The levels of polycyclic aromatic hydrocarbons (PAHs) in human milk and exposure risk to breastfed infants in petrochemical industrialized Lanzhou Valley, Northwest China

We investigated in this paper the presence of PAHs in human milk from lactating women residing in Lanzhou, a petrochemical industrialized valley city in Northwest China. The PAH concentration levels in human milk samples from 98 healthy women were determined by gas chromatography/mass spectrometry (GC/MS). The associations between the lifestyle factors and the PAHs levels of human milk were analyzed. Moreover, we applied principal component analysis (PCA) method to gain a better insight into the similarities or dissimilarities of the human milk PAH loads and different pathways of source exposure. In addition, the exposure risks of breastfed infants due to PAH ingestion via breast milk were assessed and the relative breast-feeding risk to the total intake dose of infants was addressed. The results showed that the average fat-normalized human milk ∑₁₅PAHs concentrations for the lactating women residing in four districts of Lanzhou, namely, Xigu, Anning, Qilihe, and Chengguan were 320.40, 270.36, 374.04, and 259.84 ng/g of fat, respectively. The ∑₁₅PAHs of human milk from the lactating women of Qilihe District exhibited the highest concentration level, while the concentration level for women from Xigu District is the second highest for the observed human milk ∑₁₅PAHs. And the corresponding BaPeq concentrations for women in Xigu, Anning, Qilihe, and Chengguan districts were 58.29, 47.95, 65.13, and 45.60 ng/g of fat, respectively. A significant correlation was only found between human milk and living district environment (p < 0.05). Although the Spearman correlation analysis showed that there were no significant correlation existing between other lifestyle and human milk PAHs, we confirmed that consuming barbecue food could elevate PAHs levels in human milk: the barbecue intake frequency caused 10% fluctuation of ∑₁₅PAHs concentration between high frequency and low frequency group in our study. Furthermore, the exposure to second-hand smoke can also increase the ∑₁₅PAHs levels in human milk by 4 to 11% here. Ingestion doses of PAHs by infants (19.37–77.75 ng kg⁻¹ day⁻¹) were much higher than the inhalation doses (2.83–16.48 ng kg⁻¹ day⁻¹), which indicated that the ingestion is the main exposure risk pathway for infants. Since there are limited guidelines and standards for PAHs ingestion dose in human milk by infant, we compared the ingestion dose of BaP with the upper bound estimates of BaP dietary exposure of 108 ng kg⁻¹ day⁻¹ for toddlers of ages between 1.5 and 2.5 years of age in the UK reported by Committee on Toxicity of Chemicals in Food (COT) and the data we obtained were lower than this upper bound. However, the estimated margin of exposure (MOE) values of BaP-MOE, PAH2-MOE, PAH4-MOE, and PAH8-MOE were smaller than 10,000 which indicated that there are potential hazard for breastfed infants consuming these human milk samples.