Patients with single aspergillomas generally do well with surgery to remove the aspergilloma, and are best given pre-and post-operative antifungal drugs. Often, no treatment is necessary. However, if a patient coughs up blood (haemoptysis), treatment may be required (usually angiography and embolisation, surgery or taking tranexamic acid). Angiography (injection of dye into the blood vessels) may be used to find the site of bleeding which may be stopped by shooting tiny pellets into the bleeding vessel.

For chronic cavitary pulmonary aspergillosis and chronic fibrosing pulmonary aspergillosis, lifelong use of antifungal drugs is usual. Itraconazole and voriconazole are first and second-line anti fungal agents respectively. Posaconazole can be used as third-line agent, for patients who are intolerant of or developed resistance to the first and second-line agents. Regular chest X-rays, serological and mycological parameters as well as quality of life questionnaires are used to monitor treatment progress. It is important to monitor the blood levels of antifungals to ensure optimal dosing as individuals vary in their absorption levels of these drugs.

Inhaled bronchodilators are the primary medications used, and result in a small overall benefit. The two major types are β agonists and anticholinergics; both exist in long-acting and short-acting forms. They reduce shortness of breath, wheeze, and exercise limitation, resulting in an improved quality of life. It is unclear if they change the progression of the underlying disease.

In those with mild disease, short-acting agents are recommended on an as needed basis. In those with more severe disease, long-acting agents are recommended. Long-acting agents partly work by improving hyperinflation. If long-acting bronchodilators are insufficient, then inhaled corticosteroids are typically added. With respect to long-acting agents, if tiotropium (a long-acting anticholinergic) or long-acting beta agonists (LABAs) are better is unclear, and trying each and continuing the one that worked best may be advisable. Both types of agent appear to reduce the risk of acute exacerbations by 15–25%. While both may be used at the same time, any benefit is of questionable significance.

Several short-acting β agonists are available, including salbutamol (albuterol) and terbutaline. They provide some relief of symptoms for four to six hours. Long-acting β agonists such as salmeterol, formoterol, and indacaterol are often used as maintenance therapy. Some feel the evidence of benefits is limited while others view the evidence of benefit as established. Long-term use appears safe in COPD with adverse effects include shakiness and heart palpitations. When used with inhaled steroids they increase the risk of pneumonia. While steroids and LABAs may work better together, it is unclear if this slight benefit outweighs the increased risks. Indacaterol requires an inhaled dose once a day, and is as effective as the other long-acting β agonist drugs that require twice-daily dosing for people with stable COPD.

Two main anticholinergics are used in COPD, ipratropium and tiotropium. Ipratropium is a short-acting agent, while tiotropium is long-acting. Tiotropium is associated with a decrease in exacerbations and improved quality of life, and tiotropium provides those benefits better than ipratropium. It does not appear to affect mortality or the overall hospitalization rate. Anticholinergics can cause dry mouth and urinary tract symptoms. They are also associated with increased risk of heart disease and stroke. Aclidinium, another long acting agent, reduces hospitalizations associated with COPD and improves quality of life. Aclinidinium has been used as an alternative to tiotropium, but which drug is more effective is not known.

Corticosteroids are usually used in inhaled form, but may also be used as tablets to treat and prevent acute exacerbations. While inhaled corticosteroids (ICSs) have not shown benefit for people with mild COPD, they decrease acute exacerbations in those with either moderate or severe disease. By themselves, they have no effect on overall one-year mortality. Whether they affect the progression of the disease is unknown. When used in combination with a LABA, they may decrease mortality compared to either ICSs or LABA alone. Inhaled steroids are associated with increased rates of pneumonia. Long-term treatment with steroid tablets is associated with significant side effects.

Pulmonary fibrosis creates scar tissue. The scarring is permanent once it has developed. Slowing the progression and prevention depends on the underlying cause:

- Treatment options for idiopathic pulmonary fibrosis are very limited. Though research trials are ongoing, there is no evidence that any medications can significantly help this condition. Lung transplantation is the only therapeutic option available in severe cases. Since some types of lung fibrosis can respond to corticosteroids (such as prednisone) and/or other medications that suppress the body's immune system, these types of drugs are sometimes prescribed in an attempt to slow the processes that lead to fibrosis.

- 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.

- Anti-inflammatory agents have only limited success in reducing the fibrotic progress. Some of the other types of fibrosis, such as non-specific interstitial pneumonia, may respond to immunosuppressive therapy such as corticosteroids. However, only a minority of patients respond to corticosteroids alone, so additional immunosuppressants, such as cyclophosphamide, azathioprine, methotrexate, penicillamine, and cyclosporine may be used. Colchicine has also been used with limited success. There are ongoing trials with newer drugs such as IFN-γ and mycophenolate mofetil..

- Hypersensitivity pneumonitis, a less severe form of pulmonary fibrosis, is prevented from becoming aggravated by avoiding contact with the causative material.

- Oxygen supplementation improves the quality of life and exercise capacity. Lung transplantation may be considered for some patients.

"N"-Acetylcysteine (NAC) is a precursor to glutathione, an antioxidant. It has been hypothesized that treatment with high doses of NAC may repair an oxidant–antioxidant imbalance that occurs in the lung tissue of patients with IPF. In the first clinical trial of 180 patients (IFIGENIA), NAC was shown in previous study to reduce the decline in VC and DLCO over 12 months of follow-up when used in combination with prednisone and azathioprine (triple therapy).

More recently, a large randomized, controlled trial (PANTHER-IPF) was undertaken by the National Institutes of Health (NIH) in the USA to evaluate triple therapy and NAC monotherapy in IPF patients. This study found that the combination of prednisone, azathioprine, and NAC increased the risk of death and hospitalizations and the NIH announced in 2012 that the triple-therapy arm of the PANTHER-IPF study had been terminated early.

This study also evaluated NAC alone and the results for this arm of the study were published in May 2014 in the New England Journal of Medicine, concluding that "as compared with placebo, acetylcysteine offered no significant benefit with respect to the preservation of FVC in patients with idiopathic pulmonary fibrosis with mild-to-moderate impairment in lung function".

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.

Treatment depends on the underlying cause. Treatments include iced saline, and topical vasoconstrictors such as adrenalin or vasopressin. Selective bronchial intubation can be used to collapse the lung that is bleeding. Also, endobronchial tamponade can be used. Laser photocoagulation can be used to stop bleeding during bronchoscopy. Angiography of bronchial arteries can be performed to locate the bleeding, and it can often be embolized. Surgical option is usually the last resort, and can involve, removal of a lung lobe or removal of the entire lung. Non–small-cell lung cancer can also be treated with erlotinib or gefitinib. Cough suppressants can increase the risk of choking.

The current medical treatments for aggressive invasive aspergillosis include voriconazole and liposomal amphotericin B in combination with surgical debridement.

For the less aggressive allergic bronchopulmonary aspergillosis findings suggest the use of oral steroids for a prolonged period of time, preferably for 6–9 months in allergic aspergillosis of the lungs. Itraconazole is given with the steroids, as it is considered to have a "steroid sparing" effect, causing the steroids to be more effective, allowing a lower dose.,

Other drugs used, such as amphotericin B, caspofungin (in combination therapy only), flucytosine (in combination therapy only), or itraconazole,

are used to treat this fungal infection. However, a growing proportion of infections are resistant to the triazoles. "A. fumigatus", the most commonly infecting species, is intrinsically resistant to fluconazole.

Prevention of aspergillosis involves a reduction of mold exposure via environmental infection-control. Anti-fungal prophylaxis can be given to high-risk patients. Posaconazole is often given as prophylaxis in severely immunocompromised patients.

In the majority of immunocompetent individuals, histoplasmosis resolves without any treatment. Antifungal medications are used to treat severe cases of acute histoplasmosis and all cases of chronic and disseminated disease. Typical treatment of severe disease first involves treatment with amphotericin B, followed by oral itraconazole.

Liposomal preparations of amphotericin B are more effective than deoxycholate preparations. The liposomal preparation is preferred in patients that might be at risk of nephrotoxicity, although all preparations of amphotericin B have risk of nephrotoxicity. Individuals taking amphotericin B are monitored for renal function.

Treatment with itraconazole will need to continue for at least a year in severe cases, while in acute pulmonary histoplasmosis, 6 to 12 weeks treatment is sufficient. Alternatives to itraconazole are posaconazole, voriconazole, and fluconazole. Individuals taking itraconazole are monitored for hepatic function.

Hypoxia caused by pulmonary fibrosis can lead to pulmonary hypertension, which, in turn, can lead to heart failure of the right ventricle. Hypoxia can be prevented with oxygen supplementation.

Pulmonary fibrosis may also result in an increased risk for pulmonary emboli, which can be prevented by anticoagulants.

Within all classes of medicinal drugs that possibly can lead to pulmonary toxicity as a side effect, most pulmonary toxicity is due to chemotherapy for cancer.

Many medicinal drugs can lead to pulmonary toxicity. A few medicinal drugs can lead to pulmonary toxicity frequently (in medicine defined by international regulatory authorities such as the U.S. Food and Drug Administration and the EMEA [European Union] as > 1% and 10%). These medicinal drugs can include gold and nitrofurantoin, as well as the following drugs used in chemotherapy for cancer: Methotrexate, the taxanes (paclitaxel and docetaxel), gemcitabine, bleomycin, mitomycin C, busulfan, cyclophosphamide, chlorambucil, and nitrosourea (e.g., carmustine).

Also, some medicinal drugs used in cardiovascular medicine can lead to pulmonary toxicity frequently or very frequently. These include above all amiodarone, as well as beta blockers, ACE inhibitors (however, pulmonary toxicity of ACE inhibitors usually lasts only 3–4 months and then usually disappears by itself), procainamide, quinidine, tocainide, and minoxidil.

Both oncologists and cardiologists are well aware of possible pulmonary toxicity.

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.

Radiation (radiotherapy) is frequently used for the treatment of many cancer types, and can be highly effective. Unfortunately, it also can lead to pulmonary toxicity as a side effect.

Radiotherapists are well aware of possible pulmonary toxicity, and take a number of precautions to minimise the incidence of this side effect. There are research efforts to possibly eliminate this side effect in the future.

The dual (ET and ET) endothelin receptor antagonist bosentan was approved in 2001. Sitaxentan (Thelin) was approved for use in Canada, Australia, and the European Union, but not in the United States. In 2010, Pfizer withdrew Thelin worldwide because of fatal liver complications. A similar drug, ambrisentan is marketed as Letairis in the U.S. by Gilead Sciences.

The U.S. FDA approved sildenafil, a selective inhibitor of cGMP specific phosphodiesterase type 5 (PDE5), for the treatment of PAH in 2005. It is marketed for PAH as Revatio. In 2009, they also approved tadalafil, another PDE5 inhibitor, marketed under the name Adcirca. PDE5 inhibitors are believed to increase pulmonary artery vasodilation, and inhibit vascular remodeling, thus lowering pulmonary arterial pressure and pulmonary vascular resistance.

Tadalafil is taken orally, as well as sildenafil, and it is rapidly absorbed (serum levels are detectable at 20 minutes). The T (biological half-life) hovers around 17.5 hours in healthy subjects. Moreover, if we consider pharmacoeconomic implications, patients that take tadalafil would pay two-thirds of the cost of sildenafil therapy. However, there are some adverse effects of this drug such as headache, diarrhea, nausea, back pain, dyspepsia, flushing and myalgia.

Significant disease develops in fewer than 5% of those infected and typically occurs in those with a weakened immune system. Mild asymptomatic cases often do not require any treatment, and the symptoms will go away within a few months. Those with severe symptoms may benefit from anti-fungal therapy, which usually requires 3–6 months of treatment. There is a lack of prospective studies that examine optimal anti-fungal therapy for coccidioidomycosis.

On the whole, oral fluconazole and intravenous amphotericin B are used in progressive or disseminated disease, or in immunocompromised individuals. Amphotericin B used to be the only available treatment, although now there are alternatives, including itraconazole or ketoconazole may be used for milder disease. Fluconazole is the preferred medication for coccidioidal meningitis, due to its penetration into CSF. Intrathecal or intraventricular amphotericin B therapy is used if infection persists after fluconazole treatment. Itraconazole is used for cases that involve treatment of infected person's bones and joints. The antifungal medications posaconazole and voriconazole have also been used to treat coccidioidomycosis. Because the symptoms of valley fever are similar to the common flu and other respiratory diseases, it is important for public health professionals to be aware of the rise of valley fever and the specifics of diagnosis. Greyhound dogs often get valley fever as well, and their treatment regimen involves 6–12 months of Ketoconazole, to be taken with food.

Corticosteroids are the mainstay of treatment of IPH, though they are controversial and lack clear evidence in their favour. They are thought to decrease the frequency of haemorrhage, while other studies suggest that they do not have any effect on the course or prognosis of this disease. In either case, steroid therapy has significant side effects. Small trials have investigated the use of other medications, but none has emerged as a clear standard of care. This includes immune modulators such as hydroxychloroquine, azathioprine, and cyclophosphamide. 6-mercaptopurine as a long-term therapy may prevent pulmonary haemorrhage. A 2007 scientific letter. reports preliminary success in preventing pulmonary haemorrhage with the anti-oxidant N-acetylcysteine.

Acute cardiogenic pulmonary edema often responds rapidly to medical treatment. Positioning upright may relieve symptoms. Loop diuretics such as furosemide or bumetanide are administered, often together with morphine or diamorphine to reduce respiratory distress. Both diuretics and morphine may have vasodilator effects, but specific vasodilators may be used (particularly intravenous glyceryl trinitrate or ISDN) provided the blood pressure is adequate.

Continuous positive airway pressure and bilevel positive airway pressure (BIPAP/NIPPV) has been demonstrated to reduce the need of mechanical ventilation in people with severe cardiogenic pulmonary edema, and may reduce mortality.

It is possible for cardiogenic pulmonary edema to occur together with cardiogenic shock, in which the cardiac output is insufficient to sustain an adequate blood pressure. This can be treated with inotropic agents or by intra-aortic balloon pump, but this is regarded as temporary treatment while the underlying cause is addressed.

Different treatments have been used to manage pulmonary interstitial emphysema with variable success. Admission/transfer to a neonatal intensive care unit (NICU) is common and expected for patients with PIE.

Treatments include:

- Lateral decubitus position with the affected side down

- High-frequency ventilation

- Lobectomy

- Selective Main Bronchial Intubation and Occlusion

The initial management of pulmonary edema, irrespective of the type or cause, is supporting vital functions. Therefore, if the level of consciousness is decreased it may be required to proceed to tracheal intubation and mechanical ventilation to prevent airway compromise. Hypoxia (abnormally low oxygen levels) may require supplementary oxygen, but if this is insufficient then again mechanical ventilation may be required to prevent complications. Treatment of the underlying cause is the next priority; pulmonary edema secondary to infection, for instance, would require the administration of appropriate antibiotics.

Conventional "amphotericin B desoxycholate" (AmB: used since the 1950s as a primary agent) is known to be associated with increased drug-induced Nephrotoxicity (Renal toxicity) impairing Renal function. Other formulations have been developed such as lipid soluble formulations to mitigate such side-effects as direct proximal and distal tubular cytotoxicity. These include liposomal amphotericin B, "amphotericin B lipid complex" such as Abelcet (brand) "amphotericin B phospholipid complex" also as "AmBisome Intravenous", or "Amphotec Intravenous" (Generic; Amphotericin B Cholesteryl Sul) and, "amphotericin B colloidal dispersion", all shown to exhibit a decrease in nephrotoxicity. The later was not as effective in one study as "amphotericin B desoxycholate" which had a 50% murine morbidity rate versus zero for the AmB colloidal dispersion.

The cost of AmB deoxycholate in 2015, for a patient of at 1 mg/kg/day dosage, was approximately $63.80, compared to 5 mg/kg/day of liposomal AmB at $1318.80. This may be a concern in resource-limited settings.

There is no cure available for asbestosis. Oxygen therapy at home is often necessary to relieve the shortness of breath and correct underlying low blood oxygen levels. Supportive treatment of symptoms includes respiratory physiotherapy to remove secretions from the lungs by postural drainage, chest percussion, and vibration. Nebulized medications may be prescribed in order to loosen secretions or treat underlying chronic obstructive pulmonary disease. Immunization against pneumococcal pneumonia and annual influenza vaccination is administered due to increased sensitivity to the diseases. Those with asbestosis are at increased risk for certain cancers. If the person smokes, quitting the habit reduces further damage. Periodic pulmonary function tests, chest x-rays, and clinical evaluations, including cancer screening/evaluations, are given to detect additional hazards.

Specific pretreatments, drugs to prevent chemically induced lung injuries due to respiratory airway toxins, are not available. Analgesic medications, oxygen, humidification, and ventilator support currently constitute standard therapy. In fact, mechanical ventilation remains the therapeutic mainstay for acute inhalation injury. The cornerstone of treatment is to keep the PaO2 > 60 mmHg (8.0 kPa), without causing injury to the lungs with excessive O2 or volutrauma. Pressure control ventilation is more versatile than volume control, although breaths should be volume limited, to prevent stretch injury to the alveoli. Positive end-expiratory pressure (PEEP) is used in mechanically ventilated patients with ARDS to improve oxygenation. Hemorrhaging, signifying substantial damage to the lining of the airways and lungs, can occur with exposure to highly corrosive chemicals and may require additional medical interventions. Corticosteroids are sometimes administered, and bronchodilators to treat bronchospasms. Drugs that reduce the inflammatory response, promote healing of tissues, and prevent the onset of pulmonary edema or secondary inflammation may be used following severe injury to prevent chronic scarring and airway narrowing.

Although current treatments can be administered in a controlled hospital setting, many hospitals are ill-suited for a situation involving mass casualties among civilians. Inexpensive positive-pressure devices that can be used easily in a mass casualty situation, and drugs to prevent inflammation and pulmonary edema are needed. Several drugs that have been approved by the FDA for other indications hold promise for treating chemically induced pulmonary edema. These include β2-agonists, dopamine, insulin, allopurinol, and non-steroidal anti-inflammatory drugs (NSAIDs), such as ibuprofen. Ibuprofen is particularly appealing because it has an established safety record and can be easily administered as an initial intervention. Inhaled and systemic forms of β2-agonists used in the treatment of asthma and other commonly used medications, such as insulin, dopamine, and allopurinol have also been effective in reducing pulmonary edema in animal models but require further study. A recent study documented in the "AANA Journal" discussed the use of volatile anesthetic agents, such as sevoflurane, to be used as a bronchodilator that lowered peak airway pressures and improved oxygenation. Other promising drugs in earlier stages of development act at various steps in the complex molecular pathways underlying pulmonary edema. Some of these potential drugs target the inflammatory response or the specific site(s) of injury. Others modulate the activity of ion channels that control fluid transport across lung membranes or target surfactant, a substance that lines the air sacs in the lungs and prevents them from collapsing. Mechanistic information based on toxicology, biochemistry, and physiology may be instrumental in determining new targets for therapy. Mechanistic studies may also aid in the development of new diagnostic approaches. Some chemicals generate metabolic byproducts that could be used for diagnosis, but detection of these byproducts may not be possible until many hours after initial exposure. Additional research must be directed at developing sensitive and specific tests to identify individuals quickly after they have been exposed to varying levels of chemicals toxic to the respiratory tract.

Currently there are no clinically approved agents that can reduce pulmonary and airway cell dropout and avert the transition to pulmonary and /or airway fibrosis.

Geotrichosis generally has a good prognosis and patients generally have successful recovery. However, there is not a standard treatment for geotrichosis. There are several types of antimicrobial or antifungal compounds that can be used for geotrichosis treatment. One type of treatment of geotrichosis can involve miconazole and ketoconazole, which has shown to improve cutaneous, branchopulmonary, intestinal and joint conditions. Another method of treatment involves symptomatic care, bed rest, iodine therapy, aerosol nystatin and amphotericin B. Azole drugs including isoconazole and clotrimazole are used for geotrichosis treatment. Associated treatment for pulmonary geotrichosis includes the use of potassium iodide, sulfonamides or colistin. The associated asthma can be treated with desensitization and prednisolone. Amphotericin B, clotrimazole and S-fluorocytosine have become more susceptible to "G. candidum". Antimycotic resistance can appear due to repeated treatment.