ABSTRACT
The proliferation of wireless communication technologies has raised public concern regarding potential health effects of radiofrequency (RF) exposures. This is the first report of findings from a large-cohort mortality study among employees of Motorola, a manufacturer of wireless communication products. We examined all major causes of mortality, with brain cancers, lymphomas, and leukemias as a priori outcomes of interest. Using job titles, we classified workers into high, moderate, low, and background RF exposure groups. A total of 195,775 workers contributed 2.7 million person-years during the 1976-1996 period. Using external comparisons, the standardized mortality ratios for RF-exposed workers were 0.53 [95% confidence interval (CI) = 0.21-1.09] and 0.54 (95% CI = 0.33-0.83) for central nervous system/brain cancers and all lymphomas/leukemias. Rate ratios calculated from Poisson regression models based on internal comparisons were near 1.0 for brain cancers and below 1.0 for all lymphomas and leukemias. These findings were consistent across cumulative, peak, and usual exposure classifications. We did not observe higher risk with increased exposure duration or latency. Although this study is limited by the use of a qualitative exposure matrix and the relatively young age of the cohort, our findings do not support an association between occupational RF exposure and brain cancers or lymphoma/leukemia.
Subject(s)
Brain Neoplasms/etiology , Brain Neoplasms/mortality , Communication , Occupational Exposure/adverse effects , Radio Waves/adverse effects , Brain Neoplasms/epidemiology , Cohort Studies , Death Certificates , Female , Healthy Worker Effect , Humans , Leukemia/epidemiology , Leukemia/etiology , Leukemia/mortality , Lymphoma/epidemiology , Lymphoma/etiology , Lymphoma/mortality , Male , Occupations , Poisson Distribution , Risk Factors , United States/epidemiologyABSTRACT
To characterize the role of the kallikrein-kinin system in diabetic cardiopathy, we studied the effect of streptozotocin (STZ) on the regulation of the myocardial bradykinin (BK) receptors, the B1 and B2 type, and two tissue kallikrein genes, rat kallikrein 1 (rKLK1) and rKLK7, in severely hyperglycemic rats. Experiments were performed in STZ-induced diabetic male Wistar rats (n = 7) and compared to controls (n = 7). After extraction of myocardial total RNA, specific oligonucleotides were used to generate reverse transcription PCR (RT-PCR) products from myocardial rKLK1 and rKLK7 mRNA. Southern blot analyses of these RT-PCR products were hybridized with appropriate gene-specific oligonucleotide probes. Myocardial B1 and B2 receptor expression were analyzed by RNase protection assays using specific probes from the coding region of the receptor genes. Twelve weeks after diabetes induction, the rats were normotensive and hyperglycemic and polyuric. We observed an impairment of the main myocardial kinin-forming enzymes, indicated by a reduction of the expression of both, rKLK1 and rKLK7. At this time the myocardial expression of the B1 receptor was not detectable in either group. Thus, the B1 receptor does not play a regulatory role in either the healthy or in STZ-diabetic heart. In contrast, the B2-receptor expression was detectable but did not differ significantly in either group. The reduced synthesis of myocardial tissue KLK implies a reduced capacity to generate BK in diabetic rats. This reduction is not compensated by elevated BK receptor levels. We suggest that alterations of the KKS may contribute to myocardial dysfunction in diabetes mellitus.
Subject(s)
Diabetes Mellitus, Experimental/genetics , Diabetes Mellitus, Experimental/metabolism , Gene Expression Regulation, Enzymologic , Kallikreins/genetics , Myocardium/metabolism , Receptors, Bradykinin/biosynthesis , Animals , Diabetes Mellitus, Experimental/enzymology , Kallikreins/biosynthesis , Male , Myocardium/enzymology , Rats , Rats, Wistar , Receptor, Bradykinin B1 , Receptor, Bradykinin B2ABSTRACT
We measured mortality rates in a cohort of 20,508 aerospace workers who were followed up over the period 1950-1993. A total of 4,733 workers had occupational exposure to trichloroethylene. In addition, trichloroethylene was present in some of the washing and drinking water used at the work site. We developed a job-exposure matrix to classify all jobs by trichloroethylene exposure levels into four categories ranging from "none" to "high" exposure. We calculated standardized mortality ratios for the entire cohort and the trichloroethylene exposed subcohort. In the standardized mortality ratio analyses, we observed a consistent elevation for nonmalignant respiratory disease, which we attribute primarily to the higher background rates of respiratory disease in this region. We also compared trichloroethylene-exposed workers with workers in the "low" and "none" exposure categories. Mortality rate ratios for nonmalignant respiratory disease were near or less than 1.00 for trichloroethylene exposure groups. We observed elevated rare ratios for ovarian cancer among those with peak exposure at medium and high levels] relative risk (RR) = 2.74; 95% confidence interval (CI) = 0.84-8.99] and among women with high cumulative exposure (RR = 7.09; 95% CI = 2.14-23.54). Among those with peak exposures at medium and high levels, we observed slightly elevated rate ratios for cancers of the kidney (RR = 1.89; 95% CI = 0.85-4.23), bladder (RR = 1.41; 95% CI = 0.52-3.81), and prostate (RR = 1.47; 95% CI = 0.85-2.55). Our findings do not indicate an association between trichloroethylene exposure and respiratory cancer, liver cancer, leukemia or lymphoma, or all cancers combined.
Subject(s)
Aviation/statistics & numerical data , Occupational Diseases/mortality , Occupational Exposure/adverse effects , Solvents/adverse effects , Trichloroethylene/adverse effects , Adult , Aged , Aircraft , Arizona/epidemiology , Carcinogens/classification , Cause of Death , Cohort Studies , Confidence Intervals , Female , Humans , Industry , Male , Middle Aged , Neoplasms/chemically induced , Neoplasms/mortality , Occupational Diseases/chemically induced , Occupational Exposure/statistics & numerical data , Proportional Hazards Models , Respiratory Tract Diseases/chemically induced , Respiratory Tract Diseases/mortality , RiskABSTRACT
300 hypertensive children, from newborn to 18 years old,were studied, retrospectively, from 1975 to 1992, 105 from those lost for follow-up. In 244 the diagnosis of the primary disease, predominantly glomerulopathy, was established. 122 had chronic renal failure (CRF). From them, 74 arrived at end stage renal disease (ESRD) and 13 have been transplanted. From 12 submitted to surgical treatment, hypertension has been controlled in 8. 54 died, 48 with CRF and 38 with ESRD. Difficulties in controlling those patients are discussed, mainly therapy diet, the use of hypotensive drugs on dialysis treatment. Our conclusion is for the necessity of a precocious diagnosis for hypertension and primary diseases, of a trained interprofessional team as well as availability of adequate equipment to children, mainly for dialytic therapy. For many of these children, renal transplantation is the only definite therapy.
ABSTRACT
The present study was designed to investigate the effect of intracerebroventricular (icv) and intravenous (iv) infusion of angiotensin (ANG)-(1-7), ANG III, and ANG II on the baroreceptor control of heart rate (BHR) in conscious rats. Reflex changes in HR were elicited by bolus iv injection of either phenylephrine or sodium nitroprusside before and within 1 and 3 h of icv infusion of ANG II (n = 10), ANG III (n = 9), ANG-(1-7) (n = 9), or saline (n = 9) at a rate of 3 nmol.7.5 microliter-1.h-1. In another group of animals (n = 23), iv infusion of the same amount of ANG peptides was carried out at a rate of 0.7 ml/h. The average ratio of changes in HR in beats per minute and changes in mean arterial pressure (MAP, mmHg) was used as an index of BHR sensitivity. ANG II and ANG III produced a significant increase in the basal levels of MAP, but only during the first hour of infusion (iv or icv). No significant changes in baseline HR were observed. ANG-(1-7) and saline infusion did not change basal levels of HR or MAP (iv or icv). ANG II (iv and icv) and ANG III (icv) caused a significant decrease in the BHR sensitivity for reflex bradycardia. In contrast, icv infusion of ANG-(1-7) induced a significant increase in BHR sensitivity for reflex bradycardia (-3.0 +/- 0.3, 1 h, and -2.8 +/- 0.1 beats.min-1.mmHg-1, 3 h vs. -2.1 +/- 0.2 beats.min-1.mmHg-1, before infusion).(ABSTRACT TRUNCATED AT 250 WORDS)