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PubMed1995

Ethylene oxide: induction of specific-locus mutations in the ad-3 region of heterokaryon 12 of Neurospora crassa and implications for genetic risk assessment of human exposure in the workplace.

Ethylene oxide (ETO) is an important industrial intermediate used extensively in the production of ethylene glycol, as a fumigant, and as a sterilant of choice for various medical devices. The mutagenicity of ETO was studied for the induction of specific-locus mutations in the adenine-3 (ad-3) region of a two-component heterokaryon (H-12) of Neurospora crassa. The objectives of these studies with ETO were to rank its mutagenic potency and to compare its mutational spectrum for induced specific-locus mutations with other chemical mutagens in this lower eukaryotic organism. Specific-locus mutations in the ad-3 region of heterokaryon H12 result from gene/point mutations at the closely linked ad-3A and ad-3B loci, multilocus deletion mutations and multiple-locus mutations. These major genotypic classes are similar to the types of specific-locus mutations that can be detected in higher organisms. Conidial suspensions of H-12 were treated with five different concentrations of ETO (0.1-0.35%) for 3 h at 25 degrees C. Control and ETO-treated conidial suspensions were used to obtain dose-response curves for inactivation as well as the overall induction of ad-3 forward mutations using a non-selective method based on pigment accumulation rather than a requirement for adenine. The results from these experiments are: (1) the slope of the dose-response curve for ETO-induced specific-locus mutations in the ad-3 region is 1.49 +/- 0.07, and (2) the maximum forward-mutation frequency fell between 10 and 100 ad-3 mutations per 10(6) survivors; therefore, ETO is a moderate mutagen. Classical genetic tests were used to characterize the ETO-induced ad-3 mutations from each of two treatments (0.25 and 0.35%). The overall data base demonstrates that ETO-induced ad-3 mutations result from a high percentage (96.9%) of gene/point mutations at the ad-3A and ad-3B loci, as well as from a low percentage (3.1%) of multilocus deletion mutations. The mutagenic activity of ETO is compared with the mutagenic specificity of other chemical mutagens and carcinogens in the ad-3 forward-mutation assay in Neurospora. The utilization of the Neurospora specific-locus data on ETO and those from experiments in the mouse and Drosophila, by others, is discussed for genetic risk assessment of germ-cell effects resulting from human exposure to ETO in the workplace.

Adenine↗
PubMed1985

Uptake and excretion of [14C]methyl bromide as influenced by exposure concentration.

Methyl bromide is a widely used soil fumigant and poses potential inhalation hazard to workers. Uptake of methyl bromide and pathways for excretion of 14C were investigated in male Fischer-344 rats after nose-only inhalation of 50, 300, 5700, or 10,400 nmol (1.6 to 310 ppm) of [14C]methyl bromide/liter of air for 6 hr. Fractional uptake of methyl bromide decreased at the highest concentrations, 5700 and 10400 nmol/liter, with 37 and 27% of the inhaled methyl bromide absorbed, respectively, compared to 48% at the lower levels. This resulted in the same total amount of methyl bromide being absorbed at the two higher exposure concentrations (650 mumol/kg body wt). Total methyl bromide adsorbed was 9 or 40 mumol/kg body wt after exposure to 50 or 300 nmol/liter, respectively. Elimination of 14C was linearly related to the amount of methyl bromide absorbed as determined from urine, feces, expired CO2, and parent compound collected for 66 hr after the end of exposure. Exhaled 14CO2 was the dominant route of excretion, with from 1.2 to 110 mumol (50% of amount absorbed) exhaled, and was described by a two-component negative exponential function; 85% was exhaled with a t 1/2 of 4 hr, and the remaining 15% was exhaled with a t 1/2 of 17 hr. The rate of exhalation of 14CO2 was not affected by the amount of [14C]methyl bromide absorbed. From 0.4 to 54 mumol was excreted in urine (20% of amount absorbed). The half-time for excretion of 14C in urine was approximately 10 hr, and the rate of excretion was not dependent on the amount of [14C]methyl bromide absorbed. Little 14C was exhaled as methyl bromide (less than 4% of the dose) or excreted in feces (less than 2%). At the end of 66 hr, 25% of the 14C absorbed remained in the rats. Liver, kidneys, adrenals, lungs, thymus, and turbinates (maxilloturbinates, ethmoturbinates, and nasal epithelial membrane) contained the highest concentrations of 14C. Results indicated that uptake of inhaled methyl bromide could be saturated. Any [14C]methyl bromide equivalents absorbed, however, would be excreted by concentration-independent mechanisms.

Air Pollutants, Occupational↗
PubMed1985

Disposition and metabolism of 2,3-[14C]dichloropropene in rats after inhalation.

2,3-Dichloropropene (2,3-DCP) is a constituent of some commercially available preplant soil fumigants for the control of plant parasitic nematodes. Human exposure potential exists during manufacture of the chemicals or during bulk handling activities. The purpose of this investigation was to determine the disposition and metabolism of 2,3-[14C]DCP in rats after inhalation. Male Fischer-344 rats were exposed nose-only to a vapor concentration of 250 nmol 2,3-[14C]DCP/liter air (7.5 ppm; 25 degrees C, 620 Torr) for 6 hr. Blood samples were taken during exposure, and urine, feces, expired air, and tissues were collected for up to 65 hr after exposure. Urinary excretion was the major route of elimination of 14C (55% of estimated absorbed 2,3-DCP). Half-time for elimination of 14C in urine was 9.8 +/- 0.05 hr (means +/- SE). Half-time for elimination of 14C feces (17% of absorbed 2,3-DCP) was 12.9 +/- 0.14 hr (means +/- SE). Approximately 1 and 3% of the estimated absorbed 2,3-[14C]DCP were exhaled as either 2,3-[14C]DCP or 14CO2, respectively. Concentrations of 14C in blood increased during 240 min of exposure, after which no further increases in blood concentration of 14C were seen. 14C was widely distributed in tissues analyzed after a 6-hr exposure of rats to 2,3-[14C]DCP. Urinary bladder (150 nmol/g), nasal turbinates (125 nmol/g), kidneys (84 nmol/g), small intestine (61 nmol/g), and liver (35 nmol/g) were tissues with the highest concentrations of 14C immediately after exposure. Over 90% of the 14C in tissues analyzed was 2,3-DCP metabolites. Half-times for elimination of 14C from tissues examined ranged from 3 to 11 hr. The data from this study indicate that after inhalation 2,3-DCP is metabolized in tissues and readily excreted.

Allyl Compounds↗
PubMed1986

Regression of methyl bromide-induced forestomach lesions in the rat.

There is continuing concern about the role of irritation in cancer development. Methyl bromide, a widely used fumigant and known irritant reported to cause forestomach carcinomas in rats, was dissolved in peanut oil and given by gavage at 50 mg/kg body wt to Wistar rats five times per week for 13 to 25 weeks. Starting at Week 13, methyl bromide administration was discontinued for half of the methyl bromide-treated rats (stop treatment group). After that, rats from both the continuous treatment and stop treatment groups were terminated at 4-week intervals to follow the progression of the stomach lesions. Forestomach lesions were not found in control rats receiving peanut oil and killed at 13 or 25 weeks. At 13 weeks the forestomachs from rats receiving methyl bromide were contracted and adherent to the liver and spleen. Inflammation, acanthosis, fibrosis, and a high incidence of pseudoepitheliomatous hyperplasia were found microscopically in treated animals. At 25 weeks, 100% of the rats receiving methyl bromide continuously had hyperplastic lesions of the forestomach which were more severe than those at 13 weeks. Evidence of malignancy was seen in one rat and the lesion was considered a very early carcinoma. In the stop treatment group that received methyl bromide for 13 weeks, there was regression of the stomach lesions, but at the 12-week final sacrifice, adhesions, fibrosis, and mild acanthosis remained. This study illustrates the need for regression experiments for complex forestomach lesions in rodents, especially when an irritating chemical is given by gavage.

Administration, Oral↗
PubMed1993

Human health effects of agrichemical use.

The use of pesticides and nitrogen fertilizers in agriculture has grown dramatically over the past 30 years. Currently, approximately 600 active pesticide ingredients are used, but adequate toxicologic data are available for only approximately 100 of these. Environmental exposure of humans to agrichemicals is common and results in both acute and chronic health effects, including acute and chronic neurotoxicity (insecticides, fungicides, fumigants), lung damage (paraquat), chemical burns (anhydrous ammonia), and infant methemoglobinemia (nitrate in groundwater). A variety of cancers also have been linked to exposure to various pesticides, particularly hematopoietic cancers. Immunologic abnormalities and adverse reproductive and developmental effects due to pesticides also have been reported. The health effects associated with pesticides do not appear to be restricted to only a few chemical classes. Therefore, enhanced efforts are needed to control or eliminate human exposures wherever possible. Research also is needed to better characterize and quantitate the adverse effects of agrichemicals on human health.

Abnormalities, Drug-Induced↗
PubMed1979

Potential halogenated industrial carcinogenic and mutagenic chemicals. II. Halogenated saturated hydrocarbons.

The halogenated saturated hydrocarbons analogously to the previously considered halogenated unsaturated hydrocarbons (Part I) possess considerable utility in a broad spectrum of applications including; solvents, dry-cleaning fluids, refrigerants, fumigants, degreasing agents, propellants and intermediates in the production of other chemicals, textiles and plastics. Methyl chloride, methylene chloride, chloroform, carbon tetrachloride, methyl chloroform, 1,1,2-trichloroethane, hexachloroethane, ethyl chloride and fluorocarbons were reviewed principally in terms of their synthesis (or occurrence), areas of application, stability, distribution, reactivity, levels of exposure, populations at risk, carcinogenicity, mutagenicity and metabolism.

Animals↗
PubMed1979

Potential halogenated industrial carcinogenic and mutagenic chemicals. III. Alkane halides, alkanols and ethers.

A variety of alkane halides, alkanols and ethers, analogous to the previously considered halogenated unsaturated (Part I) and saturated hydrocarbons (Part II) possess significant utility in a broad spectrum of applications including: solvents, fumigants, propellants and intermediates in the production of other chemicals, textiles, plastics and ion-exchange resins. Ethylene dichloride and dibromide, propylene dichloride; dibromochloropropane; 2-chloroethanol; 1-chloro-2-propanol; 2,3-dibromo-1-propanol; bis(chloromethyl)-, chloromethyl methyl-, bis(2-chloroisopropyl)-, and bis(2-chloroethyl-ethers were reviewed principally in terms of their synthesis, areas of utility, stability, distribution, reactivity, levels of exposure, population at risk, metabolism, carcinogenicity and mutagenicity.

Alcohols↗
PubMed1983

Mutagenicity, carcinogenicity and reproductive effects of dibromochloropropane (DBCP).

Dibromochloropropane (DBCP), a brominated organochlorine nematocide, has been used since the mid-1950s. Its primary value was its effectiveness on perennial crops without damaging the plants. DBCP also had less acute toxicity than earlier soil fumigants such as ethylene dibromide. DBCP became widely used on citrus, grapes, peaches, pineapple, soybeans and tomatoes. In Central America and Israel, banana trees were treated with DBCP. By 1975, 25 million pounds were being produced in the U.S. per year. The majority of U.S. production was applied in the Pacific Coast states, particularly California's San Joaquin Valley, and the Southern Atlantic Coast states. Animal studies in the early 1960s revealed hepatic and renal effects and testicular atrophy in DBCP-treated rates. Testicular atrophy was noted at the lowest exposure level tested (5 ppm). In 1973, DBCP was found to cause gastric carcinoma in mice and rats, and mammary adenocarcinoma in rats. A later study linked DBCP to nasal cavity tumors in rats. DBCP is an in vitro mutagen after activation with microsomal enzymes. A dominant lethal effect has been observed in rats. DBCP also induces increases in sister-chromatid exchanges and chromosomal aberrations. Mean fetal weight and maternal weight gain is decreased in pregnant rats exposed to DBCP. In mid-1977, employees in a California pesticide formulation plant were discovered to be infertile. Further investigations documented azoospermia and oligospermia among many of the workers handling DBCP. These findings were duplicated in other DBCP production plants. In the United States, the Occupational Safety and Health Administration (OSHA) and the Environmental Protection Agency (EPA) rapidly restricted the use of DBCP. The application of DBCP to all but pineapples in Hawaii was banned by the EPA in 1979. In 1982, the EPA exempted the peach crop in the Southern Atlantic coast states from the ban on DBCP use. Prior to the 1977 events, no such agent in workplace concentrations had been shown to produce infertility and sterility in otherwise healthy men. Subsequently, the interest in DBCP had led to many other studies, and has contributed to a heightened awareness about workplace hazards to both the male and female reproductive systems. This article will review the current state of knowledge of the in vitro, animal, and human toxicology of DBCP.

Animals↗
PubMed1989

Genetic toxicology of 1,2-dibromo-3-chloropropane (DBCP).

1,2-Dibromo-3-chloropropane (DBCP) is a nematocide, which has been used extensively as a soil fumigant in agriculture. Since sterility was found among male workers involved in the manufacture of DBCP, great concern has been focused on the genetic hazards of DBCP. DBCP gave positive results in many tests such as microbial, in vitro cytogenetics, and Drosophila studies. In mammalian test systems, DBCP caused chromosomal aberrations in the bone marrow cells and dominant-lethal mutations in germ cells in rats. In mice, there were no signs of DBCP-induced heritable mutation in germ cells, although point mutations were detected in somatic cells. The occurrence of Y-chromosomal non-disjunction was indicated in DBCP-exposed male workers by an increased number of sperm containing 2 Y-chromosomes.

Animals↗
PubMed1980

Dominant lethal mutation induced in male rats by 1,2-dibromo-3-chloropropane (DBCP).

1,2-Dibromoethane (DBE) and 1,2-dibromo-3-chloropropane (DBCP), soil fumigants, were investigated for their potential mutagenicity by dominant lethal studies in the rat and mouse. Dominant lethal mutation was induced by DBE in neither of the species. DBCP, on the other hand, induced dominant lethals in rats in the post-meiotic stage of spermatogenesis, especially in the early spermatid stage. However, DBCP did not cause dominant lethals in mice.

Animals↗
PubMedDate not supplied

Mutagenicity of methyl bromide in a series of short-term tests.

Methyl bromide is commonly used as a soil fumigant in greenhouses. In the framework of a toxicological evaluation, it was tested for possible genotoxic properties in two bacterial test systems (the fluctuation test using Klebsiella pneumoniae and the plate test using Salmonella typhimurium TA100 and TA98), two systems using mammalian cells in vitro (forward mutations at the TK and HPRT loci in L5178Y mouse lymphoma cells and unscheduled DNA synthesis in primary rat-liver cells) and in the sex-linked recessive lethal test using Drosophila melanogaster. Methyl bromide was active in all tests except the DNA-repair assay. The results indicate a relatively low mutagenic efficiency of the compound, as expected from its alkylating properties.

Animals↗
PubMed1986

A cytogenetic study of papaya workers exposed to ethylene dibromide.

Ethylene dibromide (EDB) has been shown to be carcinogenic in animal studies and mutagenic in vitro. One cytogenetic study of workers exposed to low levels of EDB for short durations was negative. To test whether exposure to low levels of EDB over long periods caused cytogenetic changes, we have assessed the frequencies of sister-chromatid exchanges (SCE) and chromosomal aberrations (CA) in the peripheral blood lymphocytes of 60 men occupationally exposed to EDB. These men worked in papaya-packing plants where EDB was used to fumigate the fruit after harvest to kill fruit-fly larvae. 42 other men who worked at a nearby sugar mill served as controls. The average duration of exposure of the papaya workers was 5 years. 82 full shift personal breathing-zone air samples indicated that the papaya workers were exposed to a geometric mean of 88 ppb of EDB, as an 8-h time weighted average (TWA). Peaks up to 262 ppb were measured. The proposed OSHA 8-h TWA for EDB is 100 ppb, while NIOSH recommends 45 ppb. No differences in SCE levels were found between exposed and nonexposed workers. No differences were found in the total CA frequency between exposed and nonexposed workers. SCE levels were significantly increased in men who smoked cigarettes (p = 0.0001) and in men who smoked marijuana (p = 0.01). CA levels showed a significant increasing trend with age (p = 0.03).

Adult↗
PubMed1987

Inhalation of methyl bromide gas induces mitotic recombination in somatic cells of Drosophila melanogaster.

The fumigant methyl bromide was evaluated for genotoxicity in the somatic wing-spot assay of Drosophila melanogaster. Third instar larvae trans-dihybrid for mwh and flr3 were exposed to varying concentrations (0-16 mg/l) of the gas for 1 h. Following this exposure via inhalation, the larvae were placed into vials containing Instant Medium. 7 days after the exposure, the adult flies in the vials were collected, and their wings were scored under 400X magnification for the presence of clones of cells possessing malformed wing-hairs. Such clones appeared as mwh-flr3 twin spots and single spots of either mwh or flr3 phenotype. Exposure to methyl bromide was found to result in the positive induction of both twin spots and large (greater than 2 cells) single spots. For each endpoint, a significant exponential association was obtained between concentration and frequency of spots per wing. Methyl bromide was found to be a negative inducer of small (1-2 cells) single spots at all concentrations except 16 mg/l where a positive effect was observed. Because twin spots arise exclusively from mitotic recombination, methyl bromide was identified as having recombinogenic activity in the somatic tissue of Drosophila larvae.

Animals↗
PubMed1991

Epidemiology, bacteriology and control of an outbreak of Nocardia asteroides infection on a liver unit.

An outbreak of Nocardia asteroides infection affecting seven patients is described. Over a 5-week period, five patients with liver disease admitted to a ward developed clinical and laboratory evidence of nocardiosis, and two further cases were diagnosed 3 and 5 months later. Three out of the five patients who received specific antimicrobial therapy responded to treatment; in three patients nocardia infection was considered to have contributed to death. In six out of the seven patients, nocardiosis followed immunosuppression. A common-source outbreak was considered to be responsible for infection in the first five patients. In two patients, presentation of infection 5 and 7 months after the first case may have been due to prolonged colonization or subclinical infection with Nocardia. Biotyping of the seven isolates using a fluorogenic biochemical method identified three distinct strains of N. asteroides. The most probable source of Nocardia was contaminated brick and plaster dust arising from building work in an area adjacent to the ward. However, samples of air, dust and water failed to yield N. asteroides. Infection control measures included ward closure followed by thorough cleaning, and formaldehyde fumigation.

Adult↗
PubMed1987

Injury and physiological responses of Larrea tridentata (DC) Coville exposed in situ to sulphur dioxide.

The response of shrubs of Larrea tridentata (DEC) Coville (creosotebush) exposed to sulphur dioxide (SO(2)) was evaluated using in situ plants of the Majove Desert. Larrea was exposed to acute levels of 0.3 to 2.0 microl litre(-1) SO(2) for periods up to 13 days using field chambers or an open-air fumigation system. Plants exposed in the spring exhibited considerable leaf injury (necrosis and defoliation) when exposed to 2.0 microl litre(-1) SO(2), and in the autumn had leaf injury when exposed to >0.4microl litre(-1) SO(2). Injured plants had higher transpiration rates, less negative water pressure potentials, and/or lower photosynthetic rates than control plants. It is likely that Larrea would not be injured by the typically low SO(2) concentrations and dry environmental conditions of the Mojave Desert. However, if injury were to occur, it would be accompanied by changes in plant-water relations and photosynthesis, followed by recovery after the SO(2) stress was removed.

Journal Article↗
PubMed1987

Autoradiographic studies of ethylenediurea distribution in woody plants.

Carbon-14-labelled ethylenediurea (EDU), synthesised from diethylenetriamine and (14)C-urea, was stem-injected into 2-year-old seedlings of sugar maple, white ash, flowering dogwood and flowering crabapple. At time intervals ranging from 1 h to 42 days after treatment, macroautoradiographs of leaf, stem and root tissue were made to determine relative distribution patterns of labelled chemical. Translocation of (14)C-EDU was very rapid and predominantly acropetal, especially after the first few hours. Maximum quantities of (14)C were found in leaf tissue approximately 7-10 days following injection, after which the intensity of the labelled chemical declined over the remainder of the study (42 days). Distribution patterns of (14)C-EDU were correlated with observed levels of protection afforded most plants when the chemical is injected 7 days before fumigation with ozone.

Journal Article↗
PubMed1987

Relationship between SO2 dose and growth of the pea aphid, Acyrthosiphon pisum, on peas.

A series of experiments was carried out in controlled environment cabinets to investigate the effects of SO(2) dose on the mean relative growth rate (MRGR) of pea aphids, Acyrthosiphon pisum, feeding on the pea plant, Pisum sativum. There was a significant linear increase in the MRGR of aphids feeding on SO(2)-fumigated plants, relative to control aphids feeding on plants in charcoal-filtered air. The increase in MRGR reached a maximum of 11% at SO(2) concentrations between 90 and 110 nl litre(-1). MRGR declined at higher SO(2) concentrations until above 220 nl litre(-1) it was below that of the controls. The dose-response curve is discussed in relation to reported changes in the nitrogen metabolism of plants subject to air pollution, the response of aphids to host plant nitrogen and possible toxic effects of high concentrations of SO(2) on the aphid.

Journal Article↗
PubMed1987

Effect of SO2 on the reproduction of pea aphids, Acyrthosiphon pisum, and the impact of SO2 and aphids on the growth and yield of peas.

Pea aphids feeding from birth to maturity on pea plants (Pisum sativum) exposed to SO(2) concentrations of 50 nl litre(-1) or 80 nl litre(-1) showed a significant 19% increase in the rate of nymph production during the reproductive period, compared to control aphids feeding on plants in charcoal-filtered air. The higher nymph production resulted in a mean 4.6% increase in the intrinsic rate of population increase (rm). In longer term glasshouse fumigation experiments pea aphid populations were, on average, 1.8 times greater on pea plants in ambient air plus 45 nl litre(-1) SO(2) than in ambient air alone. Aphid infestation in ambient air caused a 42% reduction in pea yield and affected most plant parameters adversely. Ambient air plus SO(2) had no direct effect on yield, but, in combination with aphid infestation, a further 10% reduction in yield was recorded.

Journal Article↗