BACKGROUND: Approximately 1% of the U.S. population has a peanut allergy. Previous studies that measured peanut protein in house dust support the hypothesis that household peanut consumption may lead to clinical sensitization through transdermal exposure. OBJECTIVE: The aim of this pilot study was to characterize Ara h2 levels in house dust from homes with and without individuals with peanut allergy. METHODS: Household dust was obtained from homes with an individual with peanut allergy and from homes with no individual with peanut allergy. Ara h2 levels were determined by using a monoclonal antibody-based immunoassay with a level of determination of 150 ng per gram of dust. Peanut consumption information was obtained by questionnaire. RESULTS: A total of 85 dust samples were collected: 38 from homes with a individual with peanut allergy and 47 from control homes. The median Ara h2 level in homes with an individual with peanut allergy was 1236 ng/g (interquartile range [IQR], 256-1342 ng/g), whereas the median Ara h2 level in homes without an individual with peanut allergy was 650 ng/g (IQR, 163-2201 ng/g). Ara h2 levels in dust from homes of individuals with peanut allergy were not significantly lower than in dust from control homes. Of the homes with an individual with peanut allergy, 15 reported complete avoidance of peanut in the home (39%). Ara h2 levels in homes that completely avoided peanuts were not significantly lower than Ara h2 levels in homes that did not restrict peanuts (p = 0.531). CONCLUSION: Although families may restrict peanuts and peanut products in the home, there was still detectable Ara h2 levels found in homes. Each subject's definition of restriction may vary, there seemed to be peanut protein entering the home, although the protein origin is not known. Possibilities include cross-reactivity with another antigen or transport into the home on some vector. Further investigation of hypotheses regarding cross-reactivity and environmental exposure to Ara h2 is necessary.
BACKGROUND: Approximately 1% of the U.S. population has a peanutallergy. Previous studies that measured peanut protein in house dust support the hypothesis that household peanut consumption may lead to clinical sensitization through transdermal exposure. OBJECTIVE: The aim of this pilot study was to characterize Ara h2 levels in house dust from homes with and without individuals with peanutallergy. METHODS: Household dust was obtained from homes with an individual with peanutallergy and from homes with no individual with peanutallergy. Ara h2 levels were determined by using a monoclonal antibody-based immunoassay with a level of determination of 150 ng per gram of dust. Peanut consumption information was obtained by questionnaire. RESULTS: A total of 85 dust samples were collected: 38 from homes with a individual with peanutallergy and 47 from control homes. The median Ara h2 level in homes with an individual with peanutallergy was 1236 ng/g (interquartile range [IQR], 256-1342 ng/g), whereas the median Ara h2 level in homes without an individual with peanutallergy was 650 ng/g (IQR, 163-2201 ng/g). Ara h2 levels in dust from homes of individuals with peanutallergy were not significantly lower than in dust from control homes. Of the homes with an individual with peanutallergy, 15 reported complete avoidance of peanut in the home (39%). Ara h2 levels in homes that completely avoided peanuts were not significantly lower than Ara h2 levels in homes that did not restrict peanuts (p = 0.531). CONCLUSION: Although families may restrict peanuts and peanut products in the home, there was still detectable Ara h2 levels found in homes. Each subject's definition of restriction may vary, there seemed to be peanut protein entering the home, although the protein origin is not known. Possibilities include cross-reactivity with another antigen or transport into the home on some vector. Further investigation of hypotheses regarding cross-reactivity and environmental exposure to Ara h2 is necessary.