The impact of the Great Recession on California domestic violence events, and related hospitalizations and emergency service visits.

OBJECTIVE: Explore the impact of the Great Recession on domestic violence (DV) related hospitalizations and emergency department (ED) visits in California. METHODS: Hospital and ED data were drawn from California's Office of Statewide Health Planning and Development (OSHPD). DV-related hospitalizations and ED visits in California were analyzed between January 2000 and September 2015 (53,596), along with total medical costs. Time series were divided into pre-recession (Jan 2000-Nov 2007) and recession/post-recession (Dec 2007-Sept 2015) periods. RESULTS: The medical cost of DV-related hospitalizations alone was estimated as $1,136,165,861. A dramatic increase in DV episodes was found potentially associated with the Great Recession. The number of ED visits per month tripled from pre- to post-recession (104.9 vs. 290.6), along with an increased number of hospitalizations (77.1 vs. 95.6); African Americans and Native Americans were disproportionally impacted. In addition, psychiatric comorbidities, severe DV episodes, in-hospital mortality and charge per hospitalization escalated. The rise in DV hospitalizations and ED visits beginning in December 2007 was mainly attributable to physical abuse episodes in adults; minors had no change in DV trends. DISCUSSION: Recessions are frequent in modern economies and are repeated cyclically. Our study provides critical information on the effects of the 2007 financial crisis on DV-related healthcare service utilization in California. Given the current financial crisis associated with COVID-19, which expert predict could extend for years, the results from this study shine a spotlight on the importance of DV-related screening, prevention and response.

Differential lung inflammation and injury with tobacco smoke exposure in Wistar Kyoto and spontaneously hypertensive rats.

OBJECTIVE: Chronic obstructive pulmonary disease (COPD) is the third leading cause of death worldwide and has been associated with periods of intense lung inflammation. The objective of this study was to characterize whether similar rat strains, possessing different genetic predispositions, might play a role in exacerbating the pathophysiology of COPD-like cellular and structural changes with progressive 12-week exposure to tobacco smoke (TS). Normotensive Wistar Kyoto (WKY) and spontaneously hypertensive (SH) rats were compared. MATERIALS AND METHODS: WKY and SH rats were exposed to filtered air or to tobacco smoke at a particulate concentration of 80 mg/m3 for 4, 8, or 12 weeks. Necropsy was performed 24 h after the last exposure to obtain cells by bronchoalveolar lavage for total cell and differential counts. Scoring of lung tissues and immunohistochemical staining for M1 (pro-inflammatory) and M2 (anti-inflammatory) macrophages were performed on paraffin-embedded lung sections. RESULTS AND DISCUSSION: With progressive exposure, TS-exposed SH rats demonstrated significant airspace enlargement, mucin production, and lung inflammation compared to their FA control and TS-matched WKY rats. Moreover, SH rats also demonstrated increased expression of the M1 marker in alveolar macrophages compared to FA control, as well as the M2 marker compared to controls and TS-exposed WKY rats. CONCLUSION: The progressive tobacco smoke exposure contributes to persistent lung injury and inflammation that can be significantly enhanced by rat strain susceptibility in the genesis of COPD.

Repeated Iron-Soot Exposure and Nose-to-brain Transport of Inhaled Ultrafine Particles.

Particulate exposure has been implicated in the development of a number of neurological maladies such as multiple sclerosis, amyotrophic lateral sclerosis, Alzheimer's disease, and idiopathic Parkinson's disease. Only a few studies have focused on the olfactory pathway as a portal through which combustion-generated particles may enter the brain. The primary objective of this study was to define the deposition, uptake, and transport of inhaled ultrafine iron-soot particles in the nasal cavities of mice to determine whether combustion-generated nanoparticles reach the olfactory bulb via the olfactory epithelium and nerve fascicles. Adult female C57B6 mice were exposed to iron-soot combustion particles at a concentration of 200 µg/m3, which included 40 µg/m3 of iron oxide nanoparticles. Mice were exposed for 6 hr/day, 5 days/week for 5 consecutive weeks (25 total exposure days). Our findings visually demonstrate that inhaled ultrafine iron-soot reached the brain via the olfactory nerves and was associated with indicators of neural inflammation.

Exposure to tobacco smoke increases bone loss in spontaneously hypertensive rats.

PURPOSE: To define if exposure to tobacco smoke (TS) could induce reduction of bone mass and impairment of bone architecture, features observed in osteoporosis in normotensive rats and the influence of TS exposure on the osteoporotic features exhibited in the spontaneously hypertensive (SH) rats. METHODS: Normotensive Wistar Kyoto (WKY) and SH rats were exposed to filtered air or TS for 8 weeks, then their proximal femurs were extracted for micro-computed tomography (micro-CT) assessment, histological and immune-histological examinations to quantify the adverse influence of TS exposure on the bone mass and density, as well as bone architecture. RESULTS: We found that TS exposure not only induced significant decreases in bone mineral density (BMD), bone volume (BV), cortical and trabecular thickness (Ct.Th and Tb.Th), trabecular surface area (Tb.Ar), expression of hypoxia-inducible factor-1α (HIF-1α) in the trabecular marrow, delayed ossification of cartilage, as well as statistical increases in trabecular separation (Tb.SP) and the number of trabecular marrow adipocytes in both WKY and SH rats, but also exacerbated multiple features of osteoporosis exhibited in SH rats, including decreased BMD, Ct.Th, Tb.Ar, HIF-1α expression, delayed cartilage ossification, and increased Tb.SP. CONCLUSIONS: Our results show that TS exposure can reduce bone mass and impair bone architecture and exacerbate multiple features of osteoporosis exhibited in SH rats.

Fine particulate matter (PM2.5) enhances allergic sensitization in BALB/c mice.

Ambient particulate matter (PM), a component of air pollution, exacerbates airway inflammation and hyperreactivity in asthmatic patients. Studies showed that PM possesses adjuvant-like properties that enhance the allergic inflammatory response; however, the mechanism (or mechanisms) by which PM enhances the allergic response remains to be determined. The aim of this study was to assess how exposure to fine PM collected from Sacramento, CA, shapes the allergic airway immune response in BALB/c mice undergoing sensitization and challenge with ovalbumin (OVA). Eight-week-old BALB/c male mice were sensitized/challenged with phosphate-buffered saline (PBS/PBS; n = 6), PM/PBS (n = 6), OVA/OVA (n = 6), or OVA + PM/OVA (n = 6). Lung tissue, bronchoalveolar lavage fluid (BALF), and plasma were analyzed for cellular inflammation, cytokines, immunoglobulin E, and heme oxygenase-1 (HO-1) expression. Mice in the OVA + PM/OVA group displayed significantly increased airway inflammation compared to OVA/OVA animals. Total cells, macrophages, and eosinophils recovered in BALF were significantly elevated in the OVA + PM/OVA compared to OVA/OVA group. Histopathological grading indicated that OVA + PM/OVA treatment induced significant inflammation compared to OVA/OVA. Both immunoglobulin (Ig) E and tumor necrosis factor (TNF) α levels were significantly increased in OVA/OVA and OVA + PM /OVA groups compared to PBS/PBS control. The number of HO-1 positive alveolar macrophages was significantly elevated in lungs of mice treated with OVA + PM /OVA compared to OVA/OVA. Our findings suggest that fine PM enhances allergic inflammatory response in pulmonary tissue through mechanisms involving increased oxidative stress.

Temporal and Spatial Expression of Transforming Growth Factor-ß after Airway Remodeling to Tobacco Smoke in Rats.

Airway remodeling is strongly correlated with the progression of chronic obstructive pulmonary disease (COPD). In this study, our goal was to characterize progressive structural changes in site-specific airways, along with the temporal and spatial expression of transforming growth factor (TGF)-ß in the lungs of male spontaneously hypertensive rats exposed to tobacco smoke (TS). Our studies demonstrated that TS-induced changes of the airways is dependent on airway generation and exposure duration for proximal, midlevel, and distal airways. Stratified squamous epithelial cell metaplasia was evident in the most proximal airways after 4 and 12 weeks but with minimal levels of TGF-ß-positive epithelial cells after only 4 weeks of exposure. In contrast, epithelial cells in midlevel and distal airways were strongly TGF-ß positive at both 4 and 12 weeks of TS exposure. Airway smooth muscle volume increased significantly at 4 and 12 weeks in midlevel airways. Immunohistochemistry of TGF-ß was also found to be significantly increased at 4 and 12 weeks in lymphoid tissues and alveolar macrophages. ELISA of whole-lung homogenate demonstrated that TGF-ß2 was increased after 4 and 12 weeks of TS exposure, whereas TGF-ß1 was decreased at 12 weeks of TS exposure. Airway levels of messenger RNA for TGF-ß2, as well as platelet-derived growth factor-A, granulocyte-macrophage colony-stimulating factor, and vascular endothelial growth factor-α, growth factors regulated by TGF-ß, were significantly decreased in animals after 12 weeks of TS exposure. Our data indicate that TS increases TGF-ß in epithelial and inflammatory cells in connection with airway remodeling, although the specific role of each TGF-ß isoform remains to be defined in TS-induced airway injury and disease.

Women and Lung Disease. Sex Differences and Global Health Disparities.

There is growing evidence that a number of pulmonary diseases affect women differently and with a greater degree of severity than men. The causes for such sex disparity is the focus of this Blue Conference Perspective review, which explores basic cellular and molecular mechanisms, life stages, and clinical outcomes based on environmental, sociocultural, occupational, and infectious scenarios, as well as medical health beliefs. Owing to the breadth of issues related to women and lung disease, we present examples of both basic and clinical concepts that may be the cause for pulmonary disease disparity in women. These examples include those diseases that predominantly affect women, as well as the rising incidence among women for diseases traditionally occurring in men, such as chronic obstructive pulmonary disease. Sociocultural implications of pulmonary disease attributable to biomass burning and infectious diseases among women in low- to middle-income countries are reviewed, as are disparities in respiratory health among sexual minority women in high-income countries. The implications of the use of complementary and alternative medicine by women to influence respiratory disease are examined, and future directions for research on women and respiratory health are provided.

Sex and strain-based inflammatory response to repeated tobacco smoke exposure in spontaneously hypertensive and Wistar Kyoto rats.

CONTEXT: Approximately four million people die every year from chronic obstructive pulmonary disease (COPD), with more than 80% of the cases attributed to smoking. OBJECT: The purpose of this study was to examine the rat strain and sex-related differences and the extended tobacco smoke exposure to induce lung injury and inflammation with the goal of finding a suitable rodent model to study COPD. METHODS: Male and female spontaneously hypertensive (SH) and male Wistar Kyoto (WKY) rats were exposed to filtered air (FA) or to tobacco smoke (TS: 90 mg/m3 particulate concentration) for 6 h/day, three days/week for 4 or 12 weeks. RESULTS: Male SH rats demonstrated an enhanced, persistent inflammatory response compared to female SH and male WKY rats with extended TS exposure. Following four weeks of TS exposure, male SH rats had significantly increased total leukocytes and macrophage numbers, levels of TNF-alpha and elevated lactate dehydrogenase activity in bronchoalveolar lavage fluid compared with female SH, male WKY rats and corresponding controls. After 12 weeks of TS exposure, male SH rats continued to show significant increase in inflammatory cells and TNF-alpha, as well as IL-6 mRNA lung expression. In addition, the alveolar airspace of male SH rats exposed to TS was significantly enlarged compared to their FA controls, female SH and WKY rats. CONCLUSION: The male SH rat demonstrates greater cellular, inflammatory and structural changes highly reminiscent of COPD compared to female SH and male WKY rats, suggesting that the male SH rat is an optimal rodent model to study COPD.

Pulmonary inflammatory effects of source-oriented particulate matter from California's San Joaquin Valley.

The EPA regulates ambient particulate matter (PM) because substantial associations have been established between PM and health impacts. Presently, regulatory compliance involves broad control of PM emission sources based on mass concentration rather than chemical composition, although PM toxicity is likely to vary depending upon PM physicochemical properties. The overall objective of this study was to help inform source-specific PM emission control regulations. For the first time, source-oriented PM was collected from the atmosphere in Fresno, CA, onto 38 source/size substrates. Mice were exposed via oropharyngeal aspiration to equivalent mass doses [50 µg] of two size fractions: ultrafine (Dp < 0.17µm) and submicron fine (0.17 < Dp < 1 µm) during summer and winter seasons. At 24 hours post-exposure, cellular and biochemical indicators of pulmonary inflammation were evaluated in the bronchoalveolar lavage fluid. Significant inflammatory responses were elicited by vehicle, regional background, and cooking PM sources that were dependent on season and particle size. This is the first study of source-oriented toxicity of atmospheric PM and supports source-specific emissions control strategies.

Developmental changes in the connective tissues of the porcine recurrent laryngeal nerve.

The recurrent laryngeal nerve (RLN) branches from the vagus cranial nerve to innervate structures important for voicing and swallowing. Damage to this nerve, commonly associated with surgery or idiopathic etiologies that largely occur with aging, results in impaired voicing and swallowing (Myssiorek, 2004). Sunderland proposed a model of peripheral nerve damage whereby a nerve's ability to resist damage from stretch and compression is determined by the quantity and composition of its epineurial connective tissues (Sunderland, 1951). Thus, it would be expected that epineurium differs depending upon the forces imposed on a nerve within its anatomical setting. The purpose of this study was to investigate RLN epineurium quantity and composition with development. A porcine model (piglet vs. juvenile) was used because of the similarity between porcine and human laryngeal innervation, anatomy and function. The entire RLN was excised bilaterally, and stereological methods were used to quantify the composition of epineurial connective tissues. Compared with the piglet, the juvenile pig RLN was double the diameter. While the piglet had no differences in the percentage of epineurial collagen and adipose between proximal and distal segments of both sides of the RLN, the juvenile pig had a greater percentage of collagen in the proximal segment of both sides of the RLN and a greater percentage of adipose in the distal segment of the left RLN compared with the proximal segment. In addition, unlike the piglet, the juvenile pig had a greater number of fascicles in the proximal than distal segment of the RLN, regardless of nerve side. These findings are consistent with predicted patterns associated with the different anatomical settings of the left and right RLN, show that the RLN changes with age, and support Sunderland's model.

Advances in diagnostic codes to document sexual assault in health care service.

OBJECTIVE: To explore trends in documented sexual abuse/assault (SA) related episodes in California hospitals and emergency departments (ED), including the impact of a change in health care service reporting codification (from ICD-9-CM to ICD-10-CM) that more clearly defined SA in October 2015. DATA SOURCES: Hospital and ED data were drawn from California's Office of Statewide Health Planning and Development (OSHPD). STUDY DESIGN: Descriptive and trend analyses of SA-related hospital and ED records (including patients' demographic information) were conducted to determine whether changes in ICD codification had an impact on documented SA-related episodes. DATA COLLECTION: All SA-related episodes (ICD-9-CM codes 995.83, 995.53; ICD-10-CM codes T74.21-T74.22, T76.21-T76.22) in California hospitals and EDs for the last decade of available data (2008-2017) were analyzed (n = 20,215). PRINCIPAL FINDINGS: An abrupt increase in documented SA episodes in hospitals and EDs began in October 2015, when specific ICD10 codes for suspected cases of SA were created. Documented SA-related episodes doubled in 1 month (164 vs. 385 episodes in September 2015 and October 2015, respectively). More than half (58.2%) of all SA-related episodes documented in Oct 2015 were coded as suspicious. The number of documented SA-related episodes continued increasing to the end of the time series (December 2017). Overall, the annual number of documented SA-related episodes increased by over 700% in only 4 years (900 vs. 6441 in 2013 and 2017, respectively), suggesting high rates of prior under-reporting and the need to introduce the new codes. African Americans were disproportionally impacted; however, the highest increases in age-adjusted rates between the ICD-9-CM and the ICD-10 codification period were found among the White population (2.46 vs. 16.53 per 100,000 inhabitants). CONCLUSIONS: SA episodes in the clinical population have been underestimated for many decades. Identifying SA victims and measuring SA-related health care utilization is a real challenge that needs further investigation.

Tolerability and pharmacokinetics of intravenous allopregnanolone with and without midazolam pretreatment in two healthy dogs.

The neurosteroid allopregnanolone (ALLO) is under investigation as a treatment for benzodiazepine-refractory status epilepticus (SE). Here, we assess the cardiopulmonary safety of intravenous ALLO by itself and after a clinically recommended dose of midazolam (MDZ) in two healthy adult beagles. Each dog received ALLO (1 mg/kg, IV), and after a washout period of 2 weeks, each dog was dosed with MDZ (0.2 mg/kg, IV) followed 10 minutes later by ALLO. Behavioral state, vital signs, arterial blood gases, blood chemistries, and plasma ALLO concentrations were monitored for up to 6 hours after dosing. The dogs appeared sleepy but were fully responsive after both treatments. No depression of mean arterial pressure or respiratory rate was noted. Blood gas measurements failed to show evidence of drug-induced acute respiratory acidosis. Estimated maximum plasma ALLO concentrations were in the range of 1500 to 3000 ng/ml. The results indicate that intravenous ALLO can be used safely to treat benzodiazepine-refractory SE, even when administered shortly after a benzodiazepine.

Can nutrition lessen the effects of secondhand smoke exposure among children?

Reducing harm from secondhand smoke (SHS) exposure is especially critical for children. Current strategies aimed at reducing SHS exposure in workplaces and public spaces have been successful in reducing adult exposure, yet infants and children, who are greatly susceptible to the adverse health effects of SHS exposure, continue to be among the most exposed in the USA. Novel strategies are needed that can work in combination with those aimed at removing SHS exposure from children, our single highest priority. The overall aim of this monograph is to demonstrate how nutrition has the potential to ameliorate adverse SHS-related outcomes in children. This aim is accomplished by providing evidence for the following: susceptibility to SHS exposure is greatest during critical windows of lung and immune system development; dietary factors act on SHS mechanisms and have the potential to reduce the risk of related adverse outcomes; the key mechanisms of adverse SHS-related outcomes include reduced nutrient status, oxidative stress, compromised immune function, and chronic inflammation; identification of nutrition-related interventions for SHS-exposed populations is a timely issue and requires future research. Our primary aim should be to eliminate SHS exposure. Until infants and children are no longer exposed to SHS, however, we propose investigating nutrition-focused interventions as a method to reduce the risk of SHS-related health outcomes for infants and children.

Susceptibility of the aging lung to environmental injury.

With an ever-increasing number of elderly individuals in the world, a better understanding of the issues associated with aging and the environment is needed. The respiratory system is one of the primary interfaces between the body and the external environment. An expanding number of studies suggest that the aging pulmonary system (>65 years) is at increased risk for adverse health effects from environmental insult, such as by air pollutants, infection, and climate change. However, the mechanism(s) for increased susceptibility in this subpopulation are not well understood. In this review, we provide a limited but comprehensive overview of how the lung ages, examples of environmental exposures associated with injury to the aging lung, and potential mechanisms underlying the increased vulnerability of the aging lung to injury from environmental factors.

Ambient particulate matter enhances the pulmonary allergic immune response to house dust mite in a BALB/c mouse model by augmenting Th2- and Th17-immune responses.

Ambient particulate matter (PM) exacerbates airway inflammation and hyper-reactivity in asthmatic patients. Studies show that PM has adjuvant-like properties that enhance the allergic inflammatory response; however, the mechanisms through which PM enhances these processes remain elusive. The objective of the study was to examine how ambient PM enhances the allergic immune response. Eight-week-old BALB/c mice were sensitized with house dust mite (HDM) or HDM and ambient particulate matter (PM, 2.5 µm; Sacramento, CA) to assess how PM modulates the development of adaptive immune responses against allergens. Both groups were challenged with HDM only. Bronchoalveolar lavage (BAL) was analyzed for extent of airway inflammation. Lung tissue was used for histological analysis, mucosubstance quantification, and heme oxygenase-1 (HO-1) localization/quantification. Gene expression was analyzed in whole lung to characterize immune markers of inflammation: cytokines, chemokines, antioxidant enzymes, and transcription factors. Cytokine and chemokine protein levels were quantified in whole lung to confirm gene expression patterns. Compared to HDM-only sensitization, exposure to PM during HDM sensitization led to significant immune cell recruitment into the airway subepithelium, IgE gene expression, mucosubstance production, and Th2-associated cytokine expression. HO-1 levels were not significantly different between the treatment groups. Gene expression profiles suggest that polycyclic aromatic hydrocarbon (PAH) content in PM activated the aryl hydrocarbon receptor (AhR) and enhanced Th17-responses in the mice that received HDM and PM compared to mice that received HDM-only. The findings suggest that PM enhances allergic sensitization via enhancement of Th2-mediated inflammation and that AhR activation by PAHs in PM promotes Th17-immune responses.

TH17-Induced Neutrophils Enhance the Pulmonary Allergic Response Following BALB/c Exposure to House Dust Mite Allergen and Fine Particulate Matter From California and China.

Asthma is a global and increasingly prevalent disease. According to the World Health Organization, approximately 235 million people suffer from asthma. Studies suggest that fine particulate matter (PM2.5) can induce innate immune responses, promote allergic sensitization, and exacerbate asthmatic symptoms and airway hyper-responsiveness. Recently, severe asthma and allergic sensitization have been associated with T-helper cell type 17 (TH17) activation. Few studies have investigated the links between PM2.5 exposure, allergic sensitization, asthma, and TH17 activation. This study aimed to determine whether (1) low-dose extracts of PM2.5 from California (PMCA) or China (PMCH) enhance allergic sensitization in mice following exposure to house dust mite (HDM) allergen; (2) eosinophilic or neutrophilic inflammatory responses result from PM and HDM exposure; and (3) TH17-associated cytokines are increased in the lung following exposure to PM and/or HDM. Ten-week-old male BALB/c mice (n = 6-10/group) were intranasally instilled with phosphate-buffered saline (PBS), PM+PBS, HDM, or PM+HDM, on days 1, 3, and 5 (sensitization experiments), and PBS or HDM on days 12-14 (challenge experiments). Pulmonary function, bronchoalveolar lavage cell differentials, plasma immunoglobulin (Ig) protein levels, and lung tissue pathology, cyto-/chemo-kine proteins, and gene expression were assessed on day 15. Results indicated low-dose PM2.5 extracts can enhance allergic sensitization and TH17-associated responses. Although PMCA+HDM significantly decreased pulmonary function, and significantly increased neutrophils, Igs, and TH17-related protein and gene levels compared with HDM, there were no significant differences between HDM and PMCH+HDM treatments. This may result from greater copper and oxidized organic content in PMCA versus PMCH.

Early postnatal exposure to allergen and ozone leads to hyperinnervation of the pulmonary epithelium.

Airway injury in infant monkeys exposed to ozone and/or house dust mite allergen (HDMA) is associated with a loss of epithelial innervation. In this study, we evaluated for persistence/recovery of the altered epithelial innervation. Thirty-day-old rhesus monkeys were exposed to repeated episodes of HDMA and/or ozone from 1 to 6 months of age and subsequently allowed to recover for 6 months in the absence of further ozone exposure and/or minimal HDMA challenge (sufficient to maintain allergen sensitization). At 1 year of age, nerve density in intrapulmonary airways was immunohistochemically evaluated using antibodies directed against protein gene product 9.5. Hyperinnervation and irregular epithelial nerve distribution was observed in both HDMA- and ozone-exposed groups; most prominent alterations were observed in animals exposed to HDMA plus ozone. Therefore, while adaptive mechanisms exist that re-establish epithelial innervation following cessation or diminution of exposure to HDMA and/or ozone, the recovery is associated with persistent proliferative mechanisms that result in hyperinnervation of the airways.

Differential pulmonary effects of wintertime California and China particulate matter in healthy young mice.

Airborne particulate matter (PM) is associated with adverse cardiorespiratory effects. To better understand source-orientated PM toxicity, a comparative study of the biological effects of fine PM (diameter≤2.5µm, PM2.5) collected during the winter season from Shanxi Province, China, and the Central Valley, California, United States, was conducted. The overarching hypothesis for this study was to test whether the chemical composition of PM on an equal mass basis from two urban areas, one in China and one in California, can lead to significantly different effects of acute toxicity and inflammation in the lungs of healthy young mice. Male, 8-week old BALB/C mice received a single 50µg dose of vehicle, Taiyuan PM or Sacramento PM by oropharyngeal aspiration and were sacrificed 24h later. Bronchoalveolar lavage, ELISA and histopathology were performed along with chemical analysis of PM composition. Sacramento PM had a greater proportion of oxidized organic material, significantly increased neutrophil numbers and elevated CXCL-1 and TNF-α protein levels compared to the Taiyuan PM. The findings suggest that Sacramento PM2.5 was associated with a greater inflammatory response compared to that of Taiyuan PM2.5 that may be due to a higher oxidice. Male, 8-week old BALB/C mice received a single 50µg dose of vehicle, Taiyuan PM or Sacramento PM by oropharyngeal aspiration and were sacrificed 24h later. Bronchoalveolar lavage, ELISA and histopathology were performed along with chemical analysis of PM composition. Sacramento PM had a greater proportion of oxidized organic material, significantly increased neutrophil numbers and elevated CXCL-1 and TNF-α protein levels compared to the Taiyuan PM. The findings suggest that Sacramento PM2.5 was associated with a greater inflammatory response compared to that of Taiyuan PM2.5 that may be due to a higher oxidized state of organic carbon and copper content.

An aerosolized fluorescent microsphere technique for evaluating particle deposition in the avian respiratory tract.

The objective of this study was to examine the feasibility of using aerosolized fluorescent microspheres to examine particle distribution in the respiratory tract of birds following aerosol exposure. Adult domestic pigeons (Columbia livia domestica; n = 5 birds per microsphere size) were exposed to aerosolized monodispersed populations of various sized carboxylate microspheres (0.5, 1.0, 2.0, 3.0, 6.0, and 10.0 microm) for 30 min. For aerosol-exposure purposes, the birds were anesthetized with injectable anesthetics, intubated, and placed on positive-pressure ventilation using a mechanical ventilator. Immediately following aerosol exposure, the birds were euthanatized, and carcasses were preserved via intravenous infusion of modified paraformaldehyde/gluteraldehyde fixative (pH = 7.2 and 340 mOsm). Initial evaluation of microsphere distribution in air sacs (cranial and caudal thoracic and abdominal) and at the level of the ostia was performed using a stereoscopic microscope with an epifluorescent module. More detailed examination of the distribution of microspheres within the respiratory tract was achieved using a confocal scanning laser microscope with a krypton argon laser and a scanning electron microscope. The results from this study revealed that positive-pressure ventilation resulted in distribution of smaller sized fluorescent microspheres (sizes 1.0, 2.0, and 3.0 microm) throughout the pigeon's respiratory tracts, and these microspheres were in highest concentration in the secondary bronchi and ostia for all of the examined air sacs. The larger sized beads (6.0 and 10.0) were confined to the upper airway (trachea and primary bronchi). The results from this study allow for a better understanding of particle deposition following positive-pressure ventilation and aerosol exposure in birds.