Eczema results from a combination of genetic, immune, and environmental factors that work together to weaken the skin’s protective barrier and trigger chronic inflammation. There is no single cause. Instead, a faulty skin barrier, an overactive immune response, and external irritants overlap in ways that vary from person to person. Around 204 million people worldwide live with atopic dermatitis, the most common form of eczema, affecting roughly 4% of children and 2% of adults globally.
A Weakened Skin Barrier Starts the Process
Healthy skin works like a brick wall. Tough, flattened cells act as bricks, and layers of fats (mostly ceramides, cholesterol, and fatty acids) act as mortar, sealing moisture in and keeping irritants out. In people with eczema, both the bricks and the mortar are defective.
The most well-studied structural problem involves a protein called filaggrin, which is responsible for bundling skin cells into a tight, flat barrier. It also breaks down into molecules that form the skin’s natural moisturizing factor. About 40 different mutations in the gene that produces filaggrin have been identified in people with eczema. These mutations prevent the body from making enough functional protein, leaving the skin barrier full of gaps. Between 20% and 30% of people with eczema carry one of these mutations, compared to 8% to 10% of the general population.
Without enough filaggrin, the skin loses water faster than it should and dries out. But the damage goes further. The fat layers between skin cells are also abnormal in eczema. Several key ceramides are reduced, and without them, the organized lipid sheets that waterproof the skin fall apart. Studies using X-ray imaging have shown that these lipid layers are simply absent in some eczema patients. The result is a “leaky” barrier that lets allergens, bacteria, and chemicals penetrate into deeper skin layers where they trigger inflammation.
An Overactive Immune Response Drives Inflammation
A broken skin barrier alone doesn’t fully explain eczema. The immune system plays an equally important role by overreacting to substances that pass through the damaged barrier. In eczema, the immune system is skewed toward a specific type of inflammatory response driven by two signaling molecules: interleukin-4 (IL-4) and interleukin-13 (IL-13).
IL-4 pushes immune cells to become a type that specializes in allergic responses. Those cells then release a cascade of additional inflammatory signals that recruit more immune cells to the skin, creating a self-reinforcing loop of inflammation. IL-13 works alongside IL-4, and together they do something the reader will recognize immediately: they directly stimulate the nerve fibers responsible for itch. This happens through pathways that don’t respond to antihistamines, which is why antihistamine pills often do little for eczema itch. The itch-scratch cycle then physically damages the barrier further, letting in more irritants and restarting the whole process.
This immune overactivity isn’t confined to the skin. It’s a systemic tendency toward allergic inflammation, which is why eczema often appears alongside other allergic conditions.
Bacteria on the Skin Make It Worse
The skin has its own ecosystem of microbes, and in eczema, that ecosystem is thrown out of balance. One bacterium in particular, Staphylococcus aureus, colonizes the skin of 30% to 100% of eczema patients depending on the study, far more than in people with healthy skin. It is one of the most influential environmental factors in the disease.
S. aureus doesn’t just sit on the skin passively. It actively worsens eczema through several mechanisms. It releases toxins that act as “superantigens,” triggering an uncontrolled activation of immune cells far beyond what a normal immune response would produce. It also produces enzymes that directly break down skin barrier proteins, widening the gaps that already exist. And it pushes the immune system further toward the allergic-type response that characterizes eczema, creating a vicious cycle: barrier damage lets the bacteria in, the bacteria damage the barrier more, and immune inflammation escalates.
Environmental Triggers That Cause Flares
Even with the underlying genetic and immune vulnerabilities in place, eczema flares are often set off by specific environmental exposures. These triggers vary widely between individuals, but several categories come up consistently.
Cold, dry weather is one of the most recognized triggers. Studies in Sweden found that colder temperatures, lower humidity, and stronger winds correlated with increased eczema-related healthcare visits. Cold exposure promotes inflammatory signaling in skin cells and increases water loss through the barrier. The International Eczema Council identifies cold, dry weather as a key environmental trigger, particularly for children.
Air pollution is another significant factor. A meta-analysis covering 42 studies across 14 countries found that elevated levels of particulate matter, nitrogen dioxide, and sulfur dioxide were consistently linked to increased outpatient and emergency visits for eczema. Pollutant particles are small enough and fat-soluble enough to penetrate the outer skin layer, where they trigger oxidative stress and inflammatory responses.
Indoor triggers matter too. Tobacco smoke, indoor mold, wool clothing, solvents, and sweat can all provoke flares. Rapid shifts in skin temperature, such as going from cold air into a hot shower, can intensify itch. Emotional stress is also listed as a recognized trigger in clinical diagnostic criteria for the condition.
Contact Allergens Cause a Different Type of Eczema
Not all eczema is atopic. Contact dermatitis, another form of eczema, occurs when the skin reacts to a specific substance it touches. Patch testing studies consistently identify metals as the most common culprits, with nickel topping the list at around 24% of cases, followed closely by cobalt at 21%. Nickel is found in jewelry, belt buckles, zippers, and phone cases.
Fragrances are the next major category. Balsam of Peru (a fragrance compound found in perfumes, lotions, and some foods) triggered reactions in about 18% of tested patients, and fragrance mixes accounted for another 14%. Rubber accelerators used in gloves and elastic, preservatives in cosmetics, and hair dye chemicals round out the most common allergens. Contact dermatitis can affect anyone, not just those with a genetic predisposition to atopic eczema.
The Link Between Eczema and Other Allergies
Eczema in early childhood often marks the beginning of what researchers call the “atopic march,” a progression from eczema to food allergies, hay fever, and asthma over several years. About one in three children with eczema develops asthma later in childhood. Among those with severe eczema, that number climbs to roughly 70%, compared to about 8% of the general population.
The timing and severity of eczema matter. Children whose eczema appears before age two, persists rather than resolving, or is severe from the start face the highest risk of progressing to respiratory allergies. The leading theory is that allergens entering through the damaged skin barrier sensitize the immune system early in life, priming it for allergic reactions in the airways and gut later on. Children who develop antibodies to common environmental allergens by age two to four are at particularly high risk of this progression.
Why Some People Get Eczema and Others Don’t
A family history of eczema, asthma, or hay fever is the single strongest predictor. But genetics alone aren’t destiny. Many people carry filaggrin mutations without ever developing eczema, and many eczema patients have no detectable filaggrin mutations at all. The current understanding is that eczema develops when genetic susceptibility overlaps with environmental exposures at the right time, particularly in early life.
What remains clear is that eczema is not caused by poor hygiene. While the “hygiene hypothesis” (the idea that overly clean environments in childhood lead to allergic diseases) has gained support for asthma and hay fever, birth cohort studies in Germany found that it does not hold up for eczema specifically. Day care attendance and having older siblings, both proxies for greater childhood germ exposure, did not protect against eczema. The environmental factors that matter appear to be disease-specific rather than following a simple “more germs equals less allergy” rule.