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BackgroundMost studies on racial disparities in childhood atopic dermatitis (AD) did not consider persistent AD or account for differences in vitamin D status.MethodsAmong 1418 children recruited from a Massachusetts HMO into the pre-birth Project Viva cohort, we examined associations of child’s race/ethnicity with maternal report of child’s AD diagnosis by annual questionnaires. We used multivariable logistic regression adjusted for socio- demographics (maternal education, household income, smoking exposure, parental atopy, breastfeeding duration, child sex) and cord blood 25-hydroxyvitamin D, to estimate odds ratios (OR) of incident AD by early childhood (median age 3.3 years), and, among young children with AD, OR of persistence through mid-childhood (median age 7.7 years).Results68% of children were non-Hispanic white, 13% were black, and 19% were other race/ethnicities. By early childhood, 497/1418 (35%) had incident AD. Among those with both AD and follow- up to mid-childhood, 58/389 (15%) had persistent AD. Black children were more likely than white children to have incident AD (OR 2.21; 95% CI 1.60, 3.04), even after adjustment for socio-demographics (2.64; 1.79, 3.89) and vitamin D levels (1.93; 1.07, 3.48). Black children also had higher odds of persistent AD (3.21; 1.63, 6.32; fully adjusted 4.60; 1.24, 17.13). Children with other race/ethnicities had non-significantly higher risk for AD incidence and persistence than white children.ConclusionIn this cohort, compared with white children, black children and children with other race/ethnicities were at higher risk for incident and persistent AD, even after accounting for differences in socio-demographic characteristics and vitamin D levels.

Rationale: Sleep-disordered breathing (SDB), the recurrent episodic disruption of normal breathing during sleep, affects as much as 17% of U.S. adults, and may be more prevalent in poor urban environments. SDB and air pollution have been linked to increased cardiovascular diseases and mortality, but the association between pollution and SDB is poorly understood.Objectives: We used data from the Sleep Heart Health Study (SHHS), a U.S. multicenter cohort study assessing cardiovascular and other consequences of SDB, to examine whether particulate air matter less than 10 μm in aerodynamic diameter (PM(10)) was associated with SDB among persons 39 years of age and older.Methods: Using baseline data from SHHS urban sites, outcomes included the following: the respiratory disturbance index (RDI); percentage of sleep time at less than 90% O(2) saturation; and sleep efficiency, measured by overnight in-home polysomnography. We applied a fixed-effect model containing a city effect, controlling for potential predictors. In all models we included both the 365-day moving averages of PM(10) and temperature (long-term effects) and the differences between the daily measures of these two predictors and their 365-day average (short-term effects).Measurements and Main Results: In summer, increases in RDI or percentage of sleep time at less than 90% O(2) saturation, and decreases in sleep efficiency, were all associated with increases in short-term variation in PM(10). Over all seasons, we found that increased RDI was associated with an 11.5% (95% confidence interval: 1.96, 22.01) increase per interquartile range increase (25.5°F) in temperature.Conclusions: Reduction in air pollution exposure may decrease the severity of SDB and nocturnal hypoxemia and may improve cardiac risk. [ABSTRACT FROM AUTHOR]

Frequently, exposure data are measured over time on a grid of discrete values that collectively define a functional observation. In many applications, researchers are interested in using these measurements as covariates to predict a scalar response in a regression setting, with interest focusing on the most biologically relevant time window of exposure. One example is in panel studies of the health effects of particulate matter (PM), where particle levels are measured over time. In such studies, there are many more values of the functional data than observations in the data set so that regularization of the corresponding functional regression coefficient is necessary for estimation. Additional issues in this setting are the possibility of exposure measurement error and the need to incorporate additional potential confounders, such as meteorological or co-pollutant measures, that themselves may have effects that vary over time. To accommodate all these features, we develop wavelet-based linear mixed distributed lag models that incorporate repeated measures of functional data as covariates into a linear mixed model. A Bayesian approach to model fitting uses wavelet shrinkage to regularize functional coefficients. We show that, as long as the exposure error induces fine-scale variability in the functional exposure profile and the distributed lag function representing the exposure effect varies smoothly in time, the model corrects for the exposure measurement error without further adjustment. Both these conditions are likely to hold in the environmental applications we consider. We examine properties of the method using simulations and apply the method to data from a study examining the association between PM, measured as hourly averages for 1-7 days, and markers of acute systemic inflammation. We use the method to fully control for the effects of confounding by other time-varying predictors, such as temperature and co-pollutants. [ABSTRACT FROM AUTHOR]

Myocardial bridging is not uncommon. However, hemodynamic instability in the setting of myocardial bridging is rare. We describe an unusual case of a 47-year-old woman whose increased use of inhaled albuterol led to a non-ST-segment elevation myocardial infarction and unmasking of hemodynamically significant myocardial bridging. We detail its diagnosis through myocardial perfusion imaging and coronary angiography. To our knowledge, this is the first time previously undiagnosed myocardial bridging has led to a myocardial infarction in the setting of inhaled albuterol use. [ABSTRACT FROM AUTHOR]

Background: Particulate air pollution has been associated with several adverse cardiovascular health outcomes, and people with diabetes may be especially vulnerable. One potential pathway is inflammation and endothelial dysfunction-processes in which cell adhesion molecules and inflammatory markers play important roles.Aim: To examine whether plasma levels of soluble intercellular adhesion molecule 1 (ICAM-1), vascular cell adhesion molecule 1 (VCAM-1) and von Willebrand factor (vWF) were associated with particle exposure in 92 Boston area residents with type 2 diabetes.Methods: Daily average ambient levels of air pollution (fine particles (PM2.5), black carbon (BC) and sulphates) were measured approximately 500 m from the patient examination site and evaluated for associations with ICAM-1, VCAM-1 and vWF. Linear regressions were fit to plasma levels of ICAM-1, VCAM-1 and vWF, with the particulate pollutant index, apparent temperature, season, age, race, sex, glycosylated haemoglobin, cholesterol, smoking history and body mass index as predictors.Results: Air pollutant exposure measures showed consistently positive point estimates of association with the inflammatory markers. Among participants not taking statins and those with a history of smoking, associations between PM(2.5), BC and VCAM-1 were particularly strong.Conclusions: These results corroborate evidence suggesting that inflammatory mechanisms may explain the increased risk of air pollution-associated cardiovascular events among those with diabetes. [ABSTRACT FROM AUTHOR]

Exposure to elevated levels of endotoxin in family-room dust was previously observed to be significantly associated with increased wheeze in the first year of life among a cohort of 404 children in the Boston, Massachusetts, metropolitan area. However, it is likely that family-room dust endotoxin was a surrogate for airborne endotoxin exposure. Therefore, a related substudy characterized the relationship between levels of airborne household endotoxin and the level of endotoxin present in house dust, in addition to identifying other significant predictors of airborne endotoxin in the home. We now reexamine the relationship between endotoxin exposure and wheeze under the assumption that the level of airborne endotoxin in the home is the exposure of interest and that the amount of endotoxin in household dust is a surrogate for this exposure. We applied a measurement error correction technique, using all available data to estimate the effect of endotoxin exposure in terms of airborne concentration and accounting for the measurement error induced by using house-dust endotoxin as a surrogate measure in the portion of the data in which airborne endotoxin could not be directly measured. After adjusting for confounding by lower respiratory infection status and race/ethnicity, endotoxin exposure was found to be significantly associated with a nearly 6-fold increase in prevalence of wheeze for a one interquartile range increase in airborne endotoxin (95% confidence interval, 1.2-26) among the 360 children in households with dust endotoxin levels between the 5th and 95th percentiles. [ABSTRACT FROM AUTHOR]

OBJECTIVES: We reported previously that 24-hr moving average ambient air pollution concentrations were positively associated with ventricular arrhythmias detected by implantable cardioverter defibrillators (ICDs). ICDs also detect paroxysmal atrial fibrillation episodes (PAF) that result in rapid ventricular rates. In this same cohort of ICD patients, we assessed the association between ambient air pollution and episodes of PAF. DESIGN: We performed a case-crossover study. PARTICIPANTS: Patients who lived in the Boston, Massachusetts, metropolitan area and who had ICDs implanted between June 1995 and December 1999 (n=203) were followed until July 2002. EVALUATIONS/MEASUREMENTS: We used conditional logistic regression to explore the association between community air pollution and 91 electrophysiologist-confirmed episodes of PAF among 29 subjects. RESULTS: We found a statistically significant positive association between episodes of PAF and increased ozone concentration (22 ppb) in the hour before the arrhythmia (odds ratio=2.08; 95% confidence interval=1.22, 3.54; p=0.001). The risk estimate for a longer (24-hr) moving average was smaller, thus suggesting an immediate effect. Positive but not statistically significant risks were associated with fine particles, nitrogen dioxide, and black carbon. CONCLUSIONS: Increased ambient O3 pollution was associated with increased risk of episodes of rapid ventricular response due to PAF, thereby suggesting that community air pollution may be a precipitant of these events. [ABSTRACT FROM AUTHOR]

Objectives: To familiarize the otolaryngologist with the evaluation and management of cervicodorsal manifestations of lipodystrophy in patients who have been treated with HIV protease inhibitor medications. In addition, to share the benefits obtainable with ultrasonic tumescent liposuction treatment. Study Design: Retrospective chart review of patients presenting to the senior author with symptomatic hypertrophic cervicodorsal fat pad attributable to HIV infection and HIV protease inhibitor use. Results: Eight patients presented for evaluation of hypertrophic cervicodorsal fat pads between January 1, 2002 and December 31, 2004. All patients had been on protease inhibitors in the past and had minimal resolution after discontinuing offending agent. Most common presenting problems include disfigurement, limited range of upper extremity and neck motion, neck and back discomfort, and difficulty with sleep including sleep-study-confirmed obstructive sleep apnea. Five of eight patients underwent ultrasonic tumescent liposuction. Three patients had satisfactory improvement of symptoms after the first surgery, whereas the other two required additional operative sessions. No complications of hematoma, seroma, infection, prolonged pain, or re-accumulation of fat pad were encountered. The primary obstacle in the three nonoperative patients was insurance denial on the basis of deemed lack of established necessity. Conclusions: Cervicodorsal lipodystrophy is a well-recognized outcome of prolonged HIV infection and side effect of certain HIV medications. Patients may present with both esthetic and functional issues related to the excess tissue. Although cessation of associated medications may halt further progression, this alone does resolve the symptoms. Ultrasonic tumescent liposuction is shown in this study to be a well-suited modality for reduction of this fibrous adipose tissue. Multiple sessions may be necessary to achieve satisfactory results because of the tenacity of the tissue. It is important for the otolaryngologist to be familiar with the head and neck issues relevant to this disorder and its treatment. [ABSTRACT FROM AUTHOR]

We investigated the association between fine particulate air pollution and oxygen saturation as measured with a peripheral oxygen saturation monitor during a 12-week repeated-measures study of 28 older Boston residents. Oxygen saturation and air pollution particulates with a mean diameter less than or equal to 2.5 microm were measured continuously during a protocol of rest, standing, exercise, postexercise rest, and 20 cycles of slow, paced breathing. In fixed-effect models, mean pollution concentration was associated with reduced oxygen saturation during the baseline rest period (6 hours: mean, -0.173%; 95% confidence interval [CI], -0.345 to -0.001), postexercise (6 hours: mean, -0.173%; 95% CI, -0.332 to -0.014), with a trend toward decrease during postexercise paced breathing (6 hours: mean, -0.142%; 95% CI, -0.292 to 0.007) but not during exercise. Participants taking beta-blockers had a greater pollution-related decrease in oxygen saturation at rest (6 hours: mean, -0.769%; 95% CI, -1.210 to -0.327) (interaction for particulates with a mean diameter less than or equal to 2.5 microm by beta-blocker, p < 0.0005) than did those not taking beta-blockers (p > 0.25). The reduction in oxygen saturation associated with air pollution may result from subtle particulate-related pulmonary vascular and/or inflammatory changes. Further investigation may contribute to our understanding of the mechanisms through which particulates may increase respiratory and cardiac morbidity among vulnerable populations. [ABSTRACT FROM AUTHOR]

The association between home dampness and lower respiratory symptoms in children has been well documented. Whether fungal exposures contribute to this association is uncertain. In a prospective birth cohort of 499 children of parents with asthma/allergies, we examined in-home fungal concentrations as predictors of lower respiratory illnesses (LRI) (croup, pneumonia, bronchitis, and bronchiolitis) in the first year. In multivariate analyses, we found a significant increased relative risk (RR) between LRI and high levels (more than the 90th percentile) of airborne Penicillium (RR = 1.73, 95% confidence interval [CI], 1.23, 2.43), dust-borne Cladosporium (RR = 1.52; CI, 1.02, 2.25), Zygomycetes (RR = 1.96; CI, 1.35, 2.83), and Alternaria (RR = 1.51; CI, 1.00, 2.28), after controlling for sex, presence of water damage or visible mold/mildew, born in winter, breastfeeding, and being exposed to other children through siblings. In a multivariate analysis, the RR of LRI was elevated in households with any fungal level at more than the 90th percentile (RR = 1.86; CI, 1.21, 2.88). Exposure to high fungal levels increased the risk of LRI in infancy, even for infants with nonwheezing LRI. Actual mechanisms remain unknown, but fungi and their components (glucans, mycotoxins, and proteins) may increase the risk of LRI by acting as irritants or through increasing susceptibility to infection. [ABSTRACT FROM AUTHOR]

Among children not selected on the basis of a parental history of atopy, day care attendance in early life is inversely associated with asthma at school age. We examined the relation between day care in the first year of life and asthma, recurrent wheezing, and eczema at the age of 6 years and wheezing in the first 6 years of life among 453 children with parental history of atopy followed from birth. Among all study participants, day care in the first year of life was inversely associated with eczema (odds ratio [OR] = 0.3, 95% confidence interval [CI] = 0.1-0.8). Day care attendance in early life was associated with a decreased risk of asthma (OR = 0.3, 95% CI = 0.1-0.7) and recurrent wheezing (OR = 0.3, 95% CI = 0.1-0.9) at the age of 6 years and with a decreased risk of any wheezing after the age of 4 years only among children without maternal history of asthma. Among children with maternal history of asthma, day care in early life had no protective effect on asthma or recurrent wheezing at the age of 6 years but was instead associated with an increased risk of wheezing in the first 6 years of life. Our findings suggest that maternal history of asthma influences the relation between day care-related exposures and childhood asthma. [ABSTRACT FROM AUTHOR]