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Abstract Reprints
1. Comparison of birth weight distributions between Chinese and Caucasian infants Shi Wu Wen, Michael S Kramer, Robert H Usher To assess the reasons for the Chinese-Caucasian differences in birth weight distributions, a cohort study was carried out involving 18,665 Caucasian and 1,597 immigrant Chinese infants born at Montreal's Royal Victoria Hospital from January 1978 to March 1990 and 1,862 native Chinese infants born at Hefei Maternal and Infant Hospital in Hefei, People's Republic of China, from September 1990 to August 1991. Mean (standard deviation) birth weights in grams were 3,369 (567), 3,195 (493), and 3,171 (428) (p < 0.01 for differences in mean and variance), and mean (standard deviation) fetal growth ratios (ratio of observed birth weight to average birth weight at the same gestational age) were 0.994 (0.124), 0.963 (0.114), and 0.935 (0.112) (p < 0.01 for differences in mean and variance), respectively, in the Caucasian, immigrant Chinese, and native Chinese groups. No important or consistent Chinese-Caucasian differences in gestational age were found. When mothers with extreme values for demographic, anthropometric, nutritional, and lifestyle determinants of fetal growth were excluded, the mean fetal growth ratio in Caucasian infants remained significantly higher (p < 0.01), but the standard deviations became more similar (p > 0.05): Mean (standard deviation) fetal growth ratios were 1.001 (0.111), 0.966 (0.108), and 0.946 (0.114), respectively. The race-specific rate of growth differed according to period of gestation, with Chinese infants showing more rapid fetal growth early in the third trimester but slower growth near and after term. The authors conclude that the lower mean birth weight in Chinese infants is due to differences in fetal growth (rather than gestational duration) and by their inherently slower growth at or after term. The tight distribution of birth weight among the Chinese is caused partly by their reduced exposure to extremes of maternal determinants of fetal growth (mediated largely by environmental mechanisms) and partly by their inherently different growth pattern, with faster growth at earlier gestations but slower growth at later gestations.
PB English, M Kharrazi Despite their more unfavorable socio-demographic profile (i.e., lower income, lower education, less prenatal care), Mexico-born Mexican-Americans have been observed to have lower rates of low birth weight (LBW) and infant mortality than non-Hispanic whites. It has been postulated that a Mexican cultural identification, along with better health behaviors, such as a lower rate of smoking during pregnancy and better nutrition, may explain this advantage. The authors conducted a population-based study of singleton infants from 1992 live birth records and supplemental questionnaires (administered to mothers around the time of birth) in four central California counties to examine factors that might explain differences in birth weight and gestational age. Although infants of Mexico-born Mexican Americans (n=2538) were of lower mean birth weight than infants of non-Hispanic whites (n=3538) (3415 grams [g] vs. 3444 g, p=0.03), they had a smaller birth weight distribution standard deviation (525 g vs. 536 g: coefficient of variation = 15.4 vs. 15.6) and fewer LBW births (<2500 g) (3.8% vs. 4.4%, p=0.26). An analysis of birth weight/gestational age categories showed that all of the advantages enjoyed by Mexico-born Mexican-American infants over whites was in the moderately LBW categories (1500-2499 g, both preterm and term; Odds Ratio (OR)=0.83, 95% confidence interval (C.I.)=0.63, 1.10). After adjusting for maternal age, education, parity, body mass index, prenatal care, and smoking during pregnancy in a logistic regression model, the advantage seen by the Mexico-born Mexican Americans disappeared (OR=1.06, 95% C.I.=0.70, 1.62).
3. The influence of maternal nativity on birth weight N Hessol, E Fuentes-Afflick Among ethnic minorities in the United States, abnormal birth weights are reportedly less common among babies delivered by foreign-born as compared to U.S.-born mothers. This study assessed the risk of low birth weight (LBW, 1500-2499 g), very low birth weight (VLBW, 1000-1499 g), and heavy birth weight (HBW, >4000 g) associated with maternal nativity and race/ethnicity. Using 1992 California birth certificate data, and restricting the analysis to 588,867 singleton births, LBW, VLBW, and HBW babies were compared in separate multiple logistic regression analyses to babies of normal birth weight (2500-4000 g), adjusting for known sociodemographic and medical risk factors. The sample was 8% African American, 6% Asian, 44% Latina/Hispanic, 3% Pacific Islander, 38% white, and <1% other. Adjusting for maternal race and other known risk factors, foreign-born mothers had a decreased risk of LBW (odds ratio (OR)=0.79, 95% confidence interval (CI) 0.76-0.83), of VLBW (OR=0.84, 95% CI 0.75-0.95), and of HBW (OR=0.95, 95% CI 0.93-0.98). Race-specific analyses found that foreign-born African Americans and Latinas had a decreased risk of LBW, foreign-born whites had a decreased risk of HBW, and foreign-born African Americans and Pacific Islanders had an increased risk of HBW. Although immigrants are often economically disadvantaged, poorly educated, and medically underserved, foreign-born mothers in California have a decreased risk of abnormal birth weight outcomes. However this risk varies across racial/ethnic groups. Understanding why foreign-born mothers have better birth weight outcomes than U.S.-born mothers needs additional study.
4. Periconceptional vitamin use, dietary folate, and the occurrence of neural tube defects Gary M Shaw, Donna Schaffer, Ellen M Velie, Kimberly Morland, John
A Harris With a case-control study, we investigated whether periconceptional intake of supplemental or dietary folate reduced the risk of having a neural tube defect (NTD)-affected pregnancy. Mothers of 549 (88% of eligible) cases and 540 (88%) controls were interviewed in person about vitamin supplements used in either the 3 months before or the 3 months after conception and also about usual diet in the 3 months before conception. Women with any use of a folic acid-containing vitamin in the 3 months before conception had a lower risk of having an NTD-affected pregnancy [odds ratio (OR) = 0.65; 95% confidence interval (CI) = 0.45-0.94]. ORs were similar for 3 levels ( < 0.4, 0.4-0.9, and > 0.9 mg per day) of average daily intake of folic acid. Any level of use in the first 3 months after conception resulted in a lowered risk as well (OR = 0.60; 95% CI = 0.46-0.79). Reduced risks were less marked for Hispanics and were not observed among women who graduated from college. Modest reduced risks were noted among non-vitamin users whose estimated daily dietary intake of folate was more than 0.227 mg. We observed decreasing risk with increasing folate intake from combined dietary sources and vitamin supplements. A reduction in NTD risk associated with folate intake is consistent with other studies; however, the reduced risk may be particular to subsets of the population, primarily non-Hispanic women and women whose education does not exceed high school.
5. Prostate cancer and prediagnostic levels of serum vitamin D metabolites (Maryland, United States) M Miles Braun, Kathy J Helzlsouer, Bruce W Hollis, George W Comstock
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.
6. Dietary factors and risk of prostate cancer: a case-control study in Ontario, Canada Thomas E Rohan, Geoffrey R Howe, J David Burch, Meera Jain The relationship between risk of prostate cancer and dietary intake of energy, fat, vitamin A, and other nutrients was investigated in a case-control study conducted in Ontario, Canada. Cases were men with a recent, histologically confirmed diagnosis of adenocarcinoma of the prostate notified to the Ontario Cancer Registry between April 1990 and April 1992. Controls were selected randomly from assessment lists maintained by the Ontario Ministry of Revenue, and were frequency-matched to the cases on age. The study included 207 cases (51.4 percent of those eligible) and 207 controls (39.4 percent of those eligible), and information on dietary intake was collected from them by means of a quantitative diet history. There was a positive association between energy intake and risk of prostate cancer, such that men at the uppermost quartile level of energy intake had a 75 percent increase in risk. In contrast, there was no clear association between the non-energy effects of total fat and monounsaturated fat intake and prostate cancer risk. There was some evidence for an inverse association with saturated fat intake, although the dose-response pattern was irregular. There was a weak (statistically nonsignificant) positive association between polyunsaturated fat intake and risk of prostate cancer. Relatively high levels of retinol intake were associated with reduced risk, but there was essentially no association between dietary, b-carotene intake and risk. There was no alteration in risk in association with dietary fiber, cholesterol, and vitamins C and E. Although these patterns were evident both overall and within age-strata, and persisted after adjustment for a number of potential confounding factors, they could reflect (in particular) the effect of nonrespondent bias.
7. Prostate cancer screening (United States) John W Waterbor, Anton J Bueschen In 1995, there will be 244,000 new cases of prostate cancer, and 40,400 deaths from prostate cancer, among men in the United States. The American Cancer Society reports that the incidence rate of prostate cancer is increasing at an accelerated pace, and was 21 percent higher in 1994 than in 1993. The major reason for this steep rise is likely to be due to increased popularity of prostate cancer screening which, by identifying latent, asymptomatic cases, may convert them into clinical cases. Is screening-an important means of cancer control for many sites-a reasonable approach for prostate cancer control? The answer is not straightforward because prostate cancer is not one, but three diseases: a latent form which will cause no harm; a progressive form which will become symptomatic and can kill; and a rapidly progressive form so malignant that it is likely to kill, whether detected early or late. Screen-detection may be worthwhile only for the second form, as tumors of the first form need never be detected, and tumors of the third form progress so rapidly that timely screen-detection is nearly impossible and, if accomplished, may be valueless. As there is no way to differentiate among the three diseases when screening, the possible deleterious effects of screen-detection must be weighed against the benefits.
Alice S Whittemore, Anna H Wu, Laurence N Kolonel, Esther M John,
Richard P Gallagher, Geoffrey R Howe, Dee W West, Chong-Ze Teh, Thomas
Stamey Increased risk of prostate cancer in men with a family history of the disease has been observed consistently in epidemiologic studies. However, most studies have been confined to white men; little is known about familial aggregation of prostate cancer in populations with unusually high incidence, such as African Americans, or in populations with low incidence, such as Asian-Americans. The authors report results from a population-based case-control study of prostate cancer among blacks, whites, and Asian-Americans in the United States and Canada. Controls were matched to cases on age (5-year groups), ethnicity (black, white, Chinese-American, Japanese-American), and region of residence (Los Angeles, San Francisco, Hawaii, Vancouver, Toronto). In the combined group of participants, 5% of controls and 13% of cases reported a father, brother, or son with prostate cancer. These prevalences were somewhat lower among Asian-Americans than among blacks or whites. A positive family history was associated with a statistically significant two-to threefold increase in risk in each of the three ethnic groups. The overall odds ratio associated with such a family history, adjusted for age and ethnicity, was 2.5 (95% confidence interval 1.9-3.3). This odds ratio varied by neither ethnicity nor age of the participants. Sera from 1,087 controls were used to examine the relations between family history and serum concentrations of androgens and prostate-specific antigen. The concentrations of sex hormone-binding globulin were slightly higher in men with than without a positive family history. Prostate-specific antigen concentrations were unrelated to family history. 9. Vasectomy and prostate cancer: results from a multiethnic case-control study Esther M John, Alice S Whittemore, Anna H Wu, Laurence N Kolonel,
T Gregory Hislop, Geoffrey R Howe, Dee W West, Jean Hankin, Darlene M
Dreon, Chong-Ze Teh, J David Burch, Ralph S Paffenbarger Background: Vasectomy, a widely used form of contraception, has been associated in some studies with increased prostate cancer risk. Purpose: We assessed this association on the basis of data collected in a large multiethnic case-control study of prostate cancer that was conducted in the United States (Los Angeles, San Francisco, and Hawaii) and Canada (Toronto and Vancouver). Methods: In home interviews conducted with newly diagnosed prostate cancer case patients and population control subjects, we obtained information on the participants' medical history, including a history of vasectomy and the age at which the procedure was performed, as well as other potential risk factors. Blood samples were collected from control subjects only and were assayed for concentration of sex hormones and sex hormone-binding globulin. Results: The present analysis was based on 1642 prostate cancer patients and 1636 control subjects. A history of vasectomy was not significantly associated with prostate cancer risk among all racial/ethnic groups combined (odds ratio [OR] = 1.1; 95% confidence interval [CI] = 0.83-1.3), whites (OR = 0.94; 95% CI = 0.69-1.3), blacks (OR = 1.0; 95% CI = 0.59-1.8), or Chinese-Americans (OR = 0.96; 95% CI = 0.42-2.2). Among Japanese-Americans, the OR was 1.8 (95% CI = 0.97-3.4), but the statistically nonsignificant elevation in risk was limited to more educated men and those with localized cancers. ORs did not vary significantly by age at vasectomy or years since vasectomy. We found a lower serum concentration of sex hormone-binding globulin and a higher ratio of dihydrotestosterone to testosterone among vasectomized control subjects than among nonvasectomized control subjects. Conclusions: The findings of this study do not support previous reports of increased prostate cancer risk associated with vasectomy. However, the altered endocrine profiles of vasectomized control subjects seen in this cross-sectional comparison warrant further evaluation in longitudinal studies.
Alice S Whittemore, Laurence N Kolonel, Anna H Wu, Esther M John,
Richard P Gallagher, Geoffrey R Howe, J David Burch, Jean Hankin, Darlene
M Dreon, Dee W West, Chong-Ze Teh, Ralph S Paffenbarger Background: International and interethnic differences in prostate cancer incidence suggest an environmental, potentially modifiable etiology for the disease. Purpose: We conducted a population-based case-control study of prostate cancer among blacks (very high risk), whites (high risk), and Asian-Americans (low risk) in Los Angeles, San Francisco, Hawaii, Vancouver, and Toronto. Our aim was to evaluate the roles of diet, physical activity patterns, body size, and migration characteristics on risk in these ethnic groups and to assess how much of the interethnic differences in risk might be attributed to interethnic differences in such lifestyle characteristics. Methods: We used a common protocol and questionnaire to administer personal interviews to 1655 black, white, Chinese-American, and Japanese-American case patients diagnosed during 1987-1991 with histologically confirmed prostate carcinoma and to 1645 population-based control subjects matched to case patients by age, ethnicity, and region of residence. Sera collected from 1127 control subjects were analyzed for levels of prostate-specific antigen (PSA) to permit comparison of case patients with control subjects lacking serological evidence of prostate disease. Odds ratios were estimated using conditional logistic regression. We estimated the proportion of prostate cancer attributable to certain risk factors and the proportion of interethnic risk differences attributable to interethnic differences in risk-factor prevalence. Results: A positive statistically significant association of prostate cancer risk and total fat intake was found for all ethnic groups combined. This association was attributable to energy from saturated fats; after adjusting for saturated fat, risk was associated only weakly with monounsaturated fat and was unrelated to protein, carbohydrate, polyunsaturated fat, and total food energy. Saturated fat intake was associated with higher risks for Asian-Americans than for blacks and whites. In all ethnic groups combined, the risk tended to be higher when only case patients with advanced disease were compared with control subjects with normal PSA levels. Among foreign-born Asian-Americans, risk increased independently with years of residence in North America and with saturated fat intake. Crude estimates suggest that differences in saturated fat intake account for about 10% of black-white differences and about 15% of white-Asian-American differences in prostate cancer incidence. Risk was not consistently associated with intake of any micronutrients, body mass, or physical activity patterns. Conclusions: These data support a causal role in prostate cancer for saturated fat intake but suggest that other factors are largely responsible for interethnic differences in risk.
Xiao Ou Shu, Mark E Nesbit, Jonathan D Buckley, Mark D Krailo, Leslie
L Robison A study of 105 patients with childhood malignant germ-cell tumors (MGCT) and 639 community controls was conducted utilizing a large epidemiologic database collected by the Childrens Cancer Group from 25 member institutions in the United States and Canada. This study was designed to explore the risk factors of this malignancy whose etiology remains poorly understood. A structured, self-administered questionnaire was used to collect exposure information, and data were analyzed using an unconditional logistic regression model with adjustment for relevant confounders. Consistent with the findings from studies of adult MGCT, gestational age was associated inversely with risk of MGCT, with a 70 to 75 percent reduction in risk for children born at term compared with those born pre-term. Parental, particularly maternal, self-reported exposure to chemicals or solvents (odds ratio [OR] = 4.6, 95 percent confidence interval [CI] = 1.9-11.3 and OR = 2.2, CI = 1.1-4.7 for maternal and paternal exposure, respectively) and plastic or resin fumes (OR = 12.0, CI = 1.9-75.0 [maternal] and OR = 2.5, CI = 1.0-6.5 [paternal]) were associated with elevated risk of MGCT. New findings, not reported previously, include a positive relationship of MGCT risk with birthweight and prolonged breastfeeding, an inverse association between MGCT risk and number of cigarettes smoked by the mother during pregnancy, and a 3.1-fold increased risk (CI = 1.5-6.6) associated with maternal urinary infections during index pregnancy. Although these findings need confirmation from future studies, they suggest a potential influence of in utero exposure to maternal endogenous hormones, parental environmental exposures, and maternal diseases during pregnancy in the development of childhood MGCT.
12. Health care utilization and disability of migraine: The Ontario Health Survey Teresa To, Keyi Wu Objective: To measure the prevalence of migraine, associated functional disabilities, use of medications and visits to physicians. Design: 135,062 migraineurs in Ontario were estimated from the Ontario Health Survey (OHS). The population demographics, use of medications and visits to physicians were compared with these measures in individuals without migraine. Results: The prevalence of migraine was estimated at 1.4% in Ontario. The migraineurs were heavy users of both prescription and non prescription drugs (98.0%). They were heavier users of pain relievers than the comparison group (91.2% versus 58.2%, p<0.0000). According to the two-week disability reports, 11% of them were bedridden for an average of 1.6 days and 9.3% were restricted from normal activities for an average of 2.4 days because of migraine. Conclusions: Severe migraine headaches may result in a $31 million loss in productivity and $2 million in hospitalization costs. The findings of this study highlight both the medical and financial impact of migraine on the individual and the health care systems.
Richard T Burnett, Robert Dales, Daniel Krewski, Renaud Vincent, Tom
Dann, Jeffrey R Brook The association of daily cardiac and respiratory admissions to 168 acute care hospitals in Ontario, Canada, with daily levels of particulate sulfates was examined over the 6-year period 1983-1988. Sulfate levels were recorded at nine monitoring stations in regions of southern and central Ontario spanned by three monitoring networks. A 13-mg/m 3 increase in sulfates recorded on the day prior to admission (the 95th percentile) was associated with a 3.7% (p < 0.0001) increase in respiratory admissions and a 2.8% (p < 0.0001) increase in cardiac admissions. Increases were observed for all age groups examined. Admissions for cardiac diseases increased 2.5% for those under 65 years and 3.5% for those 65 years and older. After adjusting for ambient temperature and ozone, similar increases in respiratory admissions were observed in the period from April to September (3.2%) and in the period from October to March (2.8%). A 3.2% increase was observed for cardiac admissions in the period from April to September, and a 3.4% increase was observed in the period from October to March after adjusting for ambient temperature and ozone.
14. Lung cancer in radon-exposed miners and estimation of risk from indoor exposure Jay H Lubin, John D Boice Jr, Christer Edling, Richard W Hornung,
Geoffrey R Howe, Emil Kunz, Robert A Kusiak, Howard I Morrison, Edward
P Radford, Jonathan M Samet, Margot Tirmarche, Alistair Woodward, Shu
Xiang Yao, Donald A Pierce Background: Radioactive radon is an inert gas that can migrate from soils and rocks and accumulate in enclosed areas, such as homes and underground mines. Studies of miners show that exposure to radon decay products causes lung cancer. Consequently, it is of public health interest to estimate accurately the consequences of daily, low-level exposure in homes to this known carcinogen. Epidemiologic studies of residential radon exposure are burdened by an inability to estimate exposure accurately, low total exposure, and subsequent small excess risks. As a result, the studies have been inconclusive to date. Estimates of the hazard posed by residential radon have been based on analyses of data on miners, with recent estimates based on a pooling of four occupational cohort studies of miners, including 360 lung cancer deaths. Purpose: To more fully describe the lung cancer risk in radon-exposed miners, we pooled original data from 11 studies of radon-exposed underground miners, conducted a comprehensive analysis, and developed models for estimating radon-associated lung cancer risk. Methods: We pooled original data from 11 cohort studies of radon-exposed underground miners, including 65 000 men and more than 2700 lung cancer deaths, and fit various relative risk (RR) regression models. Results: The RR relationship for cumulative radon progeny exposure was consistently linear in the range of miner exposures, suggesting that exposures at lower levels, such as in homes, would carry some risk. The exposure-response trend for never-smokers was threefold the trend for smokers, indicating a greater RR for exposure in never-smokers. The RR from exposure diminished with time since the exposure occurred. For equal total exposure, exposures of long duration (and low rate) were more harmful than exposures of short duration (and high rate). Conclusions: In the miners, about 40% of all lung cancer deaths may be due to radon progeny exposure, 70% of lung cancer deaths in never-smokers, and 39% of lung cancer deaths in smokers. In the United States, 10% of all lung cancer deaths might be due to indoor radon exposure, 11% of lung cancer deaths in smokers, and 30% of lung cancer deaths in never-smokers. This risk model estimates that reducing radon in all homes exceeding the U. S. Environmental Protection Agency's recommended action level may reduce lung cancer deaths about 2%-4%. These estimates should be interpreted with caution, because concomitant exposures of miners to agents such as arsenic or diesel exhaust may modify the radon effect and, when considered together with other differences between homes and mines, might reduce the generalizability of findings in miners.
Jack Siemiatycki, Daniel Krewski, Eduardo Franco, Murray Kaiserman
Background. Although the effects of cigarette smoking on cancer risk have been well documented, there remain several outstanding issues to be clarified, including the determination of which types of cancer are associated with smoking and estimation of the magnitude of the effect of smoking on different types of cancer. A further issue is whether the effects seen elsewhere can be demonstrated in Canada, where tobacco products differ somewhat from those in other countries. Methods. A case-control study was undertaken in Montreal to investigate the associations between a large number of environmental and occupational exposures on the one hand, and several types of cancer on the other. Between 1979 and 1985, interviews were carried out with incident male cases of 21 types of cancer, including 15 anatomical sites and six histological subtypes. The interview was designed to obtain detailed information on smoking histories, job histories, and other potential confounders. Altogether, 3730 cancer patients and 533 population controls were interviewed. For each type of cancer analyzed, two control groups were used: population controls and cancer controls (selected from among other cancer patients). The purpose of the present analysis is to estimate the relative risk of each of 21 types of cancer in relation to smoking and to estimate the percentage of cancer cases attributable to cigarette smoking. Results. Separate analyses conducted with the two control groups produced similar results. Of the many sites of cancer examined, the following were not associated with cigarette smoking: colon, rectum, liver, prostate, kidney and skin (melanoma). Within the lymphoreticular system, there was no excess risk of Hodgkin's lymphoma, although the results for non-Hodgkin's lymphoma were weakly suggestive of an association with smoking. The following sites were clearly associated with smoking: lung (odds ratio [OR] = 12.1), bladder (OR = 2.4), oesophagus (OR = 2.4), stomach (OR = 1.7), and pancreas (OR = 1.6). Population attributable risk percentages due to smoking were 90% for lung, 53% for bladder, 54% for oesophagus, 35% for stomach, and 33% for pancreas. Conclusions. Of the 21 types of cancer examined, the following were associated with smoking among men in Montreal: lung (including all major histological subtypes), bladder (and its main histological subtypes), oesophagus, stomach and pancreas. Smoking likely accounts for a large proportion of cancers occurring at these sites.
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