Benzo[a]pyrene-induced neurobehavioral function and neurotransmitter alterations in coke oven workers

Abstract

Occupational B[a]P exposure may reduce coke oven workers' neurobehavioral function and monoamine, amino acid and choline neurotransmitter levels. Moreover, Ach and AchE correlated with neurobehavioral function; AchE has poor specificity, but Ach is a potential biomarker of B[a]P neurotoxicity in coke oven workers.

The effect of occupational exposure to benzo[a]pyrene on neurobehavioral function in coke oven workers

“…Our findings of neurobehavioral dysfunction and high 1-OHP level in coke oven workers are consistent with previous investigations [Niu et al, 2010].…”

Neurotoxicity may be an overlooked consequence of benzo[a]pyrene exposure that is relevant to human health risk assessment

“…In addition, there has been only one report of a lack of association between prenatal exposure to BaP and a measure of neurodevelopment in children [105]. Only one published study has examined BaP neurotoxicity in adults [111]. It described impaired learning and memory in workers exposed up to 1623 ng BaP/m 3 , which is consistent with similar effects in rodents measured by the Morris water maze test.…”

“…YES: Multiple reports of AHR binding to and activation by BaP; activation of AhR (its increased gene expression) was noted in the hippocampus of in utero exposed rat pups [32,85] YES: BaP binds to human AHR to activate AHR-dependent gene expression [122] NO/Maybe: AHR targets CYP1A1 and CYP1B1 were induced in mouse, but not human neuronal progenitor cells, challenged with AhR ligand 3-methylcholanthrene [105][106][107]111] exposure to BaP in rodents leads to altered Nr1, Nr2a, and Nr2b expression in the hippocampus, accompanied by impaired learning and memory [52,[75][76][77][78] or reduction of ''anxietyrelated'' behaviour [74]. Potential inconsistency exists regarding the direction of change of NMADARs' gene expression, as discussed in Section 3.4 above.…”

New candidate proteins for Benzo(a)pyrene-induced spatial learning and memory deficits

“…Meanwhile, several studies have reported robust neurotoxic effects as evidenced by deficits in LM mechanisms subsequent to prenatal or subacute B(a)P exposure (Grova et al, 2007;Wormley et al, 2004a). Recently, studies have also suggested that neurotransmitters and morphological changes in neuronal cells played an important role in modulating the neurobehavioral effects of B(a)P (Zhang et al, 2008;Niu et al, 2010). Overall, these results from previous studies suggested that plasticity and behavioral deficits produced as a result of B(a)P exposure are at least, in part, a result of down or up-regulation of gene or protein expression.…”