Smoking is a global public health crisis driven by highly addictive nicotine. These chemical hijacks the brain's reward system, fueling intense cravings and making cessation extremely difficult. The outcome is devastating: tobacco kills up to half its regular users, causing over 7 million annual deaths, which tragically includes 1.6 million non-smokers exposed to second-hand smoke. The toxicity stems from the smoke's staggering chemical complexity, featuring over 7,000 constituents. Crucially, sidestream smoke from the burning tip comprises 85% of the mixture and carries a higher concentration of toxic gases than inhaled mainstream smoke. The core mechanism of damage is a destructive cycle of oxidative stress and chronic inflammation. Smoking triggers an excessive production of free radicals that overwhelm the body's defenses, severely damaging cellular molecules like DNA and proteins. This pathological state immediately induces proinflammatory effects, leading to chronic, destructive inflammation. This cumulative damage is the foundation for smoking's broad disease spectrum. Tobacco use is the primary cause of lung cancer and is definitively linked to 25% of all global cancer deaths. It is also a major risk factor for heart disease, stroke, COPD, and Type 2 Diabetes. This addictive practice significantly drives global mortality and imposes massive economic and healthcare burdens worldwide. This review aim to elucidate the pathological mechanisms by which cigarette smoke toxicity is mediated through oxidative stress and chronic inflammation, and to discuss the resultant range of associated diseases and their public health impact.