{"title":"Determination of o-cresol by gas chromatography and comparison with hippuric acid levels in urine samples of individuals exposed to toluene.","authors":"L C Amorim, E M Alvarez-Leite","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Hippuric acid is the most frequently used biomarker in the biological monitoring of occupational exposure to toluene. This product of solvent biotransformation may be also found in the urine of individuals who have not been exposed to the solvent. A smaller fraction of the absorbed toluene is oxidized to aromatic compounds including ortho-cresol, which is not found significantly in the urine of nonexposed individuals. An analytical methodology whereby gas chromatography with flame ionization detection is utilized for determination of o-cresol in urine of workers exposed to toluene is described. The levels obtained were subsequently compared to hippuric acid levels determined in the same urine samples. The analytical method has demonstrated an adequate precision (intra- and interassay coefficient of variation in the range of 2.4-5.4%) and average recovery of 98%. The samples for o-cresol determination were obtained from workers exposed to toluene in three different industrial activities. The concentration range found in exposed groups varied from < 0.21 to 2.8 micrograms/ml. The o-cresol values in the urine did not differ significantly among the exposed groups analyzed at the 5% level. The o-cresol and hippuric acid values found in the urine samples showed a significant correlation at the 1% level. These results may represent an additional contribution to studies for a definitive evaluation of the validity of o-cresol as a biomarker of exposure to toluene.</p>","PeriodicalId":17524,"journal":{"name":"Journal of toxicology and environmental health","volume":"50 4","pages":"401-7"},"PeriodicalIF":0.0,"publicationDate":"1997-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20068857","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Testicular effects of 1,3,5-trinitrobenzene (TNB). I. Dose response and reversibility studies.","authors":"A M Chandra, C W Qualls, G Reddy","doi":"10.1080/009841097160401","DOIUrl":"https://doi.org/10.1080/009841097160401","url":null,"abstract":"<p><p>Testicular effects of TNB were characterized after single and multiple oral doses of TNB at 0, 35.5, and 71 mg/kg. Male Fischer 344 (F344) rats were killed after a single dose or after 4 and 10 daily doses of TNB. Testicular effects were not evident at the light microscope level in rats killed after a single dose of TNB or after 4 daily doses at 35.5 mg/kg of TNB. Rats receiving 4 daily doses of TNB at 71 mg/kg had the earliest evidence of testicular damage, with necrosis and degeneration of pachytene spermatocytes including a significant decrease in testicular weight. Rats dosed at 35.5 mg/kg for 10 d had severe testicular lesions, in addition to the decrease in testicular weight. There was degeneration of round and elongate spermatids, and formation of multinucleate syncytial cells. The epididymis was devoid of sperm, instead containing exfoliated syncytial spermatids. Rats dosed at 71 mg/kg of TNB for 10 d had testicular atrophy and cessation of spermatogenesis. These rats also had apoptic cells in the ventral prostate. To assess the extent of reversibility in these atrophied testis, rats were allowed to recover for 10 or 30 d after 10 doses of TNB (71 mg/kg). A significant regenerative attempt with proliferating spermatocytes were present at 10 d and elongate spermatids were evident at 30 d. These reversibility studies indicate testicular effects of TNB are at least partially reversible.</p>","PeriodicalId":17524,"journal":{"name":"Journal of toxicology and environmental health","volume":"50 4","pages":"365-78"},"PeriodicalIF":0.0,"publicationDate":"1997-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/009841097160401","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20069556","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Testicular effects of 1,3,5-trinitrobenzene (TNB). II. Immunolocalization of germ cells using proliferating cell nuclear antigen (PCNA) as an endogenous marker.","authors":"A M Chandra, C W Qualls, G A Campbell, G Reddy","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>The applicability of PCNA as a tool for the analysis of germ cells in rats treated with 1,3,5-trinitrobenzene (TNB), a potent testicular toxicant, was evaluated. Male Fischer 344 (F344) rats were gavaged with TNB at 71 mg/kg or with corn oil (vehicle). Rats were killed after 10 daily oral doses or were allowed to recover for 10 or 30 d after the 10 doses. Testes from control rats, treated rats, and rats allowed to recover were immunohistochemically stained for PCNA. PCNA labeling in the control rats was confined to the nuclei of spermatogonia, pachytene spermatocytes, and nuclei of elongate spermatocytes. Conventional (hematoxylin and eosin) staining of testes from rats treated with TNB at 71 mg/kg for 10 d revealed loss of germ cells and cessation of spermatogenesis. Immunohistochemical staining of sections from these treated rats revealed only PCNA-positive spermatogonia. Rats allowed a 10-d recovery had both spermatogonial and spermatocytic staining, indicating partial restoration of germ-cell population. In rats allowed to recover for 30 d, the PCNA staining pattern was identical to the control rats. These results indicate that PCNA can be used to assess the proliferative status of spermatogonia (germ cells) in rodent testes exposed to testicular toxicants.</p>","PeriodicalId":17524,"journal":{"name":"Journal of toxicology and environmental health","volume":"50 4","pages":"379-87"},"PeriodicalIF":0.0,"publicationDate":"1997-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20069557","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
C Y Yang, H F Chiu, J F Chiu, W Y Kao, S S Tsai, S J Lan
{"title":"Cancer mortality and residence near petrochemical industries in Taiwan.","authors":"C Y Yang, H F Chiu, J F Chiu, W Y Kao, S S Tsai, S J Lan","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>An ecologic study design was used to investigate the relationship between cancer risks and residence in communities adjacent to petrochemical industrial counties (PICs). Directly age-adjusted mortality rates for cancer during 1982-1991 among 16 counties characterized by a heavy concentration of petrochemical industries were compared to rates among 16 matched counties with similar concentration of nonpetrochemical manufacturing industries, urbanization level, and demographic characteristics. An excess rate for liver cancer among males was found in the so-called PICs. The correlation could not be explained by confounding variables such as urbanization, socioeconomic class, or employment in nonpetrochemical industries. No other increased cancer risks were found to be associated with residence near petrochemical industries.</p>","PeriodicalId":17524,"journal":{"name":"Journal of toxicology and environmental health","volume":"50 3","pages":"265-73"},"PeriodicalIF":0.0,"publicationDate":"1997-02-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20011504","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"The toxicity of brominated and mixed-halogenated dibenzo-p-dioxins and dibenzofurans: an overview.","authors":"L W Weber, H Greim","doi":"10.1080/009841097160456","DOIUrl":"https://doi.org/10.1080/009841097160456","url":null,"abstract":"<p><p>Brominated dibenzo-p-dioxins and dibenzofurans can be formed under laboratory conditions by pyrolysis of flame retardants based on polybrominated biphenyls and biphenyl ethers. Their occurrence in the environment, however, is due to combustion processes such as municipal waste incineration and internal combustion engines. As these processes generally take place in the presence of an excess of chlorine, predominantly mixed brominated and chlorinated compounds have been identified so far in environmental samples. Brominated dibenzo-p-dioxins or dibenzofurans bind to the cytosolic Ah receptor about as avidly as their chlorinated congeners and induce hepatic microsomal enzymes with comparable potency. The same holds true for mixed brominated-chlorinated compounds. Gross pathologic symptoms-hypothyroidism, thymic atrophy, wasting of body mass, lethality-also occur at doses that, on a molar concentration basis, are virtually identical to those seen with the chlorinated compounds. Their potency to induce malformations in mice following prenatal exposure is equivalent to that of chlorinated dibenzo-p-dioxins and dibenzofurans. Possible activities as (co)carcinogens and endocrine disrupters have not been evaluated, but are likely to exist. Considering the overall similarity in action of chlorinated and brominated dibenzo-p-dioxins and dibenzofurans, environmental and health assessments should be based on molar body burdens without discrimination for the nature of the halogen.</p>","PeriodicalId":17524,"journal":{"name":"Journal of toxicology and environmental health","volume":"50 3","pages":"195-215"},"PeriodicalIF":0.0,"publicationDate":"1997-02-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/009841097160456","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20011502","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Fusaric acid increases melatonin levels in the weanling rat and in pineal cell cultures.","authors":"A M Rimando, J K Porter","doi":"10.1080/009841097160483","DOIUrl":"https://doi.org/10.1080/009841097160483","url":null,"abstract":"<p><p>Fusaric acid (FA) is produced by several Fusarium species that commonly infect cereal grains and other agricultural commodities. FA in the feed of nursing dams is lactationally transferred to the suckling offspring and alters serotonin (5-hydroxytryptamine, 5HT) in the pineal gland of the neonate rat. 5HT is involved in melatonin (MEL) production by the pineal gland. MEL is a hormone important in reproduction and seasonality in animals. Therefore, the effects of FA on MEL in the serum and pineal gland of male and female 21-d-old weanling rats from dams on an FA diet were studied. MEL was measured by enzyme-linked immunosorbent assay (ELISA), which was standardized for directly measuring MEL in rat serum and pineal homogenates. At 200 ppm in the diet of nursing dams, FA increased serum MEL in both sexes. Results obtained from ELISA were supported by high-performance liquid chromatography (HPLC) analysis with fluorescence detection. MEL analysis of the pineal gland homogenates by ELISA and HPLC supported observations in the serum. Analogously, in pineal cell monolayer cultures, FA at 1 microM and 100 microM concentrations increased MEL in a dose-dependent manner as compared to the control cells. This is the first report that FA increases MEL in vivo and in vitro and suggests that FA contamination of diets may affect mechanisms involving MEL synthesis.</p>","PeriodicalId":17524,"journal":{"name":"Journal of toxicology and environmental health","volume":"50 3","pages":"275-84"},"PeriodicalIF":0.0,"publicationDate":"1997-02-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/009841097160483","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20011505","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
K L Dreher, R H Jaskot, J R Lehmann, J H Richards, J K McGee, A J Ghio, D L Costa
{"title":"Soluble transition metals mediate residual oil fly ash induced acute lung injury.","authors":"K L Dreher, R H Jaskot, J R Lehmann, J H Richards, J K McGee, A J Ghio, D L Costa","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Identification of constituents responsible for the pulmonary toxicity of fugitive combustion emission source particles may provide insight into the adverse health effects associated with exposure to these particles as well as ambient air particulate pollution. Herein, we describe results of studies conducted to identify constituents responsible for the acute lung injury induced by residual oil fly ash (ROFA) and to assess physical-chemical factors that influence the pulmonary toxicity of these constituents. Biochemical and cellular analyses performed on bronchoalveolar lavage fluid obtained from rats following intratracheal instillation of ROFA suspension demonstrated the presence of severe inflammation, an indicator of pulmonary injury, which included recruitment of neutrophils, eosinophils, and monocytes into the airway. A leachate prepared from ROFA, containing predominantly Fe, Ni, V, Ca, Mg, and sulfate, produced similar lung injury to that induced by ROFA suspension. Depletion of Fe, Ni, and V from the ROFA leachate abrogated its pulmonary toxicity. Correspondingly, minimal lung injury was observed in animals exposed to saline-washed ROFA particles. A surrogate transition metal sulfate solution containing Fe, V, and Ni largely reproduced the lung injury induced by ROFA. Metal interactions and pH were found to influence the severity and kinetics of lung injury induced by ROFA and soluble transition metals. These findings provide direct evidence for the role of soluble transition metals in the pulmonary injury induced by the combustion emission source particulate, ROFA.</p>","PeriodicalId":17524,"journal":{"name":"Journal of toxicology and environmental health","volume":"50 3","pages":"285-305"},"PeriodicalIF":0.0,"publicationDate":"1997-02-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20011506","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
D Paustenbach, Y Alarie, T Kulle, N Schachter, R Smith, J Swenberg, H Witschi, S B Horowitz
{"title":"A recommended occupational exposure limit for formaldehyde based on irritation.","authors":"D Paustenbach, Y Alarie, T Kulle, N Schachter, R Smith, J Swenberg, H Witschi, S B Horowitz","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>In recent years, several regulatory agencies and professional societies have recommended an occupational exposure limit (OEL) for formaldehyde. This article presents the findings of a panel of experts, the Industrial Health Foundation panel, who were charged to identify an OEL that would prevent irritation. To accomplish this task, they critiqued approximately 150 scientific articles. Unlike many other chemicals, a large amount of data is available upon which to base a concentration-response relationship for human irritation. A mathematical model developed by Kane et al. (1979) for predicting safe levels of exposure to irritants based on animal data was also evaluated. The panel concluded that for most persons, eye irritation clearly due to formaldehyde does not occur until at least 1.0 ppm. Information from controlled studies involving volunteers indicated that moderate to severe eye, nose, and throat irritation does not occur for most persons until airborne concentrations exceed 2.0-3.0 ppm. The data indicated that below 1.0 ppm, if irritation occurs in some persons, the effects rapidly subside due to \"accommodation.\" Based on the weight of evidence from published studies, the panel found that persons exposed to 0.3 ppm for 4-6 h in chamber studies generally reported eye irritation at a rate no different than that observed when persons were exposed to clean air. It was noted that at a concentration of 0.5 ppm (8-h TWA) eye irritation was not observed in the majority of workers (about 80%). Consequently, the panel recommended an OEL of 0.3 ppm as an 8-h time-weighted average (TWA) with a ceiling value (CV) of 1.0 ppm (a concentration not to be exceeded) to avoid irritation. The panel believes that the ACGIH TLV of 0.3 ppm as a ceiling value was unnecessarily restrictive and that this value may have been based on the TLV Committee's interpretation of the significance of studies involving self-reported responses at concentrations less than 0.5 ppm. The panel concluded that any occupational or environmental guideline for formaldehyde should be based primarily on controlled studies in humans, since nearly all other studies are compromised by the presence of other contaminants. The panel also concluded that if concentrations of formaldehyde are kept below 0.1 ppm in the indoor environment (where exposures might occur 24 h/d) this should prevent irritation in virtually all persons. The panel could not identify a group of persons who were hypersensitive, nor was there evidence that anyone could be sensitized (develop an allergy) following inhalation exposure to formaldehyde. The panel concluded that there was sufficient evidence to show that persons with asthma respond no differently than healthy individuals following exposure to concentrations up to 3.0 ppm. Although cancer risk was not a topic that received exhaustive evaluation, the panel agreed with other scientific groups who have concluded that the cancer risk of formaldehyde is negligible ","PeriodicalId":17524,"journal":{"name":"Journal of toxicology and environmental health","volume":"50 3","pages":"217-63"},"PeriodicalIF":0.0,"publicationDate":"1997-02-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20011503","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Enhanced renal outer medullary uptake of mercury associated with uninephrectomy: implication of a luminal mechanism.","authors":"R K Zalups","doi":"10.1080/009841097160564","DOIUrl":"https://doi.org/10.1080/009841097160564","url":null,"abstract":"<p><p>In the present study, pretreatment with p-aminohippurate (PAH) and induction of stop-flow conditions (by ureteral ligation) were used as tools to determine whether the enhanced accumulation of injected inorganic mercury that occurs in the renal outer stripe of the outer medulla in rats following uninephrectomy and compensatory renal growth is due to a luminal and/or basolateral mechanism. The effects of these pretreatments on the disposition of mercury in the liver and blood were also evaluated as a secondary aim. Pretreatment of both uninephrectomized (NPX) and control rats with a 7.5 mmol/kg dose of PAH 5 min prior to the injection of a nontoxic 0.5 mumol/kg i.v. dose of mercuric chloride caused a significant decrease in the renal accumulation of mercury in both control and NPX rats during the initial 3 h after the injection of inorganic mercury. However, the concentration of mercury in the renal outer stripe of the outer medulla was significantly greater in the NPX rats than in the corresponding control rats. Induction of stop-flow conditions (by i.v. bolus injection of 2.0 mmol/kg mannitol followed 5 min later by ureteral ligation) approximately 75 min prior to the injection of inorganic mercury also resulted in decreased renal accumulation of mercury in both NPX and control rats. In contrast to the effects of PAH, induction of stop-flow conditions resulted in the concentration of mercury in the renal outer stripe of the outer medulla in the NPX rats being statistically equivalent to that in the corresponding control rats 3 h after the injection of mercury. Assuming that glomerular filtration rate was reduced to negligible levels in these animals, the fraction of mercury that was not taken up and accumulated in the outer stripe of both groups of rats represents the fraction of mercury that is taken up by a luminal mechanism. Thus, on the basis of the findings in this study, it appears that the increased accumulation of mercury that occurs in the renal outer stripe of the outer medulla in NPX rats is linked to a luminal mechanism, presumably localized in the epithelial cells lining the proximal tubule. Finally, when pretreatment with PAH and induction of stop-flow conditions were combined, there was additivity with respect to decreased renal accumulation of mercury. This additivity provides further support for the current hypothesis that there are both luminal and basolateral mechanisms involved in the renal uptake of inorganic mercury.</p>","PeriodicalId":17524,"journal":{"name":"Journal of toxicology and environmental health","volume":"50 2","pages":"173-94"},"PeriodicalIF":0.0,"publicationDate":"1997-02-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/009841097160564","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20004858","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Determination of atrazine levels in whole saliva and plasma in rats: potential of salivary monitoring for occupational exposure.","authors":"C Lu, L C Anderson, R A Fenske","doi":"10.1080/009841097160519","DOIUrl":"https://doi.org/10.1080/009841097160519","url":null,"abstract":"<p><p>Current biological monitoring techniques are often unable to provide accurate estimates of pesticide dose in exposed worker populations. This study was conducted to investigate the feasibility of pesticide biomonitoring using saliva. Atrazine [2-chloro-4-ethylamino-6-(isopropylamino)-s-triazine], a member of the triazine herbicides, was selected to investigate salivary excretion following direct gastric administration in rats. Concentrations of atrazine in whole saliva and arterial plasma samples were determined by enzyme-linked immunosorbent assay (ELISA). Atrazine reached its highest level in both arterial plasma (238 micrograms/L) and whole saliva (157 micrograms/L) 35 min after administration of 105 mg/kg of atrazine, and then decreased with time in a parallel fashion. Although saliva atrazine levels were lower than levels in arterial plasma, there was a very high correlation between whole saliva and arterial plasma atrazine concentrations (r2 = .95). In addition, pharmacokinetic analysis suggested that salivary levels of atrazine can be used to predict concentrations of atrazine in plasma. The mean whole saliva/arterial plasma atrazine concentration ratio (S/P) was 0.66 +/- 0.11 (n = 20). The S/P ratios did not vary significantly over time, and were not affected by salivary flow rate. This study demonstrates that atrazine is transported into saliva, and that a relatively constant concentration ratio between whole saliva and arterial plasma is maintained. Because the salivary concentrations of atrazine are independent of variation in salivary flow rate, salivary monitoring of atrazine in humans may prove useful and practical. Finally, this study suggests that other pesticides with chemical and physical properties similar to those of atrazine can be monitored in saliva.</p>","PeriodicalId":17524,"journal":{"name":"Journal of toxicology and environmental health","volume":"50 2","pages":"101-11"},"PeriodicalIF":0.0,"publicationDate":"1997-02-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/009841097160519","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20004925","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}