Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “BUTADIENE”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 145 records · Page 8Linked to original sources
PubMed1998

Genetic effects of 1,3-butadiene on the mouse testis.

1,3-Butadiene is a known male mouse germ-cell mutagen, to which humans may either be occupationally or environmentally exposed. Prolonged exposure to moderate or high doses in male mice can cause dominant lethal mutations and one report has indicated that 10 week inhalation administration of low doses can result in the production of malformed foetuses. The present study had dual purposes: (a) to attempt to clarify the suspected ability of sub-chronic (6 h/day, 5 days/wk, 10 weeks) low-dose exposure to 1,3-butadiene to induce heritable mutations in mouse male germ cells: (b) investigation of the relationships between testicular DNA damage, testicular DNA repair and foetal outcome. Adult male mice were exposed to low or moderate doses of 1,3-butadiene by inhalation sub-chronically or for a single 6 h period and either used for mating (sub-chronic exposure only) or for studies of DNA damage and repair. Litter size, dominant lethality and numbers of abnormal foetuses were determined the day preceding the normal day of parturition. Testicular DNA damage and repair were assessed by the Comet assay (for DNA damage) and the unscheduled DNA synthesis assay (for DNA repair). 1,3-Butadiene caused a statistically significant increase in dominant lethality at 125 ppm but not 12.5 ppm. No significant increase in DNA repair was found with either dose level or exposure period while only 6 h exposure to 125 ppm caused a small but significant increase in DNA damage as detected by the Comet assay. These effects demonstrate the reproductive genotoxicity of (125 ppm) 1,3-butadiene but do not confirm its ability to cause abnormalities in the offspring via the sperm. It is suggested that the relationship between 1,3-butadiene-induced DNA damage, DNA repair and heritable defects in the offspring may depend on the pattern of metabolites produced.

Animals↗
PubMed1997

Somatic and germ cell effects in rats and mice after treatment with 1,3-butadiene and its metabolites, 1,2-epoxybutene and 1,2,3,4-diepoxybutane.

1,3-Butadiene is produced in large quantities for use in the manufacture of synthetic rubber. It is also an environmental pollutant. There is concern about exposure to 1,3-butadiene as it has been shown to produce tumours in rats, mice and an increased risk of leukaemia in humans. It has also been shown to produce germ cell effects in mice. Differences in responses to 1,3-butadiene have been reported in rats and mice, possibly due to different metabolic capabilities. The present study thus investigated somatic and germ cell effects of 1,3-butadiene in mice and its metabolites in both rats and mice to help determine species differences using different endpoints for genotoxic effects. These included DNA strand breakage as measured in the single cell gel electrophoresis (Comet assay) in bone marrow and testicular cells, and micronuclei in bone marrow cells using both the acridine orange and Giemsa staining methods. Unscheduled DNA synthesis (UDS) was also measured in the testes of mice. CD-1 mice were exposed to 1,3-butadiene by inhalation for 6 h/day for 4 weeks, and CD-1 mice and Sprague-Dawley rats to the metabolites after i.p. injection. 1,3-Butadiene did not affect liver, bone marrow and testicular cells in mice as measured in the Comet assay. After treatment with 1,2-epoxybutene in the Comet assay, there was a response in the testes in mice but not in rats and there was little or no effect in the bone marrow assay in mice but there was in rats. After treatment with 1,2,3,4-diepoxybutane in the Comet assay in mice, there was a response in the bone marrow cells but not in the testicular cells, and in rats there was also a response only in bone marrow cells. There was an increase in micronuclei in both rats and mice with both metabolites, but clastogenicity was stronger with 1,2,3,4-diepoxybutane, occurring at lower doses, than with 1,2-epoxybutene. In the UDS assay in the testes of mice, there was an increase in response with 1,2,3,4-diepoxybutane treatment but not with 1,2-epoxybutene. These studies would appear to confirm a species difference of CD-1 mice and Sprague-Dawley rats, where mice were sensitive at lower doses than rats.

Administration, Inhalation↗
PubMed1993

Coated surface acoustic wave sensor employing a reversible mass-amplifying ligand substitution reaction for real-time measurement of 1,3-butadiene at low- and sub-ppm concentrations.

Real-time measurement of 1,3-butadiene gas using a surface acoustic wave (SAW) sensor coated with the square-planar Pt(II)-olefin pi-complex PtCl2-(1-hexene) (pyridine) and related complexes is described. Amplification of the sensor response results from displacement of two 1-hexene molecules by each butadiene molecule and formation of the bridged complex [PtCl2(pyridine)]2(1,3-butadiene). Using a 30-MHz SAW oscillator, the rate of frequency change is linearly related to the butadiene air concentration from 150 ppb to > or = 13 ppm and a calculated detection limit of 101 ppb is obtained. Using a 60-MHz oscillator, the detection limit is reduced to 24 ppb. No effect on the sensor response is observed with changes in relative humidity from 5 to 80% or changes in temperature from 25 to 35 degrees C. No interference is observed from several industrially relevant non-olefin organic gases and vapors. Responses are obtained for several olefins, but they interfere with the response to butadiene only at higher relative concentrations. The reagent can be regenerated repeatedly by brief exposure to 1-hexene vapor with retention of the original response characteristics upon subsequent exposure. The potential for using this sensor to monitor occupational 1,3-butadiene exposures is discussed in light of the recently proposed occupational exposure limit of 2 ppm.

Air Pollutants, Occupational↗
PubMed2006

The impact of domestic wood burning on personal, indoor and outdoor levels of 1,3-butadiene, benzene, formaldehyde and acetaldehyde.

The aim of this study was to quantify personal exposure and indoor levels of the suspected or known carcinogenic compounds 1,3-butadiene, benzene, formaldehyde and acetaldehyde in a small Swedish town where wood burning for space heating is common. Subjects (wood burners, n = 14), living in homes with daily use of wood-burning appliances were compared with referents (n = 10) living in the same residential area. Personal exposure and stationary measurements indoors and at an ambient site were performed with diffusive samplers for 24 h. In addition, 7 day measurements of 1,3-butadiene and benzene were performed inside and outside the homes. Wood burners had significantly higher median personal exposure to 1,3-butadiene (0.18 microg m(-3)) compared with referents (0.12 microg m(-3)), which was also reflected in the indoor levels. Significantly higher indoor levels of benzene were found in the wood-burning homes (3.0 microg m(-3)) compared with the reference homes (1.5 microg m(-3)). With regard to aldehydes, median levels obtained from personal and indoor measurements were similar although the four most extreme acetaldehyde levels were all found in wood burners. High correlations were found between personal and indoor levels for all substances (r(s) > 0.8). In a linear regression model, type of wood-burning appliance, burning time and number of wood replenishments were significant factors for indoor levels of 1,3-butadiene. Domestic wood burning seems to increase personal exposure to 1,3-butadiene as well as indoor levels of 1,3-butadiene and benzene and possibly also acetaldehyde. The cancer risk from these compounds at exposure to wood smoke is, however, estimated to be low in developed countries.

Acetaldehyde↗
PubMed1992

Lymphohematopoietic cancer in styrene-butadiene polymerization workers.

1,3-Butadiene and styrene are suspected carcinogens and common chemicals used in the synthesis of rubber. To investigate any potential human hazards from exposure to these chemicals, a case-control study of 59 lymphohematopoietic cancers was conducted within a cohort of male workers employed between 1943 and 1982 in eight North American styrene-butadiene rubber polymer-producing plants. A total of 193 controls were matched to the cases by plant, age, year of hire, duration worked, and survival to time of death of the case. Each job was assigned an estimated exposure rank, and each worker's cumulated rank score was calculated on the basis of the time spent in each job throughout his employment. "Exposure" as a dichotomous variable was defined as a log rank score above the mean of the log scores for the total population of cases and controls within a subtype of cancer. Matched-pair analysis identified a strong association between leukemia and butadiene, with an odds ratio of 9.36 (95% confidence interval 2.05-22.9) and an association between styrene and leukemia (odds ratio = 3.13, 95% confidence interval 0.84-11.2) that did not achieve statistical significance. When exposure to both styrene and butadiene was included in a conditional logistic regression model, the odds ratio for butadiene remained high (odds ratio = 7.39), but the estimated association of leukemia with styrene was small. The results of this study support the hypothesis that exposure to butadiene is associated with the risk of leukemia. There also appears to be an additional risk from work in specific subdivisions of the industry.

Butadienes↗
PubMed1994

Mortality, morbidity, and haematological results from a cohort of long-term workers involved in 1,3-butadiene monomer production.

A retrospective mortality analysis and prospective morbidity and haematological analyses were performed for Shell Deer Park Manufacturing Complex (DPMC) male employees who worked in jobs with potential exposure to 1,3-butadiene from 1948 to 1989. 614 employees qualified for the mortality study (1948-89), 438 of those were still employed during the period of the morbidity study (1982-9), and 429 of those had haematological data available for analysis. Industrial hygiene data from 1979 to 1992 showed that most butadiene exposures did not exceed 10 ppm (eight-hour time weighted average (8 hour TWA)), and most were below 1 ppm, with an arithmetic mean of 3.5 ppm. 24 deaths occurred during the mortality study period. For all causes of death, the standardised mortality ratio (SMR) was 48 (95% confidence interval (95% CI) = 31-72), and the all cancer SMR was 34 (95% CI = 9-87). There were only two deaths due to lung cancer (SMR 42, 95% CI = 5-151) and none due to lymphohaematopoietic cancer (expected = 1.2). Morbidity (illness absence) events of six days or more for the 438 butadiene employees were compared with the rest of the complex. No cause of morbidity was in excess for this group; the all cause standardised morbidity ratio (SMbR) was 85 (95% CI = 77-93) and the all neoplasms SMbR was 51 (95% CI = 22-100). Haematological results for the 429 with laboratory data were compared with results for the rest of the complex. No significant differences occurred between the two groups and the distributions of results between butadiene and non-butadiene groups were virtually identical. These results suggest that butadiene exposures at concentrations common at DPMC in the past 10-20 years do not pose a health hazard to employees.

Adult↗
PubMed1996

1,3 Butadiene, a vapor phase component of environmental tobacco smoke, accelerates arteriosclerotic plaque development.

BACKGROUND: Our recent results support predictions from epidemiology studies that thousands of excess heart disease-related deaths result yearly in the United States from involuntary exposure to environmental tobacco smoke (ETS). Limited exposures of cockerels to ETS significantly accelerate arteriosclerosis. Despite little direct in vivo support, tar fraction rather than vapor phase compounds are considered largely responsible for the plaque-promoting effects of cigarette smoke. Here, we evaluate the effects of two ETS components on plaque development: the vapor phase component, 1,3 butadiene, and the tar component, the tobacco-specific N-nitrosamine, 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK). At relatively high doses, injected NNK is carcinogenic in rodents. Epidemiology studies have identified increased mortality from arteriosclerotic heart disease among black men working in the butadiene rubber industry. Neither butadiene nor NNK has been tested experimentally for a possible role in plaque development. METHODS AND RESULTS: Cockerels inhaled butadiene (20 ppm; 16 weeks) or were injected biweekly with NNK (10 mg/kg, 16 weeks). Control cockerels were exposed to filtered air or were injected with the NNK solvent dimethylsulfoxide. Plaque incidence, prevalence, location, and size were determined double-blind. NNK had no significant effect on any of these measurements. In contrast, butadiene elicited a statistically significant increase in plaque size comparable to that seen after steady-state exposure to ETS from 5 cigarettes. CONCLUSION: (1) This study represents the first time that a single cigarette smoke component has been demonstrated to accelerate arteriosclerosis, at a dose that is environmentally relevant. (2) The plaque-promoting components of ETS may reside in the vapor phase. (3) The cockerel model should be valuable in understanding the mechanism underlying the reported increases in heart disease deaths among black workers in the butadiene rubber industry.

Air Pollutants↗
PubMed2002

Association of the blood/air partition coefficient of 1,3-butadiene with blood lipids and albumin.

Pulmonary gas uptake is a function of the blood solubility of a vapor, indicated by the blood/air partition coefficient. We hypothesized that blood lipid compositions are associated with the blood/air partition coefficients of lipophilic toxic vapors such as 1,3-butadiene. Our goal was to investigate cross-sectional and longitudinal relationships of blood triglycerides, total cholesterol, and albumin to the blood/air partition coefficient of butadiene. We collected blood samples from 24 subjects at three time points: a fasting baseline and 2 and 4 hr after drinking a standardized high-fat milk shake (107 g fat, 80 g sugar, and 27 g protein). The blood/air partition coefficient was determined using the closed vial-equilibrium technique. Triglycerides and total cholesterol were analyzed by an enzymatic method, and albumin was analyzed with an immunoassay technique. We used multiple linear regression and general linear models to examine the cross-sectional and longitudinal relationship, respectively. The results showed that the blood/air partition coefficient of butadiene was cross-sectionally associated only with triglycerides at baseline, and longitudinally related to baseline triglycerides, total cholesterol, and the change in triglycerides over time. The blood/air partition coefficient of butadiene increased, on average, by approximately 20% and up to 40% for subjects with borderline higher triglyceride levels after ingestion of a standardized milk shake. In addition, a time factor beyond lipids was also significant in predicting the blood/air partition coefficient of butadiene. This may represent the effects of other unmeasured parameters related to time or time of day on the blood/air partition coefficient of butadiene. Because the blood/air partition coefficient is a major determinant of gas uptake, ingestion of a high fat meal before this type of exposure may significantly increase an individual's absorbed dose, possibly increasing the risk of adverse effects.

Adult↗
PubMed1990

Future directions in epidemiologic studies of 1,3-butadiene-exposed workers.

To date, epidemiologic research on 1,3-butadiene has consisted of cohort mortality studies of workers in the styrene-butadiene rubber (SBR) and butadiene monomer industries. These studies have been extremely useful both in defining the focus on human health effects to the lymphopoietic cancers and in providing a perspective on which to evaluate the available animal models for human risk assessment. The next step for epidemiologic research will involve a lymphopoietic cancer case control approach to enable a more precise assessment of whether there is a relationship between 1,3-butadiene exposure and lymphopoietic cancer. In addition, periodic mortality updates of the 1,3-butadiene-exposed worker cohorts will be important to monitor trends in lymphopoietic cancer rates and to ensure that other cancers with long latency do not begin to show elevated rates. This paper describes an industry-sponsored program of case-control and cohort mortality update studies along with the critical elements in research design and analysis for each study. Epidemiological studies will play an important role in testing hypotheses developed from toxicological studies about potential biological mechanisms of 1,3-butadiene carcinogenesis in humans.

Animals↗
PubMed1990

Critical assessment of epidemiologic studies on the human carcinogenicity of 1,3-butadiene.

1,3-Butadiene, a major ingredient of synthetic rubber, has been shown to be carcinogenic in two animal species. To assess the possible human carcinogenicity of 1,3-butadiene, a critical review was undertaken of the epidemiologic literature. An early retrospective study of 8017 males employed in tire manufacturing found excess mortality for lymphatic and hematopoietic neoplasms in production workers (standardized mortality ratio, SMR = 560); these workers were exposed to 1,3-butadiene as well as to styrene and possibly to benzene. A recently updated epidemiologic study of 2568 workers at a butadiene manufacturing plant in Texas reported low mortality overall (SMR = 84) but found excess deaths for lymphosarcoma and reticulum cell sarcoma (SMR = 229). A retrospective study of workers employed at two synthetic rubber plants in Texas found excess mortality for lymphatic and hematopoietic malignancies in the older of these facilities; the excesses for lymphosarcoma (SMR = 224) and leukemia (SMR = 278) were most significant in wartime workers. A large, recently updated retrospective study of 12,113 workers employed in eight synthetic rubber manufacturing plants in the United States and Canada found excess mortality for lymphatic and hematopoietic cancer in production workers; the SMR for other lymphatic cancers in white production workers was 230, and the SMR for all lymphatic malignancies in black production workers was 507. These updated epidemiologic results strongly suggest an etiologic association between occupational exposure to 1,3-butadiene and human cancer. It is reasonable, therefore, to conclude that there now exists at least limited evidence for the human carcinogenicity of 1,3-butadiene.

Butadienes↗
PubMed1990

Studies on the mechanism of 1,3-butadiene-induced leukemogenesis: the potential role of endogenous murine leukemia virus.

Previous studies have revealed marked differences in the incidence of leukemia between rats and mice exposed to 1,3-butadiene that do not appear to be readily explained on the basis of pharmacokinetics or metabolism. Chronic exposure to 1,3-butadiene results in a high incidence of thymic lymphoma in B6C3F1 mice that is not observed in Sprague-Dawley rats. Studies at the Chemical Industry Institute of Toxicology have focused on evaluating the potential of endogenous ecotropic retroviral background to influence susceptibility to 1,3-butadiene leukemogenesis. These studies have compared the pathogenesis and incidence of thymic lymphoma between B6C3F1 and NIH Swiss mice. Proviral ecotropic sequences are truncated in the NIH Swiss mouse, and the virus is not expressed. Chronic exposure to 1,3-butadiene (1250 ppm) for up to 1 year resulted in a fourfold difference in the incidence of thymic lymphoma between B6C3F1 and NIH Swiss mice. These results provide presumptive evidence for retrovirus involvement since NIH Swiss mice lack ecotropic viruses and appear to be relatively resistant to induction of lymphoma by 1,3-butadiene. Other explanations appear to be less likely in light of the fact that target organ toxicity has been determined to be virtually identical between the two strains during the preleukemic phase of 1,3-butadiene exposure.

Animals↗
PubMed1995

Mortality study of workers in 1,3-butadiene production units identified from a chemical workers cohort.

The International Agency for Research on Cancer has given the designations of "sufficient evidence" of carcinogenicity of 1,3-butadiene in experimental animals and "limited evidence" of carcinogenicity in humans. To investigate the carcinogenic effect in humans, we conducted a cohort mortality study among 364 men who were assigned to any of three 1,3-butadiene production units located within several chemical plants in the Kanawha Valley of West Virginia, including 277 men employed in a U.S. Rubber Reserve Plant which operated during World War II. The butadiene production units included in this study were selected from an index developed by the Union Carbide Corporation, which listed for each chemical production unit within their South Charleston, West Virginia and Institute, West Virginia, plants all products, by-products, and reactants. Departments included in the study were those where butadiene was a primary product and neither benzene nor ethylene oxide was present. A total of 185 deaths were observed; the standardized mortality ratio (SMR) for all causes of death was 91, reflecting lower mortality among the study population than the U.S. population. The study found a significantly elevated standardized mortality ratio (SMR) for lymphosarcoma and reticulosarcoma based on four observed cases (SMR = 577; 95% CI = 157-1480), which persisted in an analysis using county referent rates. An excess of lymphosarcoma and reticulosarcoma among all workers and among workers with routine exposure to 1,3-butadiene was also observed in the only other cohort of 1,3-butadiene production workers previously studied.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1999

[Biological effect of exposure to butadiene].

People can be exposed to 1,3-butadiene in work place (rubber industry) as well as in natural environment (car exhausts fumes, cigarette smoke). Butadien on its own is not genotoxic, but is metabolized to mutagenic and carcinogenic epoxydes, 1,2,3,4-diepoxybutane and 3,4-epoxybutene in the organism of mammals and human. 1,3-butadiene has been shown to be a potent carcinogen in animals and human. Laboratory investigations showed also toxic and mutagenic abilities of butadiene and its metabolities. Interspecies differences in sensitivity to butadiene are caused by differences in metabolic transformations of butadiene in different species.

Butadienes↗
PubMed1990

Carcinogenicity of 1,3-butadiene in C57BL/6 x C3H F1 mice at low exposure concentrations.

The carcinogenicity of inhaled 1,3-butadiene was evaluated in C57BL/6 x C3H F1 mice exposed to concentrations of this gas ranging from 6.25 to 625 ppm. Butadiene is a high production volume chemical, used mainly in the manufacture of synthetic rubber. In these 2-yr inhalation studies, a potent multisite carcinogenic response was observed, including neoplasms of the lung at concentrations as low as 6.25 ppm. Early occurrence and extensive development of lethal lymphocytic lymphomas in mice exposed to 625 ppm of butadiene reduced the number of animals at risk for the expression of later developing neoplasms at other sites; at lower exposure concentrations, dose responses were demonstrated for hemangiosarcomas of the heart and neoplasms of the lung, forestomach, Harderian gland, preputial gland, liver, mammary gland, and ovary. So far, no long-term studies on butadiene have been conducted at exposure concentrations that have not shown a carcinogenic response. In separate experiments with reduced exposure durations, butadiene induced neoplastic responses at multiple organ sites even after only 13 wk of exposure. Because of the correspondence between these animal data and recent epidemiology findings, there is a worldwide public health need to reevaluate current workplace exposure standards for 1,3-butadiene.

Animals↗
PubMed1993

1,3-Butadiene induces cancer in experimental animals at all concentrations from 6.25 to 8000 parts per million.

1,3-Butadiene, a chemical produced in large volumes, induces cancer in many organs in rats (at 1000 and 8000 ppm) and mice (at 6.25 to 1250 ppm); however, the sites of tumour induction (seven in rats and nine in mice) and the magnitudes of response differ between the two species. Particularly noteworthy in the studies of mice exposed by inhalation were the early, extensive induction of malignant lymphomas, the induction of uncommon haemangiosarcomas of the heart and the development of malignant lung tumours at 6.25 ppm, the lowest concentration ever used in a long-term carcinogenicity study of this gas. In order to account for the impact of early mortality on the expression of late development of tumours, survival-adjusted tumour rates were computed for mice exposed to butadiene at 6.25-625 ppm. The results provide a more accurate characterization of concentration-dependent responses for butadiene-induced cancers. Stop-exposure studies revealed that the atmospheric concentration of butadiene was a greater contributing factor to the development of lymphomas than was duration of exposure. The studies in mice show a good correspondence with the reported associations between occupational exposure to butadiene and excess mortality from lymphatic and haematopoietic cancers; mice are thus a better experimental surrogate for humans. Although further work is needed to improve our understanding of the mechanisms of tumour induction by butadiene, pursuit of that research must not delay reduction of human exposure to this carcinogenic chemical.

Animals↗
PubMed1993

Critical assessment of epidemiological studies on the carcinogenicity of 1,3-butadiene and styrene.

1,3-Butadiene. The consistent finding in five epidemiological studies of workers occupationally exposed to butadiene is excess mortality from lymphohaematopoietic malignancy. This highly reproducible finding is noted despite methodological limitations in each of the published studies that tend to diminish the likelihood of observing an etiological association: (i) lack of detailed data on individual exposures to butadiene; and (ii) increasing longevity of many patients with lymphohaematopoietic malignancies, owing to treatment with modern therapeutic regimens, which results in their not being included in analysis of mortality. The observed excess in cancer mortality is most clearly evident in subpopulations heavily exposed to butadiene: production and maintenance workers as well as African-American workers. These epidemiological data strongly suggest an etiological association between exposure to butadiene and human cancer. The data amply fulfil all of Bradford Hill's criteria for causality. It is reasonable to conclude that there now exists convincing evidence for the carcinogenicity of butadiene to humans. Styrene. Epidemiological data on styrene suggest the possibility of an association with lymphohaematopoietic malignancy, although the finding has not been consistent. The most recent epidemiological study, an analysis of 35,000 European workers, suggests, however, an association between these malignancies and time elapsed since first occupational exposure to styrene. Preliminary data from a nested case-control study within the cohort also suggest an association with cumulative exposure to styrene. Although the current classification of the human carcinogenicity of styrene within the IARC Monographs programme appears to be reasonable, if the new findings are confirmed it may become necessary in the near future to revise the classification. Downgrading of the IARC classification is clearly contraindicated in light of current epidemiological and toxicological data.

Butadienes↗
PubMed2001

Reaction mechanism and structure-reactivity relationships in the stereospecific 1,4-polymerization of butadiene catalyzed by neutral dimeric allylnickel(II) halides [Ni(C3H5)X]2 (X- = Cl-, Br-, I-): a comprehensive density functional theory study.

For the first time, a comprehensive and consistent picture of the catalytic cycle of 1,4-polymerization of butadiene with neutral dimeric allylnickel(II) halides [Ni(C3H5)X]2 (X = Cl- (I), Br- (II), and I- (III)) as single-site catalysts has been derived by means of quantum chemical calculations that employ a gradient-corrected density-functional method. All crucial reaction steps of the entire catalytic course have been scrutinized, taking into account butadiene pi complex formation, symmetrical and asymmetrical splitting of dimeric pi complexes, cis-butadiene insertion, and anti-syn isomerization. The present investigation examines, in terms of located structures, energies and activation barriers, the participation of postulated intermediates, in particular it aimed to clarify whether monomeric or dimeric species are the catalytically active species. Prior qualitative mechanistic assumptions are substituted by the presented theoretically well-founded and detailed analysis of both the thermodynamic and the kinetic aspects, that substantially improve the insight into the reaction course and enlarge them with novel mechanistic proposals. From a mechanistic point of view, all three catalysts exhibit common characteristics. First, chain propagation occurs by cis-butadiene insertion into the pi-butenylnickel(II) bond with nearly identical intrinsic free-energy activation barriers. Second, the reactivity of syn-butenyl forms is distinctly higher than that of anti forms. Third, the chain-propagation step is rate-determining in the entire polymerization process, and the pre-established anti-syn equilibrium can always be regarded as attained. Accordingly, neutral dimeric allylnickel(II) halides catalyze the formation of a stereo-regular trans-1,4-polymer under kinetic control following the k1t channel with butenyl(halide)(butadiene)NiII complexes being the catalytically active species. Production of a stereoregular cis-1,4-polymer with allylnickel chloride can only be explained by making the k2c channel accessible by the formation of polybutadienyl(butadiene) complexes, which is accompanied by the coordination of the next double bond in the growing chain to the NiII center.

Journal Article↗
PubMed2003

Secondary ion and laser ablation mass spectrometry for the quantitative characterization of styrene-butadiene copolymers.

Styrene-butadiene copolymers were analyzed by static secondary ion mass spectrometry (S-SIMS) and laser ablation Fourier transform ion cyclotron resonance mass spectrometry (LA-FTICRMS) to obtain quantitative information based on specific ions. Silver deposition was performed on polystyrene, butadiene rubber and styrene-butadiene rubber. Under these experimental conditions, new secondary ions were detected, in particular silver-cationized butadiene [M(butadiene) - Ag](+) and styrene [M(styrene) - Ag](+) monomers. In contrast, LA-FTICRMS experiments did not require pretreatment. At high laser power density, UV photons (193, 266 and 355 nm) allowed the detection of styrene and butadiene monomers at m/z 104 and 54, respectively. The use of the observed ions by SIMS or LA-FTICRMS ensures that quantitative information on the relative distribution of each monomer is obtained. However, the silver coating thickness in the SIMS experiment seems to have an important influence on the quantitative information obtained. For LA-FTICRMS experiments, the best results are obtained at a wavelength of 355 nm.

Journal Article↗