• 2022-09
  • 2022-08
  • 2022-07
  • 2022-05
  • 2022-04
  • 2021-03
  • 2020-08
  • 2020-07
  • 2020-03
  • 2019-11
  • 2019-10
  • 2019-09
  • 2019-08
  • 2019-07
  • br CRP and IL concentration measurements taken


    CRP and IL-6 concentration measurements taken in the years 2, 4, 6 and 8 were analyzed at a different laboratory (Wake Forest University) than the baseline measurements (Core Laboratory at the University of Vermont). To account for possible laboratory dif-ferences, calibration was performed for both IL-6 and CRP serum concentration levels based on a set of 150 blind duplicate measure-ments obtained from both labs: one set of values was regressed on the other set to create predicted values. Calibrated values were used in our analyses and were confirmed to be significantly correlated with values from the samples at the second laboratory. Measure-ments of IL-6 were obtained from a cell pack for year 8 and from serum for baseline and years 2, 4 and 6. To account for this differ-ence in sample source, a second calibration was performed on IL-6 for year 8, based on a set of 137 samples for year 6, derived from both serum and cell packs.
    Participants were categorized in tertiles of inflammatory markers. The tertiles were updated at each time point to accurately represent the distribution of inflammatory marker levels. We also used a continu-ous log-transformed version of our inflammatory markers.
    2.3. Endpoint Ascertainment
    The primary outcome was incident lung cancer. Incident cancers and the date of diagnosis were determined directly from hospital records, or from the underlying cause of death from death certificates. Adjudication of incident cancer events, excluding non-melanoma o-Phenanthroline cancer, by the Health ABC Study Diagnosis and Disease Ascertainment Committee was completed through August 31, 2012.
    Age, gender, race, geographic site, education, body mass index (BMI), smoking status (including pack-years smoked), alcohol con-sumption, non-steroidal anti-inflammatory drug (NSAID) use, cardio-vascular disease history, and pulmonary disease history were evaluated as potential confounders. BMI, smoking status, and NSAID use were analyzed as time-updated covariates. History of pulmonary conditions was o-Phenanthroline ascertained at baseline, based on previous diagnosis of chronic bronchitis, COPD, or emphysema. History of cardiovascular con-ditions was measured at baseline, and defined as any previous diagnosis of congestive heart failure, myocardial infarction, high blood pressure or other diagnosed cardiovascular disease. BMI (kg/m2) was derived annu-ally from measured height and weight through year 4, and biennially thereafter until year 8 [22]. Smoking history was obtained from baseline interviews for former and never smokers, and updated in the years 2, 5, 8, 9, 12, and 15. Pack-years were reported at baseline along with smoking history; smoking was categorized as never, former smoking of less than 20 pack-years, former smoking of more than 20 pack-years, current smoking of less than 20 pack-years, and current smoking of more than 20 pack-years. NSAID use was measured in each group at baseline and in years 2, 3, 5, 6, 10, 12 and 13.
    2.5. Statistical Analysis
    To evaluate the long-term effects of low-grade chronic systemic inflammation on lung cancer risk, and reduce random within-person variation, we used updated exposure measures (e.g. most recent), as well as average cumulative exposure, as has been commonly done in analyses measuring the effects of repeated dietary data [23]. We also evaluated the association between baseline levels of inflammatory
    Table 1
    Comparison of baseline characteristics for 2323 participants in the health, aging and body composition (health-ABC) study.
    Tertiles of inflammatory markers
    Overall C-reactive protein (ug/ml)
    Interleukin-6 (pg/ml)
    Tumor necrosis factor-α (pg/ml)
    Education %
    Smoking Status, %
    Alcohol consumption, %