Concentrations Of Methyl Chloride Research Articles

Purge-and-Trap Gas Chromatography Method for Analysis of Methyl Chloride and Methyl Bromide in Seawater

Purge-and-trap technique coupled with gas chromatography with electron capture detector (GC-ECD) is developed for analyzing the concentrations of methyl chloride (CH3Cl) and methyl bromide (CH3Br) in seawater. The optimum conditions were established as follows: purge time (12 min), purge gas flow rate (50 mL min−1), purge temperature (40°C), desiccant (Mg(ClO4)2), liquid nitrogen trap, boiling water desorption (2 min). The detection limits were 2.7 and 0.3 pM, the precision was < 2% and < 8%, and the recoveries were 89%–97% and 75%–85% for CH3Cl and CH3Br, respectively. Experiments for sample storage were carried out to test the reliability of the storage procedure used in this study, and the results showed that there was no significant change in CH3Cl and CH3Br concentrations in seawater within 24 h using this procedure. Merits of this method are that exact concentrations could be estimated and the analysis could be completed within 6 h in situ. This method was also used to measure in situ concentrations of CH3Cl and CH3Br in the surface seawater of the Jiaozhou Bay, and the results showed that the concentrations of CH3Cl and CH3Br ranged from 130 to 346 pM and 3.90 to 20.7 pM, respectively, which were in good agreement with those values reported in literature in other coastal waters. Our study shows that this method meets the demands of the measurement of in situ concentrations of CH3Cl and CH3Br in seawater.

Seasonal and spatial variations in methyl chloride in NW Atlantic waters

Methyl chloride concentrations were measured in the upper 200 m of the water column of the NW Atlantic during three cruises along the same track in spring, summer and fall of 2003. Distinct seasonality was apparent, with the surface waters being either undersaturated or close to equilibrium with the atmosphere in spring, but with supersaturation of the warmer waters in summer and fall. Cooler waters at the more northerly stations were always undersaturated, thus representing a continual sink for atmospheric methyl chloride. Even on an annual basis, the concentration anomaly (the difference between measured concentration and equilibrium with the atmosphere) was strongly dependent on sea surface temperature (SST). This empirical relationship can be used to extrapolate fluxes globally or to estimate the influence of global warming on ocean‐to‐atmosphere fluxes of methyl chloride. The global flux of methyl chloride to the atmosphere estimate based on the full‐year relationship between concentration anomaly and SST is 17 Gmol/y, and is reduced to 6 Gmol/y if separate seasonal relationships are used. It appears that the ocean component of the flux is highly sensitive to temperature, but the actual source of the methyl chloride in ocean waters remains largely unknown.

Ocean‐atmosphere exchange of methyl chloride: Results from NW Atlantic and Pacific Ocean studies

Measurements of methyl chloride concentrations and saturations in the NW Atlantic and Pacific Ocean from 40°N to 40°S are presented. Labrador Sea waters, analyzed in July, were at or below saturation, while warmer waters south of the Gulf Stream and all Pacific samples were consistently supersaturated. We find no correlation between methyl chloride concentrations and chlorophylla, but much of the variation in methyl chloride partial pressure appears to be accounted for by variations in sea surface temperature. We estimate ocean‐atmosphere fluxes of methyl chloride, using exchange velocities for spot wind speeds and climatological wind speeds. These indicate that none of the waters we sampled support the magnitude of fluxes which have hitherto been considered to be emitted by the ocean. A simple extrapolation yields a global efflux of 0.8 to 1.1 × 1010mol yr−1(0.4 to 0.6 Tg yr−1) supplied by warm waters and a high‐latitude influx of 0.2 to 0.5 × 1010mol yr−1(0.1 to 0.3 Tg yr−1). The net global ocean source to the atmosphere is 0.3 to 0.9 × 1010mol yr−1(0.2–0.4 Tg yr−1), which accounts for 5 to 12% of the total required to balance loss by reaction with hydroxyl radicals. Unless its atmospheric reactivity has been overestimated, we conclude that other sources of methyl chloride make major contributions to its atmospheric budget.

Distribution of methylchloride, dichloromethane, trichloroethene and tetrachloroethene over the north and south Atlantic

During the cruise ANT VIII/1 of the German R/VPolarsternin August/September 1989 the latitudinal distributions of the atmospheric concentrations of methylchloride, dichloromethane, trichloroethene, and tetrachloroethene were measured over the Atlantic between 45°N and 30°S by in situ gas chromatography. With the exception of trichloroethene they showed mixing ratios well above the lower limit of detection. The methylchloride distribution was uniform with average mixing ratios of 532 ± 8 and 550 ± 12 ppt in the northern and southern Hemispheres, respectively. Dichloromethane increased linearly between the Intertropical Convergence Zone and 45°N with average mixing ratios of 36 ± 6 ppt and was almost constant in the southern hemisphere with an average of 18 ± 1 ppt. Tetrachloroethene mixing ratios were between less than 1 and 10 ppt in the northern hemisphere and always below 3 ppt in the southern hemisphere. Similar to dichloromethane, tetrachloroethene was nearly constant in the southern hemisphere and increased linearly toward northern latitudes. This is compatible with the predominantly industrial origin of these compounds. Trichloroethene varied between 0.3 ppt and about 15 ppt in the northern hemisphere with an average of 3 ± 1 ppt and was generally lower than 1 ppt in the southern hemisphere with mixing ratios often near or below the detection limit of 0.1 ppt. For CH3Cl we estimate a global turnover of 3.5 × 1012g/yr which is compatible with previous results. Using a simple model calculation our measurements imply a global turnover for CH2Cl2and C2Cl4of 0.9 × 1012g/yr and 0.6 × 1012g/yr, respectively.

Formation and repair of DNA lesions in kidneys of male mice after acute exposure to methyl chloride

The time-course of DNA lesions (DNA-protein cross-links, single-strand breaks) induced by high concentrations of methyl chloride (1000 ppm) was measured in renal tissue of male mice by means of the alkaline elution assay in order to gain an insight into repair processes. DNA-protein cross-links were removed at a fast rate, whereas single-strand breaks appeared to accumulate, even during repair of DNA-protein cross-links. However, 48 h after exposure to methyl chloride, neither of these lesions were detectable in mouse kidney. Both types of DNA damage were ascribed to the action of formaldehyde, an intermediate in methyl chloride metabolism which may react with nucleic acids and protein and interfere with DNA repair.

Biochemical effects of methyl chloride in relation to its tumorigenicity.

The biochemical effects of methyl chloride were investigated in tissues of F-344 rats and B6C3F1 mice (both sexes). Activities of GST were 2-3 times higher in livers of male B6C3F1 mice, compared with those of female mice, and with rats of both sexes. In kidneys GST activities of (male) mice were about 7 times lower than those found in livers. The activity of FDH was higher in livers of mice (both sexes) than in those of rats. No obvious sex difference was found in livers of rats and mice with respect to FDH. In kidneys, however, (minor) differences in FDH activities occurred between male and female B6C3F1 mice (4.7 vs. 3.1 nmol/min per mg). Sex differences of FDH activity in kidneys were not observed in F-344 rats. The microsomal transformation (by cytochrome P-450) of methyl chloride and S-methyl-L-cysteine to formaldehyde in tissues of B6C3F1 mice occurred preferentially in the liver. More formaldehyde was produced in liver microsomes of male, compared to those of female mice. Kidney microsomes metabolized methyl chloride to formaldehyde much less than liver microsomes. After a single exposure of mice of both sexes to 1000 ppm methyl chloride no elevation in formaldehyde concentrations was observed in livers and kidneys ex vivo. The determination of DNA lesions, using the alkaline elution technique, revealed no DNA-protein crosslinks in kidneys of male B6C3F1 mice after exposure to methyl chloride (1000 ppm, 6 h day-1, 4 days) and gave only minor evidence of single-strand breaks. Lipid peroxidation (production of TBA reactive material), induced by single exposure to methyl chloride (1000 ppm, 6 h), was very pronounced in livers of male and female mice. Smaller increases in peroxidation were observed in the kidneys of exposed mice. The theory that renal tumors observed in male mice after chronic exposure of the test animals to high (1000 ppm) concentrations of methyl chloride, are evoked by intermediates and in situ produced formaldehyde is proven unlikely by our results.

Reproduction in Fischer-344 rats exposed to methyl chloride by inhalation for two generation

Male and female Fischer-344 rats were exposed to methyl chloride by inhalation (0, 150, 475, or 1500 ppm, 6 hr/day, 5 days/week, 40 males and 80 females per group). The only treatment-related clinical signs were a 10 to 20% body weight gain depression (BWGD) in both males and females exposed to 1500 ppm at all weekly weighings after 2 weeks of exposure and a 5–7% BWGD in 475-ppm exposed animlas after Day 57. After 10 weeks the exposure schedule was changed to 6 hr/day, 7 days/week and each male was mated to two exposed females. The mating period was ended after 2 weeks, at which point 10 males/group were necropsied. The only tratment-related lesions found were severe bilateral testicular degeneration ( 10 10 ) and granulomas in the epididymis ( 3 10 ) in the 1500-ppm males. The remaining 30 males per group were then removed from exposure and mated during a 2-week period with 60 unexposed females. The exposed females were continued on exposure from the start of mating to Postnatal Day 28 (6 hr/day, 7 days/week). The females were not exposed from Gestation Day 18 to Postnatal Day 4, and the pups were never directly exposed prior to weaning. There were no significant differences between groups in the number of exposed or unexposed females that mated, as evidenced by copulation plugs. No litters were born to exposed or unexposed females mated to the 1500-ppm males. There was no significant difference in the number of litters produced by the 150-ppm groups when compared to the control groups. Fewer litters were born in the 475-ppm groups than in the control groups. No differences in litter size, sex ratio, pup viability, or pup growth were found among the 475-ppm, 150-ppm, or control F 0 groups. When bred 10 weeks after the cessation of exposures, 5 to 20 1500-ppm F 0 males had regained the ability to sire normal litters. The same number of 475-ppm F 0 males proved as fertile ( 15 20 ) as control F 0 males ( 13 20 ). After weaning, F 1 pups from the 475-, 150-, and 0-ppm groups were exposed to the same concentrations of methyl chloride for 10 weeks and then mated. A trend toward decreased fertility was found in the 475-ppm F 1 group.

DNA-binding assay of methyl chloride.

Fischer-344 rats and B6C3F1 mice of both sexes were exposed in closed chambers to 14C-labeled methyl chloride. Different clearance values from the gas phase of the system indicated that, based on body weight, mice metabolized the test compound much faster than rats. After isolation of DNA and nucleoproteins from liver and kidneys radioactivity was found in all macromolecular samples; this was ascribed to metabolic C1-incorporation. Radioactivity incorporation was particularly high in DNA of mouse kidneys, suggesting a high turnover to active C1 bodies (formaldehyde, formate) in this tissue. Analyses of DNA samples from kidneys of female and male mice showed neither 7-N-methylguanine nor O6-methylguanine. Hence, the formation of tumors in B6C3F1 mice exposed to high concentrations of methyl chloride is not based on methylation of DNA in this tissue.

Assessment of the genotoxic effects of methyl chloride in human lymphoblasts

The activity of methyl chloride was measured in 4 genotoxicity assays. In an established human lymphoblast line, a 3-h treatment with 0–5% methyl chloride resulted in a dose-related increase in mutant fraction at the thymidine kinase locus and induction of sister-chromatid exchange. No increase in DNA damage, as measured by alkaline elution, was detected in the lymphoblasts at concentrations of methyl chloride shown to be mutagenic. Also, a concentration-related increase in 8-azaguanine-resistant fraction in Salmonella typhimurium was observed following a 3-h treatment with atmospheres containing 0–20% methyl chloride. Thus, methyl chloride is a weak, direct-acting mutagen for bacteria and human cells in culture.

Reproduction in Fischer-344 Rats Exposed to Methyl Chloride by Inhalation For Two Generations

Reproduction in Fischer-344 Rats Exposed to Methyl Chloride by Inhalation For Two Generations. HAMM, T. E., JR., RAYNOR, T. H., PHELPS, M. C, AUMAN, C. D., ADAMS, W. T., PROCTOR, J. E., AND WOLKOWSKI-TYL, R. (1985) Fund. Appl. Toxicol. 5, 568–577. Male and female Fischer-344 rats were exposed to methyl chloride by inhalation (0, 150, 475, or 1500 ppm, 6 hr/day, 5 days/week, 40 males and 80 females per group). The only treatment-related clinical signs were a 10 to 20% body weight gain depression (BWGD) in both males and females exposed to 1500 ppm at all weekly weighings after 2 weeks of exposure and a 5–7% BWGD in 475-ppm exposed animals after Day 57. After 10 weeks the exposure schedule was changed to 6 hr/day, 7 days/week and each male was mated to two exposed females. The mating period was ended after 2 weeks, at which point 10 males/group were necropsied. The only tratment-related lesions Found were severe bilateral testicular degeneration (10/10) and granulomas in the epididymis (3/10) in the 1500-ppm males. The remaining 30 males per group were then removed from exposure and mated during a 2-week period with 60 unexposed females. The exposed females were continued on exposure from the start of mating to Postnatal Day 28 (6 hr/day, 7 days/week). The females were not exposed from Gestation Day 18 to Postnatal Day 4, and the pups were never directly exposed prior to weaning. There were no significant differences between groups in the number of exposed or unexposed females that mated, as evidenced by copulation plugs. No litters were born to exposed or unexposed females mated to the 1500-ppm males. There was no significant difference in the number of litters produced by the 150-ppm groups when compared to the control groups. Fewer litters were born in the 475-ppm groups than in the control groups. No differences in litter size, sex ratio, pup viability, or pup growth were Found among the 475-ppm, 150-ppm, or control F0 groups. When bred 10 weeks after the cessation of exposures, 5 to 20 1500-ppm F0 males had regained the ability to sire normal litters. The same number of 475-ppm F0 males proved as fertile (15/ 20) as control F0 males (13/20). After weaning, F1 pups from the 475-, 150-, and 0-ppm groups were exposed to the same concentrations of methyl chloride For 10 weeks and then mated. A trend toward decreased fertility was Found in the 475-ppm F1 group

Methyl halides in and over the eastern Pacific (40°N–32°S)

Methyl chloride, methyl bromide, and methyl iodide measurements in and over the eastern Pacific (40°N and 32°S latitude) show mean air concentrations of 633 parts per trillion (ppt), 23 ppt, and 2 ppt, and mean surface seawater concentrations of 11.5 ng/l, 1.2 ng/l, and 1.6 ng/l respectively. Long‐term ambient measurements at a marine Pacific site (39°N) show an essentially unchanging background, with some indication of high concentrations of methyl bromide and methyl iodide during summertime. The oceanic data indicate a mean surface supersaturation of 275%, 250%, and 340%, respectively, for these three methyl halides. Depth profiles show that methyl halides are most abundant in the top mixed layer of the ocean. Oceanic concentrations of methyl chloride and methyl bromide are significantly correlated (linear regression coefficient of 0.85), suggesting a common source. No relationship between oceanic methyl iodide concentrations and the other two halides could be found. Coexistence of high concentrations of methyl iodide with relatively low concentrations of methyl chloride and vice versa provided no direct support for the hypothesis that chloride ion reactions with methyl iodide may be the dominant oceanic source of methyl chloride. For the eastern Pacific, mean ocean to air fluxes (in units of 10−7 g cm−2 yr−1) of 13, 1, and 1 are determined for methyl chloride, methyl bromine, and methyl iodide, respectively. When extrapolated to global waters, they provide an adequate source to explain the atmospheric reservoir of these organic halides. Total organic bromine and iodine measurements would suggest that methyl bromide and methyl iodide contribute predominately to the tropospheric bromine and iodine organic reservoir.

Histopathology of acute toxic response in rats and mice exposed to methyl chloride by inhalation

Histopathology of Acute Toxic Response in Rats and Mice Exposed to Methyl Chloride by Inhalation. Morgan, K.T., Swenberg, J.A., Hamm, T.E., Jr., Wolkowski-Tyl, R. and Phelps, M. (1982). Fundam. Appl. Toxicol. 2:293–299. Both sexes of one strain of rat (F344), two strains of mice (C3H and C57BL/6) and the cross (B6C3F1) of these 2 strains of mice were exposed by inhalation to methyl chloride for 6 hours per day for up to 12 days. Methyl chloride concentrations in air were 0, 500, 1000, or 2000 ppm for mice, and 0, 2000, 3500 or 5000 ppm for rats. All male B6C3F1 mice exposed to 2000 ppm were dead or moribund by day 2, and all male and female mice in the remaining 2000 ppm groups were moribund by day 5. Prior to death many of these mice exhibited ataxia, and hematuria with the latter occurring mainly in females. Treatment associated lesions in mice included hepatocellular degeneration and necrosis, degeneration and necrosis of proximal convoluted tubules and/or basophilic tubules in the renal cortex, and focal areas of necrosis of the internal granular layer of the cerebellum. Brain lesions were most severe in female C57BL/6 mice, while hepatocellular degeneration was most severe in male C57BL/6 and B6C3F1 strains. Approximately 50% of the male and female rats exposed to 5000 ppm were killed in extremis on day 5. The principal clinical signs, which were confined to the 5000 and 3500 ppm groups, included severe diarrhea, incoordination of the fore-limbs, and in a small number of animals, hind limb paralysis and convulsions. In rats, lesions were observed in the liver, kidney and brain which resembled those seen in mice but were generally less severe. Lesions observed in tissues examined only in rats included vacuolar degeneration of the zona fasciculata of the adrenal glands and degenerative changes in the seminiferous tubules and epididymis. Rats appeared to respond in a similar manner to mice but were more resistant to methyl chloride toxicity. These findings demonstrate species, strain and sex differences in susceptibility to methyl chloride.

Experimental application of gas chromatographic headspace analysis to priority pollutants

Abstract A general procedure for the headspace analysis of volatile organic pollutants in water is examined in detail. Theoretical and practical considerations are discussed in depth. The experimental demonstration of the method is applied to the analysis of μg/l concentrations of methyl chloride, ethyl chloride and vinyl chloride. Details of field sampling, calibration, analysis, aliquot transfer and standard preparation are all addressed. Stability of prepared samples over the course of 16 days has been examined. With all data included over the course of the 16‐day investigation, the standard deviation of analyses of the individual components is approximately ± 20% of each average at nominal 30 μg/l initial concentrations.