Yueh-Ying Han, PhD, MS

Age-period-cohort analysis of cancers not related to tobacco, screening, or HIV: sex and race differences.

Yueh-Ying Han; Gregg E. Dinse; David M. Umbach; Devra Lee Davis; Joel L. Weissfeld

Published in Cancer Causes Control. 2010 Aug;21(8):1227-36. Epub 2010 Apr 7.


OBJECTIVE: To identify trends in a residual category of cancers not typically associated with tobacco, screening, or human immunodeficiency virus (HIV) infection.

METHODS: For persons aged 20-84, we used sex- and race-specific age-period-cohort (APC) models to describe temporal patterns of incidence (1975-2004) and mortality (1970-2004) in the U.S. for a residual cancer category that excluded non-Hodgkin lymphoma, Kaposi sarcoma, and cancer of the oral cavity and pharynx, esophagus, pancreas, larynx, lung and bronchus, urinary bladder, kidney and renal pelvis, colon and rectum, prostate, female breast, and cervix uteri.

RESULTS: Age-specific incidence rose (0.1-0.9% per year, on average) in every sex-race group, with factors related to both time period and birth cohort membership appearing to accelerate the increases in women. Age-specific mortality fell (0.6-0.9% per year, on average) for black and white men and women, with the declines decelerating in white women but accelerating in the other sex-race groups. Extrapolations of APC models predicted higher age-adjusted incidence rates in white women (11%), black women (5%), and white men (4%) in 2005-2009, relative to 2000-2004, and lower rates in black men (-3%), accompanied by lower age-adjusted mortality rates in every sex-race group (-8% in black men, -3% in black women, -1% in white men, and -1% in white women).

CONCLUSIONS: The possibility that increased incidence in women over time reflects changes in underlying risks, diagnostic practices, or better case ascertainment should be actively explored. Declining mortality may signify improvements in cancer care

Increased urinary 8-hydroxy-2'-deoxyguanosine excretion in long-distance bus drivers in Taiwan

Yueh-Ying Han; Maryann Donovan; Fung-Chang Sung

Published in Chemosphere. 2010 May;79(9):942-8. Epub 2010 Mar 19.

Presented at AACR International Conference on Frontiers in Cancer Prevention Research- Dec 6-9, 2009; Houston, TX [Citation Information: Cancer Prevention Research 2010;3(1 Suppl):A12]


Professional bus drivers are exposed to environments containing air pollution and reactive oxygen species (ROS) that can induce cellular oxidative stress and DNA damage. This study investigated environmental factors associated with oxidative DNA damage in a cohort of long-distance bus drivers. In a comparison study, urinary 8-hydroxydeoxyguanosine (8-OHdG), a biomarker of DNA oxidative damage, was examined in 120 male long-distance bus drivers and 58 male office workers in Taiwan. Multivariate logistic regression was used to analyze association between urinary 8-OHdG levels and environmental factors. Bus drivers had higher urinary 8-OHdG levels (adjusted odds ratio (aOR)=9.4, 95% confidence interval (CI)=3.5-28.2) compared with office workers. Increased urinary 8-OHdG level was significantly related to cigarette smoking (aOR=18.0, 95% CI=7.1-52.1), consumption of energy drinks (aOR=5.0, 95% CI=2.1-12.6), and regular exercise (aOR=3.8, 95% CI=1.5-10.2). A strong exposure-response relationship was found between urinary 8-OHdG and urinary cotinine (p<0.0001). Among nonsmokers, bus drivers (aOR=3.9, 95% CI=1.0-17.7) had higher urinary 8-OHdG than office workers. Among both bus drivers and office workers, those who drank energy drinks (aOR=3.7, 95% CI=1.2-12.2) had higher 8-OHdG levels than those who did not drink energy drinks. Adjusted for smoking, levels of 8-OHdG were increased in long-distance bus drivers exposed to traffic exhaust and ingested energy drinks. Future studies should explore what aspects of energy drinks may contribute to increased urinary 8-OHdG

Temporal and demographic patterns of non-Hodgkin's lymphoma incidence in Pennsylvania.

Published in International Journal of Occupational and Environmental Health. 2010 Jan-Mar;16(1):75-84.

Yueh-Ying Han; Gregg E. Dinse; Devra Lee Davis


Our study analyzed temporal and demographic patterns of non-Hodgkin's lymphoma (NHL) incidence in Pennsylvania and compared Pennsylvania time trends with national trends. Joinpoint and age-period-cohort analyses summarized sex- and race-specific NHL incidence time trends between 1985 and 2004. Ecologic analysis identified demographic factors associated with age-adjusted county-specific NHL incidence. NHL incidence in Pennsylvania increased annually: 1.6% and 2.5% in white and black men and 1.6% and 3.2% in white and black women. National trends were similar, except for smaller increases in white men. Diffuse lymphoma appeared to be the major contributor to the increases. NHL incidence was higher in Pennsylvania counties with greater percentages of urban residents. NHL incidence patterns in Pennsylvania were parallel to those seen nationally, with the highest rates occurring in white men and in persons residing in urban areas.

Generational risks for cancers not related to tobacco, screening, or treatment in the United States.

Published in Cancer. 2010 Feb 15;116(4):940-8.

Yueh-Ying Han; Devra Lee Davis; Joel L. Weissfeld; Gregg E. Dinse


BACKGROUND: To assess trends in cancer, the authors evaluated the risk of 1 generation compared with that 25 years earlier (generational risk) for 3 groupings of cancers: those related to tobacco; those that reflect advances in screening or treatment; and a residual category of all other cancers.

METHODS: In individuals ages 20 years to 84 years, age-period-cohort models were used to summarize time trends in terms of generational risk and average annual percentage change for US cancer incidence (1975-2004) and mortality (1970-2004) rates associated with these 3 cancer groupings.

RESULTS: Adult white men today developed 16% fewer tobacco-related cancers and had 21% fewer deaths because of those cancers than their fathers' generation, whereas adult white women experienced increases of 28% and 19%, respectively, relative to their mothers. The incidence of commonly screened cancers rose 74% in men and 10% in women, whereas mortality fell 25% in men and 31% in women. For cancers that have not been linked chiefly to tobacco or screening, the incidence was 34% and 23% higher in white men and white women, respectively, than in their parents' generation 25 years earlier. Mortality in this residual category decreased 14% in men and 18% in women. Results among blacks were qualitatively similar to those among whites.

CONCLUSIONS: Despite declining overall cancer death rates, adults are experiencing increased incidence of cancers that are not associated with tobacco or screening relative to their parents. Future research should examine whether similar patterns are exhibited in other modern nations and should identify population-wide avoidable risks that could account for unexplained increases in these residual cancers.

Cell phone use and acoustic neuroma: the need for standardized questionnaires and access to industry data.

Published in Surgical Neurology. 2009 Sep;72(3):216-22; discussion 222. Epub 2009 Mar 27.

Yueh-Ying Han; H. Kano; Devra Lee Davis; Ajay Niranjan; LD Lunsford


BACKGROUND: The capacity of radiofrequency from cell phones to be absorbed into the brain has prompted concerns that regular cell phone use may increase the risk of acoustic neuroma (AN) and other brain tumors. This article critically evaluates current literature on cell phone use and AN risks and proposes additional studies to clarify any possible linkage.

METHODS: Through a PubMed search, we identified and reviewed 10 case-control studies and 1 cohort study of AN risks associated with cell phone use and a meta-analysis of long-term mobile phone use and its association with AN and other brain tumors. RESULTS: Most studies did not find association between the development of AN and cell phone use, but some studies that followed cases for 10 years or more did show an association. Among 10 case-control studies, odds ratios for AN associated with regular cell phone use ranged from 0.5 (95% confidence interval [CI], 0.2-1.0) to 4.2 (95% CI, 1.8-10). Cell phone use was not associated with increased risk for AN in the Danish cohort study, which excluded business users from their study. The meta-analysis, which included 3 case-control studies, found that subjects who used cell phones for at least 10 years had a 2.4-fold greater risk of developing ipsilateral AN. In general, retrospective studies are limited in the ability to assess cell phone exposure because of recall bias and misclassification.

CONCLUSIONS: The evaluation of AN risk factors is challenging due to its long latency. Some studies of longer term cell phone use have found an increased risk of ipsilateral AN. Adopting a prospective approach to acquire data on cell phone use, obtaining retrospective billing records that provide independent evaluations of exposures, and incorporating information on other key potential risk factors from questionnaires could markedly advance the capacity of studies to evaluate the impact of cell phones on AN.

Indoor environmental risk factors and seasonal variation of childhood asthma.

Published in Pediatric Allergy and Immunology. 2009 Dec;20(8):748-56. Epub 2009 Feb 13.

Yueh-Ying Han; YL Lee; YL Guo


Seasonality of asthma may result from varying exposures. This cross-sectional study was designed to examine the relationship between indoor environmental factors and seasonal childhood asthma. Study subjects were participants from the International Study of Asthma and Allergies in Childhood (ISAAC) in 2004, a population-based surveillance, which included school children aged 6-15 yr in south Taiwan. Cases included 1725 children who experienced asthma symptoms in the past 12 months and the references consisted of 19,646 children who reportedly have no asthma history. By using a moving average and principal component analysis, asthmatic children were grouped into four asthma subtypes: winter, spring, summer/fall, and perennial. Multivariate logistic regression was used to evaluate the effect of indoor environmental factors on seasonality of childhood asthma. For all asthma prevalence, a peak occurred in the winter and a nadir appeared in summer. Contributing factors of asthma for children, regardless of seasonality, included younger age, parental atopy, maternal smoking during pregnancy, breast feeding, and perceived air pollution. After adjusted for salient risk factors, water damage was significantly associated with all subtypes of asthma. Presence of cockroaches was related to the summer/fall asthma (adjusted odds ratio [aOR] = 1.65, 95% confidence interval [CI] = 1.12-2.55). Visible mold on the walls was associated with an increased occurrence of winter and spring asthma (aOR = 1.53, 95% CI = 1.26-1.85 and aOR = 1.34, 95% CI = 1.10-1.62, respectively). Passive smoking was shown to be related to spring and summer/fall asthma. Water damage is a possible risk for childhood asthma year-round. Cockroaches and visible mold on the walls may play essential roles for seasonality of childhood asthma in Taiwan. Plausible mechanisms and allergic effects should be further determined. Elimination of these allergens is necessary to help prevent the development of asthma.

Arsenic levels in ground water and cancer incidence in Idaho: an ecologic study.

Published in International Archives of Occupational and Environmental Health 2009 Jul;82(7):843-9. Epub 2008 Oct 22.

Yueh-Ying Han; Joel L. Weissfeld; Devra Lee Davis; Evelyn O. Talbott


PURPOSE: Long-term exposure to arsenic above 50 microg/L in drinking water has been related to multiple types of cancers. Few epidemiologic studies conducted in the US have detected an association between regional exposures below this level in drinking water and corresponding cancer occurrence rates. This county-level ecologic study evaluates arsenic levels in ground water and its association with targeted cancer incidence in Idaho, where some regions have been found to contain higher arsenic levels.

METHODS: Using cancer incidence data (1991-2005) from the Cancer Data Registry of Idaho and arsenic data (1991-2005) from the Idaho Department of Environmental Quality, we calculated the age-adjusted incidence rate for cancers of the urinary bladder, kidney and renal pelvis, liver and bile duct, lung and bronchus, non-Hodgkin's lymphoma (NHL), and all malignant cancers according to arsenic levels in ground water. Multivariate regression analysis was applied to evaluate the relationship between arsenic levels in ground water and cancer incidence.

RESULTS: For males, but not for females, age-adjusted incidence for lung cancer and all malignant cancers was significantly higher in the intermediate arsenic counties (2-9 microg/L, n = 16) and the high arsenic counties (>or=10 microg/L, n = 5) compared to the low arsenic counties (<2.0 microg/L, n = 23). When adjusted for race, gender, population density, smoking and body mass index (BMI), no relationship was found between arsenic levels in ground water and cancer incidence.

CONCLUSIONS: In this ecological design, exposure to low-level arsenic in ground water is not associated with cancer incidence when adjusting for salient variables. For populations residing in southwestern Idaho, where arsenic has been found to exceed 10 microg/L in ground water, individual risk assessment is required in order to determine whether there is a link between long-term arsenic exposure at these levels and cancer risk.

Time Trends and Racial Differences in Female Breast Cancer Incidence in Pennsylvania, 1985-2004

Accepted for Publication by Journal of Women's Health

Presented at AACR International Conference on Frontiers in Cancer Prevention Research- Dec 6-9, 2009; Houston, TX [Citation Information: Cancer Prevention Research 2010;3(1 Suppl):A130]

Yueh-Ying Han, PhD1,2; Evelyn Talbott, DrPH1,2; Maryann Donovan, PhD, MPH2, 3


Differences in breast cancer incidence time trends can result from changes in ascertainment, new diagnostic codes, or possibly changes in underlying risk factors. Female breast cancer incidence data between 1985 and 2004 were obtained from the Pennsylvania Cancer Registry. Joinpoint regression was applied to characterize time trends of age-, race- and histologic-specific breast cancer incidence. Estimated annual percent change (APC) was calculated. Spatial analysis was applied to detect spatial clusters of county-specific incidence for breast cancer in Pennsylvania. The age-adjusted incidence of invasive breast carcinoma (IBC) and breast carcinoma in situ (BCIS) was higher in whites than in blacks. IBC incidence began to decrease significantly in 2001 (APC = -3.0%) among whites but has been stable among blacks since 1987. Among whites, the age-adjusted incidence of ductal carcinoma in situ (DCIS) increased significantly from 1985 to 1999 but was stable for lobular carcinoma in situ (LCIS). Among blacks, the incidence for DCIS and LCIS increased significantly over time. For women under the age of 40, BCIS incidence increased significantly over time (APC = 4.5% and 10.0% in whites and blacks, respectively, 1985-2004). Young black women had a higher incidence of both IBC and BCIS compared to young white women. Spatial clustering of IBC was found in Pennsylvania (p = 0.024) with regions of increased incidence rates clustered in eight southeastern counties. Although increased BCIS is partly explained by improved diagnosis and screening, other risk factors should be considered. In addition, factors responsible for higher breast cancer rates among younger black women and southeastern Pennsylvania residents should be carefully assessed.