Can occupational exposure to jet fuel, aqueous film‑forming foam (AFFF) containing per‑ and polyfluoroalkyl substances (PFAS), and legacy asbestos increase risk of coronary artery disease?

Occupational Exposure and Coronary Artery Disease Risk

Based on current evidence, PFAS exposure from AFFF is associated with increased cardiovascular disease risk through dyslipidemia and direct platelet activation, while asbestos exposure primarily causes pulmonary disease without established direct links to coronary artery disease; jet fuel exposure data regarding CAD remains insufficient for definitive conclusions.

PFAS/AFFF and Cardiovascular Risk

Established Cardiovascular Associations

PFAS exposure from firefighting foam demonstrates compelling epidemiological links to cardiovascular disease risk factors and events. 1, 2

• Dyslipidemia represents the strongest metabolic outcome associated with PFAS exposure, with the National Academies of Sciences, Engineering and Medicine recommending prioritized screening for dyslipidemia in individuals with high PFAS blood levels 1

• PFAS exposure has been associated with increased cardiovascular disease or death in both cross-sectional and longitudinal observational studies, with evidence concerning early vascular lesions and atherosclerosis 2

• Multiple mechanisms link PFAS to cardiovascular events: altered lipid and glucose metabolism, increased blood pressure, and direct promotion of thrombus formation through platelet membrane incorporation 2

Direct Thrombotic Mechanisms

PFAS directly incorporates into platelet cell membranes, providing mechanistic support for increased cardiovascular events in exposed populations. 2

• PFAS incorporation alters plasma membrane fluidity and calcium signaling, increasing platelet response to agonists both in vitro and ex vivo 2

• All functional platelet responses are enhanced by PFAS incorporation: adhesion, aggregation, microvesicle release, and experimental thrombus formation 2

Firefighter-Specific Exposure Data

Firefighters exposed to AFFF demonstrate PFOS and PFHxS levels one order of magnitude higher than the general population. 3

• Years of jobs with AFFF contact show positive associations with PFOS and PFHxS serum concentrations 3

• Firefighters may be occupationally exposed to PFAS through AFFF, smoke, dust, and turnout gear, in addition to background sources 4

• Exposure from AFFF use is particularly significant near airports and military bases where aqueous film-forming foam has been utilized 5

Asbestos and Cardiovascular Disease

Established Asbestos-Related Diseases

Asbestos exposure causes well-documented pulmonary diseases—asbestosis, pleural disease, and mesothelioma—but lacks established direct causal links to coronary artery disease. 6, 7

• Asbestos fibers induce alveolitis resulting in pulmonary fibrosis, with the degree of fibrosis being dose-dependent 6

• The primary nonmalignant manifestations are respiratory: dyspnea on exertion, nonproductive cough, restrictive lung defects, and accelerated loss of ventilatory capacity 6

• Occupational asbestos exposure historically affected shipyard workers, insulators, construction trades, power plant workers, and boilermakers from World War II through the 1970s 6

Absence of Direct CAD Evidence

The American Journal of Respiratory and Critical Care Medicine guidelines on asbestos-related disease focus exclusively on pulmonary and pleural manifestations, with no mention of coronary artery disease as a recognized outcome. 6

• Clinical evaluation emphasizes respiratory symptoms, pulmonary function tests, and chest radiographic findings rather than cardiovascular assessment 6

• The latency period for asbestos-related disease typically exceeds 15 years, with asbestosis commonly associated with 10-20 years of exposure 6

Jet Fuel Exposure

Limited Cardiovascular Evidence

While occupational exposure to carbon monoxide from gasoline combustion can cause angina and acute myocardial infarction, specific evidence linking jet fuel exposure to coronary artery disease remains insufficient. 8

• Chemical and physical workplace hazards have long been associated with increased cardiac event risk 8

• Carbon monoxide exposure (often from gasoline combustion) may trigger cardiovascular events, and methylene chloride metabolizes to carbon monoxide 8

Occupational Cardiovascular Hazards

Work-related cardiovascular risk extends beyond chemical exposures to include shift work, work pace, and unusual bursts of vigorous activity. 8

• Shift workers demonstrate a 40% increase in CVD risk compared to day workers across 17 studies 8

• Bursts of activity in untrained or at-risk workers combined with particulate exposure may explain increased on-the-job cardiac events in firefighters 8

Clinical Implications

Risk Assessment Priorities

For individuals with occupational exposure to AFFF/PFAS, prioritize screening for dyslipidemia, glucose intolerance, hypertension, and hyperuricemia as intermediate cardiovascular risk markers. 1

• Obtain comprehensive occupational history emphasizing duration, intensity, and timing of AFFF exposure, particularly in firefighting, military, and aviation settings 5, 4

• Consider biomonitoring of PFAS serum concentrations in high-risk occupational groups, as serum levels correlate with years of exposure 3

Asbestos Exposure Management

For asbestos-exposed individuals, focus clinical surveillance on pulmonary manifestations rather than cardiovascular disease, as the latter lacks established causal association. 6

• Document exposure history defining duration, intensity, time of onset, and setting, with emphasis on exposures occurring 15+ years prior 6

• Recognize that brief intense exposures (several months to 1+ year) can cause asbestosis, particularly in confined spaces like shipyards 6