Polycyclic aromatic hydrocarbon exposure and pediatric asthma in children: a case–control study

Abstract

BackgroundBronchial asthma is one of the most prevalent diseases in Arab children. Environmental pollution has been suggested to be considered causative of asthma, nasal symptoms and bronchitis in both children and adult. The objectives of this study were to evaluate the association between serum polycyclic aromatic hydrocarbons (PAHs) levels, asthma and allergic outcomes among Saudi children aged up to 15 yrs. We hypothesized that increased serum PAHs are associated with allergy, asthma, or respiratory symptoms.MethodsA total of 195 Saudi children (98 asthma pediatric patients and 97 healthy controls) were randomly selected from the Riyadh Cohort Study for inclusion. The diagnosis of Asthma was based on established pediatric diagnosis and medications taken.ResultsAsthma related markers showed highly significant differences between children with and without asthma. Thus IgE, resistin and IL-4 were significantly increased (p 0.004, 0.001 and 0.003, respectively) in children with asthma compared with non-asthma control subjects. GMCSF, IFN-γ, IL-5, IL-8 and IL-10, on the other hand, were significantly decreased in children with asthma (p 0.003, 0.03, 0.001, 0.004 and 0.03, respectively). Strong associations between serum PAHs levels and biomarkers of childhood asthma were detected in Arabic children. Data confirmed the role of naphthalene, 4H-cyclobenta[def]phenanthrene, 1,2-benzanthracene, chrysene and benzo(e)acephenanthrylene in childhood asthma; levels of these PAHs were correlated with asthma related biomarkers including IgE, resistin, GMCSF and IFN-γ as well as IL-4, IL-5, IL-8 and IL-10 cytokines.ConclusionsThis data highlight the pivotal role of specific PAHs in childhood asthma.

Exposure to polycyclic aromatic hydrocarbons (PAHs) and bladder cancer: evaluation from a gene-environment perspective in a hospital-based case-control study in the Canary Islands (Spain)

“…In addition, our study may be biased because PAHs measurements were taken at one point in time and therefore may only reflect recent exposure and not lifetime exposure. In this sense, although serum PAH levels are proposed biomarkers of PAH exposure, 4,31 our results indicate that blood does not appear to be the most adequate biological sample to assess Table 2 Distribution of polycyclic aromatic hydrocarbons (PAHs) among cases and controls…”

“…Similarly, multiple occupations have been associated with PAH exposure (including painters, machinists, mechanics, and drivers), and occupation appears to be another risk factor for bladder cancer. 15 Certain foods (charcoal broiled meats and other smoked foods and coffee) may also be a source of PAH exposure, 4 and dietary habits (such as coffee and water intake) are relevant in bladder cancer tumorigenesis. [16][17][18][19][20] Genetic polymorphisms may be important in determining individual susceptibility to bladder cancer because genetic differences in detoxification capabilities can modulate PAH-induced damage and carcinogenesis.…”

Cardiovascular and Cerebrovascular Emergency Department Visits Associated With Wildfire Smoke Exposure in California in 2015

“…In some instances, an individual county may have only 1 ground‐based air monitor for PM 2.5 . In addition, the OSHPD healthcare utilization data provided comprehensive state‐wide data of ED visits based on discharge diagnoses, whereas some other studies have relied upon syndromic surveillance 16, 26, 52. One study evaluated syndromic surveillance for cardiovascular disease in New York City and found high specificity for many of the disease entities, but often a low sensitivity and positive‐predictive value, which may underestimate the impact of wildfire smoke on cardiovascular disease 53…”

Using community level strategies to reduce asthma attacks triggered by outdoor air pollution: a case crossover analysis

“…Case cross-over analysis has drawbacks when applied to more than one pollutant at a time (e.g., diminished statistical power as pollutants are added, difficulties identifying higher order interaction, confounding from correlation) [14,16-18]. To preserve power, we focus only on five pollutants, all previously linked to asthma attack triggers.…”