Poisoning of wild birds following ingestion of lead from ammunition has long been recognised and considerable recent research has focused on terrestrial birds, including raptors and scavengers. This paper builds upon previous reviews and finds that both the number of taxa affected and geographical spread of cases has increased. Some lead may also be absorbed from embedded ammunition fragments in injured birds which risk sub-lethal and welfare effects. Some papers suggest inter-specific differences in sensitivity to lead, although it is difficult to disentangle these from other factors that influence effect severity. Sub-lethal effects have been found at lower blood lead concentrations than previously reported, suggesting that previous effect-level ‘thresholds’ should be abandoned or revised. Lead poisoning is estimated to kill a million wildfowl a year in Europe and cause sub-lethal poisoning in another ≥ 3 million. Modelling and correlative studies have supported the potential for population-level effects of lead poisoning in wildfowl, terrestrial birds, raptors and scavengers.

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Lead poisoning in birds was described in Europe at the end of the 19 th century, but the first epidemiological studies were not done until the second half of the 20 th century. So far, most work has focused on waterfowl and birds of prey, with very few reports evaluating the impact on upland game birds.

BackgroundLead is highly toxic to animals. Humans eating game killed using lead ammunition generally avoid swallowing shot or bullets and dietary lead exposure from this source has been considered low. Recent evidence illustrates that lead bullets fragment on impact, leaving small lead particles widely distributed in game tissues. Our paper asks whether lead gunshot pellets also fragment upon impact, and whether lead derived from spent gunshot and bullets in the tissues of game animals could pose a threat to human health.Methodology/Principal FindingsWild-shot gamebirds (6 species) obtained in the UK were X-rayed to determine the number of shot and shot fragments present, and cooked using typical methods. Shot were then removed to simulate realistic practice before consumption, and lead concentrations determined. Data from the Veterinary Medicines Directorate Statutory Surveillance Programme documenting lead levels in raw tissues of wild gamebirds and deer, without shot being removed, are also presented. Gamebirds containing ≥5 shot had high tissue lead concentrations, but some with fewer or no shot also had high lead concentrations, confirming X-ray results indicating that small lead fragments remain in the flesh of birds even when the shot exits the body. A high proportion of samples from both surveys had lead concentrations exceeding the European Union Maximum Level of 100 ppb w.w. (0.1 mg kg−1 w.w.) for meat from bovine animals, sheep, pigs and poultry (no level is set for game meat), some by several orders of magnitude. High, but feasible, levels of consumption of some species could result in the current FAO/WHO Provisional Weekly Tolerable Intake of lead being exceeded.Conclusions/SignificanceThe potential health hazard from lead ingested in the meat of game animals may be larger than previous risk assessments indicated, especially for vulnerable groups, such as children, and those consuming large amounts of game.

The oxidation handicap hypothesis proposes that testosterone mediates the trade‐off between the expression of secondary sexual traits and the fight against free radicals. Coloured traits controlled by testosterone can be produced by carotenoid pigments (yellow–orange–red traits), but carotenoids also help to quench free radicals. Recently, it has been shown that testosterone increases the amount of circulating carotenoids in birds. Here, a testosterone‐mediated trade‐off in the carotenoid allocation between colour expression and the fight against oxidative stress is proposed. Male red‐legged partridges were treated with testosterone, anti‐androgens or manipulated as controls. Testosterone‐treated males maintained the highest circulating carotenoid levels, but showed the palest red traits and no evidence of oxidative damage. Increased levels of a key intracellular antioxidant (i.e. glutathione) indicated that an oxidative challenge was in fact induced but controlled. The trade‐off was apparently solved by reducing redness, allowing increased carotenoid availability, which could have contributed to buffer oxidative stress.