Health and equity implications of individual adaptation to air pollution in a changing climate.

Future climate change can cause more days with poor air quality. This could trigger more alerts telling people to stay inside to protect themselves, with potential consequences for health and health equity. Here, we study the change in US air quality alerts over this century due to fine particulate matter (PM2.5), who they may affect, and how they may respond. We find air quality alerts increase by over 1 mo per year in the eastern United States by 2100 and quadruple on average. They predominantly affect areas with high Black populations and leakier homes, exacerbating existing inequalities and impacting those less able to adapt. Reducing emissions can offer significant annual health benefits ($5,400 per person) by mitigating the effect of climate change on air pollution and its associated risks of early death. Relying on people to adapt, instead, would require them to stay inside, with doors and windows closed, for an extra 142 d per year, at an average cost of $11,000 per person. It appears likelier, however, that people will achieve minimal protection without policy to increase adaptation rates. Boosting adaptation can offer net benefits, even alongside deep emission cuts. New adaptation policies could, for example: reduce adaptation costs; reduce infiltration and improve indoor air quality; increase awareness of alerts and adaptation; and provide measures for those working or living outdoors. Reducing emissions, conversely, lowers everyone's need to adapt, and protects those who cannot adapt. Equitably protecting human health from air pollution under climate change requires both mitigation and adaptation.

Longitudinal association of exclusive and dual use of cigarettes and cigars with asthma exacerbation among US adults: a cohort study.

BACKGROUND: Cigar use among adults in the United States has remained relatively stable in the past decade and occupies a growing part of the tobacco marketplace as cigarette use has declined. While studies have established the detrimental respiratory health effects of cigarette use, the effects of cigar use need further characterization. In this study, we evaluate the prospective association between cigar use, with or without cigarettes, and asthma exacerbation. METHODS: We used data from Waves 1-5 (2013-2019) of the Population Assessment of Tobacco and Health Study to run generalized estimating equation models examining the association between time-varying, one-wave-lagged cigarette and cigar use and self-reported asthma exacerbation among US adults (18+). We defined our exposure as non-established (reference), former, exclusive cigarette, exclusive cigar, and dual use. We defined an asthma exacerbation event as a reported asthma attack in the past 12 months necessitating oral or injected steroid medication or asthma symptoms disrupting sleep at least once a week in the past 30 days. We adjusted for age, sex, race and ethnicity, household income, health insurance, established electronic nicotine delivery systems use, cigarette pack-years, secondhand smoke exposure, obesity, and baseline asthma exacerbation. RESULTS: Exclusive cigarette use (incidence rate ratio (IRR): 1.26, 95% confidence interval (CI): 1.03-1.54) and dual use (IRR: 1.41, 95% CI: 1.08-1.85) were associated with a higher rate of asthma exacerbation compared to non-established use, while former use (IRR: 1.01, 95% CI: 0.80-1.28) and exclusive cigar use (IRR: 0.70, 95% CI: 0.42-1.17) were not. CONCLUSION: We found no association between exclusive cigar use and self-reported asthma exacerbation. However, exclusive cigarette use and dual cigarette and cigar use were associated with higher incidence rates of self-reported asthma exacerbation compared to non-established use. Studies should evaluate strategies to improve cigarette and cigar smoking cessation among adults with asthma who continue to smoke.

Association between cigar use, with and without cigarettes, and incident diagnosed COPD: a longitudinal cohort study.

BACKGROUND: While regular cigar smoking is believed to carry similar health risks as regular cigarette smoking, the impact of cigar use, alone or in combination with cigarettes, on obstructive pulmonary disease (COPD) has not been well characterized. The purpose of this study was to examine the prospective association between exclusive and dual cigar and cigarette use and incident self-reported diagnosed COPD. METHODS: This study used data from Waves 1-5 (2013-2019) of the Population Assessment of Tobacco and Health (PATH) Study, a nationally representative survey of U.S. adults. Longitudinal data from adults aged 40 to 79 at Wave 1, without a pre-existing COPD diagnosis who participated at follow-up interview were analyzed. A time-varying current tobacco exposure, lagged by one wave and categorized as: (a) never/non-current use; (b) exclusive cigar use; (c) exclusive cigarette use; and (d) dual cigar/cigarette use. Multivariable models adjusted for demographics (age, sex, race or ethnicity, education), clinical risk factors (asthma, obesity), and smoking-related confounders (second-hand smoke exposure, other combustible tobacco product use, e-cigarette use, time since quitting, cigarette pack-years). The incidence of self-reported diagnosed COPD was estimated using discrete-time survival models, using a general linear modeling (GLM) approach with a binomial distribution and a complementary log-log link function. RESULTS: The analytic sample consisted of 9,556 adults with a mean (SD) age of 56 (10.4), who were predominately female (52.8%) and Non-Hispanic White (70.8%). A total of 906 respondents reported a diagnosis of COPD at follow-up. In the fully adjusted model, exclusive cigar use (adjusted hazard ratio (aHR) = 1.57, 95% CI: 0.77, 3.21) was not associated with increased COPD risk compared to non-use, while exclusive cigarette use (aHR = 1.48, 95% CI: 1.13, 1.93) and dual cigar/cigarette use (aHR = 1.88, 95% CI: 1.24, 2.85) were. CONCLUSIONS: Exclusive cigarette use and dual cigar/cigarette use were associated with diagnosed incident COPD. These results suggest that cigars, when used in combination with cigarettes, may be associated with poorer COPD health outcomes. Dual use may promote a higher likelihood of inhaling cigar smoke, and future research would benefit from examining whether inhalation of cigar smoke increases COPD risk.

Review of epidemiological and toxicological studies on health effects from ingestion of asbestos in drinking water.

Asbestos is a group of naturally occurring fibrous minerals that were commonly used in the construction of cement pipes for drinking water distribution systems. These pipes deteriorate and can release asbestos fibers into drinking water, raising concerns about potential risk to human health. The objective of this work was to synthesize human, animal, and in vitro evidence on potential health risks due to ingested asbestos in drinking water and evaluate the weight of evidence (WoE) of human health risk. A systematic review of epidemiological evidence was conducted, along with critical review of animal and in vitro evidence, followed by WoE evaluation that integrated human, animal, and in vitro evidence. The systematic review included 17 human studies with health outcomes mostly related to various cancer sites, with the majority focusing on the gastrointestinal system. The WoE evaluation resulted in very low levels of confidence or insufficient evidence of a health effect for cancers in 15 organ systems and for three non-cancer endpoints. While eight studies reported possible associations with stomach cancer in males, few high-quality studies were available to verify a causal relationship. Based on high-quality animal studies, an increased risk for cancer or non-cancer endpoints was not supported, aligning with findings from human studies. Overall, the currently available body of evidence is insufficient to establish a clear link between asbestos contamination in drinking water and adverse health effects. Due to the lack of both high-quality epidemiological studies and a validated kinetic model for ingested asbestos, additional research on this association is warranted.

Dietary glycation compounds - implications for human health.

The term "glycation compounds" comprises a wide range of structurally diverse compounds that are formed endogenously and in food via the Maillard reaction, a chemical reaction between reducing sugars and amino acids. Glycation compounds produced endogenously are considered to contribute to a range of diseases. This has led to the hypothesis that glycation compounds present in food may also cause adverse effects and thus pose a nutritional risk to human health. In this work, the Senate Commission on Food Safety (SKLM) of the German Research Foundation (DFG) summarized data on formation, occurrence, exposure and toxicity of glycation compounds (Part A) and systematically assessed potential associations between dietary intake of defined glycation compounds and disease, including allergy, diabetes, cardiovascular and renal disease, gut/gastrotoxicity, brain/cognitive impairment and cancer (Part B). A systematic search in Pubmed (Medline), Scopus and Web of Science using a combination of keywords defining individual glycation compounds and relevant disease patterns linked to the subject area of food, nutrition and diet retrieved 253 original publications relevant to the research question. Of these, only 192 were found to comply with previously defined quality criteria and were thus considered suitable to assess potential health risks of dietary glycation compounds. For each adverse health effect considered in this assessment, however, only limited numbers of human, animal and in vitro studies were identified. While studies in humans were often limited due to small cohort size, short study duration, and confounders, experimental studies in animals that allow for controlled exposure to individual glycation compounds provided some evidence for impaired glucose tolerance, insulin resistance, cardiovascular effects and renal injury in response to oral exposure to dicarbonyl compounds, albeit at dose levels by far exceeding estimated human exposures. The overall database was generally inconsistent or inconclusive. Based on this systematic review, the SKLM concludes that there is at present no convincing evidence for a causal association between dietary intake of glycation compounds and adverse health effects.

Considering the implication of endogenous glycation compounds in aging and disease, dietary exposure via consumption of an "AGE (advanced glycation end product) rich diet" is increasingly suggested to pose a potential health risk. However, studies attempting to assess an association between dietary glycation compounds and adverse health effects frequently suffer from insufficient chemical analysis of glycation compounds, including inadequate structural characterization and limited quantitative data. The Senate Commission on Food Safety (SKLM) of the German Research Foundation (DFG) previously defined quality criteria for studies designed to assess the effects of dietary glycation compounds on human health. The aim of the present work is to summarize data on formation, occurrence, exposure and toxicity of glycation compounds (Part A) and to systematically evaluate if the currently available scientific database allows for a conclusive assessment of potential health effects of defined glycation compounds (Part B).The term "glycation compounds" comprises a wide range of structurally diverse compounds that derive from the Maillard reaction, a chemical reaction between reducing carbohydrates and amino compounds that occurs during food processing. In the first stage of the Maillard reaction, reducing sugars such as glucose and fructose react for instance with the ε-amino group of lysine, which is most abundant in food ("glycation" of lysine). Subsequently, these primary reaction products undergo Amadori rearrangement to yield products (ARP) such as fructosyllysine (FL) from glucose and also Heyns rearrangement products (HRPs) such as glucosyl- and mannosyllysine from fructose. While ARPs are rapidly formed during food processing, they are not stable and undergo degradation reactions, predominantly to 1,2-dicarbonyl compounds such as glyoxal (GO), methylglyoxal (MGO) and 3-deoxyglucosone (3-DG), which are highly reactive. The last stage of the Maillard reaction is characterized predominantly by the reaction of these dicarbonyl compounds with nucleophilic groups of proteins. The side-chains of lysine and arginine residues as well as the N-termini of proteins are important reaction sites. Carboxyalkylated amino acids such as N-ε-carboxymethyllysine (CML) and N-ε-carboxyethyllysine (CEL) result from reaction of the ε-amino group of lysine with the dicarbonyl compounds GO and MGO. Dicarbonyl compounds with C5 or C6 chains can form cyclic pyrrole derivatives at the ε-amino group of lysine. The most important example for this reaction is pyrraline, which is formed from reaction of 3-DG and lysine. The reaction of dicarbonyl compounds with the guanidino group of arginine mainly leads to hydroimidazolones, of which the MGO-derived hydroimidazolone 1 (MG-H1) is best described in food systems.ARPs are the most abundant glycation products found in food. Up to 55% of the lysine residues in food may be modified to ARPs at the side-chain. Food items particularly rich in ARPs include bread, rusk, biscuits, chocolate, and powdered infant formulas. Exposure estimates range between 0.6­1.6 mg/kg body weight (bw), although exposure may be as high as 14.3 mg/kg bw in individuals consuming foods with extreme ARP concentrations. Foods particularly rich in dicarbonyl compounds include heat-treated or long-term stored items rich in reducing sugars such as jams, alternative sweeteners, soft drinks, honey, candies, cookies, and vinegars, especially balsamico-type vinegars. The main contributors to the daily intake of MGO, GO, and 3-DG are coffee and bread. Dietary exposure to dicarbonyl compounds has been estimated to range between 0.02­0.29 mg/kg bw/d for MGO, 0.04­0.16 mg/kg bw/d for GO, 0.14­2.3 mg/kg bw/d for 3-DG, and 0.08­0.13 mg/kg bw/d for 3-deoxygalactosone (3-DGal). Dietary intake of 5-hydroxymethylfurfural (HMF), which can be formed from 3-DG, is estimated to range between 0.0001­0.9 mg/kg bw/d. Exposure estimates for individual glycated amino acids range from 0.03­0.35 mg/kg bw/d for CML, 0.02­0.04 mg/kg bw/d for CEL and 0.19­0.41 mg/kg bw/d for MG-H1. From a model diet consisting of 1 L milk, 500 g bakery products and 400 mL coffee, an intake of pyrraline corresponding to 0.36 mg/kg bw/d for a 70 kg person was estimated.Quantitative analysis of individual glycation compounds or their metabolites in tissues or body fluids as well as their reaction products with amino acids, proteins or DNA may serve to monitor exposure to glycation compounds. However, since glycation compounds are also formed endogenously, these biomarkers reflect the totality of the exposure, making it inherently difficult to define the body burden due to dietary intake against the background of endogenous formation.Information on the toxicokinetics and toxicity of glycation compounds is scarce and mostly limited to the reactive dicarbonyl compounds GO, MGO, 3-DG, HMF, and individual glycated amino acids such as CML and CEL. Acute toxicity of dicarbonyl compounds is low to moderate. There are some data to suggest that rapid detoxification of dicarbonyls in the gastrointestinal tract and liver may limit their oral bioavailability. Biotransformation of GO and MGO occurs predominantly via the glutathione (GSH)-dependent glyoxalase system, and to a lesser extent via glutathione-independent aldo-keto-reductases, which are also responsible for biotransformation of 3-DG. GO, MGO and 3-DG readily react with DNA bases in vitro, giving rise to DNA adducts. There is clear evidence for genotoxicity of GO, MGO and 3-DG. Repeated dose toxicity studies on GO consistently reported reduced body weight gain concomitant with reduced food and water consumption but did not identify compound related changes in clinical chemistry and hematology or histopathological lesions. There is also no evidence for systemic carcinogenicity of GO and MGO based on the available studies. However, initiation/promotion studies indicate that oral exposure to GO may exhibit genotoxic and tumor promoting activity locally in the gastrointestinal tract. From a 2-year chronic toxicity and carcinogenicity study in rats, a NOAEL for systemic toxicity of GO administered via drinking water of 25 mg/kg bw was reported based on reduced body weight and erosions/ulcer in the glandular stomach. Other non-neoplastic and neoplastic lesions were not observed. Acute toxicity of HMF is also low. From a 90-day repeated dose toxicity study in mice, a NOAEL of 94 mg/kg bw was derived based on cytoplasmic alterations of proximal tubule epithelial cells of the kidney. HMF was mostly negative in in vitro genotoxicity tests, although positive findings for mutagenicity were obtained under conditions that promote formation of the chemically reactive sulfuric acid ester 5-sulfoxymethylfurfural. There is some evidence of carcinogenic activity of HMF in female B6C3F1 mice based on increased incidences of hepatocellular adenoma, but not in male mice and rats of both sexes. Although data on oral bioavailability of glycated amino acids are mostly limited to CML, it appears that glycated amino acids may be absorbed from the gastrointestinal tract after oral exposure to their free and protein bound form. Glycated amino acids that are not absorbed in the intestine may be subject to metabolism by the gut microbiome. Glycated amino acids present in the systemic circulation are rapidly eliminated via the urine. Acute oral toxicity of CML is low. Studies in mice and rats reported changes in clinical chemistry parameters indicative of impaired renal and hepatic function. However, these changes were not dose-related and not supported by histopathological evaluation.Previous risk assessments of individual glycation compounds did not identify a health concern at estimated human exposures (GO, HMF) but also noted the lack of data to draw firm conclusions on health risks associated with exposure to MGO.To identify potential associations between dietary intake of defined glycation compounds and disease a systematic review was carried out according to the Preferred Reporting Items for Systematic reviews and Meta-Analyses (PRISMA) model, applying the quality criteria previously defined by the SKLM. Using a combination of keywords defining individual glycation compounds and relevant disease patterns linked to the subject area of food, nutrition and diet, a systematic search in Pubmed (Medline), Scopus and Web of Science was performed. Although the present systematic review identified numerous studies that investigated an association between an "AGE-rich diet" and adverse health effects, only a subset of studies was found to comply with the quality criteria defined by the SKLM and was thus considered suitable to assess potential health risks of dietary glycation compounds.For each adverse health effect considered in this assessment, only limited numbers of human studies were identified. Although studies in humans offer the advantage of investigating effects at relevant human exposures, these studies did not provide compelling evidence for adverse effects of dietary glycation compounds. Animal studies identified in this systematic review provide some evidence for induction of impaired glucose tolerance, insulin resistance, cardiovascular effects and renal injury in response to oral exposure to GO and MGO as representatives of dicarbonyl compounds. Only limited evidence points to a link between high intake of glycated amino acids and metabolic disorders. However, these effects were typically reported to occur at dose levels that exceed human dietary exposure, often by several orders of magnitude. Unfortunately, most studies employed only one dose level, precluding characterization of dose-response and derivation of a point of departure for riskassessment. While in vitro studies provide some evidence for a potential mechanistic link between individual glycation compounds and presumed adverse health effects, the clinical and toxicological relevance of the in vitro findings is often limited by the use of high concentrations of glycation compounds that by far exceed human dietary exposure and by insufficient evidence for corresponding adverse effects in vivo. A key question that has not been adequately considered in most studies investigating systemic effects of glycation compounds is the extent of oral bioavailability of dietary glycation compounds, including the form in which MRPs may be taken up (e.g. free vs. peptide bound glycated amino acids). Understanding how much dietary glycation compounds really add to the significant endogenous background is critical to appraise the relevance of dietary MRPs for human health.While it appears mechanistically plausible that glycation of dietary allergens may affect their allergenic potential, the currently available data do not support the hypothesis that dietary glycation compounds may increase the risk for diet-induced allergies. There are no human studies addressing the immunological effects of dietary AGEs. Accordingly, there are no data on whether dietary AGEs promote the development of allergies, nor whether existing allergies are enhanced or attenuated. In numerous in vitro studies, the IgG/E binding ability of antigens and therefore their allergenic potential has been predominantly reported to be reduced by glycation. However, some in vitro studies showed that glycated proteins bind to receptors of immunological cells, and thus may have promoting effects on immune response and inflammation.Although experimental data from animal studies provide some evidence that high doses of individual glycation compounds such as MGO and protein-bound CML may produce certain adverse health effects, including diabetogenic, cardiovascular, metabolic and renal effects, the doses required to achieve these effects by far exceed human dietary exposures. Of note, in the only long-term study identified, a high dose of MGO administered via drinking water to mice for 18 months had no adverse effects on the kidneys, cardiovascular system, or development of diabetes.Experimental data from animal studies provide evidence that high doses of defined glycation compounds such as MGO or protein-bound CML may affect glucose homeostasis. However, the doses required to produce these effects markedly exceed human dietary exposure. Results from human studies are inconclusive: Three short-term intervention studies suggested that diets rich in AGEs may impair glucose homeostasis, whereas one recent intervention study and two observational studies failed to show such an effect.For the cardiovascular system, there is some evidence from in vitro and in vivo studies that high concentrations of MRPs, well above the dietary exposure of humans, may enhance inflammation in the cardiovascular system, induce endothelial damage, increase blood pressure and increase the risk of thrombosis. Only a limited number of human intervention studies investigated potential effects of short-term exposure and longer-term effects of glycation compounds on the cardiovascular system, and yielded inconsistent results. The few observational studies available either found no association between dietary MRP intake and cardiovascular function or even reported beneficial effects. Therefore, currently no definitive conclusion on potential acute and chronic effects of dietary MRPs on inflammation and cardiovascular function can be drawn. However, there is currently also no convincing evidence that potential adverse effects on the cardiovascular system are triggered by dietary MRP intake.Furthermore, human studies did not provide evidence for an adverse effect of dietary MRPs on kidney function. In animal studies with high levels of oral intake, MGO was reported to cause structural and functional effects in the kidney. Several studies show that the concentration of modified proteins and amino acids, such as CML, increases significantly in kidney tissue after oral intake. One study showed a negative effect of a high-temperature-treated diet containing increased CML concentrations on kidney structure integrity and impaired glomerular filtration. The causative relationship of accumulation of dietary MRPs and a functional decline of the kidneys, however, needs further confirmation.With regard to gut health, there is some evidence for alterations in gut microflora composition and the production of individual short-chain fatty acids (SCFAs) upon dietary exposure to glycation compounds. However, this has not been linked to adverse health effects in humans and may rather reflect adaptation of the gut microbiota to changing nutrients. In particular, a human observational study and several animal studies did not find a correlation between the intake of glycation compounds and increased intestinal inflammation. In animal studies, positive effects of glycation compounds on gut tissue damage and dysbiosis during colitis were described.Considering clear evidence for DNA reactivity and genotoxicity of the dicarbonyl compounds GO, MGO and 3-DG, it is plausible to suspect that dicarbonyl compounds may induce mutations and cancer. Although there is some evidence for tumor promoting activity of GO locally in the gastrointestinal tract, the only guideline-compatible chronic rodent bioassays reported erosions and ulcer in the glandular stomach but no treatment-related neoplastic lesions. A recent multinational cohort study with focus on CEL, CML, and MG-H1 found no evidence to support the hypothesis that dietary AGEs are linked to cancer risk.Evidence for an association between human exposure to dietary glycation compounds and detrimental effects on the brain and on cognitive performance is far from being compelling. No human studies fully complying with the defined quality criteria were identified. A few experimental studies reported neuroinflammation and cognitive impairment following dietary MRP exposure, but these can be considered indicative at best and do not support firm conclusions for human health. In addition to utilizing exceedingly high dosages of individual agents like CML, harsh processing conditions causing a multitude of major process-related changes do not allow to convincingly reconcile effects observed with measured/supposed contents of free and protein-bound CML alone.Overall, although dietary glycation compounds have been claimed to contribute to a wide range of adverse health effects, the present critical evaluation of the literature allows the conclusion that the available data are insufficient, inadequate or inconclusive and do not compellingly support the hypothesis of human health risks being related to the presence of glycation compounds in food. The study limitations detailed above, together with the fact that a large number of studies did not comply with the defined quality criteria and therefore had to be excluded highlight the importance of performing adequately designed human or animal studies to inform scientifically reliable health risk assessment.To achieve this, high quality, dependable scientific cooperation within various disciplines is pivotal.

Recent advances of 3-fucosyllactose in health effects and production.

Human milk oligosaccharides (HMOs) have been recognized as gold standard for infant development. 3-Fucosyllactose (3-FL), being one of the Generally Recognized as Safe HMOs, represents a core trisaccharide within the realm of HMOs; however, it has received comparatively less attention in contrast to extensively studied 2'-fucosyllactose. The objective of this review is to comprehensively summarize the health effects of 3-FL, including its impact on gut microbiota proliferation, antimicrobial effects, immune regulation, antiviral protection, and brain maturation. Additionally, the discussion also covers the commercial application and regulatory approval status of 3-FL. Lastly, an organized presentation of large-scale production methods for 3-FL aims to provide a comprehensive guide that highlights current strategies and challenges in optimization.

Safety and protection of plasma donors: A scoping review and evidence gap map.

BACKGROUND AND OBJECTIVES: As part of a large-scale project to safely increase plasma collection in Europe, the current scoping review identifies the existing evidence (gaps) on adverse events (AEs) and other health effects in plasmapheresis donors, as well as factors that may be associated with such events/effects. MATERIALS AND METHODS: We searched six databases and three registries. Study characteristics (publication type, language, study design, population, outcomes, associated factors, time of assessment, duration of follow-up, number and frequency of donations, convalescent plasma [y/n], setting and location) were synthesized narratively and in an interactive evidence gap map (EGM). RESULTS: Ninety-four research articles and five registrations were identified. Around 90% were observational studies (57 controlled and 33 uncontrolled), and most of them were performed in Europe (55%) or the United States (20%). Factors studied in association with donor health included donor characteristics (e.g., sex, age) (n = 27), cumulative number of donations (n = 21), donation frequency (n = 11), plasma collection device or programme (n = 11), donor status (first time vs. repeat) (n = 10), donation volume per session (n = 8), time in donation programme (n = 3), preventive measures (n = 2) or other (n = 9). CONCLUSION: The current scoping review provides an accessible tool for researchers and policymakers to identify the available evidence (gaps) concerning plasmapheresis donation safety. Controlled prospective studies with long-term donor follow-up are scarce. Furthermore, additional experimental studies comparing the health effects of different donation frequencies are required to inform a safe upper limit for donation frequency.

Properties and functions of acylated starch with short-chain fatty acids: a comprehensive review.

Short-chain fatty acids (SCFAs) are the primary energy source of colonic epithelial cells, but oral SCFAs are digested, absorbed, or degraded before reaching the colon. The acylated starch with SCFAs can be fermented and release specific SCFAs under the action of colonic intestinal microbiota. This review first introduces the preparation method, reaction mechanism, and substitution factors. Second, the structure, physical and chemical properties, in vitro function, and mechanism of acylated starch were expounded. Finally, the application of acylated starch in foods is introduced, and its safety is evaluated, providing a basis for the further development of acylated starch-based foods. The acylated starch obtained by different acylation types and preparation methods is different in particle, molecular, and crystal structures, leading to changes in the function and physicochemical properties. Meanwhile, acylated starch has the functional potential of targeted delivery of SCFAs to the colon, which can increase SCFAs in feces and intestine, selectively regulate the intestinal microbiota, and produce a prebiotic effect conducive to host health. The safety of acetylated starch has been supported by relevant studies, which have been widely used in various food fields and have great potential in the food industry.

Endogenous Nitric Oxide Can Enhance Oxidative Stress Caused by Air Pollutants and Explain Higher Susceptibility of Individuals with Inflammatory Disorders.

Air pollution causes morbidity and excess mortality. In the epithelial lining fluid of the respiratory tract, air pollutants trigger a chemical reaction sequence that causes the formation of noxious hydroxyl radicals that drive oxidative stress. For hitherto unknown reasons, individuals with pre-existing inflammatory disorders are particularly susceptible to air pollution. Through detailed multiphase chemical kinetic analysis, we show that the commonly elevated concentrations of endogenous nitric oxide in diseased individuals can increase the production of hydroxyl radicals via peroxynitrite formation. Our findings offer a molecular rationale of how adverse health effects and oxidative stress caused by air pollutants may be exacerbated by inflammatory disorders.

Characterizing Chemical, Environmental, and Stimulated Subcellular Physical Characteristics of Size-Fractionated PMs Down to PM0.1.

Air pollution, especially particulate matter (PM), is a significant environmental pollution worldwide. Studying the chemical, environmental, and life-related cellular physical characteristics of size-fractionated PMs is important because of their different degrees of harmful effects on human respiratory tracts and organ systems, causing severe diseases. This study evaluates the chemical components of size-fractionated PMs down to PM0.1 collected during a biomass-burning episode, including elemental/organic carbon and trace elements. Single particle sizes and distributions of PM0.1, PM0.5-0.1, PM1.0-0.5, and PM2.5-1.0 were analyzed by scanning electron microscopy and Zeta sizer. Two commonly used cell lines, e.g., HeLa and Cos7 cells, and two respiratory-related cell lines including lung cancer/normal cells were utilized for cell cytotoxicity experiments, revealing the key effects of particle sizes and concentrations. A high-speed scanning ion conductance microscope explored particle-stimulated subcellular physical characteristics for all cell lines in dynamics, including surface roughness (SR) and elastic modulus (E). The statistical results of SR showed distinct features among different particle sizes and cell types while a E reduction was universally found. This work provides a comprehensive understanding of the chemical, environmental, and cellular physical characteristics of size-fractionated PMs and sheds light on the necessity of controlling small-sized PM exposures.

Air pollution, viral spread and health outcomes evidence from strikes in France.

To evidence the impact of air pollution on the health of urban populations, several studies use natural experiments that shift commuting from public transport to cars (or vice-versa). However, as public transport use declines, reduced interpersonal contact may lead to slower virus spread and thus lower respiratory morbidity. Using a difference-in-differences strategy, we show that respiratory hospitalisations are both positively affected by air pollution and negatively affected by viral spread following partial unavailability of public transport due to strikes in the ten most populated French cities during the period 2010-2015. Our results are in line with studies in other countries that have found a significant increase in urgent respiratory hospitalisations following a public transport strike, most likely due to car pollution, but we also find a detectable interaction with viral spread, which should not be overlooked when interpreting these studies.

Comprehensive review on toxic heavy metals in the aquatic system: sources, identification, treatment strategies, and health risk assessment.

Heavy metal pollution in water sources has become a major worldwide environmental issue, posing a threat to aquatic ecosystems and human health. The pollution of the aquatic environment is increasing as a result of industrialization, climate change, and urban development. The sources of heavy metal pollution in water include mining waste, leachates from landfills, municipal and industrial wastewater, urban runoff, and natural events such as volcanism, weathering, and rock abrasion. Heavy metal ions are toxic and potentially carcinogenic. They can also buildup in biological systems and cause bioaccumulation even at low levels of exposure, heavy metals can cause harm to organs such as the nervous system, liver and lungs, kidneys and stomach, skin, and reproductive systems. There were various approaches tried to purify water and maintain water quality. The main purpose of this article was to investigate the occurrence and fate of the dangerous contaminants (Heavy metal and metalloids) found in domestic and industrial effluents. This effluent mixes with other water streams and is used for agricultural activities and other domestic activities further complicating the issue. It also discussed conventional and non-conventional treatment methods for heavy metals from aquatic environments. Conclusively, a pollution assessment of heavy metals and a human health risk assessment of heavy metals in water resources have been explained. In addition, there have been efforts to focus on heavy metal sequestration from industrial waste streams and to create a scientific framework for reducing heavy metal discharges into the aquatic environment.

Health and economic burden of wildland fires PM2.5-related pollution in Portugal - A longitudinal study.

Portugal has been affected by wildland fires that destroy thousands of hectares of forest, causing damage to the environment and to the exposed populations. This study aims to assess the influence of wildland fire emissions on air quality, its effect on population health and the related costs, between 2015 and 2018 in Portugal. The cause-specific mortality due to PM2.5 was calculated considering the exposure for five endpoints in adults, twelve age groups for adults and considering children under five years old. The contribution of wildfire emissions to PM2.5 concentrations in Portugal was assessed through EMEP-MSC/W model. Results showed that the average annual fire emissions of PM2.5, CO, CH4, CO2 and NO2 a significant and continuous increase was observed during the first three years (2015, 2016 and 2017) for all pollutants, followed by a decrease in 2018, with values lower than those observed in 2015. Regarding the long-term exposure to PM2.5 emitted by fires a total of 32, 93, 189 and 31 deaths, corresponding to a cost of 59, 174, 360 and 60 million EUR in 2015, 2016, 2017 and 2018, respectively, were estimated. On the other hand, in the first three years an increase in years of life lost (YLL) values of 496, 1608 and 3092 was observed, corresponding to a cost of 16, 54 and 105 million EUR, respectively, followed by a decrease in 2018 with a YLL of 480, corresponding to a cost of 17 M€.

Effects of air pollution on global health: evidence from the global burden of disease study in the BRICS countries.

PURPOSE: Considering the dynamic influence of environmental, social, economic, and political factors in the emergence and growth of the BRICS countries (Brazil, Russia, India, China, and South Africa) over the years and pre-existing differences, the adverse effects of air pollution on the health and well-being of the people have remained major areas of academic inquiry and policy interventions. The present study examines the global trend of deaths and Disability Adjusted Life Years (DALYs) attributable to air pollution with particular reference to the BRICS countries for the period 1990 to 2019. METHODS: This study has used the global burden of disease estimates by using different rounds of the Global Burden of Disease (GBD) study report published by the Institute of Health Metrics Evaluation. This study has calculated the cause of death and DALYs due to environmental risk factors (i.e. Air pollution). Data analysis has been done by using the standard formula for the calculation of death (mortality) rate and DALYs rate. Similarly, we calculated the age and gender-wise death and DALYs rate by using the appropriate numerator and denominator. RESULTS: The study discovered a significant shift in disease patterns over this period, as communicable diseases like respiratory infections and tuberculosis were replaced by non-communicable diseases such as ischemic heart disease (17.2 million), chronic obstructive pulmonary disease (14.59 million), and stroke (17.02 million) as the primary causes of air pollution-related deaths in 2019 at the global level. Additionally, the study identified a worrying increase in deaths linked to neonatal disorders and respiratory infections caused by ambient particulate matter pollution in South Africa, India, and Brazil. The impact of air pollution on public health is evident across different age groups and genders, with people aged 50-69 years, those aged 70 and above, and children under 5 years being more vulnerable. Furthermore, the male population is disproportionately affected by communicable and noncommunicable diseases caused by air pollution. CONCLUSION: The study highlights the need for policymakers to implement evidence-based interventions to tackle this global health problem. The interventions should aim to reduce the emerging crisis of non-communicable diseases related to air pollution, particularly among vulnerable age groups and the male population, ultimately improving public health outcomes.

Non-dietary exposure to phthalates in primary school children: Risk and correlation with anthropometric indices, cardiovascular and respiratory diseases.

Phthalates are endocrine disruptors of increasing concern for human health; however, previous studies have only assessed the association between internal exposure and human health. We aimed to assess the non-carcinogenic and carcinogenic risks of non-dietary exposure to phthalates in indoor environments among primary school children and their correlations with health indicators. A study involving 54 children was conducted in Jinan, Shandong Province, China. Questionnaires and health examinations were conducted, dust in hard-to-clean corners of students' classrooms and homes was collected, and airborne phthalates in the middle of classrooms and family living rooms were sampled. The gas-phase phthalate concentrations, individual exposure, and non-carcinogenic and carcinogenic risks were calculated. Associations were estimated using linear mixed models. The findings revealed that phthalates posed a non-carcinogenic risk to 7.4 % of the children and a moderate carcinogenic risk to 27.8 % of the children, with higher non-carcinogenic and carcinogenic risks to girls than to boys. Five phthalates were negatively correlated with body mass index, dimethyl phthalate and diethyl phthalate (DEP) were significantly correlated with waist circumference, and di-iso-butyl phthalate (DiBP) was negatively correlated with hip circumference. DiBP, di-n-butyl phthalate, and DEP, were significantly correlated with cardiovascular disease, DEP and di (2-n-butoxyethyl) phthalate were correlated with decreased lung function, and di-n-octyl phthalate influenced airway inflammation. The findings indicated that phthalate exposure may negatively impact children's health, thereby warranting further comprehensive research on the health effects of these chemicals.

Multi-omics and gut microbiome: Unveiling the pathogenic mechanisms of early-life pesticide exposure.

The extensive application of pesticides in agricultural production has raised significant concerns about its impact on human health. Different pesticides, including fungicides, insecticides, and herbicides, cause environmental pollution and health problems for non-target organisms. Infants and young children are so vulnerable to the harmful effects of pesticide exposure that early-life exposure to pesticides deserves focused attention. Recent research lays emphasis on understanding the mechanism between negative health impacts and early-life exposure to various pesticides. Studies have explored the impacts of exposure to these pesticides on model organisms (zebrafish, rats, and mice), as well as the mechanism of negative health effects, based on advanced methodologies like gut microbiota and multi-omics. These methodologies help comprehend the pathogenic mechanisms associated with early-life pesticide exposure. In addition to presenting health problems stemming from early-life exposure to pesticides and their pathogenic mechanisms, this review proposes expectations for future research. These proposals include focusing on identifying biomarkers that indicate early-life pesticide exposure, investigating transgenerational effects, and seeking effective treatments for diseases arising from such exposure. This review emphasizes how to understand the pathogenic mechanisms of early-life pesticide exposure through gut microbiota and multi-omics, as well as the adverse health effects of such exposure.

Consumption of energy drinks by children and young people: a systematic review examining evidence of physical effects and consumer attitudes.

OBJECTIVE: To update an earlier review, published in 2016, on the health and other outcomes associated with children and young people's consumption of energy drinks (EDs). STUDY DESIGN: Review article. SYSTEMATIC REVIEW: Systematic searches of nine databases (ASSIA, CINAHL, Cochrane Library, DARE, Embase, ERIC, MEDLINE, PsycINFO and Web of Science) retrieved original articles reporting the effects of EDs experienced by children and young people up to the age of 21 years. Searches were restricted by publication dates (January 2016 to July 2022) and language (English). Studies assessed as being weak were excluded from the review. Included studies underwent narrative synthesis. RESULTS: A total of 57 studies were included. Boys consumed EDs more than girls. Many studies reported a strong positive association between ED consumption and smoking, alcohol use, binge drinking, other substance use and the intentions to initiate these behaviours. Sensation-seeking and delinquent behaviours were positively associated with ED consumption, as were short sleep duration, poor sleep quality and low academic performance. Additional health effects noted in the updated review included increased risk of suicide, psychological distress, attention-deficit hyperactivity disorder symptoms, depressive and panic behaviours, allergic diseases, insulin resistance, dental caries and erosive tooth wear. CONCLUSIONS: This review adds to the growing evidence that ED consumption by children and young people is associated with numerous adverse physical and mental health outcomes. Where feasible and ethical, additional longitudinal studies are required to ascertain causality. The precautionary principle should be considered in regulatory policy and restriction of ED sales to this population. PROSPERO REGISTRATION: CRD42021255484.

Better accounting for long-term health effects in economic assessments: an illustration for air pollution in the Canton of Geneva.

OBJECTIVES: We propose a general framework for estimating long-term health and economic effects that takes into account four time-related aspects. We apply it to a reduction in exposure to air pollution in the Canton of Geneva. STUDY DESIGN: Methodological developments on the evaluation of long-term economic and health benefits, with an empirical illustration. METHODS: We propose a unified framework-the comprehensive impact assessment (CIA)-to assess the long-term effects of morbidity and mortality in health and economic terms. This framework takes full account of four time-related issues: cessation lag, policy/technical implementation timeframe, discounting and time horizon. We compare its results with those obtained from standard quantitative health impact assessment (QHIA) in an empirical illustration involving air pollution reduction in the canton of Geneva. RESULTS: We find that by neglecting time issues, the QHIA estimates greater health and economic benefits than the CIA. The overestimation is about 50% under reasonable assumptions and increases ceteris paribus with the magnitude of the cessation lag and the discount factor. It decreases both with the time horizon and with the implementation timeframe. CONCLUSION: A proper evaluation of long-term health and economic effects is an important issue when they are to be used in cost-benefit analyses, particularly for mortality, which often represents the largest fraction. We recommend using the CIA to calculate more accurate values.

Health-based strategies for overcoming barriers to climate change adaptation and mitigation.

Climate change poses an unequivocal threat to the respiratory health of current and future generations. Human activities-largely through the release of greenhouse gases-are driving rising global temperatures. Without a concerted effort to mitigate greenhouse gas emissions or adapt to the effects of a changing climate, each increment of warming increases the risk of climate hazards (eg, heat waves, floods, and droughts) that that can adversely affect allergy and immunologic diseases. For instance, wildfires, which release large quantities of particulate matter with a diameter of less than 2.5 µm (an air pollutant), occur with greater intensity, frequency, and duration in a hotter climate. This increases the risk of associated respiratory outcomes such as allergy and asthma. Fortunately, many mitigation and adaptation strategies can be applied to limit the impacts of global warming. Adaptation strategies, ranging from promotions of behavioral changes to infrastructural improvements, have been effectively deployed to increase resilience and alleviate adverse health effects. Mitigation strategies aimed at reducing greenhouse gas emissions can not only address the problem at the source but also provide numerous direct health cobenefits. Although it is possible to limit the impacts of climate change, urgent and sustained action must be taken now. The health and scientific community can play a key role in promoting and implementing climate action to ensure a more sustainable and healthy future.

Lutein Production and Extraction from Microalgae: Recent Insights and Bioactive Potential.

Microalgae have been reported to be excellent producers of bioactive molecules. Lutein is a pigment reported to have various beneficial effects for humans, and especially for eye well-being. In the current review, we summarize various methods that have been developed to optimize its extraction and bioactivities reported for human health. Several protective effects have been reported for lutein, including antioxidant, anticancer, anti-inflammatory, and cardioprotective activity. This review also reports attempts to increase lutein production by microalgae by changing culturing parameters or by using pilot-scale systems. Genetic engineering lutein production is also discussed. Considering the increasing aging of the worldwide population will create an increased need for lutein, a viable economic and eco-sustainable method to produce lutein is needed to face this market demand.