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

Long-term exposure to elemental constituents of particulate matter and cardiovascular mortality in 19 European cohorts: Results from the ESCAPE and TRANSPHORM projects

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Modifying effect of a common polymorphism in the interleukin-6 promoter on the relationship between long-term exposure to traffic-related particulate matter and heart rate variability

Exposure to particulate matter (PM) has been associated with an increase in many inflammatory markers, including interleukin 6 (IL6). Air pollution exposure has also been suggested to induce an imbalance in the autonomic nervous system (ANS), such as a decrease in heart rate variability (HRV). In this study we aimed to investigate the modifying effect of polymorphisms in a major proinflammatory marker gene, interleukin 6 (IL6), on the relationship between long-term exposure to traffic-related PM10 (TPM10) and HRV.; For this cross-sectional study we analysed 1552 participants of the SAPALDIA cohort aged 50 years and older. Included were persons with valid genotype data, who underwent ambulatory 24-hr electrocardiogram monitoring, and reported on medical history and lifestyle. Main effects of annual average TPM10 and IL6 gene variants (rs1800795; rs2069827; rs2069840; rs10242595) on HRV indices and their interaction with average annual exposure to TPM10 were tested, applying a multivariable mixed linear model.; No overall association of TPM10 on HRV was found. Carriers of two proinflammatory G-alleles of the functional IL6 -174 G/C (rs1800795) polymorphism exhibited lower HRV. An inverse association between a 1 µg/m3 increment in yearly averaged TPM10 and HRV was restricted to GG genotypes at this locus with a standard deviation of normal-to-normal intervals (SDNN) (GG-carriers: -1.8%; 95% confidence interval -3.5 to 0.01; pinteraction(additive) = 0.028); and low frequency power (LF) (GG-carriers: -5.7%; 95%CI: -10.4 to -0.8; pinteraction(dominant) = 0.049).; Our results are consistent with the hypothesis that traffic-related air pollution decreases heart rate variability through inflammatory mechanisms