The relationship of lung function with ambient temperature

<div><p>Background</p><p>Lung function is complex trait with both genetic and environmental factors contributing to variation. It is unknown how geographic factors such as climate affect population respiratory health.</p><p>Objective</p><p>To determine whether ambient air temperature is associated with lung function (FEV₁) in the general population.</p><p>Design/Setting</p><p>Associations between spirometry data from two National Health and Nutrition Examination Survey (NHANES) periods representative of the U.S. non-institutionalized population and mean annual ambient temperature were assessed using survey-weighted multivariate regression.</p><p>Participants/Measurements</p><p>The NHANES III (1988–94) cohort included 14,088 individuals (55.6% female) and the NHANES 2007–12 cohort included 14,036 individuals (52.3% female), with mean ages of 37.4±23.4 and 34.4±21.8 years old and FEV₁ percent predicted values of 99.8±15.8% and 99.2±14.5%, respectively.</p><p>Results</p><p>After adjustment for confounders, warmer ambient temperatures were associated with lower lung function in both cohorts (NHANES III <i>p</i> = 0.020; NHANES 2007–2012 <i>p</i> = 0.014). The effect was similar in both cohorts with a 0.71% and 0.59% predicted FEV₁ decrease for every 10°F increase in mean temperature in the NHANES III and NHANES 2007–2012 cohorts, respectively. This corresponds to ~2 percent predicted difference in FEV₁ between the warmest and coldest regions in the continental United States.</p><p>Conclusions</p><p>In the general U.S. population, residing in regions with warmer ambient air temperatures was associated with lower lung function with an effect size similar to that of traffic pollution. Rising temperatures associated with climate change could have effects on pulmonary function in the general population.</p></div

Survey weighted univariate regressions.

<p>Survey weighted univariate regressions.</p

Survey weighted means (± S.E.) for study cohorts.

<p>Survey weighted means (± S.E.) for study cohorts.</p

Adjusted survey weighted multivariate regressions to assess the effect of spirometry temperature in the NHANES III cohort^*.

<p>Adjusted survey weighted multivariate regressions to assess the effect of spirometry temperature in the NHANES III cohort^{<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0191409#t004fn001" target="_blank">*</a>}.</p

Survey weighted multivariate regressions unadjusted and adjusted for potential confounders for study population.

<p>Survey weighted multivariate regressions unadjusted and adjusted for potential confounders for study population.</p

Wearable Potentiometric Chloride Sweat Sensor: The Critical Role of the Salt Bridge

The components of sweat provide an array of potential biomarkers for health and disease. Sweat chloride is of interest as a biomarker for cystic fibrosis, electrolyte metabolism disorders, electrolyte balance, and electrolyte loss during exercise. Developing wearable sensors for biomarkers in sweat is a major technological challenge. Potentiometric sensors provide a relatively simple technology for on-body sweat chloride measurement, however, equilibration between reference and test solutions has limited the time over which accurate measurements can be made. Here, we report on a wearable potentiometric chloride sweat sensor. We performed parametric studies to show how the salt bridge geometry determines equilibration between the reference and test solutions. From these results, we show a sweat chloride sensor can be designed to provide accurate measurements over extended times. We then performed on-body tests on healthy subjects while exercising to establish the feasibility of using this technology as a wearable device

Key haplotypes in <i>MSRA</i> region showing association with MI in TSS cohort.

<p><b>^a</b>Numbers in parentheses indicate physical position on chr8 in base pairs (NCBI Build 36).</p><p><b>^b</b>All observed haplotypes with frequency >1% are shown; bold indicates haplotypes noted in text.</p><p>*Protective haplotypes that reached statistical significance after Bonferroni correction for all 2,890 haplotypes tested (<i>P</i><1.73×10⁻⁵).</p>‡<p>Near significant risk haplotype containing rs614197 (italicized), the SNP that was most highly associated with MI in the initial analysis.</p

Regional association of SNPs within a region of linkage to MI on chromosome 8p23.1.

<p>The inset plot shows the locus linked to MI on chromosome 8 identified by Blackman, et al <a href="http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.1002580#pgen.1002580-Blackman1" target="_blank">[12]</a>. The green shaded region under the peak extending from 17.9 cM (8.2 Mb) to 29.0 cM (17.2 Mb), where LOD score >1, indicates the region analyzed in the main plot. The map position of <i>MSRA</i> is denoted by an arrow at ∼20.2 cM. In the main plot, <i>P</i> values are plotted in log scale versus physical location in Mb. The SNP showing the strongest association with MI, rs614197, is represented by a diamond (<i>P</i> = 8.35×10⁻⁶). SNPs surrounding rs614197 are color coded to reflect their LD with this SNP (pair-wise r² using 1000 Genomes CEU, August 2009). The dashed line indicates the threshold for region-wide significance after Bonferroni correction for 2,896 SNPs (P<1.73×10⁻⁵). Genes, exon positions, and direction of transcription are denoted below plot (human genome build 18). Nine genes outside this interval were omitted for display purposes: <i>C8orf12</i>, <i>FAM167A</i>, <i>DEFB136</i>, <i>DEFB135</i>, <i>DEFB134</i>, <i>FAM66D</i>, <i>LOC392196</i>, <i>USP17L2</i>, and <i>FAM86B1</i>. The blue shaded region represents the 2 Mb encompassing rs614197 in which haplotype association was tested (see <a href="http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.1002580#pgen.1002580.s001" target="_blank">Figure S1</a>).</p

Kaplan-Meier survival curves in CF mice according to <i>Msra</i> genotype.

<p>A. CF mice homozygous for a null <i>Cftr</i> allele (<i>Cftr</i>^−/−) and wild-type for <i>Msra</i> show high mortality due to intestinal obstruction around the time of weaning (ca. 21 days; n = 30). In contrast, survival is markedly improved in <i>Cftr</i>^−/− mice lacking one (n = 33) or two <i>Msra</i> alleles (n = 46) compared to wild-type (<i>P</i> = 0.022 and <i>P</i> = 0.0001, respectively; log-rank test). B. CF mice homozygous for a missense <i>Cftr</i> allele (<i>Cftr</i>^R117H/R117H) and wild-type for <i>Msra</i> display a low rate of mortality due to intestinal obstruction around the time of weaning (n = 14). Survival is not affected in <i>Cftr</i>^R117H/R117H mice lacking one (n = 51) or two (n = 51) <i>Msra</i> alleles compared to wild-type.</p

Patient characteristics.

<p><b>^a</b>Primary analysis included subjects from 133 “MI families” in which at least one sibling had MI.</p><p><b>^b</b><i>CFTR</i> mutation-specific analysis (i.e. p.Gly551Asp vs. p.Phe508del) utilized the entire TSS sample.</p