Birds as bioindicators of plastic pollution in terrestrial and freshwater environments: A 30-year review.

Plastic pollution is a global concern that has grown ever more acute in recent years. Most research has focused on the impact of plastic pollution in marine environments. However, plastic is increasingly being detected in terrestrial and freshwater environments with key inland sources including landfills, where it is accessible to a wide range of organisms. Birds are effective bioindicators of pollutants for many reasons, including their high mobility and high intra- and interspecific variation in trophic levels. Freshwater and terrestrial bird species are under-represented in plastic pollution research compared to marine species. We reviewed 106 studies (spanning from 1994 onwards) that have detected plastics in bird species dwelling in freshwater and/or terrestrial habitats, identifying knowledge gaps. Seventy-two studies focused solely on macroplastics (fragments >5 mm), compared to 22 microplastic (fragments <5 mm) studies. A further 12 studies identified plastics as both microplastics and macroplastics. No study investigated nanoplastic (particles <100 nm) exposure. Research to date has geographical and species' biases while ignoring nanoplastic sequestration in free-living freshwater, terrestrial and marine bird species. Building on the baseline search presented here, we urge researchers to develop and validate standardised field sampling techniques and laboratory analytical protocols such as Raman spectroscopy to allow for the quantification and identification of micro- and nanoplastics in terrestrial and freshwater environments and the species therein. Future studies should consistently report the internalised and background concentrations, types, sizes and forms of plastics. This will enable a better understanding of the sources of plastic pollution and their routes of exposure to birds of terrestrial and freshwater environments, providing a more comprehensive insight into the potential impacts on birds.

Sulfate homeostasis. I. Effect of salicylic acid and its metabolites on inorganic sulfate in rats.

Homeostasis of inorganic sulfate, a physiologic anion necessary for both detoxification and biosynthetic reactions, involves predominantly capacity-limited renal clearance mechanisms. The objective of this investigation was to examine the effect of salicylic acid (SA) and its major metabolites, salicyluric acid and salicyl phenolic glucuronide, on the serum concentrations and renal clearance of inorganic sulfate in rats. Animals were studied using a crossover design in which they received a bolus i.v. injection (75 mg/kg) and infusion (approximately 0.26 mg/min/kg) of SA or the same volume of saline (the vehicle). Blood samples were collected at 2, 3 and 4 hr after administration and urine between 2 and 4 hr. The renal clearance of sulfate and creatinine were examined at mean steady-state SA serum concentrations of 249 micrograms/ml. Although no changes in the serum concentrations and renal clearance of creatinine were observed, the renal clearance of inorganic sulfate was increased significantly (2.13 +/- 0.74 vs. 1.09 +/- 0.54 ml/min/kg in controls, mean +/- S.D., n = 7) and its serum concentration decreased (0.55 +/- 0.12 vs. 1.04 +/- 0.23 mM in controls). These changes were not due to alterations in uric acid concentrations as uric acid serum concentrations and renal clearance were unchanged when examined at similar steady-state SA serum concentrations in a subsequent study. The effects on sulfate disposition also were probably not due to the major metabolites of SA: no changes in the serum concentrations or renal clearance of sulfate were observed at mean steady-state concentrations of 52 micrograms/ml of salicyluric acid or 73.7 micrograms/ml of salicyl phenolic glucuronide after their direct administration.(ABSTRACT TRUNCATED AT 250 WORDS)

Disopyramide pharmacokinetics and metabolism: effect of inducers.

1. The disposition of orally administered disopyramide was studied in a population of smokers (n = 6) and non-smokers (n = 8) before and during phenobarbitone treatment (100 mg daily for 21 days; Cp 21st day = 13.9 +/- 2.0 micrograms ml-1). The comparative inducibility of these populations by phenobarbitone was assessed as was the inductive effect of cigarette smoking, per se. Furthermore, the determinants of the intensity of the inductive effect were examined, as well as the effect of the barbiturate on the binding of disopyramide to alpha 1-acid glycoprotein (AGP). 2. Smokers and non-smokers exhibited similar half-lives (6.48 +/- 1.49 vs 6.66 +/- 1.02 h), apparent total body clearances (0.100 +/- 0.020 vs 0.117 +/- 0.034 l h-1 kg-1), mean renal clearances (0.043 +/- 0.0093 vs 0.057 +/- 0.013 l h-1 kg-1) and apparent intrinsic metabolic clearances (0.057 +/- 0.015 vs 0.060 +/- 0.024 l h-1 kg-1) before phenobarbitone treatment. 3. Both populations responded comparably to barbiturate exposure in that apparent intrinsic metabolic clearance more than doubled. Interestingly, the magnitude of this increase was highly dependent on the observed baseline apparent intrinsic metabolic clearance, (r' = 0.81; P less than 0.001). 4. Phenobarbitone treatment of non-smokers resulted in an increase in the AUC of the active metabolite N-despropyl disopyramide (MND), but not significantly (3.8 +/- 1.6 vs 4.1 +/- 2.3 micrograms ml-1 h). Similar results were observed in smokers (3.5 +/- 1.4 vs 3.9 +/- 2.0 micrograms ml-1 h, respectively). 5. The percent of administered dose recovered in urine as disopyramide in non-smokers was significantly decreased upon phenobarbitone treatment (43 +/- 6% vs 25 +/- 5%), whereas the percent of dose recovered as MND increased significantly in this group (25 +/- 6% vs 31 +/- 5%). The population of smokers responded similarly. 6. At doses typically used to achieve hepatic microsomal enzyme induction in man, phenobarbitone treatment caused no significant change or trend towards a change in serum AGP concentrations as measured using the radial immunodiffusion method in nonsmokers (67.4 +/- 19.9 mg dl-1 vs 68.0 +/- 40.7 mg dl-1) or smokers (64.5 +/- 15.7 vs 67.9 +/- 14.9). Similarly, when AGP concentration was estimated in serum from non-smokers using a nephelometric method no effect attributable to phenobarbitone was observed (47.9 +/- 1.3 vs 47.9 +/- 16.8 mg dl-1). Consistent with this observation, disopyramide free fraction was not affected by barbiturate treatment.