Biomedical subjects
K J Rothman
Publications and source records attributed to K J Rothman.
Incidence of pelvic inflammatory disease among women treated for gonorrhea or chlamydia.
BACKGROUND: No estimate exists of the incidence of pelvic inflammatory disease (PID) after the occurrence of a recent bout of sexually transmitted disease (STD). METHODS: We used a computerized data file of prescriptions and medical encounters from the Fallon Community Health Plan to estimate the incidence rate of pelvic inflammatory disease (PID) among women with a recently treated episode of gonorrhea or chlamydia (STD). First we identified women with presumed gonorrhea or chlamydia on the basis of a combination of diagnostic codes for cervicitis, vulvovaginitis or Bartholin's abscess, and a computer record of a prescription for doxycycline. We then followed these women to estimate the incidence rate of PID after their treatment for gonorrhea or chlamydia. We estimated the number of cases of pelvic inflammatory disease in this cohort by selecting all women with an International Classification of Diseases (ICD) code of 614.9 entered for either an outpatient or inpatient diagnosis. RESULTS: We estimated the overall risk of PID to be about 9% during the 1-year period following treatment for gonorrhea or chlamydia, with a steep rise in risk coming within the first 45 days. CONCLUSION: The risk of PID in the year after an episode of treated STD is high, but the highest period of risk is in the first few weeks. The shape of the risk curve indicates that some PID cases may result from treatment-resistant infections, or possibly from untreated reinfections.
Assessment of cellular telephone and other radio frequency exposure for epidemiologic research.
Epidemiologists are now embarking on the evaluation of the hypothesis that exposure to radio frequency energy from low-power wireless communication devices, such as portable cellular telephones, causes brain cancer and other adverse health outcomes. Even in the laboratory, exposures from radio frequency sources are difficult to quantify; their measurement in large populations for epidemiologic study is challenging. In this paper, we outline the nature and magnitude of these exposures and discuss the prospects for obtaining useful measures of exposure for epidemiologic research.
Utility of telephone company records for epidemiologic studies of cellular telephones.
We conducted a survey of over 5,000 telephone users who were customers of one large cellular telephone company covering four major geographical areas. Our primary goal was to assess the utility of ascertaining information on telephone use and type from telephone company records. We compared information from 3,949 respondents with corresponding data from company billing records. We found that 48% of the account holders were sole users, and 69% were the primary user, meaning that they accounted for at least 75% of the use. Respondent reports of amount of telephone use were highly correlated with data on the billing record (r = 0.74). Respondent reports of telephone type were similarly correlated with data from the manufacturer (r = 0.92). We also inquired about telephone holding patterns, since these have implications for exposure. Most users reported favoring one side of the head when using the telephone, but the side of the head used was not strongly associated with handedness.
Overall mortality of cellular telephone customers.
Unlike mobile cellular telephones, in which the antenna is not part of the handset, a portable cellular telephone exposes the user's head to radio frequency energy transmitted from the antenna. This exposure has prompted concerns about potential biological effects, including brain cancer. As a first step in a record-based mortality surveillance of cellular telephone customers, we report on overall mortality of a cohort of more than 250,000 portable and mobile telephone customers during 1994. We found age-specific rates to be similar for users of the two types of telephones. For customers with accounts at least 3 years old, the ratio of mortality rates in 1994 for portable telephone users, compared with mobile telephone users, was 0.86 (90% confidence interval = 0.47-1.53).
Teratogenicity of high vitamin A intake.
BACKGROUND: Studies in animals indicate that natural forms of vitamin A are teratogenic. Synthetic retinoids chemically similar to vitamin A cause birth defects in humans; as in animals, the defects appear to affect tissues derived from the cranial neural crest. METHODS: Between October 1984 and June 1987, we identified 22,748 pregnant women when they underwent screening either by measurement of maternal serum alpha-fetoprotein or by amniocentesis. Nurse interviewers obtained information on the women's diet, medications, and illnesses during the first trimester of pregnancy, as well as information on their family and medical history and exposure to environmental agents. We obtained information on the outcomes of pregnancy from the obstetricians who delivered the babies or from the women themselves. Of the 22,748 women, 339 had babies with birth defects; 121 of these babies had defects occurring in sites that originated in the cranial neural crest. RESULTS: For defects associated with cranial-neural-crest tissue, the ratio of the prevalence among the babies born to women who consumed more than 15,000 IU of preformed vitamin A per day from food and supplements to the prevalence among the babies whose mothers consumed 5000 IU or less per day was 3.5 (95 percent confidence interval, 1.7 to 7.3). For vitamin A from supplements alone, the ratio of the prevalence among the babies born to women who consumed more than 10,000 IU per day to that among the babies whose mothers consumed 5000 IU or less per day was 4.8 (95 percent confidence interval, 2.2 to 10.5). Using a smoothed regression curve, we found an apparent threshold near 10,000 IU per day of supplemental vitamin A. The increased frequency of defects was concentrated among the babies born to women who had consumed high levels of vitamin A before the seventh week of gestation. CONCLUSIONS: High dietary intake of preformed vitamin A appears to be teratogenic. Among the babies born to women who took more than 10,000 IU of preformed vitamin A per day in the form of supplements, we estimate that about 1 infant in 57 had a malformation attributable to the supplement.
Preschool physical activity level and change in body fatness in young children. The Framingham Children's Study.
This study examined the effect of preschool physical activity on the change in body fatness from preschool to first grade. The Framingham Children's Study, a longitudinal study of childhood cardiovascular risk behaviors, began in 1987 with the enrollment of 106 children aged 3-5 years and their parents. The present analyses include 97 healthy children with complete data from study entry into first grade. Physical activity was assessed twice yearly for 5 days with an electronic motion sensor. The authors estimated change in the child's level of body fat from preschool to first grade by using the slopes of triceps and subscapular skinfolds and body mass index. On average, active girls (i.e., those with above-median activity levels) gained 1.0 mm in their triceps skinfolds from baseline to first grade, while inactive girls gained 1.75 mm. Active boys lost an average of 0.75 mm in their triceps, while inactive boys gained 0.25 mm. When age, television viewing, energy intake, baseline triceps, and parents' body mass indices were controlled for, inactive preschoolers were 3.8 (95% confidence interval 1.4-10.6) times as likely as active preschoolers to have an increasing triceps slope during follow up (rather than a stable or decreasing slope). This relative risk estimate was slightly higher for children with more body fat at baseline. In this study, preschool-aged children with low levels of physical activity gained substantially more subcutaneous fat than did more active children.
Research and prevention priorities for alcohol carcinogenesis.
Research conducted during the last four decades has established that consumption of alcoholic beverages causes cancer. Etiologic research questions that remain relate to increases in risk at specific sites, the effects of various types of alcoholic beverages, the effect of various concentrations of alcohol, and the mechanism(s) of action, including possible interactions with other agents such as tobacco smoke. Prevention priorities for alcohol-related cancer depend on whether alcohol causes only the upper aerodigestive cancers or whether it also causes breast and possibly colon cancers. If alcohol causes aerodigestive cancers only, existing prevention programs to prevent alcohol abuse by heavy drinkers are sufficient. The possible small cancer risk faced by moderate drinkers may be more than offset by a decrease in the risk of cardiovascular death. On the other hand, if alcohol consumption increases the occurrence of breast cancer, a prevention program aimed at women who are at high risk for breast cancer is worth considering, but the risks must be weighed against the cardiovascular benefits for moderate drinkers.
The continuing unethical use of placebo controls.
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Ethics of a prostate cancer screening trial.
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. . . and the Journal's policies.
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Mortality among synthetic fiber workers exposed to glycerol polyglycidyl ether.
We studied mortality among 8,878 employees who worked at any time from 1965 to 1988 at a synthetic fibers plant in North Carolina that used a finishing agent containing glycerol polyglycidyl ether. Some glycidyl ethers are mutagenic and tumorigenic in laboratory animals. The main route of exposure to workers was inhalation of the spray mist, although there was also skin contact. We identified 553 deaths in the cohort and the standardized mortality ratio (SMR) from all causes of death combined was 0.80. For most causes of death, mortality rates in the cohort were similar to mortality rates in the U.S. population. Among categories with at least five observed deaths, the largest effect estimate was for cancer of the central nervous system (SMR = 1.77), and the SMR for lung cancer was 0.94. The cancer categories of central nervous system (brain) and "other" lymphopoietic cancers (lymphoma and myeloma) showed weak associations with duration of employment. In case-control analyses in which we utilized work history data to compute effect estimates by duration of exposure, we found no increased risk of lung cancer or brain cancer among employees with more than 5 years of exposure. Effect estimates for lymphoma and myeloma tended to increase with duration of exposure, although there were only seven deaths in this category and the effect estimates were very imprecise. To date, this study has identified no clear carcinogenic effect of glycerol polyglycidyl ether, but plausible induction periods have not yet elapsed. The cohort should continue to be monitored to obtain more precise estimates after moderate or long induction times.
Epidemiology of pelvic inflammatory disease.
The epidemiologic study of pelvic inflammatory disease (PID) is hindered by symptoms that differ substantially from case to case, and by a substantial number of "silent" cases with few or no symptoms. Demographic data indicate that PID is primarily a disease of the young. Race also appears to be a determinant, but whether for biologic or sociologic reasons is not known. Women who are not married face a greater risk for PID than married women. The majority of PID cases are associated with sexually transmitted diseases. Consistent with this finding is the pattern of risk factors related to sexual behavior: young age at first intercourse, high frequency of intercourse, and a large number of sexual partners all increase the risk of PID. On the other hand, barrier methods of contraception appear to reduce the risk of PID, as does oral contraception. Perhaps the best publicized risk factors for PID is another contraceptive, the intrauterine device (IUD). The increased risk of PID in IUD users appears to be confined to new users and women at high risk of sexually transmitted disease infection. Douching and cigarette smoking may also be associated with the development of PID, but the evidence is weak.
Cancer occurrence among workers exposed to acrylonitrile.
A MEDLINE search identified 12 published epidemiologic studies that have reported incidence or mortality experience among workers exposed to acrylonitrile. Many of the studies contain scanty descriptions of subject ascertainment, and most do not have good information on exposure assessment. Many also may have suffered from incomplete follow-up, as evinced by an overall deficit in the number of deaths observed, compared with the number expected from general population mortality rates. Such problems are not unique to studies on acrylonitrile, and to some extent they reflect the difficulties of conducting retrospective cohort studies. Despite these drawbacks, a simplified meta-analysis of the mortality experience reported for these cohorts revealed little evidence for carcinogenicity. Approximately the same number of cancer deaths was observed as was expected according to general population mortality rates (standardized mortality ratio 1.03, 90% confidence interval 0.92-1.15). The combined information from these studies is insufficient to support confidence about a lack of carcinogenicity at all sites. Nevertheless, despite the flaws in some of the individual studies, the summarized findings offer reassurance that workers exposed to acrylonitrile face no striking increases in mortality for all cancers or for respiratory cancer.
Journal policies on conflict of interest.
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Conflict of interest. The new McCarthyism in science.
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Methodologic frontiers in environmental epidemiology.
Environmental epidemiology comprises the epidemiologic study of those environmental factors that are outside the immediate control of the individual. Exposures of interest to environmental epidemiologists include air pollution, water pollution, occupational exposure to physical and chemical agents, as well as psychosocial elements of environmental concern. The main methodologic problem in environmental epidemiology is exposure assessment, a problem that extends through all of epidemiologic research but looms as a towering obstacle in environmental epidemiology. One of the most promising developments in improving exposure assessment in environmental epidemiology is to find exposure biomarkers, which could serve as built-in dosimeters that reflect the biologic footprint left behind by environmental exposures. Beyond exposure assessment, epidemiologists studying environmental exposures face the difficulty of studying small effects that may be distorted by confounding that eludes easy control. This challenge may prompt reliance on new study designs, such as two-stage designs in which exposure and disease information are collected in the first stage, and covariate information is collected on a subset of subjects in state two. While the analytic methods already available for environmental epidemiology are powerful, analytic methods for ecologic studies need further development. This workshop outlines the range of methodologic issues that environmental epidemiologists must address so that their work meets the goals set by scientists and society at large.