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Biomedical subjects

V Riihimäki

Publications and source records attributed to V Riihimäki.

At least 19 recordsLinked to original sources

Body burden of aluminum in relation to central nervous system function among metal inert-gas welders.

OBJECTIVES: The relationship between elevated internal aluminum loads and central nervous system function was studied among aluminum welders, and the threshold level for adverse effect was defined. METHODS: For 65 aluminum welders and 25 current mild steel welders body burden was estimated, and the aluminum concentrations in serum (S-Al) and urine (U-Al) were analyzed with graphite furnace atomic absorption spectrometry with Zeeman background correction. Referents and low-exposure and high-exposure groups were defined according to an aggregated measure of aluminum body burden, the group median S-Al levels being 0.08, 0.14, and 0.46 micromol/l, respectively, and the corresponding values for U-Al being 0.4, 1.8, and 7.1 micromol/l. Central nervous system functions were assessed with a neuropsychological test battery, symptom and mood questionnaires, a visual and quantitative analysis of electroencephalography (EEG), and P3 event-related potentials with pitch and duration paradigms. RESULTS: Subjective symptoms showed exposure-related increases in fatigue, mild depression, and memory and concentration problems. Neuropsychological testing revealed a circumscribed effect of aluminum, mainly in tasks demanding complex attention and the processing of information in the working memory system and in the analysis and recall of abstract visual patterns. The visual EEG analysis revealed pathological findings only for aluminum welders. Mild, diffuse abnormalities were found in 17% of the low-exposure group and 27% of the high-exposure group, and mild to moderate epileptiform abnormalities at a frequency of 7% and 17%, respectively. CONCLUSIONS: Both objective neurophysiological and neuropsychological measures and subjective symptomatology indicated mild but unequivocal findings dose-dependently associated with increased aluminum body burden. The study indicates that the body burden threshold for adverse effect approximates an U-Al value of 4-6 micromol/l and an S-Al value of 0.25-0.35 micromol/l among aluminum welders.

Adult↗

Effects of experimental exposure to triethylamine on vision and the eye.

OBJECTIVES: To determine the effect of triethylamine (TEA) on the cornea and to evaluate the cause of blurred vision. To find the lowest observed effect concentration of exposure to TEA. METHODS: Four people were exposed to TEA for 4 hours at concentrations of 40.6, 6.5, and 3.0 mg/m3. Before and after every exposure, symptoms and ocular microscopy findings were recorded. Binocular visual acuity and contrast sensitivity at 2.5% contrast were also measured. Also, before and after the 40.6 mg/m3 exposure, corneal thickness was measured and ocular dimensions were recorded by ultrasonography, endothelial cells of the cornea were analysed, and serum and lacrimal specimens were collected for the analysis of TEA. RESULTS: After exposure to 40.6 mg/m3 TEA there was a marked oedema in the corneal epithelium and subepithelial microcysts. However, corneal thickness increased only minimally because of the epithelial oedema. The lacrimal concentrations of TEA were, on average (range) 41 (18-83) times higher than the serum TEA concentrations. The vision was blurred in all subjects and visual acuity and contrast sensitivity had decreased in three of the four subjects. After exposure to TEA at 6.5 mg/m3 two subjects experienced symptoms, and contrast sensitivity had decreased in three of the four subjects. There were no symptoms or decreases in contrast sensitivity after exposure to a TEA concentration of 3.0 mg/m3. CONCLUSIONS: TEA caused a marked oedema and microcysts in corneal epithelium but only minor increases in corneal thickness. The effects may be mediated by the lacrimal fluid owing to its high TEA concentration. Four hour exposure to a TEA concentration of 3.0 mg/m3 seemed to cause no effects, whereas exposure to 6.5 mg/m3 for the same period caused blurred vision and a decrease in contrast sensitivity.

Adult↗

Decrements in cognitive performance in metal inert gas welders exposed to aluminium.

OBJECTIVES: Often little has been discovered of the cognitive functions affected by occupational toxins because many functions cooperate to produce the single performance scores typically reported from neuropsychological tests. To facilitate the interpretation of neuropsychological scores, the issue of occupational exposure to aluminium was examined with an approach intended to increase understanding of those cognitive processes that may be affected. METHODS: The investigation was a cross sectional study of asymptomatic aluminium welders and a reference group of mild steel welders. Based on urinary aluminium concentrations, welders were classified into a reference (n = 28), low (n = 27), and high (n = 24) exposure group. The mean urinary aluminium concentrations were 0.46, 2.25, and 9.98 mumol/l, respectively. A comprehensive neuropsychological examination was undertaken to assess psychomotor function, simple visual reaction time, attention related tasks, verbal and visual or visuospatial abilities as well as verbal and visual learning and memory. RESULTS: Aluminium welders showed no impairment on the finger tapping, Santa Ana dexterity, simple visual reaction times, any of the verbal memory tasks, the similarities subtest of Wechsler adult intelligence scale, or the Stroop task. However, the low exposed group performed poorer on the memory for designs and on more difficult block design items demanding preliminary visuospatial analysis. The time limited synonym task, embedded figures, digit symbol speed, and the backward counting component of the divided attention task showed exposure-response relations. CONCLUSIONS: The impairments found were circumscribed. When the neuropsychological tasks were scored to show some of the underlying theoretical cognitive structures, the results indicated that performance difficulties were mainly detected in tasks requiring working memory, particularly that relating to processing of visuospatial information. There was also evidence that such impairments are more readily found in time limited tasks involving visually presented material, in which effective visual scanning combined with control of working memory is demanded.

Adult↗

Occupational exposure to lead and neuropsychological dysfunction.

OBJECTIVE: To evaluate the neuropsychological effects of current low level and previous higher levels of exposure to lead and evaluate the relation between effects of lead and bone lead. METHODS: A neuropsychological test battery was given to 54 storage battery workers with well documented long term exposure to lead. The effect was studied in two subgroups: those whose blood lead had never exceeded 2.4 mmol/l (the low BPbmax group, n = 26), and those with higher exposure about 10 years earlier (the high BPbmax group, n = 28). In both groups, the recent exposure had been low. Correlations between the test scores and the indices of both long term and recent exposure--including the content of lead in the tibial and calcaneal bone--and covariance analyses were used to assess the exposure-effect relation. Age, sex, and education were controlled in these analyses. RESULTS: Analyses within the low BPbmax group showed a decrement in visuospatial and visuomotor function (block design, memory for design, Santa Ana dexterity), attention (digit symbol, digit span), and verbal comprehension (similarities) associated with exposure to lead and also an increased reporting of subjective symptoms. The performance of the high BPbmax group was worse than that of the low BPbmax group for digit symbol, memory for design, and embedded figures, but there was no reporting of symptoms related to exposure, probably due to selection in this group. No relation was found between the output variables and the tibial lead concentration. The calcaneal lead concentrations were related to the symptoms in the low BPbmax group. CONCLUSIONS: Neuropsychological decrements found in subjects with high past and low present exposure indicate that blood lead concentrations rising to 2.5-4.9 mmol/l cause a risk of long lasting or even permanent impairment of central nervous system function. Milder and narrower effects are associated with lower exposures; their reversibility and time course remain to be investigated. History of blood lead gives a more accurate prediction of the neuropsychological effects of lead than do measurements of bone lead.

Adult↗

Effects of low level exposure to lead on neurophysiological functions among lead battery workers.

OBJECTIVES: Assessment of neurophysiological functions in workers with low level exposure to lead and evaluation of the efficacy of bone lead measurements in the prediction of effects of lead. METHODS: Exposure to lead of 60 workers from a lead battery battery factory was estimated from historical blood lead measurements and analysis of lead in the tibial and calcaneal bones with x ray fluorescence. Peripheral and central nervous system functions were assessed by measuring conduction velocities, sensory distal latencies, sensory amplitudes, and vibration thresholds as well as by quantitative measurement of the absolute and relative powers and mean frequencies of different electroencephalograph (EEG) channels. RESULTS: Sensory amplitudes, and to a smaller degree sensory or motor conduction velocities, showed a negative correlation with long term exposure to lead, most clearly with integrated blood lead concentration and exposure time. Vibration thresholds measured in the arm were related to recent exposure to lead, those measured in the leg to long term exposure. The alpha and beta activities of the EEG were more abundant in subjects with higher long term exposure to lead. Calcaneal lead content reflected short term exposure, tibial lead content reflected long term exposure. Blood lead history showed a closer relation with effects of lead than the tibial or calcaneal lead concentrations. CONCLUSIONS: Vibratory thresholds, quantitative EEG, and to a smaller extent the sensory amplitude, provide sensitive measures of effects of lead in occupationally exposed adults. Most accurate estimates of health risks induced by lead can be obtained from a good history of blood lead measurements. If such a history of blood lead concentrations is not available, analysis of bone lead may be used for the assessment of health risks.

Adult↗

Urinary 1-naphthol excretion in the assessment of exposure to creosote in an impregnation facility.

OBJECTIVES: This study explored the possibility of using urinary 1-naphthol excretion as a marker of complex exposure among workers handling creosote. METHODS: Urine specimens of 6 workers from a creosote impregnation plant, where railroad ties were impreganted with coal tar creosote, were collected during 1 workweek, and the concentration of 1-naphthol was determined. 1-Naphthol in spot urine samples of 5 occupationally nonexposed male smokers was used as the background reference. Concurrently, naphthalene and 10 different polycyclic aromatic hydrocarbons (PAH) were determined in personal air samples. RESULTS: The mean airborne exposure of the workers was 1.5 mg/m3 for vaporous naphthalene, 5.9 micrograms/m3 for particulate PAH and 1.4 micrograms/m3 for PAH with 4-6 aromatic rings. The mean urinary concentration of 1-naphthol at the end of the workshift was 20.5 (range 3.5-62.1) mumol/l, whereas the referents' urinary concentration was below the detection limit (0.07 mumol/l). Airborne naphthalene correlated fairly well with 1-naphthol when measured at the end of the shift (r = 0.745). CONCLUSIONS: This method of analysis for 1-naphthol is sufficiently sensitive for measuring low occupational exposures to naphthalene. Low background exposures are, however, unlikely to result in detectable urinary levels of 1-naphthol. Since naphthalene is the most abundant compound in creosote vapor, urinary 1-naphthol determination serves well as a biological marker of exposure to vaporous creosote. Urinary 1-naphthol alone is not, however, a suitable marker for inhalatory or cutaneous exposure to PAH originating from creosote.

Air Pollutants, Occupational↗

Acute effects of 1,1,1-trichloroethane inhalation on the human central nervous system.

The object of this study was to examine the immediate nervous effects of variable 1,1,1-trichloroethane (TCE) exposure combined with physical exercise. The effects on the quantitative electroencephalography (EEG), visual evoked potentials (VEP) and body sway were analyzed. Nine male volunteers were exposed to either a stable or a fluctuating exposure pattern with the same time-weighted average concentration of 200 ppm (8.1 mumol/l). In both cases, the subjects engaged in physical exercise during the exposures. Exercise alone induced an increase in the dominant alpha frequency in the EEG and, after an initial drop, an increase in the alpha percentage with a concomitant decrease in theta, whereas delta and beta bands remained unaffected. By contrast, exposure to TCI and exercise did not affect the alpha, theta or delta activities but induced changes in beta during the morning recordings at peak exposure to TCE. The body sway tended to decrease slightly during the fluctuating TCE exposure, and the later peaks in VEPs showed slight prolongations. Overall, no deleterious effects of exposure were noted.

Air Pollutants, Occupational↗

Different contributions of cytochrome P450 2E1 and P450 2B1/2 to chloroform hepatotoxicity in rat.

The contribution of cytochrome P450 isozymes CYP2E1 and CYP2B1/2 to chloroform-induced hepatotoxicity taken at 18 hr after the treatment was investigated in rats treated with n-hexane as an inducer of CYP2E1, 2-hexanone as an inducer of CYP2E1 and CYP2B1/2, and phenobarbital (PB) as an inducer of CYP2B1/2. Hepatic damage was evaluated by gross measurement of plasma alanine aminotransferase activity and histopathological examination. All treatments potentiated chloroform-induced hepatic damage. In n-hexane-pretreated rats, the damage was maximal with the middle dose of chloroform (0.2 ml/kg), whereas the damage increased with dose in rats treated with 2-hexanone or PB. The degree of hepatic damage induced with the three pretreatments was in the following order: n-hexane > 2-hexanone = PB with the middle dose of chloroform and PB >> 2-hexanone > n-hexane with the high dose (0.5 ml/kg); little difference among the pretreatments was seen with the low dose (0.1 ml/kg). These findings suggest that CYP2E1 is a low Km isoform and CYP2B1/2 a high Km isoform for chloroform activation. CYP2E1-dependent hepatic damage was characterized by ballooned hepatocytes, which were restricted to the centrilobular area; with CYP2B1/2, more necrotic than ballooned hepatocytes were seen and the necrotic hepatocytes were found not only in the centrilobular but also in the midzonal and periportal areas. Chloroform treatment did not affect the activity of N-nitrosodimethylamine N-demethylase in pretreated rats; the high dose increased the activity in control rats. In contrast, the high dose of chloroform decreased the activity of 7-pentoxyresorufin O-depentylase in all induced rats but not in controls. Immunoinhibition and immunoblot analyses showed that the high dose of chloroform induced CYP2E1 in control rats but decreased CYP2B1/2 in all pretreated rats. These results suggest that although both CYP2E1 and CYP2B1/2 contribute to chloroform-induced hepatic damage, they do so quite differently.

Alanine Transaminase↗

Urinary 1-naphthol and 1-pyrenol as indicators of exposure to coal tar products.

Chemical exposure of assemblers handling creosote-impregnated wood and of a single worker chiselling coal tar pitch layer was assessed by measuring airborne naphthalene and various polycyclic aromatic hydrocarbons (PAHs), and by measurement of urinary excretion of 1-naphthol and 1-pyrenol. The sum concentration of PAHs and of 4-6 aromatic ring-containing PAHs were high, 440 micrograms/m3 and 290 micrograms/m3, respectively, when chiselling. In the assembler's workplace, the PAH concentrations were about 1/50 of this value. Regarding airborne naphthalene concentrations the situation was reversed (assemblers, 1000 micrograms/m3; chiseller, 160 micrograms/m3). Correspondingly, the assemblers' urinary 1-napthol concentrations were 15-20 times higher than those of the chiseller. The urinary 1-pyrenol concentration of the chiseller was 2-4 times higher than among the assemblers. As the estimated pyrene inhalation doses among the assemblers could account for only about 2%-25% of the 24-h pyrenol excretion in urine, the skin was presumably the main route of uptake. For an assessment of the exposure to PAHs, air measurements, monitoring of metabolites in urine and preferably also data on the composition of the skin-contaminating product are needed.

Air Pollutants, Occupational↗

Significance of dermal and respiratory uptake in creosote workers: exposure to polycyclic aromatic hydrocarbons and urinary excretion of 1-hydroxypyrene.

OBJECTIVES: To evaluate workers' exposure in a creosote impregnation plant by means of ambient and biological monitoring. METHODS: Naphthalene (vapour phase) and 10 large molecular polycyclic aromatic hydrocarbons (PAHs) (particulate phase) were measured in the breathing zone air during an entire working week. 1-Hydroxypyrene (1-HP) was measured in 24 hour urine as a metabolite of the pyrene found in neat (dermal exposure) and airborne creosote. RESULTS: Naphthalene (0.4-4.2 mg/m3) showed 1000 times higher concentrations in air than did the particulate PAHs. In total, the geometric mean (range) of three to six ring PAHs was 4.8 (1.2-13.7) micrograms/m3; pyrene 0.86 (0.23-2.1) micrograms/m3, and benzo(a)pyrene 0.012 (0.01-0.05) micrograms/m3. There was no correlation between pyrene and gaseous naphthalene. The correlations between pyrene and the other nine particulate PAHs were strong, and gave a PAH profile that was similar in all air samples: r = 0.83 (three to six ring PAHs); r = 0.81 (three ring PAHs); r = 0.78 (four to six ring PAHs). Dermal exposure was probably very high in all workers, because the daily output of urinary 1-HP exceeded the daily uptake of inhaled pyrene by < or = 50-fold. Urinary 1-HP concentrations were very high, even on Monday mornings, when they were at their lowest (4-22 mumol/mol creatinine). 1-HP seldom showed any net increase over a workshift (except on Monday) due to its high concentrations (16 to 120 mumol/mol creatinine) in the morning samples. 1-HP was always lower at the end of the shift (19 to 85 mumol/mol creatinine) than in the evening (27 to 122), and the mean (SD) change over the working week (47 (18)) was greater than the change over Monday (35 (32)). The timing of 1-HP sampling is therefore very important. CONCLUSIONS: Urinary 1-HP proved to be a good biomarker of exposure to three to six ring PAHs but not to airborne naphthalene. Hence, biomonitoring based on 1-HP has to be completed with exposure assessment for naphthalene as a marker for creosote volatiles that mainly enter the body through the lungs.

Air Pollutants, Occupational↗

Mortality and cancer morbidity of Finnish chlorophenoxy herbicide applicators: an 18-year prospective follow-up.

An 18-year follow-up for mortality and cancer morbidity was conducted in a cohort of 1,909 men who had started spraying chlorophenoxy herbicides (mixture of 2,4-dichlorophenoxyacetic acid [2,4-D] and 2,4,5-trichlorophenoxyacetic acid [2,4,5-T]) in 1955 through 1971. In all, 384 persons had died during the follow-up, and there was a slight deficit in natural deaths (standardized mortality ratio [SMR] 0.84; 95% confidence interval [CI] 0.75-0.94). By contrast, there was a small, nonsignificant increase in accidental and violent deaths. The overall cancer mortality was slightly less than in the general population (SMR 0.83; 95% CI 0.65-1.02), and not a single case of death of non-Hodgkin's lymphomas (NHL) or soft tissue sarcomas (STS) was detected. With regard to cancer morbidity, the incident cases showed a slight deficit compared to the population figure (standardized incidence ratio [SIR] 0.81; 95% CI 0.67-0.97). One case of NHL was found (2.4 expected with 10 years of latency), but not a single case of STS (0.8 expected with 10 years of latency). While our study does not support the contention that spraying of 2,4-D and 2,4,5-T containing herbicides carries any significant risk of cancer, the medium to low statistical power of the study does not allow any far reaching negative conclusions regarding the carcinogenicity of the agents.

2,4,5-Trichlorophenoxyacetic Acid↗

Internal load of aluminum and the central nervous system function of aluminum welders.

OBJECTIVES: Because the brain is the recognized target organ for aluminum toxicity, internal aluminum load and central nervous system functions were investigated among aluminum welders in a shipyard. METHODS: Seventeen male welders with a mean age of 37 (range 24-48) years and a history of about four years of metal inert-gas welding on aluminum were the subjects. Aluminum in serum (S-Al) and urine (U-Al) was analyzed with graphite-furnace atomic absorption spectrophotometry. Central nervous system functions were examined with neuropsychological tests, symptom and mood questionnaires, quantitative electroencephalography (QEEG), and P300 evoked responses. RESULTS: The mean S-Al concentration was 0.21 (range 0.03-0.64) mumol.l-1 and the mean U-Al was 2.8 (range 0.9-6.1) mumol.l-1. Although the welders performed normally on the neuropsychological tests, there was a negative association between all four memory tests and U-Al and a positive association between the variability of visual reaction times and S-Al. In the QEEG, the amount of delta and theta activity in the frontal region correlated positively and the amount of alpha activity in the frontal region correlated negatively with S-Al. CONCLUSIONS: The S-Al and U-Al measurements indicated increased internal loads of aluminum in most of the welders. This finding is compatible with slowly eliminated aluminum from tissues. The neuropsychological assessment suggested disturbing effects of aluminum on short-term memory, learning, and attention. In the QEEG, a corresponding exposure-effect relationship was found for activity in the frontal region. Further studies are needed on the possibility that exposure to aluminum welding fumes causes harm to human health.

Adult↗

Acute effects of m-xylene inhalation on body sway, reaction times, and sleep in man.

Nine male volunteers were exposed to either a constant or a fluctuating exposure pattern of m-xylene with a time-weighted average exposure concentration of 200 ppm in both cases. The subjects remained sedentary throughout the exposure, or the exercised at 100 W for 10 min at the beginning of the morning and the afternoon sessions. In another experiment, 12 sedentary male volunteers were exposed to a fixed 200 ppm of m-xylene. The effects of m-xylene on body sway, reaction time performance, and overnight sleep were measured. Body balance was stabilized after exposure to the peaks of 400 ppm of m-xylene in both sedentary and exercising subjects. Simple visual reaction times were prolonged after the peak exposures at rest whereas auditive choice reaction times were prolonged after peaks combined with exercise. Exposure to m-xylene at a constant level of 200 ppm did not affect the ratio of "active" to "quiet" sleep in the volunteers as measured with the static charge sensitive bed recording, but decreased slightly the number of body movements in bed. On the next morning no changes were found in body sway and reaction time performance as compared to the morning before exposure.

Adult↗

Hospitalizations due to poisonings in Finland.

Poisonings constitute an important category of causes for admission of patients to the emergency room. The annual incidence of hospitalized poisonings in Finland over 2 years (1987-1988) was 11.7 for a population of 10,000 according to the Hospital Discharge Register; it was 8.7/10,000 for drugs and 3.0/10,000 for non-drugs. Children under 6 years of age were most frequently hospitalized because of poisoning (16.9/10,000), followed by adults aged 25-44 years (14.8/10,000). The leading causes of poisoning or chemical injury in children were undefined non-drug poisonings; plants, berries and mushrooms mistaken for edible food, and corrosives. In patients aged 6 years or more, mainly adults, the leading causes were psychotropic drugs, ethanol, and cardiovascular drugs. The pattern of poisoning has changed markedly during the 1980s; the rate of psychotropic and sedative drug poisoning admissions have increased from 35 to 47%, and poisonings due to analgesics have also increased significantly. Conversely, poisonings caused by cardiovascular drugs and antibiotics, solvent poisonings and incidents caused by corrosives have decreased significantly (p < 0.001).

Adolescent↗

Alcohol intoxication in hospitalized young teenagers.

The scientific literature concerning alcohol intoxication is enormous. However, less is known of alcohol-induced disturbances in children and adolescents and most of those reports concern cases of hypoglycemia in children under five years of age. We studied the clinical status and chemistry, especially acid-base balance, in 36 young teenagers treated at hospital for alcohol intoxication. On physical examination 6 patients were somnolent, 18 were comatose and 12 were in deep coma. The impairment of consciousness was directly proportional to the blood ethanol concentration. Acidosis was a central finding, and it was caused by a combination of respiratory and metabolic factors (a high blood PCO2 and a low base excess; r = 0.97, p < 0.001); the finding of respiratory acidosis dominated. Base excess correlated negatively with beta-hydroxybutyrate and lactate, as expected. All the metabolic products measured--acetate, beta-hydroxybutyrate and lactate--were significantly elevated compared with the control patients. No hypoglycemia was found. Prior treatment with intravenous glucose decreased vomiting and normalized the serum lactate concentration and PO2. Hypokalemia was the most common abnormality in serum electrolytes. In four patients the rate of fall of blood ethanol concentration was 2.8-3.3 mmol/h (0.13-0.15 g/l-1 h-1) and the mean acetate concentration was 0.8 mmol/l (SE 0.3). Biochemical disturbances in young teenage alcohol intoxicants resemble those previously found in adults. The severe toxicity by ethanol, manifesting in coma, occurs in lower blood alcohol concentrations in children than in adults.

Acetates↗

Assessment of exposure to carbon disulfide in viscose production workers from urinary 2-thiothiazolidine-4-carboxylic acid determinations.

The follow-up of environmental carbon disulfide (CS2) exposure and urinary excretion of 2-thiothiazolidine-4-carboxylic acid (TTCA) among 20 operatives over a 4-day working week in two viscose producing factories confirmed earlier observations that TTCA is a sensitive and reliable indicator of exposure to CS2. Exposure to as low as 0.5-1.0 ppm (1.6-3.2 mg/m3) of CS2 (8-hour time-weighted average [TWA]) was associated with detectable amounts of TTCA in end-of-shift urine. Moreover, the excretion of TTCA, relative to estimated CS2 uptake, appeared surprisingly constant in the studied work force. Approximately 3% (range 2-6.5%) of absorbed CS2 was detected in urine as TTCA. The proportional TTCA excretion did not show dose dependency in the estimated CS2 dose range which varied by about 20-fold. TTCA elimination exhibited both a fast (T 1/2 6 hour) and a slow (T 1/2 68 hour) phase. The slow elimination is compatible with a high lipid solubility and reversible protein binding of CS2. Consequently, urinary excretion of TTCA, relative to CS2 exposure, increased by about a third during the workweek. Urinary TTCA concentration of 4.5 mmol/mol creatinine in a postshift sample corresponded to a TWA exposure to 10 ppm CS2 towards the end of the working week.

Adult↗

In vivo measurements of lead in bone at four anatomical sites: long term occupational and consequent endogenous exposure.

Measurements of bone lead concentrations in the tibia, wrist, sternum, and calcaneus were performed in vivo by x ray fluorescence on active and retired lead workers from two acid battery factories, office personnel in the two factories under study, and control subjects. Altogether 171 persons were included. Lead concentrations in the tibia and ulna (representative of cortical bone) appeared to behave similarly with respect to time but the ulnar measurement was much less precise. In an analogous fashion, lead in the calcaneus and sternum (representative of trabecular bone) behaved in the same way, but sternal measurement was less precise. Groups occupationally exposed to lead were well separated from the office workers and the controls on the basis of calculated skeletal lead burdens, whereas the differences in blood lead concentrations were not as great, suggesting that the use of concentrations of lead in blood might seriously underestimate lead body burden. The exposures encountered in the study were modest, however. The mean blood lead value among active lead workers was 1.45 mumol l-1 and the mean tibial lead concentration 21.1 micrograms (g bone mineral)-1. The kinetics of lead in the tibia appeared to be noticeably different from that in the calcaneus. Tibial lead concentration increased consistently both as a function of intensity of exposure and of duration of exposure. Calcaneal lead concentration, by contrast, was strongly dependent on the intensity rather than duration of exposure. This indicated that the biological half life of lead in calcaneus was less than the seven to eight year periods into which the duration of exposure was split. Findings for retired workers clearly showed that endogenous exposure to lead arising from skeletal burdens accumulated over a working lifetime can easily produce the dominant contribution to systemic lead concentrations once occupational exposure has ceased.

Adult↗