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Smoking Pipe Tobacco: Exposure and Health

Silvana Barbosa, National Center for Health Research

Smoking pipe tobacco has been around for centuries. Pipe smoking typically consists of loose leaf tobacco that is fire-cured and burned in a traditional smoking pipe with a bowl and mouthpiece. Although pipe smoking has dwindled over the years, the proportion of regular users varies by state and ranges from 3% to 13%. 1  More surprising, 1.4% of high school students nationwide currently smoke a pipe. 2

Is Smoking Pipe Tobacco Safe?

While it is often assumed to be safer than smoking cigarettes, smoking pipe tobacco is still very harmful to the health of the user. Like cigarettes, pipe tobacco contains nicotine and is therefore addictive. In addition, nicotine has a harmful impact on adolescent brain development. This is especially worrisome because 90% of smokers started using tobacco before the age of 18. For pregnant women, nicotine harms the fetal brain and increases the risk of stillbirth and preterm birth. Other harmful effects of nicotine include increased risk for forming a blood clot, lightheadedness, changes in heart rate, and nausea. 3

Pipe tobacco contains toxic chemicals that increase the risk for some cancers. A study conducted by the prestigious American Association for Cancer Research found that people who smoke pipe tobacco are more likely to develop cancer of the head and neck, liver, and lung.  This risk was higher for people who smoked more often, had smoked for more years, or who inhaled more deeply. Even if users do not inhale, they are still exposed to toxic chemicals in the tobacco smoke released by the pipe. The only way to reduce the risk of these cancers is to quit smoking. Cancer risk decreases over the years following quitting. 4

According to the National Cancer Institute, the U.S. government’s major research institute on cancer, there is no safe form of tobacco, and all forms of tobacco are harmful and addictive. 5

What are the Effects of Smoking Pipe Tobacco Around Others?

Smoking pipe tobacco is not only harmful to the health of the user, but it is also a serious health risk to anyone exposed to its smoke. Secondhand smoke is classified as a known human carcinogen because it contains many of the harmful chemicals that are in the smoke directly inhaled by smokers.

Children exposed to secondhand smoke have an increased risk of sudden infant death syndrome, ear infections, respiratory infections, and far more frequent and severe asthma attacks. Adults exposed to secondhand smoke have increased risk of heart disease, stroke, lung cancer, and reduced fertility. Pregnant women are especially susceptible to the harms of secondhand smoke, because it can cause pregnancy complications such as low birth weights and preterm birth.

Since 1964, approximately 2.5 million nonsmokers have died from health problems caused by exposure to secondhand smoke. Opening windows and using air filters does not protect others from inhaling secondhand smoke. The only way to protect nonsmokers from secondhand smoke is for smokers to stop smoking. 6

There are also numerous health hazards associated with exposure to thirdhand smoke. Thirdhand smoke is residue from tobacco smoke that stays on surfaces and objects, like clothing, bedding, and furniture. The tobacco residue may remain on surfaces and objects for several months.

Children are most susceptible to thirdhand smoke. Children breathe faster and inhale more than adults, have greater hand-to-mouth contact, and absorb more chemicals through their skin. Exposed children are more likely to have coughing fits associated with mucus production.

Research also suggests that thirdhand smoke causes genetic damage that can increase the risk of developing cancer in the future. For example, studies in mice found increased risk for lung cancer and liver damage from thirdhand smoke. 7 To learn more about thirdhand smoke, please see here .

The Bottom Line

Like cigarettes, smoking pipe tobacco is not safe. Pipe tobacco contains many of the harmful chemicals found in cigarettes, including nicotine and toxic chemicals known to cause cancer. Smoking pipe tobacco is addictive, and users have an increased risk of head and neck, liver, and lung cancers.

Smoking pipe tobacco also jeopardizes the health of those around you. Secondhand smoke causes cancer and is especially harmful to pregnant women and children. Recent studies are discovering the harms of thirdhand smoke. Children face greater health risks than adults because the exposure is proportionally greater. The only way prevent harm from tobacco smoke is for the smoker to quit smoking.

For information on quitting smoking, see here.

All articles are reviewed and approved by Dr. Diana Zuckerman and other senior staff.

References: 1. Centers for Disease Control and Prevention. (2018). State-Specific Prevalence of Tobacco Product Use Among Adults – United States 2014-2015. Morbidity and Mortality Weekly Report 67(3): 97-102 https://www.cdc.gov/mmwr/volumes/67/wr/pdfs/mm6703a3-H.pdf 2. Food and Drug Administration. (2018). Pipe Tobacco. Retrieved from https://www.fda.gov/TobaccoProducts/Labeling/ProductsIngredientsComponents/ucm482580.htm . Accessed on April 25, 2019. 3. Bahl, Rajiv. (2018). From E-Cigs to Tobacco: Here’s How Nicotine Affects the Body. Retrieved from https://www.healthline.com/health-news/heres-how-nicotine-affects-the-body#5 . Accessed on April 25, 2019 4. Malhotra, Jyoti, Borron, Claire, Freedman, Neal D., Abnet, Christian C., van den Brandt, Piet A., White, Emily, Milne, Roger L., Giles, Graham G., and Boffetta,  Paolo. (2017). Association between Cigar or Pipe Smoking and Cancer Risk in Men: A Pooled Analysis of Five Cohort Studies. American Association for Cancer Research 10(12): 704-709 http://cancerpreventionresearch.aacrjournals.org/content/10/12/704 5. National Cancer Institute (2017). Harms of Cigarette Smoking and Health Benefits of Quitting. Retrieved from https://www.cancer.gov/about-cancer/causes-prevention/risk/tobacco/cessation-fact-sheet#q5 . Accessed April 25, 2019 6. Centers for Disease Control and Prevention. (2018). Secondhand Smoke Facts. Retrieved from https://www.cdc.gov/tobacco/data_statistics/fact_sheets/secondhand_smoke/general_facts/index.htm#what . Accessed April 25, 2019. 7. Drehmer, Jeremy E. , Walters , Bethany Hipple , Nabi-Burza , Emara and Winickoff , Jonathan P. (2017). Guidance for the Clinical Management of Thirdhand Smoke Exposure in the Child Health Care Setting. Journal of Clinical Outcomes Management 24(12): 551-559 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5716630/

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Article Contents

S ubjects and m ethods, d iscussion, r eferences.

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Association Between Exclusive Pipe Smoking and Mortality From Cancer and Other Diseases

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S. Jane Henley, Michael J. Thun, Ann Chao, Eugenia E. Calle, Association Between Exclusive Pipe Smoking and Mortality From Cancer and Other Diseases, JNCI: Journal of the National Cancer Institute , Volume 96, Issue 11, 2 June 2004, Pages 853–861, https://doi.org/10.1093/jnci/djh144

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Background: Although many studies have examined the adverse health effects of pipe smoking combined with other forms of tobacco use, few have included large numbers of exclusive pipe smokers. The prevalence of pipe smoking has declined since the 1960s, yet usage is still common regionally, especially among older populations. Methods: Using Cox proportional hazards models, we examined the association between pipe smoking and mortality from tobacco-related cancers and other diseases in a cohort of U.S. men enrolled in the Cancer Prevention Study II, an American Cancer Society prospective study. The cohort of 138 307 men included those who reported, in their 1982 enrollment questionnaire, exclusive current or former use of pipes (n = 15 263 men) or never use of any tobacco product (n = 123 044 men). Analyses were based on 23 589 men who died during 18 years of follow-up. Results: Current pipe smoking, compared with never use of tobacco, was associated with an increased risk of death from cancers of the lung (relative risk [RR] = 5.00, 95% confidence interval [CI] = 4.16 to 6.01), oropharynx (RR = 3.90, 95% CI = 2.15 to 7.08), esophagus (RR = 2.44, 95% CI = 1.51 to 3.95), colorectum (RR = 1.41, 95% CI = 1.15 to 1.73), pancreas (RR = 1.61, 95% CI = 1.24 to 2.09), and larynx (RR = 13.1, 95% CI = 5.2 to 33.1), and from coronary heart disease (RR = 1.30, 95% CI = 1.18 to 1.43), cerebrovascular disease (RR = 1.27, 95% CI = 1.09 to 1.48), and chronic obstructive pulmonary disease (RR = 2.98, 95% CI = 2.17 to 4.11). These risks were generally smaller than those associated with cigarette smoking and similar to or larger than those associated with cigar smoking. Relative risks of lung cancer showed statistically significant increases with number of pipes smoked per day, years of smoking, and depth of inhalation and decreases with years since quitting. Conclusion: Results from this large prospective study suggest that pipe smoking confers a risk of tobacco-associated disease similar to cigar smoking.

Clinical reports as early as 1795 linked pipe smoking with carcinoma of the lip and tongue, as noted by Doll ( 1 ). However, the risks associated with the exclusive use of pipes have been difficult to study because pipes are the least commonly used tobacco product in the United States ( 2 ), and relatively few smokers use pipes exclusively. Traditionally, men in the United States have either switched from cigarettes to pipes or smoked pipes in combination with cigarettes or cigars ( 3 ).

The prevalence of pipe smoking among adult men in the United States has decreased from 14.1% in 1965 to 2.0% in 1991 ( 4 ), and pipe smoking remains rare among U.S. women (<0.1% in 1991) ( 4 ). The prevalence of pipe smoking is highest among men aged 45 or older and in the Midwest ( 4 ). Pipes are commonly used by some populations, including American Indians (male prevalence = 6.9% in 1991) ( 5 ) and by both men and women in parts of China (20% prevalence in 1996) ( 6 ). The National Youth Tobacco Survey has measured prevalence of pipe smoking among U.S. youth since 1999. The prevalence of current pipe smoking has increased from 2.4% to 3.5% of middle school students and from 2.8% to 3.2% of high school students from 1999 to 2002; prevalence was higher among boys than girls and varied by state and ethnicity ( 7 , 8 ).

Exclusive pipe smoking has been positively associated with tobacco-related diseases in prospective ( 9 – 12 ) and case–control studies ( 13 – 23 ). The cohorts have contributed greatly to the epidemiologic evidence on tobacco and disease and include the Hammond–Horn nine-state study ( 9 ), the U.S. Veterans’ study ( 10 ), a sample of the Swedish population ( 11 ), and the Norwegian Cardiovascular Study ( 12 ). However, these studies have generally reported wide confidence intervals for the relative risk (RR) estimates associated with exclusive pipe smoking and have not been able to stratify by pipe smoking characteristics such as amount or duration because of small sample size. Case–control studies generally have not distinguished between current and former pipe smoking and present results for “ever” pipe smokers. Most published studies, especially prospective studies, have adjusted only for age and have not considered potentially important covariates such as socioeconomic status and alcohol use.

To provide a more precise estimate of the risks associated with pipe smoking, we analyzed data on a large number of exclusive pipe smokers (both current and former) from the Cancer Prevention Study II (CPS-II), an American Cancer Society prospective cohort study. We analyzed the risks of nine cancers known to be associated with tobacco as well as several other tobacco-related diseases, adjusting for potential confounding factors.

The CPS-II is an ongoing prospective cohort of approximately 1.2 million U.S. adults (676 306 women and 508 351 men) begun in the fall of 1982 ( 24 , 25 ). American Cancer Society (ACS) volunteers asked their friends, neighbors, and acquaintances who were at least 30 years old to participate in the study. Each participant completed a confidential, four-page mailed questionnaire on their smoking habits, alcohol intake, educational level, and other characteristics. This cohort is more likely to be college-educated, married, middle-class, and white than the general U.S. population ( 26 ). Informed consent to participate in the study was implied by the return of the self-administered questionnaire. All aspects of the CPS-II study protocol have been reviewed and approved by the Emory University Institutional Review Board and are renewed annually.

Information on pipe smoking was based on questionnaire responses in 1982 and was not updated during the follow-up. Men were asked “Do you now or have you ever smoked cigarettes, cigars or pipes at least one a day for one year’s time?” Current and former pipe smoking habits were assessed by asking the number of pipes smoked a day, age at which pipe smoking began, total years of pipe smoking, and depth of inhalation of pipe smoking. Former pipe smokers were asked their age at smoking cessation. Men were also asked about the use of smokeless tobacco (chewing tobacco and snuff). Users of cigarettes, cigars, or smokeless tobacco were excluded from this analysis. Women could not be included in this analysis because they were not asked whether they smoked pipes.

The vital status and cause of death of participants in CPS-II have been ascertained biennially since the month of enrollment by two methods: until 1988, via personal inquiries from ACS volunteers in September 1984, 1986, and 1988, with reported deaths verified by death certificate; since 1988, through automated linkage with the National Death Index (NDI) ( 27 ). As of December 31, 2000, 34.6% of men had died, 65.2% were still living, and 0.2% had follow-up censored on September 1, 1988, because of insufficient data for linkage with the NDI. Death certificates or multiple cause-of-death codes were obtained for 98.9% of all deaths. The underlying cause of death was coded according to the International Classification of Diseases, Ninth Revision (ICD-9) ( 28 ).

Person-years at risk were accrued from month of enrollment through the end of follow-up (December 31, 2000), the date of death, or the date lost to follow-up (because of insufficient information for NDI linkage), whichever occurred first. Age-standardized death rates were directly standardized to the age distribution of person-years among CPS-II men during the 18 years of follow-up ( 29 ).

For the purpose of this study, we restricted the cohort to the 138 307 men who reported either exclusive use of pipes (n = 15 263) or never use of any tobacco product (n = 123 044). We examined both all-cause mortality and cause-specific mortality for diseases related to cigarette smoking ( 30 , 31 ). The causes of interest included several cancers (lung, oropharynx, esophagus, larynx, stomach, colorectal, pancreas, bladder, and kidney), cardiovascular disease (coronary heart disease and stroke), and chronic obstructive pulmonary disease. Men who reported prevalent disease at enrollment in 1982 were excluded as follows: analyses of cancer mortality excluded men who reported any prevalent cancer except nonmelanoma skin cancer; analysis of coronary heart disease mortality excluded men who reported prevalent heart disease or diabetes; analysis of cerebrovascular disease mortality excluded men who reported prevalent stroke; and analysis of chronic obstructive pulmonary disease mortality excluded men who reported prevalent chronic bronchitis or emphysema. The analysis of all-cause mortality excluded men who reported a history of any of these diseases at enrollment.

Statistical Analysis

We used Cox proportional hazards models to estimate hazard ratios and 95% confidence intervals for mortality associated with pipe smoking and to adjust for other potential risk factors reported at baseline ( 32 ). We assessed the appropriateness of the Cox proportional hazards model for each cause of death by plotting log(–log) survival curves against survival time. The log(–log) survival curves were essentially parallel, suggesting that the proportional hazards assumption was met. All statistical tests were two-sided; hazard ratios were considered statistically significantly elevated if the lower limit of the 95% confidence interval was greater than 1.0, and P values less than .05 were considered statistically significant. Indicator variables were used for all independent variables. All models were adjusted for single year of age by stratification. Multivariable Cox proportional hazards models were adjusted for current alcohol consumption (none, <1 drink daily, 1 drink daily, 2–3 drinks daily, 4 or more drinks daily, and unquantifiable use), educational level (less than high school graduate, high school graduate, some college or vocational school, college graduate, and graduate school), race (white and nonwhite), and body mass index (normal or below [<25 kg/m 2 ], overweight [25–29 kg/m 2 ], and obese [≥30 kg/m 2 ]). Men who left all alcohol questions blank (“missing” alcohol use) were combined with men who reported no current alcohol consumption based on a previous analysis of CPS-II ( 33 ) in which these two groups were shown to have similar mortality patterns. In models for coronary heart disease mortality, we assessed other potential confounding factors, including occupation, current employment, vegetable and fruit consumption, dietary fat consumption, and aspirin use; these factors had little effect on the risk estimates (data not shown) and were not included in final models.

Current pipe smokers were further characterized by number of pipes smoked per day, years of smoking, and depth of inhalation, and former pipe smokers were characterized by number of years since quitting smoking and age at quitting smoking. Causes of death with fewer than 15 deaths among current or former smokers are not shown by smoking characteristic. Linear trends of smoking characteristics, excluding lifelong nonusers, were tested using the likelihood ratio test ( 34 ).

Epidemiologic evidence suggests synergism between tobacco smoking and alcohol consumption for cancers of the upper aero-digestive tract, which includes the oropharynx, esophagus, and larynx ( 30 ). Therefore we examined the joint association of pipe smoking and alcohol consumption with cancers of the upper aero-digestive tract. Men with unquantifiable alcohol consumption were excluded from this analysis. A likelihood ratio test was used to test for multiplicative interaction between pipe smoking and alcohol consumption.

Analyses of cigarette smoking in CPS-II generally use only the first 6 years of follow-up to minimize the effects of misclassification among current smokers who quit smoking during more prolonged follow-up ( 35 ). We chose to use 18 years of follow-up to maximize the number of deaths available for analysis. To examine the effect of cessation of pipe smoking over the 18-year follow-up, we compared relative risks for current and former pipe smoking associated with all causes, lung cancer, coronary heart disease, cerebrovascular disease, and chronic obstructive pulmonary disease for three six-year periods: 1982–1988; 1989–1994; and 1995–2000. If bias due to misclassification of smoking status was substantial, we would expect to see the relative risks of current smoking decrease over time. Temporal trends were tested by including interaction terms between survival time and smoking in the Cox model ( 36 ); statistical significance of interaction terms was evaluated using the Wald chi-square test.

Demographic and other characteristics of the study population according to pipe smoking status at baseline are presented in Table 1 . Men who had formerly smoked pipes were more highly educated than men who currently smoked pipes or who had never used tobacco. Both current and former pipe smokers were more likely to report alcohol consumption than never users of tobacco.

Table 2 presents death rates, adjusted for age, and hazard ratios, adjusted for age and other potentially confounding variables, comparing current and former pipe smokers with never tobacco users. Current pipe smokers experienced statistically significantly higher death rates than never users from all causes (RR = 1.33, 95% CI = 1.27 to 1.39); from cancers of the larynx (RR = 13.1, 95% CI = 5.2 to 33.1), lung (RR = 5.00, 95% CI = 4.16 to 6.01), oropharynx (RR = 3.90, 95% CI = 2.15 to 7.08), esophagus (RR = 2.44, 95% CI = 1.51 to 3.95), colorectum (RR = 1.41, 95% CI = 1.15 to 1.73), and pancreas (RR = 1.61, 95% CI = 1.24 to 2.09); from chronic obstructive pulmonary disease (RR = 2.98, 95% CI = 2.17 to 4.11); from cerebrovascular disease (RR = 1.27, 95% CI = 1.09 to 1.48); and from coronary heart disease (RR = 1.30, 95% CI = 1.18 to 1.43). Current pipe smokers also had statistically nonsignificant increases in death from cancers of the stomach (RR = 1.15, 95% CI = 0.71 to 1.87) and bladder (RR = 1.50, 95% CI = 0.94 to 2.39). No association was observed between current pipe smoking and kidney cancer mortality. Former pipe smokers experienced smaller increases in risk from most of these diseases, including cancers of the larynx (RR = 5.6, 95% CI = 1.5 to 21.2), lung (RR = 1.70, 95% CI = 1.23 to 2.36), oropharynx (RR = 1.19, 95% CI = 0.37 to 3.87), esophagus (RR = 1.60, 95% CI = 0.83 to 3.09), bladder (RR = 1.68, 95% CI = 1.03 to 2.75); and chronic obstructive pulmonary disease (RR = 1.35, 95% CI = 0.81 to 2.25).

Trends in multivariable-adjusted relative risks associated with current pipe smoking were evident in relation to the number of pipes smoked per day, duration of pipe smoking, and depth of inhalation (Table 3, 3A ). The relative risk for death from lung cancer increased from 1.99 for men who smoked 1–3 pipes daily to 7.67 for men who smoked 11 or more pipes daily ( P trend <.001). Similar increases in lung cancer mortality risk were seen with the duration of smoking ( P trend = .003) and with depth of inhalation ( P trend <.001). Statistically significant increasing dose response trends were observed with years of smoking for coronary heart disease, chronic obstructive pulmonary disease, and stomach and bladder cancers and with depth of inhalation for coronary heart disease, chronic obstructive pulmonary disease, and pancreas cancer. We observed an anomalous inverse association with depth of inhalation for cerebrovascular disease that we cannot explain.

We also analyzed the relative risks of death from tobacco-associated diseases among former pipe smokers by years since quitting pipe smoking and age at quitting (Table 4, 4A ). For most diseases, the relative risk decreased with years since quitting and with younger age at quitting. The relative risk among former pipe smokers was intermediate between that of current smokers and never tobacco users in most categories of amount, duration, and depth of inhalation (data not shown).

We assessed the potential synergism between pipe smoking and alcohol consumption for cancers of the upper aero-digestive tract (Table 5 ). The highest relative risk estimate was seen in men who reported current pipe smoking and drinking four or more drinks per day (RR = 15.1, 95% CI = 5.9 to 39.0) compared with men who use neither tobacco nor alcohol ( P interaction = .013).

To examine the effect of cessation of pipe smoking over the 18-year follow-up period, we compared the relative change in death rates among current and former pipe smokers compared with never tobacco users over three 6-year periods of follow-up (Table 6 ). Among current pipe smokers, no statistically significant trends in the relative risks of death from all causes or from any of the specific causes were evident with increasing follow-up. Among former smokers, there was a statistically significant decrease in the risk of death from lung cancer with increasing length of follow-up but also a statistically significant increase in the risk of death from cerebrovascular disease. Generally, the estimates obtained from 18 years of follow-up were similar to but more stable than those from 6 years of follow-up.

We compared the relative mortality risk estimates from smoking-attributable diseases associated with exclusive current pipe, cigarette, or cigar smoking among CPS-II men (Fig. 1 ). For most diseases, cigarette only smokers have the highest risk ( 37 , 38 ), and men who exclusively smoked pipes have risks that are similar to or higher than those associated with smokers of cigars only ( 39 ). The association between smoking and death from coronary heart disease does not differ by tobacco product ( 37 , 40 ).

Results from this large, prospective study provide more precise estimates of the relationship between pipe smoking and death from tobacco-attributable diseases than have been available previously. In this cohort, pipe smoking conferred a risk similar to or greater than that for cigar smoking for cancers of the lung, larynx, esophagus, and oropharynx and for coronary heart disease ( 39 , 40 ).

The epidemiologic literature on tobacco use, including pipe and cigar smoking, has been reviewed recently ( 30 ). Many of the studies included in that review combined pipe and cigar smokers; however, the studies that examined exclusive pipe smoking showed results similar to ours. Of the prospective studies, ours is the largest and the only one to adjust for risk factors other than age. Men who smoke pipes exclusively have higher risk of lung cancer than men who have never smoked in most published prospective ( 9 – 12 , 41 , 42 ) and case–control ( 13 – 17 ) studies. In our study, risk of lung cancer mortality in men was increased fivefold for current pipe smokers; this estimate is higher than that reported in two earlier U.S. cohorts ( 9 , 10 ) but is consistent with studies conducted in Europe ( 11 , 12 , 41 , 42 ). Like our study, two large European case–control studies ( 13 , 17 ) reported that lung cancer risk increased with years of pipe smoking, number of pipes smoked per day, and depth of inhalation and decreased with time since cessation of smoking.

Risk of death from laryngeal cancer was also strongly associated with current pipe smoking (RR = 13.1). To our knowledge, the association with laryngeal cancer has not previously been assessed among exclusive pipe smokers. Our estimates for death from cancers of the oropharynx (RR = 3.90) and esophagus (RR = 2.44) are consistent with those from other prospective studies, including Hammond–Horn ( 9 ), the U.S. Veterans’ Study ( 10 ), and a Swedish cohort ( 11 ). A hospital-based case–control study in Beijing observed a fivefold increased risk of oral cancer incidence among both male and female ever pipe smokers ( 18 ).

The risk estimate for stomach cancer mortality in this study is slightly lower than that reported in two prospective studies ( 10 , 12 ) or in a previous analysis in CPS-II men (RR = 1.3, 95% CI = 0.8 to 2.2), which was based on 14 years of follow-up ( 43 ). The risk of colorectal cancer mortality was highest for men who reported several decades of smoking or smoking 11 or more pipes per day, similar to results observed among cigarette smokers in CPS-II ( 44 ). Although no association was observed between current pipe smoking and colon or rectal cancer mortality in the Swedish study ( 11 ), Heineman et al. ( 45 ) observed an increasing risk of colon and rectal cancer death with increasing number of pipes smoked per day in a 26-year follow-up of U.S. veterans.

Risk of pancreatic cancer mortality associated with pipe smoking was increased in the Swedish prospective study ( 11 ) but not in two other prospective studies—the U.S. Veterans’ study ( 10 ) or the Norwegian Cardiovascular Study ( 12 ). A hospital-based case–control study by Muscat et al. ( 19 ) observed an increased risk for pancreatic cancer incidence associated with ever pipe smoking.

Two previous studies in U.S. cohorts ( 9 , 10 ) reported an association between pipe smoking and bladder cancer mortality similar to that seen in CPS-II (RR = 1.50); a relative risk of 4.0 was reported in the Swedish study ( 11 ). The largest study of bladder cancer, a pooled analysis of European case–control studies ( 20 ), reported statistically significantly higher risk with longer duration of pipe smoking, as was also observed in CPS-II. We did not find an association between pipe smoking and kidney cancer mortality, similar to the results of two case–control studies of kidney cancer incidence ( 22 , 23 ).

Finally, our estimates of risk for cardiovascular and pulmonary disease are similar to those reported in the large Swedish study ( 11 ) and are within the range reported by other prospective A limitation of our study is that smoking habits were reported only at baseline. For diseases such as lung cancer, in which risk increases exponentially with duration of smoking ( 46 ), the relative risk estimate among continuing smokers would be expected to increase over time. However, we found that the association between lung cancer and current pipe smoking remained relatively constant over time (Table 6 ). The expected increase may have been obscured by misclassification of exposure due to cessation of smoking among current smokers during the 18-year follow-up period. The effect of this misclassification would be to underestimate the risks of continued smoking and to attenuate dose–response gradients.

The main strength of our study was its size, which provided precise estimates of mortality risk associated with pipe smoking among men who smoked pipes exclusively and provided moderately stable estimates of risk for the more common endpoints in relation to the number of pipes smoked daily, duration of smoking, and depth of inhalation among current smokers, and age at quitting and years since quitting among former smokers.

Comprehensively documenting the deleterious health effects of pipe smoking is important in countering efforts by the tobacco industry to promote pipes as a desirable alternative to cigarettes or cigars. The tobacco industry has repeatedly demonstrated its ability to create new markets by reviving interest in tobacco products that had appeared to have become obsolete, especially among youth and young adults. Two complementary approaches used to rekindle demand for products such as moist snuff, premium cigars, bidis, and hookah pipes are to minimize the adverse health consequences of these products by presenting them as a less hazardous alternative to cigarette smoking and to glamorize use by creating positive associations with celebrity, athleticism, success, and/or internationalism ( 47 ).

Results from this large, prospective study strongly support a causal relationship between pipe smoking and mortality from cancers of the lung, larynx, esophagus, and oropharynx, and chronic obstructive pulmonary disease. Although the risk of dying from tobacco-associated diseases is lower for pipe smokers than for cigarette smokers, pipe smoking is as harmful as, and perhaps more harmful than, cigar smoking. All tobacco products cause excessive morbidity and mortality. Our findings may help deter efforts by the tobacco industry to imply, directly or indirectly, as it has with smokeless tobacco ( 48 , 49 ) and low-yield cigarettes ( 50 ), that any tobacco product has negligible adverse health effects.

Relative risk (RR) estimates for tobacco-attributable diseases associated with current exclusive cigarette, pipe, or cigar smoking among men in Cancer Prevention Study II (CPS-II). Estimates for pipe smoking are from Table 2 . The associations between cigarette and cigar smoking and tobacco-attributable diseases in CPS-II men have been published previously ( 37 – 40 ). Estimates for the association between cigarette smoking and cancer of the oropharynx, esophagus, pancreas, larynx, and bladder are from the 1989 Surgeon General’s Report, p. 150 ( 38 ); those for lung cancer and coronary heart disease are from the 1997 National Cancer Institute Smoking and Tobacco Control: Monograph No. 8, p. 395, 400 ( 37 ). Estimates for the association between cigar smoking and cancer of the lung, oropharynx, esophagus, pancreas, larynx, and bladder are from Shapiro et al. ( 39 ); the estimate for coronary heart disease is from Jacobs et al. ( 40 ).

Demographic and other characteristics of CPS-II men who, at enrollment in 1982, reported either never use of tobacco products or exclusive smoking of pipes

Mortality rates, hazard ratios (HRs), and 95% confidence intervals (CIs) comparing men who never used any tobacco product with those who smoked pipes exclusively, CPS-II, 1982–2000

Death rates are per 100000 person-years and are age-standardized to the CPS-II male person-year distribution. ICD-9 = International Classification of Diseases, 9 th edition.

From Cox proportional hazards models, adjusted for age only.

From Cox proportional hazards models, adjusted for age, race, educational level, body mass index, and alcohol consumption.

Analysis for all causes excluded men who reported prevalent cancer, heart disease, diabetes, stroke, emphysema, or chronic bronchitis in 1982.

Analyses for cancers excluded men who reported any prevalent cancer in 1982.

Analysis for coronary heart disease excluded men who reported prevalent heart disease or diabetes in 1982.

Analysis for cerebrovascular disease excluded men who reported prevalent stroke in 1982.

Analysis for chronic obstructive pulmonary disease excluded men who reported prevalent emphysema or chronic bronchitis in 1982.

Mortality hazard ratios (HRs) and 95% confidence intervals (CIs) comparing exclusive current pipe smokers with men who never used any tobacco product, by pipes smoked per day, duration of smoking, and inhalation, CPS-II, 1982–2000*

(continued).

Mortality hazard ratios (HRs) and 95% confidence intervals (CIs) comparing former pipe smokers with men who never used any tobacco product, by years since quitting and age at quitting, CPS-II, 1982–2000*

Effect of alcohol consumption on the association between upper aero-digestive tract cancer and exclusive pipe smoking, CPS-II men, 1982–2000 *

Upper aero-digestive tract cancers include oropharynx, esophagus, and larynx ( International Classification of Diseases, 9 th edition [ICD-9] codes 140–150, 161). HR = hazard ratio; CI = confidence interval.

Cox proportional hazards models are adjusted for age. P interaction = .013, based on likelihood ratio test.

Mortality hazard ratios (HRs) and 95% confidence intervals (CIs) comparing men who never used any tobacco product with men who smoked only pipes, CPS-II men, by follow-up period *

From Cox proportional hazards models, adjusted for age, race, educational level, body mass index, and alcohol consumption. ICD-9 = International Classification of Diseases, 9 th edition.

P trend is based on the Wald chi-square test.

Analysis for lung cancer excluded men who reported any prevalent cancer in 1982.

We are grateful to the 1.2 million American men and women who have participated in the Cancer Prevention Study II and to the American Cancer Society volunteers for their assistance in developing this cohort.

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• cerebrovascular disorders
• chronic obstructive airway disease
• inspiration
• lung cancer
• coronary heart disease
• cancer death rate
• pipe smoking
• cigar smoking

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• Volume 20, Issue 2
• Health consequences of pipe versus cigarette smoking
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• Aage Tverdal 1 ,
• Kjell Bjartveit 2
• 1 Norwegian Institute of Public Health, Oslo, Norway
• 2 National Health Screening Service, Oslo, Norway
• Correspondence to Dr Kjell Bjartveit, Fridtjof Nansens vei 24 B, N-0369 Oslo, Norway; kjell.bjartveit{at}getmail.no

Objectives To estimate the risk of dying from all causes and from specified smoking-related diseases in men who were exclusive daily pipe smokers at two consecutive examinations, and in men who switched from smoking cigarettes only to pipe only.

Design A prospective cohort study.

Setting Three counties in Norway.

Participants 16 932 men, aged 20–49, screened for cardiovascular disease risk factors in the mid-1970s, re-screened after 3–13 years, and followed throughout 2007.

Outcomes Absolute mortality and relative risks adjusted for confounding variables, of dying from all causes and ischaemic heart disease, stroke, cardiovascular disease, lung cancer and other smoking-related cancer.

Results Altogether, the men were observed for 403 327 years, and during the observation period, 4933 deaths occurred. With sustained never smokers as reference, the sustained smokers of a pipe only had adjusted relative risk (95% CI), of dying from any cause that was 1.99 (1.73 to 2.27). At comparable tobacco consumption, no significant difference in risk between pipe and cigarette smokers appeared. As to survival, no difference was found between sustained smokers of a pipe only and of cigarettes only. Men who switched from cigarettes only to pipe only had a risk which was not significantly different from the risk in sustained smokers of cigarettes only.

Conclusions Between pipe and cigarette smokers, no or only minor differences were found in mortality from any cause and the specified smoking-related diseases. Pipe smoking is not safer than cigarette smoking.

• Pipe smoking
• all cause mortality
• smoking-related cardiovascular disease
• smoking-related cancer
• harm reduction
• health services
• primary health care
• smoking caused disease

https://doi.org/10.1136/tc.2010.036780

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Introduction

What are the health consequences of smoking a pipe, compared to smoking cigarettes? Is there a change in risk by switching from smoking cigarettes to smoking a pipe?

The first US Surgeon General report on smoking and health issued in 1964 marginalised any risk increase in people smoking a pipe. Based upon results from seven prospective studies the report concluded ‘The death rates for pipe smokers are little if at all higher than for non-smokers, even for men who smoke 10 or more pipefuls a day and for men who have smoked pipes more than 30 years'. 1 The 1979 US Surgeon General report still concludes: ‘Overall mortality ratios for pipe-only smokers as a group are only slightly higher than for nonsmokers'. 2 The 1982 US Surgeon Report dealt with cancer, and now the conclusions are less categorical: ‘Cigar and pipe smoking are also causal factors for lung cancer’. As for oral and laryngeal cancer this report concludes that cigar and pipe smokers experience a risk similar to that of a cigarette smoker. 3 For lung cancer, the 1989 US Surgeon General Report repeats this conclusion, and adds: ‘The lower risk of lung cancer among pipe and cigar smokers compared with cigarette smokers is due to the lesser amount of tobacco smoked and the lower degree of inhalation’. 4

Results from several cohort studies in the UK, Sweden, Denmark, Norway and the USA have given more details on pipe smokers' risk, both with regard to total death and of dying from major smoking-related diseases. 5–11 Among pipe smokers, they all find increased risk of death from lung cancer, some also of coronary heart disease, 6 9 11 others not. 5

In a cohort study from the UK, it was found that smokers who switched from cigarettes to pipes or cigars halved their combined risk of dying of lung cancer, ischaemic heart disease or chronic obstructive lung disease, compared with continuing smokers, but their risk was still about 50% higher than that of lifelong non-smokers. This study did not give separate follow-up results for pipe smokers only. The authors concluded that cigarette smokers who have difficulty in giving up smoking altogether would be better off changing to cigars or pipes. 12

Except for the British Doctors' Study, the prospective cohort analyses referred to above have been based on one survey only. People may change smoking behaviour during the observation period and, thus, have an impact upon the outcome of the study. Moreover, confounding variables may have influenced the results.

In the present study we have tried, at least partly, to respond to these objections. The study is based upon smoking habits registered at two surveys, years apart. The aim is to determine the risk in sustained smokers of a pipe, compared with sustained never smokers and sustained cigarette smokers. We also examine the risk in participants who between the surveys changed their mode of smoking, in particular they who switched from smoking cigarettes to smoking a pipe. The report includes a population of 16932 men, aged 20–49 years, and living in three Norwegian counties. They were surveyed in the mid-1970s for cardiovascular disease risk factors and were screened again during the next 3–13 years at least once. These men have been followed throughout 2007 for deaths from serious smoking-related diseases and from all causes, and risk calculated after adjustment for a series of confounders registered at baseline. The mean observation period is 24 years, maximum 30 years, counting from the time of the last screening.

The study population and data collection have been described earlier 13–15 and will be repeated in the following sections.

Initial screening

Between 1974 and 1978, screening examinations for cardiovascular disease were undertaken in three Norwegian counties with a mainly rural settlement (Finnmark, Sogn og Fjordane, Oppland). All male and female residents, aged 35–49 years, were invited, and a 10% random sample of residents aged 20–34. The attendance was 88%. 16

An identical protocol was used in the screening programme in the three counties. It included a questionnaire related to well-known risk factors of cardiovascular disease. Height, weight and blood pressure were measured, and a non-fasting blood sample was drawn and serum analysed at the same laboratory for total cholesterol, triglycerides and glucose. 16 Details on the first screening were published earlier. 17

Extensive reports on this study population with relevance to smoking and mortality after 13 and 26 years of observation have been published previously. 9 18 Three other reports have been issued, concentrating on health consequences in people smoking 1–4 cigarettes per day, in heavy smokers who reduced their daily consumption by more than 50% and in sustained ex-smokers. 13–15

Second and third screening

In one county, Finnmark, two new screenings were conducted after 3 and 13 years. In the two other counties (75% of the total study population), the re-screenings were carried out 5 and 10 years after the initial screening. 19–21

At the second screening, all those invited to the initial screening were re-invited, and, in addition, a 9% random sample of people aged 20–34 years who were not invited to the first examination. The attendance was 88%. 22

At the third screening, some modifications were made of the eligibility to the study, partly due to capacity constraints. Referring to the age at the initial screening, the following were invited to the third screening: All people aged 30–44 years and all people under 30 years who were invited to the second screening. In two of the counties, a 10% random sample of people aged 45–49 years were invited; in the third county, all people in this age group were invited. The attendance was 84%. 20 23 24

All elements of the outlined screening programme, except for glucose testing, were kept unchanged throughout the screenings; in particular that part of the questionnaire covering smoking habits.

The study population

As only 18 women reported smoking a pipe at either one or both examinations, this presentation is restricted to male participants.

Further, in order to avoid influence of earlier smoking upon health, 6801 men who at the first examination were non-smokers, but reported to have smoked cigarettes daily previously, were excluded, as were 254 men who smoked cigars at either one or both examinations. Also excluded were 250 never-smoking men at both examinations, but even so they reported to have smoked for a mean of 8.6 years. In all likelihood, these men had been smoking a pipe earlier in life, but were not smoking any kind of tobacco when attending the examinations (see later under Methods, Categories of participants).

Of the remaining men, 23 038 attended two or three screenings, and of these, 22 697 had a satisfactory completion of the questions on smoking.

In order to avoid questions on reverse causality that might occur if people changed smoking habits owing to illness, the study was restricted to men who at the last examination did not report a history of myocardial infarction, angina pectoris, stroke, diabetes, atherosclerosis of legs, treatment for hypertension, use of glycerine trinitrate and symptoms indicative of angina pectoris or atherosclerosis obliterans, totalling 20 049 men. We focus on the seven smoking categories defined below, which means that 2484 men who quit smoking between the two surveys, and 633 men who reported not to have smoked a pipe only did not enter the analysis. Hence, we are left with 16 932 men. For each man who underwent two or more examinations, paired results were selected according to the following priority, on the basis of attendance at:

first and second screening (n=14 350)

second and third screening (n=2130)

first and third screening (n=452).

The follow-up period started from the last of the two examinations available.

Questions about smoking behaviour

In a special box in the questionnaire, the smokers of a pipe reported the actual packs of tobacco (50 g) smoked per week, also noting down quarters or thirds of a pack. In another box, the cigarette smokers reported the actual number of cigarettes smoked per day, allowing citing a range, such as 10–15 cigarettes.

People who stated that they did not smoke cigarettes at present were asked if they had smoked cigarettes daily before, and if they were smoking cigars daily. All present or previous smokers were asked about how many years altogether they had been smoking daily.

At the examination site, the nurses carefully checked through the questionnaire with the participants. Factory made and hand-rolled cigarettes had to be counted together. The nurses were instructed that one pack of tobacco for hand rolling (50 g) equalled 50 cigarettes. For those who gave a range of consumption, we used the highest figure.

Categories of participants

In this report we have applied the following categories:

Main categories

‘Sustainers’ : Men whose smoking behaviour did not change from the first to the second examination.

‘Switchers’ : Men who were smoking daily at both examinations, but had switched their mode of smoking from the first to the second examination.

Subcategories

Never smoked : Men who at both examinations were not smoking daily, and had never smoked cigarettes daily before

Pipe only : Men who were smoking a pipe daily, and not smoking cigarettes daily

Cigarettes only : Men who were smoking cigarettes daily, and not smoking a pipe daily

Mixed : Men who were smoking both a pipe and cigarettes daily.

Regrettably, we do not have information on men, who, before the first examination, may have smoked a pipe daily, but had stopped doing so. Likewise, we lack information on occasional, but not daily, smoking.

We carried out a mortality follow-up by linking our records with the National Causes of Death Register, using the 11-digit personal identification number as record linkage. Each person accrued person-years from the day of the last examination until date of death, date of emigration or 31 December 2007.

In addition to deaths from all causes, we studied deaths from the following:

Ischaemic heart disease : International classification of diseases (ICD), 8th edition and ICD-9: 410-414; ICD-10: I20-I25

Stroke : ICD-8 and ICD-9: 430-438; ICD-10: I60–I69

Cardiovascular disease : ICD-8: 390–444.1, 444.3–458; ICD-9: 390–459; ICD-10: I00-I99

Lung cancer : ICD-8 and ICD-9: 161–162; ICD-10: C32–C34

Other smoking-related cancer : Types of cancer that the International Agency for Research on Cancer has classed as liable to be caused by smoking, and later applied by Doll et al . 25 26 Thus, the following types of cancer were included:

– lip, oral cavity and pharynx: ICD-8 and ICD-9: 140–149; ICD-10: C00-C14

– nose and nasal sinuses: ICD-8 and ICD-9: 160; ICD-10: C30-C31

– oesophagus: ICD-8 and ICD-9: 150; ICD-10: C15

– stomach: ICD-8 and ICD-9: 151; ICD-10: C16

– pancreas: ICD-8 and ICD-9: 157; ICD-10: C25

– liver: ICD-8: 155, 197.8; ICD-9: 155; ICD-10: C22

– kidney and renal pelvis: ICD-8 and ICD-9: 189.0-1; ICD-10: C64-C65

– bladder and ureter: ICD-8 and ICD-9: 188; ICD-10: C66-C67

– myeloid leukaemia: ICD-8 and ICD-9: 205; ICD-10: C92.

Statistical methods

Age adjustments were made by the indirect method based on 5-year age intervals. Hazard ratios were estimated by the Cox proportional hazards model including potential confounders as covariates (see footnote, table 1 ). All covariates were entered as continuous linear variables, except for body mass index where dummy variables were defined based on the cut-offs 20, 25, 30 and 35 kg/m 2 . Height was included among the covariates as an indirect measure of socioeconomic status, since a previous study based on the same population found a very strong association between income, educational level and body height. 27 The proportional hazards assumption was checked by a test based on Schoenfeld residuals. 28 There was no evidence of violation of the proportional hazards assumption for stroke, lung cancer and other smoking-related cancer deaths. For total death, cardiovascular and ischaemic heart disease deaths, there was a significant violation for the category of sustained cigarettes only. Graphical inspection revealed that, after 20 years of observation, the hazard for this category approached the category of never smokers. Censoring the follow-up at 20 years gave no rejection of the proportional hazards assumption. The hazard ratios became slightly higher (cf, Results). Survival curves were produced by the Kaplan-Meier estimate.

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Adjusted relative risk* (95% CI) of death from all causes, ischaemic heart disease, stroke, cardiovascular disease, lung cancer and other smoking-related cancer, by smoking category, with sustained never smokers as reference†

Table 2 shows baseline characteristics of these men at the start of follow-up. In some of the categories, information on duration of smoking was missing for a negligible number of participants.

Background characteristics at the last examination of the participants*, by category of smoking

Men who smoked a pipe only were the oldest and had the longest duration of smoking. Subtracting mean duration of smoking from mean age gives the same mean age of smoking debut as the smokers of cigarettes only. Smokers of a pipe only had lower daily tobacco consumption than cigarette smokers.

Never smokers have the lowest mean values for systolic blood pressure and serum lipids, and the highest mean value for physical activity during leisure and for body mass index. Smokers of a pipe, both ‘sustainers’ and those who had switched to pipe smoking, have higher blood pressure values than sustained cigarette smokers.

Sustained never smokers have lower frequency of disability pension and, except for men who switched from mixed to exclusive pipe smoking, the lowest frequency of sick leave. As to family history of coronary heart disease there was some variation, but with no specific pattern.

Table 3 shows the number of men and number of person years distributed by category. The highest number of men is found among sustained never smokers and sustained smokers of cigarettes only. At the first examination, 912 men smoked a pipe exclusively. Of these, 665 (73%) were still exclusively pipe smokers at the second examination.

Number of participants and person years. Deaths from all causes, ischaemic heart disease, stroke, cardiovascular disease, lung cancer or other smoking-related cancer, number and per 100 000 person years, age adjusted. By category of smoking*

For all groups of smokers, age-adjusted mortality was distinctly higher than in never smokers. Among the ‘sustainers’, cigarette smokers had higher rates than pipe and mixed smokers. Between the ‘switchers’ no clear pattern appeared.

Table 1 displays adjusted relative risks of deaths (95% CI) from all causes and from the specified smoking-related diseases, with sustained never smokers as reference. The relative risks are adjusted for a series of confounders (see footnote in table 1 ).

Among the ‘sustainers’, the highest risks were found in men smoking cigarettes only, both for deaths from all causes and from the specified diseases. Between pipe only and mixed smokers, the risk differences were small and inconsistent, as were risks between the ‘switchers’. For all causes, the risks were twice as high in all categories of smokers as in never smokers. For lung cancer, the relative risks were between 10 and 20 times higher in smokers than in never smokers.

For all causes, the risk in sustained smokers of cigarettes only was significantly higher than in sustained smokers of a pipe only (p=0.002). For the specified smoking-related diseases, there was no significant difference between sustained smokers of a pipe only and sustained smokers of cigarettes only, except for lung cancer, where sustained smokers of cigarettes only had a significantly higher mortality (p=0.019). For all causes and the specific causes, the risks among the sustained smokers did not differ systematically from the risks in the ‘switchers’. The only exception was stroke, where the risks in all groups of ‘switchers’ were consistently higher than among the sustained smokers.

The data referred to above concern people without a history of cardiovascular disease or diabetes, or without symptoms of angina pectoris or atherosclerosis obliterans. If this group is not excluded, however, we find adjusted relative risks that are substantially the same as those presented in table 1 .

Of the 10 657 daily smokers who underwent two examinations, 7 696 (72%) also met for a third one, 5–10 years after the last of the two examinations available, or 5–10 years after the follow-up period started. Table 4 shows their smoking behaviour at the third screening.

Smoking behaviour at the third examination, by category at the second examination

As a whole, around 10% of the smokers at the second examination had quit smoking at the third examination, and there is no significant difference between the categories. The groups who had switched between smoking categories at the second examination vary somewhat; apparently some men who had switched from cigarettes to pipe only were again smoking cigarettes only at the third examination.

Table 5 is restricted to sustained smokers of a pipe only and of cigarettes only, and never smokers, altogether 16 281 men. These two categories of smokers are divided in three subgroups by daily consumption of tobacco. The subgroups of pipe and cigarette smokers correspond fairly well with each other, as can be seen from the mean weight of tobacco consumed daily (the weight of one cigarette equals 1 g). For the groups with the highest consumption, 2% of the pipe smokers consumed 2¾ packs or more per week, or 39+ g per day, whereas 27% of the cigarette smokers consumed 40 cigarettes+ per day.

Sustained smokers of a pipe and sustained smokers of cigarettes*, by amount smoked recorded at the last examination. Number of participants, person years and deaths. Adjusted relative risk† (95% CI) of death from all causes, ischaemic heart disease, stroke, cardiovascular disease, lung cancer and other smoking-related cancer, with sustained never smokers as reference

For both pipe and cigarette smokers there is a dose-response relation by amount of tobacco consumed per day. Exceptions are lung cancer and other smoking-related cancer among the sustained smokers of a pipe, where there is no increasing risk by amount smoked. Between pipe and cigarette smokers with about the same daily consumption, there is no systematic difference in risk.

In both pipe and cigarette smokers with the lowest consumption, the risks are significantly higher than in never smokers. This applies to deaths from all causes and from the specified smoking-related diseases, with the exception of stroke and other smoking-related cancer in both categories of smokers, and cardiovascular disease in cigarette smokers.

Figure 1 demonstrates survival of sustained smokers of exclusive pipe or cigarettes. The data used in the figure are adjusted as outlined in the legend. A figure based upon unadjusted data, however, gives a similar picture. The survival is roughly the same in both categories of smokers with a slightly lower survival in pipe smoker after 20 years of observation. The unadjusted 25-year survival is 66% in pipe smokers and 69% in cigarette smokers, which may be compared to 87% in never smokers.

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Survival (%) of sustained smokers of a pipe only and of cigarettes only, by observation years. The survival estimates are adjusted to age=50 years, duration of smoking=20 years, consumption=1–1.99 packs/week for pipe smokers and 5–14 cigarettes per day for cigarette smokers, cf, table 5 .

We have found that pipe smokers have a mortality that is similar to the mortality in cigarette smokers at comparable consumption levels. This observation is made both for total mortality and for the specified smoking-related diseases, with the exception of lung cancer, where smokers of only cigarettes have the highest mortality. Switching between smoking groups did not change the risk substantially.

Of particular interest is that men with the lowest daily consumption have significantly higher risk than never smokers. For cigarette smokers, this has been demonstrated before in another study based upon partly the same population, 13 and is confirmed by this new follow-up. The same observation is now made for pipe smokers with the lowest consumption, less than three pipefuls per day. For lung cancer, our findings correspond well with the US Cancer Prevention Study II, and with the Norwegian part of the Migrant Study, where significant risk increases were found in smokers of 1–3 pipes/day and 1–4 g/day, respectively. 12 7 The US study also found a significant risk increase of coronary heart disease in the said consumption group.

The higher lung cancer mortality in cigarette smokers may, at least partly, be due to the occurrence of extreme daily consumption (40 g/day+).

Generally, our findings reveal a more serious outcome for sustained pipe smokers than has been found in most other studies so far. In fact, the risk for pipe smokers is of the same order of magnitude as for cigarette smokers.

Several explanations may account for the discrepancies with other studies. Other studies are based upon only one recording of smoking habits, or refer to the participants' recall of previous smoking. People may change both their mode of smoking and their daily consumption. Recordings made at two different examinations, years apart, may give a more valid estimate of smoking habits. Another explanation may be that pipe smokers over time have changed their smoking technique; that in previous years they were merely puffing, but later started to inhale the smoke, imitating the technique they observed in cigarette smokers. We cannot elaborate on this theory, as our questionnaire did not include questions on inhaling. In our neighbouring country Sweden, however, a similar proportion of inhalers was found in cigarette smokers as in pipe smokers, in contrast to studies in the UK and USA, where the proportion of inhalers was found to be higher in cigarette smokers than in pipe smokers. 6

Other explanations for the discrepancies between our findings and results from other studies may be that we have been able to adjust for a series of confounding variables. As in the British doctors' study we excluded men who had a history of earlier smoking; also, we excluded men who reported daily smoking of cigars or cigarillos. 5 Lastly, our study has a longer follow-up period than other studies.

It is also worth noting the impact of age and consumption on the effect estimates. The crude mortality, as may be calculated from table 3 , was higher in smokers of a pipe only than in smokers of cigarettes only. Adjustment for age reversed this picture ( table 3 ). After stratifying on consumption, however, the adjusted relative risks were comparable between pipe and cigarette smokers. This underlines the importance of adequate adjustment for confounders.

Different results in different studies may also be due to changes in smoking habits during the follow-up. For 72% of smokers in our study population, we have recordings of smoking habits 5–10 years after follow-up started. At that time, quit rates in the smoking categories varied between 9% and 14%. Of the sustained smokers of a pipe only, 12.9% had quit. This shows that just a few people had given up smoking during the first third of the follow-up period. However, as the prevalence of pipe smoking has declined we cannot rule out the possibility that our risk estimates may be biased owing to changes in smoking habits during the remainder of the follow-up period.

The frequency of pipe smoking has changed considerably over time in Norway. Up to 1950 it was the dominant form of tobacco smoking; later it lost ground to cigarette smoking. Population surveys disclosed that during 1958 to 1975, the fraction of pipe smokers was halved from about 40% to about 20%. 29 Since the mid-1970s, Statistics Norway has carried out annual surveys of representative samples of the Norwegian population aged 16–74 years, applying similar questions as in our study (Norwegian Directorate of Health, 2009). In 1975, these surveys showed that 9.7% of males aged 35–49 years smoked a pipe daily (including mixed smokers), which corresponds well with the frequency observed in our study. Further results of the national surveys are shown in figure 2 , which also shows that during the last couple of years, pipe smoking in Norway is virtually non-existent. A similar trend is reported from the USA. 30

Percentage of Norwegian males aged 35–49 years smoking a pipe daily. Three yearly moving averages. Results of annual surveys of representative samples of the Norwegian population aged 16–74 years. Mean annual sample size in age group 35–49 years: 1975–86: 326; 1987–98: 325; 1999–2008: 163. Source: Norwegian Directorate of Health, Tobacco Division, 2009.

Strengths and weaknesses of the study

The strength of the study is the size of the population, 16 932 men, who were surveyed twice, years apart. They were examined according to standardised procedures, and observed for a mean of 24 years, more than 400 000 person-years. We have information on a series of relevant confounding variables, which have been adjusted for, and we have provided continuous survival rates up to 30 years after onset of the study. The follow-up is complete with respect to both death and emigration. By excluding former cigarette smokers and cigar smokers we have been able to concentrate on pipe smokers. We also have information on smoking habits for a large part of the study population up to 10 years after follow-up started.

One weakness is that, despite the size of the study population, the risk estimates for some endpoints become imprecise for several of the smoking categories. If we could have implied incidence, it would have been better for aetiological considerations, as mortality is the result of incidence and fatality. Incidence endpoints would also have increased the power of the study.

One possible bias could be that only 72% of the men from the last of the two examinations showed up for a third examination. This lack of attendance may partly be because only 10% in the age group 45–49 years (at the first examination) in two of the counties were invited to the third screening (cf,‘Study population’). Also, at the first examination, all people who could not attend the screening were asked to send in a special form provided, giving the reasons for not attending. Of the non-attendees, 55% sent such an absence note, and of these 59% stated that disease, disability or temporary absence as the reason for not showing up. 16 We have no reason to believe that the causes for non-attendance have changed substantially for the two last screenings.

Possible implications for policymakers

In the population, misconceptions undoubtedly prevail as to the risk of pipe smoking, possibly originating from the early milestone reports on smoking and health (see Introduction).

In health education and patient counselling it is important to communicate that there is only a negligible difference, if any, in risk between pipe and cigarette smokers, and that harm reduction in no way will be obtained by switching from smoking cigarettes to smoking a pipe.

It may be said that the findings of our study are of historical interest only, since pipe smoking has almost disappeared in many countries. In other countries, however, pipe smoking may still exist, and, in addition, people's smoking behaviour may change quickly so that pipe smoking may come into fashion again. In Norway, such a development has been observed for the use of moist snuff (Swedish ‘snus’). Some decades ago, this form of tobacco was used only by elderly men, but has in recent years become fashionable again in younger generations.

Exclusive pipe smokers registered at two consecutive screenings, years apart, have a risk of dying from all causes and from specified smoking-related diseases that is significantly higher than in sustained never smokers. Between pipe and cigarette smokers with comparable daily tobacco consumption, there is no consistent difference in risk. Pipe smokers with the lowest consumption, less than three pipefuls per day, have a risk that is significantly higher than in never smokers. Men who switch from cigarettes only to pipe only have a risk that is not significantly different from that of the sustained smokers of cigarettes only.

What this paper adds

This study, which includes a population of 16 932 men observed for a mean of 24 years, found that

Pipe smokers with the lowest consumption, less than three pipefuls per day, have a risk of dying from any cause and from major smoking-related causes that is significantly higher than in never smokers.

Between pipe and cigarette smokers with equivalent daily tobacco consumption, there is no significant difference in mortality risk.

Men who switch from cigarettes only to pipe only have a risk that is not significantly different from that of sustained smokers of cigarettes only.

Acknowledgments

The authors thank Rita Lindbak, senior adviser, Norwegian Directorate of Health, Tobacco Control Department, for providing survey data on Norwegian smoking habits.

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Competing interests None.

Provenance and peer review Not commissioned; externally peer reviewed.

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• Review article
• Open access
• Published: 14 September 2019

The effects of hookah/waterpipe smoking on general health and the cardiovascular system

• Hanan Qasim 1 ,
• Ahmed B. Alarabi 1 ,
• Karem H. Alzoubi 2 ,
• Zubair A. Karim 1 ,
• Fatima Z. Alshbool 1 &
• Fadi T. Khasawneh   ORCID: orcid.org/0000-0002-4027-2997 1  

Environmental Health and Preventive Medicine volume  24 , Article number:  58 ( 2019 ) Cite this article

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Hookah or waterpipe smoking or use is an emerging trend in the US population, especially among the youth. The misperception of hookah being less harmful than cigarettes and the availability of different but “appealing” flavors are considered among the main reasons for this trend. Hookah users however are exposed to many of the same toxic compounds/by-products as cigarette users, but at dramatically higher levels, which might lead to more severe negative health effects. In fact, hookah users are at risks of infections, cancers, lung disease, and other medical conditions. Moreover, because of the overlapping toxicant/chemical profile to conventional cigarettes, hookah smoke effects on the cardiovascular system are thought to be comparable to those of conventional cigarettes. A major source of tobacco addiction is nicotine, whose levels in hookah are extremely variable as they depend on the type of tobacco used. Taken together, in this review of literature, we will provide insights on the negative health effects of hookah in general, with a focus on what is known regarding its impact on the cardiovascular system.

Introduction

Hookah also known as waterpipe, narghile, argileh, shisha, hubble-bubble, goza, borry, qaylan, chica, and mada’a (Fig. 1 ) is a tobacco pipe with a long yet flexible tube that draws the smoke through water contained in a bowl [ 1 ]. Even though hookah use in the western world is a recent trend, it has existed for a millennium, emerging in the North Western provinces of India, spreading to Iran, the Arab world, and Turkey and now gaining popularity in the USA and Europe [ 2 ].

PubMed search results for different names of hookah used in the literatures. Hookah is the most common used term followed by waterpipe and shisha

Apparatus description

The hookah or hookah apparatus is composed of an upper and lower compartment connected by a pipe (Fig. 2 ). Briefly, the top consists of a bowl where tobacco or molasses are placed then covered with perforated aluminum foil above which burning charcoal is placed. On the bottom of the apparatus resides a water jar covered by a gasket, protruding a hose and a release valve (used for clearing out stagnate smoke) [ 1 , 2 , 3 ]. A detailed description of hookah components is provided in Table 1 .

A typical hookah apparatus

Even though hookah retains some of its features globally (presence of liquid through which smoke passes), there is immense variability in the consumables, sizes, and materials used to manufacture apparatus parts, due to personal preferences and cultural/regional differences [ 4 , 5 ]. It is noteworthy that manufacturing material variability may influence the levels of smoke/chemicals exposure. Indeed, one study reported that differences in pipe material affected the levels of carbon monoxide (CO) exposure, correlating the non-porous plastic hose with higher yields of CO compared to the more porous leather hose [ 6 ]. The same theory could be applied to yields of other chemicals, especially nicotine. Hence, hookah effects may be under/overestimated in some studies, so future research should take into consideration such variations to make results more relevant.

Hookah tobacco

There are three commonly used types of hookah tobacco, Mouassal, Jurak, and Tumbak, each contains different ingredients. In brief, Mouassal which is an Arabic translation for “honeyed” contains 30% tobacco and around 70% honey/sugarcane as well as glycerol and flavors [ 7 ]. Hadidi and Mohammed [ 8 ] estimated that the nicotine contents of Mouassal is about 3.4 mg/g. Jurak, on the other hand, contains tobacco, sugarcane, and around 20% other spices and dried fruits [ 8 ]. Jurak is commonly used in the Middle East and Gulf region. Finally, Tumbak, which is used mainly in Asia, is a pure form of unflavored tobacco leaves (Ajami) smoked with charcoal.

Hookah tobacco flavors

In the USA, there are different flavors used in the hookah tobacco with the most popular being the fruit flavors [ 9 ]. Similarly, among university students, fruit flavored tobacco was preferred to unflavored ones [ 10 ]. Among US women, candy/sweet and menthol are the second and third preferred flavors, respectively, with fruit flavors still the number one choice [ 11 ]. Other flavors include chocolate, clove/spice, alcohol, and other beverages [ 9 ]. This suggests that flavored tobacco plays a major role as a “motivator” for using hookah, which provides the user with the pleasant taste and smell.

Hookah preparation and mechanism of action

The user or the person preparing the hookah (Fig. 2 ) starts by loading the tobacco into the bowl before wrapping the head with aluminum foil and then perforating the foil by using a screen pincher or toothpick. After that, the “ignited” charcoal is placed on the top perforated foil to initiate the tobacco heating process [ 12 ]. During inhalation, charcoal-heated air passes through the pierced aluminum foil and through the tobacco down the pipe and towards the water. After “bubbling” through the water, the cooled smoke reaches the surface and is drawn through the hose and is inhaled [ 3 , 13 ]. Taken together, hookah smoking seems to have a complex puffing behavior when compared to conventional cigarette smoking.

Puffing topography

Both cigarette- and hookah-smoking topography serves as an indirect measure of smoke and chemical exposure [ 12 , 14 ]. In comparison to cigarettes, hookah puffing is more variable including total puffing time, number of puffs, and total smoke inhaled, all being affected by the nicotine content of tobacco, the presence of flavors, the personal preferences, and the social setting of the vaping session [ 12 , 15 , 16 ]. Regarding total puffing time, hookah use takes significantly longer periods (30–90 min/session) [ 12 , 17 , 18 , 19 , 20 ] in comparison to cigarette smoking (averages 5–6 min) [ 12 , 21 ]. Furthermore, number of puffs, mean puff duration, puff volume, and inter-puff intervals were higher in hookah [ 22 , 23 , 24 ], in contrast to conventional smoking [ 25 , 26 ]. The longer sessions of hookah smoking could explain the increase in number of puffs/session. Also, the “humid” nature of the hookah smoke makes it more pleasant than the dry cigarette smoke and facilitates higher volume uptake [ 15 , 16 , 27 ]. Importantly, this higher humidity of the smoke and its cooled down nature facilitates deeper inhalation potentially increasing the side effects of using hookah [ 2 ]. Given the behavioral complexity of hookah use/smoking, further examination of smoking patterns is warranted in order to accurately estimate users’ exposure to harmful chemicals.

Reasons and prevalence of hookah use

As mentioned before, hookah became widely popular, with its use accelerating rapidly especially among youth and women [ 28 , 29 ]. Thus, understanding the reasons/patterns of use will aid in developing strategies to better control hookah use. Although there are ample justifications in the literature for hookah use, in this section, we will include the most commonly reported, in addition to the prevalence of hookah.

Reasons of use

Many factors seem to have promoted hookahs’ spread/use, including but are not limited to perception of “no/less harm” of hookah, social acceptance/less restrictions, accessibility, use of flavored aromatic tobacco, curiosity, peer pressure, fashion, higher socioeconomic status, and need for amusement [ 28 , 30 , 31 , 32 , 33 , 34 , 35 , 36 ]. One factor that drastically contributed to the increased hookah use (similarly to e-cigarette use) is the misperception about the health risks. Majority of users believe in the “no or less harm” of hookah compared to cigarettes; this particular belief could be connected with the myths of intermittent use of hookah that reduces harm compared to constant use of cigarettes [ 37 ], the passage of smoke through water would filter it, and “the less” addictive nature of hookah [ 2 ]. Some users argue that they do not inhale the smoke (keep it in the mouth cavity), therefore protecting themselves from nicotine absorption/addictive effects. However, nicotine could be easily absorbed through the mucosal lining of oral cavity [ 2 ]. Furthermore, receiving the “positive” attributes of hookah such as socializing, relaxing, and the good taste/smell of the smoke seems to encourage and maintain hookah use [ 9 , 38 ]. To this end, a recent study conducted on social media (Twitter) found that social events and flavors were among the common contexts and experiences associated with Twitter discussions about hookah (2017–2018) [ 39 ]. Finally, one study demonstrated that participants preferred flavored hookah because the “sweet” flavored smoke smell is not viewed as offensive as cigarette smoke [ 36 ], which supports the conclusion that flavor plays an important role in promoting hookah use. Thus, clearly, there should be more emphasis on research studies that examine hookah health risks, which would inform campaigns for educating the public on the myths and the negative health effects associated with hookah use.

Worldwide, it is estimated that 100 million people use hookah on a daily bases [ 40 ]. Back in 2011 “current hookah use” among adults age > 18 years was 15% in Lebanon, 9–12% in Syria, 4–12% in Arabic gulf countries, 6% in Pakistan [ 41 ], and 30% in Jordan [ 42 ], whereas in Iran, it was found that more non-smokers transition to tobacco use including waterpipe/hookah [ 43 ]. Comparable to those levels, US adults “current use-smoking waterpipe on at least 1 day within the past 30 days” was 9.8% and “ever use-smoking waterpipe at any point in lifetime” was 1.5% between 2009 and 2010 [ 44 ] reaching levels of 12.3% and 3.3%, respectively, by 2012–2013, reflecting a gross increase within the US population [ 45 ]. Furthermore, while the majority of US hookah users are also tobacco smokers, a significant portion of hookah users are non-smokers [ 35 , 38 ]. In this connection, differences between rural and urban US in smoking hookah were also examined, and the results illustrated more prevalence of hookah use in urban areas in comparison to rural areas [ 46 ]. This difference could be attributed to the sociocultural and economic factors linked to living in urban areas. Besides that, the distribution among the states/regions was found to be variable [ 47 ] (Fig. 3 ), with west states having higher prevalence compared to south states, in particular five states, namely Arizona, California, Colorado, the District of Columbia, and Nevada, had high rates of both current hookah use ( ≥ 5%) and ever use (≥ 15%) [ 45 ]. It is difficult to determine what might be the cause behind this increase in the west, but potentially, it might derive—in part—from the higher population of Arab Americans within these regions. This notion is supported by Arab Americans having the highest rates among all racial/ethnic groups of adults identifying themselves as non-Hispanic “Other” [ 44 ]. Regardless, conducting research on hookah environment characteristics such as the number of hookah bars, methods of advertising, and social behaviors could serve as the first step in further understanding the increasing prevalence and popularity of hookah.

Distribution of hookah “ever use” in the USA, from the National Adult Tobacco Survey (NATS) 2012–2013 ( n  = 60,192) [47]

Hookah use among US youth population in schools was under scrutiny in many studies. For instance, one study surveyed a representative sample of 6th–12th grade students for hookah use, and the results showed that 10.5% reported smoking hookah [ 48 ]. Another study documented that hookah “ever use” among middle and high school students in USA included 6.8–15% of the students [ 31 ]. These results are remarkable as they show that as young as sixth grade (vulnerable population) can be a user of hookah, and potentially exposed to all associated health risks. According to the same study, household hookah users and easy access are the main motivation to use hookah in such young age [ 48 ]. Interestingly, Arab Americans had higher percentage of both “current and ever use” compared to non-Arabs, which indicates a strong influence for cultural background on hookah use [ 49 ].

College students’ prevalence of hookah use was 9.6% for “current use” and 22.9% for “ever use” between 2008 and 2009, whereas it increased to 28.4% for “past year” use and 46.4% for “ever use” in 2013 [ 50 ]. Such an alarming increase may be in part due to the belief that hookah use is less harmful/addictive with higher social approval in comparison to tobacco [ 51 , 52 ]. Notably, this belief is the major reason many adults use hookah, in addition to viewing it as a good way of socializing, and the belief that it helps quitting cigarettes, as well as being relatively cheaper than smoking cigarettes [ 34 ]. Another drastic and more concerning increase of 5.3% from 2011 to 2014 in hookah popularity was reported among adolescents in USA. This is especially troublesome as adolescents continue to be exposed to harmful tobacco product constituents, in particular nicotine that might interfere with brain development, cause addiction, and might lead to sustained future tobacco use [ 53 ]. Another recent representative sample of young adults aged 15–24 years old revealed that hookah use was 14.7% among males and 10.2% among females [ 54 ]. This increase in use could be attributed to the perception of fewer negative consequences of hookah smoking compared with cigarette smoking and the social norms regarding its acceptability among this population [ 55 , 56 , 57 ].

Importantly, developing new perhaps “more rigid” policies to regulate hookah use is not only needed in youth but must also expand to control use during pregnancy. This is rather a public health priority given hookah’s prevalence (12.4%) [ 58 ], coupled with the relatively “high” passive exposure to hookah smoke (32.8%) during gestation [ 59 ], which in turn leads to the involuntary exposure of innocent fetuses to hookah, and subjecting them to hookah’s potential harmful effects [ 60 ].

Regardless of the variability in hookah prevalence among the various populations, clearly, there is an overall drastic increase in its use over a short period. Longitudinal studies should further help in understanding and evaluating use trends, sociodemographic characteristics, and health risks in various populations being exposed to/using hookah, which would ultimately shape new “more strict” policies, especially those governing use among highly vulnerable populations, including pregnant females and youth.

Toxicants and air quality

Toxicological profile.

Even though hookah has been present for a millennium, far less studies have examined its chemical constituents/air quality relative to cigarettes. With tobacco being the main source of smoke in both hookah and cigarettes, hookah users are exposed to many of the same toxic compounds/by-products as cigarette users but at dramatically higher levels, which might in fact produce worsened health effects in users [ 23 ]. Consequently, it is important to evaluate the major compounds expelled from hookah vape, in order to aid in evaluating both acute and chronic health outcomes.

Several toxicants have been found in mainstream hookah smoke including nicotine [ 27 , 61 , 62 , 63 , 64 ], carbon monoxide [ 27 , 63 ], carcinogenic polycyclic aromatic hydrocarbons (PAHs) [ 27 , 61 , 63 , 64 , 65 ], aromatic amines [ 63 ], aldehydes [ 64 , 66 ], furanic and phenolic compounds [ 67 , 68 ], tar [ 19 , 61 ], particulate matter [ 69 ], heavy metals [ 19 ], and ammonia [ 70 ]. It is noteworthy that the amounts of these toxicants might be higher/lower in hookah compared with cigarette smoke (per cigarette/and per pack/day) due to different heating process and charcoal combustion [ 71 , 72 , 73 , 74 ] (Fig.  4 ).

Comparison of the levels of some toxicant expelled in both hookah and tobacco smoke. Levels of the toxicants ( a ) tar, CO, ( b ) carbonyl compounds (formaldehyde and acetaldehyde), and ( c ) certain PAHs are indicated. Levels of toxicants in pack/day are extrapolated by multiplying the levels in one cigarette by 20 [ 71 , 72 , 73 , 74 ]

Nicotine—the major source of tobacco addiction—content in hookah is extremely variable as it depends on the type of tobacco used. Consequently, the amount uptaken by the user depends on hookah use characteristics that are adjusted depending on nicotine levels in tobacco used in order to deliver desired doses [ 62 ]. Similar to cigarette smoking, plasma nicotine levels were found to be increased in hookah users, indicating systematic delivery of nicotine. However, these levels were much higher compared to cigarette users, which could be explained by longer “hookah” sessions with a higher puff number/volume [ 23 , 75 ]. Likewise, plasma carboxyhemoglobin levels in hookah users exceeded those of cigarette smokers’ levels [ 61 ], indicating the presence/inhalation of carbon monoxide (CO) during hookah use. This is because CO displaces O 2 from hemoglobin forming carboxyhemoglobin (CO affinity for hemoglobin is 200 times that of O 2 ) and shifting the oxygen dissociation curve to the left, thereby causing hypoxia and impairment of cellular respiration [ 76 ]. Notably, hookah use was linked to several cases of CO poisoning [ 77 , 78 , 79 , 80 , 81 ]. Furthermore, NNAL—a metabolite formed after 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) enters the body and a well known carcinogen—urinary levels increased markedly after hookah use, indicating the presence of tobacco-specific nitrosamines in hookah smoke [ 63 , 82 ]. Other well-known carcinogens/potential carcinogens are polycyclic aromatic hydrocarbons (PAHs), and they have been quantified in hookah smoke, in particular 16 of these compounds have been found [ 65 ]. Moreover, in contrast to single cigarette smoking, nicotine-free dry particulate matter (TAR) from a single 45 min hookah session reached a level of 802 mg, which represents 36.5 folds higher than that in a cigarette. This should in turn diminish marketing fads of hookah containing 0% tar [ 83 ]. Of note, levels of tar delivered vary from session to session, reaching up to 100 folds in some cases of longer hookah smoking sessions [ 84 ].

Importantly, inhaled volumes are concerning because they deliver high amounts of hazardous chemicals/session compared to cigarettes. For instance, aldehydes, such as acrolein, induce cardiopulmonary toxicity [ 85 , 86 ], are potentially carcinogenic [ 87 , 88 ], and are prothrombotic [ 89 ]. Furthermore, the PAHs are carcinogenic [ 90 ], whereas carbon monoxide induces cardiovascular disease [ 91 ], and nicotine is known for its addictive nature [ 92 ]. As for ammonia, which is a strong respiratory irritant, its levels should be measured as part of the assessment of the hookah toxicant profile, and this could be achieved using a simple colorimetric method as was recently described for determining ammonia levels in tobacco fillers and sidestream smoke in different tobacco brands [ 93 ].

Based on the aforementioned considerations, hookah use poses as many or even higher risks for the smoker as cigarette smoking. Besides tar, hookah bears additional risks such as an uptake of addictive and carcinogenic/ potentially carcinogenic chemicals, which stands in contrast to the “massive” advertisement of them as a “healthy” smoking product.

Air quality and passive exposure

Ambient concentrations of particulate matter are often used to assess pollution levels from tobacco smoke [ 94 ]. Cigarette smoking expels high levels of particulate matter in bars, exposing both customers and employees passively to hazardous levels of pollutants [ 95 ]. In similar fashion, the examined air quality in hookah lounges ranged from “unhealthy” to “hazardous” by the Environmental Protection Agency (EPA), containing high concentrations of particulate matter [ 94 , 96 , 97 ]. Such air quality poses health risks, especially among those with existing pulmonary and cardiovascular disease, and presents potential health hazard for workers who can be exposed to secondhand hookah/smoke on a daily basis and for prolonged periods of time [ 94 ]. As expected, low air quality was reported in houses of hookah users, and interestingly, toxicant levels were greater than those in cigarette smoking homes, yet less than those in lounges/bars (Fig. 5 ; [ 94 , 96 , 98 ]), which is probably due to lower numbers of hookah apparatuses used [ 98 ]. Nonetheless, such low air quality exposes non-users within the household to hazardous materials and puts them under increased risk of disease, especially if they are highly vulnerable (with chronic disease, children, and pregnant women). Consequently, there is a marked need for further research, policies, and better air quality monitoring to improve the indoor air quality in order to reduce passive exposure and its negative health consequences.

Comparison between PM2.5 levels in houses of hookah users, cigarette users, and bars in two states. NYC hookah bars ( n  = 8). Oregon hookah bars ( n  = 10) [ 94 , 96 , 98 ]

Hookah health hazards

While hookah users and those in close proximity are exposed to many of the potentially dangerous toxicants at one time, the health risks associated with its use continue to be under debate. This is—in part—attributed to the fact that the composition of tobacco smoke in hookah and its puffing patterns are variable and not well standardized. Nonetheless, several studies have provided evidence of health impairments that are associated with hookah use.

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 ]. Also, the “non-hygienic” conditions of the hose and water in the hookah apparatus could also increase mycobacteria growth, which can result in spreading/transmission of tuberculosis [ 100 , 101 ]. 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) [ 102 , 103 ]. Moreover, 48 bacterial isolates were detected from hookah hoses, and among them were virulent as well as antibiotic-resistant strains [ 104 ]. Furthermore, using hookah was linked to developing periodontal diseases in similar magnitude to cigarettes [ 105 ] as well as documented alteration in oral microbial flora [ 106 ].

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 [ 107 , 108 , 109 ]. Furthermore, hookah significantly decreases pulmonary function parameters, including FEV1, FEV1/FVC ratio, and FEF, as well as the levels of FeNO [ 110 , 111 , 112 ]. 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 [ 113 , 114 ]. Also, hookah users had lower lung diffusing capacity and elevated levels of apoptotic endothelial cell microparticles [ 109 ]. Hookah exposure induced a significant elevation of macrophages, lymphocytes, and neutrophils in broncho-alveolar lavage fluid and altered the levels of several cytokines. Thus, the levels of the pro-inflammatory cytokines TNFα, IL-1 β, IL-6, IL-12, and IL-13 were elevated, whereas the levels of the anti-inflammatory cytokine IL-10 were reduced, in the lungs of exposed mice [ 115 , 116 ]. 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-12), confirming pulmonary damage associated with hookah use [ 117 , 118 ]. Moreover, chronic (4 months) exposure to hookah smoke in mice resulted in significant increases in alveolar destructive index and mean linear intercept contributing to the chronic obstructive pulmonary disease picture in these animals [ 119 ].

Importantly, hookah hazards are not limited only to oral/pulmonary systems. 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 [ 120 ]. All of these “disorders” increase the risk of metabolic syndrome development, which is a major risk factor for developing thrombosis [ 121 ].

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. While may vary based on levels of use/exposure, a reduction of weight of the newborn (at least 100 g) in females using hookah once/day during pregnancy was evident. 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 [ 122 , 123 ]. In addition to reduction in birth weight, it was reported that hookah smoking during pregnancy contributes to a significant reduction in newborns’ other anthropometric measurements such as mean newborn length and mean newborn head circumference [ 124 ]. 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 [ 125 ]. 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 [ 126 ]. 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 [ 127 ].

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) [ 128 ], which is essential for cognition and behavior [ 128 ]. 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) [ 129 ]. Moreover, hookah tobacco smoke exposure in rats induced short- and long-term spatial memory impairment [ 130 ], which was associated with reduced hippocampal levels of major oxidative stress biomarkers and oxidative capacity enzymes [ 131 , 132 ].

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 [ 133 ]. Thus, prolonged or heavy use of hookah may induce risk of tumor development, especially in oral cavity and esophagus, which further argues against the notion that hookah has “no/less harm” if not inhaled “kept in mouth.” Indeed, incidence of benign lesions of the vocal cords was linked to the presence of cysts in 4.8% of hookah users, which was similar to cigarette smokers [ 134 ]. 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 [ 135 , 136 , 137 ]. Additionally, using hookah was linked to an average of six folds higher risk of lung cancer [ 138 , 139 , 140 , 141 ]. Moreover, it was reported that hookah use may increase the risk of gastric cancer by threefold, albeit the mechanism remains unknown [ 142 ]. 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 [ 143 , 144 ]. Exposure to hookah smoking resulted in elevated plasma and saliva levels of toxic metals, namely cadmium, copper, and zinc [ 145 ], which could contribute to its long-term carcinogenicity. Finally, another study (analyzed data collected from 152 academic institutions; n  = 100,891 students) found moderate association between hookah smoking and mental health variables, such as depression, anxiety, and addictive disorders, among college students [ 146 ]. These findings provide evidence that hookah disrupts not only the “physical” health of the user, but also their mental state.

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. Considering the cardiovascular system sensitivity and its non-linear dose-response/toxicity relationship with “smoke,” we sought to review the literature with regard to the effects of hookah on the cardiovascular system (see Fig. 6 ), both human and animal studies.

Cardiovascular effects and their underlying mechanisms. These data are compiled from what is reported in clinical studies. *In a study performed in adolescents, the reduced heart rate and blood pressure may be linked to the “abstinence of vaping” for 12 h prior to testing [ 195 ]

Cardiovascular effects of hookah use

The detrimental (acute and chronic) effects of tobacco smoking on the cardiovascular system are well established [ 147 , 148 , 149 , 150 , 151 , 152 ]. Thus, cigarette smoking predisposes to cardiovascular events and contributes significantly to cardiovascular-related mortality and morbidity, being responsible for up to 30% of heart disease-related deaths in the USA each year [ 149 , 153 ]. Importantly, hookah has overlapping toxicant/chemical profile to conventional cigarettes. 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 1.67 (95% CI = 1.25, 2.24) [ 154 ], which supports the notion that hookah is indeed detrimental to the cardiovascular system.

Clinical studies

Acute cardiovascular effects.

Acute effects of conventional smoking, such as increased blood pressure, heart rate, and vascular resistance, have been known for decades [ 155 , 156 , 157 , 158 , 159 , 160 ]. 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 , 161 , 162 , 163 , 164 , 165 , 166 ]. It is noteworthy that in one cohort study, HR elevation has exceeded 50 bpm in 6.4% of participants and reached higher than 200 bpm in 3.6% of participants after only a 30-min hookah session [ 167 ]. These effects have been attributed, in part, to the baroreflex mechanism impairment [ 164 ] or to elevated nicotine plasma level. The latter exhibits adrenergic effects that will enhance local and systemic catecholamine release [ 15 , 18 , 163 , 168 , 169 , 170 ]. 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 [ 171 ]. Additionally, in a two double-blind study, “placebo” had no effect on HR, while hookah-smoking increased it significantly [ 15 ]. 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 [ 172 ]. The cardiovascular changes were shown to be exacerbated among individuals with low habitual physical activity and physical fitness levels [ 173 ]. More recently, it has been reported that adolescents smoking hookah had significantly lower vascular endothelium growth factor (VEGF) levels [ 174 ], 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. This could be linked to local release/synthesis of oxygen-derived free radicals, cell cycle arrest, and decreased in NO activity [ 175 , 176 , 177 , 178 ]. 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 [ 177 ]. 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 [ 179 ]. This increase in TXB 2 levels would suggest an increase in platelet activity [ 180 ]. Importantly, it has been shown that an increase in platelet activity plays a major role in the pathogenesis of acute myocardial infarction (MI) [ 181 ] and acute stroke [ 182 , 183 , 184 ]. Therefore, it is not surprising to see a link between hookah smoking and acute MI in young adults [ 185 ], and among patient undergoing cardiac catheterization [ 186 ]. However, no data exist yet on the association between hookah smoking and acute stroke [ 187 ]. 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. This is thought to be due to cardiac β-adrenergic stimulation as physiological response to increased myocardial work and oxygen demand [ 188 ]. 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. Nonetheless, more research should be done to evaluate hookah’s effects, which will guide awareness campaigns regarding its negative health outcomes, including those that result from short-term use/exposure.

Cardiovascular effects of chronic use

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. In fact, individuals with more than 40 years of hookah smoking had three times more risk of having severe stenosis than non-smokers [ 189 ]. Additionally, cardiovascular disease development such as ischemic heart disease (IHD) and heart failure has been associated with heavy hookah smoking [ 190 ]. These outcomes could be explained by the continuous stress placed on the cardiovascular system as result of exposure to high amounts of CO [ 191 ]. Furthermore, death due to IHD was 1.96 folds in ever hookah smokers with higher daily intensity of hookah smoking than never users [ 192 ]. Hookah smoking was also associated with severe coronary artery disease, which was dependent on the duration/frequency of hookah smoking [ 193 ]. In accordance with the latter data, dose-response relationship between hookah-years and percent stenosis was also established [ 189 ]. Furthermore, risk of MI and stroke death was significantly increased with hookah smoking. Finally, higher fibrinogen plasma levels were reported in long-term hookah smokers (> 10 years), which elevate the incidence of pro-thrombotic/atherosclerotic events [ 194 ] and might explain in part the higher risks of stroke and MI linked with chronic 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. This might be explained by the “abstinence of” hookah smoking for 12 h prior to testing, thereby reducing nicotine levels drastically in the system, which would impact neuro-hormonal regulation (reduced cortisol and sympathetic activity). Nonetheless, the exact mechanism underlying such outcome is still unclear but warrants investigation [ 195 ].

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. Thus, hookah awareness/control should be more robust and systematic, but more importantly, further studies need to be conducted to better understand its negative health consequences and the mechanisms inducing such effects.

Animal studies

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 [ 196 ]. 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 [ 197 , 198 ]. 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 [ 197 ] is triggered. Interestingly, long-term nose-only exposure for 1 month caused a significant increase of ROS in the heart accompanied with decreased heart GSH concentrations in exposed mice, indicating depletion of the antioxidant, which increases heart tissue's vulnerability to oxygen free radical damage [ 199 ]. The increased cardiac vulnerability may explain the increased systolic blood pressure reported after long-term use, which was not seen post-short-term exposure [ 197 , 199 ].

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.

Emergence of novel hookahs (e-hookah)

Electronic nicotine delivery systems (ENDS) are battery-vaping devices that heat a liquid (e-liquid)—which may/may not be flavored and may/may not contain nicotine, thereby producing a vape that is inhaled by the user [ 200 ]. Multiple studies assessed electronic cigarettes’ (e-cigarettes) health effects which are still under debate, since they emerged in 2007 to US market [ 201 ], which is in contrast to the minimally studied electronic hookah (e-hookah) that debuted in 2014 across US markets [ 202 ]. For instance, e-cigarette use has been linked to increased health risks, including increase thrombosis risk [ 203 ] as well as throat and mouth irritation, respiratory tract irritation, and behavioral changes among others [ 153 ]. Whether e-hookah is similar to e-cigarettes in terms of exerting negative health effects is not known yet, as thus far, studies on e-hookah use/effects are limited. To this end, a recent pilot study aiming to clarify the differences (if present) between e-cigarette and e-hookah reported the following: (1) 94% of e-hookah are disposable compared to only 40% of e-cigarettes, (2) the majority of e-hookahs came with flavors compared to e-cigarettes, and (3) 91.7% of e-hookah were labeled “nicotine free” relative to 5.9% of e-cigarettes, which taken together supports the notion that the purpose of e-hookah is social/recreational in nature [ 202 ]. It is to be noted that despite the fact that most e-hookahs are labeled “nicotine free,” their safety is still unknown. Unfortunately, age restrictions on e-hookah packages apply only to 50% of the products [ 202 ], thus facilitating their purchase/use by minors. 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.

Hookah regulations and policies

Based on the scientific evidence of the toxicity associated with tobacco use (passive/active), an increasing number of states has instituted/is instituting regulations to support/expand legislation of clear indoor air quality to include hookah [ 204 , 205 ]. As mentioned before, hookah smoke may be associated with similar or even greater inhalation of toxicants in comparison to cigarettes. Since 2016, 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) [ 206 ]. However, some US legislations/policies controlling cigarettes do not similarly apply to hookah [ 31 ]. For instance, the “Prevent All Cigarette Trafficking Act” prevents US Postal Service to ship cigarettes but does not interfere with hookah shipping [ 207 ]. Additionally, nearly 90% of the largest US cities may allow hookah in bars via exemptions (whereas cigarettes are prohibited) [ 208 ]. 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 [ 209 ]. Clearly, policies and policy improvements are crucial, and research on hookah and its health effects would be helpful/important to health policy officials seeking to update/refine them.

Tobacco is a preventable cause of morbidity and mortality worldwide. In recent years, hookah use increased mainly as an alternate tobacco smoking method, under the assumption of it being “less harmful” [ 210 ]. Lately, as also noted by the American Heart Association statement [ 211 ], 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. Regarding hookah’s cardiovascular toxicity, unlike in case of smoking, little is known about those associated with hookah. Nevertheless, and based on the current evidence, it is now known that hookah emits various potentially harmful and toxic chemicals, and therefore, it should not be considered a “healthy alternative” to smoking. In fact, in light of the greater volumes expelled from hookah/session, it is still under debate whether the levels of the toxicants it emits are lower/higher than traditional smoking/day. 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. Regardless whether hookah is as toxic or less toxic than cigarettes, its harm is evident to certain extent, and it can still extend to innocent/bystander non-smokers through passive exposure, including children, pregnant women, housekeeping workers, and people with pre-existing cardiovascular and other diseases. The widespread and increasing usage of hookah in the USA is concerning. Therefore, funding should be allocated/dedicated for future research on hookah, to examine its acute/long-term effects on the cardiovascular and other systems of both active and passive users, as well as provide mechanistic insights regarding its negative health effects. Collectively, these findings can be used in educational campaigns for the public, as well as in shaping policies for further evidence-based hookah control.

Availability of data and materials

There is no “original” or unpublished data in this review article. However, the corresponding authors will share the sources of the data upon request.

Abbreviations

Brain-derived neutrophic factor

Coronary artery disease

Carcinoembryonic antigen

Carbon monoxide

Deoxyribonucleic acid

Electronic nicotine delivery systems

Environmental Protection Agency

Food and Drug Administration

Forced expiratory flow

Fractional exhaled nitric oxide

Forced expiratory volume

Flow-mediated dilation

Forced vital capacity

Glutathione

Ischemic heart disease

Interleukin

Myocardial infarction

Messenger RNA

Nitric oxide

Polycyclic aromatic hydrocarbons

Ribonucleic acid

Reactive oxygen species

Tumor necrosis factor

Thromboxane B 2

Vascular endothelium growth factor

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Qasim, H., Alarabi, A.B., Alzoubi, K.H. et al. The effects of hookah/waterpipe smoking on general health and the cardiovascular system. Environ Health Prev Med 24 , 58 (2019). https://doi.org/10.1186/s12199-019-0811-y

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Pipes and loose pipe tobacco are often advertised directly to men, and, indeed, are represented as highly masculinized and often genteel. Yello-bole pipes, for example, advertises for “The All-Male taste,” and Flying Dutchman pipe tobacco claims that their tobacco will allow men to “lead women around by the nose.” Further, one ad for Tuxedo tobacco implies that smoking a pipe is a pleasure offered only to men, while a famous actress sighs, “The fragrance of pipe tobacco makes me wish I were a man.”

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Waterpipe smoking and nicotine exposure: A review of the current evidence

The waterpipe, also known as shisha, hookah, narghile, goza, and hubble bubble, has long been used for tobacco consumption in the Middle East, India, and parts of Asia, and more recently has been introduced into the smokeless tobacco market in western nations. We reviewed the published literature on waterpipe use to estimate daily nicotine exposure among adult waterpipe smokers. We identified six recent studies that measured the nicotine or cotinine levels associated with waterpipe smoking in four countries (Lebanon, Jordan, Kuwait, and India). Four of these studies directly measured nicotine or cotinine levels in human subjects. The remaining two studies used smoking machines to measure the nicotine yield in smoking condensate produced by the waterpipe. Meta-analysis of the human data indicated that daily use of the waterpipe produced a 24-hr urinary cotinine level of 0.785 μg/ml (95% CI = 0.578–0.991 μg/ml), a nicotine absorption rate equivalent to smoking 10 cigarettes/day (95% CI = 7–13 cigarettes/day). Even among subjects who were not daily waterpipe smokers, a single session of waterpipe use produced a urinary cotinine level that was equivalent to smoking two cigarettes in one day. Estimates of the nicotine produced by waterpipe use can vary because of burn temperature, type of tobacco, waterpipe design, individual smoking pattern, and duration of the waterpipe smoking habit. Our quantitative synthesis of the limited human data from four nations indicates that daily use of waterpipes produces nicotine absorption of a magnitude similar to that produced by daily cigarette use.

Introduction

According to the World Health Organization ( WHO, 2005 ), tobacco use is responsible for about 5 million deaths per year worldwide. Furthermore, half of the people who smoke today will die prematurely.

In the midst of the present worldwide tobacco epidemic, concern is growing regarding the use of a waterpipe (referred to in various regions as shisha, hookah, narghile, and hubble bubble) to smoke tobacco, a practice dating back at least 400 years. This early form of smoking is experiencing a global revival, particularly in Middle Eastern countries ( Maziak, Ward, Soweid, & Eissenberg, 2004 ). Some of this increase in use has been attributed to the popularity of flavored or sweetened tobaccos for use in the waterpipe ( Rastam, Ward, Eissenberg, & Maziak, 2004 ). Recent reports indicate that waterpipes are commonly used in Egypt, Saudi Arabia, Jordan, Lebanon, Syria, Kuwait, Israel, Africa, India, and certain parts of Asia ( Al Mutairi, Shihab-Eldeen, Mojiminiyi, & Anwar, 2006 ; Maziak, Ward, Soweid, et al., 2004 ; Singh et al., 2006 ).

Traditionally, waterpipe smoking has been the habit of older males who, in the Middle East, often gather for waterpipe smoking in street-side cafes where they visit with friends and play table games together. Waterpipe use has recently grown in popularity and present-day waterpipe smokers include trendy youth, university students, and even high-school-aged children ( Maziak, Ward, Soweid, et al., 2004 ). Empirical observations from mainly Middle Eastern countries confirm that new chic cafes for waterpipe smoking are alive with loud music, bright lights, and frequently big screen television sets, and that such establishments are rapidly expanding to shopping malls, expensive hotels, and popular neighborhoods. It is fashionable for young people to socialize around the waterpipe.

Growing evidence indicates that women are increasingly likely to become waterpipe smokers. Some of this trend may be attributable to the introduction of sweetened and flavored waterpipe tobacco during the 1990s ( Rastam et al., 2004 ), which may be attracting female teenagers ( Hadidi & Mohammed, 2004 ). Women in general tend to perceive waterpipe use more positively than cigarette smoking, with women waterpipe users noting its positive attributes of being familiar, looking traditional, and being social ( Maziak, Ward, Soweid, et al., 2004 ). Other studies in the Middle East indicate that women find waterpipe smoking to be attractive ( Maziak, Rastam et al., 2004 ) and an occasion when they can participate with others ( Tamim, Terro et al., 2003 ). Family members’ attitudes toward women using the waterpipe appears to be shifting, with female university students thinking that adult family members would offer no particular opinion, either negative or positive, about their smoking waterpipes ( Maziak, Eissenberg et al., 2004 ).

Much of the emerging public health and medical literature on waterpipe use focuses on its impact on health. A widespread perception exists among users, as well as some physicians ( Kandela, 2000 ), that waterpipe smoking is a far less harmful habit than cigarette smoking. This notion is based on the premise that waterpipe smoke contains less tar, nicotine, and other toxins because of the “purification” ( Shihadeh, 2003 ) that occurs when the smoke passes through water before being inhaled by the user. However, this perception may be changing ( Maziak, Eissenberg et al., 2004 ). Some researchers have speculated that the health consequences are not significantly different from those associated with cigarette smoking and have presented evidence linking waterpipe smoking to cancer, abnormal pulmonary functions, elevated heart rate and blood pressure, high carboxyhemoglobin concentrations, low-birth-weight infants, respiratory ailments from environmental tobacco smoke, and decreased fertility ( Knishkowy & Amitai, 2005 ; Shafagoj, Mohammed, & Hadidi, 2002 ; Tamim, Musharrafieh, El Roueiheb, Yunis, & Almawi, 2003 ). Further studies of the morbidity and mortality associated with waterpipe smoking are needed.

In light of the current social trends toward increased waterpipe use, a number of additional questions need to be asked. For example, does waterpipe use promote nicotine addiction with the same strength as more common forms of tobacco such as cigarettes? Also relevant is whether nicotine addiction that is developed through waterpipe use leads to other forms of tobacco use (i.e., cigarette smoking). Much more needs to be learned about waterpipe dependence, but preliminary evidence suggests it has an addictive characteristic ( Maziak, Eissenberg, & Ward, 2005 ). Furthermore, it seems likely that waterpipe dependency has some unique characteristics that differ from those of cigarette dependency ( Maziak, Ward, & Eissenberg, 2004 )

We reviewed the data on nicotine exposure and waterpipe smoking from six studies that used recent, valid methodologies for measurement and collection of biospecimens ( Al Mutairi et al., 2006 ; Behera, Uppal, & Majumdar, 2003 ; Macaron, Macaron, Maalouf, Macaron, & Moor, 1997 ; Shafagoj et al., 2002 ; Shihadeh, 2003 ; Shihadeh & Saleh, 2005 ). This review aimed to (a) ascertain nicotine levels associated with waterpipe usage and (b) compare the nicotine delivery data for waterpipes with comparable data from cigarettes. This analysis will be valuable in ascertaining the public health impact of waterpipe use and its capacity to contribute to nicotine addiction in the population.

The search for articles in this review included computerized databases and references found in published articles. Databases included Medline, EBSCOhost, the Centers for Disease Control and Prevention Office on Smoking and Health, and the WHO’s Tobacco Free Initiative, as well as a general search of the Internet using Google. The waterpipe is also known as shisha, hookah, narghile, arghile, hubble bubble, or goza in various countries and parts of the world. Therefore, the search included all of these terms with their possible alternate spellings (such as sheesha or chicha).

The inclusion criterion for this comprehensive search was that the published work provided an estimate of the nicotine level associated with waterpipe use and was published since 1975. We felt that research done prior to this date would be limited by the technology of its time, raising questions about its comparability with more recent studies. Three identified articles dealing with waterpipe use, but not its nicotine delivery, were published in Hebrew and French. The final search was made in August 2006.

Our review of the literature revealed that two approaches were used to measure nicotine levels from waterpipe use. One method involved analyzing mainstream waterpipe smoke generated by machines designed to mimic human smoking patterns. This method mechanically captured the waterpipe smoke and examined it for nicotine content or other components. The second approach was to collect and analyze a waterpipe smoker’s plasma, urine, or saliva.

Six articles were identified that described studies measuring nicotine levels associated with waterpipe smoking. Two of these studies involved smoking-machine measurements and four were human studies. These studies were conducted between 1997 and 2006 in Lebanon, Jordan, Kuwait, and India. In all of these countries, waterpipe use has been a traditional form of smoking.

Data analyses

The mean urinary cotinine values from k human studies were pooled in a meta-analysis using methods described by Armitage and Berry (1987) :

where weight is given by 1/variance of the urinary cotinine value. A 95% confidence interval for the pooled mean is given by

Computing cigarette equivalency from urinary cotinine values

One of the aims of our review was to determine whether the nicotine exposure from daily use of the waterpipe is comparable with the nicotine exposure from daily use of cigarettes. Therefore, we translated our best estimate of the 24-hr urinary cotinine levels among daily waterpipe users into an equivalent number of cigarettes needed to produce the same urinary cotinine level during a 24-hr period. For this analysis we needed accurate data on the relationship between urinary cotinine and number of cigarettes smoked.

Heinrich et al. (2005) , in their study of 5,000 German adults aged 18–69 years, confirmed the data from many previous studies indicating that in the range of 1–30 cigarettes/day the relationship is linear and corresponds to urinary cotinine values of 0.075 μg/ml (≤2 cigarettes/day) to 2.1 μg/ml (21–30 cigarettes per day). In a sample of 190 Japanese males, Yang et al. (2001) found similar results, indicating a significant positive correlation between urinary cotinine and number of cigarettes smoked and a regression line indicating that urinary cotinine ranged from 0.08 μg/ml to 2.0 μg/ml for smoking 1–30 cigarettes/day.

Taken together, the slope coefficients from these studies indicated that, in the range of 1–30 cigarettes/day, each cigarette smoked produced 0.078 μg/ml of cotinine in a 24-hr urine sample. In this report, we used this value to compute the “cigarette equivalency” of waterpipe smoking.

In Lebanon, Shihadeh (2003) devised a first-generation smoking machine to determine the chemical profile of the waterpipe’s mainstream smoke ( Table 1 ). For the smoking of 10 g of waterpipe tobacco (maassel-flavored tobacco) using a standard smoking protocol (100 puffs of 3 s/per puff, 300 ml/puff, and 30 s between each puff), he measured a nicotine yield of 2.25 mg of nicotine from the smoke condensate.

Smoking machine studies that estimate the nicotine yield from the smoke condensate of a single waterpipe session.

Shihadeh (2003) noted the limitation that the true smoking patterns (i.e., puff frequency, duration, interval between puffs) of waterpipe smokers were unknown. A two-phase follow-up study ( Shihadeh, Azar, Antonios, & Haddad, 2004 ) addressed this concern by studying the smoking patterns of 52 waterpipe smokers in a Beirut cafe. Specifically, the authors studied 38 men and 14 women smokers in a busy Beirut cafe adjacent to a private university. Most of the participants were university students ( M age = 21 years), most likely from higher income strata of Beirut. These volunteers agreed to smoke a waterpipe with an attached smoking topography instrument that measured flow rate against time. The second phase consisted of inconspicuously observing 56 randomly selected waterpipe smokers in the same cafe, recording their smoking patterns. These observations were made without the smoker’s knowledge, and no contact was made before or after the smoking session. The findings from this follow-up study indicated that an “average” waterpipe session involved greater intake of smoke (171 puffs at 530 ml/puff, 2.6 s/puff, and 2.8 puffs/min) than was estimated in the previous smoking-machine study.

Using the new data that indicated a higher-intensity smoking pattern for waterpipe smokers, Shihadeh and Saleh (2005) found that the nicotine yield from a smoking session of 10 g of waterpipe tobacco was 2.94 mg ( Table 1 ). By comparison, the sales-weighted (1,294 brands) machine-measured mean nicotine yield from a single cigarette was 0.88 mg using the standard U.S. Federal Trade Commission (FTC) method that assumes taking 2-s, 35-ml puffs from a U.S. cigarette until a 23-mm butt length remained ( FTC, 2000 ). The higher volume and longer duration of a waterpipe session is noteworthy in this regard.

As a point of interest, we note findings from two early studies that used older smoking machines that are not comparable with the recent studies. Hoffmann, Rathkamp, and Wynder (1963) found that smoking 100 g of waterpipe tobacco produced 38 mg of nicotine in the smoke condensate. The results from smoking 800 mg of waterpipe tobacco showed the nicotine level in the smoke condensate to be 0.43 mg ( Galal, Youssef, & Salem, 1973 ).

Human studies

Table 2 presents the data from recent studies of adults in Lebanon, Jordan, India, and Kuwait that have measured urinary cotinine levels among water-pipe users. These studies are briefly described and summarized below, and pertinent results were included in a meta-analysis.

Human studies: Urinary cotinine values measured in waterpipe users.

Macaron et al. (1997) studied 48 adult Lebanese subjects (aged 20–68 years) to examine their intake of nicotine. The participants consisted of three equal-sized groups of waterpipe smokers (15 men and 1 woman), cigarette smokers (13 men and 3 women), and a control group of nonsmokers (12 men and 4 women). The urinary cotinine levels for the 16 waterpipe smokers ( M = 6.080 μg/ml) were not significantly different from the levels for cigarette smokers ( M = 5.980 μg/ml) but were significantly higher than those of nonsmokers ( M = 0.127 μg/ml).

Shafagoj et al. (2002) studied 14 males (aged 20–45 years) who had been smoking the waterpipe at least three times per week for more than 1 year. Subjects who used any other form of tobacco were excluded. After a single waterpipe smoking session, their blood plasma, saliva, and urine were tested for both nicotine and cotinine. Because of the washout period in this protocol (no waterpipe use 84 hr before the waterpipe session and 24 hr after the waterpipe session), the urinary cotinine levels represent the effect of a single waterpipe session occurring during a 4.5-day period. Also, because the authors provided only the total measurement of cotinine in the 24-hr urine (249 μg), we estimated the 24-hr urine volume for a healthy 28-year-old male to be an average of 1,350 ml ( Snyder et al., 1975 ) for the purpose of comparison in Table 2 .

Behera et al. (2003) measured urinary levels of nicotine and cotinine in users of various forms of tobacco. The 130 healthy adult subjects from north India ranged in age from 20 to 65 years. The study groups included 30 male cigarette smokers, 30 male bidi smokers, 10 male waterpipe smokers, 20 male tobacco chewers, 20 passive smokers (1 man and 19 women), and 20 nonsmokers (12 men and 8 women). No significant difference was found in mean urinary nicotine or cotinine levels of cigarette smokers (704 ng/ml and 2.736 μg/ml, respectively) and water-pipe smokers (548 ng/ml and 2.379 μg/ml, respectively). Mean nicotine and cotinine levels in cigarette and waterpipe smokers were, however, significantly higher compared with levels in passive smokers (110 ng/ml and 281 ng/ml) and nonsmokers (55 ng/ml and 7 ng/ml).

Al Mutairi et al. (2006) studied 168 subjects (aged 24–65 years) consisting of 77 waterpipe smokers, 75 cigarette smokers, and 16 control subjects who did not smoke. In this sample, mean urinary cotinine levels were significantly higher in cigarette smokers (1.321 μg/ml) than in waterpipe smokers (677.6 μg/ml). We found no apparent correlation between number of pipes smoked per day and urinary cotinine or nicotine. Long duration of use (>10 years) was, however, correlated with higher urinary cotinine and nicotine levels among waterpipe users.

Summary and meta-analysis of the human studies

Findings in Table 2 indicate that daily waterpipe smokers (in Kuwait, India, and Lebanon) had higher urinary cotinine levels (0.678–6.08 μg/ml) than those who engaged in a single waterpipe smoking session (0.184 μg/ml) during a 4- to 5-day period (Jordan). The data from Lebanon indicating a mean urinary cotinine of 6.08 μg/ml for daily waterpipe smokers is likely skewed upward by extreme outliers, an effect supported by the large standard deviation of 7.2 μg/ml.

To determine an overall urinary cotinine value for daily waterpipe smoking, we conducted a meta-analysis in which we pooled the data from the Kuwait, Lebanon, and India studies using the methods described in the statistical analysis section above. We found a pooled mean value for urinary cotinine among daily waterpipe smokers of 0.785 μg/ml (95% CI = 0.578–0.991).

Using the cigarette equivalency methods described earlier, we translated the cotinine values from Table 2 and the meta-analysis into the following conclusions:

• Daily waterpipe smoking produced a 24-hr urinary cotinine level that is equivalent to smoking 10 cigarettes/day (95% CI = 7–13 cigarettes/day).
• Occasional waterpipe smoking (one session of waterpipe use during a 4-day period) produced a 24-hr urinary cotinine level equivalent to having smoked two cigarettes in one pipe session.

The findings summarized in this report indicate that biologically important levels of nicotine are present in the smoke condensate of waterpipes and in the urine of daily and occasional waterpipe smokers. Specifically, smoking-machine studies ( Table 1 ) indicate that the nicotine yield (2.94 mg) from a single session of waterpipe smoking exceeds the nicotine yield from smoking an entire typical U.S. cigarette (0.88 mg). This finding alone does not provide insight into the etiologic or public health consequences of waterpipe use, since the nicotine yield from smoke condensate is not highly correlated with the amount of nicotine absorbed ( Benowitz et al., 1983 ) into the circulation of the smoker.

Therefore, we also examined the nicotine absorption of waterpipe smokers using the pooled findings ( Table 2 ) from 117 adults from four nations (Lebanon, Jordan, Kuwait, and India). These findings indicate that daily waterpipe smoking in the range of 1–10 pipeloads/day produces a 24-hr urinary cotinine level of 0.785 μg/ml, an absorption rate equivalent to daily smoking of 10 cigarettes. Additionally, occasional waterpipe smoking during a 4-day interval seems to produce a urinary cotinine level equivalent to having smoked two cigarettes in 24 hr.

Does the waterpipe filter out an important fraction of nicotine from the inhaled smoke?

The articles reviewed for this report identify long-held regional and cultural beliefs in the Middle East and other areas that waterpipe smoking is safer than cigarette smoking. This popular view is linked to the fact that nicotine is water soluble and that it and other harmful substances will be filtered out as the smoke passes through the pipe water. Taken together, the findings in this report do not support the prevalent belief that the water filtration of the commonly used waterpipe removes an important fraction of the nicotine in the tobacco. Shafagoh and Mohammed (2002) reported that less than 5% of the nicotine content of the waterpipe tobacco is trapped in the water. Shihadeh (2003) concluded that although the water does remove some nicotine from the smoke, a considerable amount (more than 2 mg in a single session) remains in the mouthpiece. Even under the assumption that the nicotine content of the smoke has been reduced (per unit volume relative to cigarettes), Macaron et al. (1997) speculated that waterpipe smokers could titrate their smoking behavior to achieve the desired dose effect. If true, then the effectiveness of water filtering out nicotine would diminish, as each smoker will continue to smoke until his or her nicotine level is satisfied. Concern also exists that this “titrating” behavior will expose the waterpipe smoker to higher levels of carbon monoxide ( Shihadeh & Saleh, 2005 ). Overall, given that titrating behavior is well documented among cigarette smokers who switch to light or ultra-light brands ( Djordjevic, Hoffman, & Hoffman, 1997 ; Scherer, 1999 ), it seems possible that waterpipe smokers might follow a similar behavior pattern.

In the studies in Lebanon and India depicted in Table 2 , the urinary nicotine and cotinine levels of waterpipe smokers and cigarette smokers were not significantly different. In Kuwait, Al Mutairi et al. (2006) reported that urinary nicotine and cotinine levels of cigarette smokers were higher than the levels in waterpipe smokers. Factors that may have contributed to the variation in the waterpipe-cigarette comparisons in these three studies include (a) puff frequency, (b) frequency and amount of tobacco used (cigarettes and water pipe), (c) variation in type and size of the waterpipe, (d) variation in nicotine exposure from other sources (i.e., environmental tobacco smoke), and (e) difference in the methodology of using a washout period (used only in the study from Kuwait), (f) small sample size criteria (studies from Lebanon and India had comparison groups of less than 40 subjects, and (g) classification of waterpipe smokers into “heavy” or “light” categories. Further large-scale comparative studies are needed to ascertain standardized measures of the nicotine absorbed by cigarette smokers and water-pipe users.

Waterpipe use and nicotine addiction

Benowitz and Henningfield’s (1994) proposal that an intake of 5 mg of nicotine per day represents an “addiction threshold” level indicates that the threshold is met for those who smoke 5 or more cigarettes per day (1 mg nicotine per cigarette). Acknowledging the numerous variables involved with smoking, the American Medical Association (1998) suggested that such a threshold will vary from person to person, and that the proposed value probably represents the highest threshold value that should be considered.

The meta-analysis in the present report suggested that daily waterpipe smoking produces nicotine absorption comparable with the daily smoking of 10 cigarettes (95% CI = 7–13 cigarettes). Thus the range of the current evidence clearly classifies daily use of the waterpipe as an addictive behavior. The meta-analysis further suggests that occasional use of the waterpipe is equivalent to smoking two cigarettes during a 24-hr period and thus is below an “addictive threshold.” These data should be interpreted with caution when considering Al Mutairi et al.’s (2006) findings that long-term waterpipe smokers (>10 years of use) absorb more nicotine than do short-term waterpipe smokers (≤10 years). These data suggest that long-term occasional use may translate into a higher nicotine exposure and cigarette equivalency than determined in the present analysis.

Limitations of the current evidence

The evidence in the present report permits a good evaluation of whether waterpipe smokers experience a biologically important level of nicotine exposure ( Tables 1 and ​ and2). 2 ). However, a number of limitations regarding the current evidence hinder investigation of more specific hypotheses about nicotine exposure and other health effects of waterpipe use. Specifically, investigations of waterpipe use need to consider in detail variables such as equipment, smoking patterns, time, and tobacco quality to ensure comparable results. Also, an increasing need exists for standardization of assessment tools, data collection procedures, and the terminology and categories used specifically for waterpipe research ( Maziak, Ward, Soweid, & Eissenberg, 2005 ; Shihadeh et al., 2004 ). Some of these issues and limitations are discussed further.

The amount of smoke inhaled from a waterpipe varies based on the size of the waterpipe, water bowl capacity, and the length of the flexible hose ( Nuwayhid, Yamout, Azar, & Kambris, 1998 ; Sajid, Akhter, & Malik, 1993 ). Constituents of the waterpipe mainstream smoke also vary depending on the type and amount of charcoal used and the point of measurement during a single waterpipe smoking session (the highest levels of particulate matter occur toward the end; Shihadeh & Saleh, 2005 ).

Smoking patterns

Given that a waterpipe session is generally characterized as a social event, puffing on the waterpipe can be intermittent, and smoking patterns can vary based on quantity, rate, depth, and duration of smoke inhalation ( Shihadeh et al., 2004 ). For example, in some areas the average duration of a waterpipe session is reported to be 45–60 min smoking time with 10–20 g of tobacco consumed ( Knishkowy & Amitai, 2005 ), whereas in other areas the average smoking time is described as 1–2 hr ( Kiter, Ucan, Ceylan, & Kiling, 2000 ) with as much as 200 g of tobacco consumed ( Zahran, Yousef, & Baig, 1982 ). These differences can influence the amount of addictive components inhaled ( Maziak, Eissenberg et al., 2005 ). Also, data indicate that a primary waterpipe smoker (one who has not previously smoked another type of tobacco) does not inhale as deeply as a secondary smoker ( Shafagoj & Mohammed, 2002 ).

Type of tobacco

An important variable that affects the delivery of nicotine is the type or brand of tobacco and its preparation for smoking. There are two general categories of waterpipe tobacco: unflavored (tumbak, or other local names) and flavored (maassel; Hadidi & Mohammed, 2004 ), the latter of which has recently become more popular. The unflavored tobacco is plain and dry, whereas the flavored tobacco mixes additives such as glycerin, honey, or molasses with flavors such as mint or fruits. The result is a moist tobacco paste that is allowed to ferment.

A study on waterpipe tobacco analyzed 13 commercial brands for their nicotine content ( Hadidi & Mohammed, 2004 ). Among the 11 tested brands of flavored tobacco, the average nicotine content was 3.35 mg/g (range 1.8 mg/g to 6.3 mg/g), which is equivalent to 67 mg for one run when using a waterpipe head that holds an average of 20 g of tobacco. Unflavored tobacco greatly increases nicotine exposure, with the two tested brands having 30 mg/g and 41 mg/g of nicotine, for a mean of 35.65 mg/g, which is equivalent to 713 mg per head. This high nicotine content is about 10 times greater than the nicotine in each gram of flavored waterpipe tobacco. In cigarette equivalency, the nicotine content in a single run of flavored tobacco is 6.5 regular cigarettes, and for unflavored tobacco, 70 cigarettes ( Hadidi & Mohammed, 2004 ).

Two factors relating to the wide variation in nicotine levels in unflavored and flavored tobacco are the added ingredients in flavored tobacco that dilute the quantity of tobacco smoked, and the use of more stems and less nicotine-rich tobacco leaves in the flavored brands. The role of glycerin in the fermentation process also is thought to affect the nicotine level ( Hadidi & Mohammed, 2004 ).

Our quantitative synthesis of the limited human data from 117 adults from Lebanon, Jordan, Kuwait, and India indicate that daily waterpipe use produces nicotine absorption of a magnitude similar to that of daily use of cigarettes. This equivalence with cigarette use of about 10 cigarettes/day further indicates that daily waterpipe use can be an effective means of initiating and maintaining nicotine addiction.

Additional research is needed to focus on the tobacco dependence associated with waterpipe smoking. For example, research is needed to examine the relationship between waterpipe smoking and other forms of tobacco use. Does cigarette smoking serve as a gateway for waterpipe use? Does initiation of a waterpipe smoking habit open the pathway to use of other tobacco products? A multiyear prospective study may be required to answer these questions. Also, what possible detrimental effects may result when various ingredients, such as glycerin, are added to maassel tobacco? More needs to be learned about the overall morbidity and mortality associated with waterpipe smoking. As more women become water-pipe smokers, studies of gender-specific issues also will be necessary.

A possible reason for the scarcity of scientific knowledge on waterpipe smoking is that the practice has traditionally been confined to certain geographic regions, affecting a relatively small portion of the world’s population ( Behera et al., 2003 ). With waterpipe smoking growing in popularity in Western Europe and North America ( Knishkowy & Amitai, 2005 ; Shihadeh et al., 2004 ), more resources will likely be invested in waterpipe research. In addition, researchers in countries where waterpipe smoking is popular are conducting and publishing new research. Tobacco research centers, with water-pipe research as one of their primary objectives, have been established recently in Egypt (Egyptian Smoking Prevention Research Institute) and Syria (Syrian Center for Tobacco Studies).

Acknowledgments

The authors had no external funding for the preparation of the article.

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Pipe Smoking Health

• 1 Chemistry and Toxicology Research
• 2.1 The highest to lowest risks from tobacco products are as follows
• 2.2 Lung cancer risk index study
• 2.3 Bladder cancer risk index
• 2.4 Do Pipe and Cigar smokers inhale?
• 2.5 Reducing the risk of tongue burn and/or tongue and mouth cancer
• 2.6 Medical examination
• 2.7 Life expectancy for Pipe Smokers
• 2.8 Other interesting facts and some to keep in mind
• 2.9 Protecting the roof of your mouth
• 3 Pipe Smoking and Health
• 4.1 PREFACE
• 5 Off site links

Chemistry and Toxicology Research

The following links are to PDFs of Dr. John Lauterbach's presentation notes to the 2015 and 2017 Tobacco Science Research Conferences. His company, Lauterbach & Associates, LLC, provides scientific and regulatory affairs support to small and medium-size manufacturers of tobacco products. He writes, "We market our services by conducting original research (generally with the help of those who have laboratories) on chemistry and toxicology of tobacco products. Over the past few years, we have focused our efforts on tobacco products other than cigarettes and moist snuff and snus. The main reason for this has been the lack of contemporary scientific knowledge of the chemistry and toxicological properties of the products that regulators might purchase at retail and then draw unwarranted scientific conclusions that could be used to reduce or eliminate products made by manufacturers other than the large multinational tobacco companies."

The following are examples of their work on pipe tobacco.

• Presentation at 2015 Tobacco Science Research Conference and Mark Ryan of Daughters and Ryan provided the samples: https://pipedia.org/images/4/47/JohnLauterbach-69th-TSRCPresentation.pdf
• Presentation at 2017 Tobacco Science Research Conference (A PRODUCT SURVEY OF 25 PIPE TOBACCOS PURCHASED FROM WEB-BASED MERCHANTS): https://pipedia.org/images/b/ba/JohnLauterbach-71st-TSRCPresentation.pdf

Contact Information:

Reducing Risks of Pipe and Cigar Smoking

Summary Notes from the lecture of Henri P. Gaboriau M.D. to the Seattle Pipe Club on March 2002, courtesy, Seattle Pipe Club

The highest to lowest risks from tobacco products are as follows

• Cigarettes: Primary Risks are Lungs, throat (Erytroplaleia)
• Cigars: Primary Risks are Lip, tongue
• Smokeless – snuff, chew etc.: Primary Risks are Gum line (Leukoplakia)
• Pipes: Primary Risks are Tongue

Lung cancer risk index study

• Non-smoker 1.0 (base number)
• Cigarette – 20 grams / day; 16.0 (i.e. 16 x the risk of non-smokers)
• Cigar – 20 grams / day; 3.2
• Pipe – if > 10 bowls per day; 6.7
• Pipe – if 5 bowls per day; 3.2
• Pipe – if 3 bowls per day; 1.5
• Pipe – if 2 bowls per day; 1.26
• typical - 2 bowls every 2-3 days; ~1.05 (almost same as non-smoker)

(Source Webline – reviewed 22 articles. 21,520 smokers studied between 1969 – 93)

Bladder cancer risk index

(although more rare in smokers than is lung and throat cancer)

• Non-smoker 1.0
• Cigarette 3.5

Do Pipe and Cigar smokers inhale?

Most Cigar and Pipe smokers do not inhale - unless they were former cigarette smokers. To test the theory, a study* was conducted with an endoscope camera down the nose and throat to observe breathing patterns in smokers. Here were the results:

• Former cigarette smokers inhaled pipes like cigarettes
• Cigar and pipe smokers – breathed normally first, then inhaled into mouth only, smoke was mostly blocked from throat by tongue, then exhaled the smoke w/o going into the lungs.
• You can test this on yourself. Take a toke on a pipe or cigar as you normally would. Now breathe in and out through your nose two or three times. Do you see smoke when you in exhale? If yes, you are inhaling. If no, now exhale the smoke from your mouth. Did smoke come out of your mouth? If yes, you are not inhaling and are tremendously decreasing your risk of lung cancer.

(Source "Pattern of inhalation of Tobacco Smoke in Pipe, Cigarette and Never Smokers” AM Rev Respir Dis 1985)

Reducing the risk of tongue burn and/or tongue and mouth cancer

• A burn or scar from hot smoke is what you are trying to avoid. This can lead to cancer.
• Don’t leave the pipe clenched in your teeth in one position touching your tongue for a long time. Move the pipe around your mouth as you smoke.
• Sip your pipe like a fine wine, don’t draw heavily.
• Find a cool burning tobacco that you enjoy. Aromatic tobaccos tend to burn hotter than do English.
• Always drink while you smoke. This helps cool the mouth, quench the thirst from dry smoke, coat the mouth from hot smoke, and wash away any hot debris. Water, sodas, coffee, tea are fine. Don’t drink anything very hot though.
• However, sorry everyone, do not drink alcohol while you smoke. The combination of alcohol and smoke is not just a linear risk, but exponential. This is a huge mistake most smokers make. The alcohol destroys the flora and protective lining of mucus in the mouth. Then the hot smoke will directly come in contact with the unprotected mouth lining. Drink alcohol only after you smoke.
• Smoking depletes the body of vitamins A and C. Take up to 3000 mg of VC a day. Also take selenium and other antioxidants that will help buffer your body from free radicals, cancer and anti-aging.

Medical examination

At least once a year, tell your physician you are a pipe smoker and would like to have your mouth and tongue examined. Schedule your teeth exams ~ 6 months after your physician’s and have your dentist give another exam. You now have two exams a year, by two different medical specialists.

Life expectancy for Pipe Smokers

Okay, sit down for this…. A US Surgeon General report “Smoking and Health” (No. 1103, page 112) noted, “Death rates for current pipe smokers were little if at all higher than for non-smokers, even with men smoking 10 pipefuls per day and with men who had smoked pipes for more than 30 years.” On page 92 the report also stated that pipe smokers who inhale live as long as nonsmokers and pipe smokers that don’t inhale live longer than non-smokers.

What? Life expectancy for pipe smokers is three years longer than… Non-Smokers! Just try to use that argument with an anti-smoking activist! Of course this is not to encourage people to smoke, but has more to do with the personality of a typical pipe smoker. Most are type “B” where most cigarette smokers are type “A”. So a pipe smoker, on average, is a more laid back person. Second, smoking a pipe is very relaxing. You just can’t be angry when you are smoking a pipe.

Cigars are also relaxing but it seems, not as much as pipes. Most cigarette smoking is not so much a relaxing experience as it is a need for nicotine.

Other interesting facts and some to keep in mind

• Pipe smoking is the lowest tobacco risk - but the risk is not zero.
• Pipe smoking risk is much like a second hand smoke risk
• Pipe tobacco has less nicotine per gram than cigarettes and contains very little of the additives.
• Wet smoking is the worst risk so be sure and clean pipe thoroughly.
• If you have any sores in your mouth or a sore throat, wait to let the mouth heal first.
• The main risks from cigars is chewing the cigar and the direct contact with the lips.
• 27% of all smokers are pipe smokers in Sweden. In US only 2%

I hope you follow the tips above. If you do, you should significantly lower your health risks from pipe and cigar smoking. Wishing you a wonderfully aromatic, relaxing and healthy enjoyment of your favorite pipe and cigar for a long lifetime.

Disclaimer: Note that the information provided in this lecture summary report are the opinions of Dr. Gaboriau. The Seattle Pipe Club has documented the lecture for informational purposes only and claims no responsibility for the accuracy of its content.

Protecting the roof of your mouth

DIY Denture experiment, Giulliano Spitaletti Smoking guard

This article shows only my experience and I am not recommending anyone to repeat what I have done without a recommendation from a doctor or dentist. I am not a scientist or a doctor so this text is not scientifically proven to be safe, is merely a personal point of view from myself a Non-professional healthcare Recently I developed a denture made of a non-expensive thermoplastic ( insta morph or. polimorph available at amazon and ebay), a material when heats up in the water can be mouldable inside the mouth providing perfect imprinting, which I use as a shield to isolate the roof of the mouth from the smoke. I call this denture Smoking guard.

A full review video can be found here:

This DIY denture intends to protect the roof of the mouth against the smoke chemicals and the smoke heat. Please before you start making your denture made out of this thermo plastic not tested by any dental organization (not proven to be safe) I strongly recommend you to consider to get made a resin denture made by a dentist. The initial point of this product came during research where I found out a disease called nicotine stomatitis has been appearing commonly in pipe smokers. Nicotine stomatitis is a condition that is hidden up on the palette and is painless. I believe a great percentage of pipe smokers might have it and not even acknowledged it. It starts with red dots, loss of colour or a blackish colouration on the palette skin. Among many types of diseases such as cancers and sores in the mouth that could potentially rise from pipe smoking, i believe By protecting the roof of the mouth a great part of the problems in pipe smoking could diminish I believe the denture won't eliminate the risk of smoking tobacco but it will decrease the area of exposition, possibly decreasing the harms. I develop this denture only as prevention and not because i have the condition.

Following is the article and the link to the article:

https://dermnetnz.org/topics/nicotine-stomatitis/

What is nicotine stomatitis? Nicotine stomatitis, also often called smoker's palate, is a reaction seen on the roof of the mouth caused by extreme heat in the mouth, most commonly from smoking. It is known by many other names including nicotinic stomatitis, stomatitis nicotina and smoker's keratosis. Nicotine stomatitis is usually seen in pipe smokers and reverse cigarette smokers (when the lit end of the cigarette is placed in the mouth). It is probably due to the concentrated heat stream hitting the roof of the mouth. Less commonly it develops with cigarette or cigar smoking and rarely with drinking extremely hot liquids. The combination of hot drinks and smoking may increase the risk. It is related to the duration and extent of the habit, requiring longterm exposure. Men and women develop nicotine stomatitis, but as pipe smoking is more common with men, so nicotine stomatitis shows a male predominance. In one large study, nicotine stomatitis was found in 60% of pipe smokers and 30% of cigarette smokers. Clinical features of nicotine stomatitis Nicotine stomatitis is often found on routine examination of the mouth as it usually does not cause any symptoms. Sometimes it may be mildly irritating. Initially there is redness of the hard palate and sometimes the adjacent soft palate. With time, the palate becomes white with a cracked appearance likened to dried mud. Characteristically there are numerous scattered red dots. These are the inflammed duct openings of minor salivary glands. Dentures protect the palate from the heat stream. The changes are then seen only towards the back of the roof of the mouth beyond the area covered by the denture. Nicotine stomatitis itself is not regarded as premalignant except with reverse smoking. However, smoking is associated with the development of oral squamous cell carcinoma so the conditions can co-exist. How is nicotine stomatitis diagnosed? Nicotine stomatitis is a clinical diagnosis based on the pattern on the palate and typical white ‘cracked’ appearance with the red dots. However a mucosal biopsy may sometimes be required to exclude dysplasia (oral leukoplakia) or oral cancer. Treatment of nicotine stomatitis The only treatment is to stop smoking. The changes then improve within 1-2 weeks. Any persistent or suspicious areas should be biopsied. Regular examination of the mouth is required because of the risk of oral cancer in smokers. See

Pipe Smoking and Health

A review of the medical literature, for the use of pipe smokers and health care professionals.

This review is in the editors original PDF, which maintains his formating: Pipe Smoking and Health

Prepared by:

Most pipe smokers consider themselves greatly different from the other users of tobacco, and as such they must be approached in a much different manner when discussing possible health consequences of their utilization of tobacco. As a result, many needs have been voiced by pipe smokers who would like to know where their type of tobacco use fits into the voluminous literature now pouring forth on the health effects of tobacco use.

In an attempt to obtain a more accurate perspective on the subject, this literature review is being compiled, which represents a current bibliography, with index, of articles dealing with the health effects of pipe smoking. The compiler of this work has a personal interest in the subject both from the perspective being a pipe smoker as well as a toxicologist. It is hoped this compilation will prove beneficial to pipe smokers, as well as health professionals who have to deal with patients who use tobacco in this form.

This review effort is a dynamic process, and the work is constantly being revised with new citations as they are published. If individuals know of any additional literature citations, please send copies of articles to the compiler listed above.

Click here to read

Off site links

• Tobacco Truth Blog, Dr. Brad Rodu
• Analysis of FDA Study at Tobacco Truth Blog
• Pipe Smoking and Health: "Risky business or casual pleasure?" by Mark Beale, MD
• The Facts About Second Hand Smoke
• Life Insurance For Smokers, a special report Interesting article on the issues of life insurance for pipe and cigar smokers.
• Reducing Risks of Pipe and Cigar Smoking, Summary Notes from the lecture of Henri P. Gaboriau M.D.
• Is Water Pipe Smoking (and inhaling) as Harmful as Cigarettes?
• Health consequences of using a pipe (and inhaling) versus cigarettes This link is just the abstract. The researchers found no significant difference in health between between cigarette smoking and pipe smoking. However the research is flawed in that they did not differentiate between pipe smokers that inhale from those that do not, and included cigarette smokers who switched to pipes, many of whom continue to inhale.

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Smoking Pipes of Eastern North America

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• Sean M. Rafferty 4  

Part of the book series: Interdisciplinary Contributions to Archaeology ((IDCA))

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Smoking pipes characterize archaeological assemblages in eastern North America at least as early as 4000 B.C. Pipes are commonly included in prehistoric Native American burials. Early pipes were finely crafted, relatively rare artifacts of stone, and became more numerous and widespread over time as ceramic technology was developed. Smoking pipes are useful sources of information regarding prehistoric ritual, symbolism, and social interaction throughout the late prehistoric period in eastern North America.

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Rafferty, S.M. (2016). Smoking Pipes of Eastern North America. In: Bollwerk, E.A., Tushingham, S. (eds) Perspectives on the Archaeology of Pipes, Tobacco and other Smoke Plants in the Ancient Americas. Interdisciplinary Contributions to Archaeology. Springer, Cham. https://doi.org/10.1007/978-3-319-23552-3_2

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Researchers discover 18th-century clay tobacco pipes were used as weapons and surgical tools

Lecturer in British Social and Cultural History and Director of the Centre of Regional and Local History, University of Leicester

Future Leaders Fellow in the School of Archaeology and Ancient History, University of Leicester

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Tobacco pipes were one of the first mass-produced, disposable objects in Britain. Through contact with indigenous peoples of the Americas, tobacco pipes and tobacco were introduced to Europe as early as the 16th century, but had been used in the Americas for centuries before this.

Pipes were adapted for European tastes using European materials, and in England the most popular material for pipes between 1600 and 1900 was clay. Shapes and styles varied over the years, but the basic design remained the same: a hand-held bowl to burn tobacco in and a stem to draw the smoke the mouth of the smoker.

Pipes were lightweight, rigid and made out of inexpensive materials. They were also rather breakable. This cheapness and breakability means they show up in large number across post-medieval archaeological sites in Britain.

The usefulness of pipes as artefacts is well established . Tobacco pipes found in archaeological digs can help researchers identify the dates when a particular site may have been occupied (based on bowl or stem size) and even who may have occupied these spaces (bite marks in stems may indicate workers holding them in their mouths while working, for example). Pipes can also inform researchers about patterns of tobacco consumption over time.

However, our research has uncovered fascinating new evidence about some of the other ways people used tobacco pipes in the past. Smoking might kill but what we found is that people routinely used tobacco pipes as weapons and as medical instruments from at least as early as the 17th century, although most of the evidence dates to the 18th century.

This new evidence brings to life the everyday experiences of those who encountered tobacco pipes. It also gives historians and archaeologists new ways of thinking about how we study historic artefacts because it encourages us to think beyond the intended functions of objects.

What these alternative uses tell us is that pipes were objects that occupied the everyday lives of men and women in the British past far beyond what we have assumed. The archaeological record has already told us that pipes were incredibly common.

By looking at evidence from archives, such as criminal records and medical texts, we understand that this commonality meant that pipes were not just used to smoke tobacco and likely played a more prominent role in everyday life than we have previously considered.

Pipes as weapons

Clay tobacco pipes were hand-held and breakable. This made them ideal for striking or stabbing with when tempers flared. In about three-quarters of the cases we looked at, attacks happened when someone holding a pipe lashed out at another person. A punch to the head, face or neck could result in a serious puncture wound, cause blindness or even death if a pipe was involved.

For example, in Caernarfonshire in Wales in 1788, a man named Sylvanus Owen was found guilty of manslaughter for striking another man with his right hand. The punch proved fatal because Owen had two pieces of a clay pipe in his had at the time, one of which entered the other man’s eye, causing a serious infection.

We also found pipes being used to intentionally burn others and as shot in pistols .

Pipes as medical instruments

Some of the same properties that made pipes excellent impromptu weapons also made them useful improvised medical instruments. The ready availability of pipes meant that one was likely always to hand and the long, narrow stems and wide bowls meant they had several uses beyond smoking.

Evidence from medical publications such as the Lancet and surgical guides suggest that pipe stems could be used as catheters to relieve both men and women of retained urine.

Pipes were also recommended for emergency tracheotomies , as straws for those who could not eat and drink on their own, and as lactation aides for nursing mothers. In 1796, Erasmus Darwin (grandfather of Charles Darwin) even recommended using the stem of a tobacco pipe to remove a guinea worm (a waterborne parasite found in certain parts of Africa) from an infected patient.

As both weapons and medical instruments, it was the combination of clay tobacco pipes’ properties and availability that made them ideal improvised tools. There is an obvious and interesting contradiction that one alternative use was to harm or end life and the other was to improve or preserve it.

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African smoking and pipes

1983, Journal of African History

This article first explains the importance of the history of smoking pipes for other historical questions, especially in West Africa, where pipe styles are used to date archaeological levels. A survey of the major theories about African smoking and pipes is presented. This is followed by a review of the published archaeological literature pertaining to smoking pipes found at various sites from around the continent. The various controversies surrounding African smoking customs are then looked at in the light of the available evidence. The most likely hypothesis is that cannabis was smoked in water pipes in eastern and southern Africa before the introduction of tobacco. Further research is called for to prove or disprove this hypothesis. Tobacco is shown to have been introduced to West Africa from eastern North America, most likely by the French coming to Senegambia, though possibly by Moroccans coming to Timbuktu.

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English Summary: Thirty years ago, a German team of scientists let the world think over the tremendous consequences of cutting-edge research findings related to the presence of substances such as cocaine, nicotine and cannabis in Pre-Columbian mummies. The first outcome was the rebuttal of the official universal history of tobacco supposed to have begun in the Old World in the wake of Columbus’ discovery of the Americas. Most recent findings confirm the presence of nicotine without totally discarding the possibility of environmental tobacco contamination, not to mention, at a more or less remote date, the use of the latter as a preservation insecticide. Nevertheless and as a whole, the results reviewed in this article, further to being contextualised with anthropological discoveries related to “exotic” forms of smoking such as the mysterious hookah (narghile, shisha) and the “dissenting” though cogent views on tobacco history, elicit an unexpected turn to the debate. For instance, leaving aside the question of actual linguistic convergences between both sides of the Atlantic Ocean, a variety of forest tobacco of the Nicotiana rustica species (vs. Nicotiana tabacum, that of the New World) was widely known in Africa long before Columbus’ discovery. The mysterious origin of the water pipe (so different by its shape and smoking techniques) also represents an extra argument supporting early transoceanic (Africa/America) Pre-Columbian contacts. Anthropological research led by separate teams from the USA, South Africa, and Tunisia, unfailingly agree on this point. Résumé en français: Il y a 30 ans, une équipe de recherche allemande eut la surprise de trouver des substances telles que la cocaïne, la nicotine et le cannabis dans des momies précolombiennes. Ces découvertes suscitèrent de nombreuses remises en question de l’histoire universelle officielle du tabac censée avoir commencé dans l’Ancien Monde après la découverte des Amériques par Christophe Colomb. Des analyses plus récentes confirment la présence de nicotine sans que soit exclue la possibilité d’une contamination environnementale par la fumée du tabac, voire de l’usage de ce dernier comme insecticide à des fins de préservation, à une date plus ou moins lointaine. Toutefois, pris dans leur ensemble, les résultats des diverses recherches passées ici en revue et une fois mises en contexte avec des découvertes anthropologiques relatives à des formes “exotiques” de tabagisme comme le mystérieux narguilé (houka, shisha/chicha), puis couplées à la prise en compte des voix de chercheurs s’opposant à l’histoire officielle du tabac, permettent d’aboutir à des conclusions iconoclastes. Par exemple, outre les convergences linguistiques de part et d’autre de l’océan atlantique, une variété de tabac forestier de l’espèce Nicotiana rustica (par opposition à Nicotiana tabacum, celle du Nouveau Monde) était largement répandue en Afrique bien avant la découverte de Colomb. L’origine mystérieuse du narguilé (si différent par sa forme et ses techniques d’usage) constitue également un argument supplémentaire en faveur de l’hypothèse, de plus en plus plausible, de voyages précolombiens transocéaniques entre l’Afrique et les Amériques. Des recherches anthropologiques menées séparément par des chercheurs aux Etats-Unis d’Amérique, en Afrique du Sud et en Tunisie, convergent inexorablement sur ce point.

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Studies of clay smoking pipes represent one of the major fields of research in post-medieval archaeology due to their frequent occurrence in the archaeological record and their suitability for typological dating. During an archaeological survey in Rua do Terreiro do Trigo, located in Lisbon’s picturesque district of Alfama, very close to the Tagus River and where many different and cosmopolitan people spent their spare time during the post-medieval period, we were able to collect a significant number of smoking pipes fragments, given the site’s dimension. Amongst the sherds recovered it is possible to identify a great number of European kaolin clay pipe fragments dated from the 17th to the 18th century and also a set of unusual black and grey earthenware chibouks of (yet) uncertain origin. Therefore, this paper seeks to report the smoking pipe assemblage recovered in Rua do Terreiro do Trigo, but also to discuss the study of smoking devices in the Portuguese post-medieval archaeological contexts.

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Research in historical archaeology has often focused on analyzing the degree to which African diaspora material culture has been shaped by the beliefs and practices of particular African cultures impacted by the trans-Atlantic slave trade. Landscapes, architecture, and objects can, at times, be analyzed to evaluate whether their design, construction, or use has been influenced by such cultural traditions. Through the concepts of innovation and creolization, material culture such as this can be reinterpreted in new ways. This article re-examines English manufactured smoking pipes recovered from Newton Plantation cemetery on Barbados. I argue that within an African diasporic burial context, unmodified European manufactured objects, such as English manufactured smoking pipes, could carry cultural significance shaped by African cultural beliefs and practices. Artifacts such as these are embedded in both diversity and situational complexity

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Smoking safer through science, weedgets demonstrates.

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The Maze-X pipe is built with a maze-like elongated pathway that cools smoke without water.

Smoking can be safer through scientific innovation without resorting to vaping or other methods that often deliver subpar results. Today Weedgets announced an industry-first partnership from American Cannabis Nurse Association (ACNA) due to the company’s focus on safer smoking methods. The Maze-X Pipe, made by Weedgets, was recently rigorously tested, approved, and officially endorsed by ACNA , marking an industry first.

"The American Cannabis Nurses Association (ACNA) is dedicated to its members, ensuring they have access to top-quality medical-grade products," Nicole Foss, President of The ACNA said in the announcement. "Partnering with Weedgets, a renowned innovator in hardware, allows us to uphold our commitment. We look forward to launching co-branded activities throughout the year for the benefit of all our registered patients."

The endorsement will lead to co-creating regional showcases, educational webinars and materials, product marketing sheets, featuring thought leadership in ongoing communications and newsletters.

Weedgets focus on safety is evident in the way the Maze-X pipe works, as well as its other products that cool and filter smoke, making it safer.

Smoking Safer

Vaporization, edibles, or other ways to consume cannabis rarely deliver the same instantaneous effect as smoking, yet smoking could lead to a list of health concerns, due to the release of unwanted resin and tar into the lungs and the high temperature of the smoke.

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So smokers transformed themselves into engineers in order to solve the problem of smoking in a safer manner. Water pipes, bubblers, and bongs—technology that’s been available for decades—attempt to cool the smoke with water. Some experienced smokers chase smoke with air because it’s too close to the flame in an attempt to cool the smoke as well. But this new patented technology provides a new approach: Creating a maze inside a pipe that forces the smoke to travel a much longer distance, in an elongated, labyrinthine path.

Weedgets is applying waterless filtration technology, using physics to cool and filter the smoke. The team designed a very deliberate, always changing direction, essentially forcing the smoke to travel through a maze. While the Maze-X pipe is the typical length of a pipe—five and a half inches, but the smoke travels 14 inches.

Weedgets CEO Michael Barenboym.

Michael Barenboym, CEO of Weedgets, a play on the word “gadgets,” has a background as a biomedical mechanical engineer who has developed artificial heart systems, steerable endoscopy and laparoscopy instrumentation, cancer ablation systems, spine reconstructive surgical instruments, steerable catheters, microvasive surgical equipment, endoscopic staplers and suturing devices. He’s also done a lot of work for pulmonary devices including implantable devices for COPD, so it's a surprising move into the field of smoking devices.

But smoking can be much safer, he says, without giving up the delivery method. “Everything that we do is tailored towards one goal: Making smoking devices safer for the consumer, because there's nothing more important to any human being than their own health,” Barenboym says in a video call.

Barenboym’s patent for the pipe shows a maze-like pathway that’s designed to cool the smoke, one of over 100 patents he’s involved in. It solves the issue of the need for smoking without some of the negative health impacts.

“So for me the approach is to develop devices exactly the same as we do in the medical field—to develop technologies that will allow people to smoke safer,” he says. “Historically, in the smoking device industry, there are two major aspects making the smoke safer and pleasant: reducing the temperature and reducing the amount of resin.”

Cooling Technology Explained

The maze-like structure inside the silicone coil in the Maze-X pipe creates an elongated pathway to ... [+] cool the smoke.

The maze-like structure inside the Maze-X pipe looks like a helix but in fact changes the direction of the smoke pathway several times as it runs its course. He explained that the longer pathway allows the air to circulate much longer, cooling the smoke, while the maze-like structure captures harmful particles. He explained that when you smoke it, it feels like air and it’s designed to be smoked slowly.

“That's the reason why you get 100 degrees compared to 300 degrees Fahrenheit,” Barenboym says. The oils and cellulose in cannabis burns at a high temperature, but the pipe provides a way to fix that.

The Maze-X pipe provides three levels of filtration, from the glass bowl to the aluminum casing, and maze coil. Weedgets released another product, their own charcoal filter, designed so people can use them frequently, and they’re disposable, and they can serve a fourth level of filtration. They last about two to three months, and people can plug them in and smoke them like regular cigarette filter.

Weedgets features a limited edition Maze-X pipe with a titanium but most models are made from aluminum, which also helps to cool the smoke as well. They offer several different models, including the Limited Edition Titanium Maze-X Pipe , the original Maze Pipe , or the Slider Pipe.

“We are the first company in the world, primarily focusing on for the end user, nobody else is paying attention to them,” he says.

"We are proud to align with the American Cannabis Nurses Association (ACNA)," stated Barenboym in the announcement. "Our range of hardware and accessories was designed with patients in mind, and this partnership will provide greater access to those in need. We are excited to progress together!" Learn more about Weedgets technology on the website .

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National News | A decade after Flint, U.S. struggles to replace…

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National news | a decade after flint, u.s. struggles to replace lead pipes.

MEMPHIS, Tenn. – Joshua Perkins was surprised one morning last summer to see trucks from Memphis Light, Gas and Water outside his home. When he went to get a glass of water from the sink, nothing came out. Then rumbles of construction on the street began, as did chimes on his phone.

Perkins, the president of his neighborhood association, learned from a group chat what was happening: The utility had sent letters saying it would soon be replacing some lead pipes in the neighborhood, though Perkins said he never received one. Three years ago, Perkins’s water test from the company came back “safe,” he said, but the recent flurry of activity reawakened his concerns about lead contamination.

“No one tells you what they are doing,” Perkins said. “They just do it.”

Even after utility workers pulled pipes from underneath the street in front of Perkins’s residence, leaving a hole in the sidewalk for months, the lead pipes under his home remain.

A decade after a crisis in Flint, Mich., triggered national alarm about the dangers of lead in U.S. drinking water, the White House estimates that more than 9 million lead pipelines still supply homes across the country. In his first year in office, President Biden secured $15 billion through the bipartisan infrastructure law to address the problem. Still, residents across the country are grappling with a patchwork system of replacing those lines – which begins in some places as a partial replacement of lead pipes – sowing confusion and uncertainty about the safety of their everyday tap water.

The cost of drinking contaminated water can last for decades. There is no safe level of exposure to lead, according to the Centers for Disease Control and Prevention. It can cause developmental delays, difficulty learning and behavioral problems. Even low-level exposure can cause permanent cognitive damage, especially in developing children, and it disproportionately harms Black and low-income families. Recent research found that school-age children affected by the crisis in Flint endured significant and lasting academic setbacks.

In 2014, Flint officials switched the city’s water source to save money but did not ensure there were corrosion-control chemicals in the new water supply. Residents in the majority-Black city, where a third of the population lives in poverty, quickly began complaining of contaminated water coming from their taps. But complaints were ignored for more than a year. Nearly 100,000 Flint residents were exposed to lead through their home water sources, according to the CDC.

Following a monumental citizen lawsuit against the city of Flint and Michigan state officials, they agreed to pay for the removal of all the city’s lead service line pipes. Though the city originally agreed to replace all of the pipes by early 2020, some residents are still waiting.

The Environmental Protection Agency has projected that replacing the nearly 10 million lead pipes that supply U.S. homes with drinking water could cost at least $45 billion. The EPA has separately proposed requiring water utilities nationwide to replace all those lead pipes within 10 years.

“Communities around the country are already engaged in efforts to replace their lead service line, and some are ahead of others, for sure,” said Bruno Pigott, the EPA’s acting assistant administrator for water.

Since 2022, Tennessee has been allotted nearly $139 million from the infrastructure law to get rid of lead pipes. But, once the money is distributed, it’s up to the state to decide how to spend and distribute funds to cities.

To be eligible for the funding, Memphis’s utility must fulfill certain requirements, said LaTricea Adams, from the White House Environmental Justice Advisory Council, like completing a comprehensive inventory of lead pipe locations. The city is still waiting for approval. Memphis Light, Gas and Water has conducted 5,843 partial replacements since 2012, according to documents provided to the city council this week, out of 24,000 lead pipes officials have said are in the city.

Doug McGowen, the utility’s president, said during a Memphis City Council committee meeting on Tuesday that replacing all the city’s pipes could cost up to $100 million.

Utility spokeswoman Ursula Madden said the company has tested 4,014 samples of water at its customers’ request and returned 24 samples, 0.5 percent, that were above 15 parts per billion, the level at which the EPA calls for replacing lead pipes.

The varying drinking water systems across the country reflect differences in state attitudes and cultures, but in a “perfect world, everyone would have the same system,” said Ronnie Levin, an environmental health instructor at Harvard University. To Levin, the piecemeal approach to lead replacement programs reflects lack of rigor on the part of federal officials.

“The EPA could have a more rigorous approach than it does, but water utilities tend to be feisty,” said Levin, who worked as a scientist at the EPA for more than 30 years. She equated the nation’s disparate public water systems to “trying to corral 60,000 teenagers with attitudes.”

Lead pipes were initially installed in cities decades ago because they were cheaper and more malleable. But the heavy metal can wear down and corrode, causing lead to leach into drinking water, which prompted Congress to ban installing them in 1986. Memphis’s utility stopped using lead for service lines in the 1950s, before Tennessee banned the use of lead service lines in 1988.

In Memphis, utilities started doing partial lead service line replacements in 2012 – a process in which some utilities have begun to replace water service lines under public property, while leaving in place any lead pipes from the property line to the home. And until federal funding kicks in to fully pay for affected lines, it’s up to owners to pay to replace any lead pipes remaining on private property.

Memphis Light, Gas and Water treats the water with phosphate to form a barrier between the pipes and the drinking water to prevent leaching of lead and copper, Madden said.

Over 200 water utilities across the country have established lead service line replacement programs, including both partial and full replacement programs, according to data compiled by the Environmental Defense Fund.

Kym Byrd, who now has copper pipes leading to her home, has lived with the consequences of lead in Memphis for more than two decades.

Byrd had no idea about the impacts when the housing projects she lived in started testing residents’ children for lead in 2002. She learned her son suffered from lead poisoning.

Byrd wasn’t sure whether it was the old paint that had chipped or water from rusted lead pipes that poisoned her son. But the damage was done.

The son, LaKendrick Young, experienced developmental delays in talking and was mute for long periods until he turned 8. Instead, he pointed.

“I wasn’t that good of a talker at first, but I’m getting better,” said Young, now 27. In school, he struggled to keep up with the material.

“I didn’t connect the dots at the time,” Byrd said.

Byrd initially was unaware of the lead pipe replacement programs in Memphis but, after researching it, said she feels as though “it’s just a Band-Aid on a gash.”

“You’ve been cut with a machete, and they take a little Band-Aid and put it on top of it,” Byrd said. “Just enough to appease some people, to make them think that they are really something.”

Many experts worry that by replacing only part of the lead line, utility companies could be introducing more lead into the water supply system.

“The lead continues to flake off small particles of lead. So you will continue having lead pipe releasing lead into your drinking water even if you partially replace it with copper,” said Erik Olson, senior strategic director for health and food at the Natural Resources Defense Council, an advocacy group.

Partial replacements can also cause lead levels in water to spike if the pipe is disturbed after the replacement.

“Anytime you disturb the pipe, you shake the ground or somebody jackhammers on the street, that’s going to release lead,” said Chet Kibble Sr., an activist and founder of the Memphis and Shelby County Lead Safe Collaborative.

The EPA understands that partial replacements are not ideal, Pigott said, and has prioritized full replacements of the lines.

Some places in the country have done full lead service line replacement at no cost to homeowners. The utility in Newark replaced 23,000 lead pipes though millions of dollars in municipal bonds, according to the New Jersey city. The process took less than three years and has been praised by the Biden administration.

But it’s unclear whether other communities can replicate that effort.

In Providence, R.I., the utility provider started by offering partial replacements, switching to full lead line replacements after receiving federal funding.

Still, it has been a confusing process for some. Providence resident Neyda DeJesus first heard that her neighborhood was doing lead pipe replacements at a community meeting. She found out that her pipes were made of lead, and testing confirmed it was seeping into her drinking water.

“I’ve been here three years, and I didn’t know about this. And my water company never informed me,” DeJesus said.

While DeJesus waits for her pipes to be replaced at the end of this year, she plans to use filtered water from her new refrigerator and continue buying bottled water.

In Memphis, residents described inconsistent communication about pipe replacements underway.

Resident Andrew Hogenboom said he was notified weeks before his replacement started. One morning, barricades blocked half of his street as the trucks came out. Utility crews offered him a water filter pitcher to use after the replacement. Utility officials said in an email that they informed customers about the work a month in advance via mail.

But like Perkins, numerous residents said they did not receive warning. To fill the gap, activists and volunteers have tried to spread the word. Each month, the nonprofit environmental justice group Young, Gifted and Green canvasses in low-income communities with known lead service lines to share information about the partial replacements and free water inspections.

Sharon Hyde, a Memphis housing program manager for the national group Green and Healthy Homes Initiative, said the utility company has failed to provide clear enough messaging to ensure residents’ safety.

“It’s a very low percentage that understand that they could be on a lead service line and understand that [the replacement] has been done or not,” Hyde said.

That information, some residents said, would provide more clarity and peace of mind.

Margaret Gatewood, who cares for her two grandchildren in North Memphis, worries about what kind of pipes lie beneath her home. The 52-year-old never thought to filter the water she uses to fill her grandson’s sippy cup and make her granddaughter’s formula – last week, she tested her water for lead for the first time.

She wonders whether any contaminated water has contributed to her grandson’s slow development. At nearly 3 years old, he just learned how to walk. He still doesn’t talk. In August, doctors diagnosed him with autism, ruling out genetics as the cause.

As she figures out whether the pipes are made of lead, she grapples with the potential cost of replacing them – a burden she wouldn’t be able to afford on her own.

“I would move out of Memphis, but I ain’t got no money, so I’m just stuck,” Gatewood said. “For people who don’t have any money, we’re just stuck.”

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