An experiment was designed to determine whether the respiratory retention of sytrene vapor, as estimated from measurements of end-exhaled air, was the same during periods of both constant and fluctuating exposure. Six human subjects were exposed to styrene inside an experimental chamber. A computer-controlled system was used to generate time-varying air concentrations of styrene over 4–5 h in both multistep sequences of constant exposure (four subjects exposed to 15–99 ppm. of styrene in 100-min steps) and fluctuating patterns representative of occupational exposures (two subjects exposed to mean concentrations of styrene of 50 ppm). In the latter case, lognormally distributed exposures, which fit one of two first-order autoregressive models, were generated at intervals of 2.5 min. It was found that the concentration of styrene in end-exhaled air was reduced by about half if the subject inhaled one to three breaths of clean air prior to sampling. This suggests that significant amounts of styrene were desorbed from the lining of the lungs during the initial exhalation. The retention of styrene vapor during constant exposures was 0.935 and was independent of the level. During each of the two sets of fluctuating exposure the retention of sytrene was also constant and was independent of both the variance and the autocorrelation coefficient. However, the retention of styrene during fluctuating exposure (estimates ranged from 0.957 to 0.973) was significantly higher than that observed during the constant exposures. It is speculated that the difference in retention between the constant and the fluctuating exposure regimens is related to non-steady-state behavior of styrene in the richly perfused tissues, as suggested by Opdam and Smolders (1986) regarding tetrachloroethylene exposure.

Methanol will be present as a new air pollutant when methanol-powered vehicles are introduced in the United States. Little is known about the effect of low-dose methanol exposure. It is controversial whether or not formate, the main metabolite responsible for methanol's acute toxicity, is a sensitive biological marker of toxicity or exposure. We studied the effect of a 4-hr exposure at rest to 200 ppm of methanol vapors on endogenous serum formate and on urinary formic acid excretion. A randomized, double-blind study of human exposure to a constant concentration of methanol was performed in a whole-body exposure chamber. Twenty-six healthy volunteers, each serving as his or her own control, participated in sham and methanol exposures. Urine (at 0, 4, 8 hr) and serum specimens (15 time points over 8 hr) collected before, during, and after the exposure were measured for formate. We found no significant differences in serum formate concentration between exposure and control conditions either at any time point or for area under the curve. Mean concentrations at the end of the exposure were: exposed 14.28 +/- 8.90 mg/l and control 12.68 +/- 6.43 mg/l. A slight, but nonsignificant (p = 0.08), increase in urine formate excretion rate was found at 4 hr (exposed 2.17 +/- 1.69 mg/4 hr and control 1.67 +/- 1.02 mg/4 hr). Age, sex, folic acid level, and smoking were not significant covariates. At 200 ppm, methanol exposure does not contribute substantially to endogenous formate quantities. Serum and urine formate determinations are not sensitive biological markers of methanol exposure at the threshold limit value.

The extent to which environmental or occupational chemical exposures affect reproductive health remains largely unknown. Teratogenic effects usually take place during critical periods of organogenesis. Common concerns of patients include the possible effects of drinking contaminated water on the fetus as well as the breast-fed infant, and the possible effects of a chemical exposure on fertility and pregnancy.

Dioxins bioaccumulate in adipose tissue and can be found in most persons. Human exposure to dioxin is a concern because dioxins cause cancer in some animals. Chloracne is the only overt clinical sign of dioxin exposure in humans.

Dermatitis accounts for about 30 percent of all illnesses in the workplace. A thorough exposure history is the most important element in accurate diagnosis of skin lesions. in certain cases, skin lesions may be valuable diagnostic clues to the presence of systemic toxicity. Irritant and allergic contact dermatitis, photosensitivity contact dermatitis, and contact urticaria are examples of skin lesions that may be caused by exposure to an environmental agent.

Because of the combustion of fossil fuels and organic waste, polycyclic aromatic hydrocarbons are ubiquitous in the environment. Some metabolites are believed to interact with DNA, causing malignancies and heritable genetic damage. Exposure to polycyclic aromatic hydrocarbons is associated with lung and skin cancers and, possibly, urologic, gastrointestinal, laryngeal and pharyngeal cancers.

Methanol is used in a variety of commercial and consumer products. Increased use of methanol as a motor fuel may lead to higher ambient air levels and a greater potential for ingestion from siphoning accidents. Methanol toxicity initially is not characterized by severe toxic manifestations. Pathophysiologically, methanol toxicity a classic example of ''lethal synthesis,'' in which toxic metabolites can cause fatality after a characteristic latent period. Methanol is well absorbed following inhalation, ingestion or cutaneous exposure. ft is oxidized in the liver to formaldehyde, then to formic acid, which contributes to the profound metabolic acidosis occurring in acute methanol poisoning. The metabolic products of methanol can produce a syndrome of delayed-onset acidosis, obtundation, visual disturbance and death. Intravenous sodium bicarbonate therapy should be considered if the patient's blood pH is below 7.2. Symptoms and history determine whether intravenous ethanol therapy and hemodialysis should be instituted.

The neurotoxicity of methylene chloride (MC) is of special interest because of its acute effects on the central nervous system (CNS) and its metabolic conversion to carbon monoxide. A cohort study of retired airline mechanics was conducted to examine the hypothesis that long term exposure to MC results in lasting effects on the CNS. Retirees were studied to eliminate effects of current occupational exposures. The total retiree population (n = 1758) was surveyed to identify mechanics who met specific occupational, demographic, and medical criteria. A group of eligible retirees having long term exposure to MC and another group with low probability of exposure to solvents were given a comprehensive battery of physiological and psychological tests. The exposure groups were similar for all potential confounders that were measured. No statistically significant differences between groups were detected on outcome measures, although subtle differences in attention and memory were identified. Thus no firm evidence was found to support the hypothesis of lasting CNS effects in retired mechanics with long term exposure to MC.

"Environmental Toxicology Case Studies for Primary Care Physicians." Journal of Toxicology: Clinical Toxicology, 28(3), pp. vii–viii

Estimating the risks of blood-borne diseases to health care workers is an important area of concern for occupational health physicians. It is best now to view this risk as an occupational injury that can be prevented. The specific numbers estimating risks are rarely as important to the worker as are methods that are available to reduce or eliminate this risk. By placing the risk of blood-borne diseases in perspective with other injuries, it can be appreciated from this information that the estimates of occupational risks of blood-borne diseases to health care workers is extremely variable, but will never be zero. The single most important variable that is preventable is exposure. Major research and educational methods are needed to continue to explore all avenues leading to exposure reduction in the health care setting.

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.

Eight hospital workers with chronic ethylene oxide exposure were age-sex matched with eight nonexposed controls with no significant differences in educational backgrounds and vocabulary scores. The exposed group performed more poorly on all eight measures of cognition, memory, attention, and coordination, with 71.3% less accuracy on the Hand-Eye Coordination Test. There was a dose-response relationship between exposure and the following: Continuous Performance Test and sural velocity. These findings suggest that neurologic dysfunction may result from long-term low-dose exposure to ethylene oxide, and that these effects may occur at exposure levels common in hospital sterilizer operations.