Ozone Exposure, Cardiopulmonary Health, and Obesity: A Substantive Review

Abstract

From 1999–2014, obesity prevalence increased among adults and youth. Obese individuals may be uniquely susceptible to the proinflammatory effects of ozone because obese humans and animals have been shown to experience a greater decline in lung function than normal-weight subjects. Obesity is independently associated with limitations in lung mechanics with increased ozone dose. However, few epidemiologic studies have examined the interaction between excess weight and ozone exposure among adults. Using PubMed keyword searches and reference lists, we reviewed epidemiologic evidence to identify potential response-modifying factors and determine if obese or overweight adults are at increased risk of ozone-related health effects. We initially identified 170 studies, of which seven studies met the criteria of examining the interaction of excess weight and ozone exposure on cardiopulmonary outcomes in adults, including four short-term ozone exposure studies in controlled laboratory settings and three community epidemiologic studies. In the studies identified, obesity was associated with decreased lung function and increased inflammatory mediators. Results were inconclusive about the effect modification when data were stratified by sex. Obese and overweight populations should be considered as candidate at-risk groups for epidemiologic studies of cardiopulmonary health related to air pollution exposures. Air pollution is a modifiable risk factor that may decrease lung function among obese individuals with implications for environmental and occupational health policy.

Examining Joint Effects of Air Pollution Exposure and Social Determinants of Health in Defining “At‐Risk” Populations Under the Clean Air Act: Susceptibility of Pregnant Women to Hypertensive Disorders of Pregnancy

“…Among those studies that did examine interactions, findings regarding differences in risk by maternal BMI are mixed, with two studies reporting no associations between air pollution and preeclampsia by BMI category using stratification, and one study that directly tested for differences reporting lower risk of preeclampsia among obese women (with pre‐pregnancy BMI ≥30 kg/m 2 ) (Mobasher et al, ). A protective effect of obesity was unexpected, as obese women are at higher risk for chronic hypertension and HDP generally and obese populations receive a greater dose of ozone and PM for the same ambient concentrations compared to other populations (Gidding et al, ; Koman & Mancuso, ; Lin & Lin, ; Salome, King, & Berend, ). Thus, we would have expected a higher risk of air pollution‐related preeclampsia with increasing weight, which was not observed in these studies (Mendola et al, ; Mobasher et al, ; Rudra et al, ).…”

“…Researchers have proposed frameworks for studying the shared etiologic path-ways of air pollution and negative social factors (Erickson, Ostry, Chan, & Arbour, 2016;Institute of Medicine, 1999;Payne-Sturges et al, 2006;Solomon, Morello-Frosch, Zeise, & Faust, 2016). To be useable in policy decisions, these research frameworks and resulting evidence must be connected to regulatory assessment methods (Koman & Mancuso, 2017).…”

Ozone Pollution: A Major Health Hazard Worldwide

“…Based on this assessment, the national ambient air quality standard for 8-h daily max ozone was revised from 75 to 70 ppb in 2015. The health effects evidence used to support these revisions include mainly the following, which has been well-demonstrated in recent reviews (25, 26).…”

Small Molecule Antipsychotic Aripiprazole Potentiates Ozone-Induced Inflammation in Airway Epithelium

“…MS parameters were optimized for the 7-DHC-PTAD adduct and were as follows: auxiliary nitrogen gas pressure at 55 psi and sheath gas pressure at 60 psi; discharge current at 22 μA and vaporizer temperature at 342 °C. Collision-induced dissociation 13 was optimized at 12 eV under 1.0 mTorr of argon. The SRM transition of precursor to product ion included m/z 560 → 365 for 7-DHC-PTAD adduct and a pseudo-SRM transition of 369 → 369 to monitor Chol since Chol does not react with PTAD.…”