RESUMEN

Volatile organic compounds (VOCs) pose potential hazards to human health and contribute significantly to odor pollution. This study examined VOC emissions from a representative recycled rubber industry, evaluating the occupational health risks for frontline workers in various workshops. Variables such as gender and workshop-specific concentration variations were considered using Monte Carlo simulation methods. Employees in the five production workshops and office areas face noncarcinogenic health risks with hazard indices (HIs) greater than 1, with the rubber compounding phase presenting the highest risk. Acetaldehyde is identified as the primary noncarcinogenic health risk substance, with hazard quotient (HQ) values exceeding 1 in all workshops. Carcinogenic health risks vary by area, with the highest risks found in compounding and refining workshops. Formaldehyde poses the greatest risk in rubber grinding workshops and offices, with cumulative weights exceeding unacceptable levels of M80.58 % and W77.56 % in grinding and M94.98 % and W92.24 % in the office. Male workers face 4-7 % greater noncarcinogenic VOC health risks than females and 5-14 % greater carcinogenic risks from individual VOCs, increasing their susceptibility to health risks caused by VOCs. Additionally, our analysis of odor identification and intensity classification revealed that 53 VOCs are capable of causing odor pollution, with several substances reaching odor levels of 2 or higher. The predominant perceived odors, as reflected in the odor wheel, include categories such as "solvent/aromatic" and "sweet/fruit," with aldehydes being the primary odor-causing substances. In summary, emissions of VOCs from rubber industrial processes not only pose substantial health risks to workers but also contribute significantly to odor pollution. Consequently, enterprises must prioritize optimizing workplace conditions to ensure the occupational health and well-being of their employees.

Asunto(s)

Exposición Profesional , Odorantes , Reciclaje , Goma , Compuestos Orgánicos Volátiles , Compuestos Orgánicos Volátiles/análisis , Odorantes/análisis , Humanos , Exposición Profesional/análisis , Goma/química , Medición de Riesgo , Femenino , Masculino , Contaminantes Ocupacionales del Aire/análisis , Formaldehído/análisis , Formaldehído/toxicidad , Acetaldehído/análisis , Monitoreo del Ambiente , Método de Montecarlo

RESUMEN

INTRODUCTION: While ambient formaldehyde (HCHO) concentrations are increasing worldwide, there was limited research on its health effects. OBJECTIVES: To assess the association of long-term exposure to ambient HCHO with the risk of respiratory (RESP) mortality and the associated mortality burden in China. METHODS: Annual and seasonal RESP death and tropospheric HCHO vertical columns data were collected in 466 counties/districts across China during 2013-2016. A difference-in-differences approach combined with a generalized linear mixed-effects regression model was employed to assess the exposure-response association between long-term ambient HCHO exposure and RESP mortality risk. Additionally, we computed the attributable fraction (AF) to gauge the proportion of RESP mortality attributable to HCHO exposure. RESULTS: This analysis encompassed 560,929 RESP deaths. The annual mean ambient HCHO concentration across selected counties/districts was 8.02×1015 ± 2.22×1015 molec.cm-2 during 2013-2016. Each 1.00×1015 molec.cm-2 increase in ambient HCHO was associated with a 1.61 % increase [excess risk (ER), 95 % confidence interval (CI): 1.20 %, 2.03 %] in the RESP mortality risk. The AF of RESP mortality attributable to HCHO was 12.16 % (95 %CI:9.33 %, 14.88 %), resulting in an annual average of 125,422 (95 %CI:96,404, 153,410) attributable deaths in China. Stratified analyses suggested stronger associations in individuals aged ≥65 years old (ER=1.87 %, 95 %CI:1.43 %, 2.32 %), in cold seasons (ER=1.00 %, 95 %CI:0.56 %, 1.44 %), in urban areas (ER=1.65 %, 95 %CI:1.15 %, 2.16 %), and in chronic obstructive pulmonary disease patients (ER=1.95 %, 95 %CI:1.42 %, 2.48 %). CONCLUSIONS: This study suggested that long-term HCHO exposure may significantly increase the risk of RESP mortality, leading to a substantial mortality burden. Targeted measures should be implemented to control ambient HCHO pollution promptly.

Asunto(s)

Contaminantes Atmosféricos , Exposición a Riesgos Ambientales , Formaldehído , Formaldehído/análisis , Formaldehído/toxicidad , Formaldehído/efectos adversos , China/epidemiología , Humanos , Contaminantes Atmosféricos/análisis , Contaminantes Atmosféricos/efectos adversos , Exposición a Riesgos Ambientales/efectos adversos , Exposición a Riesgos Ambientales/estadística & datos numéricos , Enfermedades Respiratorias/mortalidad , Enfermedades Respiratorias/inducido químicamente , Estaciones del Año , Contaminación del Aire/efectos adversos , Contaminación del Aire/estadística & datos numéricos , Anciano , Medición de Riesgo , Masculino

RESUMEN

The number of individuals with underlying medical conditions has been increasing steadily. These individuals are relatively vulnerable to harmful external factors. But it has not been proven that the effects of hazardous chemicals may differ depending on their physicochemical properties. This study determines the toxic effects of two chemicals with high indoor exposure risk and different physicochemical properties on an underlying disease model. A pulmonary arterial hypertension (PAH) model was constructed by a single subcutaneous injection of monocrotaline (MCT; 60 mg/kg) into Sprague-Dawley rats. After three weeks, formaldehyde (FA; 2.5 mg/kg) and polyhexamethylene guanidine (PHMG; 0.05 mg/kg) were administered once via intratracheal instillation, and rats were necropsied one week later. Exposure to FA and PHMG affected organ weight and the Fulton and toxicity indices in rats induced with PAH. FA promoted bronchial injury and aggravated PAH, while PHMG only induced alveolar injury. Additionally, the differentially expressed genes were altered following exposure to FA and PHMG, as were the associated diseases (cardiovascular disease and pulmonary fibrosis, respectively). In conclusion, inhaled chemicals with different physicochemical properties can cause damage to organs, such as the lungs and heart, and can aggravate underlying diseases. This study elucidates indoor inhaled exposure-induced toxicities and alerts patients with pre-existing diseases to the harmful chemicals.

Asunto(s)

Modelos Animales de Enfermedad , Formaldehído , Lesión Pulmonar , Ratas Sprague-Dawley , Animales , Ratas , Masculino , Lesión Pulmonar/inducido químicamente , Lesión Pulmonar/patología , Formaldehído/toxicidad , Guanidinas/toxicidad , Monocrotalina/toxicidad , Exposición por Inhalación , Pulmón/efectos de los fármacos , Pulmón/patología , Hipertensión Arterial Pulmonar/inducido químicamente , Sustancias Peligrosas/toxicidad

RESUMEN

Formaldehyde (FA) as a common organic compound has been shown to cause placental dysfunction and fetal defects. The potential benefits of fish oil (FOil) in protecting placental structures are attributed to its antioxidant properties. This study aimed to explore the preventive role of FOil in mitigating the adverse effects of FA in pregnant rats. Thirty pregnant Wistar rats were randomly categorized into five groups of control, sham (Normal saline; Orally and intraperitoneally), FOil (0.5 ml/day; Orally), FA (5 mg/kg/bw; intraperitoneally), FA+FOil. The treatment period was from day 0-20 of pregnancy. On the 20th day of pregnancy, placental morphometric parameters were measured. The histological and histochemical analyses were performed using H&E and PAS staining, respectively. Also, the placenta tissue was analyzed for oxidative stress biomarkers, p-53 protein levels, and the expression of caspase-3 gene. The administration of FA led to a significant decrease in the weight, diameter, and thickness of the placenta, as well as a decrease in the thickness of the decidua layer, junctional and labyrinth zone, and the number of trophoblast giant cells in rat placentas. FA led to a significant increase in placental p-53 protein levels, caspase-3 expression, and oxidative stress biomarkers. Administration of FOil to pregnant rats treated with FA led to a significant decrease in morphometric and histological changes, oxidative stress, and the expression of genes associated with apoptosis. The findings suggest that the administration of FOil to FA-treated pregnant rats can protect placental histopathological changes by enhancing the activity of the antioxidant enzymes.

Asunto(s)

Apoptosis , Caspasa 3 , Aceites de Pescado , Formaldehído , Estrés Oxidativo , Placenta , Ratas Wistar , Animales , Femenino , Placenta/efectos de los fármacos , Placenta/patología , Placenta/metabolismo , Embarazo , Estrés Oxidativo/efectos de los fármacos , Formaldehído/toxicidad , Aceites de Pescado/farmacología , Apoptosis/efectos de los fármacos , Caspasa 3/metabolismo , Antioxidantes/farmacología , Suplementos Dietéticos , Proteína p53 Supresora de Tumor/metabolismo , Proteína p53 Supresora de Tumor/genética , Ratas

RESUMEN

Formaldehyde (FA) is a carcinogen that is not only widespread in the environment, but is also produced endogenously by metabolic processes. In organisms, FA is converted to formic acid in a glutathione (GSH)-dependent manner by alcohol dehydrogenase 5 (ADH5). The abnormal accumulation of FA in the body can cause a variety of diseases, especially cognitive impairment leading to Alzheimer's disease (AD). In this study, melatonin derivative 6a (MD6a) markedly improved the survival and chemotactic performance of wild-type Caenorhabditis elegans exposed to high concentrations of FA. MD6a lowered FA levels in the nematodes by enhancing the release of covalently-bound GSH from S-hydroxymethyl-GSH in an adh-5-dependent manner. In addition, MD6a protected against mitochondrial dysfunction and cognitive impairment in beta-amyloid protein (Aß) transgenic nematodes by lowering endogenous FA levels and reducing Aß aggregation in an adh-5-dependent manner. Our findings suggest that MD6a detoxifies FA via ADH5 and protects against Aß toxicity by reducing endogenous FA levels in the C. elegans AD models. Thus, ADH5 might be a potential therapeutic target for FA toxicity and AD.

Asunto(s)

Alcohol Deshidrogenasa , Enfermedad de Alzheimer , Péptidos beta-Amiloides , Proteínas de Caenorhabditis elegans , Caenorhabditis elegans , Formaldehído , Melatonina , Animales , Caenorhabditis elegans/metabolismo , Caenorhabditis elegans/efectos de los fármacos , Melatonina/farmacología , Formaldehído/toxicidad , Péptidos beta-Amiloides/metabolismo , Péptidos beta-Amiloides/toxicidad , Enfermedad de Alzheimer/metabolismo , Enfermedad de Alzheimer/patología , Enfermedad de Alzheimer/genética , Alcohol Deshidrogenasa/metabolismo , Alcohol Deshidrogenasa/genética , Proteínas de Caenorhabditis elegans/metabolismo , Proteínas de Caenorhabditis elegans/genética , Animales Modificados Genéticamente , Glutatión/metabolismo , Modelos Animales de Enfermedad , Mitocondrias/metabolismo , Mitocondrias/efectos de los fármacos , Humanos , Formiatos

RESUMEN

The paraventricular hypothalamic nucleus (PVH) is an important neuroendocrine center involved in pain regulation, but the nociceptive afferent routes for the nucleus are still unclear. We examined the profile of PVH receiving injurious information by a combination of retrograde tracing with Fluoro-Gold (FG) and FOS expression induced by formalin stimuli. The result showed that formalin injection induced significantly increased expression of FOS in the PVH, among which oxytocin containing neurons are one neuronal phenotype. Immunofluorescent staining of FG and FOS revealed that double labeled neurons were strikingly distributed in the area 2 of the cingulate cortex (Cg2), the lateral septal nucleus (LS), the periaqueductal gray (PAG), the posterior hypothalamic area (PH), and the lateral parabrachial nucleus (LPB). In the five regions, LPB had the biggest number and the highest ratio of FOS expression in FG labeled neurons, with main subnuclei distribution in the external, superior, dorsal, and central parts. Further immunofluorescent triple staining disclosed that about one third of FG and FOS double labeled neurons in the LPB were immunoreactive for calcitonin gene related peptide (CGRP). In conclusion, the present study demonstrates the nociceptive input profile of the PVH area under inflammatory pain and suggests that neurons in the LPB may play essential roles in transmitting noxious information to the PVH.

Asunto(s)

Formaldehído , Núcleo Hipotalámico Paraventricular , Animales , Núcleo Hipotalámico Paraventricular/metabolismo , Núcleo Hipotalámico Paraventricular/efectos de los fármacos , Formaldehído/toxicidad , Masculino , Péptido Relacionado con Gen de Calcitonina/metabolismo , Ratones , Nocicepción/efectos de los fármacos , Nocicepción/fisiología , Proteínas Proto-Oncogénicas c-fos/metabolismo , Neuronas/metabolismo , Neuronas/efectos de los fármacos , Oxitocina/metabolismo , Dolor/metabolismo , Dolor/inducido químicamente , Núcleos Parabraquiales/metabolismo , Núcleos Parabraquiales/efectos de los fármacos

RESUMEN

Formaldehyde (FA) is a recognized environmental and metabolic toxin implicated in cancer development and aging. Inherited mutations in the FA-detoxifying enzymes ADH5 and ALDH2 genes lead to FA overload in the severe multisystem AMeD syndrome. FA accumulation causes genome damage including DNA-protein-, inter- and intra-strand crosslinks and oxidative lesions. However, the influence of distinct DNA repair systems on organismal FA resistance remains elusive. We have here investigated the consequence of a range of DNA repair mutants in a model of endogenous FA overload generated by downregulating the orthologs of human ADH5 and ALDH2 in C. elegans. We have focused on the distinct components of nucleotide excision repair (NER) during developmental growth, reproduction and aging. Our results reveal three distinct modes of repair of FA-induced DNA damage: Transcription-coupled repair (TCR) operating NER-independently during developmental growth or through NER during adulthood, and, in concert with global-genome (GG-) NER, in the germline and early embryonic development. Additionally, we show that the Cockayne syndrome B (CSB) factor is involved in the resolution of FA-induced DNA-protein crosslinks, and that the antioxidant and FA quencher N-acetyl-l-cysteine (NAC) reverses the sensitivity of detoxification and DNA repair defects during development, suggesting a therapeutic intervention to revert FA-pathogenic consequences.

Asunto(s)

Envejecimiento , Proteínas de Caenorhabditis elegans , Caenorhabditis elegans , Daño del ADN , Reparación del ADN , Formaldehído , Reproducción , Caenorhabditis elegans/genética , Caenorhabditis elegans/efectos de los fármacos , Caenorhabditis elegans/crecimiento & desarrollo , Formaldehído/toxicidad , Animales , Reproducción/efectos de los fármacos , Reproducción/genética , Envejecimiento/genética , Proteínas de Caenorhabditis elegans/metabolismo , Proteínas de Caenorhabditis elegans/genética , Aldehído Deshidrogenasa/genética , Aldehído Deshidrogenasa/metabolismo , Mutación , Humanos , Transcripción Genética/efectos de los fármacos , Acetilcisteína/farmacología , Aldehído Oxidorreductasas

RESUMEN

The correlation between formaldehyde (FA) exposure and prevalence of asthma has been widely reported. However, the underlying mechanism is still not fully understood. FA exposure at 2.0 mg/m3 was found to exacerbate asthma in OVA-induced murine models. IFN-γ, the cytokine produced by T helper 1 (Th1) cells, was significantly induced by FA in serum and bronchoalveolar lavage fluid (BALF) of asthmatic mice, which was different from cytokines secreted by other Th cells. The observation was also confirmed by mRNA levels of Th marker genes in CD4+ T cells isolated from BALF. In addition, increased production of IFN-γ and expression of T-bet in Jurkat T cells primed with phorbol ester and phytohaemagglutinin were also observed with 100 µM FA treatment in vitro. Upregulated STAT1 phosphorylation, T-bet expression and IFN-γ production induced by FA was found to be restrained by STAT1 inhibitor fludarabine, indicating that FA promoted Th1 commitment through the autocrine IFN-γ/STAT1/T-bet pathway in asthma. This work not only revealed that FA could bias Th lineage commitment to exacerbate allergic asthma, but also identified the signaling mechanism of FA-induced Th1 differentiation, which may be utilized as the target for development of interfering strategies against FA-induced immune disorders.

Asunto(s)

Asma , Formaldehído , Interferón gamma , Factor de Transcripción STAT1 , Proteínas de Dominio T Box , Asma/inducido químicamente , Animales , Factor de Transcripción STAT1/metabolismo , Interferón gamma/metabolismo , Ratones , Proteínas de Dominio T Box/genética , Proteínas de Dominio T Box/metabolismo , Formaldehído/toxicidad , Inflamación/inducido químicamente , Ratones Endogámicos BALB C , Humanos , Femenino , Líquido del Lavado Bronquioalveolar/citología , Líquido del Lavado Bronquioalveolar/química , Linfocitos T Colaboradores-Inductores/efectos de los fármacos , Transducción de Señal/efectos de los fármacos , Células TH1/efectos de los fármacos , Células TH1/inmunología , Células Jurkat

RESUMEN

OBJECTIVE: Cigarette smoking can lead to a host of adverse health effects such as lung and heart disease. Increased lung cancer risk is associated with inhalation of carcinogens present in a puff of smoke. These carcinogenic compounds deposit in the lung at different sites and trigger a cascade of events leading to adverse outcomes. Understanding the site-specific deposition of various smoke constituents will inform the study of respiratory diseases from cigarette smoking. We previously developed a deposition model for inhalation of aerosol from electronic nicotine delivery systems. In this study, the model was modified to simulate inhalation of cigarette smoke consisting of soluble and insoluble tar, nicotine, and cigarette-specific constituents that are known or possible human carcinogens. MATERIALS AND METHODS: The deposition model was further modified to account for nicotine protonation and other cigarette-specific physics-based mechanisms that affect smoke deposition. Model predictions showed a total respiratory tract uptake in the lung for formaldehyde (99%), nicotine (80%), and benzo[a]pyrene (60%). RESULTS: The site of deposition and uptake depended primarily on the constituent's saturation vapor pressure. High vapor pressure constituents such as formaldehyde were preferentially absorbed in the oral cavity and proximal lung regions, while low vapor pressure constituents such as benzo[a]pyrene were deposited in the deep lung regions. Model predictions of exhaled droplet size, droplet retention, nicotine retention, and uptake of aldehydes compared favorably with experimental data. CONCLUSION: The deposition model can be integrated into exposure assessments and other studies that evaluate potential adverse health effects from cigarette smoking.

Asunto(s)

Nicotina , Humanos , Nicotina/administración & dosificación , Nicotina/farmacocinética , Modelos Biológicos , Humo/análisis , Humo/efectos adversos , Formaldehído/análisis , Formaldehído/toxicidad , Productos de Tabaco/análisis , Benzo(a)pireno/farmacocinética , Benzo(a)pireno/análisis , Sistema Respiratorio/efectos de los fármacos , Sistema Respiratorio/metabolismo , Pulmón/efectos de los fármacos , Pulmón/metabolismo , Aerosoles , Administración por Inhalación , Exposición por Inhalación/efectos adversos , Fumar Cigarrillos , Sistemas Electrónicos de Liberación de Nicotina

RESUMEN

Body embalming, a practice with deep historical roots across various cultures, forms the backbone of contemporary human body donation educational programmes. In this study, we explored current embalming practices within six South African human anatomical dissection programmes, focusing on the use and volumes of key chemicals-formalin, phenol, and alcohol-and their associated health risks and potential toxicity. We measured and compared aspects of embalming practices such as the duration of body preservation and the annual intake of bodies. Variations in embalming practices and chemical ratios across different South African universities were found. However, the consistent use of formalin, phenol and alcohol were observed across all six programmes. Formaldehyde concentrations used in South African dissection programmes were within the generally acceptable international range. Regarding arterial embalming, South African dissection programmes showed widespread adherence to international embalming practices, with one programme using a substantially lower concentration of formalin. The dual nature of formaldehyde as both an effective preservative and a recognised carcinogen was underscored in relation to human health regarding chemical toxicity. Phenol, like formaldehyde, was consistently used as it is important for the inhibition of bacterial and fungal growth. Alcohol was also consistently used, but there was much greater variation in its volume across South African institutions. Our data showed a slight positive relationship between storage duration and the volumes of formalin and phenol in human embalming fluid. South African regulators enforce stricter exposure limits than those set by the World Health Organisation and various European agencies. While South African institutions operate within internationally acceptable ranges of chemical use that both maximise preservation and minimise toxicity, we acknowledge that these data are preliminary. Further investigation is encouraged to ensure embalming practices effectively protect all those involved and support the educational goals of human anatomical dissection programmes in South Africa.

Asunto(s)

Embalsamiento , Formaldehído , Fenol , Humanos , Embalsamiento/métodos , Sudáfrica , Formaldehído/toxicidad , Cadáver , Disección , Anatomía/educación , Etanol , Fijadores , Obtención de Tejidos y Órganos

RESUMEN

ETHNOPHARMACOLOGICAL RELEVANCE: Mucuna pruriens L is a wild and cultivated leguminous plant which have been used as an aphrodisiac, diuretic, nerve tonic, and antiarthritic agent. AIM: To evaluate the toxicity, antinociceptive, and anti-inflammatory activities of M. pruriens (EEMP) ethanol extract in experimental models. METHODS: M. pruriens dried leaves were extracted using aqueous ethanol (30:70). Tests for acute and subacute toxicity were conducted on rats and mice. Mice were used in hotplate, acetic acid, and formalin models to test the antinociceptive activity of EEMP. The anti-inflammatory properties of EEMP (25, 100, and 400 mg/kg) were assessed egg albumin, carrageenan, and formalin-induced oedema models. The study examined the anti-inflammatory mechanism of EEMP (25-400 mg/kg) in rats with an air pouch caused by carrageenan. Air pouch exudates were tested for total leucocytes and differential cell counts, TNF-α, IL-6, myeloperoxidase activity, malondialdehyde, nitrites, and reduced glutathione (GSH). RESULTS: The acute oral toxic dose of EEMP is greater than 2000 mg/kg. There were no significant behavioral, hematological or biochemical alterations seen after 14-days repeated administration of EEMP (200, 400 and 800 mg/kg) in mice. The EEMP demonstrated significant antinociceptive activity in hotplate, acetic acid and formalin-induced nociception in mice. The EEMP significantly and dose dependently reduced paw oedema at 2, 4 and 96 h in the egg-albumin, carrageenan- and formalin-induced paw oedema, respectively. Exudates volume, inflammatory cell counts, TNF-α, IL-6, myeloperoxidase, malondialdehyde and nitrites were significantly reduced, while GSH increased in carrageenan-air pouch of EEMP-treated rats. CONCLUSION: Mucuna pruriens leaves ethanol extract demonstrated good safety profile as well as antinociceptive and anti-inflammatory activity through mechanisms related to inhibition of oxidative stress and pro-inflammatory cytokines as well as lysosomal membrane stability.

Asunto(s)

Analgésicos , Antiinflamatorios , Edema , Mucuna , Extractos Vegetales , Hojas de la Planta , Animales , Extractos Vegetales/farmacología , Analgésicos/farmacología , Antiinflamatorios/farmacología , Antiinflamatorios/aislamiento & purificación , Masculino , Ratones , Edema/tratamiento farmacológico , Edema/inducido químicamente , Ratas , Mucuna/química , Femenino , Dolor/tratamiento farmacológico , Dolor/inducido químicamente , Carragenina , Ratas Wistar , Relación Dosis-Respuesta a Droga , Ratas Sprague-Dawley , Modelos Animales de Enfermedad , Formaldehído/toxicidad , Pruebas de Toxicidad Subaguda

RESUMEN

Pain in Parkinson's disease (PD) has been validated as one of the major non-motor dysfunctions affecting the quality of life and subsequent rehabilitation. In the present study, we investigated the role of the dopamine D3 receptor in the thalamic mediodorsal (MD) and ventromedial (VM) nuclei mediated descending control of nociception and intramuscular (i.m.) 2.5% formalin-induced persistent muscle nociception. Paw withdrawal reflexes were measured in naive rats and rats subjected to PD induced by unilateral microinjection of 6 µg 6-OHDA into the rat striatum. Formalin-induced muscle nociception in phase 1, inter-phase, and phase 2 was significantly greater in PD rats compared to naive and vehicle-treated rats (P < 0.001). PD rats exhibited bilaterally mechanical hyperalgesia and heat hypoalgesia in formalin-induced muscle nociception. Microinjection of SK609, a dopamine D3 receptor agonist, at various doses (2.5-7.5 nmol/0.5 µl) into the thalamic VM nucleus dose-dependently prolonged heat-evoked paw withdrawal latencies in both naive and PD rats. Administration of SK609 to either the MD or VM nuclei had no effect on noxious mechanically evoked paw withdrawal reflexes. Pre-treatment of the thalamic MD nucleus with SK609 significantly attenuated formalin-induced nociception, and reversed mechanical hyperalgesia, but not heat hypoalgesia. Pre-treatment of the thalamic VM nucleus with SK609 inhibited formalin-induced nociception in the late phase of phase 2 (30-75 min) and heat hypoalgesia, but not mechanical hyperalgesia (P < 0.05). It is suggested that the dopamine D3 receptors in the thalamus play an antinociceptive role in the descending modulation of nociception. Activation of D3 receptors within the thalamic MD and VM nuclei attenuates descending facilitation and enhances descending inhibition in rats during PD.

Asunto(s)

Modelos Animales de Enfermedad , Formaldehído , Nocicepción , Ratas Sprague-Dawley , Receptores de Dopamina D3 , Animales , Ratas , Masculino , Receptores de Dopamina D3/agonistas , Receptores de Dopamina D3/metabolismo , Formaldehído/toxicidad , Nocicepción/efectos de los fármacos , Nocicepción/fisiología , Hiperalgesia/inducido químicamente , Hiperalgesia/tratamiento farmacológico , Tálamo/efectos de los fármacos , Tálamo/metabolismo , Dimensión del Dolor/métodos , Oxidopamina/toxicidad

RESUMEN

Formaldehyde, a known carcinogenic compound, is commonly used in various medical settings. The objective of this study was to assess the carcinogenic and non-carcinogenic risks associated with occupational exposure to formaldehyde. This study was conducted in the pathology labs of four hospitals in Tehran. Cancer and non-cancer risks were evaluated using the quantitative risk assessment method proposed by the United States environmental protection agency (USEPA), along with its provided database known as the integrated risk information system (IRIS). Respiratory symptoms were assessed using the American thoracic society (ATS) questionnaire. The results indicated that 91.23% of exposure levels in occupational groups exceed the NIOSH standard of 0.016 ppm. Regarding carcinogenic risk, 41.03% of all the studied subjects were in the definite carcinogenic risk range (LCR > 10-4), 23.08% were in the possible carcinogenic risk range (10-5 < LCR < 10-4), and 35.90% were in the negligible risk range (LCR < 10-6). The highest index of occupational carcinogenesis was observed in the group of lab technicians with a risk number of 3.7 × 10-4, followed by pathologists with a risk number of 1.7 × 10-4. Furthermore, 23.08% of the studied subjects were within the permitted health risk range (HQ < 1.0), while 76.92% were within the unhealthy risk range (HQ > 1.0). Overall, the findings revealed significantly higher carcinogenic and non-carcinogenic risks among lab technicians and pathologists. Therefore, it is imperative to implement control measures across various hospital departments to mitigate occupational formaldehyde exposure levels proactively. These findings can be valuable for policymakers in the health sector, aiding in the elimination or reduction of airborne formaldehyde exposure in work environments.

Asunto(s)

Carcinógenos , Formaldehído , Exposición Profesional , Formaldehído/efectos adversos , Formaldehído/toxicidad , Formaldehído/análisis , Humanos , Exposición Profesional/efectos adversos , Exposición Profesional/análisis , Irán/epidemiología , Medición de Riesgo , Carcinógenos/toxicidad , Carcinógenos/análisis , Masculino , Femenino , Adulto , Hospitales , Persona de Mediana Edad , Encuestas y Cuestionarios , Laboratorios de Hospital

RESUMEN

AIMS: The preoptic area (POA) of the hypothalamus, crucial in thermoregulation, has long been implicated in the pain process. However, whether nociceptive stimulation affects body temperature and its mechanism remains poorly studied. METHODS: We used capsaicin, formalin, and surgery to induce acute nociceptive stimulation and monitored rectal temperature. Optical fiber recording, chemical genetics, confocal imaging, and pharmacology assays were employed to confirm the role and interaction of POA astrocytes and extracellular adenosine. Immunofluorescence was utilized for further validation. RESULTS: Acute nociception could activate POA astrocytes and induce a decrease in body temperature. Manipulation of astrocytes allowed bidirectional control of body temperature. Furthermore, acute nociception and astrocyte activation led to increased extracellular adenosine concentration within the POA. Activation of adenosine A1 or A2A receptors contributed to decreased body temperature, while inhibition of these receptors mitigated the thermo-lowering effect of astrocytes. CONCLUSION: Our results elucidate the interplay between acute nociception and thermoregulation, specifically highlighting POA astrocyte activation. This enriches our understanding of physiological responses to painful stimuli and contributes to the analysis of the anatomical basis involved in the process.

Asunto(s)

Astrocitos , Hipotermia , Nocicepción , Área Preóptica , Animales , Área Preóptica/efectos de los fármacos , Área Preóptica/metabolismo , Astrocitos/metabolismo , Astrocitos/efectos de los fármacos , Nocicepción/fisiología , Hipotermia/inducido químicamente , Masculino , Ratones , Receptores Purinérgicos P1/metabolismo , Ratones Endogámicos C57BL , Adenosina/metabolismo , Capsaicina/farmacología , Formaldehído/toxicidad , Formaldehído/farmacología

RESUMEN

BACKGROUND: Exposure to air pollution has been proposed as one of the potential risk factors for leukaemia. Work-related formaldehyde exposure is suspected to cause leukaemia. METHODS: We conducted a nested register-based case-control study on leukaemia incidence in the Viadana district, an industrial area for particleboard production in Northern Italy. We recruited 115 cases and 496 controls, frequency-matched by age, between 1999 and 2014. We assigned estimated exposures to particulate matter (PM10, PM2.5), nitrogen dioxide (NO2), and formaldehyde at residential addresses, averaged over the susceptibility window 3rd to 10th year prior to the index date. We considered potential confounding by sex, age, nationality, socio-economic status, occupational exposures to benzene and formaldehyde, and prior cancer diagnoses. RESULTS: There was no association of exposures to PM10, PM2.5, and NO2 with leukaemia incidence. However, an indication of increased risk emerged for formaldehyde, despite wide statistical uncertainty (OR 1.46, 95%CI 0.65-3.25 per IQR-difference of 1.2 µg/m3). Estimated associations for formaldehyde were higher for acute (OR 2.07, 95%CI 0.70-6.12) and myeloid subtypes (OR 1.79, 95%CI 0.64-5.01), and in the 4-km buffer around the industrial facilities (OR 2.78, 95%CI 0.48-16.13), although they remained uncertain. CONCLUSIONS: This was the first study investigating the link between ambient formaldehyde exposure and leukaemia incidence in the general population. The evidence presented suggests an association, although it remains inconclusive, and a potential significance of emissions related to industrial activities in the district. Further research is warranted in larger populations incorporating data on other potential risk factors.

Asunto(s)

Contaminantes Atmosféricos , Contaminación del Aire , Exposición a Riesgos Ambientales , Formaldehído , Leucemia , Material Particulado , Italia/epidemiología , Humanos , Leucemia/epidemiología , Leucemia/inducido químicamente , Leucemia/etiología , Estudios de Casos y Controles , Masculino , Incidencia , Femenino , Persona de Mediana Edad , Contaminantes Atmosféricos/análisis , Exposición a Riesgos Ambientales/efectos adversos , Adulto , Formaldehído/análisis , Formaldehído/toxicidad , Anciano , Material Particulado/análisis , Contaminación del Aire/efectos adversos , Contaminación del Aire/análisis , Dióxido de Nitrógeno/análisis , Adulto Joven

RESUMEN

After confirming that formaldehyde (FA) is carcinogenic, many studies were conducted in different countries to investigate this finding. Therefore, according to the dispersion of related studies, a bibliometric review of the current literature was performed with the aim of better understanding the exposure to FA and the resulting health risk, for the first time, using the Scopus database and the two open-source software packages, Bibliometrix R package. After screening the documents in Excel, the data was analyzed based on three aspects including performance analysis, conceptual structure, and intellectual structure, and the results were presented in tables and diagrams. A total of 468 documents were analyzed over period 1977-2023, in which 1956 authors from 56 countries participated. The number of scientific publications has grown significantly from 1977 (n = 1) to 2022 (n = 19). Zhang Y., from the Yale School of Public Health (USA), was identified as the most impactful author in this field. The Science of the Total Environment journal was identified as the main source of articles related to exposure to formaldehyde by publishing 25 studies. The United States and China were the most active countries with the most international collaboration. The main topics investigated during these 46 years included "formaldehyde" and "health risk assessment", which have taken new directions in recent years with the emergence of the keyword "asthma". The present study provides a comprehensive view of the growth and evolution of studies related to formaldehyde and the resulting health risks, which can provide a better understanding of existing research gaps and new and emerging issues.

Asunto(s)

Exposición a Riesgos Ambientales , Formaldehído , Formaldehído/toxicidad , Humanos , Medición de Riesgo , Bibliometría

RESUMEN

INTRODUCTION: Causal epidemiology for regulatory risk analysis seeks to evaluate how removing or reducing exposures would change disease occurrence rates. We define interventional probability of causation (IPoC) as the change in probability of a disease (or other harm) occurring over a lifetime or other specified time interval that would be caused by a specified change in exposure, as predicted by a fully specified causal model. We define the closely related concept of causal assigned share (CAS) as the predicted fraction of disease risk that would be removed or prevented by a specified reduction in exposure, holding other variables fixed. Traditional approaches used to evaluate the preventable risk implications of epidemiological associations, including population attributable fraction (PAF) and the Bradford Hill considerations, cannot reveal whether removing a risk factor would reduce disease incidence. We argue that modern formal causal models coupled with causal artificial intelligence (CAI) and realistically partial and imperfect knowledge of underlying disease mechanisms, show great promise for determining and quantifying IPoC and CAS for exposures and diseases of practical interest. METHODS: We briefly review key CAI concepts and terms and then apply them to define IPoC and CAS. We present steps to quantify IPoC using a fully specified causal Bayesian network (BN) model. Useful bounds for quantitative IPoC and CAS calculations are derived for a two-stage clonal expansion (TSCE) model for carcinogenesis and illustrated by applying them to benzene and formaldehyde based on available epidemiological and partial mechanistic evidence. RESULTS: Causal BN models for benzene and risk of acute myeloid leukemia (AML) incorporating mechanistic, toxicological and epidemiological findings show that prolonged high-intensity exposure to benzene can increase risk of AML (IPoC of up to 7e-5, CAS of up to 54%). By contrast, no causal pathway leading from formaldehyde exposure to increased risk of AML was identified, consistent with much previous mechanistic, toxicological and epidemiological evidence; therefore, the IPoC and CAS for formaldehyde-induced AML are likely to be zero. CONCLUSION: We conclude that the IPoC approach can differentiate between likely and unlikely causal factors and can provide useful upper bounds for IPoC and CAS for some exposures and diseases of practical importance. For causal factors, IPoC can help to estimate the quantitative impacts on health risks of reducing exposures, even in situations where mechanistic evidence is realistically incomplete and individual-level exposure-response parameters are uncertain. This illustrates the strength that can be gained for causal inference by using causal models to generate testable hypotheses and then obtaining toxicological data to test the hypotheses implied by the models-and, where necessary, refine the models. This virtuous cycle provides additional insight into causal determinations that may not be available from weight-of-evidence considerations alone.

Asunto(s)

Benceno , Formaldehído , Leucemia Mieloide Aguda , Humanos , Benceno/toxicidad , Leucemia Mieloide Aguda/epidemiología , Leucemia Mieloide Aguda/inducido químicamente , Formaldehído/toxicidad , Causalidad , Probabilidad , Medición de Riesgo , Exposición a Riesgos Ambientales , Factores de Riesgo

RESUMEN

OBJECTIVES: Korea's aquaculture sector primarily cultivates aquatic life, with fish seed production as a focus. Formalin, a parasiticide, consists of 37% formaldehyde mixed with yellow No. 4 dye. Formaldehyde vaporization poses cancer risks, classified as a carcinogen. Korea regulates formaldehyde as a hazardous substance, requiring workplace environment measurements. Few aquaculture farms have conducted these checks in recent years. In this study, we investigated actual formaldehyde exposure levels among Korean aquaculture workers, highlighting a critical safety concern. METHODS: A field survey was conducted to measure formaldehyde exposure at 10 aquaculture farms in areas where Korean aquaculture is concentrated. Short-term and long-term personal samples, local samples, and direct-reading measurements were conducted. Formaldehyde exposure levels were detected in short-term personal samples from six farms and in long-term personal samples from two farms, and formaldehyde was detected in all local samples. In direct-reading measurements, a high concentration of formaldehyde was sustained for short periods. RESULTS: Long-term (8-hour) personal samples were mostly non-detectable, except for farms A and D, which had levels of 0.0009 ppm and 0.0017 ppm, respectively. Short-term (15-minute) samples were non-detectable in four farms, with an average of 0.0158 (±0.0130) ppm in the remaining six farms. Local samples from all farms had an average of 0.0384 (±0.0957) ppm of formaldehyde. For farms A and D, where long-term sampling detected formaldehyde, real-time measurements showed a sustained high concentration in farm A for about 48 minutes before decreasing. Farm D had no detectable formaldehyde throughout the monitoring period. CONCLUSION: According to the formaldehyde exposure level assessment, short term exposure to formaldehyde during and immediately after application of formalin nearly exceeded the ACGIH TLV STEL in one farm. However, concentration of long term samples appeared at 10% of ACGIH TLV TWA. Additional study is recommended to determine whether exposure to formaldehyde poses a health risk for aquaculture workers during application of formalin.

Asunto(s)

Acuicultura , Formaldehído , Exposición Profesional , Formaldehído/análisis , Formaldehído/toxicidad , Formaldehído/efectos adversos , Humanos , República de Corea , Exposición Profesional/análisis , Monitoreo del Ambiente , Agricultores/estadística & datos numéricos , Contaminantes Ocupacionales del Aire/análisis , Adulto

RESUMEN

Lung inflammatory disorders are a major global health burden, impacting millions of people and raising rates of morbidity and death across many demographic groups. An industrial chemical and common environmental contaminant, formaldehyde (FA) presents serious health concerns to the respiratory system, including the onset and aggravation of lung inflammatory disorders. Epidemiological studies have shown significant associations between FA exposure levels and the incidence and severity of several respiratory diseases. FA causes inflammation in the respiratory tract via immunological activation, oxidative stress, and airway remodelling, aggravating pre-existing pulmonary inflammation and compromising lung function. Additionally, FA functions as a respiratory sensitizer, causing allergic responses and hypersensitivity pneumonitis in sensitive people. Understanding the complicated processes behind formaldehyde-induced lung inflammation is critical for directing targeted strategies aimed at minimizing environmental exposures and alleviating the burden of formaldehyde-related lung illnesses on global respiratory health. This abstract explores the intricate relationship between FA exposure and lung inflammatory diseases, including asthma, bronchitis, allergic inflammation, lung injury and pulmonary fibrosis.

Asunto(s)

Asma , Bronquitis , Formaldehído , Fibrosis Pulmonar , Formaldehído/toxicidad , Formaldehído/efectos adversos , Humanos , Asma/inducido químicamente , Fibrosis Pulmonar/inducido químicamente , Bronquitis/inducido químicamente , Animales , Exposición a Riesgos Ambientales/efectos adversos , Pulmón/efectos de los fármacos , Pulmón/patología , Neumonía/inducido químicamente , Estrés Oxidativo/efectos de los fármacos , Inflamación/inducido químicamente

RESUMEN

This systematic review and meta-analysis investigated studies on formaldehyde (FA) inhalation exposure in indoor environments and related carcinogenic (CR) and non-carcinogenic (HQ) risk. Studies were obtained from Scopus, PubMed, Web of Science, Medline, and Embase databases without time limitation until November 21, 2023. Studies not meeting the criteria of Population, Exposure, Comparator, and Outcomes (PECO) were excluded. The 45 articles included belonged to the 5 types of sites: dwelling environments, educational centers, kindergartens, vehicle cabins, and other indoor environments. A meta-analysis determined the average effect size (ES) between indoor FA concentrations, CR, and HQ values in each type of indoor environment. FA concentrations ranged from 0.01 to 1620 µg/m3. The highest FA concentrations were stated in water pipe cafés and the lowest in residential environments. In more than 90% of the studies uncertain (1.00 ×10-6 1.00 ×10-4) due to FA inhalation exposure was reported and non-carcinogenic risk was stated acceptable. The meta-analysis revealed the highest CR values due to inhalation of indoor FA in high-income countries. As 90% of the time is spent indoors, it is crucial to adopt effective strategies to reduce FA concentrations, especially in kindergartens and schools, with regular monitoring of indoor air quality.

Asunto(s)

Contaminación del Aire Interior , Formaldehído , Exposición por Inhalación , Formaldehído/análisis , Formaldehído/toxicidad , Contaminación del Aire Interior/análisis , Exposición por Inhalación/análisis , Medición de Riesgo , Humanos