Environmental Engineering Reference
In-Depth Information
2.7 Chemical and biochemical diagnosis of a carbofuran kill
Diagnostic confi rmation of a carbofuran kill tends to be achieved via the analysis of brain AChE,
and using chemical residue analysis. Grue and colleagues (1991) reviewed in detail the extent of
cholinesterase inhibition that is associated with acute poisoning for all cholinesterase-inhibiting pes-
ticides. Their conclusions were similar to those presented previously on the subject (e.g., by Hill and
Fleming 1982), i.e., that mortality is likely when brain depression levels of 50% or more occur. Since
diagnostic centres often deal with severely autolysed (decayed/degraded) samples, some adopt a
more stringent rule for diagnosing fatal intoxication. For instance, pathologists at the USGS National
Wildlife Health Centre use a 75% inhibition cut-off as an indication of poisoning if upper gastroin-
testinal tract contents are not available for analysis. They will attempt to have samples analysed
chemically if brain activity levels are down by two standard deviations or more from the normal
mean activity level (corresponding to approximately 20% inhibition) or when case history suggests
that it is warranted. It should be noted that, the higher the diagnostic criterion of inhibition, the more
likely bias will be introduced, namely the likelihood that cases of abuse (where concentrated bait
was involved) will be diagnosed, but not incidental intoxication from normal product use. Inhibition
of > 75%, with recovery on overnight incubation, triggers a diagnosis of 'likely carbamate intoxica-
tion', even when there is no residue analysis undertaken.
The potential for rapid, spontaneous recovery of cholinesterase activity following carbamate
intoxication means that it can be particularly diffi cult to use cholinesterase depression as a diagnos-
tic tool (in the case of carbofuran poisoning; Hill 1989). Reduced cholinesterase activity (especially
if the sample spontaneously reactivates in the laboratory) is diagnostic. However, the absence of
inhibition does not necessarily mean that there was no intoxication. For this reason, a review of all
raptor carbofuran intoxications noted between 1985 and 1995 for Canada, the US and Great Britain
(as tabulated in Mineau, Fletcher, Glazer et al. 1999), failed to show a clear/consistent relationship
between brain cholinesterase depression and carbofuran residue concentration in the gastrointestinal
tract. This could also refl ect a poor relationship between typical gastrointestinal tract residue analysis
and the amount of toxicant actually absorbed into the blood stream. There are many reasons why
reported levels in the gastrointestinal tract may not refl ect the toxicological response, not least, the
quality/representativeness of the sample analysed and the quality of the residue analysis itself, to
name but two.
In certain cases, the suitability of both the cholinesterase measurements and the residue determi-
nations can be compared. Hill and Fleming (1982) describe how 4/5 wigeons (
Anas americana
) were
picked up around 1.5 days after dying from carbofuran intoxication. In this case, their brain AChE
values had returned to normal even though carbofuran residues were still detectable in the gastro-
intestinal tract (the residue levels were not given). Wigeon picked up the day before, in a moribund
condition, exhibited brain AChE inhibition ranging from 54 to 77%.
Flickinger, Mitchell, White et al. (1986) analysed 16 carcasses of dickcissels (
Spiza Americana
)
and savannah sparrows (
Passerculus sandwichensis
). These had died when ingesting seed rice
illegally treated with carbofuran, and 12/16 carcasses analysed had > 20% brain AChE inhibition.
Residue levels in the gastrointestinal tracts of the same birds ranged from not detected (ND) to
10 ppm carbofuran.
Flickinger, King, Stout et al. (1980) diagnosed carbofuran poisoning in four shorebirds after
recording the presence of granules in their stomachs. Balcomb et al. (1983 and 1984b) used residues
in liver and the digestive tract combined to diagnose carbofuran poisoning in songbirds collected
from corn fi elds where granules had been used. The carcasses were said to be 'fresh' when collected.
Five of six carcasses collected in one of the study years were positive for carbofuran, with levels
between 1.6 and 17 ppm. Based on granule weight data (Hill and Camardese 1984), the carbofuran
extracted from each bird was between 0.2 and 1 granule (equivalent). In another year, 'selected birds'
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