ABSTRACT
OBJECTIVES: Three distinct models were utilized to investigate the combined impacts of serum aldehyde exposure and periodontitis. MATERIALS AND METHODS: We performed a cross-sectional analysis using data from 525 participants in the 2013-2014 National Health and Nutrition Examination Survey (NHANES). The directed acyclic graphs (DAG) were used to select a minimal sufficient adjustment set of variables (MSAs). To investigate the relationship between aldehydes and periodontitis, we established three models including multiple logistic regression model, restricted cubic spline (RCS) model, and Bayesian kernel machine regression (BKMR) model. RESULTS: After taking all covariates into account, the multiple logistic regression model revealed that elevated concentrations of isopentanaldehyde and propanaldehyde were strongly associated with periodontitis (isopentanaldehyde: OR: 2.38, 95% CI: 1.34-4.23; propanaldehyde: OR: 1.51, 95% CI: 1.08-2.13). Furthermore, the third tertile concentration of isopentanaldehyde was associated with a 2.04-fold increase in the incidence of periodontitis (95% CI: 1.05-3.95) compared to the first tertile concentration, with a P for trend = 0.04. RCS models showed an "L"-shaped relationship between isopentanaldehyde and periodontitis (P for nonlinear association < 0.01), with inflection point of 0.43 ng/mL. BKMR identified a strong connection between mixed aldehydes and periodontitis, with isopentanaldehyde exhibiting the greatest posterior inclusion probability (PIP) with 0.901 and propanaldehyde exhibiting a PIP with 0.775. CONCLUSIONS: Isopentanaldehyde and propanaldehyde are positively associated with the risk of periodontitis. CLINICAL RELEVANCE: Periodontitis may be associated with exposure to mixed aldehyde. This study emphasizes the important role of aldehydes in primary prevention of periodontitis.
Subject(s)
Aldehydes , Periodontitis , Humans , Bayes Theorem , Cross-Sectional Studies , Nutrition Surveys , Aldehydes/adverse effects , Periodontitis/epidemiologyABSTRACT
Fanconi anaemia (FA), a model syndrome of genome instability, is caused by a deficiency in DNA interstrand crosslink repair resulting in chromosome breakage1-3. The FA repair pathway protects against endogenous and exogenous carcinogenic aldehydes4-7. Individuals with FA are hundreds to thousands fold more likely to develop head and neck (HNSCC), oesophageal and anogenital squamous cell carcinomas8 (SCCs). Molecular studies of SCCs from individuals with FA (FA SCCs) are limited, and it is unclear how FA SCCs relate to sporadic HNSCCs primarily driven by tobacco and alcohol exposure or infection with human papillomavirus9 (HPV). Here, by sequencing genomes and exomes of FA SCCs, we demonstrate that the primary genomic signature of FA repair deficiency is the presence of high numbers of structural variants. Structural variants are enriched for small deletions, unbalanced translocations and fold-back inversions, and are often connected, thereby forming complex rearrangements. They arise in the context of TP53 loss, but not in the context of HPV infection, and lead to somatic copy-number alterations of HNSCC driver genes. We further show that FA pathway deficiency may lead to epithelial-to-mesenchymal transition and enhanced keratinocyte-intrinsic inflammatory signalling, which would contribute to the aggressive nature of FA SCCs. We propose that the genomic instability in sporadic HPV-negative HNSCC may arise as a result of the FA repair pathway being overwhelmed by DNA interstrand crosslink damage caused by alcohol and tobacco-derived aldehydes, making FA SCC a powerful model to study tumorigenesis resulting from DNA-crosslinking damage.
Subject(s)
DNA Repair , Fanconi Anemia , Genomics , Head and Neck Neoplasms , Humans , Aldehydes/adverse effects , Aldehydes/metabolism , DNA Repair/genetics , Fanconi Anemia/genetics , Fanconi Anemia/metabolism , Fanconi Anemia/pathology , Head and Neck Neoplasms/chemically induced , Head and Neck Neoplasms/genetics , Head and Neck Neoplasms/metabolism , Head and Neck Neoplasms/pathology , Papillomavirus Infections , Squamous Cell Carcinoma of Head and Neck/chemically induced , Squamous Cell Carcinoma of Head and Neck/genetics , Squamous Cell Carcinoma of Head and Neck/metabolism , Squamous Cell Carcinoma of Head and Neck/pathology , DNA Damage/drug effectsABSTRACT
Environmental pollution sources may play a key role in the pathogenesis of nephrolithiasis, although the link between environmental aldehyde exposure and the incidence of nephrolithiasis is unclear. The researchers in this study set out to see whether adult kidney stone formation was linked to environmental aldehydes. We examined data from 10,175 adult participants over the age of 20 who took part in the 2013-2014 National Health and Nutrition Examination Survey (NHANES), which was a cross-sectional research. A logistic regression model was employed in this work to examine the relationship between aldehyde exposure and kidney stones, machine learning was utilized to predict the connection of different parameters with the development of kidney stones, and a subgroup analysis was performed to identify sensitive groups. After controlling for all confounding variables, the results revealed that isopentanaldehyde, benzaldehyde, and hexanaldehyde were risk factors for kidney stone formation, with odds ratio (OR) of 2.47, 1.12, and 1.17, respectively, and 95 percent confidence intervals (95% CI) of 1.15-5.34, 1.02-1.22, and 1.00-1.36. Kidney stones may be a result of long-term exposure to aldehydes, which may cause them to form. Environmental pollution-related aldehyde exposure might give a novel notion and direction for future study into the process of kidney stone production, even if the cause is yet unknown.
Subject(s)
Benzaldehydes , Kidney Calculi , Adult , Humans , Nutrition Surveys , Cross-Sectional Studies , Kidney Calculi/epidemiology , Kidney Calculi/etiology , Aldehydes/adverse effectsABSTRACT
No treatment-related effects at the low and mid doses were observed in gestation, viability and lactation indices, duration of gestation, parturition, sex ratio, maternal care, litter size, and early postnatal pup development consisting of mortality, clinical signs, anogenital distance, areola/nipple retention, T4 thyroid hormone levels, or macroscopic examination. However, the number of litters (N = 5) at the high dose was considered too low for toxicological evaluation. Thus, based on insufficient data at 120 mg/kg/day, the NOAEL for this study was considered to be 60 mg/kg/day (RIFM, 2020d).
Subject(s)
Aldehydes/adverse effects , Cosmetics/chemistry , Environmental Exposure/adverse effects , Odorants/analysis , Perfume/adverse effects , Pregnancy Outcome , Safety , Academies and Institutes/standards , Aldehydes/analysis , Animals , Dermatitis, Photoallergic , Dermatitis, Phototoxic , Female , Household Products , Humans , Lactation/drug effects , Litter Size , Mutagenicity Tests , No-Observed-Adverse-Effect Level , Perfume/chemistry , Pregnancy , Registries , Respiratory System/drug effects , Risk Assessment , Skin/drug effects , Toxicity TestsABSTRACT
Protein kinase Cε (PKCε) is highly expressed in nociceptor neurons and its activation has been reported as pro-nociceptive. Intriguingly, we previously demonstrated that activation of the mitochondrial PKCε substrate aldehyde dehydrogenase-2 (ALDH2) results in anti-nociceptive effects. ALDH2 is a major enzyme responsible for the clearance of 4-hydroxy-2-nonenal (4-HNE), an oxidative stress byproduct accumulated in inflammatory conditions and sufficient to induce pain hypersensitivity in rodents. Here we determined the contribution of the PKCε-ALDH2 axis during 4-HNE-induced mechanical hypersensitivity. Using knockout mice, we demonstrated that PKCε is essential for the nociception recovery during 4-HNE-induced hypersensitivity. We also found that ALDH2 deficient knockin mice display increased 4-HNE-induced nociceptive behavior. As proof of concept, the use of a selective peptide activator of PKCε (ΨεHSP90), which favors PKCε translocation to mitochondria and activation of PKCε-ALDH2 axis, was sufficient to block 4-HNE-induced hypersensitivity in WT, but not in ALDH2-deficient mice. Similarly, ΨεHSP90 administration prevented mechanical hypersensitivity induced by endogenous production of 4-HNE after carrageenan injection. These findings provide evidence that selective activation of mitochondrial PKCε-ALDH2 axis is important to mitigate aldehyde-mediated pain in rodents, suggesting that ΨεHSP90 and small molecules that mimic it may be a potential treatment for patients with pain.
Subject(s)
Aldehyde Dehydrogenase, Mitochondrial/genetics , Aldehydes/adverse effects , Pain/metabolism , Protein Kinase C-epsilon/metabolism , Aldehyde Dehydrogenase, Mitochondrial/metabolism , Animals , Carrageenan/adverse effects , Disease Models, Animal , Gene Knock-In Techniques , Gene Knockout Techniques , Male , Mice , Mitochondria/metabolism , Pain/chemically induced , Protein TransportSubject(s)
Aldehydes , Octanes , Odorants , Humans , Aldehydes/adverse effects , Octanes/adverse effectsABSTRACT
Repeated activation of the hypothalamic-pituitary-adrenal axis system, sleep disturbances, and other symptoms related to posttraumatic stress disorder (PTSD) elevate reactive oxygen species, increase inflammation, and accelerate cellular aging, leading to neuroprogression and cognitive decline. However, there is no information about possible involvement of 4-hydroxynonenal (4-HNE), the product of lipid peroxidation associated with stress-associated diseases, in the complex etiology of PTSD. Therefore, the aim of this study was to compare the plasma levels of 4-HNE between war veterans with PTSD (n = 62) and age-, sex- and ethnicity- matched healthy control subjects (n = 58) in order to evaluate the potential of HNE-modified proteins as blood-based biomarker of PTSD. The genuine 4-HNE-Enzyme-Linked Immunosorbent Assay (HNE-ELISA), based on monoclonal antibody specific for HNE-histidine (HNE-His) adducts, was used to determine plasma HNE-protein conjugates. Our results revealed significantly elevated levels of 4-HNE in patients with PTSD. Moreover, the accumulation of plasma 4-HNE seems to increase with aging but in a negative correlation with BMI, showing specific pattern of change for individuals diagnosed with PTSD. These findings suggest that oxidative stress and altered lipid metabolism reflected by increase of 4-HNE might be associated with PTSD. If confirmed with further studies, elevated 4-HNE plasma levels might serve as a potential biomarker of PTSD.
Subject(s)
Aldehydes/adverse effects , Lipid Peroxidation , Stress Disorders, Post-Traumatic/etiology , Adult , Aged , Aldehydes/blood , Body Mass Index , Case-Control Studies , Humans , Male , Middle Aged , Stress Disorders, Post-Traumatic/bloodABSTRACT
This study investigated the toxic effects of trans,trans-2,4-decadienal (tt-DDE) on vascular endothelial cells as well as the underlying mechanisms involved. Human umbilical vascular endothelial cells (HUVECs) were treated with different concentrations of tt-DDE for 24 h, and cell viability, colony formation ability, apoptosis, mitochondrial function and autophagy pathway were determined. The results showed that tt-DDE dose-dependently inhibited cell viability and colony formation, and increased lactate dehydrogenase (LDH) release and apoptosis in HUVECs. Besides, tt-DDE exposure induced extensive mitochondrial damage, as evidenced by the decreased mitochondrial DNA copy number, ATP synthesis, and mitochondrial membrane potential, and increased mitochondrial reactive oxygen species (ROS) production and cytochrome c release from mitochondria. tt-DDE also induced mitochondrial fragmentation and fission by increasing DNM1L protein expression and DNM1L mitochondrial translocation. Additionally, tt-DDE treatment resulted in the blockage of autophagic flux and accumulation of autophagosomes in endothelial cells. Further investigation revealed that the inhibition of autophagy by 3-methyladenine aggravated tt-DDE-induced mitochondrial dysfunction and cell injury. However, scavenging of ROS by N-acetyl-l-cysteine (NAC) significantly prevented tt-DDE-induced mitochondrial damage, autophagy dysfunction, and cell injury. These data indicated that tt-DDE induced endothelial cell injury through impairing mitochondrial function and autophagic flux.
Subject(s)
Aldehydes/adverse effects , Autophagy/drug effects , Endothelial Cells/drug effects , Endothelial Cells/metabolism , Mitochondria/drug effects , Mitochondria/metabolism , Apoptosis/drug effects , Cell Line , Cell Survival/drug effects , Humans , Membrane Potential, Mitochondrial/drug effects , Oxidative Stress , Reactive Oxygen Species/metabolismABSTRACT
BACKGROUND: Hydroxyisohexyl 3-cyclohexene carboxaldehyde (HICC) has been the most reported fragrance chemical for two decades and will be prohibited in cosmetic products from August 2021. OBJECTIVES: To describe the time trend of HICC contact allergy in European patients with dermatitis in 2009 to 2019, and the added value of testing HICC separately in the baseline series. METHODS: Data were reviewed for 124 472 patients with dermatitis who were patch tested with HICC 5% pet. in the baseline series in the European Surveillance System on Contact Allergy (ESSCA) network (2009 to 2018) and at the Herlev-Gentofte Hospital Department of Dermatology and Allergy (2009 to 2019). RESULTS: Contact allergy to HICC was found in 1.98% of 9865 patients in Gentofte and 1.62% of 114 607 patients in the ESSCA network. Overall, the prevalence decreased annually, with 0.156 percentage points (P = .001) in Gentofte and 0.051 percentage points (P = .0002) in ESSCA. The frequency of missed contact allergy to HICC when testing only with fragrance mix II (FMII) was 0.17% (17/9865) and 0.35% (405/114607) of the whole test population in the Gentofte and ESSCA populations, respectively. CONCLUSIONS: This is the first study to demonstrate a significant decline in HICC allergy in European patients with dermatitis, most likely attributed to the upcoming European ban.
Subject(s)
Aldehydes/adverse effects , Cyclohexenes/adverse effects , Dermatitis, Allergic Contact/diagnosis , Dermatitis, Allergic Contact/epidemiology , Patch Tests/methods , Perfume/adverse effects , Age Distribution , Cosmetics/adverse effects , Cosmetics/legislation & jurisprudence , Europe/epidemiology , Humans , Perfume/legislation & jurisprudence , Prevalence , Sex DistributionABSTRACT
INTRODUCTION: Flavor aldehydes in e-cigarettes, including vanillin, ethyl vanillin (vanilla), and benzaldehyde (berry/fruit), rapidly undergo chemical reactions with the e-liquid solvents, propylene glycol, and vegetable glycerol (PG/VG), to form chemical adducts named flavor aldehyde PG/VG acetals that can efficiently transfer to e-cigarette aerosol. The objective of this study was to compare the cytotoxic and metabolic toxic effects of acetals and their parent aldehydes in respiratory epithelial cells. AIMS AND METHODS: Cell metabolic assays were carried out in bronchial (BEAS-2B) and alveolar (A549) epithelial cells assessing the effects of benzaldehyde, vanillin, ethyl vanillin, and their corresponding PG acetals on key bioenergetic parameters of mitochondrial function. The potential cytotoxic effects of benzaldehyde and vanillin and their corresponding PG acetals were analyzed using the LIVE/DEAD cell assay in BEAS-2B cells and primary human nasal epithelial cells (HNEpC). Cytostatic effects of vanillin and vanillin PG acetal were compared using Click-iT EDU cell proliferation assay in BEAS-2B cells. RESULTS: Compared with their parent aldehydes, PG acetals diminished key parameters of cellular energy metabolic functions, including basal respiration, adenosine triphosphate production, and spare respiratory capacity. Benzaldehyde PG acetal (1-10 mM) increased cell mortality in BEAS-2B and HNEpC, compared with benzaldehyde. Vanillin PG acetal was more cytotoxic than vanillin at the highest concentration tested while both diminished cellular proliferation in a concentration-dependent manner. CONCLUSIONS: Reaction products formed in e-liquids between flavor aldehydes and solvent chemicals have differential toxicological properties from their parent flavor aldehydes and may contribute to the health effects of e-cigarette aerosol in the respiratory system of e-cigarette users. IMPLICATIONS: With no inhalation toxicity studies available for acetals, data from this study will provide a basis for further toxicological studies using in vitro and in vivo models. This study suggests that manufacturers' disclosure of e-liquid ingredients at time of production may be insufficient to inform a comprehensive risk assessment of e-liquids and electronic nicotine delivery systems use, due to the chemical instability of e-liquids over time and the formation of new compounds.
Subject(s)
Aerosols/adverse effects , Aldehydes/adverse effects , Electronic Nicotine Delivery Systems/statistics & numerical data , Epithelial Cells/pathology , Flavoring Agents/adverse effects , Mitochondria/pathology , Respiratory System/pathology , Aldehydes/chemistry , Epithelial Cells/drug effects , Flavoring Agents/chemistry , Humans , Mitochondria/drug effects , Respiratory System/drug effectsABSTRACT
Specific inhalation challenge (SIC) is the reference standard for the diagnosis of occupational asthma. Current guidelines for identifying late asthmatic reactions are not evidence based. OBJECTIVES: To identify the fall in forced expiratory volume in 1 s (FEV1) required following SIC to exceed the 95% CI for control days, factors which influence this and to show how this can be applied in routine practice using a statistical method based on the pooled SD for FEV1 from three control days. METHODS: Fifty consecutive workers being investigated for occupational asthma were asked to self-record FEV1 hourly for 2 days before admission for SIC. These 2 days were added to the in-hospital control day to calculate the pooled SD and 95% CI. RESULTS: 45/50 kept adequate measurements. The pooled 95% CI was 385 mL (SD 126), or 14.2% (SD 6.2) of the baseline FEV1, but was unrelated to the baseline FEV1 (r=0.06, p=0.68), or gender, atopy, smoking, non-specific reactivity or treatment before or during SIC. Thirteen workers had a late asthmatic reaction with ≥2 consecutive FEV1 measurements below the 95% CI for pooled control days, 4/13 had <15% and 9/13 >15% late fall from baseline. The four workers with ≥2 values below the 95% CI all had independent evidence of occupational asthma. CONCLUSION: The pooled SD method for defining late asthmatic reactions has scientific validity, accounts for interpatient spirometric variability and diurnal variation and can identify clinically relevant late asthmatic reactions from smaller exposures. For baseline FEV1 <2.5 L, a 15% fall is within the 95% CI.
Subject(s)
Asthma/diagnosis , Bronchial Provocation Tests/methods , Time Factors , Acrylates/adverse effects , Adult , Aldehydes/adverse effects , Amines/adverse effects , Analysis of Variance , Asthma/physiopathology , Bronchial Provocation Tests/statistics & numerical data , Detergents/adverse effects , Disinfectants/adverse effects , Female , Forced Expiratory Volume/physiology , Humans , Isocyanates/adverse effects , Male , Plastics/adverse effectsABSTRACT
BACKGROUND: Fragrance mix II (FM II) is included in the baseline patch test series recommended by the International Contact Dermatitis Research Group (ICDRG). Hydroxyisohexyl 3-cyclohexene carboxaldehyde (HICC) is the most important sensitizer of the 6 fragrance materials included in FM II. Besides being a part of FM II, HICC is also tested separately in the ICDRG baseline series. OBJECTIVES: The aim of the study was to investigate the prevalence of contact allergy to FM II and HICC in 2012-2016 with a focus on simultaneous reactions and the percentage of missed contact allergy to HICC provided that only FM II had been tested. PATIENTS AND METHODS: A total of 25,019 consecutive dermatitis patients in 13 dermatology clinics representing 12 countries in 5 continents were patch tested with FM II and HICC in the baseline series. RESULTS: Contact allergy to FM II and HICC was found in 3.9% and 1.6%, respectively. For FM II, the frequency varied from 1.5% to 7.6% in different centers. The corresponding range for HICC was 0.2% to 3.6%. Simultaneous contact allergy to FM II and HICC was noted in 1.4% with the range 0.2% to 2.6%. Seventy-seven patients (0.31%) with contact allergy to HICC did not test positively to FM II. The range for missed HICC allergy by testing only FM II in the different centers would be 0.04% to 0.74%. The ratio between the contact allergy rates for FM II and HICC was similar for all centers, except for Montreal having significantly more contact allergy to FM II than to HICC. CONCLUSIONS: The frequency of missed contact allergy to HICC when testing only with FM II was less than 0.5%, therefore questioning the need to test HICC separately in the ICDRG baseline series.
Subject(s)
Aldehydes/adverse effects , Cyclohexenes/adverse effects , Dermatitis, Allergic Contact/etiology , Perfume/adverse effects , Allergens/adverse effects , Dermatitis, Allergic Contact/diagnosis , Female , Humans , Male , Odorants , Patch Tests , Retrospective StudiesABSTRACT
Household air pollution has adverse effects on cardiovascular health. One of the major sources of household air pollutants is the combustion of cooking oils during cooking. Trans, trans-2,4-decadienal (tt-DDE) is a type of dienaldehyde that is present in a wide range of food and food products. It is a byproduct of the peroxidation of linoleic acid following the heating of oil during cooking. The mechanisms of the associations between household air pollution and cardiac arrhythmias are currently unclear. The purpose of this study was to determine effects of tt-DDE on the ion currents in H9c2 cells. The IK and ICa,L in H9c2 cells treated with and without tt-DDE were measured using the whole-cell patch clamp method. Expressions of Kv2.1 and Cav1.2 in H9c2 cells treated with and without tt-DDE were measured by western blot analysis. After the H9c2 cells had been exposed to tt-DDE, the IK and ICa,L were significantly decreased. The expression of Kv2.1, unlike that of Cav1.2, was also significantly decreased in these cells. These changes in IK and ICa,L that were induced by tt-DDE may help to explain the association between cardiac arrhythmogenesis and cooking-oil fumes.
Subject(s)
Air Pollution, Indoor/adverse effects , Aldehydes/adverse effects , Myocytes, Cardiac/drug effects , Oils/adverse effects , Air Pollutants/adverse effects , Animals , Arrhythmias, Cardiac/etiology , Arrhythmias, Cardiac/metabolism , Calcium Channels, L-Type/metabolism , Cell Line , Cell Survival/drug effects , Cooking , Humans , Ion Transport/drug effects , Myocytes, Cardiac/metabolism , Rats , Shab Potassium Channels/metabolismABSTRACT
Cigarette smoking is the most preventable risk factor related to cardiovascular morbidity and mortality. Tobacco usage has declined in recent years; however, the use of alternative nicotine delivery methods, particularly e-cigarettes, has increased exponentially despite limited data on their short- and long-term safety and efficacy. Due to their unique properties, the impact of e-cigarettes on cardiovascular physiology is not fully known. Here, we summarize both preclinical and clinical data extracted from short- and long-term studies on the cardiovascular effects of e-cigarette use. Current findings support that e-cigarettes are not a harm-free alternative to tobacco smoke. However, the data are primarily derived from acute studies. The impact of chronic e-cigarette exposure is essentially unstudied. To explore the uniqueness of e-cigarettes, we contemplate the cardiovascular effects of individual e-cigarette constituents. Overall, data suggest that exposure to e-cigarettes could be a potential cardiovascular health concern. Further preclinical research and randomized trials are needed to expand basic and clinical investigations before considering e-cigarettes safe alternatives to conventional cigarettes.
Subject(s)
Cardiovascular Diseases/etiology , Cardiovascular System/drug effects , E-Cigarette Vapor/adverse effects , Electronic Nicotine Delivery Systems , Vaping/adverse effects , Aldehydes/adverse effects , Animals , Cardiovascular Diseases/diagnosis , Cardiovascular Diseases/physiopathology , Cardiovascular System/physiopathology , Consumer Product Safety , Flavoring Agents/adverse effects , Humans , Metals/adverse effects , Nicotine/adverse effects , Oxidants/adverse effects , Risk Assessment , Risk FactorsABSTRACT
This article gives an overview of fragrance allergy. The following subjects are discussed: composition of perfumes, contact with fragrances, diagnosing fragrance allergy, frequency of allergy, clinical picture of allergic contact dermatitis, culprit products, occupational contact dermatitis, and other adverse effects of fragrances. For diagnosing fragrance sensitization, personal products and a fragrance series may need to be tested in addition to the baseline series. In the general adult population, up to 4.5% may be allergic to fragrance materials, and in consecutive patients patch tested for suspected contact dermatitis, the frequency may reach 20% to 25%. More than 150 fragrances have caused contact allergy. The most frequent sensitizers are linalool and limonene hydroperoxides, hydroxyisohexyl 3-cyclohexene carboxaldehyde, treemoss and oakmoss absolute, isoeugenol, cinnamyl alcohol, and cinnamal. Culprit products for induction of sensitization are often deodorants, fine fragrances, and aftershaves. Occupational contact dermatitis from fragrances is seen occasionally. Other adverse effects are all discussed but occur infrequently.
Subject(s)
Dermatitis, Allergic Contact/etiology , Odorants , Perfume/adverse effects , Acyclic Monoterpenes/adverse effects , Aldehydes/adverse effects , Allergens/adverse effects , Cosmetics , Cyclohexenes/adverse effects , Deodorants , Dermatitis, Occupational/etiology , Eugenol/adverse effects , Eugenol/analogs & derivatives , Household Products , Humans , Limonene/adverse effects , Patch Tests , Propanols/adverse effects , Resins, Plant/adverse effects , Terpenes/adverse effectsABSTRACT
Aldehydes, which are present within the air as well as food and beverage sources, are highly reactive molecules that can be cytotoxic, mutagenic, and carcinogenic. To prevent harm from reactive aldehyde exposure, the enzyme aldehyde dehydrogenase 2 (ALDH2) metabolizes reactive aldehydes to a less toxic form. However, the genetic variant of ALDH2, ALDH2*2, significantly reduces the ability to metabolize reactive aldehydes in humans. Therefore, frequent environmental aldehyde exposure, coupled with inefficient aldehyde metabolism, could potentially lead to an increased health risk for diseases such as cancer or cardiovascular disease.Here, we discuss the environmental sources of reactive aldehydes and the potential health implications particularly for those with an ALDH2*2 genetic variant. We also suggest when considering the ALDH2*2 genetic variant the safety limits of reactive aldehyde exposure may have to be reevaluated. Moreover, the ALDH2*2 genetic variant can also be used as an example for how to implement precision medicine in the field of environmental health sciences.
Subject(s)
Aldehyde Dehydrogenase, Mitochondrial/genetics , Aldehydes/adverse effects , Environmental Exposure/adverse effects , HumansABSTRACT
A major pathophysiological mechanism behind the development of diabetic heart diseases is oxidative stress mediated by toxic reactive aldehydes such as 4-hydroxynonenal (4HNE). Aldehyde dehydrogenase (ALDH) 2 is a mitochondrial enzyme that has been found to detoxify these deleterious aldehydes and thereby mitigate cardiac damage. Furthermore, its protective role in cellular signaling reverses aberrations caused by hyperglycemia, thereby protecting cardiac function. This chapter assesses the role of ALDH2 in diabetic heart diseases by examining preclinical studies where ALDH2 activity is perturbed in both decreased and increased directions. In doing so, issues in improving ALDH2 activity in select human populations are elucidated, and further research directions are discussed.
Subject(s)
Aldehyde Dehydrogenase, Mitochondrial/genetics , Diabetes Mellitus/genetics , Heart Diseases/genetics , Aldehydes/adverse effects , Heart Diseases/complications , Humans , Oxidative StressABSTRACT
OBJECTIVES: Exposure to cleaning products has been associated with adverse respiratory outcomes. This study aimed to investigate the medically reported incidence, trends in incidence and occupational determinants of work-related respiratory disorders attributed to cleaning agents and to explore the role of 'Quantitative Structure Activity Relationships' (QSAR) in corroborating the identification of chemical respiratory sensitisers. METHODS: Respiratory diagnoses attributed to cleaning agents were extracted from The Health and Occupation Research (THOR) surveillance network, 1989-2017. Incidence, trends in incidence and incidence rate ratios by occupation were investigated. Agents were classified by chemical type and QSAR hazard indices were determined for specific organic chemicals. RESULTS: Approximately 6% (779 cases) of the (non-asbestos) THOR respiratory cases were attributed to cleaning agents. Diagnoses were predominantly asthma (58%) and inhalation accidents (27%) with frequently reported chemical categories being aldehydes (30%) and chlorine/its releasers (26%). No significant trend in asthma incidence (1999-2017) was observed (annual average change of -1.1% (95% CI -4.4 to 2.4)). This contrasted with a statistically significant annual decline in asthma incidence (-6.8% (95% CI -8.0 to -5.6)) for non-cleaning agents. There was a large variation in risk between occupations. 7 of the 15 organic chemicals specifically identified had a QSAR generated hazard index consistent with being a respiratory sensitiser. CONCLUSION: Specific occupations appear to be at increased risk of adverse respiratory outcomes attributed to cleaning agents. While exposure to agents such as glutaraldehyde have been addressed, other exposures, such as to chlorine, remain important. Chemical features of the cleaning agents helped distinguish between sensitising and irritant agents.
Subject(s)
Occupational Diseases/epidemiology , Occupational Exposure/adverse effects , Respiratory Tract Diseases/epidemiology , Adolescent , Adult , Aged , Aldehydes/adverse effects , Asthma/chemically induced , Asthma/epidemiology , Chlorine/adverse effects , Disinfectants/adverse effects , Female , Household Products/adverse effects , Humans , Male , Middle Aged , Occupational Diseases/chemically induced , Quantitative Structure-Activity Relationship , Respiratory Tract Diseases/chemically induced , United Kingdom/epidemiologyABSTRACT
Cooking-related emissions are associated with environmental pollution and adverse health effects. Of the various chemical species emitted during cooking, polycyclic aromatic hydrocarbons (PAHs) and aldehydes are two chemical species with carcinogenic or tumor promoting characteristics. Although PAH exposure has been studied in commercial kitchen workers, few studies have investigated simultaneous exposure to PAHs and aldehydes in these workers. The aims of this study were to compare personal concentrations of PAH and aldehyde in three commercial cooking workplaces and to estimate their corresponding cancer risks. The three cooking workplaces included western fast food restaurant kitchens, Chinese cafeteria kitchens, and street food carts. Comparisons showed that workers in western fast food restaurant kitchens and Chinese cafeteria kitchens tended to have lower personal concentrations of these pollutants compared to workers in street food carts. The geometric mean (95% CI) cancer risks in the three workplaces were, from lowest to highest, 1.36 (1.12-1.67) × 10-5 for western fast food restaurant kitchens, 1.52 (1.01-2.28) × 10-5 for Chinese cafeteria kitchens, and 3.14 (2.45-4.01) × 10-5 for street food carts. The percentage contributions of aldehyde species to cancer risk were very high (74.9-99.7%). Street food cart workers had high personal exposure to aldehyde probably due to lack of effective exhaust systems. Thus, their cancer risk was significantly higher than those of workers in western fast food restaurant kitchens (p < 0.001) and Chinese cafeteria kitchens (p = 0.013).