Smoking and Lung Cancer

Introduction

Tobacco smoking is the dominant, preventable cause of lung cancer. The relationship is dose‑dependent and modified by age at initiation, intensity, and duration. Although risk declines after cessation, it never returns fully to that of a never‑smoker. Secondhand smoke also increases lung cancer risk, underscoring the importance of smoke‑free environments.

Epidemiology and Risk Quantification

• At a population level, the majority of lung cancer deaths are attributable to cigarette smoking.
• Risk rises with cumulative exposure, commonly expressed as pack‑years (packs per day × years smoked). Higher intensity and earlier initiation further increase risk.
• Time since quitting matters: substantial risk reduction is seen within 5–10 years of cessation, with continued decline thereafter, though not to baseline never‑smoker risk.
• Other tobacco forms (cigars, pipes, waterpipes) and high‑temperature combustion products also raise risk.

Histologic Patterns

• Cigarette smoking is strongly associated with squamous cell carcinoma and small‑cell lung cancer (SCLC).
• Adenocarcinoma is now the most common histology overall and occurs in both smokers and never‑smokers; secondhand smoke exposure is linked to increased adenocarcinoma risk.

Biological Mechanisms of Carcinogenesis

• Tobacco smoke contains thousands of chemicals, including polycyclic aromatic hydrocarbons (PAHs), tobacco‑specific nitrosamines (e.g., NNK), aldehydes, metals, and oxidants.
• Procarcinogens are metabolically activated to DNA‑reactive intermediates that form DNA adducts, leading to characteristic mutational signatures when unrepaired.
• Chronic exposure promotes airway inflammation, oxidative stress, and field cancerization (widespread epithelial injury and clonal expansion), increasing the likelihood of multifocal neoplasia.

Secondhand and Thirdhand Smoke

• Secondhand smoke (sidestream + exhaled mainstream) contains many of the same carcinogens and is associated with elevated lung cancer risk in never‑smokers, particularly with prolonged household or workplace exposure.
• Thirdhand smoke (residual nicotine and other chemicals on surfaces) may re‑emit or react to form carcinogenic compounds; minimizing indoor smoking prevents accumulation.

Clinical Assessment: The Three “Rs”

• Record: document pack‑years, age of initiation, quit attempts, prior pharmacotherapy, and secondhand exposures.
• Risks: assess comorbid COPD, cardiovascular disease, and occupational exposures (asbestos, radon) that synergize with smoking.
• Readiness: determine willingness to quit and barriers; offer intensive support at every visit (Ask–Advise–Assess–Assist–Arrange).

Screening for Lung Cancer

Low‑dose computed tomography (LDCT) reduces lung cancer mortality in high‑risk populations.

• Typical eligibility (adapt to local guidelines): adults aged 50–80 years with ≥20 pack‑years who currently smoke or quit within the past 15 years.
• Frequency: annual LDCT while eligibility criteria are met; discontinue if life expectancy is limited or the patient would not pursue curative treatment.
• Program elements: shared decision‑making, smoking cessation support, standardized reporting (e.g., Lung‑RADS), and timely follow‑up of positive findings.

Smoking Cessation: What Works

Combining behavioral support with pharmacotherapy yields the highest quit rates.

First‑line Pharmacotherapies

• Varenicline: partial nicotinic agonist; start 1 week before quit date; monitor for nausea and vivid dreams.
• Bupropion SR: noradrenergic/dopaminergic agent; begin 1–2 weeks before quit date; avoid in seizure disorder.
• Nicotine Replacement Therapy (NRT): combination therapy (patch for baseline + short‑acting form for cravings) is superior to single‑agent use.

Notes
– Select agents based on patient preference, contraindications, prior response, and access.
– E‑cigarettes are not first‑line cessation therapy; evidence for long‑term safety and sustained abstinence remains evolving.

Behavioral Strategies

• Set a quit date; identify triggers; develop coping strategies; provide frequent follow‑up (in person, phone, or digital).
• Offer referral to counseling services, quitlines, and app‑based programs; engage family support and smoke‑free home policies.

Special Populations

• Pregnancy: prioritize behavioral counseling; NRT may be considered when benefits outweigh risks under clinical supervision.
• Adolescents/young adults: focus on prevention and early intervention; address vaping explicitly.
• COPD or cardiovascular disease: cessation confers rapid clinical benefits (improved FEV1 decline trajectory; reduced MI risk) and reduces perioperative risk.

Counseling Talking Points for Patients

• “Every attempt counts”—multiple tries are typical before sustained abstinence.
• “Cutting down helps, quitting helps most”—risk falls soon after cessation and continues to decline.
• “Screening complements, not replaces, quitting”—LDCT identifies cancer earlier but does not prevent it.

Key Takeaways

• Smoking is the principal modifiable driver of lung cancer; risk is dose‑ and duration‑dependent and declines with cessation.
• Secondhand smoke increases risk in never‑smokers; smoke‑free environments are essential.
• Annual LDCT screening is recommended for eligible high‑risk individuals and should be delivered within structured programs.
• Combine pharmacotherapy with behavioral support to maximize quit success.