[Paracoccidioidomicosis and multidrug-resistant tuberculosis (TBC-MDR) in patient coinfected with HIV and hepatitis C]. / Paracoccidioidomicosis y TBC-MR en portador de VIH/VHC.

A case of an adult male patient diagnosed with HIV and Hepatitis C co infection is presented. He had granu-lomatuos hepatitis and blood smear positive to Paracoccidioides brasiliensis concomitant to the detection of MDR Mycobacterium tuberculosis in sputum further complicated with reactivation of cytomegalovirus (possible pancreatitis and retinitis). Difficulties in diagnostic and therapeutic approach in a patient with multiple infections are reviewed.

Cancer induction by an organic arsenic compound, dimethylarsinic acid (cacodylic acid), in F344/DuCrj rats after pretreatment with five carcinogens.

Arsenic (As) is environmentally ubiquitous and an epidemiologically significant chemical related to certain human cancers. Dimethylarsinic acid (cacodylic acid; DMA) is one of the major methylated metabolites of ingested arsenicals in most mammals. To evaluate the effects of DMA on chemical carcinogenesis, we conducted a multiorgan bioassay in rats given various doses of DMA. One-hundred twenty-four male F344/DuCrj rats were divided randomly into 7 groups (20 rats each for groups 1-5; 12 rats each for groups 6 and 7). To initiate multiple organs and tissues, animals in groups 1-5 were treated sequentially with diethylnitrosamine (100 mg/kg body weight, i.p., single dose at the commencement) and N-methyl-N-nitrosourea (20 mg/kg body weight, i.p., 4 times, on days 5, 8, 11, and 14). Thereafter, rats received 1,2-dimethylhydrazine (40 mg/kg body weight, s.c., 4 times, on days 18, 22, 26, and 30). During the same period, the animals were sequentially administered N-butyl-N-(4-hydroxybutyl)nitrosamine (0.05% in the drinking water, during weeks 1 and 2) and N-bis(2-hydroxypropyl)nitrosamine (0.1% in the drinking water, during weeks 3 and 4; DMBDD treatment). After a 2-week interval, groups 2-5 were given 50, 100, 200, or 400 ppm DMA, respectively, in the drinking water. Groups 6 and 7, which were not given DMBDD treatment, received 100 and 400 ppm DMA during weeks 6-30. All rats were killed at the end of week 30. In the initiated groups (groups 1-5), DMA significantly enhanced the tumor induction in the urinary bladder, kidney, liver, and thyroid gland, with respective incidences in group 5 (400 ppm DMA) being 80, 65, 65, and 45%. Induction of preneoplastic lesions (glutathione S-transferase placental form-positive foci in the liver and atypical tubules in the kidney) was also significantly increased in DMA-treated groups. Ornithine decarboxylase activity in the kidneys of rats treated with 100 ppm DMA was significantly increased compared with control values (P < 0.001). In conclusion, DMA is acting as a promoter of urinary bladder, kidney, liver, and thyroid gland carcinogenesis in rats, and we speculate that this may be related to cancer induction by As in humans.

Impaired fasting glucose and the risk of hypertension in Japanese men between the 1980s and the 1990s. The Osaka Health Survey.

OBJECTIVE: To determine whether impaired fasting glucose (IFG) increased the risk for hypertension in two large Japanese cohorts during the different time periods. RESEARCH DESIGN AND METHODS: We prospectively investigated two Japanese cohorts: a 1980s population, comprising 4,130 normotensive and nondiabetic men aged 35-60 years entered between 1981 and 1983, and a 1990s population, comprising 4,319 normotensive and nondiabetic men aged 35-60 years entered between 1991 and 1992. Data on lifestyle factors were obtained from questionnaires. IFG was defined as a fasting plasma glucose level > or = 110 and < 126 mg/dl. RESULTS: During the 4-year observation period, 708 cases of hypertension were confirmed in the 1980s and 848 cases were confirmed in the 1990s. In both the 1980s and 1990s populations, IFG was associated with the risk of hypertension. The frequency of IFG in men in the 1990s group was twice as high as that in the 1980s group. The multivariate-adjusted odds ratio (OR) of hypertension was 1.54 (95% CI, 1.01-2.34) for men with IFG in the 1980s population and 1.73 (1.31-2.29) in the 1990s population, compared with those without IFG in the two populations. In the 1990s population, among lean men with a BMI < or = 23 kg/m2, men with IFG had a multivariate-adjusted OR of hypertension of 2.31 (1.46-3.65) compared with those without IFG. CONCLUSIONS: This study demonstrated direct correlation between IFG and hypertension and greater incidence of this hypertension in the 1990s group than in the 1980s group.

Daily alcohol consumption and the risk of type 2 diabetes in Japanese men: the Osaka Health Survey.

OBJECTIVE: To investigate the relationship between daily alcohol consumption and the risk of type 2 diabetes in a large Japanese cohort. RESEARCH DESIGN AND METHODS: We enrolled 6,362 Japanese men aged 35-61 years who did not have diabetes, impaired fasting glucose, hypertension, or liver cirrhosis at study entry. Type 2 diabetes was defined as a fasting plasma glucose (FPG) level > or =126 mg/dl or was diagnosed by a physician. Data on alcohol consumption were obtained from questionnaires. We confirmed 456 cases of type 2 diabetes during the 62,016 person-years of follow-up. RESULTS: The relationship between daily alcohol consumption and the risk of type 2 diabetes among lean men and among men with a higher BMI was paradoxical. Among lean men (BMI < or =22.0 kg/m2), heavy drinking was associated with an increased risk of type 2 diabetes. Men who consumed > or =50.1 ml/day of alcohol had a relative risk (RR) of 2.48 (95% CI 1.31-4.71) compared with nondrinkers after adjusting for age, BMI, regular physical exercise, parental history of diabetes, smoking habits, and FPG level. However, among men with a BMI > or =22.1 kg/m2, moderate drinking (29.1-50.0 ml/day) was associated with a decreased risk of type 2 diabetes. Daily moderate drinkers had a multiple adjusted RR of 0.58 (0.39-0.87) compared with nondrinkers. CONCLUSIONS: Among men with a BMI > or =22.1 kg/m2, moderate alcohol consumption was associated with a reduced risk of type 2 diabetes, but among lean men (BMI < or =22.0 kg/m2), heavy alcohol consumption was associated with an increased risk of type 2 diabetes.

High normal blood pressure, hypertension, and the risk of type 2 diabetes in Japanese men. The Osaka Health Survey.

OBJECTIVE: To investigate the relationship between high normal blood pressure or hypertension and the risk of developing type 2 diabetes in a large Japanese cohort. RESEARCH DESIGN AND METHODS: We enrolled 7,594 Japanese men aged 35-60 years who did not have diabetes or impaired fasting glucose at study entry. Type 2 diabetes was defined as a fasting plasma glucose level of > or = 126 mg/dl or a 2-h postload plasma glucose level of > or = 200 mg/dl. High normal blood pressure was defined as no history of hypertension and a systolic blood pressure of > or = 130 and < 140 mmHg or a diastolic blood pressure of > or = 85 and < 90 mmHg. Subjects were considered to have hypertension if they had a systolic blood pressure > or = 140 mmHg, if they had a diastolic blood pressure > or = 90 mmHg, or if they were taking anti-hypertensive medications. RESULTS: We confirmed 600 cases of type 2 diabetes during the 72,946 person-years of follow-up. Both high normal blood pressure and hypertension were associated with the risk of type 2 diabetes. Compared with normotensive men, men with high normal blood pressure had a multiple adjusted relative risk (RR) of 1.39 (95% CI 1.14-1.69), and men with hypertension had a multiple adjusted RR of 1.76 (1.43-2.16). Even among lean men (BMI < 22.7 kg/m2), men with high normal blood pressure had a multiple adjusted RR of 1.71 (1.20-2.42), and men with hypertension had a multiple adjusted RR of 2.02 (1.34-3.05) compared with normotensive men. CONCLUSIONS: High normal blood pressure and hypertension are associated with an increased risk of developing type 2 diabetes.

Structure analysis of a class II transposon encoding the mercury resistance of the Gram-positive Bacterium bacillus megaterium MB1, a strain isolated from minamata bay, Japan.

A unique transposon was found in the chromosome of Bacillus megaterium MB1, a Gram-positive bacterium isolated from mercury-polluted sediments of Minamata Bay, Japan. The transposon region of a 14.5kb DNA fragment was amplified by PCR using a single PCR primer designed from the nucleotide sequence of an inverted repeat of class II transposons. The molecular analysis revealed that the PCR-amplified DNA fragment encodes a transposition module similar to that of Tn21. The transposon also encodes a broad-spectrum mercury resistance region having a restriction endonuclease map identical to that of Bacillus cereus RC607, a strain isolated from Boston Harbor, USA. The result of a phylogenetic analysis of the amino acid sequence of putative resolvase of the transposon showed that the transposon is phylogenetically closer to the transposons of Gram-positive bacteria than those of Gram-negative bacteria. Besides the transposition module and mer operon, the transposon encodes a mobile genetic element of bacterial group II introns between the resolvase gene and mer operon. The intron, however, does not intervene in any exon gene. The discovery of this newly found combination of the complex mobile elements may offer a clue to understanding the horizontal dissemination of broad-spectrum mercury resistance among microbes.

Identification of three merB genes and characterization of a broad-spectrum mercury resistance module encoded by a class II transposon of Bacillus megaterium strain MB1.

The complete structure of a broad-spectrum mercury resistance module was shown by sequencing the Gram-positive bacterial transposon TnMERI1 of Bacillus megaterium MB1. The regions encoding organomercury resistance were identified. Upstream of a previously identified organomercurial lyase merB (merB1) region of TnMERI1, a second merR (merR2) and a second merB gene (merB2) were found. These genes constitute a second operon (mer operon 2) following a promoter/operator (P(merR2)) region. A third organomercurial lyase gene (merB3) was found immediately upstream of the mer operon (mer operon 1) followed by a promoter/operator (P(merB3)) region homologous to that of the mer operon 1 (P(merR1)-merR1-merE-like-merT-merP-merA). The complete genetic structure of the mercury resistance module is organized as P(merB3)-merB3-P(merR1)-merR1-merE-like-merT+ ++ -merP-merA-P(merR2)-merR2 -merB2-merB1. The subcloning analysis of these three merB genes showed distinct substrate specificity as different organomercury lyase genes.

Serum uric acid and the risk for hypertension and Type 2 diabetes in Japanese men: The Osaka Health Survey.

OBJECTIVE: To investigate the association of serum uric acid level with the risk for hypertension and Type 2 diabetes. DESIGN: Prospective cohort study. SETTING: Work site in Osaka, Japan. PARTICIPANTS: A total of 6,356 Japanese men, aged 35-60 years with systolic blood pressure < 140 mmHg and diastolic blood pressure < 90 mmHg, normal glucose intolerance, and no history of hypertension or diabetes at baseline. MAIN OUTCOME MEASURES: Blood pressure was measured by standard techniques, using 160/95 mmHg for diagnosis of hypertension. Type 2 diabetes was defined as a fasting plasma glucose level > or = 126 mg/dl or a 2 h post-loaded plasma glucose level > or = 200 mg/dl. RESULTS: During the 61,716 person-years follow-up period, we confirmed 639 cases of hypertension and 454 cases of Type 2 diabetes. Serum uric acid level was associated with an increased risk for hypertension but not for Type 2 diabetes. After adjustment for known risk factors, including daily alcohol consumption, the serum uric acid level was associated with an increased risk for hypertension; the relative risks for hypertension were 1.00 for quintile 1 of the serum uric acid level, 1.24 [95% confidence interval (CI), 0.94-1.65] for quintile 2, 1.34 (CI, 1.03-1.76) for quintile 3, 1.76 (CI, 1.35-2.29) for quintile 4, and 2.01 (CI, 1.56-2.60) for quintile 5 (P for trend < 0.001). Even among both non-drinkers and lean subjects, serum uric acid level was associated with an increased risk for hypertension. CONCLUSIONS: Serum uric acid level was associated with an increased risk for hypertension but not for Type 2 diabetes.

Promotion of NCI-Black-Reiter male rat bladder carcinogenesis by dimethylarsinic acid an organic arsenic compound.

Dimethylarsinic acid (DMAA) is a major metabolite of inorganic arsenicals in mammals. In the present study, we investigated its promoting effects on urinary bladder carcinogenesis in NCI-Black-Reiter (NBR) rats, which lack alpha2u-globulin synthesizing ability. Male 9-14-week-old NBR rats were treated sequentially with 0.05% N-butyl-N-(4-hydroxybutyl)-nitrosamine (BBN) for 4 weeks and then given 100 ppm DMAA in their drinking water (group 1) for 32 weeks. Induction of preneoplastic lesions (papillary or nodular hyperplasia) in this DMAA-treated group was significantly increased as compared to the carcinogen alone control group (P < 0.01). The development of carcinomas was also enhanced and a significant increase in the 5-bromo-2'-deoxyuridine (BrdU) labeling index of the urinary bladder epithelial cells was observed for the DMAA treatment group. These results indicate that DMAA has promoting effects on urinary bladder carcinogenesis even in NBR rats, so its effects are not dependent on the presence of alpha2u-globulin.

The inhibitory effect of selenium on induction of tetraploidy by dimethylarsinic acid in Chinese hamster cells.

Arsenic is a human carcinogen. On the other hand, selenium supplementation can inhibit induction of carcinogenesis by chemical carcinogens. The effect of selenium compounds on the cytotoxicity of dimethylarsinic acid (DMA) and on the induction of tetraploidy by DMA were studied using Chinese hamster V79 cells. Two selenium compounds were tested, sodium selenite and trimethylselenonium iodide (TMSeI). Trimethylselenonium is a major excretory product of selenite metabolism. The cytotoxicity of sodium selenite was 1000-fold greater than that of TMSeI. The cytotoxicity of DMA was about the same as that of TMSeI. The mitotic index for DMA administration was increased by these selenium compounds at low concentrations and decreased by them at high concentrations. The tetraploid index for DMA decreased with increasing concentrations of these selenium compounds. Tetraploidy is a form of aneuploidy, and aneuploidy is known to induce carcinogenesis. The finding that selenium inhibited induction of tetraploidy by DMA may yield clues to the role of selenium in the chemoprevention of carcinogenesis by chemical carcinogens.

Renal lesions induced in F344/DuCrj rats by 4-weeks oral administration of dimethylarsinic acid.

The nephrotoxicity of dimethylarsinic acid (cacodylic acid, DMA) was examined in male and female F344/DuCrj rats. DMA administered perorally at doses of 113, 85, and 57 mg/kg for 4 weeks produced dose-related decreases in body weight and survival rate in both sexes. Mortality was higher and appeared more quickly in females than in males. Histopathological findings in the kidney were proximal tubular degeneration and necrosis, as well as papillary necrosis, and hyperplasia of the epithelium covering the papillae. Since extensive proximal tubular necrosis was observed only in dead animals of both sexes, and not in survivors or the controls, it was therefore concluded that the main cause of death could be attributed to nephrotoxicity of DMA. The results thus show that DMA is nephrotoxic to both male and female rats.

Aneuploidy induced by dimethylarsinic acid in mouse bone marrow cells.

We investigated the cytogenetic effects of dimethylarsinic acid (DMA), which is the major metabolite of inorganic arsenic compounds, on mouse bone marrow cells after a single intraperitoneal injection to mice. DMA increased mitotic indices significantly at 16, 24 and 48 h after injection, and prolonged the average generation time 1.5 h at the 24 h. These results suggest that DMA may cause mitotic arrest in vivo as well as in vitro. However the activity of mitotic arrest induced by DMA was much weaker than that induced by colchicine. Metaphase cells obtained after administration of DMA without colchicine pretreatment were morphologically normal except for chromosome number, which varied by stage from the prophase to the telophase in M phase as seen after administration of saline. DMA significantly induced aneuploids. The frequencies of euploids with DMA and saline treatment were 55.1 and 94.0%, respectively, and in DMA treatment hyperploids with 1 or 2 extra chromosomes were over 80% of all aneuploids. These results suggest that aneuploidy induced by DMA might be associated with carcinogenicity of arsenic.

Genotoxicity of beryllium, gallium and antimony in short-term assays.

The genotoxicity of beryllium, gallium and antimony compounds was studied with the rec, Salmonella mutagenicity and SCE assays. In the rec assay, all the salts of the metals, BeCl2, Be(NO3)2, GaCl3, Ga(NO3)3, SbCl3, SbCl5, and an oxide, Sb2O3, had DNA-damaging activity. None of the compounds was mutagenic to Salmonella. In the SCE assays using V79 cells, 2 antimony(III) compounds, SbCl3 and Sb2O3, and 2 beryllium compounds, BeCl2 and Be(NO3)2, induced SCEs significantly. Sb2O3, slightly soluble in water, was positive in both the rec assay and the SCE assay at very low doses.

Possible carcinogenic potential of dimethylarsinic acid as assessed in rat in vivo models: a review.

The modifying effects of dimethylarsinic acid (DMA), the major metabolite of ingested arsenicals in most mammals, on chemical carcinogenesis were investigated using rat in vivo models and reviewed here. In a multi-organ bioassay, rats pretreated with 5 carcinogens were administered DMA at various concentrations in their drinking water. Significantly increased tumor induction due to DMA was observed in the urinary bladder, kidney, liver, and thyroid gland. This was associated with significantly elevated ornithine decarboxylase activity in the kidneys of DMA-treated animals. To estimate the hazard levels of its promoting influence, further examinations were carried out concerned with urinary bladder and liver carcinogenesis. Doses of 25 and 50 ppm, respectively, of DMA were found capable of enhancing lesion development in the two organs. In conclusion, our data indicate that DMA is a carcinogen or promoter in the urinary bladder, liver, kidney and thyroid gland, in line with previous epidemiological findings.

Genotoxicity of gardenia yellow and its components.

Gardenia fruit (Gardenia jasminoides ELLIS) is widely used as a natural food colorant and as a traditional Chinese medicine for treatment of hepatic and inflammatory diseases. "Gardenia yellow" is a natural food colorant which is extracted by ethanol from gardenia fruit. The purpose of this study was to evaluate the genotoxicity of gardenia yellow. Genotoxicity of gardenia yellow and its components, crocetin, gentiobiose (a component of crocin), geniposide and genipin (formed by hydrolysis of geniposide), was studied by Ames test, rec-assay, and sister chromatid exchange (SCE) using V79 cells. Gardenia yellow and its components were found not to be mutagenic in the Salmonella reverse mutation assay. Gardenia yellow and genipin caused damage of DNA in rec-assay. Gardenia yellow induced a significant dose-dependent increase of SCE frequency (8.6 times at 1000 microg/ml as the value for the solvent control). Only genipin induced SCEs significantly among the components of gardenia yellow. Moreover, genipin induced a significant increase of tetraploids at all doses tested (95% at 8 microg/ml). Gardenia yellow preparation was analyzed by capillary electrophoresis (CE), and geniposide was detected. However, genipin was not observed. In conclusion, we have shown that genipin possesses genotoxicity. Furthermore, there were unidentified genotoxicants in gardenia yellow.

Urinary excretion of arsenic metabolites after long-term oral administration of various arsenic compounds to rats.

The metabolism of arsenic compounds in rats was studied by comparing urinary metabolites of arsenic compounds administered for 1 wk or 7 mo. Male F344/DuCrj rats were given 100 mg As/L as monomethylarsonic acid (MMA), dimethylarsinic acid (DMA), trimethylarsine oxide (TMAO), or arsenobetaine (AsBe), or 10 mg As/L as arsenite [As(III)] via drinking water for 7 mo. Urine was collected by forced urination after 1 wk or 7 mo. Arsenic metabolites in urine were analyzed by ion chromatography with inductively coupled plasma mass spectrometry. In the case of As(III) ingestion, a small portion of all arsenic excreted in urine (about 6%) was excreted in inorganic form, while most arsenic was excreted as methylated arsenic metabolites. Following MMA treatments for 1 wk or 7 mo, the predominant products excreted were unchanged MMA and DMA accompanied by small amounts of TMAO and tetramethylarsonium (TeMA). In the case of DMA treatment the urinary compounds found were mainly the parent DMA and TMAO with minute amounts of TeMA. TMAO was methylated to TeMA to a slight extent after 1 wk and 7 mo of administration, although most TMAO was excreted in the form of unchanged TMAO. AsBe was predominantly eliminated in urine without any transformation. Two unidentified metabolites were detected in urine after 7 mo of arsenic species exposure; the amounts of these metabolites increased in the order DMA > MMA > TMAO with only small quantities of these detected in the As(III)-treated group. These results suggest that these unidentified metabolites are formed during a demethylation process, and not during methylation. Our findings indicate that long-term exposure to As(III), MMA, or DMA decreases the proportion of TMAO elimination in urine and increases that of DMA, M-1, and M-2, and that further methylation to TMAO to TeMA does occur to a slight extent following long-term exposure to arsenical compounds in rats.

Fractional clearances of low molecular weight proteins in lead workers.

Urinary alpha 1-microglobulin (alpha 1-m) and beta 2-microglobulin (beta 2-m) can be used as early indicators of renal tubular dysfunction. However, low levels of lead exposure cause an increase in urinary alpha 1-m, but not in urinary beta 2-m. In order to clarify the level of tubular dysfunction in early lead nephropathy, fractional clearances of alpha 1-m (FC-alpha 1-m) and beta 2-m (FC-beta 2-m), i.e., the ratios of these clearances to the creatinine clearance, were measured in 99 male lead workers. Blood urea nitrogen, serum creatinine, uric acid, and urinary creatinine and N-acetyl-beta-D-glucosaminidase activity were also measured to diagnose the presence of other renal dysfunction. The median of FC-alpha 1-m was 0.13% in the control group. The FC-alpha 1-m increased in lead workers with blood lead (B-Pb) levels above 20 micrograms/dl. The correlation of FC-alpha 1-m with urinary alpha 1-m was highly significant, but there was no correlation with serum alpha 1-m. The median of FC-beta 2-m was 0.065% in the control group. There was a correlation of FC-beta 2-m with FC-alpha 1-m, but there was no correlation with B-Pb, or with serum beta 2-m. These results suggest the following: There was a very low excretion rate of alpha 1-m and beta 2-m in both the control group and the lead exposed groups. The excretion rate of alpha 1-m was higher than that of beta 2-m.(ABSTRACT TRUNCATED AT 250 WORDS)

The characteristics of specific IgG to phthalic anhydride (PA)-albumin conjugate.

Phthalic anhydride (PA), used in the chemical industry, binds to proteins and causes allergic reactions. It is important to study the characteristics of antibody to PA-protein. We produced specific IgG against PA-rabbit serum albumin (RSA) by administering subcutaneous injections of PA-RSA conjugate to two rabbits. Both rabbits' sera had high titers of IgG not only to PA-RSA but also to PA-human serum albumin (HSA) and HSA. In enzyme-linked immunosorbent assay (ELISA) and ELISA HSA inhibition, specific IgG to PA-HSA revealed cross-reactivity to three other phthalyl anhydride conjugates, hexahydrophthalic anhydride (HHPA)-HSA, methylhexahydrophthalic anhydride (MHHPA)-HSA, and methyltetrahydrophthalic anhydride (MTHPA)-HSA, in both sera. Titers of IgG to HHPA-HSA, MHHPA-HSA, and MTHPA-HSA were not significantly different. On affinity chromatography, highly specific IgG to PA hapten alone was purified. In the serum not binding to PA column, specific IgG to PA-HSA was significantly less than in original serum, but levels of specific IgG to other phthalyl anhydride-HSA were unchanged. Rabbits immunized with PA-RSA produced at least two types of IgG: one is to PA hapten alone and the other may be against new antigenic determinants (NADs) on HSA.

Types of organic solvents used in workplaces and work environment conditions with special references to reproducibility of work environment classification.

A survey of solvent was conducted for 196 unit work areas in 95 plants in 1994 to 1996 in Hiroshima Prefecture, Japan. The survey had been repeated every 6 months (i.e., twice a year) during the 3-year period. Sampling and analysis of the solvent vapors were carried out after national protocols set by the regulation. Toluene was most frequently detected regardless of the type of solvent work (except for degreasing), whereas the second- and the third-most common solvents varied depending on the type of solvent works. Among chlorinated hydrocarbon solvents for degreasing, dichloromethane was most widely used. Solvent concentrations were generally low as none of the median concentrations exceeded corresponding Administrative Control Levels set by the regulation, either individually or even when the assumption of additiveness was applied. Among the 1176 cases analyzed, 80% of the unit work areas were evaluated as adequate (i.e., classified as Class I). Furthermore, about 57% stayed in Class I throughout the 3 years, suggesting that solvent exposure conditions were generally quite stable. In regulatory evaluation by classification, A-sampling was decisive in most cases, whereas the role of B-sampling was limited.

Peripheral hemodynamics evaluated by acceleration plethysmography in workers exposed to lead.

To clarify the effect of lead exposure on peripheral hemodynamics, acceleration plethysmography (APG) was performed for 48 male subjects occupationally exposed to lead (exposure group) and 43 male subjects with no history of occupational exposure to lead (control group). In the exposure group, the blood lead concentration (Pb-B) was also measured. Each APG parameter was assessed by comparing measured data with the standard aging curves. A significant negative correlation was obtained between the parameter--b/a and Pb-B. The exposure group showed significantly lower values of parameters--b/a (p < 0.01) and d/a (p < 0.05) than the control group. The parameter--b/a in the exposure group dose-dependently decreased with increases in length of working career (duration of exposure to lead) and Pb-B. The parameter--b/a significantly (p < 0.05) decreased in subjects with working careers of 5 years or more and in subjects whose Pb-B was 40 micrograms/100 ml or more. These results suggest that lead exposure affects peripheral hemodynamics as evaluated by APG.