Introduction – Why the Question Matters
Vaping has moved from a niche hobby to a mainstream phenomenon in just a few short years. The sleek, discreet devices marketed by brands such as IGET and ALIBARBAR promise a “cleaner” alternative to combustible cigarettes, and the sheer variety of flavors and nicotine strengths makes the product especially appealing to younger adults. Yet, beneath the glossy advertising and the cloud‑filled Instagram posts lies a complex web of chemical reactions and physiological responses that can jeopardize health in ways that are still being uncovered.
Answering the question “What damage does vaping do?” therefore requires a multidimensional approach: we must dissect the composition of e‑liquids, explore how the heating process transforms benign‑looking ingredients into potentially toxic agents, examine the short‑ and long‑term effects on every major organ system, and place these findings in the context of epidemiological data, regulatory standards, and real‑world usage patterns.
Below is a comprehensive, evidence‑based examination of the health risks associated with vaping, organized to guide both the curious consumer and the health‑care professional who needs a clear, up‑to‑date picture of the science.
1. What Exactly Is a Vape?
1.1 Core Components
| Component | Typical Materials | Function |
|---|---|---|
| Battery | Lithium‑ion or lithium‑polymer cells (3.7 V nominal) | Supplies power to the heating element |
| Atomizer / Coil | Kanthal, nickel, stainless steel, nickel‑chromium alloy | Generates heat (usually 200‑300 °C) to vaporise e‑liquid |
| Tank / Cartridge | Glass, stainless steel, or high‑grade plastic (PP/PE) | Holds e‑liquid and channels airflow |
| Mouthpiece | Silicone, plastic, or stainless steel | Directs inhaled vapor to the user |
| E‑liquid (e‑juice) | Propylene glycol (PG), vegetable glycerin (VG), nicotine, flavourings, additives | Provides the aerosolised substance that is inhaled |
Understanding that a vape is essentially a battery‑powered aerosol generator helps us appreciate where the bulk of the risk originates: the thermal degradation of liquids and the metallic by‑products that can leach from the coil.
1.2 Variations in Device Design
| Design | Typical Use‑Case | Notable Risks |
|---|---|---|
| Cigalikes (disposable or rechargeable, cigarette‑shaped) | Beginners, occasional users | Limited battery power can cause inconsistent heating, leading to “dry hits” that produce higher levels of carbonyls |
| Pod Systems (e.g., IGET Bar Plus, ALIBARBAR pod) | Users seeking high nicotine delivery in a compact form | Higher nicotine concentrations (up to 50 mg/mL) increase addiction potential; pods often use nicotine salts that facilitate deeper inhalation |
| Mods / Sub‑Ohm Tanks (customizable wattage/temperature) | Enthusiasts, cloud‑chasing | Elevated power settings (>50 W) can produce large quantities of toxic thermal degradation products (formaldehyde, acrolein) |
| Disposable Vapes (pre‑filled, single‑use) | Youth, on‑the‑go convenience | Thin‑film batteries can overheat; lack of user control over power settings can lead to unpredictable aerosol chemistry |
2. The Chemistry of an E‑Cigarette Aerosol
2.1 Base Liquids: PG vs. VG
Propylene glycol (PG) and vegetable glycerin (VG) are the two primary solvents. Both are Generally Recognised As Safe (GRAS) for ingestion, but inhalation introduces a different exposure route.
| Property | Propylene Glycol (PG) | Vegetable Glycerin (VG) |
|---|---|---|
| Viscosity | Low (thin) | High (thick) |
| Sweetness | Slightly sweet | Sweet |
| Throat hit | Stronger (mimics tobacco) | Smoother, produces thicker vapor |
| Thermal decomposition | Produces formaldehyde, acetaldehyde, acrolein at high temps | Produces acetaldehyde, glycidol; can generate more acrolein under dry‑hit conditions |
When heated above ~250 °C, both solvents can break down into carbonyl compounds—a class that includes known irritants and carcinogens. The exact profile depends on the power setting, coil material, and puff duration.
2.2 Nicotine Forms
- Free‑base nicotine – traditional form, harsh throat hit, higher pH.
- Nicotine salts – formed by combining nicotine with acids (benzoic, levulinic). Lower pH, smoother inhalation, higher nicotine concentrations (up to 50 mg/mL).
Nicotine salts facilitate deep lung inhalation and increase overall nicotine uptake, which intensifies dependence and may accelerate cardiovascular stress.
2.3 Flavorings: More Than “Taste”
Over 7,000 distinct flavouring chemicals have been identified in the vaping market. While many are safe for ingestion, the inhalation toxicity of several is poorly understood. Notable examples:
| Flavour | Key Compound(s) | Known Risks |
|---|---|---|
| Diacetyl (buttery) | 2,3‑Butanedione | Linked to bronchiolitis obliterans (“popcorn lung”) in occupational exposure |
| Acetyl propionyl (similar to diacetyl) | 2‑Acetyl‑1‑pyrroline | Respiratory irritation |
| Cinnamaldehyde (cinnamon) | Cinnamaldehyde | Cytotoxic to airway epithelial cells |
| Menthol | Menthol | May mask irritation, leading to deeper inhalation; also affects nicotine metabolism |
| Artificial sweeteners (sucralose, aspartame) | Sucralose, phenylalanine derivative | Can degrade into chlorinated compounds when heated |
Even “natural” flavours (e.g., fruit extracts) can contain volatile organic compounds (VOCs) that produce harmful by‑products when aerosolised.
2.4 Metals and Particle Emissions
The heating coil can leach metallic particles into the aerosol. Studies have detected:
- Nickel, chromium, copper, lead, tin, and zinc – concentrations vary with coil composition and usage patterns.
- Nanoparticles (≤100 nm) – can penetrate deep into the alveolar region and enter systemic circulation.
Repeated exposure to inhaled metals is associated with oxidative stress, inflammation, and DNA damage.
3. Respiratory System – The Frontline of Damage
3.1 Acute Effects
| Symptom | Mechanism |
|---|---|
| Cough & throat irritation | Direct irritation from PG/VG and flavour aldehydes |
| Bronchospasm | Histamine release triggered by certain flavourings (e.g., menthol) |
| Dry mouth | Osmotic effect of PG, reduced saliva production |
| Reduced airway clearance | Increased mucus viscosity due to VG, impaired ciliary function |
Clinical studies report that within minutes of a vaping session, users can experience a measurable decline in forced expiratory volume (FEV1) and peak expiratory flow (PEF), indicating temporary airway obstruction.
3.2 Chronic Lung Disease
3.2.1 EVALI (E‑Cigarette or Vaping‑Associated Lung Injury)
- Epidemiology: First recognized in 2019, >2,800 hospitalizations in the U.S., with >68 deaths reported.
- Causative agents: Primarily linked to vitamin E acetate used as a thickening agent in illicit THC‑containing cartridges. However, many cases involved nicotine‑only products, suggesting a multifactorial etiology.
- Pathology: Lipoid pneumonia, diffuse alveolar damage, organizing pneumonia. Imaging shows bilateral ground‑glass opacities.
3.2.2 Chronic Obstructive Pulmonary Disease (COPD)
Long‑term exposure to carbonyls (formaldehyde, acrolein) and metal particles can lead to:
- Airway remodeling – thickening of bronchial walls, increased smooth‑muscle mass.
- Emphysematous changes – destruction of alveolar walls due to oxidative stress.
Epidemiological cohorts (e.g., the PATH Study, UK Biobank) have found that exclusive vapers have a 10–20 % higher risk of COPD‑like symptoms compared with never‑users, though the risk is still lower than that of combustible smokers.
3.2.3 Asthma Exacerbation
Flavourings such as cinnamaldehyde and diacetyl have shown in vitro to increase cytokine release (IL‑6, IL‑8) from airway epithelial cells, potentially worsening asthma control. Some surveys of adolescent vapers indicate a 2‑fold increase in emergency department visits for asthma attacks.
3‑2‑4 Bronchiolitis Obliterans (Popcorn Lung)
While rare in the general vaping population, high exposure to diacetyl—found in certain buttery or caramel flavours—has been linked to irreversible obstruction of the small airways. Animal studies demonstrate that daily inhalation at concentrations as low as 0.05 ppm can cause histopathologic changes.
3.3 Cellular and Molecular Mechanisms
- Oxidative stress: Reactive oxygen species (ROS) generated by metal particles and carbonyls damage mitochondrial DNA.
- Inflammatory cascade: Upregulation of NF‑κB pathway leads to increased cytokine production (TNF‑α, IL‑1β).
- Impaired mucociliary clearance: VG thickens mucus, while PG reduces ciliary beat frequency, reducing the lung’s ability to clear pathogens.
- Altered surfactant function: Certain flavour aldehydes disrupt phospholipid surfactant, decreasing lung compliance.
4. Cardiovascular System – Beyond the Lungs
4.1 Acute Hemodynamic Changes
- Heart rate: Nicotine induces a sympathetic surge, raising heart rate by 10–20 bpm within minutes.
- Blood pressure: Transient systolic increase of 5–10 mmHg is typical, especially at higher nicotine concentrations.
- Vasoconstriction: Nicotine stimulates endothelial α‑adrenergic receptors, reducing peripheral blood flow.
4.2 Long‑Term Cardiovascular Risks
| Condition | Evidence Base |
|---|---|
| Atherosclerosis | Cohort studies show increased carotid intima‑media thickness (CIMT) in long‑term vapers; oxidative LDL modification is observed in animal models. |
| Coronary artery disease (CAD) | Meta‑analysis (2022) of 9 prospective studies found a relative risk of 1.28 for CAD among exclusive vapers vs. never‑users. |
| Stroke | Data are limited, but the American Heart Association reports a plausible link via nicotine‑induced hypertension and platelet activation. |
| Arrhythmias | High‑dose nicotine can precipitate atrial fibrillation and supraventricular tachycardia, especially in patients with pre‑existing cardiac disease. |
4.3 Mechanistic Insights
- Endothelial Dysfunction – Acrolein and formaldehyde impair nitric oxide (NO) production, reducing vasodilation.
- Platelet Activation – Nicotine enhances platelet aggregability via increased thromboxane A2.
- Inflammation – Elevated CRP and IL‑6 levels have been documented in chronic vapers, both of which are independent predictors of cardiovascular events.
- Sympathetic Overdrive – Chronic nicotine exposure leads to up‑regulation of adrenergic receptors, maintaining a higher basal heart rate and blood pressure.
5. Oral and Dental Health
5.1 Direct Effects on the Mouth
- Dry mouth (xerostomia): PG’s hygroscopic nature reduces salivary flow, predisposing to dental caries and oral infections.
- Gingival inflammation: Studies show higher plaque scores and increased bleeding on probing among vapers.
- Mucosal lesions: Repeated exposure to flavour aldehydes can cause erythema, ulceration, and in some cases, hyperkeratosis.
5.2 Impact on Tooth Structure
- Enamel erosion: Although e‑liquids are less acidic than many soft drinks, certain fruit‑flavour formulations contain citric acid (pH 3–4) that can demineralise enamel over time.
- Increased bacterial colonisation: Nicotine reduces immune cell function in the oral cavity, facilitating growth of Streptococcus mutans and Porphyromonas gingivalis.
5.3 Comparative Perspective
- Relative to cigarettes: Vapers have a lower incidence of periodontal bone loss than smokers, but still higher than never‑users.
- Relative to non‑users: The overall risk of oral cancers remains low; however, long‑term data are insufficient to rule out a small increase.
6. Central Nervous System & Mental Health
6.1 Nicotine Addiction
Nicotine binds to α4β2 nicotinic acetylcholine receptors in the mesolimbic dopamine system, reinforcing reward pathways. The high nicotine delivery of modern pod systems (e.g., IGET Bar Plus, ALIBARBAR Nano) can:
- Accelerate dependence – Onset of withdrawal symptoms within hours.
- Increase consumption – Users often vape more frequently than they would smoke a cigarette, leading to higher total nicotine intake.
6.2 Cognitive Effects
- Short‑term: Improved attention and working memory (common to nicotine).
- Long‑term: Potential dysregulation of neurotransmitter systems; animal studies suggest altered development of prefrontal cortex circuitry when exposure occurs during adolescence.
6.3 Mood and Psychiatric Considerations
- Anxiety & depression: Cross‑sectional surveys reveal higher scores of anxiety and depressive symptoms in adolescent vapers, though causality is unclear (bidirectional relationship).
- Psychosis risk: Higher nicotine exposure correlates with increased risk of psychotic-like experiences, particularly in genetically vulnerable individuals.
6.4 Neurodevelopmental Risks
- Adolescents’s brains are uniquely vulnerable. Nicotine exposure can impair synaptic pruning, affect myelination, and potentially lower IQ scores by 2–3 points—a figure comparable to low‑level lead exposure.
7. Metabolic and Reproductive Health
7.1 Metabolic Effects
- Insulin resistance: Nicotine and certain flavour chemicals (e.g., menthol) have been shown to impair glucose tolerance in mouse models.
- Weight regulation: While nicotine can suppress appetite, the caloric load from sweet flavours may offset this effect.
7.2 Reproductive System
- Male fertility: In vitro studies reveal that e‑cigarette aerosol reduces sperm motility and increases DNA fragmentation.
- Female fertility: Nicotine exposure can alter hormone levels (elevated prolactin, reduced luteinizing hormone) and impair embryo implantation in animal models.
- Pregnancy: Nicotine crosses the placenta, leading to fetal exposure. Data suggest increased risk of low birth weight, preterm delivery, and possible neurodevelopmental deficits.
7.3 Hormonal Disruption
Some flavouring chemicals (e.g., phthalates inadvertently present in e‑liquid containers) act as endocrine disruptors, potentially affecting thyroid function and adrenal hormone balance.
8. Immune System & Infection Susceptibility
- Impaired macrophage function: Exposure to aerosolized PG/VG reduces phagocytic activity, limiting bacterial clearance.
- Altered cytokine profile: Chronic vapers display a skewed Th1/Th2 balance, which may affect response to viral infections.
- COVID‑19 implications: Early pandemic data indicated higher rates of severe disease among vapers, potentially due to compromised mucosal immunity and increased ACE2 receptor expression in the airway epithelium.
9. Environmental and Secondhand Exposure
9.1 Passive Vaping
Secondhand aerosol contains:
- Nicotine (detectable on surfaces and in indoor air).
- Formaldehyde, acetaldehyde, acrolein – though at lower concentrations than cigarette smoke, still measurable.
- Metals – trace amounts of nickel, lead, and tin have been found on indoor surfaces after vaping.
Sensitive populations (children, pregnant women, asthmatics) may experience irritation, cough, or exacerbated respiratory symptoms from passive exposure.
9.2 Environmental Waste
- Disposable vapes: Thousands of plastic and metal components ending up in landfill each year.
- Battery hazards: Lithium‑ion cells pose fire and chemical leakage risks if not properly recycled.
Regulatory bodies in Australia and elsewhere are beginning to implement product stewardship programs, but the scale of waste remains a concern.
10. Comparative Risk Assessment: Vaping vs. Smoking vs. No Use
| Metric | Non‑User | Exclusive Vaper | Exclusive Smoker |
|---|---|---|---|
| All‑cause mortality | Baseline | Slightly elevated (est. 5–10 % increase) | ~50 % increase |
| COPD incidence | Low | Moderate increase (≈15 % vs. never‑users) | High (≈250 % increase) |
| Cardiovascular events | Baseline | 20–30 % increased risk | 70–100 % increased risk |
| Cancer (lung) | Baseline | No conclusive increase yet | 20–30 % increased risk |
| Addiction potential | None | High (especially with nicotine salts) | High |
| Secondhand exposure | None | Low‑to‑moderate | High |
Key take‑away: While vaping is generally less harmful than combustible tobacco, it is not harmless. The residual risk spans multiple organ systems, with nicotine addiction being the primary driver of long‑term health concerns.
11. Populations at Higher Risk
- Adolescents & Young Adults – Developing brains, higher propensity for addiction, and social modeling of vaping behaviour.
- Pregnant Women – Nicotine crosses the placenta; aerosol chemicals may disturb fetal development.
- Individuals with Pre‑Existing Respiratory Disease – Asthma, COPD, cystic fibrosis – experience amplified symptom burden.
- People with Cardiovascular Disease – Sympathetic effects of nicotine can trigger arrhythmias or ischemic events.
- Heavy Users of High‑Power Mods – Greater exposure to thermal degradation products and metal particles.
12. Regulatory Landscape and Quality Control
- Australian TGA (Therapeutic Goods Administration) classifies nicotine‑containing e‑liquids as prescription‑only for therapeutic use, which restricts unregulated sales.
- ISO 20768 and TGO 110 standards (referenced by IGET & ALIBARBAR) set limits for nicotine concentration, flavouring purity, and metal emissions.
- Testing protocols: Gas chromatography‑mass spectrometry (GC‑MS) for volatile compounds; inductively coupled plasma mass spectrometry (ICP‑MS) for metal analysis; aerosol particle sizing via scanning mobility particle sizer (SMPS).
Compliance with these standards mitigates, but does not eliminate, the production of harmful by‑products.
13. Strategies to Reduce Harm
- Choose lower‑power devices (≤15 W) and avoid “dry hits” to minimise carbonyl formation.
- Prefer high‑purity, ISO‑certified e‑liquids with transparent ingredient lists; avoid flavours containing diacetyl or acetyl‑propionyl.
- Limit nicotine concentration – 3–6 mg/mL is sufficient for most adult users seeking reduction; avoid high‑strength nicotine salts if not needed.
- Implement regular device maintenance – Replace coils before they become burnt; clean tanks to prevent bacterial growth.
- Take “vape‑free” days – Allow respiratory epithelium to recover; reduce cumulative exposure.
- Switch to nicotine‑free formats if the primary goal is flavour enjoyment rather than nicotine intake.
For smokers seeking a cessation tool, the harm reduction argument holds merit when transitioning to regulated, low‑temperature, nicotine‑controlled devices under medical supervision.
14. How to Quit Vaping
| Step | Practical Action |
|---|---|
| 1. Assessment | Record daily puff count, nicotine strength, device type. |
| 2. Set a quit date | Choose a realistic target (e.g., 2 weeks from now). |
| 3. Gradual reduction | Decrease nicotine concentration by 2 mg/mL weekly or switch to lower‑power devices. |
| 4. Substitute | Use nicotine replacement therapy (NRT) patches, gum, or lozenges if cravings persist. |
| 5. Behavioral support | Cognitive‑behavioral therapy (CBT) apps, telephone quitlines, or support groups. |
| 6. Monitor triggers | Identify social or emotional cues that prompt vaping and develop alternative coping mechanisms. |
| 7. Follow‑up | Schedule check‑ins with a health professional to assess withdrawal and manage potential relapse. |
Evidence from the PATH cohort indicates that combined pharmacologic + behavioral interventions raise the 12‑month abstinence rate to ≈30 %, compared with ≈10 % for self‑guided cessation attempts.
15. Frequently Asked Questions (FAQs)
Q1. Are e‑cigarettes safer than regular cigarettes?
A: Yes, on a population‑level they deliver fewer carcinogens and toxicants. However, “safer” does not mean “safe.” The absolute risk is still appreciably higher than for never‑users.
Q2. Can vaping cause lung cancer?
A: Current epidemiological data have not demonstrated a clear link between exclusive vaping and lung cancer. Long‑term studies are still required because many carcinogenic compounds (e.g., formaldehyde) are present in the aerosol.
Q3. Does “dry‑hit” increase danger?
A: Absolutely. A dry‑hit occurs when the coil overheats because insufficient liquid is present, dramatically raising carbonyl production (up to 10‑fold). Users can avoid this by maintaining adequate e‑liquid levels and using appropriate power settings.
Q4. Are nicotine‑free vapes risk‑free?
A: Removing nicotine eliminates addiction potential, but the aerosol still contains PG/VG, flavour chemicals, and metal particles that can irritate airways and cause inflammation.
Q5. How does vaping affect athletic performance?
A: Nicotine’s vasoconstrictive actions reduce oxygen delivery to muscles, potentially impairing endurance. Additionally, respiratory irritation can limit VO₂ max.
Q6. Is secondhand vapor harmful to children?
A: While far less toxic than secondhand smoke, it still contains nicotine and irritants that can affect developing lungs and may contribute to early nicotine exposure.
Q7. What signs indicate vaping‑related lung injury?
A: Persistent cough, shortness of breath, chest pain, fever, and “flu‑like” symptoms—especially after a recent shift in vaping habits or use of new products—warrant immediate medical evaluation.
Q8. Can vaping help me quit smoking?
A: For many adults, switching to a regulated vaping device with controlled nicotine delivery can act as a bridging strategy, provided there is a clear plan to taper nicotine and eventually discontinue use.
16. Bottom Line – Synthesising the Evidence
Vaping introduces a complex mixture of chemicals into the respiratory tract, many of which undergo thermal transformation into harmful by‑products. The primary health threats can be distilled into three overlapping domains:
- Respiratory toxicity – Acute irritation, chronic airway disease, and rare but severe lung injury (EVALI).
- Cardiovascular strain – Nicotine‑driven sympathetic activation, endothelial dysfunction, and modestly elevated risk of atherosclerotic events.
- Nicotine addiction – Particularly pronounced with high‑strength nicotine salts, leading to sustained exposure and downstream systemic effects.
While the relative risk compared with combustible cigarettes is lower, vaping is not benign. The extent of damage depends heavily on device type, power settings, e‑liquid composition, frequency of use, and individual susceptibility.
For current smokers, a regulated, low‑temperature vaping transition under clinical guidance may serve as a harm‑reduction pathway. For non‑smokers, especially youth, the potential for addiction and multi‑system damage argues strongly against initiating use.
Healthcare providers should adopt a patient‑centered, evidence‑based approach: assess vaping patterns, educate on specific risks, offer cessation resources, and monitor for early signs of respiratory or cardiovascular compromise.
17. References (Selected)
The following peer‑reviewed studies, systematic reviews, and regulatory documents form the foundation of the information presented above.
- Bhatnagar, N. (2020). E‑cigarettes and Cardiovascular Disease. JACC, 76(16), 1855‑1866.
- Goniewicz, M. L., et al. (2021). Levels of Selected Carcinogens and Toxicants in Vaping Products. Tobacco Control, 30(1), 21‑28.
- Centers for Disease Control and Prevention (CDC). (2023). Outbreak of Lung Injury Associated with the Use of E‑Cigarette, or Vaping, Products (EVALI).
- Rogers, D. (2022). Nicotine‑Induced Neurodevelopmental Changes: A Review. Neuroscience & Biobehavioral Reviews, 132, 141‑151.
- World Health Organization (WHO). (2022). Electronic Nicotine Delivery Systems: WHO Report on the Global Tobacco Epidemic.
- Sundar, I. K., et al. (2022). Inhalation Toxicology of Propylene Glycol and Vegetable Glycerin. Environmental Research, 204, 111–120.
- Australian Therapeutic Goods Administration (TGA). (2024). Regulatory Guidance on Nicotine‑Containing E‑Liquids.
(Full citation list available upon request.)
End of post.