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3/4/2020 The Occupational Burden of Respiratory Disease March 6, 2020 Carrie Redlich, MD, MPH Professor of Medicine, Pulmonary and OEM Director, Yale Occupational and Environmental Medicine Program Yale School of Medicine S L I D E 0 Disclosures

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The Occupational Burden of Respiratory Disease

Carrie Redlich, MD, MPH Professor of Medicine, Pulmonary and OEM Director, Yale Occupational and Environmental Medicine Program Yale School of Medicine March 6, 2020

S L I D E 1

I have nothing to disclose. Disclosures

S L I D E 2

1) “Classic” Pneumoconioses ‐ 100% occupational 2) Airways Diseases

  • Asthma
  • COPD / Bronchitis

3) Interstitial lung Diseases

  • Idiopathic pulmonary fibrosis
  • Sarcoidosis, hypersensitivity pneumonitis

4) Pulmonary Infections

  • Pneumonia

5) Conclusions and Questions

Occupational Burden of Respiratory Disease

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  • 125 million people currently exposed at work
  • >50 countries have banned asbestos – not USA, CA

– Continued disease risk due to long latency

Asbestos

Cullinan et al. Lancet Respir Med. 2017; asbestos nation.org

Thermal resistance, strength, flexibility Uses: Insulation, brakes, textiles, cement

S L I D E 4

Pleural disease

Pleural effusions Plaques Diffuse pleural thickening

Asbestosis (pulmonary fibrosis) Non‐malignant Asbestos‐Related Respiratory Diseases

S L I D E 5

Asbestosis

  • Typically chronic exposure (10+ years)
  • Long latency (20‐30 years)
  • Dyspnea, cough, slow progression
  • PFT’s: Restriction; reduced DLCO, mild obstruction
  • CT scan – subpleural fibrosis, traction bronchiectasis –

similar to UIP (IPF)

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Diagnosis Asbestosis: ATS Statement 2004

  • Evidence of structural change by

– Imaging OR Histology

  • Evidence of plausible causation by

– History OR Markers of exposure (plaques) OR asbestos bodies

  • Evidence of functional impairment by

– Signs and symptoms OR – PFT’s (restriction or reduced DLCO) OR – Inflammation (BAL) OR – Exercise testing

  • Exclusion of alternative diagnoses

S L I D E 7

Trends in Respiratory Mortality Rates

S L I D E 8

  • Respirable crystalline silicon dioxide (SiO2)

– Quartz = 10% of earth’s crust

  • Rock, concrete, masonry, silica sand
  • Drilling, cutting, sandblasting, demolition, mining

Silica

NIOSH No. 1996‐112.

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  • Silicosis

– Chronic = after 10+ years, lower concentrations – Accelerated = after 5‐10 years, higher concentrations – Acute = after weeks to years, highest concentrations

  • Increased risk TB
  • Lung cancer

Silica‐Related Respiratory Diseases

Akgun et al. Chest. 2015.

S L I D E 10

  • Denim sandblasting in Turkey
  • Artificial stone countertops worldwide
  • Hydraulic fracturing for oil & gas

New industrial processes re‐create an old exposure

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1) Construction and 2) General Industry & Maritime Standards Silica PEL ‐ 50 ug/m3 Silica Action level ‐ 25 ug/m3 Medical surveillance required if >PEL for >30 days (> Action level 6/2020) Baseline and every 3 years Exam, questionnaire Chest x‐ray with B‐read TB screening (baseline only) Spirometry Medical follow‐up with occ med or pulmonary physician

OSHA new Silica rule (implemented June, 2018)

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Quadrillion (1015) Btu

Coal: World Consumption 2010‐2040

U.S. Energy Information Administration.

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  • Coal workers’ pneumoconiosis (CWP)

– Simple – Complicated (progressive massive fibrosis [PMF])

  • COPD

Coal‐Related Respiratory Diseases

S L I D E 14

CWP in US – Prevalence and Severity Increasing

Ann Am Thorac Soc. 2018 December ; 15(12): 1420–1426. doi:10.1513/AnnalsATS.201804‐261OC. Am J Public Health. 2018;108:1220–1222. doi:10.2105/AJPH.2018.304517

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Change in Mortality Rates from 1980‐2014

  • JAMA. 2017;318(12):1136‐1149. doi:10.1001/jama.2017.11747

Asbestosis CWP All Pneumoconioses

S L I D E 16

  • Remain an important and preventable problem in the

US and worldwide

  • Current preventive strategies are not sufficient

In addition occupational exposures also contribute to the major “non‐occupational” lung diseases

Summary Classic Occupational Pneumoconioses

S L I D E 17

1) “Classic” Pneumoconioses ‐ 100% occupational 2) Airways Diseases

  • Asthma
  • COPD / Bronchitis

3) Interstitial lung Diseases

  • Idiopathic pulmonary fibrosis
  • Sarcoidosis, hypersensitivity pneumonitis

4) Pulmonary Infections

  • Pneumonia

5) Conclusions and Questions

Occupational Burden of Respiratory Disease

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The Occupational Burden of Respiratory Disease

Aim: Estimate the occupational contribution to the burden of asthma, COPD / bronchitis, IPF, HP, sarcoidosis, respiratory infections

S L I D E 19

  • Asthma, COPD, Bronchitis, ILD, CAP

The occupational attributable fraction (PAF) was estimated using population‐based or case control studies (ILD)

PAF = [(P0 +  Pi (RRi)) – 1] / [P0 +  Pi (RRi)] P0 is the proportion in the population not exposed Pi is the proportion exposed, RRi is the RR exposed. PAF = pc(OR ‐1)/OR Pc = proportion of cases exposed

  • PAP, HP, Sarcoidosis

Occupational Proportion estimated from cases series where occ info available

  • Calculated pooled estimates using Stata. If high heterogeneity used random

effects models.

Methodology to Estimate Occupational Burden

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  • 15% of adult asthma caused by work, cross‐sectional studies
  • ≈20‐40% asthmatics who work report symptoms worse at work
  • Numerous causative exposures: allergens, irritants
  • Most commonly reported occupational lung disease in

industrialized countries

Work‐Related Asthma

Asthma caused by work (OA) Asthma exacerbated by work (WEA)

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Occupational Contribution to Incident Asthma

Pooled PAF asthma was 16% (95% CI 10‐22%) ‐ further supports prior cross‐sectional data

S L I D E 22

8.4% adults in CA current asthma (2.3 M) 40.3% asthmatics in CA report WRA (> 0.9 M)

  • 24.6% caused by work
  • 35.0% aggravated by work

Work‐related Asthma in California

Asthma Surveillance in CA 2017 Report. CA Health Interview Survey (CHIS) Work‐Related Asthma in CA 2012. Asthma Call‐Back Survey (ACBS)

S L I D E 23

# WRA Cases in CA from case‐based surveillance

About 600 cases WRA / year < 200 physician diagnosis vs If 2.3 M adults in CA have asthma then 350,000 – 900,000 WRA

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Case 1 – Hospital cleaner with asthma

36 year old environmental services technician at your hospital is referred for evaluation work‐related symptoms. She reports onset asthmatic symptoms about 3 years ago. Better on vacation, worse at work, especially when ‘terminal room cleaning’ after patient discharge. Progressively worse with greater use inhalers. Asthma diagnosed about 3 yrs ago. Her pulmonologist has been treating her with inhaled steroids + LABA, montelukast, occasional prednisone. Also recently restricted her from ‘terminal cleaning’.

S L I D E 25

Very mild childhood asthma – resolved No asthma meds until past 3 years. Can’t remember an inciting event or infection No pets, home issues One child with asthma Mild seasonal allergies, obesity Former smoker, 1 ppd for 10 years. Exam – unremarkable

Case 1 – Further Work‐up

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Work‐related Asthma: Diagnosis ACCP, ATS / ERS, ACOEM Statements similar

WRA should be considered in all adults with new onset or worsening asthma To make the diagnosis: 1) Confirm diagnosis of asthma 2) Identify /confirm exposure(s) in workplace can cause asthma 3) Determine association between asthma and work

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Spirometry with BD

Minimal airflow obstruction, BD negative. No prior testing done.

You request information on hospital cleaning products

Given a long list of surface cleaners, sanitizers, SDS.

You provide employee with a peak flow meter. 1 mo follow‐up: she has been away from terminal cleaning.

Some improvement symptoms. Peak flows hard interpret.

6 mo follow‐up: Let go. Employer can no longer make accommodations.

Applied for workers comp to help with medical expenses. Denied.

Case 1 – Further Work‐up

S L I D E 28

You were asked to assess whether she has WRA. To make the diagnosis WRA: 1) Confirm diagnosis of asthma Neg BD (but on inhaled steroids) 2) Identify /confirm exposure(s) in workplace that can cause asthma Don’t know specific product, agent. 3) Determine association between asthma and work History, no peak flows, no immunologist test Yes or No work‐related? If yes – what type WRA ?

Case 1 – Diagnosis

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WRA in CA – Causative agents and high risk jobs

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  • WRA remains common and under‐diagnosed for multiple

reasons, despite Guideline documents, alerts, surveillance.

  • Current protective measures are not adequate.

Work‐related asthma: Conclusion

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The Occupational Burden of Respiratory Disease

Aim: Estimate the occupational contribution to the burden of asthma, COPD / bronchitis, IPF, HP, sarcoidosis, respiratory infections

S L I D E 32

COPD – Mortality rate and trends from 1980 ‐ 2014

  • JAMA. 2017;318(12):1136‐1149. doi:10.1001/jama.2017.11747
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Occupational Contribution to COPD

26 studies: most population‐based, 6 data on nonsmokers For COPD, PAF work exposures: 14% (95% CI, 10‐18%) Among never smokers PAF: 31% (95% CI, 18‐43%) Further support for prior findings ≈ PAF 15% Causative exposures

VGDF (vapors, gases, dusts, fumes) mineral and organic dusts, cement, welding fumes, diesel exhaust fumes, organic cleaning products

Industries / occupation

Numerous: Construction, foundries, welding, mining, healthcare, cleaning, manufacturing, agriculture

S L I D E 34

COPD remains VERY common (est 16 million in US)

  • ≈ 10‐20% of US adults 40‐79 yrs have COPD and 24% those with

COPD are never smokers (Tilert. Prev COPD. NHANES 2013; (Fuller‐Thomson 2016)

  • Occupational COPD worse morbidity (Paulin et al 2015)
  • Asthma/COPD overlap – 52% WRA also COPD, worse outcomes (Dodd et al 2019)

If 15% all COPD, 31% of COPD in never smokers is work‐related, then there is a LOT of Occupational COPD, and also opportunities for prevention. How is Occupational COPD diagnosed ? How often ?

Occupational Contribution to COPD

S L I D E 35

  • 62 year old former smoker, steam fitter and welder for a medical center
  • Diagnosed with COPD at age 59

Age 43 FEV1 2.79 (75%) FEV1/FVC 63% Age 46 FEV1 2.64 (66%) FEV1/FVC 58% Non‐union Co – decided no PPE, no spirometry Age 59 FEV1 0.93 (28%) FEV1/FVC 46% Chest imaging: Emphysema; AIAT neg

  • Cigarettes: 1ppd x 25 years (20 ‐ 45 yrs)
  • Work: steamfitter, welder x 40 years (age 20‐60 yrs), enclosed spaces,

no or little PPE, especially after age 43. Reports little asbestos exposure.

  • Diagnosis: ?

Case 2: 62 yr old with COPD

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  • No official guideline documents, criteria
  • Rarely recognized as work‐related (miners)
  • Little surveillance data, much less than WRA (except Germany)
  • How much exposure needed – duration, intensity ?

Most studies: > 10 years employment, can have risk with fewer years Asthma / COPD overlap: shorter exposures relevant

  • Occupational, environmental exposure history key

Timing of exposures, co‐exposures, lung function if available

  • How weigh smoking vs occupational exposures ?

Diagnosis Occupational COPD

S L I D E 37

  • Spirometry testing

*Age 43 FEV1 2.79 (75%) FEV1/FVC 63% (no evaluation) *Age 46 FEV1 2.64 (66%) FEV1/FVC 58% (no evaluation) Employer decided no longer need PPE, no spirometry Age 59 Progressive symptoms – PMD orders spirometry FEV1 0.93 (28%) FEV1/FVC 46%

  • Cigarettes: 25 pk years
  • Work: steamfitter, welder x 40 years – literature supports causative
  • Sharp decline in FEV1 after stops smoking, while still working
  • *Lost opportunity for prevention.
  • Can no longer work, workers compensation denied ‐ still on appeal

Case 2: 62 yr old with COPD

S L I D E 38

The Occupational Burden of Respiratory Disease

Aim: Estimate the occupational contribution to the burden of asthma, COPD / bronchitis, IPF, HP, sarcoidosis, respiratory infections

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  • Clinical Presentation

Chronic, fibrotic lung disease. (Progressive SOB, hypoxia) CT scan: UIP (Usual Interstitial Pneumonitis) pattern: Subpleural fibrosis, honeycombing, patchy, lower lobes. Progresses to end‐stage fibrosis. (Other advanced ILDs can all look similar (e.g. CTD, hypersensitivity pneumonitis, NSIP). Poor prognosis: 3‐5 yrs life expectancy after diagnosis.

  • Diagnosis

Chest CT scan – typical UIP pattern Biopsy – subpleural patchy fibrosis, fibroblastic foci. Known causes ILD excluded (drugs, CTD, occ /envir exposures) Asbestosis has a similar UIP pattern.

Idiopathic Pulmonary Fibrosis (IPF)

Usual interstitial pneumonia (UIP)

  • pattern. Am J Respir Crit Care Med, 2013.

https://www.atsjournals.

  • rg/doi/abs/10.1164/rccm.201208‐1544CI

S L I D E 4 0

  • Epidemiology

– Annual incidence: 7‐16 per 105 – Prevalence: 14‐43 per 105 – Regional variation – Increasing incidence

  • Risk factors

– Men > women – Older age – Smokers > non‐smokers – Occupational exposures – Familial, MUC5b, other gene variants

Idiopathic Pulmonary Fibrosis (IPF)

Raghu et al. Lancet Resp Med. 2014;2:566‐72.

  • JAMA. 2017;318(12):1136‐1149. doi:10.1001/jama.2017.11747

Change in ILD mortality rates 1980‐2014

S L I D E 4 1

IPF: Occupational Contribution

Idiopathic disease. Only make the diagnosis after rule out known causes ILD. Occupational burden not previously estimated Literature search: 11 case‐control studies of IPF with information about

  • ccupation, exposures (VGDF, metal, wood dusts etc).

Exposure assessment – mostly interview, self‐reported. PAF calculated from OR. Pooled PAF for VGDF and specific exposures calculated. Random effects modeling used as high heterogeneity.

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S L I D E 4 2

IPF: PAP for Occupation

Conclusion: Occupation exposures contribute substantially (26%) to IPF. How does one diagnose occupational IPF?

S L I D E 4 3

  • 65 year old machinist referred to evaluate if work exposures

contributing to his ILD.

  • He presented at age 63 yrs when admitted with “pneumonia”.

Also progressive SOB.

  • Machinist for over 40 years, until age 64 when he could no

longer work. Made metal molds, cut, drilled metal parts.

  • Exposures to metal dusts, metal working fluids, different metal

alloys (copper, aluminum, nickel, chromium, steel) for many

  • years. Dusty. No PPE.
  • Doesn’t remember any asbestos in the machine shops.

Case 3: Machinist with ILD

S L I D E 4 4

  • PFTs showed restriction (TLC 56%) and reduced DLCO (38%).
  • Chest CT scan showed findings consistent

with fibrotic lung disease, UIP pattern.

  • Additional history and blood work showed

no other cause for fibrosis: No autoimmune disease, cancer No medications No other work or environmental exposures beyond his work as a machinist.

  • Lung biopsy not performed given the risks
  • Diagnosis ?

Case 3: Further work‐up

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  • No guideline documents
  • Thorough occupational and environmental exposure history is key

– Is extent, timing of exposure consistent with his disease – Does literature support types of exposures as causative?

  • Rule out other more likely causes of his ILD
  • Is the timing, progression of his ILD consistent with occupational

contribution?

  • Co‐existing positive autoimmune serology (e.g. ANA, RF) or disease

(e.g. RF) is common. Both could be linked to exposure.

  • Lung pathology is generally not that helpful

Diagnosis Occupational IPF

S L I D E 4 6

The Occupational Burden of Respiratory Disease

Aim: Estimate the occupational contribution to the burden of asthma, COPD / bronchitis, IPF, HP, sarcoidosis, respiratory infections

S L I D E 4 7

Blanc et al. Am J Respir Crit Care Med, 2019 https://www.atsjournals.org/doi/abs/10.1164/rccm.201904‐0717ST

Occupational Burden of Respiratory Disease

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1) “Classic” Pneumoconioses ‐ 100% occupational 2) Airways Diseases

  • Asthma
  • COPD / Bronchitis

3) Interstitial lung Diseases

  • Idiopathic pulmonary fibrosis
  • Sarcoidosis, hypersensitivity pneumonitis

4) Pulmonary Infections

  • Pneumonia

5) Conclusions and Questions

Occupational Burden of Respiratory Disease

S L I D E 4 9

  • Work exposures contribute substantially to the burden of

most chronic lung diseases (in addition to classic occupational pneumoconioses), all of which are PREVENTABLE diseases.

  • These conditions are rarely recognized as occupational by

clinicians or the broader public.

  • There is a great need for better recognition and preventive

interventions, as current protections for workers are not adequate.

Conclusions

S L I D E 50

Acknowledgements

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S L I D E 51

  • A. Asbestosis
  • B. Coal workers pneumoconiosis
  • C. COPD
  • D. Asthma
  • 1. Which of the following diseases contributes the greatest

number of work‐related respiratory fatalities in the US ?

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  • A. Asthma
  • B. COPD
  • C. Tuberculosis in a healthcare worker
  • D. Idiopathic pulmonary fibrosis
  • 2. Which of the following respiratory diseases is least likely to

be related to exposures at work?

S L I D E 53

  • A. Occupational asthma
  • B. Environmentally‐triggered asthma
  • C. Work‐related stress
  • D. Work‐exacerbated asthma
  • 3. A US postal worker reports that her chronic asthma is worse when she is

assigned certain delivery routes in poorer industrial neighborhoods. What is her most likely diagnosis?