Omega-3 Fatty Acid Biomarkers and Incident Atrial Fibrillation.

BACKGROUND: The relationship between omega-3 fatty acids and atrial fibrillation (AF) remains controversial. OBJECTIVES: This study aimed to determine the prospective associations of blood or adipose tissue levels of eicosapentaenoic acid (EPA), docosapentaenoic acid (DPA), and docosahexaenoic acid (DHA) with incident AF. METHODS: We used participant-level data from a global consortium of 17 prospective cohort studies, each with baseline data on blood or adipose tissue omega-3 fatty acid levels and AF outcomes. Each participating study conducted a de novo analyses using a prespecified analytical plan with harmonized definitions for exposures, outcome, covariates, and subgroups. Associations were pooled using inverse-variance weighted meta-analysis. RESULTS: Among 54,799 participants from 17 cohorts, 7,720 incident cases of AF were ascertained after a median 13.3 years of follow-up. In multivariable analysis, EPA levels were not associated with incident AF, HR per interquintile range (ie, the difference between the 90th and 10th percentiles) was 1.00 (95% CI: 0.95-1.05). HRs for higher levels of DPA, DHA, and EPA+DHA, were 0.89 (95% CI: 0.83-0.95), 0.90 (95% CI: 0.85-0.96), and 0.93 (95% CI: 0.87-0.99), respectively. CONCLUSIONS: In vivo levels of omega-3 fatty acids including EPA, DPA, DHA, and EPA+DHA were not associated with increased risk of incident AF. Our data suggest the safety of habitual dietary intakes of omega-3 fatty acids with respect to AF risk. Coupled with the known benefits of these fatty acids in the prevention of adverse coronary events, our study suggests that current dietary guidelines recommending fish/omega-3 fatty acid consumption can be maintained.

Furan Metabolites Are Elevated in Users of Various Tobacco Products and Cannabis.

Humans are exposed to furan, a toxicant and possible human carcinogen, through multiple sources including diet and tobacco smoke. The urinary metabolites of furan are derived from the reaction of its toxic metabolite with protein nucleophiles and are biomarkers of exposure and potential harm. An established isotopic dilution liquid-chromatography mass spectrometry method was used to measure these biomarkers in urine from users of e-cigarettes, cannabis, and/or combustible tobacco with/without reduced nicotine levels. Amounts of furan mercapturic acid metabolites were higher in these individuals relative to nonsmokers, indicating that they may be at risk for potential furan-derived toxicities.

Estimating bisphenol A exposure levels using a questionnaire targeting known sources of exposure.

OBJECTIVE: To develop a BPA Exposure Assessment Module (BEAM) for use in large observational studies and to evaluate the ability of the BEAM to estimate bisphenol A (BPA) exposure levels. DESIGN: The BEAM was designed by modifying an FFQ with questions targeting known sources of BPA exposure. Frequency of intake of known dietary sources of BPA was assessed using the BEAM and three 24 h food records as a reference diet measurement tool. Urinary BPA (uBPA) levels were measured as the criterion tool in a pooled urine sample (nine spot samples per participant). Spearman correlations, linear regression and weighted kappa analysis were used to evaluate the ability of the BEAM and food records to estimate BPA exposure levels. SETTING: Minneapolis/Saint Paul, MN, USA. SUBJECTS: Sixty-eight healthy adult (20-59 years) volunteers. RESULTS: Dietary BPA intake assessed by the BEAM was not associated with uBPA levels and was unable to predict participants' rank by uBPA levels. BEAM models with all a priori predictors explained 25 % of the variability in uBPA levels. Canned food intake assessed by food records was associated with uBPA levels, but was unable to rank participants by uBPA levels. Multivariable-adjusted food record models with a priori predictors explained 41 % of the variability in uBPA levels. CONCLUSIONS: Known dietary sources of BPA exposure explained less than half the variability in uBPA levels, regardless of diet assessment method. Findings suggest that a questionnaire approach may be insufficient for ranking BPA exposure level and additional important sources of BPA exposure likely exist.