75
present during the shooting season because good estimates of
theimmaturepopulationwerenotreadilyavailable.Ourestimate
of numbers of terrestrial gamebirds birds that may potentially
ingest gunshot is therefore an underestimate. We also omitted
other potentially susceptible game species. We assumed that
hunter-shot grey and red-legged partridges would have similar
levels of gunshot ingestion (1.4%) because grey partridges
found dead would be expected to have higher levels of gunshot
ingestion if some had died of lead poisoning, and we assumed
a low 1% level of gunshot ingestion in red grouse and used
the 3% reported for pheasant. We then assumed that shooters
are twice as likely to kill birds that have ingested lead gunshot
(due to their weakened state) than to kill birds that had not
ingested gunshot, and corrected for this (this is the correction
factor for mallards that have ingested 3 shot - see Table 5 and
Bellrose 1959). We then calculated the number of birds in the
population likely to have ingested gunshot at any one time (c.
615,000). Given that we only have estimates for the proportion
of gamebirds with ingested gunshot at the time they were killed,
and gunshot has a residence time in the alimentary tract that
rarely exceeds 30 days (on average about 20 inwildfowl (Bellrose
1959)), the number of birds likely to ingest gunshot at some time
during the winter shooting season will be several times higher
than this. All birds that ingest lead gunshot may suffer some
welfare effect, and a proportion of them, perhaps of the order
of hundreds of thousands, are likely to die from lead poisoning.
We do not think that it is valid to give more precise estimates
for terrestrial birds as studies of hunting bias and shot residence
times in the intestine have not been conducted, and fewer
studies are available on levels of shot ingestion.
EFFECTS ON PREDATORY AND SCAVENGING BIRDS
AND OTHER WILDLIFE FOLLOWING INGESTION OF
AMMUNITION-DERIVED LEAD IN THE TISSUES OF
DEAD OR LIVE GAME SPECIES (EXPOSURE ROUTE 2)
Measurements of lead concentrations in tissue samples from
carcasses of dead predatory and scavenging birds have been
used, together with post mortem examinations, to assign
the cause of death to lead poisoning and other causes. Such
studies in the USA, Canada and Europe reported proportions of
deaths caused by lead in species likely to be at risk of ingesting
2 Earlier data for red-legged partridges (1933-1992) were excluded as Butler (2005) considered it possible that cases of lead ingestion were missed by the pathologists
and considered it unlikely that a detailed search was part of all post mortem examinations, particularly when no clinical signs of lead poisoning were evident.
ammunition-derived lead ranging from 3% of deaths to 35% of
deaths (Elliott et al. 1992, Wayland and Bollinger 1999, Wayland
et al. 1999, Clark and Scheuhammer 2003, Finkelstein et al.
2012, Rideout et al. 2012). In Europe the bird species with the
most consistently high proportions of deaths attributed to
lead poisoning is the white-tailed eagle (14 – 28% of deaths
attributed to effects of lead) (Elliott et al. 1992, Kenntner et al.
2001, Krone et al. 2006, Helander et al. 2009).
In the UK, Pain et al. (2007) reported lead concentrations from
tissue samples from carcasses of 44 red kites found dead or that
were captured sick and died subsequently in England between
1995 and 2003. Elevated liver lead concentrations (>15 mg/
kg dw in these birds)3 and post mortem examination analyses
indicated that four (9%) of the birds had probably died from
lead poisoning; several others had elevated liver lead but were
diagnosed as dying of other causes. Walker et al. (2012, 2013)
reported liver lead concentrations for another sample of 38
carcasses of red kites collected in England in 2010 and 2011 and
found no cases with elevated liver lead concentrations.
Pain et al. (1995) reported lead concentrations from the livers of
424 individuals of 16 raptor species found dead in Britain and
sent for analysis to the Institute of Terrestrial Ecology, Monks
Wood, from the early 1980s to the early 1990s. There were
eight species for which ten or more carcasses were analysed:
short-eared owl Asio flammeus, buzzard, little owl Athene
noctua, kestrel Falco tinnunculus, sparrowhawk, peregrine
falcon, merlin Falco columbarius and long-eared owl Asio
otus. The other eight species with fewer than ten carcasses
included three of the species most likely on the grounds of
diet to consume carrion contaminated with ammunition-
derived lead (red kite (6 carcasses), golden eagle (5), white-
tailed eagle (1)), and one species especially likely to prey upon
waterfowl with shot-in or ingested shotgun pellet-derived
lead in their tissues (western marsh harrier (1)). Of the species
with 10 or more carcasses, feeding ecology would suggest that
peregrine falcon and buzzard would be susceptible to preying
upon or scavenging (in the case of buzzards) game species.
Elevated lead concentrations in liver (>20 mg/kg dw)3, within
the range associated with lead poisoning mortality in raptors,
were recorded in one peregrine falcon (4% of species sample)
3 A review by Franson and Pain (2011) suggested that birds with no history of lead poisoning usually have liver lead concentrations of <2 mg/kg wet weight (c.
6.3ppm dry weight) and frequently of <1 mg/kg ww (c. 3.1 ppm dw). In falconiformes, these authors suggested a liver lead range for sub-clinical poisoning of 2<6
ppm ww [6.3-18.6 ppm dw] with clinical poisoning associated with liver lead concentrations exceeding >6ppm ww. ‘Elevated’ liver lead could be considered as above
background, i.e. 6.3 ppm dw with clinical poisoning occurring at levels above approximately 18.6 ppm dw. These figures can vary somewhat as there is no absolute wet
weight to dry weight conversion factor for bird livers (1ppm ww was converted to 3.1 ppm dw by Franson and Pain (2011)).
Lead poisoning of wildlife in the UK