Pub Date : 2004-11-01DOI: 10.1080/00039890409603433
James N Hyde, Doug Brugge, James Repace, William Rand
The authors sought to determine levels of urinary cotinine and its association with collateral exposure to second-hand smoke in public health workers. Urinary cotinine was measured twice at 1-wk intervals in 28 public health workers or their spouses. Information on sources of second-hand smoke exposure and a dietary history were obtained from each participant. Geometric mean and median cotinine levels were 2.74 and 2.33 ng/mL, respectively. Only 6 instances of second-hand smoke exposure were reported from a combined 204 days of potential exposure, and these did not correspond to higher cotinine values. There was no association between consumption of foods containing nicotine and log-transformed urine cotinine levels (p = .80). The authors' analysis indicates dietary sources of nicotine are not important, even for persons with very low urinary cotinine levels. Further study is needed to determine sources of variation in urinary cotinine among largely unexposed populations.
{"title":"Assessment of sources of second-hand smoke exposure in a putatively unexposed population.","authors":"James N Hyde, Doug Brugge, James Repace, William Rand","doi":"10.1080/00039890409603433","DOIUrl":"https://doi.org/10.1080/00039890409603433","url":null,"abstract":"<p><p>The authors sought to determine levels of urinary cotinine and its association with collateral exposure to second-hand smoke in public health workers. Urinary cotinine was measured twice at 1-wk intervals in 28 public health workers or their spouses. Information on sources of second-hand smoke exposure and a dietary history were obtained from each participant. Geometric mean and median cotinine levels were 2.74 and 2.33 ng/mL, respectively. Only 6 instances of second-hand smoke exposure were reported from a combined 204 days of potential exposure, and these did not correspond to higher cotinine values. There was no association between consumption of foods containing nicotine and log-transformed urine cotinine levels (p = .80). The authors' analysis indicates dietary sources of nicotine are not important, even for persons with very low urinary cotinine levels. Further study is needed to determine sources of variation in urinary cotinine among largely unexposed populations.</p>","PeriodicalId":8155,"journal":{"name":"Archives of environmental health","volume":"59 11","pages":"553-7"},"PeriodicalIF":0.0,"publicationDate":"2004-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/00039890409603433","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25960420","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}
Pub Date : 2004-11-01DOI: 10.1080/00039890409603438
Hipolito M Custodio, Karin Broberg, Maria Wennberg, Jan-Håkan Jansson, Bengt Vessby, Göran Hallmans, Birgitta Stegmayr, Staffan Skerfving
Methylmercury is eliminated from the human body as glutathione (GSH) conjugates. GSH production is mediated by glutamyl-cysteine ligase (GCL) and conjugation by glutathione S-transferases (GST). In this study, the authors tested whether polymorphisms in GCL and GST genes modify methylmercury retention. Erythrocyte mercury concentration (EryHg), plasma polyunsaturated fatty acids (PPUFA), and genotype for GCLC, GCLM, GSTA1, GSTM1, GSTP1, and GSTT1 were determined in 365 individuals. A general linear model was developed for analyzing whether genotype modified the regression of EryHg on PPUFA. The presence of one variant allele for either GCLC-129 or GSTP1-114 was associated with higher EryHg and steeper regression slope. No similar trends were shown for GCLM, GSTA1, GSTM1, or GSTT1. These findings indicate that GCLC polymorphisms that affect GSH production also affect methylmercury retention, and that GSTP1 may play a role in conjugating methylmercury with GSH.
{"title":"Polymorphisms in glutathione-related genes affect methylmercury retention.","authors":"Hipolito M Custodio, Karin Broberg, Maria Wennberg, Jan-Håkan Jansson, Bengt Vessby, Göran Hallmans, Birgitta Stegmayr, Staffan Skerfving","doi":"10.1080/00039890409603438","DOIUrl":"https://doi.org/10.1080/00039890409603438","url":null,"abstract":"<p><p>Methylmercury is eliminated from the human body as glutathione (GSH) conjugates. GSH production is mediated by glutamyl-cysteine ligase (GCL) and conjugation by glutathione S-transferases (GST). In this study, the authors tested whether polymorphisms in GCL and GST genes modify methylmercury retention. Erythrocyte mercury concentration (EryHg), plasma polyunsaturated fatty acids (PPUFA), and genotype for GCLC, GCLM, GSTA1, GSTM1, GSTP1, and GSTT1 were determined in 365 individuals. A general linear model was developed for analyzing whether genotype modified the regression of EryHg on PPUFA. The presence of one variant allele for either GCLC-129 or GSTP1-114 was associated with higher EryHg and steeper regression slope. No similar trends were shown for GCLM, GSTA1, GSTM1, or GSTT1. These findings indicate that GCLC polymorphisms that affect GSH production also affect methylmercury retention, and that GSTP1 may play a role in conjugating methylmercury with GSH.</p>","PeriodicalId":8155,"journal":{"name":"Archives of environmental health","volume":"59 11","pages":"588-95"},"PeriodicalIF":0.0,"publicationDate":"2004-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/00039890409603438","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25959300","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}
Pub Date : 2004-11-01DOI: 10.1080/00039890409603440
Alfred Körblein
Using trend analysis, the author sought a possible association between perinatal mortality rates in West Germany, 1955-1993, and the fallout from atmospheric nuclear weapons testing in the years 1952-1993. The regression model used a continuously falling trend and a superimposed extra term that reflects the average strontium content in pregnant women. Mortality rates show an upward deviation that peaked in 1970. The model attributes more than 100,000 excess perinatal deaths to strontium in the fallout. The dose-response curve is curvilinear with a power of dose of 1.81 +/- 0.23. In addition, using a combined regression model, the author analyzed the two data subsets of perinatal mortality (i.e., stillbirth rate and early neonatal mortality). The strontium effect is 3.4 times greater on early infant deaths than on stillbirths. According to the prevailing wisdom, the fetus is protected against damage from ionizing radiation by a threshold dose of 50-200 mSv, but the doses from strontium in the fallout were well below 1 mSv/yr in Germany. The results reported here seem to contradict the existence of a threshold dose for perinatal mortality at low doses.
{"title":"Perinatal mortality in West Germany following atmospheric nuclear weapons tests.","authors":"Alfred Körblein","doi":"10.1080/00039890409603440","DOIUrl":"https://doi.org/10.1080/00039890409603440","url":null,"abstract":"<p><p>Using trend analysis, the author sought a possible association between perinatal mortality rates in West Germany, 1955-1993, and the fallout from atmospheric nuclear weapons testing in the years 1952-1993. The regression model used a continuously falling trend and a superimposed extra term that reflects the average strontium content in pregnant women. Mortality rates show an upward deviation that peaked in 1970. The model attributes more than 100,000 excess perinatal deaths to strontium in the fallout. The dose-response curve is curvilinear with a power of dose of 1.81 +/- 0.23. In addition, using a combined regression model, the author analyzed the two data subsets of perinatal mortality (i.e., stillbirth rate and early neonatal mortality). The strontium effect is 3.4 times greater on early infant deaths than on stillbirths. According to the prevailing wisdom, the fetus is protected against damage from ionizing radiation by a threshold dose of 50-200 mSv, but the doses from strontium in the fallout were well below 1 mSv/yr in Germany. The results reported here seem to contradict the existence of a threshold dose for perinatal mortality at low doses.</p>","PeriodicalId":8155,"journal":{"name":"Archives of environmental health","volume":"59 11","pages":"604-9"},"PeriodicalIF":0.0,"publicationDate":"2004-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/00039890409603440","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25959302","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}
Pub Date : 2004-11-01DOI: 10.1080/00039890409603431
Tee L Guidotti
“The first rule of science is that you must not fool yourself-and you are the easiest person to fool.”Richard Feynman’ The desire to make a fundamental contribution drives all scholars-scientists more than most-but the great motivating desire to discover and innovate also renders the originator of a new theory the worst judge of its validity. Self-deception is the easiest error in science. One looks at one fact, matches it with another, links to something relevant that someone wrote several years ago, and voiM: A new theory of the universe. It all makes compelling sense to the creator, and it is very hard for the believer to abandon even if it is proven wrong. However, this used to be the way that early scientists thought until the invention of rigorous, disciplined experimentation in the late Middle Ages and the widespread adoption of hypothesis testing and reproducibility of findings as the norms by which scientists conduct studies. In Europe, in the 18th century, this systematic way of knowing crowded out the many personal theories and traditional explanations that contemporaries called, and historians of science today call, ”systems.”2 Medicine came late to the scientific method, perhaps because it developed early as a compendium of astute empirical observations united by various idiosyncratic theories. Medicine was dominated by systems until the rise of scientific medicine in the German universities of the 19th century and their subsequent influence when the scientific method began to bring reason and validity and gave birth to modern biomedical science.2 The belief in spontaneous generation gave way to the continuity of life through the experiments of Pa~teur,~ and the patchwork of therapeutic systems gave way to a rational understanding of how drugs work, which also indirectly led to modern toxi~ology.~ Even so, medicine remains plagued with untestable explanations, hypotheses, and nonscientific systems, as demonstrated by the long persistence through the 20th century of psychoanalysis and the continuing popularity of homeopathy. Science progresses in a methodical way by setting up hypotheses that can be found false whether the discipline is inherently experimental, such as chemistry and toxicology, or inherently observational, such as astrophysics and epidemiology. The test of a science rests on whether a discipline involves making predictions based on a theory and testing those predictions against observations. This is the doctrine of “falsification,” as elaborated by Popper and other students of ~c ience.~ A theory is not a science nor does a science prove a theory by working backward from an observation to string together a mechanism to explain it. Science also does not prove a theory by searching out facts that appear compatible. In truth, scientific theories cannot be proven at all, only disproven. A science does not rest on the plausibility of its argument, but is valid because the body of knowledge and i ts theory of explanation ca
{"title":"Belief, reality, and self-deception in environmental and occupational health.","authors":"Tee L Guidotti","doi":"10.1080/00039890409603431","DOIUrl":"https://doi.org/10.1080/00039890409603431","url":null,"abstract":"“The first rule of science is that you must not fool yourself-and you are the easiest person to fool.”Richard Feynman’ The desire to make a fundamental contribution drives all scholars-scientists more than most-but the great motivating desire to discover and innovate also renders the originator of a new theory the worst judge of its validity. Self-deception is the easiest error in science. One looks at one fact, matches it with another, links to something relevant that someone wrote several years ago, and voiM: A new theory of the universe. It all makes compelling sense to the creator, and it is very hard for the believer to abandon even if it is proven wrong. However, this used to be the way that early scientists thought until the invention of rigorous, disciplined experimentation in the late Middle Ages and the widespread adoption of hypothesis testing and reproducibility of findings as the norms by which scientists conduct studies. In Europe, in the 18th century, this systematic way of knowing crowded out the many personal theories and traditional explanations that contemporaries called, and historians of science today call, ”systems.”2 Medicine came late to the scientific method, perhaps because it developed early as a compendium of astute empirical observations united by various idiosyncratic theories. Medicine was dominated by systems until the rise of scientific medicine in the German universities of the 19th century and their subsequent influence when the scientific method began to bring reason and validity and gave birth to modern biomedical science.2 The belief in spontaneous generation gave way to the continuity of life through the experiments of Pa~teur,~ and the patchwork of therapeutic systems gave way to a rational understanding of how drugs work, which also indirectly led to modern toxi~ology.~ Even so, medicine remains plagued with untestable explanations, hypotheses, and nonscientific systems, as demonstrated by the long persistence through the 20th century of psychoanalysis and the continuing popularity of homeopathy. Science progresses in a methodical way by setting up hypotheses that can be found false whether the discipline is inherently experimental, such as chemistry and toxicology, or inherently observational, such as astrophysics and epidemiology. The test of a science rests on whether a discipline involves making predictions based on a theory and testing those predictions against observations. This is the doctrine of “falsification,” as elaborated by Popper and other students of ~c ience.~ A theory is not a science nor does a science prove a theory by working backward from an observation to string together a mechanism to explain it. Science also does not prove a theory by searching out facts that appear compatible. In truth, scientific theories cannot be proven at all, only disproven. A science does not rest on the plausibility of its argument, but is valid because the body of knowledge and i ts theory of explanation ca","PeriodicalId":8155,"journal":{"name":"Archives of environmental health","volume":"59 11","pages":"545-7"},"PeriodicalIF":0.0,"publicationDate":"2004-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/00039890409603431","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25959930","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}
Pub Date : 2004-11-01DOI: 10.1080/00039890409603436
Leslie London, David Bourne, Rauf Sayed, Roland Eastman
Although organophosphate (OP) insecticides have been recognized as having neuropathic potential, a relationship with Guillain-Barre syndrome (GBS) has not been previously confirmed. A cluster of 7 cases of GBS was noted over an 11-yr period in an isolated farming region in the Northern Cape Province of South Africa, an area subject to intensive aerial application of OP insecticides. Observed cases were more than 4 times higher than expected based on a Poisson probability distribution. Four cases were clustered in an area where the topography showed a marked hollow, and where spray drift of aerial OP insecticides was anticipated. The rate of GBS in this subcluster was more than 14 times higher than expected. The authors explored the hypothesis that aerial OP insecticide application was related to the raised incidence of GBS in this area and made suggestions for future research.
{"title":"Guillain-Barre syndrome in a rural farming district in South Africa: a possible relationship to environmental organophosphate exposure.","authors":"Leslie London, David Bourne, Rauf Sayed, Roland Eastman","doi":"10.1080/00039890409603436","DOIUrl":"https://doi.org/10.1080/00039890409603436","url":null,"abstract":"<p><p>Although organophosphate (OP) insecticides have been recognized as having neuropathic potential, a relationship with Guillain-Barre syndrome (GBS) has not been previously confirmed. A cluster of 7 cases of GBS was noted over an 11-yr period in an isolated farming region in the Northern Cape Province of South Africa, an area subject to intensive aerial application of OP insecticides. Observed cases were more than 4 times higher than expected based on a Poisson probability distribution. Four cases were clustered in an area where the topography showed a marked hollow, and where spray drift of aerial OP insecticides was anticipated. The rate of GBS in this subcluster was more than 14 times higher than expected. The authors explored the hypothesis that aerial OP insecticide application was related to the raised incidence of GBS in this area and made suggestions for future research.</p>","PeriodicalId":8155,"journal":{"name":"Archives of environmental health","volume":"59 11","pages":"575-80"},"PeriodicalIF":0.0,"publicationDate":"2004-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/00039890409603436","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25960427","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}
Pub Date : 2004-11-01DOI: 10.1080/00039890409603435
Richard Stephens, Balraj Sreenivasan
The health effects from prolonged low-level organophosphate exposure are unknown. We hypothesized that exposed individuals would show neuropsychological decrements when compared with unexposed individuals, and that cumulative organophosphate exposure would be correlated with neuropsychological performance. We used a quasiexperimental cross-sectional design to compare neuropsychological test scores among three groups: orchard sprayers exposed to organophosphates, and construction worker and pig farm workers who were not exposed. Relative to construction workers, orchard sprayers were significantly slower on negative statements of the syntactic reasoning test. However, we found no relationship between cumulative exposure and test response. The slower response of the orchard sprayers was apparently exposure-related, but we could not identify an underlying neurotoxic mechanism. Therefore, we are unable to conclude whether this is a specific cognitive effect, or a decrement arising on the most sensitive test employed.
{"title":"Neuropsychological effects of long-term low-level organophosphate exposure in orchard sprayers in England.","authors":"Richard Stephens, Balraj Sreenivasan","doi":"10.1080/00039890409603435","DOIUrl":"https://doi.org/10.1080/00039890409603435","url":null,"abstract":"<p><p>The health effects from prolonged low-level organophosphate exposure are unknown. We hypothesized that exposed individuals would show neuropsychological decrements when compared with unexposed individuals, and that cumulative organophosphate exposure would be correlated with neuropsychological performance. We used a quasiexperimental cross-sectional design to compare neuropsychological test scores among three groups: orchard sprayers exposed to organophosphates, and construction worker and pig farm workers who were not exposed. Relative to construction workers, orchard sprayers were significantly slower on negative statements of the syntactic reasoning test. However, we found no relationship between cumulative exposure and test response. The slower response of the orchard sprayers was apparently exposure-related, but we could not identify an underlying neurotoxic mechanism. Therefore, we are unable to conclude whether this is a specific cognitive effect, or a decrement arising on the most sensitive test employed.</p>","PeriodicalId":8155,"journal":{"name":"Archives of environmental health","volume":"59 11","pages":"566-74"},"PeriodicalIF":0.0,"publicationDate":"2004-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/00039890409603435","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25960425","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}
Pub Date : 2004-11-01DOI: 10.1080/00039890409603439
Linda P B Verhoef, Ed P F Yzerman, Jacob P Bruin, Jeroen W Den Boer
The source of infection for travelers who develop Legionnaires' disease (LD) shortly after a journey abroad is difficult to ascertain. Infection is likely to have occurred abroad, but could also have occurred at the patient's own residence. The authors conducted a case-control study to determine risk for acquiring LD at home in the Netherlands after traveling abroad. They compared homes of 44 traveling LD patients with 44 homes of nontraveling LD patients, using logistic regression models. Geographic distribution was confounding the association between traveling and presence of Legionella spp. in residences; adjustment was necessary. In traveler's homes, legionellae were present more often, with crude and adjusted OR (95% CI) being 1.6 (0.5-5.0) and 1.4 (0.4-4.4), respectively. The authors' findings indicate that the patient's residence can be a potential source of infection after traveling.
{"title":"Domestic exposure to legionellae for Dutch Legionnaires' disease patients.","authors":"Linda P B Verhoef, Ed P F Yzerman, Jacob P Bruin, Jeroen W Den Boer","doi":"10.1080/00039890409603439","DOIUrl":"https://doi.org/10.1080/00039890409603439","url":null,"abstract":"<p><p>The source of infection for travelers who develop Legionnaires' disease (LD) shortly after a journey abroad is difficult to ascertain. Infection is likely to have occurred abroad, but could also have occurred at the patient's own residence. The authors conducted a case-control study to determine risk for acquiring LD at home in the Netherlands after traveling abroad. They compared homes of 44 traveling LD patients with 44 homes of nontraveling LD patients, using logistic regression models. Geographic distribution was confounding the association between traveling and presence of Legionella spp. in residences; adjustment was necessary. In traveler's homes, legionellae were present more often, with crude and adjusted OR (95% CI) being 1.6 (0.5-5.0) and 1.4 (0.4-4.4), respectively. The authors' findings indicate that the patient's residence can be a potential source of infection after traveling.</p>","PeriodicalId":8155,"journal":{"name":"Archives of environmental health","volume":"59 11","pages":"597-603"},"PeriodicalIF":0.0,"publicationDate":"2004-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/00039890409603439","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25959301","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}
Pub Date : 2004-10-01DOI: 10.1080/00039890409605168
Ute Latza, Marcus Oldenburg, Xaver Baur
One hundred fourteen male employees of a cotton spinning mill in western Germany participated in a cross-sectional study, the purpose of which was to clarify the dose effect of endotoxin exposure on respiratory symptoms. Airborne endotoxin exposures were classified as low (< or = 100 endotoxin units [EU]/m3), medium (> 100-450 EU/m3), or high (> 450 EU/m3), on the basis of endotoxin activity in the Limulus amoebocyte lysate assay. Age- and smoking-adjusted odds ratios (ORs) and confidence intervals (CIs) were estimated. The dose-response relationship between current endotoxin exposure and prevalence of wheezing (medium: OR = 2.15, 95% CI = 0.48-9.62; high: OR = 5.49, 95% CI = 1.17- 25.81) and cough (medium: OR = 2.11; 95% CI = 0.59-7.56; high: OR = 3.93; 95% CI = 1.02-15.12) was significant (test for linear trend: p values = 0.020 and 0.040, respectively). The association between exposure and wheezing was stronger among atopic workers. The higher prevalence of chest tightness and shortness of breath among workers with medium and high current endotoxin exposure did not reach statistical significance. The results suggested that there was a dose-dependent increase in bronchial symptoms, with significant effects occurring at exposures that exceeded 450 EU/m3.
德国西部一家棉纺厂的114名男性雇员参加了一项横断面研究,目的是阐明内毒素暴露对呼吸道症状的剂量效应。根据鲎试剂中内毒素活性的测定,空气中的内毒素暴露被分为低(<或= 100内毒素单位[EU]/m3)、中(> 100-450 EU/m3)和高(> 450 EU/m3)。估计年龄和吸烟调整后的优势比(ORs)和置信区间(CIs)。当前内毒素暴露与喘息患病率之间的剂量-反应关系(中值:OR = 2.15, 95% CI = 0.48-9.62;高:OR = 5.49, 95% CI = 1.17- 25.81)和咳嗽(中:OR = 2.11;95% ci = 0.59-7.56;高:OR = 3.93;95% CI = 1.02-15.12)显著(线性趋势检验:p值分别= 0.020和0.040)。在特应性工作者中,暴露与喘息之间的联系更强。中、高电流内毒素暴露工人胸闷、呼吸短促发生率较高,无统计学意义。结果表明,支气管症状呈剂量依赖性增加,暴露量超过450 EU/m3时出现显著影响。
{"title":"Endotoxin exposure and respiratory symptoms in the cotton textile industry.","authors":"Ute Latza, Marcus Oldenburg, Xaver Baur","doi":"10.1080/00039890409605168","DOIUrl":"https://doi.org/10.1080/00039890409605168","url":null,"abstract":"<p><p>One hundred fourteen male employees of a cotton spinning mill in western Germany participated in a cross-sectional study, the purpose of which was to clarify the dose effect of endotoxin exposure on respiratory symptoms. Airborne endotoxin exposures were classified as low (< or = 100 endotoxin units [EU]/m3), medium (> 100-450 EU/m3), or high (> 450 EU/m3), on the basis of endotoxin activity in the Limulus amoebocyte lysate assay. Age- and smoking-adjusted odds ratios (ORs) and confidence intervals (CIs) were estimated. The dose-response relationship between current endotoxin exposure and prevalence of wheezing (medium: OR = 2.15, 95% CI = 0.48-9.62; high: OR = 5.49, 95% CI = 1.17- 25.81) and cough (medium: OR = 2.11; 95% CI = 0.59-7.56; high: OR = 3.93; 95% CI = 1.02-15.12) was significant (test for linear trend: p values = 0.020 and 0.040, respectively). The association between exposure and wheezing was stronger among atopic workers. The higher prevalence of chest tightness and shortness of breath among workers with medium and high current endotoxin exposure did not reach statistical significance. The results suggested that there was a dose-dependent increase in bronchial symptoms, with significant effects occurring at exposures that exceeded 450 EU/m3.</p>","PeriodicalId":8155,"journal":{"name":"Archives of environmental health","volume":"59 10","pages":"519-25"},"PeriodicalIF":0.0,"publicationDate":"2004-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/00039890409605168","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25811456","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}
Pub Date : 2004-10-01DOI: 10.1080/00039890409605167
Nachman Brautbar, Elihu D Richter, Gideon Nesher
The authors describe two patients with systemic vasculitis and prior occupational exposure to organic solvents. Systemic vasculitis should be considered a sentinel event for such exposures.
作者描述了两例全身性血管炎和先前职业暴露于有机溶剂的患者。系统性血管炎应被视为此类暴露的前哨事件。
{"title":"Systemic vasculitis and prior recent exposure to organic solvents: report of two cases.","authors":"Nachman Brautbar, Elihu D Richter, Gideon Nesher","doi":"10.1080/00039890409605167","DOIUrl":"https://doi.org/10.1080/00039890409605167","url":null,"abstract":"<p><p>The authors describe two patients with systemic vasculitis and prior occupational exposure to organic solvents. Systemic vasculitis should be considered a sentinel event for such exposures.</p>","PeriodicalId":8155,"journal":{"name":"Archives of environmental health","volume":"59 10","pages":"515-7"},"PeriodicalIF":0.0,"publicationDate":"2004-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/00039890409605167","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25811455","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}
Pub Date : 2004-10-01DOI: 10.1080/00039890409605165
Ami S Patel, Evelyn O Talbott, Jeanne V Zborowski, Juley A Rycheck, Danielle Dell, Xiaohui Xu, Joseph Schwerha
The Tranguch Gasoline Spill leaked 50,000-900,000 gallons of gasoline from underground storage tanks, potentially exposing an area of Hazle Township and Hazleton, Pennsylvania, to chronic low levels of benzene since at least 1990. A retrospective cohort study of 663 individuals representing 275 households assessed whether affected residents were at increased risk for cancer from 1990-2000 compared with the Pennsylvania populace. Age-adjusted standard incidence ratios (SIRs) were calculated using Pennsylvania rates to determine expected numbers. The age-adjusted SIR for the gasoline-affected area was 4.40 (95% confidence interval: 1.09-10.24) for leukemia. These results suggest an association between living within the area affected by the Tranguch Gasoline Spill and increased risk for leukemia.
{"title":"Risk of cancer as a result of community exposure to gasoline vapors.","authors":"Ami S Patel, Evelyn O Talbott, Jeanne V Zborowski, Juley A Rycheck, Danielle Dell, Xiaohui Xu, Joseph Schwerha","doi":"10.1080/00039890409605165","DOIUrl":"https://doi.org/10.1080/00039890409605165","url":null,"abstract":"<p><p>The Tranguch Gasoline Spill leaked 50,000-900,000 gallons of gasoline from underground storage tanks, potentially exposing an area of Hazle Township and Hazleton, Pennsylvania, to chronic low levels of benzene since at least 1990. A retrospective cohort study of 663 individuals representing 275 households assessed whether affected residents were at increased risk for cancer from 1990-2000 compared with the Pennsylvania populace. Age-adjusted standard incidence ratios (SIRs) were calculated using Pennsylvania rates to determine expected numbers. The age-adjusted SIR for the gasoline-affected area was 4.40 (95% confidence interval: 1.09-10.24) for leukemia. These results suggest an association between living within the area affected by the Tranguch Gasoline Spill and increased risk for leukemia.</p>","PeriodicalId":8155,"journal":{"name":"Archives of environmental health","volume":"59 10","pages":"497-503"},"PeriodicalIF":0.0,"publicationDate":"2004-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/00039890409605165","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25811453","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}