Participants were followed for up to 22 years for exacerbations of COPD, event of lung cancer and all-cause mortality.
If we consider association analyses for two morbidity endpoints, and one mortality endpoint, Bonferroni correction for multiple comparisons would require p values (cg05575921) methylation extent were associated with all baseline characteristics at the time blood collection for DNA extraction, except personal history of cancer (table 1).Also, pack-years corresponding to the consumption of 20 cigarettes or equivalent per day for 1 year was calculated for smokers.Thus, never, former and current smoking, quantitative smoking information and smoking history were all recorded only once, at the 1991–1994 examination.Participants reported on smoking behaviour, alcohol consumption, occupational exposure to dust and/or welding fumes, exposure to passive smoking, education, and familial cases of lung cancer.The answers were reviewed together with an examiner at the day of attendance.
Dating sex Herlev
Screening with low-dose CT scans reduces lung cancer mortality among individuals with high a priori risk, but only marginally among those at lowest risk.20 Therefore, several algorithms, which include self-reported smoking have recently been developed to predict smokers' risk of lung cancer.21 methylation extent might, therefore, provide valuable information beyond that of existing risk prediction models identifying individuals eligible for CT scan lung cancer screening, for example the 6-year predicted risk algorithm (PLCO (cg05575921) hypomethylation is associated with the risk of smoking-related morbidity and mortality in the general population.Using the published lung cancer risk prediction model,22 the 6-year lung cancer risk was calculated: we then explored if We studied 9234 consecutive individuals with available DNA from the 1991 to 1994 examination of the Copenhagen City Heart Study, a prospective study of the general population with equal emphasis on pulmonary and cardiac diseases (see flowchart in online supplementay figure 1)23 24; 98% were whites of Danish origin.cg05575921 methylation extent was measured in duplicate samples of bisulphite treated DNA from peripheral blood drawn at the 1991–1994 examination (see online supplementary appendix).Measurements were adjusted for 13 batches, and the order of individuals examined, sampling and measurements were according to the day of the month for birthday (ie, the 1st–the 31st day of the month) of the individual, thus presumably random and non-differential to We selected COPD exacerbations, lung cancer and all-cause mortality a priori because we expected these to show the strongest association with a potential smoking-related variable.Corresponding analyses using Fine–Gray regression with death and emigration as equal competing events were also conducted as sensitivity analyses.
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We applied two models adjusted for sex and age, and multifactorially additionally for the use of alcohol (continuous), body mass index (continuous), exposure to dust (no/yes), exposure to passive smoking (no/yes), history of cancer prior to attendance (no/yes), history of COPD exacerbations prior to attendance (no/yes; for lung cancer and all-cause mortality), familial history of lung cancer (no/yes), education level (categorical), smoking status (never, former current), current and cumulative consumption of tobacco.
Individuals with lung cancer prior to the date of examination were excluded from analyses of lung cancer.
Minimum, median and maximum follow-up periods were 4 days, 19 years and 22 years for COPD exacerbation, 4 days, 19 years and 21 years for lung cancer and 4 days, 19 years and 22 years for all-cause mortality.
Height and weight were measured, body mass index was calculated and blood samples were drawn for DNA.
At the day of attendance in 1991–1994 when DNA was sampled, participants were asked whether they were current or former smokers.