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PERSPECTIVES ON ANIMAL BIOSCIENCES (Open Access)

The sources and impact of microplastic intake on livestock and poultry performance and meat products: a review

Luisa Olmo https://orcid.org/0000-0001-8175-8216 A B * and Benjamin W. B. Holman https://orcid.org/0000-0002-8458-4511 C D
+ Author Affiliations
- Author Affiliations

A Elizabeth Macarthur Agricultural Institute, NSW Department of Primary Industries and Regional Development, Menangle, NSW 2568, Australia.

B School of Environmental and Rural Science, The University of New England, Armidale, NSW 2351, Australia.

C Wagga Wagga Agricultural Institute, NSW Department of Primary Industries and Regional Development, Wagga Wagga, NSW 2650, Australia.

D Gulbali Institute, Charles Sturt University, Wagga Wagga, NSW 2678, Australia.

* Correspondence to: luisa.olmo@dpird.nsw.gov.au

Handling Editor: Wayne Bryden

Animal Production Science 65, AN25022 https://doi.org/10.1071/AN25022
Submitted: 17 January 2025  Accepted: 17 August 2025  Published: 11 September 2025

© 2025 The Author(s) (or their employer(s)). Published by CSIRO Publishing. This is an open access article distributed under the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License (CC BY-NC-ND)

Abstract

Due to the large and growing quantity of microplastics being generated, their ubiquity in agricultural landscapes, their likelihood of being ingested by livestock and poultry, and their potential impacts on performance and meat products, microplastics are a potential risk to livestock and poultry production. Here, we reviewed the literature for microplastic effects on ruminant, pig and poultry health, productivity, and meat products. It was observed that controlled experimental studies show that microplastics have localised effects on livestock and poultry health, as indicated by oxidative stress, inflammation and apoptosis, following short-term exposure to concentrations higher than is environmentally typical. However, it is unclear if microplastics have gross effects on disease, productivity and welfare at natural exposure levels. Microplastics are present in livestock and poultry tissues at levels that make it a potential consumer safety issue (0–7700 mg per kg or 100–180,000 particles per kg). However, the detection methods used are prone to contamination, meaning that true concentrations remain unknown, as does the source of microplastics in terms of whether they originate from production or meat processing and packaging. Microplastics have been detected in the livestock and poultry environment, with 36–300 particles detected per kg livestock feed and 0.34–7900 particles detected per kg soil. Livestock ingest microplastics from their environments, as evidenced by microplastics being detected in chicken excreta at 667–129,800 particles per kg, in ruminant faeces at 74–50,583 particles per kg, and in pig faeces at 0–112,000 particles per kg. However, preliminary data have neither examined correlations to animal productivity, nor have they estimated the total amount and type of microplastics to which livestock and poultry are exposed. This information is needed to inform the doses used in controlled experiments aiming to understand the effect of natural exposure levels on health, productivity and meat quality. To accurately estimate microplastics in livestock supply chains, there is a need to optimise and standardise microplastic detection methods by including procedural blanks, and calculating limits of detection, recovery rate of sample digestion, sample size calculations, and reports of microplastic size, density, weight and number of particles detected. No study has investigated the sources of microplastics and effective mitigation measures in livestock supply chains. Preliminary data also show that microplastics are vectors for heavy metals, antibiotics, antibiotic resistance genes and microbes. Further research is strongly warranted to quantify the effects of microplastics as vectors. In conclusion, microplastics are present in livestock and poultry production systems, and this poses a threat to animal welfare, productivity and consumer perceptions of meat. This review has highlighted paucities in current knowledge that must be addressed to understand the scope of microplastic effects on the livestock and poultry industries, as well as the opportunities for risk mitigation.

Keywords: bioaccumulation, chickens, contamination, environment, food safety, health, pigs, plastic, red meat, routes of exposure.

Introduction

Microplastics are a real and significant threat to livestock and poultry production. This is because of their persistence within an environment, their impact on animal health and productivity, and their potential to be accumulated within meat products. Microplastics are accumulating in aquatic and terrestrial environments – these are defined as plastic particles ranging in size from 0.1 μm to 5 mm. In agricultural environments, common sources of these microplastic particles are plastic film used for greenhouses, silage and plastic mulch, biowaste for fertilisers such as sewage sludge, wastewater for irrigation, plastic pipes and faucets, general plastic equipment, and contaminated commercial feed (Rodríguez-Seijo and Pereira 2019; Beriot et al. 2021; Wu et al. 2021; Ziajahromi et al. 2024). As time passes, plastic can degrade as a result of UV radiation, natural weathering and other environmental effects to result in microplastic particle generation and distribution (Siddiqui et al. 2023). This is important, as livestock and poultry could ingest and/or absorb these environmental microplastic particles.

The European Food Safety Authority (2016) suggested that plastic particles >150 μm (0.15 mm) are excreted in faeces, whereas smaller plastic particles can penetrate the gastrointestinal barrier, and deposit in the organs and tissue of livestock. Through natural exposure, Wu et al. (2021) identified 74 microplastic particles per kg of cattle faeces, 667 microplastic particles per kg of chicken excreta and 900 microplastic particles per kg of pig faeces. Lwanga et al. (2017) identified an average of 129,800 microplastic particles per kg of chicken excreta and 31.8 microplastic particles per gizzard – based on data collected from five chickens. Beriot et al. (2021) identified 997 microplastic particles per kg of sheep faeces. Furthermore, there is evidence that ingested microplastic particles translocate from the gut; with Chen et al. (2023) reporting there to be 2.2–1751.4 mg of microplastics per kg of the jejunum, liver, leg muscle and breast muscle tissues, collected from three broilers. van der Veen et al. (2022) similarly detected microplastics at a concentration of 0.07–33.00 mg per kg in each of the 24 cattle and pig blood samples collected, and at concentrations of 53–7700 mg per kg beef and pork purchased from retail outlets (12/16 retail outlets sold meat containing microplastic particles). This is problematic, because microplastics can lead to inflammation, oxidative stress and the apoptosis of animal cells (Blackburn and Green 2022) – thereby compromising animal health and productivity. Microplastics in meat products is problematic because of the potential health risks to humans who ingest microplastics, which may result in reproductive and developmental toxicity (Blackburn and Green 2022).

It has been estimated that adult humans, in the USA, will consume 46,000–52,000 microplastic particles per year from foods that contribute 15% to their average caloric intake (Cox et al. 2019). This estimation is not exclusive to meat products, with the contribution of microplastics from livestock and poultry meat products currently unknown. One of the disincentives to addressing this paucity of information is the current lack of regulatory limits on the amount of microplastics allowable within human food. However, the regulatory landscape is evolving. For example, the European Union legislated that plastic packaging cannot release >60 mg/kg of plastic material into food they are in contact with (The European Commission 2011). The UK stipulates a maximum limit of 0.15% plastic food-grade packaging material (by weight) in human food waste used for animal feed (Parfitt et al. 2016). The Food Safety Authority of the Netherlands requires farmers to remove all plastic packaging from livestock feed prior to its provision to animals as a strategy to reduce plastic ingestion by livestock (van der Veen et al. 2022). Because microplastics in meat have the potential to impact consumer food safety, and future market access and compliance, in addition to livestock productivity, regulation affecting livestock producers must be carefully informed by robust scientific evidence.

This paper aimed to provide a comprehensive and critical review of microplastic effects on livestock and poultry. This is necessary to understand the genuine risk posed by microplastics to livestock performance and meat integrity, the key sources of microplastics and the realistic amount of microplastics that livestock are exposed to, and paucities in literature that necessitate further research to support a sustainable and robust livestock sector. For the purpose of this review, livestock refers to cattle, sheep, goats and pigs, whereas poultry refers to chickens and ducks – aquatic species; rodents or non-meat livestock products (milk, eggs and fibre) were therefore excluded. This review also only included investigations of microplastics, and excluded those studying macroplastics (plastic particles >5 mm) or nanoplastics (plastic particles <1 μm).

Microplastic effects on livestock and poultry health, productivity, and meat products

There is a general expectation that animal welfare is equal to productivity when considering the sustainability of livestock and poultry production systems. These are both a function of animal diet, namely, the combined physiochemical effects from the nutritional and non-nutritional compounds ingested by an animal – microplastics are characterised into the latter group. Few studies have investigated the effect of microplastic ingestion on livestock and poultry health, productivity, and meat products. The available studies do, however, require some examination.

Ruminants

The effect of microplastics on ruminant health and performance has been the topic of only recent investigation (Table 1). Tassone et al. (2024) performed in vitro ruminal, gastric and intestinal digestion with the Ankom DaisyII incubator to investigate the effect of three different concentrations of polyethylene terephthalate (PET) in the ruminal liquor on the digestibility of mixed hay. A chemical proximate specific response was reported as PET reduced the digestibility of crude protein and neutral detergent fibre, but had no effect on dry matter digestibility (Tassone et al. 2024). With a single digestion jar used per PET concentration, there was no true replication, and each filter bag acted as a pseudo-replicate. Also using the Ankom DaisyII incubator, L. Olmo (pers. comm.) reported no effect of four different concentrations (0.5, 1.0, 3.0 and 5.0 g/L) and two different sizes of polystyrene (PS) particles (5 and 15 μm) in the ruminal liquor on dry matter digestibility of four silage types following in vitro rumen digestion. Each treatment was replicated twice, except for the 5-g/L concentration, which was replicated once (L. Olmo, pers. comm.). This finding was consistent with additional research of the same concentrations and microplastic particle sizes that used the Tilley and Terry in vitro digestion method (L. Olmo, pers. comm.). There are limitations to the transference of in vitro findings that include a failure to take into account the absorption of nutrients by the host and effects of epithelial host–microorganism interactions on feed digestibility (Na and Guan 2022). Consequently, it is common for in vitro digestibility findings to be repeated in vivo, but then to a lesser magnitude than the former method would have indicated (Vinyard and Faciola 2022). There is a need to, therefore, confirm these in vitro research findings using a ruminant model species.

Table 1.Summary of experimental exposure studies assessing the effect of microplastics on ruminant health and productivity.

SpeciesPlastic typeSize (μm)ConcentrationDurationOrgan examinedEffectsRefs
CattlePETMean 522X−: 0 g PET/L ruminal liquor (n = 1)48, 49, 73 hIn vitro ruminal, gastric and intestinal digestion (Ankom DaisyII)
  • No effect on ruminal DM or acid detergent fibre degradability

  • Sig. ↓ CP and NDF ruminal degradability in X+1, X+2, X+3

  • No effect on gastric DM or CP digestibility

  • No effect on intestinal DM degradability and digestibility

  • Sig. ↓ intestinal CP degradability and digestibility

Tassone et al. (2024)
X+1: 5 g PET/L ruminal liquor (n = 1)
X+2: 10 g PET/L ruminal liquor (n = 1)
X+3: 15 g PET/L ruminal liquor (n = 1)
SheepPS25, 50, 100X−: 0 PS in basal diet (n = 6)60 dBlood, gastrointestinal tract, rumen fluid, longissimus lumborum (LL) muscle
  • No effect on final live weight, carcass weight, dressing %, heart, spleen lung or pancreas weight

  • Sig. ↑ liver and kidney weight

  • No effect DM intake

  • Sig. ↓ average daily gain (lowest in X+3)

  • Sig. ↑ feed conversion ratio (highest in X+3)

  • Sig. ↓ apparent digestibility of DM, NDF, ADF, and lipids

  • No effect on rumen and colon epithelium from histology

  • Damage to jejunum epithelium in treatment groups from histology (↑ with ↑ PS size)

  • Sig. ↓ ruminal pH in X+1 and X+3

  • Sig. ↓ ruminal ammonia nitrogen concentration

  • No effect on volatile fatty acids

  • Sig. changes to blood indices and metabolites suggesting oxidative stress

  • PS not detected in blood in X−, X+1, X+2 and X+3 but other plastic polymers detected

  • Sig. ↑ LL muscle pH at 48 h

  • Sig. ↓ LL muscle pH at 72 h

  • No effect on shear force at 24 and 48 h

  • Sig. ↓ shear force at 72 h (lowest in X+1)

  • Sig. ↓ meat brightness (lowest in X+1), meat redness (highest in X+1) and yellowness (highest in X+3)

  • No effect on gut microbial richness and diversity based on α-diversity, and CHAO1 and Shannon index

  • Sig. ↑ abundance of Bacteroidetes and Prevotellaceae in X+1, and Actinobacteria in X+2

  • Sig. ↓ Coriobacteriales incertae sedis in X+1, X+2 and X+3

  • No effect on total, essential, limited and branched-chain amino acids in LL muscle

  • Sig. changes to non-essential, functional and flavour amino acids

  • No effect on saturated and monounsaturated fatty acids

Chang et al. (2024)
X+1: 25 μm PS at 100 mg/day in basal diet (n = 6)
X+2: 50 μm PS at 100 mg/day in basal diet (n = 6)
X+3: 100 μm PS at 100 mg/day in basal diet (n = 6)

X−, control group, X+, treatment group; Sig., significantly; ↓, reduced; ↑, increased; d, day; h, hours; DM, dry matter; CP, crude protein; NDF, neutral detergent fibre; ADF, acid detergent fibre; PS, polystyrene; PET, polyethylene terephthalate.

Chang et al. (2024) used oral gavage to administer PS (150 mg/day) of three different microplastic particle sizes (0, 25 or 50 μm) to individually housed Hulunbuir lambs, over a 60-day feeding period. Histology demonstrated that jejunum epithelium was increasingly damaged as PS particle size increased. The authors noted the epithelial damage coincided with significant reductions to average daily liveweight gains, feed conversion efficiency, nutrient digestibility and rumen pH – despite unaltered dry matter intake or change to the rumen and colon epithelium (Chang et al. 2024). These may have contributed to the observed increases to the abundance of Bacteroidetes, Prevotellaceae and Actinobacteria, and decreases to cellulose degrading microbes, including Coriobacteriales incertae sedis, in the rumen microbiome. Concurrent changes to haematological indices suggested oxidative stress and an inflammatory response to the ingestion of larger particles of PS. The inhibitory effects of PS particle size on lamb growth and oxidative homeostasis are likely to be the drivers of tenderness (shear force), colour and pH variations reported for the longissimus lumborum muscles of the experimental lambs (Ponnampalam et al. 2022; Chang et al. 2024). The effects of PS particle size on the rumen microbiome are similarly proposed to have contributed to the variation reported to specific fatty acids and amino acids in the longissimus lumborum muscles of the experimental lambs (Chang et al. 2024). Of note was the use of a single basal diet and a single level of microplastic dosage, as it is unclear if these factors promoted or obscured the responses to microplastic ingestion. Without information pertaining to the presence of PS in the blood, meat or excretions of the lambs administered with microplastic particles, the partitioning and potential risk to the end consumer is questionable.

Pigs

There has been no investigation of microplastic ingestion or accumulation effects on pork quality; instead, the effects of microplastic particles on pig health and welfare have been the primary topic of research (Table 2). Wang et al. (2022), for example, used in vitro methods to expose swine testis cells, for a 24-h period, to PS particles of 1–10 μm at concentrations of 0–1000 μg/mL. Significant increases were observed in indicators of inflammation, apoptosis, necrosis and associated signalling pathways at all exposure groups at 24 h, noting that the lowest experimental concentration (250 mg/L) was selected based on a prior cell viability test, which identified that cell viability began reducing in a dose-dependent manner when PS concentration reached at least 125 mg/L (Wang et al. 2022). This ‘low’ concentration is high compared with other studies and it is unlikely for microplastics to achieve this concentration in situ, within the testis, meaning this research may only have application to artificial insemination practices (Wang et al. 2022). Gałęcka et al. (2024) fed pigs with 0, 0.1 or 1 g/day of PET particles, via gelatine capsules, for a total of 28 days, and found no effect on their growth or mortality rate – albeit these data were not included. Duodenum histology at Day 28 showed atypical accumulation of mucus, enterocytes on surface of villi, presence of blood-containing vessels, accumulation of goblet cells and hyperaemia in pigs fed PET at either dosage of microplastic (Gałęcka et al. 2024). These results were confirmed by significant changes to the populations of neurons in the enteric nervous system at Day 28, which suggested reduced gastric juice and intestinal motility, and increased inflammation (Gałęcka et al. 2024). It is noted that the latter study included PET particles that ranged in size (1–300 μm), and that the pigs were group fed (five pigs per pen) within their respective treatments, factors that could have contributed to these findings. In addition, virgin single type microplastic particles were used in both studies and it is unlikely that these are representative to the variety of microplastics within pig production environments.

Table 2.Summary of experimental exposure studies assessing the effect of microplastics on pig health and productivity.

SpeciesPlastic typeSize (μm)ConcentrationDurationOrgan examinedEffectsRefs
PigPS1–10X−: 0 mg/mL (n = NR)24 hTestis cells (in vitro)
  • Apoptosis and necrosis from X+1 onwards

  • Sig. changes to expression of apoptosis related genes and necroptosis marker genes with ↑ concentration (starting form X+1) suggestive of activated apoptosis and necroptosis

  • Sig. ↑ fluorescence in ROS intensity with ↑ concentration suggesting oxidative stress

  • Sig. ↑ expression of levels of primary genes in MAPK/HIF1α signalling pathway with ↑ concentration (starting form X+1) which is important for apoptosis and necroptosis

Wang et al. (2022)
X+1: 250 mg/L (n = NR)
X+2: 500 mg/L (n = NR)
X+3: 1000 mg/L medium (n = NR)
PigPET1.3–299.8X−: 0 g/day28 dSix neurons of enteric nervous system, duodenum
  • No effect on growth or mortality (anecdotally reported)

  • Accumulation of mucus, enterocytes on surface of villi, presence of blood-containing vessels, accumulation of goblet cells, hyperaemia in duodenum histology in X+1 and X+2

  • Sig. changes to populations of neurons in myenteric, outer submucous and inner submucous plexus (X+1 and/or X+2) suggesting potential:

    • ↓ in gastric juice which reduce degradation of microplastics

    • ↓ intestinal motility resulting in retention of intestinal contents which may promote the entry of microplastics into bloodstream

    • ↑ inflammation

Gałęcka et al. (2024)
X+1: 0.1 g/day via oral gelatine capsule
X+2: 1 g/day via oral gelatine capsule

X−, control group; X+, treatment group; Sig., significantly; ↓, reduced; ↑, increased; d, day; h, hours; ROS, reactive oxygen species; PS, polystyrene; PET, polyethylene terephthalate.

Poultry

Compared with ruminants and pig species, most research into the effects of microplastics has been done on poultry, primarily chickens, although some have investigated ducks (Table 3). From the literature, there were 15 controlled studies wherein chickens were administered virgin plastic; and of these, nine controlled studies used the same study design to investigate the effects of 5 μm PS particles in the drinking water of chickens at a low, medium and high concentration, following 42 days of exposure (Meng et al. 2022; Yin et al. 2022; Zhang et al. 2022a, 2022b; Li et al. 2023c; Lu et al. 2023; Yin et al. 2023; Guo et al. 2024; Lu et al. 2024). Effects were assessed by histology, transmission electron microscopy, commercial kits to assess indicators of oxidative stress, inflammation, and apoptosis, quantitative reverse transcription polymerase chain reaction and western blotting techniques. Only one of these controlled studies tested the effects of microplastic exposure duration on chickens, with only low and high concentrations tested, and the chickens exposed to microplastics in their drinking water for 28 or 48 days (Hou et al. 2022). At the conclusion of each of these studies, the experimental chickens were euthanised, and tissue samples were collected from the spleen, duodenum, caecum, liver, thymus, kidney, heart, lung, cerebellum, testis and heart. The majority of studies detected pathological damage and inflammatory cell infiltration in the tissue type analysed. These effects were evident when microplastic concentrations were low or medium and of increasing severity as microplastic concentrations increased. There were significant changes to oxidation regulation indicators, inflammatory factors and apoptosis factors, suggesting oxidative stress, inflammation and apoptosis in all of the tissue types sampled. Several studies also identified the activation of pathways involved in inflammation or apoptosis in samples collected from the microplastic exposure groups. These responses were, again, apparent when microplastic concentrations were low or medium. The exact result of each indicator measured was not uniform across studies and tissues. For example, in myocardial tissue, malondialdehyde (a marker for oxidative stress) increased significantly in the low concentration group (Zhang et al. 2022b), whereas in the thymus, it increased significantly in the medium concentration group (Li et al. 2023c). The reasons for these discrepancies were not provided, but they may reflect a tissue specific response. The three controlled studies that measured final bodyweight reported no significant effect from microplastic exposure at any of the concentrations investigated (Meng et al. 2022; Zhang et al. 2022a; Yin et al. 2023). However, there was a significant reduction to final thymus weight (Li et al. 2023c), final kidney weight (Meng et al. 2022), final heart weight (Zhang et al. 2022a) and final lung weight as a percentage of bodyweight (Lu et al. 2023) – results that indicate a potential impact on carcass yields and dressing percentages. Hou et al. (2022), Yin et al. (2022) and Yin et al. (2023) also observed significantly increased indicators of disrupted blood–testis barrier, gut vascular barrier and blood–brain barrier. It is unlikely that chickens would be exposed in situ to microplastics of uniform particle size and microplastic type, meaning that these effects remain to be confirmed under real production systems.

Table 3.Summary of experimental exposure studies assessing the effect of microplastics on poultry health and productivity.

SpeciesPlastic typeSize (μm)ConcentrationDurationOrgan examinedEffectsRefs
ChickenNRNRX−: 0 mg/kg feed (n = 30)28 dCecum content
  • Sig. ↓ body weight and average daily gain

  • No effect on daily feed intake

  • Sig. ↓ CHAO1 and abundance-based coverage estimator (ACE) indices and no change to Simpson and Shannon indices suggesting some ↓ microbial diversity

  • Sig. difference in abundance of 30 genera of microbes

  • No change to main phyla of microbiota

Zou et al. (2023)
X+: 200 mg/kg feed (n = 30)
ChickenPE1–10X−: 0 mg/kg feed (n = 30)28 dJejunal content, intestine, liver, kidney, spleen
  • Sig. ↓ body weight, average daily gain

  • Sig. ↓ serum antioxidant indicators suggesting ↓ antioxidant capacity

  • No effect on serum antioxidant indicator catalase

  • Sig. ↑ serum alanine aminotransferase, serum aspartate aminotransferase, and serum antioxidant indicator malondialdehyde

  • Liver inflammation, renal glomerular hypoplasia, and white pulp lymphopenia in histology

  • Sig. ↓ CHAO1, ACE and Shannon indices suggesting ↓ gut microbial diversity and abundance

  • No effect on main phyla of microbiota

  • Sig. difference abundance of several phyla and genera suggesting altered microbial composition

  • Sig. difference in intestinal metabolism suggesting disruptions

Li et al. (2023a)
X+: 200 mg/kg feed
ChickenPS5X−: 0 mg/L drinking water (n = 15)42 dSpleen
  • Pathological damage to spleen histology in X+2 and X+3

  • ↑ mitochondrial membrane density and ridge rupture suggesting mitochondrial damage

  • Sig. ↓ levels of ferroptosis-related factors suggesting ferroptosis

  • Sig. changes in certain oxidation regulation indicators in X+2 and X+3 suggesting oxidative stress

  • Sig. ↑ in apoptosis factors in X+1, X+2 and X+3 suggesting ↑ apoptosis

Guo et al. (2024)
X+1: 1 mg/L drinking water (n = 15)
X+2: 10 mg/L drinking water (n = 15)
X+3: 100 mg/L drinking water (n = 15)
ChickenPS5X−: 0 mg/L drinking water (n = 30)42 dDuodenum, cecum, liver
  • No effect on final body weight

  • Inflammation and damage to duodenum and cecum histology in X+1, X+2 and X+3

  • Sig. ↓ expression of intestinal tight junction proteins and sig. ↑ plasma membrane vesicle protein (X+1, X+2 and X+3) suggesting destruction of the gut vascular barrier and inhibition of the Wnt/β-catenin signalling pathway

  • Sig. ↑ in serum diamine oxidase suggesting ↑ intestinal permeability in X+2 and X+3

  • Sig. ↑ in necroptosis-related protein expression level in X+2, pyrolysis-related protein expression level in X+2, and inflammation-related protein expression level in X+2 suggesting changed mode of death from apoptosis to pyrolysis and necroptosis (inflammatory cell death)

  • No effect on apoptosis-related protein expression level in cecum

  • Some changes to indicators of intestinal microflora

  • Sig. ↑ week 6 liver injury indices and strong inflammatory cell infiltration (X+1, X+2 and X+3), liver inflammatory markers, triglycerides, and inflammation in histology, lipid accumulation and upregulation of fatty acid synthesis suggest liver damage through lipid metabolism disorder and apoptosis

  • Sig. ↓ superoxide dismutase enzyme activity, sig. ↑ malondialdehyde and enzyme activities and hepatocyte apoptosis suggesting disruption to antioxidant system balance

Yin et al. (2023)
X+1: 1 mg/L drinking water (n = 30)
X+2: 10 mg/L drinking water (n = 30)
X+3: 100 mg/L drinking water (n = 30)
ChickenPS5X−: 0 mg/L drinking water (n = 30)42 dThymus
  • Sig. ↓ final thymus weight in X+1, X+2 and X+3

  • Inflammatory cell infiltration and pathological changes to histology in X+2 and X+3

  • Sig. changes in oxidative stress-related indices in in X+1, X+2 and X+3 suggestive of oxidative stress

  • Sig. ↑ inflammatory factors in X+2 and X+3 suggesting inflammation

  • Sig. changes in multiple apoptosis related indices suggesting ↑ apoptosis (not linear PS concentration dependency)

  • Sig. ↑ autophagy proteins in X+3

Li et al. (2023c)
X+1: 1 mg/L drinking water (n = 30)
X+2: 10 mg/L drinking water (n = 30)
X+3: 100 mg/L drinking water (n = 30)
ChickenFluorescent PS (F-PS)0.5, 5, 50X−: 0 mg/L purified water by oral gavage (n = 24)1, 7, 14, 21, 28, 35 dJejunum, liver, leg muscle, breast muscle
  • F-PS accumulation in leg muscle ↓ over 35 d and remained stable in breast muscle

  • X+2 had the most F-PS accumulation in muscle, X+1 and X+3 had less

  • Sig. ↑ body weight, carcass weight, breast muscle weight, and leg muscle weight after 35 d (most consistently for X+2)

  • No effect on liver metabolism

Chen et al. (2023)
X+1: 200 μL of 0.5 μm solution at 500 mg/L by oral gavage (n = 24)
X+2: 200 μL of 5 μm solution at 500 mg/L by oral gavage (n = 24)
X+3: 200 μL of 50 μm solution at 500 mg/L by oral gavage (n = 24)
PS5X−: 0 mg/day purified water by oral gavage (n = 5)28 d
  • Sig. ↑ breast and leg muscle weight in X+2

  • No change to live and carcass weight, carcass %, breast and leg muscle growth rate

  • Sig. ↓ muscle ATP level, lactate dehydrogenase activity, total cholesterol, and triglycerides indicating inhibited muscle energy and lipid metabolism in X+2

  • Sig. ↑ activity of glutathione peroxidase indicating oxidative stress in X+2

  • Sig. ↓ activity of acetylcholinesterase suggesting neurotoxicity in X+2

  • No effect on liver metabolism or oxidative stress

  • Sig. ↓ breast muscle shear force and drip loss

  • Sig. ↑ muscle pH

  • Minor effect on muscle metabolomic profile

  • Changes to meat flavour metabolite profiles

  • Affected genes involved in neural function and muscle cell development

X+1: 0.1 mg/day by oral gavage (n = 5)
X+2: 0.5 mg/day by oral gavage (n = 5)
ChickenPS5X−: 0 mg/L drinking water (n = 30)42 dKidney
  • No effect on final body or kidney weight

  • Ruptured tubular epithelium, enlarged glomerular oedema, inflammation in kidney histology in X+1, X+2 and X+3

  • Disruption to blood-urinary barrier and microvilli swelling in X+1 from TEM

  • Mitochondrial and nuclear damage in X+2 and X+3 from TEM

  • Sig. changes to levels of protein and mRNA expression of mitochondrial function in X+1, X+2 and/or X+3 suggesting mitochondrial dysfunction

  • Sig. changes to levels of antioxidant enzymes in X+1, X+2 and/or X+3 suggesting oxidative stress by altering antioxidant enzymes in the kidney

  • Sig. ↑ nuclear factor-kappa B (NF-κB) and IκBα in kidney tissue in X+3 and protein expression levels of inflammatory factors in X+1, X+2 and/or X+3 suggesting NF-κB pathway activation and inflammation

  • Sig. ↑ in protein expression of necroptosis-associated genes in X+1, X+2 and/or X+3 and sig. ↓ in caspase8 which inhibits necroptosis suggestive of necroptosis in kidney

Meng et al. (2022)
X+1: 1 mg/L drinking water (n = 30)
X+2: 10 mg/L drinking water (n = 30)
X+3: 100 mg/L drinking water (n = 30)
ChickenPS5X−: 0 mg/L drinking water (n = 15)42 dHeart
  • No effect on final body or heart weight

  • Myocardial inflammation and injury (↑ effect with ↑ concentration) by histology and TEM

  • Changes to myocardial tissue antioxidant enzymes with ↑ concentration suggesting myocardial oxidative stress and ROS overload

  • Sig. ↑ expression of levels of mRNA markers of the NLRP3 inflammasome-dependent pyroptotic pathway with ↑ concentration suggesting myocardial pyroptosis

  • Sig. changes to levels of mRNA markers of the NF-κB inflammation pathway with ↑ concentration suggesting inflammation

  • Sig. ↑ mRNA and protein expression of pro-inflammatory factors with ↑ concentration

  • Sig. changes to mRNA protein levels with ↑ concentration and sig. changes to mitochondrial green fluorescence and AMPK-PGC-1α pathway expression in X+3 suggesting mitochondrial and energy metabolism dysfunction

  • ↓ cardiomyocyte growth after 24 hours from X+1 onwards

  • Abnormal cell morphology from X+1 onwards

  • Sig. ↑ ROS fluorescence in X+3 suggesting oxidative stress and ROS overload

  • Sig. ↑ expression of NLRP3 and GSDMD suggesting activation of pyroptotic pathway

Zhang et al. (2022b)
X+1: 1 mg/L drinking water (n = 15)4, 12, 24, 48 hCardiomyocytes (in vitro)
X+2: 10 mg/L drinking water (n = 15)
X+3: 100 mg/L drinking water (n = 15)
X−: 0 mg/mL medium (n = NR)
X+1: 0.25 mg/mL medium (n = NR)
X+2: 0.5 mg/mL medium (n = NR)
X+3: 1 mg/mL medium (n = NR)
ChickenPS5X−: 0 mg/L drinking water (n = 30)28, 48 dTestis
  • Inflammation and damage to testis histology in X+1 and X+2 after 42 d

  • Sig. ↓ proteins claudin3 and occludin after 28 d (X+2) and 48 d (X+1 and X+2) and no change to ZO-2 suggesting disrupted blood-testis barrier

  • Sig. ↓ expression of proteins Nrf2 NQO1 and HO-1 (X+2 at 42 d) and sig. ↑ Keap1 protein level by 42 d (X+1 and X+2) suggesting reduced testis antioxidant defence system which may lead to oxidative stress

  • Sig. ↑ expression of indicators of NK-κB pathway (X+1 and X+2 at 42 d, X+2 at 28 d) suggesting inflammation

  • Sig. ↓ expression of anti-apoptotic protein Bcl-2 and sig. ↑ expression of pro-apoptotic proteins suggesting apoptosis

Hou et al. (2022)
X+1: 1 mg/L drinking water (n = 30)
X+2: 100 mg/L drinking water (n = 30)
ChickenPS5X−: 0 mg/L drinking water (n = 30)42 dLung
  • Sig. ↓ lung weight as % body weight from 28 d onwards in X+2 and X+3

  • Pathological changes including inflammatory cell infiltration in lung histology from X+1 onwards

  • Apoptosis in TEM from X+1 onwards

  • Sig. changes to activity and levels of antioxidant enzymes in the lung from X+1 and X+2 onwards suggesting oxidative stress

  • Sig. changes to expression of genes associated with the PTEN/PI3K/AKT pathway (X+2 onwards) which can lead to cell death

  • Sig. changes to autophagy and apoptosis-related proteins (X+1 and X+2 onwards) suggestive of mitochondrial dysfunction

  • Sig. ↑ expression level of genes related to the MAPK signal pathway (X+2 and/or X+3) suggesting apoptosis and autophagy through the MAPK pathway

  • All effects ↑ with ↑ concentration

Lu et al. (2023)
X+1: 1 mg/L drinking water (n = 30)
X+2: 10 mg/L drinking water (n = 30)
X+3: 100 mg/L drinking water (n = 30)
ChickenPS5X−: 0 mg/L drinking water (n = 30)42 dCerebellum
  • ↓ number of Purkinje cells and ↑ haemorrhages in cerebellum tissue histology from X+1 onwards suggesting brain tissue damage and ↓ neurotransmission

  • Sig. ↓ expression levels of Occludin, Claudin 3 and ZO-1 from X+1 or X+2 onwards suggesting destruction of blood-brain barrier

  • Sig. changes to antioxidant enzyme activity from X+1, X+2 or X+3 suggesting disrupted antioxidant balance

  • Damage to mitochondria in the cerebellum from TEM from X+1 onwards and sig. changes to expression levels of ferroptosis-related proteins (X+1 or X+2 or X+3) suggesting ferroptosis in brain tissue

  • Sig. changes to expression of apoptosis-related proteins from X+2 or X+3 onwards suggesting apoptosis of cerebellar tissue

Yin et al. (2022)
X+1: 1 mg/L drinking water (n = 30)
X+2: 10 mg/L drinking water (n = 30)
X+3: 100 mg/L drinking water (n = 30)
ChickenPS5X−: 0 mg/L drinking water (n = NR)42 dLung
  • Lymphocytosis, inflammatory infiltration, and tissue necrosis in lung tissue histology from X+1 onwards suggesting lung damage

  • Pyroptosis and endoplasmic reticulum stress observed in lung by TEM

  • Sig. ↑ in expression level of heat shock proteins suggesting stress response in lungs

  • Sig. ↑ in mRNA expression of endoplasmic reticulum stress-related indexes

  • Sig. ↑ expression levels of pyroptosis-related protein and mRNA in lung tissue from X+1 onwards suggesting pyroptosis

  • Sig. changes to indicators of NF-κB signalling pathway and protein and gene expression levels of some inflammatory cytokines from X+1 onwards suggesting lung inflammation

  • All effects ↑ with ↑ concentration

Lu et al. (2024)
X+1: 1 mg/L drinking water (n = NR)
X+2: 10 mg/L drinking water (n = NR)
X+3: 100 mg/L drinking water (n = NR)
ChickenPS5X−: 0 mg/L drinking water (n = 15)42 dHeart
  • PS concentration (mg/g) in heart

    • X− = 0

    • X+1 = 0.004 ± 0.0003

    • X+2 = 0.036 ± 0.007 (Sig. ↑)

    • X+3 = 0.13 ± 0.005 (Sig. ↑)

  • Pathological manifestations in heart tissue histology from X+1 onwards suggesting myocardial damage

  • Sig. changes to mRNA and protein levels of myocardial development factors from X+1 and X+2 onwards suggesting myocardial dysplasia

  • Sig. ↑ in mRNA levels of endoplasmic reticulum stress markers in X+2 and X+3 suggesting myocardial endoplasmic reticulum stress

  • ↓ in immunofluorescence combined with sig. ↓ mRNA levels of autophagy markers from X+1 onwards suggesting activation of myocardial autophagic pathway

Zhang et al. (2022a)
X+1: 1 mg/L drinking water (n = 15)
X+2: 10 mg/L drinking water (n = 15)
X+3: 100 mg/L drinking water (n = 15)
ChickenNRNRX−: 0% daily diet via semi-cooked dough (n = 8)112 dDigestive fluids, blood
  • Sig. ↓ weight gain in X+3

  • Total white blood cell count, mean corpuscular volume, creatinine kinase, aspartate transaminase and urea were highest in X+3

  • Total red blood cell count, packed cell volume, cholesterol, total protein, albumin, alanine aminotransferase and uric acid were highest in X+2

  • Sig. ↑ level of amylase, total protease enzymes, luteinizing hormone, thyroid stimulating hormone, follicle-stimulating hormone, triiodothyronine and tetraiodothyronine in X+3

  • No effect on lipase enzyme

Malik et al. (2024)
X+1: 20% daily diet via semi-cooked dough (n = 8)
X+2: 30% daily diet via semi-cooked dough (n = 8)
X+3: 40% daily diet via semi-cooked dough (n = 8)
ChickenLow density PE50X−: 0 mg PE (n = 10)24 hCecal content (in vitro)
  • No effect of X+1, X+2, X+3, X+4 and X+5 on phylogenetic diversity and β-diversity

  • Sig. changes to metabolome in S. Typhimurium groups (X+1, X+3 and X+5) and X+2 suggesting altered metabolic activity in the cecal microbiome.

  • No effect of X+4 on metabolome suggesting greater effect of PE fibres than PE powders (i.e. effect of shape)

  • Co-exposure to PE fiber and S. Typhimurium caused greater effects than either exposure alone

Chatman et al. (2024)
X+1: Salmonella enterica Typhimurium (n = 10)
X+2: 50 mg PE fibre (n = 10)
X+3: 50 mg PE fibre + S. Typhimurium (n = 10)
X+4: 50 mg PE powder (n = 10)
X+5: 50 mg PE powder + S. Typhimurium (n = 10)
Female ducksPVCNRX−: 0 mg/kg Cd and 0 mg/L PVC in drinking water (n = 8)60 dLiver
  • Fluorescence PVC observed in liver from X+2 and X+3

  • Sig. ↑ accumulation of Cd in liver tissue in X+3 compared to X+1 suggesting that PVC promotes Cd accumulation

  • Sig. ↓ liver tissue size in X+1, X+2 and X+3

  • ↑ hepatic medullary disorders and inflammatory cell infiltration in liver histology and TEM in X+1, X+2 and X+3 (most severe in X+3)

  • Sig. ↑ serum levels of alanine transaminase in X+1 and X+3 suggesting reduced liver function

  • Sig. ↑ Cu in liver tissue in X+2 and X+3, sig. ↑ Zn in X+1, X+2 and X+3, sig. ↓ Mn in X+1 and X+3

  • Sig. ↓ levels of cellular anti-oxidative enzymes level in X+1, X+2 and X+3 suggesting oxidative stress in liver

  • Sig. ↑ lipid droplet vacuoles in liver and sig. ↑ TG levels in X+3 compared to X+1 suggesting co-exposure effect on lipid accumulation in liver

  • Sig. changes in protein expression levels affecting glycogen accumulations through the PCK1-PI3K/AKT pathway in X+1, X+2 and X+3 (X+3 had greatest effect)

  • Sig. ↑ in liver collagen fibres and protein expression associated with liver fibrosis in X+1 and X+3

  • Sig. ↑ in proportion of apoptosis-positive cells in X+1, X+2 and X+3 (X+3 had greatest effect) suggesting liver apoptosis

Chen et al. (2024)
X+1: 50 mg/kg of Cd in basal diet (n = 8)
X+2: fluorescent PVC 1 mg/L in drinking water (n = 8)
X+3: 50 mg/kg of Cd in basal diet + fluorescent PVC 1 mg/L in drinking water (n = 8)
Male ducksPS10–100X−: 0 mg/kg CTC and 0 mg/L PS (n = 6)56Breast, liver, kidney, small intestine and cecal content
  • Sig. ↓ final body weight and average daily gain in PS-treated groups (X+2 and X+3)

  • No effect on average daily feed intake

  • No effect on meat pH or colour but sig. ↓ drip loss % in PS-treated groups

  • Histopathological damage to the jejunum and sig. ↑ serum diamine oxidase and D-lactic acid and ↓ expression of tight junctions in PS-treated groups suggesting gut barrier changes and increased intestinal permeability.

  • Sig. ↑ ROS and malonaldehyde and sig. ↓ total antioxidant capacity, total superoxide dismutase, and glutathione peroxidase activity in intestine of PS-treated groups suggesting oxidative stress

  • Sig. ↑ expression of inflammatory factors in the jejunum in PS-treated groups suggesting inflammation

  • Sig. ↓ alpha diversity indices in X+1, X+2 and X+3 suggesting reduced intestinal microbiota richness and diversity

  • No effect on Simpson microbial diversity index

  • ↑ relative abundance of intestinal Prevotella, Desulfovibrio, Streptococcus, and Helicobacter in PS-treated groups

  • Sig. ↓ anti-inflammatory intestinal bacteria Clostridium and Faecalibacterium in PS-treated groups

  • Sig. ↑ abundance of antibiotic resistance genes in X+3

Liu et al. (2023)
X+1: 50 mg/kg of CTC in basal diet (n = 6)
X+2: PS 1 mg/L in drinking water (n = 6)
X+3: 50 mg/kg of CTC in basal diet + PS 1 mg/L in drinking water (n = 6)

NR, not reported; X−, control group; X+, treatment group; Sig., significantly; ↓, reduced; ↑, increased; d, day; h, hours; ATP, adenosine triphosphate; TEM, transmission electron microscopy; Cd, cadmium; CTC, chlortetracycline; ROS, reactive oxygen species; PS, polystyrene; PE, polyethylene; PVC, polyvinyl chloride.

Two studies administered microplastics through chicken feed at 200 mg/kg for 28 days, with Li et al. (2023a) investigating the effects of polyethylene (PE) particles of 1–10 μm on jejunal content, intestine, liver, kidney and spleen tissue; and Zou et al. (2023) investigating the effects on caecum content, but without describing the type or size of plastic used – making it challenging to interpret and reproduce their research. It is further noted that there may have been some microplastics in the control feed and, therefore, the treatment should be considered as additional dietary microplastics rather than total dietary microplastics. Nonetheless, both studies reported significant reductions to final bodyweight and average daily gains of chickens fed microplastic particles. Zou et al. (2023) reported no effect of microplastics on the daily feed intake of chickens. Li et al. (2023a) reported microplastic ingestion resulted in a reduced antioxidant capacity, as well as liver damage and inflammation based on oxidative biomarker concentrations and histology (Li et al. 2023a). Analyses from both studies showed there to be a decrease in chicken gut microbial diversity and abundance when fed microplastics. This was evidenced by the significant reductions in the CHAO1 and abundance-based coverage estimator indices, although only 16 samples out of the 60 chickens in the study were analysed. Li et al. (2023a) also found significantly reduced Shannon indices and intestinal metabolism.

Malik et al. (2024) fed microplastics to pullets using semi-cooked dough to encase microplastics equivalent to 0, 20, 30 and 40% of the daily diet for 112 days. The authors measured initial and final liveweights, and observed a significant reduction in weight gain for the 40% treatment group (Malik et al. 2024). This same dosage of microplastics (40%) was found to induce an immune response in chickens that can be inferred from the elevated total white blood cell count (Malik et al. 2024). The study did not report actual P-values, polymer type or size, or the how cooking the microplastics within dough affected microplastic composition. Consequently, it is unclear as to the conclusions that may be made from these research findings.

The effects of microplastics on chickens were investigated using in vitro methods by Zhang et al. (2022b) and Chatman et al. (2024). Zhang et al. (2022b) exposed cardiomyocytes to three concentrations of PS particles of 5 μm for 4, 12, 24 or 48 h. It was found that cardiomyocyte growth was reduced and abnormal cell growth occurred when PS concentrations were low (0.25 mg/L), and that these effects were intensified as PS concentrations increased (Zhang et al. 2022b). The authors also reported significant increases to indicators of oxidative stress and pyroptosis for cardiomyocytes exposed to the high and low concentrations, respectively (Zhang et al. 2022b). Chatman et al. (2024) exposed chicken caecal contents to 50 mg of 50 μm PE fibre or PE powder, with and without Salmonella enterica serovar Typhimurium, for a period of 24 h. There were no changes to microbiome diversity observed. PE fibre or powder alone did not alter metabolic activity but when exposed to caecal contents in combination with S. enterica serovar Typhimurium, a greater effect was observed than with either PS or S. enterica serovar Typhimurium exposure alone, suggesting a co-exposure effect.

Chen et al. (2023) used oral gavage to dose chickens daily with PS at a range of doses and particle sizes, in two controlled experiments assessing fluorescent and non-fluorescent PS separately (Table 3). Significantly increased final body, carcass, breast and leg muscle weight was observed at 35 days in chickens fed fluorescent PS. Fluorescent PS accumulation decreased over time in leg muscle tissue, while remaining stable in breast muscle. Non-fluorescent PS was also associated with significantly increased breast and leg muscle weight in the high-dose group, but did not affect final body or carcass weight. There were significant changes to indicators suggesting oxidative stress and neurotoxicity in the high-dose group. These potential negative health effects were not sufficient to impact on the meat products. Indeed, meat was more tender (lower shear force), some flavour metabolites were inhibited, and there were changes in genes that regulate neural function and muscle cell development for chickens administered daily with 0.1–0.5 mg of 5-μm PS particles (Chen et al. 2023). There was no effect on liver or muscle metabolism (Chen et al. 2023).

Two controlled studies investigated the effects of microplastics on ducks. Chen et al. (2024) exposed ducks to 1 mg/L of fluorescent polyvinyl chloride (PVC) through drinking water for 60 days with and without cadmium (Cd). Drinking water consumption was ad libitum, meaning that there could have been variation in the dosages between experimental ducks. Fluorescent PVC was observed in the liver of PVC exposure groups and promoted Cd accumulation (Chen et al. 2024). PVC exposure with and without Cd significantly reduced liver size, and resulted in hepatic medullary disorders and inflammatory cell infiltration in the selected histological images presented (Chen et al. 2024). Significant changes in indicators suggesting oxidative stress and apoptosis in the liver were observed in PVC exposure groups with and without Cd. Liu et al. (2023) likewise exposed ducks to 1 mg/L of 10–100-μm PS particles through drinking water, albeit for 56 days with and without chlortetracycline, an antimicrobial. Significantly reduced final bodyweight, average daily gain, and drip loss for the meat were observed in PS treatment groups with and without chlortetracycline (Liu et al. 2023). There was no effect on daily feed intake, meat pH or colour. Damage to the jejunum appeared in the selected histological images presented, and significant changes were observed in indicators suggesting gut barrier changes, and intestinal oxidative stress and inflammation in PS treatment groups with and without chlortetracycline. The interesting outcome from both of these studies with ducks was the interaction between PVC microplastics and other bioactive compounds (Cd and chlortetracycline). These interactions indicate that microplastic effects on poultry health, performance and meat quality may not be simple relationships, and require more holistic consideration of microplastic interactions with other nutritional and non-nutritional compounds.

Other effects of microplastics on livestock and poultry

A potential threat from microplastics is that they can act as vectors for pathogens, chemicals, pollutants and heavy metals to transmit to livestock, poultry and to their meat products. In the manufacturing process, microplastics are coated with chemicals to enhance durability and heat resistance, such as phthalates and bisphenol A. Phthalate is a chemical plasticiser added to plastics to increase its durability and is considered toxic. When plastics deteriorate, these chemicals are released, and the detection of these chemicals can be signatures of the presence of microplastics and vice versa. In livestock, this is an actual risk, as phthalates have been detected in pig feed (0.12–2.6 mg/kg, n = 45; Xu et al. 2022), silage (0.0002–0.03 mg/kg, n = 2), pasture and concentrate feed (0.0002–0.02 mg/kg, n = 2 each), and soil inhabited by livestock (0.00006–0.01 mg/kg, n = 2; Fierens et al. 2012).

Microplastics have hydrophobic surfaces that provide a medium for chemicals to adsorb to, or for microorganisms to form biofilms, referred to as plastispheres. In livestock, there is evidence of heavy metals adsorbing onto microplastics and being subsequently released during ruminant digestion. Liao and Yang (2022) adsorbed two concentrations of Cd onto virgin 145-μm PE, 160-μm polypropylene (PP), 170-μm PVC, 150-μm PS and 150-μm polylactic acid, which is a biodegradable biobased plastic. The Cd-loaded microplastics underwent in vitro ruminant digestion with five rumination cycles between the mouth and rumen (Liao and Yang 2022). At the lower concentration of 10 μg Cd/L, microplastics released 15–35% of their Cd by the end of digestion, whereas the higher concentration group (100 μg Cd/L) released 10–40% (Liao and Yang 2022), noting that the in vitro digestion did not include rumen microorganisms. This study did not assess aged plastic, which ruminants are more likely to ingest and which may have a stronger interaction with adsorbed Cd, leading to less release (Liao and Yang 2022).

Interactions between microplastics and bacteria have been assessed in ducks. Yu et al. (2023) exposed antibiotic resistant Escherichia coli to five concentrations of PE of three different sizes for 16 h. Transfer of antibiotic resistance genes between E. coli increased before decreasing with increasing PE concentration, and consistently increased with increasing PE particle size (Yu et al. 2023), possibly due to the larger surface area providing an environment for biofilm formation. This was accompanied by significant changes to the expression of genes regulating antibiotic resistance gene transfer and factors affecting cell permeability (Yu et al. 2023). Furthermore, on a chicken farm, the abundance of soil microplastics were significantly positively correlated to soil antibiotic resistance genes, which suggests that microplastics might promote the spread of antibiotic resistance genes (Yu et al. 2023). On a small set of samples (n = 20), Wang et al. (2024b) identified a significant positive correlation between antibiotic and microplastic concentrations in ruminant manure and soil, which was potentially due to adsorption of antibiotics onto microplastics, as well as confounding environmental factors, as the samples were from only six farms. So far, experimental exposure studies have investigated the effects of mostly virgin microplastics in isolation of the chemicals or microorganisms adsorbed to their surfaces. The vector role of microplastics is potentially more impactful on livestock health and productivity than the microplastics themselves. Delineation of these interactions is an important area for further detailed research.

Microplastic bioaccumulation in livestock and poultry tissue and meat products

The presence of microplastic is important to the safety and preference of consumers of livestock and poultry meat, irrespective to its impact on animal health, productivity and meat quality. There is evidence of microplastic bioaccumulate in livestock tissues. For example, Chen et al. (2023) used fluorescent spectroscopy to detect PS in the breast and leg muscle tissue of chickens 1 day after they were fed fluorescent PS particles of 0.5, 5 or 50 μm (n = 24, eight birds per particle size). These same authors reported that PS particles of 5 μm resulted in higher tissue concentrations to the other particle sizes – indicating a non-linear, particle size-dependent mode of accumulation. Shelver et al. (2024) fed 15 layer hens with PS particles of 0.4 μm (mean size) at 11.1 mg/kg bodyweight in a single gelatine capsule placed in the oral cavity. The PS particles were tagged with radiotracers, and radioactivity was measured 1, 2, 3, 4 and 7 days post-ingestion. Based on recoveries of radioactivity, PS particles were detected in the blood, eggs, crop, gizzard, intestinal tract, heart, kidney, liver, lung, spleen, developing ova and intestinal contents at 1 day (Shelver et al. 2024). The authors did observe that the majority of PS particles were expelled in excreta (96.8%), and that <1% of the initial dose was detected in tissues. Wang et al. (2024a) intravenously injected chicken embryos with PS particles of 0.15 or 1 μm at concentrations of 1, 2 or 5 g/mL. Analysis using fluorescence microscopy and vibratome sections identified PS in allantoic fluid, and heart, liver, kidney, intestine, brain, eye and lung tissue from Day 1.5 to 5.5, post-injection. Collectively, these studies demonstrate an acute effect of microplastic ingestion/incursion on poultry tissue concentrations, meaning there is only a short interval during which microplastic concentrations in animal tissues and meat products may be ameliorated once exposure occurs.

Ruminants

Microplastics have been identified in ruminant meat, muscle and other tissues, although little research has been applied to this investigation with four studies (Table 4). Bahrani et al. (2024) purchased cattle and sheep meat from five different retail outlets in Iran, and ensured adherence to standard microplastic contamination prevention strategies during collection – these involved cleaning of equipment with sterile liquids, covering samples with aluminium foil to protect against atmospheric microplastics and collecting blank samples from the laboratory environment. The authors reported there to be, on average, 130 microplastic particles per kg of sheep meat and 140 microplastic particles per kg of beef (Bahrani et al. 2024). A similar quantity (120 microplastic particles per kg of beef) was also reported by Milne et al. (2024) for top sirloin steak purchased from a USA supermarket, and despite a larger filter being used to isolate microplastic particles and 66% of microplastic particles detected being excluded as an adjustment based on the blank sample. van der Veen et al. (2022) employed similar blank correction and contamination prevention steps to Milne et al. (2024), in addition to the removal of the surface layer of beef samples sourced from different farms and retail outlets. Of the subset of polymers tested, these authors identified several plastic polymer types in beef that contributed to a microplastic particle concentration range of 53–7700 mg/kg (van der Veen et al. 2022). Microplastics were also detected in the blood of cattle at concentrations of 0.08–6.1 mg/kg (van der Veen et al. 2022).

Table 4.Summary of studies quantifying microplastic particles within meat, other tissues and blood from natural exposure to microplastics.

SpeciesTissue typeNQuantityQuantification methodLimit of detectionFilter size (μm)Refs
ChickenJejunum3PA6: 575.1 mg/kg PA66: 420.3 mg/kg PS: 2.2 mg/kg PET, PE, PMMA, PP, PVC, PC: 0PyGCMSPS, PET, PMMA, PC, PA6, PA66, and PVC: 0.02 μg A PP and PE: 0.5 μg A PLA and PBAT: 0.2 μg ANAChen et al. (2023)
ChickenLiver3PET: 1751.4 mg/kg PA6: 942.8 mg/kg PA66: 169.5 mg/kg PS: 5.8 mg/kg PE, PMMA, PP, PVC, PC: 0PyGCMS
ChickenLeg muscle3PA6: 884.7 mg/kg PS: 2.9 mg/kg PET, PA66, PE, PMMA, PP, PVC, PC: 0PyGCMS
ChickenBreast muscle3PA6: 561.6 mg/kg PS: 4.0 mg/kg PET, PA66, PE, PMMA, PP, PVC, PC: 0PyGCMS
33 polymer types; mostly polyamine Mostly 0–30 μm size but up to 300 μmLDIR spectroscopyNRNR
ChickenChicken nuggets12310 MP particles/kgMicroscopy and verification with Raman spectroscopy for 13% of microplastics0.84–9.39 MP particles/g (n = 14 blank samples)45Milne et al. (2024)
Chicken breast6100 MP particles/kg
CattleTop sirloin steak6120 MP particles/kg
PigPork loin6200 MP particles/kg
SheepSheep liver, meat and reticulum15130 MP particles/kg Mostly nylon, PS, PEMicroscopy and micro-Raman spectroscopyNR10Bahrani et al. (2024)
CattleBeef liver, meat and reticulum15140 MP particles/kg Mostly nylon and PE
CattleBeef8PE: 150–>7700 mg/kg PVC: 53–>2600 mg/kg PS: 77–200 mg/kg PP, PMMA, PET: 0PyGCMS0 (n = 2 blank samples) 700 nm sizeNAvan der Veen et al. (2022)
Blood12PVC: 1.2–6.1 mg/kg PE: 0.22–1.5 mg/kg PS: 0.09–1.5 mg/kg PP: 0.08–0.41 mg/kg PMMA, PET: 0PyGCMSPP: 0.05 μg PE: 0.47 μg PS: 0.1 μg (n = 9 blank samples) 700 nm size
PigPork8PE: 88–690 mg/kg PVC-P: 127 mg/kg PP: 63 mg/kg PS, PP, PMMA, PET: 0PyGCMS0 (n = 2 blank samples) 700 nm size
Blood12PE: 2.1–>33 mg/kg PVC-P: 1.7–17 mg/kg PS: 0.3–>10 mg/kg PP: 0.16–0.37 mg/kg PET: 0.07–0.34 mg/kg PMMA: 0PyGCMSPP: 0.05 μg PE: 0.47 μg PS: 0.1 μg (n = 9 blank samples) 700 nm size
PigAdult lung tissue112,000 MP particles/kg 115.1–1370.4 μmPolarised light microscopy0 (n = 10 blank samples)10Li et al. (2023b)
180,000 MP particles/kg 20.3–916.4 μm Mostly PA (64%)LDIR spectroscopy
Foetal lung tissueNR6000 MP particles/kg 138.7–438.0 μmPolarised light microscopy
97,000 MP particles/kg 20.3–501.5 μm Mostly PC (33.0%)LDIR spectroscopy
PigIntestinal tissueNR9600 MP particles/kg 72.4% <200 μm Mostly PPPolarised light microscopy or LDIR spectroscopyNR10Hua et al. (2021)

N, number of samples; MP, microplastic; PBART, polybutylene adipate terephthalate; PyGCMS, pyrolysis gas chromatography mass spectrometry; LDIR, laser direct infrared; NR, not reported; NA, not applicable; PS, polystyrene; PET, polyethylene terephthalate; PA6 and PA66, nylon; PE, polyethylene; PMMA, poly methyl methacrylate; PP, polypropylene; PVC, polyvinyl chloride; PC, polycarbonate.

A Not based on blank samples, but based on ‘experience’ of testing laboratory (Shanghai WEIPU Testing Technology Group).

Microplastics have also been isolated specifically from the surface of meat through a process of rinsing meat samples and analysing the rinse water (Table 5). Habib et al. (2022b) analysed, in triplicate, the rinse water from two cuts of beef and five cuts of chevon that had been prepared on various types of plastic cutting boards, and subjected to various cooking and washing treatments. Chevon was reported to have 70–7200 surface microplastic particles per kg, which equated to 70–1640 mg of microplastic per kg of chevon and included particles of 15.5–13,089.8 μm (Habib et al. 2022b). Beef was reported to have 1–6500 surface microplastic particles per kg, which equated to 0–1620 mg per kg of beef and included particles of 14.8–5369.8 μm. All of the microplastics identified in the beef and chevon samples were PE (Habib et al. 2022b). Hence, in addition to potential bioaccumulation, microplastic contamination post-slaughter is also a source of microplastics in livestock products. This has significant implications for ruminant meat processors and the culinary industry.

Table 5.Summary of studies quantifying microplastic particles on the surface of meat through the analysis of rinse water.

SpeciesTissue typeNQuantityQuantification methodLimit of detectionFilter size (μm)Refs
ChickenCubed whole chicken666–290 mg/kg 30–1190 MP particles/kg 74.6–178.3 μmMicroscopy, weighing and FTIR spectroscopyNR6Habib et al. (2022a)
GoatShank A11200 ± 140 mg/kg (±s.d.) 2200 ± 600 MP particles/kg 1801.3 ± 1305.9 μm 80.8–8000.3 μm (range)Microscopy, weighing and FTIR spectroscopyNR6Habib et al. (2022b)
GoatShank B1120 ± 10 mg/kg 1200 ± 600 MP particles/kg 419.2 ± 296.7 μm 15.5–1186.7 μm (range)
GoatFried shank A11640 ± 460 mg/kg 3800 ± 2600 MP particles/kg 1110.9 ± 965.2 μm 30.6–13,089.8 μm (range)
GoatPressure cooked breast A11380 ± 480 mg/kg 7200 ± 4500 MP particles/kg 1075.3 ± 899.1 μm 35.7–4884.0 μm (range)
GoatWashed shank A170 ± 50 mg/kg 70 ± 0 MP particles/kg 2580.1 ± 654.5 μm 1844.3–3097.4 μm (range)
MeatScraped from cutting board at end of day1220,400 ± 50,100 mg/kg 68,900 ± 12,100 MP particles/kg 1225.8 ± 1155.7 μm 24.5–6228.0 μm (range)
BeefRound cut A11620 ± 980 mg/kg 6500 ± 4400 MP particles/kg 742.0 ± 658.1 μm 14.8–5369.8 μm (range)
BeefCut on bamboo cutting board10
Chicken and turkeyBreast and escalope B44.0–18.7 MP particles/kg 0.02–0.4 mg/kg C 0.05–10.5 mg/kg D 300–450 μm × 130–250 μmMicroscopy and ATR-FTIR spectroscopyNR0.8Kedzierski et al. (2020)

N, number of samples; MP, microplastic; NR, not reported, FTIR, Fourier transform infrared, ATR, attenuated total reflectance; s.d., standard deviation.

A From butcher.
B From supermarket.
C Estimated assuming all microplastics are polystyrene with a density of 40 kg/m3.
D Estimated assuming all microplastics are polystyrene with a density of 1040 kg/m3.

Pigs

Microplastics have been identified in pork and pig offal in three studies (Table 4). van der Veen et al. (2022) sampled pork and pig blood using the same aforementioned methods as applied to beef. Several types of plastic polymers were identified in the purchased pork samples, and these were found to have a concentration range of 63–690 mg per kg (van der Veen et al. 2022). Similar to that observed when comparing beef and bovine blood samples, the concentration of microplastics were lower in pig blood than was found in their muscle tissue, the former having concentrations of 0.07–33.0 mg/kg (van der Veen et al. 2022). Li et al. (2023b) analysed 10 samples of lung tissue (0.05 g each) that had been collected from a single adult pig. The authors reported that polarised light microscopy identified a considerably lower concentration of 12,000 microplastic particles per kg of pig lung tissue than was identified using to laser direct infrared (LDIR) spectroscopy for these same samples, as the latter method identified 180,000 microplastic particles per kg of pig lung tissue (Li et al. 2023b). The size of microplastic particles detected in the lung tissue samples were found to be slightly smaller when determined using LDIR analysis at 20.3–916.4 μm compared with 115.1–1370.4 μm by polarised light microscopy (Li et al. 2023b). Microplastics detected in fetal lung tissue were fewer compared with adult tissue, and followed the same trend of being more concentrated with smaller particles in the LDIR analysis compared with microscopy (Table 4).

Using similar, but less detailed, methods, Hua et al. (2021) identified 9600 microplastic particles per kg of pig intestinal tissue and found that the majority of particles (72.4%) were <200 μm. It is noted that the two later studies used samples collected from pigs reared near a sewage sludge treatment plant, a locality where microplastic exposure is presumably high and potentially represent higher concentrations of microplastic accumulation in livestock tissue. This suggests caution when extrapolating these findings to pigs reared under different systems and exposure to environmental microplastics. This could be a contributing factor to the comparatively lower concentration of microplastic particles identified in pork loin (200 microplastic particles per kg of pork); although, for these samples, a larger filter was used and 66% of microplastic particles were excluded to correct for the blank standard (Milne et al. 2024). These findings also suggest caution when comparing microplastic data that have been quantified using different methods. No study has yet to investigate microplastics on the surface of pork and the potential contamination via processing or packaging systems.

Poultry

From the literature, only two studies were found to have investigated incidences of microplastics in chicken meat and tissue samples (Table 4). The first study examined three Xinghua pullets using standard contamination prevention steps, but there were no blank samples to permit correction to be made and the surface layer was not removed to reduce the potential post-hoc contamination of chicken meat (Table 2; Chen et al. 2023). Of the subset of polymers tested, PS, polyamine and PET were identified. Microplastic particles were detected in the liver (5.8–942.8 mg/kg), followed by leg muscle (2.9–884.7 mg/kg), jejunum (2.2–575.1 mg/kg) and breast muscle (4.0–561.6 mg/kg; Chen et al. 2023). Further analysis by LDIR showed that the majority of particles were 0–30 μm in size and only very few were 200–300 μm, which was the upper size limit detected. Milne et al. (2024) found lower microplastic concentrations in chicken breast (100 microplastic particles per kg), as compared with chicken nuggets (310 microplastic particles per kg). This was likely representative of the potential for microplastic contamination during processing. Indeed, like ruminants, microplastics adhered to the surface of poultry meat has been investigated, further highlighting meat processing as a source of microplastics in livestock and poultry meat products (Table 5). Habib et al. (2022a) analysed rinse water from whole chicken samples that were cubed by butchers using plastic cutting boards. These authors found a range of 30–1190 surface microplastic particles per kg of chicken meat, which weighed 66–290 mg/kg (Habib et al. 2022a). Particle sizes detected (74.6–178.3 μm) from rinse water were comparable to those detected from meat samples by Chen et al. (2023). Kedzierski et al. (2020) investigated the rinse water not only from supermarket poultry meat, but also from the internal surface of its PS packaging. They found fewer surface microplastics at 4.0–18.7 microplastic particles per kg, despite using a smaller filter size and not correcting for blank samples. These studies also provide a good example of variation in the reporting of microplastics as the number of particles or mass of microplastics per unit of mass – inconsistencies that often make it difficult to compare between studies and to standards.

Routes of microplastic ingestion and absorption by livestock and poultry

Oral, respiratory and dermal pathways of incursion are potential routes of microplastic absorption by livestock and poultry (Dong et al. 2023). Studies quantifying microplastic ingestion in livestock are highly valuable to establish the quantity, type and size of microplastic particles that livestock are exposed to across relevant production systems. At present, this base understanding is lacking. There is evidence for gastric ingestion from the microplastics identified in livestock digesta and excreta (Sheriff et al. 2023), but limited studies on other absorption routes and overall exposure. Information on environmentally relevant routes of microplastic exposure is needed to quantify the current and future threat of microplastics on livestock productivity and health.

Oral ingestion and digestive fragmentation

Ruminants

Presently, there has been no investigation of microplastics in rumen digesta reported in the literature, but there are reports of microplastics being detected in sheep and cattle faeces (Table 6). Beriot et al. (2021), for example, surveyed faeces collected from five sheep flocks, in one region of Spain, four of which grazed post-harvest vegetable crops where plastic mulch had been applied one or two times/year for 10 years. The authors identified 997 ± 971 microplastic particles per kg dry weight of faeces, although there was a high level of variation within the samples analysed (0–5000 microplastic particles/kg). Wu et al. (2021) collected duplicate faecal samples from three cattle farms and identified 74 ± 129 microplastic particles per kg wet weight of faeces. Beni et al. (2023) collected cattle faeces from a single cattle farm and identified 1500 ± 200 microplastic particles per kg dry weight of faeces. Sheehan et al. (2022) identified micro- and macroplastic particles, ranging in size from 2000–25,000 μm, in 43% (30/70) of cattle faecal samples collected from two herds, during routine worm egg testing. Wang et al. (2024b) surveyed manure from five sheep farms and one cattle farm, and identified 50,583 ± 24,318 microplastic particles per kg, of which 67% of the particles were 20–50 μm. Among these five studies, Wu et al. (2021), Beni et al. (2023) and Wang et al. (2024b) described microplastic contamination avoidance steps. Only Beni et al. (2023) assessed digestion recovery rate, but only on microplastics >500 μm in size. No studies have examined oral ingestion of microplastics in goats or other ruminants used in livestock production, nor have they compared production system effects.

Table 6.Summary of studies quantifying microplastics in livestock digesta and faeces.

SpeciesSample type NQuantityA Size detectedQuantification methodLimit of detectionFilter size (μm)Refs
DuckIntestinal contents2511–49 MPs/intestine50–100% were 2000–5000 μmDigestion with KOH and microscopyNRNR Susanti et al. (2021)
ChickenCrop and gizzard contents50 MPs/crop 31.8 ± 27.3 MPs/gizzardGizzard: 16.5% were <5 mmDigestion with demineralised water and microscopyNR2000 Lwanga et al. (2017)
Faeces2129,800 ± 82,300 MPs/kg100% were 100–1000 μm
ChickenCrop and gizzard contents2417.8 ± 12.1 MPs/crop 33.25 ± 17.8 MPs/gizzardCrop: 63% were 300–500 μm; 21% were 150–300 μm; 16% were 50–150 μm Gizzard: 47% were 300–500 μm; 39% were 50–150 μm; 14% were 150–300 μmDigestion with KOH and NaCl, microscopy and FTIR spectroscopy0 (n = 6 blank samples)NR Bilal et al. (2023)
ChickenIntestine and gizzard contents7Present in 5/7 intestines; 2/7 gizzardsNRDigestion with KOH and microscopyNRNR Leon et al. (2022)
ChickenFaeces10Present in 4/10 samplesNRDigestion with Fenton’s reagent, microscopy and Raman spectroscopy0 (n = 5 blank samples)1 Yan et al. (2020)
ChickenFaeces114,900 MPs/kg74% of total MPs were <50 μmDigested with KOH and H2O2, microscopy and LDIR spectroscopyNR10 Yu et al. (2023)
ChickenFaeces8667 ± 990 MPs/kg wet weightNRDigestion with H2O2, 10% FeSO4, NaOH & saturated NaI, microscopy and FTIR spectroscopyNR0.22 Wu et al. (2021)
PigFaeces8900 ± 1290 MPs/kg wet weight
CattleFaeces374 ± 129 MPs/kg wet weight
PigFaecesNR1250 ± 640 MPs/kg dry weightNRDigested with saturated NaCl and Nal and H2O2, microscopy and ATR-FTIR (MPs 2–5 mm) or μFTIR (MPs <2 mm)NR (n = 2 blank samples)20 Yang et al. (2021)
PigFaeces360 MPs/kgNADigested with H2O2, microscopy and FTIRNRNR Mazzoleni et al. (2023)
PigFaecesNR112,000 MPs/kgNRDigested with H2O2, microscopy and LDIRNR10 Hua et al. (2021)
CattleFaecesNR1500 ± 200 MPs/kg dry weightNRDigested with Iron Fe(II) and H2O2, microscopy and ATR-FTIRNR12 Beni et al. (2023)
CattleFaeces7030/70 faecal samplesNRDissolved in sugar faecal flotation medium and microscopyNRNR Sheehan et al. (2022)
SheepFaeces68997 ± 971 MPs/kg dry weightNRDigested with distilled water and microscopy0 (n = 6 blank samplesNR Beriot et al. (2021)
Sheep and cattleExcreta and bedding850,583 ± 24,318 MPs/kg67% were 20–50 μm, 29% were 50–100 μm, 4% were 100–500 μmDigested with HNO3 and LDIR spectroscopyNR0.45 Wang et al. (2024b)

N, number of samples; MP, microplastic; NR, not reported; KOH, potassium hydroxide; H2O2, hydrogen peroxide; NaCl, sodium chloride; FTIR, Fourier transform infrared; ATR, attenuated total reflectance; LDIR, laser direct infrared; HNO3, nitric acid; Nal, sodium iodine; NaOH, sodium hydroxide; FeSO4, iron(II) sulfate.

A Mean ± standard deviation unless specified otherwise.

Ingested plastic and microplastics may be degraded and fragmented within the ruminant digestive system, thereby creating a greater number of smaller macro- and microparticles. This was suggested by Sheehan et al. (2022), who placed 2-cm long (20,000 μm) nylon bailing rope fibres and polyethylene hay wrap films in the rumen of a single cannulated bull. After 54 days, the weight of the plastic did not diminish, but fraying of plastic fibres significantly increased and the length of plastics fibres significantly decreased (Sheehan et al. 2022). Digestive fragmentation in ruminants was also supported by an in vitro study that incubated PET with fresh rumen liquor at 40°C for up to 72 h (Quartinello et al. 2021). Rumen fluid did degrade PET to some extent, as evidenced by increased esterase activity, the formation of hydrolysis products and the detection of surface erosion (Quartinello et al. 2021), although its degradation was less intense compared with biodegradable polyesters: polybutylene adipate terephthalate and polyethylene furanoate. Likewise, Galyon et al. (2023) found that biodegradable polymers (polyhydroxyalkanoates and poly(butylene succinate-co-adipate)) fragmented after 1 day of incubation within the rumen of dry, cannulated, Holstein dairy cows and significantly degraded within 60 days of incubation. These same authors reported that low-density PE did not degrade after 150 days of incubation within the rumens of these same Holstein cows (Galyon et al. 2023); meaning that the type or blend of plastics ingested affect the presence and passage of microplastics from the ruminoreticulum.

Pigs

To date, no study has investigated microplastics in pig digesta, but four have investigated the microplastic content of pig faeces. Mazzoleni et al. (2023) analysed rectally collected faecal samples from pigs that were fed diets that contained or excluded former human food products (confectionary and baked goods). No microplastics were detected in faeces in either group, but the study used a comparatively long sample digestion duration of 1 week that may have destroyed plastic particles. Although the study did pretest the digestion procedure and reported no change in the colour or shape of spiked PP, it did not report recovery rate, and only assessed three samples and one polymer type (Mazzoleni et al. 2023). Wu et al. (2021) collected duplicate faecal samples from eight different pig farms and identified 900 ± 1290 microplastic particles per kg wet weight of faeces. Yang et al. (2021) collected pig manure from one farm and identified a higher concentration at 1250 microplastic particles per kg dry weight of faeces and used polyamine (PA) plastic filters, which may have introduced contamination. Hua et al. (2021) collected rectal faeces from an unreported number of pigs and farms, and reported a 100-fold higher concentration of microplastic particles at 112,000 per kg. Of the four studies, all reported standard contamination avoidance steps, and only one evaluated their sample digestion recovery rate, which was between 81.7 and 100% for PA, PP, PS, PE, PVC, expandable PS, PA fibre and PE film (Yang et al. 2021). No studies have investigated digestive fragmentation of microplastics in pigs.

Poultry

The incidence of microplastics in poultry digesta and excreta have been reported in the literature. Lwanga et al. (2017) were the first to publish, but excluded microplastics <2000 μm and did not specify the number of farms from which samples were collected. Although the crop was examined, only particles >5000 μm were detected (Lwanga et al. 2017). An average of 32 microplastic particles per gizzard were also detected, 84% of these particles exceeded the technical definition for microplastics, as they were >5000 μm in diameter – albeit the grinding action of the gizzard may have contributed to a reduction in size for some of the microplastic particles (Lwanga et al. 2017). Similar quantities were detected by an investigation by Bilal et al. (2023) of eight chicken farms, with 33 microplastic particles per gizzard and 18 microplastic particles per crop found, on average. Leon et al. (2022) identified microplastics in the contents of 5/7 intestines and 2/7 gizzards purchased at random from seven different wet markets. The relationship between the intestine and gizzards purchased is unclear, meaning that a within bird comparison is not possible. Susanti et al. (2021) detected microplastics in the intestinal contents of 25 ducks sourced from five different regions of Indonesia and reported there to be between 11 and 49 microplastic particles per intestine, but an overall mean was not reported.

Lwanga et al. (2017) identified microplastics in two chicken excreta samples at a high concentration of 129,800 microplastic particles per kg. Wu et al. (2021) collected duplicate faecal samples from eight chicken farms and identified a much lower concentration of 667 microplastic particles per kg wet weight, despite using a much smaller filter size (0.22 μm) than Lwanga et al. (2017). Yan et al. (2020) identified microplastics in 4/10 chicken excreta sampled from an unreported number of farms. Based on only a single excreta sample, Yu et al. (2023) identified 14,900 microplastic particles per kg excreta. All studies mentioned here reported some form of standard microplastic contamination avoidance steps but only one study reported the digestion recovery rate which were high, exceeding 97% for PE, PS, and PVC (Yan et al. 2020). The general absence of information about farming system, diet, breed, etc., does make it difficult to generalise these outcomes to other poultry species. They do, however, confirm that microplastics may be found in poultry digesta and excreta.

No studies have directly studied digestive fragmentation of microplastics in poultry. However, microplastic levels detected in the chicken gizzard were smaller than those identified in the crop (Bilal et al. 2023) potentially due to muscular grinding in the gizzard. Also, microplastics detected in chicken excreta were smaller than those identified in the gizzard (Lwanga et al. 2022) which might suggest further digestive degradation. This merits additional investigation.

Dermal and respiratory absorption

No research has yet investigated dermal absorption of microplastics by livestock and one study has investigated microplastics in livestock lung tissue (Table 4). Li et al. (2023b) identified microplastics in both adult and foetal lung tissue in pigs. The detection in the latter sample suggests that microplastics can accumulate in lungs without inhalation and that the presence of microplastics in the lung is not an exclusive indicator of a respiratory pathway of incursion. Dong et al. (2023) suggests that livestock fleece and hair is a repellent against microplastics and could therefore offer some resistance to dermal incursion.

Sources of microplastic exposure for livestock and poultry

Livestock and poultry may ingest microplastic particles from different environmental sources, including feed, soil, water, and air – the latter is also a potential pathway for exposure to microplastic particles via inhalation and transfer across mucus membranes. Post-mortem sources of microplastics may further contribute to the contamination of livestock and poultry products, for example, the plastic equipment used at slaughter and processing and the plastic used during the packaging and storage of meat products. The source and extent of exposure could influence the type, size, and amount of microplastic particles detected in livestock and poultry products. Studies that investigate sources of microplastics contamination are highly valuable because they are necessary to establish the actual levels of microplastics that livestock are exposed to. Determining the accurate exposure levels is essential to conducting experiments to assess the effects of realistic microplastic exposure levels on health, productivity, and consumer safety.

Feed and feedstuff

It is likely that feeds and feedstuff are the primary route by which livestock and poultry are exposed to microplastics. Few studies have investigated microplastic concentrations in livestock feed (Table 7). From analysis of duplicate samples collected from each of 19 farms, Wu et al. (2021) identified microplastics in cattle feed at 36 ± 63 microplastic particles per kg, in pig feed at 139 ± 115 microplastic particles per kg, and in chicken feed at 96 ± 109 microplastic particles per kg. PE was the main plastic polymer detected which was the same polymer identified in the inner layer of plastic used to package the feed (Wu et al. 2021). Xu et al. (2022) sampled 15 farms, from one region of China, and assessed the presence of only two plastic polymers in pig feed. PET was identified in 44/45 samples at a median concentration of 0.15 mg/kg dry weight; while polycarbonate (PC) was identified in 4/45 samples at a concentration of 0.006–0.09 mg/kg dry weight (Xu et al. 2022). Xu et al. (2022) estimated intake of PET as 0.80–7.79 μg/kg body weight/day based on an estimated feed intake of pigs. van der Veen et al. (2022) also assessed the presence of a discrete selection of polymer types (n = 6) and identified a higher concentration of 39–2600 mg/kg in supermarket products which consisted of PE, PS, and PVC. No microplastics were identified in fresh roughage (van der Veen et al. 2022). Sheehan et al. (2022) qualitatively identified PE treated with phthalate in commercial mineral mixes but did not quantify the amount or the number of samples tested, or describe steps to avoid microplastic contamination. Sheehan et al. (2022) also suggested that plastic microfibres may take months to move through the digestive system, as six bulls had similar microplastic faecal prevalence (50%) despite being taken off mineral supplements 5 weeks prior to sampling. Finally, Jeyasanta et al. (2024) sampled commercial animal feed samples in triplicate, from two regions of India, which included eight poultry feed samples and 12 shrimp and fish feed samples. While the study did not provide an average for poultry feed, overall concentration ranged from 90 to 330 microplastics per kg with PE being the dominant polymer type (33.7%) and 100–500 μm being the dominant particle size detected. Scanning electron microscopy showed surface cracks, brittleness, ridges, grooves, and a rough and uneven surface indicative of weathering. Of the five studies, Jeyasanta et al. (2024) was the only to report the size of the particles detected and to evaluate their sample digestion recovery rate, which was 90% for 500 μm PS, PE, and PET. Neither Wu et al. (2021) nor Jeyasanta et al. (2024) reported the proportion of microplastics from microscopy that underwent verification by Fourier transform infrared (FTIR) spectroscopy or the error rate of microscopy based on the number of microplastic identified by microscopy that did not subsequently classify as microplastics by FTIR spectroscopy.

Table 7.Summary of studies quantifying microplastics in livestock feed and foodstuff.

SpeciesSample typeNQuantity ASize detectedQuantification methodLimit of detectionFilter size (μm)Refs
ChickenFeed896 ± 109 MPs/kg wet weightNRDigested with saturated NaCl, microscopy and FTIR spectroscopyNR0.22Wu et al. (2021)
PigFeed8129 ± 115 MPs/kg wet weight
CattleFeed336 ± 63 MPs/kg wet weight
PigFeed45PET: 44/45 samples at a median value of 0.15 mg/kg dry weight PC: 4/45 samples at a range of 0.006–0.09 mg/kg dry weightNRGCMSNR0.22Xu et al. (2022)
Poultry, shrimp and fishFeed2090 ± 25.11 to 330 ± 36.12 MPs/kg10–91% were 100–500 μm, 6–33% were 500–1000 μm, 1–35% were 1000–3000 μm and 0–42% were 3000–5000 μmDigested with KOH:NaClO, microscopy and ATR- FTIR spectroscopy0 (n = NR)8Jeyasanta et al. (2024)
NRFresh feed roughage50NRPyGCMSPET: 0.53 μg (n = 7 blank samples) 700 nm sizeNAvan der Veen et al. (2022)
Shredded supermarket feed12PVC: 339–>2600 mg/kg) PE: 223‒>2400 mg/kg) PS:39–740 mg/kg PMMA, PP, PET: 0NRPET: 0.63 μg (n = 7 blank samples) 700 nm size
NRCommercial mineral mixNRPresentNRDissolved in deionised water, microscopy and FTIR spectroscopyNRNRSheehan et al. (2022)

N, number of samples; MP, microplastic; NR: not reported; NA, not applicable; FTIR, Fourier transform infrared; GCMS, gas chromatography mass spectroscopy; PyGCMS, pyrolysis gas chromatography mass spectroscopy; KOH, potassium hydroxide; NaCl, sodium chloride; ATR, attenuated total reflectance; NaClO, sodium hypochlorite; PS, polystyrene; PET, polyethylene terephthalate; PE, polyethylene; PMMA, poly methyl methacrylate; PP, polypropylene; PVC, polyvinyl chloride.

A Mean ± standard deviation unless specified otherwise.

Soil

Soil often contains microplastics and is therefore a major source by which livestock may be exposed. This is because livestock consume soil, with McConnachie et al. (2024) estimating that cattle consume 0.2–1.22 kg of soil per day. Microplastics from the application of treated sewage sludge (biosolids), compost, livestock manure, wastewater, and irrigation are accumulated in soils ‒ these each have the potential to contain high levels of microplastics (Yang et al. 2021; Ziajahromi et al. 2024). Other potential sources are the result of macroplastic deterioration, such as from plastic mulching film, silage film, bailing twine, plastic coated slow-release fertilisers and pesticides, plastic pipes, atmospheric deposition, and mismanaged farm, municipal and commercial waste (Kumar et al. 2020; Lwanga et al. 2022).

Several studies were found to have investigated microplastics concentrations in soil inhabited by livestock (Table 8). Piehl et al. (2018) identified 0.34 microplastic particles per kg dry weight of soil but the analysis had low sensitivity as a 1 mm filter was used. The main plastic identified was PE (63%) which is the main polymer in plastic films and may have been ingested by livestock and subsequently delivered to soil as manure (Piehl et al. 2018). The study site had not used fertilisers containing plastic in the last 5 years (Piehl et al. 2018). Lwanga et al. (2017) identified a much higher concentration of 870 microplastic particles per kg soil from 10 home gardens but also had low sensitivity from using a large filter (2 mm) and it was not specified if concentration was on a wet or dry weight basis. A study of Spanish soils identified an even higher microplastic concentration in soils that were mulched with PE plastic 1–2 times per year for 10 years (Beriot et al. 2021). Specifically, soil from six vegetable fields were found to contain 2116 microplastic particles per kg dry weight; although filter size and contamination avoidance steps were not mentioned (Beriot et al. 2021). Yang et al. (2021) collected duplicate soil samples from fields that had been fertilised with 1.7 tonnes/ha of pig manure for the preceding 22 years and identified a much lower concentration of 43.8 microplastics/kg despite using a finer filter (Yang et al. 2021). Unlike the previous studies, Yang et al. (2021) used chemical reagents instead of water to homogenise soil samples, which potentially destroyed 0–18.3% of PA, PP, PS, PE, PVC, expandable PS, PA fibre, PE film based on their digestion recovery test. Yu et al. (2023) also used chemical reagents and a fine filter to isolate microplastics from soil and identified a much higher concentration of 7900 microplastic particles per kg of soil samples from chicken farms from a single village in China. Finally, Wang et al. (2024b) collected soil from five sheep and two cattle farms and also identified a high microplastic concentration of 3056 ± 1746 microplastic particles per kg soil, the majority of which was PE (20.7%). These latter three studies did not specify if concentration was in wet or dry weight.

Table 8.Summary of studies quantifying microplastics in soil and water from livestock production.

SpeciesSample typeNQuantity ASize detectedQuantification methodLimit of detectionFilter size (μm)Refs
Fertilised with pig and cattle manureTop 5 cm of soil140.34 MPs/kg dry weightNRHomogenised in deionised water, microscopy and FTIR spectroscopy0 (n = 1 blank sample)1000Piehl et al. (2018)
Grazed by sheepTop 10 cm of soil182116 ± 1024 MPs/kg dry weightNRDigested with distilled water, microscopy0 (n = 6 blank samplesNRBeriot et al. (2021)
Foraged by chickensTop 10 cm of soil50870 ± 1900 MPs/kg59% were 10–20 μm, 34% were 20–50 μm, 4.8% were >50 μmDigestion with demineralised water, microscopyNR2000Lwanga et al. (2017)
Top 10–20 cm of soil50
Fertilised with pig manureTop of 20 cm1043.8 ± 16.2 MPs/kg39.1% were 1–3 mm, 34.8% were <0.5 mm, 19.6% were 0.5–1 mm, 6.5% were 3–5 mmDigested with saturated NaCl, Nal and H2O2, microscopy and ATR-FTIR (MPs 2–5 mm) or μFTIR (MPs <2 mm)NR (n = 2 blank samples)20Yang et al. (2021)
Sheep and cattle farmsTop 10 cm of soil123056 ± 1746 MPs/kg56% were 20–50 μm, 32% were 50–100 μm, 8% were 100–500 μmHomogenised with saturated NaCl, LDIR spectroscopyNR0.45Wang et al. (2024b)
Chicken farmSoil57900 MPs/kg74% of total MPs were <50 μmDigested with KOH and H2O2, microscopy and LDIR spectroscopyNR10Yu et al. (2023)
Drinking water62500 MPs/kg0.22
Livestock farmWastewater48–40 MPs/LNRDigested with H2O2 and FeSO4, microscopy and μ-Raman spectroscopy0 (n = 3 blank samples)13Wang et al. (2020)

N, number of samples; MP, microplastic; NR, not reported; FTIR, Fourier transform infrared; ATR, attenuated total reflectance; LDIR, laser direct infrared; NaCl, sodium chloride; Nal, sodium; H2O2, hydrogen peroxide; KOH, potassium hydroxide; FeSO4, iron(II) sulfate.

A Mean ± standard deviation unless specified otherwise.

Water, atmosphere, and other sources of microplastics

Livestock and poultry are routinely exposed to drinking water, air, and the plastic materials and equipment used on farms; all potential sources of microplastics. These are also possible sources of microplastics contamination of meat products during processing and handling at an abattoir or retail outlet. There has, however, been minimal investigation of these potential sources within the context of livestock and meat production. Water may become contaminated with microplastics leaching into the water from soil or from plastic water delivery systems (Dong et al. 2023). Only one study has investigated microplastics in livestock drinking water, another study investigated livestock wastewater, and no studies have investigated airborne microplastics as a pathway by which livestock are exposed (Table 8). Exposure by the respiratory route merits consideration given the reported incidences of microplastics in pig lung tissue (Li et al. 2023b) and the potential for exposure route to affect accumulation – as some compounds have been reported to accumulate more readily in the meat when inhaled rather than ingested (Maggiolino et al. 2022). Yu et al. (2023) investigated 500 mL samples of poultry drinking water, which were collected from a single village, and found 2500 microplastic particles per kg. It was unclear why the concentration was reported per water mass rather than volume. Using a larger filter size, Wang et al. (2020) analysed wastewater from several livestock farms from a highly industrialised location in China and found 8–40 microplastic particles per L, but did not report variance or particle size. Wang et al. (2020) did validate their method by testing ultra-pure water spiked with <400 μm PE and <600 μm PVC and found recovery rates of 80–100%. While wastewater is not directly consumed by livestock, it can be used to irrigate soil which could re-contaminate livestock. Furthermore, Wu et al. (2021) analysed common plastic farm equipment and identified that water delivery systems were made from PP, manure scrapers were made from PE, pipes were made from PVC, and outer and inner layers of feedbags were made of PP and PE, respectively.

Potential sources of microplastics at meat processing include plastic cutting boards, plastic gloves, plastic aprons and arm covers, plastic meat packaging, and plastic from synthetic clothing and hair nets. Only plastic cutting boards have been assessed and were identified as a source of PE microplastic contamination of meat (Habib et al. 2022b) based on consistent polymers in cutting boards and meat samples, although sample size was small (n = 7).

Opportunities and recommendations

Microplastics are present in livestock and poultry and pose a threat to animal welfare, productivity, and consumer perception of meat. This review confirmed this observation and has highlighted gaps in current knowledge that must be addressed to understand microplastic effects on livestock and poultry industries. This will only be achieved and opportunities for risk mitigation delineated when the following areas are elucidated:

  • The effects of microplastics on livestock and poultry have been determined using controlled exposure studies and only effects on tissue structure, oxidative status, inflammation, and apoptosis have been investigated. There remains a missing link between these local effects and gross pathological consequences such as the onset of disease or productivity loss. Furthermore, the limited investigation on the effects on muscle, including the rate at which microplastics accumulate in muscle, excludes the application of these research findings from the consumer experience and microplastic pathways into the human food chain. The only productivity indicator investigated was liveweight change and these results were inconclusive. Further research is needed to determine if these local effects have consequences on the economic bottom-line of livestock production as well as animal welfare. Understanding these broader effects is needed by industry to launch a proportional response to this emerging threat.

  • The concentrations, types, and particle sizes of microplastics investigated in controlled exposure studies are inconsistent to those that livestock are likely to be exposed to in real-world environments or production systems. Bucci et al. (2020) systematically reviewed 139 papers and found that only 17% of laboratory studies used environmentally relevant concentrations of microplastics and that 80% used environmentally relevant particle sizes. The effect of microplastic exposure is dependent on polymer type, shape, particle size, concentration, duration of exposure, and animal species (Bucci et al. 2020). All of these variables need to be considered when attempting to replicate natural exposure (Lenz et al. 2016). The existing research has largely focussed on virgin 5 μm particles of PS and has not investigated environmentally aged microplastics which livestock are more likely to be exposed to. Furthermore, there is no standard for the descriptors used for the different forms of microplastics analysed. This means that the studies have provided limited justification for their chosen experimental concentrations making their relevance to real-world production systems unknown.

  • While several preliminary studies have established that feed, soil, and water are sources of microplastic exposure in livestock, it remains unclear as to the total quantity and type of microplastics that livestock and poultry are exposed to and how much of these are ingested. This information is needed to inform the experimental concentrations used in controlled studies aiming to establish the impact of environmentally relevant microplastic exposure on health, productivity, and product safety outcomes. The inability to establish exposure is due to several factors in study design. Firstly, studies quantifying microplastic concentrations in the livestock environment or in livestock digesta and faeces, mostly use qualitive methods (microscopy and spectroscopy) and to a lesser frequency quantitative methods (gas chromatography). Qualitative methods result in concentration being reported in number of particles/kg while quantitative methods record concentration in mg/kg. In controlled studies, experimental concentrations are usually defined as mg/kg or mg/L. Number of particles/kg could be converted to mg/kg if particle radius and density are reported (Leusch and Ziajahromi 2021), but this is information is rarely provided. The comparability of studies is further diminished through the use of a range of filter sizes (0.22–2000 μm or not reported) which affects the minimum limit of detection; the use of a variety of different chemical reagents to separate organic matter from microplastics which affects the proportion of microplastics destroyed (recovery rate); the reporting of concentration in either wet or dry weight, feed, soil and water intake is not recorded; and limited production systems have been surveyed.

  • Studies have inconsistently employed and described validation method and quality control, which at a minimum should include a digestion recovery test and calculation of limit of detection. Digestion recovery tests assess whether and to what extent a range of relevant microplastics polymers and sizes are destroyed by the digestion method being used to extract microplastics. Limit of detection is determined based on the concentrations of microplastics detected in blank samples. Another issue with current experimental methods is an inadequate description of how particles were classified as microplastics from microscopy, given the difficulty in distinguishing synthetic fibres from natural fibres. Several studies verify microscopy against spectroscopy but may only verify a subset of particles. These studies should report the proportion of particles identified by microscopy that are subsequently verified by spectroscopy and the proportion of particles that fail to be classified as microplastics based on spectroscopy to help quantify the error rate of microscopy. Hence, there is a pressing need to optimise and standardise microplastic detection methods in order to accurately estimate the quantity of microplastics that livestock and poultry are exposed to.

  • The utility of findings on microplastic concentrations in the livestock environment or in livestock digesta and faeces could be greatly enhanced if collected and analysed with data on animal performance, health outcomes, meat quality and yield, and production system and management inputs. This could reveal impacts on productivity, health, profitability, and potential sources of microplastics in the supply chain. No study has been carried out so far. This will be particularly useful because controlled studies are restricted to using few polymer types and sizes while prevalence studies contain data on the full range of naturally aged microplastics that livestock are exposed to.

  • There are no current guidelines on microplastics in livestock or poultry meat or meat-based products. However, the limit imposed by The European Commission (2011) Regulation No. 10/2011 on the release of plastics from food packaging into food of 60 mg/kg could be considered as a guide for potential future regulation. The range of microplastics detected in beef, pork, and chicken (van der Veen et al. 2022; Chen et al. 2023) exceed these limits and highlight the emerging threat of microplastics to future market compliance and consumer safety. However, the robustness of research into the presence of microplastics in meat was inconsistent for similar reasons as described for microplastics concentrations in livestock environments, digesta and faeces. This is because not all studies had been peer-reviewed, small sample sizes were used (1–15 samples), limited range of production systems were investigated, inconsistent reporting of microplastic size detected, inconsistent contamination prevention steps taken, particularly removal of the outer layer of meat samples and the inclusion of procedural blank samples, there was inconsistent reporting of the results of blank samples and limits of detection, there were inconsistent quantification methods used with major variation in sensitivity, scope and units, there was inconsistent reporting recovery rate, and there was inconsistent reporting of mass used per sample. The main implications of these shortfalls are overestimation of microplastics from contamination with atmospheric microplastics and microplastics adhered to the surface of meat samples. This obscures whether detected microplastics originate from microplastics translocating to tissue, or from microplastics contamination at processing, and therefore, the pathway for mitigation. These shortfalls may also have resulted in an underestimation of microplastics because of microplastic destruction during sample digestion, low sensitivity (occurs when microscopy is used), exclusion of microplastics smaller than the variable filter sizes used, and exclusion of a full range of polymers [can occur when pyrolysis gas chromatography mass spectrometry (PyGCMS) is used]. Therefore, we have reached the conclusion that there is a pressing need to optimise and standardise microplastic detection methods in meat.

  • Many of the studies failed to specify the particle sizes of microplastics that translocated to or were identified in the tissue of livestock and poultry. Several reviews state that ingested microplastics greater than 150 μm (0.15 mm) are excreted in urine and faeces while only microplastics less than 150 μm can penetrate the gastrointestinal barrier (The European Commission 2011; Hirt and Body-Malapel 2020; Dong et al. 2023). Based on this assertion, the larger size range of microplastics detected in pig lung tissue (Li et al. 2023b) and chicken breast (Chen et al. 2023) represent surface contamination and not tissue accumulation through ingested microplastics. However, these size assertions are based on the maximum inert microparticle size that can penetrate the gastrointestinal barrier, and then is based on selected studies rather than an exhaustive search of literature and does not provide microplastics or livestock specific assertions (Hussain et al. 2001). Therefore, we propose that the size of microplastic particle that can penetrate the gut remains uncertain and studies should report the microplastic size detected to resolve this knowledge gap.

  • Further study on digestive fragmentation is warranted given the limited information on ruminants and absence in pigs and poultry. Monogastric digestion is speculated to have minor degrading effect on microplastics (Dong et al. 2023). This was supported by an in vitro digestion study which incubated microplastics with human saliva and gastric juices for 4 h and found no degrading effects on microplastic particles of PE, PET, PVC, PP and PS (Stock et al. 2020). However, in poultry, microplastic concentrations in intestines (667–129,800/kg), were much higher than concentrations detected in excreta (0–49/animal) and particle size was also smaller in faeces than digesta (Table 6). This could reflect digestive fragmentation of microplastics taking place following muscular grinding in the avian gizzard and warrants further investigation. Digestion fragmentation may be more pronounced in ruminants due to biodegradation from rumen microbes (Dong et al. 2023) but evidence is needed to confirm this, including a comparative analysis to the effects of the hindgut microbiome of ruminants and monogastrics.

  • Both microplastic prevalence studies and controlled experimental studies have failed to report sample size calculations. While the number of sample sizes used to quantify microplastics in excreta and faeces (n = 2–70) were larger than those used for meat studies (n = 1–15), they are low for prevalence studies. This partially explains the high variation observed in the concentration of microplastics in pig and cattle faeces (0–112,000 and 74–1500 microplastics/kg, respectively). For controlled experimental studies, it is unclear whether there was adequate statistical power to detect significant effects. To assist sample size calculations, studies need to report variance, effect sizes, and intraclass correlation where possible.

Conclusions

Microplastics indeed have effects on ruminant, pig, and poultry health but there is limited evidence of gross effects on disease and productivity outcomes from the mostly short-term, controlled experiments undertaken. Additionally, past experiments exposed livestock to new (virgin), single polymers at presumably exaggerated concentrations which are unlikely to reflect the variety of aged microplastics that livestock are exposed to in real-world or commercial production systems. Microplastics are detected in meat and edible tissues from livestock and poultry, and some research has shown that microplastic content impacts on meat quality and the oxidative status of tissue. However, without a comprehensive guideline or standard their commercial implications are unclear – albeit consumer preferences is likely to be severely impacted by heightened concentrations of microplastics in livestock and poultry meat products.

Conflicts of interest

The authors declare that they have no conflicts of interest.

Declaration of funding

This study was funded by the NSW Department of Primary Industries and Regional Development.

Acknowledgements

The authors acknowledge the support of their colleagues at the NSW Department of Primary Industries and Regional Development.

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