E-waste polycyclic aromatic hydrocarbon (PAH) exposure leads to child gut-mucosal inflammation and adaptive immune response

Abstract

Polycyclic aromatic hydrocarbon (PAH) exposure alters immunological responses. Research concerning PAH exposure on intestinal immunity of children in electronic waste (e-waste) areas is scarce. The aim of this study was to evaluate the effects of polycyclic aromatic hydrocarbon (PAH) pollutants on intestinal mucosal immunity of children in e-waste areas. Results showed higher hydroxylated PAH (OH-PAH) concentrations in e-waste-exposed children, accompanied with higher sialyl Lewis A (SLA) level, absolute lymphocyte and monocyte counts, decreased of percentage of CD4 + T cells, and had a higher risk of diarrhea. OH-PAH concentrations were negative with child growth. 1-OHNap mediated through WBCs, along with 1-OHPyr, was correlated with an increase SLA concentration. 2-OHFlu, 1-OHPhe, 2-OHPhe, 1-OHPyr, and 6-OHChr were positively correlated with secretory immunoglobulin A (sIgA) concentration. Our results indicated that PAH pollutants caused inflammation, affected the intestinal epithelium, and led to transformation of microfold cell (M cell). M cells initiating mucosal immune responses and the subsequent increasing sIgA production might be an adaptive immune respond of children in the ewaste areas. To our knowledge, this is the first study of PAH exposure on children intestinal immunity in e-waste area, showing that PAH exposure plays a negative role in child growth and impairs the intestinal immune function.

Co-Exposure of Polycyclic Aromatic Hydrocarbons and Phthalates with Blood Cell-Based Inflammation in Early Pregnant Women

“…Moreover, the co-exposure of OH-PAHs and mPAEs has been a concern due to humans being commonly exposed to a mixture of OH-PAHs and mPAEs in real environmental scenarios. However, most current studies separately explored the adverse effects of OH-PAHs or mPAEs exposure on inflammatory indicators [17,42,43]. In contrast, we explored co-exposure to OH-PAHs and mPAEs, considering the realistic exposure scenarios and the results showed that co-exposure to OH-PAHs and mPAEs was also associated with elevated inflammatory indicators, and MOP acts as a major contributor.…”

Aryl hydrocarbon receptor–kynurenine axis promotes oncogenic activity in BCP-ALL

“…However, some studies found that PAH exposure, including parental occupational exposure to car exhaust, smoking, and proximity to transportation routes, is related to the risk of childhood leukemia(Weng et al 2008 ). Although the research results are inconsistent, the relevant results suggested that PAH exposure increases the risk of ALL and affects the disease process(Chen et al 2021a ; Zhang et al 2021a ; Enuneku et al 2021 ). Moreover, its regulatory mechanism appears related to the aryl hydrocarbon receptor (AHR) (O'Driscoll et al 2018 ; Tao et al 2021 ).…”