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1.  Correlation of Insurance, Race, and Ethnicity with Pathologic Risk in a Controlled Retinoblastoma Cohort 
Ophthalmology  2016;123(8):1817-1823.
To determine whether insurance status, race, and ethnicity correlate with increased retinoblastoma invasiveness as a marker of both risk and time to diagnosis.
Retrospective case-control study.
All 203 patients from the United States enrolled in the Children's Oncology Group (COG) trial ARET0332, a study of patients with unilateral retinoblastoma requiring enucleation.
Main Outcome Measures
All surgical specimens underwent pathologic review to determine the presence of well-defined histopathologic features correlating with a higher risk of disease progression. Insurance status, race, and ethnicity were compiled from the study record for each patient.
On institutional pathologic review, nonprivate insurance, nonwhite race, and Hispanic ethnicity all correlated significantly with a greater rate of high-risk pathologic findings. Hispanic ethnicity remained a significant predictor on multivariate analysis. On central pathologic review, these correlations remained but did not reach statistical significance. The differences in results from institutional versus central pathologic reviews appeared to be due to a higher likelihood of patients in minority groups of being misclassified as high risk by institutional pathologists.
In this controlled study population of patients with retinoblastoma who had central pathologic review, our findings suggest a higher rate of more advanced disease associated with nonprivate insurance, nonwhite race, and Hispanic ethnicity; these findings may be due to delays in diagnosis for these groups. Future work should use direct methods to study the impact of other variables, including English-language proficiency and socioeconomic status. Further effort also should focus on where in the diagnostic process potential delays exist, so that interventions can be designed to overcome barriers to care for these groups. In addition, potential systematic differences in pathologic reads based on demographic variables deserve further study.
PMCID: PMC5161100  PMID: 27262763
2.  Patterns of sun protective behaviors among Hispanic children in a skin cancer prevention intervention 
Preventive medicine  2015;81:303-308.
Invasive melanoma is becoming more common in U.S. Hispanics, yet little is known about the sun protection behaviors in this population, particularly children and adolescents who incur high UV exposures. We used latent class analysis to examine patterns of sun protective behaviors in a cross-sectional survey of Hispanic elementary students participating in a sun safety intervention in Los Angeles from 2013–2014 (N=972). Five behavior indicators in two environments (school and home) representing multiple methods of sun protection were selected for the model. Results suggested a four-class model best fit the data. Classes were labeled in order of increasing risk as multiple protective behaviors (28%), clothing and shade (32%), pants only (15%), and low/inconsistent protective behaviors (25%). Children who reported high parental engagement with sun protection were significantly more likely to be classified in high overall protective categories (OR=4.77). Girls were more likely than boys to be classified in the highest protecting class (OR=3.46), but were also more likely to be in the “pants only” class (OR=2.65). Sensitivity to sunburn was associated with less likelihood of being in the “clothing and shade” class (OR=0.53). The differences amongst these classes and their predictors reveal the heterogeneity and complexity of Hispanic children’s sun protective behaviors. These findings have implications for the design and delivery of future sun protection interventions targeting Hispanic children, as strategies tailored to specific subgroups may be more effective in achieving meaningful behavioral changes.
PMCID: PMC4679689  PMID: 26436682
Children; Hispanic; Melanoma; Skin cancer; Latent class analysis
3.  Genetic Variability in ABCB1, Occupational Pesticide Exposure, and Parkinson’s Disease 
Environmental research  2015;143(Pt A):98-106.
Studies suggested that variants in the ABCB1 gene encoding P-glycoprotein, a xenobiotic transporter, may increase susceptibility to pesticide exposures linked to Parkinson’s Disease (PD) risk.
To investigate the joint impact of two ABCB1 polymorphisms and pesticide exposures on PD risk.
In a population-based case control study, we genotyped ABCB1 gene variants at rs1045642 (c.3435C/T) and rs2032582 (c.2677G/T/A) and assessed occupational exposures to organochlorine (OC) and organophosphorus (OP) pesticides based on self-reported occupational use and record-based ambient workplace exposures for 282 PD cases and 514 controls of European ancestry. We identified active ingredients in self-reported occupational use pesticides from a California database and estimated ambient workplace exposures between 1974 and 1999 employing a geographic information system together with records for state pesticide and land use. With unconditional logistic regression, we estimated marginal and joint contributions for occupational pesticide exposures and ABCB1 variants in PD.
For occupationally exposed carriers of homozygous ABCB1 variant genotypes, we estimated odds ratios of 1.89 [95% confidence interval (CI): (0.87, 4.07)] to 3.71 [95% CI: (1.96, 7.02)], with the highest odds ratios estimated for occupationally exposed carriers of homozygous ABCB1 variant genotypes at both SNPs; but we found no multiplicative scale interactions.
This study lends support to a previous report that commonly used pesticides, specifically OCs and OPs, and variant ABCB1 genotypes at two polymorphic sites jointly increase risk of PD.
PMCID: PMC4911423  PMID: 26457621
Pesticide; Epidemiology; Parkinson’s Disease; multidrug resistance protein 1 gene (ABCB1); P-glycoprotein
4.  A Statewide Nested Case–Control Study of Preterm Birth and Air Pollution by Source and Composition: California, 2001–2008 
Environmental Health Perspectives  2016;124(9):1479-1486.
Preterm birth (PTB) has been associated with exposure to air pollution, but it is unclear whether effects might vary among air pollution sources and components.
We studied the relationships between PTB and exposure to different components of air pollution, including gases and particulate matter (PM) by size fraction, chemical composition, and sources.
Fine and ultrafine PM (respectively, PM2.5 and PM0.1) by source and composition were modeled across California over 2000–2008. Measured PM2.5, nitrogen dioxide, and ozone concentrations were spatially interpolated using empirical Bayesian kriging. Primary traffic emissions at fine scale were modeled using CALINE4 and traffic indices. Data on maternal characteristics, pregnancies, and birth outcomes were obtained from birth certificates. Associations between PTB (n = 442,314) and air pollution exposures defined according to the maternal residence at birth were examined using a nested matched case–control approach. Analyses were adjusted for maternal age, race/ethnicity, education and neighborhood income.
Adjusted odds ratios for PTB in association with interquartile range (IQR) increases in average exposure during pregnancy were 1.133 (95% CI: 1.118, 1.148) for total PM2.5, 1.096 (95% CI: 1.085, 1.108) for ozone, and 1.079 (95% CI: 1.065, 1.093) for nitrogen dioxide. For primary PM, the strongest associations per IQR by source were estimated for onroad gasoline (9–11% increase), followed by onroad diesel (6–8%) and commercial meat cooking (4–7%). For PM2.5 composition, the strongest positive associations per IQR were estimated for nitrate, ammonium, and secondary organic aerosols (11–14%), followed by elemental and organic carbon (2–4%). Associations with local traffic emissions were positive only when analyses were restricted to births with residences geocoded at the tax parcel level.
In our statewide nested case–control study population, exposures to both primary and secondary pollutants were associated with an increase in PTB.
Laurent O, Hu J, Li L, Kleeman MJ, Bartell SM, Cockburn M, Escobedo L, Wu J. 2016. A statewide nested case–control study of preterm birth and air pollution by source and composition: California, 2001–2008. Environ Health Perspect 124:1479–1486;
PMCID: PMC5010414  PMID: 26895492
5.  Predictors of skin examination in California twins Prevalence and predictors of recent skin examination in a population-based twin cohort 
The incidence of melanoma is increasing worldwide. Guidelines for clinical skin exam for improving early diagnosis of melanoma remain inconsistent, and current data on factors associated with regular skin screening on a population basis are limited.
We used self-reported data from 50,044 members of the California Twin Program, a population-based cohort of twins born in California between 1908 and 1982, to identify prevalence and determinants of recent clinical screening for skin cancer.
Prevalence of skin examination was higher than national estimates, with 32% of respondents of all ages reporting ever having skin examination. Socio-demographic and constitutional risk factors including white race, educational attainment, marital status, and number of large moles were strongly associated with recent screening, as were individual and family history of skin cancer. Lower socioeconomic status, racial/ethnic minority status, and paradoxically, frequent UV-related risk behaviors in adulthood were associated with a lower likelihood of recent screening.
As the evidence concerning the efficacy of skin examination continues to evolve, attention should be paid to motivators and barriers of screening, particularly in high-risk subgroups where lack of screening may contribute to disparate rates of thicker melanomas and lower survival.
Our results demonstrate the need for prevention strategies targeted to specific at-risk groups to increase earlier detection leading to improved outcomes.
PMCID: PMC4526388  PMID: 25994738
Melanoma; prevention & control; Melanoma; diagnosis; secondary prevention; early detection of cancer
6.  In Utero and Early-Life Exposure to Ambient Air Toxics and Childhood Brain Tumors: A Population-Based Case–Control Study in California, USA 
Environmental Health Perspectives  2015;124(7):1093-1099.
Little is known about the influence of environmental factors on the etiology of childhood brain tumors.
We examined risks for brain tumors in children after prenatal and infant exposure to monitored ambient air toxics.
We ascertained all cases of medulloblastoma, central nervous system primitive neuroectodermal tumor (PNET), and astrocytoma before 6 years of age diagnosed in 1990–2007 from the California Cancer Registry and selected controls randomly from birth rolls matched by birth year. Exposures to air toxics during pregnancy/infancy for 43 PNET, 34 medulloblastoma, and 106 astrocytoma cases and 30,569 controls living within 5 mi of a monitor were determined. With factor analysis we assessed the correlational structures of 26 probable carcinogenic toxics, and estimated odds ratios by brain tumor type in logistic regression models.
PNETs (≤ 38 cases) were positively associated with interquartile range (IQR) increases in prenatal exposure to acetaldehyde [odds ratio (OR) = 2.30; 95% CI: 1.44, 3.67], 1,3-butadiene (OR = 2.23; 95% CI: 1.28, 3.88), benzene, and toluene; and with IQR increases in exposure during the first year of life to ortho-dichlorobenzene (OR = 3.27; 95% CI: 1.17, 9.14), 1,3-butadiene (OR = 3.15; 95% CI: 1.57, 6.32), and benzene. All exposures except ortho-dichlorobenzene loaded on the same factor. Medulloblastoma (≤ 30 cases) was associated with prenatal exposure to polycyclic aromatic hydrocarbons (PAHs combined: OR = 1.44; 95% CI: 1.15, 1.80). Exposures to lead and some PAHs during the first year of life were positively associated with astrocytoma, but the confidence intervals included the null value (e.g., for lead, OR = 1.40; 95% CI: 0.97, 2.03).
Our data suggest that in utero and infancy exposures to air toxics generated by industrial and road traffic sources may increase the risk of PNET and medulloblastoma, with limited support for increased risks for astrocytoma in children up to age 6.
von Ehrenstein OS, Heck JE, Park AS, Cockburn M, Escobedo L, Ritz B. 2016. In Utero and early-life exposure to ambient air toxics and childhood brain tumors: a population-based case–control study in California, USA. Environ Health Perspect 124:1093–1099;
PMCID: PMC4937846  PMID: 26505805
7.  Vitamin D receptor gene polymorphisms and Parkinson’s disease in a Population with High Ultraviolet Radiation Exposure 
A high prevalence of vitamin D deficiency has been reported in Parkinson’s disease (PD). Epidemiologic studies examining variability in genes involved in vitamin D metabolism have not taken into account level of exposure to ultraviolet radiation (UVR). We examined whether exposure to UVR (as a surrogate for vitamin D levels) and variations in the vitamin D receptor gene (VDR) are associated with PD.
Within a geographical information system (GIS) we linked participants’ geocoded residential address data to ground level UV data to estimate historical exposure to UVR. Six SNPs in VDR were genotyped in non-Hispanic Caucasian subjects.
Average lifetime UVR exposure levels were >5000 Wh/m2, which was higher than levels for populations in previous studies, and UVR exposure did not differ between cases and controls. Homozygotes for the rs731236 TT (major allele) genotype had a 31% lower risk of PD risk (OR = 0.69; 95% CI = 0.49, 0.98; p=0.04 for TT vs. TC + CC). The rs7975232 GG (minor allele) genotype was also associated with decreased risk of PD (OR = 0.63; 95% CI = 0.42, 0.93; p=0.02 for GG vs. TG + TT). The association between PD risk and a third locus, rs1544410 (BsmI), was not statistically significant after adjustment for covariates, although there was a trend for lower risk with the GG genotype.
This study provides initial evidence that VDR polymorphisms may modulate risk of PD in a population highly exposed to UVR throughout lifetime.
PMCID: PMC4478085  PMID: 25890641
vitamin D; ultraviolet radiation; Parkinson’s disease; vitamin D receptor gene polymorphisms; TaqI; ApaI
8.  Organophosphate Pesticide Exposures, Nitric Oxide Synthase Gene Variants, and Gene–Pesticide Interactions in a Case–Control Study of Parkinson’s Disease, California (USA) 
Environmental Health Perspectives  2015;124(5):570-577.
Nitric oxide synthase (NOS) genes are candidates for Parkinson’s disease (PD) because NOS enzymes produce nitric oxide (NO), a pro-oxidant that can damage neurons. Widely used organophosphate (OP) pesticides can induce oxidative stress and are reported to increase PD risk. Additionally, two single nucleotide polymorphisms (SNPs) from the PON1 (paraoxonase 1) gene influence the ability to metabolize OPs.
Here, we investigated contributions of NOS genes and OP pesticides to PD risk, controlling for PON1 status.
In 357 incident PD cases and 495 population controls, we investigated eight NOS SNPs and interactions with both household and ambient agricultural OP exposures assessed with geographic information system (GIS).
In comparing PD in homozygous variant carriers of NOS2A rs1060826 versus homozygous wild-type or heterozygotes, we estimate an adjusted odds ratio (OR) of 1.51 (95% CI: 0.95, 2.41). When considering interactions between NOS1 rs2682826 and OP exposure from household use, the OR for frequent OP use alone was 1.30 (95% CI: 0.72, 2.34) and for the CT+TT genotype alone was 0.89 (95% CI: 0.58, 1.39), and for frequent OP use combined with the CT+TT genotype the OR was 2.84 (95% CI: 1.49, 5.40) (interaction p-value 0.04). Similar results were seen for ambient OP exposure. Interactions between OP exposure and three other NOS1 SNPs and a genetic risk score combining all NOS1 SNPs reached statistical significance.
We found that OP pesticides were more strongly associated with PD among participants with variant genotypes in NOS1, consistent with the importance of oxidative stress-inducing mechanisms. Our data provide evidence for NOS1 modifying PD risk in OP exposed populations.
Paul KC, Sinsheimer JS, Rhodes SL, Cockburn M, Bronstein J, Ritz B. 2016. Organophosphate pesticide exposures, nitric oxide synthase gene variants, and gene–pesticide interactions in a case–control study of Parkinson’s disease, California (USA). Environ Health Perspect 124:570–577;
PMCID: PMC4858402  PMID: 26383258
9.  Current Data on Risk Factor Estimates Does Not Explain the Difference in Rates of Melanoma between Hispanics and Non-Hispanic Whites 
Journal of Skin Cancer  2016;2016:2105250.
United States Hispanics have seven times lower melanoma incidence rates than non-Hispanic whites (NHW). It is unclear whether this difference can be explained solely by phenotypic risk factors, like darker skin, or whether modifiable risk factors, like sun exposure, also play a role. The purpose of this paper is to summarize what is currently known about melanoma risk factors among Hispanics and NHWs, and whether or not those differences could explain the difference in melanoma incidence. Through literature review, relative risks and prevalence of melanoma risk factors in Hispanics and NHWs were identified and used to calculate the expected rate in Hispanics and rate ratio compared to NHWs. We found that melanoma risk factors either have similar frequency in Hispanics and NHWs (e.g., many large nevi) or are less frequent in Hispanics but do not explain a high proportion of disease variation (e.g., red hair). Considering current knowledge of risk factor prevalence, we found that melanoma incidence rates in the two groups should actually be similar. Sun exposure behavior among Hispanics may contribute to the explanation for the 7-fold difference in melanoma rates. Currently, limited data exist on sun exposure behavior among Hispanics, but possibilities for improving primary prevention by further studying these practices are substantial.
PMCID: PMC4820624  PMID: 27092276
10.  Retinoblastoma and ambient exposure to air toxics in the perinatal period 
We examined ambient exposure to specific air toxics in the perinatal period in relation to retinoblastoma development. Cases were ascertained from California Cancer Registry records of children diagnosed 1990–2007 and matched to California birth certificates. Controls were randomly selected from state birth records for the same time period. We chose 27 air toxics for the present study that had been listed as possible, probable, or established human carcinogens by the International Agency for Research on Cancer. Children (103 cases and 30,601 controls) included in the study lived within 5 miles (~8K) of an air pollution monitor. Using logistic regression analyses, we modeled the risk of retinoblastoma due to air toxics exposure, separately for exposures in pregnancy and the first year of life. With a per interquartile range increase in air toxics exposure, retinoblastoma risk was found to be increased with pregnancy exposure to benzene (OR=1.67, 95%CI 1.06, 2.64) and other toxics which primarily arise from gasoline and diesel combustion: toluene, 1,3 butadiene, ethyl benzene, ortho-xylene, and meta/para-xylene; these 6 toxics were highly correlated. Retinoblastoma risk was also increased with pregnancy exposure to chloroform (OR=1.35, 95%CI 1.07, 1.70), chromium (OR=1.29, 95%CI 1.04, 1.60), para-dichlorobenzene (OR=1.24, 95%CI 1.04, 1.49), nickel (OR=1.48, 95%CI 1.08, 2.01), and in the first year of life, acetaldehyde (OR=1.62, 95%CI 1.06, 2.48). Sources of these agents are discussed.
PMCID: PMC4059784  PMID: 24280682
Retinoblastoma; Air pollution; Benzene; Chromium; Nickel; Xylenes
11.  Tanning bed use and melanoma: Establishing risk and improving prevention interventions☆ 
Preventive Medicine Reports  2016;3:139-144.
Exposure to ultraviolet radiation (UVR) from indoor tanning devices is thought to cause melanoma and other negative health consequences. Despite these findings, the practice of indoor tanning in the United States remains prevalent. In this paper we aim to present a clear discussion of the relationship between indoor tanning and melanoma risk, and to identify potential strategies for effective melanoma prevention by addressing indoor tanning device use.
Basic procedures
We reviewed relevant literature on the risks of indoor tanning, current indoor tanning legislation, and trends in indoor tanning and melanoma incidence. Study was conducted at the University of Southern California, Los Angeles, CA between the years of 2014 and 2015.
Main findings
Our findings reaffirm the relationship between indoor tanning and melanoma risk, and suggest a widespread public misunderstanding of the negative effects of indoor tanning.
Principal conclusions
This review argues for an aggressive initiative to reduce indoor tanning in the United States, to design prevention efforts tailored towards specific high risk groups, and the need to better inform the public of the risks of indoor tanning.
•We present a concise review of current evidence on the risks of indoor tanning.•We identify populations most at risk of negative outcomes from indoor tanning.•We evaluate current legislation aimed to reduce the prevalence of indoor tanning.•We argue for aggressive anti-tanning initiatives targeting specific high risk groups.•We reaffirm the need for widespread public education on the health risks of indoor tanning.
PMCID: PMC4929140  PMID: 27419006
Melanoma; Tanning; Risk factors; Prevention; Adolescents
12.  In Utero Exposure to Toxic Air Pollutants and Risk of Childhood Autism 
Epidemiology (Cambridge, Mass.)  2014;25(6):851-858.
Genetic and environmental factors are believed to contribute to the development of autism, but relatively few studies have considered potential environmental risks. Here we examine risks for autism in children related to in utero exposure to monitored ambient air toxics from urban emissions.
Among the cohort of children born in Los Angeles County, California 1995–2006, those whose mothers resided during pregnancy in a 5km buffer around air-toxics monitoring stations were included (n=148,722). To identify autism cases in this cohort, birth records were linked to records of children diagnosed with primary autistic disorder at the California Department of Developmental Services between 1998 and 2009 (n=768). We calculated monthly average exposures during pregnancy for 24 air toxics selected based on suspected or known neurotoxicity or neurodevelopmental toxicity. Factor analysis helped us identify the correlational structure among air toxics, and we estimated odds ratios (ORs) for autism from logistic regression analyses.
Autism risks were increased per interquartile-range increase in average concentrations during pregnancy of several correlated toxics mostly loading on one factor, including 1,3-butadiene (OR=1.59 [95% confidence interval=1.18–2.15]), meta/para-xylene (1.51 [1.26–182]), other aromatic solvents, lead (1.49 [1.23–1.81]), perchloroethylene (1.40 [1.09–1.80]), and formaldehyde (1.34 [1.17–1.52]), adjusting for maternal age, race/ethnicity, nativity, education, insurance type, maternal birth place, parity, child sex, and birth year.
Risks for autism in children may increase following in utero exposure to ambient air toxics from urban traffic and industry emissions, as measured by community-based air -monitoring stations.
PMCID: PMC4698150  PMID: 25051312
13.  Epidemiologic study of residential proximity to transmission lines and childhood cancer in California: description of design, epidemiologic methods and study population 
We conducted a large epidemiologic case-control study in California to examine the association between childhood cancer risk and distance from the home address at birth to the nearest high-voltage overhead transmission line as a replication of the study of Draper et al. in the United Kingdom. We present a detailed description of the study design, methods of case ascertainment, control selection, exposure assessment and data analysis plan. A total of 5788 childhood leukemia cases and 3308 childhood central nervous system cancer cases (included for comparison) and matched controls were available for analysis. Birth and diagnosis addresses of cases and birth addresses of controls were geocoded. Distance from the home to nearby overhead transmission lines was ascertained on the basis of the electric power companies’ geographic information system (GIS) databases, additional Google Earth aerial evaluation and site visits to selected residences. We evaluated distances to power lines up to 2000 m and included consideration of lower voltages (60–69 kV). Distance measures based on GIS and Google Earth evaluation showed close agreement (Pearson correlation >0.99). Our three-tiered approach to exposure assessment allowed us to achieve high specificity, which is crucial for studies of rare diseases with low exposure prevalence.
PMCID: PMC4617228  PMID: 24045429
childhood leukemia; electromagnetic fields; geographic information system; childhood cancer; power lines; case-control study
14.  Risk of leukemia in relation to exposure to ambient air toxics in pregnancy and early childhood 
There are few established causes of leukemia, the most common type of cancer in children. Studies in adults suggest a role for specific environmental agents, but little is known about any effect from exposures in pregnancy to toxics in ambient air. In our case-control study, we ascertained 69 cases of acute lymphoblastic leukemia (ALL) and 46 cases of acute myeloid leukemia (AML) from California Cancer Registry records of children < age 6, and 19,209 controls from California birth records within 2km (1.3 miles) (ALL) and 6km (3.8 miles) (AML) of an air toxics monitoring station between 1990–2007. Information on air toxics exposures was taken from community air monitors. We used logistic regression to estimate the risk of leukemia associated with one interquartile range increase in air toxic exposure. Risk of ALL was elevated with 3rd trimester exposure to polycyclic aromatic hydrocarbons (OR=1.16, 95%CI 1.04, 1.29), arsenic (OR=1.33, 95%CI 1.02, 1.73), benzene (OR=1.50, 95%CI 1.08, 2.09), and three other toxics related to fuel combustion. Risk of AML was increased with 3rd trimester exposure to chloroform (OR=1.30, 95%CI 1.00, 1.69), benzene (1.75, 95%CI 1.04, 2.93), and two other traffic-related toxics. During the child’s first year, exposure to butadiene, ortho-xylene, and toluene increased risk for AML and exposure to selenium increased risk for ALL. Benzene is an established cause of leukemia in adults; this study supports that ambient exposures to this and other chemicals in pregnancy and early life may also increase leukemia risk in children.
PMCID: PMC4071125  PMID: 24472648
Childhood leukemia; pregnancy; polycyclic aromatic hydrocarbons; benzene; toluene; lead; chloroform; xylenes; arsenic; childhood cancer epidemiology
15.  Exposure to infections and Risk of Leukemia in Young Children 
Epidemiologic studies indicate that infections in early childhood may protect against pediatric acute lymphoblastic leukemia (ALL).
We identified 3,402 ALL cases among children 0–5 years using the California Cancer Registry. From California birth records we randomly selected controls in a 20:1 ratio and frequency matched them to cases by birth year. We investigated markers of exposure to infections, including month of birth, timing of birth in relation to influenza and respiratory syncytial virus (RSV) seasons, and birth order based on data from California birth certificates and national infection surveillance systems.
We observed an increased risk of ALL for spring and summer births, and for those first exposed to an influenza or RSV season at nine to twelve months of age compared to those exposed during the first three months of life, and this association was stronger among first born children (OR and 95% CI 1.44 [1.13, 1.82] for influenza exposure at nine to twelve months of age). Decreased risk was observed with increasing birth order among non-Hispanic whites but not Hispanics (OR and 95% CI 0.76 [0.59, 096] for fourth or higher birth order among whites).
Our results support the hypothesis that infections in early childhood decrease risk of ALL.
Our findings implicate early life exposure to infections as protective factors for ALL in young children.
PMCID: PMC4100471  PMID: 24793957
Children; Epidemiology; Infant; Influenza; Human; Leukemia; Lymphoid; Respiratory Syncytial Virus
16.  Prenatal exposure to air toxics and risk of Wilms’ tumor in 0-5 year old children 
To study prenatal air toxics exposure and Wilms’ tumor in children.
We identified 337 Wilms’ tumor cases among children <6 years (1988-2008) from the California Cancer Registry, randomly selected 96,514 controls from California birth rolls in 20:1 ratio matched to all cancer cases, then linked birth addresses to air monitors within 15 miles to assess exposures. Multiple logistic regressions were applied to estimate effects.
Children prenatally exposed to formaldehyde, polycyclic aromatic hydrocarbons, perchloroethylene, or acetaldehyde in the third trimester had an increased odds of Wilms’ tumor per interquartile increase in concentration (OR [95%CI]: 1.28 [1.12, 1.45], 1.10 [0.99, 1.22], 1.09 [1.00, 1.18], 1.25 [1.07, 1.45] respectively).
We found positive associations for four air toxics. This is the first study of this kind. Future studies are needed to confirm our findings.
PMCID: PMC4204106  PMID: 24854250
17.  The Effect of Neighborhood and Individual Characteristics on Pediatric Critical Illness 
Journal of community health  2014;39(4):753-759.
The relationship between neighborhood/individual characteristics and pediatric intensive care unit (PICU) outcomes is largely unexplored. We hypothesized that individual- level racial/ethnic minority status and neighborhood-level low socioeconomic status and minority concentration would adversely affect children’s severity of illness on admission to the PICU. Retrospective analyses (1/1/2007–5/ 23/2011) of clinical, geographic, and demographic data were conducted at an academic, tertiary children’s hospital PICU. Clinical data included age, diagnosis, insurance, race/ethnicity, Pediatric Index of Mortality 2 score on presentation to the PICU (PIM2), and mortality. Residential addresses were geocoded and linked with 2010 US Census tract data using geographic information systems geocoding techniques. Repeated measures models to predict PIM2 and mortality were constructed using three successive models with theorized covariates including the patient’s race/ethnicity, the predominant neighborhood racial/ethnic group, interactions between patient race/ethnicity and neighborhood race/ethnicity, neighborhood socioeconomic status, and insurance type. Of the 5,390 children, 57.8 %were Latino and 70.1 %possessed government insurance. Latino children (β = 0.31; p < 0.01), especially Latino children living in a Latino ethnic enclave (β = 1.13; p < 0.05), had higher PIM2 scores compared with non-Latinos. Children with government insurance (β = 0.29; p < 0.01) had higher PIM2 scores compared to children with other payment types and median neighborhood income was inversely associated with PIM2 scores (β = −0.04 per $10,000/year of income; p < 0.05). Lower median neighborhood income, Latino ethnicity, Latino children living in a predominantly Latino neighborhood, and children possessing government insurance were associated with a higher severity of illness on PICU admission. The reasons why these factors affect critical illness severity require further exploration.
PMCID: PMC4443908  PMID: 24488647
Neighborhood; Geocoding; Pediatric; Intensive care; Health care disparities
18.  Impact of neighborhood and individual socioeconomic status on survival after breast cancer varies by race/ethnicity: The Neighborhood and Breast Cancer Study 
Research is limited on the independent and joint effects of individual- and neighborhood-level socioeconomic status (SES) on breast cancer survival across different racial/ethnic groups.
We studied individual-level SES, measured by self-reported education, and a composite neighborhood SES (nSES) measure in females (1,068 non-Hispanic whites, 1,670 Hispanics, 993 African-Americans, and 674 Asian-Americans), aged 18–79 years and diagnosed 1995–2008, in the San Francisco Bay Area. We evaluated all-cause and breast cancer-specific survival using stage-stratified Cox proportional hazards models with cluster adjustment for census block groups.
In models adjusting for education and nSES, lower nSES was associated with worse all-cause survival among African-Americans (p-trend=0.03), Hispanics (p-trend=0.01) and Asian-Americans (p-trend=0.01). Education was not associated with all-cause survival. For breast cancer-specific survival, lower nSES was associated with poorer survival only among Asian-Americans (p-trend=0.01). When nSES and education were jointly considered, women with low education and low nSES had 1.4 to 2.7-times worse all-cause survival than women with high education and high nSES across all races/ethnicities. Among African-Americans and Asian-Americans, women with high education and low nSES had 1.6 to 1.9-times worse survival, respectively. For breast cancer-specific survival, joint associations were found only among Asian-Americans with worse survival for those with low nSES regardless of education.
Both neighborhood and individual SES are associated with survival after breast cancer diagnosis, but these relationships vary by race/ethnicity.
A better understanding of the relative contributions and interactions of SES with other factors will inform targeted interventions towards reducing long-standing disparities in breast cancer survival.
PMCID: PMC4018239  PMID: 24618999
breast cancer survival; neighborhood socioeconomic status; education; race/ethnicity
19.  The Association Between Ambient Exposure to Organophosphates and Parkinson’s Disease Risk 
There is a general consensus that pesticides are involved in the etiology of Parkinson’s disease (PD), although associations between specific pesticides and the risk of developing Parkinson’s disease have not been well studied. This study examines the risk of developing PD associated with specific organophosphate pesticides and their mechanisms of toxicity.
This case-control study uses a geographic information system (GIS)-based exposure assessment tool to estimate ambient exposure to 36 commonly used organophosphates (OPs) from 1974-1999. All selected OPs were analyzed individually and also in groups formed according to their presumed mechanisms of toxicity.
The study included 357 incident PD cases and 752 population controls living in the Central Valley of California. Ambient exposure to each OP evaluated separately increased the risk of developing PD. However, most participants were exposed to combinations of OPs rather than a single pesticide. Risk estimates for OPs grouped according to different presumed functionalities and toxicities were similar and did not allow us to distinguish between them. However, we observed exposure-response patterns with exposure to an increasing number of OPs.
This study adds strong evidence that OPs are implicated in the etiology of idiopathic PD. However, studies of OPs at low doses reflective of real-world ambient exposure are needed to determine the mechanisms of neurotoxicity.
PMCID: PMC4351788  PMID: 24436061
20.  Preliminary evidence for mediation of the association between acculturation and sun-safe behaviors 
Archives of dermatology  2011;147(7):814-819.
To identify and test mediators of the relationship between acculturation and sun-safe behaviors among Latinos in the United States. We hypothesized that the effect of acculturation on use of sunscreen, shade, and sun-protective clothing would be mediated by perceived health status, educational level, access to healthcare, and contact with social networks regarding health matters.
The 2005 Health Information National Trends Survey, implemented by the National Cancer Institute.
Nationwide survey.
A probability-based sample of the US civilian, noninstitutionalized adult population, comprising 496 Latino respondents.
Main outcome measures
Use of sunscreen, shade, and sun-protective clothing when outdoors on sunny days, assessed by self-reports on frequency scales.
The positive association between acculturation and sunscreen use and the negative association between acculturation and use of sun-protective clothing were mediated by educational level (P<0.05 for both). Perceived health status and contact with social networks regarding health matters were supported as mediators only for sunscreen use (P<0.05). Health care access was not supported as a mediator for any of the outcomes.
Structural equation models revealed distinct direct and indirect paths between acculturation and each sun-safe practice. Our findings place an emphasis on behavior-specific mediated associations and could inform sun safety programming for Latinos with low and high levels of acculturation. The models support education level, contact with social networks regarding health matters, and perceived health status as mediators primarily for sunscreen use. Future research should test different mediators for use of shade or sun-protective clothing.
PMCID: PMC4353392  PMID: 21768480
21.  Molecular characteristics of diffuse large B-cell lymphoma in human immunodeficiency virus-infected and -uninfected patients in the pre-highly active antiretroviral therapy and pre-rituximab era 
Leukemia & lymphoma  2013;55(3):551-557.
Human immunodeficiency virus (HIV) infection substantially elevates diffuse large B-cell lymphoma (DLBCL) risk, but its impact on the distinct DLBCL subtypes defined by cell of origin is unclear. We compared DLBCL molecular characteristics and prognosis in 51 HIV-infected and 116 HIV-uninfected cases diagnosed during 1977-2003. Using immunohistochemistry to classify cell of origin based on the Tally algorithm, activated B-cell (ABC)-DLBCL was substantially more common in HIV-infected (83%) than in HIV-uninfected (54%) cases (p< 0.001). Epstein-Barr virus (EBV) was detected in 63% of DLBCLs in HIV-infected cases, occurring almost exclusively in ABC-DLBCL (74% vs. 13% of germinal center B-cell [GCB]-DLBCL, p=0.002), but was rarely detected in DLBCLs among HIV-uninfected cases (3%). Among HIV-uninfected cases, MYC/IgH[t(8;14)(q24;q32)] and IgH/BCL2[t(14;18)(q32;q21)] translocations were significantly more common and BCL6/IgH[t(3;14)(q27;q32)] significantly less common in GCB-DLBCL than in ABC-DLBCL (p= 0.010, < 0.001 and = 0.039, respectively). Among HIV-infected cases, translocations other than MYC/IgH[t(8;14)(q24;q32)] (21%) were rare (≤6%) and unrelated to cell of origin. ABC-DLBCL was associated with adverse overall survival compared with GCB-DLBCL regardless of HIV status (pHIV-infected= 0.066;pHIV-uninfected= 0.038). Our data demonstrate key differences in the molecular characteristics, cell of origin and prognosis of DLBCL by HIV status in the pre-highly active antiretroviral therapy (HAART) and pre-rituximab era, supporting biologic differences in lymphomagenesis in the presence of HIV.
PMCID: PMC3936016  PMID: 23772639
Diffuse large B-cell lymphoma; Epstein-Barr virus; activated B-cell; germinal center B-cell
22.  Epstein-Barr virus patterns in U.S. Burkitt lymphoma tumors from the SEER Residual Tissue Repository during 1979-2009 
Burkitt lymphoma (BL) occurs at all ages, but the patterns of Epstein-Barr virus (EBV) positivity in relation to human immunodeficiency virus (HIV), immunoprofiles and age have not been fully explored.
Design and methods
BL tissues from residual tissue repositories, and 2 academic centers in the United States were examined by expert hematopathologists for morphology, immunohistochemistry, MYC rearrangement, EBV early RNA (EBER), and diagnosed according to the 2008 WHO lymphoma classification. Analysis was done using frequency tables, Chi-squared statistics, and Student’s t-test.
Of 117 cases examined, 91 were confirmed as BL. The age distribution was 26%, 15%, 19%, and 29% for 0-19, 20-34, 35-59, 60+ years, and missing in 11%. MYC rearrangement was found in 89% and EBER positivity in 29% of 82 cases with results. EBER positivity varied with age (from 13% in age-group 0-19 to 55% in age-group 20-34, and fell to 25% in age-group 60+ years, P=0.08); with race (56% in Blacks/Hispanics versus 21% in Whites/Asians/Pacific Islanders, P=0.006); and by HIV status (64% in HIV positive versus 22% in HIV negative cases, P=0.03).
EBER positivity was demonstrated in about one-third of tumors and it was strongly associated with race and HIV status, and marginally with age-group.
PMCID: PMC3723754  PMID: 23607450
23.  An exploratory study of ambient air toxics exposure in pregnancy and the risk of neuroblastoma in offspring 
Environmental research  2013;127:1-6.
Little is known about the etiology of neuroblastoma, the most common cancer in infancy. In this study, we examined maternal exposure to ambient air toxics in pregnancy in relation to neuroblastoma in the child. We ascertained all cases of neuroblastoma listed in the California Cancer Registry 1990-2007 that could be linked to a California birth certificate, and controls were selected at random from California birth records. Average air toxics exposures during pregnancy were determined based upon measures from community-based air pollution monitors. The study included 75 cases and 14,602 controls who lived with 5 kilometers of an air pollution monitor, and we additionally examined results for those living within a smaller radius around the monitor (2.5 km). Logistic regression was used to determine the risk of neuroblastoma with one interquartile range increase in air toxic exposure. Neuroblastoma risk was increased with higher maternal exposure to carbon tetrachloride (OR=2.65, 95%CI 1.07, 6.53) and polycyclic aromatic hydrocarbons (OR=1.39, 95%CI 1.05, 1.84), particularly indeno(1,2,3-cd)pyrene and dibenz(a,h)anthracene. Hexavalent chromium was associated with neuroblastoma at the 5 km distance (OR=1.32, 95%CI 1.00, 1.74) but not at the 2.5 km distance. This is one of the first studies to report associations between neuroblastoma and these air toxics.
PMCID: PMC3960946  PMID: 24139061
Air pollution; Benzene; Embryonal neoplasms; Neuroblastoma; Prenatal Exposure; Childhood cancer epidemiology; Risk factors
24.  Trends in Childhood Brain Tumor Incidence, 1973-2009 
Journal of neuro-oncology  2013;115(2):153-160.
In the mid 1980s, there was a rise in incidence rates of childhood brain tumors (CBT) in the United States that appeared to stabilize at a higher rate in the early 1990s. An updated analysis of the pattern of CBT over the past 2 decades, with commentary on whether the elevated incidence rate has continued, is past due.
We used Surveillance Epidemiology and End Results (SEER) data to examine trends in incidence of CBT from 1973 through 2009. We examined age-adjusted incidence rates (AAIRs) and secular trends for all malignant brain tumors combined (SEER classification) by histologic tumor type and anatomic site.
The incidence of CBT remained stable from 1987-2009 (annual percent change (APC)=0.10; 95% confidence intervals (CI): −0.39, 0.61) with an AAIR for all CBT of 3.32 (95%CI: 3.22, 3.42). The stability of rates in these two decades contrast the change that occurred in the mid-1980s (1983-1986), when the incidence of CBT increased by 53% (APC=14.06; 95%CI: 4.05, 25.0). From 1983-1986, statistically significant rate increases were observed for pilocytic astrocytoma, PNET/medulloblastoma, and mixed glioma. Further, the rate of increase in pilocytic astrocytoma was similar to the rate of decrease for astrocytomas NOS from 1981-2009, suggesting a change from a more general to more specific classification.
After the increase in rates in the mid-1980s, rates of CBT over the past two decades have stabilized. Changes in incidence rates of subtypes of tumors over this time period reflect changes both in classification of CBT and in diagnostic techniques.
PMCID: PMC4056769  PMID: 23925828
childhood brain tumors; gender; histology; incidence rates; pediatric cancer; secular trends; SEER
25.  Prenatal Exposure to Traffic-related Air Pollution and Risk of Early Childhood Cancers 
American Journal of Epidemiology  2013;178(8):1233-1239.
Exposure to air pollution during pregnancy has been linked to the risk of childhood cancer, but the evidence remains inconclusive. In the present study, we used land use regression modeling to estimate prenatal exposures to traffic exhaust and evaluate the associations with cancer risk in very young children. Participants in the Air Pollution and Childhood Cancers Study who were 5 years of age or younger and diagnosed with cancer between 1988 and 2008 were had their records linked to California birth certificates, and controls were selected from birth certificates. Land use regression–based estimates of exposures to nitric oxide, nitrogen dioxide, and nitrogen oxides were assigned based on birthplace residence and temporally adjusted using routine monitoring station data to evaluate air pollution exposures during specific pregnancy periods. Logistic regression models were adjusted for maternal age, race/ethnicity, educational level, parity, insurance type, and Census-based socioeconomic status, as well as child's sex and birth year. The odds of acute lymphoblastic leukemia increased by 9%, 23%, and 8% for each 25-ppb increase in average nitric oxide, nitrogen dioxide, and nitrogen oxide levels, respectively, over the entire pregnancy. Second- and third-trimester exposures increased the odds of bilateral retinoblastoma. No associations were found for annual average exposures without temporal components or for any other cancer type. These results lend support to a link between prenatal exposure to traffic exhaust and the risk of acute lymphoblastic leukemia and bilateral retinoblastoma.
PMCID: PMC3792733  PMID: 23989198
air pollution; epidemiology; leukemia; neoplasms; retinoblastoma

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