1. Chemical and Physical Data

1.2. Structural and molecular formulae and molecular weight

2. Production, Use, Occurrence and Analysis

2.1. Production and use

(a) Production

Bromoform can be prepared by reacting chloroform (see IARC, 1987) with aluminium tribromide at less than or equal to 60°C; by reacting ethanol with sodium hypobromite; or by the redistribution reaction between chloroform and ethyl bromide (Harlow & Ross, 1932; Soroos & Hinkamp, 1945; Sherman & Kavasmaneck, 1980).

(b) Use

Bromoform has been used as an intermediate in organic synthesis, as an ingredient in fire-resistant chemicals, as a gauge fluid in geological assaying, as a solvent for waxes, greases and oils, and as a sedative (Sittig, 1985; Sax & Lewis, 1987).

(c) Regulatory status and guidelines

Standards have been established for trihalomethanes (including bromoform) in drinking-water (see monograph on chlorinated drinking-water, p. 59) in several countries. Occupational exposure limits and guidelines for bromoform are presented in Table 1.

Table 1.

Occupational exposure limits and guidelines for bromoform.

2.2. Occurrence

(a) Natural occurrence

Mean levels of bromoform in the tissues of temperate marine macroalgae (Ascophyllum nodosum, Fucus vesiculosis, Enteromorpha linza, Ulva lacia, Gigartina stellata) ranged from 8 to 120 ng/g dry weight. Bromoform was released to seawater at a rate of 0.14–14 µg/g of dry algae per day (Gschwend et al, 1985).

Macroalgae collected near the Bermuda Islands (Fucales sargassum) and at the Cape of Good Hope (Laminariales laminaria) showed a specific pattern of emissions of volatile organohalides into the air. The main components were bromoform, bromodichloromethane and chlorodibromomethane (Class et al., 1986).

(b) Air

The volatilization half-time of bromoform from rivers and streams has been estimated to range from 63 min to 24 days, depending on turbulence and temperature. A typical half-time, based on actual data, was 66 h (Kaczmar et al., 1984).

Ullrich (1982) studied the organohalogen compound concentrations in the air of four public indoor swimming pools in western Berlin. Mean bromoform concentrations ranged from 0.7 to 6 µg/m³.

In a review of data on the presence of volatile organic chemicals in the atmosphere of the USA in 1970–80, a median concentration of 0.64 µg/m³ bromoform was reported for the four urban/suburban data points examined and below the limit of detection for industrial areas (74 data points) (Brodzinsky & Singh, 1983).

Bromoform levels in air samples collected in 1985 over the Atlantic Ocean were 0.6–460 ppt (6.2–4.8 µg/m³); baseline levels of biogenic bromoform in air were 0.6–6.6 ppt (6.2–68.2 ng/m³). The highest levels were found in samples taken at beaches with intense algal populations. Air samples collected in 1985 from a forest area in southern Germany contained 1.2 ppt (12.4 ng/m³) bromoform (Class et al., 1986).

In the USA, air samples collected 2 cm above the surface of five outdoor pools contained < 0.1 µg/m³ bromoform; those above four indoor pools contained < 0.1–20 µg/m³ and those above four spas (whirlpools or hot tubs) contained < 0.1–62 µg/m³. Samples collected 2 m above the surface contained < 0.1 µg/m³, < 0.1–14 µg/m³ and < 0.1–14 µg/m³, respectively (Armstrong & Golden, 1986).

Air samples collected in the USA between 1984 and 1987 showed that the atmospheric concentrations of bromoform averaged 6.3 ng/l at Point Barrow, Alaska, and 3.1 ng/l at Cape Kumukahi, Hawaii. Large pulses of organic bromine (mainly bromoform) enter the atmosphere during the three-month Arctic spring (Fogelqvist, 1985; Cicerone et al., 1988).

(c) Water and sediments

The formation of trihalomethanes in drinking-water (see also the monograph on Chlorinated drinking-water, p. 56 et seq.) and the effects of temperature and pH have been discussed extensively (Williams, 1985). The formation of bromoform during drinking-water chlorination depends on the presence of bromide in untreated water.

Bromoform was detected (but not quantified) in headspace analysis of nine of ten Pacific seawater samples collected in 1983 (Hoyt & Rasmussen, 1985).

Bromoform has been measured or detected in many drinking-water systems, both in samples collected at treatment facilities or along the distribution system (Table 2) and in samples collected from natural and untreated water sources (Table 3). Concentrations in treated drinking-water typically ranged from < 1 to 10 µg/l (with higher values in some locations), compared with concentrations in untreated (natural) waters which are typically less than 1 µg/l.

Table 2.

Bromoform concentrations in treated^a drinking-water,1973–89.

Table 3.

Bromoform concentrations in untreated (natural) water, 1973–79.

Rook (1974) demonstrated that bromoform, observed at concentrations ranging from 0.5 to 10 µg/l following chlorination of stored surface waters, was a product of chlorination of the humic substances in natural waters.

In the 1975 US National Organics Reconnaissance Survey of water supplies in 80 US cities, bromoform was not found in any of the raw water samples (minimum quantifiable concentration, 1–4 µg/l) (Symons et al., 1975).

According to the US Environmental Protection Agency STORET system concentrations of bromoform in 131 samples of surface water in 1970–79 ranged from 0.1 to 1 µg/l in 1% of the samples, 1–10 µg/l in 97% of the samples, and 10–100 µg/l in 2% of the samples (Perwak et al., 1980).

In the 1982 US Nationwide Urban Runoff Program, bromoform was detected in samples from one of the 15 reporting cities at a concentration of 1 µg/l (Cole et al., 1984).

The US Environmental Protection Agency estimated that 17 tonnes of bromoform were generated in the US in 1978 by water chlorination. On the basis of the 1976 National Organic Monitoring Survey, the general population was estimated to be exposed to 7 µg bromoform per day from drinking-water, assuming a maximal concentration of 280 µg/l and an intake of 2.18 1 per day, the daily exposure increased to 600 µg per day (Perwak et al, 1980).

Bromoform levels in tap water collected at four locations in a Swedish community ranged from 0.24 to 0.34 µg/l; when the treatment facility briefly changed the disinfectant from chlorine to chlorine dioxide, bromoform was not detected (detection limit, 0.01 µg/l) (Norin et al., 1981).

Samples of water were collected between August and October 1980 from one supply system in São Paulo State, Brazil. Mean levels of bromoform were 0 1 µg/l in treated water (after chlorination) and 0.06 µg/l in treated water from the reservoir (II) (de Fernicola & de Azevedo, 1984).

Bromoform has been identified as the major halogenated organic compound produced as a result of chlorinating seawater. Potential daily bromoform producation by a Pilot plant for conversion of ocean thermal energy was estimated to be 1300 g/day; the bromoform concentration contained in the diluted discharge water was estimated to be 0.93 µg/l (Hartwig & Valentine, 1983).

Bromoform concentrations in samples of chlorinated seawater at a desalination test facility on Wrightsville Beach, NC, USA, were 23–209 µg/l. In general, bromoform concentrations increased through the various pretreatment processes; in effluents from activated carbon columns, however, levels ranged from not detected to 36 µg/l (Singer, 1982).

Pretreatment of seawater with chlorine at a pilot desalination facility in the USA produced average concentrations of bromoform ranging from 13 to 110 µg/l dining the different steps of the two pretreatment processes (Chang & Singer,

Samples of chlorinated intake and discharge seawater collected in 1980 from a power plant in Port Everglades, FL, contained bromoform at levels ranging from 75 to 78 µg/l and from 32 to 86 µg/l, respectively. The concentration of bromoform in the unchlorinated intake water was 1 µg/l. Chlorination of the seawater in the laboratory with 1, 2, and 4 mg/l chlorine resulted in corresponding bromoform concentrations of 6.5, 107 and 272 µg/l (Carpenter et al, 1981).

In 1980, the mean concentrations of bromoform in Arctic seawater were 9.8 ng/l in open surface water and 58 ng/l in surface water close to the Svalbard shore (Fogelqvist, 1985).

Water samples were collected from five outdoor pools, four indoor pools, and four spas (whirlpools or hot tubs) in Lubbock, TX, USA. The concentrations of bromoform in the outdoor pools, which used chlorine-based chemicals for chlorination, were < 0.1–1 µg/l. Two of the indoor pools in which only chlorination was used had levels of < 0.1–1 µg/l; one indoor pool in which only bromination (sodium hypobromite) was used had levels of 8–60 µg/l; and the fourth indoor pool, in which chlorination and bromination were alternated had levels of 11–49 µg/l. The spa in which only chlorination was used had levels of < 0.1–1 µg/l; the two spas in which only bromination was used had levels of 3–183 µg/l; and the spa in which the combination was used had levels of 50–89 µg/l. The average concentration of bromoform in Lubbock, TX, tap water was < 0.1 µg/l (Armstrong & Golden, 1986).

Bromination (3 mg bromine/1) of the water in a Swedish public swimming pool resulted in the formation of bromoform at 400 µg/l (Norin & Renberg, 1980).

Water samples were collected in 1978–79 from eight covered swimming pools in Bremen, Germany, to determine the concentration of bromoform. The source of fresh water was mixed river and groundwater for four pools and groundwater for four pools. The level of bromoform in the pools with mixed sources was 45 µg/l, and that for the pools with groundwater, not detectable (ND). The range of means of bromoform in the four pools with a mixed water source was 0.5–12 µg/l (total range, ND-88 µg/l); that in the four pools with a groundwater source was ND-0.1 µg/l (total range, ND-0.2 µg/l) (Lahl et al, 1981).

The concentrations of bromoform in three thermal spas in western Germany in which the initial bromide concentration was 0.5–0.7 mg/l were 2.3–9.6 µg/l (Weil et al, 1980).

Scotte (1984) studied the concentrations of organohalogen compounds in the water of 10 covered swimming pools in France. The mean concentrations of bromoform were 0.1 µg/l in the four pools treated with Surchlor GR 60 (anhydrous sodium dichloroisocyanurate), none in the two treated with gaseous chlorine, 1.0 µg/l in two treated with sodium hypochlorite and 481.2 µg/l in two treated with bromine.

Effluents from a wastewater treatment plant on Boston Harbor, MA, USA sampled in 1984 and 1985, contained a mean bromoform level of 165 µg/l (range, not detected to 6.9 µg/l and had an estimated mass input rate of 1.39 kg per day (Kossik et al.,1986)

Heating water to prepare food has been shown to eliminate a large part of trihalomethanes in the water, particularly as a function of temperature and heating time. Bromoform levels were reduced from 35.9 µg/l in tap water to 21.3 µg/l after heating at 80°C for 1 min, to 13.9 µg/l after heating to 100°C, to 13 5 µg/l after boiling for 1 min, and to 6.8 µg/l after boiling for 5 min (Lahl et al., 1982).

(d) Animals

Bioaccumulation of bromoform has been studied in five marine species The uptake and depuration is rapid (equilibrium is reached in 24–48 h) and the concentration factor are relatively low (<1–10 times the water concentration)(Gibson et al.,1980).

(e) Human tissues and secretions

Analysis of whole blood samples collected from a population of 250 patients with no known exposure to volatile organic compounds revealed a mean bromoform level of 0.6 ng/ml (range, ND-3.4 ng/ml); the number of individuals with detected levels of bromoform was not specified, but 11 had significantly elevated levels (greater than two standard deviations above the mean) (Antoine et al., 1986).

2.3. Analysis

Selected methods for the analysis of bromoform in air, water and other matrices are presented in Table 4. The US Environmental Protection Agency methods for analysing water (Methods 8010 and 8240) have also been used for liquid and solid wastes. Volatile components of solid waste samples are first extracted with methanol, prior to purge-and-trap concentration and analysis by gas chromatography-electrolytic conductivity detection (Method 8010) or gas chromatography-mass spectrometry (Method 8240). The detection limit for bromoform using Method 8010 is 0.20 µg/l, and the practical quantification limit using Method 8240 is 5 µg/l for groundwater and for soil/sediment samples (US Environmental Protection Agency, 1986a,b).

Table 4.

Methods for the analysis of bromoform.

US Environmental Protection Agency Method 624 has also been adapted to the analysis of bromoform in fish, with an estimated detection limit of 10 µg/kg (Easley et al., 1981).

Sorbent tube sampling is the approved method of the National Institute for Occupational Health/Occupational Safety and Health Administration (USA) for collecting the most hazardous gases and vapours from the air—in this case bromoform. A sample is collected by drawing air through a tube, where the airborne chemical is trapped in the sorbent. The trapped chemical is solvent-extracted from the tube and analysed using gas chromatography with a flame ionization detector to determine the amount of chemical present. A direct-reading system is available with colour detector tubes to monitor and detect bromoform in air (SKC Inc., 1990).

Bromoform can be determined in water by glass capillary column gas chromatography and electron capture detection, with a detection limit of 1 ng/l (Eklund et al., 1978b,c).

3. Biological Data Relevant to the Evaluation of Carcinogenic Risk to Humans

3.1. Carcinogenicity studies in animals (Table 5)

Table 5.

Summary of carcinogenicity studies of bromoform in experimental animals.

(a) Oral administration

Mouse: Groups of 50 male and 50 female B6C3F₁ mice, eight weeks old, were given bromoform (> 95% pure) in corn oil by gavage at 50 or 100 mg/kg bw (males) and 100 or 200 mg/kg bw (females) on five days per week for 103 weeks. Survival at 105 weeks was: males—vehicle control, 41/50; low-dose, 37/50; high-dose, 36/50; females—control, 25/50; low-dose, 13/50; high-dose, 20/50. Decreased survival in female mice was associated in part with utero-ovarian abscesses. No tumour occurred in a significantly larger proportion of treated than of control mice. The proportion of high-dose male mice with alveolar/bronchiolar neoplasms of the lung was significantly lower than that of controls (p < 0.015, incidental tumour test) (National Toxicology Program, 1989).

Rat: Groups of 50 male and 50 female Fischer 344 rats, seven to eight weeks old, were given bromoform (> 95% pure) in corn oil by gavage at 100 or 200 mg/kg bw on five days per week for 103 weeks. Survival at 105 weeks was: males—vehicle control, 34/50; low-dose, 30/50; high-dose, 11/50; females—control, 33/50; low-dose, 28/50; high-dose, 28/50. Adenomatous polyps of the large intestine occurred in 0/50 control, 0/50 low-dose and 2/50 high-dose male rats, and adenocarcinoma of the large intestine occurred in one additional high-dose male rat. Adenomatous polyps occurred in 0/50 control, 1/50 low-dose and 6/50 high-dose female rats, and adenocarcinomas occurred in two additional high-dose animals. The proportion of high-dose female rats with neoplasms of the large intestine was significantly larger than in controls (p = 0.004, pairwise comparison; p < 0.001, trend test, logistic regression). Neoplasms of the large intestine are uncommon in controls of this strain (males—study laboratory, 0/285; all National Toxicology Program laboratories, 3/1873 (0.2%); females—all National Toxicology Program laboratories, 0/1888). The incidence of preputial gland neoplasms was significantly decreased in high-dose male rats (control, 10/41; low-dose, 5/38; high-dose, 1/34; p = 0.014, pairwise comparison, logistic regression). In female rats, the incidences of stromal polyps of the uterus, fibroadenomas of the mammary gland and adenomas of the anterior pituitary gland were significantly decreased in the high-dose group (stromal polyps—vehicle control, 10/49; low-dose, 9/50; high-dose, 2/50; p = 0.019, logistic regression; fibroadenomas—vehicle control, 22/50; low-dose, 17/50; high-dose, 6/50; p < 0.001, logistic regression; pituitary adenomas—vehicle control, 29/48; low-dose, 12/46; high-dose, 16/48; p = 0.011, logistic regression) (National Toxicology Program, 1989).

(b) Intraperitoneal administration

Mouse: In a screening assay based on the enhanced induction of lung tumours, groups of 20 male strain A/St mice, six to eight weeks old, were injected intraperitoneally three times per week with bromoform (> 95% pure) in tricaprylin at 4, 48 or 100 mg/kg bw for a total of 18, 23 or 24 injections (total doses, 72, 1100 or 2400 mg/kg bw). Twenty males given tricaprylin only served as controls. All surviving mice were killed 24 weeks after the first injection, at which time survival was 15/20 of controls, 17/20 in the low-dose, 15/20 in the mid-dose and 15/20 in the high-dose group. The average numbers of lung tumours per mouse were 0.27 ± 0.15 (SE) in controls, 0.53 ± 0.21 at the low dose, 1.13 ± 0.36 at the mid-dose and 0.67 ± 0.21 at the high dose [proportion of mice with tumours not given]; the average number of lung tumours in the mid-dose group was significantly higher than that in controls (p < 0.05, Student’s t test). In a positive control group given a single intraperitoneal injection of urethane at 1000 mg/kg bw, the average number of lung tumours per mouse was 19.6 ± 2.4 (Theiss et al., 1977).

3.2. Other relevant data

(a) Experimental systems

(i) Absorption, distribution, excretion and metabolism

Bromoform at 0.008–0.04 mmol/kg bw (2–10 mg/kg bw) given by gavage as an aqueous solution to rats was rapidly absorbed and distributed to liver, brain, kidney, blood and fat; the highest concentrations were found in fat 30 min after administration (Parra et al., 1986). ¹⁴C-Bromoform at 0.39 mmol/kg bw (16 µCi/kg bw; 100 mg/kg bw) administered orally in corn oil to rats by gavage was absorbed and eliminated in the expired air as unchanged bromoform (67% of dose) or as 14C-carbon dioxide (4% of dose) in 8 h; radiolabel amounting to about 2% of the dose was eliminated in the urine, and about 2% of the dose was retained in body tissues. 14C-Bromoform administered similarly to mice (0.59 mmol/kg bw; 32 µCi/kg bw; 150 mg/kg bw) was absorbed and eliminated in the expired air as unchanged bromoform (6% of dose) or as ¹⁴C-carbon dioxide (40% of dose) in 8 h; about 5% of the administered radiolabel was eliminated in the urine, and 12% was retained in body tissues (Mink et al., 1986). Bromoform is metabolized to carbon monoxide in vivo (Anders et al, 1978; Stevens & Anders, 1981) and in vitro; the latter reaction requires NADPH and oxygen and is stimulated eight fold by glutathione (Ahmed et al., 1977). Bromoform was metabolized to dibromocarbonyl, the bromine analogue of phosgene, by rat hepatic microsomal fractions (Stevens & Anders, 1979; Pohl et al., 1980).

(ii) Toxic effects

The LD₅₀ of a single subcutaneous injection of bromoform in olive oil was estimated to be 7.2 mmol/kg (1.82 g/kg) bw in male Swiss mice (Kutob & Plaa, 1962); the single intraperitoneal 48-h LD₅₀ in corn oil was 414 µl/kg bw in male Sprague-Dawley rats (CR-1 strain; Agarwal & Mehendale, 1983). The single-dose oral LD₅₀s (Emulphor:ethanol:saline 1:1:8 administered by gavage) were 1400 mg/kg bw in male and 1500 mg/kg bw in female ICR Swiss mice (Bowman et al., 1978). Oral LD₅₀ values (in corn oil) were 1388 and 1147 mg/kg bw in male and female Sprague-Dawley rats (Chu et al., 1980,1982a) and 933 mg/kg bw in male and female Fischer 344/N rats (National Toxicology Program, 1989); the values for male and female B6C3F₁ mice were 707 and 1072 mg/kg bw bromoform, respectively. Signs of acute toxicity included sedation, prostration, lachrymation, lethargy, shallow breathing, reduction in peripheral lymphocyte count and liver damage (Agarwal & Mehendale, 1983; Bowman et al, 1978; Chu et al, 1982a; National Toxicology Program, 1989).

Daily oral treatment of male and female CD-I mice with 50–250 mg/kg bw bromoform (in 10% Emulphor in water) for 14 days resulted in decreased fibrinogen levels in blood, liver damage (increased ASAT), decreased serum glucose and blood urea nitrogen and decreased cellular and humoral immunity at 250 mg/kg bw (Munson et al., 1982). Similarly, administration of 145 and 289 mg/kg bw bromoform in corn oil per day for 14 days to male CD-I mice resulted in centrilobular pallor, focal inflammation and increased mitosis in the liver. Tubular hyperplasia and glomerular degeneration and reduced uptake of organic acids were observed in the kidney after administration of the high dose (Condie et al., 1983).

Daily oral administration of 600 and 800 mg/kg bw bromoform by gavage for 14 days induced lethargy, shallow breathing and ataxia and was lethal to all male and female Fischer 344/N rats. Body weight reduction was observed at 400 mg/kg bw; enlargement of the thyroid gland was observed at 400 and 800 mg/kg bw. B6C3F₁ mice receiving similar treatment were less sensitive. In a 13-week study, male and female Fischer 344/N rats were administered 12–200 mg/kg bw bromoform and male and female B6C3F₁ mice were administered 25–400 mg/kg bw bromoform by gavage on five days per week. Body weight reduction was observed in male mice treated with the high dose. Hepatocellular vacuolization was observed in male rats at all doses and in male mice at 200 and 400 mg/kg bw (National Toxicology Program, 1989).

Male and female Sprague-Dawley rats received 5–2500 mg/l bromoform in drinking-water for 90 days. The highest dose, which corresponded to an approximate daily intake of 29–55 mg/rat, resulted in liver lesions, reduced lymphocyte counts (after a 90-day recovery period) and a reduction in serum lactic dehydrogenase activity (Chu et al., 1982b).

Administration of bromoform for two years (see section 3.1) resulted in hepatic fatty changes, including vacuolization, in male and female rats and in female but not male mice in all treated groups (National Toxicology Program, 1989).

In a screening assay based on the production of γ-glutamyltranspeptidase-positive foci in the liver, nine male rats were given a single dose of bromoform at 1 mmol/kg (250 mg/kg) bw [route of administration unspecified] following a two-thirds hepatectomy. Bromoform did not have a significant effect (Herren-Freund & Pereira, 1986).

(iii) Effects on reproduction and prenatal toxicity

Swiss CD-I mice were given bromoform by gavage in corn oil at daily doses of 0, 50, 100 or 200 mg/kg bw in a reproductive study using a continuous breeding protocol. Treatment was continued for 18 weeks: one week prior to cohabitation, 14 weeks of cohabitation and three weeks thereafter. Toxicity was observed at the two higher levels, as decreased body weight and kidney weight and increased liver weight, but there was no adverse effect on fertility in either the parental or F₁ generation. A decrease in neonatal (F₁) survival was noted in the high-dose group. The body weights of treated F₁ males were significantly lower than the corresponding control values (Gulati et al., 1989).

Sprague-Dawley rats were administered bromoform in corn oil by gavage at daily doses of 0, 50, 100 or 200 mg/kg bw on gestation days 6–15. No maternal toxicity was observed, and bromoform did not alter the incidence of resorptions, litter size or fetal weight. There was a dose-related increase in the incidence of skeletal variations, primarily involving the sternum, the interparietal bones and ribs (Ruddick et al., 1983). [The Working Group noted that too few fetuses (12–16 per dose level) were examined for visceral malformations for a conclusion about lack of malformations in soft tissues to be drawn.]

(iv) Genetic and related effects (Table 6)

Table 6.

Genetic and related effects of bromoform.

Bromoform was mutagenic to Salmonella typhimurium occasionally, especially when tested in closed containers. In single studies, bromoform caused mitotic arrest (c-mitosis) in Allium cepa, mutation in Drosophila melanogaster and mouse lymphoma L5178Y cells, and sister chromatid exchange in human lymphocytes and (weakly) in Chinese hamster CHO cells. In two of three studies with cultured Chinese hamster cells, chromosomal aberrations were reported. Sister chromatid exchange was induced in mice in vivo in two reports, and induction of micronuclei was seen in one but not in a second study. In one study, chromosomal aberrations were not induced in bone-marrow cells of mice treated in vivo. No DNA binding was observed in livers of bromoform-treated rats.

(b) Humans

No data were available to the Working Group.

4. Summary of Data Reported and Evaluation

5. References

• Agarwal A.K., Mehendale H.M. Absence of potentiation of bromoform hepatotoxicity and lethality by chlordecone. Toxicol. Lett. 1983;15:251–257. [PubMed: 6187108]
• Ahmed A.E., Kubic V.L., Anders M.W. Metabolism of haloforms to carbon monoxide I. In vitro studies. Drug Metab. Disposition. 1977;5:198–204. [PubMed: 15814]
• Aldrich Chemical Co. (1990) 1990–1991 Aldrich Handbook of Fine Chemicals, Milwaukee, WI, p. 200.
• American Conference of Governmental Industrial Hygienists (1989) TLVs Threshold Limit Values and Biological Exposure Indices for 1989–1990, Cincinnati, OH, p. 14.
• American Tokyo Kasei (1988) TCI American Organic Chemicals 88/89 Catalog, Portland, OR, p. 187.
• Anders M.W., Stevens J.L., Sprague R.W., Shaath Z., Ahmed A.E. Metabolism of haloforms to carbon monoxide II. In vivo studies. Drug Metab. Disposition. 1978;6:556–560. [PubMed: 30605]
• Antoine S.R., DeLeon I.R., O'Dell-Smith R.M. Environmentally significant volatile organic pollutants in human blood. Bull. environ. Contam. Toxicol. 1986;36:364–371. [PubMed: 3955247]
• Armstrong D.W., Golden T. Determination of distribution and concentration of trihalomethanes in aquatic recreational and therapeutic facilities by electron-capture GC. LC-GC. 1986;4:652–655.
• Barkley J., Bunch J., Bursey J.T., Castillo N., Cooper S.D., Davis J.M., Erickson M.D., Harris B.S.H. III, Kirkpatrick M., Michael L.C., Parks S.P., Pellizzari E.D., Ray M., Smith D., Tomer K.B., Wagner R., Zweidinger R.A. Gas chromatography mass spectrometry computer analysis of volatile halogenated hydrocarbons in man and his environment—a multimedia environmental study. Biomed. Mass Spectrometry. 1980;7:139–147. [PubMed: 7448328]
• Bauer U. Human exposure to environmental chemicals—Investigations on volatile organic halogenated compounds in water, air, food, and human tissues III. Communication: results of investigations. Zentralbl. Bakteriol. Mikrobiol. Hyg. Abt. 1 Orig. B. 1981;174:200–237. [PubMed: 7331583]
• Bowman F.J., Borzelleca J.F., Munson A.E. The toxicity of some halomethanes in mice. Toxicol. appl. Pharmacol. 1978;44:213–215. [PubMed: 675691]
• Brass, A.J., Feige, M.A., Halloran, T., Mello, J.W., Munch, D. & Thomas, R.F. (1977) The National Organic Monitoring Survey: samplings and analyses for purgeable organic compounds. In: Pojasek, R.B., ed., Drinking Water Quality Enhancement Through Source Protection, Ann Arbor, MI, Ann Arbor Science, pp. 393–416.
• Brodzinsky, R. & Singh, H.B. (1983) Volatile Organic Chemicals in the Atmosphere: An Assessment of Available Data (EPA-600/3-83-027a; NTIS PB83-195503), Research Triangle Park, NC, US Environmental Protection Agency.
• Budavari, S., ed. (1989) The Merck Index, 11th ed., Rahway, NJ, Merck & Co., p. 215.
• Bunn W.W., Haas B.B., Deane E.R., Kleopfer R.D. Formation of trihalomethanes by chlorination of surface water. Environ. Lett. 1975;10:205–213. [PubMed: 1213009]
• Carpenter, J.H., Smith, C.A. & Zika, R.G. (1981) Reaction Products from the Chlorination of Seawater (EPA-600/4-81-010; NTIS PB81-172280), Gulf Breeze, FL, US Environmental Protection Agency.
• Cech I., Smith V., Henry J. Spatial and seasonal variations in concentration of trihalomethanes in drinking water. Pergamon Ser. environ. Sci. 1982;7:19–38.
• Chang N.-W., Singer P.C. Formation and fate of bromoform during desalination. J environ. Eng. 1984;110:1189–1193.
• Chu I., Secours V., Marino I., Villeneuve D.C. The acute toxicity of four trihalomethanes in male and female rats. Toxicol. appl. Pharmacol. 1980;52:351–353. [PubMed: 7361328]
• Chu I., Villeneuve D.C., Secours V.E., Becking G.C. Toxicity of trihalomethanes: I The acute and subacute toxicity of chloroform, bromodichloromethane, chlorodibromomethane and bromoform in rats. J. environ. Sci. Health. 1982a;B17:205–224. [PubMed: 7096898]
• Chu I., Villeneuve D.C., Secours VE., Becking G.C. Trihalomethanes: II Reversibility of toxicological changes produced by chloroform, bromodichloromethane, chlorodibromomethane and bromoform in rats. J. environ. Sci. Health. 1982b;B17:225–240. [PubMed: 7096899]
• Cicerone R.J., Heidt L.E., Pollock W.H. Measurements of atmospheric methyl bromide and bromoform. J. geophys. Res. 1988;93:3745–3749.
• Class T., Kohnle R., Ballschmiter K. Chemistry of organic traces in air VII: Bromo- and bromochloroethanes in air over the Atlantic. Ocean. Chemosphere. 1986;15:429–436.
• Cole R.H., Frederick R.E., Healy R.P., Rolan R.G. Preliminary findings of the Priority Pollutant Monitoring Project of the Nationwide Urban Runoff Program. J. Water Pollut. Control Fed. 1984;56:898–908.
• Coleman W.E., Munch J.W., Kaylor W.H., Streicher R.P., Ringhand H.P., Meier J.R. Gas chromatography/mass spectroscopy analysis of mutagenic extracts of aqueous chlorinated humic acid A comparison of the byproducts to drinking water contaminants. Environ. Sci. Technol. 1984;18:674–681.
• Comba M.E., Kaiser K.L.E. Determination of volatile contaminants at the ng/l level in water by capillary gas chromatography with electron capture detection. Int. J. environ, anal. Chem. 1983;16:17–31.
• Condie L.W., Smallwood C.L., Laurie R.D. Comparative renal and hepatotoxicity of halomethanes: bromodichloromethane, bromoform, chloroform, dibromochloro-methane and methylene chloride. Drug chem. Toxicol. 1983;6:563–578. [PubMed: 6653442]
• Cook, W.A. (1987) Occupational Exposure Limits—Worldwide, Cincinnati, OH, American Industrial Hygiene Association, pp. 85, 130, 166.
• Easley D.M., Kleopfer R.D., Carasea AM. Gas chromatographic-mass spectrometric determination of volatile organic compounds in fish. J. Assoc. off. anal. Chem. 1981;64:653–656. [PubMed: 7240070]
• Eklund G., Josefsson B., Roos C. Trace analysis of volatile organic substances in Goeteborg municipal drinking water. Vatten. 1978a;3:195–206.
• Eklund G., Josefsson B., Roos C. Determination of volatile halogenated hydrocarbons in environmental water by glass capillary column gas chromatography and electron capture detection. Chromatogr. Newsl. 1978b;6:39–41.
• Eklund G., Josefsson B., Roos C. Determination of volatile halogenated hydrocarbons in tap water, seawater and industrial effluents by glass capillary gas chromatography and electron capture detection. J. high Resolut. Chromatogr. Chromatogr. Commun. 1978c;1:34–40.
• Eller, P.M. (1987) NIOSH Manual of Analytical Methods, 3rd ed., Vol. 2, rev. 1 (DHHS (NIOSH) Publ. No. 84–100), Washington DC, US Government Printing Office, pp. 1003-1-1003-6.
• de Fernicola N.A.G.G., de Azevedo F.A. Water levels of trihalomethanes (THM) in four different supply systems from Sao Paulo State, (Brazil). J. environ. Health. 1984;46:187–188.
• Fogelqvist E. Carbon tetrachloride, tetrachloroethylene, 1,1,1-trichloroethane and bromoform in Arctic seawater. J. geophys. Res. 1985;90:9181–9193.
• Furlong E.A.-N., D'Itri EM. Trihalomethane levels in chlorinated Michigan drinking water. Ecol. Modelling. 1986;32:215–225.
• Gabel B., Lahl U., Baetjer K., Cetinkaya M., von Dueszeln J., Kozicki R., Podbielski A., Stachel B., Thiemann W. Volatile halogenated compounds (VOHal) in drinking waters of the FRG. Sci. total Environ. 1981;18:363–366. [PubMed: 7233175]
• Gibson, C.L, Tone, F.C, Schirmer, R.E. & Blaylock, J.W. (1980) Bioaccumulation and depuration of bromoform in five marine species. In: Jolley, R.L., Brungs, W.A., Cumming, R.B. & Jacobs, V.A., eds, Water Chlorination: Environmental Impact and Health Effects, Vol. 3, Ann Arbor, MI, Ann Arbor Science, pp. 517–533.
• Glaze W.H., Rawley R. A preliminary survey of trihalomethane levels in selected East Texas water supplies. J. Am. Water Works Assoc. 1979;71:509–515.
• Gschwend P.M., MacFarlane J.K., Newman K.A. Volatile halogenated organic compounds released to seawater from temperate marine macroalgae. Science. 1985;227:1033–1035. [PubMed: 17794227]
• Gulati, D.K., Hope, E., Barnes, L.H., Russell, S. & Poonacha, K.B. (1989) Bromoform: Reproductive and Fertility Assessment in Swiss CD-1 Mice When Administered by Gavage (NTP-86-FACB-053), Research Triangle Park, NC, National Institute for Environmental Health Sciences.
• Hagenmaier H., Werner G., Jäger W. Quantitative determination of volatile halogenated hydrocarbons in water samples by capillary gas chromatography and electron capture detection. Z. Wasser Abwasser Forsch. 1982;15:195–198.
• Harlow, I.F. & Ross, O.C. (1932) Preparation of Brominated Hydrocarbons (US Patent 1,891,415 to Dow Chemical Co)
• Hartwig, E.O. & Valentine, R. (1983) Bromoform production in tropical open-ocean waters: ocean thermal energy conversion chlorination. In: Jolley, R.L., Brungs, W.A., Cotruvo, J.A., Cumming, R.B., Mattice, J.S. & Jacobs, V.A., eds, Water Chlorination: Environmental Impact and Health Effects, Vol. 4, Book 1, Chemistry and Water Treatment, Ann Arbor, MI, Ann Arbor Science, pp. 311–330.
• Haworth S., Lawlor T., Mortelmans K., Speck W., Zeiger E. Salmonella mutagenicity test results for 250 chemicals. Environ. Mutagenesis, Suppl. 1983;1:3–142. [PubMed: 6365529]
• Hayashi M., Kishi M., Sofuni T., Ishidate M. Jr. Micronucleus tests in mice on 39 food additives and eight miscellaneous chemicals. Food chem. Toxicol. 1988;26:487–500. [PubMed: 3169648]
• Health and Welfare Canada (1977) National Survey for Halomethanes in Drinking Water (Report 77-EHD-9), Ottawa, Environmental Health Directorate, Health Protection Branch.
• Henderson, J.E., Peyton, G.R. & Glaze, W.H. (1976) A convenient liquid-liquid extraction method for the determination of halomethanes in water at the parts-per-billion level. In: Keith, L.H., ed., Identification and Analysis of Organic Pollutants in Water, Ann Arbor, MI, Ann Arbor Science, pp. 105–111.
• Herren-Freund S.L., Pereira M. A. Carcinogenicity of by-products of disinfection in mouse and rat liver. Environ. Health Perspect. 1986;69:59–65. [PMC free article: PMC1474319] [PubMed: 2880712]
• Hoyt S.D., Rasmussen R.A. Determining trace gases in air and seawater. Adv. chem. Ser. Mapping Strategies chem. Oceanogr. 1985;209:31–56.
• IARC (1987) IARC Monographs on the Evaluation of Carcinogenic Risks to Humans, Suppl. 7, Overall Evaluations of Carcinogenicity: An Updating of IARC Monographs Volumes 1 to 42, Lyon, pp. 152–154. [PubMed: 3482203]
• Isacson, P., Bean, J.A. & Lynch, C. (1983) Relationship of cancer incidence rates in Iowa municipalities to chlorination status of drinking water. In: Jolley, R.L., Brungs, W.A., Cotruvo, J.A., Cumming, R.B., Mattice, J.S. & Jacobs, V.A., eds, Water Chlorination: Environmental Impact and Health Effects, Vol. 4, Book 2, Environment, Health, and Risk, Ann Arbor, MI, Ann Arbor Science, pp. 1353–1364.
• Ishidate, M., Jr (1987) Data Book of Chromosomal Aberration Test in vitro rev. ed., Tokyo, Life-Science Information Center, pp. 421–422.
• Kaczmar S.W., D'Itri F.M., Zabik M.J. Volatilization rates of selected haloforms from aqueous environments. Environ. Toxicol. Chem. 1984;3:31–35.
• Kaiser K.L.E., Comba M.E. Volatile contaminants in the Welland River watershed. J. Great Lakes Res. 1983;9:274–280.
• Kaiser K.L.E., Comba M.E., Huneault H. Volatile halocarbon contaminants in the Niagara River and in Lake Ontario. J. Great Lakes Res. 1983;9:212–223.
• Kossik, R.E, Gschwend, P.S. & Adams, E.E. (1986) Tracing and Modeling Pollutant Transport in Boston Harbor (Report No. MITSG-86/16; NTIS PB87-136891), Rockville, MD, National Oceanic and Atmospheric Administration.
• Krasner, S.W., McGuire, M.J., Jacangelo, J.G., Patania, N.L., Reagan, K.M. & Aieta, E.M. (1989) The occurrence of disinfection by-products in drinking water in a nationwide study. In: Annual Conference of the American Water Works Association, Los Angeles, CA, Denver, CO, American Water Works Association.
• Kutob S.D., Plaa G.L. A procedure for estimating the hepatotoxic potential of certain industrial solvents. Toxicol. appl. Pharmacol. 1962;4:354–361. [PubMed: 14460943]
• Lahl U., Bätjer K., von Düszeln J., Gabel B., Stachel B., Thiemann W. Distribution and balance of volatile halogenated hydrocarbons in the water and air of covered swimming pools using chlorine for water disinfection. Water Res. 1981;15:803–814.
• Lahl U., Cetinkaya M., von Düszeln J., Gabel B., Stachel B., Thiemann W. Health risks for infants caused by trihalomethane generation during chemical disinfection of feeding utensils. Ecol. Food Nutr. 1982;12:7–17.
• Loy, E.W, Jr, Brown, D.W., Stephenson, J.H.M. & Little, J.A. (1976) Uses of wastewater discharge compliance monitoring data. In: Keith, L.H., ed., Identification and Analysis of Organic Pollutants in Water, Ann Arbor, MI, Ann Arbor Science, pp. 499–516.
• Mabey, W.R., Smith, J.H., Podoll, R.T., Johnson, H.L., Mill, T., Chou, T.W., Gates, J., Waight Partridge, I. & Vandenberg, D. (1982) Aquatic Fate Process Data for Organic Priority Pollutants (EPA-440/4-81-014; NTIS PB87-169090), Washington DC, Office of Water Regulations and Standards, US Environmental Protection Agency, pp. 183–184.
• McConnell G. Haloorganics in water supplies. J. Inst. Water Eng. Sci. 1976;30:431–445.
• Mersch-Sunderman V. Examination of the mutagenicity of organic micro-contaminations inn the environment II. The mutagenicity of halogenated aliphatic hydrocarbons with the Salmonella-microsome test (Ames test) in relation to contamination of ground- and drinking-water (Ger.). Zbl. Bakt. Hyg B. 1989;187:230–243.
• Minear, R.A. & Morrow, CM. (1983) Raw Water Bromide: Levels and Relationship to Distribution of Trihalomethanes in Finished Drinking Water (OWRT-A-063-TENN; NTIS PB83-256735), Washington DC, US Environmental Protection Agency.
• Mink F.L., Brown TJ., Rickabaugh J. Absorption, distribution, and excretion of ¹⁴C-trihalomethanes in mice and rats. Bull. environ. Contam. Toxicol. 1986;37:752–758. [PubMed: 3779162]
• Morimoto K., Koizumi A. Trihalomethanes induce sister chromatid exchanges in human lymphocytes in vitro and mouse bone marrow cells in vivo. Environ. Res. 1983;32:72–79. [PubMed: 6617620]
• Munson A.E., Sain L.E., Sanders V.M., Kauffmann B.M., White K.L. Jr, Page D.G., Barnes D.W., Borzelleca J.F. Toxicology of organic drinking water contaminants: trichloromethane, bromodichloromethane, dibromochloromethane and tribromomethane. Environ. Health Perspect. 1982;46:117–126. [PMC free article: PMC1569032] [PubMed: 7151752]
• National Toxicology Program (1989) Toxicology and Carcinogenesis Studies of Tribromomethane (Bromoform) (CAS No. 75-25-2) in F344/N Rats B6C3F₁ Mice (Gavage Studies) (NTP Technical Report No. 350), Research Triangle Park, NC. [PubMed: 12704434]
• Norin H., Renberg L. Determination of trihalomethanes (THM) in water using high efficiency solvent extraction. Water Res. 1980;14:1397–1402.
• Norin H., Renberg L., Hjort J., Lundblad P.O. Factors influencing formation of trihalomethanes in drinking water with special reference to Swedish conditions. Chemosphere. 1981;10:1265–1273.
• Östergren C. Colchicine mitosis chromosome contraction, narcosis and protein chain folding. Hereditas. 1944;30:429–467.
• Otson R. Purgeable organics in Great Lakes raw and treated water. Int. J. environ. anal. Chem. 1987;31:41–53.
• Otson R., Williams D.T., Bothwell P.D. Volatile organic compounds in water at thirty Canadian potable water treatment facilities. J. Assoc. off. anal. Chem. 1982;65:1370–1374.
• Page G.W. Comparison of groundwater and surface water for patterns and levels of contamination by toxic substances. Environ. Sci. Technol. 1981;15:1475–1481.
• Parra P., Martinez E., Suñol C., Artigas E., Tusell J.M., Gelpi E., Albaigés J. Analysis, accumulation and central effects of trihalomethanes I. Bromoform. Toxicol. environ. Chem. 1986;24:79–91.
• Peoples A.J., Pfaffenberger CD., Shafik T.M., Enos H.F. Determination of volatile purgeable halogenated hydrocarbons in human adipose tissue and blood serum. Bull. environ. Contam. Toxicol. 1979;23:244–249. [PubMed: 497433]
• Pereira M.A., Lin L.-H.C., Lippitt J.M., Herren S.L. Trihalomethanes as initiators and promoters of carcinogenesis. Environ. Health Perspect. 1982;46:151–156. [PMC free article: PMC1569022] [PubMed: 7151756]
• Perwak, J., Goyer, M., Harris, J., Schimke, G., Scow, K., Wallace, D. & Slimak, M. (1980) An Exposure and Risk Assessment for Trihalomethanes: Chloroform, Bromoform, Bromodichloromethane, Dibromochloromethane (EPA-440/4-81-018; NTIS PB85-211977), Washington DC, Office of Water Regulations and Standards, US Environmental Protection Agency.
• Pohl, L.R., Martin, J.L., Taburet, A.M. & George, J.W. (1980) Oxidative bioactivation of haloforms into hepatotoxins. In: Coon, M.J., Conney, A.H., Estabrook, R.W, Gelboin, H.V., Gillette, J.R. & O'Brien, P.J., eds, Microsomes, Drug Oxidations, and Chemical Carcinogenesis, Vol. II, New York, Academic Press, pp. 881–884.
• Pouchert, C.J., ed. (1974) The Aldrich Library of NMR Spectra, Vol. 1, Milwaukee, WI, Aldrich Chemical Co., p. 64B.
• Pouchert, C.J., ed. (1981) The Aldrich Library of Infrared Spectra, 3rd ed., Milwaukee, WI, Aldrich Chemical Co., p. 51H.
• Pouchert, C.J., ed. (1985) The Aldrich Library of FT-IR Spectra, Vol. 3, Milwaukee, WI, Aldrich Chemical Co., p. 117B.
• Quaghebeur D., De Wulf E. Volatile halogenated hydrocarbons in Belgian drinking waters. Sci. total Environ. 1980;14:43–52.
• Rapson W.H., Nazar M.A., Butsky VV. Mutagenicity produced by aqueous chlorination of organic compounds. Bull. environ. Contam. Toxicol. 1980;24:590–596. [PubMed: 6991030]
• Reding, R., Fair, P.S., Shipp, C J. & Brass, H.J. (1989) Measurement of dihaloacetonitriles and chloropicrin in US drinking waters. In: Disinfection By-products: Current Perspectives, Denver, CO, American Waterworks Association, pp. 11–22.
• Riedel-de Haën (1986) Laboratory Chemicals 1986, Seelze 1/Hannover, pp. 161–162.
• Rodriguez-Flores, M. (1983) Characterization of Organic Contaminants in Selected Potable Water Supplies in Puerto Rico (OWRT-A-057-PR; NTIS PB83-178038), Washington DC, US Environmental Protection Agency.
• Rook J.J. Formation of haloforms during chlorination of natural waters. Water Treat. Exam. 1974;23:234–243.
• Ruddick J.A., Villeneuve D.C., Chu I. A teratological assessment of four trihalomethanes in the rat. J. environ. Sci. Health. 1983;B18:333–349. [PubMed: 6875216]
• Sadtler Research Laboratories (1980) The Sadtler Standard Spectra, 1980 Cumulative Index, Philadelphia, PA.
• Sax, N.I. & Lewis, R.J., Sr (1987) Hawley’s Condensed Chemical Dictionary, 11th ed., New York, Van Nostrand Reinhold, p. 172.
• Scotte P. Study of halogenated organic compounds in covered swimming pools (Fr.). Eau. Ind. Nuisances. 1984;86:37–41.
• Sherman, P.D., Jr & Kavasmaneck, PR. (1980) Ethanol. In: Mark, H.F., Othmer, D.F., Overberger, C.G., Seaborg, G.T. & Grayson, M., eds, Kirk-Othmer Encyclopedia of Chemical Technology, 3rd ed., Vol. 9, New York, John Wiley & Sons, pp. 341–342.
• Simmon, VE, Kauhanen, K. & Tardiff, R.G. (1977) Mutagenic activity of chemicals identified in drinking water. In: Scott, D., Bridges, B.A. & Sobeis, F.H., eds, Progressin Genetic Toxicology, Amsterdam, Elsevier/North-Holland Biomedical Press, pp. 249–258.
• Singer, PC. (1982) Formation and Removal of Bromoform During Desalination (OWRT-C-90013-S(9507); NTIS PB87-197646), Washington DC, US Environmental Protection Agency.
• Sittig, M. (1985) Handbook of Toxic and Hazardous Chemicals and Carcinogens, 2nd ed., Park Ridge, NJ, Noyes Publications, pp. 149–150.
• SKC Inc. (1990) Comprehensive Catalog and Guide. Mr Sampling Products for Worker Monitoring, Chemical Hazard Detection and Industrial Hygiene, Eighty Four, PA.
• Soroos H., Hinkamp J.B. The redistribution reaction XI. Application to the preparation of carbon tetraiodide and related halides. J. Am. chem. Soc. 1945;67:1642–1643.
• Stevens, A.A., Moore, L.A., Slocum, C.J., Smith, B.L., Seeger, D.R. & Ireland, J.C. (1989) By-products of chlorination at ten operating utilities. In: Disinfection By-Products: Current Perspectives, Denver, CO, American Water Works Association, pp. 23–61.
• Stevens J.L., Anders M.W. Metabolism of haloforms to carbon monoxide III. Studies on the mechanism of the reaction. Biochem. Pharmacol. 1979;28:3189–3194. [PubMed: 526325]
• Stevens J.L., Anders M.W. Metabolism of haloforms to carbon monoxide IV. Studies on the reaction mechanism in vivo. Chem.-biol. Interact. 1981;37:365–374. [PubMed: 7296701]
• Symons J.M., Bellar T.A., Carswell J.K., DeMarco J., Kropp K.L., Robeck G.G., Seeger D.R., Slocum CJ., Smith B.L., Stevens A.A. 1975National Organics Reconnaissance Survey for halogenated organics J. Am. Water Works Assoc. 67634.–647.
• Theiss J.C., Stoner G.D., Shimkin M.B., Weisburger E.K. Test for carcinogenicity of organic contaminants of United States drinking waters by pulmonary tumor response in strain A mice. Cancer Res. 1977;37:2717–2720. [PubMed: 872098]
• Trussell, A.R., Cromer, J.L., Umphres, M.D., Kelley, P.E. & Moncur, J.G. (1980) Monitoring of volatile halogenated organics: a survey of twelve drinking waters from various parts of the world. In: Jolley, R.L., Brungs, W.A., Cumming, R.B. & Jacobs, V.A., eds, Water Chlorination: Environmental Impact and Health Effects, Vol. 3, Ann Arbor, MI, Ann Arbor Science, pp. 39–53.
• Ullrich D. 7 Organohalogenated compounds in the air of some public swimming pools of Berlin (Ger.). WaBoLu-Ber. 1982;1:50–52.
• US Environmental Protection Agency (1986a) Method 8010. Halogenated volatile organics. In: Test Methods for Evaluating Solid Waste—Physical/Chemical Methods, 3rd ed. (EPA No. SW-846), Washington DC, Office of Solid Waste and Emergency Response.
• US Environmental Protection Agency (1986b) Method 8240. Gas chromatography/mass spectrometry for volatile organics. In: Test Methods for Evaluating Solid Waste—Physical/Chemical Methods, 3rd ed. (EPA No. SW-846), Washington DC, Office of Solid Waste and Emergency Response.
• US Environmental Protection Agency (1988a) Method TO-1. Method for the determination of volatile organic compounds in ambient air using Tenax(R) absorption and gas chromatography/mass spectrometry (GC/MS). In: Compendium of Methods for the Determination of Toxic Organic Compounds in Ambient Air (EPA-600/4-89-017; NTIS PB90-116989), Research Triangle Park, NC, Atmospheric Research and Exposure Laboratory, Office of Research and Development.
• US Environmental Protection Agency (1988b) Methods for organic chemical analysis of municipal and industrial wastewater. Method 601. Purgeable halocarbons. US Code fed. Regul., Title 40, Part 136, Appendix A, pp. 267–281.
• US Environmental Protection Agency (1988c) Methods for organic chemical analysis of municipal and industrial wastewater. Method 624. Purgeables. US Code fed. Regul., Title 40, Part 136, Appendix A, pp. 432–446.
• US Environmental Protection Agency (1988d) Method 502.2. Volatile organic compounds in water by purge and trap capillary column gas chromatography with photoionization and electrolytic conductivity detectors in series. Revision 2.0. In: Methods for the Determination of Organic Compounds in Drinking Water (EPA-600/4-88-039; PB89-220461), Cincinnati, OH, Environmental Monitoring Systems Laboratory, pp. 31–62.
• US Environmental Protection Agency (1988e) Method 524.2. Measurement of purgeable organic compounds in water by capillary column gas chromatography/mass spectrometry. Revision 3.0. In: Methods for the Determination of Organic Compounds in Drinking Water (EPA-600/4-88-039; PB98-220461), Cincinnati, OH, Environmental Monitoring Systems Laboratory, pp. 285–323.
• US Environmental Protection Agency (1988f) Methods for organic chemical analysis of municipal and industrial wastewater. Method 1624 Revision B. Volatile organic compounds by isotope dilution GC/MS. US Code fed. Regid., Title 40, Part 136, Appendix A, pp. 475–488.
• US Environmental Protection Agency (1988g) Analysis of trihalomethanes. Part II—Analysis of trihalomethanes in drinking water by liquid/liquid extraction. US Code fed. Regul., Title 40, Part 141, Appendix C, pp. 563–571.
• US Occupational Safety and Health Administration (1989) Air contaminants—permissible exposure limits (Report No. OSHA3112). US Code fed. Regul., Title 29, Part 1910.1000.
• Varma M.M., Ampy F.R., Verma K., Talbot W.W. In vitro mutagenicity of water contaminants in complex mixtures. J. appl. Toxicol. 1988;8:243–248. [PubMed: 3183290]
• Verschueren, K. (1983) Handbook of Environmental Data on Organic Chemicals, 2nd ed., New York, Van Nostrand Reinhold, pp. 291–292.
• Weast, R.C., ed. (1989) CRC Handbook of Chemistry and Physics, 70th ed., Boca Raton, FL, CRC Press, pp. C-350, D-198.
• Weil L., Jandik J., Eichelsdoefer D. Organic halogenated compounds in swimming pool water I. Determination of volatile halogenated hydrocarbons (Ger.). Z. Wasser Abwasser Forsch. 1980;13:141–145.
• Westrick J.J., Mello J.W., Thomas R.F. The groundwater supply survey. J. Am. Water Works Assoc. 1984;76:52–59.
• Williams, D.T. (1985) Formation of trihalomethanes in drinking water. In: Fishbein, L. & O'Neill, I.K., eds, Environmental Carcinogens. Selected Methods of Analysis, Vol. 7, Some Volatile Halogenated Hydrocarbons (IARC Scientific Publications No. 68), Lyon, IARC, pp. 69–88.
• Woodruff R.C., Mason J.M., Valencia R., Zimmering S. Chemical mutagenesis testing in Drosophila. V Results of 53 coded compounds tested for the National Toxicology Program. Environ. Mutagenesis. 1985;7:677–702. [PubMed: 3930237]

Footnotes

1

In square brackets, spectrum number in compilation

2

Calculated from: mg/m³ = (molecular weight/24.45) × ppm, assuming standard temperature (25 °C) and pressure (760 mm Hg)

1

For definition of the italicized terms, see Preamble, pp. 30–33.