The effect of body weight (W) upon the oxygen cost of activity ([vdot]o2) is analyzed with respect to the authors’ data on stepping and bicycle ergometry, and Brown’s results for five industrial activities. Net oxygen consumption is proportional to Wn, where n = 0 for activities with little body movement and 1.0 for activities with substantial body movement; the oxygen cost of unit work is also increased by inexperience and obesity. The new method for the standardization of energy costs is somewhat superior to the adjustment of gross [vdot]o2 by W1.0 or W0.75, particularly in light work; however, there remains a challenging percentage of undescribed interindividual variation in the oxygen cost of industrial activities.
Rats and hamsters were exposed to 0.1 ppm bis(chloromethyl)ether (BCME) six hours per day, five days per week throughout their lifetime. Additional groups of rats were given 10, 20, 40, 60, 80, and 100 exposures to 0.1 ppm BCME and then held until death. Forty cancers originating in the respiratory tract were found in the 200 rats involved in these studies. These included 14 cancers of the lung and 26 cancers of the nasal cavity. They occurred in dose-related fashion. A single undifferentiated carcinoma of the lung was seen in a hamster.
Weanling male Sprague-Dawley rats were fed either a synthetic diet supplemented with 11 mg vitamin E/kg body weight (to approximate average U.S. human dietary intake) or a commercial rat chow for 5 wk. At 2 months of age, rats were exposed to either 0.0, 0.1, or 0.2 ppm ozone continuously for 7 days. Morphological lesions were consistently present in centriacinar regions of lungs of both groups of rats at the 0.2 ppm level. At 0.1 ppm ozone, two of six rats fed the synthetic diet and two of five fed lab chow had minimal centriacinar lesions. Biochemical assays showeed that the activities of glutathione (GSH) peroxidase, GSH reductase, and G-6-P dehydrogenase and level of nonprotein sulfhydryls in the lungs of rats fed the synthetic diet and exposed to 0.1 ppm were elevated to about one-half the level that was produced by 0.2 ppm. The authors conclude that the level whereby there are no observable morphologic effects for short-term exposure to ozone in 2-month-old rats is less than, but close to, 0.1 ppm.
Swiss Webster male mice were exposed to intermittent 0.34 ppm nitrogen dioxide for 6 wk. Quantitative image analysis showed increased Type 2 cell numbers in each of the three lobes measured, with and without adjustment to alveolar wall measurements for lung volume normalization (e.g., P less than .037 for Type 2 cell number adjusted to alveolar wall perimeters, combined lobe analysis of variance). The exposed animals dominated the upper quartile ranking of the cell number/alveolar area ratio computations (P less than .025), which implied the presence of an especially susceptible subpopulation of animals. The Type 2 cell increase is believed to result from damage and loss of Type 1 cells, the reversibility and progression of which are presently unknown. The data also suggest an increased size of the Type 2 cell, and possibly slight atelectasis and/or edema of the alveolar walls.
Lung lavage and disc-gel electrophoresis of the lavage fluid were carried out in a study of 18 guinea pigs, half of which were exposed continuously over a one-week period to 0.4 ppm nitrogen dioxide. Of the nine animal pairs, eight were characterized by higher protein levels for the exposed animals (P < .001). The values for eight of nine control animals were .1097 (arbitrary units) or less, whereas those for eight of nine exposed animals had levels .1164 or higher, with a maximum of .1698. The methodologies represent a relatively simple means of detecting a physiologically important alteration and have the potential of greater sensitivity to and specificity of protein content through new advances in electrophoretic techniques.
Forty-four mice were continuously exposed to 0.47 ppm nitrogen dioxide for ten, 12, and 14 days. The protein content of homogenized lung tissue was assayed fluorometrically after the animals had received intravenous injections of fluorescamine, a new reagent for protein assay. The mean protein value of all exposed animals was higher than that of the control animals (P less than .025). No correlation was noted between serum fluorophor levels and those in the lung homogenate.
Urinary proteins were quantitated by disc-gel electrophoresis, chemical tests, and specific gravity determinations. In the first of two experiments, the seven animals exposed to continuous 0.5 ppm NO2, three for seven days and four for 14 days, had consistently higher levels of urinary protein than control animals (P <.01). The increase involved all three of the major protein groups demonstrated by the discgel procedure, putatively albumins, combined α-and β-globulins, and γ-globulins. A second experiment involving 12 pairs of guinea pigs gave similar results for two of three animal groups (P < .05) despite a decrease in exposure to only four hours a day. Routine histological studies of the kidneys showed negative results.
Of 31 young, health male volunteers who participated in this study 15 were exposed to air (control) and 16 to 0.75ppm (2.15mg/m3) SO2 for 2 hr at 21 degrees C and 60% relative humidity. At the end of the first hour, the subjects exercised for 15 min on a treadmill at 6.4 kmph, with a 10% grade. Methods employed in evaluation of pulmonary function included body plethysmography, spirometry, and multigas rebreathing test. From the battery of 15 pulmonary function parameters, only the pattern of airway resistance changes was significantly altered by SO2 exposure, although spirometric parameters followed a similar pattern. Eight of the SO2-exposed ubjects, with one or more positive allergen skin tests, appeared to be significantly more reactive to SO2 than skin test-negative subjects. All subjects remained asymptomatic. The small number of changes observed appeared to be reversible and do not suggest a significant health hazard to normal human subjects exposed to SO2 under these conditions.
Nine rats were exposed to 0.8 ppM NO/sub 2/ and allowed to live out life-span of up to 33 months. There were 12 control animals. No emphysema or other overt changes were noted due to exposure. The animals were also normal otherwise except for an increase in respiration rate of about 20% (tachypnea).
p-Dichlorobenzene is used widely in the United States as a room deodorizer, a moth repellent, and a precursor for a polymer. In a previous study of selected children in Arkansas, we found that 96% of the children had detectable urinary concentrations of 2,5-dichlorophenol, the metabolite of p-dichlorobenzene. In the current study, we found that, in a sample of 1,000 adults who lived throughout the United States, 98% had detectable levels of 2,5-dichlorophenol in their urine, and 96% had detectable levels of p-dichlorobenzene in their blood. Urinary 2,5-dichlorophenol concentrations ranged up to 8,700 micrograms/l (median and mean concentrations of 30 micrograms/l and 200 micrograms/l, respectively). p-Dichlorobenzene blood concentrations ranged up to 49 micrograms/l, with median and mean concentrations of 0.33 micrograms/l and 2.1 micrograms/l, respectively. The Pearson correlation coefficient for 2,5-dichlorophenol in urine and p-dichlorobenzene in blood was .82 (p < .0001), thus demonstrating a strong association between these exposure measurements. Neither age nor gender was related to urinary 2,5-dichlorophenol or blood p-dichlorobenzene concentrations (p > .40). When these results are viewed with data from other studies, the collective data show that p-dichlorobenzene is a common, worldwide contaminant. The high prevalence of exposure to p-dichlorobenzene, coupled with its potential for adverse health effects, indicate the need for more detailed studies, including studies of long-term health effects on exposed populations.
Relationships between blood lead concentrations in 1,047 children aged 2 mo to 16 y and age, sex, and province (i.e., residence) were examined. The relationships were consistent with other studies, in which mean blood lead concentrations reportedly increased during the first 5 y of life, after which began to decrease, reaching a minimum at approximately 16 y of age. However, boys who were more than 6 y of age had higher blood lead concentrations than similarly aged girls. Blood lead levels of children living in the Eastern Province were higher than levels found in children from other provinces. Most of the children in this study who had elevated blood lead concentrations resided in small towns, e.g., Ehssa, Abqiq, Hofouf, rather than in cities such as Dammam and Dahran. Factors, such as socioeconomic status and cultural habits (e.g., diet, use of traditional remedies and cosmetics), may have contributed to this result.
To assess the relationship between altitude, atherogenic, and anti-atherogenic lipoprotein cholesterols (low- [C-LDL] and high [C-HDL] density lipoprotein cholesterols, respectively), 136 and 94 Venezuelan Mestizos living at 1,000 and 3,500 in elevation were studied. The two groups did not differ in regard to height, weight, ethnic origin, social or economic status, nutritional patterns, age, or occupation. Both groups had a high level of daily physical exertion, an imperative in their subsistence rural agricultural economy. Due to the mountainous terrain, high altitude residents were thought to have increased levels of physical activity. Males and females at high altitude had significantly lower plasma total cholesterol and C-LDL levels, and slightly lower C-HDL levels than those at low altitudes. It is speculated that reduced coronary heart disease event rates at high altitude might be related to lower levels of the atherogenic lipoprotein cholesterol, C-LDL.
This study was conducted to identify risk factors for paraquat-related occupational illnesses. Pesticide-related illness is a reportable disease in California. A total of 231 skin (26.0%), eye (32.0%), local respiratory (3.5%), and systemic (38.5%) paraquat-related cases were reported to the Worker Health and Safety Branch, California Department of Food and Agriculture, during 1971 through 1985. Following paraquat exposure, we found no cases of pulmonary fibrosis. Annual numbers of cases ranged between 1 and 33 (median = 14 cases/y). Information on illnesses reported during 1981 through 1985 (n = 62) was merged with detailed information on paraquat use in agricultural settings (111,716 applications) for the same years. We found that crop treated, method of application, and season of application all contributed independently to the risk of reported illness. Hand application was associated with a higher risk of illness, compared with air application (RR = 99.1, 95% CI = 22.16-443.47); summer application was associated with a higher risk of illness than was winter application (RR = 4.1, 95% CI = 1.91-8.61); and fruit trees were associated with higher risk of illness than were other crops (mainly cotton) (RR = 3.6, 95% CI = 1.18-11.21).
The organochlorine pesticide 2,2-bis(p-chlorophenyl)-1,1,1,-trichloroethane (DDT) and its metabolite 1,1-dichloro-2,2-bis(p-chlorophenyl)ethylene (DDE) are examples of an environmental contaminant that may have hormonal properties. Bone metabolism is both estrogen- and androgen-dependent. Exposures to various environmental endocrine disrupters can affect bone metabolism in animals, but there are no published data concerning the effect of DDE exposure on bone metabolism in humans. We hypothesized that high levels of DDE would be associated with lower bone density in peri- and postmenopausal women than in premenopausal women. Study subjects were drawn from the cohort of women who had participated in the Mount Sinai Medical Center Longitudinal Normative Bone Density Study (1984-1987). We used serum samples obtained at study entry to measure DDE levels in 103 (50 black, 53 white) women (mean age = 54.5 y [standard deviation = 5 y]). Measurements of bone mineral density at the lumbar spine and radius were made at 6-mo intervals during a 2-y period. DDE concentrations were significantly (p < .001) higher in blacks (13.9 ng/ml) than in whites (8.4 ng/ml), but there was no correlation between DDE concentration and bone density at the spine (mean levels = 1.065 g/cm2 and 1.043 g/cm2 in the lowest and highest quartiles, respectively, of DDE [trend p value = .85]) or at the radius (mean levels = 0.658 g/cm and 0.664 g/cm in the lowest and highest quartiles, respectively, of DDE [trend p value = .34]). Longitudinal analyses revealed no correlation between DDE and the rate of bone loss at either bone site. Similar results were seen in race-stratified analyses, as well as in analyses in which we controlled for lactation history and other potential confounders. We found little evidence that chronic low-level DDT exposure is associated with bone density in peri- and postmenopausal women.
Fatty fish species, e.g., salmon and herring, in the Baltic Sea have high levels of polychlorinated biphenyls (PCBs) and 1,1,1-trichloro-2,2-bis(p-chlorophenyl)ethane (p,p'-DDT), and its main metabolite: 1,1-dichloro-2,2-bis(p-chlorophenyl)-ethylene (p,p'-DDE). We determined levels of 10 different PCB congeners, including non- and mono-ortho-PCBs, as well as DDT and DDE, in human blood plasma from 37 subjects with varying intake of fish (0-1 750 g/wk) from the Baltic Sea. With respect to all of the PCB congeners we investigated, as well as for DDT and DDE, there were statistically significant associations with fish intake. Thus, fish from the Baltic Sea is a major source of exposure to these compounds in Swedes. Polychlorinated dibenzo-p-dioxins (PCDD) and dibenzofurans (PCDF) had been determined earlier in 29 of the subjects. The PCB contribution to "dioxin-like" effects among high consumers of fish (calculated as Nordic TCDD equivalents) was almost 80%, whereas that from PCDD and PCDF was only 20%.
The organochlorine pesticide 1,1,1-trichloro-2,2-bis (p-chlorophenyl)-ethane (DDT), is a well-known and widely dispersed "environmental estrogen" (World Health Organization Criteria no. 9; Geneva, Switzerland ). Kelce et al. (Nature, 1995; 375:581-85) recently identified the DDT metabolite, 1,1-dichloro-2,2-bis(p-chlorophenyl)ethylene (DDE), has also recently been identified as a potent androgen receptor antagonist. The authors examined the relationship between serum levels of DDE and bone mineral density in 68 sedentary women who reported adequate dietary intake of calcium. Reduced bone mineral density was correlated significantly with age (r = -.36, p = .004), as well as with increases in the log of DDE levels in serum (r = -.27, p = .03). The authors also used multiple-regression analysis to examine the influence of other predictor variables on the relationship between log DDE and bone mineral density. The strongest model (p = .002) included log DDE (p = .018), age (p = .002), and years on hormone replacement therapy (p = .10) as predictor variables, and this model afforded prediction of 21% of bone mineral density variation. These results suggest that past community exposures to DDT may be associated with reduced bone mineral density in women.
The effects of 1,1,1-trichloroethane (1,1,1-TCE) inhalation on total peripheral vascular resistance and the possibility of the peripheral vessels being a site of action for 1,1,1-TCE were investigated in anesthetized dogs. In acute inhalation experiments, a decrease in total peripheral vascular resistance was observed following inhalation of 1,1,1-TCE concentrations sufficient to induce systemic hypotension. The threshold concentration of 1,1,1-TCE required to produce a decrease in perfusion pressure of the isolated hindlimb was approximately 0.4-0.5% in inspired air. A dose-response relationship between the decrease in perfusion pressure and 1,1,1-TCE concentration, which exceeded the threshold level, was observed. It is suggested that the decrease in total peripheral vascular resistance is related to systemic hypotension following 1,1,1-TCE inhalation; further, this vasodilator effect may be induced in the peripheral vessels, which is one of the sites where 1,1,1-TCE acts.
The response of heart rate to acute 1,1,1-trichloroethane (1,1,1-TCE) inhalation and its mechanism via the autonomic nervous system were studied in anesthetized dogs in acute inhalation experiments. Concentrations of 1,1,1-TCE in inspired air of 1.32 +/- 0.14% (mean +/- S.E.) increased heart rate, but 2.79 +/- 0.24% decreased heart rate. Opposite reactions of heart rate were observed when blood pressure decreased to 70-80 mm Hg following inhalation. Moreover, both tachycardia from relatively low concentrations and bradycardia from higher concentrations were blocked by pre-administration of adrenergic beta blocker, but were only slightly affected by vagotomy. It is suggested that both tachycardia and bradycardia following 1,1,1-TCE inhalation may be controlled by the sympathetic nervous system.
The effects of 1,1,1-trichloroethane (1,1,1-TCE) inhalation on respiration and afferent activity of the lung stretch receptor were investigated in anesthetized dogs. In acute inhalation experiments, rapid and shallow breathing was observed following inhalation of high 1,1,1-TCE concentrations. The threshold concentration of 1,1,1-TCE to produce an increase in respiratory rate was approximately 0.9% in inspired air. Moreover, a dose-response relationship was observed between the increase in respiratory rate and concentrations which exceeded the threshold level. An inspiratory action of respiration markedly decreased for high 1,1,1-TCE concentrations. Both the increase in respiratory rate and the decrease in the inspiratory action for high 1,1,1-TCE concentrations were significantly inhibited, however, these reactions were not completely blocked by bilateral vagotomy. Afferent impulses of the lung stretch receptor in the vagus nerve obviously increased following 1,1,1-TCE whose concentrations were more than 0.9% in inspired air. It is suggested that rapid and shallow breathing following higher 1,1,1-TCE concentrations may be related to the increase in the activity of the lung stretch receptor. It is further suggested that a part of rapid and shallow breathing is not based on anesthetic effects but enhancement of Hering Breuer reflex following 1,1,1-TCE inhalation.
An epidemiologic study of 151 matched pairs of employees was conducted in two adjacent textile plants, one of which used inhibited 1,1,1-trichloroethane as a general cleaning solvent. Employees in the study population had exposures to the solvent for 6 yrs or less at varying concentrations which were measured by breathing zone sampling and personal monitoring. While cardiovascular and hepatic observations were of primary interest, other health parameters were also studied. Application of sensitive statistical techniques and careful examination of all data did not reveal any clinically pertinent findings that were associated with exposure to 1,1,1-trichloroethane. The statistically significant associations that were observed between health measures and nonexposure factors emphasize the need to consider age, sex, race, and other variables in designing epidemiologic studies.
Two fatal poisonings resulting from exposure to 1,1,1-trichloroethane are described. Each case occurred at a separate workplace where the solvent was used as a degreasing agent. These cases are considered in light of other 1,1,1-trichloroethane poisonings reported to Her Majesty's Factory Inspectorate. Factors common to these and other incidents are discussed.
The effect of acute 1,1,1-trichloroethane (1,1,1-TCE) inhalation on left ventricular contractility and influence on heart rate were investigated in anesthetized dogs. In the acute inhalation experiment, a decrease in the maximum left ventricular dp/dt (peak dp/dt) was observed following inhalation of higher 1,1,1-TCE contentrations. The threshold concentration of 1,1,1-TCE that decreased peak dp/dt was approximately 0.2% in inspired air. A dose-response relationship was observed between the decrease in peak dp/dt and 1,1,1-TCE concentration. Heart rate recorded simultaneously increased with relatively low concentrations and decreased with higher concentrations. Increase or decrease in peak dp/dt was observed to be dependent on changes in heart rate induced by right atrial pacing. Thus, the degree of the decrease in peak dp/dt during pacing experiments was compared with those of nonpacing experiments. At low concentrations, peak dp/dt during pacing decreased more than in nonpacing experiments. With higher concentrations, the decreases in peak dp/dt during pacing was slightly less than in the nonpacing experiments. Heart rate may be important in regulating peak dp/dt for relatively low 1,1,1-TCE concentrations. However, the effect of heart rate on peak dp/dt is slight at higher concentrations.
Acute exposure of anesthetized dogs to 1,1,1-trichlorothane (TCE) results in a dose-dependent, biphasic decline in arterial pressure similar to that observed following exposure to a commercial solvent containing TCE. The initial phase of pressure decline is associated with peripheral vasodilation whose magnitude exceeds concomitant, reflex, positive chronotropic and inotropic effects on myocardial function. The peripheral dilation could be reversed by injection of the α-agonist, phenylephrine hydrochloride. The second phase of pressure decline is primarily associated with a depression of myocardial function; heart rate, stroke output, and myocardial contractility declined. Injection of Ca++ ameliorated the TCE-induced alteration of myocardial contractility and blood pressure was protected. The data suggest that comprehension of the mech- anism(s) by which TCE induces cardiovascular depression may lead to more effective clinical management of the toxic effects of this compound.
The effects of 1,1,1-trichloroethane (1,1,1-TCE) inhalation on arterial blood pressure and renal sympathetic nerve activity were investigated in anesthetized dogs. In acute inhalation experiments, the threshold concentration of 1,1,1-TCE required to produce a decrease in blood pressure was 0.4 to 0.5% in inspired air; moreover, a dose-response relationship between the decrease in blood pressure and 1,1,1-TCE concentration which exceeded the threshold level was observed. In addition, renal nerve activity increased and was associated with a slight decrease in blood pressure following inhalation of relatively low concentrations of 1,1,1-TCE. Following inhalation of relatively high concentrations of 1,1,1-TCE, however, renal nerve activity decreased and was accompanied by a marked decrease in blood pressure. Opposite reactions of renal nerve activity were observed when blood pressure decreased to 70-80 mm Hg following inhalation. It is suggested that systemic hypotension resulting from 1,1,1-TCE inhalation may be controlled by two different reactions of sympathetic nerve activity.
A case is described of peripheral sensory neuropathy in a woman who had daily exposure to 1,1,1-trichloroethane, used as a degreasing agent. Although previous reviews of the health effects of 1,1,1-trichloroethane have not indicated long-term neurotoxicity, there are recent animal studies that suggest chronic central neurotoxic effects and previous case reports of peripheral neuropathy in three exposed workers in one plant. Our case provides additional evidence that 1,1,1-trichloroethane exposure may be associated with peripheral sensory neuropathy. Reporting of similar cases is encouraged and investigation of the neurotoxic effects of 1,1,1-trichloroethane is recommended.
A scale based upon the induction of anti-tumor cellular immune responses has been described which relates the in vivo mutagenic/carcinogenic potential of an environmental agent with that of ionizing radiation. Such a potential (radiation equivalency) has now been determined in rats for the gastrointestinal carcinogen 1, 2,-dimethylhydrazine as compared with the effects induced by X-irradiation of only the small intestine. The preliminary results suggest that such scales may be readily constructed based upon environmental immunology concepts which relate the potential hazard of an agent to be weighed alongside the maximum allowable population limits of ionizing radiation.
High doses of 2,4,5 trichlorophenoxy acetic acid (2,4,5 T) (6.25, 12.5, or 25 mg/kg ten times daily) were administered orally to mature male mice. The herbicide 2,4,5 T significantly reduced the assimilation of radioactive androgen by the proslate gland (P ≤ .05). This was reflected not only in a reduction in the total accumulation of testosterone-1,2-3H2 (T-3H2) by the prostate gland, but also in a decrease in the levels of its labeled metabolites.
Ground-water contamination with the pesticides 1,2 dibromo-3-chloropropane (DBCP) and ethylene dibromide (EDB) affects Fresno/Clovis city in California. The spatial and temporal distribution of DBCP and EDB in public wells in Fresno/Clovis was examined, using mapping and time-series analyses of chemical test results, during the time periods 1979-1980 and 1992-1993. Health risks were estimated from mean concentrations, lifetime cancer risks were estimated, and monitoring and control programs were reviewed. Mean DBCP concentrations in selected wells declined from 0.56 ppb in 1979-1980 to 0.18 ppb in 1992-1993. Closure of wells and wellhead filtration caused levels to be reduced further (i.e., to 0.06 ppb). Mean EDB concentrations declined from 0.25 ppb to 0.15 ppb during the same time periods. The estimated lifetime cancer risk for DBCP was 1 excess death per 125 000 population in 1992-1993, but this risk varied within the city. The risk for EDB was 1 excess death per 2.2 million. Recommendations were made for the modeling of pesticide movement in ground water and for epidemiological studies.
An adolescent drank a few milliliters of a volatile hydrocarbon in the expectation of getting “high.” Despite deceptively few symptoms and signs on admission and sophisticated therapy later, his condition ran a rapid, downhill course and he died after five days. Two prominent clinical features were hypoglycemia and hypercalcemia. At autopsy, the major findings were florid liver necrosis, renal tubular necrosis, and focal adrenal degeneration and necrosis. The pathologic findings are correlated with the clinical features except for hypercalcemia. The reasons for this and many similar tragedies lie not only in personality problems, but also in the failure to provide aεleqyate warning on the product labels.
Three groups composed of rats, rabbits, and monkeys were exposed for 26 weeks to 1,2,4-trichlorobenzene (-TCB), and one group of each species was used as a control group. The nominal exposure concentrations of 1,2,4-TCB were 25.0, 50.0, and 100.0 ppm. Pulmonary function and operant behavior tests in monkeys, ophthalmoscopic examinations in rabbits and monkeys, and measurement of body weights and hematologic and serum biochemical determinations in all species were conducted before and during the exposure period. At termination of 1, 3, and 6 months of exposure, microscopic examination of selected rat tissues was performed. Microscopic changes were seen in the parenchymal of livers and kidneys from all groups of rats exposed to 1,2,4-TCB when sacrificed after 4 and 13 weeks of exposure, but no exposure-related abnormalities or other effects were seen after 26 weeks of exposure in any species.
In a study to evaluate its acnegenic potential, increasing concentrations of 1,2,4-trichlorobenzene were applied topically to the ventral surface of the rabbit ear three times weekly for 13 weeks. Additional groups of rabbits received similar treatment with petroleum ether (solvent controls), received no treatment (negative controls), and received four once-weekly treatments with hexachlorodiphenyloxide, a known chloracnegenic agent (positive controls). Skin response to 1,2,4-trichlorobenzene was characterized grossly by dermal irritation directly related to the concentration of test material; there were the associated histologic changes of acanthosis and hyperkeratosis; there was no primary follicular involvement characteristic of acneform dermatitis. Dermal responses to hexachlorodiphenyloxide consisted of gross follicular enlargement, with waxy excretion on pressure, and severe scaling. The affected ear appeared thickened up to three times normal size and histologic sections showed primary follicular involvement characterized by marked thickening of the sheath and marked distention of the follicles with keratin, with resultant comedone formation, typical of chloracne.
Potential adverse health effects from occupational exposure to 1,3-dichloro-propene (DCP) are reviewed and hazards assessed. Further toxicologic evaluations should be conducted using only high-purity material that is free from possibly confounding impurities and stabilizers. Safety considerations when handling the material are included.
A gas chromatographic-mass spectrometric assay was developed to identify and measure the N-acetyl cysteine conjugate of cis-1,3-dichloropropene. The assay was used to show that individuals exposed to 1,3-dichloropropene vapor during field applications excrete this conjugate in their urine. The recoveries of the conjugate were correlated with the product of airborne concentrations and the duration of exposure (r = 0.83).
1,3-dichloropropene (DCP), the primary constituent of Telone II, is a subsoil fumigant that has supplanted 1,2-dibromo-3-chloropropane (DBCP) and ethylene dibromide (EDB) as primary fumigant in Hawaiian pineapple culture. To determine the potential for adverse health effects, an environmental survey was done to assess worker exposures. Exposures were predominantly below 1 ppm, which is the no-effect level determined with experimental animals, and the Threshold Limit Value (TLV) recommended by the American Conference of Governmental Industrial Hygienists (ACGIH).
A comparison was made of the effects of acrolein and aqueous cigarette smoke extracts on amino acid incorporation into protein by rabbit pulmonary alveolar macrophages. Studies were on cells maintained in vitro as adherent monolayers. Freshly prepared acrolein inhibited amino acid incorporation by significant amounts after approximately 30 min and aqueous smoke extracts after approximately 15 min of incubation. Fifty percent inhibition by acrolein occurred with a dose of 5.5 microgram acrolein/ml, an amount four times that in the amount of aqueous smoke extract required for 50% inhibition according to previously reported findings. Analysis by a dual-isotope technique and sodium dodecyl sulfate polyacrylamide gel electrophoresis showed the inhibitory effect of acrolein to be nonspecific, as had previously been found for aqueous smoke extracts. The presence of the sulfhydryl reagent cysteine, reduced the inhibitory effect of acrolein by 57.5%, but reduced inhibition induced by aqueous smoke extracts by only 12.2%. These results suggest the effects of acrolein are both quantitatively and qualitatively different than those of aqueous smoke extracts.
The immunotoxicological effects of cadmium suggest that it may alter immunosurveillance. However, the studies contributing to this conclusion have been conducted at relatively high cadmium concentrations and for extended periods of exposure. Cadmium was administered in the drinking water of Balb/c mice at 0.01, 0.10, and 1.0 ppm for 4 to 5 wk. Under these conditions, there was a cadmium dose-dependent change in the mortality rate of mice when challenged with an intraperitoneal injection of 5 X 10(3), 5 X 10(4), or 5 X 10(5) MOPC-104E plasmacytoma cells. There was a maximum decrease in mortality at the 0.01 ppm dose level, while at the higher cadmium concentrations there was little or no change. At the two highest tumor cell doses, there was a decrease in the incubation time of the illness in animals exposed to 0.01 ppm cadmium. This returned to control values at the higher concentration of cadmium. The data indicate that at very low concentrations cadmium can alter tumor growth by more than one mechanism that may involve immunocompetence.
Distribution of subcutaneously injected cadmium 109 (109Cd) was studied in mature rats over a period of 14 days. Tthe isotope was primarily deposited in the kidneys, liver, and pancreas. Within four hours after injection, cadmium appeared in the wall and in the contents of the small intestine. In the colon and in its contents, the concentration of the isotope increased gradually over a period of 24 hours. Cadmium content in the intestinal tract decreased progressively between 30 and 336 hours after injection. The stomach wall concentrated and retained 109Cd, and only traces of the isotope appeared in the contents of the stomach. From the blood plasma, cadmium disappeared rapidly, whereas the blood cells showed an increase in cadmium concentration between 24 and 336 hours after injection.