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. Author manuscript; available in PMC: 2024 Apr 1.
Published in final edited form as: Curr Opin Allergy Clin Immunol. 2023 Jan 11;23(2):164–171. doi: 10.1097/ACI.0000000000000889

Impact of the exposome on food allergy development

Timothy P Moran 1,2
PMCID: PMC9985871  NIHMSID: NIHMS1862970  PMID: 36728313

Abstract

Purpose of review:

The increasing global prevalence of food allergy indicates that environmental exposures are likely contributing to food allergy development. This review summarizes recent studies on how specific factors within the external exposome may impact the development of food allergy.

Recent findings:

There is strong evidence that non-oral exposure to food allergens within the living environment is a risk factor for food sensitization and food allergy. The role of air pollution in food allergy development remains unclear, as cohort studies have not found consistent relationships between air pollutant exposure and food sensitization. Early-life microbial exposures linked to a rural lifestyle are likely protective against food allergy development, possibly through alteration of the infant microbiome. In contrast, factors associated with urbanization and decreased exposure to microbes may contribute to food allergy development. Recent studies on the role of residential greenness in food allergy development suggest either no relationship or a possible increased risk for food allergy.

Summary:

The external exposome comprises a number of exposures that can modify food allergy risk. Improved understanding of how complex environmental exposures interact with genetic factors will be necessary for developing effective interventions aimed at preventing food allergy development in children.

Keywords: Food allergy, exposome, environment, air pollution, microbiome

INTRODUCTION

IgE-mediated food allergy is a potentially life-threatening disease that is a global health problem affecting up to 10% of children and adults in some populations (1, 2). While there is geographic variability, epidemiological studies suggest that food allergy rates have increased significantly over the past few decades (3). The recent increase in food allergy prevalence cannot be explained by genetics alone, indicating that environmental factors are likely driving the food allergy epidemic (4). Beginning at conception and continuing throughout life, individuals encounter a wide range of environmental exposures that can impact allergic disease development (5). The external exposome refers to the totality of these environmental exposures and encompasses several non-genetic factors including diet, pollution, microbes, allergens, climate change, psychosocial stressors, and socioeconomic factors (6, 7). This review will highlight recent reports regarding the role of the external exposome in food allergy, with a particular focus on how environmental food exposure, air pollution, microbial exposures, and residential greenness impact food allergy development.

ENVIRONMENTAL FOOD EXPOSURE

There is strong evidence that exposure to food allergens within the living environment is a risk factor for food sensitization and food allergy (8, 9). Food allergens, including peanut, cow’s milk, hen’s egg and fish, are present in dust samples collected throughout the home including children’s play areas and bedrooms (10–15). Recent studies also show that food allergens, including peanut, tree nuts, milk and egg, are detectable in table wipe and floor dust samples from school classrooms and cafeterias, indicating that environmental food exposure occurs outside of the home (13, 15). While food allergen levels in dust typically correlate with household consumption of the food (14, 16), food allergens are still detectable in homes and classrooms where those foods are excluded (15, 17), indicating that food allergens are dispersed throughout the living environment.

The dual allergen exposure hypothesis postulates that cutaneous exposure to environmental food allergens is a risk factor for allergic sensitization, whereas consumption of the food leads to immunological tolerance (18). Epicutaneous exposure to environmental peanut has been associated with peanut sensitization and development of peanut allergy, particularly in infants with an impaired skin barrier due to atopic dermatitis (AD) or filaggrin loss-of-function mutations (19, 20). There is less evidence that environmental exposure to food allergens other than peanut is a risk factor for food allergy. Recently, a cross-sectional study of 159 children in Japan found that egg protein levels in house dust correlated with maternal egg consumption, but there was no association with egg allergy at 6 years of age (16). In addition to the presence of food allergens, co-exposure to immunostimulatory agents (adjuvants) within the indoor environment, such as house dust mite or fungal proteases, may be an important determinant for whether epicutaneous food exposure results in allergic sensitization (21).

Given the associations between AD and peanut sensitization, strategies that prevent or reduce the severity of AD may reduce peanut allergy risk. Initial studies suggested that early application of emollients to neonates at high-risk for AD reduced the incidence of AD by up to 50% (22, 23). However, recent randomized controlled trials have not found a protective effect of early emollient application on AD or food allergy development (24–26). In the BEEP (Barrier Enhancement for Eczema Prevention) study, 1394 infants at high-risk for AD were randomized to either daily emollient application or standard skin care (24). At 2 years of age, no difference in rates of AD (aRR 0.95; 95% CI, 0.78–1.16) were observed between the groups. Interestingly, there was a trend for higher rates of food allergies to milk, egg or peanut in the emollient group (aRR 1.47, 95% CI 0.93–2.33). In the PreventADALL (Preventing Atopic Dermatitis and ALLergies in Children) study, 2397 newborn infants were randomized to four different intervention groups: no intervention, frequent application of emollients (skin intervention), early complementary feeding of allergenic foods at 3 months of age (food intervention), or combined skin and food interventions (25, 26). No difference in rates of AD was observed between any of the groups at 12 months of age (25). At 36 months of age, food allergy was reduced in the food intervention group compared to the no intervention group (OR 0.4; 95% CI, 0.2–0.8), but not in the skin intervention group (OR 1.3; 95% CI, 0.7–2.3) (26)●●. In a post-hoc analysis of the EAT (Enquiring About Tolerance) study, the frequency of parent-reported moisturizer usage at 3 months of age showed a dose-dependent association with food allergy development (OR 1.20; 95% CI, 1.13–1.27) (27). Taken together, these studies indicate that regular emollient use during infancy is not protective against food allergy, and may actually increase food allergy risk, possibly by facilitating transcutaneous sensitization to food allergens in the environment.

Recent studies also suggest that the airway may be another route for sensitization to environmental food allergens (28). In preclinical animal models, airway exposure to peanut can induce allergic sensitization and development of peanut allergy (29, 30). Co-exposure to environmental adjuvants within house dust, such as microbial products that stimulate Toll-like receptors, can also promote airway sensitization to peanut (31, 32). In humans, pathogenic peanut-specific CD4+ T helper cells from peanut allergic individuals express the skin- and lung-homing chemokine receptor CCR4, but express low levels of the skin-homing molecule cutaneous lymphocyte antigen, suggesting that these cells may have been primed in the lungs rather than the skin (33). Further studies are needed to determine the mechanisms by which skin and airway exposure to foods contributes to food allergy development, and whether reducing environmental levels of food allergens mitigates food allergy risk.

AIR POLLUTION

Air pollution is a significant public health problem in many countries, with 90% of the world’s population living in areas of low air quality (34). The combustion of fossil fuels is a major source of air pollutants, including particulate matter with an aerodynamic diameter ≤2.5 μm (PM2.5), sulfur dioxide, nitrogen dioxides, polycyclic aromatic hydrocarbons, and ground-level ozone (35). Children are particularly vulnerable to the negative health effects of air pollution, especially those from poor communities and certain racial and ethnic groups (36). While air pollution is a well-known risk factor for asthma and other respiratory diseases (34), it could also play a role in food allergy development. PM2.5 can disrupt epithelial barrier function and activate type 2 inflammatory responses in the skin and mucosal surfaces, which could lead to the immune system encountering food proteins under T helper 2 (Th2)-polarizing conditions, resulting in sensitization rather than tolerance (37). Prenatal exposure to ambient air pollution can also alter early-life immune responses at mucosal tissues, conferring an increased risk for allergic sensitization later in life (38).

Despite the potential pro-allergic effects of air pollutants, consistent evidence for an association between air pollution exposure and food allergy is lacking. A prospective birth cohort study of nearly 4,000 children in the Netherlands (PIAMA) found positive associations between traffic-related air pollutant exposure (PM2.5, NO2 and soot) and sensitization to common food allergens at 4 years of age (39). However, these associations were no longer observed in the same cohort at 8 years of age (40). In a Swedish birth cohort study including over 2,500 children (BAMSE), exposure to PM10 and nitrogen oxides was associated with increased risk of food sensitization at age 8 years (OR 2.30; 95% CI, 1.10–4.82) (41), but not at age 4 years (42). Recently, a US birth cohort study including 996 mother-child pairs (Project Viva) found that prenatal exposure to black carbon (OR 1.4; 95% CI, 1.1–1.7) or PM2.5 (OR 1.3; 95% CI, 1.1–1.7) was associated with increased the risk of sensitization to foods and aeroallergens combined; rates of food allergy were not reported (43).

Meta-analyses of birth cohort studies have also yielded conflicting results. A meta-analysis of five European birth cohort studies, including the BAMSE and PIAMA cohorts, found no association between air pollution exposure and food allergen sensitization during the first 10 years of life (44). In contrast, a 2015 meta-analysis of 11 birth cohort studies, which also included the BAMSE and PIAMA cohorts, reported that increasing exposure to PM2.5 was associated with sensitization to food allergens at ages 4 and 8 years (45). More recently, a meta-analysis of 6163 children from four European birth cohorts participating in the Mechanisms of the Development of Allergy (MeDALL) consortium found no association between air pollution exposure and sensitization to common food allergens in children up to 16 years of age (46)●●. A limitation of these studies is the inability to accurately assess air pollution exposure at the individual or household level. As technologies for personal environmental monitoring improve, it will be important to determine how individual air pollutant exposures impact food allergy development.

The increasing prevalence of wildfires, which is likely being driven by climate change, is also an emerging cause of air pollution (47). Wildfire smoke can be significant source of ambient air pollution in some parts of the world, accounting for nearly half of PM2.5 exposure (48). Wildfire smoke also contains volatile organic compounds and other toxic substances that can induce inflammation and damage epithelial barriers (49). While an association between wildfires and food allergy has yet to be investigated, a recent cross-sectional study of 4147 patients at an academic dermatology clinic found that exposure to wildfire-associated air pollution was associated with exacerbations of AD (50). Given that AD is a risk factor for epicutaneous sensitization to foods, it will be important to investigate whether early-life wildfire exposure is associated with food allergy development.

MICROBIAL EXPOSURES

Urbanization and the modern lifestyle are leading to decreased exposure to microbes during early life, which has been associated with increased risk for allergies and other chronic noncommunicable diseases, likely due to alterations in the human microbiome (51). Early-life microbial colonization plays an important role in immune system development and helps determine whether exposure to allergens results in tolerance or immunity (52). Several factors can alter the infant microbiota, including early-life antibiotic exposures, cesarean section and formula feeding (53). While these factors are important, none alone have consistently been shown to significantly increase the risk for food allergy, indicating the complexity of the microbiome-immune axis.

Urbanization is associated with increased risk for food allergy (54), and recent studies have investigated whether this may be due to changes in the microbiome. Using longitudinal data from a birth cohort of 700 children in Denmark (COPSAC2010), Lehtimaki et al. (55)● investigated whether the degree of urbanization (based on land cover from satellite imaging) during infancy altered the microbiome and how this related to atopy. They observed differences in airway and gut microbiota between urban and rural infants, which was associated with an increased risk of asthma in the urban cohort. However, no relationship between urbanization and food allergen sensitization was found, and food allergy prevalence was not reported. Recently, Seppo et al. (56)● compared the gut microbiome of infants from urban/suburban homes in Rochester, New York, to those from nearby rural Old Order Mennonite (OOM) communities who practice a traditional farming lifestyle and have low rates of food allergy (57). They observed significant differences in stool microbiome at a median of 2 months of age, with OOM infants having enrichment of Bifidobacteriaceae and high rates of B. infantis colonization. OOM infants had lower rates of food allergy, but there was no association between B. infantis colonization and food allergy, likely due to the overall low rates of food allergy in the cohort (56). Changes in the home microbiota due to urbanization could also affect the host microbiome. Analysis of dust samples from a subset of subjects in the South African Food Allergy (SAFFA) study, a cohort of urban and rural toddlers screened for challenge-proven food allergy, demonstrated significant differences in microbial composition between urban and rural homes, with urban house dust having decreased relative abundance of Clostridiales, Lachnospiraceae, Ruminococcaceae, and Bacteroidales (58). While an association between the microbial composition of the house dust and food allergy was not assessed, other studies have shown that the indoor microbiota can impact risk for allergic disease such as asthma (59).

Pacifiers are another potential source of microbial exposure early in life. A Swedish birth cohort study had found lower rates of food sensitization in children whose parents used their own mouths to clean the child’s pacifier, which was associated with changes in the child’s salivary microbiota (60). Expanding upon these findings, Soriano et al. (61)●● investigated whether pacifier usage and sanitation methods were associated with challenge-proven food allergy in 787 infants from an Australian birth cohort. They found that any pacifier use was associated with food allergy at 6 months (aOR 1.94; 95% CI, 1.04–3.61), but this was primarily driven by the concurrent use of antiseptics for pacifier sanitation (aOR 4.83; 95% CI, 1.10–21.18), as other pacifier sanitation methods were not associated with food allergy. The mechanisms responsible for this association were not investigated, and thus it will be important to determine if pacifier sanitation methods alter the oral or gut microbiome of infants.

Other components of the exposome that can impact microbial exposure include mode of birth, antibiotic use, pet ownership, livestock exposure, family size, daycare attendance and consumption of unpasteurized milk. Using data from the previously mentioned SAFFA study, Levin et al. (62) examined the association of several of these factors with food allergy. They found that the relative impact of environmental exposures on food allergy varied between urban and rural populations. For example, antenatal or childhood exposure to farm animals was protective against food allergy in the rural cohort. Consumption of unpasteurized milk was uncommon in the rural cohort, indicating that this was unlikely responsible for the observed protection of the rural environment. In the urban cohort, birth by cesarean section was associated with food allergy, possibly due to higher cesarean section rates in this cohort (40.5% in urban vs. 18.8% in rural cohorts). Antibiotic exposure was also associated with increased food allergy in the urban cohort, despite higher rates of antibiotic use in the rural cohort. Recently, Lyons et al. (63) investigated the associations between several environmental exposures and food sensitization using data from 2196 children enrolled in the cross-sectional EuroPrevall project. They found that childhood food sensitization was inversely associated with dog ownership (OR 0.65; 95% CI, 0.48–0.90), but no associations were observed with family size, daycare attendance, antibiotic use, or exposure to a farm environment. Overall, these studies suggest a complex interplay between different environmental exposures, and that the relative contribution of specific exposures to food allergy development varies between the rural and urban setting.

RESIDENTIAL GREENNESS

Residential greenness refers to the natural vegetation surrounding the home. Green environments are thought to promote human health by facilitating physical and social activities, reducing stress, and mitigating adverse effects of air pollution and extreme heat (64). Greenspaces may also increase exposure to a variety of environmental microbes that foster normal immune development and provide protection against atopic and inflammatory diseases: a core tenet of the biodiversity hypothesis (65). While residential greenness has been associated with a number of health benefits, including a reduction in all-cause mortality (64), its effect on allergic disease development is unclear, with some studies showing protection against atopy while others report an increased risk (66).

Recent studies have begun to investigate whether there is an association between residential greenness and food sensitization or food allergy. Using data collected from 631 children in the German birth cohort LISA Leipzig, Markevych et al. (67) assessed whether residential greenness (as determined by Normalized Difference Vegetation Index, NVDI) and exposure to allergenic trees during early-life was associated with allergic sensitization to aeroallergens and foods. There was no association between greenness and food sensitization, but they did find a positive relationship between exposure to allergenic trees and food sensitization in a single-exposure model (OR 1.59; 95% CI, 1.05–2.42), possibly due to cross-reactivity between certain pollens and food allergens. Analysis of early-life residential greenness by NVDI and the Enhanced Vegetation Index (EVI) for 522 mother-child pairs in a Chinese birth cohort found no association with physician-diagnosed food allergy at 2 years of age (68), although a positive association between greenness and eczema was observed (OR 1.26; 95% CI, 1.02–1.56). More recently, Peters et al. (69)●● analyzed NDVI data from 5097 infants enrolled in the HealthNuts Study, a large population-based cohort in Melbourne, Australia, that performed oral food challenges to confirm food allergy in 12-month-old infants sensitized to either peanut, egg or sesame. The researchers found that increasing environmental greenness was associated with challenge-proven peanut allergy (aOR 1.78; 95% CI, 1.13–2.82 for the highest tertile) and egg allergy (aOR 1.38; 95% CI, 1.05–1.82 for the highest tertile). The authors postulated that increased exposure to pollens in greenspace areas could stimulate innate immunity and promote Th2 skewing of immune responses to foods. Overall, the results of recent studies suggest either no link or a possible association of residential greenness with food allergy. A limitation of these studies is that residing near greenspaces does not equate to a person using the greenspaces, and other confounders may be present. More research is needed to determine what role if any residential greenness has in food allergy development.

CONCLUSION

Recent studies indicate that specific exposures with in the external exposome can impact the development of food allergy (Table 1). There is strong evidence that exposure to environmental food allergens can lead to epicutaneous sensitization. Studies also suggest that the airway may be another route for sensitization to environmental food allergens, and that co-exposures to adjuvants within the indoor environment, such as microbial products and proteases, can further modify food allergy risk. Birth cohort studies have not found a consistent association with air pollution exposure and food sensitization, although further studies are needed to better define pollutant exposure at the individual level and whether this affects food allergy risk. Wildfires and other environmental disasters associated with climate change may impact the developing immune system in children, and studies are needed to determine whether these exposures could contribute to food allergy development. Early-life microbial exposures associated with a rural lifestyle appear to be protective against food allergy development in some cohorts. In contrast, there is concern that urbanization and other components of the modern lifestyle may contribute to food sensitization, possibly by modifying the infant microbiome. Although residential greenness is associated with several health benefits, current evidence does not support a protective role against food allergy. While environmental exposures play a critical role in food allergy development, it will also be important to consider how gene-environment interactions modify food allergy risk (Figure 1). Identifying those children at highest risk for food allergy based on both genetic and environmental factors will likely improve the efficacy of interventions aimed at mitigating the risk for food allergy development.

Table I:

Recent studies of select environmental exposures and impact on food sensitization or food allergy

Reference Study population Exposure(s) Findings
(19) UK birth cohort of 623 children Environmental peanut allergen  • Positive association between peanut dust levels and peanut sensitization/allergy in children with filaggrin loss-of-function mutations
(20) US cohort of 359 atopic children (CoFAR) Environmental peanut allergen  • Exposure-response relationship between peanut levels in dust and peanut sensitization and allergy
 • Strongest association found in children with eczema
(16) Japanese cohort of 159 children Environmental egg exposure  • Maternal egg consumption and number of home inhabitants was associated with higher egg levels in house dust
 • No association between egg allergy and egg dust levels at 6 years
(39,40) Netherlands birth cohort of 4146 children (PIAMA) Air pollutants  • Positive associations between PM2.5, NO2 and soot exposure and food sensitization at 4 years, but not at 8 years
(41,42) Swedish birth cohort of 2545 children (BAMSE) Air pollutants  • Exposure to NO2 and particulate matter (PM) was associated with increased risk for food sensitization at 8 years, but not at 4 years
(43) US cohort of 996 mother-child pairs (Project Viva) Air pollutants  • Black carbon and PM2.5 exposure was associated with increased risk of food and aeroallergen sensitization
(55) Danish birth cohort of 700 children (COPSAC2010) Urbanization, microbiome  • Composition of airway and gut microbiome significantly differed between urban and rural infants
 • No effect of urbanization on food sensitization
(56) US cohort of 39 Rochester and 65 Old Order Mennonite (OOM) mother-infant pairs Urbanization, microbiome  • Lower rates of food allergy in OOM infants
 • High rates of B. infantis colonization in OOM infants, but did not correlate with food allergy
(61) Australian birth cohort of 787 infants Microbial exposures (pacifier use)  • Pacifier use was associated with food allergy at 6 months likely due to use of antiseptics for pacifier sterilization
(62) South African cohort of 1185 urban and 398 rural toddlers (SAFFA) Farm animal exposure, unpasteurized milk consumption, birth by cesarean section, antibiotic use, maternal smoking  • Antenatal and childhood exposure to farm animals was protective against food allergy in rural cohort
 • Consumption of unpasteurized milk was not associated with protection in rural cohort
 • Birth by cesarean section and use of antibiotics was associated with increased risk for food allergy in urban cohort
 • Maternal smoking during pregnancy was associated with increased food allergy risk in both urban and rural cohorts
(63) 2323 children enrolled in European cross-sectional cohort study (EuroPrevall) Pet ownership, family size, daycare attendance, antibiotic use, farm environment, parental smoking  • Dog ownership associated with decreased risk for food sensitization
 • No association of other exposures with food sensitization
(67) German birth cohort of 631 children (LISA Leipzig) Residential greenness  • No association between greenness and food sensitization
 • Positive relationship between allergenic tree exposure and food sensitization
(68) Chinese birth cohort of 522 mother-child pairs Residential greenness  • No association between greenness and physician-diagnosed food allergy at 2 years
 • Positive relationship between greenness and eczema
(69) Australian cohort study of 5097 infants (HealthNuts) Residential greenness  • Increasing environmental greenness associated with challenge-proven peanut and egg allergy at 12 months
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Figure 1: Food allergy risk is dependent upon environment-gene interactions.

Figure 1:

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Environmental exposures, including environmental food allergens, air pollution, microbes and residential greenness, interact with host genetic factors to determine food allergy risk. Created with BioRender.com.

KEY POINTS:

  • The external exposome plays a critical role in food allergy development.

  • Cutaneous and possibly airway exposures to environmental food allergens are risk factors for food sensitization and allergy.

  • Microbial exposures associated with a rural lifestyle are likely protective against food allergy development.

  • The role of air pollution and residential greenness in food allergy development is unclear and warrants further investigation.

2. Financial support and sponsorship:

This work was supported by funding from the National Institute of Health (R01-ES032544).

Footnotes

3.

Conflicts of interest: None.

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