Blueprint for the design, construction, and validation of a plastic and phthalate-minimised laboratory

Microplastics are ubiquitous environmental contaminants leading to inevitable human exposure. Even so, little is known about the effects of microplastics in human health. Thus, in this work we review the evidence for potential negative effects of microplastics in the human body, focusing on pathways of exposure and toxicity. Exposure may occur by ingestion, inhalation and dermal contact due to the presence of microplastics in products, foodstuff and air. In all biological systems, microplastic exposure may cause particle toxicity, with oxidative stress, inflammatory lesions and increased uptake or translocation. The inability of the immune system to remove synthetic particles may lead to chronic inflammation and increase risk of neoplasia. Furthermore, microplastics may release their constituents, adsorbed contaminants and pathogenic organisms. Nonetheless, knowledge on microplastic toxicity is still limited and largely influenced by exposure concentration, particle properties, adsorbed contaminants, tissues involved and individual susceptibility, requiring further research.

Endocrine-disrupting chemicals (EDCs) can increase the risk of childhood diseases by disrupting hormone-mediated processes critical for growth and development. Here, Joseph Braun discusses epidemiological evidence of associations between early-life exposure to EDCs and childhood neurodevelopmental disorders and obesity.

Since reports published in 2015 and 2016 identified 15 probable exposure–outcome associations, there has been an increase in studies in humans of exposure to endocrine-disrupting chemicals (EDCs) and a deepened understanding of their effects on human health. In this Series paper, we have reviewed subsequent additions to the literature and identified new exposure–outcome associations with substantial human evidence. Evidence is particularly strong for relations between perfluoroalkyl substances and child and adult obesity, impaired glucose tolerance, gestational diabetes, reduced birthweight, reduced semen quality, polycystic ovarian syndrome, endometriosis, and breast cancer. Evidence also exists for relations between bisphenols and adult diabetes, reduced semen quality, and polycystic ovarian syndrome; phthalates and prematurity, reduced anogenital distance in boys, childhood obesity, and impaired glucose tolerance; organophosphate pesticides and reduced semen quality; and occupational exposure to pesticides and prostate cancer. Greater evidence has accumulated than was previously identified for cognitive deficits and attention-deficit disorder in children following prenatal exposure to bisphenol A, organophosphate pesticides, and polybrominated flame retardants. Although systematic evaluation is needed of the probability and strength of these exposure–outcome relations, the growing evidence supports urgent action to reduce exposure to EDCs.