Faculty Bibliography

OBJECTIVES: Intensivist-performed focused sonography, including renal sonography, is becoming accepted practice. Whether internal medicine residents can be trained to accurately rule out renal obstruction and identify sonographic findings of chronic kidney disease is unknown. The purpose of this study was to test the ability of residents to evaluate for this specific constellation of findings. METHODS: Internal medicine residents were trained in a 5-hour module on focused renal sonography evaluating renal length, echogenicity, hydronephrosis, and cysts on a convenience sample of medical ward, intermediate care, and medical intensive care unit patients. All patients underwent comprehensive sonography within 24 hours. The primary outcome was represented by the Fleiss kappa statistic, which indicated the degree of interobserver agreement between residents and radiologists. Sensitivity, specificity, and positive and negative predictive values were calculated using the comprehensive radiologist-read examination as the reference. RESULTS: Seventeen internal medicine residents imaged 125 kidneys on 66 patients. The average number of studies performed was 7.3 (SD, 6.6). Residents demonstrated excellent agreement with radiologists for hydronephrosis (kappa = 0.73; P < .001; SE, 0.15; sensitivity, 94%; specificity, 93%), moderate agreement for echogenic kidneys (kappa = 0.43; P < .001; SE, 0.13; sensitivity, 40%; specificity, 98%), and substantial agreement for renal cysts (kappa = 0.61; P < .001; SE, 0.12; sensitivity, 60%; specificity, 96%). Residents showed sensitivity of 100% and specificity of 88% for identification of atrophic kidneys, defined as length less than 8 cm. CONCLUSIONS: After a 5-hour training course, medical residents accurately identified hydronephrosis and key sonographic findings of chronic kidney disease in a cohort of medical patients. Screening for hydronephrosis and renal atrophy can be performed by medical residents after adequate training.

Particulate matter (PM*), an ambient air criteria pollutant, is a complex mixture of chemical components; particle sizes range from nanometer-sized molecular clusters to dust particles that are too large to be aspirated into the lungs. Although particle composition is believed to affect health risks from PM exposure, our current health-based air quality standards for PM are limited to (1) the mass concentrations of PM2.5 (particles 2.5 microm or smaller in aerodynamic diameter), which are largely attributable to combustion products; and (2) PM10 (10 microm or smaller), which includes larger-sized mechanically generated dusts. Both of these particle size fractions are regulated under the National Ambient Air Quality Standards (NAAQS) and both have been associated with excess mortality and morbidity. We conducted four studies as part of HEI's integrated National Particle Component Toxicity (NPACT) Initiative research program. Since 1999, the Chemical Speciation Network (CSN), managed by the U.S. Environmental Protection Agency (U.S; EPA), has routinely gathered air monitoring data every third or sixth day for the concentrations of numerous components of PM2.5. Data from the CSN enabled us to conduct a limited time-series epidemiologic study of short-term morbidity and mortality (Ito study); and a study of the associations between long-term average pollutant concentrations and annual mortality (Thurston study). Both have illuminated the roles of PM2.5 chemical components and source-related mixtures as potentially causal agents. We also conducted a series of 6-month subchronic inhalation exposure studies (6 hours/day, 5 days/week) of PM2.5 concentrated (nominally) 10 x from ambient air (CAPs) with apolipoprotein E-deficient (ApoE(-/-)) mice (a mouse model of atherosclerosis) (Chen study). The CAPs studies were conducted in five different U.S. airsheds; we measured the daily mass concentrations of PM2.5, black carbon (BC), and 16 elemental components in order to identify their sources and their roles in eliciting both short- and long-term health-related responses. In addition, from the same five air-sheds we collected samples of coarse (PM10-2.5), fine (PM2.5-0.2), and ultrafine (PM0.2) particles. Aliquots of these samples were administered to cells in vitro and to mouse lungs in vivo (by aspiration) in order to determine their comparative acute effects (Gordon Study). The results of these four complementary studies, and the overall integrative analyses, provide a basis for guiding future research and for helping to determine more targeted emission controls for the PM components most hazardous to acute and chronic health. Application of the knowledge gained in this work may therefore contribute to an optimization of the public health benefits of future PM emission controls. The design of each NPACT study conducted at NYU was guided by our scientific hypotheses, which were based on our reviews of the background literature and our experience in conducting studies of associations between ambient PM and health-related responses. These hypotheses guided the development and conduct of the four studies. Hypothesis 1. Coarse, fine, and ultrafine PM are each capable of producing acute health effects of public health concern, but the effects may differ according to particle size and composition. (Applies to all studies.) Hypothesis 2. Long-term PM2.5 exposures are closely associated with chronic health effects. (Applies to studies 1 and 4.) Hypothesis 3. The source-apportionment techniques that we have developed and refined in recent years provide a useful basis for identifying major categories of sources of PM in ambient air and specific chemical components that have the greatest impacts on a variety of acute and chronic health effects. (Applies to all studies.) Hypothesis 4. The health effects due to ambient PM exposures can best be seen in sensitive subgroups within overall human populations and in animal models of such populations. (Applies to studies 1, 3, and 4.) Overall, the studies have demonstrated that the toxicity of PM is driven by a complex interaction of particle size range, geographic location, source category, and season. These findings suggest that the components of PM--associated with certain categories of sources--are responsible for the observed adverse health effects. Most importantly, the responsible components and source categories vary with the health-related endpoints being assessed. Across all studies, fossil-fuel combustion source categories were most consistently associated with both short- and long-term adverse effects of PM2.5 exposure. The components that originate from the Residual Oil Combustion and Traffic source categories were most closely associated with short-term effects; and components from the Coal Combustion category were more closely associated with long-term effects.

OBJECTIVES: We sought to analyze how early exposure to the 1918 influenza pandemic is associated with old-age mortality by cause of death. METHODS: We analyzed the National Health Interview Survey (n = 81,571; follow-up 1989-2006; 43,808 deaths) and used year and quarter of birth to assess timing of pandemic exposure. We used Cox proportional and Fine-Gray competing hazard models for all-cause and cause-specific mortality, respectively. RESULTS: Cohorts born during pandemic peaks had excess all-cause mortality attributed to increased noncancer mortality. We found evidence for a trade-off between noncancer and cancer causes: cohorts with high noncancer mortality had low cancer mortality, and vice versa. CONCLUSIONS: Early disease exposure increases old-age mortality through noncancer causes, which include respiratory and cardiovascular diseases, and may trigger a trade-off in the risk of cancer and noncancer causes. Potential mechanisms include inflammation or apoptosis. The findings contribute to our understanding of the causes of death behind the early disease exposure-later mortality association. The cancer-noncancer trade-off is potentially important for understanding the mechanisms behind these associations.

OBJECTIVE: To describe the prevalence of physical function limitations among a nationally representative sample of adults with prediabetes. RESEARCH DESIGN AND METHODS: We performed a cross-sectional analysis of 5,991 respondents>/=53 years of age from the 2006 wave of the Health and Retirement Study. All respondents self-reported physical function limitations and comorbidities (chronic diseases and geriatric conditions). Respondents with prediabetes reported no diabetes and had a measured glycosylated hemoglobin (HbA1c) of 5.7-6.4%. Descriptive analyses and logistic regressions were used to compare respondents with prediabetes versus diabetes (diabetes history or HbA1c>/=6.5%) or normoglycemia (no diabetes history and HbA1c<5.7%). RESULTS: Twenty-eight percent of respondents>/=53 years of age had prediabetes; 32% had mobility limitations (walking several blocks and/or climbing a flight of stairs); 56% had lower-extremity limitations (getting up from a chair and/or stooping, kneeling, or crouching); and 33% had upper-extremity limitations (pushing or pulling heavy objects and/or lifting>10 lb). Respondents with diabetes had the highest prevalence of comorbidities and physical function limitations, followed by those with prediabetes, and then normoglycemia (P<0.05). Compared with respondents with normoglycemia, respondents with prediabetes had a higher odds of having functional limitations that affected mobility (odds ratio [OR] 1.48), the lower extremities (OR 1.35), and the upper extremities (OR 1.37) (all P<0.01). The higher odds of having lower-extremity limitations remained after adjusting for age, sex, and body mass index (OR 1.21, P<0.05). CONCLUSIONS: Comorbidities and physical function limitations are prevalent among middle-aged and older adults with prediabetes. Effective lifestyle interventions to prevent diabetes must accommodate physical function limitations.