Dentists can be exposed to hazardous chemicals, airborne particulates, and bioaerosols known to be risk factors for respiratory disease. Vapors from solvents and acrylic resins, such as methyl methacrylate, can be released during procedures involving caries restorations, implants, and dental prosthetics as well as during environmental cleaning in dental settings.^1,2 The dental dust generated during carious tissue removal and grinding/polishing dental materials can contain nanoparticles and respirable dusts from teeth, dental composite, glass ionomers, and metal alloys (containing nickel, chromium, cobalt, and molybdenum).^3–7 Additionally, dental instruments such as ultrasonic scalers and high speed hand pieces can be sources of bioaerosols in the dental environment.^8,9 Inhalational exposures are common among dentists; 55% of general dentists have reported their job required being exposed to contaminants (such as pollutants, gases, dust, or odors) every day, and another 19% reported these exposures occurred once a week or more but not every day.¹⁰

Studies among dental personnel have reported associations between materials used in dental settings and respiratory disease, including work-related upper and lower respiratory symptoms, occupational asthma, and other respiratory hypersensitivies.^11–15 Pneumoconiosis, a type of interstitial lung disease (ILD) caused by dust exposures and characterized by pulmonary fibrosis, has been documented among dental personnel.^3,16 Idiopathic pulmonary fibrosis (IPF) is one of the most common ILDs and is a chronic, progressive disease with no cure, a median survival of 3–5 years, and lung transplantation is the only means of prolonging survival.^17,18 Despite requirement for a specific set of clinical, radiologic, and histologic characteristics with a limited range of phenotypes for a diagnosis of IPF,¹⁹ patients continue to experience misdiagnosis.²⁰ This misdiagnosis may occur when these specific characteristics are absent, yet the diagnosis is applied based on some other pattern of pulmonary fibrosis on imaging or histology. Additionally, clinicians may inappropriately use this term when the correct patterns of pulmonary fibrosis are present on imaging or histology, but where a search for a cause is incomplete.¹⁹ A cluster of nine cases of IPF was identified among dental personnel treated at a tertiary care center during 2000–2017. The number of cases identified in that patient population was approximately 23-times higher than expected in the United States.²¹ Increased proportionate mortality ratios (PMRs) for dentists who died of “other interstitial pulmonary diseases with fibrosis,” which includes IPF, have also been previously described, indicating dentists might be occupationally exposed to hazards associated with pulmonary fibroses.²¹

In 2022, there were approximately 202,500 dentists employed in the United States, and the number of dentists in the United States potentially exposed to respiratory hazards is expected to increase over time because of increased demand for dental treatments.^22,23 Despite known occupational exposures to hazardous compounds, few mortality studies of United States dentists have been published; furthermore, of those studies that have been published, the vast majority were prior to 1980 and limited to specific states.²⁴ To further understand the relationship between occupation as a dentist and respiratory disease, our objective was to describe the patterns and causes of mortality, focusing on non-malignant respiratory diseases (NMRD) including pulmonary fibrosis, among dentists who died in the United States during 1979–2018.

During 1979–2018, dentists had lower proportionate mortality than the general U.S. population for all NMRDs, except the non-specific “other respiratory diseases” category. Dentists had higher proportionate mortality than the general U.S. population for this “other respiratory diseases” category, which was primarily composed of underlying causes of death of pulmonary diseases with fibrosis (PF group), a particular interest in this study as potentially being occupationally related, and pneumonitis due to food and vomit, which we would not expect to be occupationally related. Because we could not separate deaths from pulmonary fibrosis from deaths due to other causes in the “other respiratory diseases” category using standard LTAS rate files, we a priori designed a PF group of ICD codes to most closely approximate IPF as possible. These more specific analyses on pulmonary fibrosis, in both our main and sensitivity analyses, revealed dentists had higher proportionate mortality than the general U.S. population for pulmonary diseases with fibrosis, both overall and during each calendar period with at least one death from a PF group UCOD, with most reaching statistical significance.

Our study is the first mortality study of its size among dentists in the United States in almost 50 years. A previous study commissioned by NIOSH published in the 1970s included over 102,000 dentists and examined causes of death among the 8,945 dentists who died during the study period 1960–1965. That study revealed significantly reduced mortality among dentists from NMRD overall, compared to the general U.S. population.³³ Our results are also similar to smaller studies in Taiwan, Japan, Europe, and the United States that found reduced mortality among dentists, compared with the general population, for COPD, pneumonia, influenza, bronchitis, and asthma.^34–37 The authors of these other studies suggest the findings of reduced mortality from respiratory diseases might be because of dentists’ high socioeconomic status and access to healthcare. In the United States, a low smoking prevalence of approximately 6% among dentists, compared with 19.6% among all U.S. working adults and 15.9% among U.S. adults working in the healthcare and social assistance industry, might also contribute to these findings in our study.^38,39

Our study is also the first to specifically examine mortality from NMRD with a focus on fibrotic pulmonary diseases, following a cluster of IPF cases identified among dental personnel.²¹ Although historically dental practices have not been considered settings where potentially harmful exposures that could contribute to ILDs occur, occupational pneumoconiosis linked to dental dust has been documented among dental professionals, particularly dental technicians, across multiple studies in various countries.³ Additionally, a case report from the United States described a 79-year-old retired dentist with severe interstitial pulmonary fibrosis of unknown cause who died from respiratory failure, and a necropsy with scanning electron microscopy of his lung tissue revealed inclusions consistent with alginate impression powders the dentist used during his career.⁴⁰ If we made assumptions about state and year of death from this case report, we could conclude this dentist was included in our study in the PF group.

In our study of dentists, no decedent had silicosis or other pneumoconiosis as the UCOD. Still, given dentists’ known occupational exposures to dental dust and previous case reports/series of ILDs including IPF among dental personnel, our pulmonary fibroses (PF group) results corroborate concerns about a potential relationship between occupational exposures and pulmonary fibrosis among dentists. Our PF group results are also consistent with elevated PMRs previously reported by NIOSH using surveillance data for “other interstitial pulmonary disease with fibrosis” (which included IPF), both among those with the occupation of dentist (PMR, 1.78; 95% CI, 1.45 to 2.20) and those who worked in the offices of dentists (PMR, 1.44; 95% CI, 1.22 to 1.69).²¹ Future studies examining pulmonary fibrosis in dentists is warranted to investigate if the decreased PMR for the most recent calendar period represents an overall decreasing trend of pulmonary fibrosis among dentists, especially given the increasing proportion of female dentists over time (16.0% in 2001 to 31.8% in 2018) and binary sex differences in IPF survival.^23,41 We also acknowledge other dental personnel could also be exposed to similar occupational hazards warranting future investigation.

Our study’s strengths include its sample size of over 38,000 dentist decedents, 40 years of included data, national scope, and specific analyses on pulmonary fibroses that is a topic of recent concern to the occupation. Although the proportion of dentist deaths captured by ADA is uncertain, this proportion is estimated to be greater than 50%; while we do not anticipate the captured deaths to be systematically different from non-captured deaths, the number of dentist deaths during the study period may be an undercount, and we cannot make conclusions about the representativeness of the included decedents.

Our study is also subject to at least four limitations. First, for some decedents, NDI returned multiple potential death record matches. Although the NDI-recommended probability score cutoffs and date of death were used to select a single death record, we acknowledge misclassification is possible. Second, misclassification of causes(s) of death on death certificates is possible, and some decedents could have had pulmonary fibrosis not indicated by the UCOD ICD code;⁴² this limitation would result in an undercount of decedents with any pulmonary fibrosis in our study. We also did not exclude decedents with contributing causes of death associated with known causes of pulmonary fibrosis, as has been done in previous studies attempting to examine IPF specifically.^30,32,43 These types of multiple-cause-of-death analyses were beyond the scope of the current study, and furthermore, the UCOD is the recommended unit of primary tabulation to examine opportunities for public health intervention for the precipitating cause of death.⁴⁴ Third, while we defined the PF group ICD codes a priori, based on previous IPF studies,³¹ to most closely approximate IPF as possible for the UCOD, the PF group likely includes decedents whose UCOD was pulmonary fibrosis, but not specifically IPF. This limitation was acceptable in our current study, because decedents with IPF are often either coded to one of these more general pulmonary fibrosis ICD codes and additional ICD codes on death certificates are inadequately sensitive to determine pulmonary fibrosis etiology.^29,30,32 Finally, a general limitation of PMRs is that cause-specific PMRs are mutually dependent, meaning an elevated PMR for one cause could result in a decreased PMR for another cause. If dentists’ mortality overall is lower than the general U.S. population, for example because of the healthy worker effect, then PMRs might differ from SMRs, which are more reliable estimates of mortality but require data on the entire at-risk population.⁴⁵ Future analyses could benefit from identifying sources of denominator data for dentists and calculating SMRs to confirm these findings.

Given the known occupational risks for interstitial lung disease among dental personnel, possible inadequate ascertainment of occupational history from patients, and potential for misdiagnosis of IPF,^19,46–48 our mortality results might indicate IPF among dentists may not truly be idiopathic and instead may be related to a common underlying occupational exposure. Measuring actual dust and bioaerosol exposures in dental practice settings would provide information on specific respiratory hazards in these workplaces that could guide design and implementation of effective engineering controls.