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Biomedical subjects

R Hoover

Publications and source records attributed to R Hoover.

At least 55 records · Page 3Linked to original sources
PubMed1989

The risk of breast cancer after estrogen and estrogen-progestin replacement.

To examine the risk of breast cancer after noncontraceptive treatment with estrogen, we conducted a prospective study of 23,244 women 35 years of age or older who had had estrogen prescriptions filled in the Uppsala region of Sweden. During the follow-up period (mean, 5.7 years) breast cancer developed in 253 women. Compared with other women in the same region, the women in the estrogen cohort had an overall relative risk of breast cancer of 1.1 (95 percent confidence interval, 1.0 to 1.3). The relative risk increased with the duration of estrogen treatment (P = 0.002), reaching 1.7 after nine years (95 percent confidence interval, 1.1 to 2.7). Estradiol (used in 56 percent of the treatment periods in the cohort) was associated with a 1.8-fold increase in risk after more than six years of treatment (95 percent confidence interval, 0.7 to 4.6). No increase in risk was found after the use of conjugated estrogens (used in 22 percent of the treatment periods) or other types, mainly estriols (used in 22 percent of the treatment periods). Although the numbers of women were smaller, the risk of breast cancer was highest among the women who took estrogen and progestin in combination for extended periods. The relative risk was 4.4 (95 percent confidence interval, 0.9 to 22.4) in women who used only this combination for more than six years. Among women who had previously used estrogens alone, the relative risk after three years or more of use of the combination regimen was 2.3 (95 percent confidence interval, 0.7 to 7.8). We conclude that in this cohort, long-term perimenopausal treatment with estrogens (or at least estradiol compounds) seems to be associated with a slightly increased risk of breast cancer, which is not prevented and may even be increased by the addition of progestins.

Adult↗
PubMed1989

Lung cancer risk, occupational exposure, and the debrisoquine metabolic phenotype.

The risk of lung cancer in smokers was examined based on the debrisoquine metabolic phenotype and on exposure to occupational lung carcinogens, specifically asbestos and polycyclic aromatic hydrocarbons. Extensive metabolizers of debrisoquine are at a 4-fold increased risk for lung cancer compared to poor metabolizers, after adjustment for age, sex, and smoking (pack-years), when only occupationally unexposed subjects are considered. Increased risk related to the debrisoquine metabolic phenotype was greatest for squamous and small cell histologies, and least for the adenocarcinoma subtype. Men with a history of exposure to occupational carcinogens had significantly increased risk of lung cancer (relative risk = 2.8), after adjustment for age and smoking. Considering the combined effect of the high risk extensive metabolizers debrisoquine metabolic phenotype and likely occupational exposure to asbestos, the relative excess risk for lung cancer was 18-fold. This finding is consistent with a synergism in risk between the ability to extensively metabolize debrisoquine and occupational exposure to lung carcinogens in male smokers. Debrisoquine phenotyping has potential for identifying carcinogen-exposed workers at high risk of lung cancer.

Asbestos↗
PubMed1989

Risk of endometrial cancer after treatment with oestrogens alone or in conjunction with progestogens: results of a prospective study.

OBJECTIVE: To determine the relative risk of developing endometrial neoplasia after treatment with oestrogens alone or in conjunction with progestogens. DESIGN: Prospective cohort follow up study, average observation period 5.7 years for each patient. To have a 90% chance of detecting a relative risk of 2.0 with 95% significance the study required 78,000 person years of observation. SETTING: Community based cohort. PATIENTS: Women aged over 35 who were prescribed non-contraceptive oestrogens in the Uppsala health care region during April 1977 to March 1980 were identified from pharmacy records. Of all prescriptions issued, 95% were identified. Patients from the cohort who developed endometrial neoplasia were identified from the cancer registry of the Uppsala health care region. Compliance, sociodemographic data, and lifetime exposures to oestrogen and cyclically added progestogen were assessed by questionnaire in a sample of the cohort. The final cohort consisted of 23,244 patients (133,373 person years). The prevalence of university education, oophorectomy, and hysterectomy was higher in the cohort than the general population; no other confounding factors were identified. MEASUREMENTS: The total number of person years was divided into exposure groups by inference from the data from the questionnaire. Compensation was made for the excess of hysterectomies. Specimens from all cases of endometrial neoplasia in the cohort and 90% of cases in the general population were studied blind histopathologically. Characteristics of treatment of all women who had endometrial neoplasia were assessed by questionnaire. Relative risks and 95% confidence intervals were calculated. RESULTS: Seventy four cases of carcinoma and 33 cases of premalignant lesions occurred in the cohort. The relative risk of endometrial carcinoma was 1.8 (95% confidence interval 1.1 to 3.2) after exposure to any oestrogen compound without progestogen for more than six years; 2.2 (1.2 to 4.4) after more than three years' exposure to conjugated oestrogens without progestogen; and 2.7 (1.4 to 5.1) after more than three years' exposure to oestradiol compounds without progestogen. When carcinoma and premalignant lesions were considered together the results were similar but the relative risk was higher. Risk of carcinoma did not increase when progestogens were cyclically added to oestrogens for the entire treatment period (relative risk 0.9 (0.4 to 2.0]. CONCLUSIONS: Use of oestrogens without progestogens is associated with a twofold to threefold increase in risk of endometrial neoplasia. Use of progestogens either removes this increased risk or delays its onset. A further follow up of the cohort is essential to analyse the risks with greater statistical power.

Adult↗
PubMed1989

In vitro effects of endotoxin on bovine and sheep lung microvascular and pulmonary artery endothelial cells.

A single infusion of Escherichia coli endotoxin into sheep results in structural evidence of pulmonary endothelial injury, increases in both prostacyclin and prostaglandin E2 (PGE2) in lung lymph, and an increase in pulmonary microvascular permeability. Endotoxin-induced lung endothelial damage can also be induced in vitro, but to date these studies have utilized endothelium from large pulmonary vessels. In the present study, we have grown endothelial cells from peripheral lung vessels of cows and sheep and exposed these microvascular endothelial cells to endotoxin. Controls included lung microvascular endothelium without endotoxin and endothelial cells from bovine and sheep main pulmonary artery with and without addition of endotoxin. We found that endotoxin caused significant increases in release of prostacyclin and PGE2 from both bovine and sheep lung microvascular and pulmonary artery endothelium. Normal bovine and sheep pulmonary artery and bovine lung microvascular endothelium released greater levels of prostacyclin than PGE2 (ng/ng); release of PGE2 from the microvascular cells was greater than from the pulmonary artery endothelium in both species. Exposure of endothelial cells from cow and sheep main pulmonary artery to endotoxin results in endothelial cell retraction and pyknosis, a loss of barrier function, increased release of prostacyclin and PGE2 and eventual cell lysis. In lung microvascular cells, the increases in prostanoids were accompanied by changes in cell shape but occurred in the absence of either detectable alterations in barrier function or cytolysis. Thus, while endotoxin causes alterations to endothelial cells from both large and small pulmonary vessels, the effects are not identical suggesting site specific phenotypic expression of endothelial cells even within a single vessel. To determine whether the response of either the large or small pulmonary vessel endothelial cells in culture mimics most closely the in vivo response of the lung to endotoxin requires further study.

Animals↗
PubMed1989

A case-control study of epithelial ovarian cancer.

With data from a study of 296 patients with primary epithelial ovarian cancer and 343 patients hospitalized because of other conditions, we estimated ovarian cancer risk in accordance with reproductive and other factors. Risk was greatest among women of lower parity, especially among women who said they planned to have children but could not. The protective effect of oral contraceptives seen in other studies was observed only in subgroups of our study population. Women who had breastfed their children had decreased risk, but the number of months of breastfeeding was not related to risk. Incomplete pregnancies did not provide the protection seen for live births. A family history of ovarian cancer and a medical history of breast cancer were both strong risk factors. None of the nonreproductive factors that we examined, including childhood illnesses, tobacco and alcohol consumption, obesity, and selected adult diseases, was convincingly associated with risk.

Adult↗
PubMed1989

Cancer risk following pernicious anaemia.

A computer-based file of all Veterans Administration (VA) hospitalisation records for the period 1969-1985 was used to identify and follow for cancer development a cohort of 5,161 white males with pernicious anaemia. A total of 34,915 person-years were accrued, with an average length of follow-up of 6.8 years. A total of 481 cancers were diagnosed, slightly higher than the number expected (SIR = 1.2). Significant excesses were observed for cancers of the buccal cavity and pharynx (1.8) and stomach (3.2), and for melanoma (2.1), multiple myeloma (2.1), myeloid leukaemia (3.7) and other and unspecified leukaemia (4.0). Although the excess for stomach cancer was highest in the first year after diagnosis in a VA hospital, risks of 2-fold or greater persisted throughout the study period. The majority of leukaemias occurred in the first year of follow-up, but some excess risk continued beyond this time. The elevated risk of buccal and pharyngeal cancers may relate to heavy alcohol intake among this population, although risks remained high even when the cohort was restricted to patients without an admission for alcoholism. Although an elevated risk of stomach cancer among pernicious anaemia patients is consistent with most previous surveys, the low absolute risk suggests that the cost-effectiveness of intensive screening should be reassessed.

Adolescent↗
PubMed1989

Cancer risk after evaluation for infertility.

To evaluate cancer risk by various causes of infertility, the authors conducted a retrospective cohort study among 2,335 women evaluated for infertility at the Mayo Clinic between 1935 and 1964. Most cancers occurred at expected frequencies, with the exception of cancers of the thyroid (standardized incidence ratio (SIR) = 2.6) and other endocrine glands (SIR = 6.7), although analyses were based on small numbers. Patients with progesterone deficiencies (31 per cent of the study subjects) had a 20 per cent higher cancer risk than did those with other causes of infertility, with excesses deriving primarily from cancers of the lung, cervix, ovary, and thyroid and from melanoma. Breast cancer risk, however, was not elevated in either patients with progesterone deficiencies (SIR = 0.9) or patients with other causes of infertility (SIR = 1.0). Examination of other parameters of infertility, including age at evaluation, type of infertility (primary vs. secondary), and years of attempted conception, showed no elevated risks of breast cancer in any subgroup. These results fail to support previous studies that have linked progesterone deficiencies among infertile women to elevated breast cancer risk. However, the data suggest a possible involvement of a progesterone deficiency in the etiology of other cancers, particularly thyroid cancer and melanoma.

Adult↗
PubMed1988

Effects of timing and type of tobacco in cigarette-induced bladder cancer.

We analyzed a case-control study of bladder cancer in Torino (512 male and 55 female cases; 596 male and 202 female controls) with emphasis on the timing of cigarette smoking and the use of black or blond tobacco. The risk of bladder cancer was 2 to 3 times higher among smokers of black tobacco than among smokers of blond tobacco. Both groups of smokers showed a beneficial effect of smoking cessation, with an immediate decline in risk. This pattern is consistent with a late-stage effect of smoking. Among smokers of black tobacco, there was a gradient of risk with early exposure, and smokers who had quit never showed a drop to base-line levels of risk. These patterns, not apparent in users of blond tobacco, suggest an early stage effect of black tobacco, perhaps due to the higher concentration of aromatic amines in black than blond tobacco smoke and the higher blood levels of the hemoglobin adduct with 4-aminobiphenyl (a human bladder carcinogen) among smokers of black tobacco.

Age Factors↗
PubMed1988

Menopause and ovarian cancer.

Using data from a study of 296 patients diagnosed in greater Washington, D.C., from 1978 to 1981 with primary epithelial ovarian cancer and 343 patients hospitalized for other conditions, the authors estimated the rate ratios according to various characteristics of the menopause. Menopause induced by hysterectomy with preservation of both ovaries was associated with a 30 per cent reduction in risk of later development of ovarian cancer. Age at natural menopause was not consistently related to risk. Women who used menopausal estrogens showed a 40 per cent decreased risk.

Actuarial Analysis↗
PubMed1988

Risk factors in ovarian cancer.

For 50 years, the three- and five-year survival rates of under 40% for invasive ovarian cancer in the USA have not significantly changed. Identifying those women who have a greater probability of developing the disease should contribute to improving survival. Our 3-year case-control study of 298 women from the metropolitan Washington, DC, area with primary epithelial ovarian cancer revealed a woman is at greater risk of developing ovarian cancer if she has a family history of the disease, experiences difficulty becoming pregnant, and has a normal menopause with hot flashes. Her risk for the disease is diminished with multiparity, a history of dysmenorrhea, and hysterectomy. Physicians should consider these risk factors when performing pelvic examinations in women and coordinate them with known changes in ovarian size and procedures to view the ovaries which may permit earlier recognition of ovarian cancer.

Adult↗
PubMed1987

Myoglobin recombination at low temperature. Two phases revealed by Fourier transform infrared spectroscopy.

The low-temperature recombination of CO with myoglobin was studied using Fourier transform infrared spectroscopy. The bound state of carbon monoxide myoglobin has two distinct conformers observed at 1926 and 1945 cm-1 with an intensity ratio of 1 to 8. The recombination of these bands after complete photolysis at 10 K followed by a temperature jump shows distinct kinetics for the two bands. Although both bands apparently follow the nonexponential kinetics originally described by Frauenfelder and co-workers (Austin, R., Beeson, K., Eisenstein, L., Frauenfelder, H., and Gunsalus, I. (1975) Biochemistry 14, 5355-5373), the 1926 cm-1 band does not appear appreciably below 70 K. In fact, after 20 min of recombination at 70 K the 1945 cm-1 band is fully recovered, while no detectable amount of the 1926 cm-1 band is present. This is the first association of a spectroscopic marker of protein substructure with reaction kinetics.

Carbon Monoxide↗
PubMed1987

Changing cigarette habits and bladder cancer risk: a case-control study.

With the use of data from the 8,764 subjects in the National Bladder Cancer Study, the separate contribution of various aspects of a person's cigarette smoking history to his increased risk of bladder cancer was estimated. These estimates have not been previously available, owing to the smaller sizes of earlier studies. Our data indicated that people who have only smoked unfiltered cigarettes have higher risks than those who have only smoked filtered cigarettes but that people who have switched from unfiltered to filtered have experienced no reduction in risk. Our data also indicated that smoking cessation substantially reduced the risk. The former smoker appeared to benefit both because he stopped adding to the burden of irreversible damage and because he ceased being exposed to some reversible hazard. Thus the former smoker had a lower risk than the current smoker even though they had smoked the same number of cigarettes daily for the same number of years, but the former smoker's risk remained higher than the risk of a person who never smoked. Our data suggest that one-half of the bladder cancer occurring among men in the United States and one-third of that among women is caused by cigarette smoking.

Adult↗
PubMed1987

The National Bladder Cancer Study: employment in the chemical industry.

The relationship between bladder cancer employment in the chemical industry was assessed in a study of 2,982 incident cases and 5,782 population controls. There were 190 cases and 369 controls who had ever been employed in the chemical industry [odds ratio (OR) = 1.0; 95% confidence interval (CI) = 0.8, 1.2]. Employment in the production of organic chemicals was associated with a 1.3-fold increased risk among men (95% CI = 0.8, 2.1). Risk increased with duration of employment, reaching an OR of 2.4 for 20 or more years (chi for trend = 1.57; P = .06). Women who had worked in the plastics industry had a 3.3-fold increased bladder cancer risk. Within the plastics and rubber industry, increased risks for bladder cancer were found for men in mixing, filtering, grinding, and other dusty operations (OR = 4.6; 95% CI = 1.0, 20.4) and men in heat-associated operations (OR = 2.8; 95% CI = 0.5, 15.3). A 1.4-fold risk among men in agricultural chemicals was attributable to risks in the pesticides subdivision (OR = 2.3; 95% CI = 0.6, 8.2). Men performing dusty operations (i.e., mixing, filtering, sifting, grinding, and crushing) in any industry had an OR of 1.4 (95% CI = 0.8, 2.7). Despite the large number of study subjects, few statistically significant findings were observed and should be evaluated with consideration of the large number of comparisons made in the analysis. The statistical power of case-control studies to detect risks associated with particular occupational exposures is limited by the small proportion of the population employed in any specific occupation or industry.

Adult↗
PubMed1987

Dietary fat and breast cancer in the National Health and Nutrition Examination Survey I Epidemiologic Follow-up Study.

The relationship between dietary fat intake and breast cancer incidence was examined in the National Health and Nutrition Examination Survey I (NHANES I) Epidemiologic Follow-up Study cohort. This cohort is derived from adults (greater than or equal to 25 yr) examined in the NHANES I (1970-75) cross-sectional survey of the U.S. population and provides a mean follow-up time of 10 years. An analytic sample of 5,485 women, including 99 breast cancer cases (34 premenopausal and 65 postmenopausal at NHANES I baseline), was examined for associations with dietary intake of fat, percent energy from fat, total energy, saturated fat, polyunsaturated fat, monounsaturated fat, and cholesterol on the basis of a 24-hour recall administered at the baseline NHANES I examination. No significant differences in dietary fat intake between cases and noncases were evident when mean intakes for each group were compared. For total fat (g) and saturated fat (g), a significant inverse association was indicated in proportional hazards analyses. Adjustment of fat for total energy intake resulted in a smaller effect that was no longer statistically significant. Adjustment for accepted breast cancer risk factors did not change these findings. This prospective study of a sample from the U.S. population does not support the hypothesis that high dietary fat intake increases breast cancer risk. Indeed, some lower risk associated with high fat intake may be indicated, although this result may be influenced by methodologic problems with the dietary assessment.

Adult↗
PubMed1987

Bladder cancer, drinking water source, and tap water consumption: a case-control study.

Data from a population-based case-control interview study of incident bladder cancer in 10 areas of the United States were used to estimate relative risks among white men (2,116 cases, 3,892 controls) and women (689 cases, 1,366 controls) according to beverage intake level and type of water source. Individual year-by-year profiles of water source and treatment were developed by linking lifetime residential information with historical water utility data from an ancillary survey. Risk of bladder cancer increased with intake level of beverages made with tap water. The odds ratio (OR) for the highest vs. lowest quintile of tap water consumption was 1.43 [95% confidence interval (CI) = 1.23, 1.67; chi 2 for trend = 26.3, P less than .001]. The risk gradient with intake was restricted to persons with at least a 40-year exposure to chlorinated surface water and was not found among long-term users of nonchlorinated ground water. The ORs for the highest vs. lowest quintiles of tap water intake were 1.7 and 2.0, respectively, among subjects with 40-59 and greater than or equal to 60 years' exposure. Duration of exposure to chlorinated surface water was associated with bladder cancer risk among women and nonsmokers of both sexes. Among non-smoking respondents with tap water consumption above the population median, the OR increased with exposure duration to a level of 3.1 (CI = 1.3, 7.3; chi 2 for trend = 6.3, P = .01) for greater than or equal to 60 years of residence at places served by chlorinated surface water (vs. non-chlorinated ground water users). These results extend findings of earlier epidemiologic studies and are consistent with environmental chemistry and toxicologic data demonstrating the presence of genotoxic by-products of chlorine disinfection in treated surface waters.

Chlorine↗
PubMed1986

Long-term use of oral contraceptives and risk of invasive cervical cancer.

To evaluate the relationship between use of oral contraceptives and risk of invasive cervical cancer, a case-control study involving 479 patients and 789 population controls was undertaken in 5 geographic regions of the US. Initially, the relationship was obscured by confounding variables, particularly the interval since last Pap smear. Control for this variable as well as for sexual and sociodemographic factors revealed an RR of 1.5 overall, with long-term users (5 or more years) being at a 2-fold higher risk than non-users. Pill associations prevailed for both adenocarcinomas and squamous-cell tumors, and risks were highest for those using pills containing high estrogen potencies. In addition, there was some evidence that pill associations were most pronounced among women who had never used barrier methods of contraception or who had histories of genital infections, suggesting that oral contraceptives may act as co-carcinogens with transmissible agents. Our findings provide further evidence that long-term use of oral contraceptives may have a carcinogenic effect on cervical epithelium, but emphasize the need for careful evaluation of confounding influences.

Adenocarcinoma↗
PubMed1986

Agricultural herbicide use and risk of lymphoma and soft-tissue sarcoma.

A population-based case-control study of soft-tissue sarcoma (STS), Hodgkin's disease (HD), and non-Hodgkin's lymphoma (NHL) in Kansas found farm herbicide use to be associated with NHL (odds ratio [OR], 1.6; 95% confidence interval [CI], 0.9, 2.6). Relative risk of NHL increased significantly with number of days of herbicide exposure per year and latency. Men exposed to herbicides more than 20 days per year had a sixfold increased risk of NHL (OR, 6.0; 95% CI, 1.9, 19.5) relative to nonfarmers. Frequent users who mixed or applied the herbicides themselves had an OR of 8.0 (95% CI, 2.3, 27.9) for NHL. Excesses were associated with use of phenoxyacetic acid herbicides, specifically 2,4-dichlorophenoxyacetic acid. Neither STS nor HD was associated with pesticide exposure. This study confirms the reports from Sweden and several US states that NHL is associated with farm herbicide use, especially phenoxyacetic acids. It does not confirm the case-control studies or the cohort studies of pesticide manufacturers and Vietnam veterans linking herbicides to STS or HD.

Adult↗