Allergies are caused by the immune system mistakenly treating a harmless substance, like pollen, pet dander, or a food protein, as a dangerous invader. In 2024, nearly one in three American adults (31.7%) had a diagnosed seasonal allergy, eczema, or food allergy. The underlying cause involves a chain reaction of immune events, but genetics, early childhood environment, and even air pollution all play a role in determining who develops allergies and who doesn’t.
How the Immune System Creates an Allergy
An allergy develops in two stages. The first is sensitization: your immune system encounters a substance (an allergen) for the first time and incorrectly flags it as harmful. During this silent phase, which produces no symptoms, your body manufactures a specific type of antibody called IgE that’s custom-built to recognize that particular allergen. These IgE antibodies then attach themselves to mast cells, which are immune cells packed with inflammatory chemicals and found throughout your skin, airways, and gut lining. You’re now “primed” for an allergic reaction, though you won’t know it yet.
The second stage is the reaction itself. The next time you encounter the same allergen, it latches onto those waiting IgE antibodies on your mast cells. When enough allergen molecules bind at once, they bridge multiple antibodies together in a process called cross-linking. This acts like flipping a switch. Within minutes, the mast cells burst open (degranulate) and flood the surrounding tissue with histamine and other inflammatory chemicals, including prostaglandins and leukotrienes.
What Histamine and Other Mediators Do to Your Body
Histamine is the chemical most people associate with allergies, and for good reason. It’s responsible for many of the classic symptoms: itching, sneezing, a runny nose, and watery eyes. But mast cells release a cocktail of chemicals, not just histamine, and each one targets different tissues. Prostaglandins cause flushing and contribute to nasal congestion. Leukotrienes tighten the smooth muscles in your airways, leading to wheezing and shortness of breath. Other signaling molecules recruit more immune cells to the area, which is why allergic inflammation can build over hours even after the initial trigger is gone.
Where these chemicals are released determines what kind of allergic reaction you experience. In the nasal passages, the result is hay fever. In the lungs, it can trigger asthma symptoms. In the skin, you get hives or eczema flares. In the gut, you get cramping, nausea, and diarrhea. In severe cases, mast cells throughout the body activate simultaneously, causing a dangerous drop in blood pressure, throat swelling, and rapid pulse, which is anaphylaxis.
Why Some People Get Allergies and Others Don’t
Genetics is one of the strongest predictors. If one parent has allergies, a child is 30 to 50% more likely to develop them. If both parents have allergies, the risk jumps to 60 to 80%. What’s inherited isn’t necessarily a specific allergy to cats or peanuts, but rather a general tendency for the immune system to produce excessive IgE in response to environmental proteins. A child with this inherited tendency might develop entirely different allergies than their parents did, depending on what they’re exposed to.
But genetics alone doesn’t explain the rapid rise in allergy rates over the past few decades. One of the most studied explanations is the hygiene hypothesis, which proposes that children raised in overly clean environments don’t get enough early exposure to diverse bacteria and other microbes. This microbial exposure appears to train the immune system toward a balanced response. Certain gut bacteria, for instance, stimulate the production of regulatory immune cells that actively suppress allergic inflammation. Without that microbial education early in life, the immune system is more likely to overreact to harmless proteins like pollen or food.
How Food Allergies Develop Differently
Your gut is designed to tolerate foreign proteins. Every time you eat, your digestive system breaks down food and presents its components to immune cells in the intestinal lining. Normally, specialized immune cells respond by releasing anti-inflammatory signals that teach the rest of the immune system to accept these proteins as safe. This process is called oral tolerance, and it works seamlessly for most people with most foods.
Food allergies develop when this tolerance process breaks down. One key factor is the integrity of the gut lining itself. The cells lining your intestines are held together by tight junctions that control what passes through. When these junctions are damaged, whether by infection, inflammation, or other factors, large, undigested food proteins can slip through into deeper tissue where the immune system encounters them in a context that looks more like an invasion than a meal. This triggers an allergic sensitization response instead of a tolerance response, priming the body to react the next time that food is eaten.
This is one reason early introduction of allergenic foods to infants has become a standard recommendation. Exposing the gut to potential allergens like peanut protein during infancy, when the immune system is still learning, appears to promote tolerance rather than sensitization.
Climate Change Is Making Pollen Allergies Worse
If your seasonal allergies feel worse than they used to, that’s not your imagination. A study analyzing pollen data from 60 stations across North America between 1990 and 2018 found that pollen seasons have lengthened by about 20 days, and pollen concentrations have increased by roughly 21%. Warmer temperatures cause plants to start releasing pollen earlier in the spring and continue later into fall. Higher carbon dioxide levels also cause plants to produce more pollen per plant.
The researchers estimated that human-driven climate change was responsible for about half of the lengthening of pollen seasons. This trend is expected to continue, meaning seasonal allergy sufferers are facing a progressively longer and more intense exposure window each year.
Air Pollution Acts as an Allergy Amplifier
Pollution doesn’t just irritate your airways on its own. Diesel exhaust particles, the fine particulate matter from vehicle emissions, actively make allergic reactions worse through a specific biological mechanism. Research published in the Journal of Allergy and Clinical Immunology found that when people were exposed to diesel particles alongside an allergen, their symptom scores nearly tripled compared to the allergen alone. Sneezing, for instance, jumped from an average of 2.2 episodes with allergen alone to 6.4 when diesel particles were also present.
This isn’t just a generic irritant effect. When researchers tested pure carbon particles (the same size but without the chemical coating found on diesel exhaust), there was no increase in symptoms. The organic chemicals on diesel particles are what cause the problem. They directly activate mast cells to release more histamine, boost the production of allergen-specific IgE antibodies, and push the immune response further toward the allergic pathway. Diesel exhaust also lowers the threshold at which an allergen triggers symptoms, meaning you react to smaller amounts of pollen or dust than you otherwise would. For people living near busy roads or in high-traffic urban areas, this pollution effect layers on top of the allergen exposure itself.
Common Allergy Triggers by Category
- Airborne allergens: tree, grass, and weed pollen; dust mites; mold spores; pet dander; cockroach waste
- Food allergens: peanuts, tree nuts, milk, eggs, wheat, soy, fish, shellfish, and sesame (the nine major allergens recognized in the U.S.)
- Contact allergens: nickel, latex, fragrances, and certain preservatives in skincare products
- Insect venom: stings from bees, wasps, hornets, and fire ants
A quarter of American adults have a diagnosed seasonal allergy, 7.7% have eczema, and 6.7% have a confirmed food allergy. Many people have more than one type, and developing a new allergy in adulthood is common, particularly after moving to a new region or after a significant illness that may alter immune function.