A system linking occupation history questionnaire data and magnetic field monitoring data.

A method is presented which links on-site electromagnetic field monitoring data with pre-existing work history data. The linkage is used to estimate cumulative and average annualized magnetic field exposure for a case-control study. On-site electromagnetic field monitoring data for 1,966 volunteer utility employees, at 59 sites in the United States and three other countries, were obtained from a large project (the EMDEX project) designed to collect, analyze, and document 60-Hz electric and magnetic field exposures for a diverse population. These data represent 9 primary work environments, and 16 job classification categories, amounting to 144 unique job categories which were consolidated using the job-exposure matrix presented into 282 three-digit Dictionary of Occupational Title (DOT) codes. The DOT code categories were then linked to lifetime occupational histories from a case-control study of leukemia. The method may be extended to link additional job titles with monitoring information. Job titles linked with electromagnetic field monitoring information provide more specific estimates of exposure intensity than previous ordinal estimates of exposure. Therefore, estimates of cumulative electromagnetic field exposure are achievable, as well as high and low level exposure estimates.

Excess leukemia and multiple myeloma in a mining county in northeast Texas.

From 1950 to 1979, cancer mortality rates in Titus County, Texas, increased with a significant excess of deaths from leukemia, lymphoma, brain and liver cancers, and melanoma. County residents requested this study to verify the apparent excess of cancer. Newly diagnosed cases of cancer among white residents from 1977 to 1984 were ascertained from the Texas Cancer Registry, hospital records, and death certificates. Direct and indirect methods were used to calculate incidence rates and standardized incidence ratios (SIR). We identified 663 cancers for 148,470 person-years of observation. No overall excess of cancer was found. However, we found a significant excess of leukemia (SIR = 2.53, 95% confidence interval [CI] = 1.86, 3.30) and multiple myeloma (SIR = 1.87, 95% CI = 1.02, 3.14). The reasons for the increased SIRs are unknown. However, the excess of cancers in this mining community may be relevant to the ongoing debate on the health effects of the disposal of combustion wastes from mining and fossil fuel and on the need for stricter regulations. Other potential risk factors include the presence of petrochemical and poultry industries. regulations. Other potential risk factors include the presence of petrochemical and poultry industries.

Mortality among workers at a butadiene facility.

Several studies of styrene-butadiene rubber (SBR) workers have reported excess cancers at various sites; however, little could be concluded concerning specific etiologic agents because of the multiple exposures encountered by these groups. The current study examined cause-specific mortality in a cohort of 2,586 male workers employed for at least 6 months between 1943 and 1979 in a butadiene manufacturing plant that supplied butadiene to two SBR plants. Standardized mortality ratios were calculated using national (NSMR) and local (LSMR) comparison populations. The all-cause NSMR was 80 (p less than 0.05) and the all-cancer NSMR was 84; the corresponding LSMRs were 96 and 76 (p less than 0.05). No significant excesses were observed for any cause of death except lymphosarcoma and reticulum cell sarcoma (NSMR = 235). When the cohort was subdivided into routine, nonroutine, and low-exposure groups, the SMRs were consistently elevated for this cause of death in all three groups. However, direct comparisons between each of the two exposure groups and the low-exposure group were inconsistent. This suggests butadiene may not be responsible for the excess, but the association deserves close attention in future studies.

Analyses of rat Pneumocystis carinii antigens recognized by human and rat antibodies by using western immunoblotting.

The major Pneumocystis carinii antigens inducing antibody responses in infected hosts were identified by Western immunoblotting techniques. The biochemical nature of these antigens was also elucidated. Sodium dodecyl sulfate-polyacrylamide gel electrophoresis followed by protein staining revealed a major component with a molecular weight (MW) of greater than 205,000. This major component disappeared and a new major protein staining component of approximately 110,000 to 116,000 MW appeared when electrophoresis was done in the presence of beta-mercaptoethanol. Periodic acid-Schiff staining revealed that this major component contains carbohydrate moieties. A major component in the 55,000- to 60,000-MW region was visible with periodic acid-Schiff stain, but not with a protein stain, after electrophoresis in the presence of beta-mercaptoethanol. The majority of sera tested from humans with diagnosed pneumocystosis and from rats allowed to recover from steroid-induced pneumocystosis reacted strongly with 110,000- to 116,000-, and 55,000- to 60,000-MW components. These sera often, but not always, detected antigens with MWs of approximately 170,000, 125,000, and 30,000 to 32,000. The data suggest that the antigenic composition of P. carinii is relatively complex and that rat and human P. carinii probably share antigenic determinants. Competitive studies between infection-derived human and rat antisera for the major rat P. carinii components revealed competition; rat antisera appeared to recognize a greater range of antigenic epitopes than did human antisera. Protease treatment of the antigenic components that had been immobilized on nitrocellulose paper destroyed their antigenic reactivity with rat antibody. Treatment with sodium periodate decreased reactivity of this 110,000- to 116,000-MW component and completely destroyed the reactivity of the 55,000- to 60,000-MW component with rat antibody.

Mortality and influenza.

Systematic virologic surveillance in Houston over the past seven years has revealed that influenza virus infections have been epidemic during each respiratory disease season. The peak of the occurrence of acute respiratory illnesses that caused patients to seek medical care always coincided with the peak of influenza virus activity. The peak number of deaths attributed to pneumonia or influenza followed the peak of influenza virus activity by about two weeks. This relationship was constant even though the time of the epidemic peak ranged from as early as the third week of December to as late as the second week of March. No increase in deaths occurred in the absence of influenza virus activity. Therefore, the methods used to predict base-line mortality that show a seasonal rise in the absence of influenza activity may be inaccurate and, if so, lead to underestimation of mortality associated with influenza virus infections.

Time as a factor in atmospheric sampling.

Differences in results of simultaneous air monitoring of ozone with three different methods in the field are described. The argument is advanced that the differences are due largely to sampling turbulent atmospheres with instruments utilizing different sampling intervals and time constants. It is concluded that when sampling natural turbulent atmospheres, a stable mean value can only be achieved through integrated sampling periods of greater than ten minutes.

Circadian rhythmicity in heart rate and duration of cardiac cycle (P-P interval) in donor and recipient cardiac tissue of heart homograft patients.

Chronobiologic analyses of data collected during one or more continuous 72-hr spans from 3 heart-transplant patients adhering at diurnal activity (0700-2230) and nocturnal rest (2230-0700) reveal statistically significant circadian rhythmicity in the P-P time interval of recipients (P-P)R and the donor (P-P)D, as well as in the reciprocal measure of the latter, the heart rate. The circadian acrophase for (P-P)D and (P-P)R differ slightly (the 95% confidence arcs overlap). For the group, the acrophases for (P-P)D and heart rate at 0344 (2056 to 0528) and 1656 (0940 to 2100) agree in anti-phase, as expected. For 1 patient studied during 3 separate occasions -1,5 and 12 months post-transplant--the period of the rhythm for the (P-P)R time interval progressively elongated from 23.7 hr (1 month post-transplant) to 26.1 hour (5 months post-transplant) and finally to 32.3 hr (12 months post-transplant and 4 months prior to death) while the (P-P)D remained around 24.0 hr (range 23.8 to 24.6 hr). Change in the rhythm's period in (P-P)R may reflect events associated with rejection, continuing necrosis of cardiac tissue and/or medications, among others.