Environmental Exposures: Evolving Evidence for Their Roles in Adult Allergic Disorders

Kaoru Harada; Rachel L. Miller


Curr Opin Allergy Clin Immunol. 2022;22(1):24-28. 

In This Article

Epidemiologic Associations


Despite the importance of allergen exposure to multiple allergic diseases, recent research among adults has focused mostly on asthma. For example, one retrospective study evaluated short-term effects of aeroallergens gathered from 3 pollen-collecting stations in Seoul on asthma exacerbation visits to emergency rooms (ERs) in 2008–2012. Among cases, 8,639 (29.97%) were adults aged 18–59 years, and 6,675 (23.16%) were in elderly adults aged 60 years or older. Tree, but not grass or weed, allergen was associated with asthma exacerbations in adults aged 18–59 years only.[5] These results suggest that specific allergic triggers of ER visits for asthma may vary across aeroallergens.

Roberts et al. elucidated the relationship between allergic sensitization and current allergy symptoms by assessing component-resolved diagnostics that detect immunoglobulin (Ig) E for individual allergens. Machine learning was used to study interactions across over 100 allergenic components, and network analyses were applied to determine whether connectivity differed by asthma severity, including among the 509 (65.26%) in their cohort that were adults. There was no relationship between an elevated IgE level to any single allergen and asthma severity. But in severe asthma, there was weak connectivity among IgE levels to proteins that were structurally unrelated, whereas in mild or moderate asthma, there were fewer but stronger connections between structurally similar proteins.[6] The number, structural similarity, and strength of connectivity patterns among allergenic components may be useful biomarkers of disease severity in patients with allergic asthma.

Air Pollution

Despite conflicting evidence,[7] an American Thoracic Society workshop published a report in 2020 writing that there was inconclusive evidence regarding outdoor air pollution exposure and new onset asthma in adults.[8] Findings regarding air pollution and eczema are inconsistent and may reflect differences by asthma phenotype, particularly atopic versus nonatopic eczema. The Study on the influence of Air pollution on Lung function, Inflammation and Aging (SALIA) reported on a cohort of adult women in Germany who was followed for 19 years. Traffic-related air pollution (TRAP) exposure was estimated from residential addresses using land-use regression models based on 3 two weeks' measurements of nitrogen oxides (NOX), NO2, and particulate matter (PM). TRAP exposure at baseline was estimated using back-extrapolation algorithm. The incidence of patient-reported eczema after age 55 years was associated with NO2, NOx, PM2.5 (PM diameter ≤ 2.5 μm), and PM10 (PM diameter ≤ 10 μm).[9] A subsequent study was done in this cohort of older women using three increasingly strict definitions to exclude atopy: participants who never had hay fever, participants who never had hay fever and did not have IgE levels greater than 100 IU/mL at baseline, and participants who never had hay fever and did not have IgE levels greater than 100 IU/mL at baseline and follow-up. When these stricter definitions were applied, the previously described association between air pollutants (NO2, NOx, PM2.5, PM10) at baseline and eczema incidence after age 55 years grew stronger. Thus, TRAP may influence the development of nonatopic eczema more than atopic eczema in older women.[10] However, these findings were not replicated by Lopez et al. when they conducted a prospective study on air pollution and eczema in Tasmania, Australia. The participants were 43 years old at baseline, and eczema were evaluated 10 years later. Air pollution exposure at residential address was measured using distance from a major road and NO2 and PM2.5 levels from satellite-based land-use regression models. Atopic eczema was defined as having at least one positive skin prick testing to common aeroallergens. NO2 exposure was associated with increased odds of prevalent eczema and for atopic eczema specifically at follow-up in males, but not females. Similarly, NO2 and PM2.5 were associated with increased odds of persistent atopic eczema in males only. Unlike the findings from SALIA, no significant association was observed between ambient air pollution and incident eczema.[11]

The association between air pollution and rhinitis may depend on phenotype. A cross-sectional study of two European cohorts after twenty years of follow-up found that higher exposures to PM10 and PM2.5 were associated with higher levels of rhinitis severity. When participants were stratified by allergic sensitization, the effects of pollutants strengthened for participants with nonallergic rhinitis. Increasing levels of NO2, PM10, PM2.5, PMcoarse and traffic intensity on the nearest road were associated with increased severity score of rhinitis in nonallergic participants, whereas only PM2.5 was associated with severity in participants with allergic sensitization. A similar pattern was observed when participants were stratified by asthma status; increases in NO2, PM10, PM2.5, and traffic load and intensity were associated with increased severity score of rhinitis only among the nonasthmatics.[12] Overall, it appears that air pollution may contribute more to rhinitis severity in individuals with nonatopic phenotypes.


The National Health and Nutritional Examination Survey (NHANES) has yielded abundant cross-sectional findings on chemical exposures from a diverse and large sample across the United States. Overall, the association between chemical exposures and asthma appears to vary by age and sex. For example, one study measured spot urine phthalate metabolite concentrations and found no significant associations between phthalate levels and self-reported asthma in adults overall. However, in stratified analyses, mono-ethyl phthalate (MEP) was associated with current asthma in adult males. In contrast, mono-(3-carboxylpropyl) phthalate (MCPP) and mono-(carboxynonyl) phthalate (MCNP) were negatively associated with current asthma in adult females.[13] Mendy and colleagues found that spot urine levels of bisphenol (BP) F, but not BPA, was associated with higher odds of current asthma. This association was strongest in adults aged 18–59 years compared to younger and older age groups. When stratified by sex, higher BPS levels were associated with increased odds of asthma in males, but not females.[14]

Among the same cohort of patients, Mendy et al. found that higher urinary BPF levels were associated with self-reported symptoms of allergic rhinitis after adjustment by age.[14] Another study evaluating allergic symptoms in relation to urinary nitrate, thiocyanate, and perchlorate levels found that urinary thiocyanate was positively associated with the prevalence of sneeze regardless of age and sex.[15]


Recent research generated from NHANES also suggested that exposure to endotoxin may synergize with other environmental toxicants to cause allergies.[16,17] Mendy and colleagues investigated the contributions of endotoxin measured from bedroom dust with air pollution exposure predominantly (75.8%) among adults participating in NHANES. Annual average exposures to PM2.5, ozone (O3) and NO2 at participants' addresses were estimated using air quality modeling systems from the Environmental Protection Agency. PM2.5, O3, and NO2 were associated with higher ER visits for asthma in the past 12 months. Interestingly, co-exposure to elevated concentrations of residential endotoxin and ambient PM2.5 increased the odds of ER visits for asthma in the past 12 months by fivefold. This association was stronger than the sum of endotoxin alone and PM2.5 alone, suggesting that these environmental exposures interacted synergistically.[18]


The influence of the microbiome, part of our internal exposome, on the development of allergic diseases continues to be delineated. A cross-sectional study of adult farmers and their spouses from North Carolina and Iowa found that bedroom dust bacterial diversity was lower in participants with seroatopy or allergic rhinitis, but not asthma. The bacterial composition differed as well, with the genera Bacteroides, Porphyromonas, and Fusobacterium more abundant in homes of participants with asthma and allergic rhinitis.[19]

A cross-sectional study of the adult nasopharyngeal microbiome found that the composition of the microbiome, but not its diversity, differed by asthma diagnosis. Additionally, different patterns were observed by age group. In young adults aged 18–45 years, phylum Proteobacteria was more abundant in asthmatics, whereas genera Corynebacteriales was higher in nonasthmatics. In the elderly group aged 65 years or older, genera Moraxella was more common in nonasthmatics. The relative abundance of genes whose functions related to N-glycan biosynthesis, peroxisome proliferator-activated receptor gamma signaling and degradation of toxins were lower in asthmatics. In contrast, genes whose functions related to pentose phosphate pathway, lipopolysaccharide biosynthesis, flagellar assembly, and bacterial chemotaxis were higher in asthmatics.[20] These findings suggest that bacterial composition, not diversity, may play a functional role in asthma.