Department of Chemical Engineering, University of Science and Technology of Mazandaran, Behshahr, Iran
Abstract: (42 Views)
The discovery of plastic debris in the marine environment half a century ago has evolved into one of the globally most growing environmental pollution concerns of our time. There is an increasing awareness of not only environmental but also human health risks associated to microplastics and nanoplastics (MNPs) exposures, with MNP being identified in human tissues, including blood, placenta, brain, and thrombi. However, critical knowledge gaps currently limit the ability to reliably assess human health impacts caused by MNP uptake, including lacking understanding of: (i) the range of truly environmentally realistic concentrations of MNP in different environmental compartments; (ii) environmental, societal, behavioral impacts on often highly variable individual exposures at acute and chronic levels; (iii) major uptake mechanisms of MNPs and associated chemicals of concern through respiratory, digestive or dermatological routes; and resulting from this (iv) the realistic range of MNP and associated chemicals in specific organ systems.
Inferences of human health risks can therefore not reliably be made purely based on knowledge of the environmental presence of MNP. Humans are exposed to MNP in indoor and outdoor, domestic and occupational environments with the risk of inhalation and ingestion of particles through food, water, and air. A recent synthesis argues that uptake and internalization of MNP resulting from these exposures may amplify chronic inflammatory disease, potentially exacerbating the global burden of non-communicable diseases6. However, key elements of the exposure-uptake-impact causation chain are often missing, resulting in highly fragmented knowledge and limiting global ability to link MNP exposures to human health outcomes. Close interaction between environmental exposure science and human health research and (eco)toxicology will be required to determine at what exposure dose, by which uptake route, and through which mechanisms MNPs become clinically relevant, and how this health relevance varies for different populations
In cardiovascular research for instance, MNPs have been detected in carotid plaques and thrombi, and their presence has been associated with subsequent cardiovascular events and disease severity.5˒7 These are important findings of course that suggest that MNPs may participate in disease processes; but they do not establish whether MNPs could have caused the disease or merely accompanied it or, in fact, MNP have been trapped particularly because the progress of cardiovascular disease. Such distinctions are of direct clinical and public health relevance of course as they determine actions such as initiation of interventions such as wider monitoring or broader regulatory action. Experimental models provide additional capacity to strengthen the case for biological plausibility.
MNP exposure has been linked to the induction of oxidative stress, mitochondrial dysfunction, inflammation, and barrier disruption.⁸˒⁹ Yet these effects have often been observed at doses that are difficult to compare with real world human exposure, in particular since the range of environmentally realistic acute and chronic exposures are largely unknown, especially with regards to smallest microplastic fractions and nanoplastics. Similar observational evidence can therefore be interpreted to provide mechanistic understanding and support the creation of conceptual models.
In addition, most human studies remain small, cross-sectional, or case-control in design and analytically heterogeneous. A limited number of prospective observational studies have begun to explore associations between MNP burden or exposure and subsequent clinical outcomes 10, 11. Another challenge persists in the lack of commonly agreed analytical laboratory and reporting standards, with different laboratories measuring different MNP particle size ranges, reporting of either particle counts or polymer mass, use of different digestion and extraction protocols that vary in recovery and contamination control. These differences currently limit abilities for comparing reported concentrations across studies and to define meaningful human exposure levels.
These methodological challenges must not be seen as a reason to dismiss the human health concerns. On the contrary, they are underline the need for rigorous attempts to link exposure and impact research outcomes and justify calls for following precautionary principles when it comes to assessing MNP human and environmental health risks.
We are calling here for a three-tiered approach:
First – development of standardised analytical methods and requirements of routine reporting of blanks (procedural and analytical), recovery tests, and lower detection limits for MNP particle sizes based on respective analytical methods.
Second – moving from cross-sectional studies that primarily detect MNPs in human samples prospective observational designs that can examine whether measured MNP exposure or burden is associated with subsequent health outcomesThird – using increasing knowledge of possible ranges of acute and chronic MNP exposures to inform experimental designs of exposure and impact studies to target environmentally realistic MNP concentrations (as well as polymer types and associated chemicals of concern) that yield mechanistic understanding can be translated into risk estimates.
Following such strategies will help distinguishing genuine biological effects and reduce uncertainties arising from methodological differences, contamination, or exposure scenarios that are not representative of human populations.
Inferences of human health risks can therefore not reliably be made purely based on knowledge of the environmental presence of MNP. Humans are exposed to MNP in indoor and outdoor, domestic and occupational environments with the risk of inhalation and ingestion of particles through food, water, and air. A recent synthesis argues that uptake and internalization of MNP resulting from these exposures may amplify chronic inflammatory disease, potentially exacerbating the global burden of non-communicable diseases6. However, key elements of the exposure-uptake-impact causation chain are often missing, resulting in highly fragmented knowledge and limiting global ability to link MNP exposures to human health outcomes. Close interaction between environmental exposure science and human health research and (eco)toxicology will be required to determine at what exposure dose, by which uptake route, and through which mechanisms MNPs become clinically relevant, and how this health relevance varies for different populations
In cardiovascular research for instance, MNPs have been detected in carotid plaques and thrombi, and their presence has been associated with subsequent cardiovascular events and disease severity.5˒7 These are important findings of course that suggest that MNPs may participate in disease processes; but they do not establish whether MNPs could have caused the disease or merely accompanied it or, in fact, MNP have been trapped particularly because the progress of cardiovascular disease. Such distinctions are of direct clinical and public health relevance of course as they determine actions such as initiation of interventions such as wider monitoring or broader regulatory action. Experimental models provide additional capacity to strengthen the case for biological plausibility.
MNP exposure has been linked to the induction of oxidative stress, mitochondrial dysfunction, inflammation, and barrier disruption.⁸˒⁹ Yet these effects have often been observed at doses that are difficult to compare with real world human exposure, in particular since the range of environmentally realistic acute and chronic exposures are largely unknown, especially with regards to smallest microplastic fractions and nanoplastics. Similar observational evidence can therefore be interpreted to provide mechanistic understanding and support the creation of conceptual models.
In addition, most human studies remain small, cross-sectional, or case-control in design and analytically heterogeneous. A limited number of prospective observational studies have begun to explore associations between MNP burden or exposure and subsequent clinical outcomes 10, 11. Another challenge persists in the lack of commonly agreed analytical laboratory and reporting standards, with different laboratories measuring different MNP particle size ranges, reporting of either particle counts or polymer mass, use of different digestion and extraction protocols that vary in recovery and contamination control. These differences currently limit abilities for comparing reported concentrations across studies and to define meaningful human exposure levels.
These methodological challenges must not be seen as a reason to dismiss the human health concerns. On the contrary, they are underline the need for rigorous attempts to link exposure and impact research outcomes and justify calls for following precautionary principles when it comes to assessing MNP human and environmental health risks.
We are calling here for a three-tiered approach:
First – development of standardised analytical methods and requirements of routine reporting of blanks (procedural and analytical), recovery tests, and lower detection limits for MNP particle sizes based on respective analytical methods.
Second – moving from cross-sectional studies that primarily detect MNPs in human samples prospective observational designs that can examine whether measured MNP exposure or burden is associated with subsequent health outcomesThird – using increasing knowledge of possible ranges of acute and chronic MNP exposures to inform experimental designs of exposure and impact studies to target environmentally realistic MNP concentrations (as well as polymer types and associated chemicals of concern) that yield mechanistic understanding can be translated into risk estimates.
Following such strategies will help distinguishing genuine biological effects and reduce uncertainties arising from methodological differences, contamination, or exposure scenarios that are not representative of human populations.
Type of Study: Letter |
Subject:
Environmental Health
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