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Waterpipe smoking is increasingly popular and understanding how chemicals found in hookah smoke may be harmful to human bronchial epithelial cells is of great importance. 4,4'-Oxydianiline (ODA), is an aromatic amine which is present at comparatively high levels in hookah smoke. The metabolism and the subsequent toxicity of ODA in human bronchial epithelial cells remains unknown. Given that ODA is an aromatic amine, we hypothesized that ODA is N -acetylated and induces DNA damage following exposure to immortalized human bronchial epithelial cells (BEP2D cells). We measured the N -acetylation of ODA to mono-acetyl-ODA and the N -acetylation of mono-acetyl-ODA to diacetyl-ODA by BEP2D cells following separation and quantitation by high performance liquid chromatography. For ODA, the apparent K M in cells was 12.4 ± 3.7 µM with a V max of 0.69 ± 0.03 nmol/min/106 cells, while for mono-acetyl-ODA, the apparent K M was 111.2 ± 48.3 µM with a V max of 17.8 ± 5.7 nmol/min/106 cells ODA exposure for 24 h resulted in DNA damage to BEP2D cells following concentrations as low as 0.1 µM as measured by yH2Ax protein expression These results demonstrate that ODA, the most prevalent aromatic amine identified in hookah smoke, is N -acetylated and induces DNA damage in human bronchial epithelial cells. • 4,4'-Oxydianiline (ODA) is present at comparatively high levels in hookah smoke. • N -acetylation of ODA was determined in human bronchial epithelial cells. • ODA exposure resulted in DNA damage to human bronchial epithelial cells. [ABSTRACT FROM AUTHOR]

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]

Introduction: Although communal smoking of hookah by means of water pipes is perceived to be a safe alternative to cigarette smoking, the effects of hookah smoke in respiratory epithelia have not been well characterized. This study evaluated epigenomic and transcriptomic effects of hookah smoke relative to cigarette smoke in human respiratory epithelial cells. Methods: Primary normal human small airway epithelial cells from three donors and cdk4 and hTERT-immortalized small airway epithelial cells and human bronchial epithelial cells were cultured for 5 days in normal media with or without cigarette smoke condensates (CSCs) or water pipe condensates (WPCs). Cell count, immunoblot, RNA sequencing, quantitative real-time reverse-transcriptase polymerase chain reaction, methylation-specific polymerase chain reaction, and quantitative chromatin immunoprecipitation techniques were used to compare effects of hookah and cigarette smoke on cell proliferation, global histone marks, gene expression, and promoter-related chromatin structure. Results: CSC and WPC decreased global H4K16ac and H4K20me3 histone marks and mediated distinct and overlapping cancer-associated transcriptome signatures and pathway modulations that were cell line dependent and stratified across lung cancer cells in a histology-specific manner. Epiregulin encoding a master regulator of EGFR signaling that is overexpressed in lung cancers was up-regulated, whereas FILIP1L and ABI3BP encoding mediators of senescence that are repressed in lung cancers were down-regulated by CSC and WPC. Induction of epiregulin and repression of FILIP1L and ABI3BP by these condensates coincided with unique epigenetic alterations within the respective promoters. Conclusions: These findings support translational studies to ascertain if hookah-mediated epigenomic and transcriptomic alterations in cultured respiratory epithelia are detectable and clinically relevant in hookah smokers.

To investigate the demographic characteristics, concentration of Benzene, Toluene, Ethyl benzene and Xylenes (BTEX) in output smoke and health risk assessment in hookah smokers in hookah cafés, Iran. We checked hookah cafés in the different parts of Hamadan city and analyzed location and social station of each cafés in 2016. Finally, 20 cafés selected and five samples on each cafés (total of 100 samples). BTEX compounds were sampled in output smoke from mouth smokers using charcoal and analyzed by GC- MS according to NIOSH1501 method. The quantitative risk assessment of exposure to BTEX as recommended by the United State Environmental Protection Agency method was used. The smokers' demographic characteristics collected using a self-designed questionnaire. The average concentrations of benzene, toluene, ethyl benzene, o, m-Xylene and p- Xylene were 6.45, 7.02, 10.07, 7.21 and 8.36 mg/m3, respectively. The mean cancer risk for benzene was estimated as 529 × 10-5 and mean non-carcinogenic risks for toluene, ethyl benzene and o, m-Xylene and p–Xylene (TEXs) were 17.57, 5.03, 24.03 and 27.88, respectively. Hookah smoking is prevalent among youths and smokers are exposed to benzene level higher than the threshold limit value recommended by ACGIH. Cancer risk for benzene and non-carcinogenic risk for TEXs were much higher than recommended limits. Thus, in order to prevent diseases stemming from hookah smoking, urgent and increased notification about its adverse health effects and intensified regulatory laws are needed to decrease hookah smoking in hookah cafés.

The purpose of present study was to evaluate the toxic, teratogenic and histopathological effects of shisha smoking on some organs (uterine horns, liver, lung, heart and kidneys) of pregnant white mice Mus musculus and their fetus. Twenty pregnant female mice were used and they were divided into twice experimental groups. The first one as a control group was exposed to fresh air, while the second was exposed to shisha smoke once daily at 7th to 18th gestation day for 30 minutes for each exposed period per day. Exposed mice to shisha smokes showed increase locomotors activity. Fetal malformations were recorded at rate 86% appearance of malformed fetuses, like water nymph, aborted embryos, head defects with cephalomegaly, meningomeningo myelocele, sunken eye, cyanotic skin, skeletal deformity. Histopathological lesions in pregnant mice organs included, infiltration of inflammatory mononuclear cells, accumulation of serous fluid between the pulmonary alveoli, coagulated necrosis and thickening into alveolar septa, necrosis in the myocardial fibers, pyknosis, binuclated hepatocytes megakaryocyte. The histopathological effects in fetal organs were similar to that of the pregnant mice. In conclusion, shisha smokes increase locomotor activity, fetal malformations with prominent histopathological features in multiple organs pregnant mice and their fetuses. [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.

In this study, Air-agitated liquidâliquid microextraction (AALLME) with low solvent consumption was demonstrated for gas chromatographic determination of some polycyclic aromatic hydrocarbons (PAHs) as carcinogenic and mutagenic compounds in aqueous samples. Factors affecting the extraction process, such as extracting solvent type, extracting solvent volume, number of agitation, ionic strength, and centrifugation time, were investigated thoroughly and optimized. Under the optimized conditions, the method provided a good linearity in the range of 0.05 to 120 ng mL-1 (R2 ⥠0.995), low limits of detection (0.015 to 0.05 ng mL-1), good repeatability of the extractions (RSDs below 9.8%, n = 5), and the enrichment factors (EFs) were found to be in the range of 327 to 773. This is the first report on the utilization of AALLME for extraction of PAHs and results showed that AALLME can be a good choice for efficient micro-extraction of these compounds. In order to investigate this common view among some of people that hookah smoke can be healthy due to passing through water, both the hookah water and the hookah smoke were analyzed.

In this work, two disperser-free microextraction methods, namely, air-agitated liquid-liquid microextraction and ultrasound-assisted emulsification microextraction are compared for the determination of a number of polycyclic aromatic hydrocarbons in aqueous samples, followed by gas chromatography with flame ionization detection. The effects of various experimental parameters upon the extraction efficiencies of both methods are investigated. Under the optimal conditions, the enrichment factors and limits of detection were found to be in the ranges of 327-773 and 0.015-0.05 ng/mL for air-agitated liquid-liquid microextraction and 406-670 and 0.015-0.05 ng/mL for ultrasound-assisted emulsification microextraction, respectively. The linear dynamic ranges and extraction recoveries were obtained to be in the range of 0.05-120 ng/mL ( R2 ≥ 0.995) and 33-77% for air-agitated liquid-liquid microextraction and 0.05-110 ng/mL ( R2 ≥ 0.994) and 41-67% for ultrasound-assisted emulsification microextraction, respectively. To investigate this common view among some people that smoking hookah is healthy due to the passage of smoke through the hookah water, samples of both the hookah water and hookah smoke were analyzed. [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. [ABSTRACT FROM AUTHOR]

Introduction: Although communal smoking of hookah by means of water pipes is perceived to be a safe alternative to cigarette smoking, the effects of hookah smoke in respiratory epithelia have not been well characterized. This study evaluated epigenomic and transcriptomic effects of hookah smoke relative to cigarette smoke in human respiratory epithelial cells., Methods: Primary normal human small airway epithelial cells from three donors and cdk4 and hTERT-immortalized small airway epithelial cells and human bronchial epithelial cells were cultured for 5 days in normal media with or without cigarette smoke condensates (CSCs) or water pipe condensates (WPCs). Cell count, immunoblot, RNA sequencing, quantitative real-time reverse-transcriptase polymerase chain reaction, methylation-specific polymerase chain reaction, and quantitative chromatin immunoprecipitation techniques were used to compare effects of hookah and cigarette smoke on cell proliferation, global histone marks, gene expression, and promoter-related chromatin structure., Results: CSC and WPC decreased global H4K16ac and H4K20me3 histone marks and mediated distinct and overlapping cancer-associated transcriptome signatures and pathway modulations that were cell line dependent and stratified across lung cancer cells in a histology-specific manner. Epiregulin encoding a master regulator of EGFR signaling that is overexpressed in lung cancers was up-regulated, whereas FILIP1L and ABI3BP encoding mediators of senescence that are repressed in lung cancers were down-regulated by CSC and WPC. Induction of epiregulin and repression of FILIP1L and ABI3BP by these condensates coincided with unique epigenetic alterations within the respective promoters., Conclusions: These findings support translational studies to ascertain if hookah-mediated epigenomic and transcriptomic alterations in cultured respiratory epithelia are detectable and clinically relevant in hookah smokers.