In experimental studies, caffeine increases blood pressure in caffeine-naive or nontolerant individuals, but not in regular caffeine consumers. Using an epidemiologic approach, we examined the hypothesis that serum-caffeine concentration would be positively associated with blood pressure in infrequent (but not habitual) caffeine users in a group of bus drivers. Infrequent and habitual users of caffeine showed no differences in systolic or diastolic blood pressures when there is no measurable caffeine in the serum. However, at serum concentrations of caffeine typical of those achieved after one to two cups of coffee, infrequent users demonstrated greater systolic and diastolic pressures, averaging +5.3 mm Hg and +3.6 mm Hg, respectively, compared with habitual users. The magnitude of difference remained after adjustment for age, body mass index, race, sex, and tobacco and alcohol use. These elevations are large enough to exaggerate the prevalence of hypertension, if such assessments are based on cross-sectional surveys that fail to assess both proximate caffeine consumption and usual caffeine consumption habits.

The relationship between blood pressure (BP) and blood lead concentration (PbB) was examined in 51 bus drivers who were treated for hypertension. These drivers were a subset of a representative sample (N = 342) of the driver population (N = approximately 2,000), and were not selected for hypertension or lead exposure. Blood lead concentrations ranged from 2-24 micrograms/dl (median: 6.9 micrograms/ld). There were 33 subjects treated primarily with diuretics, and 18 subjects were treated with beta blockers. Adjusted regression coefficients relating systolic BP with PbB were -6.4 +/- 11.4 and 4.5 +/- 12.9 mmHg/In(micrograms/dl) in each group, respectively, but were not statistically significant. The adjusted coefficients for diastolic BP were 1.12 +/- 3.89 and 14.3 +/- 5.69 mmHg/In(micrograms/dl) (p = 0.036), respectively. The latter relationship represents an average increment of 12 mmHg in diastolic BP over the range of observed PbBs (2.0 to 11.4 micrograms/dl) in subjects treated with beta blockers. Thus, beta blocker therapy may be less effective in reducing diastolic pressure in individuals with higher PbBs and suggests an action of lead at PbBs below current standards.

San Francisco bus drivers have an increased prevalence of hypertension. This study examined relationships between blood lead concentration and blood pressure in 342 drivers. The analysis reported in this study was limited to subjects not on treatment for hypertension (n = 288). Systolic and diastolic pressures varied from 102 to 173 mm Hg and from 61 to 105 mm Hg, respectively. The blood lead concentration varied from 2 to 15 micrograms/dL. The relationship between blood pressure and the logarithm of blood lead concentration was examined using multiple regression analysis. Covariates included age, body mass index, sex, race, and caffeine intake. The largest regression coefficient relating systolic blood pressure and blood lead concentration was 1.8 mm Hg/ln (micrograms/dL) [90% C. I., -1.6, 5.3]. The coefficient for diastolic blood pressure was 2.5 mm Hg/ln (micrograms/dL) [90% C. I., 0.1, 4.9]. These findings suggest effects of lead exposure at lower blood lead concentrations than those concentrations that have previously been linked with increases in blood pressure.

Lead is a common element in the earth's crust, serving useful purposes in industry, but serving no purpose in the human body. Increase in blood pressure is an important public health problem with numerous factors contributing to many facets of the disease. The relationship of lead exposure and increased blood pressure has long been considered, but only recently critically investigated. Reports of subtle changes in calcium metabolism and renal function, as well as in vitro studies examining end-arteriolar smooth muscle contractility, link lead exposure and increased blood pressure. This paper critically examines the evidence associating chronic low-level lead exposure and increased blood pressure. The review focuses on epidemiological, clinical, and toxicological data. The epidemiological evidence is consistent with low-level exposure to lead causing an elevation in blood pressure. The strength of that association, and the dose-response characteristics, are less certain. Individual resistance and susceptibility could affect the degree of blood pressure elevation. The results of animal and in vitro studies are consistent with the epidemiological evidence, and suggest biologically plausible mechanisms for the association. The most probable mechanisms are intracellular perturbations in calcium metabolism mediated by direct lead effects at the end-arteriole, and indirect effects via renal dysfunction. Better indices of lead exposure and lead activity are needed to quantify these effects in humans. New and safer methods of chelating lead suggest interesting approaches for studying the relationship between lead and hypertension. This link could have significant implications in determining what constitutes a 'safe' level of environmental lead exposure, and whether a proportion of essential hypertension could be 'cured' by chelation therapy.

In recent decades, there has been remarkable growth in scientific research examining the multiple ways in which racism can adversely affect health. This interest has been driven in part by the striking persistence of racial/ethnic inequities in health and ...Read More

Clarity and scientific validity are two criteria for assessing the quality of communications between scientists and risk managers. Regulating permissible exposures on the basis of very-low-dose risk extrapolation uses scientific information that may not meet either criterion. With regard to clarity, it is difficult for an individual to conceive of the meaning of risks on the order of 1 in 1,000,000 lifetime excess. With regard to scientific validity, the uncertainties of extrapolating risks at very low doses are evident in the wide variation in results produced depending on the statistical and pharmacokinetic assumptions made. An alternative approach is to fix benchmarks from which safety factors are chosen (Gaylor, 1983). For epidemiological data, we propose a benchmark of that exposure which would cause 1% cancer excess with 10 yr of exposurefollowed by 30 yr of further followup. These values have been chosen at this stage of development since they are close to observable values in many cancer epidemiology studies. In the first stage, excess cancer risk versus duration of exposure is plotted and the excess risk is estimated for a exposure duration of 10 yr. The next step involves a short linear extrapolation from the exposure levels linked with this excess risk to the exposure levels that would cause a 1% excess risk over a duration of 10 yr. We have established preliminary benchmarks from published data for benzene and radon daughter exposure. Permissible exposure levels might then be set by deciding on safety factors. Although low-dose extrapolation will aid in selecting a safety factor for carcinogenic exposures, it should be acknowledged that the actual risk at the permissible level is not known. The risk might be zero, it might be between zero and a linear extrapolation value, or it might possibly be a little higher than the value from a linear projection (Gaylor and Kodell, 1980; Gaylor, 1983).