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Background: The global incidence of thyroid cancer has increased over the past several decades. While this increase is partially due to increased detection, environmental pollutants have also emerged as a possible contributing factor. Our goal was to perform a systematic review to assess the relationship between environmental air pollution and thyroid cancer. Methods: Systematic literature search was performed using PubMed, EMBASE, Cochrane Library, Web of Science, and Scopus databases for original articles published prior to March 2024, investigating outdoor air pollution and thyroid cancer/nodules (PROSPERO CRD42024517624). Inclusion criteria included quantitative reporting of pollutant levels and effect size. Specific pollutants included ozone (O 3 ), particulate matter less than 2.5 (PM 2.5 ) or 10 microns in diameter (PM 10 ), sulfur dioxide (SO 2 ), nitric oxides (NO x ), carbon monoxide (CO), and polyaromatic hydrocarbons (PAHs). Study design, sample size, pollution assessment method, covariates, and strength/direction of associations between pollutants and thyroid cancer/nodule detection were extracted, and descriptive synthesis was utilized to summarize pertinent findings. Risk of bias was assessed using the National Heart, Lung, and Blood Institute quality assessment tool. Results: Of 1294 identified studies, 11 met inclusion criteria. Over 6 million patients from diverse regions were represented across studies. Pollutants studied included O 3 in 5 studies; PM 2.5 , PM 10 , SO 2 , and NO x in 3 studies; unspecified PM and CO in 2 studies; and PAHs in 1 study. Primary outcome was thyroid cancer diagnosis among 9 studies and thyroid nodule detection in 2. All studies examining NO x and O 3 reported increased risks ranging from 1.03 to 1.5-fold and 1.1 to 1.3-fold, respectively. Both studies assessing PM 2.5 reported 1.18 to 1.23-fold increased odds of thyroid cancer diagnosis, and the magnitude of association increased with increasing duration or concentration of PM 2.5 Inconsistent results were observed for levels of CO, PM 10 , and SO 2 . Conclusion: While an emerging body of literature suggests a potential association between air pollution and thyroid cancer, the quality of evidence is limited by study design constraints, variability in exposure assessment, and inconsistent adjustment for potential confounding factors. The heterogeneity in study designs and methodologies present challenges in interpreting results, underscoring the need for standardized approaches in future research.

Background: Chronic rhinosinusitis (CRS) is a prevalent upper respiratory condition that manifests in two primary subtypes: CRS with nasal polyps (CRSwNP) and CRS without nasal polyps (CRSsNP). While previous studies indicate a correlation between air pollution and CRS, the role of genetic predisposition in this relationship remains largely unexplored. We hypothesized that higher air pollution exposure would lead to the development of CRS, and that genetic susceptibility might modify this association., Methods: This cohort study involving 367,298 adult participants from the UK Biobank, followed from March 2006 to October 2021. Air pollution metrics were estimated at residential locations using land-use regression models. Cox proportional hazard models were employed to explore the associations between air pollution exposure and CRS, CRSwNP, and CRSsNP. A polygenic risk score (PRS) was constructed to evaluate the joint effect of air pollution and genetic predisposition on the development of CRS., Results: We found that the risk of CRS increased under long-term exposure to PM 2.5 [the hazard ratios (HRs) with 95 % CIs: 1.59 (1.26-2.01)], PM 10 [1.64 (1.26-2.12)], NO 2 [1.11 (1.04-1.17)], and NO x [1.18 (1.12-1.25)], respectively. These effects were more pronounced among participants with CRSwNP, although the differences were not statistically significant. Additionally, we found that the risks for CRS and CRSwNP increased in a graded manner among participants with higher PRS or higher exposure to PM 2.5 , PM 10 , or NO x concentrations. However, no multiplicative or additive interactions were observed., Conclusions: Long-term exposure to air pollution increases the risk of CRS, particularly CRSwNP underscoring the need to prioritize clean air initiatives and environmental regulations., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024. Published by Elsevier B.V.)

This review article highlights air pollution as a critical global health concern with emphasis on its effects and role in the development and exacerbation of upper airway and lower airway disease with a focus on allergic rhinitis and asthma. This review underscores the World Health Organization's recognition of air pollution as the biggest environmental threat to human health. It discusses the various components and categories of air pollutants and the evidence-based effects they have on asthma and allergic rhinitis, ranging from pathogenesis to exacerbation of these conditions across various age groups in different geographic locations., (Copyright © 2023 Elsevier Inc. All rights reserved.)

Background: Chronic exposure to particulate matter air pollution (PM 2.5 ) is associated with chronic rhinosinusitis (CRS). Elevated ambient temperature may increase PM 2.5 levels and thereby exacerbate sinonasal symptoms. This study investigates the association between high ambient temperature and the risk of CRS diagnosis., Methods: Patients with CRS were diagnosed at Johns Hopkins hospitals from May to October 2013-2022, and controls were matched patients without CRS meanwhile. A total of 4752 patients (2376 cases and 2376 controls) were identified with a mean (SD) age of 51.8 (16.8) years. The effect of maximum ambient temperature on symptoms was estimated with a distributed lag nonlinear model (DLNM). Extreme heat was defined as 35.0°C (95 th percentile of the maximum temperature distribution). Conditional logistic regression models estimated the association between extreme heat and the risk of CRS diagnosis., Results: Exposure to extreme heat was associated with increased odds of exacerbation of CRS symptoms (odds ratio [OR] 1.11, 95% confidence interval [CI] 1.03-1.19). The cumulative effect of extreme heat during 0-21 lag days was significant (OR 2.37, 95% CI 1.60-3.50) compared with the minimum morbidity temperature (MMT) at 25.3°C. Associations were more pronounced among young and middle-aged patients and patients with abnormal weight., Conclusions: We found that short-term exposure to high ambient temperature is associated with increased CRS diagnosis, suggesting a cascading effect of meteorological phenomena. These results highlight climate change's potentially deleterious health effects on upper airway diseases, which could have a significant public health impact., (© 2023 ARS-AAOA, LLC.)

Background: Limited data exists suggesting that cumulative exposure to air pollution in the form of fine particulate matter (aerodynamic diameter ≤ 2.5 μm [PM 2.5 ]) may be associated with papillary thyroid carcinoma (PTC), although this relationship has not been widely established. This study aims to evaluate the association between PM 2.5 and PTC and determine the subgroups of patients who are at the highest risk of PTC diagnosis., Methods: Under IRB approval, we conducted a case-control study of adult patients (age ≥ 18) newly diagnosed with PTC between 1/2013-12/2016 across a single health care system were identified using electronic medical records. These patients were compared to a control group of patients without any evidence of thyroid disease. Cumulative PM 2.5 exposure was calculated for each patient using a deep learning neural networks model, which incorporated meteorological and satellite-based measurements at the patients' residential zip code. Adjusted multivariate logistic regression was used to quantify the association between cumulative PM 2.5 exposure and PTC diagnosis. We tested whether this association differed by gender, race, BMI, smoking history, current alcohol use, and median household income., Results: A cohort of 1990 patients with PTC and a control group of 6919 patients without thyroid disease were identified. Compared to the control group, patients with PTC were more likely to be older (51.2 vs. 48.8 years), female (75.5% vs 46.8%), White (75.2% vs. 61.6%), and never smokers (71.1% vs. 58.4%) (p < 0.001). After adjusting for age, sex, race, BMI, current alcohol use, median household income, current smoking status, hypertension, diabetes, COPD, and asthma, 3-year cumulative PM 2.5 exposure was associated with a 1.41-fold increased odds of PTC diagnosis (95%CI: 1.23-1.62). This association varied by median household income (p-interaction =0.03). Compared to those with a median annual household income <$50,000, patients with a median annual household income between $50,000 and < $100,000 had a 43% increased risk of PTC diagnosis (aOR = 1.43, 95%CI: 1.19-1.72), and patients with median household income ≥$100,000 had a 77% increased risk of PTC diagnosis (aOR = 1.77, 95%CI: 1.37-2.29)., Conclusions: Cumulative exposure to PM 2.5 over 3 years was significantly associated with the diagnosis of PTC. This association was most pronounced in those with a high median household income, suggesting a difference in access to care among socioeconomic groups., (© 2023. Crown.)

Background: The association between exposure to air pollution and papillary thyroid carcinoma is unknown. We sought to estimate the relationship between long-term exposure to the fine (diameter ≤ 2.5 μm) particulate matter component of air pollution and the risk of papillary thyroid cancer., Methods: Adult (age ≥18) patients with newly diagnosed papillary thyroid carcinoma between January 1, 2013 and December 31, 2016 across a single health system were identified using electronic medical records. Data from 1,990 patients with papillary thyroid carcinoma were compared with 3,980 age- and sex-matched control subjects without any evidence of thyroid disease. Cumulative fine (diameter <2.5 μm) particulate matter exposure was estimated by incorporating patients' residential zip codes into a deep learning neural networks model, which uses both meteorological and satellite-based measurements. Conditional logistic regression was performed to assess for association between papillary thyroid carcinoma and increasing fine (diameter ≤2.5 μm) particulate matter concentrations over 1, 2, and 3 years of cumulative exposure preceding papillary thyroid carcinoma diagnosis., Results: Increased odds of developing papillary thyroid carcinoma was associated with a 5 μg/m 3 increase of fine (diameter ≤2.5 μm) particulate matter concentrations over 2 years (adjusted odds ratio = 1.18, 95% confidence interval: 1.00-1.40) and 3 years (adjusted odds ratio = 1.23, 95% confidence interval: 1.05-1.44) of exposure. This risk differed by smoking status (p interactio n = 0.04). Among current smokers (n = 623), the risk of developing papillary thyroid carcinoma was highest (adjusted odds ratio = 1.35, 95% confidence interval: 1.12-1.63)., Conclusion: Increasing concentration of fine (diameter ≤2.5 μm) particulate matter in air pollution is significantly associated with the incidence of papillary thyroid carcinoma with 2 and 3 years of exposure. Our novel findings provide additional insight into the potential associations between risk factors and papillary thyroid carcinoma and warrant further investigation, specifically in areas with high levels of air pollution both nationally and internationally., (Copyright © 2021 Elsevier Inc. All rights reserved.)

Purpose of Review: Chronic rhinosinusitis (CRS) is a highly prevalent disease with large social and financial burdens. The pathophysiology is multifactorial. Environmental pollutants have been suggested to play a role in the inflammatory component of the disease process., Recent Findings: Recent work has focused on exposure to various pollutants, primarily particulate matter (PM). Exposure to environmental pollutants leads to upregulation of inflammatory markers and ciliary dysfunction at the cellular level. Mouse models suggest a role for epithelial barrier dysfunction contributing to inflammatory changes after pollutant exposure. Clinical studies support the role of pollutants contributing to disease severity in certain populations, but the role in CRS incidence or prevalence is less clear. Research is limited by the retrospective nature of most studies. This review focuses on recent advancements in our understanding of the impact of environmental pollutants in CRS, limitations of the available data, and potential opportunities for future studies., (© 2021. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.)

Importance: Anosmia, the loss of the sense of smell, has profound implications for patient safety, well-being, and quality of life, and it is a predictor of patient frailty and mortality. Exposure to air pollution may be an olfactory insult that contributes to the development of anosmia., Objective: To investigate the association between long-term exposure to particulate matter (PM) with an aerodynamic diameter of no more than 2.5 μm (PM2.5) with anosmia., Design, Setting, and Participants: This case-control study examined individuals who presented from January 1, 2013, through December 31, 2016, at an academic medical center in Baltimore, Maryland. Case participants were diagnosed with anosmia by board-certified otolaryngologists. Control participants were selected using the nearest neighbor matching strategy for age, sex, race/ethnicity, and date of diagnosis. Data analysis was conducted from September 2020 to March 2021., Exposures: Ambient PM2.5 levels., Main Outcomes and Measures: Novel method to quantify ambient PM2.5 exposure levels in patients diagnosed with anosmia compared with matched control participants., Results: A total of 2690 patients were identified with a mean (SD) age of 55.3 (16.6) years. The case group included 538 patients with anosmia (20%), and the control group included 2152 matched control participants (80%). Most of the individuals in the case and control groups were women, White patients, had overweight (BMI 25 to <30), and did not smoke (women: 339 [63.0%] and 1355 [63.0%]; White patients: 318 [59.1%] and 1343 [62.4%]; had overweight: 179 [33.3%] and 653 [30.3%]; and did not smoke: 328 [61.0%] and 1248 [58.0%]). Mean (SD) exposure to PM2.5 was significantly higher in patients with anosmia compared with healthy control participants at 12-, 24-, 36-, 60-month time points: 10.2 (1.6) μg/m3 vs 9.9 (1.9) μg/m3; 10.5 (1.7) μg/m3 vs 10.2 (1.9) μg/m3; 10.8 (1.8) μg/m3 vs 10.4 (2.0) μg/m3; and 11.0 (1.8) μg/m3 vs 10.7 (2.1) μg/m3, respectively. There was an association between elevated PM2.5 exposure level and odds of anosmia in multivariate analyses that adjusted for age, sex, race/ethnicity, body mass index, alcohol or tobacco use, and medical comorbidities (12 mo: odds ratio [OR], 1.73; 95% CI, 1.28-2.33; 24 mo: OR, 1.72; 95% CI, 1.30-2.29; 36 mo: OR, 1.69; 95% CI, 1.30-2.19; and 60 mo: OR, 1.59; 95% CI, 1.22-2.08). The association between long-term exposure to PM2.5 and the odds of developing anosmia was nonlinear, as indicated by spline analysis. For example, for 12 months of exposure to PM2.5, the odds of developing anosmia at 6.0 µg/m3 was OR 0.79 (95% CI, 0.64-0.97); at 10.0 µg/m3, OR 1.42 (95% CI, 1.10-1.82); at 15.0 µg/m3, OR 2.03 (95% CI, 1.15-3.58)., Conclusions and Relevance: In this study, long-term airborne exposure to PM2.5 was associated with anosmia. Ambient PM2.5 represents a potentially ubiquitous and modifiable risk factor for the loss of sense of smell.

Background: Air pollution exposure may contribute to rhinoconjunctivitis morbidity in children with underlying airways disease. Prior studies have not assessed rhinoconjunctivitis-related quality of life (QOL) in children with asthma chronically exposed to air pollution., Methods: Children ages 9-19 years with asthma from peri-urban Peru, self-reporting rhinoconjunctivitis symptoms (n = 484), were administered the Rhinoconjunctivitis QOL Questionnaire (RQLQ) at repeated intervals over one year, with scores dichotomized into bothered (>0) and not bothered (= 0). Individual weekly exposures to particulate matter<2.5μm (PM2.5) and its black carbon (BC) component were estimated by inverse distance weighted methods. Generalized estimating equations, adjusting for covariates, estimated associations of PM2.5 and BC with QOL., Results: Participants were on average 13 years old, 55% female, and majority were atopic (77%). Mean (SD) PM2.5 and BC concentrations were 21(3.2) μg/m3 and 4.4(1.5) μg/m3, respectively. In adjusted multi-pollutant models, each 10μg/m3 increase in PM2.5 was associated with increased odds of worse rhinoconjunctivitis QOL (OR;[95% CI]: 1.83;[1.33,2.52]). A 10% increase in the BC proportion was associated with higher rhinitis burden (OR;[95% CI]: 1.80;[1.22,2.66]), while increases in the non-BC component of PM did not significantly impact rhinoconjunctivitis QOL. Associations were similar regardless of atopy., Conclusion: Higher PM2.5 and BC exposure is associated with worse rhinitis QOL among asthmatic children.