Occurrence of organic ultraviolet absorbers in the particle and gas samples from plastic greenhouses: Human inhalation intake risk assessment.

The environmental pollution of organic ultraviolet absorbers (UVAs) has attracted global attention. However, the distribution, sources and risk assessment of UVAs in air from plastic greenhouses are rarely reported. This study was the first to investigate the concentrations of ten UVAs in the air samples from plastic greenhouses. The total concentrations of ten UVAs (∑10UVAs) in the air samples ranged from 5.7 × 103 ng/m3 to 6.3 × 103 ng/m3 (median 5.7 × 103 ng/m3) in greenhouses covered with biodegradable mulch film, 288.2 ng/m3 to 376.4 ng/m3 (median 333.9 ng/m3) in greenhouses covered with PE mulch film, and 97.9 ng/m3 to 142.6 ng/m3 (median 114.9 ng/m3) in greenhouses covered without mulch film. The concentrations of ten UVAs in 65 commercial agricultural films were simultaneously analyzed. Additionally, the potential health risks for greenhouse workers exposed to UVAs were estimated. And the migration simulations showed that the health risk in greenhouses may be higher even if only one UVA is added to the biodegradable mulch film. Therefore, the exposure risk of UVAs in plastic greenhouses needs to be highly prioritized.

Characterization of the inhalable fraction (< 10 µm) of soil from highly urbanized and industrial environments: magnetic measurements, bioaccessibility, Pb isotopes and health risk assessment.

Soil in urban and industrial areas is one of the main sinks of pollutants. It is well known that there is a strong link between metal(loid)s bioaccessibility by inhalation pathway and human health. The critical size fraction is < 10 µm (inhalable fraction) since these particles can approach to the tracheobronchial region. Here, soil samples (< 10 µm) from a highly urbanized area and an industrialized city were characterized by combining magnetic measurements, bioaccessibility of metal(loids) and Pb isotope analyses. Thermomagnetic analysis indicated that the main magnetic mineral is impure magnetite. In vitro inhalation analysis showed that Cd, Mn, Pb and Zn were the elements with the highest bioaccessibility rates (%) for both settings. Anthropogenic sources that are responsible for Pb accumulation in < 10 µm fraction are traffic emissions for the highly urbanized environment, and Pb related to steel emissions and coal combustion in cement plant for the industrial setting. We did not establish differences in the Pb isotope composition between pseudo-total and bioaccessible Pb. The health risk assessment via the inhalation pathway showed limited non-carcinogenic risks for adults and children. The calculated risks based on pseudo-total and lung bioaccessible concentrations were identical for the two areas of contrasting anthropogenic pressures. Carcinogenic risks were under the threshold levels (CR < 10-4), with Ni being the dominant contributor to risk. This research contributes valuable insights into the lung bioaccessibility of metal(loids) in urban and industrial soils, incorporating advanced analytical techniques and health risk assessments for a comprehensive understanding.

Worse pulmonary function in association with cumulative exposure to nanomaterials. Hints of a mediation effect via pulmonary inflammation.

BACKGROUND: Today, nanomaterials are broadly used in a wide range of industrial applications. Such large utilization and the limited knowledge on to the possible health effects have raised concerns about potential consequences on human health and safety, beyond the environmental burden. Given that inhalation is the main exposure route, workers exposed to nanomaterials might be at risk of occurrence of respiratory morbidity and/or reduced pulmonary function. However, epidemiological evidence regarding the association between cumulative exposure to nanomaterials and respiratory health is still scarce. This study focused on the association between cumulative exposure to nanomaterials and pulmonary function among 136 workers enrolled in the framework of the European multicentric NanoExplore project. RESULTS: Our findings suggest that, independently of lifelong tobacco smoking, ethnicity, age, sex, body mass index and physical activity habits, 10-year cumulative exposure to nanomaterials is associated to worse FEV1 and FEF25 - 75%, which might be consistent with the involvement of both large and small airway components and early signs of airflow obstruction. We further explored the hypothesis of a mediating effect via airway inflammation, assessed by interleukin (IL-)10, IL-1ß and Tumor Necrosis Factor alpha (TNF-α), all quantified in the Exhaled Breath Condensate of workers. The mediation analysis results suggest that IL-10, TNF-α and their ratio (i.e., anti-pro inflammatory ratio) may fully mediate the negative association between cumulative exposure to nanomaterials and the FEV1/FVC ratio. This pattern was not observed for other pulmonary function parameters. CONCLUSIONS: Safeguarding the respiratory health of workers exposed to nanomaterials should be of primary importance. The observed association between cumulative exposure to nanomaterials and worse pulmonary function parameters underscores the importance of implementing adequate protective measures in the nanocomposite sector. The mitigation of harmful exposures may ensure that workers can continue to contribute productively to their workplaces while preserving their respiratory health over time.

Exposure to tungsten particles via inhalation triggers early toxicity marker expression in the rat brain.

OBJECTIVE: Our work is focused on tungsten, considered as an emerging contaminant. Its environmental dispersion is partly due to mining and military activities. Exposure scenario can also be occupational, in areas such as the hard metal industry and specific nuclear facilities. Our study investigated the cerebral effects induced by the inhalation of tungsten particles. METHODS: Inhalation exposure campaigns were carried out at two different concentrations (5 and 80 mg/m3) in single and repeated modes (4 consecutive days) in adult rats within a nose-only inhalation chamber. Processes involved in brain toxicity were investigated 24 h after exposure. RESULTS AND DISCUSSION: Site-specific effects in terms of neuroanatomy and concentration-dependent changes in specific cellular actors were observed. Results obtained in the olfactory bulb suggest a potential early effect on the survival of microglial cells. Depending on the mode of exposure, these cells showed a decrease in density accompanied by an increase in an apoptotic marker. An abnormal phenotype of the nuclei of mature neurons, suggesting neuronal suffering, was also observed in the frontal cortex, and can be linked to the involvement of oxidative stress. The differential effects observed according to exposure patterns could involve two components: local (brain-specific) and/or systemic. Indeed, tungsten, in addition to being found in the lungs and kidneys, was present in the brain of animals exposed to the high concentration. CONCLUSION: Our data question the perceived innocuity of tungsten relative to other metals and raise hypotheses regarding possible adaptive or neurotoxic mechanisms that could ultimately alter neuronal integrity.

Aristolochic Acid Exposure via Dermal Contact or Inhalation of Herbal Powders: Evidence of Occupational Exposure in Herbalists with Urothelial Cancer.

Emerging evidence showing urothelial cancer in herbalists is linked to aristolochic acid (AA) exposure; however, the exposure pathway remains unclear. Here, we show that dermal contact and inhalation of fine powders of AA-containing herbs are significant occupational AA exposure pathways for herbalists. We initiated the study by quantifying the amount of AA in the AA-containing powder deposited on gloves and face masks worn by the operators of an AA-containing herb grinding machine. Then, we measured the kinetics of dermal absorption and dissolution of AA from fine powders of AA-containing herbs into artificial sweat and surrogate lung fluid. Lastly, we quantified the mutagenic AA-DNA adduct levels formed in the kidneys of mice exposed to AA-containing fine powders through dermal contact. Our findings highlight an urgent occupational risk that should demand implementation of safety standards for herbalists exposed to AA-containing fine powders.

Differences in the anatomy and physiology of the human and rat respiratory tracts and impact on toxicological assessments.

Inhalation is a critical route through which substances can exert adverse effects in humans; therefore, it is important to characterize the potential effects that inhaled substances may have on the human respiratory tract by using fit for purpose, reliable, and human relevant testing tools. In regulatory toxicology testing, rats have primarily been used to assess the effects of inhaled substances as they-being mammals-share similarities in structure and function of the respiratory tract with humans. However, questions about inter-species differences impacting the predictability of human effects have surfaced. Disparities in macroscopic anatomy, microscopic anatomy, or physiology, such as breathing mode (e.g., nose-only versus oronasal breathing), airway structure (e.g., complexity of the nasal turbinates), cell types and location within the respiratory tract, and local metabolism may impact inhalation toxicity testing results. This review shows that these key differences describe uncertainty in the use of rat data to predict human effects and supports an opportunity to harness modern toxicology tools and a detailed understanding of the human respiratory tract to develop testing approaches grounded in human biology. Ultimately, as the regulatory purpose is protecting human health, there is a need for testing approaches based on human biology and mechanisms of toxicity.

Increased mortality risk from airborne exposure to polycyclic aromatic hydrocarbons.

BACKGROUND: The potential health effects of airborne polycyclic aromatic hydrocarbons (PAHs) among general population remained extensively unstudied. This study sought to investigate the association of short-term exposure to low-level total and 7 carcinogenic PAHs with mortality risk. METHODS: We conducted an individual-level time-stratified case-crossover study in Jiangsu province of eastern China, by investigating over 2 million death cases during 2016-2019. Daily concentrations of total PAH and its 7 carcinogenic species including benzo[a]anthracene (BaA), benzo[a]pyrene (BaP), benzo[b]fluoranthene (BbF), benzo[k]fluoranthene (BkF), chrysene (Chr), dibenz[a,h]anthracene (DahA), and indeno[1,2,3-cd]pyrene (IcdP), predicted by well-validated spatiotemporal models, were assigned to death cases according to their residential addresses. We estimated mortality risk associated with short-term exposure to increase of an interquartile range (IQR) for aforementioned PAHs using conditional logistic regression. RESULTS: An IQR increase (16.9 ng/m3) in 2-day (the current and prior day) moving average of total PAH concentration was associated with risk increases of 1.90% (95% confidence interval [CI]: 1.71-2.09) in all-cause mortality, 1.90% (95% CI: 1.70-2.10) in nonaccidental mortality, 2.01% (95% CI: 1.72-2.29) in circulatory mortality, and 2.53% (95% CI: 2.03-3.02) in respiratory mortality. Risk increases of cause-specific mortality ranged between 1.42-1.90% for BaA (IQR: 1.6 ng/m3), 1.94-2.53% for BaP (IQR: 1.6 ng/m3), 2.45-3.16% for BbF (IQR: 2.8 ng/m3), 2.80-3.65% for BkF (IQR: 1.0 ng/m3), 1.36-1.77% for Chr (IQR: 1.8 ng/m3), 0.77-1.24% for DahA (IQR: 0.8 ng/m3), and 2.96-3.85% for IcdP (IQR: 1.7 ng/m3). CONCLUSIONS: This study provided suggested evidence for heightened mortality risk in relation to short-term exposure to airborne PAHs in general population. Our findings suggest that airborne PAHs may pose a potential threat to public health, emphasizing the need of more population-based evidence to enhance the understanding of health risk under the low-dose exposure scenario.

Dry deposition fluxes and inhalation risks of toxic elements in total suspended particles in the Bohai Rim region: Long-term trends and potential sources.

Long-term changes in dry deposition fluxes (DDF) and health risks for toxic elements (TE) in total suspended particles (TSP) in the Bohai Rim region are important for assessing control effects of pollution sources. Thus, we investigated the trends in DDF and concentrations for TSP and TE and health risks of TE in eight cities in the region from 2011-2020. TSP concentration and DDF showed general downward trends. Compared to the before Clear Air Action Plan (BCAAP, 2011-2012) period, concentration and DDF of TE over the Clear Air Action Plan (CAAP, 2013-2017) period substantially decreased, with the highest decrease rates in Zn, Cd, and Cr. During the study period, non-carcinogenic (HI) and total carcinogenic (TCR) risks for children and adults were 0.09 and 0.04, and 1.54 × 10-5 and 2.65 × 10-5, respectively, with Cr6+ and As being dominant contributors. Compared to the BCAAP period, HI and TCR over the CAAP period decreased by 36.8 % and 32.4 %, respectively. However, their risks increased over the Blue Sky Protection Campaign (BSPC, 2018-2020) period. Potential source contribution function suggested substantial changes in potential risk areas over different control periods, with the BSPC primarily being on land and the Yellow Sea.

Characterization and health risks of short- and medium-chain chlorinated paraffins in the gas and size-fractionated particulate phases in ambient air.

Short-chain and medium-chain chlorinated paraffins (SCCPs and MCCPs) have garnered significant attention because they have persistence and potential toxicity, and can undergo long-distance transport. Chlorinated paraffins (CPs) inhaled in the size-fractionated particulate phase and gas phase can carry different risks to human health due to their ability to accumulate in different regions of the respiratory tract and exhibit varying deposition efficiencies. In our study, large-volume ambient air samples in both the size-fractionated particulate phase (Dp < 1.0 µm, 1.0-2.5 µm, 2.5-10 µm, and Dp ≥ 10 µm) and gas phase were collected simultaneously in Beijing using an active sampler. The overall levels of SCCPs and MCCPs were relatively high, the ranges being 57-881 and 30-385 ng/m3, respectively. SCCPs tended to be partitioned in the gas phase (on average 75% of the ΣSCCP concentration), while MCCPs tended to be partitioned in the particulate phase (on average 62% of the ΣMCCP concentration). Significant correlations were discovered between the logarithm-transformed gas-particle partition coefficients (KP) and predicted subcooled vapor pressures (PL0) (p < 0.01 for SCCPs and MCCPs) and between the logarithm-transformed KP values and octanol-air partition coefficients (KOA) (p < 0.01 for SCCPs and MCCPs). Thus, the slopes indicated that organic matter absorption was the dominant process involved in gas-particle partitioning. We used the ICRP model to calculate deposition concentrations for particulate-associated CPs in head airways region (15.6-71.4 ng/m³), tracheobronchial region (0.8-4.8 ng/m³), and alveolar region (5.1-21.9 ng/m³), then combined these concentrations with the CP concentrations in the gas phase to calculate estimated daily intakes (EDIs) for inhalation. The EDIs for SCCPs and MCCPs through inhalation of ambient air for the all-ages group were 67.5-184.2 ng/kg/day and 19.7-53.7 ng/kg/day, respectively. The results indicated that SCCPs and MCCPs in ambient air do not currently pose strong risks to human health in the study area.

Biomarkers of Organophosphate and Polybrominated Diphenyl Ether (PBDE) Flame Retardants of American Workers and Associations with Inhalation and Dermal Exposures.

This study evaluated workers' exposures to flame retardants, including polybrominated diphenyl ethers (PBDEs), organophosphate esters (OPEs), and other brominated flame retardants (BFRs), in various industries. The study aimed to characterize OPE metabolite urinary concentrations and PBDE serum concentrations among workers from different industries, compare these concentrations between industries and the general population, and evaluate the likely route of exposure (dermal or inhalation). The results showed that workers from chemical manufacturing had significantly higher (p <0.05) urinary concentrations of OPE metabolites compared to other industries. Spray polyurethane foam workers had significantly higher (p <0.05) urinary concentrations of bis(1-chloro-2-propyl) phosphate (BCPP) compared to other industries. Electronic scrap workers had higher serum concentrations of certain PBDE congeners compared to the general population. Correlations were observed between hand wipe samples and air samples containing specific flame-retardant parent chemicals and urinary metabolite concentrations for some industries, suggesting both dermal absorption and inhalation as primary routes of exposure for OPEs. Overall, this study provides insights into occupational exposure to flame retardants in different industries and highlights the need for further research on emerging flame retardants and exposure reduction interventions.

A novel approach to assess the health risk of aryl hydrocarbon receptor-bound contaminants via inhalation exposure using CYP1A1 expression as a biomarker.

Polycyclic aromatic hydrocarbons (PAHs) and dioxins are potential causes of multiple diseases by activating the aryl hydrocarbon receptor (AhR) pathway. Health risk assessment of chemicals primarily relies on the relative potency factor (RPF), although its accuracy may be limited when solely using EC50 values. The induction of cytochrome P4501A1 (CYP1A1) serves as a biomarker for AhR activation and is an integrator of dioxin-like toxicity. Here, we present a method for evaluating the risks associated with AhR activation using mathematical models of dose-CYP1A1 induction. The dose-effect curves for certain PAHs and dioxins, including Ant, BghiP, 1,2,3,4,7,8-HxCDD, and others, exhibited a non-classical S-shaped form. The toxic equivalent factor (TEF) profiles revealed a broad range of toxic equivalent factor values. The TEFs for PAHs ranged from approximately 0.01 to 6, with higher values being observed when the concentration was less than 10-10 M, with the exceptions of Ace, Phe, and BghiP. Most congeners of dioxins got the lowest TEF value at around 10-10 M, ranging from 0.04 to 1.00. The binding affinity of AhR to ligands did not display a strong correlation with the EC50 of CYP1A1 expression, suggesting that the AhR-mediated effects of PAHs and dioxins are not fixed but instead fluctuate with the dose. Air samples acquired from a parking area were used to compare the proficiency of RPF and our current approach. In the current method, naphthalene and chrysene were the primary contributors of PAHs to AhR-mediated risks in parking lots air samples, respectively. However, the contributions of naphthalene and chrysene could be disregarded in the RPF approach.

Proposals for new spray drift exposure values in orchards and vineyards for residents and bystanders.

In the EU, predicted exposure to spray drift for residents and bystanders from applications in orchards and vineyards is based on data from one study published in 1987, where one downwind distance (8 m) was considered. CropLife Europe conducted sixteen new GLP compliant studies in 4 EU countries, 8 in orchards, 8 in vineyards with early and late season applications, using adult and child mannequins located 5, 10 and 15 m downwind from the last row to measure dermal and inhalation exposures. The resulting "Bystander Resident Orchard Vineyard (BROV)" database comprises 288 observations and offers a more comprehensive option for exposure prediction. There were differences between adult and child, crop type, leaf cover and distance from the sprayer, supporting the derivation of mean, median, 75th and 95th percentile exposures for each subset. Exposures did not generally correlate with wind speed, wind direction, sprayer type, spray quality, spray concentration or amount applied. Dermal and inhalation exposure were lower in vineyards than in orchards and further analysis is required to understand why.

Investigating the temporal link between PM2.5 exposure and acceleration of myocardial ischemia reperfusion injury: Emphasizing the hazardous presence of metals in inhaled air.

Exposure to PM2.5 is widely acknowledged to induce cardiotoxic effects, leading to decreased myocardial tolerance to revascularization procedures and subsequent ischemia reperfusion injury (IR). However, the temporal relationship between PM2.5 exposure and vulnerability to IR, along with the underlying mechanisms, remains unclear and is the focus of this study. Female Wistar rats were exposed to PM2.5 at a concentration of 250 µg/m³ for 3 h daily over varying durations (7, 14, and 21 days), followed by IR induction. Our results demonstrated a significant increase in cardiac injury, as evidenced by increased infarct size and elevated cardiac injury markers, starting from day 14 of PM2.5 exposure, accompanied by declined cardiac function. These adverse effects were associated with apoptosis and impaired mitochondrial function, including reduced bioenergetics, mitochondrial DNA copy number and quality control mechanisms, along with inactivation of the PI3K/AKT/AMPK signalling pathways. Furthermore, analysis of myocardial tissue revealed elevated metal accumulation, particularly within mitochondria. Chelation of PM2.5 -associated metals using EDTA significantly mitigated the toxic effects on cardiac IR pathology, as confirmed in both rat myocardium and H9c2 cells. These findings suggest that metals in PM2.5 play a crucial role in inducing cardiotoxicity, impairing myocardial resilience to stress through mitochondrial accumulation and dysfunction.

Nasal filter reveal exposure risks of inhalable particulates and heavy metals in urban women.

Urban populations, especially women, are vunerable to exposure to airborne pollution, particularly inhalable particulates (PM10). Thus, more accurate measurement of PM10 levels and evaluating their health effects is critical for guiding policy to improve human health. Previous studies obtained personal PM10 with time-weighted average by air filter-based sampling (AFS), which ignores individual differences and behavioral patterns. Here, we used nasal filters instead of AFS to obtain actual inhaled PM10 under short-term exposure for urban dwelling women during a severe haze event in Beijing in 2016. The levels of six heavy metals such as As, Cd, Ni, Cr, Pb, and Co in PM10 were investigated, and carcinogenic and non-carcinogenic risks evaluated based on an adjusted US EPA health risk assessment model. The health endpoints for urban dwelling women were further assessed through an exposure-reponse model. We found that the hourly inhaled dose of PM10 obtained through the nasal filter was about 2.5-17.6 times that obtained by AFS, which also resulted in 4.41-11.30 times more morbidity than estimated by AFS (p < 0.05). Proximity to traffic emissions resulted in greater exposure to particulate matter (>18.8 µg/kg·h) and heavy metals (>2.2 ng/kg·h), and these populations are therefore at greatest risk of developing non-cancer (HI = 4.16) and cancer (Rt = 7.8 × 10-3) related morbities.

Probabilistic Estimation of Airborne Micro- and Nanoplastic Intake in Humans.

Little research exists on the magnitude, variability, and uncertainty of human exposure to airborne micro- and nanoplastics (AMNPs), despite their critical role in human exposure to MNPs. We probabilistically estimate the global intake of AMNPs through three main pathways: indoor inhalation, outdoor inhalation, and ingestion during indoor meals, for both children and adults. The median inhalation of AMPs is 1,207.7 (90% CI, 42.5-8.48 × 104) and 1,354.7 (90% CI, 47.4-9.55 × 104) N/capita/day for children and adults, respectively. The annual intake of AMPs is 13.18 mg/capita/a for children and 19.10 mg/capita/a for adults, which is approximately one-fifth and one-third of the mass of a standard stamp, assuming a consistent daily intake of medians. The majority of AMP number intake occurs through inhalation, while the ingestion of deposited AMPs during meals contributes the most in terms of mass. Furthermore, the median ANP intake through outdoor inhalation is 9,638.1 N/day (8.23 × 10-6 µg/d) and 5,410.6 N/day (4.62 × 10-6 µg/d) for children and adults, respectively, compared to 5.30 × 105 N/day (5.79 × 10-4 µg/d) and 6.00 × 105 N/day (6.55 × 10-4 µg/d) via indoor inhalation. Considering the increased toxicity of smaller MNPs, the significant number of ANPs inhaled warrants great attention. Collaborative efforts are imperative to further elucidate and combat the current MPN risks.

Systemic immunological responses are dependent on sex and ovarian hormone presence following acute inhaled woodsmoke exposure.

BACKGROUND: Rural regions of the western United States have experienced a noticeable surge in both the frequency and severity of acute wildfire events, which brings significant challenges to both public safety and environmental conservation efforts, with impacts felt globally. Identifying factors contributing to immune dysfunction, including endocrinological phenotypes, is essential to understanding how hormones may influence toxicological susceptibility. METHODS: This exploratory study utilized male and female C57BL/6 mice as in vivo models to investigate distinct responses to acute woodsmoke (WS) exposure with a focus on sex-based differences. In a second set of investigations, two groups were established within the female mouse cohort. In one group, mice experienced ovariectomy (OVX) to simulate an ovarian hormone-deficient state similar to surgical menopause, while the other group received Sham surgery as controls, to investigate the mechanistic role of ovarian hormone presence in driving immune dysregulation following acute WS exposure. Each experimental cohort followed a consecutive 2-day protocol with daily 4-h exposure intervals under two conditions: control HEPA-filtered air (FA) and acute WS to simulate an acute wildfire episode. RESULTS: Metals analysis of WS particulate matter (PM) revealed significantly increased levels of 63Cu, 182W, 208Pb, and 238U, compared to filtered air (FA) controls, providing insights into the specific metal components most impacted by the changing dynamics of wildfire occurrences in the region. Male and female mice exhibited diverse patterns in lung mRNA cytokine expression following WS exposure, with males showing downregulation and females displaying upregulation, notably for IL-1ß, TNF-α, CXCL-1, CCL-5, TGF-ß, and IL-6. After acute WS exposure, there were notable differences in the responses of macrophages, neutrophils, and bronchoalveolar lavage (BAL) cytokines IL-10, IL-6, IL-1ß, and TNF-α. Significant diverse alterations were observed in BAL cytokines, specifically IL-1ß, IL-10, IL-6, and TNF-α, as well as in the populations of immune cells, such as macrophages and polymorphonuclear leukocytes, in both Sham and OVX mice, following acute WS exposure. These findings elucidated the profound influence of hormonal changes on inflammatory outcomes, delineating substantial sex-related differences in immune activation and revealing altered immune responses in OVX mice due to ovarian hormone deficiency. In addition, the flow cytometry analysis highlighted the complex interaction between OVX surgery, acute WS exposure, and their collective impact on immune cell populations within the hematopoietic bone marrow niche. CONCLUSIONS: In summary, both male and female mice, alongside females subjected to OVX and those who had sham surgery, exhibit significant variations in the expression of proinflammatory cytokines, chemokines, lung mRNA gene expression, and related functional networks linked to signaling pathways. These differences potentially act as mediators of sex-specific and hormonal influences in the systemic inflammatory response to acute WS exposure during a wildfire event. Understanding the regulatory roles of genes expressed differentially under environmental stressors holds considerable implications, aiding in identifying sex-specific therapeutic targets for addressing acute lung inflammation and injury.

Cross-shift changes in pulmonary function and occupational exposure to particulate matter among e-waste workers in Ghana.

Introduction: Little is known on the association between cross-shift changes in pulmonary function and personal inhalation exposure to particulate matter (PM) among informal electronic-waste (e-waste) recovery workers who have substantial occupational exposure to airborne pollutants from burning e-waste. Methods: Using a cross-shift design, pre- and post-shift pulmonary function assessments and accompanying personal inhalation exposure to PM (sizes <1, <2.5 µm, and the coarse fraction, 2.5-10 µm in aerodynamic diameter) were measured among e-waste workers (n = 142) at the Agbogbloshie e-waste site and a comparison population (n = 65) in Accra, Ghana during 2017 and 2018. Linear mixed models estimated associations between percent changes in pulmonary function and personal PM. Results: Declines in forced expiratory volume in one second (FEV1) and forced vital capacity (FVC) per hour were not significantly associated with increases in PM (all sizes) among either study population, despite breathing zone concentrations of PM (all sizes) that exceeded health-based guidelines in both populations. E-waste workers who worked "yesterday" did, however, have larger cross-shift declines in FVC [-2.4% (95%CI: -4.04%, -0.81%)] in comparison to those who did not work "yesterday," suggesting a possible role of cumulative exposure. Discussion: Overall, short-term respiratory-related health effects related to PM exposure among e-waste workers were not seen in this sample. Selection bias due to the "healthy worker" effect, short shift duration, and inability to capture a true "pre-shift" pulmonary function test among workers who live at the worksite may explain results and suggest the need to adapt cross-shift studies for informal settings.

Low-Level Respirable Crystalline Silica and Silicosis: Long-Term Follow-Up of Vermont Granite Workers.

The lifetime risk of silicosis associated with low-level occupational exposure to respirable crystalline silica remains unclear because most previous radiographic studies included workers with varying exposure concentrations and durations. This study assessed the prevalence of silicosis after lengthy exposure to respirable crystalline silica at levels ≤ 0.10 mg/m3. Vermont granite workers employed any time during 1979-1987 were traced and chest radiographs were obtained for 356 who were alive in 2017 and residing in Vermont. Work history, smoking habits and respiratory symptoms were obtained by interview, and exposure was estimated using a previously developed job-exposure matrix. Associations between radiographic findings, exposure, and respiratory symptoms were assessed by ANOVA, chi-square tests and binary regression. Fourteen workers (3.9%) had radiographic evidence of silicosis, and all had been employed ≥30 years. They were more likely to have been stone cutters or carvers and their average exposure concentrations and cumulative exposures to respirable crystalline silica were significantly higher than workers with similar durations of employment and no classifiable parenchymal abnormalities. This provides direct evidence that workers with long-term exposure to low-level respirable crystalline silica (≤0.10 mg/m3) are at risk of developing silicosis.

Toxicological inhalation studies in rats to substantiate grouping of zinc oxide nanoforms.

BACKGROUND: Significant variations exist in the forms of ZnO, making it impossible to test all forms in in vivo inhalation studies. Hence, grouping and read-across is a common approach under REACH to evaluate the toxicological profile of familiar substances. The objective of this paper is to investigate the potential role of dissolution, size, or coating in grouping ZnO (nano)forms for the purpose of hazard assessment. We performed a 90-day inhalation study (OECD test guideline no. (TG) 413) in rats combined with a reproduction/developmental (neuro)toxicity screening test (TG 421/424/426) with coated and uncoated ZnO nanoforms in comparison with microscale ZnO particles and soluble zinc sulfate. In addition, genotoxicity in the nasal cavity, lungs, liver, and bone marrow was examined via comet assay (TG 489) after 14-day inhalation exposure. RESULTS: ZnO nanoparticles caused local toxicity in the respiratory tract. Systemic effects that were not related to the local irritation were not observed. There was no indication of impaired fertility, developmental toxicity, or developmental neurotoxicity. No indication for genotoxicity of any of the test substances was observed. Local effects were similar across the different ZnO test substances and were reversible after the end of the exposure. CONCLUSION: With exception of local toxicity, this study could not confirm the occasional findings in some of the previous studies regarding the above-mentioned toxicological endpoints. The two representative ZnO nanoforms and the microscale particles showed similar local effects. The ZnO nanoforms most likely exhibit their effects by zinc ions as no particles could be detected after the end of the exposure, and exposure to rapidly soluble zinc sulfate had similar effects. Obviously, material differences between the ZnO particles do not substantially alter their toxicokinetics and toxicodynamics. The grouping of ZnO nanoforms into a set of similar nanoforms is justified by these observations.

Probabilistic Reference and 10% Effect Concentrations for Characterizing Inhalation Non-cancer and Developmental/Reproductive Effects for 2,160 Substances.

Chemicals assessment and management frameworks rely on regulatory toxicity values, which are based on points of departure (POD) identified following rigorous dose-response assessments. Yet, regulatory PODs and toxicity values for inhalation exposure (i.e., reference concentrations [RfCs]) are available for only ∼200 chemicals. To address this gap, we applied a workflow to determine surrogate inhalation route PODs and corresponding toxicity values, where regulatory assessments are lacking. We curated and selected inhalation in vivo data from the U.S. EPA's ToxValDB and adjusted reported effect values to chronic human equivalent benchmark concentrations (BMCh) following the WHO/IPCS framework. Using ToxValDB chemicals with existing PODs associated with regulatory toxicity values, we found that the 25th %-ile of a chemical's BMCh distribution (PODp25BMCh) could serve as a suitable surrogate for regulatory PODs (Q2 ≥ 0.76, RSE ≤ 0.82 log10 units). We applied this approach to derive PODp25BMCh for 2,095 substances with general non-cancer toxicity effects and 638 substances with reproductive/developmental toxicity effects, yielding a total coverage of 2,160 substances. From these PODp25BMCh, we derived probabilistic RfCs and human population effect concentrations. With this work, we have expanded the number of chemicals with toxicity values available, thereby enabling a much broader coverage for inhalation risk and impact assessment.