Pneumoconiosis: Diagnosis and Management

00:00 So how do we make the diagnosis of pneumoconiosis? There are four basic criteria.

00:06 One, we need to have a documented exposure history.

00:10 You need to go back in time because, as we talked about earlier, it's a very long, latent period between the primary exposure and the subsequent development of the disease, the fibrosis or the malignancy.

00:24 We also need to have the clinical radiologic features compatible with the known elements of the disease, and we'll show some of that in the next few slides.

00:32 We need to exclude other diseases that could explain the findings.

00:36 Primary pulmonary fibrosis is a thing.

00:39 Primary pulmonary hypertension is a thing.

00:42 And so we need to exclude those before we say, oh, they got exposed to the particles and that's what caused this.

00:50 Finally, being a pathologist, you need to do a pulmonary biopsy and a particulate analysis.

00:56 When I say that, you're not just looking down the microscope and saying, oh, I think that's silica or I think that's asbestos.

01:02 You take a hunk of lung or a little piece of lung, a biopsy, and ash it.

01:07 You burn it up and count the number of residual particles that are left after you've completely burned out the rest of the organic material.

01:18 Silicosis, I've already seen a picture of this previously.

01:22 The CT on the left-hand side shows typical nodular fibrosis.

01:27 A test X-ray may show ground glass opacity, particularly in the perihilar and basilar regions.

01:34 The H and E shows diffuse dense fibrosis with the very bright white speckling that is the residual silica.

01:43 In asbestosis, you may see asbestosis plaques.

01:47 Those are the fibrotic plaques that are typically in the pleura.

01:52 Those are indicated by the arrows.

01:54 But you may also see interstitial fibrosis.

01:57 And keep in mind, all of the pneumoconiosis will drive macrophage activation, drive a pro-fibrotic process.

02:05 In asbestos, when we look at the lungs, we can also see the asbestos fibers rather large.

02:12 We get these so-called ferruginous bodies, iron-encrusted asbestos, and then around them, you see all these rather large and activated macrophages.

02:22 Secondary to that macrophage activation, we are getting release of pro-fibrotic, pro-inflammatory cytokines, which drive inflammation but also interstitial fibrosis.

02:34 Cold workers' pneumoconiosis typically have rather large nodules that are well seen here on the chest X-ray.

02:45 You can see rather large nodules that you think, oh my goodness, that's malignancy.

02:50 No, those are collections of dense fibrosis with a lot of carbon in them.

02:55 You can have progressive disease.

02:57 What is shown on the right-hand side is a lot of carbon deposition with associated emphysema.

03:05 The emphysema can be due to the activation of the macrophages with the release of pro-inflammatory mediators that degrade the parenchyma.

03:15 But frequently, too, coal miners also smoke and may have kind of a confounding interaction between the coal and the impurities in the coal as well as their smoking.

03:29 And finally, borreliosis, the least common of our four most common pneumoconiosis.

03:34 Typically with a relatively long latency period, the interstitial fibrosis, pleural thickening, ground glass capacities that we've seen with the other pneumoconiosis.

03:45 With the pro-inflammatory state, we will also tend to get higher lymphadenopathy.

03:49 However, I would suggest that you use Dr.

03:52 Google and see what this looks like.

03:54 Pulmonary function tests are important.

03:57 These will typically show a restrictive pattern with a diminished forced vital capacity, a diminished total lung capacity, and the diffusion is also going to be down.

04:09 There may be a normal ratio of the forced expiratory volume to the forced vital capacity.

04:15 But again, because a lot of these same individuals that have got particular exposure are also smokers, that may confound the analysis.

04:25 Lab tests overall have relatively limited diagnostic value.

04:29 You can do a borrelium lymphocyte proliferation test if you suspect borrelium is the agent.

04:34 And you're looking for sensitization of an individual to the borrelium particulates and management.

04:41 What do we do about this? The problem is that there's not really good definitive treatment.

04:48 You want to cease exposure or limit exposure and wearing masks to prevent the initial exposure and not trying to wear masks after the horse is already out of the barn.

04:59 I think you also want to have your patients quit smoking if that's another confounding variable.

05:04 You can consider lung transplantation.

05:07 Things that you can practically do is make sure that they don't get secondary infections.

05:12 So make sure they get all their vaccinations for influenza and pneumococcal bacteria.

05:17 If they have some obstructive component, bronchodilators may be helpful.

05:23 Many will end up on permanent, lifelong supplemental oxygen.

05:27 Steroids are, you would think that because of the inflammatory component of the pneumoconiosis, steroids may be helpful, usually at the point where it makes the diagnosis.

05:39 The fibrosis is already well established.

05:42 So anti-inflammatories are not going to be all that helpful.

05:46 Same thing goes for other immunosuppressants.

05:49 Once we have fibrosis, that's not reversible.

05:52 And so I think mainly you want to prevent the fibrosis in the first place.

05:59 And then once it has occurred, give them as much support with vaccination bronchodilators and oxygen as possible.

06:05 And so with that, we've reached the end of the discussion of pneumoconiosis.

06:11 If you are involved in public health issues, this is a really significant element and something that we really need to protect the workers who are getting the front-line exposure to these agents.