Developmental Brain and Behavior Toxicity of Air Pollutants: A Focus on the Effects of Polycyclic Aromatic Hydrocarbons (PAHs)

Schroeder, Henri

doi:10.1080/10643389.2010.495644

Cited by 39 publications

(19 citation statements)

References 79 publications

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“…These differences may be related to multiple factors including both variations in molecular structure, ways of metabolism, toxicokinetic characteristics, brain targets of interactions, way of administration and levels of exposure. Whereas BaP has been demonstrated to modify several functional endpoints in the brain including neuronal excitability, oxidative stress, and several neurotransmitter systems [7], little is known about the brain cellular and/or molecular toxicity of fluorene, requiring the testing of the effects of this compound [30].…”

Section: Discussionmentioning

confidence: 99%

“…In contrast, the potential neurotoxicity of PAHs has received much less attention despite some human and animal evidence (for review, see reference [7]). In humans, PAH-related neurological symptoms were reported in residents living near two dumping sites in Texas [8] or a waste oil reprocessing plant in California [9], and in workers of a coke processing plant in Poland [10].…”

Section: Introductionmentioning

confidence: 99%

“…Such results were associated with concomitant dose-related changes in the expression of the NR1 and NR2A subunits of the NMDA glutamate receptor in regions involved in memory and anxiety. Taken all together, these observations have led to speculations about a possible relationship between neurobehavioral alterations and exposure to environmental PAHs [7], [16].…”

Section: Introductionmentioning

confidence: 99%

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Neurobehavioral Toxicity of a Repeated Exposure (14 Days) to the Airborne Polycyclic Aromatic Hydrocarbon Fluorene in Adult Wistar Male Rats

et al. 2013

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Fluorene is one of the most abundant polycyclic aromatic hydrocarbons in air and may contribute to the neurobehavioral alterations induced by the environmental exposure of humans to PAHs. Since no data are available on fluorene neurotoxicity, this study was conducted in adult rats to assess the behavioral toxicity of repeated fluorene inhalation exposure. Male rats (n = 18/group) were exposed nose-only to 1.5 or 150 ppb of fluorene 6 hours/day for 14 consecutive days, whereas the control animals were exposed to non-contaminated air. At the end of the exposure, animals were tested for activity and anxiety in an open-field and in an elevated-plus maze, for short-term memory in a Y-maze, and for spatial learning in an eight-arm maze. The results showed that the locomotor activity and the learning performances of the animals were unaffected by fluorene. In parallel, the fluorene-exposed rats showed a lower level of anxiety than controls in the open-field, but not in the elevated-plus maze, which is probably due to a possible difference in the aversive feature of the two mazes. In the same animals, increasing blood and brain levels of fluorene monohydroxylated metabolites (especially the 2-OH fluorene) were detected at both concentrations (1.5 and 150 ppb), demonstrating the exposure of the animals to the pollutant and showing the ability of this compound to be metabolized and to reach the cerebral compartment. The present study highlights the possibility for a 14-day fluorene exposure to induce some specific anxiety-related behavioral disturbances, and argues in favor of the susceptibility of the adult brain when exposed to volatile fluorene.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Neurobehavioral Toxicity of a Repeated Exposure (14 Days) to the Airborne Polycyclic Aromatic Hydrocarbon Fluorene in Adult Wistar Male Rats

et al. 2013

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“…The main mechanism of these negative health effects was found to involve their effects on enzymes, especially on the cytochrome P450 (CYP) family of enzymes, including CYP1A [18,19,20,21]. Research has also shown that PAHs could be transferred from their mothers to newborns and young infants, and cause brain and behavior toxicity [1,22]. Moreover, the diet may be the major source of exposure to PAHs for people who are non-tobacco-smokers and non-occupationally exposed.…”

Section: Introductionmentioning

confidence: 99%

Evaluation of Benzo[a]pyrene in Food from China by High-Performance Liquid Chromatography-Fluorescence Detection

Chen

Xia

et al. 2012

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The occurrence and levels of benzo[a]pyrene in various heat-treated foods from China were evaluated by high-performance liquid chromatography-fluorescence detection. In a total of 119 samples, 105 were found to contain benzo[a]pyrene at levels of 0.03 to 19.75 µg/kg. The benzo[a]pyrene contents in 12 animal source foods were higher than the Chinese maximum permissible level in food (5 µg/kg) and the highest level was 19.75 µg/kg, nearly four times the maximum permissible level. The results revealed a widespread carinogenic public health risk from benzo[a]pyrene in heat-treated foods. The highest benzo[a]pyrene levels were found in animal source samples such as charcoal-grilled and smoked meats, especially pork, beef and sausage, while trace levels of benzo[a]pyrene were present in grain food. Charcoal-grilled vegetables were found to also contain certain levels of benzo[a]pyrene. This study provided new information on benzo[a]pyrene content of a variety of heat-treated foods from China.

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“…21 Regarding the specific effects of gestational PAH exposure on neurodevelopment in laboratory animals, potential mechanisms include impairment in N-methyl-Daspartate receptor-1 (NMDAR1) subunit expression and impaired long-term potentiation (LTP) generation (reviewed in ref 71).…”

Section: Figurementioning

confidence: 99%

Prenatal Exposure to Air Pollution, Maternal Psychological Distress, and Child Behavior

2013

PEDIATRICS

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WHAT'S KNOWN ON THIS SUBJECT: Prenatal exposures to diverse pollutants and psychosocial stressors have been shown independently to adversely affect child development. Less is known about the potential interactions between these factors, although they commonly co-occur, especially in disadvantaged populations. WHAT THIS STUDY ADDS:The combination of high prenatal exposure to environmental polycyclic aromatic hydrocarbons and maternal demoralization adversely affects child behavior, and maternal demoralization has a greater effect among children with high prenatal polycyclic aromatic hydrocarbon exposure for a majority of behavioral symptoms. abstract BACKGROUND: Airborne polycyclic aromatic hydrocarbons (PAHs) are pollutants generated by combustion of fossil fuel and other organic material. Both prenatal PAH exposure and maternal psychological distress during pregnancy have each been associated with neurodevelopmental problems in children. The goal was to evaluate potential interactions between prenatal exposure to airborne PAHs and maternal psychological distress during pregnancy on subsequent behavioral problems in children. METHODS:In a longitudinal birth cohort study, 248 children of nonsmoking white women in the coal-burning region of Krakow, Poland, were followed from in utero until age 9. Prenatal PAH exposure was measured by personal air monitoring during pregnancy, maternal demoralization during pregnancy by the Psychiatric Epidemiology Research Instrument-Demoralization, and child behavior by the Child Behavior Checklist. RESULTS:Significant interactions between maternal demoralization and PAH exposure (high versus low) were identified for symptoms of anxious/ depressed, withdrawn/depressed, social problems, aggressive behavior, internalizing problems, and externalizing problems. The effects of demoralization on syndromes of anxious/depressed, withdrawn/depressed, rule-breaking, aggressive behavior, and the composite internalizing and externalizing scores were seen only in conjunction with high PAH exposure. Fewer significant effects with weaker effect sizes were observed in the low-PAH-exposure group.CONCLUSIONS: Maternal demoralization during pregnancy appears to have a greater effect on child neurobehavioral development among children who experienced high prenatal PAH exposure. The results provide the first evidence of an interaction between prenatal exposure to maternal demoralization and air pollution on child neurobehavioral development, indicating the need for a multifaceted approach to the prevention of developmental problems in children. Pediatrics 2013;132:e1284-e1294 AUTHORS:

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Developmental Brain and Behavior Toxicity of Air Pollutants: A Focus on the Effects of Polycyclic Aromatic Hydrocarbons (PAHs)

Cited by 39 publications

References 79 publications

Neurobehavioral Toxicity of a Repeated Exposure (14 Days) to the Airborne Polycyclic Aromatic Hydrocarbon Fluorene in Adult Wistar Male Rats

Neurobehavioral Toxicity of a Repeated Exposure (14 Days) to the Airborne Polycyclic Aromatic Hydrocarbon Fluorene in Adult Wistar Male Rats

Evaluation of Benzo[a]pyrene in Food from China by High-Performance Liquid Chromatography-Fluorescence Detection

Prenatal Exposure to Air Pollution, Maternal Psychological Distress, and Child Behavior

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