Many of the products we use have common antibacterial chemicals found. They can be found in soap, toothpaste, mouthwash and other personal-care products. A new study from Johns Hopkins says that exposures to these antibacterials may make children more prone to a wide range of food and environmental allergies.
The study authors looked at data from a national health survey of 860 children ages 6 to 18 and looked at the relationship between a child’s urinary levels of antibacterials and preservatives found in many personal-hygiene products and the presence of IgE antibodies in the child’s blood. These IgE antibodies are immune chemicals that rise in response to an allergen and are markedly elevated in people with allergies.
The authors saw a link between level of exposure, measured by the amount of antimicrobial agents in the urine, and allergy risk, indicated by circulating antibodies to specific allergens in the blood.
The researchers caution that the findings do not prove that antibacterials and preservatives themselves cause the allergies, but instead suggest that these agents play a role in the immune system development.
The so-called hygiene hypothesis suggests that early childhood exposure to common pathogens is essential in building healthy immune responses. Lack of such exposure, according to the theory, can lead to an overactive immune system that misfires against harmless substances such as food proteins, pollen or pet dander. It is as if our immune system becomes too vigilant. Bacteria are required to promote the shift from the TH2-biased immune response present at birth (pro-allergic) to a balanced TH1/TH2 pattern (the essence of the hygiene hypothesis).
This link between allergy risk and antimicrobial exposure suggests that these agents may affect the balance between beneficial and bad bacteria in the body and lead to immune system dysregulation, which in turn raises the risk of allergies.
In the study, those with the highest urine levels of triclosan — an antibacterial agent used in soaps, mouthwash and toothpaste — had the highest levels of food IgE antibodies, and therefore the highest allergy risk, compared with children with the lowest triclosan levels. Children with the highest urinary levels of parabens — preservatives with antimicrobial properties used in cosmetics, food and medications — were more likely to have detectable levels of IgE antibodies to environmental allergens like pollen and pet dander, compared with those with low paraben levels.
The team initially zeroed in on seven ingredients previously shown to disrupt endocrine function in lab and animal studies. These compounds were bisphenol A — found in plastics — and triclosan, benzophenone-3 and propyl, methyl, butyl and ethyl parabens, found in personal-hygiene products and some foods and medications. Interestingly, triclosan and propyl and butyl parabens, all of which have antimicrobial properties, were the only ones associated with increased allergy risk in the current study, the researchers noted.
This finding highlights the antimicrobial properties of these agents as a probable driving force behind their effect on the immune system.
Children with the highest urine levels of triclosan had nearly twice the risk of environmental allergies as children with the lowest urinary concentrations. Those with highest levels of propyl paraben in the urine had twice the risk of an environmental allergy. Food allergy risk was more than twice as pronounced in children with the highest levels of urinary triclosan as in children with the lowest triclosan levels. High paraben levels in the urine were not linked to food allergy risk.
The researchers are planning a long-term study in babies exposed to antibacterial ingredients at birth, following them throughout childhood.
In speaking with another expert , Dr David Golden, he cautions against extending the conclusion to triclosan causing clinical allergy. IgE is necessary but not sufficient for allergic reactions. More than half the population has positive allergy skin tests but less than 25% have clinical allergy. Hence the emphasis in this report on the "risk" of allergy rather than an actual cause of allergy . As well we cannot ignore the role of genetic factors (family history) in the observed response. This turned out to be a significant factor in the studies showing reduced risk of allergy and asthma in kids who grow up with pets in the home (the risk was actually increased when the parents had animal allergy).
Still we might be well off to reduce these antimicrobial products.
