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.

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.

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.

Background

It has been demonstrated that ambient particulate matter (PM) can act as an adjuvant for allergic sensitization. Redox-active organic chemicals on the particle surface play an important role in PM adverse health effects and may determine the adjuvant effect of different particle types according to their potential to perturb redox equilibrium in the immune system.

Objectives

We determined whether the adjuvant effect of ambient fine particles versus ultrafine particles (UFPs) is correlated to their prooxidant potential.

Methods

We have established an intranasal sensitization model that uses ambient PM as a potential adjuvant for sensitization to ovalbumin (OVA), which enhances the capacity for secondary OVA challenge to induce allergic airway inflammation.

Results

UFPs with a greater polycyclic aromatic hydrocarbon (PAH) content and higher oxidant potential enhanced OVA sensitization more readily than did fine particles. This manifests as enhanced allergic inflammation upon secondary OVA challenge, leading to eosinophilic inflammation and mucoid hyperplasia starting at the nasal turbinates all the way down to the small pulmonary airways. The thiol antioxidant N-acetyl cysteine was able to suppress some of these sensitization events.

Conclusions

The adjuvant effects of ambient UFP is determined by their oxidant potential, which likely plays a role in changing the redox equilibrium in the mucosal immune system.

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.

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.

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.