Abstract
Background
Little is known about the role of waterpipe smoking and cardiovascular (CVD) risk. We evaluated the association between ever-smoking waterpipe and risk of death from incident CVD using data from the Hanoi Prospective Cohort Study, a prospective cohort study in Northen Vietnam.
Methods
The current analysis included 35,646 Vietnamese aged 18 years and older who were recruited during 2007–2019 period. Cox proportional hazard regression model was used to calculate the hazard ratio (HR) and 95% confidence intervals (95% CIs) for risk of CVD mortality related to ever-smoking waterpipe.
Results
After a median follow-up of 11.01 years (range: 0.13–11.64 years), we identified 344 CVD deaths. Overall, compared with never-smokers, ever-WTP smokers were about 60% higher risk of CVD deaths (HR=1.57; 95% CI: 1.16–2.13), 44% higher risk of deaths from cerebrovascular disease (HR=1.44; 95% CI: 1.08–1.93) and the highest of CVD deaths was among dual ever-smokers of waterpipe and cigarette (HR=1.77, 95% CI: 1.21–2.60). Also, compared with non-smokers & no alcohol user, the CVD risk was the highest among WTP smokers who smoked ≥11 pack-years (i.e., 1 pack/day x11 years) & ever-alcohol drinkers (HR=2.19, 95% CI: 1.42–3.38).
Conclusion
In a large prospective cohort study, we showed that ever-waterpipe smoking was associated with increased risk of CVD deaths, particularly deaths from cerebrovascular disease; and higher among dual smokers of cigarettes and waterpipe. Additionally, smoking cigarette and drinking alcohol doubled risk of CVD death. These findings suggest that waterpipe smoking should receive equal attention as cigarette smoking in tobacco control and prevention programs.
Keywords: Waterpipe and cigarette smoking, Risk, Cardiovascular disease deaths, Prospective cohort study, Viet Nam
Graphical abstract
Lay summary
Though cigarette smoking is a well-established risk factor for cardiovascular disease (CVD), little is known about the role of waterpipe smoking, a non-cigarette product with rising prevalence, and the risk of CVD mortality. This study aimed to determine the association between ever-smoking of waterpipe (WTP) and risk of CVD mortality using data from an on-going prospective cohort study, comprising approximately to 36,000 Vietnamese men and women.
- Overall, compared with never-smokers, ever-WTP smokers had the highest risk of CVD mortality, particularly deaths from cerebrovascular disease.
-Among dual ever-smokers of waterpipe and cigarette, the risk of CVD mortality were higher in those who began smoking before age 21, smoked ≥15 sessions/day, had smoked for ≥10 years, and accumulated ≥11 pack-years.
1. Introduction
Cardiovascular disease (CVD) is a significant public health issue, accounting for millions of deaths worldwide 1]. Notably, more than 75 % of CVD deaths occur in the low-and middle income countries (LMICs) [1,2]. Vietnam, a LMIC in Southeast Asia with a total population more than 103 million, is ranked the 14th most populous country globally and recorded approximately 170,000 CVD deaths, accounting for 31 % of all deaths in 2016 [3].
While cigarette smoking is considered a well-established risk factor for CVD mortality [4,5], waterpipe (WTP) smoking in CVD mortality remains poorly understood. Waterpipe smoking is a popular form of tobacco use in different regioins of the world, particularly in Middle East, North Africa, South Asian and part of East Asia, including Vietnam. Vietnam ranks among top ten countries worldwide in terms of smoking prevalence and has one of the highest rates of male WTP smokers among LMICs [6]. A recent National Health Survey in Vietnam reported that among smokers, the majority were exclusive cigarette smokers, followed by exclusive WTP smokers (23.2 %) and ever-dual smokers of cigarettes and WTP (7.7 %) [7]. There is, therefore, an urgent unmet need to investigate the public health impact of waterpipe smoking.
Evidence regarding the impact of waterpipe smoking on CVD mortality remains extremely limited. There have been several efforts investigating the relationship between waterpipe smoking and the severity of coronary artery disease in the hospital-based studies [[8], [9], [10]]. Another study, using data from the Cancer Prevention Study II, an American Cancer Society prospective co+hort study, found that pipe smoking was associated with increased risk of deaths from coronary heart disease, cerebrovascular disease, and chronic obstructive pulmonary disease [11]. To our knowledge, there has been no prospective cohort study that has evaluated the impact of waterpipe smoking on the risk of CVD mortality.
The current study, aimed to fill this gap of knowledge by examining the association between ever-smoking of waterpipe and risk of incident CVD mortality using data from the Hanoi Prospective Cohort Study (HPCS), an ongoing study of more than 52,000 participants residing in Northern Vietnam.
2. Methods
2.1. Study population
The HPCS is an on-going prospective cohort study conducted in Northern Vietnam. Details of its design and methods had been described previously [[12], [13], [14]]. Briefly, between April 2007 and November 2008, the HPCS recruited 52,325 Vietnamese participants aged one year or older from nine communities, including five in the urban areas of Hanoi, three in the rural regions of Hung Yen province, and one in the mountain area of Phu Tho province. In the parent prospective cohort study, we included children under 15 in the cohort because injury-related mortality accounted for approximately 12 % of total deaths in Vietnam at the time [15], and prior evidence suggested that smoking was associated with increased risk of injury [16]. The HPCS was approved by the Institutional Review Boards of the Hanoi Medical University and the International University of Health and Welfare, Japan.
At baseline, train interviewers conducted in-home interviews using a structured questionnaire to obtain information on sociodemographic, body weight and height, lifetime use of tobacco smoking (i.e., cigarette smoking and waterpipe smoking), family history of cancer, medical history, and diet. In the current analysis, we excluded 13,682 participants aged 18 or younger and 2997 individuals who migrated out of the communities. The final sample size included 35,646 study participants for our analysis (Fig. 1 and Supplementary Methods).
Fig. 1.
Workflow Chart of Study Participants in the Current Study.
2.2. Smoking assessment
We used the structured questionnaire, which included items on demographic and lifestyle factors as well as semi-quantitative food frequency questionnaire (FFQ), to collect information on tobacco use, diet, and related information. Two main types of tobacco use, including cigarette and waterpipe smoking were assessed in the HPCS [17].
The following questions were used to obtain information on cigarette smoking: 1) “Do you currently smoke cigarettes every day?” (Yes/no); if “yes,” “What is the average number of cigarettes smoked daily?” “Number of years smoked?”; 2) “Do you currently smoke cigarettes weekly?” (Yes/no); if “yes,” “what is the average number of cigarettes smoked weekly?” “Number of years smoked?”; 3) “If you do not currently smoke cigarettes daily or weekly, in the past, did you smoke cigarettes daily?” (Yes/no); if “yes,” “what is the average number of cigarettes smoked daily?” “Number of years smoked?” “The number of years you have quit smoking?”. We used the same set of questions to collect the information on waterpipe smoking.
We also conducted a validation study of the smoking questionnaire among 147 participants, each of whom completed two interviews administered two weeks apart to evaluate the agreement between two interviews (or test-retest reliability). The interviews were conducted by two independent and experienced interviewers. The kappa statistics (κ) and corresponding 95 % confidence intervals (CIs) for current and former tobacco smoking (including both cigarette and waterpipe smoking) were 0.97 % (0.94–0.99), P < 0.01) and 0.96 (0.93–0.99; P < 0.01), respectively, indicating excellent agreement between the two assessments.
In the current analysis, smoking status was categorized as ever-smokers and never-smokers. We defined a never-smoker as an individual who had never smoked tobacco of any type and ever smokers of cigarettes and/or waterpipe, or dual smoking of cigarette and waterpipe. Former smokers were defined as individuals who had smoked during their lifetime but did not smoke for at least six months prior to the interview date. Smoking frequency was defined as smoking intensity daily reported during any period of life. Cumulative smoking was calculated by multiplying the average daily smoking session and the duration of tobacco (in years).
We compared the proportions of ever-tobacco smokers between the current dataset (after excluding 2997 participants who were either lost to follow-up or migrated out of the communities) and with that in the full baseline dataset (or before such exclusion) to assess potential selection bias. The difference between these two proportions was 0.44 % (P-value=0.09), indicating that the exclusion of these 2997 participants did not materially affect the distribution of smoking status in the current analysis.
2.3. Deaths ascertainment from cardiovascular disease (CVD)
All-cause of mortality information, including CVD-related deaths, was identified based on medical records available at the community health station (CHS), district hospitals, provincial hospitals, and other health facilities. Detailed information regarding mortality included date of death (day, month and year), place of final medical examination and diagnosis, treatment received, and the medical certificate issued by the health facility. Cause-specific mortality was classified using the International Classification of Diseases, Tenth Revision (ICD-10) code. A prior validation study of the mortality registry reported completeness, sensitivity, and specificity of 93.9 %, 75.4 %, and 98.4 %, respectively. To improve accuracy, an additional review was conducted in consultations with an independent second opinion to clarify the underlying cause of CVD-related deaths, particularly for cases classified as false negatives (24.6 %) or incompleteness (6.1 %). In the current study, 344 CVD-related deaths were identified. For individuals who migrated out of the study communities, we collected the following information: 1) the move date (day, month, and year) and 2) the new address.
In our analysis, the last follow-up was on December 31, 2019, or at the time when the information on those who died or had events or moved out of the community was confirmed. Follow-up time was defined by years from enrolment (or baseline survey) to the date of death, loss-to-follow-up, or end of follow-up, whichever came first.
2.4. Assessment of other covariates
Potential confounding was identified from prior studies on mortality risks [12,18,19]. The following covariates were included in the current analysis: 1) age (i.e., 10–49, 50–59, 60–69, ≥70), 2) education level (i.e., primary and secondary or higher), 4) body mass index (BMI) (in kg/m2 calculated as weight in kilograms divided by height in meters squared) that was grouped into <18.5, 18.5 to <23, and ≥23, 4) alcohol drinking status (i.e., yes versus no), 5) history of hypertension (i.e., yes versus no), 6) history of type 2 diabetes (i.e., yes versus no), 7) total energy intake (in Kcal/day and quintiles), 8) dietary protein intake (in g/day and quintiles), 9) dietary fat intake (in g/day and quintiles), and 10) dietary carbohydrate intake (in g/day and quintiles).
2.5. Statistical analysis
We calculated means and standard deviations (SDs) for continuous variables and counts and proportions for categorical variables. We used t-test and χ2 test to compare the difference in distributions of continuous and categorical variables, respectively, between CVD deaths versus survived participants and across categories of smoking types (i.e., never-smokers, dual ever-smokers of cigarette and waterpipe, exclusive cigarette smokers and exclusive waterpipe smokers). We also calculated the person-years at risk for each participant from the interview date to the date of death, migration out of communities, or December 31, 2019, whichever occurred first.
In the main analysis, we utilized Cox proportional hazard regression model to determine the association between smoking (i.e., exclusive cigarette smoking, exclusive waterpipe smoking and dual ever-smoking of cigarette and waterpipe) and risk of CVD deaths. We calculated the hazard ratios (HRs) and their 95 % CIs for risk of CVD deaths according to smoking types. We included the above set of 10 covariates in the multivariable Cox regression models to control for potential confounding effect. We also performed additional analysis to evaluate the impact of waterpipe smoking with other types of tobacco smoking, including exclusive cigarette smoking and dual ever-smoking of cigarette when exclusive WTP smoking was treated as a reference group. To further understand the impact of smoking on CVD deaths, we conducted analysis by age at start smoking (in years), frequency of smoking (session per day), duration of smoking (in years), and the intensity of smoking (in pack-years) by specific types of tobacco (i.e., overall or ever-smoking of cigarette and/or ever-smoking of waterpipe, exclusive cigarette smoking, exclusive WTP smoking, and dual ever-smoking of cigarette). For models of waterpipe smoking in relation to CVD deaths, we further adjusted for ever cigarette smoking status. Similarly, models of cigarette smoking in relation to CVD deaths, we further adjusted for ever waterpipe smoking status.
We further conducted stratified analysis by age (<60 vs. ≥60 years old), BMI status (<23 vs. ≥ 23 kg/m2), history of hypertension (yes vs. no), history of type 2 diabetes (yes vs. no) and types of disease (cerebrovascular diseases vs. other heart diseases). We could not perform a stratified analysis by race/ethnicity because almost 100 % study participants were Kinh ethnicity, a major ethnic group in Vietnamese population.
Stata statistical package, version 14.0 (StataCorp LP., College Station, TX) was used for all statistical analyses. All P values were two-sided, and P-values (or alpha level) less than 0.05 were considered statistically significant.
3. Results
After a median (range) follow-up of 11.01 (0.13–11.64) years, 344 CVD deaths (203 among men and 141 among women) were identified. Compared with never-smokers, smokers were older, had higher BMI, and were more likely to be drinkers and had histories of hypertension and type 2 diabetes (All P’s<0.05). Waterpipe smokers had lower education levels than never-smokers (P < 0.0001) (Table 1).
Table 1.
Selected baseline characteristics of study participants by types of smoking, the Hanoi prospective cohort study.
| Never smoker (n = 26,359) |
Ever-Dual smokers (n = 2719) |
Exclusive Waterpipe smokers (n = 3061) |
Exclusive cigarette smokers (n = 3507) |
Total (N = 35,646) |
P-value | |
|---|---|---|---|---|---|---|
| Waterpipe and cigarette smoking | ||||||
| Intensity (pack-years), mean (SD) | - | 17.6 (19.0) | 12.5 (13.8) | 7.9 (11.3) | - | <0.001 |
| Age at started smoking, mean (SD) | - | 24.1 (6.1) | 25.9 (6.6) | 25.2 (6.1) | - | <0.001 |
| Frequency (session per day), mean (SD) | - | 18.7 (13.2) | 11.6 (8.9) | 9.6 (8.4) | - | <0.001 |
| Duration of smoking (years), mean (SD) | - | 17.3 (10.7) | 19.9 (12.6) | 14.2 (11.1) | - | <0.001 |
| Sex | ||||||
| Male | 8072 (30.6) | 2612 (96.1) | 2920 (95.4) | 3346 (98.2) | 16,950 (47.5) | <0.001 |
| Female | 18,287 (69.4) | 107 (3.9) | 141 (4.6) | 161 (1.8) | 18,696 (52.5) | |
| Age, mean (SD) | 41.7 (18.6) | 45.3 (14.2) | 49.1 (14.4) | 45.3 (15.4) | 42.97 (17.85) | <0.001 |
| 18–39 | 13,852 (33.9) | 1005 (37.0) | 809 (26.4) | 1399 (39.9) | 17,065 (47.9) | |
| 40–49 | 4346 (25.2) | 801 (29.5) | 915 (29.9) | 823 (23.5) | 6885 (19.3) | |
| 50–59 | 3247 (12.3) | 478 (17.5) | 666 (21.8) | 609 (17.3) | 5000 (14.0) | |
| 60–69 | 1926 (7.3) | 223 (8.2) | 303 (9.9) | 362 (10.3) | 2814 (7.9) | |
| ≥70 | 2988 (11.3) | 212 (7.8) | 368 (12.0) | 314 (9.0) | 3882 (10.9) | |
| Highest level of education | ||||||
| Primary school | 5058 (19.2) | 435 (16.0) | 718 (23.5) | 333 (9.5) | 6544 (18.4) | <0.001 |
| Middle school or higher | 21,301 (80.8) | 2284 (84.0) | 2343 (76.5) | 3174 (90.5) | 29,102 (81.6) | |
| History of hypertension | ||||||
| No | 25,278 (95.9) | 2577 (94.8) | 2927 (95.6) | 3312 (94.4) | 34,094 (95.6) | |
| Yes | 1081 (4.1) | 142 (5.2) | 134 (4.4) | 195 (5.6) | 1552 (4.4) | <0.001 |
| History of type 2 diabates | ||||||
| No | 26,201 (99.4) | 2698 (99.2) | 3045 (99.5) | 3472 (99.0) | 35,416 (99.4) | 0.006 |
| Yes | 158 (0.6) | 21 (0.8) | 16 (0.5) | 35 (1.0) | 230 (0.6) | |
| BMI, mean (SD)a | 20 (3.9) | 20.5 (4) | 20.1 (3.6) | 20.7 (3) | 20.1 (3.78) | <0.001 |
| <18.5 | 5728 (21.7) | 462 (17.0) | 612 (20.0) | 556 (15.9) | 7358 (20.6) | |
| 18.5–22.9 | 14,363 (54.5) | 1517 (55.8) | 1689 (55.2) | 1954 (55.7) | 19,523 (54.8) | |
| ≥23 | 6268 (23.8) | 740 (27.2) | 760 (24.8) | 997 (28.4) | 8765 (24.6) | |
| Alcohol drinking statusa | ||||||
| Never | 22,305 (89.2) | 589 (21.7) | 866 (29.3) | 1128 (33.9) | 24,888 (73.2) | <0.001 |
| Ever | 2708 (10.8) | 2130 (78.3) | 2094 (70.7) | 2198 (66.1) | 9130 (26.8) | |
| Energy intake (Kcal/day) mean (SD) | 1759.9 (427.6) | 1751.8 (413.6) | 1758.8 (433.5) | 1764.5 (415.5) | 1759.66 (425.9) | 0.28 |
| Protein intake (g/day), mean (SD) | 65.2 (18.7) | 65.3 (18.6) | 64.4 (19.0) | 66.5 (18.2) | 65.24 (18.7) | 0.11 |
| Fat intake (g.day) mean (SD) | 23.7 (10.1) | 24.4 (10.4) | 23.6 (10.6) | 24.4 (9.8) | 23.83 (10.2) | 0.001 |
| Carbohydrate intake (g daily, mean (SD) | 325 (85.9) | 321.3 (82.4) | 325.8 (86.6) | 323.4 (83.6) | 324.66 (85.4) | 0.03 |
Abbreviation: BMI: Body mass index; SD: standard deviation.
Based on reported data.
Compared with participants who survived during the study period (referred to as surviving participants), those who died from CVD were older, had lower levels of education, were more likely to have histories of hypertension or type 2 diabetes, and were more likely to be alcohol drinkers. They also had lower intakes of protein and fat (all P’s<0.05). There were no statistically significant differences between CVD deaths and surviving participants in BMI or carbohydrate intake (Supplementary Table 1).
Compared with non-smokers, ever-smokers had significantly increased risk of CVD deaths (HR=1.33; 95 % CI, 1.01–1.74). This observation was also seen in ever-waterpipe smokers (HR=1.57; 95 % CI, 1.16–2.13). Also, dual ever-smokers of cigarette and WTP had a 64 % higher risk of CVD deaths (HR=1.64; 95 % CI, 1.14–2.36), compared with never-smokers. (Table 2).
Table 2.
Associations between smoking status of cigarette and waterpipe with risk of CVD deaths in men and women combined and in men only, the Hanoi prospective cohort study.
| Person- years | # Deaths | Rate per 1000 | Age-adjusted Model HR (95 % CI) |
Multivariable model HR (95 % CI) |
|
|---|---|---|---|---|---|
| Ever Cigarette and/or Waterpipe Smokinga | |||||
| Never smoker | 286,012 | 207 | 0.72 | 1.00 | 1.00 |
| Ever cigarette and/or waterpipe smokers | 99,139 | 137 | 1.38 | 1.26 (0.97–1.65) | 1.33 (1.01–1.74) |
| Former cigarette and/or waterpipe smokers | 21,762 | 56 | 2.57 | 1.27 (0.90–1.78) | 1.25 (0.89–1.76) |
| Current cigarette and/or waterpipe smokers | 77,377 | 81 | 1.05 | 1.26 (0.93–1.71) | 1.39 (1.02–1.88) |
| Ever Waterpipe Smoking Statusb | |||||
| Never smoker | 286,012 | 207 | 0.72 | 1.00 | 1.00 |
| Ever smokers | 57,312 | 85 | 1.48 | 1.52 (1.13–2.06) | 1.57 (1.16–2.13) |
| Smoking Status of Cigarettes and Waterpipe | |||||
| By Types of Smokinga | |||||
| Never smoker | 286,012 | 207 | 0.72 | 1.00 | 1.00 |
| Dual ever-smokers of waterpipe and cigarettes (mean: 17.6 pack-years) | 28,867 | 45 | 1.56 | 1.62 (1.13–2.32) | 1.64 (1.14–2.36) |
| Exclusive waterpipe smokers (mean: 12.5 pack-years) | 32,374 | 48 | 1.48 | 1.18 (0.83–1.67) | 1.25 (0.88–1.78) |
| Exclusive cigarette smokers (mean: 7.9 pack-years) | 37,897 | 44 | 1.18 | 1.11 (0.77–1.60) | 1.18 (0.82–1.70) |
| Waterpipe versus cigarette smoking statusc | |||||
| Exclusive waterpipe smokers | 37,897 | 44 | 1.16 | 1.00 | 1.00 |
| Exclusive cigarette smokers | 32,374 | 48 | 1.48 | 1.06 (0.71–1.60) | 1.04 (0.68–1.59) |
| Ver-dual waterpipe & cigarette smokers | 28,867 | 45 | 1.56 | 1.45 (0.96–2.20) | 1.41 (0.92–2.15) |
Abbreviation: CI: confidence interval); HR: hazard ratio.
Model adjusted for: age groups (18–39, 40–49, 50–59, 60–69, ≥70), an education level (Primary school, middle school or higher, unknown), BMI (kg/m2, <18.5, 18.5-<23, ≥23, unknown), alcohol consumption (yes/no, unknown), history of hypertension (yes vs. no), history of diabetes (yes vs. no), total energy intake (kcal/day, quintiles), protein intake (g/day, quintiles), fat intake (g/day, quintiles), and carbohydrate intake (g/day, quintiles).
Model adjusted for: age groups (18–39, 40–49, 50–59, 60–69, ≥70), an education level (Primary school, middle school or higher, unknown), BMI (kg/m2, <18.5, 18.5-<23, ≥23, unknown), alcohol consumption (yes/no, unknown), history of hypertension (yes vs. no), history of diabetes (yes vs. no), total energy intake (kcal/day, quintiles), protein intake (g/day, quintiles), fat intake (g/day, quintiles), carbohydrate intake (g/day, quintiles) and ever cigarette smoking.
Model adjusted for: age groups (18–39, 40–49, 50–59, 60–69, ≥70), education level (Primary school, middle school or higher, unknown), BMI (kg/m2, <18.5, 18.5-<23, ≥23, unknown), alcohol consumption (yes/no, unknown), history of hypertension (yes vs. no), history of diabetes (yes vs. no), total energy intake (kcal/day, quintiles), protein intake (g/day, quintiles), fat intake (g/day, quintiles), carbohydrate intake (g/day, quintiles) and smoking session per day.
Bold numbers: statistically significant (P < 0.05).
Compared with never-smokers, the risk of CVD deaths was particularly increased in ever-smokers of cigarette and/or ever-smokers of waterpipe who started smoking at early age (<25 years old; HR=1.41, 95 % CI: 1.00–2.00), smoked 10 sessions per day or more (HR=1.35, 95 % CI: 0.97–1.88), smoked 13 years or more (HR=1.53, 95 % CI: 1.10–2.14) and smoked 7 pack-years or more (HR=1.47, 95 % CI: 1.09–1.99). Similar observations were also found among dual ever-smokers of cigarette and waterpipe (Table 3, Fig. 2A-C). The estimated survival proportion among ever smokers was lowest among male who smoked 10 pack-years or more (Supplementary Figure 1).
Table 3.
Associations between smoking status, frequency, duration, and intensity of cigarette and waterpipe with risk of CVD deaths, the Hanoi prospective cohort study.
| Person- years | # Deaths | Rate per 1000 | Age-adjusted Model HR (95 % CI) |
Multivariable model HR (95 % CI) |
|
|---|---|---|---|---|---|
| Ever Cigarette and/or Waterpipe Smokinga | |||||
| Age at started smoking | |||||
| Never smoker | 286,012 | 207 | 0.72 | 1.00 | 1.00 |
| <25 years old | 38,748 | 57 | 1.47 | 1.35 (0.95–1.90) | 1.41 (1.00–2.00) |
| ≥25 years old | 45,279 | 40 | 0.88 | 1.39 (0.94–2.04) | 1.49 (1.01–2.21) |
| Continuous scale (Per SD increment) | 1.03 (1.00–1.07) | 1.04 (1.01–1.07) | |||
| Ptrend | 0.05 | 0.02 | |||
| Frequency (session per day) | |||||
| Never smoker | 286,012 | 207 | 0.72 | 1.00 | 1.00 |
| <10 sessions/day | 54,337 | 67 | 1.23 | 1.20 (0.87–1.65) | 1.28 (0.93–1.77) |
| ≥10 sessions/day | 40,123 | 60 | 1.50 | 1.30 (0.94–1.81) | 1.35 (0.97–1.88) |
| Continuous scale (Per SD increment) | 1.14 (0.97–1.35) | 1.17 (0.99–1.38) | |||
| Ptrend | 0.11 | 0.06 | |||
| Duration of smoking (years) | |||||
| Never smoker | 286,012 | 207 | 0.72 | 1.00 | 1.00 |
| <13 years | 31,945 | 20 | 0.63 | 1.17 (0.72–1.91) | 1.21 (0.74–1.97) |
| ≥13 years | 29,867 | 64 | 2.14 | 1.47 (1.06–2.05) | 1.53 (1.10–2.14) |
| Continuous scale (Per SD increment) | 1.21 (1.03–1.43) | 1.24 (1.05–1.46) | |||
| Ptrend | 0.02 | <0.001 | |||
| Intensity (pack-years) | |||||
| Never smoker | 286,012 | 207 | 0.72 | 1.00 | 1.00 |
| <7 pack-years | 46,066 | 34 | 0.74 | 1.05 (0.70–1.56) | 1.10 (0.74–1.64) |
| ≥7 pack-years | 44,549 | 89 | 2.00 | 1.39 (1.03–1.88) | 1.47 (1.09–1.99) |
| Continuous scale (Per SD increment) | 1.18 (1.02–1.37) | 1.21 (1.04–1.41) | |||
| Ptrend | 0.03 | 0.01 | |||
| Ever Waterpipe Smoking, Intensity (pack-years)b | |||||
| Never smoker | 286,012 | 207 | 0.72 | 1.00 | 1.00 |
| <10 pack-year | 31,891 | 24 | 0.75 | 1.01 (0.64–1.58) | 1.07 (0.68–1.68) |
| ≥10 pack-year | 25,421 | 61 | 2.40 | 1.58 (1.14–2.21) | 1.63 (1.16–2.28) |
| Continuous scale (Per SD increment) | 1.25 (1.06–1.48) | 1.27 (1.07–1.51) | |||
| Ptrend | 0.01 | 0.01 | |||
| Exclusive Waterpipe Smokingb | |||||
| Age at started smoking | |||||
| Never smoker | 286,012 | 207 | 0.14 | 1.00 | 1.00 |
| <21 years old | 12,367 | 19 | 0.59 | 1.46 (0.88–2.42) | 1.46 (0.88–2.42) |
| ≥21 years old | 14,889 | 15 | 0.29 | 1.16 (0.67–2.03) | 1.18 (0.68–2.06) |
| Continuous scale (Per SD increment) | 1.05 (0.96–1.16) | 1.06 (0.96–1.17) | |||
| Ptrend | 0.29 | 0.27 | |||
| Frequency (session per day) | |||||
| Never smoker | 286,012 | 207 | 0.60 | 1.00 | 1.00 |
| <15 sessions/day | 19,960 | 27 | 0.20 | 1.12 (0.73–1.74) | 1.14 (0.73–1.76) |
| ≥15 sessions/day | 10,853 | 17 | 0.19 | 1.41 (0.83–2.37) | 1.45 (0.86–2.44) |
| Continuous scale (Per SD increment) | 1.12 (0.94–1.33) | 1.13 (0.95–1.34) | |||
| Ptrend | 0.19 | 0.16 | |||
| Duration of smoking (years) | |||||
| Never smoker | 286,012 | 207 | 0.15 | 1.00 | 1.00 |
| <10 years | 10,722 | 2 | 0.09 | 0.36 (0.09–1.45) | 0.36 (0.09–1.46) |
| ≥10 years | 19,205 | 41 | 0.10 | 1.39 (0.95–2.02) | 1.41 (0.97–2.06) |
| Continuous scale (Per SD increment) | 1.11 (0.98–1.27) | 1.12 (0.99–1.27) | |||
| Ptrend | 0.10 | 0.08 | |||
| Intensity (pack-years) | |||||
| Never smoker | 286,012 | 207 | 0.72 | 1.00 | 1.00 |
| <8 pack-years | 15,050 | 12 | 0.80 | 1.01 (0.55–1.85) | 1.11 (0.60–2.04) |
| ≥8 pack-years | 14,587 | 30 | 2.06 | 1.24 (0.82–1.89) | 1.32 (0.86–2.01) |
| Continuous scale (Per SD increment) | 1.11 (0.90–1.36) | 1.14 (0.93–1.41) | |||
| Ptrend | 0.33 | 0.21 | |||
| Exclusive Cigarette Smokingc | |||||
| Age at started smoking | |||||
| Never smoker | 286,012 | 207 | 0.06 | 1.00 | 1.00 |
| <21 years old | 14,085 | 20 | 0.94 | 1.62 (0.98–2.66) | 1.60 (0.97–2.64) |
| ≥21 years old | 16,033 | 8 | 0.29 | 1.03 (0.49–2.14) | 1.05 (0.50–2.19) |
| Continuous scale (Per SD increment) | 1.06 (0.95–1.19) | 1.06 (0.95–1.19) | |||
| Ptrend | 0.20 | 0.28 | |||
| Frequency (session per day) | |||||
| Never smoker | 286,012 | 207 | 0.68 | 1.00 | 1.00 |
| <15 sessions/day | 18,198 | 18 | 0.33 | 1.11 (0.67–1.86) | 1.07 (0.64–1.79) |
| ≥15 sessions/day | 18,632 | 24 | 0.32 | 1.25 (0.79–1.98) | 1.24 (0.78–1.96) |
| Continuous scale (Per SD increment) | 1.08 (0.93–1.26) | 1.07 (0.92–1.25) | |||
| Ptrend | 0.32 | 0.36 | |||
| Duration of smoking (years) | |||||
| Never smoker | 286,012 | 207 | 0.83 | 1.00 | 1.00 |
| <10 years | 20,661 | 11 | 0.09 | 0.93 (0.50–1.75) | 0.91 (0.48–1.71) |
| ≥10 years | 15,817 | 33 | 0.10 | 1.42 (0.95–2.13) | 1.39 (0.92–2.09) |
| Continuous scale (Per SD increment) | 1.12 (0.98–1.29) | 1.11 (0.97–1.28) | |||
| Ptrend | 0.10 | 0.12 | |||
| Intensity (pack-years) | |||||
| Never smoker | 286,012 | 207 | 0.72 | 1.00 | 1.00 |
| <4 pack-years | 17,485 | 8 | 0.46 | 0.69 (0.33–1.43) | 0.7 (0.34–1.44) |
| ≥4 pack-years | 15,818 | 30 | 1.90 | 1.39 (0.91–2.11) | 1.51 (0.98–2.32) |
| Continuous scale (Per SD increment) | 1.15 (0.93–1.42) | 1.19 (0.96–1.49) | |||
| Ptrend | 0.21 | 0.11 | |||
| Dual Ever-Cigarette & Waterpipe Smokinga | |||||
| Age at started smoking | |||||
| Never smoker | 286,012 | 207 | 0.06 | 1.00 | 1.00 |
| <21 years old | 10,488 | 17 | 1.62 | 1.66 (0.98–2.83) | 1.68 (0.99–2.87) |
| ≥21 years old | 16,163 | 18 | 1.11 | 2.21 (1.31–3.73) | 2.25 (1.33–3.82) |
| Continuous scale (Per SD increment) | 1.17 (1.07–1.29) | 1.18 (1.07–1.30) | |||
| Ptrend | <0.001 | <0.001 | |||
| Frequency (session per day) | |||||
| vNever smoker | 286,012 | 207 | 0.13 | 1.00 | 1.00 |
| <15 sessions/day | 9056 | 11 | 1.21 | 1.63 (0.87–3.07) | 1.63 (0.86–3.08) |
| ≥15 sessions/day | 19,696 | 33 | 1.67 | 1.82 (1.21–2.73) | 1.84 (1.22–2.76) |
| Continuous scale (Per SD increment) | 1.22 (1.07–1.40) | 1.23 (1.07–1.40) | |||
| Ptrend | <0.001 | <0.001 | |||
| Duration of smoking (years) | |||||
| Never smoker | 286,012 | 207 | 0.06 | 1.00 | 1.00 |
| <10 years | 11,894 | 10 | 0.84 | 1.87 (0.97–3.61) | 1.90 (0.98–3.67) |
| ≥10 years | 15,973 | 34 | 2.13 | 1.84 (1.22–2.75) | 1.85 (1.23–2.79) |
| Continuous scale (Per SD increment) | 1.23 (1.07–1.40) | 1.23 (1.08–1.41) | |||
| Ptrend | <0.001 | <0.001 | |||
| Intensity (pack-years) | |||||
| Never smoker | 286,012 | 207 | 0.72 | 1.00 | 1.00 |
| <11 pack years | 14,061 | 11 | 0.78 | 1.43 (0.76- 2.69) | 1.42 (0.75–2.67) |
| ≥11 pack years | 13,614 | 32 | 2.35 | 1.76 (1.17–2.66) | 1.76 (1.16–2.67) |
| Continuous scale (Per SD increment) | 1.33 (1.09–1.63) | 1.33 (1.08–1.63) | |||
| Ptrend | 0.01 | 0.01 | |||
Abbreviation: CI: confidence interval); HR: hazard ratio.
Model adjusted for: age groups (18–39, 40–49, 50–59, 60–69, ≥70), sex (if possible), an education level (Primary school, middle school or higher, unknown), BMI (kg/m2, <18.5, 18.5-<23, ≥23, unknown), alcohol consumption (yes/no, unknown), history of hypertension (yes vs. no), history of diabetes (yes vs. no), total energy intake (kcal/day, quintiles), protein intake (g/day, quintiles), fat intake (g/day, quintiles), and carbohydrate intake (g/day, quintiles).
Model adjusted for: age groups (18–39, 40–49, 50–59, 60–69, ≥70), sex (if possible), an education level (Primary school, middle school or higher, unknown), BMI (kg/m2, <18.5, 18.5-<23, ≥23, unknown), alcohol consumption (yes/no, unknown), history of hypertension (yes vs. no), history of diabetes (yes vs. no), total energy intake (kcal/day, quintiles), protein intake (g/day, quintiles), fat intake (g/day, quintiles), carbohydrate intake (g/day, quintiles) and ever cigarette smoking.
Model adjusted for: age groups (18–39, 40–49, 50–59, 60–69, ≥70), sex (if possible), an education level (Primary school, middle school or higher, unknown), BMI (kg/m2, <18.5, 18.5-<23, ≥23, unknown), alcohol consumption (yes/no, unknown), history of hypertension (yes vs. no), history of diabetes (yes vs. no), total energy intake (kcal/day, quintiles), protein intake (g/day, quintiles), fat intake (g/day, quintiles), carbohydrate intake (g/day, quintiles) and ever waterpipe smoking.
Bold numbers: statistically significant (P < 0.05).
Fig. 2.
Cubical Spline Curves of Association Between Ever Waterpipe Smoking and Risk of CVD Deaths, the Hanoi Prospective Cohort Study by (A) smoking session per day; (B) smoking duration; and (C) smoking pack-years.
In the stratified analysis in ever-smokers of waterpipe, we also found that the risk of CVD deaths was more apparent in individuals who were younger than 60 years old, those with BMI<23 kg/m2, individuals without history of hypertension and those without history of type 2 diabetes. The respective HRs and 95 % CIs were 2.16 (1.11-*4.24), 1.78 (1.23–2.57), 1.64 (1.16–2.30), and 1.61 (1.18–2.18) (All P’sheterogeneity> 0.05 (Supplementary Table 2).
Also, in the stratified analysis by type of disease, overall smoking and waterpipe smoking were associated with cerebrovascular disease only but not with other heart diseases. The respective HRs and 95 % CIs were 1.32 (1.01–1.74) and 1.45 (1.07–1.96) (Supplementary Table 3).
In the evaluation of joint effect between ever alcohol users and ever-smokers of waterpipe smoking, we found that the CVD risk was the highest among ever-smokers of waterpipe who smoked ≥11 pack-years & ever-drinkers of alcohol, compared with never smokers & no alcohol drinkers (HR=2.05, 95 % CI: 1.36–3.08) (Pheterogeneity=0.48) (Supplementary Table 4).
4. Discussion
In this large on-going prospective cohort study of close to 36,000 Vietnamese men and women, we found that overall, ever smokers significantly increased risk of CVD deaths and ever waterpipe smoker were at the highest risk of CVD deaths, particularly risk of deaths from cerebrovascular disease, compared with never smokers. The risk of CVD deaths for dual ever-smokers of waterpipe and cigarettes increased among those who started smoking before 21 years of age, smoked ≥15 sessions/day, smoked ≥10 years, and smoked ≥11 pack-years.
To the best of our knowledge, the current study might be the first effort to determine the association between waterpipe smoking and risk of CVD deaths in a large prospective cohort study design. Prior hospital-based studies have examined the association between waterpipe smoking and the severity of coronary artery disease (CAD) 0.8–10 For instance, in a large hospital-based study of 1210 CAD patients in Lebanon, Sibai et al. [10] found that lifetime exposure exceeding 40 waterpipe-years was associated with a threefold increase in the odds of having severe stenosis (≥70 %) compared with non-smokers (OR=2.94, 95 % CI: 1.04–8.33) as well as with the CAD Index (β=7.835, P = 0.03). Similarly, in a hospital-based study of 287 CAD patients in Egypt, Selim et al. [8] reported that patients who smoked shisha had significantly higher Duke Jeopardy Score, representing the severity of coronary angiography than those who were non-shisha smoker (Mean±SD: 6.961±3.238 vs. 5.762±3.062, P = 0.004). In addition, in an analysis of the Gulf Registry of Acute Coronary Events (Gulf RACE) survey, comprising 6704 patients with acute coronary syndrome (ACS) in six Middle-Eastern countries, Al Suwaidi et al. [9] reported that the in-hospital mortality rate was highest among waterpipe smokers, (5.2 %), followed by combined smokers (waterpipe and cigarette smoking) (3.5 %) and cigarette smokers (2.8 %), compared with non-smokers 4.1 %). Finally, Henley et al. analyzed data from the Cancer Prevention Study II-an American Cancer Society prospective cohort study (n = 138,307 men) and reported that current pipe smoking was associated with increased risk of deaths from coronary heart disease (HR=1.30, 95 % CI: 1.18–1.43) and cerebrovascular disease (HR=1.27, 95 % CI: 1.09–1.48)[11].
Compared with non-smokers, dual ever-smokers of waterpipe and cigarettes were associated with a 164 % increased risk of CVD deaths, followed by exclusive waterpipe smoking (125 %) and exclusive cigarette smoking (118 %). The heightened risk associated with waterpipe smoking might be explained by a strong addition to waterpipe tobacco, reflecting higher intensity, frequency and duration of smoking. Compared with exclusive cigarette smokers, both exclusive waterpipe smokers and dual ever-smokers of waterpipe and cigarette have higher intensity (Mean pack-years: 7.9 vs. 12.5 and 17.5, P < 0.001); higher frequency of session per day (Mean: 9.8 vs. 11.6 and 18.7, P < 0.001) and higher duration of smoking (Mean in years: 14.2 vs. 19.9 and 17.3, P < 0.001) (Table 1). Indeed, waterpipe smoking is recognized as a carcinogen and has been previously associated with risk of cancer incidence and mortality in this cohort [13,14,20].
Different mechanisms have been proposed regarding the role of cigarette smoking in CVD. One of the primary mechanisms is the induction of atherogenesis, in which smoking impair vascular function by reducing nitric oxide availability, resulting in increased adhesion molecular production and endothelial dysfunction[21,22]. Another mechanism involved the creation of a procoagulant and inflammatory environment through effects on platelets activation and macrophage adhesion [23]. Importantly, macrophages migrate through the endothelium, become activated, take up oxidized lipoproteins, and transform into foam cells[ 24,25]. Additionally, cigarette smoking induces tissue remodelling, promotes prothrombotic processes, and activates systemic inflammatory signalling activation; collectively contributing to atherosclerotic changes in arterial walls [[26], [27], [28]]. Moreover, atherosclerosis is strongly associated with CVD incidence and mortality [21].
Several studies have shown that waterpipe smoking has comparable adverse effects on the cardiovascular systems as cigarette smoking [[29], [30], [31]]. Patients who smoke both cigarettes and waterpipes have greater levels of low-density lipoprotein (LDL) cholesterol than those who smoke exclusively cigarettes [32]. A prior study by Zhang et al. reported that the likelihood of developing coronary heart disease later in life increases in correlation with the cumulative LDL levels across adolescent and middle-age [33]. Another study also found that waterpipe smoking might decrease total antioxidant capacity and vitamin C levels, which increase serum low-density lipoprotein levels [34]. Additionally, smokers of both cigarettes and shisha (a type of waterpipe smoking) were found to have a significantly higher heart rate and systolic blood pressure, compared with smokers of exclusive cigarettes, exclusive shisha, or non-smokers [8].
Waterpipe smoking delivers higher amounts of compounds that adversely affect the cardiovascular systems than cigarette smoking, including aromatic hydrocarbons (PAH), benzenes, and nicotine [[35], [36], [37]]. Vietnam has a relatively high prevalence of waterpipe smoking (6.4 %) compared with other Asian countries, such as China (i.e., no reported use) and Eastern Mediterranean countries (3.3 %)[37]. Vietnamese waterpipe smokers typically used raw tobacco leaves of Nicotiana rustica, which contains extremely high concentrations of nicotine[38]. Nicotine plays a significant role in cardiovascular dysfunction through multiple pathways, including increasing cardiac output or damage[39,40]. One mechanism is the evaluation of sympathetic nervous system activity, induced by nicotine exposure, which can lead to acute hemodynamic changes such as increase heart rate, myocardial contractility, and cardiac output [41]. Waterpipe smoking has also been shown to induce acute hemodynamic changes comparable to those observed with cigarette smoking [42,43]. In addition to its toxic effects, nicotine is a highly addictive, producing withdrawal symptoms that makes cessation difficult [44].
Similar to other observational studies, our study has several limitations. First, we were unable to evaluate the impact of changes in smoking habit over time because we only collected smoking information at baseline. Second, misclassification of smoking status and/or dietary patterns might have occurred due to reliance on participant recall during interview. Third, interpretation of the spline curves should be cautious, as the confidence intervals for those who smoked 30 sessions/day or more, or smoked more than 25 years or smoked 30 pack-years or more were wider than those who smoked less than 30 sessions/day, smoked less than 25 years or those who smoked less than 30 pack-years; therefor the trends showed in spline curves might not be fully accurate. Finally, we were unable to ascertain the diagnosis of CVD during the follow up. The inability to capture temporal sequence from the date of CVD diagnosis to the dates of death or the last day of follow-up resulted in lower estimates, or hazard ratios toward the null.
Our study also has several strengths, including a prospective design with large sample size and detailed data on tobacco smoking habits [12]. The prevalence of waterpipe smoking among men in Northern Vietnam exceeded 45 %, allowing for the evaluation of the independent impact of waterpipe versus cigarette smoking on CVD mortality [45]. The use of a structured questionnaire enabled us to collect comprehensive information, including socioeconomic status, BMI, alcohol habit, and dietary factors, which were used in the multivariate models to control for potential confounding effects.
Although this analysis might be the first effort to comprehensively examine the harmful effects of waterpipe smoking on CVD mortality in Vietnam, it reinforces an important point that waterpipe smoking is unsafe and represents a significant public health concern.
In summary, in a prospective cohort study of 35,646 Vietnamese men and women, we found that, compared with never smokers, waterpipe smoking, either in the forms of exclusive or in combination with cigarettes, was associated with increased risk of CVD mortality, particularly deaths from cerebrovascular disease. To our knowledge, this might be the first prospective cohort study to comprehensively examine the harmful effects of waterpipe smoking on CVD mortality. These findings reassure that waterpipe smoking is a significant public health concern and should receive equal attention as cigarette smoking in tobacco control and prevention programs, particularly in similar settings and countries.
Funding/Support
NT Le was the PI of Grant Agreement No.: 18/FIRST/1a/HMU, Under the Project: "Fostering Innovation through Research, Science, and Technology; Viet Nam Ministry of Science and Technology, 2017–2019, and the Project of Viet Nam Ministry of Science and Technology supported the baseline survey for 2006–2011. This work has also been supported by a UICC 2013 American Cancer Society Beginning Investigators Fellowship funded by the American Cancer Society, a UICC 2015 Yamagiwa-Yoshida Memorial International Cancer Study Grant, and a UICC technical fellowship 2023 to NT Le. YT-H Pham was supported by the NIH T32CA186873 (PI: J-M Yuan) training grant in cancer epidemiology and prevention.
Role of the funder/sponsor
The funding organizations had no role in the design and conduct of the study; collection, management, analysis, and interpretation of the data; preparation, review, or approval of the manuscript; and decision to submit the manuscript for publication.
Data sharing statement
Data is available from the corresponding authors on request.
Abbreviations
BMI, body mass index; CHS, commune health station; CI, confidence interval; CO, carbon monoxide; DLQ, demographic lifestyle questionnaire; GATS, Global Adult Tobacco Survey; ICD-10, International Classification of Diseases, Tenth Revision; HPCS, Hanoi Prospective Cohort Study; HR, hazard ratio; LMICs, Low- and middle-income countries; OR, odds ratio; PAH, polycyclic aromatic hydrocarbon; PM, particulate matter; SQFFQ, semi-quantitative food frequency questionnaires; WHO, World Health Organization; WTP, Waterpipe tobacco smoking.
Author agreement
The authors have agreed to the submission of this manuscript - Waterpipe Smoking and Risk of Cardiovascular Disease Mortality: Findings from a Prospective Cohort Study -and the materials in this manuscript have not been previously published nor are in consideration for publication elsewhere.
CRediT authorship contribution statement
Ngoan Tran Le: Writing – review & editing, Writing – original draft, Visualization, Validation, Supervision, Software, Resources, Project administration, Methodology, Investigation, Funding acquisition, Formal analysis, Data curation, Conceptualization. Hieu Lan Nguyen: Writing – review & editing, Writing – original draft, Investigation, Formal analysis, Conceptualization. Linh Thuy Le: Writing – review & editing, Validation, Methodology, Investigation. Thinh Gia Nguyen: Writing – review & editing, Methodology, Investigation. Dung Thi-Thuy Truong: Writing – review & editing, Methodology, Investigation. Phuoc Hong Le: Writing – review & editing, Methodology, Investigation. Lang Wu: Writing – review & editing, Methodology, Investigation. Yen Thi-Hai Pham: Writing – review & editing, Writing – original draft, Methodology, Investigation, Formal analysis. Hung N. Luu: Writing – review & editing, Writing – original draft, Visualization, Validation, Supervision, Software, Resources, Project administration, Methodology, Investigation, Formal analysis, Data curation, Conceptualization.
Declaration of competing interest
Dr. Le reported receiving grants from the American Cancer Society and the Union for International Cancer Control during the conduct of the study. Dr. Pham reported receiving a grant from the National Institutes of Health (NIH) during the conduct of the study.
Acknowledgments
The authors thank all study participants in the three northern provinces of Viet Nam for their participation. We also thank Ha Nguyen (Auburn University) for generating figures of cubical restricted splines.
Footnotes
Supplementary material associated with this article can be found, in the online version, at doi:10.1016/j.ajpc.2026.101516.
Contributor Information
Ngoan Tran Le, Email: v.dir.srm@vinmec.com.
Hung N. Luu, Email: hluu2@houstonmethodist.org.
Appendix. Supplementary materials
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