OBJECTIVEThere are limited data on the risk of pulmonary disease in patients with diabetes. The aim of this study was to evaluate and compare the incidence of asthma, chronic obstructive pulmonary disease (COPD), pulmonary fibrosis, pneumonia, and lung cancer in patients with and without a diagnosis of diabetes.RESEARCH DESIGN AND METHODSWe conducted a retrospective, longitudinal cohort study using the electronic records of a large health plan in northern California. Age and sex data were available for all cohort members (n = 1,811,228). Data on confounders were available for a subcohort that responded to surveys (n = 121,886), among whom Cox proportional hazards regression models were fit.RESULTSAge- and sex-adjusted incidence rates and 95% CIs were calculated for members with and without diabetes in the full cohort and the subcohort. No difference was observed for lung cancer, but the incidence of asthma, COPD, fibrosis, and pneumonia was significantly higher in those members with a diagnosis of diabetes. These differences remained significant in regression models adjusted for age, sex, race/ethnicity, smoking, BMI, education, alcohol consumption, and outpatient visits (asthma hazard ratio [HR] 1.08 [95% CI 1.03–1.12], COPD HR 1.22 [1.15–1.28], pulmonary fibrosis HR 1.54 [1.31–1.81], and pneumonia HR 1.92 [1.84–1.99]). The risk of pneumonia and COPD increased significantly with increasing A1C.CONCLUSIONSIndividuals with diabetes are at increased risk of several pulmonary conditions (asthma, COPD, fibrosis, and pneumonia) but not lung cancer. This increased risk may be a consequence of declining lung function in patients with diabetes.

We examined whether ischemic heart disease (IHD) hospital admissions were associated with air pollutants in those with and without secondary diagnoses of arrhythmia (ARR) or congestive heart failure (CHF). We assessed the occurrence of increased vulnerability among persons with these conditions to daily variations in ozone, carbon monoxide, nitrogen dioxide, or particulate matter less than or equal to 10 micro m in aerodynamic diameter (PM10). The study population consisted of members of a large health maintenance organization residing in the South Coast Air Basin of California from 1988 to 1995. After adjustment for day of week, study year, and smoothing splines for day of study, temperature, and relative humidity, CO and NO2 were both associated with admissions with the greatest effects for CO. A 1-ppm increase in 8-hr average CO was associated with a 3.60% [95% confidence interval (CI), 1.62-5.63%] increase in same-day IHD admissions in persons with a secondary diagnosis of CHF, a 2.99% (95% CI, 1.80-4.19%) increase in persons with a secondary diagnosis of ARR, and a 1.62% (95% CI, 0.65-2.59%) increase in IHD admissions in persons without either secondary diagnosis. Air pollution was most strongly associated with myocardial infarction hospital admissions. The vulnerability of the secondary CHF subgroup may be due to a greater prevalence of myocardial infarction primary diagnoses and not the modifying effect of CHF. This study suggests that people with IHD and accompanying CHF and/or ARR constitute a sensitive subgroup in relation to the effects of criteria ambient air pollutants associated with motor vehicle combustion.

deaths due to NHL in the United States. 1 The overall incidence rate of NHL is increasing worldwide, especially in developed countries, 2-4 whereas the rate in the United States has been relatively stable during 1995 to 2003. 5 NHL disproportionately affects males and is more common in white non-Hispanics than in other racial or ethnic groups. 5 For the period of 1995 to 2002, the median age of NHL diagnosis in the United States was 67 years. 5 Immune suppression and pesticide/insecticide exposure are thought to be related to NHL development, and there is strong evidence that infections with human T-cell leukemia virus, Epstein-Barr virus, helicobacter pylori, and hepatitis C virus (HCV) are involved in the etiology of NHL. 2 Infection with hepatitis B virus (HBV) 6,7 is a major global public health problem with 50 million people infected per year 8 and more than 350 million people chronically infected worldwide. 9 In the United States, chronic HBV infection is more common in Asians than in other racial-ethnic groups. Among the common sequelae of chronic HBV infection are cirrhosis of the liver 10 and hepatocellular carcinoma (HCC). 11 Given the relationship between chronic HCV infection and NHL, [12][13][14][15][16] an association between HBV infection and NHL is quite plausible. HCV infection is thought to promote the development of NHL by inducing chronic lymphoprolifAbbreviations: HBV, hepatitis B virus; HCC, hepatocellular carcinoma; HCV, hepatitis C virus; HBsAg, hepatitis B surface antigen; HFHS, Henry Ford Health System; HIV, human immunodeficiency virus; KPMCP, Kaiser Permanente Medical Care Program; NHL, non-Hodgkins lymphoma; SEER, Surveillance Epidemiology and End Results. From

A genome-wide association study of prostate cancer in Kaiser Permanente health plan members (7,783 cases, 38,595 controls; 80.3% non-Hispanic white, 4.9% African-American, 7.0% East Asian, 7.8% Latino) revealed a new independent risk indel rs4646284 at the previously-identified locus 6q25.3 that replicated in PEGASUS (N=7,539) and MEC (N=4,679) (p=1.0×10−19, OR=1.18). Across the 6q25.3 locus, rs4646284 exhibited the strongest association with expression of SLC22A1 (p=1.3×10−23) and SLC22A3 (p=3.2×10−52). At the known 19q13.33 locus rs2659124 (p=1.3×10−13, OR=1.18) nominally replicated in PEGASUS. A risk score of 105 known risk SNPs was strongly associated with prostate cancer (p<1.0×10−8). Comparing the highest to lowest risk score deciles, the OR was 6.22 for non-Hispanic Whites, 5.82 for Latinos, 3.77 for African-Americans, and 3.38 for East Asians. In non-Hispanic whites, the 105 risk SNPs explained ~7.6% of disease heritability. The entire GWAS array explained ~33.4% of heritability, with a 4.3-fold enrichment within DNaseI hypersensitivity sites (p=0.004).

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Background:Ecologic analyses, case–case comparisons, and animal experiments suggest positive associations between air pollution and tuberculosis.Objectives:We evaluated this hypothesis in a large sample, which yielded results that are applicable to the general population.Methods:We conducted a case–control study nested within a cohort of Kaiser Permanente of Northern California members. All active pulmonary tuberculosis (TB) cases newly diagnosed between 1996 and 2010 (n = 2,309) were matched to two controls (n = 4,604) by age, sex, and race/ethnicity on the index date corresponding with the case diagnosis date. Average individual-level concentrations of carbon monoxide (CO), nitrogen dioxide (NO2), sulfur dioxide (SO2), ozone (O3), and particulate matter with aerodynamic diameter ≤ 2.5 μm (PM2.5) and 10 μm (PM10) for 2 years before diagnosis/entry into the study were estimated using measurements from the California Air Resources Board monitor closest to the participant’s residence.Results:In single-pollutant adjusted conditional logistic regression models, the pulmonary TB odds ratios (95% confidence intervals) for the highest quintile (vs. lowest) were 1.50 (95% CI: 1.15, 1.95) for CO and 1.42 (95% CI: 1.10, 1.84) for NO2. Corresponding estimates were higher among never [1.68 (95% CI: 1.26, 2.24)] than ever [1.19 (95% CI: 0.74, 1.92)] smokers for CO. In contrast, for NO2, estimates were higher among ever [1.81 (95% CI: 1.13, 2.91)] than never [1.29 (95% CI: 0.97, 1.71)] smokers. O3 was inversely associated for smokers [0.66 (95% CI: 0.43, 1.02)] and never smokers [0.65 (95% CI: 0.52, 0.81)]. No other consistent patterns were observed.Conclusions:In this first, to our knowledge, U.S. nested case–control study on air pollution and pulmonary TB, we observed positive associations with ambient CO and NO2, which require confirmation.Citation:Smith GS, Van Den Eeden SK, Garcia C, Shan J, Baxter R, Herring AH, Richardson DB, Van Rie A, Emch M, Gammon MD. 2016. Air pollution and pulmonary tuberculosis: a nested case-control study among members of a Northern California health plan. Environ Health Perspect 124:761–768; http://dx.doi.org/10.1289/ehp.1408166

The Multigroup Ethnic Identity Measure-Revised (MEIM-R), a brief instrument assessing affiliation with one’s ethnic group, is a promising advance in the ethnic identity literature. However, equivalency of its measurement properties across specific racial and ethnic groups should be confirmed before using it in diverse samples. We examined a) the psychometric properties of the MEIM-R including factor structure, measurement invariance, and internal consistency reliability, and b) levels of and differences in ethnic identity across multiple racial and ethnic groups and subgroups. Asian (n = 630), Black/African American (n = 58), Hispanic (n = 240), multiethnic (n = 160), and White (n = 375) women completed the MEIM-R as part of the “Gestational diabetes’ Effect on Moms” diabetes prevention trial in the Kaiser Permanente Northern California health care setting (N = 1,463; M age 32.5 years, SD = 4.9). Multiple-groups confirmatory factor analyses provided provisional evidence of measurement invariance, i.e., an equal, correlated two-factor structure, equal factor loadings, and equal item intercepts across racial and ethnic groups. Latent factor means for the two MEIM-R subscales, exploration and commitment, differed across groups; effect sizes ranging from small to large generally supported the notion of ethnic identity as more salient among people of color. Pending replication, good psychometric properties in this large and diverse sample of women support the future use of the MEIM-R. Preliminary evidence of measurement invariance suggests that the MEIM-R could be used to measure and compare ethnic identity across multiple racial and ethnic groups.

Using computerized data systems in a large integrated health delivery system, we found that the rate of ectopic pregnancy in 1997-2000 was similar to the national rate in 1990-1992, when national data were last available. These data suggest that the ectopic pregnancy rate is not increasing, although differences in the study populations need to be kept in mind. Medical treatment seems to be increasing over time.