Racial and ethnic differences in access to medical care.

The authors' review of the health services literature since the release of the landmark Report of the Secretary's Task Force Report of Black and Minority Health in 1985 revealed significant differences in access to medical care by race and ethnicity within certain disease categories and types of health services. The differences are not explained by such factors as socioeconomic status (SES), insurance coverage, stage or severity of disease, comorbidities, type and availability of health care services, and patient preferences. Under certain circumstances when important variables are controlled, racial and ethnic disparities in access are reduced and may disappear. Nonetheless, the literature shows that racial and ethnic disparities persist in significant measure for several disease categories and service types. The complex challenge facing current and future researchers is to understand the basis for such disparities and to determine why disparities are apparent in some but not other disease categories and service types.

Genetic epidemiologic methods to screen for matrilineal inheritance in mitochondrial disorders.

We propose a method to screen for the matrilineal inheritance in mitochondrial disorders by comparing the risk of disease in a person whose mother is affected or whose maternal grandmother or aunt or uncle is affected to the risk of disease in a person whose father is affected or whose paternal grandmother or aunt or uncle is affected using a modification of the reconstructed cohort design. Sampling of pedigrees is accomplished via probands and must not be influenced by family history. The cohort of the proband's offspring, and offspring of the proband's siblings, can be analyzed using survival analysis. Cox proportional hazards model, Bonney's [(1986) Biometrics 42:611-625] model, and Liang's [(1991) Genet Epidemiol 8:329-338] model. Mitochondrial transmission can be distinguished from X-linked transmission by examining sex-specific patterns of disease expression in matrilineally transmitted diseases. To illustrate our epidemiologic method, we apply our screening method to pedigrees of two disorders which have been proposed to have a mitochondrial DNA component to their inheritance.

Risk of childhood cancer for infants with birth defects. I. A record-linkage study, Atlanta, Georgia, 1968-1988.

To evaluate the risk of childhood cancer among infants with serious birth defects, the authors linked records of the population-based registry of the Georgia Center for Cancer Statistics for 1975 to 1988 with records of the population-based Metropolitan Atlanta Congenital Defects Program for 1968 to 1987. During the study period, birth defects were diagnosed in 19,373 infants younger than 1 year of age, and cancer was diagnosed in 400 children younger than 15 years of age. The observed number of children with a defect who developed cancer was compared with the number expected on the basis of the cancer registry rates. Of the 19,373 children with birth defects, 31 developed cancer (standardized incidence ratio (SIR) = 2.2, 95% confidence interval (CI) 1.5-3.2). Two associations were found: of 532 children with Down's syndrome (trisomy 21), three developed acute leukemia (SIR = 50.8, 95% CI 10.5-148.5) while of 746 children with pyloric stenosis, four developed cancer (SIR = 7.5, 95% CI 2.0-19.3). These data show that children with selected birth defects are at increased risk for specific childhood cancers. Such record-linkage can reveal new associations, which can in turn help researchers understand underlying mechanisms common to teratogenesis and carcinogenesis.

Risk of childhood cancer for infants with birth defects. II. A record-linkage study, Iowa, 1983-1989.

To attempt to confirm associations found in a companion study in Atlanta, Georgia between Down's syndrome and acute leukemia and between pyloric stenosis and childhood cancer, the authors used the State Health Registry of Iowa to link the records of infants and children with cancer for 1983 to 1989 with the records of infants with birth defects for 1983 to 1988. During the study period, birth defects were diagnosed in 10,891 infants younger than 1 year of age, and cancer was diagnosed in 396 children younger than 8 years of age. The authors compared the observed number of children with a defect who developed cancer with the number expected on the basis of the cancer registry rates. Of the 10,891 children with birth defects, 16 developed cancer (standardized incidence ratio (SIR) = 2.0, 95% confidence interval (CI) 1.2-3.3). Of 251 children with Down's syndrome (trisomy 21), two developed leukemia (SIR = 32.1, 95% CI 3.9-116.0). None of the infants with cancer had pyloric stenosis (SIR = 0.0, 95% CI 0.0-6.7). The results of this study supported the association found in the Atlanta study between Down's syndrome and leukemia, but did not support the association found there between pyloric stenosis and childhood cancer. This study, however, had a shorter follow-up period and a smaller number of subjects than the Atlanta study.

The associations of alcohol drinking and drinking cessation to measures of the immune system in middle-aged men.

To estimate the association between the immunologic responses of the cell-mediated and humoral systems and alcohol drinking, we used data from the Vietnam Experience Study conducted by the Centers for Disease Control. That study, conducted from 1985 to 1986, was based on a random sample of 4462 male, Vietnam-era, U.S. veterans. By using linear regression, we evaluated how (1) the number of alcoholic drinks the subjects consumed per month and (2) the drinking cessation of certain subjects were associated with their relative and absolute T, B, CD4, and CD8 lymphocyte counts and immunoglobulin A (IgA), IgM, and IgG levels. We used geometric means and percentage differences in geometric means of immune status to measure the associations and adjusted these values to account for the effect of covariates. The results indicated that measures of immune status differed among the drinking categories and that, generally, the differences changed after adjustment for covariates. These differences consisted, as alcohol consumption increased, of higher IgA and IgM levels, relative T and CD4 lymphocytes, and the ratio of CD4 to CD8 cells, and of lower IgG levels, relative B and CD8 lymphocytes, absolute lymphocyte, and lymphocyte subset counts after adjusting for other covariates. Among former drinkers, we found no clear-cut pattern in measures of immunity for a few years after cessation and then found that values of former drinkers tended to return toward values of nondrinkers as they continued to abstain.

Prevalence of birth defects among low-birth-weight infants. A population study.

Major birth defects are diagnosed in about 3% to 4% of infants during their first year of life. Because many infants with birth defects have intrauterine growth retardation, are born prematurely, or both, the rate of birth defects undoubtedly varies according to the infant's birth weight. Nevertheless, the magnitude of such variation has not, to our knowledge, been adequately studied in well-defined populations. We analyzed data from the population-based Metropolitan Atlanta (Ga) Congenital Defects Program for 1978 through 1988. These data included information on 11,398 infants who were diagnosed with serious birth defects among 317,499 singleton live-born infants. Although the overall rate of birth defects was 3.6%, we observed a striking inverse relationship between the birth defects rate and the infants' birth weights. The birth defect rates were 16.2% for newborns weighing less than 1500 g at birth, 13.2% for newborns weighing from 1500 g to 1999 g, 6.2% for newborns weighing from 2000 g to 2499 g, 3.2% for newborns weighing from 2500 g to 3999 g, and 2.8% for newborns weighing 4000 g or more. Analyses by type of defect indicated that most birth defects were significantly associated with low birth weight. The higher risk of birth defects among low-birth-weight infants demonstrates that birth defects contribute to excess morbidity among low-birth-weight infants. Because of the overlap between birth defects and low birth weight, the prevention of low birth weight in the population depends greatly on a better recognition of the complex etiology of low birth weight and, in part, on the delineation of risk factors that influence the occurrence of birth defects.

The associations of race, cigarette smoking, and smoking cessation to measures of the immune system in middle-aged men.

To estimate the association between the immunologic responses of the cell-mediated and humoral systems and race or tobacco smoking, we used data from the Vietnam Experience Study conducted by the Centers for Disease Control. That study, done from 1985 to 1986, was based on a random sample of 4462 male, Vietnam-era, U.S. veterans. Racial groups were white, black, Hispanic, Asian, and American Indian. We used linear regression to evaluate how (i) the race of the subjects, (ii) the number of pack-years of cigarettes the subjects smoked, and (iii) the smoking cessation of certain subjects were associated with their relative and absolute T, B, CD4, and CD8 lymphocyte counts and immunoglobulin A (IgA), IgM, and IgG levels. The results indicated that immune status was associated with race and smoking history and that, generally, the associations remained after adjustment for covariates. For example, the average IgA level and absolute CD8 lymphocyte count for blacks were, respectively, 19 and 16% higher than those for whites. On the other hand, smokers had lower immunoglobulin levels and relative CD8 cell counts and higher counts for other lymphocytes of the cell-mediated system than nonsmokers. For example, the average absolute B count of heavy smokers was 37% higher than that of nonsmokers. The pattern after cigarette smoking cessation was consistent with a reversible effect of smoking and a return toward immune levels of nonsmokers.

The effect of environmental temperature on the rate of healing of fractures in tail vertebrae of mice.

The effect of the environmental temperature on the healing of fractures was assessed in vertebrae of tails of young albino mice. It was found that fractures in animals kept at 33 degrees Celsius healed very rapidly (bony callus by 14 days) while in animals kept in the cold (8 degrees Celsius) fractures were still at the stage of granulation tissue at this time. Controls were at an intermediate stage. This result might have a clinical application.