Reducing socio-economic inequalities in all-cause mortality: a counterfactual mediation approach

Background: Socio-economic inequalities in mortality are well established, yet the contribution of intermediate risk factors that may underlie these relationships remains unclear. We evaluated the role of multiple modifiable intermediate risk factors underlying socio-economic-associated mortality and quantified the potential impact of reducing early all-cause mortality by hypothetically altering socio-economic risk factors.Methods: Data were from seven cohort studies participating in the LIFEPATH Consortium (total n = 179 090). Using both socio-economic position (SEP) (based on occupation) and education, we estimated the natural direct effect on all-cause mortality and the natural indirect effect via the joint mediating role of smoking, alcohol intake, dietary patterns, physical activity, body mass index, hypertension, diabetes and coronary artery disease. Hazard ratios (HRs) were estimated, using counterfactual natural effect models under different hypothetical actions of either lower or higher SEP or education.Results: Lower SEP and education were associated with an increase in all-cause mortality within an average follow-up time of 17.5 years. Mortality was reduced via modelled hypothetical actions of increasing SEP or education. Through higher education, the HR was 0.85 [95% confidence interval (CI) 0.84, 0.86] for women and 0.71 (95% CI 0.70, 0.74) for men, compared with lower education. In addition, 34% and 38% of the effect was jointly mediated for women and men, respectively. The benefits from altering SEP were slightly more modest.Conclusions: These observational findings support policies to reduce mortality both through improving socio-economic circumstances and increasing education, and by altering intermediaries, such as lifestyle behaviours and morbidities.</p

Reducing socioeconomic inequalities in all-cause mortality: a counterfactual mediation approach

Background: Socioeconomicinequalities inmortality arewell established, yet the contribution of intermediate risk factors that may underlie these relationships remains unclear.We evaluated the role of multiple modifiable intermediate risk factors underlyingsocioeconomicassociated-mortality and quantifiedthe potentialimpact of reducing early all-cause mortality by hypothetically altering socioeconomic risk factors. Methods: Data were fromsevencohort studies participating in the LIFEPATH consortium (total n=179,090). Using bothsocioeconomic position (SEP) (based on occupation) and education, we estimated thenaturaldirect effect on all-cause mortality, and thenatural indirect effect via the joint mediatingrole of smoking, alcohol intake, dietary patterns, physical activity, body mass index,hypertension, diabetes, and coronary artery disease.Hazard ratios(HR)were estimated, using counterfactual natural effect modelsunder different hypothetical actions of either lower or higher SEP or education. Results: Lower SEP and educationwereassociated with anincreaseinall-cause mortalitywithin an average follow up time of 17.5 years.Mortality wasreducedviamodelled hypothetical actions of increasing SEP oreducation. Through higher educationtheHR was0.85(95% confidence interval (CI) 0.84, 0.86) for women and 0.71(95% CI 0.70, 0.74)for men,compared to lower education. In addition, 34% and 38% of the effect was jointlymediatedfor womenand men, respectively. The benefits from alteringSEP were slightly more modest.Conclusions: Theseobservational findings supportpoliciesto reducemortalityboththrough improving socioeconomic circumstances and increasing education,andby altering intermediaries, such as lifestyle behaviours and morbidities

Smoking, secondhand smoke, and cotinine levels in a subset of EPIC cohort.

BACKGROUND: Several countries are discussing new legislation regarding the ban on smoking in public places, based on the growing evidence of the hazards of secondhand smoke (SHS) exposure. The objective of the present study is to quantitatively assess the relationship between smoking, SHS, and serum cotinine levels in the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort. METHODS: From a study on lung cancer in the EPIC cohort, questionnaire information on smoking was collected at enrolment, and cotinine was measured in serum. Three statistical models were applied by using samples available in a cross-section design: (i) cotinine levels by categories combining smoking and SHS (n = 859); (ii) the effect of hours of passive smoking exposure in nonsmokers only (n = 107); (iii) the effect of the number of cigarettes consumed per day in current smokers only (n = 832). All models were adjusted for country, sex, age, and body mass index. RESULTS: Among nonsmokers, passive smokers presented significant differences in cotinine compared with nonexposed, with a marked (but not significant) difference among former-smokers. A one hour per day increment of SHS gave rise to a significant 2.58 nmol/L (0.45 ng/mL) increase in mean serum cotinine (P &lt; 0.001). In current smokers, a one cigarette per day increment gave rise to a significant 22.44 nmol/L (3.95 ng/mL) increase in cotinine mean (P &lt; 0.001). CONCLUSIONS: There is clear evidence that not only tobacco smoking but also involuntary exposure increases cotinine levels. IMPACT: This study strengthens the evidence for the benefits of a smoking ban in public places