**Haloaldehydes**

**JA Cotruvo, RJ Bull, J Crook, M Whittaker**

**WateReuse Foundation 06-004**

**Background**

Over the years a series of halogenated aldehydes have been identified as
chlorination by-products. These potential toxicological effects of these
compounds have attracted little attention.

**Occurrence**

Dichloroacetaldehyde and bromochloroacetaldehyde have been found in
chlorinated drinking water at concentrations as high as 11 and 1.3 µg/L,
respectively (see DBP-1). However, these DBPs are not measured in
routine monitoring of DBPs. As a consequence, we were unable to locate
data to their concentrations that might be expected in the product
waters of potable reuse projects. Nevertheless, it is highly probable
that they would occur. The molecular weight of dichloroacetaldehyde
suggests that it would be likely to penetrate reverse osmosis membranes
used in many potable reuse projects. The stability of this compound to
biological degradation in the environment does not appear to have been
studied.

Trihaloacetaldehydes are also known to be chlorination by-products.
However, chloral hydrate has been extensively studied, is a very weak
carcinogen only in mice. IRIS reviews of chloral hydrate indicate an RfD
much higher than the concentrations that is seen to occur.

Other aldehydes, such as 2-chloropropenal, are known to be formed in the
chlorination of drinking water (Meier, 1988). 2-chloropropenal is highly
mutagenic, but there has been no systematic survey of the concentrations
that occur in chlorinated drinking waters.

**TTC analysis**

Dichloroacetaldyde is mutagenic in the Salmonella/microsome assay and
occurs at concentrations above 0.75 µg/L. No tests of
bromochloroacetaldehyde appear to have been performed, but it is
probable that it is also mutagenic. Therefore, assessment of the risks
for these compounds requires chemical-specific evaluation of data.

Dichloroacetaldehyde is an established metabolite of vinylidene choride
(Liebler et al., 1985; Dowsley et al., 1995), but its role in the
carcinogenic effects of this chemical are overshadowed by the apparent
reactivity of other metabolites.

We were unable to identify data that would establish whether the
dihaloacetaldehydes are carcinogenic or not. No entry has been made in
the Carcinogenic Potency Database, consistent with our inability to
locate appropriate data.

There appear to be no conventional toxicology studies of the
dihaloacetaldehydes.

Bull et al. (2006) subjected a number of DBPs to QSAR study as
carcinogens and/or developmental toxicants. Dichloroacetaldehyde met the
criteria as a probable carcinogen. A chronic LOAEL of 5.8 mg/kg was also
predicted. This LOAEL is approximately 1/10 that observed with commonly
regulated haloacetic acid and THM DBPs. The QSAR program did not
identify dichloroacetaldehyde as a probable developmental toxicant.

**Research Recommendation**

The occurrence of dihaloacetaldehydes has not been surveyed in potable
reuse projects. As a consequence, it is not known whether these DBPs are
produced in greater or lesser amounts than in drinking water systems
drawing their water from surface sources. Given the concentrations that
are found in the more conventionally derived drinking waters and the
mutagenic activity of the compound, we must identify it as a DBP
deserving some research. It will be difficult to make a case for this
compound without a more extensive database on its occurrence in potable
reuse projects.

Based upon its relationship with several other known carcinogenic
compounds, either as a metabolite or as a product (dichloroacetaldehyde
should be easily oxidized to dichloroacetic acid), the only nomination
that makes sense at this time would be a lifetime bioassay of its
carcinogenic properties in rodents by the National Toxicology Program.

**References**

Bull, R.J., Reckhow, D.A., Rotello, V., Bull, O.M., and Kim, J. (2006).
Use of Toxicological and Chemical Models to Prioritize DBP Research.
Report for AWWA Research Foundation Project 2867. Awwa Research
Foundation, Denver CO

Dowsley, T.F., Forkert, P.G., Benesch, L.A., and J.L. Bolton. 1995.
Reaction of glutathione with the electrophilic metabolites of
1,1-dichloroethylene. Chem. Biol. Interact.95(3):227-244.

Liebler, D.C, M.J. Meredith, and F.P. Guengerich. 1985. Formation of
glutathione conjugates by reactive metabolites of vinylidene chloride in
microsomes and isolated hepatocytes. Cancer Res. 45(1)186-193.

Löforth, G. 1978. The mutagenicity of dichloroacetaldehyde. Z.
Naturforsch. (C) 33:(9-10):783-785.

Meier, J.R. 1988. Genotoxic activity of organic chemicals in drinking
water. Mutat. Res. 196:211-245.