Director of Global and Environmental Public Health
Clinical Associate Professor of Global Health
Dr. Chris Dickey is an international development innovator and public health entrepreneur whose work seeks to develop sustainable public health models and to forge bonds between the academic community and practitioners in the field. He sees the challenges facing public health - vast health inequities, applied skills gaps among public health professionals, weak community health systems, and shrinking research budgets - and seeks to reimagine sustainable solutions through a multidisciplinary approach. This is reflected by the fact that he has worked in more than 20 countries with the United Nations (UN) and other agencies and co-founded a company that provides clean water and primary care in villages in India.
Dr. Dickey is developing a public health entrepreneurship program to address the demand for a new generation of public health practitioners with the skill sets and opportunities to create innovative and sustainable business models as stand-alone entities or within a larger corporation.
Through a learning model that combines lectures, group exercises, real-time simulations, and implementable course projects and in partnership with the UN and World Food Programme, Dr. Dickey leads an Applied Food System and Nutrition course in which international public health professionals and public health students learn and work together on real world problems. Additionally, Dr. Dickey coordinates the Applied Global Health and Development Lab, where have the opportunity to work on universal health coverage policy, a new data-driven decision support tool, supply chain and logistics analysis, social network and knowledge management analyses, and the development of a business model for online public health programs.
DrPH, Molecular Cancer Epidemiology, Columbia University, New York, NYMBA, Finance and Entrepreneurial Management, University of Pennsylvania, Philadelphia, PAMA, Journalism, New York University, New York, NY
Global HealthInter-organizational NetworksPublic Health EntrepreneurshipSustainabilitySystems Interventions
Behavioral Communication Strategies for Global Epidemics: An Innovative Model for Public Health Education and Humanitarian ResponseDickey, C., Holzman, E., Bedford, J., Manoncourt, E., Shirky, C., Petit, V., Guirguis, S., Bloch, K., & Obregon, R.
Journal titleHealth promotion practiceIn response to a number of growing global health challenges, New York University and UNICEF designed a Behavioral Communication Strategies for Global Epidemics course that brings together United Nations professionals, government staff, and MPH (Master of Public Health) students to design innovative social behavior change communication (SBCC) strategies that address disease outbreaks and humanitarian challenges around the world. Applying a systems approach, participants in the course work on interdisciplinary teams to design strategies, develop skills, and engage in global learning. At the culmination of the course, all teams present strategies to UNICEF country offices for implementation. This innovative model for disease outbreak, public health education, and humanitarian response provides professionals with an opportunity to develop a wide range of competencies, including systems thinking, behavior change, and human-centered design and equips them with the necessary tools to develop more novel approaches to SBCC. As the number of outbreaks and humanitarian challenges increase each year, this format for learning can serve as a model for how professionals can effectively address these complex crises.
Addressing equitable access through innovation: case studies from Ghana, Uganda and Rwanda.Dickey, C., Bedford, J., Thiede, M., & O’Connell, T.
Integrating an approach to assess UHC access barriers into district health systems strengthening in Uganda, Ghana and Rwanda.Dickey, C., O’Connell, T., Bedford, J., & Thiede, M.
What would it really take to halt Ebola and prevent future epidemics?Healton, C., & Dickey, C.
Journal titleThe Huffington Post
Aromatic DNA adducts in foundry workers in relation to exposure, life style and CYP1A1 and glutathione transferase M1 genotypeHemminki, K., Dickey, C., Karlsson, S., Bell, D., Hsu, Y., Tsai, W. Y., Mooney, L. V. A., Savela, K., & Perera, F. P.
Page(s)345-350Levels of aromatic DNA adducts in foundry workers and controls were followed at four annual samplings. During this time exposure to polycyclic aromatic hydrocarbons (PAH) decreased and the level of DNA adducts decreased accordingly. In the total group exposure was related to the level of adducts. Adduct levels correlated with urinary 1-hydroxypyrene (LOGU1OH), air benzo[a]pyrene, weekly working hours and daily cigarette consumption. In a multivariate model 1-hydroxypyrene had a consistent effect. Neither glutathione transferase M1 (GSTM1) nor cytochrome P450 1A1 (CYP1A1) genotypes had clear effects. Yet the individuals lacking GSTM1 had a stronger effect of LOGU1OH and some effect by other sources of PAH, such as charcoal broiled food, although all these variables were not significant in the multivariate model. The rare individuals with a CYP1A1 polymorphism MspI containing an amino acid change at isoleucine had an increased level of adducts. The results showed that the postlabelling method used was able to detect an increase in aromatic DNA adducts in leukocytes when exposure to benzo[a]pyrene in air was ~5 ng/m3. At such low levels smoking and charcoal broiled food may be important contributors to adducts.
Molecular epidemiology and occupational healthPerera, F. P., & Dickey, C.
Journal titleAnnals of the New York Academy of Sciences
Molecular epidemiology in environmental carcinogenesisPerera, F. P., Mooney, L. V. A., Dickey, C. P., Santella, R. M., Bell, D., Blaner, W., Tang, D., & Whyatt, R. M.
Journal titleEnvironmental health perspectives
Page(s)441-443Molecular epidemiology has significant potential in preventing cancer and other diseases caused by environmental exposures (related to lifestyle, occupation, or ambient pollution). This approach attempts to prevent cancer by incorporating laboratory methods to document the molecular dose and preclinical effects of carcinogens, as well as factors that increase individual susceptibility to carcinogens. Recently we have carried out validation studies of biologic markers such as carcinogen-DNA and carcinogen-protein adducts, gene and chromosomal mutations, alterations in target oncogenes or tumor suppressor genes, polymorphisms in putative susceptibility genes (individual P450s, glutathione transferase M1), and serum levels of micronutrients. This research involves adults, infants, and children exposed to varying levels of carcinogens, as well as cancer cases and controls. On a group level, dose-response relationships have frequently been seen between various biomarkers and environmental exposures such as polycyclic aromatic hydrocarbons, cigarette smoke (active and passive), and ambient indoor and workplace air pollution. However, there is significant interindividual variation in biomarkers that appears to reflect a modulating effect on biomarkers (hence potential risk) by genetic and acquired susceptibility factors. Ongoing retrospective and nested case-control studies of lung and breast cancer are examining the association between biomarkers and cancer risk. Results of these studies are encouraging; they suggest that biomarkers, once validated, can be useful in identifying populations and individuals at risk in time to intervene effectively.
CYP1A1 Messenger RNA Levels in Placental Tissue as a Biomarker of Environmental ExposureWhyatt, R. M., Garte, S. J., Cosma, G., Bell, D. A., Jedrychowski, W., Wahrendorf, J., Randall, M. C., Cooper, T. B., Ottman, R., Tang, D., Tsai, W. Y., Dickey, C. P., Manchester, D. K., Crofts, F., & Perera, F. P.
Journal titleCancer Epidemiology Biomarkers and Prevention
Page(s)147-153The human CYP1A1 gene codes for an inducible enzyme system involved in biotransformation of certain xenobiotics, including polycyclic aromatic hydrocarbons; some of the metabolites are carcinogenic and mutagenic. Effects of environmental exposures (smoking, air pollution, and diet) on CYP1A1 gene induction in placental tissue and the modulation of induction by the CYP1A1 Mspl RFLP were evaluated in two groups from Poland: 70 mother-child pairs from Krakow, a city with elevated air pollution; and 90 pairs from Limanowa, a less polluted area. Compared to placentas from nonsmoking women, CYP1A1 mRNA levels were significantly increased in placentas from current smokers (P < 0.001). Ex-smokers also had significantly higher placental mRNA levels, including women who quit smoking prior to pregnancy (P < 0.01). A marginal increase in CYP1A1 mRNA with environmental tobacco smoke exposure was evident. Within Krakow, there was an increase in CYP1A1 mRNA with ambient pollution at the place of residence for each woman, which was significant among women who were not employed away from the home (P < 0.05 controlling for smoking status, diet, and use of coal for heating). Significant increases in mRNA were associated with dietary consumption of smoked meat, cheese, and fish (P < 0.01). The CYP1A1 Mspl RFLP was not a significant determinant of CYP1A1 mRNA levels after controlling for smoking and other variables. Human placenta provides a readily available and responsive system that can serve as a model for evaluating environmental and genetic determinants of CYP1A1 induction.
Carcinogen-DNA adducts and gene mutation in foundry workers with low-level exposure to polycyclic aromatic hydrocarbonsPerera, R. R., Dickey, C., Santella, R., O’neill, J. P., Albertini, R. J., Ottman, R., Tsai, W. Y., Mooney, L. A., Savela, K., & Hemminki, K.
Page(s)2905-2910Carcinogen-DNA adducts and somatic gene mutation at the hypoxanthine guanine phosphoribosyl transferase (HPRT) locus were evaluated in peripheral leukocytes of workers in an iron foundry with exposure to benzo[a]pyrene (B[a]P) and other polycyclic aromatic hydrocarbons (PAHs). During the two year study period, B[α]P exposure declined by ∼40%, from a maximum of 60 ng/m3 in the first year to <36 ng/m3 1 year later. A total of 64 persons were sampled in November/December of the two successive study years; 24 of them gave two samples one year apart. The biomarkers included carcinogen-DNA adducts in leukocytes (PAH-DNA measured by an immunoassay, aromatic-DNA by the 32P-postlabeling method) and HPRT mutation in lymphocytes. After adjusting for smoking, levels of PAH-DNA, aromatic-DNA and HPRT mutation frequency (Mf) increased with exposure among the 64 workers sampled during the 2 year period (P ≤ 0.05). However, the markers showed a differential response to the change in exposure, consistent with their individual biology. For example, among the 24 workers sampled in both years, carcinogen-DNA adducts (which have a halflife on the order of several months) were markedly reduced from the first to the second year (PAH-DNA, 6.2 versus 2.3/108; aromatic-DNA, 2.5 versus 1.4/108; P <0.01). HPRT Mf (a longer-lived marker) was somewhat less affected by the decline in exposure (13 versus 0.8, P < 0.05). Moreover, in the second year several long-term workers had low levels of adducts, but elevated HPRT Mf. Thus, PAH-DNA and HPRT Mf were highly correlated in the first year (n = 17; r = 0.67;P <0.01), but not in the second year or in the two years combined. However, when analysis was restricted to workers with detectable levels of adducts (who included the more highly exposed workers) the correlation was significant between PAH-DNA and HPRT (n = 17; r = 0.65; P = 0.005). In contrast, aromatic-DNA adducts and HPRT were not correlated in either year. These results suggest a molecular link between somatic gene mutation and PAHs; and they highlight the need in such molecular epidemiologic studies to consider the varying lifetimes of the individual markers.
Polycyclic aromatic hydrocarbon-DNA adducts in smokers and their relationship to micronutrient levels and the glutathione-s-transferase m1 genotypeGrinberg-funes, R. A., Singh, V. N., Perera, F. P., Bell, D. A., Young, T. L., Dickey, C., Wang, L. W., & Santella, R. M.
Page(s)2449-2454Sixty-three male cigarette smokers were entered into a cross-sectional study to determine whether inverse associations existed between polycydlic aromatic hydrocarbon (PAH)-DNA adduct levels and intake/serum levels of vitamin A, vitamin C and vitamin E. Associations between PAH-DNA adducts and intakes of carotene, as well as serum levels of β-carotene, were also determined. Fasting blood samples were collected for assays of PAH-DNA adducts in circulating mononuclear cells, plasma cotinine and serum levels of vitamin A, β-carotene, vitamin C and vitamin E. Since genetic deficiency in the detoxifying enzyme glutathione S-traasferase M1 (GSTM1) has been associated with increased risk of lung cancer, GSTM1 genotype was also determined. Analysis of PAH-DNA adducts by competitive enzyme-linked immunosorbent assay (ELISA) indicated that 70% of the subjects had detectable adducts, with a mean of 4.38 adducts/108 nucleotides (range 1.00-24.1/108 Pearson's method was utilized to determine whether any associations existed between the various host variables and PAH-DNA adducts. Previously, no significant associations were found between PAH-DNA adducts and cigarettes smoked/day, pack-years, daily/life time tar exposures or plasma cotinine levels (Santella et al., Carcinogenesis, 13, 2041-2045, 1992). PAH-DNA adducts were inversely associated with serum cholesterol-adjusted vitamin E levels (r = -0.25, P ≤ 0.05) and with smoking-adjusted vitamin C serum levels (r = -0.22, ≤ 0.09). Stratification by GSTM1 genotype indicated that these associations were limited to subjects with the null genotype. The relationship between adducts and serum cholesterol-adjusted vitamin E was significant in those of the null genotype (r = -0.38, ≤ 0.04), but not in those with the gene present (r = -0.12, P = 0.5). Similarly, for smoking-adjusted vitamin C, the relationship with adducts was stronger in subjects with the null genotype (r = -035, P ≤.0.06) than in those with GSTM1 present (r = -0.05, P = 0.77). These results are consistent with findings of prior epidemiological studies Identifying significant inverse associations between anti-oxidant micronutrient status or GSTM1 genotype and the incidence of lung cancer. Additional studies should be conducted to confirm a possible role for vitamin E in PAH-DNA adduct formation and to explore further the possible roles of vitamin A, β-carotene and vitamin C in modulating adduct formation and lung cancer risk.
Hprt and glycophorin a mutations in foundry workers: Relationship to pah exposure and to pah-DNA adductsPerera, F. P., Tang, D. L., O’neill, J. P., Bigbee, W. L., Albertini, R. J., Santella, R., Ottman, R., Tsai, W. Y., Dickey, C., Mooney, L. A., Savela, K., & Hemminki, K.
Page(s)969-973Mutations were evaluated in workers in an iron foundry with exposure to polycyclic aromatic hydrocarbons (PAHs), measured by personal and area monitoring, ranging from <5 to 60 ng/m3 of benzo[a]pyrene (B[a]P). Mutation at the hypoxanthine guanine phosphoribosyl transferase (HPRT) and glycophorin A (GPA) loci (measures of molecular effect in lymphocytes and erythrocytes respectively) were assessed to demonstrate their relationship to external exposure at lower levels than previously analyzed in foundry workers at this plant (<50-200 ng/m3). The relationship between mutations and PAH - DNA adducts measured by immunoassay (as a measure of the biologically effective dose) was also investigated. The markers were analyzed for dose-response and interindividual variability. Workers were classified into three exposure categories (low, medium and high). PAH-DNA adduct values for the low, medium and high exposure groups were 5.19, 6.10 and 9.57×10-8 nucleotides respectively (r = 0.28; P = 0.08). HPRT mutant frequencies (adjusted for age and cloning efficiency) for the low, medium and high exposure groups were 1.04, 1.13 and 1.82×10-6 cells respectively and demonstrated an upward trend with increasing exposure that was of borderline significance (r = 0.46, P = 0.06). In contrast, HPRT mutations were highly correlated with PAH-DNA adducts (r = 0.67; P = 0.004). Interindividual variability in mutant frequencies ranged from 1.5- to 4.5-fold within the three exposure categories. With respect to GPA variants, NN frequency (Vf) in erythrocytes (which reflects chromosomal loss and duplication, recombination or gene conversion) was not positively correlated with PAH exposure. The level of NØ Vf (arising from small-scale structural mutations in the GPA gene or from larger-scale chromosomal rearrangements or deletions) increased slightly, but not significantly, over the three exposure groups from 8.2 to 10.7 to 11.8/106 cells (P = 0.32). Interindividual variation in GPA NN Vf ranged from 2- to 18-fold and in GPA NØ from 4- to 5-fold. NN and NØ Vf were highly correlated (P = 0.001) but no correlation was seen between GPA and HPRT or between GPA and PAH-DNA adducts. Thus, the most interesting and novel finding is that, even at relatively low exposures to PAH, HPRT mutations were increased in parallel with PAH-DNA adducts. The observed association between PAH-DNA adducts and HPRT gene mutation in humans is consistent with experimental data for PAHs. These results support the use of both biomonitoring and personal ambient monitoring in further molecular epidemiology studies.
Molecular epidemiology of lung cancer and the modulation of markers of chronic carcinogen exposure by chemopreventive agentsPerera, F. P., Tang, D., Grinberg‐Funes, R. A., Blackwood, M. A., Dickey, C., Blaner, W., & Santella, R. M.
Journal titleJournal of Cellular Biochemistry
Page(s)119-128Chronic inhalation exposure to environmental carcinogens such as polycyclic aromatic hydrocarbons (PAHs), cigarette smoke, 4‐aminobiphenyl (4‐ABP), ethylene oxide, and styrene is associated with elevations in biomarkers such as DNA adducts, protein adducts, sister chromatid exchanges (SCEs), chromosomal aberrations, gene mutation, and/or oncogene activation. These biomarkers indicate an increased cancer risk for the exposed population, although quantitative estimates cannot be made with certainty. There is convincing epidemiological evidence that the antioxidant and free radical‐scavenging vitamins C and E and β‐carotene (β‐C) protect against cancer of the lung and other epithelial tissues, with somewhat weaker evidence for retinol. Experimental studies demonstrate that these micronutrients are capable of blocking or reducing tumor formation caused by diverse carcinogens. A variety of mechanisms appear to be involved, including suppression of carcinogen activation, enhancement of carcinogen detoxification, induction of cellular differentiation, inhibition of mutagenesis, enhancement of immunologic function, and/or reduction of the formation of carcinogen–DNA adducts, SCEs, micronuclei, and other markers of genotoxic damage. Therefore, we have recently investigated the possible modifying effect of serum vitamins C and E, β‐C, and retinol on a number of such biomarkers in a case‐control study of lung cancer, and in a cross‐sectional study of heavy smokers. Preliminary results indicate an inhibitory effect of certain vitamins on DNA adduct formation. A significant number of human intervention trials are ongoing involving these vitamins. It appears that biomarkers can provide useful intermediate endpoints for assessment of both the mechanisms and the efficacy of chemopreventive agents.
Polycyclic Aromatic Hydrocarbon-DNA Adducts in White Blood Cells and Urinary 1-Hydroxypyrene in Foundry WorkersSantella, R. M., Tang, D. L., Young, T. L., Dickey, C., Whyatt, R., Perera, F. P., Paik, M., Ottman, R., Hemminki, K., Vodickova, L., Hemminki, K., & Savela, K.
Journal titleCancer Epidemiology Biomarkers and Prevention
Page(s)59-62In an ongoing comprehensive evaluation of biological markers, workers in or near an iron foundry with varying exposure to polycyclic aromatic hydrocarbons (PAH) were analyzed for molecular response to this exposure. Exposure to benzo(a)pyrene, determined by personal monitors worn by the workers (2 to 60 ng/ m3), was considerably lower than in a previous study at this foundry (≤50 to 200 ng/m3) (F. P. Perera ef al., Cancer Res., 48: 2288–2291, 1988). Two biomarkers, 1-hydroxypyrene in urine measured by high-performance liquid chromatography with fluorescence detection (a measure of internal dose) and PAH-DNA adducts in WBC measured by immunoassay (a measure of biologically effective dose) were assessed to demonstrate their relationship to the lowest exposures yet analyzed in foundry workers. In addition, these markers were analyzed for dose response and interindividual variability. Cigarette smoking, but not age or charbroiled food, influenced the level of 1-hydroxypyrene but not PAH-DNA adducts. When workers were classified into three exposure categories (low, medium, and high), mean 1-hydroxypyrene levels were 2.7, 1.8, and 3.6 junol/mol creatinine, respectively. Comparisons by analysis of variance showed a significant difference between the groups after controlling for smoking (P = 0.02), but a trend test using multivariate linear regression analysis was not significant (r = 0.27; P = 0.07). Substantial interindividual variation was demonstrated by the 19-to 20-fold range in the values within each of the three exposure groups. PAH-DNA adducts showed an increasing trend, with exposure from 5.2 to 6.1 to 9.6 adducts/108 nucleotides in the low-, medium-, and high-exposure groups, respectively (P 0.08). The three exposure groups did not significantly differ from each other by analysis of variance (P 0.23). There was a 10- to 35-fold range in PAH-DNA adducts within exposure groups, reflecting the interindividual variability in this molecular response to PAH exposure. The correlation (r) between the two markers was 0.15 (P = 0.37). These results indicate that even at relatively low levels of benzo(a)pyrene (approximately 30-fold lower than in the previous study), we continue to observe a dose-response relationship between external exposure and the biologically effective dose of PAH.
Cigarette smoking related polycyclic aromatic hydrocarbon-DNA adducts in peripheral mononuclear cellsSantella, R. M., Grinberg-funes, R. A., Young, T. L., Dickey, C., Singh, V. N., Wang, L. W., & Perera, F. P.
Page(s)2041-2045Studies on cigarette smoking related polycyclic aromatic hydrocarbon-DNA adducts in blood have produced conflicting results. To determine whether a subset of specific white blood cells is a useful marker for monitoring exposure to cigarette smoke, blood was obtained from 63 heavy smokers and 27 non-smokers. Adduct levels were determined by competitive enzyme-linked immunosorbent assay with a polyclonal antiserum recognizing benzo[a]pyrene and structurally related diolepoxide-DNA adducts. Analysis of the lymphocyte plus monocyte fraction from smokers indicated 70% had detectable adducts with a mean of 4.38 ± 4.29 adducts/108 nucleotides, while in non-smokers the corresponding values were 22% and 1.35 ± 0.78/108 (P < 0.001). Plasma cotinine levels differed significantly in smokers (286 ± 90 μg/l) compared to non-smokers (4.4 ± 3.3 μg/l) (P < 0.001). However, cotinine was not correlated with self-reported smoking history in these heavy smokers. Nor were DNA adducts in smokers correlated with cigarettes per day, pack-years and plasma cotinine, indicating large interindividual variation in DNA adduct formation. These data demonstrate lymphocytes plus monocytes from smokers have elevated levels of polycyclic aromatic hydrocarbon diolepoxide-DNA adduct levels compared to non-smokers.
Molecular and genetic damage in humans from environmental pollution in PolandPerera, F. P., Hemminki, K., Gryzbowska, E., Motykiewicz, G., Michalska, J., Santella, R. M., Young, T. L., Dickey, C., Brandt-Rauf, P., Devivo, I., Blaner, W., Tsai, W. Y., & Chorazy, M.
Page(s)256-258EXTREME environmental pollution such as that found in the highly industrialized Silesian region of Poland has been associated with increased risk of cancer and adverse reproductive outcomes1,2. Among the most prevalent carcinogenic and mutagenic air pollutants in Silesia are the polycyclic aromatic hydrocarbons (PAH) which are largely produced by industrial and residential combustion of coal1. Molecular epidemiology aims to prevent disease by using biological markers to identify risks well before clinical onset to allow effective intervention3-7. Here, we use a battery of biological markers to measure molecular and genetic damage in peripheral blood samples from residents of Silesia and from persons living in a rural, less polluted area of Poland. The results show that their exposure to environmental pollution is associated with significant increases in carcinogen-DNA adducts (PAH-DNA and aromatic adducts), in sister chromatid exchange including high-frequency cells, and in chromosomal aberrations as well as a doubling in the frequency of ras oncogene overexpression. We found that aromatic adducts on DNA were significantly correlated with chromosomal mutation, providing us with a molecular link between environmental exposure and a genetic alteration relevant to cancer and reproductive risk.