Gynecologists have experience managing human papillomavirus–associated diseases of the lower genital tract. However, HPV also causes warty disease, dysplasia, and carcinoma of the head and neck. Risk factors for head and neck cancer include smoking and smokeless tobacco use, alcohol consumption, periodontal disease, radiation exposure, and HPV. The incidence of HPV-associated head and neck cancer is rising, particularly among men, at a rate of 2.7% per year.1 The incidence of HPV-associated squamous cell carcinoma of the oropharynx now surpasses that of cervical cancer. Concerns exist regarding occupational exposure to HPV by health care providers (HCP) who perform smoke-generating procedures on HPV-infected tissues, and the potential for them to develop head and neck pathology.
In March of 2020, the American Society for Colposcopy and Cervical Pathology made the recommendation that clinicians who are routinely exposed to HPV should protect themselves against the sequela of occupationally acquired HPV by receiving the HPV vaccine.2 They advocate for the “complete provider team” including physicians, advanced practice providers, nurses, operative technicians, and residents and fellows to be considered for protective vaccination.
Similar to disease patterns in the genital tract, different strains of HPV have differing propensity to cause benign, premalignant, and malignant disease states. HPV 6 and 11 are more commonly associated with warty disease in the nares, pharynx, and tonsillar tissues. HPV 16, 18, 31, and 33 (most commonly 16) are considered high risk for carcinoma formation, particularly of the tonsils and base of the tongue.
The procedures most implicated in occupational HPV exposure include ablative procedures for anogenital warts, laser ablation of vaginal and vulvar dysplasia, and electrosurgical excisional procedures for cervical dysplasia. Smoke plumes from HPV-associated procedures are known to contain HPV for both laser and electrocautery sources.3 A study of 134 patients undergoing surgical procedures for laser ablation of HPV-infected tissues detected concordant strains of HPV in approximately 30% of smoke plumes and approximately 1.5% of surgeons’ nares.4 Not all procedures appear to carry the same risk. Electrocoagulation procedures appear to yield fewer postprocedural positive mucosal swabs for HPV, compared with those taken after CO2 laser.5
Animal studies have shown that papilloma virus procured from smoke plume has the capacity to generate disease. When 10 calves were inoculated with bovine papillary virus obtained from smoke plumes from laser ablation of bovine papillomavirus lesions, all calves manifested BPV fibropapilloma lesions at the sites of inoculation.6
There appears to be an increased incidence of HPV-associated head and neck disease among surgeons who perform procedures on HPV tissues, and there have been multiple case reports that have cited examples of HPV-associated benign and malignant disease among HCPs with frequent occupational exposure to HPV anogenital ablative and excisional procedures.7 While these observations are not proof of causation, they are cause for concern.
While the ASCCP guidelines advocate for HPV vaccination as a strategy for prevention of occupationally related HPV-associated disease, there are other strategies in place to minimize risk. The CDC guidelines for environmental infection control in health care facilities include the following recommendations:
- In settings where surgical lasers are used, wear appropriate personnel protective equipment (PPE), including N95 or N100 respirators to minimize exposure to laser plumes.
- Use central wall suction units with in-line filters to evacuate minimal laser plumes.
- Use a mechanical smoke evaluation system with a high efficiency filter to manage the generation of large amounts of laser plume, when ablating tissue infected with HPV.
- Use local exhaust ventilation (LEV).8
When closely adhered to, these methods appear to provide high-level protection. Data suggest that, when HCPs can access appropriate protective equipment, risks for HPV exposure are low. However, this is more feasible for larger hospital facilities, and may be more limited in outpatient settings. This has led to the consideration of background protection in the form of HPV vaccination for at-risk HCPs. This is analogous to mandates for HCPs to receive hepatitis B vaccination despite the concomitant practice of universal precautions in health care settings. Preventative strategies are typically most efficacious when performed in concert.
After nearly 2 decades of widespread use, we have confidence in the safety of the HPV vaccination. Its benefit through age 45 has been established, leading to the 2018 FDA approval for the 9-valent HPV vaccine, Guardisil-9, for this expanded age group. It would seem logical that systematic administration of the HPV vaccine for at-risk HCPs would be both feasible and safe. There are well-established systems for administering vaccines for HCPs in all health care systems. Perhaps health system administrators should consider routinely offering HPV vaccination for at-risk employees as part of their occupational health care responsibilities. One important caveat being the cost and efficacy of HPV vaccination in this group has not been not established.
In the meantime, it is critical that gynecology providers be aware of their risk for occupational exposure to HPV when using laser and electrocautery techniques on HPV-infected tissues and the potential for them developing head and neck pathology. They should strictly adhere to preventative measures such as use of fit-tested N-95 respirators, mechanical smoke evacuators with high-efficiency filters and work in environments with adequate room ventilation. We all should individually evaluate what role HPV vaccination may play for us in augmenting our own safety.
Dr. Rossi is assistant professor in the division of gynecologic oncology at the University of North Carolina at Chapel Hill.
1. Van Dyne EA et al..
3. Fox-Lewis A et al..
4. Zhou Q et al.
5. Bergbrant I et al..
6. Garden J et al.
7. Harrison R, Huh W..
8. CDC. 1996. DHHS (NIOSH).