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PubMed2026

Environmental benzene exposure induces a conserved neutrophil degranulation program across species.

Immune systems have evolved under constant pressure from pathogens and environmental challenges, leading to the emergence of conserved defense mechanisms across diverse organisms. Evidence indicates that environmental exposures perturb immune regulatory networks, particularly during development, when transcriptional programs governing hematopoiesis, immune cell differentiation, and inflammatory signaling are highly dynamic and sensitive to external stressors. Volatile organic compounds represent an important but incompletely understood source of immunological perturbation. Among these, benzene is a ubiquitous environmental contaminant associated with hematotoxicity and immune dysregulation; however, transcriptional responses to environmentally relevant low-level exposures during development remain poorly characterized. To determine whether benzene exposure engages conserved cross-species immune regulatory pathways, we performed a comparative transcriptomic analysis integrating developmental tissues from 3 vertebrate systems: human placenta, murine placenta, and zebrafish larvae. Bulk RNA sequencing datasets were analyzed to identify transcriptional responses associated with benzene exposure in experimental models (≤5 ppm) and with benzene adduct levels in maternal plasma for human samples. Because placental gene expression exhibits strong sexual dimorphism, murine datasets were stratified by fetal sex. Pathway- and network-level analyses were used to identify conserved biological responses. We observed a striking convergence on activation of innate immune pathways associated with neutrophil degranulation, IL-8 signaling, and Rho GTPase-mediated inflammatory responses. Further, network analyses identified CXCL8 and ERK1/2 as shared regulatory hubs linking transcriptional responses across datasets. Together, these findings uncover an evolutionarily conserved innate immune signature associated with benzene exposure during vertebrate development, suggesting that environmental chemical perturbations may disrupt fundamental immune regulatory programs across species.

Animals↗
PubMed1979

Documentation of environmental particulate exposures in humans using SEM and EDXA.

There is increasing awareness of health hazards from environmental and occupational exposures to particulates. Scanning electron microscopy (SEM) and energy dispersive x-ray analysis (EDXA) can document these exposures by analysis of small portions of cells, tissues and environmental samples. Previous work is briefly reviewed and special attention is given to discussion, with examples, of the various types of particulates which may be found in tissues (exogenous, endogenous, inhaled, injected, ingested, inorganic, organic), the different tissues in which they may be found (lung, heart, liver, skin, brain, kidney, lymph nodes, etc.), methods of tissue sampling (e.g. pulmonary lavage, transbronchial biopsy, open biopsy, percutaneous biopsy, autopsy), specimen preparation (fixation, embedding, sectioning, choice of substrate), SEM and EDXA data collection (backscattered electron imaging, etc.) data interpretation (artefacts, limitations of SEM and EDXA) and other new techniques (ion microprobe, laser Raman microprobe).

Air Pollutants↗
PubMed1977

Biochemical studies on populations with long- or short-term exposure to environmental pollution.

Three groups of populations were studied: I. living for about 10 years, II. living for about 3 years near copper smelteries, and III. living in rural area, far from any source of air pollution. Lead content in blood was found to be 182.0 and copper 274.6 microgram/100 ml for group I, Pb - 69.2 and Cu - 253.3 microgram/100 ml for group II, and Pb - 43.8 and Cu - 143.3 microgram/100 ml for group III. Inhibition of glycolytic cycle enzymes and delta-aminolevulinic acid dehydratase was proportional to the duration of exposure to environmental pollution. Ceruloplasmin concentration in serum, as well as serum and red cells aminotransferases activities, were increased in group II and decreased in group I, suggesting certain mechanism of adaptation.

Air Pollutants↗
PubMed2026

Urban Design Quality and Clinical Mental Health: A Systematic Review.

ObjectivesThis systematic review synthesizes empirical evidence on core urban design dimensions that affect clinical mental health outcomes and examines how environmental exposures mediate or moderate these relationships.BackgroundUrban design has increasingly been recognized as a determinant of psychological well-being, yet a standardized framework to evaluate its mental health impact remains underdeveloped.MethodsFollowing PRISMA 2020 guidelines, we systematically reviewed 19 quantitative empirical studies published through January 2025, examining relationships between outdoor urban design features and validated clinical mental health indicators across four major databases.ResultsFindings reveal that urban design influences clinical mental health outcomes (depression, anxiety, stress, cognitive decline) through two objective spatial scales: street-level features (imageability, enclosure, human scale, complexity) and neighborhood environments (land use mix, density, green infrastructure). Environmental exposures (traffic, noise, air pollution) operate as perceptual and experiential mechanisms that mediate or moderate the mental health effects of these spatial design features.ConclusionsWe propose an integrated three-domain conceptual framework distinguishing objective spatial design scales from subjective exposure mechanisms. This framework provides evidence-based guidance for urban planners and policymakers toward creating mentally healthier urban environments.

Humans↗
PubMed1975

Impacts of environmental stress exposure on central nervous functional patterns. A quantitative approach to evoked potential data.

Albino rats and rhesus monkeys with chronically implanted electrodes in cortical and subcortical, vasomotory and emotionally relevant brain regions were subjected to psycho-nerval stress (short-term stressful CR learning experiments on rats, long-term environmental stress with disturbances of the diurnal rhythm and social hierarchy on rhesus monkeys). Applying average computer techniques and discriminance analyses to evoked potentials (average evoked potentials = AEP to standardized optic-acoustic test stimuli) we were able to objectify the effect of different stress categories on central nervous functional patterns. These phenomena of electrical activity of the CNS proved to be extremely responsive to the stress exposure (avoidance conditioned learning experiments or socio-emotional overstrain). Under moderated stress (CR phases of acquisition and stabilization), time-space patterns of a primary facilitation of AEP could be established, expressing an improved energetic capacity of the CNS (adaptive effect). On the other hand, there was a generalized impairment of bioelectric information processing in temporal correlation with an increase in psycho-nervous stress exposure to rats (CR phases of differentiation). During long-term socio-emotional stress exposure of rhesus monkeys the highly significant changes of AEP-patterns (increasing fall short of the set point of the bioelectric level of activity with segmental differences in the multiphasic evoked potential) are to be interpreted as maladaptive processes in central nervous function under long lasting high stress conditions.

Adaptation, Physiological↗
PubMed1979

Perinatal period and pregnancy: intervals of high risk for chemical carcinogens.

Experiments in rodents indicate that during the post-embryonic period of prenatal development, the fetus is more sensitive than the adult to certain carcinogens, by several decimal orders of magnitude. Most such agents are direct-acting and independent of metabolism. To other substances, often those which require enzyme-mediated metabolic conversion to a chemically reactive derivative in order to effect carcinogenesis, the fetus may be less vulnerable than the adult. The neonate is also more susceptible than adults to some carcinogens, and may be more susceptible than the fetus to certain agents. Both rodent and primate studies indicate that gravid females are also at elevated risk for carcinogenesis, in part because of the presence in the placenta of trophoblastic tissue which may become malignant. The contributions of rapid growth rate, changing metabolic competence, and tissue differentiation to elevated perinatal susceptibility to carcinogens in rodents and primates are discussed, together with the implications of these findings for human beings subjected to industrial or environmental exposures to such chemicals.

Adult↗
PubMed1977

[Determination of the pneumoconiosis hazard in the cork industry].

The AA. have carried out an epidemiological investigation in order to control the prevalence of chronic respiratory diseases on a group of 385 people working in several cork industries in North Sardinia. At the same time an environmental investigation has been carried out. Standard questionnaire (CECA questionnaire) for chronic bronchitis and pulmonary emphysema, standard chest X-ray film, spyrographic investigation, ECG and sputum analysis for acid resistent bacteria have been used for epidemiological investigation. Environmental dust concentration and individual dust exposure, environmental concentration of sulphur oxides, nitrogen oxides, carbon mono- and dioxide, ammonia nad microclimatic conditions have been studied. Examination of medical data shows only a low degree of respiratory pathology in contrast with results of other authors, probably because of different methods used for epidemiological investigation and data interpretation and because of different environmental and working conditions.

Air Pollutants↗
PubMed1979

Arsenic exposure in multiple environmental media in children near a smelter.

A nationwide survey of heavy-metal exposure in children living near primary nonferrous metal smelters demonstrated high urine arsenic levels in children living near a copper smelter in Ajo, Arizona. Airborne smelter emissions and drinking water were the apparent sources of exposure. To determine whether increased arsenic absorption had produced adverse health effects, we conducted an evaluation of 132 Ajo children 5 to 18 years old and compared results with those of 47 children from a comparison town with low arsenic exposure. Environmental testing showed that Ajo's municipal water supply contained arsenic in concentrations of 0.09 mg/l (the EPA standard is 0.05 mg/l); arsenic concentrations in dust averaged 342.2 microgram/g. Urine arsenic levels in Ajo children correlated positively with amount of tap-water consumed (r = .32, p less than. 0002) and with distance of residence from the smelter (r = .20, p less than .02). Tap-water drinkers had significantly higher urine arsenic levels than bottled water drinkers (t = 4.21 p less than .001). Mean urine arsenic levels were significantly higher for children in Ajo (4.75 microgram/100 ml) than for children in the comparison town (1.17 microgram/100 ml). Hair arsenic levels correlated poorly with arsenic exposure. Despite the study population's chronic exposure to elevated environmental levels of arsenic, no clinical or hematologic abnormalities attributable to arsenic were found.

Adolescent↗
PubMed2024

Gene-environment interactions within a precision environmental health framework.

Understanding the complex interplay of genetic and environmental factors in disease etiology and the role of gene-environment interactions (GEIs) across human development stages is important. We review the state of GEI research, including challenges in measuring environmental factors and advantages of GEI analysis in understanding disease mechanisms. We discuss the evolution of GEI studies from candidate gene-environment studies to genome-wide interaction studies (GWISs) and the role of multi-omics in mediating GEI effects. We review advancements in GEI analysis methods and the importance of large-scale datasets. We also address the translation of GEI findings into precision environmental health (PEH), showcasing real-world applications in healthcare and disease prevention. Additionally, we highlight societal considerations in GEI research, including environmental justice, the return of results to participants, and data privacy. Overall, we underscore the significance of GEI for disease prediction and prevention and advocate for integrating the exposome into PEH omics studies.

Humans↗