In the differential diagnosis (finding the correct diagnosis between diseases that have overlapping features) of some obstructive lung diseases, DPB is often considered. A number of DPB symptoms resemble those found with other obstructive lung diseases such as asthma, chronic bronchitis, and emphysema. Wheezing, coughing with sputum production, and shortness of breath are common symptoms in such diseases, and obstructive respiratory functional impairment is found on pulmonary function testing. Cystic fibrosis, like DPB, causes severe lung inflammation, excess mucus production, and infection; but DPB does not cause disturbances of the pancreas nor the electrolytes, as does CF, so the two diseases are different and probably unrelated. DPB is distinguished by the presence of lesions that appear on X-rays as nodules in the bronchioles of both lungs; inflammation in all tissue layers of the respiratory bronchioles; and its higher prevalence among individuals with East Asian lineage.

DPB and bronchiolitis obliterans are two forms of primary bronchiolitis. Specific overlapping features of both diseases include strong cough with large amounts of often pus-filled sputum; nodules viewable on lung X-rays in the lower bronchi and bronchiolar area; and chronic sinusitis. In DPB, the nodules are more restricted to the respiratory bronchioles, while in OB they are often found in the membranous bronchioles (the initial non-cartilaginous section of the bronchiole, that divides from the tertiary bronchus) up to the secondary bronchus. OB is a bronchiolar disease with worldwide prevalence, while DPB has more localized prevalence, predominantly in Japan. Prior to clinical recognition of DPB in recent years, it was often misdiagnosed as bronchiectasia, COPD, IPF, phthisis miliaris, sarcoidosis or alveolar cell carcinoma.

Positive indications on patient assessment:

- Shortness of breath

- Chest X-ray may show a characteristic patchy, subpleural, bibasilar interstitial infiltrates or small cystic radiolucencies called honeycombing.

Pneumoconiosis in combination with multiple pulmonary rheumatoid nodules in rheumatoid arthritis patients is known as Caplan's syndrome.

The diagnosis of DPB requires analysis of the lungs and bronchiolar tissues, which can require a lung biopsy, or the more preferred high resolution computed tomography (HRCT) scan of the lungs. The diagnostic criteria include severe inflammation in all layers of the respiratory bronchioles and lung tissue lesions that appear as nodules within the terminal and respiratory bronchioles in both lungs. The nodules in DPB appear as opaque lumps when viewed on X-rays of the lung, and can cause airway obstruction, which is evaluated by a pulmonary function test, or PFT. Lung X-rays can also reveal dilation of the bronchiolar passages, another sign of DBP. HRCT scans often show blockages of some bronchiolar passages with mucus, which is referred to as the "tree-in-bud" pattern. Hypoxemia, another sign of breathing difficulty, is revealed by measuring the oxygen and carbon dioxide content of the blood, using a blood test called arterial blood gas. Other findings observed with DPB include the proliferation of lymphocytes (white blood cells that fight infection), neutrophils, and foamy histiocytes (tissue macrophages) in the lung lining. Bacteria such as "H. influenzae" and "P. aeruginosa" are also detectable, with the latter becoming more prominent as the disease progresses. The white blood, bacterial and other cellular content of the blood can be measured by taking a complete blood count (CBC). Elevated levels of IgG and IgA (classes of immunoglobulins) may be seen, as well as the presence of rheumatoid factor (an indicator of autoimmunity). Hemagglutination, a clumping of red blood cells in response to the presence of antibodies in the blood, may also occur. Neutrophils, beta-defensins, leukotrienes, and chemokines can also be detected in bronchoalveolar lavage fluid injected then removed from the bronchiolar airways of individuals with DPB, for evaluation.

UIP may be diagnosed by a radiologist using computed tomography (CT) scan of the chest, or by a pathologist using tissue obtained by a lung biopsy. Radiologically, the main feature required for a confident diagnosis of UIP is honeycomb change in the periphery and the lower portions (bases) of the lungs. The histologic hallmarks of UIP, as seen in lung tissue under a microscope by a pathologist, are interstitial fibrosis in a "patchwork pattern", honeycomb change and fibroblast foci (see images below).

The differential diagnosis includes other types of lung disease that cause similar symptoms and show similar abnormalities on chest radiographs. Some of these diseases cause fibrosis, scarring or honeycomb change. The most common considerations include:

- chronic hypersensitivity pneumonitis

- non-specific interstitial pneumonia

- sarcoidosis

- pulmonary Langerhans cell histiocytosis

- asbestosis

The diagnosis is based upon a history of symptoms after exposure to the allergen and clinical tests. A physician may take blood tests, seeking signs of inflammation, a chest X-ray and lung function tests. The sufferer shows a restrictive loss of lung function.

Precipitating IgG antibodies against fungal or avian antigens can be detected in the laboratory using the traditional Ouchterlony immunodiffusion method wherein 'precipitin' lines form on agar plate. The ImmunoCAP technology has replaced this time consuming, labor-intensive method with their automated CAP assays and FEIA (Fluorescence enzyme immunoassay) that can detect IgG antibodies against Aspergillus fumigatus (Farmer's lung or for ABPA) or avian antigens (Bird Fancier's Lung).

Although overlapping in many cases, hypersensitivity pneumonitis may be distinguished from occupational asthma in that it is not restricted to only occupational exposure, and that asthma generally is classified as a type I hypersensitivity. Unlike asthma, hypersensitivity pneumonitis targets lung alveoli rather than bronchi.

Given the constant threat of bioterrorist related events, there is an urgent need to develop pulmonary protective and reparative agents that can be used by first responders in a mass casualty setting. Use in such a setting would require administration via a convenient route for e.g. intramuscular via epipens. Other feasible routes of administration could be inhalation and perhaps to a lesser extent oral – swallowing can be difficult in many forms of injury especially if accompanied by secretions or if victim is nauseous. A number of in vitro and in vivo models lend themselves to preclinical evaluation of novel pulmonary therapies.

Lung biopsies can be diagnostic in cases of chronic hypersensitivity pneumonitis, or may help to suggest the diagnosis and trigger or intensify the search for an allergen. The main feature of chronic hypersensitivity pneumonitis on lung biopsies is expansion of the interstitium by lymphocytes accompanied by an occasional multinucleated giant cell or loose granuloma.

When fibrosis develops in chronic hypersensitivity pneumonitis, the differential diagnosis in lung biopsies includes the idiopathic interstitial pneumonias. This group of diseases includes usual interstitial pneumonia, non-specific interstitial pneumonia and cryptogenic organizing pneumonia, among others.

The prognosis of some idiopathic interstitial pneumonias, e.g. idiopathic usual interstitial pneumonia (i.e. idiopathic pulmonary fibrosis), are very poor and the treatments of little help. This contrasts the prognosis (and treatment) for hypersensitivity pneumonitis, which is generally fairly good if the allergen is identified and exposures to it significantly reduced or eliminated. Thus, a lung biopsy, in some cases, may make a decisive difference.

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.

Pneumoconiosis is an occupational lung disease and a restrictive lung disease caused by the inhalation of dust, often in mines and from agriculture.

In 2013, it resulted in 260,000 deaths, up from 251,000 deaths in 1990. Of these deaths, 46,000 were due to silicosis, 24,000 due to asbestosis and 25,000 due to coal workers pneumoconiosis.

Initially, the disease appears as alveolitis, and then progresses to emphysema.

Patients may develop pneumothorax (collapsed lung).

Lycoperdonosis is a respiratory disease caused by the inhalation of large amounts of spores from mature puffballs. It is classified as a hypersensitivity pneumonitis (also called extrinsic allergic alveolitis)—an inflammation of the alveoli within the lung caused by hypersensitivity to inhaled natural dusts. It is one of several types of hypersensitivity pneumonitis caused by different agents that have similar clinical features. Typical progression of the disease includes symptoms of a cold hours after spore inhalation, followed by nausea, rapid pulse, crepitant rales (a sound like that made by rubbing hairs between the fingers, heard at the end of inhalation), and dyspnea. Chest radiographs reveal the presence of nodules in the lungs. The early symptoms presented in combination with pulmonary abnormalities apparent on chest radiographs may lead to misdiagnosis of the disease as tuberculosis, histiocytosis, or pneumonia caused by "Pneumocystis carinii". Lycoperdonosis is generally treated with corticosteroids, which decrease the inflammatory response; these are sometimes given in conjunction with antimicrobials.

The disease was first described in the medical literature in 1967 by R.D. Strand and colleagues in the "New England Journal of Medicine". In 1976, a 4-year-old was reported developing the disease in Norway after purposely inhaling a large quantity of "Lycoperdon" spores to stop a nosebleed. "Lycoperdon" species are sometimes used in folk medicine in the belief that their spores have haemostatic properties. A 1997 case report discussed several instances of teenagers inhaling the spores. In one severe case, the individual inhaled enough spores so as to be able to blow them out of his mouth. He underwent bronchoscopy and then had to be on life support before recovering in about four weeks. In another instance, a teenager spent 18 days in a coma, had portions of his lung removed, and suffered severe liver damage. In Wisconsin, eight teenagers who inhaled spores at a party presented clinical symptoms such as cough, fever, shortness of breath, myalgia, and fatigue within a week. Five of the eight required hospitalization; of these, two required intubation to assist in breathing. The disease is rare, possibly because of the large quantity of spores that need to be inhaled for clinical effects to occur. Lycoperdonosis also occurs in dogs; in the few reported cases, the animals had been playing or digging in areas known to contain puffballs. Known species of puffballs implicated in the etiology of the published cases include the widespread "Lycoperdon perlatum" (the "devil's snuff-box", "L. gemmatum") and "Calvatia gigantea", both of the Lycoperdaceae family.

Aspiration pneumonia is typically diagnosed by a combination of clinical circumstances (a debilitated or neurologically impaired person), radiologic findings (an infiltrate in the proper location), and sometimes with the help of microbiologic cultures. Some cases of aspiration pneumonia are caused by aspiration of food particles or other particulate substances like pill fragments; these can be diagnosed by pathologists on lung biopsy specimens.

Bauxite pneumoconiosis, also known as Shaver's disease, corundum smelter's lung, bauxite lung or bauxite smelters' disease, is a progressive form of pneumoconiosis usually caused by occupational exposure to bauxite fumes which contain aluminium and silica particulates.

It is typically seen in workers involved in the smelting of bauxite to produce corundum.

Mold health issues are potentially harmful effects of molds.

Molds (US usage; British English "moulds") are ubiquitous in the biosphere, and mold spores are a common component of household and workplace dust. The United States Centers for Disease Control and Prevention reported in its June 2006 report, 'Mold Prevention Strategies and Possible Health Effects in the Aftermath of Hurricanes and Major Floods,' that "excessive exposure to mold-contaminated materials can cause adverse health effects in susceptible persons regardless of the type of mold or the extent of contamination." When mold spores are present in abnormally high quantities, they can present especially hazardous health risks to humans after prolonged exposure, including allergic reactions or poisoning by mycotoxins, or causing fungal infection (mycosis).

Infants may develop respiratory symptoms as a result of exposure to a specific type of fungal mold, called Penicillium. Signs that an infant may have mold-related respiratory problems include (but are not limited to) a persistent cough and/or wheeze. Increased exposure increases the probability of developing respiratory symptoms during their first year of life. Studies have shown that a correlation exists between the probability of developing asthma and increased exposure to "Penicillium". The levels are deemed ‘no mold’ to ‘low level’ , from ‘low’ to ‘intermediate’ , and from ‘intermediate’ to ‘high’.

Mold exposures have a variety of health effects depending on the person. Some people are more sensitive to mold than others. Exposure to mold can cause a number of health issues such as; throat irritation, nasal stuffiness, eye irritation, cough and wheezing, as well as skin irritation in some cases. Exposure to mold may also cause heightened sensitivity depending on the time and nature of exposure. People at higher risk for mold allergies are people with chronic lung illnesses, which will result in more severe reactions when exposed to mold.

There has been sufficient evidence that damp indoor environments are correlated with upper respiratory tract symptoms such as coughing, and wheezing in people with asthma.

The illness is generally self-limiting. Management on the whole is preventative, by limiting exposure to mouldy environments with ventilation, or by wearing respiratory protection such as facemasks.

It was recognised as a distinct clinical syndrome in the 1980s. Previously, cases had been reported and given various names such as pulmonary mycotoxicosis, silo unloader’s syndrome, grain fever, toxin fever, humidifier fever, mill fever, toxic alveolitis or allergic alveolitis. In 1994, the National Institute for Occupational Safety and Health published case reports and highlighted the urgency for study of the syndrome.

Research and data collection in the agricultural industry is difficult, as many workers are casual.

Aspiration pneumonia is often caused by a defective swallowing mechanism, often due to a neurological disease or as the result of an injury that directly impairs swallowing or interferes with consciousness. Examples of the former are stroke, Parkinson's disease, and multiple sclerosis, and examples of the latter are some types of dementia, seizures, intoxication, and general anaesthesia. For many types of surgical operations, patients are therefore instructed to take nothing by mouth (nil per os, abbreviated as NPO) for at least four hours before surgery.

While sick building syndrome (SBS) encompasses a multitude of non-specific symptoms, building-related illness (BRI) comprises specific, diagnosable symptoms caused by certain agents (chemicals, bacteria, fungi, etc.). These can typically be identified, measured, and quantified. There are usually 4 causal agents in BRI; 1.) Immunologic, 2.) Infectious, 3.) toxic, and 4.) irritant. For instance, Legionnaire's disease, usually caused by "Legionella pneumophila", involves a specific organism which could be ascertained through clinical findings as the source of contamination within a building. SBS does not have any known cure; alleviation consists of removing the affected person from the building associated with non-specific symptoms. BRI, on the other hand, utilizes treatment appropriate for the contaminant identified within the building (e.g., antibiotics for Legionnaire's disease). In most cases, simply improving the indoor air quality (IAQ) of a particular building will attenuate, or even eliminate, the acute symptoms of SBS, while removal of the source contaminant would prove more effective for a specific illness, as in the case of BRI. Building-Related Illness is vital to the overall understanding of Sick Building Syndrome because BRI illustrates a causal path to infection, theoretically. Office BRI may more likely than not be explained by three events: “Wide range in the threshold of response in any population (susceptibility), a spectrum of response to any given agent, or variability in exposure within large office buildings." Isolating any one of the three aspects of office BRI can be a great challenge, which is why those who find themselves with BRI should take three steps, history, examinations, and interventions. History describes the action of continually monitoring and recording the health of workers experiencing BRI, as well as obtaining records of previous building alterations or related activity. Examinations go hand in hand with monitoring employee health. This step is done by physically examining the entire workspace and evaluating possible threats to health status among employees. Interventions follow accordingly based off the results of the Examination and History report.

The following are causes of BHL:

- Sarcoidosis

- Infection

- Tuberculosis

- Fungal infection

- Mycoplasma

- Intestinal Lipodystrophy (Whipple's disease)

- Malignancy

- Lymphoma

- Carcinoma

- Mediastinal tumors

- Inorganic dust disease

- Silicosis

- Berylliosis

- Extrinsic allergic alveolitis

- Such as bird fancier's lung

- Less common causes also exist:

- Eosinophilic granulomatosis with polyangiitis

- Human immunodeficiency virus

- Extrinsic allergic alveolitis

- Adult-onset Still's disease

Bilateral hilar lymphadenopathy is a bilateral enlargement of the lymph nodes of pulmonary hila. It is a radiographic term that describes the enlargement of mediastinal lymph nodes and is most commonly identified by a chest x-ray.

Some studies have shown a small difference between genders, with women having slightly higher reports of SBS symptoms compared to men. However, many other studies have shown an even higher difference in the report of sick building syndrome symptoms in women compared to men. It is not entirely clear, however, if this is due to biological, social, or occupational factors.

A 2001 study published in the Journal Indoor Air 2001 gathered 1464 office-working participants to increase the scientific understanding of gender differences under the Sick Building Syndrome phenomenon. Using questionnaires, ergonomic investigations, building evaluations, as well as physical, biological, and chemical variables, the investigators obtained results that compare with past studies of SBS and gender. The study team found that across most test variables, prevalence rates were different in most areas, but there was also a deep stratification of working conditions between genders as well. For example, men’s workplace tend to be significantly larger and have all around better job characteristics. Secondly, there was a noticeable difference in reporting rates, finding that women have higher rates of reporting roughly 20% higher than men. This information was similar to that found in previous studies, indicating a potential difference in willingness to report.

There might be a gender difference in reporting rates of sick building syndrome because women tend to report more symptoms than men do. Along with this, some studies have found that women have a more responsive immune system and are more prone to mucosal dryness and facial erythema. Also, women are alleged by some to be more exposed to indoor environmental factors because they have a greater tendency to have clerical jobs, wherein they are exposed to unique office equipment and materials (example: blueprint machines), whereas men often have jobs based outside of offices.

In 1980, the American College of Rheumatology agreed on diagnostic criteria for scleroderma.

Diagnosis is by clinical suspicion, presence of autoantibodies (specifically anti-centromere and anti-scl70/anti-topoisomerase antibodies) and occasionally by biopsy. Of the antibodies, 90% have a detectable anti-nuclear antibody. Anti-centromere antibody is more common in the limited form (80-90%) than in the diffuse form (10%), and anti-scl70 is more common in the diffuse form (30-40%) and in African American patients (who are more susceptible to the systemic form).

Other conditions may mimic systemic sclerosis by causing hardening of the skin. Diagnostic hints that another disorder is responsible include the absence of Raynaud's phenomenon, a lack of abnormalities in the skin on the hands, a lack of internal organ involvement, and a normal antinuclear antibodies test result.

Cyanosis is defined as the bluish or purplish discolouration of the skin or mucous membranes due to the tissues near the skin surface having low oxygen saturation. Based on Lundsgaard and Van Slyke's work, it is classically described as occurring if 5.0 g/dL of deoxyhemoglobin or greater is present. This was based on an estimate of capillary saturation based on a mean of arterial versus peripheral venous blood gas measurements. Since estimation of hypoxia is usually now based either on arterial blood gas measurement or pulse oximetry, this is probably an overestimate, with evidence that levels of 2.0 g/dL of deoxyhemoglobin may reliably produce cyanosis. Since, however, the presence of cyanosis is dependent upon there being an absolute quantity of deoxyhemoglobin, the bluish color is more readily apparent in those with high hemoglobin counts than it is with those with anemia. Also, the bluer the color, the more difficult it is to detect on deeply pigmented skin. When signs of cyanosis first appear, such as on the lips or fingers, intervention should be made within 3–5 minutes because a severe hypoxia or severe circulatory failure may have induced the cyanosis.

The name "cyanosis" literally means "the blue disease" or "the blue condition". It is derived from the color cyan, which comes from κυανός, "kyanós", the Greek word for "blue".