Faculty Bibliography

Rationale: Air quality improvements are increasingly difficult to come by as modern pollution control technologies and measures have been widely implemented in the United States. Although there have been dramatic improvements in air quality over the last several decades, it is important to evaluate changes in the health impacts of air pollution for a more recent time period to better understand the current trajectory of air quality improvements. Objectives: To provide county-level estimates of annual air pollution-related health outcomes across the United States and to evaluate these trends from 2008 to 2017, presented as part of the annual American Thoracic Society (ATS)/Marron Institute "Health of the Air" report. Methods: Daily air pollution values were obtained from the U.S. Environmental Protection Agency's Air Quality System for monitors in the United States from 2008 to 2017. Concentration-response functions used in the ATS/Marron Institute "Health of the Air" report were applied to the pollution increments corresponding to differences between the rolling 3-year design values (reported as the third year) and ATS-recommended levels for annual particulate matter less than or equal to 2.5 μm in aerodynamic diameter (PM_2.5; 11 μg/m³), short-term PM_2.5 (25 μg/m³), and ozone (O₃; 60 ppb). Health impacts were estimated at the county level in locations with valid monitor data. Results: Annual excess mortality in the United States due to air pollution levels greater than recommended by the ATS decreased from approximately 12,600 (95% confidence interval [CI], 5,470-21,040) in 2010 to 7,140 (95% CI, 2,290-14,040) in 2017. This improvement can be attributed almost entirely to reductions in PM_2.5-related mortality, which decreased by approximately 60% (reduced from 8,330 to 3,260 annual deaths), whereas O₃-related mortality remained largely unchanged, other than year-to-year variability, over the same time period (reduced from 4,270 to 3,880 annual deaths). Conclusions: Improvements in health impacts attributable to ambient PM_2.5 concentrations have been observed across most regions of the United States over the last decade, although the rate of these improvements has leveled off in recent years. Despite two revisions of the National Ambient Air Quality Standards strengthening the standard for O₃ in 2008 and 2015, there has not yet been a substantial improvement in the health impacts attributable to O₃ during this time period. In many U.S. cities, an increase in the exposed population over the last decade has outpaced the improvements in ambient O₃ concentrations, resulting in a net increase in O₃-related health impacts over time.

Air quality conditions in the U.S. are reported to the general public via the regulatory-based Air Quality Index (AQI). The accuracy of AQI as a risk communication tool is dependent, in part, on an assumption of equivalent health risks for each of the index pollutants. Time-series analyses of 858,030 emergency department visits from 2005–2010 for respiratory diseases in two New York counties (Bronx and Queens) were completed using a Poisson generalized linear model in order to assess the equivalency of respiratory morbidity risk for four index pollutants. Excess respiratory risk per 1-AQI unit was approximately twice as high for ozone (0.16%, 95% confidence interval [CI] [0.08, 0.24]) as compared with sulfur dioxide (0.09%, 95% CI [0.01, 0.16], nitrogen dioxide (0.07%, 95% CI [0.01, 0.15]), and fine particulate matter (0.07%, 95% CI [0.02, 0.12]). Unequal respiratory risks on a per-AQI-unit basis resulted in inconsistencies between reported AQI values and public health risks, especially during the ozone season. While still useful in reporting general air quality conditions to the public, AQI may be insufficiently precise to inform optimal daily behavior modification decisions

Environmental justice efforts in the United States seek to provide equal protection from environmental hazards, such as air pollution, to all groups, particularly among traditionally disadvantaged populations. To accomplish this objective, the U.S. EPA has previously required states to use an environmental justice screening tool as part of air quality planning decision-making. The generally utilized approach to assess potential areas of environmental justice concern relies on static comparisons of environmental and demographic information to identify areas where minority and low income populations experience elevated environmental exposures, but does not include any additional information that may inform the trade-offs that sub-populations of varying socio-demographic groups make when choosing where to reside in cities. In order to address this limitation, job accessibility (measured by a mobility index defining the number of jobs available within a set commuting time) was developed as a novel environmental justice indicator of environmental justice priority areas at the local level. This approach is modeled using real-world data in Allegheny County, PA (USA), and identifies areas with relatively high levels of outdoor air pollution and low access to jobs. While traditional tools tend to flag the poorest neighborhoods for environmental justice concerns, this new method offers a more refined analysis, targeting populations suffering from the highest environmental burden without the associated benefits of urban living.

BACKGROUND: Emerging experimental evidence suggests that air pollution may contribute to development of obesity and diabetes, but studies of children are limited. OBJECTIVES: We hypothesized that pollution effects would be magnified after bariatric surgery for treatment of obesity, reducing benefits of surgery. METHODS: In 75 obese adolescents, excess weight loss (EWL), high-density lipoprotein (HDL) cholesterol, triglycerides, alkaline phosphatase (ALP) and hemoglobin A1c (HbA1c ) were measured prospectively at baseline and following laparoscopic adjustable gastric banding (LAGB). Residential distances to major roads and the average two-year follow-up exposure to particulate matter <2.5 mum (PM2.5 ), nitrogen dioxide (NO2 ) and ozone were estimated. Associations of exposure with change in outcome and with attained outcome two years post-surgery were examined. RESULTS: Major-roadway proximity was associated with reduced EWL and less improvement in lipid profile and ALP after surgery. NO2 was associated with less improvement in HbA1c and lower attained HDL levels and change in triglycerides over two years post-surgery. PM2.5 was associated with reduced EWL and reduced beneficial change or attained levels for all outcomes except HbA1c . CONCLUSIONS: Near-roadway, PM2.5 and NO2 exposures at levels common in developed countries were associated with reduced EWL and metabolic benefits of LAGB. This novel approach provides a model for investigating metabolic effects of other exposures.

BACKGROUND:The Mexico City Metropolitan Area has an expansive urban population and a long history of air quality management challenges. Poor air quality has been associated with adverse pulmonary and cardiac health effects, particularly among susceptible populations with underlying disease. In addition to reducing pollution concentrations, risk communication efforts that inform behavior modification have the potential to reduce public health burdens associated with air pollution. METHODS:This study investigates the utilization of Mexico's IMECA risk communication index to inform air pollution avoidance behavior among the general population living in the Mexico City Metropolitan Area. Individuals were selected via probability sampling and surveyed by phone about their air quality index knowledge, pollution concerns, and individual behaviors. RESULTS:The results indicated reasonably high awareness of the air quality index (53% of respondents), with greater awareness in urban areas, among older and more educated individuals, and for those who received air quality information from a healthcare provider. Additionally, behavior modification was less influenced by index reports as it was by personal perceptions of air quality, and there was no difference in behavior modification among susceptible and non-susceptible groups. CONCLUSIONS:Taken together, these results suggest there are opportunities to improve the public health impact of risk communication through an increased focus on susceptible populations and greater encouragement of public action in response to local air quality indices.

Inhalation of ozone (O₃), a gaseous air pollutant, causes lung injury, lung inflammation, and airway hyperresponsiveness. Macrophages, mast cells, and neutrophils contribute to one or more of these sequelae induced by O₃ Furthermore, each of these aforementioned cells express chemokine (C-C motif) receptor-like 2 (Ccrl2), an atypical chemokine receptor that facilitates leukocyte chemotaxis. Given that Ccrl2 is expressed by cells essential to the development of O₃-induced lung pathology and that chemerin, a Ccrl2 ligand, is increased in bronchoalveolar lavage fluid (BALF) by O₃, we hypothesized that Ccrl2 contributes to the development of lung injury, lung inflammation, and airway hyperresponsiveness induced by O₃ To that end, we measured indices of lung injury (BALF protein, BALF epithelial cells, and bronchiolar epithelial injury), lung inflammation (BALF cytokines and BALF leukocytes), and airway responsiveness to acetyl-β-methylcholine chloride (respiratory system resistance) in wild-type and mice genetically deficient in Ccrl2 (Ccrl2-deficient mice) 4 and/or 24 hours following cessation of acute exposure to either filtered room air (air) or O₃ In air-exposed mice, BALF chemerin was greater in Ccrl2-deficient as compared to wild-type mice. O₃ increased BALF chemerin in mice of both genotypes, yet following O₃ exposure, BALF chemerin was greater in Ccrl2-deficient as compared to wild-type mice. O₃ increased indices of lung injury, lung inflammation, and airway responsiveness. Nevertheless, no indices were different between genotypes following O₃ exposure. In conclusion, we demonstrate that Ccrl2 modulates chemerin levels in the epithelial lining fluid of the lungs but does not contribute to the development of O₃-induced lung pathology.