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A specially designed method for measuring infant mortality among families with subsequent siblings of sudden infant death syndrome (SIDS) victims in the state of Washington, 1969 to 1984, yielded results similar to those from an earlier study in Norway. In both studies the SIDS rates among siblings were substantially lower than prior estimates. The rate of SIDS in siblings of infants who died of SIDS did not differ significantly from the SIDS rate among control infants matched for maternal age and birth order. Total infant mortality rates in the two groups were virtually identical. From the data at hand, it appears that earlier estimates of the risk of SIDS in siblings were inflated and that parents of SIDS victims can be counseled accordingly.

During a 12-year period (1969 through 1980), 431 episodes of sudden infant death syndrome (SIDS) occurred in King County, Washington. Longitudinal analysis of these data confirms the inverse association of SIDS occurrence with maternal age, which has been reported repeatedly from previous cross-sectional analyses. Risk of SIDS increases with increasing birth order, but the inverse maternal age gradient remains constant within each birth-order category. Available evidence suggests that maternal age may be a more important clue to SIDS causation than previously supposed. Assessment of established SIDS risk factors in relation to maternal age deserves further attention. The role of nutrition of pregnancy in relation to maternal age and SIDS risk may also be a productive avenue for future investigation.

All 1998 resident infant deaths in the 1969--1977 King County, Washington birth cohort of 139,132 resident live births comprise the data base for epidemiologic comparisons of the sudden infant death syndrome (SIDS) with eight other major infant mortality components: hyaline membrane disease; respiratory distress syndrome; asphyxia of the newborn; immaturity; birth injury; congenital malformation; infection; and "all other." These components were compared with respect to age at death; sex; race; prior fetal loss; prior live-born, now dead; birth plurality; birth weight; maternal age; birth order; marital status; prenatal care; and season of death in an attempt to determine the uniqueness of these purported SIDS risk factors. Only the age at death distribution unequivocally distinguished SIDS from the other components. The combination of low maternal age and multiparity was demonstrated to be putatively synergistic for risk of SIDS, hyaline membrane disease, and respiratory disease syndrome. Only deaths from infection exhibited seasonal variation similar to SIDS. These observations probably reflect secondary associations with as yet unidentified primary risk factors relatable to maternal experience.

The relationship of acute urinary tract infection occurring during pregnancy and the incidence of adverse fetal outcomes was examined with the use of birth certificate data from Washington state for the years 1980 and 1981. The two-year fetal mortality rate among urinary tract infection-associated pregnancies was found to be 17.9 per thousand livebirths, 2.4 times the rate for the state as a whole. Low birth weight newborns and small for gestational age newborns were, respectively, 2.04 and 1.57 times more frequent in urinary tract infection-associated pregnancies compared to controls. These estimates of risk were unchanged when adjusted for maternal age, race, and past obstetric history. The risk of prematurity in women with urinary tract infection and no history of fetal loss was 2.4 times the control risk. Sepsis was rare in both the urinary tract infection and control groups. These results add to the evidence implicating maternal urinary tract infection as a threat to fetal well-being.

In a follow-up study of 1,852 men with coronary heart disease, 195 deaths occurred within the first 3 years (33 +/- 13 months [mean +/- standard deviation]). Analysis of these cases indicated that the risk of sudden cardiac death in ambulatory men with clinical manifestations of coronary heart disease may be readily estimated from noninvasive clinical and exercise criteria. The important predictors are indexes of the severity of coronary heart disease and impairment of peak left ventricular function demonstrated with symptom-limited maximal exercise. The advantages of these predictors are that they may be elicited on the initial study as well as on follow-up noninvasive examinations of ambulatory patients. The appearance of nonelectrocardiographic predictors in serial examinations may provide an indication for invasive studies and be a more important finding than the ischemic S-T reponse to exertion.

A unique opportunity to study proven infant apnoea (PIA) and Sudden Infant Death Syndrome (SIDS) occurrences epidemiologically in 12 Counties in north-western Washington State during the same time period during which 180,017 live births were recorded revealed markedly dissimilar distribution patterns. The overall incidence of SIDS exceeded that of PIA by a factor of 3. Five PIA babies subsequently succumbed to SIDS. Statistical analysis reveals that these five events cannot be explained as random coincidences; they represent 3% of 163 PIA cases but only 1% of 503 SIDS occurrences. Infant apnoea is an infrequent precursor of SIDS. These results do not support the view that SIDS and infant apnoea are related conditions caused by a common underlying disorder. Aetiological models other than infant apnoea must be devised if the momentum of SIDS research is to be sustained.

Data from six geographically dispersed metropolitan areas in the United States in which special sudden infant death syndrome (SIDS) surveillance programs for detection and autopsy diagnosis existed during the period 1965 through 1974 reveal considerable diversity in overall ten-year incidence rates as well as in annual rate distribution patterns. A downward trend in SIDS incidence occurred in some areas but not in others. Non-SIDS postneonatal death rates, which were used for comparison, also decreased in some areas. Rate trends for whites and nonwhites were not consistent. During the same period, the fertility rate in the United States decreased by about a third for both whites and nonwhites. To explain the observed trends we postulate that concomitants of the fertility rate decline may have reduced the number of "high mortality risk babies" to a variable degree in different places and at different times.