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Wise et al.

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followed standard feeding practices, infants in the food-avoidance arm showed a significant reduction in rates food allergy and milk sensitization before age 2 years. However, by the age of 7 years, the prevalence of food allergy was no longer different between the 2 groups. Furthermore, there was no difference in rates of AR, AD, asthma, and other atopic disease at age 7 years. 573 Based on the presented meta-analysis, prospective randomized studies, and a large prospective birth cohort study, there is no data to support maternal diet as a contributing factor for the development of food allergy and AR; however, there is some evidence that the presence of food allergy during childhood (greater than 2 years old) is a risk factor for AR. • Aggregate Grade of Evidence: A (Level 1b: 3 studies; Level 2a: 1 study; Level 2b: 1 study; Table VI.C). The relationship between pollution and AR has received increasing attention over the past decade. Environmental air pollutants contain several compounds; however, most studies have primarily focused on particulate matter <10 μ m (PM 10 ), particulate matter <2.5 μ m (PM 2.5 ), nitrogen dioxide (NO 2 ), sulfur dioxide (SO 2 ), carbon monoxide (CO), and ozone (O 3 ). These particles may potentiate atopy through multiple mechanisms, including injuring the nasal epithelium, altering the immune response, and increasing the allergenicity of certain antigens. 574,575 For example, pollution may damage the nasal mucosa and impair MCC, thereby facilitating the access of inhaled allergens to cells of the immune system. 576 Additionally, airborne particles, including diesel fuel exhaust, are also able to carry allergens, thus potentially increasing the spread of allergens or the duration of their exposure. 574 In nasal provocation studies of HDM-sensitive individuals, a combined nasal challenge with HDM allergens and diesel exhaust particles led to enhanced mast cell degranulation and increased severity of rhinitis symptoms compared to a challenge with HDM alone. 577 Numerous studies have examined the effects of air pollutants on the development of AR in both pediatric and adult patients (Table VI.D). However, 3 prospective cohort studies (the highest level of evidence identified for this topic) found no significant correlation. 578-580 Codispoti et al. 578 specifically looked at the relationship between exposure to diesel exhaust particles (DEP) at 1 year of age and the subsequent development of AR at 2, 3, and 4 years of age. While they found that DEP had a marginally positive association with aeroallergen sensitization at 2 and 3 years, and increased aeroallergen sensitization increased the risk of AR, they failed to identify a significant direct correlation between DEP and AR development. Additionally, Kim et al. 579 evaluated exposure to NO 2 , SO 2 , CO, and PM 10 in children and found no significant association with a new diagnosis of AR after 2 years. However, they did note a positive association between increased levels of O 3 and an AR diagnosis in industrial areas only; O 3 was also significantly associated with the development of new sensitizations to outdoor allergens, which may explain the mechanism for the related increase in AR prevalence. Finally, Gehring et al. 580 pooled 4 prospective pediatric birth cohort studies with 14 to 16 year follow-up and found no indication that NO 2 , PM 2.5 , or PM 10 levels influenced the development of rhinoconjunctivitis.

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VI.D. Pollution

Int Forum Allergy Rhinol . Author manuscript; available in PMC 2020 June 10.