The hygiene hypothesis attempts to explain the increased rates of asthma worldwide as a direct and unintended result of reduced exposure, during childhood, to non-pathogenic bacteria and viruses. It has been proposed that the reduced exposure to bacteria and viruses is due, in part, to increased cleanliness and decreased family size in modern societies. Exposure to bacterial endotoxin in early childhood may prevent the development of asthma, but exposure at an older age may provoke bronchoconstriction. Evidence supporting the hygiene hypothesis includes lower rates of asthma on farms and in households with pets.

Use of antibiotics in early life has been linked to the development of asthma. Also, delivery via caesarean section is associated with an increased risk (estimated at 20–80%) of asthma—this increased risk is attributed to the lack of healthy bacterial colonization that the newborn would have acquired from passage through the birth canal. There is a link between asthma and the degree of affluence which may be related to the hygiene hypothesis as less affluent individuals often have more exposure to bacteria and viruses.

Many environmental factors have been associated with asthma's development and exacerbation including allergens, air pollution, and other environmental chemicals. Smoking during pregnancy and after delivery is associated with a greater risk of asthma-like symptoms. Low air quality from factors such as traffic pollution or high ozone levels has been associated with both asthma development and increased asthma severity. Over half of cases in children in the United States occur in areas with air quality below EPA standards. Low air quality is more common in low-income and minority communities.

Exposure to indoor volatile organic compounds may be a trigger for asthma; formaldehyde exposure, for example, has a positive association. Also, phthalates in certain types of PVC are associated with asthma in children and adults. While exposure to pesticides is linked to the development of asthma it is unclear if this is a cause and effect relationship.

There is an association between acetaminophen (paracetamol) use and asthma. The majority of the evidence does not, however, support a causal role. A 2014 review found that the association disappeared when respiratory infections were taken into account. Use by a mother during pregnancy is also associated with an increased risk as is psychological stress during pregnancy.

Asthma is associated with exposure to indoor allergens. Common indoor allergens include dust mites, cockroaches, animal dander (fragments of fur or feathers), and mold. Efforts to decrease dust mites have been found to be ineffective on symptoms in sensitized subjects. Certain viral respiratory infections, such as respiratory syncytial virus and rhinovirus, may increase the risk of developing asthma when acquired as young children. Certain other infections, however, may decrease the risk.

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.

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.

Chronic bronchitis has a 3.4% to 22% prevalence rate among the general population. Individuals over the age of 45, smokers, those that live in areas with high air pollution and those have asthma have a higher risk of developing chronic bronchitis. This wide range is due to the different definitions of chronic bronchitis which can be defined based on signs and symptoms or the clinical diagnosis of the disorder. Chronic bronchitis tends to affect men more often than women. While the primary risk factor for chronic bronchitis is smoking, there is still a 4%-22% chance that people with chronic bronchitis were never smokers. This might suggest other risk factors such as the inhalation of fuels, dusts, and fumes. Obesity has also been linked to an increased risk in the onset of chronic bronchitis. In the United States in the year 2014 per 100,000 population the death rate of chronic bronchitis was 0.2%.

Poorly ventilated cooking fires, often fueled by coal or biomass fuels such as wood and dung, lead to indoor air pollution and are one of the most common causes of COPD in developing countries. These fires are a method of cooking and heating for nearly 3 billion people, with their health effects being greater among women due to more exposure. They are used as the main source of energy in 80% of homes in India, China and sub-Saharan Africa.

People who live in large cities have a higher rate of COPD compared to people who live in rural areas. While urban air pollution is a contributing factor in exacerbations, its overall role as a cause of COPD is unclear. Areas with poor outdoor air quality, including that from exhaust gas, generally have higher rates of COPD. The overall effect in relation to smoking, however, is believed to be small.

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.

At present, over 400 workplace substances have been identified as having asthmagenic or allergenic properties. Their existence and magnitude vary by region and industry and can include diisocyanates, acid anhydrides, plicatic acid, and platinum salts (all low molecular weight agents), and animal protein, enzymes, wheat, and latex (high-molecular weight agents). For example, in France the industries most affected are bakeries and cake-shops, automobile industry and hairdressers, whereas in Canada the principal cause is wood dust, followed by isocyanates. Furthermore, the most common cause of occupational asthma in the workplace are isocyanates. Isocyanates are used in the production of motor vehicles and in the application of orthopaedic polyurethane and fibreglass casts.

The occupations most at risk are: adhesive handlers (e.g. acrylate), animal handlers and veterinarians (animal proteins), bakers and millers (cereal grains), carpet makers (gums), electronics workers (soldering resin), forest workers, carpenters and cabinetmakers (wood dust), hairdressers (e.g. persulfate), health care workers (latex and chemicals such as glutaraldehyde), janitors and cleaning staff (e.g. chloramine-T), pharmaceutical workers (drugs, enzymes), seafood processors, shellac handlers (e.g. amines), solderers and refiners (metals), spray painters, insulation installers, plastics and foam industry workers (e.g. diisocyanates), textile workers (dyes) and users of plastics and epoxy resins (e.g. anhydrides)

The following tables show occupations that are known to be at risk for occupational asthma, the main reference for these is the Canadian Centre for Occupational Health and Safety.

Approximately 21% of the adults affected by asthma report an aggravation of their symptoms while at work and an improvement when away, which implies that they may be suffering from occupational asthma. In the United States, occupational asthma is the most common occupational lung disease. Today, asthma affects as much as 15% of the Canadian population, a statistic reflective of other developed countries, and has increased fourfold in the last 20 years. Various reasons can be identified for this increase, including increase environmental pollution, better diagnostic ability, and greater awareness.

Feline asthma and other respiratory diseases may be prevented by cat owners by eliminating as many allergens as possible. Allergens that can be found in a cat’s habitual environment include: pollen, molds, dust from cat litter, perfumes, room fresheners, carpet deodorizers, hairspray, aerosol cleaners, cigarette smoke, and some foods. Avoid using cat litters that create lots of dust, scented cat litters or litter additives. Of course eliminating all of these can be very difficult and unnecessary, especially since a cat is only affected by one or two. It can be very challenging to find the allergen that is creating asthmatic symptoms in a particular cat and requires a lot of work on both the owner’s and the veterinarian's part. But just like any disease, the severity of an asthma attack can be propelled by more than just the allergens, common factors include: obesity, stress, parasites and pre-existing heart conditions. Dry air encourages asthma attacks so keep a good humidifier going especially during winter months.

Studies show that cats between the ages of two and eight years have the greatest risk of developing a respiratory disease. As well as Siamese and Himalayan breeds and breed mixes seem to be most prone to asthma. Some studies also indicate that more female cats seem to be affected by asthma than male cats.

Tuberculosis, pneumonia, inhaled foreign bodies, allergic bronchopulmonary aspergillosis and bronchial tumours are the major acquired causes of bronchiectasis. Infective causes associated with bronchiectasis include infections caused by the Staphylococcus, Klebsiella, or Bordetella pertussis, the causative agent of whooping cough and nontuberculous mycobacteria.

Aspiration of ammonia and other toxic gases, pulmonary aspiration, alcoholism, heroin (drug use), various allergies all appear to be linked to the development of bronchiectasis.

Various immunological and lifestyle factors have also been linked to the development of bronchiectasis:

- Childhood Acquired Immune Deficiency Syndrome (AIDS), which predisposes patients to a variety of pulmonary ailments, such as pneumonia and other opportunistic infections.

- Inflammatory bowel disease, especially ulcerative colitis. It can occur in Crohn's disease as well, but does so less frequently. Bronchiectasis in this situation usually stems from various allergic responses to inhaled fungal spores. A Hiatal hernia can cause Bronchiectasis when the stomach acid that is aspirated into the lungs causes tissue damage.

- People with rheumatoid arthritis who smoke appear to have a tenfold increased rate of the disease. Still, it is unclear as to whether or not cigarette smoke is a specific primary cause of bronchiectasis.

- Case reports of Hashimoto's thyroiditis and bronchiectasis occurring in the same persons have been published.

No cause is identified in up to 50% of non-cystic-fibrosis related bronchiectasis.

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.

In infants under one year of age, acute bronchitis was the most common reason for admission to the hospital after an emergency department visit in the US in 2011.

To help the bronchial tree heal faster and not make bronchitis worse, smokers should quit smoking completely.

The disease affects between 1 per 1000 and 1 per 250,000 adults. The disease is more common in women and increases as people age. It became less common since the 1950s, with the introduction of antibiotics. It is more common among certain ethnic groups such as indigenous people.

The exact rates of bronchiectasis are often unclear as the symptoms are variable. Rates of disease appeared to have increased in the United States between 2000 and 2007.

The best treatment is to avoid the provoking allergen, as chronic exposure can cause permanent damage. Corticosteroids such as prednisolone may help to control symptoms but may produce side-effects.

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).

Eosinophilic pneumonia is a rare disease. Parasitic causes are most common in geographic areas where each parasite is endemic. AEP can occur at any age, even in previously healthy children, though most patients are between 20 and 40 years of age. Men are affected approximately twice as frequently as women. AEP has been associated with smoking. CEP occurs more frequently in women than men and does not appear to be related to smoking. An association with radiation for breast cancer has been described.

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

In addition to any issues of treatment compliance, and maximised corticosteroids (inhaled or oral) and beta agonist, brittle asthma treatment also involves for type 1 additional subcutaneous injections of beta2 agonist and inhalation of long acting beta-adrenoceptor agonist, whilst type 2 needs allergen avoidance and self-management approaches. Since catastrophic attacks are unpredictable in type 2, patients may display identification of the issue, such as a MedicAlert bracelet, and carry an epinephrine autoinjector.

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.

Medications, substance abuse, and environmental exposures may all trigger eosinophil dysfunction. Medications such as NSAIDs (e.g. ibuprofen), nitrofurantoin, phenytoin, L-tryptophan, daptomycin and ampicillin and drugs of abuse such as inhaled heroin and cocaine may trigger an allergic response which results in EP. Chemicals such as sulfites, aluminum silicate, and cigarette smoke can cause EP when inhaled. A New York City firefighter developed EP after inhalation of dust from the World Trade Center on September 11, 2001.

Hypersensitivity pneumonitis may also be called many different names, based on the provoking antigen. These include:

Of these types, Farmer's Lung and Bird-Breeder's Lung are the most common. "Studies document 8-540 cases per 100,000 persons per year for farmers and 6000-21,000 cases per 100,000 persons per year for pigeon breeders. High attack rates are documented in sporadic outbreaks. Prevalence varies by region, climate, and farming practices. HP affects 0.4–7% of the farming population. Reported prevalence among bird fanciers is estimated to be 20-20,000 cases per 100,000 persons at risk."

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.

Tobacco smoke is a known carcinogen. Workers in the hospitality industry may be exposed to tobacco smoke in the workplace, especially in environments like casinos and bars/restaurants.