DOCSLIB.ORG

Reactive Airways Dysfunction Syndrome After Hydrofluoric Acid

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Reactive Airways Dysfunction Syndrome After Hydrofluoric Acid Allergology International 65 (2016) 343e344 Contents lists available at ScienceDirect Allergology International journal homepage: http://www.elsevier.com/locate/alit Letter to the Editor Reactive airways dysfunction syndrome after hydrofluoric acid inhalation Dear Editor, symptoms are present for 1e2 days after exposure, fever, cough, dyspnea, cyanosis, and pulmonary edema may occur later.1 There A 44-year-old man who had been working in a glass washing are few reports of adverse health effects from inhalation exposure factory visited our hospital with cough, sputum, and dyspnea after to a consumer product containing HF. One report described a single accidental exposure to hydrofluoric acid of 50% concentration 10 case of chemical pneumonitis and adult respiratory distress syn- days ago. drome following household use of an HF-containing rust stain He was ex-smoker who quit smoking 10 years ago and had 5 remover. Another reported a case of adult-onset asthma immedi- pack years smoking history. He had usually been working in the ately following use of the same household rust stain remover.4 glass washing factory in position of office based job. At this time Reactive airways dysfunction syndrome (RADS), or irritant he was exposed to 50% concentration of HF during opening of cap induced asthma without latency, is characterized by the immediate of HF bottle. After opening for approximately 1e2 min, he experi- onset of asthma following a single exposure (or possibly several ex- e enced a burning sensation in his eyes, nose, and mouth and he posures) to irritating vapor, fume, or smoke.5 7 developed chest tightness and dyspnea. He had persistent prob- RADS was originally described by Brooks and Lockers5 in 1981 as lems on breathing for previous 10 days, and he finally came to sudden onset of non-immunological asthma resulting from an hospital. exposure to high-level irritant gases. Many cases occurred after His initial blood pressure was 130/70 mmHg, pulse rate 70/min, the 9/11 collapse of the New York World Trade Center, resulting respiratory rate 20/min, and body temperature 36.8 C. There were from the inhalation of fumes and particulate matters.8 Symptoms no abnormal findings in physical examinations. Chest radiography persist for at least 12 weeks but there is no previously documented and PNS water's view showed normal findings. White blood cell evidence of asthma or other chronic lung disease.8 count was 9590 cells/mL (neutrophil, 65.1%; lymphocyte, 24.5%; According to ACCP9 RADS can be diagnosed by following condi- monocyte, 8.6%; eosinophil, 1.5%) and other laboratory measure- tions: (1) A documented absence of preceding respiratory com- ments were within normal ranges. Measuring bronchodilator plaints; (2) Onset of symptoms after a single exposure incident; response with pulmonary function test was done; FEV1/FVC 89%; (3) Exposure to very high concentrations of a mixture of sodium hy- FVC 5.10L (101%); FEV1 4.56L (121%). He showed positive reaction pochlorite and hydrochloric acid; (4) Onset of symptoms within to Dermatophagoides farinae and Dermatophagoides pteronyssinus 24 h after the exposure, with persistence of symptoms for at least on allergen skin prick test. A non-specific bronchial challenge test 12 weeks; (5) Symptoms simulating asthma with cough, wheeze, with methacholine was performed to evaluate airway hyperres- and dyspnea; (6) Presence of airflow obstruction; and (7) Absence ponsiveness and the result was positive (PC20 ¼ 7.78 mg/ml). of all other pulmonary diseases. RADS is also a subcategory of HF (hydrofluoric acid) is a weak acid and is colorless, potent res- irritant-induced occupational asthma (OA), and irritant-induced piratory irritant with an unpleasant odor.1,2 The boiling point of OA can be classified by exposure concentration and duration of anhydrous HF is 19.5 C and it is miscible with water, and HF fumes exposure.8,10 RADS is characterized by extremely high exposure strongly in moist air.2 The odor threshold is reported to be concentration which is over occupational exposure limit and the 0.5e3.0 parts per million.2 HF is a toxic substance used widely in duration of exposure is below one day.8,10 both industrial and domestic settings, and is used to produce a va- The patient described in this report developed adult onset riety of chemicals and in numerous industrial processes.1,2 It is most asthma based on his history of symptoms, dyspnea improvement largely used in production of fluorocarbon compounds.2 HF is with inhaled steroid medication, and the positive tests for non- unique among acids because its toxicity is mostly attributed to an specific bronchial hyperreactivity. His asthma had immediate onset anion and fluoride, not to a cation and a hydrogen ion responsible following the exposure of high concentration of HF, and the symp- for toxicity in many other acids.2 Most acids cause burns and necro- toms had persisted for at least 3 months. Therefore, based on the sis from liberated hydrogen ions. Generally, HF is produced by the history and medical findings he appears to be suitable for the reaction of sulfuric acid with calcium fluoride.2 criteria for RADS. In conclusion, we report a 44-year old man HF is strong irritant to eyes, nose, throat, and skin. HF causes var- with RADS including bronchial asthma with cough, sputum, and iable symptoms tears, eye redness, rhinorrhea, sore throat, cough, dyspnea after exposure to high concentration of hydrofluoric acid. headache, and dermatalgia.1,3,4 Even in cases in which no He was educated from avoiding exposure of HF, and now well controlled treated with normal lung function by step downing inhaled steroids. Peer review under responsibility of Japanese Society of Allergology. http://dx.doi.org/10.1016/j.alit.2016.02.002 1323-8930/Copyright © 2016, Japanese Society of Allergology. Production and hosting by Elsevier B.V. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/ licenses/by-nc-nd/4.0/). 344 Letter to the Editor / Allergology International 65 (2016) 343e344 Acknowledgements 2. Carolyn AT, Dennis J, Lisa I, Gloria S, Lara C. Toxicological Profile for Fluorides, Hydrogen Fluoride, and Fluorine. U.S. Department of Health and Human Ser- vices, Public Health Service, Agency for Toxic Substances and Disease Registry; This study was supported by Soonchunhyang University September 2003. Available from: http://www.atsdr.cdc.gov/ToxProfiles/tp11. Research Fund. pdf. 3. Bennion JR, Franzbiau A. Chemical pneumonitis following household exposure to hydrofluric Acid. Am J Ind Med 1997;31:474e8. Conflict of interest 4. Franzbiau A, Sanhakian N. Asthma following household exposure to hydroflu- fl The authors have no con ict of interest to declare. oric acid. Am J Ind Med 2003;44:321e4. 5. Brooks SM, Lockey J. Reactive airways dysfunction syndrome (RADS): a newly defined occupational disease. Am Rev Respir Dis 1981;123(Suppl):A133. Tae-Kyu Lee, Hae-Won Yoo, Seong-Hwan Bae, Min-Jung Kim, 6. Bardana EJ. Reactive airways dysfunction syndrome (RADS): fact or fantasy? Al- * lergy 1999;54:33e5. Gyu-Hyung Kim, An-Soo Jang 7. Brooks SM, Hammad Y, Richards I, Giovireo-Barbas J, Jenkins K. The spectrum of irritant-induced asthma: sudden and not-so-sudden onset and the role of al- Division of Allergy and Respiratory Medicine, Department of Internal Medicine, lergy. Chest 1998;113:42e9. Soonchunhyang University Bucheon Hospital, Bucheon, South Korea 8. Varney VA, Evans J, Bansal AS. Successful treatment of reactive airways dysfunction syndrome by high-dose vitamin D. J Asthma Allergy 2011;4:87e91. * Corresponding author. Division of Allergy and Respiratory Medicine, Department 9. Chan-Yeung M. Assesment of asthma in the workplace. Chest 1995;108: of Internal Medicine, Soonchunhyang University Bucheon Hospital, 170 Jomaru-ro, 1084e117. Wonmi-gu, Bucheon , Gyeonggi-do 420-767, South Korea. 10. Baur X, Bakehe P, Vellguth H. Bronchial asthma and COPD due to irritants in the E-mail address: [email protected] (A.-S. Jang). workplace e an evidence-based approach. J Occup Med Toxicol 2012;7:19. References Received 21 December 2015 Received in revised form 28 January 2016 1. Wing JS, Brender JD, Sanderson LM, Perrotta DM, Beauchamp RA. Acute health Accepted 3 February 2016 effects in a community after a release of hydrofluoric acid. Arch Environ Health Available online 2 March 2016 1991;46:155e60..
Load more

Recommended publications
  • Siphoning Diesel: a Fatal Mistake
    CASE REPORT Siphoning diesel: a fatal mistake Leong Wei Cheng, MRCP, Brian Cheong Mun Keong, FRCP Department of Medicine, Hospital Teluk Intan cervical lymphadenopathy and auscultation of his lungs SUMMARY revealed normal findings. Examination of other systems did Diesel is commonly used as fuel for engines and is distilled not reveal any abnormalities. from petroleum. Diesel has toxic potential and can affect multiple organs. Exposure can occur after ingestion, Initial blood investigations showed evidence of acute kidney inhalation or through the dermal route. The practice of injury (urea: 16.7 mmol/l, sodium 129 mmol/l, potassium 3.7 siphoning diesel using a rubber tubing and the mouth is mmol/l and creatinine 937 µmol/l). There was presence of common in rural communities. This can lead to accidental protein and erythrocytes (2+) in his urine. His full blood count ingestion and aspiration. Here we report a case of a patient showed elevated white cell count of 11,600/µl (neutrophil who accidentally ingested diesel during siphoning, which 85%) with normal haemoglobin concentration (15.9 g/dl) caused extensive erosion of the oral cavity and oesophagus and platelets (185,000/µl). Liver transaminases were normal. leading to pneumomediastinum and severe chemical lung Chest radiograph showed clear lung fields. His provisional injury. The patient responded well initially to steroids and diagnosis was acute tonsillitis with post- infectious Rapidly supportive care but required prolonged hospitalisation. He Progressive Glomerolonephritis (RPGN). Intravenous (IV) developed complications of nosocomial infection and Ceftriaxone 2 g daily was started. succumbed 23 days after admission. He became progressively more tachypnoeic in the ward with KEY WORDS: Diesel; siphon; chemical pneumonitis; oesophageal perforation; worsening renal function and metabolic acidosis.
    [Show full text]
  • Occupational Dusts Other Than Silica* by Kenneth M
    Thorax: first published as 10.1136/thx.2.2.91 on 1 June 1947. Downloaded from Thorax (1947), 2, 91. DISEASES OF THE LUNG RESULTING FROM OCCUPATIONAL DUSTS OTHER THAN SILICA* BY KENNETH M. A. PERRY London It is only in recent years that considerable interest has been given to the dusts to which men are exposed at their work, even though silicosis is known to have occurred in prehistoric times. Many dusts are now recognized as dangerous, and in the extreme it may even be doubted whether any dust can be regarded as harmless. It is rational at least to suppose that the lung cannot become a physiological dust trap and yet retain its elasticity. It seems possible that any dust, no matter how innocuous in small concentrations, would in large enough quantity eventually overwhelm the defences of the lung and accumulate in such amounts as to impair function; such a form of lung disease would be the result of causes of a mechanical nature-the physical presence of large amounts of inert foreign material. The term "benign pneumoconiosis " has been given to this type of disease in order to contrast it with diseases resulting http://thorax.bmj.com/ from the inhalation of siliceous matter. But besides this group of conditions occupational dust may give rise to inflammatory lesions, allergic responses, and neoplastic changes. INFLAMMATORY CHANGES Inflammatory changes may be caused by inorganic metals, such as manganese, on September 24, 2021 by guest. Protected copyright. beryllium, vanadium, and osmium, giving.rise to a chemical pneumonitis; and by organic matter, such as decaying hay and grain, bagasse, cotton fibre, and similar substances where the aetiology is somewhat obscure, though fungi are frequently blamed.
    [Show full text]
  • Airbag Pneumonitis
    Hindawi Publishing Corporation Case Reports in Medicine Volume 2010, Article ID 498569, 2 pages doi:10.1155/2010/498569 Case Report Airbag Pneumonitis Raghav Govindarajan, Gustavo Ferrer, Laurence A. Smolley, Eduardo Araujo Oliveira, and Franck Rahaghi Department of Pulmonary Medicine, Cleveland Clinic Florida, 2950 Cleveland Clinic Boulevard, Weston, FL 33331, USA Correspondence should be addressed to Raghav Govindarajan, [email protected] Received 29 June 2010; Accepted 13 September 2010 Academic Editor: Steven A. Sahn Copyright © 2010 Raghav Govindarajan et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. The widespread and mandatory use of airbags has resulted in various patterns of injuries and complications unique to their use. Airbags have been implicated in a spectrum of pulmonary conditions ranging from exacerbation of asthma, reactive airway diseases to new onset asthma. We report a case of inhalational chemical pneumonitis that developed after exposure to the airbag fumes. 1. Introduction room air. There were no significant electrolyte abnormalities. Chest X-ray PA and lateral view revealed left lower lobe and ffi The 2001 United States national highway tra csafety retocardiac infiltrate. CT chest noncontrast revealed tree in administration report estimated that airbags reduce driver bud opacities in the right middle lobe, left lingual. Ground fatality by 12%–14% [1].The widespread and mandatory glass opacity was also seen in the posterior basal segment of use of airbags has resulted in various patterns of injuries the left lower lobe (Figure 1).
    [Show full text]
  • Thirty Workers in Missouri Popcorn Plant Diagnosed With
    Occupational Lung SSSEEENNNSSSOOORRR Disease Bulletin Massachusetts Department of Public Health Occupational Health Surveillance Program, 250 Washington Street, 6th Floor, Boston, MA 02108 Tel: (617) 624-5632 Fax: (617) 624-5696 www.mass.gov/dph/ohsp June 2006 Dear Health Care Provider, An investigation of the workplace revealed that diacetyl, Welcome to the June issue of the SENSOR an artificial butter flavoring ingredient, was linked with the Occupational Lung Disease Bulletin! In this issue, we employees’ symptoms. Animal studies conducted by focus on the topic of bronchiolitis obliterans, a severe lung flavoring manufacturers as early as 1993 showed that disease that can occur in workers that make or handle inhalation of diacetyl resulted in severe lung injury. food flavoring. Bronchiolitis obliterans has been linked to Additional studies completed in 2002 confirmed these diacetyl, an artificial butter flavoring ingredient. The findings1. The National Institute for Occupational Safety illness has been called “popcorn lung disease” because of and Health (NIOSH) issued an alert in 2004, warning of the clusters of workers in popcorn plants that have been the danger posed by vapors, dusts or sprays of flavorings diagnosed with the disease. However, workers in plants and recommending controls to ensure worker safety in making food ranging from pastries and frozen food to plants using or making flavorings. NIOSH recommended nacho chips and candy may be exposed to the chemicals substituting less hazardous flavoring ingredients as the in food flavorings, and therefore may be at risk for best option for controlling health risks to workers. bronchiolitis obliterans. In addition, workers who use Additional options include local exhaust ventilation or, if diacetyl to produce artificial flavorings are also at risk.
    [Show full text]
  • Occupational Lung Disease Bulletin
    Occupational Lung Disease Bulletin Massachusetts Department of Public Health Winter 2017 The objective of the IARC is to identify hazards that are Dear Healthcare Provider, capable of increasing the incidence or severity of malignant neoplasms. The IARC classifications are not Dr. Neil Jenkins co-wrote this Occupational Lung Disease based on the probability that a carcinogen will cause a Bulletin, during his rotation at MDPH from Harvard School cancer or the dose-response, but rather indicate the of Public Health. He brought expertise in welding from a strength of the evidence that an agent can possibly cause materials science and occupational medicine background, a cancer. as well as involvement in welding oversight with the The IARC classifies the strength of the current evidence American Welding Society. that an agent is a carcinogen as: Remember to report cases of suspected work-related lung Group 1 Carcinogenic to humans disease to us by mail, fax (617) 624-5696 or phone (617) Group 2A Probably carcinogenic to humans 624-5632. The confidential reporting form is available on Group 2B Possibly carcinogenic to humans our website at www.mass.gov/dph/ohsp. Group 3 Not classifiable as to carcinogenicity To receive your Bulletin by e-mail, to provide comments, Group 4 Probably not carcinogenic to humans or to contribute an article to the Bulletin, contact us at [email protected] In 1989, welding fume was classified as Group 2B Elise Pechter MPH, CIH because of "limited evidence in humans" and "inadequate evidence in experimental animals." Since that time, an additional 20 case-control studies and nearly 30 cohort studies have provided evidence of increased risk of lung Welding—impact on occupational health cancer from welding fume exposure, even after Neil Jenkins and Elise Pechter accounting for asbestos and tobacco exposures.3 Studies of experimental animals provide added limited evidence 3 Welding joins metals together into a single piece by for lung carcinogenicity.
    [Show full text]
  • RESPIRATORY TRACT RELATED INFECTIOUS SYNDROMES Acute
    RESPIRATORY TRACT RELATED INFECTIOUS SYNDROMES Acute or Acute on Chronic Bronchitis Antibiotics are NOT RECOMMENDED as >99% of acute bronchitis is caused by viruses. Asthma Exacerbation Supportive care. Antibiotics are NOT RECOMMENDED in the absence of pneumonia. COPD Exacerbation (COPDE) without evidence of pneumonia Per GOLD Guidelines, only the following patients presenting with COPDE may benefit from antibiotics - Increased sputum purulence WITH increased dyspnea or sputum volume - Severe exacerbation requiring invasive or non-invasive (e.g. BIPAP) mechanical ventilation - Pneumonia as indicated by symptoms and imaging findings Common causative pathogens: S. pneumoniae, H. influenzae, M. catarrhalis, viruses Antibiotics, in order of preference Comments Doxycycline 100 mg PO/IV BID x 5 days Has MRSA and atypical activity, some anti-inflammatory effects, may be protective against C. difficile Azithromycin 500 mg PO/IV Q24 x 5 days Has atypical activity Some anti-inflammatory effects Levofloxacin* 750 mg PO/IV Q24 x 3-5 days Increased risk of C. difficile and MRSA Black box warning for tendonitis, especially if >60 years old or concomitant steroids *Routine use levofloxacin is discouraged. Levofloxacin may be considered in patients at high risk of adverse events from COPDE such as those with poor baseline functional status, >3 exacerbations/year, FEV1 <50%. PNEUMONIA Signs/symptoms: cough +/- purulent sputum, shortness of breath, hypoxia/hypoxemia, fever >38⁰C, leukocytosis, wheezing, diminished breath sounds, pleuritic chest pain, rales/rhonchi,
    [Show full text]
  • Community-Acquired Pneumonia ©Adam Spivak/Ambulatory Curriculum 2014
    Community-Acquired Pneumonia ©Adam Spivak/Ambulatory Curriculum 2014 Section 1: Diagnostic criteria of community-acquired pneumonia (CAP) Radiographic finding of new infiltrate plus at least two of: fever; cough; chest pain; dyspnea. To qualify as "community- acquired", patient should not o have been hospitalized in an acute care hospital for >2D in past 90 days o be a nursing home or long-care facility resident o received intravenous antibiotic therapy/chemo/wound care in past 30 days o attended a hospital or hemodialysis clinic. Section 2: Most common etiologic agents of CAP Streptococcus pneumoniae Haemophilus pneumoniae Mycoplasma pneumoniae Chlamydophila pneumoniae Staphylococcus aureus Moraxella catarrhalis Section 3: Common pathogens in specific clinical scenarios Alcoholism Streptococcus pneumoniae and anaerobes COPD / smoking S. pneumoniae, Haemophilus influenzae, Moraxella catarrhalis and Legionella Nursing Home residency S. pneumoniae, gram-negative bacilli, H. influenzae, Staphylococcus aureus, anaerobes, and Chlamydophila pneumoniae Poor dental hygiene Anaerobes HIV infection (early stage) S. pneumoniae, H. influenzae, and Mycobacterium tuberculosis HIV infection (late stage) Above plus P. jiroveci, Cryptococcus, and Histoplasma species Travel to southwestern US Coccidioides species Influenza active in community Influenza, S. pneumoniae, S. aureus, S. pyogenes, and H. influenzae Suspected large volume aspiration Anaerobes (chemical pneumonitis, obstruction) Structural disease of lung Pseudomonas aeruginosa, Burkholderia (Pseudomonas) cepacia, S. aureus Injection drug use S. aureus, anaerobes, M. tuberculosis, and S. pneumoniae Airway obstruction Anaerobes, S. pneumoniae, H. influenzae, and S. aureus Section 4: Risk stratification in CAP management Step 1: If none of below present, outpatient mgmt. Step 2: Use if any positives in Step 1. Admit if score>70 ok Predictors of increased risk 1 pt.
    [Show full text]
  • Airborne Dust WHO/SDE/OEH/99.14 Chapter 1 - Dust: Definitions and Concepts
    Hazard Prevention and Control in the Work Environment: Airborne Dust WHO/SDE/OEH/99.14 Chapter 1 - Dust: Definitions and Concepts Airborne contaminants occur in the gaseous form (gases and vapours) or as aerosols. In scientific terminology, an aerosol is defined as a system of particles suspended in a gaseous medium, usually air in the context of occupational hygiene, is usually air. Aerosols may exist in the form of airborne dusts, sprays, mists, smokes and fumes. In the occupational setting, all these forms may be important because they relate to a wide range of occupational diseases. Airborne dusts are of particular concern because they are well known to be associated with classical widespread occupational lung diseases such as the pneumoconioses, as well as with systemic intoxications such as lead poisoning, especially at higher levels of exposure. But, in the modern era, there is also increasing interest in other dust-related diseases, such as cancer, asthma, allergic alveolitis, and irritation, as well as a whole range of non-respiratory illnesses, which may occur at much lower exposure levels. This document aims to help reduce the risk of these diseases by aiding better control of dust in the work environment. The first and fundamental step in the control of hazards is their recognition. The systematic approach to recognition is described in Chapter 4. But recognition requires a clear understanding of the nature, origin, mechanisms of generation and release and sources of the particles, as well as knowledge on the conditions of exposure and possible associated ill effects. This is essential to establish priorities for action and to select appropriate control strategies.
    [Show full text]
  • Foreign Body Management
    Foreign Body Management NYSGE Fellows Summer Course Susana Gonzalez, MD Assistant Professor of Medicine 1 Objectives • Timing of endoscopy When ? • Anatomic location Where ? • High risk objects What ? • Choosing accessories Which ? • Airway protection Who ? 2 Foreign Bodies in the GI Tract • 1500 people die annually • High risk: – Pediatric age group (80%) – Edentulous adults – Eosinophilic esophagitis – Alcoholics – Prisoners – Psychiatric patients 3 Ingested Foreign Bodies Outcomes: – Pass spontaneously 80-90% – Endoscopy 10-20% – Surgery ~1% Complications: Perforation <1% Mediastinitis Lung abscess Fistula Aspiration Always consider the possibility of more than one foreign body 4 Commonly Ingested Objects Children Adults • Coins • Food impaction* – Meat • Toys/ Magnets – Bones • Crayons – Fibrous husks • Ball point pen – Fish and chicken bones caps • Dentures • Batteries • Sharp Objects 5 Patient Presentation • Symptoms – 92% Dysphagia: location of object – 60% Neck tenderness – Odynophagia: impaction, esophageal tear, spasm – Hypersalivation/inability to tolerate oral secretions – Regurgitation – Abdominal pain • History – Objects swallowed – Timing of object swallowed 6 Patient Presentation • Physical examination: – Mental Status – Respiratory status • Airway compromise – Subcutaneous emphysema • esophageal perforation – Drooling • complete esophageal obstruction – Peritoneal signs • gastrointestinal perforation 7 Patient Presentation • Radiologic imaging – Location of object – Subcutaneous air – Pneumomediastinum – Pleural effusion
    [Show full text]
  • Occupational Chemical Respiratory Exposures & Asthma
    Occupationally Related Asthma, Bronchitis or Respiratory Hypersensitivity Reaction (Occupationally related respiratory conditions due to inhalation of chemicals, gases, fumes, and vapors; Occupationally Related Asthma) Other Names/Conditions: Work-related chemical pneumonitis, chemical bronchitis, or toxic pneumonitis. Work-related asthma, work-aggravated asthma, and reactive airways dysfunction syndrome are conditions that will also be described in this reference. Responsibilities: Hospital: Report by phone, fax, or mail Lab: Report by phone, fax, or mail Physician/Health care providers: Report by phone, fax, or mail Medical Examiners: Report by phone, fax, or mail Poison Control Centers: Report by phone, fax, or mail Occupational Nurses: Report by phone, fax, or mail Local Public Health Agency (LPHA): No follow-up required, unless outbreak occurrence Report to the IDPH Bureau of Environmental Health Services: Iowa Department of Public Health Bureau of Environmental Health Services Lucas State Office Building 321 E. 12th Street Des Moines, Iowa 50319-0075 Phone (Mon-Fri 8 am - 4:30 pm): 800-972-2026 Fax: 515-281-4529 24-hour Disease Reporting Hotline: (For use outside of EHS office hours) 800-362-2736 Web: https://idph.iowa.gov/ehs/reportable-diseases Report Form: Environmental & Occupational Report Form on web Note: This revised document reflects provisional language in reference to the current Iowa Administrative Code [641] Chapter 1: “Occupationally related asthma, bronchitis or respiratory hypersensitivity reaction” means any extrinsic asthma or acute chemical pneumonitis due to exposure to toxic agents in the workplace. (ICD-10 codes J67.0 to J67.9).” The diagnostic coding currently listed is inappropriate for the narrative of the condition described.
    [Show full text]
  • Chemical Pneumonia Due to Paint Thinner Ingestion: a Case Report and Literature Review
    EURASIAN JOURNAL OF EMERGENCY MEDICINE DO I: 10.4274/eajem.galenos.2018.24482 Case Report Eurasian J Emerg Med. 2019;18(1): 55-7 Chemical Pneumonia Due to Paint Thinner Ingestion: A Case Report and Literature Review Mehmet Koçak1, Kurtuluş Açıksarı2 1Clinic of Emergency Medicine, Fatih Sultan Mehmet Training and Research Hospital, İstanbul, Turkey 2Department of Emergency Medicine, İstanbul Medeniyet University Faculty of Medicine, İstanbul, Turkey Abstract Paint thinner is an organic solvent which includes aromatic hydrocarbons and is widely used in the paint, varnish, and plastic products industries. Regular inhalation of such solvents is known to cause chronic intoxication. Oral thinner over-exposure is rare but quite fatal. Volatile liquids can cause pulmonary complications even with oral ingestion. Therefore, in patients with oral volatile liquid thinner intake, emergency physicians should be aware of local complications as well as the systematic effect even with initial normal physical or radiological findings. In this report, we present a patient with chemical pneumonia due to self-vomiting after accidentally drinking paint thinner. Keywords: Chemical pneumonitis, thinner, hydrocarbons, ingestion Introduction admitted to our hospital with complaint of fever with the history of paint thinner ingestion. Exposure to hydrocarbons is common in modern society. Thinner is an organic solvent that contains aromatic hydrocarbons such Case Report as toluene and xylene and is easily accessible in products such as gasoline, paint, varnish, and plastic production industries. A 54-year-old male patient presented to the emergency Types of exposure include unintentional ingestion, intentional department (ED) with fever. He had drunk half bottle of paint recreational abuse, unintentional inhalation, and dermal thinner (approximately 100 mL) accidentally 9 hours before exposure or oral ingestion in a suicide attempt.
    [Show full text]
  • Vaping Induced Pathological Changes in the Lung Comparing with Imaging Finding-A Case Report Study
    Bhuyan RR, et al., J Clin Stud Med Case Rep 2020, 7: 092 DOI: 10.24966/CSMC-8801/100092 HSOA Journal of Clinical Studies and Medical Case Reports Case Study and Prevention (CDC) website posted on January 20, 2020 [1]. 27 Vaping Induced Pathological confirmed death cases have been reported due to severe and acute pulmonary disease associated with e-cigarettes in all 50 states, the Changes in the Lung Comparing District of Columbia, and two U.S. territories (Puerto Rico and the U.S. Virgin Islands) [1]. with Imaging Finding-A Case Although chemical exposure has been postulated as a definitive cause, the acute incidence of pulmonary disease has brought national Report Study attention to this epidemic and warrants more studies of clinical course, radiological findings and unique pathological changes in the Rashmi R Bhuyan*, Kumkum Vadehra and Ningdong Kang lungs, that will help in immediate medical management for VAPI with appropriate support, as reported in the case below [2]. Department of Pathology and Department of Surgery, Harbor-UCLA Medical Center, California, USA Case Report A 30 year old female with history of anxiety, depression and marijuana use presented in the ED with dyspnea and hypoxic respiratory Abstract failure with presumed How did the author know if it is ‘presumed Vaping Associated Pulmonary Injury (VAPI) is a group of respi- etiology’? etiology of inhalation of injury vs hypersensitivity ratory symptoms like shortness of breath and tachypnea and, often- pneumonia. CT chest showed diffuse bilateral ground-glass changes times, it is associated with non-specific symptoms like generalized with differential diagnosis of multifocal pneumonia vs interstitial fatigue, body ache, fever, nausea, diarrhea, vomiting and chills.
    [Show full text]