In a recent study published in BMJ Public Health, researchers quantified the effect of smoking on stroke prevalence. They investigated the association between smoking-related characteristics and the risk of stroke, including an examination of demographic differences that influence the association.
Study: From smoke to stroke: quantifying the impact of smoking on stroke prevalence. Image Credit: africa_pink/Shutterstock.com
Background
Stroke leads to considerable morbidity and mortality worldwide. Stroke may be ischemic or hemorrhagic and occurs due to injury to the blood vessels and tissues of the brain.
Causes of ischemic stroke are thrombosis and arteriosclerosis due to microvascular disease and restricted blood flow. Hemorrhagic stroke causes include vascular abnormalities, hypertension, and cerebral aneurysm ruptures.
Oxidative stress, inflammation, autophagy, and apoptosis characterize stroke risk. High smoking rates, family smoking, and high amounts of toxic tobacco components, including carbon monoxide, nicotine, and tar, all raise the risk of a stroke.
These parameters indicate the ambient exposure to and frequency of smoking, as well as the potential damage caused by inhaled smoke.
About the study
In the present study, researchers investigated associations between smoking indicators and the risk of stroke.
The study analyzed data from 9,176 adults participating in the 2003–2018 National Health and Nutrition Examination Survey (NHANES). Exclusion criteria were the absence of stroke status and missing information on smoking-associated indicators.
The researchers compared clinical variables to smoking-related parameters such as smoking duration and amounts of carbon monoxide, nicotine, and tar. The smoker variable was derived from the multiplication of the total number of smoking days in the previous month by the mean count of tobacco cigarettes smoked daily, based on study participant replies.
Additional smoking-associated data, such as cigarette length, cigarette filter, tar, carbon monoxide, and nicotine concentration, were gathered directly through questionnaire replies. The researchers assessed family smoking using questions on the smoking habits of the family members of the participants.
Stroke diagnosis was determined using self-administered questionnaires and participant declarations of medically verified stroke diagnoses. Weighted logistic regression modeling determined the odds ratios (OR) for analysis.
Covariates in the study were age, biological sex, body mass index (BMI), race, educational attainment, marital status, poverty-to-income ratio (PIR), alcohol use, and comorbidities such as diabetes, hyperlipidemia, and hypertension.
The team conducted subgroup studies to determine the association between household smoking practices and stroke development risk. The researchers used the restricted cubic spline method to simulate non-linear associations of smoking-related factors with stroke risk.
Results and discussion
The stroke prevalence in the studied population was 3.40%. The researchers discovered statistically significant relationships between stroke incidence and factors like age, biological sex, educational achievement, and marital status.
The adjusted logistic regressions revealed that greater levels of carbon monoxide and nicotine were associated with an increased stroke development risk.
Specifically, OR values increased from 2.4 in the unadjusted model to 2.6 in the fully adjusted model for nicotine and ranged between 1.10 and 1.11 for carbon monoxide. The limited cubic spline cut-off analysis identified critical thresholds for an increase in stroke risk at 410 units of smoke exposure, 12 mg of tar, 1.1 mg of nicotine, and 12 ppm of carbon monoxide.
Above these cutoffs, stroke risk increased considerably. Family smoking increased stroke risk with odds ratios of 1.88 in the unadjusted model and 1.7 in the fully adjusted model, demonstrating a statistically significant but diminishing influence across models.
Logistic regressions revealed that the risk of stroke was considerably higher among males aged above 60 years with comorbidities. Smoking-related features such as carbon monoxide and nicotine levels and duration (long and ultralong) are associated with a significantly increased stroke risk. Higher educational attainment, unmarried status, and PIR above 3.5 lowered stroke risk.
Tobacco, which primarily contains nicotine, has serious health consequences, notably for cardiovascular tissues. It stimulates neuronal nicotinic acetylcholine receptor (nAChR) molecules, which release noradrenaline and adrenaline, raising blood pressure and heart rate and increasing the risk of developing stroke.
Nicotine also increases blood viscosity, which raises the risk of thrombosis. Smoking produces carbon monoxide, which lowers blood oxygen-carrying ability and causes hypoxia in tissues and several organs, notably the brain.
Tobacco burning creates tar, a mixture of hazardous substances, including polycyclic aromatic hydrocarbons (PAHs), heavy metals, and free radicals, which raise the risk of developing stroke by inducing vascular endothelial cell damage and lowering nitric oxide generation while increasing oxidative stress.
Conclusion
The study demonstrates that smoking significantly increases strop development risk, primarily due to exposure to carbon monoxide and nicotine.
The increased stroke risk among elderly males with concomitant illnesses and a family history of smoking highlights the importance of tailored stroke preventive methods that consider demographic susceptibilities.
Stroke risk assessments must include smoking-associated indicators to increase prediction accuracy and inform preventative efforts. Further studies could explore the genetic and biological factors enhancing the effects of smoking on the risk of stroke among more diverse populations to improve the generalizability of the study findings.
Stroke survivors more likely to experience abnormal sleep patterns