Bronchiolitis typically affects infants and children younger than two years, principally during the fall and winter . Bronchiolitis hospitalization has a peak incidence between two and six months of age and remains a significant cause of respiratory disease during the first two years of life. It is a leading cause of hospitalization in infants and young children.

The term usually refers to acute viral bronchiolitis, a common disease in infancy. This is most commonly caused by respiratory syncytial virus (RSV, also known as human pneumovirus). Other viruses which may cause this illness include metapneumovirus, influenza, parainfluenza, coronavirus, adenovirus, and rhinovirus.

Children born prematurely (less than 35 weeks), with a low birth weight or who have from congenital heart disease may have higher rates of bronchiolitis and are more likely to require hospital admission. There is evidence that breastfeeding provides some protection against bronchiolitis.

The primary risk factor for COPD globally is tobacco smoking. Of those who smoke, about 20% will get COPD, and of those who are lifelong smokers, about half will get COPD. In the United States and United Kingdom, of those with COPD, 80–95% are either current smokers or previously smoked. The likelihood of developing COPD increases with the total smoke exposure. Additionally, women are more susceptible to the harmful effects of smoke than men. In nonsmokers, secondhand smoke is the cause of about 20% of cases. Other types of smoke, such as, marijuana, cigar, and water-pipe smoke, also confer a risk. Water-pipe smoke appears to be as harmful as smoking cigarettes. Problems from marijuana smoke may only be with heavy use. Women who smoke during pregnancy may increase the risk of COPD in their child. For the same amount of cigarette smoking, women have a higher risk of COPD than men.

Acute bronchitis is one of the most common diseases. About 5% of adults are affected and about 6% of children have at least one episode a year. It occurs more often in the winter. More than 10 million people in the United States visit a doctor each year for this condition with about 70% receiving antibiotics which are mostly not needed. There are efforts to decrease the use of antibiotics in acute bronchitis.

Bronchiolitis obliterans has many possible causes, including collagen vascular disease, transplant rejection in organ transplant patients, viral infection (respiratory syncytial virus, adenovirus, HIV, cytomegalovirus), Stevens-Johnson syndrome, Pneumocystis pneumonia, drug reaction, aspiration and complications of prematurity (bronchopulmonary dysplasia), and exposure to toxic fumes, including diacetyl, sulfur dioxide, nitrogen dioxide, ammonia, chlorine, thionyl chloride, methyl isocyanate, hydrogen fluoride, hydrogen bromide, hydrogen chloride, hydrogen sulfide, phosgene, polyamide-amine dyes, mustard gas and ozone. It can also be present in patients with rheumatoid arthritis. Certain orally administrated emergency medications, such as activated charcoal, have been known to cause it when aspirated. The ingestion of large doses of papaverine in the vegetable Sauropus androgynus has caused it. Additionally, the disorder may be idiopathic (without known cause).

There are many industrial inhalants that are known to cause various types of bronchiolitis, including bronchiolitis obliterans.

Industrial workers who have presented with bronchiolitis:

- nylon-flock workers

- workers who spray prints onto textiles with polyamide-amine dyes

- battery workers who are exposed to thionyl chloride fumes

- workers at plants that use or manufacture flavorings, e.g. diacetyl butter-like flavoring

Intense and prolonged exposure to workplace dusts, chemicals, and fumes increases the risk of COPD in both smokers and nonsmokers. Workplace exposures are believed to be the cause in 10–20% of cases. In the United States, they are believed to be related to more than 30% of cases among those who have never smoked and probably represent a greater risk in countries without sufficient regulations.

A number of industries and sources have been implicated, including high levels of dust in coal mining, gold mining, and the cotton textile industry, occupations involving cadmium and isocyanates, and fumes from welding. Working in agriculture is also a risk. In some professions, the risks have been estimated as equivalent to that of one-half to two packs of cigarettes a day. Silica dust and fiberglass dust exposure can also lead to COPD, with the risk unrelated to that for silicosis. The negative effects of dust exposure and cigarette smoke exposure appear to be additive or possibly more than additive.

Pneumonia is due to infections caused primarily by bacteria or viruses and less commonly by fungi and parasites. Although there are more than 100 strains of infectious agents identified, only a few are responsible for the majority of the cases. Mixed infections with both viruses and bacteria may occur in up to 45% of infections in children and 15% of infections in adults. A causative agent may not be isolated in approximately half of cases despite careful testing.

The term "pneumonia" is sometimes more broadly applied to any condition resulting in inflammation of the lungs (caused for example by autoimmune diseases, chemical burns or drug reactions); however, this inflammation is more accurately referred to as pneumonitis.

Conditions and risk factors that predispose to pneumonia include smoking, immunodeficiency, alcoholism, chronic obstructive pulmonary disease, asthma, chronic kidney disease, and liver disease. The use of acid-suppressing medications—such as proton-pump inhibitors or H2 blockers—is associated with an increased risk of pneumonia. The risk is also increased in old age.

Bacteria are the most common cause of community-acquired pneumonia (CAP), with "Streptococcus pneumoniae" isolated in nearly 50% of cases. Other commonly isolated bacteria include "Haemophilus influenzae" in 20%, "Chlamydophila pneumoniae" in 13%, and "Mycoplasma pneumoniae" in 3% of cases; "Staphylococcus aureus"; "Moraxella catarrhalis"; "Legionella pneumophila" and Gram-negative bacilli. A number of drug-resistant versions of the above infections are becoming more common, including drug-resistant "Streptococcus pneumoniae" (DRSP) and methicillin-resistant Staphylococcus aureus (MRSA).

The spreading of organisms is facilitated when risk factors are present. Alcoholism is associated with "Streptococcus pneumoniae", anaerobic organisms, and "Mycobacterium tuberculosis"; smoking facilitates the effects of "Streptococcus pneumoniae", "Haemophilus influenzae", "Moraxella catarrhalis", and "Legionella pneumophila". Exposure to birds is associated with "Chlamydia psittaci"; farm animals with "Coxiella burnetti"; aspiration of stomach contents with anaerobic organisms; and cystic fibrosis with "Pseudomonas aeruginosa" and "Staphylococcus aureus". "Streptococcus pneumoniae" is more common in the winter, and should be suspected in persons aspirating a large amount of anaerobic organisms.

Most cases of chronic bronchitis are caused by smoking cigarettes or other forms of tobacco. Additionally, chronic inhalation of air pollution or irritating fumes or dust from hazardous exposures in occupations such as coal mining, grain handling, textile manufacturing, livestock farming, and metal moulding may also be a risk factor for the development of chronic bronchitis. Protracted bacterial bronchitis is usually caused by "Streptococcus pneumoniae", "Non-typable Haemophilus influenzae", or "Moraxella catarrhalis".

CAP is common worldwide, and a major cause of death in all age groups. In children, most deaths (over two million a year) occur in newborn period. According to a World Health Organization estimate, one in three newborn deaths are from pneumonia. Mortality decreases with age until late adulthood, with the elderly at risk for CAP and its associated mortality.

More CAP cases occur during the winter than at other times of the year. CAP is more common in males than females, and more common in black people than Caucasians. Patients with underlying illnesses (such as Alzheimer's disease, cystic fibrosis, COPD, tobacco smoking, alcoholism or immune-system problems) have an increased risk of developing pneumonia.

When comparing the bacterial-caused atypical pneumonias with these caused by real viruses (excluding bacteria that were wrongly considered as viruses), the term "atypical pneumonia" almost always implies a bacterial cause and is contrasted with viral pneumonia.

Known viral causes of atypical pneumonia include respiratory syncytial virus (RSV), influenza A and B, parainfluenza, adenovirus, severe acute respiratory syndrome (SARS)

and measles.

Mycoplasma is found more often in younger than in older people.

Older people are more often infected by Legionella.

As the lungs tend to be vulnerable organs due to their exposure to harmful particles in the air, several things can cause an acute exacerbation of COPD:

- Respiratory infection, being responsible for approximately half of COPD exacerbations. Approximately half of these are due to viral infections and another half appears to be caused by bacterial infections. Common bacterial pathogens of acute exacerbations include "Haemophilus influenzae", "Streptococcus pneumoniae" and "Moraxella catarrhalis". Less common bacterial pathogens include "Chlamydia pneumoniae" and "MRSA". Pathogens seen more frequently in patients with impaired lung function (FEV<35% of predicted) include "Haemophilus parainfluenzae" (after repeated use of antibiotics), "Mycoplasma pneumoniae" and gram-negative, opportunistic pathogens like "Pseudomonas aeruginosa" and "Klebsiella pneumoniae".

- Allergens, e.g., pollens, wood or cigarette smoke, pollution

- Toxins, including a variety of different chemicals

- Air pollution

- Failing to follow a drug therapy program, e.g. improper use of an inhaler

In one-third of all COPD exacerbation cases, the cause cannot be identified.

Flock worker's lung is caused by exposure to small pieces of flock, usually nylon, created during the flocking process and inhaled. Exposure to rotary-cut flock particulates is the main risk factor; whether or not other types of flock cause this pulmonary fibrosis is not yet determined. Other types of flock include rayon, polypropylene, and polyethylene. Workers exposed to nylon, polypropylene, polyethylene, and rayon flocking debris have developed flock worker's lung. Exposure to higher concentrations of respirable flock particles is associated with more severe disease.

Whether or not smoking affects the progression or incidence of flock worker's lung is a topic of ongoing research as of 2015. Research in rats has shown that nylon flocking is a causative agent.

A full spectrum of microorganisms is responsible for CAP in adults, and patients with certain risk factors are more susceptible to infections of certain groups of microorganisms. Identifying people at risk for infection by these organisms aids in appropriate treatment.

Many less-common organisms can cause CAP in adults, and are identified from specific risk factors or treatment failure for common causes.

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.

The rate of BPD varies among institutions, which may reflect neonatal risk factors, care practices (e.g., target levels for acceptable oxygen saturation), and differences in the clinical definitions of BPD.

Flock worker's lung can be prevented with engineering controls that protect workers from inhaling flock. Engineering controls to prevent inhalation of flock can include using guillotine cutters rather than rotary cutters, and ensuring that blades are sharp, since dull blades shear off more respirable particles. Flocking plants have also implemented medical surveillance programs for workers to diagnose cases at an earlier stage. Another technique for preventing flock worker's lung is cleaning the workplace with alternatives to compressed air in order to avoid resuspending particulates in the air.

According to a recent study, the main risk factors for RA-ILD are advancing age, male sex, greater RA disease activity, rheumatoid factor (RF) positivity, and elevated titers of anticitrullinated protein antibodies such as anticyclic citrullinated peptide. Cigarette smoking also appears to increase risk of RA-ILD, especially in patients with human leukocyte antigen DRB1.

A recently published retrospective study by a team from Beijing Chao-Yang Hospital in Beijing, China, supported three of the risk factors listed for RA-ILD and identified an additional risk factor. In that study of 550 RA patients, logistic regression analysis of data collected on the 237 (43%) with ILD revealed that age, smoking, RF positivity, and elevated lactate dehydrogenase closely correlated with ILD.

Recent studies have identified risk factors for disease progression and mortality. A retrospective study of 167 patients with RA-ILD determined that the usual interstitial pneumonia (UIP) pattern on high-resolution computed tomography (HRCT) was a risk factor for progression, as were severe disease upon diagnosis and rate of change in pulmonary function test results in the first 6 months after diagnosis.

A study of 59 RA-ILD patients found no median survival difference between those with the UIP pattern and those without it. But the UIP group had more deaths, hospital admissions, need for supplemental oxygen, and decline in lung function.

The following are precautionary measures that can be taken to avoid the spread of bagassosis:

1. Dust control-prevention /suppression of dust such as wet process, enclosed apparatus, exhaust ventilation etc. should be used

2. Personal protection- masks/ respirators

3. Medical control- initial medical examination & periodical checkups of workers

4. Bagasse control- keep moisture content above 20% and spray bagasse with 2% propionic acid

Clinically, the most serious and immediate complication is acute respiratory distress syndrome (ARDS), which usually occurs within 24 h. Those with significant lower airway involvement may develop bacterial infection. Importantly, victims suffering body surface burn and smoke inhalation are the most susceptible. Thermal injury combined with inhalation injury compromises pulmonary function, producing microvascular hyperpermeability that leads to a significant increase in lung lymph flow and pulmonary edema. The terrorist attack on the World Trade Center on September 11, 2001 left many people with impaired lung function. A study of firefighters and EMS workers enrolled in the FDNY WTC Medical Monitoring and Treatment Program, whose lung function was tested prior to 9/11, documented a steep decline in lung function in the first year after 9/11. A new study that includes a thousand additional workers shows that the declines have persisted over time. Prior to 9/11, 3% of firefighters had below-normal lung function, one year after 9/11 nearly 19% did, and six years later it stabilized at 13%. Ten to 14 days after acute exposure to some agents (e.g. ammonia, nitrogen oxides, sulfur dioxide, mercury), some patients develop bronchiolitis obliterans progressing to ARDS. Bronchiolitis obliterans with organized pneumonia can ensue when granulation tissue accumulates in the terminal airways and alveolar ducts during the body's reparative process. A minority of these patients develop late pulmonary fibrosis. Also at enhanced risk are persons with co-morbidities. Several studies report that both aged persons and smokers are especially vulnerable to the adverse effects of inhalation injury.

It was identified in 1985, although its symptoms had been noted before but not recognised as a separate lung disease. The risk of BOOP is higher for people with inflammatory diseases like lupus, dermatomyositis, rheumatoid arthritis, and scleroderma.

The cause of IPF is unknown but certain environmental factors and exposures have been shown to increase the risk of getting IPF. Cigarette smoking is the best recognized and most accepted risk factor for IPF, and increases the risk of IPF by about twofold. Other environmental and occupation exposures such as exposure to metal dust, wood dust, coal dust, silica, stone dust, biologic dusts coming from hay dust or mold spores or other agricultural products, and occupations related to farming/livestock have also been shown to increase the risk for IPF. There is some evidence that viral infections may be associated with idiopathic pulmonary fibrosis and other fibrotic lung diseases.

The clinical course of IPF can be unpredictable. IPF progression is associated with an estimated median survival time of 2 to 5 years following diagnosis.

The 5-year survival for IPF ranges between 20–40%, a mortality rate higher than that of a number of malignancies, including colon cancer, multiple myeloma and bladder cancer.

Recently a multidimensional index and staging system has been proposed to predict mortality in IPF. The name of the index is GAP and is based on gender [G], age [A], and two lung physiology variables [P] (FVC and DL that are commonly measured in clinical practice to predict mortality in IPF. The highest stage of GAP (stage III) has been found to be associated with a 39% risk of mortality at 1 year. This model has also been evaluated in IPF and other ILDs and shown good performance in predicting mortality in all main ILD subtypes. A modified ILD-GAP Index has been developed for application across ILD subtypes to provide disease-specific survival estimates. In IPF patients, the overall mortality at 5 years rate is high but the annual rate of all-cause mortality in patients with mild to moderate lung impairment is relatively low. This is the reason why change in lung function (FVC) is usually measured in 1-year clinical trials of IPF treatments rather than survival.

In addition to clinical and physiological parameters to predict how rapidly patients with IPF might progress, genetic and molecular features are also associated with IPF mortality. For example, it has been shown that IPF patients who have a specific genotype in the mucin MUC5B gene polymorphism (see above) experience slower decline in FVC and significantly improved survival. Even if such data are interesting from a scientific point of view, the application in the clinical routine of a prognostic model based on specific genotypes is still not possible.