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PubMed1994

Bacterial mutagenicity of 2-chloro-1,3-butadiene (chloroprene) caused by decomposition products.

Since the literature on genotoxicity of 2-chloro-1,3-butadiene (chloroprene) is controversial, the mutagenicity of this compound was reinvestigated with respect to its chemical stability. Because of the volatility of chloroprene, Ames tests with S. typhimurium TA 100 were carried out with gas-tight preincubation. Propylene oxide, a volatile direct mutagen, served as a positive control. Benzo[a]pyrene was used as a control for an indirect mutagen. Using this experimental regimen, freshly distilled chloroprene was not mutagenic. However, a mutagenic effect occurred linearly with increasing age of the chloroprene distillates. Aged chloroprene gave the same positive results whether preincubation was gas-tight or not. Analysis by gas chromatography (GC) revealed several decomposition products in aged chloroprene distillates. The direct mutagenicity towards TA 100 correlated with the integrated amounts of four of these substances; these substances always occurred in the same relative ratio. When chloroprene was kept under anaerobic conditions, products occurred with time which were partly different from those obtained under aerobic conditions. The direct mutagenicity of anaerobically aged chloroprene was only weak, but the mutagenic effect was enhanced about two- to threefold by addition of S9 mix. Partial identification of chloroprene decomposition products was done by gas chromatography-mass spectrometry (GC-MS): major byproducts of chloroprene, probably responsible for mutagenic properties of aged chloroprene samples, were cyclic chloroprene dimers.

Chloroprene↗
PubMed1999

Multiple organ carcinogenicity of inhaled chloroprene (2-chloro-1,3-butadiene) in F344/N rats and B6C3F1 mice and comparison of dose-response with 1,3-butadiene in mice.

Chloroprene (2-chloro-1,3-butadiene) is a high production chemical used almost exclusively in the production of polychloroprene (neoprene) elastomer. Because of its structural similarity to 1,3-butadiene, a trans-species carcinogen, inhalation studies were performed with chloroprene to evaluate its carcinogenic potential in rats and mice. Groups of 50 male and female F344/N rats and 50 male and female B6C3F1 mice were exposed to 0, 12.8, 32 or 80 p.p.m. chloroprene (6 h/day, 5 days/week) for 2 years. Under these conditions, chloroprene was carcinogenic to the oral cavity, thyroid gland, lung, kidney and mammary gland of rats, and to the lung, circulatory system (hemangiomas and hemangiosarcomas), Harderian gland, kidney, forestomach, liver, mammary gland, skin, mesentery and Zymbal's gland of mice. Survival adjusted tumor rates in mice were fit to a Weibull model for estimation of the shape of the dose-response curves, estimation of ED10 values (the estimated exposure concentration associated with an increased cancer risk of 10%) and comparison of these parameters with those for 1,3-butadiene. Butadiene has been identified as a potent carcinogen in mice and has been associated with increased risk of lymphatic and hematopoietic cancer in exposed workers. Shape parameter values for most of the neoplastic effects of chloroprene and 1,3-butadiene were consistent with linear or supralinear responses in the area near the lowest tested exposures. The most potent carcinogenic effect of 1,3-butadiene was the induction of lung neoplasms in female mice, which had an ED10 value of 0.3 p.p.m. Since the ED10 value for that same response in chloroprene exposed mice was also 0.3 p.p.m., we conclude that the carcinogenic potency of chloroprene in mice is similar to that of 1,3-butadiene. Cancer potency of chloroprene is greater in the mouse lung than in the rat lung, but greater in the rat kidney than in the mouse kidney and nearly equivalent in the mammary gland of each species.

Administration, Inhalation↗
PubMed1996

Toxicity of inhaled chloroprene (2-chloro-1,3-butadiene) in F344 rats and B6C3F(1) mice.

Chloroprene (2-chloro-1,3-butadiene) is a high production chemical used almost exclusively in the production of polychloroprene (neoprene) elastomer. Because of its structural similarity to isoprene (2-methyl-1,3-butadiene) and to 1,3-butadiene, a potent trans-species carcinogen, inhalation studies were performed on chloroprene to characterize its toxicological potential and to provide a basis for selecting exposure concentrations for chronic toxicity and carcinogenicity studies. Thirteen-week inhalation toxicology studies were conducted in male and female F344 rats and B6C3F(1) mice at exposure concentrations of 0, 5, 12, 32 or 80 ppm (6 h/day; 5 days/week). A 200 ppm exposure group was also included for rats only, because a previous study showed that this concentration of chloroprene is lethal to mice. In mice, exposure to 80 ppm chloroprene caused a marginal decrease in body weight gain in males and epithelial hyperplasia of the forestomach in males and females. This lesion has been observed in mice exposed to isoprene or 1,3-butadiene. In rats, exposure to 80 ppm chloroprene or higher concentrations caused degeneration and metaplasia of the olfactory epithelium and exposure to 200 ppm caused anemia, hepatocellular necrosis and reduced sperm motility. These lesions have not been observed in rats exposed to isoprene or 1,3-butadiene. The profile of toxic effects of chloroprene is considerably different from that of isoprene or 1,3-butadiene; this may be due to differences in exposure concentrations that were used in toxicology studies of these compounds and /or to the influence of the chlorine substitution on the toxicokinetics of these compounds, on their biotransformation, or on the reactivity of metabolic intermediates with tissue macromolecules.

Administration, Inhalation↗
PubMed2006

The metabolism and molecular toxicology of chloroprene.

Chloroprene (2-chloro-1,3-butadiene, 1) is oxidised by cytochrome P450 enzymes in mammalian liver microsomes to several metabolites, some of which are reactive towards DNA and are mutagenic. Much less of the metabolite (1-chloroethenyl)oxirane (2a/2b) was formed by human liver microsomes compared with microsomes from Sprague-Dawley rats and B6C3F1 mice. Epoxide (2a/2b) was a substrate for mammalian microsomal epoxide hydrolases, which showed preferential hydrolysis of the (S)-enantiomer (2b). The metabolite 2-chloro-2-ethenyloxirane (3a/3b) was rapidly hydrolysed to 1-hydroxybut-3-en-2-one (4) and in competing processes rearranged to 1-chlorobut-3-en-2-one (5) and 2-chlorobut-3-en-1-al (6). The latter compound isomerised to (Z)-2-chlorobut-2-en-1-al (7). In microsomal preparations from human, rat and mouse liver, compounds 4, 5 and 7 were conjugated by glutathione both in the absence and presence of glutathione transferases. There was no evidence for the formation of a chloroprene diepoxide metabolite in any of the microsomal systems. The major adducts from the reaction of (1-chloroethenyl)oxirane (2a/2b) with calf thymus DNA were identified as N7-(3-chloro-2-hydroxy-3-buten-1-yl)-guanine (20) and N3-(3-chloro-2-hydroxy-3-buten-1-yl)-2'-deoxyuridine (23), with the latter being derived by alkylation at N-3 of 2'-deoxycytidine, followed by deamination. Adducts in DNA were identified by comparison with those derived from individual deoxyribonucleosides. The metabolite (Z)-2-chlorobut-2-en-1-al (7) formed principally two adducts with 2'-deoxyadenosine which were identified as a pair of diastereoisomers of 3-(2'-deoxy-beta-d-ribofuranosyl)-7-(1-hydroxyethyl)-3H-imidazo[2,1-i]purine (25). The chlorine atom of chloroprene thus leads to different intoxication and detoxication profiles compared with those for butadiene and isoprene. The results infer that in vivo oxidations of chloroprene catalysed by cytochrome P450 are more important in rodents, whereas hydrolytic processes catalysed by epoxide hydrolases are more pronounced in humans. The reactivity of chloroprene metabolites towards DNA is important for the toxicology of chloroprene, especially when detoxication is incomplete.

Animals↗
PubMed1999

High frequency of codon 61 K-ras A-->T transversions in lung and Harderian gland neoplasms of B6C3F1 mice exposed to chloroprene (2-chloro-1,3-butadiene) for 2 years, and comparisons with the structurally related chemicals isoprene and 1,3-butadiene.

Chloroprene is the 2-chloro analog of 1,3-butadiene, a potent carcinogen in laboratory animals. Following 2 years of inhalation exposure to 12.8, 32 or 80 p.p.m. chloroprene, increased incidences of lung and Harderian gland (HG) neoplasms were observed in B6C3F1 mice at all exposure concentrations. The present study was designed to characterize genetic alterations in the K- and H-ras proto-oncogenes in chloroprene-induced lung and HG neoplasms. K-ras mutations were detected in 80% of chloroprene-induced lung neoplasms (37/46) compared with only 30% in spontaneous lung neoplasms (25/82). Both K- and H-ras codon 61 A-->T transversions were identified in 100% of HG neoplasms (27/27) compared with a frequency of 56% (15/27) in spontaneous HG neoplasms. The predominant mutation in chloroprene-induced lung and HG neoplasms was an A-->T transversion at K-ras codon 61. This mutation has not been detected in spontaneous lung tumors of B6C3F1 mice and was identified in only 7% of spontaneous HG neoplasms. In lung neoplasms, greater percentages (80 and 71%) of A-->T transversions were observed at the lower exposures (12.8 and 32 p.p.m.), respectively, compared with 18% at the high exposure. In HG neoplasms, the percentage of A-->T transversions was the same at all exposure concentrations. The chloroprene-induced ras mutation spectra was similar to that seen with isoprene, where the predominant base change was an A-->T transversion at K-ras codon 61. This differed from 1,3-butadiene, where K-ras codon 13 G-->C transitions and H-ras codon 61 A-->G transitions were the predominant mutations. The major finding of K-ras A-->T transversions in lung and Harderian gland neoplasms suggests that this mutation may be important for tumor induction by this class of carcinogens.

Adenoma↗
PubMed1981

Biochemical and hematological evaluation of chloroprene workers.

Swedish and Russian investigators have reported a variety of biochemical and hematological alterations in choloroprene-exposed workers. In view of their findings, an evaluation of the biochemical and hematological status of active chloroprene workers at a Du Pont Company plant was undertaken. The distributions of biochemical and hematological values of 336 currently exposed and 227 previously exposed chloroprene workers were compared to those of 283 workers never exposed to chloroprene. The comparative analysis did no indicate or suggest that chloroprene workers have biochemical or hematological alterations, or both, of medical significance. Some of the biochemical and hematological alterations cited by other researchers were investigated in the current study. Of those alterations investigated, none were found among the current cohort of chloroprene-exposed workers.

Adult↗
PubMed2006

Spatial and temporal trend evaluation of ambient concentrations of 1,3-butadiene and chloroprene in Texas.

This paper provides information on 1,3-butadiene (BD) and chloroprene as atmospheric pollutants in Texas and reviews available emission estimates and monitoring data. Ambient BD concentrations in most areas of Texas are predominantly influenced by on-road and off-road vehicular emissions or biomass burning, since BD is a product of combustion. However, large industrial point sources of BD emissions in Texas locally influence ambient concentrations. Total industrial BD emissions to the atmosphere in Texas for 2003 were estimated at 695 tonnes per year (TPY), approximately 70% of the total reported national industrial BD air emissions. Since 1998, there have not been any large industrial sources of chloroprene emissions in Texas, and total industrial chloroprene emissions for 2003 was estimated at only 0.09 TPY. Chloroprene was never detected at air monitoring sites. In 2003, the Texas Commission on Environmental Quality (TCEQ) monitored BD ambient air concentrations at 57 sites, some of which have been operational since 1992. These air monitors provide information on ambient BD concentrations in Texas and allow spatial and temporal trend evaluation. In 2003, annual average concentrations at monitoring sites in Texas ranged from less than the reporting limit of 0.01 to 3.2 parts per billion by volume (ppbv) with an overall average of 0.2 ppbv. This overall average is reduced to 0.1 ppbv if BD data from monitoring sites in Port Neches and Milby Park in Houston, which are located downwind of significant point sources of BD, are excluded. Ambient air monitoring has been conducted in Port Neches and in Milby Park in Houston since 1996 and 1999, respectively. At the Port Neches monitor, trend evaluation indicates that ambient concentrations of BD have declined since 1996 due to cooperative agreements with industries emitting BD. Annual average BD concentrations at the Port Neches monitor decreased from 8.3ppbv in 1996 to 1.3 ppbv in 2003, giving an 8-year average of 3.8 ppbv. Annual average BD concentrations at the Milby Park monitor varied between 2.1 and 4.4 ppbv from 1999 through 2003, giving a 5-year average of 3.1 ppbv. The results of cancer cluster studies based on Cancer Registry 1995-2001 incidence data and 1993-2002 mortality data conducted by the Texas Department of State Health Services for zip codes 77017/77012 (Houston) and 77651 (Port Neches) will be presented.

Air Pollutants↗
PubMed2001

Comparative carcinogenicity of 1,3-butadiene, isoprene, and chloroprene in rats and mice.

1,3-Butadiene, isoprene (2-methyl-1,3-butadiene), and chloroprene (2-chloro-1,3-butadiene) are high-production-volume chemicals used mainly in the manufacture of synthetic rubber. Inhalation studies have demonstrated multiple organ tumorigenic effects with each of these chemicals in mice and rats. Sites of tumor induction by these epoxide-forming chemicals were compared to each other and to ethylene oxide, a chemical classified by the National Toxicology Program (NTP) and by the International Agency for Research on Cancer (IARC) as carcinogenic to humans. For this group of chemicals, there are substantial species differences in sites of neoplasia; neoplasia of the mammary gland is the only common tumorigenic effect in rats and mice. Within each species, there are several common sites of tumor induction; these include the hematopoietic system, circulatory system, lung, liver, forestomach, Harderian gland, and mammary gland in mice, and the mammary gland and possibly the brain, thyroid, testis, and kidney in rats. For studies in which individual animal data were available, mortality-adjusted tumor rates were calculated, and estimates were made of the shape of the exposure-response curves and ED10 values (i.e. exposure concentrations associated with an excess risk of 10% at each tumor site). Most tumorigenic effects reported here were consistent with linear or supralinear models. For chloroprene and butadiene, the most potent response was for the induction of lung neoplasms in female mice, with ED10 values of 0.3 ppm. Based on animal cancer data, isoprene and chloroprene are listed in the NTP's Report on Carcinogens (RoC) as reasonably anticipated to be a human carcinogen. Butadiene is listed in the RoC as known to be a human carcinogen 'based on sufficient evidence of carcinogenicity from studies in humans, including epidemiological and mechanistic information', with support from experimental studies in laboratory animals. Epidemiology data for isoprene and chloroprene are not considered adequate to evaluate the potential carcinogenicity of these agents in humans.

Administration, Inhalation↗
PubMed1988

Chloroprene and isoprene: cytogenetic studies in mice.

Groups of male B6C3F1 mice (n = 15) were exposed for 6 h per day to ambient air, to chloroprene (12, 32, 80, 200 p.p.m.) or to isoprene (438, 1750 and 7000 p.p.m.) on 12 days. These compounds are the 2-chloro and the 2-methyl analogues, respectively, of 1,3-butadiene, a genotoxic and carcinogenic chemical in B6C3F1 mice. Exposure to chloroprene resulted in a 100% incidence of mortality among the mice exposed to 200 p.p.m. At concentrations of 80 p.p.m. and below, chloroprene neither induced a significant increase in chromosomal aberrations (CA), sister chromatid exchanges (SCE) or micronucleated erythrocytes, nor significantly altered the rate of erythropoiesis or of bone marrow cellular proliferation kinetics. However, the mitotic index (MI) in the bone marrow of chloroprene-exposed mice was significantly increased. Under similar conditions, exposure to isoprene induced significant increases at all concentrations in the frequency of SCE in bone marrow cells and in the levels of micronucleated polychromatic erythrocytes (PCE) and of micronucleated normochromatic erythrocytes in peripheral blood. In addition, a significant lengthening of the bone marrow average generation time and a significant decrease in the percentage of circulating PCE was detected. However, exposure to isoprene did not induce in bone marrow a significant increase in the frequency of CA nor did the exposure significantly alter the MI. The dose-response curves for SCE and micronuclei induction were non-linear, appearing to saturate at 438 and 1750 p.p.m., respectively. These results suggest that, similarly to butadiene, inhaled isoprene can be expected to induce tumors at multiple sites in B6C3F1 mice.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

Results of NTP-sponsored mouse cytogenetic studies on 1,3-butadiene, isoprene, and chloroprene.

Studies were conducted to determine the cytotoxic and cytogenetic effects of 1,3-butadiene and two structural analogs, chloroprene and isoprene, in the bone marrow cells of B6C3F1 mice exposed to the chemicals by inhalation. In one study, animals were exposed to 1,3-butadiene concentrations of 6.25, 62.5, or 625 ppm 6 hr/day on 10 exposure days and in the second study, to the same concentrations on weekdays for 13 weeks. Chloroprene and isoprene treatments involved 6 hr/day exposures on 12 exposure days at concentrations of 0, 12, 32, 80, and 200 ppm for chloroprene and 0, 438, 1750, and 7000 ppm for isoprene. In the 10-day study, 1,3-butadiene induced significant increases in sister chromatid exchange (SCE) at 6.25 ppm, micronuclei at 62.5 ppm, and chromosomal aberrations at 625 ppm. In the 13-week study, the frequency of micronucleated normochromatic erythrocytes in the peripheral blood was significantly elevated in all exposure groups including the 6.25-ppm group. Isoprene induced both SCE and micronuclei, whereas chloroprene gave negative results for all cytogenetic end points assessed in bone marrow cells.

Animals↗
PubMed1989

Epidemiologic study of cancer mortality among chloroprene workers.

Both case-control and cohort studies were undertaken from July 1, 1969 to June 30, 1983 to ascertain whether exposure to chloroprene increases the risk of cancer. Fifty-five cases of cancer deaths were verified, 16 of which had histories of exposure to chloroprene ranging from 3 to 23 years (median 11 years) with a latent period of 8-27 years, except for one case of 3 years (median 12.5 years). Fifty-four pairs were obtained by matching the cancer deaths to noncancer deaths in accordance with strict requirements. The odds ratio for the paired data was 13, X2 = 8.64, P less than 0.005. The average age at death from cancer of workers exposed to chloroprene was 12.7 years younger than that of unexposed workers, t' = 2.98, P less than 0.001. The total cohort consisted of 1213 persons, among whom 149 (11.6%) had histories of exposure for over 25 years, 381 (31.5%) for over 20 years, and 852 (70.2%) for over 15 years. The SMR for the total cohort was 2.38 (P less than 0.01), and all SMRs for the high-exposure occupations were of significance (P less than 0.05 or P less than 0.01), in contrast to those of the low-exposure grups whose SMRs were low or zero. Thus, a dose-response relationship existed. Among the high-exposure occupations, maintenance mechanics seem to have the highest risk of cancers, and SMRs for liver, lung, and lymphatic cancers were significant in this group. These results suggested that chloroprene exposure increases the risk of developing cancer.

Butadienes↗
PubMed2001

1,3-Butadiene, isoprene and chloroprene: reviews by the IARC monographs programme, outstanding issues, and research priorities in epidemiology.

1,3-Butadiene, isoprene and chloroprene have all been evaluated more than once by the IARC Monographs Programme on the Evaluation of Carcinogenic Risks to Humans, most recently in February 1998 (Volume 71). Summaries are available on-line at http://monographs.iarc.fr. 1,3-Butadiene is currently classified in Group 2A (probably carcinogenic to humans), on the basis of limited evidence for increased occupational cancer risk in humans plus sufficient evidence of carcinogenicity at multiple organ sites in rats and especially in mice exposed by inhalation. Four epidemiologic studies are available on cancer risk among workers exposed to 1,3-butadiene, one large study among styrene-butadiene rubber (SBR) workers, and one large and two small studies among 1,3-butadiene production workers. The results of the study of SBR workers suggest an association between butadiene exposure and leukaemia risk, which is consistent with the results of the large study of production workers. This latter study also suggested an increased risk of lymphoreticulosarcoma (ICD-8, 200). The major factors hampering the assessment of the available results are (i) possible misclassification of lymphoid and haematopoietic neoplasms, (ii) limitations in the assessment of past exposure (with the exception of the study of SBR workers) and (iii) a potential confounding effect of agents other than butadiene. Future research priorities include (i) the incorporation of newly developed biomarkers of exposure, (ii) the possible application of intermediate biomarkers, (iii) the replication of the study among SBR workers, possibly in Europe, and (iv) reanalysis of existing data in light of revisions of the classifications of leukaemias and lymphomas in the International Classification of Diseases for Oncology, Third Edition (2000). Isoprene is classified in Group 2B (possibly carcinogenic to humans), on the basis of sufficient evidence for carcinogenicity at multiple organ sites in both mice and rats, especially male mice, exposed by inhalation. No epidemiologic studies are available on cancer risk from occupational exposure to isoprene. Such studies could be conducted within the framework of existing or future studies of SBR workers, assuming that isoprene exposure can be disentangled from butadiene and styrene exposure. Chloroprene is classified in Group 2B on the basis of sufficient evidence for carcinogenicity at multiple organ sites in both mice and rats exposed by inhalation. Studies of chloroprene exposed workers now include chemical workers from the United States, China and Armenia as well as shoe workers from Russia. The results of the studies from China, Armenia and Russia suggest an excess risk of liver cancer. The risk of other neoplasms was not consistently increased. Limitations of available studies include possible bias from cohort enumeration, follow-up, and choice of reference population. In most studies the exposure assessment was poor, the possible confounding effect of co-exposures was not addressed and the statistical power was low. The pathology of the cases of liver cancer should be reviewed. Future research priorities include a replication of available studies in well-defined populations and the development of biomarkers of exposure.

Animals↗
PubMed2003

Detoxication pathways involving glutathione and epoxide hydrolase in the in vitro metabolism of chloroprene.

Chloroprene (2-chloro-1,3-butadiene, 1) is an important industrial chemical, which is carcinogenic in experimental animals and possibly in humans. It is metabolized to the monoepoxides, 2-chloro-2-ethenyloxirane (2a,b) and (1-chloroethenyl)oxirane (3a,b), together with electrophilic chlorinated aldehydes and ketones. This study has investigated the detoxication of these chloroprene metabolites in vitro by glutathione (GSH) and epoxide hydrolase (EH) in liver microsomes from Sprague-Dawley rats, B6C3F1 mice, and humans. In incubations of chloroprene with liver microsomes containing GSH, several GSH conjugates were identified. These were 1-hydroxy-4-(S-glutathionyl)butan-2-one (13), 1,4-bis-(S-glutathionyl)butan-2-one (15), and (Z)-2-(S-glutathionyl)but-2-en-1-al (16). A fourth GSH conjugate was identified as either 2-chloro-3-hydroxy-4-(S-glutathionyl)butene (12a,b) or 1-chloro-4-(S-glutathionyl)-butan-2-one (14), which were indistinguishable by LC/MS. Structural assignments of metabolites were based on chromatographic and spectroscopic comparisons with synthetic standards. There were significant differences between species in the amounts of 3a,b formed in microsomal incubations, the order being mouse > rat > human. Hydrolysis by microsomal EHs showed a distinct selectivity for S-(1-chloroethenyl)oxirane (3b) resulting in an accumulation of the R-enantiomer; the ratio of the amounts between species was 20:4:1 for mouse:rat:human, respectively.

Animals↗
PubMed2000

[Exposure to chloroprene as an occupational hazard (a cohort epidemiologic study)].

A cancer epidemiological study was conducted in chloroprene workers in Yerevan. In a cohort of male workers, the total morbidity rates for all tumor patterns were significantly lower (32%) than expected, which was attributed to the effect of "the healthy worker". Risk for hepatic tumor was 3.83 times the expected level among male operators of the chloroprene production equipment. A direct "dose-effective" correlation was established between liver cancer risk and length of record for occupational exposure to chloroprene. The highest risk was among males who came into contact with the substance under the age of 30.

Adult↗
PubMed1989

Short-term test for the induction of lung tumor in mouse by chloroprene.

In a previous study by the authors, positive results from both a case-control study and a cohort study were reported. In the present study a short-term test for the induction of mouse lung tumor by chloroprene was conducted to confirm whether chloroprene monomer itself can induce tumors. Kunming albino mice weaned at 2 weeks were subjected to inhaling 0, 2.9 +/- 0.3, 19.2 +/- 1.9, and 189.0 +/- 13.3 mg/m3 chloroprene (GC purity, 99.8%) 4 h daily (except Sunday) for 7 months. All survivors were killed at the end of the 8th month or when moribund. No lung tumors were found before the 6th month. Thus, survivors at the 6th month were counted as effective animals. Most lung tumors observed were papilloadenomas (50/57), and a few were adenomas (7/57). The tumor incidence in the 2.9 mg/m3 group was 8.1% in comparison to 1.3% in the control group, with the significance level at P less than 0.05. The higher the concentration, the higher the incidence. Examination of the multiplicity of tumor induction also demonstrated a dose-response relationship, and the number of tumors per mouse in the 189 mg/m3 group was significant at P less than 0.01.

Animals↗
PubMed1989

[Lung tumors induction short-term test of chloroprene in mice].

In a previous report by the authors, positive results in both case-control study mouse lung tumor induction short-term test of chloroprene for carcinogenicity was conducted to determine whether chloroprene monomer itself could induce tumor. Kuangming albino mice weaned 2 wk were subjected to inhale 0.0, 2.9 +/- 0.34, 19.18 +/- 1.89, 189.00 +/- 13.26 mg/m3, chloroprene (GC purity 99.69%) 4 h daily (except Sunday) for 7 month. All survivors were killed at the end of the 8th month or when moribund. No lung tumor was found before the 6th month. Thus survivors at the 6th month were counted as effective animals. Most lung tumors observed were papillo-adenoma (50/57), and a few were adenoma (7/57). Tumor incidence of the 2.9 mg/m3 group increased to 8.1% in comparison with that of the control group (1.3%) at a significant level of P less than 0.05; and the higher the concentration the higher the incidence. Examination of the multiplicity of tumors also demonstrated the dose-response relationship, and the number of tumors per mouse in the 189 mg/m3 group was significant at P less than 0.01.

Animals↗
PubMed1976

Aspects of the toxicology of chloroprene: immediate and long-term effects.

The maximum permissible concentration (MPC) of chloroprene was set at 2 mg/m3 in the USSR in the 1940's. The existing MPC is 4 mg/m3. The threshold of systemic effects as a result of chronic chloroprene exposure is l.69 mg/m3. However, the threshold for embryotoxic and mutagenic effects is 0.15 mg/m3. In consideration of this information, setting a new MPC for chloroprene at 0.05 mg/m3 is recommended.

Adult↗
PubMed1977

Toxicity of chloroprene, 1,3-dichlorobutene-2, and 1,4-dichlorobutene-2.

A review of the toxicity of 1,3-dichlorobutene-2 (1,3-DCB), 1,4-dichlorobutene-2 (1,4-dcb), and 2-chlorobutadiene, 1,3 (beta-chloroprene) was undertaken with an emphasis on assessing the hazards of these materials in the industrial situation. 1,3-DCB is a by-product of beta-chloroprene from the acetylene route, with 1,4-DCB is an intermediate in the production of beta-chloroprene from the butadiene route, the production route used in the U.S. Presented in the review is a summary of the acute toxicity including mutagen testing, skin, eye, and inhalation testing of these compounds. In addition, subacute inhalation testing, embryotoxicity, teratogenicity, and carcinogenicity are also reviewed where the information is available.

Abnormalities, Drug-Induced↗