Exposure to endocrine disruptors (EDs) is associated with increased susceptibility to obesity and metabolic dysfunction in epidemiological and preclinical studies. Accumulating evidence supports that various EDs promote energy intake and fat storage, but little is known about how they affect energy expenditure (EE). This systematic review examined the effect of EDs on EE in murine models and on mitochondrial bioenergetics in cell-based studies. We included 12 in vivo studies, which assessed the effect of phytoestrogens, DDT, tolylfluanid, benzene, bisphenol A, bisphenol S, butyl-phthalate, deltamethrin, and the mixtures of 23 chemicals and of organophosphate flame retardants. DDT, tolylfluanid, benzene, and the mixtures of 23 chemicals and of flame retardants decreased; bisphenol A, bisphenol S, and butyl-phthalate had a neutral effect; and phytoestrogens and deltamethrin increased EE. The effects of some EDs were sexually dimorphic, dose-dependent, and interacted with diet. Nine cell-based studies were included and indicated that mitochondrial bioenergetics was impaired by tolylfluanid, bisphenol A, and DDT in muscle cells; by bisphenol AF, BDE-99, DDT, DDE, and the mixture of DDE, trans-nonachlor, and oxychlordane in adipocytes; by bisphenol A in hepatocytes; and by tributyltin in pluripotent cells. Our findings indicate that EDs affect EE in mice in a sexually dimorphic pattern and impair mitochondrial bioenergetics in cellular models which are representative of key tissues involved in energy balance. While further studies are needed to fully elucidate the impact of EDs on energy balance and mitochondrial function, this review underscores the plausibility of mitochondrial dysfunction and altered EE as key pathways linking ED exposure to metabolic diseases.

Chronic fluorosis, characterized by excessive exposure to fluoride, is associated with a greater risk of frailty in endemic populations. While fluoride correlates with inflammation and frailty, the mediating role of interleukins (ILs) remains unclear. This study investigated the potential multiple mediation pathways of ILs on the relationship between fluoride exposure and frailty in skeletal fluorosis patients.

The widespread use of pesticides, including glyphosate-based herbicides (e.g., Roundup®, R) and chlorpyrifos-based insecticides (e.g., Clorpi48®, C), has raised concerns about their environmental and human health impacts. Growing evidence links pesticide exposure to cancer development. Given the critical role of immune surveillance in tumor growth control, environmental pollutants such as pesticides should also be evaluated for immunotoxicity. Moreover, while individual pesticides have been extensively studied, the effects of pesticide mixtures on human immune cells remain poorly explored. Here, we assessed the impact of environmentally relevant doses of R, C, or their combination (R+C) on immune cell functions.

The prevalence of autism spectrum disorder has risen in recent decades. Given the growing evidence that prenatal fluoride exposure may be neurotoxic, we examined associations between prenatal fluoride exposure and parent-reported autistic behaviors in preschool-aged children.

Firefighters have frequent exposure to carcinogens and an increased risk of cancer. Wildland-urban interface (WUI) fires, which involve both structures and undeveloped wildland fuels, pose unique challenges to the health of firefighters. However, the extent of health risks associated with these fires remains underexplored.

Lead is a well-known neurotoxicant with no identified safe level. Prior studies found that childhood lead exposure is associated with decreased intelligence quotient (IQ) scores. However, most studies rely on a limited number of blood lead measurements. In this prospective pregnancy and birth cohort, we estimated cumulative childhood lead exposure using repeated blood lead concentrations and regression calibration, allowing for more accurate assessment of lead burden over time and its association with IQ.

Exposure to air pollution poses a serious threat to maternal and child health, particularly during critical developmental periods. Extracellular vesicles (EVs), as key mediators of intercellular communication, have emerged as a novel mechanism through which environmental exposures, including air pollutants, exert systemic effects. This review synthesizes current evidence on the role of small EVs (sEVs) in mediating the biological impacts of prenatal air pollution exposure, with a focus on their molecular profile, including the presence of signaling molecules like miRNAs and proteins, and their implications for childhood health outcomes. In this review, we explore mechanisms involving sEVs in transplacental exposure, signaling and epigenetic modifications, linking exposure to adverse developmental and health effects in early life. Furthermore, we highlight the potential of sEVs as biomarkers for exposure assessment and predictors of adverse health outcomes. Relevant studies were identified through a comprehensive literature search and systematic review of experimental and epidemiological evidence. By integrating insights from toxicology, epidemiology, and molecular biology, we identify specific needs for further research into sEVs, both as mechanistic mediators and diagnostic tools for air pollution-related health risks.

In Italy, the area of Casale Monferrato in the Piedmont Region has experienced a high burden of malignant mesothelioma (MM) due to environmental contamination from Eternit, the country's largest asbestos-cement plant, which operated from 1907 to 1986. The severity of the health impact led to the area's designation as a Site of National Interest (SIN) for environmental and health concerns. Despite the 1992 asbestos ban, the MM epidemic persists, driven by the disease's long latency. Using data from the Piedmont Malignant Mesothelioma Registry (RMM), we describe MM trends in Casale Monferrato's SIN from 1990 to 2021 and project future incidence through 2042 using Age-Period-Cohort (APC) models.

Air pollution, in particular due to traffic, is suspected of increasing the risk of childhood acute leukemia (AL), most of the evidence coming from epidemiological studies and literature reviews that focused on the time around diagnosis. Using data on the national scale, we tested the hypothesis that prenatal exposure to traffic-related air pollution increases the risk of childhood AL.

Vinyl acetate (VA) is a synthetic chemical that can be metabolized to form the carcinogen acetaldehyde (AA). This paper summarizes the key evidence relevant to the evaluation of VA’s carcinogenicity.

The ethical obligation of reporting back research results (RBRR) is established. Yet the ethical dimensions of how RBRR is implemented remain largely unexplored. The Environmental influences on Child Health Outcomes (ECHO) program has identified logistical challenges in RBRR, citing limited guidance resources as a key obstacle. The objective of this research was to characterize and assess ethical considerations for RBRR: (i) with or without clinical significance; (ii) within a pregnancy cohort, and; (iii) within a study population with diverse cultural and traditional contexts.

In the context of global warming and escalating urbanization, occurrences of extreme ozone (EO) and heatwave (HW) events are increasingly frequent. However, studies on the impact of consecutive extreme ozone and heatwave (EO-HW) events on hospitalizations for neurological disorders (ND) and related economic burdens remains limited. Our study aimed to explore the impacts of these events on ND hospitalizations, length of stay, and related costs, with a specific focus on quantifying the impacts of consecutive extreme events of varying durations.

Exposome research seeks to understand how cumulative environmental exposures across the life course shape health outcomes. Most studies however, adopt a unidirectional, top-down model, conceptualizing individuals as passive recipients of exposure, which overlooks the social, cultural, and behavioral dynamics through which people engage with their environments and thus underestimates the human agency of those exposed in mitigating exposures.

Chlordecone is a persistent organochlorine insecticide that was widely used to control banana root borer in the French West Indies until 1993. Animal studies have reported an impact of chlordecone exposure on female fertility, but no data are available for humans. Here, we investigated the association between chlordecone exposure in women and time to pregnancy (TTP).

Ultraviolet radiation (UVR), primarily from sunlight, is a natural component of environmental exposure and can cause genomic damage, photoaging, and skin cancer. Sunscreens containing UV-filters are widely used to prevent these effects and are also found in many personal care products. Despite their protective role, concerns have emerged regarding the accumulation of UV-filters in the environment and human matrices, along with their ability to act as endocrine disruptors, which main target include also thyroid hormone regulation.

Higher fluoride in plasma has been associated with lower eGFR among adolescents in the National Health and Nutrition Examination Survey (NHANES); however, whether fluoride exposure may contribute to decreased kidney function or fluoride may accumulate in plasma from lower kidney filtration could not be parsed. We examined the presence of dental fluorosis (DF; reflecting chronic fluoride exposure during tooth development) among adolescents and young adults and urinary fluoride (UF) levels among adolescents in relation to kidney and liver parameters in the United States (US).

Exposure to phthalates and non-phthalate plasticizers as well as bisphenols may be relevant to the development of behavioural symptoms in childhood with sex-specific effects, although the results of existing studies are not consistent. The aim of the study was to evaluate the cross-sectional association between childhood exposure to these compounds and behavioral outcomes in the REPRO_PL cohort (Poland).

Asbestos is a well-established occupational carcinogen, with strong evidence linking its exposure to lung cancer. Despite increasing awareness of its health risks, asbestos continues to be used in many countries. We aimed to evaluate the global burden of lung cancer attributable to occupational asbestos exposure and to analyze its epidemiological patterns across time and by regions, sex, and age.

The International Agency for Research on Cancer classifies formaldehyde as a human carcinogen, with sufficient evidence for nasopharyngeal cancer and leukaemia. However, the association with lymphoma subtypes has been less thoroughly investigated. We explored this link in an Italian multicentre case-control study.