question: How do lungs manage to heal themselves when someone has quit smoking after being a smoker and inhaling tar for multiple years?
comment: The tar is constantly being cleaned by cilia and mucous, so the cleaning part isn't really a major surprise. The body finally wins when the crap is no longer constantly added. The "healing" part though is not quite true. Lots of damage cannot be repaired. You won't regain elasticity to lungs that lost it, and the scar tissue won't ever get returned to normal. Sometimes it is too late when the smoker quits.
passages: Section::::Induced regeneration in humans.:Lung.
  
  Chronic obstructive pulmonary disease (COPD) is one of the most widespread health threats today. It affects 329 million people worldwide, which makes up nearly 5% of the global population. Having killed over 3 million people in 2012, COPD was the third greatest cause of death. Worse still is that due to increasing smoking rates and the aging populations in many countries, the number of deaths as a result of COPD and other chronic lung diseases is predicted to continue increasing. Therefore, developments in the lung’s capacity for regeneration is in high demand.
   In some cases the specific cause of the disease can be diagnosed, but in others the probable cause cannot be determined, a condition called idiopathic pulmonary fibrosis. There is no known cure for the scars and damage in the lung due to pulmonary fibrosis.
  
  Section::::Signs and symptoms.
  
  Symptoms of pulmonary fibrosis are mainly:
  
  BULLET::::- Shortness of breath, particularly with exertion
  
  BULLET::::- Chronic dry, hacking coughing
  
  BULLET::::- Fatigue and weakness
  
  BULLET::::- Chest discomfort including chest pain
  
  BULLET::::- Loss of appetite and rapid weight loss
   Section::::Clinical significance.:Lung cancer.
  
  Some of these cancers have environmental causes such as smoking. When a tobacco product is inhaled, the smoke paralyzes the cilia, causing mucus to enter the lungs. Frequent smoking, over time causes the cilia hairs to die and can no longer filter mucus. Tar from the smoke inhaled enters the lungs, turning the pink-coloured lungs black. The accumulation of this tar could eventually lead to lung cancer, or chronic obstructive pulmonary disease.
  
  Section::::Clinical significance.:Chronic obstructive pulmonary disease.
   The use of tobacco can also cause the damage of the skin's collagen. It causes the skin around the lips to loose collagen when it comes into contact with the smoke. It may also cause the vessels of blood to constrict and reduce the flow of blood. Due to this occurrence, collagen may become rigid and die off. When collagen is lost in large amounts it may cause wrinkles to emerge, dryness and may result to discolored skin. It has also been noted that tobacco also causes a slow or none collagen healing.
  
  Section::::Treatment the loss of collagen.
   It has been shown that bone marrow-derived cells could be the source of progenitor cells of multiple cell lineages, and a 2004 study suggested that one of these cell types was involved in lung regeneration. Therefore, a potential source of cells for lung regeneration has been found; however, due to advances in inducing stem cells and directing their differentiation, major progress in lung regeneration has consistently featured the use of patient-derived iPSCs and bioscaffolds.
   There is no cure for pulmonary siderosis or other interstitial lung diseases. Any damage is thus permanent. Symptoms can be treated.
  
  Section::::Prognosis.
  
  Outcome of pulmonary siderosis is often good if the inhalation of iron or rust dust is permanently avoided. However, welding has been associated with lung cancer, a condition which may have a poor outcome. Still, it is not known if pulmonary siderosis causes cancer in welders specifically or if these cases of cancer appear due to entirely different factors.
  
  Section::::See also.
  
  BULLET::::- Idiopathic pulmonary haemosiderosis - a disease caused by lung capillary bleeding
   On spirometry, as a restrictive lung disease, both the FEV1 (forced expiratory volume in 1 second) and FVC (forced vital capacity) are reduced so the FEV1/FVC ratio is normal or even increased in contrast to obstructive lung disease where this ratio is reduced. The values for residual volume and total lung capacity are generally decreased in restrictive lung disease.
  
  Section::::Treatment.
  
  Pulmonary fibrosis creates scar tissue. The scarring is permanent once it has developed. Slowing the progression and prevention depends on the underlying cause:
   When the appearance is caused by heat, the lesion is usually completely reversible within a few weeks if the smoking habit is stopped. This is the case even if the condition has been present for decades. Without stopping smoking, spontaneous remission of the lesion is unlikely. If the lesion persists despite stopping smoking, this is usually then considered to be a true leukoplakia rather than a reactionary keratotis, and may trigger the decision to carry out a biopsy to confirm the diagnosis. Since this condition almost always develops in the setting of long term heavy smoking, it usually indicates the need for regular observation for cancers associated with smoking, e.g. lung cancer.
   COPD is generally irreversible although lung function can partially recover if the patient stops smoking. Smoking cessation is an essential aspect of treatment. Pulmonary rehabilitation programmes involve intensive exercise training combined with education and are effective in improving shortness of breath. Severe emphysema has been treated with lung volume reduction surgery, with some success in carefully chosen cases. Lung transplantation is also performed for severe COPD in carefully chosen cases.
   One of the most known diseases caused by smoking is lung cancer. A few carcinogens commonly found in tar include benzene, acrylamide and acrylonitrile. Smoking exposes delicate cells inside the lungs directly to these compounds. This causes mutations in the DNA of the cells, which leads to cancer. According to the World Health Organization's report, "Tobacco Smoke and Involuntary Smoking", 90 percent of all cases of lung cancer are attributable to smoking.
  
  Section::::Long term effects.:Third-hand smoking and its effects.
   Apart from stopping the habit, no other treatment is indicated. Long term follow-up is usually carried out. Some recommend biopsy if the lesions persists more than 6 weeks after giving up smokeless tobacco use, or if the lesion undergoes a change in appearance (e.g. ulceration, thickening, color changes, especially to speckled white and red or entirely red). Surgical excision may be carried out if the lesion does not resolve.
  
  Section::::Prognosis.
   It is hypothesized that the initial or repetitive injury in IPF occurs to the lung cells, called alveolar epithelial cells (AECs, pneumocytes), which line the majority of the alveolar surface. When type I AECs are damaged or lost, it is thought that type II AECs undergo proliferation to cover the exposed basement membranes. In normal repair, the hyperplastic type II AECs die and the remaining cells spread and undergo a differentiation process to become type I AECs. Under pathologic conditions and in the presence of transforming growth factor beta (TGF-β), fibroblasts accumulate in these areas of damage and differentiate into myofibroblasts that secrete collagen and other proteins. In the past, it was thought that inflammation was the first event in initiating lung tissue scarring. Later findings showed that the development of fibroblastic foci precedes the accumulation of inflammatory cells and the consequent deposition of collagen. This pathogenetic model is indirectly supported by the clinical features of IPF, including an insidious onset over several years, relatively infrequent acute exacerbations, and failure to respond to immunosuppressive therapy. A number of therapies that target fibroblast activation or the synthesis of extracellular matrix are currently in early testing or are being considered for development.
   BULLET::::- Pulmonary fibrosis, fatal respiratory disease in which scars are formed in the lung tissues, leading to serious breathing problems. Scar formation, the accumulation of excess fibrous connective tissue (the process called fibrosis), leads to thickening of the walls, and causes reduced oxygen supply in the blood. As a consequence patients suffer from perpetual shortness of breath. There is no known cure for the scars and damage in the lung due to pulmonary fibrosis.
  
  BULLET::::- Postural Orthostatic Tachycardia Syndrome
  
  Section::::R.
   BULLET::::- Two pharmacological agents intended to prevent scarring in mild idiopathic fibrosis are pirfenidone, which reduced reductions in the 1-year rate of decline in FVC. Pirfenidone also reduced the decline in distances on the 6-minute walk test, but had no effect on respiratory symptoms. The second agent is nintedanib, which acts as antifibrotic, mediated through the inhibition of a variety of tyrosine kinase receptors (including platelet-derived growth factor, fibroblast growth factor, and vascular endothelial growth factor). A randomized clinical trial showed it reduced lung-function decline and acute exacerbations.
   Recent studies have suggested the involvement of immunological mechanisms in COPD. An increase in Th17 cells was observed in patients with COPD compared with current smokers without COPD and healthy subjects, and inverse correlations were found between Th17 cells with lung function. Gene expression profiling of bronchial brushings obtained from COPD patients also linked lung function to several Th17 signature genes such as SAA1, SAA2, SLC26A4 and LCN2. Animal studies have shown that cigarette smoke promotes pathogenic Th17 differentiation and induces emphysema, while blocking IL-17A using neutralizing antibody significantly decreased neutrophil recruitment and the pathological score of airway inflammation in tobacco-smoke-exposed mice.
   Usually this lesion is reversible if the tobacco habit is stopped completely, even after many years of use. In one report, 98% of lesions disappeared within 2 weeks of stopping tobacco use. The risk of the lesion developing into oral cancer (generally squamous cell carcinoma and its variant verrucous carcinoma) is relatively low. Indeed, veruccous carcinoma is sometimes term "snuff dipper's cancer". In most reported cases, malignant transformation has occurring in individuals with a very long history of chewing tobacco or who use dry snuff.
   Smoking leads to an increased risk of bone fractures, especially hip fractures. It also leads to slower wound-healing after surgery, and an increased rate of postoperative healing complication.
  
  Section::::Health effects of smoking.:Benefits.
  
  In addition to the numerous documented negative health effects of smoking, several types of "smoker's paradoxes" (cases where smoking appears to have specific beneficial effects) have been observed. Smoking may prevent Parkinson's disease.
  
  Section::::Mechanism.
  
  Section::::Mechanism.:Chemical carcinogens.
   Tar, when in the lungs, coats the cilia causing them to stop working and eventually die, causing conditions such as lung cancer as the toxic particles in tobacco smoke are no longer trapped by the cilia but enter the alveoli directly. Thus, the alveoli cannot come through with the process that is called ‘gas exchange’ which is the cause of rough breathing.
  
  Cannabis when burned also creates biological residue that is very similar to the "tar" created by tobacco smoke.
  
  Section::::Long term effects.
  
  Section::::Long term effects.:Lung cancer.
   Some smokers can achieve long-term smoking cessation through willpower alone. Smoking, however, is highly addictive, and many smokers need further support. The chance of quitting is improved with social support, engagement in a smoking cessation program, and the use of medications such as nicotine replacement therapy, bupropion, or varenicline. Combining smoking-cessation medication with behavioral therapy is more than twice as likely to be effective in helping people with COPD stop smoking, compared with behavioral therapy alone.
  
  Section::::Prevention.:Occupational health.
   Some types of chronic lung diseases are classified as restrictive lung disease, because of a restriction in the amount of lung tissue involved in respiration. These include pulmonary fibrosis which can occur when the lung is inflamed for a long period of time. Fibrosis in the lung replaces functioning lung tissue with fibrous connective tissue. This can be due to a large variety of occupational lung diseases such as Coalworker's pneumoconiosis, autoimmune diseases or more rarely to a reaction to medication.
   In fire curing, smoke from a low-burning fire on the barn floor permeates the leaves. This gives the leaves a distinctive smoky aroma and flavor. Fire curing takes three to ten weeks and produces a tobacco low in sugar and high in nicotine. Pipe tobacco, chewing tobacco, and snuff are fire cured.
   There is no cure or discovered treatments for Pneumoconiosis. Some patients are given oxygen to help with their breathing and are advised to stop smoking to prevent further decline in lung function. In the most extreme cases a lung transplant could be done to help prolong the patient's life expectancy. 
  
  Section::::Diagnosis.:Prevention of Pneumoconiosis.
   Stress can influence the course of Crohn's disease. Smoking has also been associated with the disease, and smokers with Crohn's are encouraged to explore smoking cessation programs. Smoking can not only make Crohn's disease worse in people who do it, but also increase the risk of recurrence after surgery. If a Crohn's disease patient who undergoes surgery does not quit smoking, the disease is likely to recur more aggressively.
  
  Section::::Helminthic therapy.
   Classic lung diseases are a complication of HIV/AIDS with emphysema being a source of disease. HIV is cited as a risk factor for the development of emphysema regardless of smoking status. HIV associated emphysema occurs over a much shorter time than that associated with smoking. It is thought that an understanding of the mechanisms that underlie the triggering of HIV associated emphysema may help in the understanding of the mechanisms of the development of smoking-related emphysema.
  
  Section::::By location.:Lungs.:Ritalin lung.
   Full recovery is common with proper treatment. Pulmonary laceration usually heals quickly after a chest tube is inserted and is usually not associated with major long-term problems. Pulmonary lacerations usually heal within three to five weeks, and lacerations filled with air will commonly heal within one to three weeks but on occasion take longer. However, the injury often takes weeks or months to heal, and the lung may be scarred. Small pulmonary lacerations frequently heal by themselves if material is removed from the pleural space, but surgery may be required for larger lacerations that do not heal properly or that bleed.
  
presuppositions: Once smokers quit smoking they are able to heal the damage they inflicted upon themselves during the time they smoked.
corrections: While the body is able to clean the effected areas, the body isn't really able to heal the areas as lots of damage can't be repaired or healed. 
raw_presuppositions: Once smokers quit smoking they are able to heal the damage they inflicted upon themselves during the time they smoked. Lungs heal themselves after smokers quit smoking.
raw_corrections: While the body is able to clean the effected areas, the body isn't really able to heal the areas as lots of damage can't be repaired or healed.  Lungs have permanent damage that cannot be healed even after smokers quit smoking.