Department of Health and Human Services. Ward KD, et al. TC; , 24 S1 :i1-i2. Food and Chemical Toxicology; , Schubert J, et al. Toxicology Letters; , 3 Jacob P, et al. CEBP; , Shihadeh A. Cobb CO, et al. American Journal of Health Behavior; , 34 3 — Centers for Disease Control and Prevention.
February 15, ; 68 6 November 9, ; 67 44 American College Health Association. Ambrose BK, et al. American Lung Association. February Primack BA, et al. AJPM; , 42 2 We also use third-party cookies that help us analyze and understand how you use this website. These cookies will be stored in your browser only with your consent.
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Theoretically, sharing the mouthpiece during hookah group smoking can be a probable source of transmission of pathogens such as viruses, bacteria, and fungi. For instance, a study reported a potential risk for transmission of communicable diseases such as hepatitis C when sharing the mouthpiece between users with bleeding gum [ 99 ]. Other studies have also linked hookah to transmission of Helicobacter pylori main cause of peptic ulcer and Aspergillus spores cause of pneumonia in immunocompromised patients [ , ].
Moreover, 48 bacterial isolates were detected from hookah hoses, and among them were virulent as well as antibiotic-resistant strains [ ]. Furthermore, using hookah was linked to developing periodontal diseases in similar magnitude to cigarettes [ ] as well as documented alteration in oral microbial flora [ ]. Similar to cigarette smoking, hookah use is also linked to a harmful impact on the pulmonary system.
Thus, hookah users complain of symptoms such as wheezing, cough, sputum, and shortness of breath [ , , ]. FeNO is an essential marker of eosinophilic airway inflammation, and reduction in its levels may be due to rapid conversion of nitric oxide to peroxynitrite by reactive oxygen and nitrogen species or downregulation of nitric oxide synthase [ , ]. Also, hookah users had lower lung diffusing capacity and elevated levels of apoptotic endothelial cell microparticles [ ].
Hookah exposure induced a significant elevation of macrophages, lymphocytes, and neutrophils in broncho-alveolar lavage fluid and altered the levels of several cytokines. It also increased catalase activity in the lung and resulted in changes in the level and mRNA of major matrix metalloproteinases MMP-1, MMP-9, and MMP , confirming pulmonary damage associated with hookah use [ , ].
To this end, in a population-based study, hookah use was associated with metabolic syndrome development. Thus, hookah users had significantly higher incidence of hypertriglyceridemia and hyperglycemia, as well as hypertension and abdominal obesity, which was observed after controlling for age, sex, social class, and area of residence [ ].
Unfortunately and as stated before, the number of hookah users among the vulnerable populations of pregnant females and adolescents is increasing. In fact, pregnant females still use hookah during pregnancy, regardless of its reported hazards.
Moreover, the risk of delivering low birth babies tripled, in addition to reported neonatal respiratory distress that is linked to hookah use during the first trimester [ , ]. In a rat exposure model, hookah smoke exposure was shown to be associated with low birth weight, increased neonatal death rate, and lower growth rate among offspring [ ]. Additionally, prenatal exposure to hookah smoke in a murine model of asthma in adult mice offspring also induced airway inflammation and adversely affected lung function [ ].
In utero exposure to hookah tobacco smoke in rats resulted in impaired memory and decreased brain-derived neurotrophic factor in hippocampus of adult male offspring rats [ ].
A study of hookah use among 7th—10th grade students indicated that it may impair adolescent brain development, given that it reduces the levels of the brain-derived neutrophic factor BDNF [ ], which is essential for cognition and behavior [ ]. A relatively recent study also reported a reduction in BDNF serum levels in students reflecting a possibility of systematic adverse health alterations in adolescence, coupled with behavioral changes low attention and aggression [ ].
Moreover, hookah tobacco smoke exposure in rats induced short- and long-term spatial memory impairment [ ], which was associated with reduced hippocampal levels of major oxidative stress biomarkers and oxidative capacity enzymes [ , ]. With respect to carcinogenicity of hookah, it was reported that carcinoembryonic antigen CEA levels were higher in hookah smokers, in comparison to non-smokers, yet not as high as in cigarette smokers [ ]. Furthermore, three case-control studies reported a link between the risk of esophageal cancer and hookah use, with the risk increasing with cumulative use, higher frequency, and the duration of use [ , , ].
Additionally, using hookah was linked to an average of six folds higher risk of lung cancer [ , , , ]. Moreover, it was reported that hookah use may increase the risk of gastric cancer by threefold, albeit the mechanism remains unknown [ ].
In addition, hookah smoking was shown to be genotoxic, leading to DNA damage in lymphocytes, where the magnitude of its genotoxicity was higher than that induced by cigarette smoking [ , ]. Exposure to hookah smoking resulted in elevated plasma and saliva levels of toxic metals, namely cadmium, copper, and zinc [ ], which could contribute to its long-term carcinogenicity.
It is noteworthy that many of the aforementioned studies had limitations, for example, no control over use of other forms of tobacco and lack adjustments of the cofounding factors in some case studies, as well as limited assessment of gender and age as cofounders.
Nonetheless and taken together, there is sufficient evidence in support of the association of hookah use with negative human health outcomes. Cardiovascular effects and their underlying mechanisms. These data are compiled from what is reported in clinical studies. The detrimental acute and chronic effects of tobacco smoking on the cardiovascular system are well established [ , , , , , ].
In light of that, it has been shown that hookah smoke effects on the cardiovascular system are comparable to those of conventional cigarettes. It is noteworthy that a recent meta-analysis reported an odds ratio of association between hookah tobacco smoking and heart disease of 1. Acute effects of conventional smoking, such as increased blood pressure, heart rate, and vascular resistance, have been known for decades [ , , , , , ].
As with tobacco smoking, the instantaneous effects of hookah use include higher systolic and mean arterial blood pressure, as well as elevated heart rate HR [ 17 , 23 , , , , , , ]. These effects have been attributed, in part, to the baroreflex mechanism impairment [ ] or to elevated nicotine plasma level. The latter exhibits adrenergic effects that will enhance local and systemic catecholamine release [ 15 , 18 , , , , ].
Supporting the latter notion, mean post-hookah-smoking HR elevation was doubled in participants using nicotine-containing hookah in comparison to nicotine-free hookah smokers [ ].
Another study reported that changes in the cardiovascular central and peripheral components occur immediately after hookah smoking and include increases in HR, blood pressure, and after occlusion vascular resistance, whereas after occlusion blood flow and outflow were decreased [ ].
The cardiovascular changes were shown to be exacerbated among individuals with low habitual physical activity and physical fitness levels [ ]. More recently, it has been reported that adolescents smoking hookah had significantly lower vascular endothelium growth factor VEGF levels [ ], which might adversely affect vascular growth and function in this population.
Acute use of hookah also induced changes in the peripheral vascular system in similar fashion to cigarette smoking, such that it increased vascular resistance and reduced post-occlusion blood flow. In a manner comparable to cigarette smoking, short-term hookah use significantly impaired flow-mediated dilation FMD , which indicates endothelial dysfunction, but hookah was a weaker predictor for high risk profile [ ].
Furthermore, it was reported that short-term hookah use both tobacco-based and tobacco-free products disrupts the autonomic nervous system regulation on the cardiac cycle, thereby causing a reduction in HRvariability, which—in turn—might aggravate the risk of coronary artery disease development [ 18 ].
Moreover, a significant increase in TXB 2 levels, a metabolite of the biologically active TXA 2 , and an index of oxidative injury were reported after a single hookah smoking session [ ]. This increase in TXB 2 levels would suggest an increase in platelet activity [ ]. Importantly, it has been shown that an increase in platelet activity plays a major role in the pathogenesis of acute myocardial infarction MI [ ] and acute stroke [ , , ]. Therefore, it is not surprising to see a link between hookah smoking and acute MI in young adults [ ], and among patient undergoing cardiac catheterization [ ].
However, no data exist yet on the association between hookah smoking and acute stroke [ ]. Interestingly, and contrary to the hypothesis that hookah decreases myocardial blood flow because of the charcoal combustion nanoparticles vasoconstrictor , a study found that hookah use acutely increased myocardial blood flow. In light of the aforementioned evidence, it is clear that even short-term use of hookah disrupts normal cardiovascular function, as repetitive short-term hookah exposure may be the triggering point of causal chain of reactions ultimately leading to the chronic effects.
With regard to the adverse cardiovascular effects associated with longer-term of hookah use, they are comparable to those associated with cigarette smoking. In this connection, a link between chronic use of hookah and coronary artery disease CAD development has been shown, with the frequency and duration of exposure being critical risk factors to CAD.
Additionally, cardiovascular disease development such as ischemic heart disease IHD and heart failure has been associated with heavy hookah smoking [ ]. These outcomes could be explained by the continuous stress placed on the cardiovascular system as result of exposure to high amounts of CO [ ]. Furthermore, death due to IHD was 1. In accordance with the latter data, dose-response relationship between hookah-years and percent stenosis was also established [ ].
Furthermore, risk of MI and stroke death was significantly increased with hookah smoking. Notably and interestingly, a recent cross-sectional study aimed to examine the relationship between chronic hookah smoking and cardiovascular hemodynamics in adolescents found a reduction in both BP and HR of adolescent hookah smokers versus non-smokers, which is in contrast to previously reported results in adults.
Nonetheless, the exact mechanism underlying such outcome is still unclear but warrants investigation [ ]. Together, hookah use has been associated with many cardiovascular effects that influence or contribute to the decline of the overall health status of members of our communities. Unfortunately, despite studies documenting cardiovascular disease risks associated with hookah, people continue to assume that it is safer than cigarettes, mainly due to being unaware of its negative health effects.
Acute and chronic exposures to hookah smoke resulted in significant changes in kidney function biomarkers such as creatinine and blood urea nitrogen, in mice. This was associated with reduction in antioxidant enzymes and biomarkers including superoxide dismutase for acute and chronic hookah smoke exposures, and catalase, glutathione peroxidase, and thiobarbituric acid reactive substances for chronic exposure [ ].
Acute and chronic exposure of mice to hookah corroborates with the clinical findings that suggest cardiovascular dysfunction. Thus, short-term nose-only exposure to mainstream hookah for 5 consecutive days induced a significant decrease in platelet numbers and amplified in vitro platelet aggregation indicating a prothrombotic state [ , ].
Furthermore, cardiac inflammation with an increase in reactive oxygen species ROS was observed, which consequently caused an elevation in heart glutathione GSH; an antioxidant concentrations. This seems to indicate that an initial adaptive response that counterbalances the potentially damaging activity of ROS [ ] is triggered.
The increased cardiac vulnerability may explain the increased systolic blood pressure reported after long-term use, which was not seen post-short-term exposure [ , ]. In summary, both clinical and animal studies have provided substantial evidence of a link between cardiovascular disease development and hookah short- and long-term use.
However, there remain some knowledge gaps; firstly, there is a lack of well-designed studies addressing the association between hookah use and cardiovascular diseases. Second, the pathophysiologic mechanisms underlying the cardiovascular adverse effect are not fully understood, and thus, studies to address these issues are not only warranted but also critical at this point. For instance, e-cigarette use has been linked to increased health risks, including increase thrombosis risk [ ] as well as throat and mouth irritation, respiratory tract irritation, and behavioral changes among others [ ].
As for the use of e-liquids in e-hookah, that would be expected to produce the same toxicity as e-cigarettes. The evolving nature of these devices supports the notion that investigating their use patterns, purpose, prevalence, and potential health effects is crucial. Meanwhile, the public health experts should educate the public about the possible yet unknown health hazards of these products, whereas policy makers should limit their access to youth.
As mentioned before, hookah smoke may be associated with similar or even greater inhalation of toxicants in comparison to cigarettes. Since , the FDA finalized a rule extending their control of all tobacco products, including hookah tobacco. FDA now regulates the manufacture, import, packaging, labeling, advertising, promotion, and sale, as well as distribution of hookah tobacco and of all hookah apparatus parts except the accessories; lighters and tongs [ ]. Unfortunately, youth represent a large portion of the hookah user population, and their accessibility is facilitated through online ordering.
To control such means of access, major credit card companies should ban online payments for hookah, as they did with cigarettes [ ]. Tobacco is a preventable cause of morbidity and mortality worldwide.
Lately, as also noted by the American Heart Association statement [ ], hookah has been considered a global threat—in part—due to the high increase of its use, in addition to the deleterious effects it has on human body such as frequent respiratory infections, persistent cough, oral and esophageal cancer, and induction of a pro-inflammatory state.
In this connection, recent studies have shown that the levels of hookah-emitted chemicals vary depending on multiple factors such as topography, experience, session length, and type of tobacco used during each session. The widespread and increasing usage of hookah in the USA is concerning. Collectively, these findings can be used in educational campaigns for the public, as well as in shaping policies for further evidence-based hookah control.
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