Jayanta Gupta

Featured Application This pilot study provides preliminary evidence that integrating chemical (TMVOC) and biological (ATP) indicators can enhance post-disaster indoor air quality assessments. For environmental engineering, the findings suggest potential applications in refining building assessment tools and moisture diagnostics to better identify hidden microbial contamination. For environmental health, the approach offers early insight into how combined TMVOC and ATP measurements may complement visual inspection methods in flood-damaged homes. Although based on a small sample of residential homes affected by Hurricane Ian, these results demonstrate a methodological framework that could be expanded in larger studies and aid future disaster response strategies. Flooding from hurricanes creates damp indoor environments that support mold growth and microbial contamination, posing long-term health risks for occupants. This pilot study evaluated TMVOCs, microbial activity, and environmental conditions in 13 Hurricane Ian-affected residences across multiple flood-affected neighborhoods. Air samples were collected using sorbent tubes and analyzed by gas chromatography-mass spectrometry, while microbial activity on surfaces was assessed via ATP bioluminescence. Visible mold and dampness were documented with the CDC/NIOSH Dampness and Mold Assessment Tool, and environmental measurements included temperature, relative humidity, and surface as well as hidden moisture. Median (IQR) TMVOC concentrations were 12 (8) mu g/m(3), with 61% of homes exceeding the 10 mu g/m(3) benchmark set by previous researchers despite minimal visible contamination. Spearman's correlation revealed significant negative relationships between odor and surface microbial activity (rho = -0.569, p < 0.05), indicating that organic debris may play a more crucial role in microbial activity within the tested homes, and that odors might originate from hidden microbes instead of surface microbial growth. Our study emphasizes the necessity of utilizing both chemical (TMVOC) and biological (ATP) indicators to evaluate poor air quality caused by molds in flood-affected homes, serving as a supplement to routine visible mold assessments.

Carbon nanomaterials (CNMs) particularly carbon nanotubes (CNTs) have found widespread applications in diversified fields including biomedical, industrial, and agriculture sectors, because of their unique physicochemical attributes. However, these high-volume nanomaterials have the propensity to become airborne as carbon nanoparticles (CNPs) during manufacturing, handling, and usage and pose exposure hazards in occupational and nonoccupational settings. Consequently, CNPs are deemed as emerging members of the toxic particulate matter in air pollution. Animal model studies have shown that inhaled CNPs have the potential to cause respiratory (tissue injury, inflammation, fibrosis) and systemic health effects including various organ toxicities and gut dysbiosis; the respiratory effects have been corroborated in emerging human epidemiological studies in CNM-exposed individuals. Inhaled CNT nanoparticles have been shown to cause immunotoxicity, oxidative stress, DNA damage, and other cellular changes, though the specific underlying molecular mechanisms continue to emerge. In this direction, we have compared the available Omics-based studies and presented an account of adverse outcome pathways (AOPs) impacted by CNT exposures. In particular, activation of specific immune signaling pathways varies with the CNT particle type/shape (rods versus tangles), as well as exposure duration. In conclusion, while CNMs offer significant benefits across various fields, their propensity to become airborne posing exposure risks via air pollution and health consequences must not be overlooked. Continued research is crucial to fully understand the underlying molecular mechanisms of their health effects and to develop effective strategies for safe handling and use.

Excerpt: Fibrosis of the kidney is the hallmark and the final common pathway of chronic kidney disease (CKD) progression, regardless of underlying etiology. Fibrosis is characterized by excessive production and deposition of extracellular matrix (ECM) proteins mainly in the kidney interstitium and results in structural damage, impairment of renal function, and eventually end-stage renal disease (ESRD). The most abundant collagens in the interstitial matrix of the kidney are collagen type I (COL I) and III (COL III). In renal fibrosis, these collagens are upregulated and the activity of the proteases responsible for their remodeling is altered. In this study, we used a sub-cohort of the Chronic Renal Insufficiency Cohort (CRIC) to examine the association of serum PRO-C6, a biomarker for type VI collagen formation and urine C3M, a biomarker for type III collagen degradation with a composite endpoint (ESRD or 50% decline in eGFR).

BACKGROUND AND AIM[|]After a flood, dampness in homes can lead to mold growth on building surfaces and behind the walls. These molds can produce volatile organic compounds (VOCs), which may cause symptoms of sick building syndrome and other building-related illnesses among occupants. This study aimed to measure the levels of total mold-specific VOCs (TMVOC) in residential buildings affected by Hurricane Ian in relation to visible molds on different surfaces.[¤]METHOD[|]Air samples from 13 flooded homes were collected using sorbent tubes following US EPA TO-17 and ISO 16000-6 methods. Gas chromatography/mass spectrometry (GC/MS) was used to identify and quantify mold-specific organic compounds. Visible molds in buildings were assessed using the {Dampness and Mold Assessment Screening Tool} developed by the CDC/NIOSH.[¤]RESULTS[|]Initial flood water levels in homes ranged from 3 to 10 ft. The mean (±SD) TMVOC and total VOC (TVOC) values were 11.84 (±6.57) ng/L of air and 2,131.53 (±1,365.33) ng/L of air, respectively. The most common types of mold-specific VOC compounds were methyl ethyl ketone, 1-pentanol, 2-heptanone, 2-pentyl furan, and 2-ethyl-1-hexanol. While molds could be observed in damp areas in a few homes, most homes were free from visible mold growths on walls, floors, and ceilings.[¤]CONCLUSIONS[|]Data collected with the CDC/NIOSH survey tool showed that visible molds and dampness were not evident in most homes, probably because they had been renovated and painted. In a previous large-scale indoor air quality study, the TMVOC values in over 45,000 air samples had ranged from <LOD to 55 ng/L of air. In the current study, 61% of sampled homes had moderate levels of TMVOC, with concentrations of >10 ng/L of air. This finding indicates that 61% of tested homes had actively growing molds – possibly hidden behind walls or under the floors – and individuals sensitive to molds could likely be affected.

Background Differences in death rate and cardiovascular disease (CVD) between Black and White patients with chronic kidney disease is attributed to sociocultural factors, comorbidities, genetics, and inflammation. Methods and Results We examined the interaction of race, plasma IL-6 (interleukin-6), and TMPRSS6 genotype as determinants of CVD and mortality in 3031 Chronic Renal Insufficiency Cohort study participants. The primary outcomes were all-cause mortality and a composite of incident myocardial infarction, peripheral artery disease, stroke, and heart failure. During the median follow-up of 10 years, Black patients with chronic kidney disease experienced a significantly higher mortality (34% versus 26%) and CVD composite (41% versus 28%) compared with White patients. After adjustment, TMPRSS6 genotype did not associate with the outcomes. The adjusted hazard ratio for mortality (4.11 [2.48-6.80], P<0.001) and CVD composite (2.52 [1.96-3.24], P<0.001) were higher for the highest versus lowest IL-6 quintile. The adjusted hazards for death per 1-quintile increase in IL-6 in White and Black individuals were 1.53 (1.42-1.64) versus 1.29 (1.20-1.38) (P<0.001), respectively. For CVD composite they were 1.61 (1.50-1.74) versus 1.30 (1.22-1.39) (P<0.001), respectively. In Cox proportional hazard models that included IL-6, there was no longer a racial disparity for death (1.01 [0.87-1.16], P=0.92), but significant unexplained mediation remained for CVD (1.24 [1.07-1.43]; P=0.004). Path models that included IL-6, diabetes, and urine albumin to creatinine ratio were able to identify variables responsible for racial disparity in mortality and CVD. Conclusions Racial differences in mortality and CVD among patients with chronic kidney disease could be explained by good-fitting path models that include selected mediator variables including diabetes and plasma IL-6.

Excerpt: Atopic dermatitis (AD) is a common pruritic skin disease characterized by acute disease flares and remissions.1,2 The worldwide prevalence of childhood AD ranges from 7% to 25%.1,3,4 AD is also common in adults; it may begin in adulthood or persist from childhood, and it has a prevalence of about 10%.1 AD is observed across all races and ethnicities, and in the United States it is likely more common in Black children than in White children.1,2,5 AD has been associated with the sequential progression to asthma and/or allergic rhinitis (AR), which is referred to as the ‘‘atopic march’’ and is thought to occur because of a common atopic pathophysiology linked to epithelial barrier defect, genetic predisposition, and environmental and immunologic factors.2,3,5 How the march is defined may vary depending on the article.2 The march classically includes the onset of asthma and AR after AD, but it can include other illnesses such as food allergies (FAs), eosinophilic esophagitis, allergic conjunctivitis, pet allergies, and specific sequential progressions of these illnesses in individuals with AD.2,3 Understanding the march is thought to be critically important for preventing the onset of these other atopic illnesses among individuals with AD. Patients can develop asthma or AR.

Approximately 1 billion tons of phosphogypsum (PG), a by-product of the fertilizer industry, are currently stacked in Florida. PG emits radon gas, which is a risk factor for lung cancer and can also increase particulate matter (PM) associated non-cancer mortality in exposed individuals. We measured concentrations of atmospheric radon and particulate matter near PG stacks and their short-term variations at different distances to estimate exposures in nearby communities. Specifically, we measured atmospheric levels of radon, and mass concentrations of PM
, PM
, and PM
, and number concentrations of PM
, PM
, PM
PM
, PM
, and PM
near three large PG stacks in Florida. Atmospheric radon was collected at distances of 2.5, 5.0, and 7.5 miles downwind from three large PG stacks using charcoal-based kits and measured by liquid scintillation counting. A professional radon monitor was used to take 24-h-average radon reading at 5.0 miles from each stack for comparison purposes. The median (IQR) radon levels were 0.325 (0.150, 0.675), 0.150 (0.150, 0.650), and 0.500 (0.150, 0.700) pCi/L at 2.5, 5, and 7.5 miles, respectively. The median (IQR) PM
levels were 5 (4, 6), 5 (3, 7), and 5 (2, 9) µg/m
at 2.5, 5, and 7.5 miles, respectively. Non-parametric Kruskal-Wallis test could not detect any association between radon or PM levels and distances (2.5-7 miles) from PG stacks. With scintillation counting, median radon levels detected were above the US Environmental Protection Agency (EPA) recommended standard in some of the sites; however, much higher levels were detected through the more advanced digital monitor. PM
levels were below the US-EPA 24-h average national ambient air quality standard in the study area. We conclude that ambient radon levels near PG stacks could exceed US EPA recommended outdoor standards and do not vary within a short distance from the sources, implying similar exposures in nearby communities.

Human trafficking is a major crime with millions of victims globally. The issue has come to increased attention in the past twenty-five years, and much progress has been made in rescue efforts by law enforcement agencies. Unfortunately, the same pace has not been seen in understanding the public health crisis associated with this, nor has much attention been paid to the psychological consequences and treatment. Although a number of risk and protective factors for the health consequences of human trafficking victims have been identified, there is still a dearth of information in the area of intervention and treatment. In reviewing current literature, we could not find articles comparing the different components of prevailing trauma treatment strategies, and the potential usefulness of these strategies in the treatment of human trafficking victims. To this end, we surveyed mental health professionals from Florida about their experience in working with this population and treatment strategies they have found effective in working with this population. Based on prevailing research, we also tried to understand the usefulness of current treatment strategies and methods used with this population. Based on the results of our study, we conclude that mental health providers who work with human trafficking victims should become aware of treatment efficacy. Further research on the effectiveness of treatment strategies used with victims/survivors of human trafficking is needed to validate our recommendations.

Mutations in the Filaggrin gene can cause absent or reduced filaggrin protein, leading to impaired keratinization and skin barrier defect, which produce characteristic phenotypes. In this short review, we report current evidence on the topic with special reference to atopic dermatitis, suggest future directions, and discuss therapeutic implications. Numerous candidate gene association studies, genome-wide association studies, studies on copy number variations and most recently, sequencing studies, have confirmed the robust association of mutations in the Filaggrin gene with atopic dermatitis, and have also linked these mutations with several other disorders. Filaggrin gene defects remain the strongest identified genetic risk factors for atopic dermatitis. Taken in conjunction with other genes found to be associated with this condition, genetic screening and identification of individuals at risk for atopic dermatitis could lead to personalized therapy. Manipulation of genetic regulatory elements to increase the amount of filaggrin protein in deficient individuals is an attractive treatment option for the future.