We found strong support for the two hypotheses we posited with respect to plastic ingestion based on our necropsy data. First, animals that had plastic ingestion listed as the cause of death had higher concentrations of plastic debris in their gastro-intestinal tract than animals that died of known non-plastic ingestion related causes. We found that the causes of death are segregated in terms of plastic concentration (Fig. 1). Second, when we regressed the probability of death due to plastic on the concentration of plastic in the gastro-intestinal tract, we found strong support for a positive relationship, suggesting that higher concentrations of plastic items in the gastro-intestinal tract lead to a higher probability of mortality. Analysis of the government strandings database (Strandnet) generally supported the results from our necropsy data. The proportion of animals with plastics in their gut increased as we hypothesized, with unknown and known not due to plastics < indeterminate < known due to plastics.

Our results can be used to predict the mortality probability for any turtle, given a CCL, age class and load of plastic items in the gastro-intestinal tract (see SI). For instance, for a juvenile animal with a CCL of 43.5 cm (the median size in our dataset), the probability of mortality rises to 0.5 (i.e. 50% of animals would be expected to die) with a load of 17 items. This increases to a probability of 1.0 (i.e. certain death) at 226 items. Our results also indicate that animals can die due to the effects of plastic ingestion, even when they have ingested a single item. For example, two animals had ingested only one plastic item, yet this item had caused the animal’s death. In one case this was due to a gut perforation, and in the other it was due to gut impaction. Our analysis suggests that at this lower end, there is a 22% chance of dying due to ingesting a single debris item.

The structure of the sea turtle gastro-intestinal tract and the mixture of anthropogenic debris items they ingest both play a role in the relationship between plastic ingestion and the chance of mortality. The alimentary canal in sea turtles is particularly prone to plication and accumulation of debris items due to the inability of turtles to regurgitate items and their convoluted gastrointestinal tracts. The nature and type of debris can have compounding effects in the accumulation of debris. For example, normal gut passage time for sub adult and juvenile loggerhead turtles is estimated to be between approximately five and 23 days15,17. However, transit time for items through the GIT is strongly influenced by the individual characteristics of the item ingested (e.g. density, size, shape)17. One feeding experiment found that, rather than passing through the GIT individually, pieces of soft plastic could compound together and pass as a single compacted item, despite being ingested at separate intervals15. Their capacity to form an obstruction is also fuelled by the extended time until elimination, noted to be up to four months for small pieces of soft latex15 and even up to six months for 10 × 10 cm plastic sheets18.

In addition to the interaction between plastic type and gut passage time, plastics themselves differ widely in their likelihood of causing perforation or impaction. For instance, a single piece of monofilament fishing line or a metal hook can cause plication as it passes through the gut19. In contrast, small hard plastic fragments may pass quickly through the gut with little incident. Furthermore, turtles likely differ in their exposure to amounts and types of plastic, based on their feeding location in the water column and with respect to the coastal zone. Plastic fragments on the water surface have been found to be larger near coastal zones and in the gyres, presumably due to their proximity to coastal sources or collection points in the gyres1,20. As such, one would expect turtles feeding in surface waters near coastal margins to be more likely to ingest larger fragments that would be more likely to cause mortality.

This interaction between feeding location, plastic characteristics, and life history stage is reflected in our data. Twenty-three percent of the juveniles and fifty-four percent of post-hatchling stage turtles in our necropsies ingested plastic, in comparison with fifteen percent of the sub-adults and sixteen percent of adults. The younger animals are feeding in the water column nearer the surface, and in some cases in coastal environments where debris is potentially bigger or in convergence zones where plastics accumulate. Thus, in using our results to translate rates of plastic ingestion into probability of mortality, it is important to consider both the life history stage of the animal and the location where it is feeding.

There have been discussions on sea turtles and debris selectivity. A study on the visual similarities between their natural prey items and the plastic debris ingested suggests sea turtles will actively seek out plastic debris that appear similar to their food sources, particularly flexible film-like items13. However, this does not preclude instances where ingestion occurs incidentally. Regardless, post hatchlings and juveniles are shown to have higher incident rates of ingestion9. These turtles occupy pelagic environments and are more likely to feed in areas where debris accumulates (surface waters and convergence zones)9.

Pelagic juveniles caught in longline fisheries operating in convergence zones in many parts of the world show relatively high rates of plastic ingestion10,21 suggesting that high volumes of debris in seemingly healthy juveniles is a widespread phenomenon. All four pelagic juvenile turtles that drowned on longlines included in our data are consistent with these findings, showing relatively high levels of debris ingestion (between 24 and 39 pieces, Table 2). Our model would suggest these animals have relatively high mortality probabilities from plastic ingestion, between 0.69 and 0.90 (Fig. 4), yet plastic ingestion was not fatal for these turtles, as the animals died from drowning.

This apparent contradiction may point to one bias in our data and analysis. Most of the animals we necropsied, and those included in StrandNet, were sourced from coastal areas where they have washed up either incapacitated or dead. These coastal animals have died from a mixture of causes, with the cause of death not strongly related to the likelihood of sampling the animal. The pelagic juveniles differ, as the cause of death is directly related to the chance of sampling an animal. Only animals caught in pelagic longlines were recovered and necropsied. This implies we have no samples of animals that have died due to plastic ingestion which would correspond to the longline caught animals. If plastic debris in offshore regions is smaller and more compactly shaped, it might be that there is a significant difference (reduction) in the likelihood of mortality due to ingestion of plastic debris in these regions. This again suggests that our model should be used primarily in coastal regions, and if applied offshore should be considered an upper bound on the probability of mortality.

Nearly 700 species are now known to interact with anthropogenic debris22 and as more species are investigated, the number continues to rise. As global plastic production increases, so too does our understanding of the ubiquity and impacts of anthropogenic debris on marine fauna such as seabirds2,23, fish24,25, marine mammals2,26, and a range of invertebrates27,28 including corals29. This work provides a critical next step in quantifying the risk plastic pollution poses to the world’s declining sea turtle populations, by linking plastic debris loads and the likelihood of mortality. The model has broad applicability and can be adapted for other taxa to understand dose responses to plastic ingestion for other marine taxa of interest.