ENVIRONMENTAL EXPOSURES AND LUNG CANCER RISK AMONG WOMEN IN HARRIS COUNTY, TEXAS, 1977-1980 (OCCUPATION, SMOKING, BYSTANDER)

Excessively high, accelerating lung cancer rates among women in Harris County, Texas, prompted this case-comparison study. Objectives were to compare patterns of employment, indirect exposures, and sociodemographic variables of lung cancer cases with comparison subjects (compeers) after standardizing for possible confounders, such as age and cigarette smoking. Lung cancer cases were microscopically confirmed, white, Harris County residents. Compeers, chosen from Medicare records and Texas Department of Public Safety records, were matched on gender, race, age, resident and vital status. Personal interviews were conducted with study subjects or next-of-kin. Industries and occupations were categorized as high risk, based on previous studies.^ Almost all cases (95.0%) and 60.0% of compeers smoked cigarettes. The odds ratio for lung cancer and smoking is 13.9. Stopping smoking between ages 30-50 years carries a lower risk than stopping at age 58 or more years. Women's employment in a high risk industry or occupation results in consistently elevated, smoking-adjusted odds ratios. Frequency and duration of employment demonstrate a moderate dose-response effect. A temporal association exists with employment in a high risk occupation during 1940-1949.^ No increased risk appeared with passive smoking. Husband's employment in a construction industry or a structural occupation significantly increased the smoking-adjusted odds ratios among cases and compeers (O.R. = 2.9, 2.2). Smoking-adjusted odds ratios increased significantly when women had resided with persons employed in cement (O.R. = 3.2) or insulation (O.R. = 5.5) manufacturing, or a high rise construction industry (O.R. = 2.4). A family history of lung cancer resulted in a two-fold increase in smoking-adjusted odds ratios. Vital status of compeers affected the odds ratios.^ Work-related exposures appear to increase the risk of lung cancer in women although cigarette smoking has the single highest odds ratio. Indirect exposure to certain employment also plays a significant role in lung cancer in women. Investigations of specific direct and indirect hazardous exposures in the workplace and home are needed. Cigarette smoking is as hazardous for women as for men. Smoking should be prevented and eliminated. ^

The relationship between enterotoxigenic {\it Escherichia coli\/} infection and environmental risk factors in Bilbeis, Egypt, 1981--1983

Diarrheal disease associated with enterotoxigenic Escherichia coli (ETEC) infection is one of the major public health problems in many developing countries, especially in infants and young children. Because tests suitable for field laboratories have been developed only relatively recently, the literature on the environmental risk factors associated with ETEC is not as complete as for many other pathogens or for diarrhea of unspecified etiology.^ Data from a diarrheal disease surveillance project in rural Egypt in which stool samples were tested for a variety of pathogens, and in which an environmental questionnaire was completed for the same study households, provided an opportunity to test for an association between ETEC and various risk factors present in those households. ETEC laboratory-positive specimens were compared with ETEC laboratory-negative specimens for both symptomatic and asymptomatic children less than three years of age at the individual and household level using a case-comparison design.^ Individual children more likely to have LT infection were those who lived in HHs that had cooked food stored for subsequent consumption at the time of the visit, where caretakers used water but not soap to clean an infant after a diarrheal stool, and that had an indoor, private water source. LT was more common in HHs where the caretaker did not clean an infant with soap after a diarrheal stool, and where a sleeping infant was not covered with a net. At both the individual and HH level, LT was significantly associated with good water supply in terms of quantity and storage.^ ST was isolated more frequently at the individual level where a sleeping infant was covered with a net, where large animals were kept in or around the house, where water was always available and was not potable, and where the water container was not covered. At the HH level, the absence of a toilet or latrine and the indiscriminate disposal of animal waste decreased risk. Using animal feces for fertilizer, the presence of large animals, and poor water quality were associated with ST at both the individual and HH level.^ These findings are mostly consistent with those of other studies, and/or are biologically plausible, with the obvious exception of those from this study where poorer water supplies are associated with less infection, at least in the case of LT. More direct observation of how animal ownership and feces disposal relates to different types of water supply and usage might clarify mechanisms through which some ETEC infection could be prevented in similar settings. ^

Zoning and the built environment: A public health analysis of zoning in Austin, Texas

The built environment is part of the physical environment made by people and for people. Because the built environment is such a ubiquitous component of the environment, it acts as an important pathway in determining health outcomes. Zoning, a type of urban planning policy, is one of the most important mechanisms connecting the built environment to public health. This policy analysis research paper explores how zoning regulations in Austin, Texas promote or prohibit the development of a healthy built environment. A systematic literature review was obtained from Active Living Research, which contained literature published about the relationships between the built environment, physical activity, and health. The results of these studies identified the following four components of the built environment that were associated to health: access to recreational facilities, sprawl and residential density, land use mix, and sidewalks and their walkability. A hierarchy analysis was then performed to demonstrate the association between these aspects of the built environment and health outcomes such as obesity, cardiovascular disease, and general health. Once these associations had been established, the components of the built environment were adapted into the evaluation criteria used to conduct a public health analysis of Austin's zoning ordinance. A total of eighty-eight regulations were identified to be related to these components and their varying associations to human health. Eight regulations were projected to have a negative association to health, three would have both a positive and negative association simultaneously, and nine were indeterminable with the information obtained through the literature review. The remaining sixty-eight regulations were projected to be associated in a beneficial manner to human health. Therefore, it was concluded that Austin's zoning ordinance would have an overwhelmingly positive impact on the public's health based on identified associations between the built environment and health outcomes.^

Industrial benzene emissions in Houston: Legal barriers to reducing a public health threat

Decades of research show that environmental exposure to the chemical benzene is associated with severe carcinogenic, hematoxic and genotoxic effects on the human body. As such, the Environmental Protection Agency (EPA) has designated the chemical as a Hazardous Air Pollutant and prescribed benzene air concentration guidelines that provide cities with an ideal ambient level to protect human health. However, in Houston, Texas, a city home to the top industrial benzene emitters in the US who undoubtedly contribute greatly to the potentially unsafe levels of ambient benzene, regulations beyond the EPA’s unenforceable guidelines are critical to protecting public health. Despite this, the EPA has failed to establish National Ambient Air Quality Standards (NAAQS) for benzene. States are thus left to regulate air benzene levels on their own; in the case of Texas, the Texas Commission on Environmental Quality (TCEQ) and state legislature have failed to proactively develop legally enforceable policies to reduce major source benzene emissions. This inaction continues to exacerbate a public health problem, which may only be solved through a legal framework that restricts preventable benzene emissions to protect human health and holds industrial companies accountable for violations of such regulations and standards. This analysis explores legal barriers that the City of Houston and other relevant agencies currently face in their attempt to demand and bring about such change. ^

Logistic regression with Markov chains as covariates

The tobacco-specific nitrosamine 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) is an obvious carcinogen for lung cancer. Since CBMN (Cytokinesis-blocked micronucleus) has been found to be extremely sensitive to NNK-induced genetic damage, it is a potential important factor to predict the lung cancer risk. However, the association between lung cancer and NNK-induced genetic damage measured by CBMN assay has not been rigorously examined. ^ This research develops a methodology to model the chromosomal changes under NNK-induced genetic damage in a logistic regression framework in order to predict the occurrence of lung cancer. Since these chromosomal changes were usually not observed very long due to laboratory cost and time, a resampling technique was applied to generate the Markov chain of the normal and the damaged cell for each individual. A joint likelihood between the resampled Markov chains and the logistic regression model including transition probabilities of this chain as covariates was established. The Maximum likelihood estimation was applied to carry on the statistical test for comparison. The ability of this approach to increase discriminating power to predict lung cancer was compared to a baseline "non-genetic" model. ^ Our method offered an option to understand the association between the dynamic cell information and lung cancer. Our study indicated the extent of DNA damage/non-damage using the CBMN assay provides critical information that impacts public health studies of lung cancer risk. This novel statistical method could simultaneously estimate the process of DNA damage/non-damage and its relationship with lung cancer for each individual.^

Detecting genetic and nutritional lung cancer risk factors related to folate metabolism using Bayesian generalized linear models

Complex diseases, such as cancer, are caused by various genetic and environmental factors, and their interactions. Joint analysis of these factors and their interactions would increase the power to detect risk factors but is statistically. Bayesian generalized linear models using student-t prior distributions on coefficients, is a novel method to simultaneously analyze genetic factors, environmental factors, and interactions. I performed simulation studies using three different disease models and demonstrated that the variable selection performance of Bayesian generalized linear models is comparable to that of Bayesian stochastic search variable selection, an improved method for variable selection when compared to standard methods. I further evaluated the variable selection performance of Bayesian generalized linear models using different numbers of candidate covariates and different sample sizes, and provided a guideline for required sample size to achieve a high power of variable selection using Bayesian generalize linear models, considering different scales of number of candidate covariates. ^ Polymorphisms in folate metabolism genes and nutritional factors have been previously associated with lung cancer risk. In this study, I simultaneously analyzed 115 tag SNPs in folate metabolism genes, 14 nutritional factors, and all possible genetic-nutritional interactions from 1239 lung cancer cases and 1692 controls using Bayesian generalized linear models stratified by never, former, and current smoking status. SNPs in MTRR were significantly associated with lung cancer risk across never, former, and current smokers. In never smokers, three SNPs in TYMS and three gene-nutrient interactions, including an interaction between SHMT1 and vitamin B12, an interaction between MTRR and total fat intake, and an interaction between MTR and alcohol use, were also identified as associated with lung cancer risk. These lung cancer risk factors are worthy of further investigation.^

EMPLOYMENT AND EXPOSURES IN THE PETROLEUM REFINING AND PETROCHEMICAL INDUSTRIES AND THE RISK OF LUNG CANCER (EPIDEMIOLOGY, ASSESSMENT)

This dissertation addresses the risk of lung cancer associated with occupational exposures in the petroleum refining and petrochemical industries. Earlier epidemiologic studies of this association did not adjust for cigarette smoking or have specific exposure classifications. The Texas EXposure Assessment System (TEXAS) was developed with data from a population-based, case-comparison study conducted in five southeast Texas counties between 1976 and 1980. The Texas Exposure Assessment System uses job and process categories developed by the American Petroleum Institute, as well as time-oriented variables to identify high risk groups.^ An industry-wide, increased risk for lung cancer was associated with jobs having low-level hydrocarbon exposure that also include other occupational inhalation exposures (OR = 2.0--adjusted for smoking and latency effects). The prohibition of cigarette smoking for jobs with high-level hydrocarbon exposure might explain part of the increased risk for jobs with low-level hydrocarbon exposures. Asbestos exposure comprises a large part of the risk associated with jobs having other inhalation exposures besides hydrocarbons. Workers in petroleum refineries were not shown to have an increased, occupational risk for lung cancer. The increased risk for lung cancer among petrochemical workers (OR = 3.1--smoking and latency adjusted) is associated with all jobs that involve other inhalation exposure characteristics (not only low-level hydrocarbon exposures). Findings for contract workers and workers exposed to specific chemicals were inconclusive although some hypotheses for future research were identified.^ The study results demonstrate that the predominant risk for lung cancer is due to cigarette smoking (OR = 9.8). Cigarette smoking accounts for 86.5% of the incident lung cancer cases within the study area. Workers in the petroleum industry smoke significantly less than persons employed in other industries (p << 0.001). Only 2.2% of the incident lung cancer cases may be attributed to petroleum industry jobs; lifestyle factors (e.g., nutrition) may be associated with the balance of the cases. The results from this study also suggest possible high risk time periods (OR = 3.9--smoking and occupation adjusted). Artifacts in time-oriented findings may result because of the latency interval for lung cancer, secular peaks in age-, sex-specific incidence rates, or periods of hazardous exposures in the petroleum industry. ^

Risk of second primary tumors following treatment of non-small cell lung cancer

Background. The rise in survival rates along with more detailed follow-up using sophisticated imaging studies among non-small lung cancer (NSCLC) patients has led to an increased risk of second primary tumors (SPT) among these cases. Population and hospital based studies of lung cancer patients treated between 1974 and 1996 have found an increasing risk over time for the development of all cancers following treatment of non-small cell lung cancer (NSCLC). During this time the primary modalities for treatment were surgery alone, radiation alone, surgery and post-operative radiation therapy, or combinations of chemotherapy and radiation (sequentially or concurrently). There is limited information in the literature about the impact of treatment modalities on the development of second primary tumors in these patients. ^ Purpose. To investigate the impact of treatment modalities on the risk of second primary tumors in patients receiving treatment with curative intent for non-metastatic (Stage I–III) non-small cell lung cancer (NSCLC). ^ Methods. The hospital records of 1,095 NSCLC patients who were diagnosed between 1980–2001 and received treatment with curative intent at M.D. Anderson Cancer Center with surgery alone, radiation alone (with a minimum total radiation dose of at least 45Gy), surgery and post-operative radiation therapy, radiation therapy in combination with chemotherapy or surgery in combination with chemotherapy and radiation were retrospectively reviewed. A second primary malignancy was be defined as any tumor histologically different from the initial cancer, or of another anatomic location, or a tumor of the same location and histology as the initial tumor having an interval between cancers of at least five years. Only primary tumors occurring after treatment for NSCLC will qualified as second primary tumors for this study. ^ Results. The incidence of second primary tumor was 3.3%/year and the rate increased over time following treatment. The type of NSCLC treatment was not found to have a striking effect upon SPT development. Increased rates were observed in the radiation only and chemotherapy plus radiation treatment groups; but, these increases did not exceed expected random variation. Higher radiation treatment dose, patient age and weight loss prior to index NSCLC treatment were associated with higher SPT development. ^

A case-control study of tea/coffee consumption and lung cancer risk

Background. Despite the increasing attention to the effects of dietary factors on lung cancer risk, epidemiological research on the role of black/green tea and coffee intake and lung cancer risk is scarce. The purpose of this study was to explore the following three hypotheses: (1) the preventive (protective) effect from lung cancer is higher in green tea than in black tea and coffee consumption. (2) brewed tea (either black or green) daily drinkers have lower odds of lung cancer than non-drinkers of brewed tea (3) regular black and green tea have more preventive effect against lung cancer than decaffeinated teas due to the synergistic effect of caffeine and other tea components. ^ Methods. Data on 1,088 lung cancer cases and 1,127 controls from an ongoing epidemiological study of lung cancer by the Department of Epidemiology of the University of Texas M.D. Anderson Cancer were analyzed. Multiple logistic regressions were performed for testing associations between frequency of specific types of tea/coffee consumption and the risk of lung cancer. ^ Results. We observed that more than a cup a week of green tea and decaffeinated black tea were significantly associated with reduced odds of lung cancer by 64% for green tea (adjusted OR = 0.44; 95% CI = 0.31–0.64), 36% for decaffeinated black tea (OR = 0.64; 95% CI = 0.45–0.90), when compared with non-drinkers and those who drank less than a cup a week. On the other hand, increasing intake of regular coffee (more than 3 cups a day) was associated with a 30% higher odds ratio of lung cancer (OR = 1.30; 95% CI = 1.01–1.09). No association was found between regular black tea, decaffeinated coffee consumption and the odds ratio of lung cancer. However, when drinkers of other tea/coffee beverages were excluded from each model in order to explore the independent effect of each type of tea/coffee, green tea and decaffeinated black tea-lung cancer associations remained but no association was observed for drinkers of regular coffee. ^ Conclusion. We report the chemopreventive effects of more than a cup a week of green tea and decaffeinated black tea on lung cancer. ^

Hormone therapy and physical activity as predictors of lung cancer risk and survival: The California Teachers Study

Cigarette smoking is responsible for the majority of lung cancer cases worldwide; however, a proportion of never smokers still develop lung cancer over their lifetime, prompting investigation into additional factors that may modify lung cancer incidence, as well as mortality. Although hormone therapy (HT), physical activity (PA), and lung cancer have been previously examined, the associations remain unclear. This study investigated exposure to HT and PA that may modulate underlying mechanisms of lung cancer etiology and progression among women by using existing, de-identified data from the California Teachers Study (CTS).^ The CTS cohort, established in 1995–1996, has 133,479 active and retired female teachers and administrators, recruited through the California State Teachers Retirement System, and followed annually for cancer diagnosis, death, and change of address. Each woman enrolled in the CTS returned a questionnaire covering a wide variety of issues related to cancer risk and women's health, including recent and past HT use and physical activity, as well as active and environmental cigarette smoke exposure. Complete data to assess the associations between HT and lung cancer risk and survival were available for 60,592 postmenopausal women. Between 1995 and 2007, 727 of these women were diagnosed with invasive lung cancer; 441 of these died. Complete data to assess the associations between PA and lung cancer risk and survival were available for 118,513 women. Between 1995 and 2007, 853 of these women were diagnosed with invasive lung cancer; 516 of these died.^ After careful adjustment for smoking habits and other potential confounders, no measure of HT use was associated with lung cancer risk; however, any HT use (vs. no use) was associated with a decrease in lung-cancer-specific mortality. Specifically, among women who only used estrogen (E-only), decreases in lung cancer mortality were seen for recent use, but not for former use; no association was observed for estrogen plus progestin (E+P). Furthermore, among former users of HT, a statistically significant decrease in lung cancer mortality was observed for E-only use within 5 years prior to baseline, but not for E-only use >5 years prior to baseline. Neither long-term recreational PA nor recent recreational PA alone were associated with lung cancer risk; however, among women with a BMI<25 and ever smokers, high long-term moderate+strenuous PA was associated with a decrease in lung cancer risk. Women with non-local disease showed a decrease in lung cancer mortality associated with increasing duration of strenuous long-term activity, and 1.50-3.00 h/wk/y of recent moderate or recent strenuous PA. Long-term moderate PA was associated with decreased lung cancer mortality in never smokers, whereas recent moderate PA was associated with increased lung cancer mortality in current smokers. ^ Placing our findings in the context of the current literature, HT does not appear to be associated with lung cancer risk and previous studies reporting a protective effect of HT use on lung cancer risk may be subject to residual confounding by smoking. Looking at our findings regarding PA overall, the evidence still remains inconclusive regarding whether or not physical activity influence lung cancer risk or mortality. Our results suggest that recreational PA may associated with decreased lung cancer risk among women with BMI<25 and ever smoking-women; however, residual confounding by smoking should be strongly considered. To our knowledge, this is the first study to investigate lifetime recreational PA and lung cancer mortality among women. Our results contribute to the growing body of knowledge regarding non-smoking-related risk factors for lung cancer incidence and mortality among women. Given the potential clinical and interventional significance, further study and validation of these findings is warranted.^

The effect of specific carotenoids on lung cancer risk

A population-based case-comparison study of histologically confirmed lung cancer among white male and female residents of six Texas coastal counties was conducted from 1979-1982. Dietary information as well as information concerning smoking, alcohol consumption, occupational and residential exposures, and family history of cancer was obtained from 149 living cases and 359 comparison subjects.^ These data support the findings of previous studies that reported a protective association of total carotene intake with lung cancer (OR = 4.07, CI = 3.36-4.78), and no association for total Vitamin A or retinol. Of six specific carotenoids examined, these data reveal a statistically significant protective effect for alpha carotene (OR = 3.58, CI = 2.85-4.31), and an elevated, although non-significant effect for beta carotene (OR = 1.46, CI = 0.61-2.31). No consistent significant effect was found for cryptoxanthin, other xanthins, lutein or lycopene.^ Similar results were found for both males and females, and for both squamous cell and adenocarcinoma subtypes, although loss of power resulting from stratification may have rendered the celltype specific results more imprecise. These results should be considered with caution until confirmed by other studies, however, they suggest the importance of evaluating specific carotenoids in future diet-lung cancer investigations. ^

Genetic Predictors of Clinical Outcomes in Non-Small Cell Lung Cancer Patients

Lung cancer is the leading cause of cancer-related mortality in the US. Emerging evidence has shown that host genetic factors can interact with environmental exposures to influence patient susceptibility to the diseases as well as clinical outcomes, such as survival and recurrence. We aimed to identify genetic prognostic markers for non-small cell lung cancer (NSCLC), a major (85%) subtype of lung cancer, and also in other subgroups. With the fast evolution of genotyping technology, genetic association studies have went through candidate gene approach, to pathway-based approach, to the genome wide association study (GWAS). Even in the era of GWAS, pathway-based approach has its own advantages on studying cancer clinical outcomes: it is cost-effective, requiring a smaller sample size than GWAS easier to identify a validation population and explore gene-gene interactions. In the current study, we adopted pathway-based approach focusing on two critical pathways - miRNA and inflammation pathways. MicroRNAs (miRNA) post-transcriptionally regulate around 30% of human genes. Polymorphisms within miRNA processing pathways and binding sites may influence patients’ prognosis through altered gene regulation. Inflammation plays an important role in cancer initiation and progression, and also has shown to impact patients’ clinical outcomes. We first evaluated 240 single nucleotide polymorphisms (SNPs) in miRNA biogenesis genes and predicted binding sites in NSCLC patients to determine associations with clinical outcomes in early-stage (stage I and II) and late-stage (stage III and IV) lung cancer patients, respectively. First, in 535 early-stage patients, after correcting multiple comparisons, FZD4:rs713065 (hazard ratio [HR]:0.46, 95% confidence interval [CI]:0.32-0.65) showed a significant inverse association with survival in early stage surgery-only patients. SP1:rs17695156 (HR:2.22, 95% CI:1.44-3.41) and DROSHA:rs6886834 (HR:6.38, 95% CI:2.49-16.31) conferred increased risk of progression in the all patients and surgery-only populations, respectively. FAS:rs2234978 was significantly associated with improved survival in all patients (HR:0.59, 95% CI:0.44-0.77) and in the surgery plus chemotherapy populations (HR:0.19, 95% CI:0.07-0.46).. Functional genomics analysis demonstrated that this variant creates a miR-651 binding site resulting in altered miRNA regulation of FAS, providing biological plausibility for the observed association. We then analyzed these associations in 598 late-stage patients. After multiple comparison corrections, no SNPs remained significant in the late stage group, while the top SNP NAT1:rs15561 (HR=1.98, 96%CI=1.32-2.94) conferred a significantly increased risk of death in the chemotherapy subgroup. To test the hypothesis that genetic variants in the inflammation-related pathways may be associated with survival in NSCLC patients, we first conducted a three-stage study. In the discovery phase, we investigated a comprehensive panel of 11,930 inflammation-related SNPs in three independent lung cancer populations. A missense SNP (rs2071554) in HLA-DOB was significantly associated with poor survival in the discovery population (HR: 1.46, 95% CI: 1.02-2.09), internal validation population (HR: 1.51, 95% CI: 1.02-2.25), and external validation (HR: 1.52, 95% CI: 1.01-2.29) population. Rs2900420 in KLRK1 was significantly associated with a reduced risk for death in the discovery (HR: 0.76, 95% CI: 0.60-0.96) and internal validation (HR: 0.77, 95% CI: 0.61-0.99) populations, and the association reached borderline significance in the external validation population (HR: 0.80, 95% CI: 0.63-1.02). We also evaluated these inflammation-related SNPs in NSCLC patients in never smokers. Lung cancer in never smokers has been increasingly recognized as distinct disease from that in ever-smokers. A two-stage study was performed using a discovery population from MD Anderson (411 patients) and a validation population from Mayo Clinic (311 patients). Three SNPs (IL17RA:rs879576, BMP8A:rs698141, and STK:rs290229) that were significantly associated with survival were validated (pCD74:rs1056400 and CD38:rs10805347) were borderline significant (p=0.08) in the Mayo Clinic population. In the combined analysis, IL17RA:rs879576 resulted in a 40% reduction in the risk for death (p=4.1 × 10-5 [p=0.61, heterogeneity test]). We also validated a survival tree created in MD Anderson population in the Mayo Clinic population. In conclusion, our results provided strong evidence that genetic variations in specific pathways that examined (miRNA and inflammation pathways) influenced clinical outcomes in NSCLC patients, and with further functional studies, the novel loci have potential to be translated into clinical use.

Hormonal risk factors and testicular cancer

The cause of testicular cancer is not known and recent hypotheses have suggested an altered hormonal milieu may increase the risk of testis cancer. This study examined modulation of testicular cancer risk by hormonal factors, specifically: environmental xenoestrogens (e.g. organochlorines), prenatal maternal estrogens, testosterone indices (age at puberty, severe adolescent acne, self-reported balding), sedentary lifestyle and dietary consumption of fats and phytoestrogens.^ A hospital based friend matched case-control study was conducted at the University of Texas M. D. Anderson Cancer Center in Houston, Texas, between January 1990 and October 1996. Cases had a first primary testis tumor diagnosed between age 18 to 50 years and resided in Texas, Louisiana, Oklahoma or Arkansas.^ Cases and friend controls completed a mail questionnaire and case/control mothers were contacted by phone regarding pregnancy related variables. The study population comprised 187 cases, 148 controls, 147 case mothers and 86 control mothers. Odds ratios were virtually identical whether the match was retained or dissolved, thus the analyses were conducted using unconditional logistic regression.^ Cryptorchidism was a strong risk factor for testis cancer with an age-adjusted odds ratio (OR) of 7.7 (95% confidence interval (CI): 2.3-26.3). In a final model (adjusted for age, education, and cryptorchidism), history of severe adolescent acne and self-reported balding were both significantly protective, as hypothesized. For acne (yes vs. no) the OR was 0.5 (CI: 0.3-1.0) and for balding (yes vs. no) the OR was 0.6 (CI: 0.3-1.0). Marijuana smoking was a risk factor among heavy, regular users (17 times/week, OR = 2.4; CI: 0.9-6.4) and higher saturated fat intake increased testis cancer risk (saturated fat intake $>$ 15.2 grams/day vs. $<$ 11.8 grams/day, OR = 3.3; CI: 1.5-7.1). Early puberty, xenoestrogen exposure, elevated maternal estrogen levels, sedentary lifestyle and dietary phytoestrogen intake were not associated with risk of testicular cancer.^ In conclusion, testicular cancer may be associated with endogenous androgen metabolism although environmental estrogen exposure can not be ruled out. Further research is needed to understand the underlying hormonal mechanisms and possible dietary influences. ^

Primary lung cancer after breast cancer: The role of radiation therapy and cigarette smoking

The magnitude of the interaction between cigarette smoking, radiation therapy, and primary lung cancer after breast cancer remains unresolved. This case control study further examines the main and joint effects of cigarette smoking and radiation therapy (XRT) among breast cancer patients who subsequently developed primary lung cancer, at The University of Texas M. D. Anderson Cancer Center (MDACC) in Houston, Texas. Cases (n = 280) were women diagnosed with primary lung cancer between 1955 and 1970, between 30–89 years of age, who had a prior history of breast cancer, and were U.S. residents. Controls (n = 300) were randomly selected from 37,000 breast cancer patients at MDACC and frequency matched to cases on age at diagnosis (in 5-year strata), ethnicity, year of breast cancer diagnosis (in 5-year strata), and had survived at least as long as the time interval for lung cancer diagnosis in the cases. Stratified analysis and unconditional logistic regression modeling were used to calculate the main and joint effects of cigarette smoking and radiation treatment on lung cancer risk. Medical record review yielded smoking information on 93% of cases and 84% of controls, and among cases 45% received XRT versus 44% of controls. Smoking increased the odds of lung cancer in women who did not receive XRT (OR = 6.0, 95%CI, 3.5–10.1) whereas XRT was not associated with increased odds (OR = 0.5, 95%CI, 0.2–1.1) in women who did not smoke. Overall the odds ratio for both XRT and smoking together compared with neither exposure was 9.00 (9 5% CI, 5.1–15.9). Similarly, when stratifying on laterality of the lung cancer in relation to the breast cancer, and when the time interval between breast and lung cancers was >10 years, there was an increased odds for both smoking and XRT together for lung cancers on the same side as the breast cancer (ipsilateral) (OR = 11.5, 95% CI, 4.9–27.8) and lung cancers on the opposite side of the breast cancer (contralateral) (OR= 9.6, 95% CI, 2.9–0.9). After 20 years the odds for the ipsilateral lung were even more pronounced (OR = 19.2, 95% CI, 4.2–88.4) compared to the contralateral lung (OR = 2.6, 95% CI, 0.2–2.1). In conclusion, smoking was a significant independent risk factor for lung cancer after breast cancer. Moreover, a greater than multiplicative effect was observed with smoking and XRT combined being especially evident after 10 years for both the ipsilateral and contralateral lung and after 20 years for the ipsilateral lung. ^

An analysis of Texas's school based HPV vaccine mandate: A public health risk communication failure: HPVETO!

Genital human papillomavirus (HPV) is of public health concern because persistent infection with certain HPV types can cause cervical cancer. In response to a nationwide push for cervical cancer legislation, Texas Governor Rick Perry bypassed the traditional legislative process and issued an executive order mandating compulsory HPV vaccinations for all female public school students prior to their entrance in the sixth grade. By bypassing the legislative process Governor Perry did not effectively mitigate the risk perception issues that arose around the need for and usefulness of the vaccine mandate. This policy paper uses a social policy paradigm to identify perception as the key intervening factor on how the public responds to risk information. To demonstrate how the HPV mandate failed, it analyzes four factors, economics, politics, knowledge and culture, that shape perception and influence the public's response. By understanding the factors that influence the public's perception, public health practitioners and policy makers can more effectively create preventive health policy at the state level. ^