Exposure to man-made combustion products, including secondhand tobacco smoke, maternal smoking during pregnancy, and near-roadway air pollution (NRAP), have been associated with increased body mass index and obesity in children and have been shown to result in excess weight gain in animal models. Potential mechanisms include pro-inflammatory central nervous system effects of airborne particles on appetite control, resulting in increased caloric intake, or changes in basal metabolism due to effects on mitochondria and brown adipose tissue. Combustion-derived polyaromatic hydrocarbons have also been linked to altered lipid metabolism, epigenetic effects on PPARγ expression, particle-induced estrogenic effects, and alterations in the distribution of visceral fat. Emerging evidence that a broad spectrum of environmental chemicals have “obesogenic” properties and alter the metabolic profile of adipose tissue challenges the prevailing model that the childhood obesity epidemic is explained solely by increased caloric density of food and decreased physical activity. Research on environmental obesogens could identify novel targets for intervention and yield public health benefits, since NRAP and SHS exposure are both common in populations most at-risk for development of obesity.
Objectives. As part of a community-based participatory research effort, we estimated the preventable burden of childhood asthma associated with air pollution in the southern California communities of Long Beach and Riverside. Methods. We calculated attributable fractions for 2 air pollution reduction scenarios to include assessment of the newly recognized health effects associated with residential proximity to major roads and impact from ship emissions. Results. Approximately 1600 (9%) of all childhood asthma cases in Long Beach and 690 (6%) in Riverside were attributed to traffic proximity. Ship emissions accounted for 1400 (21%) bronchitis episodes and, in more modest proportions, health care visits for asthma. Considerably greater reductions in asthma morbidity could be obtained by reducing nitrogen dioxide and ozone concentrations to levels found in clean coastal communities. Conclusions. Both Long Beach and Riverside have heavy automobile traffic corridors as well as truck traffic and regional pollution originating in the Los Angeles–Long Beach port complex, the largest in the United States. Community-based quantitative risk analyses can improve our understanding of health problems and help promote public health in transportation planning.
Population growth and the proliferation of roadways in Southern California have facilitated a glut of mobile air pollution sources (cars and trucks), resulting in substantial atmospheric pollution. Despite successful efforts over the past 40 years to reduce pollution, an alarming set of health effects attributable to air pollution have been described in Southern California. The Children's Health Study indicates that reduced lung function growth, increased school absences, asthma exacerbation, and new-onset asthma are occurring at current levels of air pollution, with sizable economic consequences. We describe these findings and urge a more aggressive effort to reduce air pollution exposures to protect our children's health. Lessons from this "case study" have national implications.
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