Guidelines for Canadian Drinking Water Quality: Guideline Technical Document - Haloacetic Acids

9.0 Health effects in humans

A limited population-based case-control study conducted in Nova Scotia and eastern Ontario did not find an association between HAA exposures and stillbirth risk when controlling for total THM exposures (King et al., 2005). The analysis included 112 stillbirth cases and 398 live birth controls that occurred between 1999 and 2001. No other specific information was available on the teratogenic, reproductive or embryotoxic effects of chlorinated HAAs in humans (CHEMINFO, 2003a, b, c, d, e). Epidemiological studies have been conducted with CDBPs to determine if exposure contributes to reproductive and developmental effects in humans (Bove et al., 1995; Mills et al., 1998). No other information was available to assess the effects of individual HAAs, nor have HAAs been satisfactorily dissociated from the many other by-products (hundreds, if not thousands) that are produced by chlorination. Therefore, it is difficult to infer causality between specific HAAs and adverse reproductive and developmental health outcomes in humans based on one limited study.

Epidemiological studies on the incidence of cancer have been conducted with CDBPs, but not specifically with chlorinated HAAs. Cohort and descriptive studies have also been conducted with TCE and PCE. Biological monitoring of exposure to both these compounds was done by measuring the urinary levels of DCA or TCA, which have been identified as metabolites of these two compounds (TCE and PCE) in humans (IARC, 1995). TCA has also been identified as a metabolite of other chlorine-containing ethanes and ethylenes (ACGIH, 2001).

Most chlorinated HAAs are found in drinking water (where the pH range of 6-9 is close to neutral) almost exclusively in the ionized form (anion) due to their very low pK_a values (IPCS, 2000). HAAs are found in drinking water at very low concentrations, which means that the dilution of HAAs in drinking water and the buffer capacity of drinking water would mostly counter the irritative properties described below for concentrated acid solutions of HAAs.

9.1 Monochloroacetic acid

The probable lethal oral dose for MCA (acid) in humans is in the range of 50-500 mg/kg bw (Gosselin et al., 1984). In one fatal case, a 5-year-old girl ingested a teaspoon (5-6 mL) of a wart remover composed of 80% MCA (acid); she began vomiting, collapsed and died 8 hours later. The cause of her death was attributed to metabolic acidosis and cardiac arrhythmia. The autopsy revealed that the liver was damaged, and the stomach had signs of marked irritation (Feldhaus et al., 1993; Rogers, 1995).

The sodium salt of MCA is not corrosive to the skin and has limited skin absorption (ECETOC, 2001). MCA does not easily form a vapour (CHEMINFO, 2003 a, b). No cases of acute intoxication from MCA (sodium salt) have been located in the literature (ECETOC, 2001).

Three adult volunteers who drank 300 mL of a 0.05% aqueous solution of MCA (acid) daily for a period of 60 days (corresponding to 2 mg/kg bw per day) experienced no adverse health effects (Morrison and Leake, 1941; NTP, 1992). Dilute solutions of MCA (acid) (i.e., up to 1% aqueous) failed to produce irritation of human skin (Morrison and Leake, 1941).

9.2 Dichloroacetic acid

Patients diagnosed with genetic disorders, such as familial hypercholesterolaemia (a common disorder of lipid metabolism associated with a high risk of early mortality from coronary artery disease) or various mitochondrial disorders and, as a result, treated daily with DCA (sodium salt) for periods longer than 4 months were found to develop peripheral neuropathy (loss of reflexes and muscle weakness) and in one case hepatomegaly (enlarged liver) (Moore et al., 1979; Spruijt et al., 2001; Izumi et al., 2003).

Humans exposed in an occupational setting to concentrated DCA mist or vapour may develop pulmonary oedema several hours after exposure (CHEMINFO, 2003c).

9.3 Trichloroacetic acid

In an occupational setting, concentrated solutions and/or mists of TCA (acid) have caused skin effects (redness, swelling, pain and possibly burns), eye effects (severe irritation or corrosive injury) or damage to the gastrointestinal tract due to accidental ingestion (CHEMINFO, 2003d, e). According to CHEMINFO (2003d, e), the severity of the injury (dermal, oral, ocular) increases with the concentration of the acid and the duration of exposure.

TCA did not induce chromosomal aberrations in human lymphocytes (IARC, 1995). No reports were available on in vivo mutagenicity studies in humans (CHEMINFO, 2003d, e).

No long-term studies on humans exposed to TCA were located in the literature (IARC, 1995; OEHHA, 1999).

9.4 Monobromoacetic acid

No studies reporting human health effects from exposure to MBA were reported.

9.5 Dibromoacetic acid

No studies were located in the literature on the health effects of DBA in humans (IPCS, 2000).