Pesticide exposures and multiple myeloma in Iowa men

A population-based case-control study of 173 White men with multiple myeloma (MM) and 650 controls was conducted in Iowa (United States), an area with a large farming population, to evaluate the association between MM, agricultural risk factors, and exposure to individual pesticides. A slight nonsignificantly elevated risk for MM was seen among farmers (odds ratio [OR]=1.2, 95 percent confidence interval [CI]=0.8–1.7). Although slight excesses were observed, there were no significant associations between MM and handling either classes of pesticides or specific pesticides. Thus, this study found little evidence to suggest an association between risk of MM and farming or pesticides.Ms Brown and Dr Blair are with the Epidemiology and Biostatistics Program, National Cancer Institute, Bethesda, MD, USA. Dr Burmoistor is with the Department of Preventive Medicine, University of Iowa, Iowa City, IA, USA. Dr Everett is with the Department of Internal Medicine, Orlando Regional Medical Center, Orlando, FL, USA. Address correspondence to Ms Brown, Epidemiology and Biostatistics Program, National Cancer Institute, Executive Plaza North, Room 415, Bethesda, MD, USA. This project was supported in part by a grant from the National Institute of Environmental Health Sciences (ES 03099).     

Cigarette smoking and leukemia: results from the Lutheran Brotherhood Cohort Study

In a 20-year follow-up (1966–86) of 17,633 White males who described tobacco use in a mailed questionnaire sent in 1966, there were 74 deaths from leukemia (including 30 myeloid, 30 lymphatic, and 14 other and unspecified leukemia). Among men who ever smoked cigarettes, increased risks were observed for lymphatic (relative risk [RR]=2.7), and other and unspecified leukemia (RR=1.5); risks rose with increasing number of cigarettes smoked, although the dose-response relationship was statistically significant only for total leukemia. Mortality from myeloid leukemia was not elevated, except among those smoking over a pack of cigarettes per day. Results from this cohort support a relationship between cigarette smoking and leukemia. Further studies are needed to elucidate subtype associations with cigarette smoking.Drs Linet, McLaughlin, Hsing, Wacholder, and Blot are with the Epidemiology and Biostatistics Program, National Cancer Institute. Dr Co-Chien is at Westat, Inc., Rockville, Maryland, USA, Dr Schuman is at the University of Minnesota, Minneapolis, Minnesota, USA. Dr Bjelke is with the Center for Epidemiologic Research, University of Bergen, Norway. Address correspondence to Dr Linet, Epidemiology and Biostatistics Program, National Cancer Institute, Executive Plaza North Room 415B, Bethesda, MD 20892, USA.     

Leukemia,lymphoma, and multiple myeloma following selected medical conditions

The role of selected prior medical conditions in the etiology of hematopoietic malignancies was examined in a case-control study of members of two regional branches of the Kaiser Permanente Medical Care Program (USA). Past history of chronic infectious, autoimmune, allergic, and musculoskeletal disorders was abstracted from medical records for leukemia (n = 299), non-Hodgkin's lymphoma (NHL, n = 100), and multiple myeloma (n = 175) cases and matched controls (n = 787). Little difference was found between cases and controls for most of the chronic conditions evaluated, including sinusitis, carbuncles, urinary tract infections, pelvic infections, herpes zoster, asthma, rheumatoid arthritis, psoriasis, bursitis, and gout. Only three statistically significant elevated risks were found, i.e., with combined disc disease myeloma among patients with prior eczema and disk and other musculoskeletal conditions, and NHL following tuberculosis. Only two of these associations showed consistent patterns by sex and geographic region (myeloma with eczema and with musculoskeletal conditions). While prior history of eczema and musculoskeletal conditions may slightly increase risk of myeloma, this study provided little if any support for an association of chronic infectious, autoimmune, allergic, and musculoskeletal conditions with subsequent occurrence of the leukemias or NHL. Additionally, these data did not support a role for chronic antigenic stimulation, as defined in previous epidemiologic studies, in the etiology of hematopoietic malignancies.Ms Doody and Drs Linet, Pottern, Boice, and Fraumeni are with the Epidemiology and Biostatistics Program, National Cancer Institute. Dr Glass is with the Kaiser Permanente Medical Care Program, Northwest Region, Portland, Oregon, USA. Dr Friedman is with the Kaiser Permanente Medical Care Program, Northern California Region, Oakland, California, USA. Address correspondence to Ms Doody, Radiation Epidemiology Branch, National Cancer Institute, Executive Plaza North, Room 408, Bethesda, MD 20892, USA. This research was supported in part by National Cancer Institute contracts NO1-CP-01047, NO1-CP-01054, NO1-CP-11009, NO1-CP-11037, NO1-CP-31035, and NO1-CP-61006.     

Reproductive factors and risk of brain,colon, and other malignancies in Iowa (United States)

The influence of parity on the risk of cancers of the female breast and reproductive organs is well established. However, non-reproductive sites have received less attention. Mail questionnaire data gathered from incident female cases (169 brain; 332 colon; 260 rectal; 145 kidney; and 169 pancreas cancers), and 821 populationbased controls in Iowa (United States) were used to measure the effect of parity and age at first birth on risk of these malignancies. Relative to nulliparous women, ever-parous women were at significantly decreased risk of brain cancer (odds ratio [OR]=0.44, 95 percent confidence interval [CI]=0.3–0.7) and of colon cancer (OR=0.67, CI=0.5–0.97), after adjustment for age and other risk factors. The OR for the other sites did not differ significantly from 1.0. The lower risk of brain cancer among parous women was similar in younger and older age groups, in patients diagnosed with glioblastoma and astrocytoma, and among ever- and never-smokers. The findings for colon cancer are consistent with observations from other studies. In the context of limited laboratory and clinical evidence implicating hormones in brain neoplasia, these findings may suggest a role for hormonal factors in brain cancer etiology. Hormonal factors deserve more detailed future consideration as risk factors in brain cancer.Dr Cantor is with the Environmental Epidemiology Branch, National Cancer Institute, Bethesda, MD, USA. Dr Lynch and Ms Johnson are with the Department of Preventive Medicine and Environmental Health, University of Iowa, Iowa City, IA, USA. Address correspondence to Dr Cantor, Environmental Epidemiology Branch, National Cancer Institute, Executive Plaza North, Suite 443, Bethesda, MD 20892, USA. Supported in part by United States National Cancer Institute research contracts (NCI-NO1-CP-51026 and NCI NO1-CP-85614) and by a Public Health Service Preventive Oncology Academic Award (5 KO7 CA01181-05).     

Cigarette smoking and liver cancer among US veterans

The relationship of tobacco use with risk of primary liver cancer was investigated using data from a 26-year mortality follow-up of nearly 250,000 US veterans, mostly from World War I. Significantly increased risks for liver cancer (289 deaths) were associated with most forms of tobacco use, including pipe and cigar smoking. Elevated relative tisks (RRs) were seen for current cigarette smokers (RR=2.4; 95 percent confidence interval [CI] 1.6–3.5) and former cigarette smokers (RR=1.9, 1.2–2.9). A strong dose-response relationship (P<0.001) was found for cigarette smoking, with smokers of 40 or more cigarettes per day having almost a fourfold risk (RR=3.8, 1.9–8.0). Risks were also found to increase significantly with years of cigarette use and with earlier age at the start of cigarette smoking. These results are consistent with those of other cohort and case-control studies, suggesting that cigarette smoking may be related to the risk of liver cancer.All authors are in the Epidemiology and Biostatistics Program, Division of Cancer Etiology, National Cancer Institute. Address correspondence to Dr Hsing at Executive Plaza North, Room 415, Bethesda, MD 20892, USA.     

A cohort study of smoking,alcohol consumption,and dietary factors for pancreatic cancer (United States)

Risk factors for pancreatic cancer were evaluated in a cohort study of 17,633 White men in the United States who responded to a mailed questionnaire in 1966 and were followed-up through 1986 for mortality. Cigarette smoking and alcohol consumption were found to be important risk factors for pancreatic cancer. Risks increased significantly with number of cigarettes smoked, reaching fourfold for smokers of 25 or more cigarettes per day relative to nonsmokers. Alcohol intake also was related significantly to risk, with consumers of 10 or more drinks per month having three times the risk of nondrinkers, but dose-response trends among drinkers were not smooth. Coffee consumption was unrelated to risk. Dietaryanalyses revealed a rising rate of pancreatic cancer mortality with increasing consumption of meat after adjustment for other risk factors. Men in the highest quartile of meat intake had about three times the risk of those in the lowest quartile. No consistent association, however, was observed for consumption of fruits, vegetables, or grains. This study confirms cigarette smoking as an important risk factor for pancreatic cancer, and provides evidence that elevated intake of alcohol and meat may increase the risk of this fatal malignancy.Drs Zheng (at the time of this study), McLaughlin, Gridley, Silverman, Wacholder, Blot, and Fraumeni Jr. are with the Epidemiology and Biostatistics Program, National Cancer Institute, Bethesda, MD, USA. Dr Zheng is currently with the School of Public Health, University of Minnesota, Minneapolis, MN, USA, as is Dr Schuman. Dr Bjelke is with the Center for Epidemiologic Research, University of Bergen, Bergen, Norway. Mr Co-Chien is with Westat, Inc., Rockville, MD, USA. Address correspondence to Dr McLaughlin, Biostatistics Branch, National Cancer Institute, 6130 Executive Blvd., Room 415, Bethesda, MD 20892, USA.     

Tobacco smoking,alcohol consumption,and risk of oral cancer: a case-control study in Beijing,People's Republic of China

A case-control study of oral cancer was conducted in Beijing, People's Republic of China (PRC). The study was hospital-based and controls were hospital in-patients matched for age and gender with the cases. The response rates for cases and controls were 100 percent and 404 case/control pairs were interviewed. Tobacco smoking and alcohol consumption emerged as independent risk factors for oral cancer. For tobacco smoking, the association was considerably stronger for smokers of pipes than for smokers of cigarettes. For all kinds of tobacco, expressed as cigarette equivalents, the odds ratio (OR) for total pack-years smoked, among males, rose from 1.0 in never-smokers to 3.7 (95 percent confidence interval, 1.8–7.4) in the highest quintile of exposure. Similar results were found for females. The association with tobacco consumption was strong for squamous cell carcinoma but there was no trend in risk associated with tobacco for adenocarcinomas and other histologic types. So few women reported consuming alcohol that this variable could be examined only in male. Risk in the highest category of total lifetime intake of alcohol relative to than in lifetime abstainers was 2.3 (1.1–4.8) with a significant trend in risk with increasing dose (P<0.002). The combined effects of tobacco and alcohol appear to be approximately multiplicative in males. The attributable risk of oral cancer for tobacco among tobacco smokers was estimated as 34 percent (45 percent among males and 21 percent among females); for alcohol consumption in males the estimate was 23 percent.Drs Zheng, Hu, and Niu are from the Department of Epidemiology, National Institute for Enviromental Health and Engineering, Chinese Academy of Pieventive Medicine, Beijing, People's Republic of China. Dr Boyle is with the Unit of Analytical Epidemiology, Internationat Agency for Research on Cancer, Lyon, France, where Dr Zheng beld a fellowship. Dr Duan is with the Beijing Union Hospital. Dr Jian is with the Cancer Institute, Chinese Academy of Medical Sciences. Dr Ma is with the Beijing Medical University Stomatological Hospital, Dr Shui is with the Beijing Municipal Stomatological Hospital, Dr MacMabon is in the Department of Epidemiology, Harvard School of Public Health where Dr Zbeng was a graduate student. Address reprint requests to Dr Zheng at the Cancer Prevention Research Unit, Department of Epidemiology and Public Health, Yale University, School of Medicine, B.O. Box 3333, New Haven, CT 06310, USA, Dr Zbeng was supported, in part by a grant from the DuPont Company.     

A prospective study of tobacco use and multiple myeloma: evidence against an association

The relationship between the use of cigarettes and other tobacco products and the risk of multiple myeloma was examined in a cohort of nearly 250,000 American veterans followed prospectively for 26 years. Compared with men who had never used tobacco, the risk of death from myeloma was not increased among current (relative risk [RR]=0.9, 95 percent confidence interval [CI]=0.8–1.2) or former (RR=1.0, CI=0.8–1.3) cigarette smokers, nor among users of chewing tobacco or snuff (RR=1.0, CI=0.4–2.3). Risk was only slightly and nonsignificantly increased among pipe or cigar smokers (RR=1.2, CI=0.9–1.5). There was no indication of increasing risk with amount of tobacco used or earlier age at first use. With over 90 percent power to detect a 30 percent increased risk of this tumor occuring among current cigarette smokers, this study provides the strongest evidence to date against an association of cigarette smoking with multiple myeloma.Epidemiology and Biometry Program, Division of Cancer Etiology, National Cancer Institute. Westat, Inc. Rockville, MD. National Cancer Institute, 6130 Executive Blvd, Room 418, Rockville, MD 20892, USA.     

Race and sex differences in associations of vegetables,fruits, and carotenoids with lung cancer risk in New Jersey (United States)

We used data from a case-control study conducted in New Jersey between 1980 and 1983 to evaluate race and sex differences in associations of vegetable, fruit, and carotenoid consumption with lung cancer. Cases included 736 White males, 860 White females, 269 Black males, and 86 Black females with incident, histologically confirmed, primary cancer of the trachea, bronchus, or lung. Controls were identified through drivers' license and Health Care Financing Administration files and included 548 White males, 473 White females, 170 Black males, and 47 Black females. Usual intakes of vegetables (predominantly yellow/green) and fruit (predominantly yellow/orange) as well as other food sources of carotenoids were ascertained by a food frequency questionnaire. White females showed significant inverse associations of lung cancer with vegetables, fruit, and carotenoids. White males showed nonsignificant inverse associations with vegetables and carotenoids, and Black females just with vegetables. No inverse associations were found for Black males. Vegetable consumption was associated with risk of all histologic types of lung cancer, but the pattern of increasing risk with decreasing intake was limited to smokers. We infer that consumption of yellow/green vegetables and carotenoids may confer protection from lung cancer to White male and White female smokers. Further studies are needed to clarify the effect in Blacks.Drs Dorgan and Shaw are with the Division of Cancer Prevention and Control, and Drs Ziegler and Hartge, and Ms Falk are with the Division of Cancer Etiology, National Cancer Institute, Bethesda, MD, USA. Authors also are affiliated with the Special Epidemiology Program, New Jersey State Department of Health, Trenton, NJ, USA (Ms Schoenberg and Mr Wilcox) and Information Management Services, Inc., Silver Spring, MD, USA (Ms McAdams). Address correspondence to Dr Dorgan, Division of Cancer Prevention and Control, National Cancer Institute, Executive Plaza North, Room 211, Bethesda, MD 20892, USA.     

Soft tissue sarcoma and tobacco use: data from a prospective cohort study of United States veterans

A report of an increased risk of soft tissue sarcoma (STS) among users of smokeless tobacco led us to evaluate this association and the role of other types of tobacco in a prospective cohort mortality-study of United States veterans. A total of 248,046 veterans provided tobacco-use histories on a mail questionnaire in 1954 or 1957. Data on subsequent tobacco use were not collected. By 1980, 119 deaths from STS had occurred among the cohort members. Veterans who had ever chewed tobacco or used snuff had a nonsignificant 40 percent excess of STS (95 percent confidence interval [CI]=0.8–2.6; 21 deaths) in comparison with veterans who had never used any tobacco products. Risk was limited to former users (relative risk [RR]=1.5) with no excess seen among current users (RR=0.9). Frequent former users had higher risk (RR=1.9) than infrequent users (RR=1.3). Risk was slightly higher in persons who started using smokeless tobacco at younger ages, but did not increase with duration of use or with late age at cessation of use. Most veterans who used chewing tobacco or snuff also used some other form of tobacco. No STS deaths occurred among the 2,308 veterans who used smokeless tobacco only. An unexpected finding of the study was the significant excess of STS deaths among cigarette smokers (RR=1.8, CI=1.1–2.9). Risk was higher among ex-smokers (RR=2.2) than among current smokers (RR=1.5) and was not related to number of cigarettes per day, age started smoking, duration, or pack-years. Pipe and cigar smokers also experienced a nonsignificant excess risk (RR=1.6). The study findings may have been affected by limitations in the histories of tobacco use, the quality of death certificate data on STS, and the small number of STS deaths, particularly among users of smokeless tobacco.Drs Zahm and heineman are with the Occupational Studies Section, Environmental Epidemiology Branch, Epidemiology and Biostatistics Program, National Cancer Institute, Rockville, MD, USA. Dr Vaught is with Westat, Inc., Rockville, MD. USA. Address correspondence to Dr Zahm, Occupational Studies Section, National Cancer Institute, Executive Plaza North, Room 418, Rockville, MD 20892, USA.     

Use of a job-exposure matrix to evaluate parental occupation and childhood cancer

We examined the association between parental occupation and childhood cancer among 252 incident cases of childhood cancer (ages 0–14, diagnosed 1976–83) and 222 controls selected by random digit dialing in Denver, Colorado (USA). A job-exposure matrix was used to assign parental exposures based on job titles, emphasizing chemicals that were implicated in previous studies. All cancers, acute lymphocytic leukemia (ALL), and brain cancer were examined in relation to parental occupation during the year prior to the birth of the child. Elevated odds ratios (OR), all with confidence intervals extending below the null, were found for maternal exposure to benzene (OR=1.9), petroleum/coke pitch/tar (OR=2.2), and soot (OR=3.3) in relation to total cancers. The ORs for total cancer and paternal exposure to all hydrocarbons combined was 1.0. Results for individual hydrocarbons and ALL showed larger odds ratios, including aniline (OR=2.1), benzene (OR=1.6), and petroleum/coke pitch/tar (OR=1.6). Potential exposure to creosote was strongly associated with brain cancer (OR=3.7) based on five exposed cases (95 percent confidence interval = 0.8–16.6). Control for other potential childhood cancer risk factors did not alter the results substantially. In spite of uncertainties due to small numbers and errors in exposure classification, results tend to corroborate past research that suggests an association between specific parental occupational exposures and childhood cancer.Ms Feingold, is with the Department of Community Health, Brown University, Providence, RI, USA. Dr Savitz is with the Department of Epidemiology, University of North Carolina School of Public Health, Chapel Hill, NC, USA. Dr John is with the Department of Health Research and Policy, Stanford University, Stanford, CA, USA. Address correspondence to Dr Savitz, Department of Epidemiology, CB 7400, University of North Carolina School of Public Health, Chapel Hill, NC 27599-7400, USA. Ms Feingold's work was supported in part by National Cancer Institute grant 5-T32-CA09330, a cancer epidemiology training grant.     

Bladder cancer,parity, and age at first birth

The excess of bladder cancer in males (M:F ratio of 4:1 in the United States) is not explained fully by gender differences in smoking habits or occupational exposures. Laboratory studies suggest that some androgenic hormones stimulate (or do not inhibit) oncogenesis in bladder tissue, and that estrogenic hormones have the opposite effect. These observations suggest that bladder cancer risk in females may be modified by sex hormones which undergo profound changes during and following pregnancy. Mail-questionnaire data from 317 incident female cases, and 833 population-based controls in Iowa were used to measure the effect of parity and maternal age at first birth on bladder cancer risk. Parous women were at decreased risk relative to nulliparous women (odds ratio [OR]=0.67, 95 percent confidence interval [CI]=0.44–1.00), after adjustment for age, tobacco use, and previous bladder infection. The overall risk reduction was restricted to women who had never smoked (OR=0.51, CI=0.30–0.88), with no apparent effect of parity among ever-smokers (OR=0.93, CI=0.49–1.77). Risk appeared to decrease with increasing age at first birth, but did not vary with increasing parity after the first birth. Our findings are consistent with the hypothesis that oncogenesis in transitional cell tissue of the human bladder is influenced by sex hormones, and that hormonal changes related to pregnancy thereby can decrease risk.Dr Cantor is with the Environmental Epidemiology Branch, National Cancer Institute. Dr Lynch and Ms Johnson are in the Department of Preventive Medicine, University of Iowa School of Medicine, Iowa City, Iowa. Address correspondence to Dr Cantor at NCI, Executive Plaza North, Suite 443, Bethesda, MD 20892, USA. This research was supported in part by National Cancer Institute research contracts NCI-NO1-CP-51026 and NCI-NO1-CP-85614, and by a Public Health Service Preventive Oncology Academic Award, 5 KO7 CA01181-04.     

Cigarette smoking and risk of non-Hodgkin's lymphoma--a population-based case-control study.

BACKGROUND: Epidemiologic evidence of an association between tobacco smoking and non-Hodgkin's lymphoma has been conflicting. This may reflect that non-Hodgkin's lymphoma comprises several distinct disease entities with different etiologies, as some studies have indicated an association between smoking and follicular lymphoma. OBJECTIVE: To investigate the association between cigarette smoking and non-Hodgkin's lymphoma risk, overall and by subtype. METHODS: As part of a nationwide Danish-Swedish population-based case-control study, we interviewed 3,055 incident non-Hodgkin's lymphoma patients and 3,187 population controls. All lymphomas were uniformly classified according to the WHO classification. We used unconditional logistic regression to estimate adjusted odds ratios (OR) and 95% confidence intervals (95% CI) for the association between cigarette smoking and risk of non-Hodgkin's lymphoma. RESULTS: Cigarette smoking was not associated with the risk of non-Hodgkin's lymphoma overall (OR, 0.97; 95% CI, 0.87-1.08) nor with the major subgroups such as diffuse large B-cell lymphoma (OR, 0.94; 95% CI, 0.79-1.10), chronic lymphocytic leukemia (OR, 0.86; 95% CI, 0.72-1.02), or follicular lymphoma (OR, 1.03; 95% CI, 0.85-1.24). Female smokers were at a marginally increased risk of follicular lymphoma (OR, 1.41; 95% CI, 1.04-1.92). Men who had ever smoked had a significantly increased risk of T-cell lymphoma (OR, 1.67; 95% CI, 1.11-2.51). No dose-response association with cigarette smoking could be established for any lymphoma subgroup. CONCLUSION: We found little evidence of an association between cigarette smoking and non-Hodgkin's lymphoma risk overall. Although increased risks of follicular lymphoma in female smokers and of T-cell lymphoma in male smokers were suggested, no dose-response relationship was observed, leaving limited support for causality.     

Extremely low-frequency electric and magnetic fields and cancer

Dr Poole is with the Epidemiology and Biostatistics Section, Boston University School of Public Health, 80 East Concord Street, Boston, MA 02118-2394, USA. Dr Trichopoulos is with the Department of Epidemiology, Harvard School of Public Health, Boston, MA, USA. Address correspondence to Dr Poole.     

Alcohol consumption and risk of leukemia, non-Hodgkin's lymphoma, and multiple myeloma.

Population-based case-control interview studies of white men, 578 with leukemia, 622 with non-Hodgkin's lymphoma, and 820 controls from Iowa and Minnesota and 173 with multiple myeloma and 452 controls from Iowa, offered the opportunity to investigate the relationship of these cancers with alcohol consumption. Although drinkers had non-significantly elevated risks for specific subtypes of leukemia (acute lymphocytic leukemia (OR = 3.0), myelodysplasia (OR = 1.6), and other leukemia (OR = 1.5)) and multiple myeloma (OR = 1.3), there were no statistically significant findings and no dose-response gradients with amount of alcohol consumed. Thus, these data suggest that alcohol is not an important contributor to the etiology of lymphatic and hematopoietic tumors.     

Differences between Black and White patients with cancer of the uterine corpus in interval from symptom recognition to initial medical consultation (United States)

To determine whether Black women with symptoms of uterine corpus cancer had longer times from symptom recognition to initial medical consultation than did White women in the United States, 331 newly diagnosed patients living in Atlanta (GA), New Orleans (LA), and San Francisco/Oakland (CA) during 1985–87 were interviewed to collect information on symptoms, dates of recognition and consultation, and other factors that might affect the interval. Data were analyzed to estimate medical consultation rates and rate ratios following sysptom recognition. Median recalled times between symptom recognition and consultation were 16 days for Black women and 14 days for White women. Although poverty, having no usual source of healthcare, and other factors were associated with lower consultation rates, the adjusted rate among Black women was only somewhat lower (0.87) than among White women, and the 95 percent confidence interval (CI=0.58–1.31) was consistent with no true difference between the races. In addition, the median time to consultation for women with stage IV cancer was only 15 days longer than the time (14 days) for the women with stage I cancer. These results suggest that time from symptom recognition to initial medical consultation does not contribute importantly to the more advanced stage cancer of the uterine corpus commonly found among Black women.Drs Coates and Eley and Ms Click are with the Department of Epidemiology, Rollins School of Public Health of Emory University, Atlanta, GA (USA). Authors are also with the Division of Cancer Prevention & Control, National Cancer Institute, Rockville, MD (Drs Harlan and Edwards); Department of Pathology Obstetrics and Gynecology, Duke University Medical Center, Durham, NC (Dr Robboy); Forsyth Medical Park, Winston-Salem, NC (Dr Barrett); Environmental Epidemiology Section, California State Department of Health Services, Emeryville, CA (Dr Reynolds); Department of Pathology, Louisiana State University Medical Center, New Orleans, LA (Dr Chen); School of Public Health, University of Massachusetts, Amberst, MA (Dr Darity); Office of the President, Northeastern Ohio Universities College of Medicine, Rootstown, OH (Dr Blacklow). Address correspondence to Dr Coates, Department of Epidemiology, Rollins School of Public Health of Emory University, 1518 Clifton Road, NE, Atlanta, GA 30322, USA. This research was supported in part by contracts N01CN-35042-46, N01CN-05227, N01CN-45174, and N01CN-45176 from the National Cancer Institute, US National Institutes of Health.     

Epidemiology of the M-component immunoglobulin types of multiple myeloma

The purpose of this population-based case-control study was to learn whether risk factors differ for the individual immunoglobulin types of multiple myeloma. In particular, we sought to determine whether IgA and IgG myeloma were related to a history of exposure to reported IgA- and IgG-stimulating conditions, respectively, or to a history of selected occupational and physicochemical exposures. The M-component immunoglobulin type was determined from immunoelectrophoresis as reported in medical records, and exposure status was obtained through in-person interviews. IgG (56 percent) and IgA (22 percent) M-components predominated. For 17 percent of cases, no peak was found on immunoelectrophoresis; they were presumed to have light-chain myeloma. Persons with these three types of myeloma did not differ with respect to distributions of age or race, but a somewhat higher proportion of light-chain cases were women (58 percent cf 45 percent of all other cases). Detailed analysis of the IgA and IgG subtypes provided little evidence that they differ with respect to prior immune stimulation or employment in several specific jobs. IgA myeloma, but not IgG myeloma, was associated modestly with a history of exposure to chest and dental X-rays. Our study provides little evidence that IgA and IgG myeloma differ with respect to the risk factors examined.Ms Herrinton and Drs Koepsell, Weiss, and Daling are with the Department of Epidemiology, University of Washington, Seattle, WA, USA, and the Division of Public Health Sciences, Fred Hutchinson Cancer Research Center, Seattle, WA, USA. Dr Demers is with the Department of Environmental Health, University of Washington, Seattle, WA, USA. Dr Taylor is with Group Health Cooperative of Puget Sound, Seattle, WA, USA. Dr Lyon is with the School of Medicine, University of Utah, Salt Lake City, UT, USA. Dr Swanson is with the Cancer Center, Michigan State University, East Lansing, MI, USA. Dr Greenberg is with the School of Public Health, Emory University, Atlanta, GA, USA. Address correspondence to Ms Lisa Herrinton, Fred Hutchinson Cancer Research Center, 1124 Columbia MP-381, Seattle, WA 98104, USA. The project was supported by grants CA23350, CA39779, and CA09168 from the US National Cancer Institute.     

Are the known bladder cancer risk-factors associated with more advanced bladder cancer?

Risk factors for superficial and invasive bladder cancer were examined in a case-control study of 470 cases Identified in 1967–68 in the Brockton and Boston Standard Metropolitan Areas (MA, United States) and of 500 population-based controls. Histologic specimens were reviewed and classified as superficial or invasive, following a standardized protocol. The tobacco-associated risk for superficial bladder cancer was odds ratio (OR)=2.6 (95 percent confidence interval [CI]=1.7–4.1) and the risk for invasive bladder cancer was OR=1.7 (CI=1.1–2.5). For subjects less than 60 years of age, the risks were greater for invasive tumors (OR=4.3, CI=1.2–15) than for superficial tumors (OR=0, CI=0.9–4.2), but this pattern for tobacco use was not found in older subjects. A strong trend of increased risk with increased amount of cigarettes smoked was shown only for invasive bladder tumors. No clear pattern of excess risk for invasive bladder tumors was seen for age at first use and years since last use of tobacco. The risk associated with occupational exposure to aromatic amine bladder carcinogens was OR=1.7 (CI=0.8–3.3) for superficial and OR=1.5 (CI=0.8–3.0) for invasive bladder cancer. For subjects less than 60 years of age, the risks were greater for invasive (OR=12.0, CI=2.1–65) than for superficial tumors (OR=4.3, CI=0.8–24), but this pattern for occupational exposure was not found in older subjects. Risk by age at first exposure to occupational aromaticamine, bladder carcinogens was similar for superficial and invasive tumors. Overall, there was no association between known bladder-cancer risk-factors and more advanced bladder cancer. The relative risk associated with cigarette smoking and occupational exposure to aromatic amines was higher for invasive than superficial cancer only for men less than 60 years of age.Drs Hayes and Zahm are with the Environmental Epidemiology Branch, National Cancer Institute, Bethesda, MD, USA. Authors are affiliated also with the Lucille P. Markey Cancer Center, Lexington, KN, USA (Dr Friedell) and the Department of Epidemiology, University of Alabama, Birmingham, AL, USA (Dr Cole). Address correspondence to Dr Hayes, Environmental Epidemiology Branch, National Cancer Institute, EPN 418, Bethesda, MD 20892, USA.     

Occupational risk factors for lung cancer among nonsmoking women: a case-control study in Missouri (United States)

Occupationally related risk of lung cancer among women and among nonsmokers has not been widely studied. A recently conducted population-based, case-control study in Missouri (United States) provided the opportunity to evaluate risk of lung cancer associated with several occupational factors. Incident cases (n=429) were identified through the Missouri Cancer Registry for the period 1986 through 1991, and included 294 lifetime nonsmokers and 135 ex-smokers who had stopped at least 15 years prior to diagnosis or had smoked for less than one pack-year. Controls (n=1,021) were selected through driver's license and Medicare files. Risk was elevated among women exposed to asbestos (ever: odds ratio [OR]=3.5, 95 percent confidence interval [CI]=1.2–10.0; >9 yrs: OR=4.6, CI=1.1–19.2) and pesticides (ever: OR=2.4, CI=1.1–5.6; >17.5 yrs: OR=2.4, CI=0.8–7.0). Risk also was elevated among dry cleaning workers (ever: OR=1.8, CI=1.1–3.0; >1.125 yrs: OR=2.9, CI=1.5–5.4). Occupational risks for lung cancer among women merit further study.Drs Brownson and Chang are with the Missouri Department of Health, Columbia, MO, USA. Dr Alavanja is with the Epidemiology and Biostatistics Program, National Cancer Institute, Rockville, MD, USA. Dr Chang directs the Missouri Cancer Registry with the Missouri Department of Health. Address correspondence to Dr Brownson, Division of Chronic Disease Prevention and Health Promotion, Missouri Department of Health, 201 Business Loop 70 West, Columbia, MO 65203, USA. This study was supported in part by US National Cancer Institute contracts NO1-CP7-1096-01 and NO1-CP7-1096-02.     

Prostate cancer and prediagnostic levels of serum vitamin D metabolites (Maryland,United States)

An hypothesis has been forwarded linking prostate cancer to low serum levels of vitamin D metabolites. We sought to test this hypothesis using sera obtained in a large, prospective cohort study. A serum bank in Washington County, Maryland (United States) has stored sera obtained from 20,305 county residents during a blood collection campaign undertaken in August through November 1974. We studied sera obtained from 61 residents who were diagnosed with prostate cancer during the period 1980 through 1992. Each prostate cancer case was matched to two controls on age (±1 yr) and race. Controls had donated blood in the same blood-collection campaign and had not been diagnosed with prostate cancer through 1992. Serum levels of vitamin D metabolites did not differ significantly between cases and controls. Mean 25-hydroxyvitamin D (25-D) levels were 34.3 ng/ml and 33.2 ng/ml, and mean 1,25-dihydroxyvitamin D (1,25-D) levels were 41.0 pg/ml and 40.1 pg/ml, in cases and controls, respectively. No statistically significant trends or differences between cases and controls were found in an analysis by quintile of serum level. We also did not observe the association of vitamin D metabolites with prostate cancer to be strongest among older men with more severe disease, as previously has been reported. In summary, although our study's power was limited, our findings provide little support for the hypothesis that vitamin D metabolite levels are associated strongly with subsequent risk for prostate cancer.Dr Braun is with the Epidemiology and Biostatistics Program, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA. Authors are also affiliated with the Department of Epidemiology, Johns Hopkins University School of Hygiene and Public Health, Baltimore, MD, USA (Drs Helzlsouer and Comstock), and the Department of Pediatrics, Medical University of South Carolina, Charleston, SC, USA (Dr Hollis). Address correspondence to Dr Braun, Epidemiology and Biostatistics Program, National Cancer Institute, EPN 443, Bethesda, MD 20892-7374, USA.