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Wise et al.

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Several international case-control and cross-sectional studies have also evaluated the relationship between pollution and AR with varied results. Anderson et al. 581 performed the largest cross-sectional study evaluating the effect of PM 10 levels on the development of rhinoconjunctivitis in 322,529 children from 51 countries. There was no between-country association of rhinitis with modeled pollution levels, and within countries (24 countries had more than 1 study center) there were weakly positive associations between PM 10 levels and rhinoconjunctivitis symptoms in 6-year-olds to 7-year-olds and diagnosed hay fever in 13 year-olds to 14-year-olds. Interestingly, they did show a positive association between high PM 10 levels and the development of atopy. 581 Some pediatric studies have identified a positive correlation between increased exposure to various pollutants and an increased diagnosis of AR during childhood. 476,557,582-589 Liu et al. 586 and Deng et al. 557 even found that prenatal/gestational exposure to high concentrations of NO 2 were associated with a higher prevalence of AR diagnosis during childhood. However, almost all of these studies utilize nearby traffic density or home address geocodes to estimate local pollution exposure. In many countries, people living in more polluted areas with high levels of traffic may also be more likely to have other confounding features that influence their development of AR (ie, socioeconomic status [SES], exposure to different aeroallergens) and not all studies fully adjust for these potential confounders. Additionally, several of these studies were restricted to specific cities in Asia, in turn, limiting generalizability. Overall, the relationship between pollution exposure and the development AR is currently unclear. More prospective pediatric and adult studies in diverse geographic locations are needed to better understand this complex relationship. • Aggregate Grade of Evidence: C (Level 2b: 3 studies; Level 3b: 2 studies; Level 4: 9 studies; Table VI.D). AR has frequently been associated with both active and passive (secondhand) exposure to tobacco smoke. However, the pathophysiology behind this relationship is complex and, at times, contradictory. Studies have shown that tobacco smoke exposure can propagate the development of atopic diseases via several mechanisms including direct surface damage to nasal mucosa, altered epigenetic mechanisms through histone acetylation, expression of microRNA, and DNA methylation. 590,591 Alternatively, it has also been shown that nicotine may exert an immunosuppressive effect on allergic disease by suppressing eosinophil trafficking and Th2 cytokine/chemokine responses. 592 Recently, 2 large meta-analyses were published which sought to better define the relationship between tobacco and AR (Table VI.E). Saulyte et al. 593 identified a significant correlation between passive smoke exposure and the development of AR, but no significant relationship between active smoking or maternal prenatal passive smoke exposure and AR. However, they did find a significant correlation between active smoking and non-allergic/ chronic rhinitis. Hur et al. 594 also systematically evaluated the relationship between secondhand smoke and AR and that meta-analysis of studies in adults showed an association between passive smoke and AR, while a similar analysis of pediatric studies did not. This raises the possibility that the atopic effects of secondhand smoke in the nasal mucosa may

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VI.E. Tobacco smoke

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