personal inhalation exposures to particle-bound PAH (PB-PAH) using data from global positioning system (GPS) time-activity tracking data, traffic activity, and questionnaire information. METHODS: We conducted real-time (1-min interval) personal PB-PAH exposure sampling coupled with GPS tracking in 28 non-smoking women for one to three sessions and one to nine days each session from August 2009 to November 2010 in Los Angeles and Orange Counties, California. Each subject filled out a baseline questionnaire and environmental and behavior questionnaires on their typical activities in the previous three months. A validated model was used to classify major time-activity patterns (indoor, in-vehicle, and other) based on the raw GPS data. Multiple-linear regression and mixed effect models were developed to estimate averaged daily and subject-level PB-PAH exposures. The covariates we examined included day of week and time of day, GPS-based time-activity and GPS speed, traffic- and roadway-related parameters, meteorological variables (i.e. temperature, wind speed, relative humidity), and socio-demographic variables and occupational exposures from the questionnaire. RESULTS: We measured personal PB-PAH exposures for 180 days with more than 6 h of valid data on each day. The adjusted R2 of the model was 0.58 for personal daily exposures, 0.61 for subject-level personal exposures, and 0.75 for subject-level micro-environmental exposures. The amount of time in vehicle (averaging 4.5% of total sampling time) explained 48% of the variance in daily personal PB-PAH exposure and 39% of the variance in subject-level exposure. The other major predictors of PB-PAH exposures included length-weighted traffic count, work-related exposures, and percent of weekday time. CONCLUSION: We successfully developed regression models to estimate PB-PAH exposures based on GPS-tracking data, traffic data, and simple questionnaire information. Time in vehicle was the most important determinant of personal PB-PAH exposure in this population. We demonstrated the importance of coupling real-time exposure measures with GPS time-activity tracking in personal air pollution exposure assessment.

Linking In-Vehicle Ultrafine Particle Exposures to On-Road Concentrations.

For traffic-related pollutants like ultrafine particles (UFP, Dp < 100 nm), a significant fraction of overall exposure occurs within or close to the transit microenvironment. Therefore, understanding exposure to these pollutants in such microenvironments is crucial to accurately assessing overall UFP exposure. The aim of this study was to develop models for predicting in-cabin UFP concentrations if roadway concentrations are known, taking into account vehicle characteristics, ventilation settings, driving conditions and air exchange rates (AER). Particle concentrations and AER were measured in 43 and 73 vehicles, respectively, under various ventilation settings and driving speeds. Multiple linear regression (MLR) and generalized estimating equation (GEE) regression models were used to identify and quantify the factors that determine inside-to-outside (I/O) UFP ratios and AERs across a full range of vehicle types and ages. AER was the most significant determinant of UFP I/O ratios, and was strongly influenced by ventilation setting (recirculation or outside air intake). Inclusion of ventilation fan speed, vehicle age or mileage, and driving speed explained greater than 79% of the variability in measured UFP I/O ratios.

Predictive model for vehicle air exchange rates based on a large, representative sample.

The in-vehicle microenvironment is an important route of exposure to traffic-related pollutants, particularly ultrafine particles. However, significant particle losses can occur under conditions of low air exchange rate (AER) when windows are closed and air is recirculating. AERs are lower for newer vehicles and at lower speeds. Despite the importance of AER in affecting in-vehicle particle exposures, few studies have characterized AER and all have tested only a small number of cars. One reason for this is the difficulty in measuring AER with tracer gases such as SF(6), the most common method. We developed a simplified yet accurate method for determining AER using the occupants' own production of CO(2), a convenient compound to measure. By measuring initial CO(2) build-up rates and equilibrium values of CO(2) at fixed speeds, AER was calculated for 59 vehicles representative of California's fleet. AER measurements correlated and agreed well with the largest other study conducted (R(2) = 0.83). Multivariable models captured 70% of the variability in observed AER using only age, mileage, manufacturer, and speed. These results will be useful to exposure and epidemiological studies since all model variable values are easily obtainable through questionnaire.

Vehicle and driving characteristics that influence in-cabin particle number concentrations.

In-transit microenvironments experience elevated levels of vehicle-related pollutants such as ultrafine particles. However, in-vehicle particle number concentrations are frequently lower than on-road concentrations due to particle losses inside vehicles. Particle concentration reduction occurs due to a complicated interplay between a vehicle's air-exchange rate (AER), which determines particle influx rate, and particle losses due to surfaces and the in-cabin air filter. Accurate determination of inside-to-outside particle concentration ratios is best made under realistic aerodynamic and AER conditions because these ratios and AER are determined by vehicle speed and ventilation preference, in addition to vehicle characteristics such as age. In this study, 6 vehicles were tested at 76 combinations of driving speeds, ventilation conditions (i.e., outside air or recirculation), and fan settings. Under recirculation conditions, particle number attenuation (number reduction for 10-1000 nm particles) averaged 0.83 ± 0.13 and was strongly negatively correlated with increasing AER, which in turn depended on speed and the age of the vehicle. Under outside air conditions, attenuation averaged 0.33 ± 0.10 and primarily decreased at higher fan settings that increased AER. In general, in-cabin particle number reductions did not vary strongly with particle size, and cabin filters exhibited low removal efficiencies.

Personal endotoxin exposure in a panel study of school children with asthma.

BACKGROUND: Endotoxin 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. METHODS: We 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. RESULTS: We 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. CONCLUSIONS: Daily 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.

Traffic-related air pollution and blood pressure in elderly subjects with coronary artery disease.

BACKGROUND: Associations between blood pressure (BP) and ambient air pollution have been inconsistent. No studies have used ambulatory BP monitoring and outdoor home air-pollutant measurements with time-activity-location data. We address these gaps in a study of 64 elderly subjects with coronary artery disease, living in retirement communities in the Los Angeles basin. METHODS: Subjects were followed up for 10 days with hourly waking ambulatory BP monitoring (n = 6539 total measurements), hourly electronic diaries for perceived exertion and location, and real-time activity monitors (actigraphs). We measured hourly outdoor home pollutant gases, particle number, PM2.5, organic carbon, and black carbon. Data were analyzed with mixed models controlling for temperature, posture, actigraph activity, hour, community, and season. RESULTS: We found positive associations of systolic and diastolic BP with air pollutants. The strongest associations were with organic carbon (especially its estimated fossil-fuel- combustion fraction), multiday average exposures, and time periods when subjects were at home. An interquartile increase in 5-day average organic carbon (5.2 microg/m) was associated with 8.2 mm Hg higher mean systolic BP (95% confidence interval = 3.0-13.4) and 5.8 mm Hg higher mean diastolic BP (3.0-8.6). Associations of BP with 1-8 hour average air pollution were stronger with reports of moderate to strenuous physical exertion but not with higher actigraph motion. Associations were also stronger among 12 obese subjects. CONCLUSIONS: Exposure to primary organic components of fossil fuel combustion near the home were strongly associated with increased ambulatory BP in a population at potential risk of heart attack. Low fitness or obesity may increase the effects of pollutants.

Associations of primary and secondary organic aerosols with airway and systemic inflammation in an elderly panel cohort.

BACKGROUND: Exposure-response information about particulate air-pollution constituents is needed to protect sensitive populations. Particulate matter <2.5 mm (PM2.5) components may induce oxidative stress through reactive-oxygen-species generation, including primary organics from combustion sources and secondary organics from photochemically oxidized volatile organic compounds. We evaluated differences in airway versus systemic inflammatory responses to primary versus secondary organic particle components, particle size fractions, and the potential of particles to induce cellular production of reactive oxygen species. METHODS: A total of 60 elderly subjects contributed up to 12 weekly measurements of fractional exhaled nitric oxide (NO; airway inflammation biomarker), and plasma interleukin-6 (IL-6; systemic inflammation biomarker). PM2.5 mass fractions were PM0.25 (<0.25 µm) and PM0.25-2.5 (0.25-2.5 µm). Primary organic markers included PM2.5 primary organic carbon, and PM0.25 polycyclic aromatic hydrocarbons and hopanes. Secondary organic markers included PM2.5 secondary organic carbon, and PM0.25 water soluble organic carbon and n-alkanoic acids. Gaseous pollutants included carbon monoxide (CO) and nitrogen oxides (NOx; combustion emissions markers), and ozone (O3; photochemistry marker). To assess PM oxidative potential, we exposed rat alveolar macrophages in vitro to aqueous extracts of PM0.25 filters and measured reactive-oxygen-species production. Biomarker associations with exposures were evaluated with mixed-effects models. RESULTS: Secondary organic markers, PM0.25-2.5, and O3 were positively associated with exhaled NO. Primary organic markers, PM0.25, CO, and NOx were positively associated with IL-6. Reactive oxygen species were associated with both outcomes. CONCLUSIONS: Particle effects on airway versus systemic inflammation differ by composition, but overall particle potential to induce generation of cellular reactive oxygen species is related to both outcomes.

Characterization of the asthmatic population of St. Vincent and the Grenadines: asthma severity levels and atopic sensitization.

BACKGROUND: The developing country of St. Vincent and the Grenadines (SVG) reported a 4.5-fold increase in wheezing incidence between 1986 and 2002. It is unknown whether aeroallergens play a significant role in asthma in SVG. OBJECTIVE: The objective of the study is to investigate the importance of aeroallergens and the association between age and persistence of asthma into adulthood. Methods. Subjects were recruited from the National Asthma Clinic. Asthma was diagnosed in 525 participants and severity levels assigned according to the National Heart, Lung, and Blood Institute guidelines. Participants were separated into three age groups [≤6 years (n=176), 7-18 years (n=164), and ≥19 years (n=185)]. Skin testing was performed on 171 participants to dust mite, cat, dog, cockroach, pollens, and mold. Age of asthma onset was obtained. RESULTS: Persistent asthma was diagnosed in 235 participants (44.8%) and increased with increasing age group (p<.0001). Atopy was identified in 121/171 (70.8%) participants and was significantly higher in persistent asthma (p<.004). A significant positive association was seen between atopy and age group (p<.0004) in participants with intermittent asthma but not in participants with persistent asthma. The most common allergen among the atopic participants was house dust mite (93.4%), followed by cockroach (47.9%). Adult participants reporting asthma onset in adulthood were less atopic than those whose asthma developed ≤18 years of age (p<.05). CONCLUSIONS: The predominance of asthma with atopy in SVG implicates a role for atopy in the sudden rise in asthma cases. This asthma characteristic and the increase in persistent asthma with age in SVG are similar to those reported in the developed countries.

Ethane and n-pentane in exhaled breath are biomarkers of exposure not effect.

The relationship of exhaled ethane and n-pentane to exhaled NO, carbonylated proteins, and indoor/outdoor atmospheric pollutants were examined in order to evaluate ethane and n-pentane as potential markers of airway inflammation and/or oxidative stress. Exhaled NO and carbonylated proteins were found to have no significant associations with either ethane (p = 0.96 and p = 0.81, respectively) or n-pentane (p = 0.44 and 0.28, respectively) when outliers were included. In the case where outliers were removed n-pentane was found to be inversely associated with carbonylated proteins. Exhaled hydrocarbons adjusted for indoor hydrocarbon concentrations were instead found to be positively associated with air pollutants (NO, NO(2) and CO), suggesting pollutant exposure is driving exhaled hydrocarbon concentrations. Given these findings, ethane and n-pentane do not appear to be markers of airway inflammation or oxidative stress.

Determination of metal-based hydroxyl radical generating capacity of ambient and diesel exhaust particles.

Numerous studies have suggested the association of reactive oxygen species (ROS) with adverse health effects derived from exposure to airborne particulate matter (PM) and diesel exhaust particles (DEP). This redox activity has been attributed to both inorganic and organic species present in these particles, but a clear distinction has not been established between the contribution of each. This article describes an application of an analytical procedure, based on the reaction of salicylic acid with hydroxyl radical to form dihydroxybenzoate (DHBA) isomers, to measure transition metal-based redox activity associated with ambient and diesel exhaust particles. In the procedure, ascorbic acid (AA) is used as electron source for reduction of metal ions and oxygen to generate superoxide, which is further reduced to hydroxyl radical in the presence of transition metal ions. Hydroxyl radical reacts with salicylate to generate DHBA isomers, which are measured by high-performance liquid chromatography (HPLC) with electrochemical detector. Both copper (Cu) and iron (Fe) ions generated DHBA isomers in a concentration-dependent manner but at different rates. The procedure was applied to DEP and ambient particles and the results showed Cu ion to be the major contributor to DHBA formation. The procedure provides a quantitative measure of transition metal-based redox activity associated with ambient samples with different physicochemical properties.

Associations between personal, indoor, and residential outdoor pollutant concentrations: implications for exposure assessment to size-fractionated particulate matter.

The physical and chemical characteristics of indoor, outdoor, and personal quasi-ultrafine (<0.25 microm)-, accumulation (0.25-2.5 microm)-, and coarse (2.5-10 microm)-mode particles were studied at four different retirement communities in southern California between 2005 and 2007. Linear mixed-effects models and Spearman's correlation coefficients were then used to elucidate the relationships among size-segregated particulate matter (PM) levels, their particle components, and gaseous co-pollutants. Seasonal and spatial differences in the concentrations of all measured species were evaluated at all sites on the basis of P values for product terms. Outdoor quasi-ultrafine (UF) and, to a lesser extent, accumulation-mode particles were the two fractions that best correlated with outdoor concentrations of carbon monoxide (CO), nitrogen dioxide (NO2), nitrogen oxides (NOx; during both phases of the study), and ozone (O3; only during the warmer months). Outdoor and indoor concentrations of CO, NO2, and NOx were more positively correlated to personal quasi-UF particles than larger size fractions. Despite these findings, it seems unlikely that these gaseous co-pollutants could confound epidemiologic associations between quasi-UF particles and adverse health effects. Overall, measured gaseous co-pollutants were weak surrogates of personal exposure to accumulation-mode PM, at least for subjects with similar exposure profiles and living in similar urban locations. Indoor sources were not significant contributors to personal exposure of accumulation and quasi-UF PM, which is predominantly influenced by primary emitted pollutants of outdoor origin. Correlations between personal coarse-mode PM and both outdoor and indoor gaseous co-pollutant concentrations were weak at all sites and during all seasons.

Personal and ambient air pollution exposures and lung function decrements in children with asthma.

BACKGROUND: Epidemiologic studies have shown associations between asthma outcomes and outdoor air pollutants such as nitrogen dioxide and particulate matter mass < 2.5 microm in diameter (PM(2.5)). Independent effects of specific pollutants have been difficult to detect because most studies have relied on highly correlated central-site measurements. OBJECTIVES: This study was designed to evaluate the relationship of daily changes in percent-predicted forced expiratory volume in 1 sec (FEV(1)) with personal and ambient air pollutant exposures. METHODS: For 10 days each, we followed 53 subjects with asthma who were 9-18 years of age and living in the Los Angeles, California, air basin. Subjects self-administered home spirometry in themorning, afternoon, and evening. We measured personal hourly PM(2.5) mass, 24-hr PM(2.5) elemental and organic carbon (EC-OC), and 24-hr NO(2), and the same 24-hr average outdoor central-site(ambient) exposures. We analyzed data with transitional mixed models controlling for personal temperature and humidity, and as-needed beta(2)-agonist inhaler use. RESULTS: FEV(1) decrements were significantly associated with increasing hourly peak and daily average personal PM(2.5), but not ambient PM(2.5). Personal NO(2) was also inversely associated with FEV(1). Ambient NO(2) was more weakly associated. We found stronger associations among 37 subjects not taking controller bronchodilators as follows: Personal EC-OC was inversely associated with morning FEV(1); for an interquartile increase of 71 microg/m(3) 1-hr maximum personal PM(2.5), overall percent-predicted FEV(1) decreased by 1.32% [95% confidence interval (CI), -2.00 to -0.65%]; and for an interquartile increase of 16.8 ppb 2-day average personal NO(2), overall percent-predicted FEV(1) decreased by 2.45% (95% CI, -3.57 to -1.33%). Associations of both personal PM(2.5) and NO(2) with FEV(1) remained when co-regressed, and both confounded ambient NO(2). CONCLUSIONS: Independent pollutant associations with lung function might be missed using ambient data alone. Different sets of causal components are suggested by independence of FEV(1) associations with personal PM(2.5) mass from associations with personal NO(2).