The Poverty-Benefit Effects of the Integration of Three Rural Sector Industries: The Case of China

This paper aims to empirically substantiate the poverty-benefit effects of the integration of the three rural sector industries in China. The study results show that the integration of three rural industries has a significant poverty-benefiting impact. The heterogeneity analysis shows that the age, gender, education level, and region of the household head also have a certain degree of influence on the poverty-benefit effect of the integration of the three rural industries. The study of the poverty-benefit impacts of the integration of the three rural industries can provide theoretical support for China to consolidate its poverty-eradication achievements, promote the integration of the three rural industries, and comprehensively promote rural revitalization and accelerate agricultural and rural modernization. At the same time, China's experience also has implications for developing rural industrial integration in other countries.

PATHOPHYSIOLOGY OF LACTIC ACIDOSIS IN PATIENTS WITH ASTHMA

SESSION TITLE: Challenges in Asthma SESSION TYPE: Rapid Fire Case Reports PRESENTED ON: 10/18/2022 10:15 am - 11:10 am INTRODUCTION: Asthma is a chronic illness affecting 334 million people worldwide[1]. Asthma affects the respiratory gas exchange, which plays a significant role in acid-base balance. Acid-base disorders in asthma involve respiratory alkalosis, respiratory acidosis, and AG acidosis[2]. CASE PRESENTATION: A 37 years old Hispanic male with a PMH of intermittent asthma presents with progressive dyspnea for three days, worse with activity and decreases with rest. He reported no [cough, fever, rhinorrhea, chest pain]. No orthopnea. He is vaccinated for COVID ( 2 Pfizer doses), has no sickness exposure, and works as a driver. The patient is not a smoker. Physical Exam: Blood pressure 124/72 mmHg. Heart Rate 100 PPM. Temperature 97.1 F.Respiratory Rate 21BPM.SPO2 90% General appearance: acute distress with nasal flaring. Heart: Normal S1, S2. RRR. Lung: Poor air entry with diffuse wheeze bilaterally. He was placed on a 6 LPM NC. CBC and differential were unremarkable. He was started on methylprednisone, Ceftriaxone, and azithromycin. The patient was started on inhaled Salbutamol and Budesonide. Chest X-ray was unremarkable, Chemistry was unremarkable except for elevated Lactic acid 4.7, There was no concern for reduced tissue perfusion or hypoxia, with no evidence of an infectious process because both viral and bacterial causes for pneumonia were excluded, and antibiotics were stopped. A serial lactic acid level trend was 4.5/4.3/ 4.1/ 4 on the first day, while on the next day, it was 3.1/ 2.9/ 2.7/ 2.5/ 3.5, we stopped trending his lactic acid level. He improved and was discharged on an oral taper steroid and inhaled steroids with a B2 agonist. DISCUSSION: There are two types of Lactic acidosis in patients with asthma: 1- Type-A results from impaired oxygen delivery to tissues and reduced tissue perfusion in severe acute asthma may be accompanied by reduced cardiac output. 2- Type B where oxygen delivery is normal, but the cellular function is impaired due to increased norepinephrine in plasma, increasing metabolic rate and lactate production, drugs like beta-agonists increase glycogenolysis leading to an increased pyruvate concentration;pyruvate is converted to lactic acid. B2 agonist increases lipolysis and increases Acetyl CoA, this increase in Acetyl CoA inhibits the conversion of pyruvate to Acetyl CoA, increasing pyruvate which will be converted to lactic acid[2], Theophylline is a non-selective 5'-phosphodiesterase inhibitor and potentiates the activity of ß-adrenergic agents by increasing the intracellular concentration of cAMP, Glucocorticoids are also known to increase the ß-receptor's sensitivity to ß-adrenergic agonists. CONCLUSIONS: Providers are increasingly challenged by hyperlactatemia,it is not harmful but elevated Lactic acid levels and clearance rate is used for prognostication,hyperlactatemia might be misleading,and all possible causes of elevated lactic acid levels must be explored. Reference #1: 10.5334/aogh.2412 Reference #2: https://doi.org/10.3390/jcm8040563 Reference #3: Edwin B. Liem, Stephen C. Mnookin, Michael E. Mahla;Albuterol-induced Lactic Acidosis. Anesthesiology 2003;99:505–506 doi: https://doi.org/10.1097/00000542-200308000-00036 DISCLOSURES: No relevant relationships by Vasudev Malik Daliparty No relevant relationships by Abdallah Khashan No relevant relationships by Samer Talib No relevant relationships by MATTHEW YOTSUYA

CHLORINE GAS EXPOSURE AND OBSTRUCTIVE AIRWAY DISEASE: A CASE REPORT AND CASE-BASED DISCUSSION

SESSION TITLE: Occupational and Environmental Lung Disease Cases SESSION TYPE: Rapid Fire Case Reports PRESENTED ON: 10/18/2022 12:25 pm - 01:25 pm INTRODUCTION: Chlorine gas is a pulmonary irritant with pungent odor that damages the respiratory tract. Chlorine gas exposure occurs in industrial or household exposures,Chlorine gas has two forms either a liquid or gas, toxicity of chlorine gas depends on the dose and duration of exposure. Chlorine gas used in manufacturing products like paper, insecticides, Chlorine is used to treat bottled and swiming pool water. CASE PRESENTATION: A 37 Y.O Male, no PMH presents with progressive dyspnea for three days worse with activity,decreases with rest, denied cough fever or chest pain he is vaccinated for COVID,no smoking history. The patient worked at a chlorine gas factory in the Dominican Republic for 15 years. Exam: Vitals: BP 124/72 mmHg. HR 100 BPM. RR 21 BPM. SpO2 84%. General: acute distress. Heart: normal S1, S2. RRR. Lung: wheeze bilaterally. Abdomen: Soft. Musculoskeletal: no pitting edema. he was placed on 6 LPM NC saturation improved to 90%. CBC and Chemistry were unremarkable, he was started on steroid, breathing treatment with antibiotics. ABG showed hypoxemia. he was placed on Venturi mask and his saturation improved to 95%.CTA was negative for PE. EKG, troponin were unremarkable. A proBNP normal. The antibiotics were discontinued because of a negative workup. A TTE study was normal. HRCT scan of the chest, showed atelectasis and infiltrates of lower lobes. No interstitial fibrosis.A PFT showed obstructive airway disease. He was discharged on oral and inhaled steroids.Hi new onset obstructive airway could be due to chlorine gas exposure. DISCUSSION: Chlorine gas causes cellular injury through oxidative damage but further damage results from activation and recruitment of inflammatory cells with subsequent release of oxidants and proteolytic enzymes. Humans can detect chlorine gas odor at a concentration between 0.1-0.3 ppm. At 1-3 ppm,it causes irritation of oral,eye mucosal membranes. At 30-40 ppm causes cough, chest pain, and SOB. At 40-60 ppm, toxic pneumonitis and pulmonary edema and can be fatal at 430 ppm concentration or higher within thirty minutes. Chronic exposure to chlorine gas lead to chest pain, cough, sore throat, hemoptysis, recurrent asthma. Physical exam findings include tachypnea cyanosis, wheezing, intercostal retractions, decreased breath sounds. Pulmonary function tests may reveal obstructive lung function disease. Chronic exposure to a low level was found to be associated with an increased risk of asthma in swimmers. CONCLUSIONS: Chlorine exposure results in direct chemical toxicity to the airways with acute airways obstruction or airways hyperreactivity, presentation varies from acute overwhelming intoxication with acute lung injury and or death, occupational exposure increase the likelihood of chronic bronchitis or isolated wheezing attacks. Treatment for chlorine exposure is largely supportive. Reference #1: 1- Center of disease control and prevention website/emergency preparedness and response/ https://emergency.cdc.gov/agent/chlorine/basics/facts.asp Reference #2: 2- C- Morim A, Guldner GT. Chlorine Gas Toxicity. [Updated 2021 Jul 25]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing;2022 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK537213/. Reference #3: A- Gummin DD, Mowry JB, Beuhler MC, et al. 2020 Annual Report of the American Association of Poison Control Centers’ National Poison Data System (NPDS): 38th Annual Report. Clin Toxicol (Phila). 2021;59(12):1282-1501. doi:10.1080/15563650.2021.1989785 DISCLOSURES: No relevant relationships by Abdallah Khashan No relevant relationships by Samer Talib no disclosure on file for Matthew Yotsuya;

BABESIA MICROTI INFECTION WITH LOW-GRADE PARASITEMIA CAUSING ARDS IN AN IMMUNOCOMPETENT PATIENT

SESSION TITLE: Unusual Critical Care SESSION TYPE: Rapid Fire Case Reports PRESENTED ON: 10/18/2022 10:15 am - 11:10 am INTRODUCTION: Babesiosis can have a clinical spectrum ranging from mild illness in most cases to more severe manifestations in immunosuppressed individuals or in those with high-grade parasitemia. This patient had severe babesiosis resulting in ARDS and shock in spite of being immunocompetent and having low-grade parasitemia, making it a rare presentation. CASE PRESENTATION: A 49-year-old, previously healthy woman, was admitted with high-grade fevers. Physical exam findings were normal, except for fever (103 F). Initial lab results were significant for hemolytic anemia and thrombocytopenia. Chest radiography was normal. Other microbiology studies, including COVID-19, were negative. Empiric antibiotic therapy with piperacillin-tazobactam and doxycycline was started. Peripheral smear identified rare, minute intracellular ring forms, suspicious for babesia. IV azithromycin and oral atovaquone were started. PCR was done to confirm the diagnosis and Babesia microti DNA was detected. As peripheral smear showed parasitemia of only 1% (percentage of red blood cells infected), exchange transfusion was not considered as a treatment option. Two days after admission, worsening hemodynamic and respiratory status was noted with increasing oxygen requirements. CT chest now revealed diffuse interstitial infiltrates. ARDS ensued and the patient was intubated and started on mechanical ventilation with vasopressor support. Immunodeficiency workup was normal. In view of clinical deterioration, the antimicrobials were switched from atovaquone and azithromycin to IV clindamycin and quinidine for 14 days. After a protracted ICU stay, the patient showed gradual clinical improvement, parasitemia resolved, and she was eventually discharged to a rehabilitation facility. DISCUSSION: Babesiosis is a tick-borne infectious disease endemic to the North-East and Midwest United States. Majority of the infections are self-limited. However, in immunocompromised individuals and in those with high-grade parasitemia (>10%), it manifests as a severe illness with ARDS, severe hemolysis, or shock. Diagnosis is made by identifying parasites on thin peripheral blood smears with Giemsa/Wright stains. PCR can be used for species identification and for confirming the diagnosis in cases with low-grade parasitemia (<4%). IV azithromycin plus oral atovaquone is the preferred initial regimen and IV clindamycin plus quinidine is an alternative combination that can be used in severe infection. Red blood cell exchange transfusion can be considered in patients with high-grade parasitemia or organ failure. CONCLUSIONS: Babesiosis can very rarely cause ARDS and shock in immunocompetent patients with low-grade parasitemia. Prompt diagnosis and escalation of antimicrobial regimens to clindamycin and quinidine in such cases can lead to improved clinical outcomes. Exchange transfusion can serve as a treatment option in patients with high-grade parasitemia. Reference #1: Ord RL, Lobo CA. Human babesiosis: Pathogens, prevalence, diagnosis, and treatment. Current clinical microbiology reports. 2015 Dec;2(4):173-81. Reference #2: Ripoll JG, Rizvi MS, King RL, Daniels CE. Severe Babesia microti infection presenting as multiorgan failure in an immunocompetent host. Case Reports. 2018 May 30;2018:bcr-2018. Reference #3: Sanchez E, Vannier E, Wormser GP, Hu LT. Diagnosis, treatment, and prevention of Lyme disease, human granulocytic anaplasmosis, and babesiosis: a review. Jama. 2016 Apr 26;315(16):1767-77. DISCLOSURES: No relevant relationships by Shankar Chhetri No relevant relationships by Vasudev Malik Daliparty No relevant relationships by Preethi Dendi No relevant relationships by samer talib

Influence of the Development of Human Capital and Social Identification of the Rural Laborers' Mobility on Rural Strategy Revitalization in China

This paper presents an empirical analysis of the relationship between human capital and rural laborers' willingness to return to their hometowns based on the moderating effect of identity in China. The results show that the level of human capital significantly affects the willingness of the mobile population to return to their hometowns, but this effect is reversed, i.e., the increase in the level of human capital reduces the willingness of rural laborers to return to their hometowns. The urban identity of rural laborers after flowing into cities has a significant positive moderating effect on their willingness to return to their hometowns. Improving the carrying capacity of economic development in rural areas, further strengthening infrastructure construction in rural areas to provide the material basis for rural revitalization and labor force return, and at the same time strengthening the education and training of farmers to enhance their main status is recommended.