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Children are extremely liable to indoor air pollutants as their physiology and a few metabolic pathways are different from those of adults. The present cross-sectional study aimed to assess exposure of children living with parents who use hookah tobacco smoke to polycyclic aromatic hydrocarbons (PAHs) using a biomonitoring approach. The study was conducted on 25 children (7–13 years of age) exposed to hookah smoke at home and 25 unexposed age-matched children. Urinary levels of five metabolites of PAHs were quantified via headspace gas chromatography-mass spectrometry (GC–MS). Urinary malondialdehyde (MDA) was measured, as well. Information regarding the sociodemographic and lifestyle conditions was collected through interviews using managed questionnaires. The urinary 1-OH-NaP and 9-OH-Phe concentrations were respectively 1.7- and 4.6-folds higher in the case samples compared to the control group (p < 0.05). In addition, urinary MDA levels were 1.4 times higher in the exposed children than in the unexposed group, but the difference was not statistically significant (p > 0.05). Increasing the consumption of grilled and meat food in the diet increased the participants' urinary 2-OH-Flu and 1-OH-Pyr levels, respectively. Moreover, sleeping in the living room instead of the bedroom at night was a significant predictor of high 1-OH-NaP and 2-OH-NaP concentrations in the children's urine. Overall, the findings confirmed that children living in their homes with hookah-smoking parents were significantly exposed to naphthalene and phenanthrene. Hence, implementing protective measures is critical to reduce the exposure of this group of children. [ABSTRACT FROM AUTHOR]

We investigated some reproductive actions of hookah smoke (HS) exposure (30 min/day, for 30 days) in male mice, and the possible mitigative effect of the prebiotic agent gum acacia (GA) thereon. Control mice were air-exposed (AE). Twenty-four hours after the last exposure, the levels of some plasma reproductive hormones, biochemical markers of inflammation, oxidative and nitrosative stress and testicular histopathology were assessed. The urinary level of cotinine, a major nicotine metabolite, was also measured. HS exposure induced significant decreases in testosterone, estradiol, luteinizing hormone, and androgen binding protein, as well as glutathione reductase activity and levels of nitrite and total nitrite. Plasma inhibin B, alkaline phosphatase, lipopolysaccharide binding protein, uric acid, lactate dehydrogenase, lipid peroxidation, 8-oxo-2’-deoxyguanosine, and cytochrome C were significantly increased following HS exposure. In testicular homogenate, nuclear factor-κB (NF-ĸB), nuclear factor erythroid 2–related factor 2 (Nrf2), interleukin- 6 (IL-6), interleukin-1β (IL-1β), transforming growth factor-β1(TGF- β1), and tumor necrosis factor-α (TNF- α) were all significantly elevated, and the steroidogenic acute regulatory protein (StAR) significantly decreased. Histopathologically, there was slight impairment and disorganization of spermatogenesis. Urinary cotinine concentration was elevated significantly in the HS-exposed group compared with the air-exposed group. GA co-administration mitigated the adverse actions of HS measured. In conclusion, daily exposure to HS at the above dose induced adverse actions on the reproductive system of male mice. GA co-administration significantly mitigated these effects by reducing the inflammation, oxidative and nitrosative stress, via a mechanism involving Nrf2, and reduction of StAR expression.

We investigated some reproductive actions of hookah smoke (HS) exposure (30 min/day, for 30 days) in male mice, and the possible mitigative effect of the prebiotic agent gum acacia (GA) thereon. Control mice were air-exposed (AE). Twenty-four hours after the last exposure, the levels of some plasma reproductive hormones, biochemical markers of inflammation, oxidative and nitrosative stress and testicular histopathology were assessed. The urinary level of cotinine, a major nicotine metabolite, was also measured. HS exposure induced significant decreases in testosterone, estradiol, luteinizing hormone, and androgen binding protein, as well as glutathione reductase activity and levels of nitrite and total nitrite. Plasma inhibin B, alkaline phosphatase, lipopolysaccharide binding protein, uric acid, lactate dehydrogenase, lipid peroxidation, 8-oxo-2'-deoxyguanosine, and cytochrome C were significantly increased following HS exposure. In testicular homogenate, nuclear factor-κB (NF-ĸB), nuclear factor erythroid 2–related factor 2 (Nrf2), interleukin- 6 (IL-6), interleukin-1β (IL-1β), transforming growth factor-β1(TGF- β1), and tumor necrosis factor-α (TNF- α) were all significantly elevated, and the steroidogenic acute regulatory protein (StAR) significantly decreased. Histopathologically, there was slight impairment and disorganization of spermatogenesis. Urinary cotinine concentration was elevated significantly in the HS-exposed group compared with the air-exposed group. GA co-administration mitigated the adverse actions of HS measured. In conclusion, daily exposure to HS at the above dose induced adverse actions on the reproductive system of male mice. GA co-administration significantly mitigated these effects by reducing the inflammation, oxidative and nitrosative stress, via a mechanism involving Nrf2, and reduction of StAR expression. [ABSTRACT FROM AUTHOR]