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.

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.

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.

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.

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.

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.

Health care professionals are at risk of occupational influenza exposure; during a pandemic influenza, anyone in a close environment is at risk, including those in an office environment.

Beginning shortly after the opening of the first complex in 1956, severe cases of chronic obstructive pulmonary disease, chronic bronchitis, pulmonary emphysema, and bronchial asthma rose quickly among the local inhabitants. Taller smokestacks were implemented, but these simply spread the pollution over a wider area and did not help alleviate the reported health issues.

Fish caught in Ise Bay developed a bad taste, causing local fishermen to petition the government for compensation for their unsaleable fish in 1960.

Thunderstorm asthma is the triggering of an asthma attack by environmental conditions directly caused by a local thunderstorm. It has been proposed that during a thunderstorm, pollen grains can absorb moisture and then burst into much smaller fragments with these fragments being easily dispersed by wind. However, there is no experimental evidence confirming this theory. While larger pollen grains are usually filtered by hairs in the nose, the smaller pollen fragments are able to pass through and enter the lungs, triggering the asthma attack.

There have been events where thunderstorms have caused asthma attacks across cities such that emergency services and hospitals have been overwhelmed. The phenomenon was first recognised and studied after three recorded events in the 1980s; in Birmingham, England, in 1983 and in Melbourne, Australia in 1987 and 1989. Since then there have been further reports of widespread thunderstorm asthma in Wagga Wagga, Australia; London, England; Naples, Italy; Atlanta, United States; and Ahvaz, Iran. A further outbreak in Melbourne, in November 2016, that overwhelmed the ambulance system and some local hospitals, resulted in at least nine deaths. There was a similar incident in Kuwait in early December, 2016 with at least 5 deaths and many admissions to the ICU.

Many of those affected during a thunderstorm asthma outbreak may have never experienced an asthma attack before.

It has been found 95% of those that were affected by thunderstorm asthma had a history of hayfever, and 96% of those people had tested positive to grass pollen allergies, particularly rye grass. A rye grass pollen grain can hold up to 700 tiny starch granules, measuring 0.6 to 2.5 μm, small enough to reach the lower airways in the lung.

In 1955, the Ministry of International Trade and Industry began its policy to transition Japan's primary fossil fuel source from coal to petroleum. To accomplish that goal, construction of the Daichi Petrochemical Complex was begun in 1956. The complex contained an oil refinery, a petrochemical plant, and a power station. This was the first petrochemical complex constructed in Japan.

In 1960, the government of Prime Minister Hayato Ikeda accelerated the growth of petrochemical production as part of its goal to double individual incomes of Japanese citizens over a 10-year period. Also in 1960, MITI announced that a second complex was to be constructed on reclaimed land in northern Yokkaichi. The second complex went online in 1963. As demand for ethylene and other petrochemicals rose, a third complex was constructed which began production in 1972. Yokkaichi transferred its energy production from coal to oil more quickly than the rest of the nation. The oil used in Yokkaichi was primarily imported from the Middle East, which contained 2% sulfur in sulfur containing compounds, resulting in a white-colored smog developing over the city.

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.

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.

Medication challenge tests, such as the methacholine challenge test, have a lower sensitivity for detection of exercise-induced bronchoconstriction in athletes and are also not a recommended first-line approach in the evaluation of exercise-induced asthma.

Mannitol inhalation has been recently approved for use in the United States.

It should be noted, however, that a relatively recent review of the literature has concluded that there is currently insufficient available evidence to conclude that either mannitol inhalation or eucapnic voluntary hyperventilation are suitable alternatives to exercise challenge testing to detect exercise-induced bronchoconstriction and that additional research is required.

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%.

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 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.

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.

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."

In 1973, Breslin et al. tested the effects of alcoholic beverage consumption on the respiratory symptoms of 11 asthmatic subjects who gave a history of asthma attacks following certain alcoholic beverages. In response to ingesting the type of beverage that the subjects reported to provoke their symptoms, six developed the asthmatic symptom of chest tightness, two developed a symptom often associated with asthma, rhinitis, and one subject developed both chest tightness and rhinitis. Symptoms developed almost immediately after ingestion, inhalation of fumes from the beverages did not precipitate symptoms, and bronchoconstriction in response to the ingestion was confirmed in the three patients evaluated by pulmonary function tests. The study suggested that these reactions were induced by non-alcoholic allergens that were contained in or contaminated the beverages. In 1978 a non-asthmatic female of Japanese descent with a history of moderately severe bronchoconstriction responses to various alcoholic beverages and in 1981 an asthmatic Japanese male with a similar history beer or 95% pure ethanol were studied and found to develop bronchoconstriction after drinking apple juice but not after drinking apple juice per se; intravenous infusion or inhalation of ethanol also caused bronchospasm responses in the male subject. These studies suggested that alcohol itself caused the asthmatic symptoms triggered by alcoholic beverages. A subsequent study in 1986 found that 9 of 18 patients with a history of red wine-induced asthma symptoms showed bronchoconstriction in response to ingesting red wine; the response correlated positively with the amount of sulfur dioxide contained in the provocative wine. The study suggested that the reaction was not allergen-induced but rather triggered by sulfur dioxide, a sulfur dioxide-related agent, or an agent whose levels in alcohol beverages correlated positively with those of sulfur dioxide. Finally, a questionnaire survey of 366 asthmatic patients conducted in 2000 found that 33% reported asthma symptoms in response to alcoholic beverages; there was a significant association between wine-induced asthma and asthma triggered by sulfite-containing foods, by aspirin, and by nonsteroidal anti-inflammatory drugs (NSAID) other than aspirin. The study suggested the salicylate-"contaminates" in wine may contribute to these responses. In other studies, D.P. Agarwal and colleagues associated race-based variations in the activity alcohol-metabolizing enzymes with the occurrence of alcohol flush reactions to alcohol and alcoholic beverages in certain Asian populations. This early work is the basis for further studies that have defined not only many alcohol-induced flush reactions but also many alcohol-induced respiratory reactions as due to racially associated genetic differences in alcohol-metabolizing enzymes.

Avoidance of ethanol is the safest, surest, and cheapest treatment. Indeed, surveys find a positive correlation between high incidences of glu487lys ALDH2 allele-related alcohol-induced respiratory reactions as well as other causes of these reactions and low levels of alcohol consumption, alcoholism, and alcohol-related diseases. Evidently, people suffering these reaction self-impose avoidance behavior. There is a proviso here: ethanol, at surprisingly high concentrations, is used as a solvent to dissolve many types of medicines and other ingredients. This pertains particularly to liquid cold medicines and mouthwashes. Ethanol avoidance includes avoiding the ingestion of and, depending on an individual's history, mouth washing with, such agents.

Type H1 antagonists in the histamine antagonist family of drugs were tested in Japanese volunteers with alcohol-induced asthma (who presumably have glu487lys ALDH2 allele-associated asthma) and found to be completely effective in blocking bronchoconstriction responses to alcoholic beverages; these blockers, it is suggested, may be taken 1–2 hours before consumption of alcohol beverages as a preventative of alcohol-induced respiratory reactions. In the absence of specific studies on the prevention of classical alcohol induced rhinitis and asthma due to allergens in alcoholic beverages, see asthma section on Prevention and rhinitis section on Prevention of allergen-induced reactions.

In the absence of specific studies on the treatment of acute alcohol-induced bronchoconstriction and rhinitis, treatment guidelines should probably follow those of their comparable allergen-induced classical allergic reactions (see asthma section on Treatment and rhinitis section on Treatment) but possibly favoring the testing of H1 antagonist anti-histamines as part of the initial protocol.

The International Olympic Committee recommends the eucapnic voluntary hyperventilation (EVH) challenge as the test to document exercise-induced asthma in Olympic athletes. In the EVH challenge, the patient voluntarily, without exercising, rapidly breathes dry air enriched with 5% for six minutes. The presence of the enriched compensates for the losses in the expired air, not matched by metabolic production, that occurs during hyperventilation, and so maintains levels at normal.

Each home contains possible allergens that can develop into allergies after exposure to:

- Dust mites

- Dogs and cats

- Other furry pets

- Cockroaches

- Mice and rats)

- Plants

- Mold

Vitamin D deficiency at the time of birth and exposure to egg white, milk, peanut, walnut, soy, shrimp, cod fish, and wheat makes a child more susceptible to allergies. Soy-based infant formula is associated with allergies in infants.

A child's allergy is an immune system reaction. The child is reacting to a specific substance, or allergen. The immune system of a child responds to the invading allergen by releasing histamine and other chemicals that typically trigger symptoms in the nose, lungs, throat, sinuses, ears, eyes, skin, or stomach lining. In some children, allergies can also trigger symptoms of asthma—a disease that causes wheezing or difficulty breathing. If a child has allergies and asthma, controlling the allergies is important because the lack of treatment may make the allergies worse. Compounds such as phthalates are associated with asthma in children. Asthma in children is associated with exposure to indoor allergens. in early childhood may prevent the development of asthma, but exposure at an older age may provoke bronchoconstriction. Use of antibiotics in early life has been linked to the development of asthma. Exposure to indoor volatile organic compounds may be a trigger for asthma; formaldehyde exposure, for example, has a positive association.

Some people have reported relief of symptoms by following a low-salicylate diet such as the Feingold diet. Aspirin is quickly converted in the body to salicylic acid, also known as 2-Hydroxybenzoic acid. Sommer "et al." reported a multi-center prospective randomized cross-over trial with 30 patients following a low-salicylate diet for 6 weeks. This study demonstrated a clinically significant decrease in both subjective and objective scoring of severity of disease, but made note of the challenge for patients in following what is a fairly stringent diet.

A diet low in omega-6 oils (precursors of arachidonic acid), and high in omega-3 oils, may also help. In a small study, aspirin-sensitive asthma patients taking 10 grams of fish oil daily reported relief of most symptoms after six weeks, however symptoms returned if the supplement was stopped.