When David Lloyd, 62, was told he had terminal lung cancer in January 2006, his wife, Annette Edwards, contacted their bank, the Halifax, to let them know of his predicament and that he would no longer be able to work. They applied for a payout on an insurance policy, and for state benefits, but while they waited for the money to arrive they went overdrawn.

Lloyd and Edwards, who had been a Halifax account holder for 15 years, claim the debt is around £800, but the bank says it is £4,000. The bank and its agents telephoned the couple 762 times over seven months in what they say is aggressive pursuit of the debt in calls made “morning, noon and night”.

Lloyd, who worked for the Institute of Civil Engineers until his cancer diagnosis, has developed a phobia of telephones and suffers from anxiety and depression. Edwards says the couple feel dehumanised because their situation was ignored.

In May, the couple obtained a court undertaking at Leeds county court ensuring the Halifax would not contact them. Despite the undertaking, a letter from the Halifax arrived last Wednesday at the couple’s home in Sale, Greater Manchester.

At Manchester Justice Centre yesterday, the Bank of Scotland, the parent company of the Halifax, appeared before a judge in a contempt of court hearing instigated by the couple. The bank’s barrister, James Counsell, said: “The bank issues its wholehearted fulsome apology for the error and the serious breach of the undertaking which it very much regrets.”

He said the bank had taken extensive steps to stop the correspondence and there had been no telephone calls since summer 2007. The bank paid £1,150 costs to the claimants and made a new undertaking to write to HBOS and ask its subsidaries not to contact the claimants using the Halifax logo.

The couple also claim that their daughter, Stefanie Moore, 29, received 60 to 100 phone calls and two text messages, yet wasn’t even a customer.

It is doubtful that Lloyd, who has not been able to eat for 48 hours, will be alive when the harassment case comes to a full hearing in February. Edwards says of her husband: “He is prepared to put his head above the parapet because he doesn’t want other people to go through what he has had to go through.”

Money | The Guardian

Chronic obstructive pulmonary disease (COPD) is often caused by smoking and kills about 30,000 UK residents a year.

US scientists found that sulforapane increases the activity of the NRF2 gene in human lung cells which protects cells from damage caused by toxins.

The same broccoli compound was recently found to be protective against damage to blood vessels caused by diabetes.

Brassica vegetables such as broccoli have also been linked to a lower risk of heart attacks and strokes.

Cell pollutants

In the latest study, a team from Johns Hopkins School of Medicine found significantly lower activity of the NRF2 gene in smokers with advanced COPD.

Writing in the American Journal of Respiratory and Critical Care Medicine, they said the gene is responsible for turning on several mechanisms for removing toxins and pollutants which can damage cells.

Previous studies in mice had shown that disrupting the NRF2 gene caused early onset severe emphysema – one of the conditions suffered by COPD patients.

Increasing the activity of NRF2 may lead to useful treatments for preventing the progression of COPD, the researchers said.

In the study, they showed that sulforapane was able to restore reduced levels of NRF2 in cells exposed to cigarette smoke.

“Future studies should target NRF2 as a novel strategy to increase antioxidant protection in the lungs and test its ability to improve lung function in people with COPD,” said study leader Dr Shyam Biswal.

A spokeswoman for the British Lung Foundation said: “This is an important study for the 3 million people in the UK with COPD because of its findings about the imbalance of oxidants and antioxidants in the lungs.

“We know broccoli naturally contains important compounds but studies so far have taken place in the test tube and further research is needed to find if you can produce the same effect in humans.”

They found that male nonsmokers were about 25 percent more likely to die from lung cancer than women nonsmokers even though they developed the disease at similar rates.

Men who had never smoked had a 1.1 percent risk of dying from lung cancer, compared to 0.8 percent for the women, the study found. This compares to about 22 percent among men who smoke and 12 percent of women who smoke.

The study in North America, Europe and Asia was the largest ever done on nonsmokers and lung cancer.

“Lung cancer is a significant public health and medical problem even beyond the overwhelming disease burden caused by tobacco smoking,” Dr. Michael Thun of the American Cancer Society, who led the study, said in a telephone interview.

Thun said it is unclear why male nonsmokers are more likely to die from lung cancer than women.

“That’s an interesting and unresolved question,” he said.

In this study, a person was considered a lifelong nonsmoker if he or she reported never smoking, regardless of exposure to secondhand smoke, Thun’s team reported in the Public Library of Science journal PLoS Medicine

The study also indicated that death rates among lifelong nonsmokers have remained stable over the past several decades.

Factors other than smoking are estimated to account for 10 to 15 percent of lung cancer deaths. In the United States, for example, that translates to between 16,000 and 24,000 of the more than 161,000 lung cancer deaths forecast this year.

Lung cancer is the leading cause of cancer death in men and the second leading cause of cancer death among women worldwide, according to the American Cancer Society, with about 975,000 men and 376,000 women forecast to die annually.

Risk factors unrelated to smoking include workplace or environmental exposures to radon and asbestos, certain metals such as chromium, cadmium and arsenic, some chemicals, radiation, air pollution, coal smoke or indoor emissions from burning certain fuels, the American Cancer Society said.

The findings were based on combined data from 13 studies done from 1960 to 2004.