Smoking during pregnancy is associated with higher dietary intake of polycyclic aromatic hydrocarbons and poor diet quality

Abstract

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 nonsmokers, passive or active smokers. Linear regression was used to assess factors related to higher intake, and associations between dietary PAH and birth weight. 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: b 5 2142?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.

A review of airborne polycyclic aromatic hydrocarbons (PAHs) and their human health effects

“…Likewise, ten volunteers eating charbroiled beef for five days had a 10-80 fold increase in 1-OH-pyrene glucuronide excretion in urine which returned to background level within 24-72 h (Kang et al, 1995). The intake of pyrene from cigarette smoking (12 nmol day −1 ) was comparable to that of a diet of normal foods (9.4 nmol day −1 ) (Duarte-Salles et al, 2010). Tobacco smokers who are not exposed to PAHs have about twice the level of 1-hydroxypyrene in their urine relative to non-smokers (Hecht, 2002;Srogi, 2007;Van Rooij et al, 1994).…”

Increased susceptibility to hyperoxic lung injury and alveolar simplification in newborn rats by prenatal administration of benzo[a]pyrene

“…Oral exposure to BP is known to induce developmental and reproductive toxicity in experimental studies in animals, including fetal growth (Duarte-Salles et al, 2013). Recent epidemiological studies suggest an association between dietary BP intake and lower birth weight in children (Duarte-Salles et al, 2013; Duarte-Salles et al, 2010). PAHs, by themselves are inert, but they induce enzymes such as cytochrome P450 (CYP)1A1, 1A2, and 1B1, which are involved in the activation of BP to reactive metabolites that in turn bind to protein and DNA, leading to carcinogenesis (Guengerich, 1988; Smerdova et al, 2013; Xue and Warshawsky, 2005)).…”

Polycyclic Aromatic Hydrocarbon Residues in Serum Samples of Autopsied Individuals from Tennessee

“…The variations in PAH residue levels could be due to inter-individual differences in dietary habits [ 10 ], exposure to mainstream or side stream cigarette smoke [ 11 ], uptake and biotransformation of the PAHs [ 12 ] and other preexisting pathophysiological conditions [ 13 ]. Use of autopsy samples for estimating the body burden of PAHs rests on the premise that the PAH concentrations found at postmortem are a measure of the amount of PAHs present at the time of death.…”