There is not much data referring to the asbestos exposure situation in Korea and internationally. Also most of the data was concerns about asbestos exposure in asbestos mines, the textile industry, shipbuilding industry and automobile maintenance service rather than the construction industry. In the case of Dutch workers working in the asbestos cement industry, the groups working with the raw materials were exposed to an average of 7.5 f/cc of asbestos in the 1970s and the exposure level gradually decreased [13]. In a study of malignant mesothelioma, which is an indicator of asbestos exposure, the incidence rate was 5.8 times (95 % PI 5.3–6.5) higher in construction site workers [14]. In this case, because of absence of working environment measurement, we need to estimate asbestos exposure through exposure reconstruction using literature reviews. There are asbestos Exposure assessment studies according to industry. In the American workers, Considering the entire dataset that contained air sampling data from 1984 to 2011, not accounting for outliers, personal asbestos concentrations ranged from non-detectable (ND) to a maximum of 175 f/cc [15]. From 1984 to 1989, personal air samples of operative builder with detectable asbestos concentrations ranged from 0.001 to 16.1 f/cc. From 1990 to 1999, concentrations ranged from 0.003 to 13.2 f/cc, and from 0.0024 to 0.32 f/cc in the 2000s, respectively. Finally, from 2010 to 2011, personal air samples ranged in concentrations from 0.13 to 0.19 f/cc. In the Iran’s construction workers, during demolition of old house, Personal monitoring of asbestos fiber levels indicated a range from 0.01 to 0.15 PCM f/ml (0.02–0.42 SEM f/ml) [16]. In Korea, a study of Job exposure-matrix of asbestos was conducted by reviewing about literatures reported [17]. Construction industry was classified as third exposed group, in 1996 in 18 samples concentrations ranged from 0.01 to 0.32 f/cc (GM 0.05), in 2001 in the two samples concentrations were detected by 0.01 f/cc, in 2006 in the twelve samples concentrations ranged from 0.00 to 0.06 f/cc (GM 0.01) [17]. However, About the exposure study of building demolition workers which was expected to be exposed to a high concentration of asbestos, In 2002, concentrations ranged from 0.014 to 0.419 f/cc. In the case of the worker, because it is not enough to reconstruct job exposure matrix, we couldn’t estimate asbestos exposure dose. But, estimating asbestos exposure from historical data by year, from 1971 to 1995 there is no previous exposure data in the construction industry, so using previous exposure data in the shipbuilding and automobile maintenance services, we estimated minimum asbestos concentration ranged from 0.046 to 0.866 f/cc, from 1995 to 2000 concentrations ranged from 0.1 to 0.2 f/cc, after 2000, concentrations ranged from 0.01 to 0.05 f/cc. And during demolition that account one-third of the total construction process, it is estimated that asbestos concentration was twice to five times than that of construction process. Based on this, we estimated approximately that cumulative asbestos exposure of this worker was minimum 10 f/cc*year.
The worker in this case did not have pleural plaques or pleural thickening in chest X-rays. However, pleural plaques can be an indicator of asbestos exposure, they are not observed in all workers exposed to asbestos [18], and general radiographic examinations of the chest do not have high sensitivity or specificity [19]. This worker underwent endoscopy, biopsy and PET-CT so chest CT exam was not performed as it did not seem useful for the diagnosis.
Since smoking and drinking are the most important risk factors for laryngeal cancer, occupational risk factors have not been much studied in Korea. However, one factor identified in other countries is asbestos exposure, and others include exposure to diesel combustion material, polycyclic aromatic hydrocarbons (PAH), silica, welding fumes, nickel, sulfuric acid mist, rubber manufacturing, etc. and tree dust, formaldehyde, cement dust are known to make a small contribution [20–22].
Asbestos is a representative factor in relation to laryngeal cancer in an occupational and environmental medicine perspective. Various epidemiologic studies have examined about the correlation between laryngeal cancer and asbestos exposure. In a case–control study conducted in France on 1,833 patients with head and neck squamous cell carcinoma, asbestos exposure increased the risk of laryngeal cancer (OR 2.1, 95 % CI 1.6–2.8), and the risk increased with the length and severity of asbestos exposure [23]. Also in a study conducted on 307,799 Swedish industrial workers, 227 workers were diagnosed with laryngeal cancer, and asbestos exposure increased its incidence by RR 1.9, 95 % CI 1.2–3.1 [24].
However until recently there has been controversy over the relation between laryngeal cancer and asbestos exposure. In a Dutch study conducted on 58,279 patients, glottic cancer was correlated with organ exposure to asbestos, and supraglottic cancer was more strongly correlated [25]. However a meta-analysis of 69 studies referring to asbestos found no significant dose–response relationship between asbestos and laryngeal cancer [26].
Until 2009, the IARC accepted only limited evidence of asbestos being carcinogenic for laryngeal cancer. However in 2009, a report of a discussion about cancer and asbestos among 27 scientists from 8 countries held during an IARC was published in Lancet Oncology. In the report, it was suggested that there was adequate evidence that lung cancer, mesothelioma, ovarian cancer and laryngeal cancer could be caused by asbestos [12]. The IARC described the evidence in an IARC monograph (100C, 2012) citing cohort studies, case control studies, meta-analysis studies, etc.. In a meta-analysis of cohort studies by the Institutive of Medicine (IOM), the RR of the exposed group to the non-exposed group was 1.4 (95 % CI: 1.17–1.64), and the RR of the group exposed to high concentrations was 2.02 (95 % CI: 1.64–2.47) when applying the low standard, and 2.57 (95 % CI: 1.47–4.49) when applying the high standard (Some studies reported dose–response relationship on multiple gradient metrics. In computing the summary RR, “lower standard” calculation used the smallest “high vs. none” RR, and “high standard” calculation used largest “high vs. none” RR). In the meta-analysis of case control studies, the RR before adjusting for drinking and smoking was 1.43 (95 % CI: 1.15–1.78) and 1.18 (95 % CI: 1.01–1.37) after adjusting [27]. There is a need for additional quantitative exposure studies, such as studies of cumulative asbestos exposure, but it is now generally accepted that high concentration of asbestos or long term exposure to asbestos can cause laryngeal cancer in exposed occupational clusters.
The worker in this case worked as a supervisor for 38 years from the age of 19 in 1971 in material inspection, site inspection and site management. He did not handle asbestos directly but was constantly exposed to asbestos while inspecting asbestos-containing materials and working on site. In particular he participated in the entire process of demolition of previous buildings from site inspection to completion of demolition so he can be assumed to have been exposed to large amounts of asbestos. Therefore the laryngeal cancer which occurred in this worker is considered to be work-related.
This study has some limitations. First, in his occupational history before 1996, the worker’s activities in supervision and design were not defined. Therefore we could not calculate the precise exposure time. Second, we assumed that the risk factors for head and neck tumors and laryngeal cancer were similar, and this assumption needs more investigation. Third, level of the construction work environment was not measured, and past asbestos exposure was estimated from the statements of the worker. Fourth, there were no pleural plaques or pleural thickenings in the chest X-rays, so that exposure could not be proved by an objective standard. Finally, for this worker, we can’t rule out the laryngeal cancer due to other risk factors such as cement and silica in the workplace. Also, it could have been caused by the interaction between asbestos and other factors.
Despite these limitations, this study is the first case report suggesting a relation between exposure to asbestos and the development of laryngeal cancer in Korea. However, further epidemiological and experimental studies are needed in order to prove this connection definitively.