Gestational exposure to nicotine and/or benzo[a]pyrene causes long‐lasting neurobehavioral consequences

Abstract

Tobacco smoke is a complex mixture that includes thousands of compounds. Previously, we have found that gestational exposure to the complex mixture of tobacco smoke extract caused long‐term neurobehavioral impairments. In this study, we examined the interaction of two of the most biologically active, nicotine and benzo[a]pyrene (BaP). Developmental effects were determined in Sprague–Dawley rats prenatally exposed to low doses of BaP and nicotine (0.03 mg/kg/day of BaP and 2 mg/kg/day of nicotine) via maternal osmotic minipumps throughout gestation. Behavioral function was assessed in the offspring via a battery of tests through adolescence into adulthood. There were sex‐selective effects in four of the behavioral tests. In the elevated plus maze, there was a significant interaction of BaP and sex, where BaP‐treated males showed a trend for increased activity. In the novelty suppressed feeding test, there were significant sex selective effects in males such that the normal sex difference in the behavior in this test was eliminated. Male offspring with prenatal exposure to either nicotine or BaP showed significant reductions in fear response. In the Figure‐8 locomotor activity test, BAP‐exposed male offspring were significantly hyperactive. This also eliminated the sex difference typically seen in this test. This effect persisted into adulthood. In the attention task, males exposed to nicotine during gestation showed a significant percent hit impairment. BaP reversed this effect. No significant effects were seen with percent correct rejection. These data show that both nicotine and BaP cause persisting sex‐selective behavioral effects that persist into adulthood.

Associations between household incense burning and delayed motor development among preterm infants modified by gestational age and maternal educational status

“…Previous animal studies have demonstrated neuroinflammatory changes, ventriculomegaly, and increased repetitive behaviors in mice exposed with fine and ultrafine particulate matter 40‐42 . Gestational exposure to PAH and its constituents exhibited decreased learning and responses in zebra fish, and hyperactivity and reductions in fear response among rats 43,44 . Furthermore, altered cerebellar development in metabolomic and myelination patterns after perinatal particulate matter and benzo(a)pyrene exposure were also observed as possible mechanism of cerebellar neuropathy 45,46 …”

“…Cumulating toxicological evidences reported neurotoxicity for major incense burning emissions, such as PM and PAH, which provided possible pathophysiological mechanism for the adverse health effects of incense burning exposure. [40][41][42][43][44][45][46] and ultrafine particulate matter. [40][41][42] Gestational exposure to PAH and its constituents exhibited decreased learning and responses in zebra fish, and hyperactivity and reductions in fear response among rats.…”

“…[40][41][42] Gestational exposure to PAH and its constituents exhibited decreased learning and responses in zebra fish, and hyperactivity and reductions in fear response among rats. 43,44 Furthermore, altered cerebellar development in metabolomic and myelination patterns after perinatal particulate matter and benzo(a)pyrene exposure were also observed as possible mechanism of cerebellar neuropathy. 45,46 There are cumulating evidences reporting societal determinants and environmental exposures, and indoor air pollutant exposure distributed disproportionately across different socioeconomic groups.…”

“…Cumulating toxicological evidences reported neurotoxicity for major incense burning emissions, such as PM and PAH, which provided possible pathophysiological mechanism for the adverse health effects of incense burning exposure 40‐46 . Previous animal studies have demonstrated neuroinflammatory changes, ventriculomegaly, and increased repetitive behaviors in mice exposed with fine and ultrafine particulate matter 40‐42 .…”

Maternal nicotine exposure aggravates metabolic associated fatty liver disease via PI3K/Akt signaling in adult offspring mice

“…Studies have shown that maternal nicotine exposure (MNE) is associated with a series of adverse pregnancy outcomes, such as spontaneous abortion, preterm birth, stillbirth, fetal growth restriction, low birth weight, and sudden infant death syndrome 15 . MNE can also cause fetal behavior and learning deficits after birth, 16 and this impairment persists into adulthood 17 . Moreover, MNE enhances the susceptibility of adult offspring to chronic metabolic diseases such as metabolic syndrome, 18 lipid metabolism disorder, 19 and steatosis 20 .…”