Faculty Bibliography

Power outages can impact health, and certain populations may be more at risk. Personal preparedness may reduce impacts, but information on power outage preparedness and risk perception among vulnerable populations is limited. We examined power outage preparedness and concern among New York City residents, including vulnerable populations defined as older adults (≥ 65 years), and respondents with household members who require assistance with daily activities or depend on electric medical devices. A random sample telephone survey was conducted during November-December 2016. Preparedness was defined as having a three-day supply of drinking water, non-perishable food, and a working flashlight. Among all respondents (n = 887), 58% were prepared and 46% expressed concern about health. Respondents with electric-dependent household members (9% of all respondents) tended to have higher preparedness (70 vs. 56% of respondents without electric-dependent household members). Among this group, only 40% reported being registered with a utility company to receive early notification of outages. While the subgroup sample was small, respondents with registered electric-dependent household members had lower preparedness than those with non-registered users (59 vs. 76%). Respondents with household members who needed assistance had comparable levels of preparedness to respondents without someone who needed assistance (59 vs. 57%). Older adults had greater preparedness than younger adults (65 vs. 56%). Health concerns were greater among all vulnerable groups than the general population. Levels of preparedness varied among vulnerable respondents, and awareness of power outage notification programs was low. Our findings highlight the need to increase awareness and preparedness among at-risk people.

Previous studies have shown that higher ambient air temperature is associated with increased incidence of gastrointestinal illnesses, possibly as a result of leaving potentially hazardous food in the temperature danger zone for too long. However, little is known about the effect of hot weather on restaurant practices to maintain safe food temperatures. We examined hot weather impacts on restaurant food safety violations and operations in New York City using quantitative and qualitative methods. We used data from 64,661 inspections conducted among 29,614 restaurants during May to September, 2011 to 2015. We used Poisson time-series regression to estimate the cumulative relative risk (CRR) of temperature-related food safety violations across a range of daily maximum temperature (13 to 40°C [56 to 104°F]) over a lag of 0 to 3 days. We present CRRs for an increase in daily maximum temperature from the median (28°C [82°F]) to the 95th percentile (34°C [93°F]) values. Maximum temperature increased the risk of violations for cold food holding above 5°C (41°F) (CRR, 1.19; 95% CI, 1.14, 1.25) and insufficient refrigerated or hot holding equipment (CRR, 2.37; 95% CI, 2.02, 2.79). We also conducted focus groups among restaurant owners and managers to aid interpretation of findings and identify challenges or knowledge gaps that prevent hot weather preparedness. Focus group participants cited refrigeration issues as a common problem during hot weather. Participants expressed the need for more guidance on hot weather and power outages to be delivered concisely. Our findings suggest that hotter temperatures may compromise cold and hot food holding, possibly by straining refrigeration or other equipment. The findings have public health implications because holding potentially hazardous foods in the temperature danger zone allows foodborne pathogens to proliferate and increases risk for foodborne illness. Distribution of simple guidelines that can be easily accessed during emergencies could help restaurants respond better.

BACKGROUND:Previous studies investigated potential health effects of large-scale power outages, including the massive power failure that affected the northeastern United States and Ontario, Canada, in August 2003, and outages associated with major storms. However, information on localized outages is limited. OBJECTIVE:The study sought to examine potential health impacts of citywide and localized outages in New York City (NYC). METHODS:Along with the citywide 2003 outage, localized outages in July 1999 and July 2006 were identified. We additionally investigated localized, warm- and cold-weather outages that occurred in any of 66 NYC electric-grid networks during 2002-2014 using New York State Public Service Commission data. Mortality and hospitalizations were geocoded and linked to the networks. Associations were estimated using Poisson time-series regression, including examining distributed lags and adjusting for temperature and temporal trends. Network-specific estimates were pooled by season. RESULTS:CRR=0.77 (95% CI: 0.61, 0.97)]. CONCLUSIONS:Localized outages may affect health. This information can inform preparedness efforts and underscores the public health importance of ensuring electric grid resiliency to climate change. https://doi.org/10.1289/EHP2154.

BACKGROUND: Fine particulate matter (PM2.5) air pollution exposure has been identified as a global health threat. However, the types and sources of particles most responsible are not yet known. In this work, we sought to identify the causal characteristics and sources of air pollution underlying past published associations in the American Cancer Society's Cancer Prevention Study-II cohort between long-term PM2.5 exposure and Ischemic Heart Disease (IHD) mortality. METHODS: Individual risk factor data were evaluated for 445,860 adults in 100 U.S. metropolitan areas followed from 1982 to 2004 for vital status and cause of death. Using Cox proportional hazard models, IHD mortality hazard ratios (HRs) were derived for PM2.5, trace constituents, and pollution source-associated PM2.5, as derived from air monitoring at central stations throughout the nation during 2000-2005. RESULTS: Associations with IHD mortality varied by PM2.5 mass constituent and source. A coal combustion PM2.5 IHD HR = 1.05 (95% CI=1.02, 1.08) per microg/m3, versus an IHD HR = 1.01 (95% CI=1.00, 1.02) per microg/m3 PM2.5 mass, indicated a risk roughly five times higher for coal combustion PM2.5 than for PM2.5 mass in general, on a per microg/m3 PM2.5 basis. Diesel traffic-related elemental carbon (EC) soot was also associated with IHD mortality (HR = 1.03; 95% CI: 1.00, 1.06 per 0.26 mug/m3 EC increase). However, PM2.5 from both wind-blown soil and biomass combustion were not associated with IHD mortality. CONCLUSIONS: Long-term PM2.5 exposures from fossil fuel combustion, especially coal burning, but also from diesel traffic, were associated with increases in IHD mortality in this nationwide population. Results suggest that PM2.5 - mortality associations can vary greatly by source, and that the largest IHD health benefits per microg/m3 from PM2.5 air pollution control may be achieved via reductions of fossil fuel combustion exposures, especially from coal-burning sources.

BACKGROUND: Long-term exposure to ambient particulate matter (PM) air pollution is associated with increased cardiovascular disease (CVD); however, the impact of PM on clinical risk factors for CVD in healthy subjects is unclear. We examined the relationship of PM with levels of circulating lipids and blood pressure in the Third National Health and Nutrition Examination Survey (NHANES III), a large nationally-representative US survey. METHODS: This study was based on 11,623 adult participants of NHANES III (1988-1994; median age 41.0). Serum lipids and blood pressure were measured during the NHANES III examination. Average exposure for 1988-1994 to particulate matter <10microm in aerodynamic diameter (PM10) at the residences of participants was estimated based on measurements from U.S. Environmental Protection Agency monitors. Multivariate linear regression was used to estimate the associations of PM10 with lipids and blood pressure. RESULTS: An interquartile range width (IQRw) increase in PM10 exposure (11.1 microg/m) in the study population was associated with 2.42 percent greater serum triglycerides (95% confidence interval [CI]: 1.09-3.76); multivariate adjusted means of triglycerides according to increasing quartiles of PM10 were 137.6, 142.5, 142.6, and 148.9 mg/dL, respectively. An IQRw increase in PM10 was associated with 1.43 percent greater total cholesterol (95% CI: 1.21-1.66). These relationships with triglycerides and total cholesterol did not differ by age or region. Associations of PM10 with blood pressure were modest. CONCLUSIONS: Findings from this large diverse study indicate that greater long-term PM10 exposure is associated with elevated serum triglycerides and total cholesterol, potentially mediating air pollution-related effects on CVD.

Particulate matter (PM*), an ambient air criteria pollutant, is a complex mixture of chemical components; particle sizes range from nanometer-sized molecular clusters to dust particles that are too large to be aspirated into the lungs. Although particle composition is believed to affect health risks from PM exposure, our current health-based air quality standards for PM are limited to (1) the mass concentrations of PM2.5 (particles 2.5 microm or smaller in aerodynamic diameter), which are largely attributable to combustion products; and (2) PM10 (10 microm or smaller), which includes larger-sized mechanically generated dusts. Both of these particle size fractions are regulated under the National Ambient Air Quality Standards (NAAQS) and both have been associated with excess mortality and morbidity. We conducted four studies as part of HEI's integrated National Particle Component Toxicity (NPACT) Initiative research program. Since 1999, the Chemical Speciation Network (CSN), managed by the U.S. Environmental Protection Agency (U.S; EPA), has routinely gathered air monitoring data every third or sixth day for the concentrations of numerous components of PM2.5. Data from the CSN enabled us to conduct a limited time-series epidemiologic study of short-term morbidity and mortality (Ito study); and a study of the associations between long-term average pollutant concentrations and annual mortality (Thurston study). Both have illuminated the roles of PM2.5 chemical components and source-related mixtures as potentially causal agents. We also conducted a series of 6-month subchronic inhalation exposure studies (6 hours/day, 5 days/week) of PM2.5 concentrated (nominally) 10 x from ambient air (CAPs) with apolipoprotein E-deficient (ApoE(-/-)) mice (a mouse model of atherosclerosis) (Chen study). The CAPs studies were conducted in five different U.S. airsheds; we measured the daily mass concentrations of PM2.5, black carbon (BC), and 16 elemental components in order to identify their sources and their roles in eliciting both short- and long-term health-related responses. In addition, from the same five air-sheds we collected samples of coarse (PM10-2.5), fine (PM2.5-0.2), and ultrafine (PM0.2) particles. Aliquots of these samples were administered to cells in vitro and to mouse lungs in vivo (by aspiration) in order to determine their comparative acute effects (Gordon Study). The results of these four complementary studies, and the overall integrative analyses, provide a basis for guiding future research and for helping to determine more targeted emission controls for the PM components most hazardous to acute and chronic health. Application of the knowledge gained in this work may therefore contribute to an optimization of the public health benefits of future PM emission controls. The design of each NPACT study conducted at NYU was guided by our scientific hypotheses, which were based on our reviews of the background literature and our experience in conducting studies of associations between ambient PM and health-related responses. These hypotheses guided the development and conduct of the four studies. Hypothesis 1. Coarse, fine, and ultrafine PM are each capable of producing acute health effects of public health concern, but the effects may differ according to particle size and composition. (Applies to all studies.) Hypothesis 2. Long-term PM2.5 exposures are closely associated with chronic health effects. (Applies to studies 1 and 4.) Hypothesis 3. The source-apportionment techniques that we have developed and refined in recent years provide a useful basis for identifying major categories of sources of PM in ambient air and specific chemical components that have the greatest impacts on a variety of acute and chronic health effects. (Applies to all studies.) Hypothesis 4. The health effects due to ambient PM exposures can best be seen in sensitive subgroups within overall human populations and in animal models of such populations. (Applies to studies 1, 3, and 4.) Overall, the studies have demonstrated that the toxicity of PM is driven by a complex interaction of particle size range, geographic location, source category, and season. These findings suggest that the components of PM--associated with certain categories of sources--are responsible for the observed adverse health effects. Most importantly, the responsible components and source categories vary with the health-related endpoints being assessed. Across all studies, fossil-fuel combustion source categories were most consistently associated with both short- and long-term adverse effects of PM2.5 exposure. The components that originate from the Residual Oil Combustion and Traffic source categories were most closely associated with short-term effects; and components from the Coal Combustion category were more closely associated with long-term effects.

Exposure to ambient fine particulate matter (PM2.5) increases risks for cardiovascular disorders (CVD). However, the mechanisms and components responsible for the effects are poorly understood. Based on our previous murine exposure studies, a translational pilot study was conducted in female residents of Jinchang and Zhangye, China, to test the hypothesis that specific chemical component of PM2.5 is responsible for PM2.5 associated CVD. Daily ambient and personal exposures to PM2.5 and 35 elements were measured in the two cities. A total of 60 healthy nonsmoking adult women residents were recruited for measurements of inflammation biomarkers. In addition, circulating endothelial progenitor cells (CEPCs) were also measured in 20 subjects. The ambient levels of PM2.5 were comparable between Jinchang and Zhangye (47.4 and 54.5microg/m(3), respectively). However, the levels of nickel, copper, arsenic, and selenium in Jinchang were 82, 26, 12, and 6 fold higher than Zhangye, respectively. The levels of C-reactive protein (3.44+/-3.46 vs. 1.55+/-1.13), interleukin-6 (1.65+/-1.17 vs. 1.09+/-0.60), and vascular endothelial growth factor (117.6+/-217.0 vs. 22.7+/-21.3) were significantly higher in Jinchang. Furthermore, all phenotypes of CEPCs were significantly lower in subjects recruited from Jinchang than those from Zhangye. These results suggest that specific metals may be important components responsible for PM2.5-induced cardiovascular effects and that the reduced capacity of endothelial repair may play a critical role.

With the advent of multicity studies, uniform statistical approaches have been developed to examine air pollution-mortality associations across cities. To assess the sensitivity of the air pollution-mortality association to different model specifications in a single and multipollutant context, the authors applied various regression models developed in previous multicity time-series studies of air pollution and mortality to data from Philadelphia, Pennsylvania (May 1992-September 1995). Single-pollutant analyses used daily cardiovascular mortality, fine particulate matter (particles with an aerodynamic diameter