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.

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.

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.

Nrf2-related gene expression and exposure to traffic-related air pollution in elderly subjects with cardiovascular disease: An exploratory panel study.

Gene expression changes are linked to air pollutant exposures in in vitro and animal experiments. However, limited data are available on how these outcomes relate to ambient air pollutant exposures in humans. We performed an exploratory analysis testing whether gene expression levels were associated with air pollution exposures in a Los Angeles area cohort of elderly subjects with coronary artery disease. Candidate genes (35) were selected from published studies of gene expression-pollutant associations. Expression levels were measured weekly in 43 subjects (≤ 12 weeks) using quantitative PCR. Exposures included gaseous pollutants O3, nitrogen oxides (NOx), and CO; particulate matter (PM) pollutants elemental and black carbon (EC, BC); and size-fractionated PM mass. We measured organic compounds from PM filter extracts, including polycyclic aromatic hydrocarbons (PAHs), and determined the in vitro oxidative potential of particle extracts. Associations between exposures and gene expression levels were analyzed using mixed-effects regression models. We found positive associations of traffic-related pollutants (EC, BC, primary organic carbon, PM 0.25-2.5 PAH and/or PM 0.25 PAH, and NOx) with NFE2L2, Nrf2-mediated genes (HMOX1, NQO1, and SOD2), CYP1B1, IL1B, and SELP. Findings suggest that NFE2L2 gene expression links associations of traffic-related air pollution with phase I and II enzyme genes at the promoter transcription level.

Fine and ultrafine particulate organic carbon in the Los Angeles basin: Trends in sources and composition.

In this study, PM2.5 and PM0.18 (particles with dp<2.5 µm and dp<0.18 µm, respectively) were collected during 2012-2013 in Central Los Angeles (LA) and 2013-2014 in Anaheim. Samples were chemically analyzed for carbonaceous species (elemental and organic carbons) and individual organic compounds. Concentrations of organic compounds were reported and compared with many previous studies in Central LA to quantify the impact of emissions control measurements that have been implemented for vehicular emissions over the past decades in this area. Moreover, a novel hybrid approach of molecular marker-based chemical mass balance (MM-CMB) analysis was conducted, in which a combination of source profiles that were previously obtained from a Positive Matrix Factorization (PMF) model in Central LA, were combined with some traditional source profiles. The model estimated the relative contributions from mobile sources (including gasoline, diesel, and smoking vehicles), wood smoke, primary biogenic sources (including emissions from vegetative detritus, food cooking, and re-suspended soil dust), and anthropogenic secondary organic carbon (SOC). Mobile sources contributed to 0.65 ± 0.25 µg/m(3) and 0.32 ± 0.25 µg/m(3) of PM2.5 OC in Central LA and Anaheim, respectively. Primary biogenic and anthropogenic SOC sources were major contributors to OC concentrations in both size fractions and sites. Un-apportioned OC ("other OC") accounted for an average 8.0 and 26% of PM2.5 OC concentration in Central LA and Anaheim, respectively. A comparison with previous studies in Central LA revealed considerable reduction of EC and OC, along with tracers of mobile sources (e.g. PAHs, hopanes and steranes) as a result of implemented regulations on vehicular emissions. Given the significant reduction of the impacts of mobile sources in the past decade in the LA Basin, the impact of SOC and primary biogenic emissions have a larger relative impact and the new hybrid model allows the impact of these sources to be better quantified.

Oxidative potential of coarse particulate matter (PM(10-2.5)) and its relation to water solubility and sources of trace elements and metals in the Los Angeles Basin.

In this study, potential sources of water-soluble (WS) and water-insoluble (WI) fractions of metals and trace elements in coarse particulate matter (CPM) (PM(10-2.5), 2.5 < dp < 10 µm) were identified and their association with the redox properties of CPM, measured by means of reactive oxygen species (ROS), was explored. CPM was collected during 2012-2013 in Central Los Angeles (LA) and 2013-2014 in Anaheim, CA. Generally, WI components contributed to a larger fraction of CPM ROS activity (as much as 64% and 54% at Central LA and Anaheim, respectively). Two major source factors were identified by principal component analysis for both the WS and WI fractions: vehicular abrasion and re-suspended road dust. Univariate analysis indicated that several species were correlated with CPM ROS activity: in WS fraction, metals such as Mn, Fe, Cd and Zn were associated with WS ROS, while in WI fraction Ti, Fe, Ni, Pb and Cr had the highest correlations with WI ROS activity. Multiple linear regression analysis revealed that both vehicular abrasion and re-suspension of road dust were associated with WS ROS activity, while only vehicular abrasion contributed significantly to the WI ROS activity. Moreover, comparison with previous studies indicated that the ROS activity of CPM has increased in the past 5 years in Central LA. We attribute this increase mainly to the elevated levels of re-suspension of road dust caused by the increase in vehicle speed and number of trucks in recent years in this area, reaffirming the growing importance of non-tailpipe traffic emissions on CPM toxicity.

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.

Chemical characterization and source apportionment of indoor and outdoor fine particulate matter (PM(2.5)) in retirement communities of the Los Angeles Basin.

Concurrent indoor and outdoor measurements of fine particulate matter (PM2.5) were conducted at three retirement homes in the Los Angeles Basin during two separate phases (cold and warm) between 2005 and 2006. Indoor-to-outdoor relationships of PM2.5 chemical constituents were determined and sources of indoor and outdoor PM2.5 were evaluated using a molecular marker-based chemical mass balance (MM-CMB) model. Indoor levels of elemental carbon (EC) along with metals and trace elements were found to be significantly affected by outdoor sources. EC, in particular, displayed very high indoor-to-outdoor (I/O) mass ratios accompanied by strong I/O correlations, illustrating the significant impact of outdoor sources on indoor levels of EC. Similarly, indoor levels of polycyclic aromatic hydrocarbons (PAHs), hopanes, and steranes were strongly correlated with their outdoor components and displayed I/O ratios close to unity. On the other hand, concentrations of n-alkanes and organic acids inside the retirement communities were dominated by indoor sources (e.g. food cooking and consumer products), as indicated by their I/O ratios, which exceeded unity. Source apportionment results revealed that vehicular emissions were the major contributor to both indoor and outdoor PM2.5, accounting for 39 and 46% of total mass, respectively. Moreover, the contribution of vehicular sources to indoor levels was generally comparable to its corresponding outdoor estimate. Other water-insoluble organic matter (other WIOM), which accounts for emissions from uncharacterized primary biogenic sources, displayed a wider range of contributions, varying from 2 to 73% of PM2.5, across all sites and phases of the study. Lastly, higher indoor than outdoor contribution of other water-soluble organic matter (other WSOM) was evident at some of the sites, suggesting the production of secondary aerosols as well as direct emissions from primary sources (including cleaning or other consumer products) at the indoor environments.

Diurnal and seasonal trends in the apparent density of ambient fine and coarse particles in Los Angeles.

Diurnal and seasonal variations in the apparent density of ambient fine and coarse particulate matter (PM2.5 and CPM [PM2.5-10], respectively) were investigated in a location near downtown Los Angeles. The apparent densities, determined by particle mass-to-volume ratios, showed strong diurnal and seasonal variations, with higher values during the warm phase (June to August 2013) compared to cold phase (November 2012 to February 2013). PM2.5 apparent density showed minima during the morning and afternoon rush hours of the cold phase (1.20g cm(-3)), mainly due to the increased contribution of traffic-emitted soot particles, and highest values were found during the midday in the warm phase (2.38g cm(-3)). The lowest CPM apparent density was observed during the morning rush hours of the cold phase (1.41g cm(-3)), while highest in early afternoon during the warm phase (2.91g cm(-3)), most likely due to the increased wind-induced resuspension of road dust.

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).

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.

Relations between isoprene and nitric oxide in exhaled breath and the potential influence of outdoor ozone: a pilot study.

The role of endogenous isoprene in the human body, if any, is unclear because previous research is inconsistent and mechanistic evidence for the biologic function of isoprene is lacking. Given previous evidence that exhaled isoprene is elevated in systemic inflammatory states, we hypothesized that exhaled isoprene would be positively associated with a breath biomarker of airway inflammation, the fractional concentration of exhaled nitric oxide (FENO). We examined relationships of exhaled breath isoprene with FENO and with outdoor ozone given that ozone chemically reacts with isoprene and has been positively associated with FENO in past studies. Sixteen elderly subjects were followed with ≤12 weekly exhaled hydrocarbon and FENO collections at the subjects' retirement community. Outdoor ozone concentrations were measured continuously on site. Mixed-effects regression analyses tested relations of FENO with isoprene, and FENO and isoprene with ozone, adjusted for temperature. We found FENO was inversely associated with isoprene, and this was not confounded by ozone. Isoprene was inversely related to ozone. FENO was positively related to ozone and this relation was not confounded by isoprene. In contrast to hypothesized relations, we conclude that exhaled isoprene is inversely associated with FENO as well as outdoor ozone, which suggests possible protective ozone-scavenging functions of endogenous isoprene. Findings may indicate chemical reactions of isoprene oxidation by ozone and by hydroxyl radicals in the presence of O2 that is dependent on NO concentration. These preliminary results need to be confirmed in additional studies of human subjects, particularly as they apply to FENO monitoring in asthma.

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.

Particulate air pollution, ambulatory heart rate variability, and cardiac arrhythmia in retirement community residents with coronary artery disease.

BACKGROUND: Decreased heart rate variability (HRV) has been associated with future cardiac morbidity and mortality and is often used as a marker of altered cardiac autonomic balance in studies of health effects of airborne particulate matter. Fewer studies have evaluated associations between air pollutants and cardiac arrhythmia. OBJECTIVES: We examined relationships between cardiac arrhythmias, HRV, and exposures to airborne particulate matter. METHODS: We measured HRV and arrhythmia with ambulatory electrocardiograms in a cohort panel study for up to 235 hr per participant among 50 nonsmokers with coronary artery disease who were ≥ 71 years of age and living in four retirement communities in the Los Angeles, California, Air Basin. Exposures included hourly outdoor gases, hourly traffic-related and secondary organic aerosol markers, and daily size-fractionated particle mass. We used repeated measures analyses, adjusting for actigraph-derived physical activity and heart rate, temperature, day of week, season, and community location. RESULTS: Ventricular tachycardia was significantly increased in association with increases in markers of traffic-related particles, secondary organic carbon, and ozone. Few consistent associations were observed for supraventricular tachycardia. Particulates were significantly associated with decreased ambulatory HRV only in the 20 participants using ACE (angiotensin I-converting enzyme) inhibitors. CONCLUSIONS: Although these data support the hypothesis that particulate exposures may increase the risk of ventricular tachycardia for elderly people with coronary artery disease, HRV was not associated with exposure in most of our participants. These results are consistent with previous findings in this cohort for systemic inflammation, blood pressure, and ST segment depression.

Airway inflammation and oxidative potential of air pollutant particles in a pediatric asthma panel.

Airborne particulate matter (PM) components from fossil fuel combustion can induce oxidative stress initiated by reactive oxygen species (ROS). Reported associations between worsening asthma and PM2.5 mass could be related to PM oxidative potential to induce airway oxidative stress and inflammation (hallmarks of asthma pathology). We followed 45 schoolchildren with persistent asthma in their southern California homes daily over 10 days with offline fractional exhaled nitric oxide (FENO), a biomarker of airway inflammation. Ambient exposures included daily average PM2.5, PM2.5 elemental and organic carbon (EC, OC), NO2, O3, and endotoxin. We assessed PM2.5 oxidative potential using both an abiotic and an in vitro bioassay on aqueous extracts of daily particle filters: (1) dithiothreitol (DTT) assay (abiotic), representing chemically produced ROS; and (2) ROS generated intracellularly in a rat alveolar macrophage model using the fluorescent probe 2'7'-dicholorohidroflourescin diacetate. We analyzed relations of FENO to air pollutants in mixed linear regression models. FENO was significantly positively associated with lag 1-day and 2-day averages of traffic-related markers (EC, OC, and NO2), DTT and macrophage ROS, but not PM2.5 mass. DTT associations were nearly twice as strong as other exposures per interquartile range: median FENO increased 8.7-9.9% per 0.43 nmole/min/m(3) DTT. Findings suggest that future research in oxidative stress-related illnesses such as asthma and PM exposure would benefit from assessments of PM oxidative potential and composition.

Mitochondrial genetic background modifies the relationship between traffic-related air pollution exposure and systemic biomarkers of inflammation.

BACKGROUND: Mitochondria are the main source of reactive oxygen species (ROS). Human mitochondrial haplogroups are linked to differences in ROS production and oxidative-stress induced inflammation that may influence disease pathogenesis, including coronary artery disease (CAD). We previously showed that traffic-related air pollutants were associated with biomarkers of systemic inflammation in a cohort panel of subjects with CAD in the Los Angeles air basin. OBJECTIVE: We tested whether air pollutant exposure-associated inflammation was stronger in mitochondrial haplogroup H than U (high versus low ROS production) in this panel (38 subjects and 417 observations). METHODS: Inflammation biomarkers were measured weekly in each subject (≤ 12 weeks), including interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), C-reactive protein, interleukin-6 soluble receptor and tumor necrosis factor-soluble receptor II. We determined haplogroup by restriction fragment length polymorphism analysis. Air pollutants included nitrogen oxides (NOx), carbon monoxide (CO), organic carbon, elemental and black carbon (EC, BC); and particulate matter mass, three size fractions (<0.25 µm, 0.25-2.5 µm, and 2.5-10 µm in aerodynamic diameter). Particulate matter extracts were analyzed for organic compounds, including polycyclic aromatic hydrocarbons (PAH), and in vitro oxidative potential of aqueous extracts. Associations between exposures and biomarkers, stratified by haplogroup, were analyzed by mixed-effects models. RESULTS: IL-6 and TNF-α were associated with traffic-related air pollutants (BC, CO, NOx and PAH), and with mass and oxidative potential of quasi-ultrafine particles <0.25 µm. These associations were stronger for haplogroup H than haplogroup U. CONCLUSIONS: Results suggest that mitochondrial haplogroup U is a novel protective factor for air pollution-related systemic inflammation in this small group of subjects.

A comparative assessment of PM2.5 exposures in light-rail, subway, freeway, and surface street environments in Los Angeles and estimated lung cancer risk.

According to the U.S. Census Bureau, 570000+ commuters in Los Angeles travel for over 60 minutes to work. Studies have shown that a substantial portion of particulate matter (PM) exposure can occur during this commute. This study represents the integration of the results from five commute environments in Los Angeles. Personal PM exposures are discussed for the: (1) METRO gold line, a ground-level light-rail route, (2) METRO red line, a subway line, (3) the 110, a high volume freeway with low heavy-duty vehicle (HDV) fraction, (4) the 710, a major corridor for HDVs from the Port of Los Angeles, and (5) Wilshire/Sunset Boulevards, major surface streets. Chemical analysis including total and water-soluble metals and trace elements, elemental and organic carbon (EC/OC), and polycyclic aromatic hydrocarbons (PAHs) was performed. The focus of this study is to compare the composition and estimated lung cancer risk of PM2.5 (dp < 2.5 µm) for the five differential commute environments. Metals associated with stainless steel, notably Fe, Cr, and Mn, were elevated for the red line (subway), most likely from abrasion processes between the rail and brakes; elements associated with tire and brake wear and oil additives (Ca, Ti, Sn, Sb, and Pb) were elevated on roadways. Elemental concentrations on the gold line (light-rail) were the lowest. For water-solubility, metals observed on the red line (subway) were the least soluble. PAHs are primarily derived from vehicular emissions. Overall, the 710 exhibited high levels of PAHs (3.0 ng m−3), most likely due to its high volume of HDVs, while the red and gold lines exhibited low PAH concentrations (0.6 and 0.8 ng m−3 for red and gold lines, respectively). Lastly, lung cancer risk due to inhalation of PAHs was calculated based on a commuter lifetime (45 years for 2 hours per workday). Results showed that lung cancer risk for the 710 is 3.8 and 4.5 times higher than the light-rail (gold line) and subway (red line), respectively. With low levels of both metal and PAH pollutants, our results indicate that commuting on the light-rail (gold line) may have potential health benefits when compared to driving on freeways and busy roadways.

Examining the representativeness of home outdoor PM(2.5), EC, and OC estimates for daily personal exposures in Southern California.

Recent studies have linked acute respiratory and cardiovascular outcomes to measurements or estimates of traffic-related air pollutants at homes or schools. However, few studies have evaluated these outdoor measurements and estimates against personal exposure measurements. We compared measured and modeled home outdoor concentrations with personal measurements of traffic-related air pollutants in the Los Angeles air basin (Whittier and Riverside). Personal exposure of 63 children with asthma and 15 homes were assessed for particulate matter with an aerodynamic diameter less than 2.5 µm (PM(2.5)), elemental carbon (EC), and organic carbon (OC) during sixteen 10-day monitoring runs. Regression models to predict daily home outdoor PM(2.5), EC, and OC were constructed using home outdoor measurements, geographical and meteorological parameters, as well as CALINE4 estimates at outdoor home sites, which represent the concentrations from local traffic sources. These home outdoor models showed the variance explained (R(2)) was 0.97 and 0.94 for PM(2.5), 0.91 and 0.83 for OC, and 0.76 and 0.87 for EC in Riverside and Whittier, respectively. The PM(2.5) outdoor estimates correlated well with the personal measurements (Riverside R(2) = 0.65 and Whittier R(2) = 0.69). However, excluding potentially inaccurate samples from Riverside, the correlation between personal exposure to carbonaceous species and home outdoor estimates in Whittier was moderate for EC (R(2) = 0.37) and poor for OC (R(2) = 0.08). The CALINE4 estimates alone were not correlated with personal measurements of EC or other pollutants. While home outdoor estimates provide good approximations for daily personal PM(2.5) exposure, they may not be adequate for estimating daily personal exposure to EC and OC. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1007/s11869-010-0099-y) contains supplementary material, which is available to authorized users.

Characterization of organic, metal and trace element PM2.5 species and derivation of freeway-based emission rates in Los Angeles, CA.

On-road particulate matter (PM) was collected during a sampling campaign in March-April of 2011 on two major Los Angeles freeways, I-710 and Route 110. I-710 is a major route for heavy-duty vehicles (HDVs) traveling to and from the Ports of Long Beach and Los Angeles, while Route 110 has a much lower HDV fraction -3.9% versus 11.4%. Two sets of samples were collected for each roadway, each set representing approximately 50°h of on-road sampling. Concurrent sampling at a fixed site at the University of Southern California's (USC) downtown Los Angeles campus provided estimates of urban background levels. Chemical analysis was performed for elemental carbon (EC), organic carbon (OC), polycyclic aromatic hydrocarbons (PAHs), hopanes and steranes, and metals and trace elements. Freeway-based emission rates (ERs) - mass per kilometer of freeway per hour - were calculated using mass concentrations, fuel characteristics, and traffic flow rates. These ERs are presented such that freeways could be treated as a line source of emissions for use in predictive models of population exposure for nearby communities. This data could also be used to assess the exposure of commuters to traffic-related PM2.5 emissions. ERs are compared to data from a previous fixed-site roadside study of I-710 as well as to reconstructed values from a tunnel study. ERs were generally lower (or comparable) on the gasoline-vehicle dominated freeway (Route 110) than the freeway with more diesel trucks (I-710), with EC and pyrene being notably lower on Route 110, findings consistent with the Route 110's lower HDV fraction. We found EC emission rates decreased over time suggesting that efforts to reduce diesel emissions from HDVs at the Ports of Los Angeles and Long Beach have been successful. While ERs for most of the organic species were within the range of values reported by previous studies, the present study found much higher ERs for metals and trace elements. This suggests that the sampling methods employed in this campaign are more efficient at capturing particles from sources such as resuspended road dust and wear from tires and brakes, which are usually not included in traditional sampling methodologies for assessing vehicular emissions (e.g. dynamometer studies).

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.