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Current legislative controls and monitoring of industrial,
municipal and agricultural lead emissions in the UK are such
that cases of clinical lead poisoning from these sources in
wildlife are likely to be rare. High concentrations of lead derived
from sources other than ammunition and fishing weights exist
in some soils in urban areas and near centres of current and
historical industrial activity, especially mining and smelting.
Some lead derived from anglers’ lead weights used before
restrictions on their sale and use were introduced in 1987 is
present in some wetlands and rivers, but additional lead from
this source has probably been added at a low rate since then
through a small amount of permitted use, and any illegal use
that may have occurred. The mute swan Cygnus olor is the
species reported to have been significantly affected by the
ingestion of anglers’ lead weights in the UK (Birkhead 1982,
Birkhead and Perrins 1986) probably because of their habit of
frequenting urban rivers and lakes where fishing activity is high.
The recorded decrease in the incidence of lead poisoning in
mute swans (Sears and Hunt 1990) and corresponding increase
in their populations following the 1987 restrictions (Kirby et al.
1994) suggests that restrictions were largely successful. Newth
et al. (2012) similarly found that the proportion of deaths
attributable to lead poisoning in a sample of mute swans
decreased significantly over time after restrictions, i.e. from 25%
between 1971 and 1987 (pre-restrictions) to 4.6%between 1988
and 1999 and 2% between 2000 and 2010.
Beyond these sources, lead derived from ammunition now
appears to be the only significant, geographically widespread
and common source of unregulated environmental lead
contamination to which wildlife is exposed.
This paper aims to bring together a broad range of evidence
to illustrate the pathways by which wildlife is exposed to
ammunition-derived lead and review the extent and impact of
the problem in the UK.
PHYSIOLOGICAL EFFECTS OF LEAD
Lead is a non-essential metal that has no biological benefit to
living organisms and is toxic to all vertebrates. Lead is also toxic
to invertebrates but sensitivities appear to vary considerably
(Eisler 1988). It is an accumulative metabolic poison that is non-
specific, affecting a wide range of physiological and biochemical
systems. These include the haematopoietic, vascular, nervous,
renal and reproductive systems (Eisler 1988, USATSDR 2007,
EFSA 2010, Franson and Pain 2011). Lead occurs primarily in
inorganic form in the environment and lead in ammunition is in
its elemental metallic form. In this paper, the term“lead”refers to
inorganic lead. Following absorption, the effects of lead upon an
animal’s body systems are independent of source.
The toxic effects of lead are broadly similar in all vertebrates.
In wild animals these effects are well known from numerous
experimental and field studies. These have been reviewed many
times (e.g. Eisler 1988, Pattee and Pain 2003, Franson and Pain
2011, Ma 2011). Although the present paper deals withwildlife in
general, we have focussed upon birds because they are by far the
most significantly studied taxon and are significantly affected.
Clinical signs of poisoning are often associated with chronic
exposure to lead in birds. Chronic exposure is extended exposure
at a level that is not necessarily likely to cause immediate failure of
biological functioning or death, although death may eventually
result. Signs include anaemia, lethargy, muscle wasting and loss
of fat reserves, green diarrhoea staining the vent, wing droop,
lack of balance and coordination and other neurological signs
such as leg paralysis or convulsions (e.g. Locke and Thomas 1996,
Wobeser 1997, Friend and Franson 1999, Eisler 2000, Pattee
and Pain 2003). In cases where birds die rapidly following acute
exposure to high levels of lead, many of these signs may be
absent.
Numerous experiments have been conducted where captive
birds frommany taxa, including wildfowl and raptors, have been
dosed with lead gunshot and blood lead concentrations and
physiological responses reported relative to controls (e.g. Pattee
et al. 2006, Hoffman et al. 1981, 1985, reviews in Eisler 1988,
see also Pattee and Pain 2003, and Franson and Pain 2011). In
some instances, lead ammunition or ammunition fragments are
eliminated rapidly from a bird’s alimentary canal with little lead
absorption, but they are also often retained until completely
eroded,withtheleadbecomingsolublesaltsandmuchofitbeing
absorbed by the bird. The acidic conditions in birds’ stomachs
and the strong mechanically grinding action in the gizzards of
certain bird species facilitate erosion and solubilisation of lead
ammunition, and blood lead concentrations can rapidly become
elevated after ingestion of gunshot (e.g. see Hoffman et al. 1981,
1985, Pain and Rattner 1988, Pattee et al. 2006). Absorbed lead is
transported in the bloodstream and deposited rapidly into soft
tissues, primarily the liver and kidney, intobone, and thegrowing
feathers of birds. Lead in bone is retained for long periods and
bone lead concentrations increase over an animal’s lifetime,
whereas lead in soft tissues has a much shorter half-life (often
Lead poisoning of wildlife in the UK