Search Results (4)

Several studies have shown the presence of aldehydes (i.e., formaldehyde, acrolein) in mainstream emissions of some e-cigarettes. For this reason, concerns have been raised regarding potential toxicity. The purpose of this research was to measure levels of carbonyls in exhaled breath of e-cigarette users during “vaping” sessions and estimate the respiratory tract (RT) uptake of specific aldehydes, including formaldehyde and acetaldehyde. We measured concentrations of 12 carbonyls in e-cigarette aerosols produced directly by e-cigarettes and in the exhaled breath of 12 participants (19 sessions). Carbonyls were sampled on 2,4-dinitrophenylhydrazine (DNPH) cartridges and analyzed with high performance liquid chromatography (HPLC) coupled with a UV/Vis photodiode detector. We found that in most cases, levels of aldehydes and methyl ethyl ketone (MEK) were significantly higher (2–125 times) in exhaled e-cigarette breaths than in pre-exposed breath. Exposure levels for the most abundant individual carbonyls in e-cigarette emissions—formaldehyde, acetaldehyde, acrolein—were between the limit of quantification (LOQ) and 24.4 μg·puff⁻¹. The mean retention of formaldehyde in the respiratory tract was 99.7 ± 0.9% for all participants, while acetaldehyde retention was 91.6 ± 9.9%. Within the limitation of a small number of participants, our results showed that there is an increase in breath carbonyls during e-cigarette use. Full article

Arsenic methylation capacity is associated with metabolic syndrome and its components among highly exposed populations. However, this association has not been investigated in low to moderately exposed populations. Therefore, we investigated arsenic methylation capacity in relation to the clinical diagnosis of metabolic syndrome in a low arsenic exposure population. Additionally, we compared arsenic methylation patterns present in our sample to those of more highly exposed populations. Using logistic regression models adjusted for relevant biological and lifestyle covariates, we report no association between increased arsenic methylation and metabolic syndrome in a population in which arsenic is regulated at 10 ppb in drinking water. However, we cannot rule out the possibility of a positive association between arsenic methylation and metabolic syndrome in a subsample of women with normal body mass index (BMI). To our knowledge this is the first investigation of arsenic methylation capacity with respect to metabolic syndrome in a low exposure population. We also report that methylation patterns in our sample are similar to those found in highly exposed populations. Additionally, we report that gender and BMI significantly modify the effect of arsenic methylation on metabolic syndrome. Future studies should evaluate the effectiveness of arsenic policy enforcement on subclinical biomarkers of cardiovascular disease. Full article

Arsenic is a potent cardiovascular toxicant associated with numerous biomarkers of cardiovascular diseases in exposed human populations. Arsenic is also a carcinogen, yet arsenic trioxide is used as a therapeutic agent in the treatment of acute promyelotic leukemia (APL). The therapeutic use of arsenic is limited due to its severe cardiovascular side effects. Many of the toxic effects of arsenic are mediated by mitochondrial dysfunction and related to arsenic’s effect on oxidative stress. Therefore, we investigated the effectiveness of antioxidants against arsenic induced cardiovascular dysfunction. A growing body of evidence suggests that antioxidant phytonutrients may ameliorate the toxic effects of arsenic on mitochondria by scavenging free radicals. This review identifies 21 antioxidants that can effectively reverse mitochondrial dysfunction and oxidative stress in cardiovascular cells and tissues. In addition, we propose that antioxidants have the potential to improve the cardiovascular health of millions of people chronically exposed to elevated arsenic concentrations through contaminated water supplies or used to treat certain types of leukemias. Importantly, we identify conceptual gaps in research and development of new mito-protective antioxidants and suggest avenues for future research to improve bioavailability of antioxidants and distribution to target tissues in order reduce arsenic-induced cardiovascular toxicity in a real-world context. Full article

The use of solid biomass fuels in cookstoves has been associated with chronic health impacts that disproportionately affect women worldwide. Solid fuel stoves that use wood, plant matter, and cow dung are commonly used for household cooking in rural Bangladesh. This study investigates the immediate effects of acute elevated cookstove emission exposures on pulmonary function. Pulmonary function was measured with spirometry before and during cooking to assess changes in respiratory function during exposure to cookstove emissions for 15 females ages 18–65. Cookstove emissions were characterized using continuous measurements of particulate matter (PM_2.5—aerodynamic diameter <2.5 μm) concentrations at a 1 s time resolution for each household. Several case studies were observed where women ≥40 years who had been cooking for ≥25 years suffered from severe pulmonary impairment. Forced expiratory volume in one second over forced vital capacity (FEV1/FVC) was found to moderately decline (p = 0.06) during cooking versus non-cooking in the study cohort. The study found a significant (α < 0.05) negative association between 3- and 10-min maximum PM_2.5 emissions during cooking and lung function measurements of forced vital capacity (FVC), forced expiratory volume in one second (FEV1), and FEV1/FVC obtained during cooking intervals. This study found that exposure to biomass burning emissions from solid fuel stoves- associated with acute elevated PM_2.5 concentrations- leads to a decrease in pulmonary function, although further research is needed to ascertain the prolonged (e.g., daily, for multiple years) impacts of acute PM_2.5 exposure on immediate and sustained respiratory impairment. Full article