Grass pollen concentrations associated with food reactivity, eczema flares in children
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Increases in concentrations of grass pollen were associated with increases in risk for food skin prick test reactivity and eczema flares in children, according to a study published in Pediatric Allergy and Immunology.
Exposure to grass pollen also may have a bigger impact among children who already have a peanut allergy, according to Nur Sabrina Idrose, MSc, PhD student and research assistant, allergy and lung health unit, Melbourne School of Population and Global Health, and colleagues.
“We hypothesized that high pollen exposure may result in an inflammatory response that may lower the threshold for manifestation of other allergic diseases such as food allergy and eczema, and this may include those without pre-existing respiratory conditions or known grass pollen sensitization,” Idrose told Healio.
Previous research only investigated long-term associations, such as pollen exposure at birth or in utero and the risk for food allergy later in childhood, Idrose explained.
“We did this study because population-based studies investigating the role of short-term pollen exposure in food allergy and eczema are lacking,” she added.
Study results
The researchers examined 1,108 infants aged 1 year, 675 of whom had data at age 6 years. These examinations occurred during grass pollen seasons, with grass pollen concentrations recorded on the day of testing (lag 0), up to 3 days before (lag 1 to lag 3) and cumulatively (lag 0-3).
Although there was no overall association between grass pollen exposure and food SPT reactivity at age 1 year, the researchers found interactions among infants with a family history of peanut allergy (P for interaction = .03). At lag 0, infants with a family history of food allergy experienced 1.3 times (95% CI, 1-2.4) greater odds for peanut SPT reactivity with each 29 grains/m3 increase in grass pollen concentrations.
Infants with peanut allergies experienced an association between grass pollen concentrations and higher median serum food-specific IgE levels at lag 1 (coefficient, 5.8 kUA/L; 95% CI, 0.3-12) and lag 0-3 (coefficient, 1.2 kUA/L; 95% CI, 0.6-2), although there was no evidence for a similar association among infants with egg allergies.
Also, infants with peanut allergies, but not those with egg allergies, experienced a nonlinear association between grass pollen concentrations and lower median reaction thresholds to oral food challenges at lag 0 (P < .001).
At age 6 years, each 20 grains/m3 increase in grass pollen concentrations at lag 0-3 increased odds for SPT reactivity to peanut (OR = 1.17; 95% CI, 1-1.3 ), cashew (OR = 1.13; 95% CI, 1-1.24), hazelnut (OR = 1.15; 95% CI, 1-1.35), almond (OR = 1.17; 95% CI, 1-1.37), egg (OR = 1.22; 95% CI, 1-1.43) and sesame (OR = 1.17; 95% CI, 1-1.4).
Also, researchers observed a 1.13 times (95% CI, 1.13-1.22) increased risk for eczema flares with grass pollen at lag 0-3 among the 6 year olds, although they didn’t observe this association at age 1 year.
At 6-year follow-up, grass pollen concentrations did not show persistent associations with IgE levels or reaction thresholds to OFCs.
Interpretations
Idrose said that some of these findings were surprising.
“The associations between grass pollen concentration and food SPT reactivity were not restricted to or amplified in children with grass pollen sensitization,” she said. “Similarly, the associations with eczema flares were not limited to children with reported eczema in the past 12 months or grass pollen sensitization.”
The researchers said these results could be attributed to several causes.
“Firstly, this could be due to small sample bias or residual confounding,” Idrose said. “Secondly, increased awareness in parents of children with allergic disease may have led to adoption of preventive measures during the pollen season to reduce the burden of exposure.”
The researchers also only performed SPTs to ryegrass and Bermuda grass pollen, Idrose continued, although some children may be sensitized to other types of grass pollen.
“Furthermore, we did not have quantitative data on sensitization such as the serum allergen-specific IgE for grass pollen,” she continued. “Lastly, pollen has nonallergenic properties, which can trigger non-IgE mediated responses, and this could not have been distinguished by skin prick tests.”
Still, Idrose called the study’s findings significant.
“Persistent grass pollen exposure may trigger dysregulation of immune responses leading to increased odds of food SPT reactivity and eczema flares in children, but the impact on food may be greater if peanut allergy is already present,” she said.
Before these findings can be applied to clinical guidelines, however, Idrose said that they first need to be replicated and confirmed.
“In the interim, there is no harm in advising patients to take preventive measures such as limiting time spent outdoors, using indoor air filters and/or closing windows during the grass pollen season,” Idrose said. “Additional caution for peanut avoidance may also need to be taken for peanut-allergic children.”
The researchers also called for further research into the physiological mechanisms that occur after pollen exposure.
“It would be interesting to investigate the severity of food allergy and eczema as outcomes since we did not have sufficient sample size for this,” Idrose said. “It would also be interesting to investigate the role of other aeroallergens in food allergy and eczema, such as weed pollen, tree pollen and fungi.”
For more information:
Nur Sabrina Idrose, MSc, can be reached at sabrina.idrose@unimelb.edu.au.