Large-scale evaluation of microorganism inactivation by bipolar ionization and photocatalytic devices.

The COVID-19 pandemic has raised awareness in the spread of disease via airborne transmission. As a result, there has been increasing interest in technologies that claim to reduce concentrations of airborne pathogens in indoor environments. The efficacy of many of these emerging technologies is not fully understood, and the testing that has been done is often conducted at a small scale and not representative of applied settings. There is currently no standard test method for evaluating air treatment technologies, making it difficult to compare results across studies or technology types. Here, a consistent testing approach in an operational-scale test chamber with a mock recirculating heating, ventilation, and air conditioning (HVAC) system was used to evaluate the efficacy of bipolar ionization and photocatalytic devices against the non-enveloped bacteriophage MS2 in the air and on surfaces. Statistically significant differences between replicate sets of technology tests and control tests (without technologies active) are apparent after 1 h, ranging to a maximum of 0.88 log10 reduction for the bipolar ionization tests and 1.8 log10 reduction for the photocatalytic device tests. It should be noted that ozone concentrations were elevated above background concentrations in the test chamber during the photocatalytic device testing. No significant differences were observed between control and technology tests in terms of the amount of MS2 deposited or inactivated on surfaces during testing. A standardized, large-scale testing approach, with replicate testing and time-matched control conditions, is necessary for contextualizing laboratory efficacy results, translating them to real-world conditions, and for facilitating technology comparisons.

Mutagenicity of the organic fraction of World Trade Center dust.

Most studies of the health effects and chemical characterization of the dust resulting from the catastrophic collapse of the World Trade Center (WTC) on September 11, 2001, have focused on the large inorganic fraction of the dust; however, chemical analyses have identified mutagens and carcinogens in the smaller organic fraction. Here, we determined the mutagenicity of the organic fraction of WTC dust in Salmonella. Only 0.74% of the mass of the particulate matter (PM) <53 µm in diameter was extractable organic matter (EOM). Because the EOM was 10 times more mutagenic in TA100 +S9 than in TA98 +S9 and was negative in TA98 -S9, we inferred, respectively, that polycyclic aromatic hydrocarbons (PAHs) played a role in the mutagenicity and not nitroarenes. In TA98 +S9, the mutagenic potency of the EOM (0.1 revertant/µg EOM) was within the range of EOMs from air and combustion emissions. However, the EOM-based mutagenic potency of the particles (0.0007 revertants/µg PM) was 1-2 orders of magnitude lower than values from a review of 50 combustion emissions and various air samples. We calculated that 37 PAHs analyzed previously in WTC EOM were 5.4% of the EOM mass and 0.04% of the PM mass; some air contained 0.3 µg WTC EOM/m3 (0.02 µg PAHs/m3 ). Populations exposed to WTC dust have elevated levels of prostate and thyroid cancer but not lung cancer. Our data support earlier estimates that PAH-associated cancer risk among this population, for example, PAH-associated lung cancer, was unlikely to be significantly elevated relative to background PAH exposures.

Plants, animals, and fisheries waste-mediated bioremediation of contaminants of environmental and emerging concern (CEECs)-a circular bioresource utilization approach.

The release of contaminants of environmental concern including heavy metals and metalloids, and contaminants of emerging concern including organic micropollutants from processing industries, pharmaceuticals, personal care, and anthropogenic sources, is a growing threat worldwide. Mitigating inorganic and organic contaminants, which can be coined as contaminants of environmental and emerging concern (CEECs), is a big challenge as traditional physicochemical processes are not economically viable for managing mixed contaminants of low concentrations. As a result, low-cost materials must be designed to provide high CEEC removal efficiency. One of the environmentally viable and energy-efficient approaches is biosorption, which involves using biomass or biopolymers isolated from plants or animals to decontaminate heavy metals in contaminated environments using inherent biological mechanisms. Among chemical constituents in plant biomass, cellulose, lignin, hemicellulose, proteins, polysaccharides, phenolic compounds, and animal biomass include polysaccharides and other compounds to bind heavy metals covalently and non-covalently. These functional groups include carboxyl, hydroxyl, carbonyl, amide, amine, and sulfhydryl. Cation-exchange capacities of these bioadsorbents can be improved by applying chemical modifications. The relevance of chemical constituents and bioactives in biosorbents derived from agricultural production such as food and fodder crops, bioenergy and cash crops, fruit and vegetable crops, medicinal and aromatic plants, plantation trees, aquatic and terrestrial weeds, and animal production such as dairy, goatery, poultry, duckery, and fisheries is highlighted in this comprehensive review for sequestering and bioremediation of CEECs, including as many as ten different heavy metals and metalloids co-contaminated with other organic micropollutants in circular bioresource utilization and one-health concepts.

Impact of test methodology on the efficacy of triethylene glycol (Grignard Pure) against bacteriophage MS2.

The COVID-19 pandemic has raised interest in using chemical air treatments as part of a strategy to reduce the risk of disease transmission, but more information is needed to characterize their efficacy at scales translatable to applied settings and to develop standardized test methods for characterizing the performance of these products. Grignard Pure, a triethylene glycol (TEG) active ingredient air treatment, was evaluated using two different test protocols in a large bioaerosol test chamber and observed to inactivate bacteriophage MS2 in air (up to 99.9% at 90 min) and on surfaces (up to 99% at 90 min) at a concentration of approximately 1.2 - 1.5 mg/m3. Introducing bioaerosol into a TEG-charged chamber led to overall greater reductions compared to when TEG was introduced into a bioaerosol-charged chamber, although the differences in efficacy against airborne MS2 were only significant in the first 15 min. Time-matched control conditions (no TEG present) and replicate tests for each condition were essential for characterizing treatment efficacy. These findings suggest that chemical air treatments could be effective in reducing the air and surface concentrations of infectious pathogens in occupied spaces, although standard methods are needed for evaluating their efficacy and comparing results across studies. The potential health impacts of chronic exposure to chemicals should also be considered, but those were not evaluated here.

Does restricting arm motion compromise short sprint running performance?

BACKGROUND: Synchronized arm and leg motion are characteristic of human running. Leg motion is an obvious gait requirement, but arm motion is not, and its functional contribution to running performance is not known. Because arm-leg coupling serves to reduce rotation about the body's vertical axis, arm motion may be necessary to achieve the body positions that optimize ground force application and performance. RESEARCH QUESTION: Does restricting arm motion compromise performance in short sprints? METHODS: Sprint performance was measured in 17 athletes during normal and restricted arm motion conditions. Restriction was self-imposed via arm folding across the chest with each hand on the opposite shoulder. Track and field (TF, n = 7) and team sport (TS, n = 10) athletes completed habituation and performance test sessions that included six counterbalanced 30 m sprints: three each in normal and restricted arm conditions. TS participants performed standing starts in both conditions. TF participants performed block starts with extended arms for the normal condition and elevated platform support of the elbows for the crossed-arm, restricted condition. Instantaneous velocity was measured throughout each trial using a radar device. Average sprint performance times were compared using a Repeated Measures ANOVA with Tukey post-hoc tests for the entire group and for the TF and TS subgroups. RESULTS: The 30 m times were faster for normal vs. restricted arm conditions, but the between-condition difference was only 1.6% overall and < 0.10 s for the entire group (4.82 ± 0.46 s vs. 4.90 ± 0.46 s, respectively; p < 0.001) and both TF (4.55 ± 0.34 vs. 4.63 ± 0.32 s; p < 0.001) and TS subgroups (5.01 ± 0.46 vs. 5.08 ± 0.47 s; p < 0.001). SIGNIFICANCE: Our findings suggest that when arm motion is restricted, compensatory upper body motions can provide the rotational forces needed to offset the lower body angular momentum generated by the swinging legs. We conclude that restricting arm motion compromised short sprint running performance, but only marginally.

Artificially long legs directly enhance long sprint running performance.

This comment addresses the incomplete presentation and incorrect conclusion offered in the recent manuscript of Beck et al. (R. Soc. Open Sci. 9, 211799 (doi:10.1098/rsos.211799)). The manuscript introduces biomechanical and performance data on the fastest-ever, bilateral amputee 400 m runner. Using an advantage standard of not faster than the fastest non-amputee runner ever (i.e. performance superior to that of the intact-limb world record-holder), the Beck et al. manuscript concludes that sprint running performance on bilateral, lower-limb prostheses is not unequivocally advantageous compared to the biological limb condition. The manuscript acknowledges the long-standing support of the authors for the numerous eligibility applications of the bilateral-amputee athlete. However, it does not acknowledge that the athlete's anatomically disproportionate prosthetic limb lengths (+15 cm versus the World Para Athletics maximum) are ineligible in both Olympic and Paralympic track competition due to their performance-enhancing properties. Also not acknowledged are the slower sprint performances of the bilateral-amputee athlete on limbs of shorter length that directly refute their manuscript's primary conclusion. Our contribution here provides essential background information and data not included in the Beck et al. manuscript that make the correct empirical conclusion clear: artificially long legs artificially enhance long sprint running performance.

Global Health Security Capacity and Capability Measurement Framework Within the Biological Threat Reduction Program.

The Biological Threat Reduction Program, part of the Nunn-Lugar Cooperative Threat Reduction Program since 1991, is mandated by the US Congress to regularly provide public reporting as part of its accountability. The Biological Threat Reduction Program recently designed a metrics and evaluation framework to measure its impact and effectiveness in partner countries. The framework focuses on capacity and capability strengthening related to biosafety, biosecurity, and biosurveillance. This is a marked shift from the previous approach, which relied on more tangible outcomes such as the elimination of weapons of mass destruction production assets, delivery devices, munitions, and construction activities. The new metrics and evaluation framework tracks the program's impact across 24 biosafety, biosecurity, and biosurveillance metrics and numerous capability, capacity, sustainability, and regional leadership indicators for human and animal health systems. The framework uses quantitative and qualitative inputs to generate measurement scores for program investment in partner countries. Overall, the framework provides a robust feedback loop between requirements, plans, and implementation processes throughout each step of the program's annual management lifecycle.

Biomarkers of exposure, effect, and susceptibility in workers exposed to nitrotoluenes.

Nitrotoluenes, such as 2-nitrotoluene, 2,4-dinitrotoluene (24DNT), and 26DNT, are carcinogenic in animal experiments. Humans are exposed to such chemicals in the workplace and in the environment. It is therefore important to develop methods to biomonitor people exposed to nitrotoluenes to prevent the potential harmful effects. For the present study, workers exposed to high levels of these chemicals were investigated. The external dose (air levels), the internal dose (urine metabolites), the biologically effective dose [hemoglobin (Hb) adducts and urine mutagenicity], and biological effects (chromosomal aberrations and health effects) were determined. Individual susceptibility was assessed by determining genetic polymorphisms of enzymes assumed to function in nitrotoluene metabolism, namely glutathione S-transferases (GSTM1, GSTT1, GSTP1), N-acetyltransferases (NAT1, NAT2), and sulfotransferases (SULT1A1, SULT1A2). The levels of urinary metabolites did not correlate with the air levels. The urinary mutagenicity levels determined in a subset of workers correlated with the levels of a benzylalcohol metabolite of DNT. The Hb-adducts correlated with the urine metabolites but not with the air levels. The frequency of chromosomal aberrations (gaps included) was increased (P < 0.05) in the exposed workers in comparison with a group of factory controls and correlated with the level of 24DNT Hb-adducts in young subjects (<31 years). The GSTM1-null genotype was significantly more prevalent in the controls than in the exposed group, which probably reflected an elevated susceptibility of the GSTM1-null genotype to adverse health effects of DNT exposure, such as nausea (odds ratio, 8.8; 95% confidence interval, 2.4-32.2). A statistically significant effect was seen for SULT1A2 genotype on a 24DNT Hb-adduct; GSTP1 genotype on a 2,4,6-trinitrotoluene Hb-adduct; and SULT1A1, SULT1A2, NAT1, GSTT1, and GSTP1 genotypes on chromosomal aberrations in the exposed workers.

Urinary biomarkers in charcoal workers exposed to wood smoke in Bahia State, Brazil.

Charcoal is an important source of energy for domestic and industrial use in many countries. Brazil is the largest producer of charcoal in the world, with approximately 350,000 workers linked to the production and transportation of charcoal. To evaluate the occupational exposure to wood smoke and potential genotoxic effects on workers in charcoal production, we studied urinary mutagenicity in Salmonella YG1041 +S9 and urinary levels of 2-naphthol and 1-pyrenol in 154 workers of northeastern Bahia. Workers were classified into three categories according to their working location, and information about socio-demographic data, diet, alcohol consumption, and smoking was obtained using a standard questionnaire. Spot urine samples were collected to evaluate urinary mutagenicity and urinary metabolites. Urinary mutagenicity increased significantly with exposure to wood smoke and was modified by smoking. The prevalence odds ratio was 5.31, and the 95% confidence interval was 1.85; 15.27 for urinary mutagenicity in the highly exposed group relative to the nonexposed group. The levels of urinary metabolites increased monotonically with wood smoke exposure and were associated with the GSTM1 null genotype, which was determined previously. The prevalence odds ratio (95% confidence interval) for higher levels of 2-naphtol among the highly exposed was 17.13 (6.91; 42.44) and for 1-hydroxyprene 11.55 (5.32; 25.08) when compared with nonexposed workers. Urinary 2-naphthol was the most sensitive indicator of wood smoke exposure. This is the first reported measurement of internal exposure to wood smoke among charcoal workers, and the results showed that these workers receive a systemic exposure to genotoxic compounds.

Urinary mutagenicity and colorectal adenoma risk.

We investigated urinary mutagenicity and colorectal adenoma risk in a clinic-based, case-control study of currently nonsmoking cases (n = 143) and controls (n = 156). Urinary organics were extracted by C18/methanol from 12-h overnight urine samples, and mutagenicity was determined in Salmonella YG1024 +S9 (Ames test). Adenoma risk was 2.4-fold higher in subjects in the highest versus the lowest quintile of urinary mutagenicity (95% confidence interval = 1.1-5.1). Combining urinary mutagenicity with intake of meat-derived mutagenicity (from our earlier analysis) resulted in a 5.6-fold increase in adenoma risk (95% confidence interval = 2.2-13.9, comparing the highest with the lowest quintile). In our study population, diet may have contributed to mutagenic exposure, which was positively associated with colorectal adenoma risk.

Bioassay-directed fractionation and salmonella mutagenicity of automobile and forklift diesel exhaust particles.

Many pulmonary toxicity studies of diesel exhaust particles (DEPs) have used an automobile-generated sample (A-DEPs) whose mutagenicity has not been reported. In contrast, many mutagenicity studies of DEPs have used a forklift-generated sample (SRM 2975) that has been evaluated in only a few pulmonary toxicity studies. Therefore, we evaluated the mutagenicity of both DEPs in Salmonella coupled to a bioassay-directed fractionation. The percentage of extractable organic material (EOM) was 26.3% for A-DEPs and 2% for SRM 2975. Most of the A-EOM (~55%) eluted in the hexane fraction, reflecting the presence of alkanes and alkenes, typical of uncombusted fuel. In contrast, most of the SRM 2975 EOM (~58%) eluted in the polar methanol fraction, indicative of oxygenated and/or nitrated organics derived from combustion. Most of the direct-acting, base-substitution activity of the A-EOM eluted in the hexane/dichloromethane (DCM) fraction, but this activity eluted in the polar methanol fraction for the SRM 2975 EOM. The direct-acting frameshift mutagenicity eluted across fractions of A-EOM, whereas > 80% eluted only in the DCM fraction of SRM 2975 EOM. The A-DEPs were more mutagenic than SRM 2975 per mass of particle, having 227 times more polycyclic aromatic hydrocarbon-type and 8-45 more nitroarene-type mutagenic activity. These differences were associated with the different conditions under which the two DEP samples were generated and collected. A comprehensive understanding of the mechanisms responsible for the health effects of DEPs requires the evaluation of DEP standards for a variety of end points, and our results highlight the need for multidisciplinary studies on a variety of representative samples of DEPs.

The carcinogenic response of Tsc2 mutant Long-Evans (Eker) rats to a mixture of drinking water disinfection by-products was less than additive.

Cancer risk assessment methods for chemical mixtures in drinking water are not well defined. Current default risk assessments for chemical mixtures assume additivity of carcinogenic effects, but this may not represent the actual biological response. A rodent model of hereditary renal cancer (Eker rat) was used to evaluate the carcinogenicity of mixtures of water disinfection by-products (DBPs). Male and female Eker rats were treated with individual DBPs or a mixture of DBPs for 4 or 10 months. Potassium bromate, 3-chloro-4-(dichloromethyl)-5-hydroxy-2(5H)-furanone, chloroform, and bromodichloromethane were administered in drinking water at low concentrations of 0.02, 0.005, 0.4, and 0.07 g/l, respectively, and high concentrations of 0.4, 0.07, 1.8, and 0.7 g/l, respectively. Low and high dose mixture solutions comprised all four chemicals at either the low or the high concentrations, respectively. Body weights, water consumption, and chemical concentrations in the water were measured monthly. All tissues were examined macroscopically for masses and all masses were diagnosed microscopically. Total renal lesions (adenomas and carcinomas) were quantitated microscopically in male and female rats treated for 4 or 10 months. A dose response for renal tumors was present in most treatment groups after 4 or 10 months of treatment. Treatment with the mixture produced on average no more renal, splenic, or uterine tumors than the individual compound with the greatest effect. This study suggests that the default assumption of additivity may overestimate the carcinogenic effect of chemical mixtures in drinking water.

Urinary mutagenesis and fried red meat intake: influence of cooking temperature, phenotype, and genotype of metabolizing enzymes in a controlled feeding study.

Meat cooked at high temperatures contains potential carcinogenic compounds, such as heterocyclic amines (HCAs) and polycyclic aromatic hydrocarbons (PAHs). Samples from a 2-week controlled feeding study were used to examine the relationship between the intake of mutagenicity from meat fried at different temperatures and the levels of mutagenicity subsequently detected in urine, as well as the influence of the genotype of drug metabolizing enzymes on urinary mutagenicity. Sixty subjects consumed ground beef patties fried at low temperature (100 degrees C) for 1 week, followed by ground beef patties fried at high temperature (250 degrees C) the second week. Mutagenicity in the meat was assayed in Salmonella typhimurium TA98 (+S9), and urinary mutagenicity was determined using Salmonella YG1024 (+S9). Genotypes for NAT1, NAT2, GSTM1, and UGT1A1 were analyzed using blood samples from the subjects. Meat fried at 100 degrees C was not mutagenic, whereas meat fried at 250 degrees C was mutagenic (1023 rev/g). Unhydrolyzed and hydrolyzed urine samples were 22x and 131x more mutagenic, respectively, when subjects consumed red meat fried at 250 degrees C compared with red meat fried at 100 degrees C. We found that hydrolyzed urine was approximately 8x more mutagenic than unhydrolyzed urine, likely due to the deconjugation of mutagens from glucuronide. The intake of meat cooked at high temperature correlated with the mutagenicity of unhydrolyzed urine (r = 0.32, P = 0.01) and hydrolyzed urine (r = 0.34, P = 0.008). Mutagenicity in unhydrolyzed urine was not influenced by NAT1, NAT2, or GSTM1 genotypes. However, a UGT1A1*28 polymorphism that reduced UGT1A1 expression and conjugation modified the effect of intake of meat cooked at high temperature on mutagenicity of unhydrolyzed urine (P for interaction = 0.04). These mutagenicity data were also compared with previously determined levels of HCAs (measured as MeIQx, DiMeIQx, and PhIP) and polycyclic aromatic hydrocarbons (PAHs) in the meat, levels of HCAs in the urine, and CYP1A2 and NAT2 phenotypes. The levels of mutagenicity in the meat fried at low and high temperatures correlated with levels of HCAs, but not levels of PAHs, in the meat. Also, levels of mutagenicity in unhydrolyzed urine correlated with levels of MeIQx in unhydrolyzed urine (r = 0.36; P = 0.01), and the levels of mutagenicity of hydrolyzed urine correlated with levels of MeIQx (r = 0.34; P = 0.01) and PhIP (r = 0.43; P = 0.001) of hydrolyzed urine. Mutagenicity in unhydrolyzed urine was not influenced by either the CYP1A2 or NAT2 phenotype. The data from this study indicate that urinary mutagenicity correlates with mutagenic exposure from cooked meat and can potentially be used as a marker in etiological studies on cancer.

Evidence for the presence of mutagenic arylamines in human breast milk and DNA adducts in exfoliated breast ductal epithelial cells.

Aromatic and heterocyclic amines are ubiquitous environmental mutagens present in combustion emissions, fried meats, and tobacco smoke, and are suspect human mammary carcinogens. To determine the presence of arylamines in breast tissue and fluid, we examined exfoliated breast ductal epithelial cells for DNA adducts and matched human milk samples for mutagenicity. Breast milk was obtained from 50 women who were 4-6 weeks postpartum, and exfoliated epithelial-cell DNA was evaluated for bulky, nonpolar DNA adducts by (32)P-postlabeling and thin-layer chromatography. Milk was processed by acid hydrolysis, and the extracted organics were examined in the standard plate-incorporation Ames Salmonella assay using primarily strain YG1024, which detects frameshift mutations and overexpresses aryl amine N-acetyltransferase. DNA adducts were identified in 66% of the specimens, and bulky adducts migrated in a pattern similar to that of 4-aminobiphenyl standards. The distribution of adducts did not vary by NAT2 genotype status. Of whole milk samples, 88% (22/25) had mutagenic activity. Among the samples for which we had both DNA adduct and mutagenicity data, 58% (14/19) of the samples with adducts were also mutagenic, and 85% (11/13) of the mutagenic samples had adducts. Quantitatively, no correlation was observed between the levels of adducts and the levels of mutagenicity. Separation of the milk showed that mutagenic activity was found in 69% of skimmed milk samples but in only 29% of the corresponding milk fat samples, suggesting that the breast milk mutagens were moderately polar molecules. Chemical fractionation showed that mutagenic activity was found in 67% (4/6) of the basic fractions but in only 33% (2/6) of acidic samples, indicating that the mutagens were primarily basic compounds, such as arylamines. Although pilot in nature, this study corroborates previous findings of significant levels of DNA adducts in breast tissue and mutagenicity in human breast milk and indicates that breast milk mutagens may be moderately polar basic compounds, such as arylamines.