Faculty Bibliography

BACKGROUND:Tobacco remains a leading cause of preventable death in the U.S., responsible for more than 440,000 deaths each year. Approximately 10% of these deaths are attributable to exposure of non-smokers to secondhand smoke (SHS). Residents living in public multi-unit housing (MUH) are at excess risk for SHS exposure compared to the general population. On November 30, 2016, the U.S. Department of Housing and Urban Development (HUD) passed a rule requiring all public housing agencies to implement smoke-free housing (SFH) policies in their housing developments by July 30, 2018. METHODS:As part of a larger natural experiment study, we designed a protocol to evaluate indoor SHS levels before and after policy implementation through collection of repeat indoor air samples in non-smoking apartments and common areas of select high-rise NYCHA buildings subject to the HUD SFH rule, and also from socio-demographically matched private-sector high-rise control buildings not subject to the rule. A baseline telephone survey was conducted in all selected buildings to facilitate rapid recruitment into the longitudinal study and assess smoking prevalence, behaviors, and attitudes regarding the SFH policy prior to implementation. Data collection began in early 2018 and will continue through 2021. DISCUSSION/CONCLUSIONS:The baseline survey was completed by 559 NYCHA residents and 471 comparison building residents (response rates, 35, and 32%, respectively). Smoking prevalence was comparable between study arms (15.7% among NYCHA residents and 15.2% among comparison residents). The majority of residents reported supporting a building-wide smoke-free policy (63.0 and 59.9%, respectively). We enrolled 157 NYCHA and 118 comparison non-smoking households into the longitudinal air monitoring study and performed air monitoring in common areas. Follow up surveys and air monitoring in participant households occur every 6 months for 2.5 years. Capitalizing on the opportunity of this federal policy rollout, the large and diverse public housing population in NYC, and robust municipal data sources, this study offers a unique opportunity to evaluate the policy's direct impacts on SHS exposure. Methods in this protocol can inform similar SFH policy evaluations elsewhere.

Recent epidemiological data indicate that the popularity of electronic cigarettes (e-cigarettes), and consequently nicotine use, is rising in both adolescent and adult populations. As nicotine is a known developmental neurotoxin, these products present a potential threat for those exposed during early life stages. Despite this, few studies have evaluated the toxicity of e-cigarettes on the developing central nervous system (CNS). The goal of this study was to assess neurotoxicity resulting from early life exposure to electronic cigarette aerosols in an in vivo model. Specifically, studies here focused on neuro-parameters related to neuroinflammation and neurotrophins. To accomplish this, pregnant and neonatal C57BL/6 mice were exposed to aerosols produced from classic tobacco flavor e-cigarette cartridges (with [13 mg/ml] and without nicotine) during gestation ( approximately 3-wk) and lactation ( approximately 3-wk) via whole-body inhalation. Exposure to e-cigarette aerosols with and without nicotine caused significant reductions in hippocampal gene expression of Ngfr and Bdnf, as well as in serum levels of cytokines IL-1beta, IL-2 and IL-6. Exposure to e-cigarette aerosols without nicotine enhanced expression of Iba-1, a specific marker of microglia, in the CA1 region of the hippocampus. Overall, our novel results indicate that exposure to e-cigarette aerosols, with and without nicotine, poses a considerable risk to the developing CNS. Consequently, e-cigarettes should be considered a potential public health threat, especially early in life, requiring further research and policy considerations.

Annual increases in global travel have resulted in more individuals being exposed to varying environmental conditions abroad and, thereby, subject to air pollution related health risks. Individuals who travel abroad may be exposed to varying levels of air pollution within a matter of hours. We wish to consider whether exposure to air pollution could be a significant contributor to the risk of illness and death in travelers, particularly those who travel to highly polluted cities. We report the findings of a study in which the peak expiratory flow (PEF) of a traveler decreased in Shanghai relative to baseline in New York City; the decline in PEF correlated to concentration of particulate matter (PM2.5). We discuss the health implication of these results on global travel.

Silver nanoparticles (AgNPs) are employed in a variety of consumer products; however, in vivo rodent studies indicate that AgNPs can cause lung inflammation and toxicity in a strain- and particle type-dependent manner, but mechanisms of susceptibility remain unclear. The aim of this study was to assess the variation in AgNP-induced lung inflammation and toxicity across multiple inbred mouse strains and to use genome-wide association (GWA) mapping to identify potential candidate susceptibility genes. Mice received doses of 0.25 mg/kg of either 20-nm citrate-coated AgNPs or citrate buffer using oropharyngeal aspiration. Neutrophils in bronchoalveolar lavage fluid (BALF) served as markers of inflammation. We found significant strain- and treatment-dependent variation in neutrophils in BALF. GWA mapping identified 10 significant single-nucleotide polymorphisms (false discovery rate, 15%) in 4 quantitative trait loci on mouse chromosomes 1, 4, 15, and 18, and Nedd4l (neural precursor cell expressed developmentally downregulated gene 4-like; chromosome 18), Ano6 (anocatmin 6; chromosome 15), and Rnf220 (Ring finger protein 220; chromosome 4) were considered candidate genes. Quantitative RT-PCR revealed significant inverse associations between mRNA levels of these genes and neutrophil influx. Nedd4l, Ano6, and Rnf220 are candidate susceptibility genes for AgNP-induced lung inflammation that warrant additional exploration in future studies.-Scoville, D. K., Botta, D., Galdanes, K., Schmuck, S. C., White, C. C., Stapleton, P. L., Bammler, T. K., MacDonald, J. W., Altemeier, W. A., Hernandez, M., Kleeberger, S. R., Chen, L.-C., Gordon, T., Kavanagh, T. J. Genetic determinants of susceptibility to silver nanoparticle-induced acute lung inflammation in mice.

United States soldiers are returning from the Greater Middle East with respiratory illnesses ranging from new onset asthma to constrictive bronchiolitis. The etiology of the diseases is unknown. A study was conducted to determine the possible role of local mineral dust in the development of abnormal respiratory illnesses in soldiers during and after deployment in Iraq. A dust sample obtained in proximity to a burn pit in Camp Victory, Iraq, (CVD) was characterized both chemically and mineralogically. For comparison, a dust sample from Fort Irwin, California, (FID) was also collected. The ability of the dust samples to generate reactive oxygen species (ROS) was quantified, as well as their ability to generate an inflammatory stress response (ISR) in human lung epithelial cells. Both samples are comprised of common silicate and carbonate minerals and contain heavy metals with concentration ranges expected for mineral dust. The ISR generated by each sample was within the range of inert material with the minimal stress generated associated with the carbonate phases. The findings based on this one sample suggest that the origin of the disease is not driven by the particles ability to generate ROS. However it is likely that particle overload, and associated complications, or endotoxin contribute extensively to pathogenesis.

Exposure to fine particulate matter (PM2.5) and black carbon (BC) have been linked to negative health risks, but exposure among professional taxi drivers is understudied. This pilot study measured drivers' knowledge, attitudes, and beliefs (KAB) about air pollution compared with direct measures of exposures. Roadside and in-vehicle levels of PM2.5 and BC were continuously measured over a single shift on each subject, and exposures compared with central site monitoring. One hundred drivers completed an air pollution KAB questionnaire, and seven taxicabs participated in preliminary in-cab air sampling. Taxicab PM2.5 and BC concentrations were elevated compared with nearby central monitoring. Average PM2.5 concentrations per 15-min interval were 4-49 mug/m3. BC levels were also elevated; reaching>10 mug/m3. Fifty-six of the 100 drivers surveyed believed they were more exposed than non-drivers; 81 believed air pollution causes health problems. Air pollution exposures recorded suggest that driver exposures would likely exceed EPA recommendations if experienced for 24 h. Surveys indicated that driver awareness of this was limited. Future studies should focus on reducing exposures and increasing awareness among taxi drivers.Journal of Exposure Science and Environmental Epidemiology advance online publication, 11 May 2016; doi:10.1038/jes.2016.23.

BACKGROUND: Despite the increasing popularity of hookah bars, there is a lack of research assessing the health effects of hookah smoke among employees. This study investigated indoor air quality in hookah bars and the health effects of secondhand hookah smoke on hookah bar workers. METHODS: Air samples were collected during the work shift of 10 workers in hookah bars in New York City (NYC). Air measurements of fine particulate matter (PM2.5), fine black carbon (BC2.5), carbon monoxide (CO), and nicotine were collected during each work shift. Blood pressure and heart rate, markers of active smoking and secondhand smoke exposure (exhaled CO and saliva cotinine levels), and selected inflammatory cytokines in blood (ineterleukin (IL)-1b, IL-6, IL-8, interferon gamma (IFN-gamma), tumour necrosis factor (TNF-alpha)) were assessed in workers immediately prior to and immediately after their work shift. RESULTS: The PM2.5 (gravimetric) and BC2.5 concentrations in indoor air varied greatly among the work shifts with mean levels of 363.8 microg/m3 and 2.2 microg/m3, respectively. The mean CO level was 12.9 ppm with a peak value of 22.5 ppm CO observed in one hookah bar. While heart rate was elevated by 6 bpm after occupational exposure, this change was not statistically significant. Levels of inflammatory cytokines in blood were all increased at postshift compared to preshift testing with IFN-Upsilon increasing from 0.85 (0.13) to 1.6 (0.25) (mean (standard error of the mean; SEM)) pg/mL (p<0.01). Exhaled CO levels were significantly elevated after the work shift with 2 of 10 workers having values >90 ppm exhaled CO. CONCLUSIONS: These results demonstrate that hookah bars have elevated concentrations of indoor air pollutants that appear to cause adverse health effects in employees. These data indicate the need for further research and a marked need for better air quality monitoring and policies in such establishments to improve the indoor air quality for workers and patrons.