Background:Prenatal polybrominated diphenyl ethers (PBDEs) and polychlorinated biphenyls (PCBs) exposures may influence children’s neurodevelopment.Objective:We examined the association of prenatal PBDE and PCB exposures with children’s reading skills at ages 5 and 8 years, Full-Scale Intelligence Quotient (FSIQ), and externalizing behavior problems at age 8 years.Methods:From 239 mother–child pairs recruited (2003–2006) in Cincinnati, Ohio, we measured maternal serum PBDE and PCB concentrations, assessed child’s reading skills using the Woodcock–Johnson Tests of Achievement III (WJ-III) at age 5 years and the Wide Range Achievement Test-4 (WRAT-4) at age 8 years, tested FSIQ using the Wechsler Intelligence Scale for Children-IV (WISC-IV), and externalizing behavior problems using the Behavioral Assessment System for Children-2 (BASC-2) at age 8 years. We used multiple linear regression to examine the association of prenatal PBDE and PCB concentrations and reading, FSIQ, and externalizing behavior problems after adjusting for covariates.Results:An increase of Sum4PBDEs (BDE-47, BDE-99, BDE-100, and BDE-153) by 10 times was not significantly associated with reading scores at age 5 years at the p = 0.05 level but was inversely associated with Reading Composite scores (β: –6.2, 95% CI: –11.7, –0.6) and FSIQ (β: –5.3, 95% CI: –10.6, –0.02) at age 8 years; it was positively associated with the score for externalizing behavior problems (β: 3.5, 95% CI: –0.1, 7.2) at age 8 years. Prenatal Sum4PCBs (PCB-118, -153, -138-158, and -180) was not significantly associated with a child’s reading skills, FSIQ, and externalizing behavior problems.Conclusion:Prenatal PBDE concentration was inversely associated with reading skills and FSIQ and positively associated with externalizing behavior problems at age 8 years. No significant associations were found in prenatal PCB concentration.Citation:Zhang H, Yolton K, Webster GM, Sjödin A, Calafat AM, Dietrich KN, Xu Y, Xie C, Braun JM, Lanphear BP, Chen A. 2017. Prenatal PBDE and PCB exposures and reading, cognition, and externalizing behavior in children. Environ Health Perspect 125:746–752; http://dx.doi.org/10.1289/EHP478

Benzo[a]pyrene (B[a]P), a well-known carcinogen, is widespread in the environment. Although the neurotoxic effect of B[a]P has not drawn much attention, toxic effects of B[a]P on learning and memory have been reported. Since it is well known that neuronal apoptosis plays a major role in impairment of learning and memory triggered by many stimuli, an effort has been made to examine whether the B[a]P-induced neurotoxicity occurs through mitochondria-mediated apoptosis. Cultured newborn rat cerebral neurons were used to clarify the apoptosis induced by B[a]P in the study. After incubating with different doses of B[a]P in presence of S9 for 40 h, the apoptotic rates of B[a]P-treated neurons increased in a dose-dependent manner. Further analysis showed that B[a]P-induced apoptosis was accompanied by loss of mitochondrial membrane potential, release of cytochrome c from mitochondria to the cytosol, downregulation of antiapoptotic protein B-cell lymphoma-2 (Bcl-2) levels with concurrent upregulation in proapoptotic Bcl-2-associated X protein (Bax) levels, and increase in the levels and activities of caspases-9 and -3. However, there was no difference in the activity of caspase-8 between B[a]P-exposed neurons and controls. Collectively, these results showed that B[a]P upregulates Bax and downregulates Bcl-2 expression in cultured cerebral neurons, which leads to mitochondrial release of cytochrome c, caspase-3 activation and neuronal apoptotic death.

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To detect the blood genomic DNA methylation in coke oven workers and find a possible early screening index for occupational lung cancer, 74 coke oven workers as the exposed group and 47 water pump workers as the controls were surveyed, and urine samples and peripheral blood mononuclear cells (PBMCs) were collected. Airborne benzo[a]pyrene (B[a]P) levels in workplace and urinary 1-hydroxypyrene (1-OH-Py) levels were determined by high-performance liquid chromatography. DNA damage of PBMCs and the p14(ARK), p15(INK4b) and p16(INK4a) gene CpG island methylation in the promoter region were detected by comet assay and methylation-specific polymerase chain reaction techniques, respectively. Results show that compared with the controls, concentration of airborne B[a]Ps was elevated in the coke plant, and urinary 1-OH-Py’s level and DNA olive tail moment in comet assay were significantly increased in the coke oven workers, and p14(ARK), p15(INK4b) and p16(INK4a) gene methylation rates were also significantly increased. With the working years and urinary 1-OH-Py’s level, the rates of p14(ARK) and p16(INK4a) gene methylation were significantly increased while that of p15(INK4b) gene methylation displayed no statistical change. We conclude that PBMCs’ p14(ARK) and p16(INK4a) gene methylation may be used for screening and warning lung cancer in coke oven workers.

, immune toxicity and neurotoxicity 3,4) . Immune cell apoptosis is one of the hot spots in immune toxicity research, and peripheral blood mononuclear cell (PBMC) apoptosis can reflect the immune system's stability. Reduced apoptosis would result in excessive proliferation of immune cells and formation of autoimmunity, while increased apoptosis can cause immunodeficiency and formation of immune tolerance 5) . To assess the immune function of coke oven workers, we detected and analyzed the changes in PBMC apoptosis. Subjects and Methods SubjectsThe exposed groups consisted of 129 middle-school educated, 23-49-year-old male coke oven workers employed at least 1 year in the coke plant of a large state-owned company, who were divided into the oven-bottom group (34 subjects), oven-side group (48 subjects) and oven-top group (47 subjects) according to their working sites and environmental monitoring data. A working shift lasted 8 h, and each worker's tasks were relatively constant over 1 yr. The controls were 37 warehouse workers from the raw materials plant at same company who were not occupationally exposed to PAHs from the coking operation and had not visited the coke plant in the previous 3 mo, were The aim of the present study was to determine the peripheral blood mononuclear cell (PBMC) apoptosis in coke oven workers so that we can take effective measures to protect coke oven workers. Methods: The subjects, 129 coke oven workers and 37 warehouse workers (controls), were investigated using a questionnaire to collect information about their age, working years, smoking and drinking habits, vocational history and other general information. The coke oven workers were divided into the oven-bottom group (34), oven-side group (48) and oven-top group (47) according to their working sites and environmental monitoring data. The concentration of benzo[a]pyrene (B[a]P) and the subjects' urinary 1-hydroxypyrene (1-OH-Py) levels were determined by HPLC. Additionally, the PBMCs were separated from blood samples, and the early and late apoptosis rates were determined by flow cytometry. Results: The airborne B[a]P concentrations were 19.5 ± 13.2, 185.9 ± 38.6 and 1,623.5 ± 435.8 ng/m 3 at the bottom, side and top of the oven, respectively, and were higher than in the controls' workplaces 10.2 ± 7.6 ng/m 3 . Urinary 1-OH-Py, indicating the B[a]P's internal exposure level, was significantly higher in the exposed groups than in the controls (p<0.05). Compared with the controls, the coke oven workers' PBMC apoptosis rates were significantly increased and increased in association with the B[a]P level. PBMC apoptosis increased in association with the 1-OH-Py level and coking operation years and decreased in association with years of alcohol consumption. Conclusions: PBMC apoptosis in the coke oven workers was associated with the 1-OH-Py level, coke operation years and