Surgical spirit

BackgroundEarly life exposure to lead, mercury, polychlorinated biphenyls (PCBs), polybromide diphenyl ethers (PBDEs), organophosphate pesticides (OPPs), and phthalates have been associated with lowered IQ in children. In some studies, these neurotoxicants impact males and females differently. We aimed to examine the sex-specific effects of exposure to developmental neurotoxicants on intelligence (IQ) in a systematic review and meta-analysis.MethodWe screened abstracts published in PsychINFO and PubMed before December 31st, 2021, for empirical studies of six neurotoxicants (lead, mercury, PCBs, PBDEs, OPPs, and phthalates) that (1) used an individualized biomarker; (2) measured exposure during the prenatal period or before age six; and (3) provided effect estimates on general, nonverbal, and/or verbal IQ by sex. We assessed each study for risk of bias and evaluated the certainty of the evidence using Navigation Guide. We performed separate random effect meta-analyses by sex and timing of exposure with subgroup analyses by neurotoxicant.ResultsFifty-one studies were included in the systematic review and 20 in the meta-analysis. Prenatal exposure to developmental neurotoxicants was associated with decreased general and nonverbal IQ in males, especially for lead. No significant effects were found for verbal IQ, or postnatal lead exposure and general IQ. Due to the limited number of studies, we were unable to analyze postnatal effects of any of the other neurotoxicants.ConclusionDuring fetal development, males may be more vulnerable than females to general and nonverbal intellectual deficits from neurotoxic exposures, especially from lead. More research is needed to examine the nuanced sex-specific effects found for postnatal exposure to toxic chemicals.

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BackgroundAutism Spectrum Disorder (ASD) is a lifelong neurodevelopmental condition affecting communication, social interaction, and behavior. Evidence suggests that environmental pollutants are associated with ASD incidence. This review aimed to analyze the effect of environmental pollutants on ASD.MethodsSystematic review and meta-analysis of cohort studies evaluated the association between exposure to environmental pollutants and ASD. We searched COCHRANE CENTRAL, MEDLINE, CINAHL, LILACS, EMBASE, PsycINFO, Web of Science, SciELO, and gray literature from inception to January 2023. The model used for meta-analysis was inverse variance heterogeneity (IVhet). The effect measures were the beta coefficient (β) and the relative risk (RR) with their 95% confidence intervals (95% CI). Sensitivity analyses were carried out using an instrument to screen or diagnose autism.ResultsA total of 5,780 studies were identified; 27 were included in the systematic review, and 22 were included in the meta-analysis. These studies included 1,289,183 participants and 129 environmental pollutants. Individual meta-analyses found a significant association between nitrogen dioxide RR = 1.20 (95% CI: 1.03 to 1.38; I2: 91%), copper RR = 1.08 (95% CI: 1.03 to 1.13; I2: 0%), mono-3-carboxy propyl phthalate β = 0.45 (95% CI: 0.20 to 0.70; I2: 0%), monobutyl phthalate β = 0.43 (95% CI: 0.13 to 0.73; I2: 0%) and polychlorinated biphenyl (PCB) 138 RR = 1.84 (95% CI: 1.14 to 2.96; I2:0%) with ASD. Subgroup meta-analyses found a significant association with carbon monoxide RR = 1.57 (95% CI: 1.25 to 1.97; I2: 0%), nitrogen oxides RR = 1.09 (95% CI: 1.04 to 1.15; I2: 34%) and metals RR = 1.13 (95% CI: 1.01 to 1.27; I2:24%).ConclusionThis study found positive associations nitrogen dioxide, copper, mono-3-carboxypropyl phthalate, monobutyl phthalate, and PCB 138, and the development of ASD, likewise, with subgroups of pollutants carbon monoxide, nitrogen oxides, and metals. Therefore, it is important to identify these risk factors in children and adolescents to contribute to ASD and identify prevention strategies effectively.

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Objectives: This systematic review aims to assess the relationship between prenatal and childhood exposure to phthalates and neurodevelopmental outcomes, identifying periods of heightened susceptibility. Data sources considered studies examining repeated phthalate exposure during pregnancy and childhood on neurodevelopment. Methods: Evaluation included bias risk and study quality criteria. Evidence was synthesized by groups of low and high phthalate molecular weight and exposure measured prenatally and postnatally and outcome measured in childhood. Beta coefficients and their standard errors were extracted, leading to meta-analyses of various neurodevelopmental outcomes: cognition, motor skills, language, behavior, and temperament. Results: Eleven pregnancy and birth cohort studies were identified as relevant. For each phthalate group and outcome combination, there was low or very low evidence of an association, except for prenatal and postnatal phthalate exposure and behavioral development and postnatal exposure and cognition. Conclusion: The estimated effects sizes were relatively small and strong evidence for periods of heightened susceptibility could not be elucidated. No distinction between phthalates of low molecular weight and those of high molecular weight with regards to the outcomes was found.

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Polycystic ovary syndrome (PCOS) is an endocrine disorder manifesting with symptoms such as irregular menstrual cycles, hyperandrogenism, and/or polycystic ovaries. The exact cause of PCOS remains unknown, but it is believed to result from a combination of genetic predisposition, insulin resistance, low-grade inflammation, and excessive androgen production. Various environmental factors, especially endocrine-disrupting chemicals (EDCs), in addition to genetic and hormonal ones, also may influence PCOS. This is one of the first systematic reviews dealing with the exposure to non-persistent endocrine disrupting chemicals and PCOS. The review summarizes the existing knowledge about the association of EDCs with PCOS based on significant findings on the toxicity of various non-persistent environmental EDCs and polycyclic ovarian syndrome risk. A systematic search of the literature was conducted in order to identify proper studies using PubMed, Scopus, Elsevier, and Springer databases. The results of the studies suggest that there is a positive association between bisphenol A (BPA), phthalates, octocrylene, and PCOS. The data concerning triclosan and PCOS were inconclusive. Additionally, no link between the exposures to parabens and PCOS was observed. These results of the presented studies highlight the urgent need for continued research on EDCs and their role in PCOS. Int J Occup Med Environ Health. 2025;38(2):98-121.

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ObjectiveTo summarize the available evidence on the association between endocrine disruptors and polycystic ovary syndrome (PCOS).MethodsA search was conducted in the MEDLINE (via PubMed); Science direct, Scopus and LILIACS databases for relevant studies published between 2013 and 2025. The inclusion criteria covered cohort, cross-sectional, and case-control studies published in English or Spanish. Data extraction and quality assessment were performed using the Joanna Briggs Institute (JBI) checklists, and the results were synthesized descriptively. The articles retrieved were reviewed by two evaluators; 49 were chosen for full-text review, 30 were included in the qualitative analysis.ResultsThis systematic review found that bisphenol A (BPA) is the most frequently associated endocrine disruptor with PCOS. This compound interferes with steroidogenesis by mimicking estrogen, which may contribute to insulin resistance and androgen dysfunction. Additionally, phthalates were found to be related to elevated androgen levels and ovarian dysfunction, while triclosan and cadmium were associated with hormonal imbalances affecting ovarian reserve and testosterone levels. Furthermore, perfluoroalkyl and polyfluoroalkyl substances (PFAS) were linked to reduced ovarian reserve and a higher prevalence of PCOS.ConclusionsThe results of this review highlight the role of endocrine disruptors in the pathophysiology of polycystic ovary syndrome, emphasizing the need for further research to identify emerging disruptors and their potential mechanisms in the development of this disease. Therefore, it is crucial to adopt public health measures aimed at minimizing exposure to these compounds, particularly in women who are more susceptible to developing PCOS.

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Chemical simulants have long been used in human trials of mass decontamination to determine the efficacy of decontamination interventions against more toxic agents. Until now, reliance has mostly been on individual chemicals as surrogates to specific agents (e.g., methyl salicylate for sulphur mustard). A literature review was conducted to identify chemicals that had been previously tested on human volunteers and that represent diverse physicochemical characteristics in order to create a repository for chemical simulants. Of the 171 unique chemicals identified, 78 were discounted for the risk they could pose to human volunteers, 39 were deemed suitable for use, and a further 54 were considered to be possible simulants but would require further research. Suitable simulants included both solid and liquid chemicals spanning a wide range of physicochemical properties including molecular weight, octanol/water partition coefficient, vapour pressure, and solubility. This review identifies an array of potential simulants suitable for use in human volunteer decontamination studies and is of relevance to future studies on systemic absorption and surface decontamination.

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The everyday use of plastic products exposes us to plastic-associated chemicals (PACs), which have been associated with risks to human health. We present the results of the Plastic Exposure Reduction Transforms Health Trial, with an observational cohort of 211 Australian participants and a 7-day pilot randomized controlled trial in 60 participants. Intervention groups received combinations of plastic-free kitchenware, low-plastic personal-care products and food sourced from more than 100 producers that minimized all plastic touchpoints from paddock to plate, while the control group received no intervention. The primary trial outcome was a reduction in urinary plastics-associated chemicals levels. In the cohort study, highly processed, plastic-packaged and canned foods were important modifiable factors for urinary PAC metabolite levels. Additionally, we observed negative associations between cardiometabolic biomarkers and higher urinary di(2-ethylhexyl) phthalate metabolites. Our randomized controlled dietary intervention maintained participants' daily energy intake while decreasing plastic exposure (P < 0.001) and urinary levels of mono-n-butyl phthalate, monobenzyl phthalate and bisphenol A by 37.5% (95% confidence interval (CI): -55.6, -12.0; P = 0.007), 53.5% (95% CI: -72.7, -20.6; P = 0.005) and 59.7% (95% CI: -82.5, -6.87; P = 0.033), respectively. Intervention groups provided with foods that had minimal to no contact with plastic had the broadest effect on PAC excretion, and replacing low-plastic personal-care products alone led to an independent decrease in urinary mono-n-butyl phthalate, compared to no intervention. Despite constant plastic exposures, limiting food plastics touchpoints decreases select PACs in 7 days. Australian and New Zealand Clinical Trials Registry: ACTRN12622001252707 .

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Phthalic acid esters (PAEs) are a class of lipophilic chemicals widely used as plasticizers and additives to improve various products' mechanical extensibility and flexibility. At present, synthesized PAEs, which are considered to cause potential hazards to ecosystem functioning and public health, have been easily detected in the atmosphere, water, soil, and sediments; PAEs are also frequently discovered in plant and microorganism sources, suggesting the possibility that they might be biosynthesized in nature. In this review, we summarize that PAEs have not only been identified in the organic solvent extracts, root exudates, and essential oils of a large number of different plant species, but also isolated and purified from various algae, bacteria, and fungi. Dominant PAEs identified from natural sources generally include di-n-butyl phthalate, diethyl phthalate, dimethyl phthalate, di(2-ethylhexyl) phthalate, diisobutyl phthalate, diisooctyl phthalate, etc. Further studies reveal that PAEs can be biosynthesized by at least several algae. PAEs are reported to possess allelopathic, antimicrobial, insecticidal, and other biological activities, which might enhance the competitiveness of plants, algae, and microorganisms to better accommodate biotic and abiotic stress. These findings suggest that PAEs should not be treated solely as a "human-made pollutant" simply because they have been extensively synthesized and utilized; on the other hand, synthesized PAEs entering the ecosystem might disrupt the metabolic process of certain plant, algal, and microbial communities. Therefore, further studies are required to elucidate the relevant mechanisms and ecological consequences.

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