Most epidemiological studies of human papillomavirus (HPV) infections rely on HPV DNA detection. Recent studies have reported very high prevalence and acquisition rates in men.1 However, presence of HPV DNA is not proof of infection, as it might represent environmental contamination.

Studies of HPV DNA on environmental surfaces could provide insights of the possible magnitude of this problem. We studied surfaces that frequently contact anogenital skin: toilet seats in airport restrooms. Apparently clean seats in 23 airports located in 13 countries (Belgium, Denmark, Finland, France, Germany, Italy, Jordan, the Netherlands, Russia, Sweden, Switzerland, Spain and UK) were sampled with the same cytobrush sampling procedure as typically used in HPV-epidemiological studies. β-globin real-time PCR detected human DNA in 101/113 (89%) of samples. PCR using HPV general primers 2 with genotyping using Luminex3 with probes for 13 oncogenic, high-risk HPV types (16, 18, 31, 33, 35 39, 45, 51, 52, 56, 58, 59 and 68, including variants) and 23 non-oncogenic types (6, 11, 26, 30, 40, 42, 43, 53, 54, 61, 66, 67, 70, 73, 74, 81, 82, 83, 86, 87, 89, 9, and 91) was used with 11 negative (water) and 8 positive (HPV plasmid pools) controls run in each assay. The method was proficient in the WHO HPV LabNet global proficiency panel. HPV DNA was found in 22.8% of the 101 β-globin positive samples, with high-risk HPVs being found in 15.8%, HPV-16 in 12.9% and multiple HPV types in 3.0%.

STI particles deposited on environmental surfaces may stay temporarily infectious: for up to 30 h for Chlamydia trachomatis 4 and up to 7 days for HPV.5 A clinical experiment exploring the likelihood of environmental or patient cross-contamination of C trachomatis in clinical samples found that this appeared to be rare if not neglible4 but similar assessments of the proportion of HPV-positives that may be caused by environmental contamination are lacking. Presence of HPV DNA does not necessarily indicate the presence of infectious virus. The present study therefore does not provide any evidence regarding routes of HPV transmission.

Data on incidence, prevalence and clearance of HPV infection in men are essential for the development of models estimating the effect of male HPV vaccination.1

The fact that our environmental surface survey found HPV DNA prevalence comparable with those reported from high sexual risk-taking groups in humans implies that caution is required when interpreting presence of HPV DNA as an ‘infection’.