Black lung disease also known as Coal workers' pneumoconiosis, is a legal term describing a preventable, occupational lung disease that is contracted by prolonged breathing of coal mine dust. There are two forms: simple CWP and complicated CWP, which also involves progressive massive fibrosis (PMF). Coal dust provides a sufficient stimulus for the macrophage to release various products, including enzymes, cytokines, oxygen radicals, and fibroblast growth factors, which are important in the inflammation and fibrosis of CWP. The centres of dense lesions may become necrotic due to ischemia, leading to large cavities within the lung. There is no proven effective treatment for Black lung disease, although complications can be treated. Avoiding further exposure to the dust is the only one of treatment. Black lung disease can be prevented by controlling dust and having good ventilation in the workplace. In the late 1970s, about 35 percent of miners acquired CWP, but stricter safety measures caused a decline in the number of cases until the late 1990s, when the rate reached 7 percent. However, by the mid-2000s, the rate had increased to more then 10 percent again. The bulk of all deaths from CWP are in Pennsylvania, Kentucky, Virginia and West Virginia, with Pennsylvania accounting for most of them. Of the men in the Big Branch disaster, 17 of 24 had some form of the disease, including men as young as 25. Five of the men found to have CWP in those autopsies had been involved in mining for less than 10 years. Black lung normally only affects those who have been mining for decades. Work to investigate the relationship between respirable dust exposure and coal worker's pneumoconiosis was carried out in Britain by the Institute of Occupational Medicine. This research was known as the Pneumoconiosis Field Research (PFR).