Daily hospital admissions for asthma and upper respiratory infections, air pollutants, outdoor pollen, and temperature in New York City, from 1999 to 2009.

<p>Daily hospital admissions for asthma and upper respiratory infections, air pollutants, outdoor pollen, and temperature in New York City, from 1999 to 2009.</p

Confounding effects of hospital admissions for Upper Respiratory Infections (URI) on the associations between asthma hospital admissions in school-age children and ozone (top) and PM_2.5 (bottom).

<p>URI is included in the main model as log-transformed daily counts of all-age URI HA. Squares are point estimates for relative risks of asthma hospital admissions associated with increases in air pollutants. The dashed lines represent ±10% changes in the point estimates from the main model.</p

Relative risks^a of hospital admissions for asthma per 10 ppb increase in ozone concentrations or per 10 μg/m³ increase in PM_2.5 concentrations in New York City, from 1999 to 2009.

<p>Relative risks<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0180522#t002fn002" target="_blank">^a</a> of hospital admissions for asthma per 10 ppb increase in ozone concentrations or per 10 μg/m³ increase in PM_2.5 concentrations in New York City, from 1999 to 2009.</p

Relative risks^a of hospital admissions for asthma per 10 ppb increase in ozone concentrations or per 10 μg/m3 increase in PM_2.5 concentrations at Lag 0–1 in New York City, stratified by socioeconomic status, during warm seasons from 2002 to 2006.

<p>Relative risks<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0180522#t003fn002" target="_blank">^a</a> of hospital admissions for asthma per 10 ppb increase in ozone concentrations or per 10 μg/m3 increase in PM_2.5 concentrations at Lag 0–1 in New York City, stratified by socioeconomic status, during warm seasons from 2002 to 2006.</p

Confounding effects of outdoor pollen on the associations between asthma hospital admissions in school-age children and ozone (top) and PM_2.5 (bottom).

<p>Squares are point estimates for relative risks of asthma hospital admissions associated with increases in air pollutants. The dashed lines represent ±10% changes in the point estimates from the main model.</p

Additional file 1: Fig. S1. of Ambient ozone and asthma hospital admissions in Texas: a time-series analysis

Histograms of pollen counts. A. Original data. B. Log-transformed data. Fig. S2 Histograms of aeroallergen counts. A. Original data. B. Log-transformed data. Table S1 Descriptive statistics of asthma HAs, ambient O3, pollen, and meteorological factors in Dallas, Houston, and Austin, Texas, from 2003 to 2011. Table S2 Associationsa between asthma HAs and ambient O3 concentrations in Dallas, Houston, and Austin, Texas, from 2003 to 2011. Table S3 Associationsa between asthma HAs and ambient O3 concentrations, with adjustment for pollen, in Dallas, Houston, and Austin, Texas, from 2003 to 2011. Table S4 Associations between asthma HAs and ambient O3 concentrations, with adjustment for pollen using alternative dataa for Dallas. Table S5 Associations between asthma HAs and ambient O3 concentrations, with adjustments for pollen and respiratory infection HAs, in Dallas, Houston, and Austin, Texas, from 2003 to 2011. Table S6 Results of asthma HAs per 10 ppb increase in O3 concentrations, with adjustment for aeroallergen, in Dallas and Houston, Texas, from 2003 to 2011. Table S7 Sensitivity analyses with different specifications of temperature and dew point . Table S8 Sensitivity analysesa with different specifications of temporal trend. Table S9 Sensitivity analysesa with O3 concentrations at lag −1 day. Table S10 Associationsa between acute appendicitis HAs and ambient O3 in Dallas, Houston, and Austin, Texas, from 2003 to 2011. (XLSX 95 kb

DataSheet_1_Molecular epidemiology study of programmed death ligand 1 and ligand 2 protein expression assessed by immunohistochemistry in extensive-stage small-cell lung cancer.pdf

ObjectivesPrevalence of tumor PD-L1 expression in extensive-stage small-cell lung cancer (ES-SCLC) is variable, and data on PD-L2 expression are limited. The prognostic values of these biomarkers are not well understood. The current study was conducted to address these data gaps.MethodsA retrospective cohort study of Danish patients with histologically confirmed ES-SCLC and evaluable tumor samples who were receiving usual care before the introduction of immunotherapy was conducted. Protein expression of PD-L1 and PD-L2 was determined by immunohistochemistry (IHC) using the PD-L1 IHC 22C3 pharmDx assay and a PD-L2 IHC assay using a propriety mouse monoclonal antibody. A combined positive score (CPS) of ≥1 was used to define biomarker positivity. Kaplan-Meier plots and Cox proportional hazard models were employed to assess the relationship between PD-L1 and PD-L2 protein expression and OS.ResultsAmong 80 patients, 31% (n=25) and 36% (n=29) had disease positive for PD-L1 and PD-L2, respectively. Overall, 85% (n=68) of patients had concordant PD-L1/PD-L2 status; 26% (n=21) had double positive disease (both PD-L1 and PD-L2 CPS ≥1) and 59% (n=47) had double negative disease (both PD-L1 and PD-L2 CPS ConclusionPD-L1 and PD-L2 positivity were observed in approximately one-third of assessed ES-SCLC tumor samples and were highly congruent. Patients with PD-L1 and PD-L2 positivity, alone or combined, were associated with longer OS, independent of other prognostic factors.</p

Ozone exposure and systemic biomarkers: Evaluation of evidence for adverse cardiovascular health impacts

<div><p></p><p>The US Environmental Protection Agency (EPA) recently concluded that there is likely to be a causal relationship between short-term (< 30 days) ozone exposure and cardiovascular (CV) effects; however, biological mechanisms to link transient effects with chronic cardiovascular disease (CVD) have not been established. Some studies assessed changes in circulating levels of biomarkers associated with inflammation, oxidative stress, coagulation, vasoreactivity, lipidology, and glucose metabolism after ozone exposure to elucidate a biological mechanism. We conducted a weight-of-evidence (WoE) analysis to determine if there is evidence supporting an association between changes in these biomarkers and short-term ozone exposure that would indicate a biological mechanism for CVD below the ozone National Ambient Air Quality Standard (NAAQS) of 75 parts per billion (ppb). Epidemiology findings were mixed for all biomarker categories, with only a few studies reporting statistically significant changes and with no consistency in the direction of the reported effects. Controlled human exposure studies of 2 to 5 hours conducted at ozone concentrations above 75 ppb reported small elevations in biomarkers for inflammation and oxidative stress that were of uncertain clinical relevance. Experimental animal studies reported more consistent results among certain biomarkers, although these were also conducted at ozone exposures well above 75 ppb and provided limited information on ozone exposure-response relationships. Overall, the current WoE does not provide a convincing case for a causal relationship between short-term ozone exposure below the NAAQS and adverse changes in levels of biomarkers within and across categories, but, because of study limitations, they cannot not provide definitive evidence of a lack of causation.</p></div