Occupational Lung Diseases: Guillermo Do Pico Md Fccp Professor Of Medicine

Occupational Lung Diseases Guillermo do Pico MD FCCP Professor of Medicine

10/02/09

INHALATION EXPOSURE

Airways Bronchioles Alveoli Interstitium Blood Systemic effects

Site & intensity of the injury  Physico-chemical ◆ ◆ ◆ ◆ ◆

properties

Particle size…<5u go deeper Concentration… Solubility Density… lighter (as) go deeper Reactivity… higher (NH4) more damage

 Duration

of exposure Signs of alertness  Rate / depth of breathing  Host response variability / susceptibility  Host defense mechanisms

Mechanisms Toxic Inflammatory Irritant : Allergic : Sensitizers : Infectious : Carcinogenic

farm dust, chemicals flour (bakers) toluene di-isocyanates brucellosis uranium,

Symptoms Cough Expectoration Hemoptysis Dyspnea at rest and/or on exertion Wheezing Chest tightness / pain Upper airways symptoms Fever, chills, other

Threshold limit values ACGIH or OSHA TLV-TWA: time-weighted average concentration for 8 hours.Most workers will have adverse effects TLV-STEL: max concentration for up to 15 min that can cause chronic or irreversible changes in tissues or narcosis

UPPER ITIS 

AIRWA YS EXPOSU RE SYSTEMIC



ALVEO LI

BRONCHITIS  ASTHMALIKE  PULM ASTHMA BRONCHIOL EDEMA  ITIS PNEUMONI  BOOP TIS FIBROSIS ●NEUROTOXINS ●FEVERS

●

BRONCHOGE NIC

AIRWA YS

Asbestos + Smoking Uranium + •Smoking MESOTHELI ●

●

carcinog enic

PLEURA

OMA

•Asbestos

SYSTEMIC

● ●

LIVER Ca

Polyvinyl chloride

●

AIRWA YS

NEUROTOXINS Malathion ●CO

●

FEVERS

●

EXPOSU RE

ALVEO LI

SYSTEMIC

Grain ●Moldy hay ●Endotoxin ●Tephlon fumes ●Metal fumes ●

Occupational diseases Acute Chronic Progressive Regressive Intermitent Reversible Irreversible

Asthma Bronchitis Silicosis HP Asthma Asthma Silicosis

Airways exposure Acute massive

Chronic low

Acute low

chemical bronchitis Complete recovery

Chronic Bronchitis Asthma-like disease Allergic asthma

POPULATION STUDIES CHRONIC BRONCHITIS 80

GRAIN workers SM NS

CONTROL S NS

FARMER S

NS

70

SMOKERS

60 50 40 30

NONSMOKER

20 10 0 GS

GNS

CS

CNS

FS

FNS

Definition Occupational asthma A. Asthma

B. Onset after entering workplace C. Association of symptoms to workplace D1. Agent known to cause OA or D2. Work-related changes in lung function

No latency……………..irritant exposure Latency…………………….allergic nonallergic sensitization

Etiology Mechanism Inducers Immunologic IgE mediated High molecular wght

Low molecular haptens ? Cell mediated Low molecular

Nonimmunologic Irritant-toxic

Grain, crab, castor beans Woods, gum acacia Animal dander, urine Epoxy resins Chloramine T Platinum salts di-isocyanates Red Cedar Cobalt Ammonia, chlorine

Occupational Asthma in Finland Mean annual incidence 17/100000 workers

Bakers, food industry Painters, Lacquerers Veterinarians Chemical workers Farmers Animal husbandry Welders Plastics industry

60 % related to: Animal epithelia hair secretions

Flours Grains Fodder

Kajalainen et al Am J Industr Med 2000

MILK TANK INSULATION

Grain elevator Superior-Duluth

CARGO SHIP

Next slide

Truck unloading grain

No mask NIOSH tech w/mask

● ● ● ● ● ■

History Exam Lung Functions Skin tests Therapeutic trial

● ●

Obstructive pattern ◆ On spirometry Bronchodilatadors Provocation tests

IMMEDIATE REACTION FEV1

LATE REACTION

O

DUAL REACTION

PROGRESSIVE-PROLONGE

HOME-------------WORK-----HOME— WORK--HOMEWORK

Rx

therapy Same as other asthma Most important=avoidance of exposure

Prognosis Can not be predicted by severity, exposure, type,... Progress

Exposure ceases

Persistent Recurrent Resolves

HIGH IRRITANT UNCONDITIONED Stimulus RESPONSE

GAS VAPOR

Autonomic LOW Activation ODORANT “PANIC” Event-triggered reaction CONDITIONED

OCCUPATIONAL ALVEOLAR INJURY ◆ORGANIC DUSTS: ◆ Allergic

pneumonitis

◆INORGANIC DUSTS: ◆ Pneumoconiosis

◆CHEMICALS: ◆ Pulmonary

edema or Diffuse Alveolar Damage

Hypersensitivity Pneumonitis Lung disease resulting from sensitization and recurrent exposures to organic dusts Symptoms hours after exposure Fever,chills, dyspnea, cough Xray = bilateral pneumonitis Abnormal lung functions Acute, subacute or chronic

Organic Dust Toxic Syndrome Flu-like syndrome During exposure or delayed High level single exposure to dust No Xray or lung function changes Recovery without sequelae

Incidence of Allergic Alveolitis or“Farmers Lung Disease” and Organic Dust Toxic Syndrome or Inhalation Fever EAA = 2-3/10000 farmers/year ODTS = 1/1000 farmers/year 6702 swedish farmers Malmberg et al 1988

Hypersensitivity Pneumonitis Farmer’s Lung Bird Breeder’s Metal worker’s Hot tub Mushroom workers Rodent handlers Cheese washers Bagassosis

Summertype Humidifier Lung Suberosis Coptic Lung Malt workers Bathtub refinisher Composter’s lung Sauna takers

Hypersensitivity Pneumonitis Microbial “moldy” Bacteria Thermophiles • S. rectivirgula NonThermophiles • P. fluorescens • B. cereus, B subtilis

Fungi : Aspergillus sp,Penicillium,

Amebae Mycobacteria avium Contaminated fluids

Animal Birds, rats dander,feathers, droppings, urine Insects:weevil

Chemicals Metal fluid Diisocyanates Pyrethrum

Salami worker’s lung Rivero et al Medicina 1999 Biopsy proven Penicillium spp

Water reservoirs related HP Hot tub Humidifiers home, office, industry Saunas Showers Swimming pools Air conditioning systems Endotoxin or Specific antigen?………..

Metal working fluid Metal working fluids Cool and lubricate machine parts Removal of metal waste

Water-oil emulsions w/ soluble synthetic oils and biocide to reduce microbial contamination

Respiratory symptoms Asthma Hypersensitivity Pneumonitis

Hypersensitivity Pneumonitis to Metal working fluids Biopsy proven > 20 cases (US-Canada)

– Hodgson et al Am J Industr Med 2001 39:616 – Fox et al Am J Industr Med 1999 35:58- Wi

Causative agent: unknown

Solutions

Technical improvements • avoid cooling mists, • enclosures, • improve ventilation

Workers education Surveillance for sentinel cases

Treatment Corticosteroids for subacute or severe acute

PROGNOSIS- OUTCOME Resolve Recurrent disease= outcome determinant Fibrosis / COPD

Fatal,progressive

Treatment –Avoidance of exposure –Corticosteroids

Flock worker’s Lung Flocking Industry

Flock=powder of fibers .2-5 mm Nylon, rayon, polyester, textile waste….. Precision-cut Random-cut • Dull rotary blade • <10 μm particles

Adhesive coated fabrics

Fleeced fabrics

Clothing, carpets upholstery, cars …

FLEECE

INORGANIC DUST-INDUCED LUNG DISEASE barium •LOW-FIBROGENIC

•FIBROGENIC

Deposits: iron, tin,

titanium, glass wool Granulomatous: Berillium Silica (silicon dioxide) upper Silicates: Asbestos, lower Talc, Kaolin upper Coal dust Aluminum

Silica exposure

HOST

Minning Foundry work Sand blasting Ceramics

Silicosis Calcified lymph nodes Upper lobe nodules

Silicosis Massive fibrosis

Acute silicosis quarry worker Kim et la

Silicoproteinosis 25 yo dental technician Majo Barcelona

Simple Carbomonoxide-fires Methane, CO2-manure pits Chemical (interfere with cell respiration H cyanide-burning plastics H sulfide-manure pits Neurotoxins Pesticides, herbicides, fumigants

Irritants gases •Acrolein-burning plastics •Ammonia-fertilizer, transport •Chlorine-transport accidents paper mills •M-isocyanates plastics, fertilizers •N oxides=Farm silo, missile silo Zamboni disease •Phosgene=paint stripping, fires

Industrial or transportation accidents or intentional in wars

Mustard gas

Mustard Gas - Iran-Iraq war 10 years after single exposure 197 iranian veterans asthma 11% chronic bronchitis 59% bronchiectasis 9% airway scars or granulation 10% pulmonary fibrosis 12% Emad et al Chest 97

Complex exposures

Complex exposures

Site and extent of damage depend on : Duration Concentration Depth of inhalation Solubility Reactivity Warning properties

MASSIVE TOXIC INHALATION ASPHYXIA

PULMONARY IRRITATION UPPER AIRWAYS EDEMA LOWER AIRWAYS

LARYNGOSPA VENTILATORY OBSTRUCTION SM FAILURE ANOXIA

DEATH

MECHANICAL RECOVERY VENTILATION

Pulmonary edema Hemorrhagic alveolitis Acetaldehide Acrolein Ammonia Cadmium oxide Cobalt fumes Chlorine H chloride H fluoride H sulfide

Methyl bromide Methylisocyanate Nickel carbonyl Nitrogen dioxide Organophosphates Sulfur dioxide Toluene diisocyanate Trimellitic anhidride Zinc chloride

Exposure to Nitrous dioxide Silo Fillers Disease Within 10 days

Went to rescue P.edema burns †

Titan ll missile

Missile Silo McConnel Accident Both pulmonary edema 1 †

20th Century castle for sale 2.3 million

Diffuse alveolar Damage Non cardiogenic pulmonary edema=ARDS

can be delayed

OCCUPATIONAL LUNG DISEASES ARE PREVENTABLE

Defective-Zamboni disease

NO2

“Zamboni disease” 96 Hockey Players

Cough 97 % Hemoptysis 38 % Dyspnea-rest 50 % Dyspnea-exertion 70 % Epistaxis 11 % Headache 42 % Nausea20 % Weakness 38 % Chest pain 70 %

PIGS

PIG FEE D

NH3 H2S

CO2 CH4

Occupational Lung diseases are preventable