Acute exacerbations can be partially prevented. Some infections can be prevented by vaccination against pathogens such as influenza and "Streptococcus pneumoniae". Regular medication use can prevent some COPD exacerbations; long acting beta-adrenoceptor agonists (LABAs), long-acting anticholinergics, inhaled corticosteroids and low-dose theophylline have all been shown to reduce the frequency of COPD exacerbations. Other methods of prevention include:

- Smoking cessation and avoiding dust, passive smoking, and other inhaled irritants

- Yearly influenza and 5-year pneumococcal vaccinations

- Regular exercise, appropriate rest, and healthy nutrition

- Avoiding people currently infected with e.g. cold and influenza

- Maintaining good fluid intake and humidifying the home, in order to help reduce the formation of thick sputum and chest congestion.

Oxygen therapy should be initiated if there is significantly low blood oxygen. High flow oxygen may be harmful in those with an acute exacerbation of COPD. In the prehospital environment those given high flow O rather than titrating their O saturations to 88% to 92% had worse outcomes.

Prevention is by not smoking and avoiding other lung irritants. Frequent hand washing may also be protective. Treatment of acute bronchitis typically involves rest, paracetamol (acetaminophen), and NSAIDs to help with the fever. Cough medicine has little support for its use and is not recommended in children less than six years of age. There is tentative evidence that salbutamol may be useful in those with wheezing; however, it may result in nervousness and tremors. Antibiotics should generally not be used. An exception is when acute bronchitis is due to pertussis. Tentative evidence supports honey and pelargonium to help with symptoms. Getting plenty of rest and fluids is also often recommended.

Evidence suggests that the decline in lung function observed in chronic bronchitis may be slowed with smoking cessation. Chronic bronchitis is treated symptomatically and may be treated in a nonpharmacologic manner or with pharmacologic therapeutic agents. Typical nonpharmacologic approaches to the management of COPD including bronchitis may include: pulmonary rehabilitation, lung volume reduction surgery, and lung transplantation. Inflammation and edema of the respiratory epithelium may be reduced with inhaled corticosteroids. Wheezing and shortness of breath can be treated by reducing bronchospasm (reversible narrowing of smaller bronchi due to constriction of the smooth muscle) with bronchodilators such as inhaled long acting β-adrenergic receptor agonists (e.g., salmeterol) and inhaled anticholinergics such as ipratropium bromide or tiotropium bromide. Mucolytics may have a small therapeutic effect on acute exacerbations of chronic bronchitis. Supplemental oxygen is used to treat hypoxemia (too little oxygen in the blood) and has been shown to reduce mortality in chronic bronchitis patients. Oxygen supplementation can result in decreased respiratory drive, leading to increased blood levels of carbon dioxide (hypercapnia) and subsequent respiratory acidosis.

Interventions include intravenous (IV) medications (e.g. magnesium sulfate), aerosolized medications to dilate the airways (bronchodilation) (e.g., albuterol or ipratropium bromide/salbutamol), and positive-pressure therapy, including mechanical ventilation. Multiple therapies may be used simultaneously to rapidly reverse the effects of status asthmaticus and reduce permanent damage of the airways. Intravenous corticosteroids and methylxanthines are often given. If the person with a severe asthma exacerbation is on a mechanical ventilator, certain sedating medications such as ketamine or propofol, have bronchodilating properties. According to a new randomized control trial ketamine and aminophylline are also effective in children with acute asthma who responds poorly to standard therapy.

Infliximab, an immune-suppressing antibody, has been tested in COPD; there was a possibility of harm with no evidence of benefit.

Roflumilast, cilomilast, and phosphodiesterase 4 inhibitors act as a bronchodilator and as an anti-inflammatory. They show promise in decreasing the rate of exacerbations, but do not appear to change a persons quality of life. Roflumilast and cilomilast may be associated with side effects such as gastrointestinal issues and weight loss. Sleep disturbances and mood disturbances related to roflumilast have also been reported.

Several new long-acting agents are under development. Treatment with stem cells is under study. While there is tentative data that it is safe, and the animal data is promising, there is little human data as of 2017. The human data has shown poor results.

A procedure known as target lung denervation, which involves decreasing the parasympathetic nervous system supply of the lungs, is being studied but does not have sufficient data to determine its use. The effectiveness of alpha-1 antitrypsin augmentation treatment for people who have alpha-1 antitrypsin deficiency is unclear.

Research continues into the use of telehealthcare to treat people with COPD when they experience episodes of shortness of breath; treating people remotely may reduce the number of emergency-room visits and improve the person's quality of life.

Status asthmaticus is slightly more common in males and is more common among people of African and Hispanic origin. The gene locus glutathione dependent S-nitrosoglutathione (GSNOR) has been suggested as one possible correlation to development of status asthmaticus.

Supplemental oxygen is recommended in those with low oxygen levels at rest (a partial pressure of oxygen less than 50–55 mmHg or oxygen saturations of less than 88%). In this group of people, it decreases the risk of heart failure and death if used 15 hours per day and may improve people's ability to exercise. In those with normal or mildly low oxygen levels, oxygen supplementation may improve shortness of breath when given during exercise, but may not improve breathlessness during normal daily activities or affect the quality of life. A risk of fires and little benefit exist when those on oxygen continue to smoke. In this situation, some recommend against its use. During acute exacerbations, many require oxygen therapy; the use of high concentrations of oxygen without taking into account a person's oxygen saturations may lead to increased levels of carbon dioxide and worsened outcomes. In those at high risk of high carbon dioxide levels, oxygen saturations of 88–92% are recommended, while for those without this risk, recommended levels are 94–98%.

In order to prevent bronchiectasis, children should be immunized against measles, pertussis, pneumonia, and other acute respiratory infections of childhood. While smoking has not been found to be a direct cause of bronchiectasis, it is certainly an irritant that all patients should avoid in order to prevent the development of infections (such as bronchitis) and further complications.

Treatments to slow down the progression of this chronic disease include keeping bronchial airways clear and secretions weakened through various forms of pneumotherapy. Aggressively treating bronchial infections with antibiotics to prevent the destructive cycle of infection, damage to bronchial tubes, and more infection is also standard treatment. Regular vaccination against pneumonia, influenza and pertussis are generally advised. A healthy body mass index and regular doctor visits may have beneficial effects on the prevention of progressing bronchiectasis. The presence of hypoxemia, hypercapnia, dyspnea level and radiographic extent can greatly affect the mortality rate from this disease.

Underlying disease must be controlled to prevent exacerbation and worsening of ABPA, and in most patients this consists of managing their asthma or CF. Any other co-morbidities, such as sinusitis or rhinitis, should also be addressed.

Hypersensitivity mechanisms, as described above, contribute to progression of the disease over time and, when left untreated, result in extensive fibrosis of lung tissue. In order to reduce this, corticosteroid therapy is the mainstay of treatment (for example with prednisone); however, studies involving corticosteroids in ABPA are limited by small cohorts and are often not double-blinded. Despite this, there is evidence that acute-onset ABPA is improved by corticosteroid treatment as it reduces episodes of consolidation. There are challenges involved in long-term therapy with corticosteroids—which can induce severe immune dysfunction when used chronically, as well as metabolic disorders—and approaches have been developed to manage ABPA alongside potential adverse effects from corticosteroids.

The most commonly described technique, known as sparing, involves using an antifungal agent to clear spores from airways adjacent to corticosteroid therapy. The antifungal aspect aims to reduce fungal causes of bronchial inflammation, whilst also minimising the dose of corticosteroid required to reduce the immune system’s input to disease progression. The strongest evidence (double-blinded, randomized, placebo-controlled trials) is for itraconazole twice daily for four months, which resulted in significant clinical improvement compared to placebo, and was mirrored in CF patients. Using itraconazole appears to outweigh the risk from long-term and high-dose prednisone. Newer triazole drugs—such as posaconazole or voriconazole—have not yet been studied in-depth through clinical trials in this context.

Whilst the benefits of using corticosteroids in the short term are notable, and improve quality of life scores, there are cases of ABPA converting to invasive aspergillosis whilst undergoing corticosteroid treatment. Furthermore, in concurrent use with itraconazole, there is potential for drug interaction and the induction of Cushing syndrome in rare instances. Metabolic disorders, such as diabetes mellitus and osteoporosis, can also be induced.

In order to mitigate these risks, corticosteroid doses are decreased biweekly assuming no further progression of disease after each reduction. When no exacerbations from the disease are seen within three months after discontinuing corticosteroids, the patient is considered to be in complete remission. The exception to this rule is patients who are diagnosed with advanced ABPA; in this case removing corticosteroids almost always results in exacerbation and these patients are continued on low-dose corticosteroids (preferably on an alternate-day schedule).

Serum IgE can be used to guide treatment, and levels are checked every 6–8 week after steroid treatment commences, followed by every 8 weeks for one year. This allows for determination of baseline IgE levels, though it’s important to note that most patients do not entirely reduce IgE levels to baseline. Chest X-ray or CT scans are performed after 1–2 months of treatment to ensure infiltrates are resolving.

Treatment of bronchiectasis includes controlling infections and bronchial secretions, relieving airway obstructions, removal of affected portions of lung by surgical removal or artery embolization and preventing complications. The prolonged use of antibiotics prevents detrimental infections and decreases hospitalizations in people with bronchiectasis, but also increases the risk of people becoming infected with drug-resistant bacteria.

Other treatment options include eliminating accumulated fluid with postural drainage and chest physiotherapy. Postural drainage techniques, aided by physiotherapists and respiratory therapists, are an important mainstay of treatment. Airway clearance techniques appear useful.

Surgery may also be used to treat localized bronchiectasis, removing obstructions that could cause progression of the disease.

Inhaled steroid therapy that is consistently adhered to can reduce sputum production and decrease airway constriction over a period of time, and help prevent progression of bronchiectasis. This is not recommended for routine use in children. One commonly used therapy is beclometasone dipropionate.

Although not approved for use in any country, mannitol dry inhalation powder, has been granted orphan drug status by the FDA for use in people with bronchiectasis and with cystic fibrosis.

Reactive airways dysfunction syndrome (RADS) is a term proposed by Stuart M. Brooks and colleagues in 1985

It can also manifest in adults with exposure to high levels of chlorine, ammonia, acetic acid or sulphur dioxide, creating symptoms like asthma. These symptoms can vary from mild to fatal, and can even create long-term airway damage depending on the amount of exposure and the concentration of chlorine. Some experts classify RADS as occupational asthma. Those with exposure to highly irritating substances should receive treatment to mitigate harmful effects.

The evidence for the effectiveness of measures to prevent the development of asthma is weak. The World Health Organization recommends decreasing risk factors such as tobacco smoke, air pollution, and the number of lower respiratory infections. Other efforts that show promise include: limiting smoke exposure in utero, breastfeeding, and increased exposure to daycare or large families, but none are well supported enough to be recommended for this indication.

Early pet exposure may be useful. Results from exposure to pets at other times are inconclusive and it is only recommended that pets be removed from the home if a person has allergic symptoms to said pet.

Dietary restrictions during pregnancy or when breast feeding have not been found to be effective and thus are not recommended. Reducing or eliminating compounds known to sensitive people from the work place may be effective. It is not clear if annual influenza vaccinations affects the risk of exacerbations. Immunization; however, is recommended by the World Health Organization. Smoking bans are effective in decreasing exacerbations of asthma.

The neurotransmitter acetylcholine is known to decrease sympathetic response by slowing the heart rate and constricting the smooth muscle tissue. Ongoing research and successful clinical trials have shown that agents such as diphenhydramine, atropine and Ipratropium bromide (all of which act as receptor antagonists of muscarinic acetylcholine receptors) are effective for treating asthma and COPD-related symptoms .

Macrolide antibiotics, such as erythromycin, are an effective treatment for DPB when taken regularly over an extended period of time. Clarithromycin or roxithromycin are also commonly used. The successful results of macrolides in DPB and similar lung diseases stems from managing certain symptoms through immunomodulation (adjusting the immune response), which can be achieved by taking the antibiotics in low doses. Treatment consists of daily oral administration of erythromycin for two to three years, an extended period that has been shown to dramatically improve the effects of DPB. This is apparent when an individual undergoing treatment for DPB, among a number of disease-related remission criteria, has a normal neutrophil count detected in BAL fluid, and blood gas (an arterial blood test that measures the amount of oxygen and carbon dioxide in the blood) readings show that free oxygen in the blood is within the normal range. Allowing a temporary break from erythromycin therapy in these instances has been suggested, to reduce the formation of macrolide-resistant "P. aeruginosa". However, DPB symptoms usually return, and treatment would need to be resumed. Although highly effective, erythromycin may not prove successful in all individuals with the disease, particularly if macrolide-resistant "P. aeruginosa" is present or previously untreated DPB has progressed to the point where respiratory failure is occurring.

With erythromycin therapy in DPB, great reduction in bronchiolar inflammation and damage is achieved through suppression of not only neutrophil proliferation, but also lymphocyte activity and obstructive mucus and water secretions in airways. The antibiotic effects of macrolides are not involved in their beneficial effects toward reducing inflammation in DPB. This is evident because the treatment dosage is much too low to fight infection, and in DPB cases with the occurrence of macrolide-resistant "P. aeruginosa", erythromycin therapy still reduces inflammation.

A number of factors are involved in suppression of inflammation by erythromycin and other macrolides. They are especially effective at inhibiting the proliferation of neutrophils, by diminishing the ability of interleukin 8 and leukotriene B4 to attract them. Macrolides also reduce the efficiency of adhesion molecules that allow neutrophils to stick to bronchiolar tissue linings. Mucus production in the airways is a major culprit in the morbidity and mortality of DPB and other respiratory diseases. The significant reduction of inflammation in DPB attributed to erythromycin therapy also helps to inhibit the production of excess mucus.

There is ongoing research on the treatment of ARDS by interferon (IFN) beta-1a to aid in preventing leakage of vascular beds. Traumakine (FP-1201-lyo), is a recombinant human IFN beta-1a drug developed by Faron pharmaceuticals, is undergoing international phase-III clinical trials after an open-label, early-phase trial showed a 81% reduction-in-odds of 28-day mortality in ICU patients with ARDS. The drug is known to function by enhancing lung CD73 expression and increasing production of anti-inflammatory adenosine, such that vascular leaking and escalation of inflammation are reduced.

Avoidance of triggers is a key component of improving control and preventing attacks. The most common triggers include allergens, smoke (tobacco and other), air pollution, non selective beta-blockers, and sulfite-containing foods. Cigarette smoking and second-hand smoke (passive smoke) may reduce the effectiveness of medications such as corticosteroids. Laws that limit smoking decrease the number of people hospitalized for asthma. Dust mite control measures, including air filtration, chemicals to kill mites, vacuuming, mattress covers and others methods had no effect on asthma symptoms. Overall, exercise is beneficial in people with stable asthma. Yoga could provide small improvements in quality of life and symptoms in people with asthma.

Beta2-adrenergic agonists are recommended for bronchospasm.

- Short acting (SABA)

- Terbutaline

- Salbutamol

- Levosalbutamol

- Long acting (LABA)

- Formoterol

- Salmeterol

- Others

- Dopamine

- Norepinephrine

- Epinephrine

Along with the measure above, systemic immediate release opioids are beneficial in emergently reducing the symptom of shortness of breath due to both cancer and non cancer causes; long-acting/sustained-release opioids are also used to prevent/continue treatment of dyspnea in palliative setting. Pulmonary rehabilitation may alleviate symptoms in some people, such as those with COPD, but will not cure the underlying disease. There is a lack of evidence to recommend midazolam, nebulised opioids, the use of gas mixtures, or cognitive-behavioral therapy.

Untreated DPB leads to bronchiectasis, respiratory failure, and death. A journal report from 1983 indicated that untreated DPB had a five-year survival rate of 62.1%, while the 10-year survival rate was 33.2%. With erythromycin treatment, individuals with DPB now have a much longer life expectancy due to better management of symptoms, delay of progression, and prevention of associated infections like "P. aeruginosa". The 10-year survival rate for treated DPB is about 90%. In DPB cases where treatment has resulted in significant improvement, which sometimes happens after about two years, treatment has been allowed to end for a while. However, individuals allowed to stop treatment during this time are closely monitored. As DPB has been proven to recur, erythromycin therapy must be promptly resumed once disease symptoms begin to reappear. In spite of the improved prognosis when treated, DPB currently has no known cure.

In those who are not palliative the primary treatment of shortness of breath is directed at its underlying cause. Extra oxygen is effective in those with hypoxia; however, this has no effect in those with normal blood oxygen saturations, even in those who are palliative.

ILD is not a single disease, but encompasses many different pathological processes. Hence treatment is different for each disease.

If a specific occupational exposure cause is found, the person should avoid that environment. If a drug cause is suspected, that drug should be discontinued.

Many cases due to unknown or connective tissue-based causes are treated with corticosteroids, such as prednisolone. Some people respond to immunosuppressant treatment. Patients with a low level of oxygen in the blood may be given supplemental oxygen.

Pulmonary rehabilitation appears to be useful. Lung transplantation is an option if the ILD progresses despite therapy in appropriately selected patients with no other contraindications.

On October 16, 2014, the Food and Drug Administration approved a new drug for the treatment of Idiopathic Pulmonary Fibrosis (IPF). This drug, Ofev (nintedanib), is marketed by Boehringer Ingelheim Pharmaceuticals, Inc. This drug has been shown to slow the decline of lung function although the drug has not been shown to reduce mortality or improve lung function. The estimated cost of the drug per year is approximately $94,000.

Respiratory disease is a common and significant cause of illness and death around the world. In the US, approximately 1 billion "common colds" occur each year. A study found that in 2010, there were approximately 6.8 million emergency department visits for respiratory disorders in the U.S. for patients under the age of 18. In 2012, respiratory conditions were the most frequent reasons for hospital stays among children.

In the UK, approximately 1 in 7 individuals are affected by some form of chronic lung disease, most commonly chronic obstructive pulmonary disease, which includes asthma, chronic bronchitis and emphysema.

Respiratory diseases (including lung cancer) are responsible for over 10% of hospitalizations and over 16% of deaths in Canada.

In 2011, respiratory disease with ventilator support accounted for 93.3% of ICU utilization in the United States.

There are limited national and international studies into the burden of ABPA, made more difficult by a non-standardized diagnostic criteria. Estimates of between 0.5–3.5% have been made for ABPA burden in asthma, and 1–17.7% in CF. Five national cohorts, detecting ABPA prevalence in asthma (based on GINA estimates), were used in a recent meta-analysis to produce an estimate of the global burden of ABPA complicating asthma. From 193 million asthma sufferers worldwide, ABPA prevalence in asthma is estimated between the extremes of 1.35–6.77 million sufferers, using 0.7–3.5% attrition rates. A compromise at 2.5% attrition has also been proposed, placing global burden at around 4.8 million people affected. The Eastern Mediterranean region had the lowest estimated prevalence, with a predicted case burden of 351,000; collectively, the Americas had the highest predicted burden at 1,461,000 cases. These are likely underestimates of total prevalence, given the exclusion of CF patients and children from the study, as well as diagnostic testing being limited in less developed regions.

A Cochrane review comparing pirfenidone with placebo, found a reduced risk of disease progression by 30%. FVC or VC was also improved, even if a mild slowing in FVC decline could be demonstrated only in one of the two CAPACITY trials. A third study, which was completed in 2014 found reduced decline in lung function and IPF disease progression. The data from the ASCEND study were also pooled with data from the two CAPACITY studies in a pre-specified analysis which showed that pirfenidone reduced the risk of death by almost 50% over one year of treatment.