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Michael J Thun

Publications and source records attributed to Michael J Thun.

At least 19 recordsLinked to original sources

Cardiovascular mortality and long-term exposure to particulate air pollution: epidemiological evidence of general pathophysiological pathways of disease.

BACKGROUND: Epidemiologic studies have linked long-term exposure to fine particulate matter air pollution (PM) to broad cause-of-death mortality. Associations with specific cardiopulmonary diseases might be useful in exploring potential mechanistic pathways linking exposure and mortality. METHODS AND RESULTS: General pathophysiological pathways linking long-term PM exposure with mortality and expected patterns of PM mortality with specific causes of death were proposed a priori. Vital status, risk factor, and cause-of-death data, collected by the American Cancer Society as part of the Cancer Prevention II study, were linked with air pollution data from United States metropolitan areas. Cox Proportional Hazard regression models were used to estimate PM-mortality associations with specific causes of death. Long-term PM exposures were most strongly associated with mortality attributable to ischemic heart disease, dysrhythmias, heart failure, and cardiac arrest. For these cardiovascular causes of death, a 10-microg/m3 elevation in fine PM was associated with 8% to 18% increases in mortality risk, with comparable or larger risks being observed for smokers relative to nonsmokers. Mortality attributable to respiratory disease had relatively weak associations. CONCLUSIONS: Fine particulate air pollution is a risk factor for cause-specific cardiovascular disease mortality via mechanisms that likely include pulmonary and systemic inflammation, accelerated atherosclerosis, and altered cardiac autonomic function. Although smoking is a much larger risk factor for cardiovascular disease mortality, exposure to fine PM imposes additional effects that seem to be at least additive to if not synergistic with smoking.

Adult↗

Multivitamin use and colorectal cancer incidence in a US cohort: does timing matter?

Multivitamins contain several nutrients, including folic acid, that are hypothesized to reduce the risk of colorectal cancer. Previous studies suggest that multivitamin use may reduce colorectal cancer risk but only after a long latency period. The authors examined the association between regular multivitamin use (four or more times per week) and colorectal cancer incidence among 145,260 men and women in the Cancer Prevention Study II Nutrition Cohort. Current multivitamin use was reported on a questionnaire at enrollment in 1992-1993. All participants had also reported multivitamin use on a questionnaire completed for a different study approximately 10 years earlier (in 1982). The authors observed 797 incident cases of colorectal cancer during follow-up from 1992 to 1997. After multivariate adjustment, regular multivitamin use at enrollment was not associated with risk of colorectal cancer (rate ratio = 1.04, 95% confidence interval: 0.87, 1.23), whereas regular multivitamin use 10 years before enrollment was associated with reduced risk (rate ratio = 0.71, 95% confidence interval: 0.57, 0.89). Regular multivitamin users 10 years before enrollment were at similarly reduced risk whether they were still regular multivitamin users at enrollment or had stopped. These results are consistent with the hypothesis that past, but not recent, multivitamin use may be associated with modestly reduced risk of colorectal cancer.

Aged↗

Lung cancer mortality in relation to age, duration of smoking, and daily cigarette consumption: results from Cancer Prevention Study II.

The magnitude of the effect of smoking duration on lung cancer mortality relative to that of intensity (cigarettes/day) has practical implications for both tobacco control policy and research. This issue was addressed by R. Doll and R. Peto (J. Epidemiol. Commun. Health, 32: 303-313, 1978) in their historic analysis of one of the few large cohort studies in which intensity and duration were estimated separately. Their findings have been interpreted to mean that smoking duration is much more important than smoking intensity in causing lung cancer. The separate contributions of smoking duration and intensity to lung cancer risk have not been evaluated in other large prospective studies. We studied participants in the Cancer Prevention Study II, followed from 1982 through 1988. After restricting to people 40-79 years old who smoked < or =40 cigarettes per day at enrollment, we fit Poisson models for four age groups and evaluated lung cancer mortality (M) in relation to smoking duration (D) and intensity (I) on a double-log scale, as suggested by the Armitage-Doll multistage carcinogenesis model. The age-specific mortality estimates for men (M(m)) and for women (M(w)), when transformed to the original scale, were: ages 40-49: M(m) = e(-17.9) x D(1.9) x I(0.95), M(w) = e(-20.2) x D(2.8) x I(0.96); ages 50-59: M(m) = e(-17.4) x D(2.6) x I(0.52), M(m) = e(-17.2) x D(2.2) x I(0.75); ages 60-69: M(m) = e(-15.7) x D(2.4) x I(0.37), M(m) = e(-14.1) x D(1.5) x I(0.78); ages 70-79: M(m) = e(-13.0) x D(1.8) x I(0.39), M(m) = e(-13.2) x D(1.3) x I(0.95). Our study confirms that years of cigarette smoking is far more important than the number of cigarettes smoked per day in predicting lung cancer risk in United States men, regardless of age, and provides new evidence that a qualitatively similar pattern holds for women. The results support measures to prevent the uptake of smoking by adolescents and increase cessation. We discuss reasons why the associations we observe are lower than those reported by R. Doll and R. Peto (J. Epidemiol. Commun. Health, 32: 303-313, 1978).

Adult↗

Annual report to the nation on the status of cancer, 1975-2000, featuring the uses of surveillance data for cancer prevention and control.

BACKGROUND: The American Cancer Society, the Centers for Disease Control and Prevention (CDC), the National Cancer Institute (NCI), and the North American Association of Central Cancer Registries (NAACCR) collaborate annually to update cancer rates and trends in the United States. This report updates statistics on lung, female breast, prostate, and colorectal cancers and highlights the uses of selected surveillance data to assist development of state-based cancer control plans. METHODS: Age-adjusted incidence rates from 1996 through 2000 are from state and metropolitan area cancer registries that met NAACCR criteria for highest quality. Death rates are based on underlying cause-of-death data. Long-term trends and rates for major racial and ethnic populations are based on NCI and CDC data. Incidence trends from 1975 through 2000 were adjusted for reporting delays. State-specific screening and risk factor survey data are from the CDC and other federal and private organizations. RESULTS: Cancer incidence rates for all cancer sites combined increased from the mid-1970s through 1992 and then decreased from 1992 through 1995. Observed incidence rates for all cancers combined were essentially stable from 1995 through 2000, whereas the delay-adjusted trend showed an increase that had borderline statistical significance (P =.05). Increases in the incidence rates of breast cancer in women and prostate cancer in men offset a long-term decrease in lung cancer in men. Death rates for all cancer sites combined decreased beginning in 1994 and stabilized from 1998 through 2000, resulting in part from recent revisions in cause-of-death codes. Death rates among men continued to decline throughout the 1990s, whereas trends in death rates among women were essentially unchanged from 1998 through 2000. Analysis of state data for the leading cancers revealed mixed progress in achieving national objectives for improving cancer screening, risk factor reduction, and decreases in mortality. CONCLUSIONS: Overall cancer incidence and death rates began to stabilize in the mid- to late 1990s. The recent increase in the delay-adjusted trend will require monitoring with additional years of data. Further reduction in the burden of cancer is possible but will require the continuation of strong federal, state, local, and private partnerships to increase dissemination of evidence-based cancer control programs to all segments of the population.

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Long-term trends in cancer mortality in the United States, 1930-1998.

BACKGROUND: Progress against cancer can be examined by analyzing long-term trends in cancer incidence and mortality. The recent directive from the U.S. Department of Health and Human Services to adopt the 2000 U.S. standard population for the age adjustment of death rates prompted the American Cancer Society to update historical cancer mortality statistics using the new standard. METHODS: Mortality data were abstracted by race, gender, year, and age at death for 1930 through 1959 from annual volumes of Vital Statistics of the United States. For 1960 through 1998, these data were obtained from data tapes provided by the National Center for Health Statistics. Two U.S. standard million populations (1970 and 2000) were used to calculate age-adjusted rates. Average annual percent change was estimated for each decade by site, gender, and age, and the statistical significance of the change was assessed at p < 0.05. RESULTS: After long-term increases or mostly level trends that date from the 1930s for some sites, death rates for cancers of the lung (in males), prostate, female breast, colon-rectum, pancreas, leukemia, and ovary were decreasing in the 1990s. Liver cancer death rates were increasing in the 1990s. Throughout the study period, death rates for female lung cancer increased, while death rates for stomach and uterine cancers declined. CONCLUSIONS: The trends of decreasing cancer death rates for the leading cancer sites in the 1990s are encouraging. However, surveillance researchers must continue to monitor these declines to assess whether the progress seen in this decade persists. Efforts also must be made to study the sites with increasing trends and identify potential underlying causes.

Adolescent↗

Diet Quality Index as a predictor of short-term mortality in the American Cancer Society Cancer Prevention Study II Nutrition Cohort.

The Diet Quality Index (DQI) was developed to measure overall dietary patterns and to predict chronic disease risk. This study examined associations between DQI and short-term all-cause, all-circulatory-disease, and all-cancer mortality in the American Cancer Society Cancer Prevention Study II Nutrition Cohort, a cohort of US adults aged 50-79 years enrolled in a prospective study. After 4 years of follow-up (1992-1996), there were 869 deaths among 63,109 women and 1,736 deaths among 52,724 men. All study participants reported being disease free at baseline in 1992-1993. In age-adjusted Cox models, a higher DQI, which was indicative of a poorer quality diet, was positively related to all-cause and all-circulatory-disease mortality rates in both women and men and to cancer mortality in men only. However, in fully adjusted Cox models, only circulatory disease mortality was clearly positively related to DQI and only in women (medium-low-quality diet vs. highest-quality diet: rate ratio = 1.86, 95% confidence interval: 1.19, 2.89). Although trend tests indicated significant positive relations between DQI and all-cause mortality, effects were small (rate ratios </= 1.31), and confidence intervals were wide, generally including 1.0. DQI was unrelated to cancer mortality. As currently constructed, the DQI may have limited ability to predict mortality.

Aged↗

Overweight, obesity, and mortality from cancer in a prospectively studied cohort of U.S. adults.

BACKGROUND: The influence of excess body weight on the risk of death from cancer has not been fully characterized. METHODS: In a prospectively studied population of more than 900,000 U.S. adults (404,576 men and 495,477 women) who were free of cancer at enrollment in 1982, there were 57,145 deaths from cancer during 16 years of follow-up. We examined the relation in men and women between the body-mass index in 1982 and the risk of death from all cancers and from cancers at individual sites, while controlling for other risk factors in multivariate proportional-hazards models. We calculated the proportion of all deaths from cancer that was attributable to overweight and obesity in the U.S. population on the basis of risk estimates from the current study and national estimates of the prevalence of overweight and obesity in the U.S. adult population. RESULTS: The heaviest members of this cohort (those with a body-mass index [the weight in kilograms divided by the square of the height in meters] of at least 40) had death rates from all cancers combined that were 52 percent higher (for men) and 62 percent higher (for women) than the rates in men and women of normal weight. For men, the relative risk of death was 1.52 (95 percent confidence interval, 1.13 to 2.05); for women, the relative risk was 1.62 (95 percent confidence interval, 1.40 to 1.87). In both men and women, body-mass index was also significantly associated with higher rates of death due to cancer of the esophagus, colon and rectum, liver, gallbladder, pancreas, and kidney; the same was true for death due to non-Hodgkin's lymphoma and multiple myeloma. Significant trends of increasing risk with higher body-mass-index values were observed for death from cancers of the stomach and prostate in men and for death from cancers of the breast, uterus, cervix, and ovary in women. On the basis of associations observed in this study, we estimate that current patterns of overweight and obesity in the United States could account for 14 percent of all deaths from cancer in men and 20 percent of those in women. CONCLUSIONS: Increased body weight was associated with increased death rates for all cancers combined and for cancers at multiple specific sites.

Adult↗

Correlates of underutilization of colorectal cancer screening among U.S. adults, age 50 years and older.

BACKGROUND: Although effective screening for colorectal cancer (CRC) exists, only 37% of incident CRC are diagnosed at a localized stage at which treatment is effective. We identified demographic and other characteristics of adults (> or = 50 years old) who reported no CRC screening. METHODS: We calculated the prevalence of never having had a fecal occult blood test and/or a sigmoidoscopy or colonoscopy by age, sex, and other factors using the 1999 Behavioral Risk Factor Surveillance System data. RESULTS: CRC screening tests were underutilized across all segments of the population. Underutilization was highest in persons aged 50-64 years and those with lower education and a lack of health insurance and preventive services. CONCLUSIONS: The data indicate that large proportions of average-risk adults across various sociodemographics and behavioral factors are not utilizing recommended CRC screening tests. There is a need to increase the awareness of the importance of utilizing effective CRC screening tests for the early detection of colorectal cancers.

Aged↗

Calcium, vitamin D, dairy products, and risk of colorectal cancer in the Cancer Prevention Study II Nutrition Cohort (United States).

OBJECTIVE: Calcium, vitamin D, and dairy product intake may reduce the risk of colorectal cancer. We therefore examined the association between these factors and risk of colorectal cancer in a large prospective cohort of United States men and women. METHODS: Participants in the Cancer Prevention Study II Nutrition Cohort completed a detailed questionnaire on diet, medical history, and lifestyle in 1992-93. After excluding participants with a history of cancer or incomplete dietary information, 60,866 men and 66,883 women remained for analysis. During follow-up through 31 August 1997 we documented 421 and 262 cases of incident colorectal cancers among men and women, respectively. Multivariate-adjusted rate ratios (RR) were calculated using Cox proportional hazards models. RESULTS: Total calcium intake (from diet and supplements) was associated with marginally lower colorectal cancer risk in men and women (RR = 0.87, 95% CI 0.67-1.12, highest vs lowest quintiles, p trend = 0.02). The association was strongest for calcium from supplements (RR = 0.69, 95% CI 0.49-0.96 for > or = 500 mg/day vs none). Total vitamin D intake (from diet and multivitamins) was also inversely associated with risk of colorectal cancer, particularly among men (RR = 0.71, 95% CI 0.51-0.98, p trend = 0.02). Dairy product intake was not related to overall risk. CONCLUSIONS: Our results support the hypothesis that calcium modestly reduces risk of colorectal cancer. Vitamin D was associated with reduced risk of colorectal cancer only in men.

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Lung cancer trends in young adults: an early indicator of progress in tobacco control (United States).

OBJECTIVE: Tobacco smoking is known to increase lung cancer occurrence beginning in young adulthood, although age-specific rates have not been used to monitor the early consequences of tobacco control efforts in the United States. We evaluated state trends in lung cancer death rates among young adults in relation to an index of state tobacco control activities and conventional indices of current smoking and cessation. METHODS: We calculated lung cancer death rates in young adults (age 30-39 years) over two time intervals from 1990-1994 through 1995-1999 in states with at least 25 deaths per interval. We measured the correlation of an index of state tobacco control in 1992-1993 with absolute rates and with total percent change during the two time intervals. RESULTS: Both lung cancer death rates during the recent time interval (1995-1999) and the change in these rates from 1990-1994 correlated strongly and inversely with the index of state tobacco control efforts measured in 1992-1993. Lung cancer death rates decreased in states with high tobacco control efforts, but increased in states with low tobacco control efforts. Tobacco control indices were strongly and positively correlated with cessation of smoking by age 30-39 years. CONCLUSIONS: Lung cancer death rates among young adults are strongly and inversely correlated with recent indices of tobacco control. Future monitoring of the effectiveness of statewide comprehensive tobacco control programs should assess trends in lung cancer rates in young adults as well as youth and adult smoking prevalence.

Adolescent↗

Recreational physical activity and risk of postmenopausal breast cancer in a large cohort of US women.

Due to its potential effects on ovarian hormone production, physical activity has been proposed as a modifiable risk factor for breast cancer. The authors analyzed data from the American Cancer Society Cancer Prevention Study II (CPS-II) Nutrition Cohort to examine the association between various measures of physical activity and postmenopausal breast cancer risk. Information on physical activity was obtained in 1992 via a self-administered questionnaire for 72,608 postmenopausal female participants who were cancer-free. During the five year prospective follow-up, 1520 incident breast cancer cases were identified among these women. Cox proportional hazards modeling was used to compute hazard rate ratios (RR) and to adjust for potential confounding factors including mammography. Women who were most physically active (> 42.0 MET-h/week) at baseline had 29% lower incidence rates than active women with the least activity (> 0-7.0 MET-h/week) (95% CI, 0.49-1.02). The difference in risk was largest for localized breast cancer, and for women who did not use hormone replacement therapy (HRT) at enrollment. Our findings are consistent with other studies that show lower risk of postmenopausal breast cancer associated with regular physical activity.

Aged↗

Alcohol, folate, methionine, and risk of incident breast cancer in the American Cancer Society Cancer Prevention Study II Nutrition Cohort.

Recent studies suggest that the increased risk of breast cancer associated with alcohol consumption may be reduced by adequate folate intake. We examined this question among 66,561 postmenopausal women in the American Cancer Society Cancer Prevention Study II Nutrition Cohort. A total of 1,303 incident cases had accrued during the first 5 years of follow-up. Cox proportional hazards models and stratified analysis were used to examine the relationship between alcohol, dietary and total folate intake, multivitamin use, dietary methionine, and breast cancer. We observed an increasing risk of breast cancer with increasing alcohol consumption (P for trend = 0.01). In the highest category of consumption (15 or more grams of ethanol/day), the risk of breast cancer was 1.26 (95% confidence interval, 1.04-1.53) compared with nonusers. We observed this association with higher alcohol consumption for in situ, localized, and regional disease. We found no association between risk of breast cancer and dietary folate, total folate, multivitamin use, or methionine intake. Furthermore, we found no evidence of an interaction between levels of dietary folate (P for interaction = 0.10) or total folate (P for interaction = 0.61) and alcohol. Nor did we find evidence of an interaction between alcohol consumption and recent or long-term multivitamin use (P for interaction = 0.27). Our results are consistent with a positive association with alcohol but do not support an association with folate or methionine intake or an interaction between folate and alcohol intake on risk of breast cancer.

Adult↗

Dietary glycemic index, glycemic load, and risk of incident breast cancer in postmenopausal women.

Insulin and insulin-like growth factor-I (IGF-I) are associated with increased risk of breast cancer in several studies. Circulating concentrations of insulin increase with dietary consumption of high glycemic index foods, which, in turn, may influence IGF-I levels or activity, but the relevance of such dietary patterns for breast cancer risk is unclear. We investigated whether consumption of carbohydrates with high dietary glycemic index would predict risk of postmenopausal breast cancer among 63,307 United States women in the Cancer Prevention Study II Nutrition Cohort. From baseline in 1992, participants 40-87 years of age and free from cancer and diabetes, were followed for 5 years; 1442 incident breast cancer cases were documented. Diet was assessed at baseline by a validated 68-item food frequency questionnaire from which we calculated dietary glycemic index and glycemic load. Dietary glycemic index and load were not associated with increased risk of postmenopausal breast cancer (rate ratio = 1.03; 95% confidence interval, 0.87-1.22 and rate ratio = 0.90; 95% confidence interval, 0.76-1.08, respectively) after adjustment for multiple breast cancer risk factors. Associations were not modified by body mass index, physical activity, hormone use, or stage of disease. Future evaluations of glycemic index and breast cancer risk may be strengthened by longer follow-up, more complete dietary information, and measurement of plasma insulin and IGF-I levels.

Adult↗

Calcium, dairy products, and risk of prostate cancer in a prospective cohort of United States men.

Intake of calcium and/or dairy products has been associated with increased risk of prostate cancer in some epidemiological studies. One potential biological mechanism is that high calcium intake down-regulates 1,25 dihydroxy vitamin D(3), which may increase cell proliferation in the prostate. We examined the association between calcium, dairy intake, and prostate cancer incidence in the Cancer Prevention Study II Nutrition Cohort, a prospective cohort of elderly United States adults. Participants in the study completed a detailed questionnaire on diet, medical history, and lifestyle at enrollment in 1992-1993. After excluding men with a history of cancer or incomplete dietary information, 65,321 men remained for analysis. During follow-up through August 31, 1999, we documented 3811 cases of incident prostate cancer. Multivariate-adjusted rate ratios (RRs) were calculated using Cox proportional hazards models. Total calcium intake (from diet and supplements) was associated with modestly increased risk of prostate cancer [RR = 1.2, 95% confidence interval (CI) = 1.0-1.6 for >or=2000 versus <700 mg/day, P trend = 0.02). High dietary calcium intake (>or=2000 versus <700 mg/day) was also associated with increased risk of prostate cancer (RR = 1.6, 95% CI = 1.1-2.3, P trend = 0.10), although moderate levels of dietary calcium were not associated with increased risk. Dairy intake was not associated with prostate cancer risk. The association between prostate cancer and total calcium intake was strongest for men who reported not having prostate-specific antigen testing before 1992 (RR = 1.5, 95% CI = 1.1-2.0, P trend < 0.01 for >or= 2000 mg/day of total calcium; RR = 2.1, 95% CI = 1.3-3.4 >or=2000 mg/day of dietary calcium, P trend = 0.04). Our results support the hypothesis that very high calcium intake, above the recommended intake for men, may modestly increase risk of prostate cancer.

Aged↗

Vitamin C and vitamin E supplement use and bladder cancer mortality in a large cohort of US men and women.

Some epidemiologic studies suggest that use of vitamin C or vitamin E supplements, both potent antioxidants, may reduce the risk of bladder cancer. The authors examined the association between use of individual vitamin C and vitamin E supplements and bladder cancer mortality among 991,522 US adults in the Cancer Prevention Study II (CPS-II) cohort. CPS-II participants completed a self-administered questionnaire at enrollment in 1982 and were followed regarding mortality through 1998. During follow-up, 1,289 bladder cancer deaths occurred (962 in men and 327 in women). Rate ratios were adjusted for age, sex, cigarette smoking, education, and consumption of citrus fruits and vegetables. Regular vitamin C supplement use (>or=15 times per month) was not associated with bladder cancer mortality, regardless of duration (rate ratio (RR) = 0.91, 95% confidence interval (CI): 0.68, 1.20 for <10 years' use; RR = 1.25, 95% CI: 0.91, 1.72 for >or=10 years' use). Regular vitamin E supplement use for >or=10 years was associated with a reduced risk of bladder cancer mortality (RR = 0.60, 95% CI: 0.37, 0.96), but regular use of shorter duration was not (RR = 1.04, 95% CI: 0.77, 1.40). Results support the hypothesis that long-duration vitamin E supplement use may reduce the risk of bladder cancer mortality.

Adult↗