Hr Mean Research Articles

Using PM2.5 concentrations to estimate the health burden from solid fuel combustion, with application to Irish and Scottish homes.

BackgroundThis study estimates the potential population health burden from exposure to combustion-derived particulate air pollution in domestic settings in Ireland and Scotland.MethodsThe study focused on solid fuel combustion used for heating and the use of gas for cooking. PM2.5 (particulate matter with an aerodynamic diameter < 2.5 μm) was used as the pollutant mixture indicator. Measured PM2.5 concentrations in homes using solid fuels were adjusted for other sources of PM2.5 by subtracting PM2.5 concentrations in homes using gas for cooking but not solid fuel heating. Health burden was estimated for exposure indoors 6 pm - midnight, or all day (24-hour), by combining estimated attributable annual PM2.5 exposures with (i) selected epidemiological functions linking PM2.5 with mortality and morbidity (involving some re-scaling from PM10 to PM2.5, and adjustments ‘translating’ from concentrations to exposures) and (ii) on the current population exposed and background rates of morbidity and mortality.ResultsPM2.5 concentrations in coal and wood burning homes were similar to homes using gas for cooking, used here as a baseline (mean 24-hr PM2.5 concentrations 8.6 μg/m3) and so health impacts were not calculated. Concentrations of PM2.5 in homes using peat were higher (24-hr mean 15.6 μg/m3); however, health impacts were calculated for the exposed population in Ireland only; the proportion exposed in Scotland was very small. The assessment for winter evening exposure (estimated annual average increase of 2.11 μg/m3 over baseline) estimated 21 additional annual cases of all-cause mortality, 55 of chronic bronchitis, and 30,100 and 38,000 annual lower respiratory symptom days (including cough) and restricted activity days respectively.ConclusionNew methods for estimating the potential health burden of combustion-generated pollution from solid fuels in Irish and Scottish homes are provided. The methodology involves several approximations and uncertainties but is consistent with a wider movement towards quantifying risks in PM2.5 irrespective of source. Results show an effect of indoor smoke from using peat (but not wood or coal) for heating and cooking; but they do not suggest that this is a major public health issue.

High Dietary Sodium Reduces Flow Mediated Dilation Similarly in Humans with Salt Sensitive &amp; Salt Resistant Blood Pressure

Recent studies demonstrate that high dietary sodium (HS) impairs endothelial function in those with salt‐resistant (SR) blood pressure (BP), suggesting that the effect of dietary sodium on endothelial function may be independent of BP. We hypothesized that HS would impair flow mediated dilation (FMD) more in those with salt sensitive (SS) BP compared to those with SR BP. Five SS (2M 3W, 43±5yrs) &amp; 7 SR (3M 4W, 45±2.4yrs) subjects were enrolled in a controlled feeding study consisting of a run‐in diet followed by a two phase randomized crossover 7‐day diet perturbation: low dietary sodium (LS) (20 mmol/d) &amp; HS (300 or 350 mmol/d). Brachial artery FMD and 24‐hr BP were assessed on the last day of each diet. SS BP was defined as a change in 24‐hr mean arterial pressure of &gt;; 5 mmHg between LS &amp; HS diets. HS attenuated FMD in both the SS (LS: 12.8±2.4%, HS: 8.2±1.4%, p&lt;0.05) &amp; SR (LS: 10.5±1.8%, HS: 6.9±1.1%, p&lt;0.05) groups. The decline in FMD was not different between groups for the change in FMD (SS: Δ‐4.6±1.2%, SR: Δ‐3.6±1.2%, p&gt;;0.05). These data indicate a HS diet impairs FMD to a similar extent in SS &amp; SR individuals, providing additional evidence suggesting a BP independent effect of dietary sodium on endothelial function.Research funded by NIH grants 2 P20 RR016472–11 &amp; R01 HL104106.

The clinically-tested S1P receptor agonists, FTY720 and BAF312, demonstrate subtype-specific bradycardia (S1P₁) and hypertension (S1P₃) in rat.

Sphingosine-1-phospate (S1P) and S1P receptor agonists elicit mechanism-based effects on cardiovascular function in vivo. Indeed, FTY720 (non-selective S1PX receptor agonist) produces modest hypertension in patients (2–3 mmHg in 1-yr trial) as well as acute bradycardia independent of changes in blood pressure. However, the precise receptor subtypes responsible is controversial, likely dependent upon the cardiovascular response in question (e.g. bradycardia, hypertension), and perhaps even species-dependent since functional differences in rodent, rabbit, and human have been suggested. Thus, we characterized the S1P receptor subtype specificity for each compound in vitro and, in vivo, the cardiovascular effects of FTY720 and the more selective S1P1,5 agonist, BAF312, were tested during acute i.v. infusion in anesthetized rats and after oral administration for 10 days in telemetry-instrumented conscious rats. Acute i.v. infusion of FTY720 (0.1, 0.3, 1.0 mg/kg/20 min) or BAF312 (0.5, 1.5, 5.0 mg/kg/20 min) elicited acute bradycardia in anesthetized rats demonstrating an S1P1 mediated mechanism-of-action. However, while FTY720 (0.5, 1.5, 5.0 mg/kg/d) elicited dose-dependent hypertension after multiple days of oral administration in rat at clinically relevant plasma concentrations (24-hr mean blood pressure = 8.4, 12.8, 16.2 mmHg above baseline vs. 3 mmHg in vehicle controls), BAF312 (0.3, 3.0, 30.0 mg/kg/d) had no significant effect on blood pressure at any dose tested suggesting that hypertension produced by FTY720 is mediated S1P3 receptors. In summary, in vitro selectivity results in combination with studies performed in anesthetized and conscious rats administered two clinically tested S1P agonists, FTY720 or BAF312, suggest that S1P1 receptors mediate bradycardia while hypertension is mediated by S1P3 receptor activation.

Time-Series Analyses of Air Pollution and Mortality in the United States: A Subsampling Approach

Background: Hierarchical Bayesian methods have been used in previous papers to estimate national mean effects of air pollutants on daily deaths in time-series analyses.Objectives: We obtained maximum likelihood estimates of the common national effects of the criteria pollutants on mortality based on time-series data from ≤ 108 metropolitan areas in the United States.Methods: We used a subsampling bootstrap procedure to obtain the maximum likelihood estimates and confidence bounds for common national effects of the criteria pollutants, as measured by the percentage increase in daily mortality associated with a unit increase in daily 24-hr mean pollutant concentration on the previous day, while controlling for weather and temporal trends. We considered five pollutants [PM10, ozone (O3), carbon monoxide (CO), nitrogen dioxide (NO2), and sulfur dioxide (SO2)] in single- and multipollutant analyses. Flexible ambient concentration–response models for the pollutant effects were considered as well. We performed limited sensitivity analyses with different degrees of freedom for time trends.Results: In single-pollutant models, we observed significant associations of daily deaths with all pollutants. The O3 coefficient was highly sensitive to the degree of smoothing of time trends. Among the gases, SO2 and NO2 were most strongly associated with mortality. The flexible ambient concentration–response curve for O3 showed evidence of nonlinearity and a threshold at about 30 ppb.Conclusions: Differences between the results of our analyses and those reported from using the Bayesian approach suggest that estimates of the quantitative impact of pollutants depend on the choice of statistical approach, although results are not directly comparable because they are based on different data. In addition, the estimate of the O3-mortality coefficient depends on the amount of smoothing of time trends.

Abstract 27: Leptin Reduces Food Intake but Fails to Raise Blood Pressure In Mice With Deficiency of Insulin Receptor Substrate (IRS2) In the Entire Brain or Specifically in Pomc Neurons

Insulin receptor substrate (IRS2) is one of three major leptin receptor signaling pathways. However, its role in mediating the chronic effects of leptin on appetite, blood pressure and glucose regulation is unclear. In the present study we tested whether deletion of IRS2 in the whole brain or specifically in proopiomelanocortin (Pomc) neurons attenuates the chronic cardiovascular and metabolic responses to leptin. Mice with IRS2 deletion in the entire brain (IRS2 flox/flox /Nestin-Cre, n=7), specifically in Pomc neurons (IRS2 flox/flox /Pomc-Cre, n=7) and control IRS2 flox/flox mice (n=9) were instrumented with telemetry probes for measurement of 24-hr mean arterial pressure (MAP) and heart rate (HR) and venous catheters for saline or leptin infusions. After a 5-day control period, mice received leptin infusion (2 μg/kg/min, iv) for 7 days. Compared to IRS2 flox/flox , IRS2 flox/flox /Pomc-Cre mice had similar body weight and food intake (33±1 vs 35±1g and 3.6±0.5 vs 3.8±0.2 g/day) and higher MAP and HR (110±2 vs 102±2 mmHg and 641±9 vs 616±5 bpm). IRS2 flox/flox /Nestin-Cre mice were heavier (38±1.5 g), had increased food intake (4.5±1.0 g/day), and higher MAP and HR (108±1.5 mmHg and 659±9.0 bpm) compared to control mice. Leptin infusion for 7 days in control IRS2 flox/flox mice gradually increased MAP by 5 mmHg despite decreasing food intake by 31%. In contrast, leptin infusion did not change MAP in IRS2 flox/flox /Nestin-Cre and IRS2 flox/flox /Pomc-Cre mice. The anorexic effect of leptin, however, was not attenuated in IRS2 flox/flox /Pomc-Cre or IRS2 flox/flox /Nestin-Cre mice (-35% and -34%, respectively). In addition, deletion of IRS2 in the whole brain or Pomc neurons did not impair the ability of leptin to reduce plasma glucose levels (IRS2 flox/flox : 170±15 to 130±12; IRS2 flox/flox /Pomc-Cre: 180±20 to 150±15; IRS2 flox/flox /Nestin-Cre: 160±10 to 131±20 mg/dL) These results indicate that activation of IRS2 signaling in the CNS, and particularly in Pomc neurons, is essential for the long-term actions of leptin to raise MAP and HR but not for its anorexic or antidiabetic effects. (NHLBI-PO1HL51971/ AHA SDG5680016)

Abstract 605: Calcitonin Gene Related Peptide (cgrp) And Its Role In Cardiovascular And Autonomic Regulation

Calcitonin gene related peptide (CGRP) is the most potent microvascular vasodilator known. It exerts effects centrally as well as in the gastrointestinal, respiratory and endocrine system. However, its role in cardiovascular regulation remains controversial. We studied the hemodynamic and autonomic function in CGRP knockout (KO) mice. Blood pressure (BP), heart rate (HR) and activity level were assessed at least one week after mice were implanted with telemeters. Ten CGRP KO and ten wild type (WT) mice (3-4month old) were used in this study. After the recording period, 24-hr urine and blood were collected for assessment of catecholamine and their metabolites. To study the baroreflex sensitivity, phenylephrine and sodium nitroprusside were administered in an acute study with seven mice from each group. We found higher blood pressure at rest during daytime in the CGRP KO mice (102.4 ± 1.652mmHg, vs. 110.5 ± 3.242mmKg, p = 0.039), though not in 24-hr mean arterial pressure (MAP) (105.0 ± 1.789mmHg, vs. 112.1 ± 3.123mmHg, p = 0.05). There was no difference in HR in the two groups (KO: 566.4 ± 12.09; WT: 581.9 ± 8.544, p = 0.31). Norepinephrine was greatly elevated in both plasma and 24-hr urine in KO mice (in urine: KO: 956.7 ± 90.65 pg/ml, WT: 618.1 ± 46.15pg/ml, p = 0.004; in plasma: KO: 2505 ± 596.3pg/ml, n=6, WT: 1168 ± 98.05 pg/ml, p = 0.04). Baroreflex sensitivity was higher in the KO mice (KO: 3.217 ± 0.6852 ms/mmHg, n=7, WT: 1.398 ± 0.2583 ms/mmHg, n=7, p=0.03). The activities level was slightly lower in the KO mice (KO: 6.717 ± 1.059 counts/min, WT: 10.59 ± 1.787 counts/min p = 0.08). However, KO mice that were 6-8 month old were heavier compared to WT mice of the same age (KO: 30.65 ± 0.6009 g, n=17, WT: 27.89 ± 0.6345 g, n=17, p = 0.004). While CGRP might seem to contribute less to the physiological regulation of blood pressure in young adult mice due to their better baroreflex function, it likely contributes to blood pressure and sympathetic activation in older mice. Therefore, further study in BP, HR and metabolic syndromes in old CGRP KO mice is required.

Estimating Mortality Effects of Fine Particulate Matter in Japan: A Comparison of Time-Series and Case-Crossover Analyses

Small particles can reach alveoli without being trapped in the upper respiratory tract and may have a greater impact on health than larger particles. Given the limited knowledge on health effects of fine particulate matter (PM2.5) in Japan, the short-term effects of PM2.5 on daily mortality using the generalized additive model (GAM), generalized linear model (GLIM), and time-stratified case-crossover analysis were estimated. Daily mortality data were obtained from the Ministry of Health, Labor, and Welfare. Air pollution and meteorological data in 20 areas were obtained from the National Institute for Environmental Studies and the Japan Meteorological Agency, respectively. The three methods were compared, adjusting for meteorological variables and co-pollutants, for area-specific analyses and combined area-specific results using meta-analysis with a random-effects model. Daily mortality for elderly aged 65 and over varied from 0.5 to 127.3 by area. The 24-hr mean concentration of PM2.5 ranged from 11.8 to 22.8 μg/m3. Area-specific analyses revealed regional heterogeneity. Furthermore, combined results showed that a 10-μg/m3 increase in PM2.5 for the single-pollutant model at lag1 was associated with a 0.53, 0.77, and 0.88% increase in all-cause mortality for the GAM, GLIM, and case-crossover analysis, respectively. These findings provide robust evidence for the short-term effects of air pollutants on daily mortality in Japan and suggest that differences in estimates obtained from different statistical models should be considered when multipollutant models are used.

Comparison of Commonly Used Placement Sites for Activity Monitoring

No accepted standard exists to evaluate nonsleep-related activity in nursing facility residents where monitors are variously placed at the ankle, waist, wrist, thigh, or embedded in sheeting and set to record activity frequency. To determine optimal placement of activity monitors by site-at the ankle, waist, or wrist for nursing facility residents. Nursing facility residents (N = 16) wore accelerometers at three sites: the nondominant ankle, waist, and wrist, while recording activity in three modes: frequency, duration, and intensity. The natural log activity mean for each mode by site and time revealed no significant differences between the three sites for activity intensity, F(2, 62.78) = .15, p = .86; activity duration, F(2, 69.84) = .50, p = .61; and activity frequency, F(2, 70.04) = 1.25, p = .29. There were no significant site-time interactions. The natural log activity by site and mode indicated no significant differences by site for the 24-hr mean, F(2, 107.64) = .20, p = .82; activity median, F(2, 100.42) = .47, p = .63; and activity standard deviation, F(2, 108.69) = 1.5, p = .23. A significant difference was seen by site for the acceleration index, F(2, 106.32) = 9.57, p < .001. No significant site-mode interactions were found. Similarity between ankle, waist, or wrist sites when measuring activity by various modes, frequency, duration, or intensity, suggests the monitors measure nonsleep-related activity equally well at any of the sites.

대기오염 지표로서의 시정과 일별 호흡기계 사망간의 연관성에 관한 시계열적 연구

There seems to be a consensus among most people that visibility impairment is the most obvious indicator of air pollution. While considerable evidence on the association between air pollution and health outcomes including death and disease have been established, based on industrial complex areas or huge urban cities, time-series, case-crossover and cohort studies, scarce literature exists on the direct evidence for the association between visibility and adverse health outcomes. Our study is assessed the effect of air pollution measured by visibility impairment on respiratory mortality over a period of six years. Relative risks in respiratory deaths were estimated by a Poisson regression model of daily deaths between <TEX>$1999{\sim}2004$</TEX>. Daily counts of respiratory deaths as dependent variable was modelled with daily 24-hr mean visibility measurements (kilometers) as independent variable by means of Poisson regression. This model is controlled for confounding factors such as day of weeks, weather variables, seasonal variables and <TEX>$PM_{10}$</TEX>. The results in this study is observed the statistically significant association between an inverse health effect and visibility during the study period for respiratory mortality (percentage change in the relative risk for all aged -0.57%, 95% Cl, <TEX>$-1.01%{\sim}-0.12%$</TEX>; for <TEX>$0{\sim}15$</TEX> aged -7.12%, 95% Cl, <TEX>$-13.29%{\sim}-0.51%$</TEX>; for 65+ aged -0.43%, 95% Cl, <TEX>$-0.93%{\sim}-0.06%$</TEX> per 1 km increased in visibility). The effect size was much reduced during warm season. Visibility impairment resulting from air pollution is strongly associated with respiratory mortality, especially for children may be spent at outdoor. Our result provides a quick and useful indicator for eliciting the contribution of air pollution to the excess risk of respiratory mortality in Seoul, Korea.

A Pilot Home Study of Temporal Variations of Symptoms in Chronic Obstructive Lung Disease

The purposes of this pilot study are to describe the 24-hr patterns of dyspnea, fatigue, and peak expiratory flow rate (PEFR) in patients with chronic obstructive pulmonary disease (COPD) and examine their interrelationships. The repeated-measures design protocol involved 10 patients with moderate to severe COPD who self-assessed dyspnea, fatigue, and PEFR five times a day for 8 days. Circadian rhythms were documented by single cosinor analysis in 40% of the participants for dyspnea, 60% for fatigue, and 60% for PEFR. The 8-day, 24-hr means of dyspnea and fatigue were moderately correlated; 70% of the sample displayed significant correlations. The means of PEFR and both dyspnea and fatigue were weakly negatively correlated. The findings suggest that circadian rhythm in lung function may not be temporally coupled with the circadian rhythm in dyspnea and fatigue in all patients and that the mean self-perceived levels of dyspnea and fatigue are moderately related.

24-hr ambulatory mean blood pressure vs. pulse pressure as a predictor of silent cerebral infarcts in older Japanese hypertensives

Pulse pressure (PP), an indicator of arterial stiffness, increases with aging. But the impact of PP on the risk of silent cerebral infarct (SCI) remained unclear in Japanese older hypertensives. We performed brain magnetic resonance image and 24-hr ambulatory blood pressure (BP) to 514 old hypertensive subjects in 6 institutes. SCI was detected in 257 subjects (50%) and multiple SCI (≥2 SCI) was detected in 102 subjects (19.8%). Multiple SCI subjects had higher level of age, diabetes, clinic systolic BP, 24-hr ambulatory systolic and diastolic BP, 24-hr mBP and PP than the others. In logistic regression, after adjusting for confounding factors, the odds ratios of multiple SCI for the second, third and forth quartiles of 24-hr mBP to the first were 1.42 (95% confidence interval (CI) 6.52–30.93, p=0.38), 2.19 (95% CI 10.41–46.15, p=0.04) and 4.42 (95% CI 21.85–90.55, P<0.001), and those of 24-hr PP were 1.49 (95% CI 6.54–34.00, p=0.34), 3.54 (95% CI 16.47–76.00, p=0.001), 3.18 (95% CI 14.80–68.12, p=0.003). When 24-hr PP and 24-hr mBP were entered into the same model, only the odds ratios of the forth quartile of mBP to the first remained significant (odds ratio 3.42, 95% CI 1.33–8.81, p=0.01). 24-hr mean blood pressure is a better predictor of multiple silent cerebral infarcts than 24-hr pulse pressure even in older Japanese hypertensives.

Systemic Nitric Oxide Production and 24-Hr Blood Pressure Relationship Following Aerobic Exercise in African-American Hypertensives

1673 We previously showed that hypertensive Caucasians significantly reduced their 24-hr ambulatory blood pressure (ABP) following acute aerobic exercise. It is not known if this type of exercise provides similar BP reductions or if the physiological mechanisms underlying this reduction are the same in African-American hypertensives. PURPOSE: To determine the effects of acute aerobic exercise on 24-hr ABP and whether changes in ABP were related to urinary nitric oxide (NO) excretion levels in African-American hypertensives. METHODS: Seventeen African-Americans with high normal blood pressure or stage 1 hypertension, but otherwise healthy, underwent 50 minutes of treadmill exercise at 65–70% of heart rate reserve. Subjects completed a 24-hr ABP monitoring and urine collection period that was divided into 5 time intervals on a day following exercise and on a day without prior exercise (baseline day). Urine samples were ultrafiltered and assayed for NO end-products (NOX) using the Greiss assay. NOX levels have been used as an index of systemic NO production. RESULTS: There were no significant differences in 24-hr mean arterial BP (MAP) between the exercise and baseline day during any of the time periods. NOX excretion was significantly greater during the first 4-hr time period on the exercise day compared to the baseline day (17.8 ± 5 μmol vs. 7.5 ± 3 μmol, p = 0.009) but not significantly different during the remaining time periods. There was no relationship between 24-h MAP and 24-hr NOX excretion on the baseline day, however there was a significant positive relationship (r = 0.32, p<0.003) during the exercise day. CONCLUSION: In contrast to similar studies in hypertensive Caucasians, acute aerobic exercise did not significantly reduce ABP in hypertensive African-Americans, indicating that the mechanisms underlying acute exercise-induced reductions in blood pressure may be different in African- Americans. It appears that acute exercise may have stimulated the NO system for the 4 hrs following exercise, however, ABP was not affected.

Effects of particulate air pollution on blood pressure and heart rate in subjects with cardiovascular disease: a multicenter approach.

Given the hypothesis that air pollution is associated with elevated blood pressure and heart rate, the effect of daily concentrations of air pollution on blood pressure and heart rate was assessed in 131 adults with coronary heart disease in Helsinki, Finland; Erfurt, Germany; and Amsterdam, the Netherlands. Blood pressure was measured by a digital monitor, and heart rate was calculated as beats per minute from an electrocardiogram recording with the patient in supine position. Particle concentrations were measured at central measuring sites. Linear regression was used to model the association between 24-hr mean concentrations of particles and blood pressure and heart rate. Estimates were adjusted for trend, day of week, temperature, barometric pressure, relative humidity, and medication use. Pooled effect estimates showed a small significant decrease in diastolic and systolic blood pressure in association with particulate air pollution; a slight decrease in heart rate was found. Of the three centers, Erfurt revealed the most consistent particle effects. The results do not support findings from previous studies that had shown an increase in blood pressure and heart rate in healthy individuals in association with particles. However, particle effects might differ in cardiac patients because of medication intake and disease status, both affecting the autonomic control of the heart.

Leptin and exercise.

Short-term exercise (<60 min) studies suggest that leptin concentrations are not acutely affected in healthy males and females. Most reports of reductions in serum leptin may be attributed to circadian rhythms or hemoconcentration. For long-term (> or =60 min) exercise, a reduction in leptin concentrations reported from 1 to 3 hr of running or cycling has been attributed to diurnal reduction in circulating leptin, independent of exercise. Exercise that produces a sufficient energy imbalance (kilocalorie intake versus kilocalorie expenditure) suppresses 24-hr mean and amplitude of the diurnal rhythm of leptin in women. Suppression of leptin concentrations may be counterbalanced by feeding and may explain consistent reports of reductions in leptin concentrations following extreme bouts of exercise such as marathons or ultramarathons. In addition, leptin concentrations are reduced 48 hr after long-term aerobic exercise and long-term resistance exercise is associated with delayed leptin reduction 9 hr postexercise. Training studies have documented that short-term exercise training (< or =12 weeks) does not affect leptin levels, with the exception of patients with type 2 diabetes. Exercise training protocols that result in reduced fat mass will lower leptin concentrations, thus, most investigators have reported leptin concentrations after accounting for fat loss. There are disparate findings concerning long-term (>12 weeks) training studies, with a number of studies finding no effect of training on leptin concentrations other than effects induced by fat loss, and other studies finding reductions in leptin concentrations after accounting for fat loss. Exercise training-induced reductions in leptin levels have been attributed to alterations in energy balance, improvements in insulin sensitivity, alterations in lipid metabolism, and unknown factors. Hormone replacement does not seem to affect leptin adaptations to training. Patients with type 2 diabetes show delayed effects of short-term resistance exercise on leptin concentrations, reduced leptin levels with long-term training, and appear to be more sensitive to training-induced leptin adaptations than other populations.

Association of asthma symptoms with peak particulate air pollution and effect modification by anti-inflammatory medication use.

Maxima of hourly data from outdoor monitors may capture adverse effects of outdoor particulate matter (PM) exposures in asthmatic children better than do 24-hr PM averages, which form the basis of current regulations in the United States. Also, asthmatic children on anti-inflammatory medications may be protected against the proinflammatory effects of air pollutants and aeroallergens. We examined strengths of pollutant associations with asthma symptoms between subgroups of asthmatic children who were on versus not on regularly scheduled anti-inflammatory medications, and tested associations for different particle averaging times. This is a daily panel study of 22 asthmatic children (9-19 years of age) followed March through April 1996 (1,248 person-days). They lived in nonsmoking households in a semirural area of Southern California within the air inversion mixing zone (range, 1,200-2,100 feet) with transported air pollution from urban areas of Southern California. The dependent variable derived from diary ordinal scores is episodes of asthma symptoms that interfered with daily activities. Minimum to 90th-percentile levels of exposures at the outdoor monitoring site were 12-63 microg/m(3) for 1-hr PM < 10 microm in aerodynamic diameter (PM(10)); 8-46 microg/m(3) for 8-hr PM(10); 7-32 microg/m(3) for 24-hr PM(10); 45-88 ppb for 1-hr O(3); 6-26 ppb for 8-hr NO(2); 70-4,714 particles/m(3) for 12-hr daytime fungi; and 12-744 particles/m(3) for 24-hr pollen. Data were analyzed with generalized estimating equations controlling for autocorrelation. There was no confounding by weather, day of week, or linear time trend. Associations were notably stronger in 12 asthmatic children who were not taking anti-inflammatory medications versus 10 subjects who were. Odds ratios (95% confidence intervals) for asthma episodes in relation to lag 0 minimum to 90th-percentile pollutant changes were, respectively, 1-hr maximum PM(10), 1.92 (1.22-3.02) versus 0.96 (0.25-3.69); 8-hr maximum PM(10), 1.68 (0.91-3.09) versus 0.75 (0.18-3.04); 24-hr average PM(10), 1.35 (0.82-2.22) versus 0.80 (0.24-2.69); 1-hr maximum O(3), 1.28 (0.75-2.17) versus 0.76 (0.24-2.44); 8-hr maximum NO(2), 1.91 (1.07-3.39) versus 1.08 (0.30-3.93); 12-hr fungi, 1.89 (1.24-2.89) versus 0.90 (0.35-2.30); 24-hr pollen, 1.90 (0.99-3.67) versus 0.85 (0.18-3.91). Pollutant associations were stronger during respiratory infections in subjects not on anti-inflammatory medications. Although lag 0 1-hr maximum PM(10) showed the strongest association, the most robust associations were for lag 0 and 3-day moving averages (lags 0-2) of 8-hr maximum and 24-hr mean PM(10) in sensitivity analyses testing for thresholds. Most pollutant effects were largely driven by concentrations in the upper quintile. The divergence of exposure-response relationships by anti-inflammatory medication use is consistent with experimental data on inflammatory mechanisms of airborne pollutants and allergens.

Daily rhythm of glucose-induced insulin secretion by isolated islets from intact and pinealectomized rat.

It is well known that pinealectomy induces in rats a diminished glucose tolerance, insulin resistance, a reduction in GLUT4 content in adipose and muscular tissues, a decrease in hepatic and muscular glycogenesis, impairment of glucagon action and an increase in blood pyruvate concentration. In addition, it has been shown that melatonin suppresses insulin secretion in several experimental conditions. The objective of the present study was to investigate the daily rhythm of glucose-induced insulin secretion and glucose oxidation by isolated pancreatic islets and to investigate the effect of chronic absence of melatonin (30 days of pinealectomy) on this rhythmic process. The data obtained confirmed the presence of a strong 24-hr rhythm of insulin secretion by isolated pancreatic islets. In addition, it was demonstrated that the glucose-metabolizing ability of the B-cell follows a daily rhythm phase locked to insulin secretion rhythm. Most interesting, however, was the demonstration that the daily rhythmic processes of insulin secretion and B-cell -[U-14C]-glucose oxidation by isolated pancreatic islets is completely modified by the chronic absence of the pineal gland. Thus, pinealectomy induced in all groups an increase in 24-hr mean glucose-stimulated insulin secretion and [U-14C]-glucose oxidation, in addition to some alterations in the rhythmic amplitude and a remarkable phase-advancing of the daily curves for 8.3 mm glucose (a condition similar to that observed in fed animals and where the B-cells are supposedly more active). These observations strongly suggest that the presence of the pineal gland may be necessary for the proper synchronization of these metabolic rhythms with other circadian rhythms like activity-rest and feeding.

Health Effects of Residential Exposure to Aluminum Plant Air Pollution

In this study, the authors evaluated the relative risk of residential exposure to air pollution from an aluminum plant. The authors used government-compiled data to compare hospital admissions in 1997 for selected respiratory diseases for 2 communities in Brazil. One community, Ouro Preto, was located near an aluminum plant, and the other, Diamantina, was located far from any source of industrial air pollution. The relative risk of hospital admissions for selected respiratory diseases was 4.11 (95% confidence interval = 2.96, 5.70). The risk was highest among individuals between 30 and 39 yr of age (relative risk = 11.70; 95% confidence interval = 1.52, 89.96). Admissions per thousand residents were highest for individuals under 10 yr of age and for individuals older than 70 yr of age. The authors assessed exposure with environmental measurements. Dust deposition was collected in the residences of participants (n = 36 in each location), and the dust was analyzed for aluminum, manganese, magnesium, and calcium content. There were significantly different (p < .05) levels of aluminum in the 2 communities; the highest quantities were found near the aluminum plant. Measurements from independent studies indicated that both 24-hr maximum values and annual mean concentrations of suspended particulate matter exceeded the average of international standards in Ouro Preto (i.e., aluminum plant area). These results suggested that exposure to greater air pollution in the aluminum plant area (i.e., Ouro Preto, Brazil) versus the control area resulted in statistically significant health effects in those individuals who resided in Ouro Preto.

Effect of Air Pollution on Daily Mortality in Hong Kong

In different weather conditions, constituents and concentrations of pollutants, personal exposure, and biologic responses to air pollution may vary. In this study we assessed the effects of four air pollutants on mortality in both cool and warm seasons in Hong Kong, a subtropical city. Daily counts of mortality, due to all nonaccidental causes, and cardiovascular and respiratory diseases were modeled with daily pollutant concentrations [24-hr means for nitrogen dioxide, sulfur dioxide, and particulate matter &lt; 10 microm in aerodynamic diameter (PM(10)); 8-hr mean for ozone]. using Poisson regression. We controlled for confounding factors by fitting the terms in models, in line with those recommended by the APHEA (Air Pollution and Health: a European Approach) protocol. Exposure-response relationships in warm and cool seasons were examined using generalized additive modeling. During the cool season, for a linear extrapolation of 10th-90th percentiles in the pollutant concentrations of all oxidant pollutants, NO(2), SO(2), and O(3), we found significant effects on all the mortality outcomes under study, with relative risks (RR) of 1.04-1.10 (p &lt; 0.038, except p = 0.079 for SO(2) on respiratory mortality). We observed consistent positive exposure-response relationships during the cool season but not during the warm season. The effects of PM(10) were marginally significant (RR = 1.06; p = 0.054) for respiratory mortality but not for the other outcomes (p &gt; 0.135). In this subtropical city, local air quality objectives should take into account that air pollution has stronger health effects during the cool rather than warm season and that oxidant pollutants are more important indicators of health effects than particulates.

Effect of air pollution on daily mortality in Hong Kong.

In different weather conditions, constituents and concentrations of pollutants, personal exposure, and biologic responses to air pollution may vary. In this study we assessed the effects of four air pollutants on mortality in both cool and warm seasons in Hong Kong, a subtropical city. Daily counts of mortality, due to all nonaccidental causes, and cardiovascular and respiratory diseases were modeled with daily pollutant concentrations [24-hr means for nitrogen dioxide, sulfur dioxide, and particulate matter < 10 microm in aerodynamic diameter (PM(10)); 8-hr mean for ozone]. using Poisson regression. We controlled for confounding factors by fitting the terms in models, in line with those recommended by the APHEA (Air Pollution and Health: a European Approach) protocol. Exposure-response relationships in warm and cool seasons were examined using generalized additive modeling. During the cool season, for a linear extrapolation of 10th-90th percentiles in the pollutant concentrations of all oxidant pollutants, NO(2), SO(2), and O(3), we found significant effects on all the mortality outcomes under study, with relative risks (RR) of 1.04-1.10 (p < 0.038, except p = 0.079 for SO(2) on respiratory mortality). We observed consistent positive exposure-response relationships during the cool season but not during the warm season. The effects of PM(10) were marginally significant (RR = 1.06; p = 0.054) for respiratory mortality but not for the other outcomes (p > 0.135). In this subtropical city, local air quality objectives should take into account that air pollution has stronger health effects during the cool rather than warm season and that oxidant pollutants are more important indicators of health effects than particulates.

Day-to-Day Particulate Exposures and Health Changes in Los Angeles Area Residents with Severe Lung Disease

ABSTRACT We measured particulate matter (PM2.5 and PM10) exposures, home temperature, arterial blood oxygen saturation, blood pressure, and lung function in 30 volunteer Los Angeles area residents during four-day intervals. Continuous Holter electrocardiograms were recorded in a subgroup on the first two days. Subjects recorded symptoms and time-activity patterns in diaries during monitoring, and during a reference period one week earlier/later. All subjects had severe chronic obstructive pulmonary disease. PM10 (24-hr mean) at monitoring stations near subjects’ homes averaged 33 μg/m3, and ranged from 9 to 84 μpg/m3. In longitudinal analyses, day-to-day changes in PM2.5 and PM10 outside subjects’ homes significantly tracked concurrent station PM10 (r2 = 0.22 and 0.44, respectively). Indoor and personal concentrations were less related to station readings (r2 ≤ 0.1), but tracked each other (r2 ≥ 0.4). In-home temperatures tracked outdoor temperatures more for lows (r2 = 0.27) than for highs (r2 = 0.10). These longitudinal relationships of subject-oriented and station PM measurements were generally similar to cross-sectional relationships observed previously in similar subjects. Among health measurements, only blood pressure showed reasonably consistent unfavorable longitudinal associations with particulates, more with station or outdoor PM than with indoor or personal PM.