This study found that the prevalence estimate of clinical allergy to peanut, milk, egg, and/or shrimp was 2.5% and was associated with childhood, male gender, and non-Hispanic black race/ethnicity. We also found an association of Likely FA with current asthma and emergency room (ER) visits for asthma in the prior year.
For the first time in a US nationally representative sample, specific serum IgE levels were used to quantify allergic sensitization to common foods. This is important because clinical studies have demonstrated that higher food-specific IgE levels indicate a greater likelihood of clinical FA. While age-specific distinctions in food sensitization and FA have long been suspected, this was also the first time in a US national study that food sensitization was assessed in younger children (1–5 years old) together with older adults (at least 60 years old). These cohort strengths allowed for a comprehensive, contemporary US public health perspective on the prevalence of and risks associated with higher food-specific serum IgE levels, indicative of PFA or LFA.
This investigation estimated clinical FA rates of 2.5% in the US population. They are highest in children (4.2% in 1–5 year olds, 3.8% in 6–19 year olds), and lowest in older adults (1.3% in 60+ year olds). These overall estimates are lower than some other studies. Sampson estimated the prevalence of FA in the US to be 3.5 to 4.0%.1
Bock et al. reported a 6% prevalence of food challenge-confirmed FA in infants less than 3 years of age.7
Our estimates were remarkably similar to those reported by Branum and colleagues from the 2007 National Health Interview Survey, in which the prevalence of self-reported food or digestive allergy in children was 3.9%.2
Our US prevalence of peanut sensitization of 7.6% is consistent with that observed by Arbes and colleagues in NHANES III (1988–1994). These investigators reported an 8.6% prevalence of peanut sensitization in 6–59 year olds by allergy prick skin testing. Importantly, NHANES III did not include younger children or older adults, whereas our data indicate that peanut sensitization is less prevalent in these age groups5
and excluding them to achieve a comparable age population to NHANES III increases the estimated peanut sensitization prevalence to 8.3%. Our clinical peanut allergy estimate of 1.3% is higher than in a US telephone survey in 2002 by Sicherer and colleagues that determined self-reported peanut allergy to be present in 0.6% of the population.6
While there were limited shrimp-specific data upon which to base our threshold partitioning PFA and LFA, our clinical shrimp allergy estimate of 1.0% appears consistent with another US telephone survey conducted by Sicherer and colleagues, which found 2.0% prevalence of physician-diagnosed or convincing reactions to any type of shellfish.3
Furthermore, a sensitivity analysis showed that the estimated prevalence of clinical food allergy reported in this paper is very robust to the particular choice of threshold used to differentiate PFA and LFA to shrimp.
Prevalence differences between studies are attributable to differences in cohort enrollment, how food sensitization or FA was determined, and the panel of foods tested. Our study was strengthened by the nationally representative nature of the cohort, the consistent methodologies employed by the NHANES, and by using standardized food-specific serum IgE, increasing levels of which predict an increasing probability of clinical food reactivity.1, 11, 12
Those with low-level sensitization (0.35–2 kU/L) were excluded from clinical FA estimates in order to minimize the impact of low-level sensitization, which is thought to be associated with a relatively low probability of clinical allergic reactivity, on the results. This study was limited by the fact that the NHANES relied solely on IgE levels for determination of clinical FA estimates, without detailed clinical or questionnaire-based information to corroborate the relevance of these findings. Moreover, there are no predictive values available from studies of adults. Therefore, this study might overestimate FA prevalence since it is possible that higher IgE levels in adults do not correlate as highly with allergy, or it might underestimate FA prevalence by measuring specific IgE to only 4 common foods. Including other common allergenic foods (e.g., tree nuts, sesame, fish, wheat, soy) would likely have increased overall prevalence estimates. Nevertheless, this study provides a consistent, contemporary picture of FA prevalence in the US.
Childhood (1–19 years old), male gender, and non-Hispanic black race/ethnicity were identified as significant risk factors for FA. In fact, the odds of black male children having FA were 4.4 times higher than others in the general population. Childhood is well recognized as a time when food allergies, especially to milk and egg, are more prevalent. Our study's observation of the high peanut allergy prevalence through childhood (1.8% in 1–5 year olds, 2.7% in 6–19 year olds), and the low peanut allergy prevalence in older adults (0.3% in 60+ year olds) has not been previously observed.6
The overall decreasing trend in FA with increasing age may reflect a combination of two factors: (1) the general loss of sensitization with age, noting that allergy to foods such as milk and egg typically resolve over time whereas peanut and shellfish more typically persist, together with (2) a possible cohort effect associated with the increasing prevalence of allergy in children in recent years.16
Male gender and black race/ethnicity were significant risk factors for inhalant allergen sensitization in NHANES II17
and NHANES III.5
With specific regard to FA, Sicherer et al3
found that self-reported shellfish allergy was more prevalent among blacks than whites, while Branum and Lukacs2
found higher rates of sensitization to shrimp, milk, and peanuts among non-Hispanic black children than other children. Our results are consistent with these but are supported by, to our knowledge, the first population-based study among all ages using objective clinical data to identify male gender and black race/ethnicity as risk factors for FA. FA may be under-recognized in blacks, males, and children, because it was self-reported in the other US-wide studies instead of being determined by food-specific serum IgE levels.
The higher prevalence of food sensitization and FA risk categories in participants with asthma, hay fever and eczema is consistent with other national studies.18, 19
In our study, the link between FA and asthma appeared especially strong. There was increased prevalence of all food sensitization and FA risk categories in those with diagnosed asthma, as well as, increased prevalence and likelihood of FA in those with current asthma (indicative of asthma persistence) and ER visits for asthma in the prior year (indicative of severe asthma exacerbations). Indeed, the odds of asthmatics with FA experiencing a recent severe asthma exacerbation were 6.9 times higher than those without FA.
This relationship between FA and asthma severity may or may not be causal in nature. For example, severe asthma may be associated with greater atopy in general.20, 21
In this context, FA might be a marker for a generalized atopic phenotype of severe asthma, but ingesting the allergenic food might not be directly responsible for the asthma severity and severe asthma attacks.
Alternatively, the relationship between FA and asthma severity could be causal, noting that asthma symptoms are induced by foods in food-allergic people up to 30% of the time, although usually with other allergic symptoms.4, 22
However, bronchial hyperreactivity and asthma worsening can be induced, in the absence of immediate bronchospasm, by the ingestion of small amounts of food allergens in sensitized individuals.23, 24
FA has been recently found to be a major risk factor for severe asthma and life-threatening asthma episodes. Several smaller studies have identified food sensitization as a significant risk factor for severe asthma.25, 26
Roberts and colleagues reported 54% of children with asthma requiring intubation for a severe asthma exacerbation had food sensitization, compared with 10% of hospitalized children with asthma at the same hospital.27
Asthma is coincident in nearly all people who suffer fatal anaphylactic reactions and severe asthma is a common manifestation.28, 29
Thus, while the relationship may or may not be causal, this study provides further credence and a national perspective to the concern that FA may be an under recognized trigger of severe asthma exacerbations. Offending foods are notoriously occult and are often hidden in other foods, leading to accidental ingestion. Food-allergic reactions might only be triggered when combined with exercise. In these circumstances, the onset of food-induced symptoms can often be delayed by 2–4 hours after ingestion and only manifest after vigorous physical exertion.30, 31
With these challenges to clinical detection of food-triggered asthma, heightened suspicion is necessary to identify food-triggered asthma episodes. Recognition of FA-triggered asthma exacerbations might improve preventive and therapeutic management and result in better clinical outcomes.
In summary, this NHANES investigation provides a comprehensive, contemporary US public health perspective on the prevalence and risks associated with higher food-specific serum IgE levels indicative of PFA or LFA. Black race/ethnicity and male gender were identified as important risk factors for FA. Along with childhood, these risk factors might identify at-risk populations in which FA is under recognized. A US population-level association between FA and severe asthma exacerbations was also identified. Because the cross-sectional design of this study does not substantiate inferences of causation, prospective clinical investigation of this association is needed. Nevertheless, these findings raise awareness that FA may be contributing to severe asthma episodes.