DOI: https://doi.org/https://doi.org/10.57187/4935
Plastics are all around us. They are used in almost every sector, including product and food packaging, building and construction materials, textiles, consumer products such as cosmetics, transportation, electrical and electronics sectors, and industrial machinery [1]. Plastic use is increasing worldwide; of particular concern, the global plastics treaty, which aimed to address growing plastic pollution, did not reach an agreement [2]. Additionally, this “plastic crisis” is accompanied by growing concerns regarding emissions and exposure across the plastic lifecycle and their potential adverse effects on the environment and health [3]. Microplastics are tiny plastic particles smaller than 5 mm and larger than 1 micrometer, whereas nanoplastics are defined as either 1–100 nm or 1–1000 nm [4]. Herein, we refer to both sizes as microplastics.
Microplastics are classified as either primary microplastics, which are produced intentionally (e.g. for cosmetics), or as secondary microplastics, which are formed through the fragmentation or abrasion of larger plastics or plastic waste [5]. Microplastics have been studied in water and soil for a while [6]. However, few studies have measured microplastics in the air [5].
The Swiss Federal Office for the Environment commissioned a report summarising the state of knowledge regarding the health effects of microplastics in ambient air from LUDOK – the literature database and services on health effects of ambient air pollution at the Swiss Tropical and Public Health Institute (https://www.swisstph.ch/de/projects/ludok). This review summarises key findings of the larger report published in German in February 2025 [7].
The systematic collection and selection of studies regarding exposure and possible health effects of microplastics in the air were based on the work and expertise of LUDOK. LUDOK systematically searches for, collects, and summarises important research on ambient air pollution and health since 1985 [8].
The literature search for the microplastics review used five complementary approaches to find relevant literature on the topic.
Studies and reviews reporting on measured exposure to microplastics in ambient or indoor air, or on microplastics detected in the human body (biomonitoring data) were included, along with studies examining the health effects of (micro)plastics in occupational settings and the health effects of non-exhaust emissions with a focus on the indicator metals copper, zinc, and barium for tyre wear [9–11]. Microplastics from tyre wear are an important component of non-exhaust traffic emissions, alongside brake and road wear [11, 12]. Because this study was interested in the health effects of microplastics in ambient air, it was hypothesised that, as in research on the health effects of particulate air pollution or its components, studies in occupational settings and studies that analysed non-exhaust traffic-related air pollution could provide insights into the potential health effects of airborne microplastics.
Microplastics in the environment are a highly complex mixture of materials and chemicals that differ in size, shape, material composition, additives, and surface properties, depending on their origin or source and the process through which they are formed.
In Switzerland, the improper disposal of plastics, such as littering or plastics in organic waste disposal, is the primary source of macroplastics (>5 mm) in the environment. Due to communal cleaning services, most of these plastics are removed and burned in waste incineration plants. In Switzerland, the largest sources of microplastics that are contaminating water, soil, and air are tyre wear and the degradation of plastics used in agriculture, construction, and households [13, 14]. In other countries, relevant microplastic sources mentioned include tyre abrasion from road and air traffic, artificial turf, road markings (thermoplastics), waste incineration, construction, landfills, industrial emissions, and tumble dryer exhaust [15, 16], as well as the fragmentation and abrasion of macroplastics by wind, the resuspension of tyre, brake, and road surface abrasion, and the abrasion of textile furnishing and synthetic clothing by human movement [17]. The dispersion of microplastics from water bodies through sea spray or on the surface of water bodies is also mentioned [18]. However, the contribution of water bodies to airborne microplastics has recently been challenged, with evidence indicating that it is overestimated [19]. No reliable statements can be made on the quantitative contributions of all these sources [18].
Estimates suggest that tyre wear contributes between 0.1% and 10% of PM10 air pollution in the form of microplastics [5]. Manoli and Voutsa [20] estimated that 28% of particulate matter in PM10 corresponds to resuspended road dust, including tyre wear. Wik and Dave [21] estimated that approximately 5% of tyre abrasion can enter the air. Grigoratos and Martini [11] and Kole and Lohr [22] estimated that 0.1–10% of PM10 and 3–7% of PM2.5 in the air consists of tyre and road abrasion, which is likely to be at the upper limit. For Switzerland, Rausch and Jaramillo-Vogel [23] quantified tyre abrasion particles at an urban road site (NABEL monitoring station Bern-Bollwerk) and at an urban background site (NABEL monitoring station Zurich-Kaserne). The proportion of tyre abrasion particles in PM10 was 11% at the road site and 2% at the urban background site, with values of 2.24 and 0.28 μg/m3, respectively. Measurements in indoor and outdoor air identifying plastic fibres in air samples suggest that the wear and tear of synthetic textiles and furniture finishings are also important contributors to airborne microplastic exposure [24, 25].
Regarding the processes leading to ever smaller plastic particles, the degradation depends on parameters such as temperature, wind, relative humidity, colonisation by microbes, additives, surface area, size, and shape. Photo-oxidative degradation is the most important mechanism in the air and requires sunlight (UV radiation). Degradation is generally very slow [4]. This leads to plastic accumulation in the environment that is expected to persist for hundreds to thousands of years, depending on the plastic type [26]. Air is therefore considered not a sink but a transport medium [13]. Prevailing meteorological parameters, including wind, temperature, relative humidity, and rainfall, along with particle solubility, shape, size, and structures, affect the transport of atmospheric microplastics [4].
The World Health Organisation [27] has summarised the different attributes of microplastics in a figure (figure 1). Toxicity can vary depending on these characteristics. Some authors additionally mention the ageing of the materials or colonisation by bacteria as traits influencing toxicity [28].

Figure 1Attributes of microplastics that are relevant for assessing both exposure and hazard (from: WHO. Dietary and inhalation exposure to nano- and microplastic particles and potential implications for human health. Geneva: World Health Organization, 2022 [27], under Creative Commons licence CC BY-NC-SA 3.0).
There are no standardised measurement methods for microplastics in the air. Depending on the research question, such as differentiating between sizes, quantities, shapes, or chemical features of plastics, different methods for sampling, pre-treatment, and identification are used. A review by Luo and Wang [29] provides a good overview of existing methods. Because of the variety of methods, it is difficult to compare measurements [30]. Additionally, there are major challenges in terms of quality assurance, for example, in avoiding sample contamination [31].
Exposure measurement studies from Europe, North America, the Middle East, and Asia indicate that microplastics are present in the air. Pollution is higher in areas with greater human activity, which means that higher levels are observed in cities than in rural areas [25] (appendix 2). The fact that microplastics are also found in remote areas, such as glaciers, and that their number has increased in recent years, indicates that they are transported by wind and removed from the atmosphere by dry and wet deposition, and that emissions have increased [32]. The number of inhalable particles (i.e. particles smaller than 10 μm in diameter, PM10) is unclear. However, to date, microplastics likely only account for a small fraction of human exposure to particulate pollution in PM2.5 or PM10. Indoor exposure, particularly from textile fibres, is higher than ambient exposure because of indoor air sources and closed rooms with minimal air exchange [33–35].
Taking the results of various measurement studies and assuming an average breathing volume of 15 m3 per day for an adult [27], the inhaled quantity of microplastics per day and year was estimated (table 1).
Exposure studies from Europe report an annual average exposure of a few thousand particles (3285-5091 particles/year, with 1259 particles at a remote location such as the Pic Du Midi). Asian studies generally show larger numbers, which can partly be attributed to the inclusion of the total load, including large particles. Nevertheless, the average pollution in five major cities in China remains high, with over 900,000 particles, when taking into account that about 61% (over 1.5 million particles) were smaller than 30 μm [36].
Table 1Calculation of the annual exposure to the number of microplastic particles or fibres based on selected exposure measurement data (assumption of a daily breathing volume of an adult of 15 m3 per day).
| Reference | Place /country | Particle size | Concentration (particles/m³) | Dailye exposure (particles/day) | Annual exposur (particles inhaled/year) |
| [32] | Pic du Midi, Pyrenees, France | More than half ≤10 μm | 0.23 (range: 0.09–0.66) | 3.45 (range: 1.35–9.9) | 1259.25 (range: 492–3613) |
| [37] | Indoor air, Aarhus, Denmark | Median: 21 and 36 μm (smaller/larger particles) | Avg. 9.3 ± 5.8 (range: 1.7–16.2) | Avg. 139.5 (range: 25.5–243) | Avg. 50917 (range: 9307–88695) |
| [34] | Coastal California, USA | Fibres: 616 μm (30%: 100–300 μm), Fragments: 104 μm | Fibres: 0.6, Fragments: 5.6 | Fibres: 9, Fragments: 84 | Fibres: 3285, Fragments: 30660 |
| [33] | Paris, France | Outdoor air fibres <1650 μm | 0.9 (range: 0.3–1.5) | 13.5 (range: 4.5–22.5) | 4927 (range: 1642–8212) |
| [38] | Asaluyeh, Iran | <100 – >1000 μm (air: 2–100 μm, dust: 75% <100 μm) | 1 (range: 0.3–1.1) | 15 (range: 4.5–16.5) | 5475 (range: 1642–6022) |
| [39] | Nagpur, Central India | n/a | Residential: 116.25 particles/day, Industrial: 99.25 particles/day | Same as concentration | Residential: 42431, Industrial: 36226 |
| [40] | Beijing, China | 80%: 5–20 μm, range: 5–200 μm | 14100–16700 fibres/m³ | 211500–250500 fibres/day | 77197500–91432500 |
| [41] | Wenzhou, China | 5–1794 μm (65.1% <30 μm, 29.4%: 30–100 μm) | 188.7 | 2830.5 | 1033132 |
| [36] | 5 major cities in China | 5.9–1475 μm, 61.6% <30 μm | Range: 104–650, Avg: 282 | Range: 1560–9750, Avg: 4230 | 1543950 (range: 569400–3558750) |
| [42] | Shanghai, China | 23.07–9955 μm, Avg: 597.5 μm at 1.7m | 0–4.18, Avg: 1.42 | 0–62.7, Avg: 21.3 | 7774 (range: 0–22885) |
| [43] | Shanghai, China | Avg: 246.52 μm (12.35–2191.32) | 0–2, Avg: 0.41 | 0–30, Avg: 6.15 | 2244 (range: 0–10950) |
Abbreviations: Avg, average; n/a, not available; μm, micrometre; m, metre; m3, cubic metre.
There are various alternative calculations of the total human exposure to microplastics, which produce very different figures depending on the assumptions and models used. Cox and Covernton [44] calculated that a North American ingests 39,000–52,000 particles per year via food and that the total exposure increases to 74,000–121,000 particles if exposure via respiration is taken into account (based on numbers from [33] and [45]). Zhang and Xu [46] calculated an intake through food, specifically from salt and water, of up to 77,700 particles and over 30 million through respiration. These figures are subject to great uncertainty. Whether the consumption of water drunk from plastic bottles is added can make a huge difference (up to 90,000 additional particles per year [44]). What is striking, however, is that estimated exposures from air can play a major role in total exposure, given that microplastics can enter the organism both through inhalation via the lungs and through the gastrointestinal tract by swallowing particles removed by the respiratory tract’s cleaning mechanisms.
Humans are exposed to microplastics via food, air, and skin, whereby, depending on the authors, food [13] and (indoor) air [47] are discussed as the main routes of exposure. Airborne microplastics can (1) be inhaled, (2) be inhaled and trapped in the mucus of the lining of the upper respiratory system and removed by mucociliary transport to be swallowed, and (3) settle on meals [48] or surfaces. The latter is especially relevant for the exposure of infants, who can ingest microplastics through typical mouthing behaviours [49]. The latter two mechanisms result in exposure of the gastrointestinal tract.
In general, inhalable particles larger than 10 µm in aerodynamic diameter are deposited mainly in the extrathoracic region, whereas particles under 10 µm can reach the tracheobronchial regions of the lung [50]. Small particles measuring less than 2.5 µm can reach the alveolar region of the lung, where clearance mechanisms are not as successful [15]. Particles below 1–1000 nanometers (nanoplastics) can cross the alveolar-capillary barrier [51] and, once in the bloodstream, can also cross the blood-brain or placental barrier [52].
The detection of microplastics in various organs and body fluids indicates exposure and transport within the body. Microplastics were first detected in human lung tissue of workers in the textile industry in 1975 [53]. Since then, microplastics have also been found in the lung tissues of the general population [54–56] and in other organs, such as blood [57–59], the gut [60], liver tissue [61], faeces [62, 63], breast milk [64], the placenta [65, 66], and the first stool of a newborn (meconium) [67, 68]. This suggests that microplastic particles are transferred via the placenta and the umbilical cord. Reviews by Jung and Sampath [69], Prata [70], and Barceló and Picó [71] cover important studies on the detection of microplastics in the human body.
Table 2 shows the types of microplastics that have been detected in different organs and body fluids.
Table 2Types of plastic detected that have passed the human body’s biological barriers or were excreted (adapted from: Krause S, Ouellet V, Allen D, Allen S, Moss K, Nel HA, et al. The potential of micro- and nanoplastics to exacerbate the health impacts and global burden of non-communicable diseases. Cell Rep Med. 2024 Jun;5(6):101581 [51] under Creative Commons licence CC BY-NC-SA 4.0).
| Type of microplastic | Placenta | Meconium | Breast milk | Blood | Faeces |
| Polyamide | X | X | X | X | X |
| Polyurethane | X | X | X | X | X |
| Polyethylene | X | X | X | X | X |
| Polyethylene terephthalate | X | X | X | X | X |
| Polypropylene | X | X | X | X | X |
| Polyvinyl chloride | X | X | X | – | X |
| Polyoxymethylene | X | X | – | – | X |
| Ethylene vinyl acetate copolymer | X | X | – | – | X |
| Polytetrafluoroethylene | X | X | – | – | X |
| Chlorinated polyethylene | X | X | – | – | X |
| Polybutadiene | X | X | – | – | X |
| Polycarbonate | – | – | X | – | – |
| Polystyrene | – | – | X | – | X |
| Polymethyl methacrylate | X | X | – | X | X |
| Polylactic acid | X | X | – | X | X |
| Polysulfones | X | X | – | X | X |
| Nitrocellulose | – | – | – | X | – |
| Sizes detected | 5–10 μm/50–240 nm | >50 μm | 2–50 μm | ~700 nm | infant: 20–50 μm, adult: 50–500 μm |
X indicates that the plastic type has been detected, whereas cells with dashes (–) indicate that no evidence of the presence of the microplastic type was found in the corresponding medium.
Abbreviations: μm, micrometres; nm, nanometres
More recently, microplastics have been detected in the olfactory nerve [72] and in the brain, sparking discussion on their potential role in the development of dementia, as a greater accumulation of microplastics was observed in a cohort of decedent brains with a documented dementia diagnosis than in those without a diagnosis. Notable deposition was observed in cerebrovascular walls and immune cells [73]. The authors confirmed the presence of microplastics in the human kidney, liver, and brain using robust complementary methods for detecting microplastics. Most of the total mass consisted of polyethylene, with lesser but relevant concentrations of other polymers. In brain tissues, they observed the highest proportions of polyethylene, which are presented largely as nanoscale, shard-like fragments. Plastic concentrations in these decedent tissues were not influenced by age, sex, race/ethnicity, or cause of death. The time of death (2016 vs 2024) was a significant factor, with increasing microplastic concentrations over time in both liver and brain samples [73].
However, no reliable statement can be made about the general level and distribution of exposure. Similar to the challenges of measurement of microplastics in ambient air, measurements of microplastics in body fluids are not based on standardised methods either [52].
Microplastics are a mixture of materials and additives that can have very different effects depending on their size, shape, composition, age, and surface properties or the materials present on their surface. It is virtually impossible to separate the effects of chemicals and particles [74].
Various mechanisms of action can lead to damage and impaired health. These include physical or chemical irritation by the particles themselves, as well as adhering chemicals from production or components such as proteins or heavy metals accumulated from the environment or within the body [38, 75, 76]. Non-toxic material that is inert per se can accumulate and trigger inflammatory reactions and systemic changes, such as in the microbiome [77].
To date, no reliable epidemiological studies on the general population are available that describe a connection between environmental exposure to microplastic particles and health consequences for humans, including exposure from air. Occupational health studies and studies investigating non-exhaust components of particulate matter are used here as proxies for airborne microplastic exposure and suggest comparable effects to those described for exposure to particulate matter, as described below.
Occupational health studies, typically from the textile, flocking, tyre producing, or vinyl (PVC) industry, have primarily described respiratory symptoms such as allergic or asthma-like reactions, (chronic) cough, bronchitis, changes in lung function, wheezing, inflammation of the airways, pulmonary fibrosis [53, 78], and even lung cancer [79, 80]. Cancers of the liver, bladder, and digestive tract have been reported [81, 82]. Increased mortality from respiratory diseases [83] and cancer [79, 84] has also been described. However, according to a WHO report [27], the evidence for a link between microplastic exposure and cancer is still inadequate. Individual studies additionally point to links with mortality from cardiovascular diseases and possible effects on the brain (dementia) [85, 86].
Occupational studies point to possible health effects. However, their results cannot be transferred to the general population, which includes susceptible people such as children, pregnant women, individuals with pre-existing conditions, and older adults. Exposure in the general population is often characterised by long-term exposure to low levels of pollution, whereas occupational exposure typically is characterised by higher exposure levels over shorter time periods, with recovery time when not working. In addition, it is difficult to assess exposure-response relationships in occupational studies and rule out effects from other co-pollutants in the workplace or other confounding factors.
Epidemiological studies that examine exposure from traffic using specific metals in particulate matter as indicators for (brake and) tyre wear (e.g. zinc and barium), or that use other methods to calculate the contribution of non-exhaust emissions from traffic to PM exposure, might be considered proxies for microplastics exposure from ambient air. The 90 studies selected from the LUDOK database describe various health endpoints.
Respiratory effects related to pneumonia [87, 88] and reduced lung function [89, 90] were found to be associated with non-exhaust particles and zinc in adults and children. Results on asthma and wheezing were mixed, with some studies showing increased risks of asthma, as well as increased symptoms [91–93] or emergency events [94]; however, these associations were not observed in other studies examining asthma-related emergencies [95–98].
The mortality risk in the general population was increased in association with long-term exposure to zinc in PM or non-exhaust emissions in Rome [99] and Massachusetts (USA) [100], as well as in the European studies ESCAPE [101] and ELAPSE [102, 103] and in heart patients [104]. However, a UK study in the general population in London found no association with non-exhaust primary particles (PM2.5 and PM10) [105].
The ELAPSE study observed an increased lung cancer risk associated with zinc [106], and the ESCAPE study found increased risk with copper, zinc, and nickel [107]. Zinc in PM was also found to increase liver cancer risk in the ELAPSE study [108], but no associations were found regarding brain [109] or breast cancer risk in the ESCAPE study [110].
A review of toxicological studies found that microplastics affected cardiac function and caused toxicity at (micro)vascular sites. Direct cardiac toxicity included abnormal heart rate, cardiac function impairment, pericardial oedema, and myocardial fibrosis. At (micro)vascular sites, microplastics induced haemolysis, thrombosis, blood coagulation, and vascular endothelial damage [111]. Epidemiological studies with indicators of non-exhaust traffic exposure have found mixed results regarding heart rate variability [112–114] and for effects on hospital admissions or emergency events related to cardiovascular diseases [94, 98], stroke [115, 116], mortality due to CVD [99, 117] or of patients with CVD [104, 118], and the development of CVD [88, 119, 120].
Microplastics may alter hormonal balance and metabolism. In particular, the additives bisphenol A and phthalates are known endocrine disruptors that may lead to lower birth weight, preterm birth, insulin resistance, high blood pressure, and obesity [69]. Only a few individual studies in LUDOK support these findings regarding non-exhaust exposures. A Spanish study found higher risks for preeclampsia in association with traffic and brake dust exposure [121]. Studies conducted in London and Sweden found lower term birth weight with non-exhaust emissions [122, 123].
Recently, as mentioned above, the migration and accumulation of microplastic particles in the brain have been discussed, and a higher content of microplastics has been observed in the brains of individuals with a diagnosis of dementia than in those without a diagnosis [73]. A cohort study in children found a higher risk for autism diagnoses with non-exhaust emissions during pregnancy [124]. Flame retardants, another common additive in plastics, have also been discussed in association with neurodevelopmental diseases [125]. Mortality from dementia was non-significantly elevated in association with zinc in PM in the ELAPSE study [126], but dementia incidence was not associated with traffic exposure in London [127]. Cognitive function in children was not associated with zinc in PM in the ESCAPE study [128] or the Spanish BREATHE study [129]. Other health endpoints that may be associated with microplastics exposure include altered digestion due to an altered gut microbiome [130–132], as well as altered liver and kidney function [133] and alterations in the immune system [49, 69].
Overall, epidemiological studies examining the effects of non-exhaust traffic emissions and indicators of tyre wear show similar effects to those reported in occupational studies. However, the results are often mixed, and the number of studies investigating a specific outcome is too low to draw firm conclusions. Additionally, the interpretation of the results of the occupational and epidemiological studies mentioned above as proxies for the harmful effects of ambient airborne microplastics should be approached with caution. Epidemiological studies that allow linking exposure to ambient airborne microplastics with acute and chronic preclinical and clinical phenotypes are lacking and urgently needed, but face several challenges.
Microplastic pollution in the air and its association with health and diseases remain poorly understood because of several challenges.
First, the measurement and characterisation of microplastics in the air are still in their infancy. Major challenges remain in the areas of sampling, identification, measurement, and characterisation of microplastics [5]. The lack of comprehensive standardisation of measurement and analysis methods with proper quality assurance, as well as representative reference materials, impairs both the comparison of results from different regions and their general reproducibility [27, 31]. The focus of research on airborne microplastics should be specifically on the particle fraction of <10 μm, which is the most relevant to health [29]. However, only a few studies in Europe or North America [32, 35, 134–137] and Asia [36, 39–41, 138] have examined this.
Second, it is generally considered unlikely that, currently, without extensive standardisation, representative reference materials, and the inclusion of physico-chemical properties and associated substances, a realistic assessment of human health risks is possible [26]. Additionally, the biokinetics of the absorption, distribution, metabolism, and excretion of these particles are still poorly understood [139]. This also relates to the understanding of the ability of microplastics to overcome barriers such as the epithelia of the respiratory tract and the digestive tract [140].
Third, the complex mixtures of different chemicals found in environmental samples of microplastics present a very high hurdle for separating the different effects of combinations of chemicals and particles [26]. It requires an exposome science approach to connect health effects to single chemicals or mixtures thereof, given that humans are exposed to numerous chemicals from a multitude of sources [141].
The fourth challenge, which is linked to those above, is that it remains very challenging to study the effects of microplastics in the air in epidemiological studies, which would provide insights into exposure under real-world conditions over longer time frames and into effects in susceptible populations.
Given the potentially increasingly diverse composition of ambient particulate matter, it is crucial that efforts in air pollution research investigate particle composition and sources and take microplastics into consideration. The chemical composition and context, as well as the level of exposure, in part driven by the availability of exposure adaptation measures (e.g. masks carried in occupational settings), differ substantially depending on the context of exposure (occupational settings versus general population settings; non-tailpipe traffic-derived versus textile-derived particles). Therefore, occupational studies or studies on non-exhaust traffic exposure do not allow for clear conclusions regarding the health effects of microplastic exposure in the general population. The population health effects of ambient air microplastic exposure for estimating their risk burden and supporting targeted policies require novel, fine-grained exposure models and their application in large-scale cohorts with associated biobanks to facilitate exposome science [142, 143].
Sources
Measurement
Exposure
Dosage
Health effects
Microplastic pollution is linked to human activity. Textile wear is an important source of microplastics, particularly indoors. In outdoor air, tyre wear and the abrasion and decomposition of materials from the agricultural and construction industries or larger plastics (e.g. littering) are also important sources. Exact quantification remains difficult, but biomonitoring and pathology studies indicate that the general public is exposed to microplastics from air and food. Although occupational health studies, animal studies, and studies from medical and implant research cannot replace epidemiological studies in the general population, the diverse adverse health effects observed raise concerns despite their limitations. The extent to which microplastic particles and their additives are more toxic than other particles remains an important focus of environmental research.
With the decrease in particulate matter pollution from exhaust gases, it can be assumed that the contribution and proportion of microplastics from tyre wear will increase in future. Additionally, increased use and disposal of plastics and increasing levels of microplastics in human tissue suggest that plastic pollution (from the air) might become more important in future. Interdisciplinary research is urgently needed to better understand the level of exposure and health effects of microplastic pollution from ambient air.
The authors would like to thank Luc Lutz, who helped with the literature screening and data extraction process.
Author contributions: MKJ and NPH conceptualised the review. MKJ conducted the literature search and drafted the initial manuscript. NPH critically revised the manuscript for important intellectual content. All authors contributed to the writing, reviewed the final manuscript, and approved it for publication.
The original report on which this overview is based was commissioned and funded by the Swiss Federal Office for the Environment under the LUDOK contract.
Both authors have completed and submitted the International Committee of Medical Journal Editors form for disclosure of potential conflicts of interest. No potential conflict of interest related to the content of this manuscript was disclosed.
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The appendix is available in the pdf version of the article at https://doi.org/10.57187/4935.