OBJECTIVE: To estimate the dietary intake of total polycyclic aromatic hydrocarbons (PAH) and benzo(a)pyrene (BaP), and to characterise factors associated with higher intake during pregnancy. Recent studies suggest that prenatal exposure to PAH is associated with adverse reproductive outcomes. Other than tobacco smoke and occupational exposures, diet is the main source of human PAH exposure. DESIGN: Prospective birth cohort study. Dietary exposure to total PAH and BaP was calculated combining food consumption data and estimated PAH concentrations in foods. One-way ANOVA was used to assess differences in intake among non-smokers, passive or active smokers. Linear regression was used to assess factors related to higher intake, and associations between dietary PAH and birth weight. SETTING: Sabadell, Spain, 2004-2006. SUBJECTS: Women (n 657) recruited during the first trimester of pregnancy. RESULTS: The mean dietary intake of BaP and total PAH was significantly higher among active (0·199 and 10·207 μg/d, respectively) and passive smokers (0·196 and 9·458 μg/d) than among non-smokers (0·181 and 8·757 μg/d; P value < 0·005). Maternal age, educational level and region of origin were also associated with higher BaP intake. In all women, major contributors to PAH intake were processed/cured meats, cereals/potatoes and shellfish. Elevated first trimester dietary BaP was associated with a significant reduction in birth weight (fourth v. first quartile: β = -142·73 g, P value < 0·05). CONCLUSIONS: Active and passive smokers had higher dietary PAH exposure during pregnancy because of higher intake of processed meats and shellfish. As tobacco smoke is an additional route of PAH exposure, the added dietary burden in these women is of concern.
OBJECTIVE: To estimate the dietary intake of total polycyclic aromatic hydrocarbons (PAH) and benzo(a)pyrene (BaP), and to characterise factors associated with higher intake during pregnancy. Recent studies suggest that prenatal exposure to PAH is associated with adverse reproductive outcomes. Other than tobacco smoke and occupational exposures, diet is the main source of humanPAH exposure. DESIGN: Prospective birth cohort study. Dietary exposure to total PAH and BaP was calculated combining food consumption data and estimated PAH concentrations in foods. One-way ANOVA was used to assess differences in intake among non-smokers, passive or active smokers. Linear regression was used to assess factors related to higher intake, and associations between dietary PAH and birth weight. SETTING: Sabadell, Spain, 2004-2006. SUBJECTS:Women (n 657) recruited during the first trimester of pregnancy. RESULTS: The mean dietary intake of BaP and total PAH was significantly higher among active (0·199 and 10·207 μg/d, respectively) and passive smokers (0·196 and 9·458 μg/d) than among non-smokers (0·181 and 8·757 μg/d; P value < 0·005). Maternal age, educational level and region of origin were also associated with higher BaP intake. In all women, major contributors to PAH intake were processed/cured meats, cereals/potatoes and shellfish. Elevated first trimester dietary BaP was associated with a significant reduction in birth weight (fourth v. first quartile: β = -142·73 g, P value < 0·05). CONCLUSIONS: Active and passive smokers had higher dietary PAH exposure during pregnancy because of higher intake of processed meats and shellfish. As tobacco smoke is an additional route of PAH exposure, the added dietary burden in these women is of concern.
Authors: Simone H Crouch; Lisa J Ware; Lebo F Gafane-Matemane; Herculina S Kruger; Tertia Van Zyl; Bianca Van der Westhuizen; Aletta E Schutte Journal: J Clin Hypertens (Greenwich) Date: 2018-07-01 Impact factor: 3.738
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