Coarse Particles and Heart Rate Variability among Older Adults with Coronary Artery Disease in the Coachella Valley, California

Alterations in cardiac autonomic control, assessed by changes in heart rate variability (HRV), provide one plausible mechanistic explanation for consistent associations between exposure to airborne particulate matter (PM) and increased risks of cardiovascular mortality. Decreased HRV has been linked with exposures to PM(10) (PM with aerodynamic diameter ≤ 10 μm) and with fine particles (PM with aerodynamic diameter ≤ 2.5 μm) originating primarily from combustion sources. However, little is known about the relationship between HRV and coarse particles [PM with aerodynamic diameter 10–2.5 μm (PM(10–2.5))], which typically result from entrainment of dust and soil or from mechanical abrasive processes in industry and transportation. We measured several HRV variables in 19 nonsmoking older adults with coronary artery disease residing in the Coachella Valley, California, a desert resort and retirement area in which ambient PM(10) consists predominantly of PM(10–2.5). Study subjects wore Holter monitors for 24 hr once per week for up to 12 weeks during spring 2000. Pollutant concentrations were assessed at nearby fixed-site monitors. We used mixed models that controlled for individual-specific effects to examine relationships between air pollutants and several HRV metrics. Decrements in several measures of HRV were consistently associated with both PM(10) and PM(10–2.5); however, there was little relationship of HRV variables with PM(2.5) concentrations. The magnitude of the associations (~ 1–4% decrease in HRV per 10-μg/m(3) increase in PM(10) or PM(10–2.5)) was comparable with those observed in several other studies of PM. Elevated levels of ambient PM(10–2.5) may adversely affect HRV in older subjects with coronary artery disease

Air Pollution and Lymphocyte Phenotype Proportions in Cord Blood

Effects of air pollution on morbidity and mortality may be mediated by alterations in immune competence. In this study we examined short-term associations of air pollution exposures with lymphocyte immunophenotypes in cord blood among 1,397 deliveries in two districts of the Czech Republic. We measured fine particulate matter < 2.5 μm in diameter (PM(2.5)) and 12 polycyclic aromatic hydrocarbons (PAHs) in 24-hr samples collected by versatile air pollution samplers. Cord blood samples were analyzed using a FACSort flow cytometer to determine phenotypes of CD3(+) T-lymphocytes and their subsets CD4(+) and CD8(+), CD19(+) B-lymphocytes, and natural killer cells. The mothers were interviewed regarding sociodemographic and lifestyle factors, and medical records were abstracted for obstetric, labor and delivery characteristics. During the period 1994 to 1998, the mean daily ambient concentration of PM(2.5) was 24.8 μg/m(3) and that of PAHs was 63.5 ng/m(3). In multiple linear regression models adjusted for temperature, season, and other covariates, average PAH or PM(2.5) levels during the 14 days before birth were associated with decreases in T-lymphocyte phenotype fractions (i.e., CD3(+) CD4(+), and CD8(+)), and a clear increase in the B-lymphocyte (CD19(+)) fraction. For a 100-ng/m(3) increase in PAHs, which represented approximately two standard deviations, the percentage decrease was −3.3% [95% confidence interval (CI), −5.6 to −1.0%] for CD3(+), −3.1% (95% CI, −4.9 to −1.3%) for CD4(+), and −1.0% (95% CI, −1.8 to −0.2%) for CD8(+) cells. The corresponding increase in the CD19(+) cell proportion was 1.7% (95% CI, 0.4 to 3.0%). Associations were similar but slightly weaker for PM(2.5). Ambient air pollution may influence the relative distribution of lymphocyte immunophenotypes of the fetus

Resistant pathogens in biliary obstruction: Importance of cultures to guide antibiotic therapy

Background . Cholangitis, infection of the bile ducts, is a serious condition that necessitates prompt and efficacious treatment for a good clinical outcome. A single center retrospective study of cholangitis was conducted to better define the spectrum of responsible pathogens and their antibiotic sensitivities. Methods . We studied all patients at our hospital who had cholangitis from January 1998 to June 2004. Patients were identified by ICD-9 codes and the cause of the cholangitis, the treatment and culture data were noted by review of the medical record. Results . Thirty patients presented with cholangitis as noted by the clinical symptoms of jaundice, fever and abdominal pain. The cause of the biliary obstruction was gallstones in 18 patients, benign biliary strictures in 5 and malignant obstruction in 7. All the patients with malignant obstruction with cholangitis had stents; there were no cases of cholangitis in malignant obstruction unless prior instrumentation had been performed. The most common isolates were Enterococcus>E. coli>Enterobacter>Klebsiella. Sixty-four percent of blood cultures and all but one of the bile cultures grew organisms. Seventy-two percent of patients had positive blood cultures with at least one resistant organism present and 36% had organisms resistant to multiple antibiotics. Fifty percent of patients with benign biliary disease and positive blood cultures had multiple organisms growing in their blood. Three-quarters of the isolates were resistant to one or more antibiotics and one-quarter of isolates were resistant to three or more antibiotics. Resistant organisms were found regardless of the cause of the biliary obstruction. Discussion . For all causes of cholangitis, there is a high incidence of positive blood cultures and a high rate of antibiotic resistance. For optimal treatment, blood and/or bile cultures should be routinely performed to optimize antibiotic therapy.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/73375/1/13651820510028792.pd

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Air pollution exposure during critical time periods in gestation and alterations in cord blood lymphocyte distribution: a cohort of livebirths

<p>Abstract</p> <p>Background</p> <p>Toxic exposures have been shown to influence maturation of the immune system during gestation. This study investigates the association between cord blood lymphocyte proportions and maternal exposure to air pollution during each gestational month.</p> <p>Methods</p> <p>Cord blood was analyzed using a FACSort flow cytometer to determine proportions of T lymphocytes (CD3⁺cells and their subsets, CD4⁺and CD8⁺), B lymphocytes (CD19⁺) and natural killer (NK) cells. Ambient air concentrations of 12 polycyclic aromatic hydrocarbons (PAH) and particulate matter < 2.5 micrometer in diameter (PM_2.5) were measured using fixed site monitors. Arithmetic means of these pollutants, calculated for each gestational month, were used as exposure metrics. Data on covariates were obtained from medical records and questionnaires. Multivariable linear regression models were fitted to estimate associations between monthly PAH or PM_2.5and cord blood lymphocytes, adjusting for year of birth and district of residence and, in further models, gestational season and number of prior live births.</p> <p>Results</p> <p>The adjusted models show significant associations between PAHs or PM_2.5during early gestation and increases in CD3⁺and CD4⁺lymphocytes percentages and decreases in CD19⁺and NK cell percentages in cord blood. In contrast, exposures during late gestation were associated with decreases in CD3⁺and CD4⁺fractions and increases in CD19⁺and NK cell fractions. There was no significant association between alterations in lymphocyte distribution and air pollution exposure during the mid gestation.</p> <p>Conclusions</p> <p>PAHs and PM_2.5in ambient air may influence fetal immune development via shifts in cord blood lymphocytes distributions. Associations appear to differ by exposure in early versus late gestation.</p

Lung cancer risk in never-smokers: a population-based case-control study of epidemiologic risk factors

<p>Abstract</p> <p>Background</p> <p>We conducted a case-control study in the greater Toronto area to evaluate potential lung cancer risk factors including environmental tobacco smoke (ETS) exposure, family history of cancer, indoor air pollution, workplace exposures and history of previous respiratory diseases with special consideration given to never smokers.</p> <p>Methods</p> <p>445 cases (35% of which were never smokers oversampled by design) between the ages of 20-84 were identified through four major tertiary care hospitals in metropolitan Toronto between 1997 and 2002 and were frequency matched on sex and ethnicity with 425 population controls and 523 hospital controls. Unconditional logistic regression models were used to estimate adjusted odds ratios (OR) and 95% confidence intervals (CI) for the associations between exposures and lung cancer risk.</p> <p>Results</p> <p>Any previous exposure to occupational exposures (OR total population 1.6, 95% CI 1.4-2.1, OR never smokers 2.1, 95% CI 1.3-3.3), a previous diagnosis of emphysema in the total population (OR 4.8, 95% CI 2.0-11.1) or a first degree family member with a previous cancer diagnosis before age 50 among never smokers (OR 1.8, 95% CI 1.0-3.2) were associated with increased lung cancer risk.</p> <p>Conclusions</p> <p>Occupational exposures and family history of cancer with young onset were important risk factors among never smokers.</p