| 11. |
- Gallo, Valentina, et al.
(författare)
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Second-hand Smoke, Cotinine Levels, and Risk of Circulatory Mortality in a Large Cohort Study of Never-Smokers.
- 2010
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Ingår i: Epidemiology. - 1531-5487 .- 1044-3983. ; 21, s. 207-214
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND:: Exposure to second-hand smoke has been shown to be associated with increased cardiovascular mortality in several, but not all, epidemiologic studies. Our aim was to investigate the risk of circulatory death associated with exposure to second-hand smoke in never-smokers in a very large prospective study, the European Prospective Investigation into Cancer and Nutrition. A secondary aim was to use cotinine levels for cross-validating self-reported second-hand smoke exposure. METHODS:: Cox proportional hazard models were used to investigate the risk of death due to circulatory causes associated with second-hand smoke exposure in 135,233 never-smokers. Exposure to second-hand smoke was assessed through a questionnaire at enrollment and then validated against plasma cotinine measurements in a subsample. RESULTS:: Study participants who reported second-hand smoke exposure at home had higher cotinine levels (median plasma cotinine concentration in exposed = 0.82 mug/L; in those unexposed 0.02 mug/L). Second-hand smoke exposure at home was associated with an increased risk of dying from cardiovascular diseases (hazard ratio [HR] = 1.38 [95% confidence interval = 1.01-1.90]), all circulatory diseases (1.28 [0.98-1.69]), and coronary heart disease (1.31 [0.83-2.08]) after adjustment for age, sex, education, physical activity, and body mass index. Dose-response relationships were observed between exposure to second-hand smoke at home and risk of circulatory death (HR per each additional hour/d = 1.25 [1.04-1.50]). Having a partner who smokes more than 30 cigarettes per day considerably increased the risk of a circulatory death (2.94 [1.11-7.78]). Second-hand smoke exposure at home was not associated with total mortality (1.03 [0.93-1.13]). DISCUSSION:: Exposure to second-hand smoke at home (as confirmed by plasma cotinine levels) increases the risk of cardiovascular mortality.
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| 12. |
- Hardell, Lennart, 1944-, et al.
(författare)
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Long-Term Mobile Phone Use and Acoustic Neuroma
- 2014
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Ingår i: Epidemiology. - : Lippincott Williams & Wilkins. - 1044-3983 .- 1531-5487. ; 25:5, s. 778-778
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Tidskriftsartikel (refereegranskat)
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| 13. |
- Hardell, Lennart, 1944-, et al.
(författare)
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Mobile Phones and Cancer : Next Steps
- 2014
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Ingår i: Epidemiology. - : Lippincott Williams & Wilkins. - 1044-3983 .- 1531-5487. ; 25:4, s. 617-618
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Tidskriftsartikel (refereegranskat)
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| 14. |
- Hergens, Maria-Pia, et al.
(författare)
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Use of Scandinavian Moist Smokeless Tobacco (Snus) and the Risk of Atrial Fibrillation
- 2014
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Ingår i: Epidemiology. - 1044-3983 .- 1531-5487. ; 25:6, s. 872-876
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: Snus is a smokeless tobacco product, widely used among Swedish men and increasingly so elsewhere. There is debate as to whether snus is an acceptable "harm-reduction" tobacco product. Since snus use delivers a dose of nicotine equivalent to cigarettes, and has been implicated in cardiac arrhythmia because of associations with sudden cardiovascular death, a relation with atrial fibrillation is plausible and important to investigate.METHODS:: To assess the relation between use of snus and risk of atrial fibrillation, we carried out a pooled analysis of 7 prospective Swedish cohort studies. In total, 274,882 men, recruited between 1978 and 2004, were followed via the National Patient Register for atrial fibrillation. Primary analyses were restricted to 127,907 never-smokers. Relative risks were estimated using Cox proportional hazard regression.RESULTS:: The prevalence of snus use was 25% among never-smokers. During follow-up, 3,069 cases of atrial fibrillation were identified. The pooled relative risk of atrial fibrillation was 1.07 (95% confidence interval = 0.97-1.19) in current snus users, compared with nonusers.CONCLUSION:: Findings from this large national pooling project indicate that snus use is unlikely to confer any important increase in risk of atrial fibrillation.
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| 15. |
- Häggström, Christel, et al.
(författare)
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Prostate Cancer, Prostate Cancer Death, and Death from Other Causes, Among Men with Metabolic Aberrations
- 2014
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Ingår i: Epidemiology. - 1044-3983 .- 1531-5487. ; 25:6, s. 823-828
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Tidskriftsartikel (refereegranskat)abstract
- Background: Few previous studies of metabolic aberrations and prostate cancer risk have taken into account the fact that men with metabolic aberrations have an increased risk of death from causes other than prostate cancer. The aim of this study was to calculate, in a real-life scenario, the risk of prostate cancer diagnosis, prostate cancer death, and death from other causes.Methods: In the Metabolic Syndrome and Cancer Project, prospective data on body mass index, blood pressure, glucose, cholesterol, and triglycerides were collected from 285,040 men. Risks of prostate cancer diagnosis, prostate cancer death, and death from other causes were calculated by use of competing risk analysis for men with normal (bottom 84%) and high (top 16%) levels of each factor, and a composite score.Results: During a mean follow-up period of 12 years, 5,893 men were diagnosed with prostate cancer, 1,013 died of prostate cancer, and 26,328 died of other causes. After 1996, when prostate-specific antigen testing was introduced, men up to age 80 years with normal metabolic levels had 13% risk of prostate cancer, 2% risk of prostate cancer death, and 30% risk of death from other causes, whereas men with metabolic aberrations had corresponding risks of 11%, 2%, and 44%.Conclusions: In contrast to recent studies using conventional survival analysis, in a real-world scenario taking risk of competing events into account, men with metabolic aberrations had lower risk of prostate cancer diagnosis, similar risk of prostate cancer death, and substantially higher risk of death from other causes compared with men who had normal metabolic levels.
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| 16. |
- Johansson, ALV, et al.
(författare)
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Smoking and Miscarriage Risk response
- 2010
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Ingår i: EPIDEMIOLOGY. - 1044-3983. ; 21:6, s. 919-919
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Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)
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| 17. |
- Jokela, Markus, et al.
(författare)
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From midlife to early old age : health trajectories associated with retirement.
- 2010
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Ingår i: Epidemiology. - 1044-3983 .- 1531-5487. ; 21:3, s. 284-90
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: Previous studies report contradictory findings regarding health effects of retirement. This study examines longitudinally the associations of retirement with mental health and physical functioning. METHODS: The participants were 7584 civil servants from the Whitehall II cohort study aged 39-64 years at baseline and 54-76 years at the last follow-up. Self-reported mental health and physical functioning were assessed using the Short Form Medical Outcomes Survey questionnaire, and the scales were scored as T-scores (mean [SD] = 50 [10]). Retirement status and health were assessed with 6 repeated measurements over a 15-year period. RESULTS: The associations between retirement and health were dependent on age at retirement, reason for retirement, and length of time spent in retirement. Compared with continued employment, statutory retirement at age 60 and early voluntary retirement, respectively, were associated with 2.2 (95% confidence interval = 1.7 to 2.8) and 2.2 (1.7 to 2.7) points higher mental health and with 1.0 (0.6 to 1.5) and 1.1 (0.8 to 1.4) points higher physical functioning. Retirement due to ill health was associated with poorer mental health (-0.7 points [-1.62 to 0.2]) and physical functioning (-4.5 points [-5.1 to -3.9]). Within-subject analyses suggested a causal interpretation for statutory and voluntary retirement, but health selection for retirement due to ill health. CONCLUSIONS: Longitudinal analyses of repeat data suggest that health status improves after statutory and voluntarily retirement, although the improvement seems to attenuate over time. By contrast, the association between retirement due to ill health and subsequent poor health seems to reflect selection rather than causation.
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| 18. |
- Julin, Bettina, et al.
(författare)
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Cadmium in Diet and Risk of Cardiovascular Disease in Women
- 2013
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Ingår i: Epidemiology. - : LIPPINCOTT WILLIAMS & WILKINS. - 1044-3983 .- 1531-5487. ; 24:6, s. 880-885
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Tidskriftsartikel (refereegranskat)abstract
- Background: The toxic metal cadmium is suggested to increase the risk of cardiovascular disease, but only one incidence study has explored this association. We evaluated the association between quartiles of food frequency questionnaire-based estimates of cadmium exposure from food (the predominant source of exposure to the metal) and incident cardiovascular disease and its subtypes. Methods: From the population-based Swedish Mammography cohort, 33,333 women were followed prospectively from baseline (1997) through 2010. We estimated relative risks (RRs) with 95% confidence intervals (CIs) using Cox proportional hazard models. Results: During 12 years of follow-up, we identified 3155 incident cases of total cardiovascular disease (1322 cases of myocardial infarction and 1833 cases of total stroke [1485 ischemic and 208 hemorrhagic stroke]). Dietary cadmium exposure was not associated with risk of total cardiovascular disease, myocardial infarction, or total stroke or its subtypes. For total cardiovascular disease, the multivariable-adjusted RR comparing the highest quartile of cadmium exposure with the lowest was 0.96 (95% CI = 0.85-1.09). The corresponding RRs were 1.07 (0.88-1.29) for myocardial infarction, 0.90 (0.76-1.05) for total stroke, 0.89 (0.74-1.06) for ischemic stroke, and 1.11 (0.68-1.80) for hemorrhagic stroke. Conclusions: Our study lends no support to an overall association between low-level exposure to cadmium via food and incident cardiovascular disease.
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| 19. |
- Modig, L., et al.
(författare)
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Short-Term Exposure to Ozone and Levels of Exhaled Nitric Oxide
- 2014
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Ingår i: Epidemiology. - : Ovid Technologies (Wolters Kluwer Health). - 1044-3983. ; 25:1, s. 79-87
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Tidskriftsartikel (refereegranskat)abstract
- Background: Adverse effects of air pollution include respiratory inflammation. A few epidemiologic studies have shown elevations in the fraction of exhaled nitric oxide, a marker of airway inflammation, after exposure to traffic-related pollutants. Methods: We examined whether short-term exposures to ozone (O-3), oxides of nitrogen (NOx), or particulate matter <10 m (PM10) were associated with proximal and distal airway inflammation. The study included 5841 randomly selected Swedish adults from 25 to 75 years of age. Fraction of exhaled nitrogen was measured at two flow rates: 50 ml/s representing the proximal airways and 270 ml/s representing the distal airways. Air pollution data were obtained from an urban monitoring site. We applied linear regression to estimate short-term associations of O-3, NOx, and PM10 with fractions of exhaled NO at 50 and 270 ml/s. Results: An interquartile range increase in 120-hour average O-3 levels was associated with a 5.1% (95% confidence interval = 1.7% to 8.5%) higher level of fraction of exhaled NO at 270 ml/s and 3.6% (-0.4% to 3.4%) higher level of the fraction of exhaled NO at 50 ml/s. For NOx, a small effect was seen for the 24-hour average on the fraction of exhaled NO at 270 ml/s, while for PM10 no clear effects were seen. There was a tendency for a weaker effect of ozone and a stronger effect of NOx in subjects with asthma. Conclusions: Exposure to O-3 was associated with a marker of distal airway inflammation, while the association was less obvious for inflammation of the proximal airways.
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| 20. |
- Modig, Lars, et al.
(författare)
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Short-Term Exposure to Ozone and Levels of Exhaled Nitric Oxide
- 2014
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Ingår i: Epidemiology. - : Lippincott Williams & Wilkins. - 1044-3983 .- 1531-5487. ; 25:1, s. 79-87
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Tidskriftsartikel (refereegranskat)abstract
- Background: Adverse effects of air pollution include respiratory inflammation. A few epidemiologic studies have shown elevations in the fraction of exhaled nitric oxide, a marker of airway inflammation, after exposure to traffic-related pollutants. Methods: We examined whether short-term exposures to ozone (O-3), oxides of nitrogen (NOx), or particulate matter <10 m (PM10) were associated with proximal and distal airway inflammation. The study included 5841 randomly selected Swedish adults from 25 to 75 years of age. Fraction of exhaled nitrogen was measured at two flow rates: 50 ml/s representing the proximal airways and 270 ml/s representing the distal airways. Air pollution data were obtained from an urban monitoring site. We applied linear regression to estimate short-term associations of O-3, NOx, and PM10 with fractions of exhaled NO at 50 and 270 ml/s. Results: An interquartile range increase in 120-hour average O-3 levels was associated with a 5.1% (95% confidence interval = 1.7% to 8.5%) higher level of fraction of exhaled NO at 270 ml/s and 3.6% (-0.4% to 3.4%) higher level of the fraction of exhaled NO at 50 ml/s. For NOx, a small effect was seen for the 24-hour average on the fraction of exhaled NO at 270 ml/s, while for PM10 no clear effects were seen. There was a tendency for a weaker effect of ozone and a stronger effect of NOx in subjects with asthma. Conclusions: Exposure to O-3 was associated with a marker of distal airway inflammation, while the association was less obvious for inflammation of the proximal airways.
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