Investigation of mainstream smoke aerosol of the argileh water pipe. Food and Chemical Toxicology ;41 1 —52 [accessed Feb 10]. World Health Organization. Tobacco Regulation Advisory Note. Tobacco Control Mar 24 [accessed Feb 10]. Drug and Alcohol Dependence external icon ; 1—3 —9 [accessed Mar 18].
For Further Information. Fact Sheets. What's this. Related CDC Sites. Social Media. Links with this icon indicate that you are leaving the CDC website. Linking to a non-federal website does not constitute an endorsement by CDC or any of its employees of the sponsors or the information and products presented on the website.
You will be subject to the destination website's privacy policy when you follow the link. CDC is not responsible for Section compliance accessibility on other federal or private website.
In hookah smokers, overall, GM urinary cotinine levels increased significantly 8. Among daily and weekly hookah smokers, GM urinary cotinine levels increased significantly 2. The highest increase post a hookah event was among occasional hookah smokers in which GM urinary cotinine levels increased significantly The highest pre and post hookah event GM urinary cotinine levels were among daily hookah smokers Pre hookah event GM urinary cotinine levels among daily hookah smokers were significantly 53 and times higher, respectively, than those found in occasional smokers and non-smokers.
Also, post hookah event GM urinary cotinine levels among daily hookah smokers were significantly 4. Among non-smokers, overall, GM urinary cotinine levels increased significantly 2. Creatinine-corrected cotinine values pre and post a hookah event by smoking status and location of event are presented in Table 3 see supplementary file Appendix 2 for uncorrected cotinine values. Among hookah smokers, GM urinary cotinine levels increased significantly 8. Among non-smokers, GM urinary cotinine levels increased significantly 3.
Responses ranged from doing smoke tricks, smoking while watching TV, smoke at home for fun and when bored, and smoking at home while socializing with friends or family members. A total of Other reasons included owning a hookah and hookah tobacco 7. We quantified uptake of nicotine in hookah smokers and non-smokers exposed exclusively to hookah tobacco SHS in indoor hookah smoking social events in natural settings: private homes and hookah lounges.
Our results demonstrated higher exposures to nicotine post hookah events in both hookah smokers and non-smokers exposed to hookah tobacco SHS in both home and hookah lounge settings.
Both before and after hookah events, GM urinary cotinine levels in daily and weekly hookah smokers were significantly higher than in non-smokers. Furthermore, among hookah smokers overall, pre-to-post event change in cotinine levels was positively correlated with number of hookah heads smoked at home events.
These results suggest that hookah tobacco smoking is a source of exposure to the addictive drug nicotine and should be included in tobacco control strategies. We identified only one study in the U. The overall trend is higher in our study, showing an 8.
This variability may be explained in part in that participants in our study spent more time during the hookah lounge visit mean, minutes vs. To date, we did not identify studies in the U. We did not find a significant difference in change in urine cotinine levels pre-to-post hookah event between hookah smokers in hookah lounges vs.
Therefore, future research and hookah tobacco preventive measures and control should include both natural locations where hookah smoking is allowed in hookah lounges and in homes.
We also were not able to find data on urinary cotinine levels in tobacco smokers and non-tobacco smokers exposed to tobacco SHS in a nationally representative sample of the U. Because collecting urine samples are less invasive than blood samples, and in order to compare our results to a representative sample of tobacco smokers and non-tobacco users exposed to SHS in the U.
To date, research focusing on the impact of SHS exposure from hookah tobacco smoking on non-smokers, particularly in natural settings is limited We found that passive exposure to hookah tobacco SHS in non-smokers resulted in a significant increase, 3.
Urine cotinine levels among non-smokers exposed to hookah tobacco SHS ranged from 0. Since there is no level of exposure to tobacco smoke considered to be risk free 30 , exposure to SHS should be minimized in order to protect the health of non-smoker adults and children socializing or living with hookah smokers.
Furthermore, optimal cut-off points for biomarker values to distinguish tobacco use versus no tobacco use have been determined for tobacco use other than hookah use.
We suggest that future research identify urine cotinine cut-off values to distinguish among hookah smokers, non-smokers exposed to hookah tobacco SHS, and non-smokers. Additionally, for disease epidemiology, it will be important to consider investigating the adverse effect of the cumulative dose of low cotinine levels due to chronic exposure to hookah tobacco SHS.
The causes of nicotine dependence among hookah smokers are likely multidimensional 3 , 20 , Therefore, studies are needed to investigate the effect of chronic nicotine exposure within the context of various stimuli that may induce tobacco dependence in daily hookah smokers versus in occasional hookah smokers with intermittent nicotine exposure.
We found that among daily hookah smokers, GM urinary cotinine levels increased 2. This variation by hookah smoking status in changes in GM urinary cotinine levels due to smoking hookah was partly the result of differences in pre hookah event cotinine levels; pre-event GM urinary cotinine levels were 53 times higher in daily hookah smokers than in occasional smokers We have previously identified stimuli to practice the habit of hookah smoking in hookah lounges, such as the high density of hookah lounges and proximity to colleges and homes, social aspects, and the availability of a variety of hookah tobacco flavors These stimuli could be included as points of intervention in public health programs to curb the spread of hookah use in private homes.
A few of our participants tried to save money by smoking in their private homes. Such stimulus that encourages hookah smoking at home suggests raising excise taxes on hookah tobacco products to increase the burden of smoking. Hookah tobacco smoke inside homes is hazardous to the health of non-smokers who live or socialize with hookah smokers in their homes While previously we suggested curbing the spread of hookah lounges 15 , 27 , our previous and present findings reported in this paper suggest encouraging banning hookah tobacco smoking inside private homes Efforts to pass regulations to ban smoking in public housing, and to encourage voluntary bans of smoking in private homes 36 , should be extended to include hookah tobacco smoking.
Generalizability of this study is limited by convenience sampling. Additional research is needed with larger sample sizes by smoking frequency status to enable a more rigorous assessment of nicotine exposure from hookah tobacco smoking. Hookah tobacco smoke is a source of nicotine exposure. Those attending social smoking events in hookah lounges and private homes are at risk of nicotine intake from exposure to hookah tobacco SHS, and smokers absorb even more nicotine through direct inhalation.
GM urinary cotinine levels in hookah smokers and non-smokers increased significantly 8. Among hookah smokers, the greatest change in urinary cotinine levels was found in occasional hookah smokers, in which GM levels increased Melbourne F Hovell.
Declaration of Interests: The authors declare no competing interests associated with this study. National Center for Biotechnology Information , U. Author manuscript; available in PMC May A Find articles by Noura O Kassem.
A Find articles by Sandy Liles. A Find articles by Sheila R Jackson. A Find articles by Dale A Chatfield. A Find articles by Melbourne F Hovell. Author information Copyright and License information Disclaimer. Copyright notice. This is an open-access article distributed under the terms of the Creative Commons Attribution-NonCommercial 4.
See other articles in PMC that cite the published article. Associated Data Supplementary Materials Supplemental. Abstract Background Nicotine, an addictive drug, is present in all forms of tobacco products, including hookah tobacco, which is not yet regulated in the United States.
Objectives This study aimed to investigate the uptake of nicotine in hookah smokers and non-smokers exposed to secondhand smoke SHS at indoor hookah social events in natural settings where hookah tobacco was smoked exclusively. Patients and Methods We quantified cotinine, a metabolite of nicotine, in the urine of hookah smokers and non-smokers. Results Following a social event where exclusively hookah tobacco was smoked, urinary cotinine levels increased significantly 8.
Dokha is manufactured by drying fine tobacco leaves in the desert region. Since the tobacco leaves are not processed much, it appears virtually unaltered and contains higher levels of nicotine, tar and carbon monoxide. A medwakh pipe Figure 1 , which consists of a bowl, stem and mouthpiece, is used to smoke dokha. Smokers typically smoke 6 g of dokha per day 8. Hookah is a pipe used to smoke shisha; it consists of a head, body, water bowl and vapor tube.
Shisha is a molasses-based tobacco mixture that is flavored with fruits or vegetables. In a hookah, the charcoal-heated tobacco mixture is passed through a water pipe and finally through a water-filled chamber. The burning embers are placed on the top of a pricked aluminum foil and the tobacco mixture is placed below. The smoker inhales the water-filtered smoke through the vapor tube via a mouthpiece and the smoke is cooled as it passes through the water 9.
Traditional medwakh and shisha pipes have no filters, so a variety of toxicants in tobacco smoke, such as tar, carbon monoxide, hydrogen cyanide HCN , nitrosamines, volatile organic compounds and toxic heavy metals can quickly enter the lungs 10 , Shisha manufacturers add a wide variety of fruit flavors to attract youth and falsely present shisha as a healthier and more natural alternative to cigarettes 9.
Nicotine is the most abundant alkaloid in tobacco leaves. The tobacco leaf position, leaf type and blend affect the amount of nicotine in each tobacco product 12 , Due to the high alkaloid content in tobacco plants, these alkaloids can be used as a natural pharmacological defense against vertebrates, insects and microorganisms. In fact, nicotine extracted from the tobacco plant is toxic to many insects, so it can be used as a commercial pesticide Nicotine binds to nicotinic acetylcholine receptors in brain tissue and exerts agonistic activity, so nicotine is addictive for humans According to Bulletin No.
In older processing methods, the nicotine content of the leaves was 1. The nicotine content of tobacco leaves can vary from 1. Tar is a sticky, partially combusted, particulate substance produced from the burning of tobacco during smoking. Tar also damages the mouth by decomposing and blackening teeth, damaging the gums and desensitizing taste buds. In tobacco products, smoke tar contains most of the toxic, mutagenic and carcinogenic agents Tar typically refers to the total aerosol residue As it enters the lungs, tar coats the cilia and causes them to stop working and eventually die.
Once gone, the cilia no longer trap toxic particles and the poisons can enter the alveoli directly, leading to lung cancer Smoking causes lung cancer due to a wide variety of carcinogenic substances found in tar, such as acrylonitrile, benzene and acrylamide. The carcinogenic substances in tobacco smoke, when directly exposed to delicate lung cells, mutate the DNA and leads to cancer.
The rate of coronary artery disease CAD in smokers is much higher in comparison to non-smokers because of the nicotine and tar from tobacco products. Some of the tar compounds are absorbed through the lungs and enter the bloodstream, promoting chemical changes to the cholesterol plaques formed on the walls of arteries, including coronary arteries.
Therefore, smoking and high cholesterol are multiplicative risk factors for CAD Pumice, paraffin and deionized water used in this work. Dilute hydrochloric acid was also prepared with deionized water. An Airpo mini vacuum pump 12 V-DC with pressure range 0—32 psi, separatory funnel mL , medwakh pipe and analytical balance was used to trap the tar particles released from tobacco smoke.
Tobacco smoke has carcinogenic and mutagenic agents; therefore, the extraction of tar and nicotine should be performed in a fume hood. Personal protective equipment must be worn during the extraction. Never taste the extracted nicotine from tobacco samples. The extracted samples should be stored in a secure container.
Chapin It is a rapid and accurate analytical method 16 , 23 , In the year , Association of Official Analytical Chemists International officially adopted the SAM method to quantify nicotine in tobacco products 25 , The SAM consists of three stages:. Extraction and Distillation, 2. Precipitation and Filtration and 3. The tobacco samples were homogenized by grinding to mesh sized particles using an agate mortar and pestle.
About 5 g of finely powdered sample or 2. Alcoholic sodium hydroxide solution 2. Alcoholic sodium hydroxide should be added in a quantity which is enough to liberate nicotine.
In the case of tobacco extracts, a sufficient quantity of powdered calcium carbonate was added to form a moist, but not lumpy mass; then, the mixture was thoroughly crushed with a pestle or spatula and was transferred into a suitable soxhlet extractor Figure 2. Experimental setup for the extraction of nicotine and trapping of tar particles from dokha and shisha tobacco samples. The sample was exhaustively extracted with diethyl ether.
Once the extraction was complete, the exhausted sample was removed and the excess ether was recovered. To obtain a higher percentage of nicotine from the samples, the cooling temperature of the circulating water should be maintained at a low temperature. The residue was diluted with sodium hydroxide solution 4 g NaOH in 1, mL deionized water.
Then, it was transferred using deionized water to a Kjeldahl flask, capable of holding mL, and steam distilled using a condenser through which water was flowing rapidly. A three-bend outflow tube was used, and a few pieces of pumice and paraffin were added to prevent bumping and frothing. Distillation was carried out until all the nicotine was extracted and the distillate was collected in a receiving flask. The crucible was accurately weighed to the fourth decimal point [0.
The precipitate was removed from the sides of the beaker and the stirring rod by washing with 0. The distillate was mixed thoroughly, and an aliquot was acidified with dilute hydrochloric acid [] or more. The mixture was thoroughly stirred and left standing for 18 h One end of the L-blend tube Figure 2 was fitted at the top of a mL separatory funnel, and the other end was attached to the medwakh pipe filled with 0.
The stopper is removed and a piece of glass wool was inserted to trap the tar residue. Before inserting the glass wool, the mass of the glass wool was measured up to four decimal places using an analytical balance. The bottom of the stopcock tap of the separatory funnel was fitted to an electronically controlled Airpo mini vacuum pump to simulate the inhaling of tobacco smoke. The vacuum pump outlet was connected to a properly vented exhaust.
The vacuum pump was turned on, and the tobacco sample was lit with a Bunsen burner flame. Gradually, the sample smoke accumulated in the body of the separatory funnel. Tar particles were trapped on the glass wool as the smoke passed through the stopcock tap. The collected smoke entered the inlet of the vacuum pump and exhausted via the outlet. The weight of the glass wool with tar residue was measured and the amount of tar in the dokha and shisha smoke samples was thus obtained.
The nicotine and tar levels in the dokha and shisha samples of various brands are tabulated in Table I. Table I. Nicotine and tar levels in various dokha and shisha tobacco brands. Figure 3 shows the nicotine and tar levels found experimentally from the various dokha and shisha tobacco products. The amount of nicotine and tar in the samples were significantly higher in comparison with the data provided by the Federal Trade Commission cigarette data 27 and commercially available tobacco products in the USA, UAE and India, as tabulated in Table II.
The min—max box plots of the tobacco products Figure 4 give the range of nicotine and tar levels in the various tobacco products. From the plots, dokha and shisha brands have surprisingly high nicotine and tar levels in comparison with cigarettes and smokeless tobacco products.
There is no precise data available regarding the amount of nicotine and tar present in dokha and shisha brands available in the UAE; however, neither dokha and shisha manufacturers nor the Public Health Department have provided any information to consumers regarding the nicotine and tar levels.
Dokha and shisha are readily available in different flavors. Most adults consuming these products are assuming that they are natural and have less nicotine and tar in comparison with cigarettes; thus, they believe that consuming dokha and shisha will not affect their health 7.
Therefore, it is logical and scientific to presume that dokha smokers are at a high risk of getting addicted to nicotine and of developing lung cancer. The box plots show that the amount of nicotine in the different dokha brands is surprisingly very high in comparison with cigarettes and other tobacco products.
0コメント