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Biomedical subjects

T D Sterling

Publications and source records attributed to T D Sterling.

At least 19 recordsLinked to original sources
PubMed1992

Computation of relative risk based on simultaneous surveys: an alternative to cohort and case-control studies.

If the same information on the distribution of risk factors is available for both the general population and a subset distinguished by some disease outcome, it becomes possible to derive relative risk estimates applicable to the entire population with the assurance that the data upon which the estimates are based is representative of that population. To illustrate this approach, data from the 1986 National Mortality Follow-back Survey and the 1987 National Health Interview Survey were used to compute rate ratios for several causes of death for work in dirtyier as compared with cleaner occupations by three methods commonly employed in cohort and case-control studies: the usual standardized rate ratio, the Mantel-Haenszel estimate of the rate ratio, and a multiplicative model fit to an appropriate cross-classification. Properly placed questions in appropriate surveys might very well serve as a substitute for cohort studies and could be performed at less cost and with less overall effort, and completed in a shorter time. Moreover, this approach is less subject to problems of representativeness than cohort and case-control studies.

Epidemiologic Methods↗
PubMed1992

Analysis of the relationship between smokeless tobacco and cancer based on data from the National Mortality Followback Survey.

This study investigates the potential link between the use of smokeless tobacco and oral cancer and cancer of digestive organs. The combined data of the National Mortality Followback Survey (NMFS), a probability sample of the U.S. deaths, and the coincident National Health Interview Survey (NHIS), a probability sample of the living, non-institutionalized U.S. population, are used to compute risk estimates for cancer, oral cancer, and cancer of the digestive organs associated with use of smokeless tobacco based on a cross sectional study design, simultaneously controlled for potential confounding from active smoking, alcohol consumption, and occupational exposure. Use of smokeless tobacco (either as snuff or chewing tobacco) does not increase the risk of oral cancer or cancer of the digestive organs. Alcohol emerges as a major risk factor for oral cancer with a strong dose-response relationship between the amount of drinking and risk. The same is true to a lesser extent for cancer of the digestive organs. Smoking is associated with increased risk of oral cancer but not of cancer of the digestive organs. Blue collar, technical, and service workers have significantly increased risk of cancer of the digestive organs relative to professional, managerial, and clerical workers, but not of oral cancer. Differences between findings based on the NMFS/NHIS and those obtained from other data very likely are due to inadequate control for confounding. Other reasons for differences between the NMFS/NHIS data and other studies are discussed.

Adult↗
PubMed1992

Bias in the attribution of lung cancer as cause of death and its possible consequences for calculating smoking-related risks.

Most published calculations of mortality risk, especially those for lung cancer associated with smoking, are based almost exclusively on the underlying cause as recorded on death certificates. Such risk calculations implicitly assume that the conditional probability of recording lung cancer as the underlying cause of death, given that it really is the underlying cause, is the same for all exposure groups. If these probabilities are not equal for all exposure groups, we call the resulting bias a cause of death attribution bias. We analyzed the 1986 National Mortality Followback Survey, a sample of 18,733 U.S. death certificates, and the 1954-1962 Dorn study, a follow-up study of approximately 250,000 holders of U.S. Veterans Life Insurance. Both data sets include information on the smoking habits of decedents and on the underlying and contributing causes of their deaths. We found that lung cancer as an underlying cause is recorded with a much smaller relative frequency if the decedent is known to be a never-smoker and with a much larger relative frequency when the decedent is known to be a smoker. On the other hand, lung cancer as a contributing cause is recorded with a much larger frequency if the decedent is known to be a never-smoker and with a much smaller frequency when the decedent is known to be a smoker. The reverse is true for cancers other than of the lung. There is no similar pattern related to smoking for other causes of death (specifically for myocardial infarction, other chronic ischemic heart disease, diabetes, or cerebrovascular disease).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1991

A practical approach to estimating the true effect of exposure despite imprecise exposure classification.

Accurate information on actual exposure to some possibly toxic agent usually is not available in long-term occupational studies. Any strategy for assigning exposure levels or categories necessarily results in misclassification, where some individuals classified as exposed have no real exposure and some individuals classified as not exposed have some exposure to the agent. Both misclassification errors serve to reduce the estimate of risk associated with exposure. The question arises, "How much does the true risk depart from the observed estimate given an assumed level of misclassification?" This paper quantifies the effect of such misclassification on several forms of standardized risk ratios. Our results express the true risk as a function of the apparent risk based on imprecise exposure classification and parameters representing the proportion of each of the groups that are correctly classified. In any practical situation, the apparent risk can be computed based on whatever classification scheme is being used. On the other hand, the proportions of the imprecisely classified groups actually exposed cannot. However, the investigator may have information or may make assumptions for likely ranges of values for these proportions. Given the apparent risk, estimated true risks can be calculated and plotted or represented in tabular form as a function of the proportions of actual exposure. The resulting graph or table enables the investigator to read off the range of possible true risk values based on what he is prepared to believe or what other information indicates about the range of proportions of misclassified subjects. For instance, results for a typical value of apparent risk of 1.8 show that the true risk may be twice the apparent risk with only 23% misclassification in each exposure group. The value of the true risk that would be necessary to be consistent with a given apparent risk increases rapidly as the extent of misclassification increases. We also show that, if the extent of misclassification is large, the apparent relative risk is close to 1.0 regardless of the actual value of the true risk. Therefore, a small apparent risk does not necessarily indicate that there is no occupational hazard.

Bias↗
PubMed1991

A graphical approach to the interpretation of age-period-cohort data.

Two major obstacles to the routine application of age-period-cohort models are (1) the identification problem, and (2) the fact that separate interpretation of the coefficients of the model is seldom possible. We offer a practical solution to these obstacles that involves plotting the relation between the variable of interest and the age, period, and cohort variables in such a manner that nontrivial age, period, or cohort effects are readily recognized as particular types of features in the graph. These features remain recognizable in the presence of normal sampling variability. Examples are given for applying the technique to previously published mortality data.

Age Factors↗
PubMed1991

[Epidemiology of "sick buildings"].

The indoor environment of modern buildings, especially those designed for commercial and administrative purposes, constitutes a unique ecological niche with its own biochemical environment, fauna and flora. Sophisticated construction methods and the new materials and machinery required to maintain the indoor environment of these enclosed structures produce a large number of chemical by-products and permit the growth of many different microorganisms. Because modern office buildings are sealed, the regulation of humidification and temperature of ducted air presents a dilemma, since difference species of microorganisms flourish at different combinations of humidity and temperature. If the indoor environment of modern office buildings is not properly maintained, the environment may become harmful to its occupants' health. Such buildings are classified as "Sick Buildings". A review of the epidemiology of building illness is presented. The etiology of occupant illnesses, sources of toxic substances, and possible methods of maintaining a safe indoor environment are described.

Absenteeism↗
PubMed1990

Age related changes in age of starting to smoke.

The Average Age of Starting to Smoke (AASS) has been reported to decline for younger birth cohorts. That apparent decline has been used to support a conclusion of an increase in smoking among younger individuals. However, in some cases the apparent decline is an artifact of the method of computation which arises when the quantity being averaged is related to a quantity used to classify subjects for comparison. In one other case, a second type of error arises because the distribution of smoking initiation with age changed in such a way that the proportion of individuals taking up smoking at older ages declined more rapidly than the proportion starting at younger ages. In fact, comparison of the 1970 National Health Interview Survey (NHIS) to the 1979/80 NHIS shows a uniform decrease in starting to smoke among teens and preteens. Examples are discussed which show that estimates of possible disease related factors actually experienced by a cohort are possible only if other suitable data are available for comparable representative sections of the population at different time periods and for different ages.

Adolescent↗
PubMed1990

The sick person effect.

Very often criteria by which subjects are selected for epidemiological studies are associated in some manner with their health. The Healthy Worker Effect (HWE) or Healthy Person Effect (HPE) is well known. Little has been said about the converse case in which selection is associated with decreased health status, the Sick Person Effect (SPE). The SPE may introduce a bias for some cohort, most clinical follow-up, and some case-control studies when risks are standardized against an inappropriate referent. We demonstrate the existence of the SPE in two studies. Study 1 compares the incidence of a number of different diseases among individuals who were selected as children for medical treatment with that among their siblings. Study 2 computes the Standardized Morbidity Ratios (SmRs) for various acute and chronic diseases for individuals who have reported particular chronic symptoms. The SPE is clearly apparent for all instances where the general population is taken as the referent. The HPE and SPE may present serious problems for the validity of conclusions with respect to risk levels.

Bias↗
PubMed1989

Comparison of smoking-related risk factors among black and white males.

The lung cancer risk factors of smoking prevalence, amount smoked, and age started to smoke were compared for blacks and whites, using the 1970 and 1979/80 National Health Interview Survey (NHIS) survey data. For both survey years, proportionally more blacks were never smokers and fewer were ever smokers (although more were current and fewer former smokers). The average adult black smoker smoked approximately 65% of the number of cigarettes smoked by the average white adult. Blacks started smoking later than whites for almost all occupational categories. Thus, it could be argued that whites had higher smoking-associated risk factors than did blacks. At the same time, a much greater proportion of blacks than whites were in the types of occupation where they would have been exposed to occupational hazards. The sharp rise in and the larger incidence of lung cancer among blacks compared to whites may not be due to differences in black and white smoking, but more likely are a reflection of occupational differences.

Black or African American↗
PubMed1989

Reanalysis of lung cancer mortality in a National Cancer Institute Study on "Mortality among industrial workers exposed to formaldehyde".

The analysis of an historical cohort study of mortality among individuals occupationally exposed to formaldehyde by Blair et al. (2) in 1986 failed to allow properly for the Healthy Worker Effect and to evaluate time integrated exposure and length of exposure simultaneously. In our reanalysis of the same data we find a risk for lung cancer, increasing with increasing cumulative exposure to formaldehyde.

Adult↗
PubMed1988

Concentrations of nicotine, RSP, CO and CO2 in nonsmoking areas of offices ventilated by air recirculated from smoking designated areas.

The exposure of nonsmokers to environmental tobacco smoke (ETS) when smoking is relegated to designated areas that are not separately ventilated is of considerable interest. Concentrations of nicotine, respirable suspended particles (RSP), carbon monoxide (CO), and carbon dioxide (CO2) were measured in offices under different conditions of smoking regulation: smoking prohibited; smoking prohibited areas receiving recirculated air from designated smoking areas; smoking and nonsmoking sections of these designated smoking areas. Nicotine was collected by pumping air for periods of 1-8 hr at 1 L/min through sampling tubes containing a styrene divinylbenzene copolymer. RSPs (5 micron cut-off) were measured using an optical side scattering instrument. CO was measured by a direct reading electrochemical analyzer and CO2 by colorimetric detector tubes. Detection of nicotine in nonsmoking office areas that received recirculated air from smoking designated areas required sampling times of 4 hr or more. Nicotine levels in such offices were approximately 1.0 micrograms/m3. RSP, CO and CO2 concentrations were approximately the same in these offices as compared to nonsmoking offices not exposed to recirculated air from smoking areas. Providing a designated but not separately ventilated smoking area appears to be effective in eliminating most components of ETS from nonsmoking office work areas.

Air Pollutants, Occupational↗
PubMed1988

Reanalysis of lung cancer mortality in a National Cancer Institute study on mortality among industrial workers exposed to formaldehyde.

The results of an historical cohort study of mortality among individuals occupationally exposed to formaldehyde were announced in 1986 by Blair et al (JNCI 1986; 76:1071-1084). The study was a joint undertaking of the National Cancer Institute and the Formaldehyde Institute, and concluded, ". . .this large multiplant cohort study provided little evidence to suggest that formaldehyde exposure affected the mortality experience of these industrial workers." However, there were concerns by a number of workers that the design and analysis of the study had possibly masked an existing occupational hazard. Analyzing time-integrated exposure to formaldehyde without simultaneously considering length of exposure and comparing mortality of formaldehyde workers to mortality of the general population could have masked an increase in cancer risks because of the healthy worker effect. A copy of the data of the study was obtained from the principal investigator and reanalyzed. We find a significantly increased risk for all cancers and for lung cancer as a function of cumulative exposure when workers with higher levels of exposure are compared with those with little or no exposure while simultaneously considering length of exposure. When the risk ratio (RR) for lung cancer at less than or equal to 0.1 ppm cumulative exposure (CX) is taken as 1.0, the lung cancer RR for CX of 0.1 to 0.5 ppm is 1.41 (1.20 to 1.66), the RR for CX of 0.5 to 2.0 ppm is 1.73 (1.42 to 2.11), and the RR for CX greater than or equal to 2.0 is 1.70 (1.32 to 2.18). Hourly workers have a significantly higher RR than salaried workers (RR = 1.58).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗