Vaping has moved from a niche hobby into a mainstream consumer product, and the question “What do vapes do to you?” now appears on search engines, health forums, and in everyday conversation. Answering it requires a multidisciplinary approach that combines toxicology, physiology, epidemiology, and product engineering. Below, the narrative walks through the fundamentals of how vaping devices work, dissects the chemical cocktail delivered to the lungs, examines acute and chronic biological responses, compares vaping to combustible cigarettes, explores the regulatory and safety frameworks that shape product quality, and finally addresses the practical concerns of users who want to understand the true impact of a puff. The discussion is grounded in peer‑reviewed research, clinical observations, and industry standards, offering a comprehensive, evidence‑based portrait of the effects of vaping on the human body.
1. The Mechanics of a Vape – From Power Supply to Inhaled Aerosol
1.1 Core components
A typical modern vape (also called an electronic cigarette or e‑cigarette) consists of four primary components:
| Component | Function | Typical Materials |
|---|---|---|
| Battery | Supplies electrical energy to heat the coil | Lithium‑ion cells (3.7 V nominal) |
| Atomizer/Coil | Converts electrical energy into heat, vaporising the e‑liquid | Kanthal, Nickel‑Chrome, Stainless steel, or Nichrome wires, sometimes wrapped around cotton or silica wicks |
| E‑liquid (e‑juice) | Source of vapor‑phase chemicals | Propylene glycol (PG), vegetable glycerin (VG), nicotine, flavorings, and optional additives |
| Mouthpiece/Flow channel | Guides aerosol to the user’s mouth | Plastic, stainless steel or resin‑based couplings |
When the user activates the device (by pressing a button or inhaling in “draw‑activated” models), the battery delivers a current that heats the coil to temperatures typically ranging from 150 °C to 300 °C. At these temperatures, the PG/VG base mixtures become a fine aerosol that carries dissolved nicotine and flavor compounds into the respiratory tract.
1.2 Generation of the aerosol
The transformation from liquid to aerosol is not a simple boiling process; it is a thermophysical atomisation event where droplets are formed via rapid volatilisation and nucleation. The size distribution of the resulting particles is critical:
- Mass Median Aerodynamic Diameter (MMAD): 1–2 µm for most devices, ensuring deep lung penetration.
- Number median diameter: 30–150 nm for ultrafine particles, which can cross alveolar barriers and enter systemic circulation.
The aerosol is therefore a mixture of liquid droplets, solid particles (e.g., trace metals shed from the coil), and gaseous constituents (volatile organic compounds, nicotine, and potentially carbonyls formed by thermal degradation).
1.3 Device variability
The performance of a vape can vary dramatically based on power settings, coil resistance, and e‑liquid composition. High‑wattage “sub‑ohm” devices (≤ 0.5 Ω coils) can push temperatures above 350 °C, increasing the formation of toxic carbonyls such as formaldehyde and acrolein. By contrast, low‑wattage, closed‑system pod devices (e.g., IGET Bar Plus, ALIBARBAR disposable vapes) generally operate at lower power levels, limiting the generation of harmful degradation products but still delivering nicotine efficiently.
2. Chemical Landscape of Vaping Aerosol
2.1 Propylene Glycol (PG) and Vegetable Glycerin (VG)
Both PG and VG are regarded as “Generally Recognised as Safe” (GRAS) for ingestion, but inhalation exposes the respiratory epithelium to a different set of physicochemical stresses.
- PG is hygroscopic and contributes to a “throat hit.” Inhalation can cause mild irritation in susceptible individuals, particularly at high concentrations.
- VG yields denser vapor, providing a smoother feel. However, its higher viscosity can promote the production of larger droplets, potentially altering deposition patterns in the lungs.
Studies using in vitro air‑liquid interface (ALI) cultures have demonstrated that prolonged exposure to PG/VG aerosol can modestly reduce ciliary beat frequency, impairing mucociliary clearance. The effect, however, is generally dose‑dependent and less severe than that observed with cigarette smoke.
2.2 Nicotine
Nicotine is the primary psychoactive ingredient in most vaping products, delivering the well‑documented cardiovascular and neurochemical effects seen in traditional cigarettes.
| Pharmacokinetic Parameter | Vaping vs. Smoking |
|---|---|
| Peak plasma nicotine | 10–15 ng/mL (similar) |
| Time to peak (Tmax) | 2–5 min (slightly slower) |
| Half‑life | 1–2 h (unchanged) |
The absorption pathway differs: nicotine in vapor is deposited predominantly on the oropharyngeal mucosa and alveoli, where it diffuses rapidly into the bloodstream. The resulting systemic exposure mirrors that of smoked cigarettes, but the rapidity of delivery can be modulated by device temperature and puff duration.
2.3 Flavoring Compounds
Flavorings are the most diverse component class, ranging from natural extracts (e.g., menthol, vanilla) to synthetic chemicals (e.g., cinnamaldehyde, diacetyl). While the majority are approved for food use, their safety upon inhalation is less well‑established.
- Cinnamaldehyde has been shown to inhibit mitochondrial respiration in bronchial cells at concentrations as low as 0.1 mg/mL.
- Diacetyl and acetyl propionyl, linked to “popcorn lung” (bronchiolitis obliterans), have been detected in many fruit‑flavoured vapes; however, concentrations are typically below occupational exposure limits. Nonetheless, chronic exposure in susceptible individuals remains a concern.
2.4 Thermal Degradation Products
When the coil temperature exceeds certain thresholds, PG, VG, and nicotine undergo pyrolysis, forming carbonyl compounds such as:
- Formaldehyde
- Acetaldehyde
- Acrolein
- Acetone
Heavy‑metal particles (nickel, chromium, lead) may also be liberated from the coil material itself, especially in older or poorly manufactured devices. For instance, a systematic review of 45 vaping devices identified mean lead concentrations of 0.2 µg per puff in high‑wattage models, a level that, while low, could accumulate with chronic use.
3. Acute Physiological Effects – What Happens When You Take a Puff
3.1 Respiratory Tract Response
- Airway Irritation: Immediate sensation of mild throat irritation or “dry cough” is common, especially with high‑PG liquids or high‑temperature aerosol. Cytokine release (IL‑6, IL‑8) from airway epithelial cells can be transiently elevated.
- Bronchodilation vs. Bronchoconstriction: Nicotine exerts a bronchodilatory effect via β2‑adrenergic stimulation, yet some flavor additives cause reflex bronchoconstriction. Spirometric studies have reported a 2–4 % increase in forced expiratory volume (FEV1) within 10 minutes of a nicotine‑containing puff, but a subsequent 1–2 % decline after exposure to certain menthol or cinnamaldehyde flavours.
- Mucociliary Clearance: As mentioned, PG/VG can reduce ciliary beat frequency by 10–15 % after a 30‑minute exposure, potentially impairing clearance of pathogens and particulates.
3.2 Cardiovascular Impact
Nicotine’s sympathomimetic activity triggers:
- Increased heart rate (average +5–10 bpm) within minutes.
- Elevated systolic and diastolic blood pressure (5–8 mmHg rise) lasting 15–30 minutes.
- Enhanced arterial stiffness, measurable via pulse wave velocity, reflecting transient endothelial dysfunction.
Acute vaping has also been associated with reduced flow‑mediated dilation (FMD) of the brachial artery, an indicator of endothelial health. The magnitude of FMD reduction (≈ 2 %) mirrors that seen after a single cigarette, suggesting comparable short‑term vascular stress.
3.3 Central Nervous System Effects
Nicotine binds to nicotinic acetylcholine receptors (nAChRs) in the brain, producing:
- Increased dopamine release in the mesolimbic pathway, reinforcing the rewarding sensation.
- Elevated alertness, reduced appetite, and a sense of relaxation after the initial stimulant phase.
- Withdrawal reversal in dependent users, manifesting as reduced irritability and anxiety after vaping.
Neuroimaging studies using functional MRI have demonstrated activation of the insular cortex and ventral striatum within 3 minutes of inhalation, aligning with patterns observed in conventional smoker cohorts.
3.4 Metabolic and Hormonal Shifts
Nicotine stimulates catecholamine release (epinephrine, norepinephrine), leading to:
- Increased basal metabolic rate (≈ 5–7 % rise in resting energy expenditure).
- Transient hyperglycemia, due to hepatic glycogenolysis, which normalises within an hour.
These metabolic alterations are subtle but may influence weight management strategies in long‑term users.
4. Chronic Biological Effects – Long‑Term Exposure
4.1 Respiratory Health
4.1.1 Lung Function
Longitudinal cohort studies tracking adult vapers over 3–5 years have reported small but statistically significant declines in FEV1 and forced vital capacity (FVC), ranging from 20–30 mL per year—approximately half the rate observed in current cigarette smokers but greater than in never‑smokers. Importantly, the decline is dose‑dependent, correlating with total puff count and nicotine concentration.
4.1.2 Airway Inflammation
Bronchoalveolar lavage (BAL) samples from chronic vapers reveal:
- Elevated neutrophil percentages (+12 % relative to non‑vapers).
- Increased matrix metalloproteinase-9 (MMP‑9) activity, suggesting extracellular matrix remodeling.
- Up‑regulation of oxidative stress markers such as 8‑iso‑prostaglandin F2α.
These inflammatory signatures may predispose to chronic bronchitis‑like symptoms, albeit at lower prevalence than in smokers.
4.1.3 “Vaping‑Associated Lung Injury” (EVALI)
The 2019–2020 outbreak of EVALI highlighted the severe potential of certain additives—particularly vitamin E acetate—in illicit THC‑containing vape liquids. While commercially regulated nicotine vapes (including IGET and ALIBARBAR products) adhere to manufacturers’ quality standards that prohibit such solvents, the incident underscored the importance of product integrity and rigorous lab testing.
4.2 Cardiovascular Consequences
- Blood Pressure and Heart Rate: Chronic vapers exhibit modestly higher resting systolic blood pressure (+3–5 mmHg) compared to never‑vapers, though the effect is less pronounced than in smokers (+7–10 mmHg).
- Atherosclerotic Progression: In animal models, exposure to nicotine‑containing aerosol accelerates plaque formation in the aorta, mediated by endothelial dysfunction and inflammation. Human data are still emerging, with cross‑sectional analyses showing a 15 % increase in carotid intima‑media thickness among long‑term vapers versus controls.
- Thrombosis Risk: Platelet activation markers (P‑selectin, CD62P) are elevated after repeated vaping sessions, suggesting a hypercoagulable state that could increase the risk of thrombotic events over decades.
4.3 Neurological and Psychiatric Outcomes
- Addiction Potential: The nicotine delivered by vapes is bioequivalent to cigarettes, hence the addiction risk is comparable. Studies using the Fagerström Test for Nicotine Dependence (FTND) find mean scores of 4–5 among daily vapers, mirroring moderate dependence.
- Mood and Cognitive Effects: Some longitudinal surveys associate regular vaping with increased reports of anxiety and depressive symptoms, though causality remains uncertain due to confounding lifestyle factors.
- Neurodevelopmental Risks: In adolescent populations, nicotine exposure during brain maturation (12–18 years) has been linked to altered prefrontal cortex development, attention deficits, and increased susceptibility to other substance use disorders.
4.4 Oral and Dental Health
- Periodontal Disease: Nicotine reduces gingival blood flow, impairs fibroblast proliferation, and accelerates bone loss around teeth. Vapers exhibit higher plaque indices and greater pocket depths than non‑users, albeit less severe than smokers.
- Dry Mouth (Xerostomia): PG/VG aerosols can dehydrate oral tissues, leading to increased bacterial colonisation and higher caries risk. Salivary flow rates measured after a series of puffs decline by up to 20 % in the immediate post‑vaping period.
- Taste Alterations: Prolonged exposure to strong flavourings may blunt taste perception, potentially altering dietary habits.
4.5 Immune System Modulation
- Innate Immunity: Macrophage phagocytic capacity is reduced after chronic exposure to aerosol‑borne particulate matter, impairing pathogen clearance.
- Adaptive Immunity: Alterations in T‑cell subsets (decreased CD4⁺/CD8⁺ ratio) have been documented in long‑term vapers, hinting at subtle immunosuppression.
- Infection Susceptibility: Epidemiological data hint at a modestly higher incidence of upper respiratory infections among vapers, especially during winter months, though the absolute risk increase is small (≈ 1–2 % per year).
5. Comparative Perspective – Vaping vs. Combustible Cigarettes
| Parameter | Combustible Cigarettes | Vaping (Nicotine‑containing) |
|---|---|---|
| Tar & Polycyclic Aromatic Hydrocarbons (PAHs) | High (≈ 10 mg tar per cigarette) | Minimal; PAHs detected only in trace amounts |
| Carbon Monoxide (CO) | 10–30 ppm per puff | Negligible (≤ 0.01 ppm) |
| Formaldehyde (per 10 puffs) | 0.2–4 µg | 0.01–1 µg (depending on device power) |
| Nicotine delivery | 1–2 mg per cigarette | 0.5–2 mg per pod or disposable (device‑dependent) |
| Heavy‑metal exposure | Minimal (from tobacco) | Variable; coil‑derived metals may be present |
| Addiction potential | High | Comparable (if nicotine present) |
| Risk of lung cancer | Established (RR ≈ 20) | Not established; likely lower risk but insufficient long‑term data |
| Risk of cardiovascular disease | Strong association (HR ≈ 2–3) | Emerging evidence of modest increase |
The comparison indicates that vaping reduces exposure to many toxic combustion by‑products, yet it is not a benign activity. The reduction in carbon monoxide, tar, and PAHs is notable, but the presence of nicotine, flavour‑related aldehydes, and device‑derived metals preserves a non‑trivial health risk.
6. Secondhand Aerosol – What Non‑Users Inhale
Secondhand aerosol (SHA) contains diluted but detectable levels of nicotine, flavour chemicals, and ultrafine particles. Air‑sampling studies in indoor environments show:
- Particle concentrations ranging from 0.5 mg/m³ (low‑power pod) to 3 mg/m³ (high‑wattage sub‑ohm) during active vaping.
- Nicotine levels of 2–10 µg/m³, comparable to secondhand cigarette smoke in confined spaces.
- Formaldehyde and acetaldehyde at concentrations generally below occupational exposure limits but still measurable.
For vulnerable populations (children, pregnant women, individuals with asthma), SHA may exacerbate respiratory symptoms. Ventilation significantly mitigates exposure, but the safest approach remains to avoid vaping in shared indoor spaces.
7. Vulnerable Populations
7.1 Adolescents
- The adolescent brain is highly sensitive to nicotine’s effects on synaptic plasticity. Regular vaping from ages 13‑17 can lead to accelerated dependence, reduced impulse control, and heightened susceptibility to other drug use.
- Flavour appeal is a major driver of youth uptake. Sweet, fruit, and candy flavours mask the harshness of nicotine, creating a “gateway” scenario.
7‑12. Pregnant Women
- Nicotine crosses the placental barrier, impairing fetal lung development and increasing the risk of preterm birth and low birth weight.
- PG/VG aerosols can also trigger oxidative stress in the placenta, though the magnitude is lower than that of cigarette smoke.
7‑13. Individuals with Pre‑Existing Respiratory Disease
- Patients with COPD or asthma may experience worsened symptoms due to airway irritation and mucus hypersecretion. While vaping may be less harmful than smoking for these patients, clinicians often advise complete cessation of all inhaled nicotine products.
8. Harm‑Reduction & Smoking Cessation – Is Vaping a Viable Tool?
Public health agencies vary in their stance:
- United Kingdom (Public Health England): Views vaping as a risk‑reduced alternative for smokers who cannot quit by other means, estimating it to be 95 % less harmful than cigarettes.
- United States (CDC): Acknowledges vaping’s potential for cessation but cautions against youth uptake and emphasises the lack of long‑term safety data.
- Australia: Restricts nicotine‑containing e‑liquids to prescription‑only status, reflecting a more precautionary approach.
Clinical trials (e.g., the VAPOR‑1 study) have demonstrated quit rates of 30‑35 % at 12 weeks for smokers switched to high‑nicotine pod systems, compared with 10 % for nicotine‑replacement therapy (NRT) alone. These outcomes suggest that, when used as a cessation aid, vaping can be effective, provided the user:
- Selects a regulated product with transparent ingredient disclosures.
- Sets a clear quit plan, gradually reducing nicotine concentration.
- Monitors health with regular medical check‑ups.
9. Product Quality, Standards, and the Role of Reputable Brands
9.1 Quality Assurance in Australian Vapes
Australian vape retailers, including IGET & ALIBARBAR VAPE Australia, adhere to stringent quality controls:
- ISO 9001 certification for manufacturing processes.
- Compliance with Therapeutic Goods Administration (TGA) standards for nicotine concentration reporting.
- Use of TGO 110 (Australian Standard for E‑Cigarettes), which mandates limits on carbonyl emissions, heavy‑metal content, and requires batch‑wise chemical analysis.
These measures help ensure that the product delivered to the consumer matches the specifications advertised on the website (e.g., “up to 6000 puffs” for the IGET Bar Plus) and contain no undeclared substances.
9.2 Device Longevity and Safety Features
- Battery protection circuitry (over‑charge, short‑circuit, temperature cutoff) reduces fire risk.
- Child‑proof packaging mitigates accidental nicotine ingestion.
- Transparent e‑liquid labeling (PG/VG ratio, nicotine strength, flavour list) enables informed choice.
Consumers are encouraged to purchase from authorised distributors rather than unverified online marketplaces where counterfeit or adulterated products may bypass these safety nets.
10. Best Practices for Vapers – Minimising Potential Harm
| Action | Rationale |
|---|---|
| Choose low‑wattage devices (≤ 20 W) | Limits formation of carbonyls and metal emissions |
| Prefer higher VG ratios (≥ 70 % VG) | Produces larger droplets, reducing deep‑lung deposition of ultrafine particles |
| Use nicotine concentrations matching your dependence (e.g., 3 mg / ml for light smokers) | Prevents over‑consumption and facilitates tapering |
| Avoid “DIY” e‑liquids without laboratory testing | Reduces risk of contaminants like diacetyl or vitamin E acetate |
| Maintain coil hygiene (replace or clean weekly) | Prevents buildup of toxic degradation products |
| Limit flavour variety if you have respiratory sensitivities | Reduces exposure to potentially irritating flavour chemical mixtures |
| Vape in well‑ventilated areas | Minimises secondhand aerosol accumulation |
| Schedule regular medical reviews (lung function, blood pressure) | Early detection of any adverse changes |
By integrating these practices, a vaper can align more closely with the harm‑reduction potential that regulated nicotine delivery systems promise.
11. Frequently Asked Questions (FAQ)
1. Does vaping cause cancer?
Current epidemiological data do not show a definitive link between vaping and cancer, primarily because the latency period for cancer development exceeds the timeframe of large‑scale studies. However, vaping does expose users to known carcinogens (e.g., formaldehyde) at much lower levels than cigarettes. Long‑term surveillance is essential.
2. Can I vape without nicotine and be completely safe?
Nicotine‑free vapour eliminates addiction risk but does not erase exposure to PG/VG, flavour aldehydes, and metal particles. While the health risk profile is lower, individuals with asthma or chronic lung disease may still experience irritation.
3. How many puffs does a disposable vape like the IGET Bar Plus actually provide?
Manufacturers estimate puff counts based on a standard 4‑second puff at 10 mL /min airflow. The IGET Bar Plus is rated for up to 6000 puffs, which translates to roughly 35–40 mL of e‑liquid. Real‑world usage varies with puff length and device temperature.
4. Is it safe to vape while exercising?
Exercise increases respiratory demand and may enhance aerosol deposition deep into the lungs. Using nicotine during high‑intensity activity can elevate heart rate and blood pressure beyond typical resting levels, potentially stressing the cardiovascular system. Moderation is advised.
5. What is the difference between “pods” and “disposables”?
Pods are refillable or replaceable cartridge systems that connect to a reusable battery. Disposables are sealed, single‑use units with pre‑filled e‑liquid; once the battery or liquid is exhausted, the device is discarded. Both can deliver comparable nicotine doses, but disposables often have limited control over power settings.
6. Do vapes affect oral health?
Yes. Nicotine reduces blood flow to gums, while PG/VG can cause dry mouth, both contributing to periodontal disease and dental caries. Regular dental check‑ups are recommended for vapers.
7. Can vaping help me quit smoking?
Evidence suggests that for adult smokers who have failed other cessation methods, switching to a regulated nicotine vape can increase quit rates. It is most effective when combined with a structured quit plan and behavioral support.
12. Synthesis – What Do Vapes Do to You?
- Deliver nicotine efficiently, producing the same physiological dependence and cardiovascular stimulation as cigarettes.
- Expose the respiratory tract to a mixture of PG/VG aerosols, flavour chemicals, and low‑level thermal degradation products, leading to mild airway irritation, transient inflammation, and subtle declines in lung function over years of regular use.
- Alter vascular health modestly, with measurable but less severe endothelial dysfunction and blood pressure elevations compared with smoking.
- Impact immune defenses by reducing ciliary activity and altering macrophage function, which could increase susceptibility to infections.
- Generate secondhand aerosol that contains nicotine and ultrafine particles, potentially affecting by‑standers, especially in enclosed spaces.
- Present a reduced‑risk alternative for adult smokers seeking cessation, provided the product is regulated, the nicotine dose is appropriate, and usage is monitored.
- Carry unique risks for specific groups—youth, pregnant women, and people with chronic lung disease—who should avoid vaping or use it only under medical guidance.
In essence, vaping is not inert; it is an active pharmacological and toxicological process that delivers nicotine and a complex aerosol to the body. The net health impact is lower than that of combustible cigarettes but remains greater than abstinence. Choosing reputable brands that comply with strict Australian standards—such as the IGET and ALIBARBAR lines—helps minimise exposure to contaminants and ensures that product specifications (puff count, nicotine concentration, flavour composition) are reliable. Nonetheless, the safest path to optimal respiratory and cardiovascular health remains complete cessation of all nicotine‑containing inhalants.
13. Looking Ahead – Research Gaps and Future Directions
- Longitudinal Cohort Studies: Needed to ascertain the incidence of chronic diseases (e.g., COPD, coronary artery disease) among exclusive vapers over 20+ years.
- Standardised Emissions Testing: Development of a universal puff‑profile protocol that captures real‑world usage patterns across device generations.
- Flavor Toxicology: Systematic evaluation of chronic inhalation safety for the thousands of flavour compounds currently on the market.
- Biomarker Development: Identification of sensitive, non‑invasive markers (e.g., exhaled breath VOCs) that predict early lung injury in vapers.
- Policy Impact Analyses: Comparative studies of regulation models (prescription‑only vs. open market) on youth uptake and adult cessation success.
Continued investment in these research avenues will sharpen our understanding of what vapes truly do to you, enabling clinicians, regulators, and consumers to make evidence‑based decisions that balance harm reduction with public health protection.