Examining the representativeness of home outdoor PM2.5, 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 2.5μm (PM2.5), elemental carbon (EC), and organic carbon (OC) during sixteen 10-day monitoring runs. Regression models to predict daily home outdoor PM2.5, 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 PM2.5, 0.91 and 0.83 for OC, and 0.76 and 0.87 for EC in Riverside and Whittier, respectively. The PM2.5 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 PM2.5 exposure, they may not be adequate for estimating daily personal exposure to EC and O

PM10 source apportionment in a Swiss Alpine valley impacted by highway traffic

Although trans-Alpine highway traffic exhaust is one of the major sources of air pollution along the highway valleys of the Alpine regions, little is known about its contribution to residential exposure and impact on respiratory health. In this paper, source-specific contributions to particulate matter with an aerodynamic diameter < 10μm (PM10) and their spatio-temporal distribution were determined for later use in a pediatric asthma panel study in an Alpine village. PM10 sources were identified by positive matrix factorization using chemical trace elements, elemental, and organic carbon from daily PM10 filters collected between November 2007 and June 2009 at seven locations within the village. Of the nine sources identified, four were directly road traffic-related: traffic exhaust, road dust, tire and brake wear, and road salt contributing 16%, 8%, 1%, and 2% to annual PM10 concentrations, respectively. They showed a clear dependence with distance to highway. Additional contributions were identified from secondary particles (27%), biomass burning (18%), railway (11%), and mineral dust including a local construction site (13%). Comparing these source contributions with known source-specific biomarkers (e.g., levoglucosan, nitro-polycyclic aromatic hydrocarbons) showed high agreement with biomass burning, moderate with secondary particles (in winter), and lowest agreement with traffic exhaus

Transportation noise (in particular railway noise) and blood pressure in REGICOR compared to SAPALDIA

Peer ReviewedPostprint (author's final draft

Transportation Noise and Blood Pressure in a Population-Based Sample of Adults

Background: There is some evidence for an association between traffic noise and ischemic heart disease; however, associations with blood pressure have been inconsistent, and little is known about health effects of railway noise

Different genes interact with particulate matter and tobacco smoke exposure in affecting lung function decline in the general population

BACKGROUND: Oxidative stress related genes modify the effects of ambient air pollution or tobacco smoking on lung function decline. The impact of interactions might be substantial, but previous studies mostly focused on main effects of single genes. OBJECTIVES: We studied the interaction of both exposures with a broad set of oxidative-stress related candidate genes and pathways on lung function decline and contrasted interactions between exposures. METHODS: For 12679 single nucleotide polymorphisms (SNPs), change in forced expiratory volume in one second (FEV(1)), FEV(1) over forced vital capacity (FEV(1)/FVC), and mean forced expiratory flow between 25 and 75% of the FVC (FEF(25-75)) was regressed on interval exposure to particulate matter >10 microm in diameter (PM10) or packyears smoked (a), additive SNP effects (b), and interaction terms between (a) and (b) in 669 adults with GWAS data. Interaction p-values for 152 genes and 14 pathways were calculated by the adaptive rank truncation product (ARTP) method, and compared between exposures. Interaction effect sizes were contrasted for the strongest SNPs of nominally significant genes (p(interaction)>0.05). Replication was attempted for SNPs with MAF<10% in 3320 SAPALDIA participants without GWAS. RESULTS: On the SNP-level, rs2035268 in gene SNCA accelerated FEV(1)/FVC decline by 3.8% (p(interaction) = 2.5x10(-6)), and rs12190800 in PARK2 attenuated FEV1 decline by 95.1 ml p(interaction) = 9.7x10(-8)) over 11 years, while interacting with PM10. Genes and pathways nominally interacting with PM10 and packyears exposure differed substantially. Gene CRISP2 presented a significant interaction with PM10 (p(interaction) = 3.0x10(-4)) on FEV(1)/FVC decline. Pathway interactions were weak. Replications for the strongest SNPs in PARK2 and CRISP2 were not successful. CONCLUSIONS: Consistent with a stratified response to increasing oxidative stress, different genes and pathways potentially mediate PM10 and tobac smoke effects on lung function decline. Ignoring environmental exposures would miss these patterns, but achieving sufficient sample size and comparability across study samples is challengin

Simulation of population-based commuter exposure to NO2 using different air pollution models

We simulated commuter routes and long-term exposure to traffic-related air pollution during commute in a representative population sample in Basel (Switzerland), and evaluated three air pollution models with different spatial resolution for estimating commute exposures to nitrogen dioxide (NO2) as a marker of long-term exposure to traffic-related air pollution. Our approach includes spatially and temporally resolved data on actual commuter routes, travel modes and three air pollution models. Annual mean NO2 commuter exposures were similar between models. However, we found more within-city and within-subject variability in annual mean (±SD) NO2 commuter exposure with a high resolution dispersion model (40 ± 7 µg m−3, range: 21–61) than with a dispersion model with a lower resolution (39 ± 5 µg m−3; range: 24–51), and a land use regression model (41 ± 5 µg m−3; range: 24–54). Highest median cumulative exposures were calculated along motorized transport and bicycle routes, and the lowest for walking. For estimating commuter exposure within a city and being interested also in small-scale variability between roads, a model with a high resolution is recommended. For larger scale epidemiological health assessment studies, models with a coarser spatial resolution are likely sufficient, especially when study areas include suburban and rural areas

Airborne Emissions from 1961 to 2004 of Benzo[a]pyrene from U.S. Vehicles per km of Travel Based on Tunnel Studies

We identified 13 historical measurements of polycyclic aromatic hydrocarbons (PAHs) in U.S. vehicular traffic tunnels that were either directly presented as tailpipe emission factors in μg per vehicle-kilometer or convertible to such a form. Tunnel measurements capture fleet cruise emissions. Emission factors for benzo[a]pyrene (BaP) for a tunnel fleet operating under cruise conditions were highest prior to the 1980s and fell from more than 30-μg per vehicle-km to approximately 2-μg/km in the 1990s, an approximately 15-fold decline. Total annual U.S. (cruise) emissions of BaP dropped by a lesser factor, because total annual km driven increased by a factor of 2.7 during the period. Other PAH compounds measured in tunnels over the 40-year period (e.g., benzo[ghi]perylene, coronene) showed comparable reduction factors in emissions. PAH declines were comparable to those measured in tunnels for carbon monoxide, volatile organic compounds, and particulate organic carbon. The historical PAH “source terms” determined from the data are relevant to quantifying the benefits of emissions control technology and can be used in epidemiological studies evaluating the health effects of exposure, such as those undertaken with breast cancer in New York State

Estimates of CO2 from fires in the United States: implications for carbon management

<p>Abstract</p> <p>Background</p> <p>Fires emit significant amounts of CO₂to the atmosphere. These emissions, however, are highly variable in both space and time. Additionally, CO₂emissions estimates from fires are very uncertain. The combination of high spatial and temporal variability and substantial uncertainty associated with fire CO₂emissions can be problematic to efforts to develop remote sensing, monitoring, and inverse modeling techniques to quantify carbon fluxes at the continental scale. Policy and carbon management decisions based on atmospheric sampling/modeling techniques must account for the impact of fire CO₂emissions; a task that may prove very difficult for the foreseeable future. This paper addresses the variability of CO₂emissions from fires across the US, how these emissions compare to anthropogenic emissions of CO₂and Net Primary Productivity, and the potential implications for monitoring programs and policy development.</p> <p>Results</p> <p>Average annual CO₂emissions from fires in the lower 48 (LOWER48) states from 2002–2006 are estimated to be 213 (± 50 std. dev.) Tg CO₂yr^-1and 80 (± 89 std. dev.) Tg CO₂yr^-1in Alaska. These estimates have significant interannual and spatial variability. Needleleaf forests in the Southeastern US and the Western US are the dominant source regions for US fire CO₂emissions. Very high emission years typically coincide with droughts, and climatic variability is a major driver of the high interannual and spatial variation in fire emissions. The amount of CO₂emitted from fires in the US is equivalent to 4–6% of anthropogenic emissions at the continental scale and, at the state-level, fire emissions of CO₂can, in some cases, exceed annual emissions of CO₂from fossil fuel usage.</p> <p>Conclusion</p> <p>The CO₂released from fires, overall, is a small fraction of the estimated average annual Net Primary Productivity and, unlike fossil fuel CO₂emissions, the pulsed emissions of CO₂during fires are partially counterbalanced by uptake of CO₂by regrowing vegetation in the decades following fire. Changes in fire severity and frequency can, however, lead to net changes in atmospheric CO₂and the short-term impacts of fire emissions on monitoring, modeling, and carbon management policy are substantial.</p

Adult lung function and long-term air pollution exposure. ESCAPE: a multicentre cohort study and meta-analysis.

The chronic impact of ambient air pollutants on lung function in adults is not fully understood. The objective of this study was to investigate the association of long-term exposure to ambient air pollution with lung function in adult participants from five cohorts in the European Study of Cohorts for Air Pollution Effects (ESCAPE). Residential exposure to nitrogen oxides (NO\u2082, NOx) and particulate matter (PM) was modelled and traffic indicators were assessed in a standardised manner. The spirometric parameters forced expiratory volume in 1 s (FEV\u2081) and forced vital capacity (FVC) from 7613 subjects were considered as outcomes. Cohort-specific results were combined using meta-analysis. We did not observe an association of air pollution with longitudinal change in lung function, but we observed that a 10 \u3bcg\ub7m(-3) increase in NO\u2082 exposure was associated with lower levels of FEV\u2081 (-14.0 mL, 95% CI -25.8 to -2.1) and FVC (-14.9 mL, 95% CI -28.7 to -1.1). An increase of 10 \u3bcg\ub7m(-3) in PM10, but not other PM metrics (PM2.5, coarse fraction of PM, PM absorbance), was associated with a lower level of FEV\u2081 (-44.6 mL, 95% CI -85.4 to -3.8) and FVC (-59.0 mL, 95% CI -112.3 to -5.6). The associations were particularly strong in obese persons. This study adds to the evidence for an adverse association of ambient air pollution with lung function in adults at very low levels in Europe