Allergic sinusitis and severe asthma caused by occupational exposure to locust bean gum: Case report.

We present a case that highlights the difficulties with diagnosis and the dangers of occupational allergic sinusitis and asthma left unrecognized. We describe the case history of a man who experienced work-related symptoms 1 year after beginning work as a cheesemaker at a creamery, and whose respiratory symptoms progressively worsened over 16 years before an occupational cause of his asthma was identified. His initial discrete episodes of sinusitis and acute bronchitis evolved into persistent asthma of increasing severity with exacerbations requiring repeated emergency room treatment. The case described in our report emphasizes the importance of clinician diagnosis of OA, and subsequent removal from exposure, such that asthma severity does not progress to near-fatal or fatal asthma in the sensitized worker. As demonstrated by this case report, identification of an occupational cause of asthma relies on a high degree of suspicion and excellent detective work by the clinician.

Notes from the Field: Respiratory Symptoms and Skin Irritation Among Hospital Workers Using a New Disinfection Product - Pennsylvania, 2015.

In March 2014, a new disinfection product, consisting of hydrogen peroxide, peroxyacetic acid, and acetic acid, was introduced at a Pennsylvania hospital to aid in the control of health care-associated infections. The product is an Environmental Protection Agency-registered non-bleach sporicide advertised as a one-step cleaner, disinfectant, and deodorizer. According to the manufacturer's safety data sheet, the product requires no personal protective equipment when it is diluted with water by an automated dispenser before use. On January 30, 2015, CDC's National Institute for Occupational Health (NIOSH) received a confidential employee request to conduct a health hazard evaluation at the hospital. The request cited concerns about exposure of hospital environmental services staff members to the product and reported symptoms among persons who had used the product that included eye and nasal problems, asthma-like symptoms, shortness of breath, skin problems, wheeze, chest tightness, and cough.

Differential response of human nasal and bronchial epithelial cells upon exposure to size-fractionated dairy dust.

Exposure to organic dusts is associated with increased respiratory morbidity and mortality in agricultural workers. Organic dusts in dairy farm environments are complex, polydisperse mixtures of toxic and immunogenic compounds. Previous toxicological studies focused primarily on exposures to the respirable size fraction; however, organic dusts in dairy farm environments are known to contain larger particles. Given the size distribution of dusts from dairy farm environments, the nasal and bronchial epithelia represent targets of agricultural dust exposures. In this study, well-differentiated normal human bronchial epithelial cells and human nasal epithelial cells were exposed to two different size fractions (PM10 and PM>10) of dairy parlor dust using a novel aerosol-to-cell exposure system. Levels of proinflammatory transcripts (interleukin [IL]-8, IL-6, and tumor necrosis factor [TNF]-α) were measured 2 h after exposure. Lactate dehydrogenase (LDH) release was also measured as an indicator of cytotoxicity. Cell exposure to dust was measured in each size fraction as a function of mass, endotoxin, and muramic acid levels. To our knowledge, this is the first study to evaluate the effects of distinct size fractions of agricultural dust on human airway epithelial cells. Our results suggest that both PM10 and PM>10 size fractions elicit a proinflammatory response in airway epithelial cells and that the entire inhalable size fraction needs to be considered when assessing potential risks from exposure to agricultural dusts. Further, data suggest that human bronchial cells respond differently to these dusts than human nasal cells, and therefore that the two cell types need to be considered separately in airway cell models of agricultural dust toxicity.

Potential Hazards Not Communicated in Safety Data Sheets of Flavoring Formulations, Including Diacetyl and 2,3-Pentanedione.

Objectives: Workers using flavoring formulations containing diacetyl and 2,3-pentanedione may be at risk of inhalational exposure, as these volatile hazardous chemicals are emitted from the bulk material, especially at elevated temperatures. However, flavoring formulations that contain diacetyl and 2,3-pentanedione might not list these ingredients because they are generally recognized as safe to ingest, may be part of a proprietary mixture deemed a trade secret, or may not be required to be listed if they are present at <1% composition. The objective of this study was to investigate whether potential inhalational hazards present in flavoring samples were reported as chemical ingredients on their corresponding safety data sheets (SDSs). Methods: A convenience sample of 26 bulk liquid flavorings obtained from two coffee roasting and packaging facilities in the USA was analyzed for 20 volatile organic chemicals present in the headspaces of vials containing flavoring liquids using gas chromatography-mass spectrometry. Flavoring samples were included in the study if headspace analysis results and SDSs were available. Flavoring samples included hazelnut, French vanilla, amaretto, chocolate, and caramel as well as some flavoring mixtures containing added fruit flavors such as cherry and raspberry. The presence of a chemical in the flavoring formulation was then compared to the ingredient list on the SDSs. Results: All the flavoring SDSs contained trade secret designations. None of the SDSs listed diacetyl or 2,3-pentanedione. Headspace analyte concentrations revealed that diacetyl was present in 21 of 26 samples (81%) with a maximum concentration of 5.84 × 10(4) µg m-3 in flavor 18 (caramel). 2,3-Pentanedione was present in 15 flavors (58%) with a maximum concentration of 3.79 × 10(5) µg m-3 in flavor 24 (oatmeal cookies). Conclusions: A majority of the flavorings tested had diacetyl, 2,3-pentanedione, or both as volatile constituents in the headspace. These chemicals were not listed on the SDSs, but inclusion of diacetyl and 2,3-pentanedione on SDSs would serve to protect downstream users from unrecognized exposure and potential respiratory disease. The headspace technique presented here is a viable tool to rapidly screen for volatile hazardous chemicals that may be present in flavoring formulations. Facilities that use flavorings should be aware that constituents in flavorings may present a potential inhalational hazard even if not identified as such by the SDS. A precautionary approach is warranted when working with flavorings, including exposure monitoring and effective exposure control strategies such as containment and local exhaust ventilation.

Health problems and disinfectant product exposure among staff at a large multispecialty hospital.

BACKGROUND: Hospital staff expressed health concerns after a surface disinfectant product containing hydrogen peroxide, peracetic acid, and acetic acid was introduced. We sought to determine if this product posed a health hazard. METHODS: An interviewer-administered questionnaire on work and health characteristics was completed by 163 current staff. Symptoms that improved away from work were considered work-related. Forty-nine air samples were taken for hydrogen peroxide, peracetic acid, and acetic acid. Prevalence ratios (PRs) were calculated using Poisson regression, and standardized morbidity ratios (SMRs) were calculated using nationally representative data. RESULTS: Product users reported higher prevalence of work-related wheeze and watery eyes than nonusers (P < .05). Workers in the department with the highest air measurements had significantly higher prevalence of watery eyes (PR, 2.88; 95% confidence interval [CI], 1.18-7.05) than those in departments with lower air measurements, and they also had a >3-fold excess of current asthma (SMR, 3.47; 95% CI, 1.48-8.13) compared with the U.S. CONCLUSIONS: This disinfectant product was associated with mucous membrane and respiratory health effects. Risks of mucous membrane irritation and asthma in health care workers should be considered in development of disinfection protocols to protect patients from hospital-acquired infections. Identification of optimal protocols that reduce worker exposures while maintaining patient safety is needed.

Respiratory Symptoms in Hospital Cleaning Staff Exposed to a Product Containing Hydrogen Peroxide, Peracetic Acid, and Acetic Acid.

Cleaning and disinfecting products consisting of a mixture of hydrogen peroxide (HP), peracetic acid (PAA), and acetic acid (AA) are widely used as sporicidal agents in health care, childcare, agricultural, food service, and food production industries. HP and PAA are strong oxidants and their mixture is a recognized asthmagen. However, few exposure assessment studies to date have measured HP, PAA, and AA in a health care setting. In 2015, we performed a health and exposure assessment at a hospital where a new sporicidal product, consisting of HP, PAA, and AA was introduced 16 months prior. We collected 49 full-shift time-weighted average (TWA) air samples and analyzed samples for HP, AA, and PAA content. Study participants were observed while they performed cleaning duties, and duration and frequency of cleaning product use was recorded. Acute upper airway, eye, and lower airway symptoms were recorded in a post-shift survey (n = 50). A subset of 35 cleaning staff also completed an extended questionnaire that assessed symptoms reported by workers as regularly occurring or as having occurred in the previous 12 months. Air samples for HP (range: 5.5 to 511.4 ppb) and AA (range: 6.7 to 530.3 ppb) were all below established US occupational exposure limits (OEL). To date, no full-shift TWA OEL for PAA has been established in the United States, however an OEL of 0.2 ppm has been suggested by several research groups. Air samples for PAA ranged from 1.1 to 48.0 ppb and were well below the suggested OEL of 0.2 ppm. Hospital cleaning staff using a sporicidal product containing HP, PAA, and AA reported work-shift eye (44%), upper airway (58%), and lower airway (34%) symptoms. Acute nasal and eye irritation were significantly positively associated with increased exposure to the mixture of the two oxidants: HP and PAA, as well as the total mixture (TM)of HP, PAA, and AA. Shortness of breath when hurrying on level ground or walking up a slight hill was significantly associated with increased exposure to the oxidant mixture (P = 0.017), as well as the TM (P = 0.026). Our results suggest that exposure to a product containing HP, PAA, and AA contributed to eye and respiratory symptoms reported by hospital cleaning staff at low levels of measured exposure.

Murine precision-cut lung slices exhibit acute responses following exposure to gasoline direct injection engine emissions.

Gasoline direct injection (GDI) engines are increasingly prevalent in the global vehicle fleet. Particulate matter emissions from GDI engines are elevated compared to conventional gasoline engines. The pulmonary effects of these higher particulate emissions are unclear. This study investigated the pulmonary responses induced by GDI engine exhaust using an ex vivo model. The physiochemical properties of GDI engine exhaust were assessed. Precision cut lung slices were prepared using Balb/c mice to evaluate the pulmonary response induced by one-hour exposure to engine-out exhaust from a laboratory GDI engine operated at conditions equivalent to vehicle highway cruise conditions. Lung slices were exposed at an air-liquid interface using an electrostatic aerosol in vitro exposure system. Particulate and gaseous exhaust was fractionated to contrast mRNA production related to polycyclic aromatic hydrocarbon (PAH) metabolism and oxidative stress. Exposure to GDI engine exhaust upregulated genes involved in PAH metabolism, including Cyp1a1 (2.71, SE=0.22), and Cyp1b1 (3.24, SE=0.12) compared to HEPA filtered air (p<0.05). GDI engine exhaust further increased Cyp1b1 expression compared to filtered GDI engine exhaust (i.e., gas fraction only), suggesting this response was associated with the particulate fraction. Exhaust particulate was dominated by high molecular weight PAHs. Hmox1, an oxidative stress marker, exhibited increased expression after exposure to GDI (1.63, SE=0.03) and filtered GDI (1.55, SE=0.04) engine exhaust compared to HEPA filtered air (p<0.05), likely attributable to a combination of the gas and particulate fractions. Exposure to GDI engine exhaust contributes to upregulation of genes related to the metabolism of PAHs and oxidative stress.

Time course of bronchial cell inflammation following exposure to diesel particulate matter using a modified EAVES.

Electrostatic deposition of particles onto the surface of well-differentiated airway cells is a rapid and efficient means to screen for toxicity associated with exposure to fine and ultrafine particulate air pollution. This work describes the development and application of an electrostatic aerosol in vitro exposure system (EAVES) with increased throughput and ease-of-use. The modified EAVES accommodates standard tissue culture plates and uses an alternating electric field to deposit a net neutral charge of aerosol onto air-interface cell cultures. Using this higher-throughput design, we were able to examine the time-course (1, 3, 6, 9, and 24 h post-exposure) of transcript production and cytotoxicity in well-differentiated human bronchial cells exposed to diesel particulate matter at levels of 'real-world' significance. Statistically significant responses were observed at exposure levels (∼0.4 µg/cm(2)) much lower than typically reported in vitro using traditional submerged/resuspended techniques. Levels of HO-1, IL-8, CYP1A1, COX-2, and HSP-70 transcripts increased immediately following diesel particulate exposure and persisted for several hours; cytotoxicity was increased at 24h. The modified EAVES provides a platform for higher throughput, more efficient and representative testing of aerosol toxicity in vitro.

Oxidative stress and aromatic hydrocarbon response of human bronchial epithelial cells exposed to petro- or biodiesel exhaust treated with a diesel particulate filter.

The composition of diesel exhaust has changed over the past decade due to the increased use of alternative fuels, like biodiesel, and to new regulations on diesel engine emissions. Given the changing nature of diesel fuels and diesel exhaust emissions, a need exists to understand the human health implications of switching to "cleaner" diesel engines run with particulate filters and engines run on alternative fuels like biodiesel. We exposed well-differentiated normal human bronchial epithelial cells to fresh, complete exhaust from a diesel engine run (1) with and without a diesel particulate filter and (2) using either traditional petro- or alternative biodiesel. Despite the lowered emissions in filter-treated exhaust (a 91-96% reduction in mass), significant increases in transcripts associated with oxidative stress and polycyclic aromatic hydrocarbon response were observed in all exposure groups and were not significantly different between exposure groups. Our results suggest that biodiesel and filter-treated diesel exhaust elicits as great, or greater a cellular response as unfiltered, traditional petrodiesel exhaust in a representative model of the bronchial epithelium.