Young smokers risk greater genetic damage

Scientists are not sure why smokers who start young are susceptible to more long-term damage, but they think it could be linked to the impact of smoking at an age when the lungs are still developing.

Alternatively, it might be because of the cumulative effect of cancer-causing chemicals on lung tissue.

Changes to genetic material

The study appears in the Journal of the (US) National Cancer Institute. It was led by Dr John Wiencke, associate professor of epidemiology at the University of California at San Francisco.

It examined DNA damage in former smokers who have lung cancer.

Dr Wiencke said: "Our finding suggests that young smokers incur more severe or persistent DNA damage than adult smokers do.

"Smoking during adolescence may produce physiological changes that lead to persistent increased DNA damage, or young smokers may be markedly susceptible to DNA damage formation and have higher burdens of damage after they quit smoking than those who started smoking later in life."

Damage affects all smokers

All smokers suffer damage to their DNA, but once they quit they experience some level of repair.

However, the researchers found that less repair - or less successful repair - occurs in people who smoked as adolescents.

Their study aimed to clarify what links existed between lung cancer and the known risk factors for the disease, including the number of years ex-smokers smoked and the amount they smoked.

Dr Wiencke said: "The ability to identify those current and former smokers with the highest risk of developing cancer has substantial preventive implications."

The damaged segments of DNA, known as DNA adducts, are parts of genes that are known to be caused by exposure to carcinogens.

They are believed to be one of the first steps towards the formation of tumours.

Cancer-causing chemicals

Carcinogens known as polynuclear aromatic hydrocarbons (PAHs) attach themselves to genes and are strongly suspected of initiating tumour formation.

The researchers examined DNA adduct levels in non-tumourous lung tissue samples from 143 lung cancer patients and blood samples from 57 of these patients.

Fifty-seven of the patients were current smokers, 79 were ex-smokers and seven had never smoked.

In those who had never smoked, there were low DNA adduct levels in the lung tissue.

DNA adduct levels were eight times higher in current smokers and 3.5 times higher in ex-smokers.

Risk varies with consumption

For current smokers, the number of cigarettes smoked per day was the variable most closely related to high adduct levels.

But in former smokers, it was the age at which the subject started smoking that most seemed to influence DNA adduct levels.

The highest levels of damage were observed in those who started between the ages of nine and 12.

The researchers hope the findings will spur others to investigate how precisely DNA adduct levels interact with the various factors suspected of contributing to susceptibility to lung cancer.

They say such factors include smoking history, genetics, diet and occupation and now, in light of their own findings, perhaps the age at which smoking starts.

Dr Wiencke said: "To our knowledge, no other study has considered the age at which smoking was initiated as a potential predictor of tobacco smoke-related DNA damage in former smokers."