A community study of the effect of particulate matter on blood measures of inflammation and thrombosis in an elderly population

BACKGROUND: The mechanism behind the triggering effect of fine particulate matter (PM) air pollution on cardiovascular events remains elusive. We postulated that elevated levels of PM would be associated with increased blood levels of inflammatory and thrombotic markers in elderly individuals. We also hypothesized that elevated PM would increase levels of cytokines in individuals with heart disease. METHODS: We measured these blood markers in 47 elderly individuals with (23) and without (16 COPD and 8 healthy) cardiovascular disease (CVD) on 2 or 3 mornings over a 5 or 10-day period between February 2000 and March 2002. Blood measures were paired with residence level outdoor PM measured by nephelometry. Analyses determined the within-individual effect of 24-hour averaged outdoor PM on blood measures. RESULTS: Analyses found no statistically significant effect of a same day 10 ug/m(3 )increase in fine PM on log transformed levels of CRP 1.21 fold-rise [95% CI: 0.86, 1.70], fibrinogen 1.02 fold-rise [95% CI: 0.98, 1.06], or D-dimer 1.02 fold-rise [95% CI: 0.88, 1.17] in individuals with CVD. One-day lagged analyses in the CVD subgroup found similar null results. These same models found no change in these blood markers at the same-day or 1-day lag in the group without CVD. In 21 individuals with CVD, a 10 μg/m(3 )increase in same-day PM was associated with a 1.3 fold-rise [95% CI: 1.1, 1.7] in the level of monocyte chemoattractant protein-1. CONCLUSION: We did not find consistent effects of low ambient levels of PM on blood measures of inflammation or thrombosis in elderly individuals

Intermediate-mass dilepton spectra and the role of secondary hadronic processes in heavy-ion collisions

We carry out a study of intermediate-mass (between 1 and 2.5 GeV) dilepton spectra from hadronic interactions in heavy-ion collisions. The processes considered are $\pi\pi\to l{\bar l}$, $\pi\rho\to l{\bar l}$, $\pi a_1\to l{\bar l}$, $\pi\omega\to l{\bar l}$, $K{\bar K}\to l{\bar l}$, and $K{\bar K^*}+c.c \to l{\bar l}$. The elementary cross sections for those are obtained from chiral Lagrangians involving pseudoscalar, vector, and axial-vector mesons. The respective electromagnetic form factors are determined by fitting to experimental data for the reverse processes of $e^+e^-\to hadrons$. Based on this input we calculate cross sections and thermal dilepton emission rates and compare our results with those from other approaches. Finally we use these elementary cross sections with a relativistic transport model and calculate dilepton spectra in S+W collisions at SPS energies. The comparison of our results with experimental data from the HELIOS-3 collaboration indicates the importance of the secondary hadronic contributions to the intermediate-mass dilepton spectra.Comment: 25 pages, including 20 postscript figure

Pulmonary Effects of Indoor- and Outdoor-Generated Particles in Children with Asthma

Most particulate matter (PM) health effects studies use outdoor (ambient) PM as a surrogate for personal exposure. However, people spend most of their time indoors exposed to a combination of indoor-generated particles and ambient particles that have infiltrated. Thus, it is important to investigate the differential health effects of indoor- and ambient-generated particles. We combined our recently adapted recursive model and a predictive model for estimating infiltration efficiency to separate personal exposure (E) to PM(2.5) (PM with aerodynamic diameter ≤2.5 μm) into its indoor-generated (E(ig)) and ambient-generated (E(ag)) components for 19 children with asthma. We then compared E(ig) and E(ag) to changes in exhaled nitric oxide (eNO), a marker of airway inflammation. Based on the recursive model with a sample size of eight children, E(ag) was marginally associated with increases in eNO [5.6 ppb per 10-μg/m(3) increase in PM(2.5); 95% confidence interval (CI), −0.6 to 11.9; p = 0.08]. E(ig) was not associated with eNO (−0.19 ppb change per 10μg/m(3)). Our predictive model allowed us to estimate E(ag) and E(ig) for all 19 children. For those combined estimates, only E(ag) was significantly associated with an increase in eNO (E(ag): 5.0 ppb per 10-μg/m(3) increase in PM(2.5;) 95% CI, 0.3 to 9.7; p = 0.04; E(ig): 3.3 ppb per 10-μg/m(3) increase in PM(2.5); 95% CI, −1.1 to 7.7; p = 0.15). Effects were seen only in children who were not using corticosteroid therapy. We conclude that the ambient-generated component of PM(2.5) exposure is consistently associated with increases in eNO and the indoor-generated component is less strongly associated with eNO