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Heat exposure of a population is often estimated by applying temperatures from outdoor monitoring stations. However, this can lead to exposure misclassification if residents do not live close to the monitoring station and temperature varies over small spatial scales due to land use/built environment variability, or if residents generally spend more time indoors than outdoors. Here, we compare summertime temperatures measured inside 145 homes in low-income households in Baltimore city with temperatures from the National Weather Service weather station in Baltimore. There is a large variation in indoor temperatures, with daily-mean indoor temperatures varying from 10 °C lower to 10 °C higher than outdoor temperatures. Furthermore, there is only a weak association between the indoor and outdoor temperatures across all houses, indicating that the outdoor temperature is not a good predictor of the indoor temperature for the residences sampled. It is shown that much of the variation is due to differences in the availability of air conditioning (AC). Houses with central AC are generally cooler than outdoors (median difference of − 3.4 °C) while those with no AC are generally warmer (median difference of 1.4 °C). For the collection of houses with central or room AC, there is essentially no relationship between indoor and outdoor temperatures, but for the subset of houses with no AC, there is a weak relationship (correlation coefficient of 0.36). The results presented here suggest future epidemiological studies of indoor exposure to heat would benefit from information on the availability of AC within the population. [ABSTRACT FROM AUTHOR]

Indoor air pollution has been linked to adverse chronic obstructive pulmonary disease ( COPD) health, but specific causative agents have not yet been identified. We evaluated the role of indoor endotoxin exposure upon respiratory health in former smokers with COPD. Eighty-four adults with moderate to severe COPD were followed longitudinally and indoor air and dust samples collected at baseline, 3 and 6 months. Respiratory outcomes were repeatedly assessed at each time point. The associations between endotoxin exposure in air and settled dust and health outcomes were explored using generalizing estimating equations in multivariate models accounting for confounders. Dust endotoxin concentrations in the main living area were highest in spring and lowest in fall, while airborne endotoxins remained steady across seasons. Airborne and dust endotoxin concentrations were weakly correlated with one another ( r s = +0.24, P = 0.005). Endotoxin concentrations were not significantly associated with respiratory symptoms, rescue medication use, quality of life, or severe exacerbations. In vitro whole-blood assays of the pro-inflammatory capacity of PM10 filters with and without endotoxin depletion demonstrated that the endotoxin component of indoor air pollution was not the primary trigger for interleukin-1 β release. Our findings support that endotoxin is not the major driver in the adverse effects of indoor PM upon COPD morbidity. [ABSTRACT FROM AUTHOR]

Background Vitamin D deficiency may be associated with an increased risk of asthma. Objective We studied the association between 25-hydroxy (25- OH) vitamin D deficiency and asthma prevalence in two Peruvian populations close to the equator but with disparate degrees of urbanization. Methods We conducted a population-based study in 1441 children in two communities in Peru, of which 1134 (79%) provided a blood sample for 25- OH vitamin D analysis. Results In these 1134 children, mean age was 14.8 years; 52% were boys; asthma and atopy prevalence was 12% in Lima vs. 3% in Tumbes ( P < 0.001) and 59% in Lima vs. 41% in Tumbes ( P < 0.001), respectively; and, mean 25-OH vitamin D level was 20.8 ng/ mL in Lima vs. 30.1 ng/ mL in Tumbes ( P < 0.001). Prevalence of 25-OH vitamin D deficiency (< 20 ng/ mL) was 47% in Lima vs. 7% in Tumbes ( P < 0.001). In multi-variable logistic regression, we found that lower 25-OH vitamin D levels were associated with an increased odds of asthma (OR = 1.7 per each 10 ng/ mL decrease in 25-OH vitamin D levels, 95% CI 1.2-2.6; P < 0.01). In stratified analyses, the association between lower 25-OH vitamin D levels and asthma was limited to children with atopy (OR = 2.2, 95% CI 1.3-3.6) and not in those without atopy (OR = 0.9, 95% CI 0.5-2.0). We did not find associations between 25- OH vitamin D levels and other clinical biomarkers for asthma, including exhaled nitric oxide, total serum IgE and pulmonary function. Conclusion and Clinical Relevance Both asthma and 25- OH vitamin D deficiency were common among children living in Lima (latitude = 12.0°S) but not among those in Tumbes (3.6°S). The relationship between 25- OH vitamin D deficiency and asthma was similar in both sites and was limited among children with atopy. Future supplementation trials may need to consider stratification by atopy at the time of design. [ABSTRACT FROM AUTHOR]

Background Allergic rhinitis is a disease with a high global disease burden, but risk factors that contribute to this condition are not well understood. Objective To assess the prevalence and risk factors of allergic rhinitis in two Peruvian populations with disparate degrees of urbanization. Methods We conducted a population-based, cross-sectional study on 1441 children aged 13-15 years at enrollment (mean age 14.9 years, 51% boys) to investigate the prevalence of allergic disease. We used a standardized, Spanish validated questionnaire to determine the prevalence of allergic rhinitis and asked about sociodemographics and family history of allergies. Children also underwent spirometry, exhaled nitric oxide, allergy skin testing to 10 common household allergens and provided a blood sample for measurement of 25 OH vitamin D and total serum IgE. Results Overall prevalence of allergic rhinitis was 18% (95% CI 16% to 20%). When stratified by site, the prevalence of allergic rhinitis was 23% Lima vs. 13% in Tumbes ( P < 0.001); however, this difference was no longer significant after controlling for subject-specific factors ( P = 0.95). There was a strong association with other allergic diseases: 53% of children with asthma had allergic rhinitis vs. 15% in those without asthma ( P < 0.001) and 42% of children with eczema vs. 17% of those without eczema ( P < 0.001). Important risk factors for allergic rhinitis were parental rhinitis (adjusted OR = 3.0, 95% CI 1.9-4.7 for 1 parent and adjusted OR = 4.4, 95% CI 1.5-13.7 for 2 parents); allergic sensitization to common household aeroallergens (1.6, 1.1-2.3); being overweight (1.5, 1.0-2.3); exhaled nitric oxide ≥20 ppb (1.9, 1.3-2.7); and total serum IgE ≥ 95th percentile (2.4, 1.2-4.8). Population attributable risk of important factors for allergic rhinitis were 25% for high exhaled nitric oxide, 22% for allergic sensitization to common household aeroallergens, 22% for paternal rhinitis, 10% for being overweight and 7% for an elevated total serum IgE. Conclusion and Clinical Relevance Allergic rhinitis was prevalent in both settings, and important risk factors include elevated exhaled nitric oxide, allergic sensitization to common household aeroallergens, parental rhinitis, being overweight and high total serum IgE. When considering subject-specific factors, the difference in prevalence between the urban and rural settings became non-important. [ABSTRACT FROM AUTHOR]

Nitrogen dioxide ( NO2), a by-product of combustion produced by indoor gas appliances such as cooking stoves, is associated with respiratory symptoms in those with obstructive airways disease. We conducted a three-armed randomized trial to evaluate the efficacy of interventions aimed at reducing indoor NO2 concentrations in homes with unvented gas stoves: (i) replacement of existing gas stove with electric stove; (ii) installation of ventilation hood over existing gas stove; and (iii) placement of air purifiers with high-efficiency particulate air ( HEPA) and carbon filters. Home inspection and NO2 monitoring were conducted at 1 week pre-intervention and at 1 week and 3 months post-intervention. Stove replacement resulted in a 51% and 42% decrease in median NO2 concentration at 3 months of follow-up in the kitchen and bedroom, respectively ( P = 0.01, P = 0.01); air purifier placement resulted in an immediate decrease in median NO2 concentration in the kitchen (27%, P < 0.01) and bedroom (22%, P = 0.02), but at 3 months, a significant reduction was seen only in the kitchen (20%, P = 0.05). NO2 concentrations in the kitchen and bedroom did not significantly change following ventilation hood installation. Replacing unvented gas stoves with electric stoves or placement of air purifiers with HEPA and carbon filters can decrease indoor NO2 concentrations in urban homes. [ABSTRACT FROM AUTHOR]

Context: Endothelial function is abnormal in chronic obstructive pulmonary disease (COPD); whether endothelial dysfunction causes COPD is unknown. Objective: Test associations of endothelial biomarkers with FEV1 using instrumental variables. Methods: Among 26 907 participants with spirometry, ICAM-1, P-selectin, E-selectin and endothelin-1 were measured in subsets. Results: ICAM-1 and P-selectin were inversely associated with FEV1 among European-Americans (−29 mL and −34 mL per standard deviation of log-transformed biomarker, p < 0.001), as was endothelin-1 among African-Americans (−22 mL, p = 0.008). Genetically-estimated ICAM-1 and P-selectin were not significantly associated with FEV1. The instrumental variable for endothelin-1 was non-informative. Conclusion: Although ICAM-1, P-selectin and endothelin-1 were inversely associated with FEV1, associations for ICAM-1 and P-selectin do not appear causal. [ABSTRACT FROM AUTHOR]

Background: Allergic diseases are thought to involve dysregulated activation of T cells including CD4+ lymphocytes. T-cell activation results in changes in gene expression, but the optimal method to study gene expression profiles in T cells, and how this changes over time, are not known. Methods: Circulating CD4+ T cells were obtained from subjects with atopic asthma, nonatopic asthma or nonallergic controls, and total mRNA was rapidly isolated. Atopy was defined as positive skin prick test to one of nine allergens. Gene expression was analyzed using hybridization and Affymetrix® oligonucleotide arrays (Hu133A and Hu133B chips, n = 84), or by reverse transcription-polymerase chain reaction (RT-PCR) with a pathway-targeted array (Human Th1–Th2–Th3 RT2 ProfilerTM PCR Array, Superarray, n = 16). Results: Using Affymetrix arrays, it was difficult to discern a dominant allergy-associated profile because of heterogeneity in gene expression profiles. In contrast, a Th2-like signature was evident using RT-PCR arrays with increased expression of expected genes (e.g. IL-4, 5, 9, and 13, all P < 0.05) as well as unexpected gene transcripts (e.g. osteopontin). Gene expression profiles were relatively stable over time in circulating CD4+ T cells from two subjects using both platforms. Conclusions: Unstimulated CD4+ T cells isolated from allergic subjects express a characteristic profile of genes when analyzed using RT-PCR based microarrays. [ABSTRACT FROM AUTHOR]