Childhood Eczema: An Environmental Scan

Table of Contents

3.2.2 Causes and Triggers of Childhood Eczema

3.2.2.1 Personal Hygiene

Among eczema research it is now well understood that an individual’s use of soap and other bathing products (shower gels, bubble baths) along with baby wipes are all linked to both the development and flare ups associated with eczema. Simple breakdown in the skin’s barriers leave cracks and the ability for irritates to penetrate the protective barrier of the skin, which can result in the development of lesions. Estimates suggest 1 in 5 children develops eczema because of the increase in using such products.

3.2.2.2 Pharmacology

Regarding the use of acetaminophen (paracetamol), a recent study (the ISSAC programme) found that among children who were 6-7 years old, the use of acetaminophen in the first year of life was associated with both an increase in the likelihood of eczema and asthma. In addition, the researchers stated that children with eczema, asthma and nasal allergies were more likely to use acetaminophen thus, research into pharmacology is still necessary and on-going and further investigation into the relationship between acetaminophen and possible increases in the likelihood of asthma is warranted (11) (12).

3.2.2.3 Hygienic Hypothesis

Dr. Sami Baha, the chief of Allergy and Immunology at Louisiana State University Health Sciences Centre and other leading clinicians suggests the ‘hygienic hypothesis’ is responsible for impacting the current increasing prevalence trends of childhood eczema. The hypothesis is based on the fact that many children, especially those living in the West have immune systems that are deficient in normal processes of identifying and attacking ‘invaders’ of the body. When children are increasingly exposed to sterile environments from birth, their immune systems do not develop normally by being challenged by various pathogens. Factors such as the use antibiotics and vaccinations, along with an emphasis on antibacterial soaps, creams and cleaners produce an environment whereby the immune system does not receive adequate exposure to develop normally and fight infection. As a result the overall system can become hyperactive (13;14).

Specifically concerning vaccines, some researchers have focused on possible links between vaccinations and the incidence of both eczema and asthma. A study published in the UK in 2004, examined vaccinations for diphtheria, polio, whooping cough, measles, mumps and tetanus and found that there were no significant risk factors for either eczema or asthma (15). Similarly, Bernsen reported a lower risk of atopic disorders in the whole-cell pertussis vaccine when comparing results with children who did not have the immunization (16) However, it is widely understood that individuals with eczema should not receive the smallpox vaccine. A U.S. study noted the importance of knowing an individual’s dermatological history with respect to atopic dermatitis and specifically eczema before receiving the smallpox vaccine as individuals with eczema may develop eczema vaccinatum when either they themselves or someone who is in close contact receives the vaccine (17).

3.2.2.4 Genetics

Although the definitive cause of childhood eczema remains complicated and unclear, research during the past 25 years has led to many hypotheses including genetic factors, environmental triggers, allergic origins and stress conditions (8). Family history is widely accepted as the strongest predictor of whether or not a child will develop eczema. Genetic predisposition, such as whether the child has a parent or sibling who has eczema, asthma or hayfever is associated with a higher risk of developing the disease. Specifically, estimates suggest that if either parents (or a sibling) are afflicted with eczema, hayfever or asthma, their child has a 50% chance of also having eczema. Similarly, if only one parent has any of the former conditions and older siblings are not afflicted, the child’s risk falls to 25% (18).

Specifically, research in the area of the association between genetics and the development of eczema has identified particular variants in the fillagrin (FLG) gene as factor in the predisposition to eczema and has been replicated in numerous studies (19-21). A mutation in the fillagrin gene impairs a barrier within the skin that results in penetration of allergens and irritants. Additionally, the variant is also believed to be associated with food allergies. Importantly, research out of Ireland had noted that when an individual has two specific mutations of the fillagrin gene together they are very susceptible to atopic conditions, which increases their risk of eczema and specifically may be associated with a form that begins in infancy and continues through to adulthood (21). The variant in the FLG gene alone however does not explain the development of eczema. Under normal conditions, fillagrin is found in the skin and performs the function of a protective barrier protein. For individuals with the variant, researchers believe a catalyst, such as an exposure to allergen triggers eczema and then the variant in the gene prevents the immune system from working effectively.

Additionally, genetic research has also uncovered the gene associated with itching or the ‘itch-sensation’ as the GRPR (gastrin-releasing peptide receptor). The hope in this area of research is to develop treatment options that will effectively impair the messaging of the itch in the body and bring relief to those who suffer chronic itching symptoms such as eczema patients (22). The exact association between genetic factors and eczema are not well understood; however, there is consensus among researchers and clinicians that having a genetic predisposition can make a child more susceptible to developing eczema but genetic factors may not be sufficient on their own to cause the disease (9).

3.2.2.5 Allergies

A substantial trigger associated with eczema is allergies. Numerous agents causing allergic reactions are thought to have an association with eczema including environmental allergens such as house dust, dust mites, cockroach allergens, outdoor air pollen and pet dander; however, the true relationship between atopic sensitizations and allergic disease is poorly understood (23). A particularly difficult situation surrounds dust and dust mites as they are near impossible to avoid. When an individual already has eczema and the skin is damaged, the exposure to an allergen further impairs the protective layer of the skin to heal thus leading to more severe symptoms.

It is well known that pet dander causes an allergic reaction for many individuals and that an exposure to animals for people suffering with eczema and asthma can be a very serious reaction. Research out of the University of Manchester and Copenhagen has specifically examined the link between cats and eczema. Importantly, researchers have found that in children who are predisposed genetically to eczema and who are also exposed within the first year of life to cats increased the risk of developing eczema to that 4 times greater than for children who are not exposed. The exposure to dogs had no effect. Other research has suggested exposure to not only cats but other animals in fact provides a protective effect against eczema by exposing children to various allergens and bacteria early in life to stimulate a healthy immune responses (to contradict the effects of the hygienic hypothesis discussed above). Conversely, additional studies focused on pets have suggested that having a bird in the home may reduce eczema. The hypothesis is that when children are exposed at a young age to the bird feathers, which contain toxins their immune system responds and during early development this exposure may prevent allergies. Finally, another body of investigations in the area of the correlation between allergies and the severity of eczema showed that only those children who were considered severely afflicted with eczema and who may also report difficulties in responding to treatments are likely to be further adversely affected by allergens such as grass and domestic animals (24).

Another extremely difficult issue to manage in the area of childhood eczema and allergies is the area of food sensitization. In 2008, the CDC reported that 27% of children who had food allergies also reported either eczema or a skin allergy (25). Any child with a food allergy is estimated to have 2 to 4 times a higher risk of having eczema, asthma or other allergies. Data briefs out of the CDC state between 1997 and 2007 the diagnosed cases of food allergies in children in the United States rose 18%, which translates into approximately 3 million children or 4 in every 100. Similarly, in 2008, Dr. Hanifin speaking at a dermatology conference in the US estimated that up to 40% of children, who experience eczema as infants and young children will go on to develop food allergies. He emphasized that public education must include dispelling the common myth that food allergies cause eczema and that in fact the sequence of events is the other way around. Similarly, research in Australia has reported that the earlier a child develops eczema in their life and the greater the severity of their condition are both markers for increased prevalence of food sensitivities (26)

Notably, parents experience, on a daily basis the impact food their child has eaten and associations with eczema albeit do not necessarily know which food is causing a specific reaction. It is extremely frustrating and difficult for parents to manage this issue of their child’s disease. Clinicians state that the skin is highly susceptible to the food we ingest and that a person’s skin is a reflection of not only their overall health but of the specific state of the bodies’ hormone balance and immune system. It is understood that certain foods are known to have a clear association with eczema and 90% of all food allergies are attributed to 8 foods: milk, eggs, peanuts, soybeans, fish, shellfish, wheat and tree nuts (25); however, the specific mechanisms by which the reactions take place are elusive. Importantly, some food allergic reactions are not restricted to having to ingest the allergen. For example, some children may be so sensitive to certain food items that simply having their skin come in contact with such a trigger can cause anything from a flare up of hives and/or an outburst of eczema all the way to a life threatening anaphylactic shock reaction. Furthermore, not all food allergens are confined to edible items. Some elements can be found in other areas of their environment such as cosmetics, making the avoidance of certain allergens very difficult as the overriding concern is the severity or sensitivity of food allergies that continues to rise.