Hay fever, medically known as allergic rhinitis, is a common condition triggered by the immune system overreacting to harmless airborne particles (allergens). These allergens are typically pollen, dust mites, or pet dander. The resulting immune response causes familiar symptoms like sneezing, a runny nose, and itchy eyes. While environmental exposure is necessary for the condition to manifest, a person’s likelihood of developing hay fever is rooted in inherited traits. Hay fever shows a strong genetic component that establishes a predisposition for the allergy.
Statistical Risk of Inheritance
The likelihood of a child developing hay fever is significantly influenced by the allergic history of their parents. In the general population, the risk of developing allergic rhinitis is approximately 10 to 20 percent. This baseline risk increases when one or both parents have a history of allergies. If a child has only one allergic parent, their probability of developing an allergy, including hay fever, increases to a range of 30 to 50 percent.
The risk becomes substantially higher when both parents are affected by allergies. In this scenario, the child’s chance of developing an allergy can rise to 60 to 80 percent, with some studies estimating the likelihood of developing allergic rhinitis specifically to be as high as 75 percent. This pattern of escalating risk suggests a complex interaction of multiple genes rather than a single, dominant gene.
Twin studies provide further evidence of genetic influence. Identical twins, who share 100 percent of their genes, are much more likely to both suffer from hay fever than fraternal twins, who share only about half. Analyses of this data estimate that genetic effects account for up to 71 percent of an individual’s susceptibility to hay fever.
Genetic Predisposition and Atopy
The inherited tendency to develop hay fever and other related allergic diseases, such as asthma and atopic dermatitis (eczema), is collectively termed atopy. Atopy is a genetically influenced predisposition characterized by a heightened immune response to common environmental allergens. This immune overreaction is driven by the overproduction of a specific class of antibodies known as Immunoglobulin E (IgE).
The inheritance of hay fever is polygenic, meaning that susceptibility is governed by the combined effect of many different genes, each contributing a small risk. Genome-wide association studies have identified numerous genetic variants, or single nucleotide polymorphisms, that increase the risk of allergic rhinitis. Over 40 risk genes involved in various immune pathways have been identified.
Many of these genes regulate the body’s IgE response and immune cell function. For example, variants in cytokine genes like IL4 and IL13 are implicated because the proteins they encode promote an allergic response phenotype, stimulating B cells to produce allergen-specific IgE. Other genes affect the receptors for IgE on immune cells, making them more sensitive to triggering an allergic reaction.
Research also focuses on genes that maintain the integrity of the airway lining, or epithelial barrier function. The nasal and bronchial epithelia act as a physical shield against inhaled particles. Genetic variations in genes, such as C11orf30, can compromise this protective layer, allowing allergens to penetrate more easily into the tissue below. This increases the likelihood of sensitization and allergic response.
Gene-Environment Interaction
While the genetic predisposition for hay fever sets the stage, external factors determine whether the condition develops and how severe it becomes. The expression of inherited susceptibility is heavily modulated by the environment, showcasing a classic gene-environment interaction. This means a person with high genetic risk may never develop hay fever if they live in a protective environment, while someone with moderate risk may develop it due to intense exposure to triggers.
Environmental pollutants play a significant role in this interaction. Exposure to components of air pollution, such as nitrogen oxides and fine particulate matter from traffic, can increase the permeability of the respiratory lining. For a genetically predisposed individual, this damage to the epithelial barrier allows allergens to more easily cross into the underlying tissue. This effectively lowers the threshold needed to trigger an allergic response.
The “Hygiene Hypothesis” further illustrates this gene-environment interplay by focusing on early life microbial exposure. This concept suggests that sanitized environments of modern life prevent the immune system from being properly trained by exposure to microorganisms early in childhood. Epidemiological data noted an inverse correlation between hay fever risk and the number of older siblings, suggesting that greater exposure to infectious agents early on was protective.
This lack of microbial exposure, sometimes referred to as the “microflora hypothesis,” is thought to steer the developing immune system toward an allergic-prone state. Inherited genetic susceptibility, combined with changes in early-life microbial stimulation and exposure to irritants like pollution, contributes to the rapid increase in hay fever prevalence seen in industrialized nations.