Smoke, or any partially burnt organic matter, is carcinogenic (cancer-causing). The damage a continuing smoker does to their lungs can take up to 20 years before its physical manifestation in lung cancer. Women began smoking later than men, so the rise in death rate amongst women did not appear until later. The male lung cancer death rate decreased in 1975 — roughly 20 years after the fall in cigarette consumption in men. A fall in consumption in women also began in 1975 but by 1991 had not manifested in a decrease in lung cancer related mortalities amongst women.

 

Smoke contains several carcinogenic pyrolysis products, particularly the polynuclear aromatic hydrocarbons (PAH), which are toxicated to mutagenic epoxides. The first PAH to be
identified as a carcinogen in tobacco smoke was benzopyrene, which been shown to permanently attach to nuclear DNA, which may either kill the cell or cause a genetic mutation. If the
mutation inhibits programmed cell death, the cell can survive to become a cancer cell.

 

The carcinogenity of tobacco smoke is not explained by nicotine per se, which is not carcinogenic or mutagenic. However, it inhibits apoptosis, therefore accelerating existing cancers. Also, NNK, a nicotine derivative converted from nicotine, can be carcinogenic.

 

Lung dysfunction

 

Chronic obstructive pulmonary disease (COPD) caused by smoking, known as tobacco disease, is a permanent, incurable reduction of pulmonary capacity characterized by shortness of breath, wheezing, persistent cough with sputum, and damage to the lungs, including emphysema and chronic bronchitis.