Abstract
Cancer of the oral cavity and pharynx is one of the ten most common in the world. In 2008, the age-standardized incidence rate was 8.7 per 100,000 men and 3.4 per 100,000 women, and mortality rate was 7.0 per 100,000 men and 1.7 per 100,000 women. About 90 % of oral cavity and pharynx tumors are histological squamous cell type. Incidence increases with age and peaks between ages of 50 and 70 years. Incidence is higher in more developed regions for males than less developed regions, while mortality is similar between the more and less developed regions. In women, incidence and mortality are higher in less developed regions. In India, these tumors are a heavy health burden in both urban and rural areas. They are responsible for the highest cancer mortality rates in men and are third after breast and uterine cervix tumors in women. Other high-incidence areas are Eastern, Western, and Southern Europe, Australia and New Zealand, and Melanesia. Latin America and the Caribbean have intermediate incidence rates of oral and pharynx cancers; however, rates vary widely between countries in the region and even within those countries. In Brazil, mortality rates from oral cavity cancer are stable in both men and women; however, pharynx cancer is increasing. Increasing incidence of oral and pharynx cancers has been observed in some Western Europe countries. Incidence of oral cavity and pharynx tumors in the United States has been decreasing over the last 30 years. However, increasing incidence in cancer of the tongue, base of the tongue, and the tonsils has been observed in patients under 45 years of age. Nordic countries have also shown increasing incidence of tongue cancer in both male and female young adults.
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Keywords
- Oral cancer
- Pharyngeal cancer
- Occupation
- Asbestos
- Diesel engine exhaust
- Leather dust
- Cotton dust
- Occupational risk factors
- Formaldehyde
- Wood dust
- Welding fumes
Overview
Oral Cavity and Pharynx Cancer
Cancer of the oral cavity and pharynx is one of the ten most common in the world. In 2008, the age-standardized incidence rate was 8.7 per 100,000 men and 3.4 per 100,000 women, and mortality rate was 7.0 per 100,000 men and 1.7 per 100,000 women [1]. About 90 % of oral cavity and pharynx tumors are histological squamous cell type. Incidence increases with age and peaks between ages of 50 and 70 years. Incidence is higher in more developed regions for males than less developed regions, while mortality is similar between the more and less developed regions. In women, incidence and mortality are higher in less developed regions [2]. In India, these tumors are a heavy health burden in both urban and rural areas. They are responsible for the highest cancer mortality rates in men and are third after breast and uterine cervix tumors in women [1]. Other high-incidence areas are Eastern, Western, and Southern Europe, Australia and New Zealand, and Melanesia [3]. Latin America and the Caribbean have intermediate incidence rates of oral and pharynx cancers; however, rates vary widely between countries in the region and even within those countries [4, 5]. In Brazil, mortality rates from oral cavity cancer are stable in both men and women; however, pharynx cancer is increasing [6]. Increasing incidence of oral and pharynx cancers has been observed in some Western Europe countries [7–10]. Incidence of oral cavity and pharynx tumors in the United States has been decreasing over the last 30 years [11]. However, increasing incidence in cancer of the tongue, base of the tongue, and the tonsils has been observed in patients under 45 years of age [12, 13]. Nordic countries have also shown increasing incidence of tongue cancer in both male and female young adults [14, 15].
Nasopharynx Cancer
Incidence of nasopharynx cancer is higher for those in their 50s. Worldwide incidence rates are about 1.7 per 100,000 in men and 0.8 per 100,000 in women, and mortality rates are 1.1 and 0.4 per 100,000, respectively, in men and women [1]. However, incidence is much higher in Southern China, Southeast Asia, the Middle East, and North Africa. In some regions of Southern China, such as Hong Kong, incidence in men reached levels higher than 20 per 100,000, but there has been a remarkable continuous downward trend for these tumors [16–18]. This can mainly be attributed to changes in environmental risk factors within the Chinese population, such as a diet that has been changing to a more Western style; thus, preserved salted fish is no longer a common food for most Chinese households [16]. This downward trend has also been seen in the United States among Chinese Americans living in California [19, 20]. The World Health Organization classifies nasopharyngeal carcinoma into three types according to histology: squamous cell carcinoma (Type I), nonkeratinizing carcinoma (Type II), and undifferentiated carcinoma (Type III). Nonkeratinizing and undifferentiated carcinomas are the most common (>90 %) in high-incidence areas [20–22], and squamous cell carcinoma is the most common (>70 %) in low-incidence regions [20, 21, 23].
Nonoccupational Risk Factors
Oral Cavity and Pharynx Cancer
For a long time, tobacco smoking and alcohol consumption have been recognized as the main causal factors for oral cavity and pharynx tumors; recent pooled analysis and multicenter studies have confirmed this [24–26]. Tobacco smoking and alcohol intake have a dose-response relationship in the occurrence of these tumors; there is also an evident interaction between these two risk factors [27]. Environmental exposure to tobacco smoke in homes and workplace is also associated with oral cavity and pharynx tumors. A pooled analysis of case-control studies has shown the carcinogenic effect of involuntary smoking on head and neck anatomical sites, particularly the pharynx and larynx [28]. Incidence of oral cavity and pharynx cancer is higher among groups of low socioeconomic status [29]. This can be partly explained by higher prevalence of smoking and alcohol consumption in individuals from socially disadvantaged groups [30]. Other factors related to these tumors have also been reported: for instance, diet, where consumption of fruit and vegetables is inversely associated to the risk of these tumors [31]; being underweight, where individuals with low BMI are at increased risk of head and neck cancer (including oral cavity, pharynx, and larynx) [32, 33]; chewing betel quid with or without tobacco, where products commercially available in India are considered carcinogenic to humans, affecting the oral cavity and pharynx with tobacco and just the oral cavity without tobacco [34–36]; and periodontal disease and regular gum bleeding, as well as daily mouthwash use, which may be independent risk factors for oral cavity and pharynx cancer [37, 38]. Poor mouth condition and missing teeth indicate low mouth health care and limited access to dental assistance, both correlated with low socioeconomic status. Human papillomavirus (HPV), particularly HPV16, is associated with oropharyngeal cancer [39]. Increasing incidence of tongue and tonsil tumors seen among those under 45 has been attributed to increasing prevalence of HPV infection in developing countries, practice of oral sex, and number of sexual partners [2, 40, 41]. In addition to environmental factors, familial clustering of oral cavity and pharynx cancer is related to increased risk of oral cavity and pharynx cancer [42].
Nasopharynx Cancer
Nasopharynx cancer is a complex disease; some environmental factors are involved in its origin, probably interacting, and there is also some type of genetic susceptibility. Consumption of salted fish starting in childhood is an important cause of nasopharyngeal cancer in the Chinese population [35, 36], but in contrast to salted fish and other preserved foods, frequent consumption of fresh fruit and vegetables has been linked to a lower risk [21]. Epstein-Barr virus is associated with nasopharynx cancer, but other cofactors must also be present for the disease to manifest [20, 39, 43]. Other factors also associated with nasopharynx cancer are previous chronic ear or nose diseases, such as chronic rhinitis or otitis media [23, 44]; active and passive smoking [23, 36, 44–47]; and the use of Chinese nasal oil and traditional herbal medicine [45, 48]. Additionally, family history of nasopharynx cancer has also been related to increased risk of nasopharynx cancer [44, 45, 49].
Occupational Risk Factors
Oral Cavity and Pharynx Cancer
Some studies have investigated the relationship between occupation and oral cavity and pharynx cancer considering broad categories; Garrote et al. [50] divided subjects into white-collar and blue-collar workers, farmers and housewives, and others, and Menvielle et al. [51] classified their study population into three groups, manual, nonmanual, and agricultural. Tables 4.1 and 4.2 describe 20 case-control and 24 cohort studies which reported an association between specific occupations and industries and oral cavity and pharynx cancer. Several occupations, work in specific industries, and exposure to specific agents have been screened for their carcinogenic potential.
Formaldehyde
Formaldehyde is widely used to manufacture building materials and household products. Most of formaldehyde production is for manufacture of resins, used to make adhesives for pressed wood products. Formaldehyde is also used as a preservative in medical laboratories and mortuaries.
Three of the four case-control studies in Table 4.1, which examined the effect of exposure to formaldehyde in oral and pharynx cancers, found relative risks (RR) of around 1.0 [52–54], whereas Vlajinac et al. [55] found a high risk (RR 4.4, 95 % confidence interval [95 % CI] 0.6–31.6). In a cohort study of workers from ten formaldehyde-producing or formaldehyde-using plants in the United States, Blair et al. [56] found standardized mortality ratio (SMR) of 443 (p < 0.05) for oropharynx cancer in those exposed to cumulative doses of 0.5 parts per million-years (ppm-years) or less; however, SMRs were lower than 100 for those exposed to higher cumulative dose levels. Gardner et al. [57] in a cohort study of six formaldehyde-producing companies in the United Kingdom observed increased SMRs for oral and pharynx cancers in those employed before 1965 and for oral cancer in those employed after 1964. Andjelkovich et al. [58] found SMR 131 (95 % CI 48–286) for workers exposed to formaldehyde in an automotive iron foundry. Marsh et al. [59] in a cohort of workers in a plastic-producing plant found for oral and pharynx cancers SMR of 1.80 (95 % CI 1.22–2.55). Other results from this study, including exposure duration and cumulative exposure to formaldehyde, are difficult to interpret as analysis for pharynx cancer included nasopharyngeal carcinoma. A cohort study in the United Kingdom [60] found SMRs below 2.0 for men with high exposures (estimated as greater than 2.0 ppm). Hauptmann et al. [61] expanded the follow-up from previously cited Blair et al.’s [56] cohort study. Even though risks for oral cavity cancer above 2.0 were found for some average-intensity exposure levels, no dose-response effect was detected. Stayner et al. [62] conducted a mortality cohort study in garment manufacturers, as workers in this industry are potentially exposed to formaldehyde. They concluded that there was a possible relationship between formaldehyde and oral cavity cancer (SMR 343, 95 % CI 118–786). An extension of this cohort until 1998 [63] confirmed increased risks, particularly for oral cavity cancer SMR (3.53, 95 % CI 0.96–9.02), for the original cohort exposure period, but revealed decreased SMRs for the updated period. Several other cohorts were conducted specifically with formaldehyde-exposed professionals, such as pathologists, anatomists, medical laboratory technicians, embalmers, and funeral directors [64–68], but revealed decreased risks of oral and pharynx cancers. A Finnish cohort population [69] did not find any increased risk at the lowest, middle, or highest exposure levels to formaldehyde for oral cavity and pharynx cancer. Innos et al. [70] in a cohort of furniture workers in Estonia detected slight risks for those with possible exposure to formaldehyde. Bosetti et al. [71] conducted the most recent meta-analysis of cohort studies on formaldehyde and cancer risk; related to oral cavity and pharynx, they found RR of 1.09 (95 % CI 0.88–1.34) for industrial workers and RR of 0.96 (95 % CI 0.75–1.23) for professionals. The results of all available studies are inconsistent, and no clear association could be established between exposure to formaldehyde and oral and pharynx cancers [72, 73].
Leather Dust and Leather Industry Work
A case-control study conducted in the United States [74] showed evidence of oral and pharynx cancers in leather industry workers (RR 3.58; p < 0.01). However, three subsequent case-control studies reporting specifically on the leather industry or exposure to leather dust showed less emphatic results: in Brazil [75] the risk was low (RR 1.3), in Italy [53] risk deficits were observed (RR 0.4 for any exposure to leather dust and RR 0.9 for probable or definitive exposure), and in Sweden [54] risks higher than 2.0 were observed, but they were not statistically significant. A cohort study in Finland [69] reported increase risk of oral and pharynx cancers from exposure to leather dust as standardized incidence ratio (SIR) 1.75 (95 % CI 0.36–5.13) for those with medium-category exposure, as no cases were observed at high exposure level. There is no specific cohort study with workers in leather industry. Even though leather dust has been classified by the International Agency for Research on Cancer (IARC) as definitively carcinogenic for humans, into Group 1 [76, 77], from results of available case-control and cohort studies which have investigated exposure to leather dust and oral and pharynx cancers, no conclusive association can be assumed.
Wood Dust and Wood Industry Work
Many case-control studies that have reported an association between wood dust exposure or jobs in wood-related work and oral and pharynx cancers have revealed decreased risks or risks around unity [53, 54, 75, 78–81]. Other studies have found risks ranging from 1.5 to 2.0 for pharyngeal cancer [55, 82, 83]. A case-control study [84] observed a high risk for oral cavity cancer in wood and wood product workers (RR 5.5, 95 % CI 1.2–25.0); and other case-control study [53] found increased risk (RR 5.5, 95 % CI 0.7–44.6) for those exposed for 16 years or more in wood furniture production. A cohort study of United States Coast Guard shipyard workmen [85] detected a high risk (RR 6.20, 95 % CI 2.27–13.50) of oral and pharynx cancers in woodworkers, but analysis included nasopharynx cancer. In Finland, two cohort studies did not reveal any risks of oral and pharynx cancers in woodworkers. In the first [86], decreased risks for oral cancer in construction carpenters and pharynx cancer in woodworkers were found. In the second [69], authors found a protection (SIR 0.79, 95 % CI 0.62–0.99) for oral and pharynx cancers in woodworkers but SIR 1.3 (95 % CI 0.7–2.1) for men and women in the highest category of exposure to hardwood dust. Innos et al. [70] conducted a cohort study in two large furniture factories; they found increased risk of pharynx cancer in men (RR 1.82, 95 % CI 0.83–3.46) and oral cavity cancer in women (RR 1.84, 95 % CI 0.50–4.71). Brown et al. [87] observed increased risk of oral cancer in male wood lacquerers (SIR 2.1, 95 % CI 1.0–3.9), but probably in the context of this cohort study, agents other than those habitually used in wood industry were involved, such as the basic components of paint, varnish, and lacquer, including pigments, resins, and solvents. In general, the risks of oral and pharynx cancers for wood dust or wood industry exposure were imprecise, and no dose-response effect could be observed considering level or time of exposure.
Gustavsson et al. [54] speculated that lowered risk to wood dust exposure could be due to residual confounding from low smoking levels in these workers because of the obvious fire hazard in this activity; however, after subdividing smoking habits into eight increasing cumulative tobacco classes, low RR associated with exposure to wood dust persisted. IARC has classified wood dust in Group 1 [77]; however, specifically for oral and pharynx cancers, results from studies conducted until now do not allow conclusive answers on a causal relationship between wood dust exposure and oral and pharynx cancers.
Cotton Dust and Textile Work
A case-control study of women in the United States [88] found increased risk (RR 3.9, 95 % CI 1.2–12.0) of oral cancer in those with presumed exposure to dust in textile industry for 1–4 years, but no risk was observed for those exposed for 10 years or more. Increased risks were also found in France [78] for pharynx cancer (RR 2.4, 95 % CI 1.0–5.7) and in Italy [53] for oral cancer (RR 2.5, 95 % CI 0.5–9.9). However, many other case-control studies have revealed risk deficits or close to unity values for oral and pharynx cancers in textile dust exposure or textile work [54, 75, 80, 82, 83]. Tarvainen et al. [69] in a cohort study also found risk deficits in men and women exposed to any level of textile dust. This inconsistency in results does not allow the supposition of a causal relationship between cotton dust exposure or textile work and oral and pharynx cancers.
Welding Fumes and Welding as an Occupation
There are many different welding methods which involve exposure to chemicals, such as irritant gases, chromium, polycyclic aromatic hydrocarbons, and metal dust. A case-control study in Sweden [54] found risk excess of pharynx cancer (RR 2.26, 95 % CI 1.09–3.69) in workers exposed to welding fumes for more than 8 years. In another case-control study in Sweden [84], increased risk of oral cancer was detected in welders (RR 2.3, 95 % CI 0.6–9.1). There is little consistency between these findings and results from other case-control [53, 80, 82, 83] and cohort studies [85, 89]. Exposure to welding fumes clearly needs further investigation in order to arrive at a definite conclusion of carcinogenicity for the oral cavity and pharynx anatomical regions.
Diesel Engine Exhaust and Vehicle Repair Mechanics
Recently, IARC considered the evidences of causal association between diesel engine exhaust and cancer as sufficient, particularly for lung cancer [90]. This decision was taken considering a large US National Cancer Institute/National Institute for Occupational Safety and Health study conducted among underground miners [91, 92].
Boffetta et al. [93] conducted a cohort study to evaluate exposure to diesel engine emissions in a Swedish population and found a general SIR of 1.64 (95 % CI 1.11–2.33) for oral and pharynx cancers in women, but no risk was detected for men. Using a job-exposure matrix, exposure was categorized according to probability and intensity as low, medium, and high. Some tenuous positive relative risks were observed, but without a dose-response effect. A cohort study in Finland [69] detected increased risks of mouth and pharynx cancer in men and women with medium levels of exposure to engine exhaust (SIR 1.34, 95 % CI 1.08–1.66) and at the highest level of exposure to engine exhaust (SIR 1.68, 95 % CI 1.09–2.48). Vaughan [82] in a case-control study found a risk higher than 2.0 for vehicle mechanics in repair services, but they examined oral cavity, pharynx, and nasopharynx tumors all together. In a case-control study in Brazil, Andreotti et al. [80] found increased risks, greater than 2.0, for oral and pharynx cancers in every occupation of vehicle mechanic, and for every vehicle repair service job, these risks were augmented considering the restrictions of 10 or more years of exposure and induction period (equal to or greater than 20 years before diagnosis). Vehicle mechanics are potentially exposed to diesel and gasoline engine exhaust, but they are also exposed to other hazardous agents, such as solvents, mineral oils, strong acid fumes, and metal dust. They are therefore exposed to a complex mixture of potential carcinogens. Vehicle mechanics in repair and diesel and gasoline exhaust services are potentially at increased risk of contracting oral and pharynx cancers, but more studies are needed to confirm this relationship.
Other Occupations
Several other occupations, industries, and agents have been linked to oral cavity and pharynx cancer. Certainly, all these circumstances require further studies before a definitive view can be taken on their possible role in the causal chain for the disease.
Exposures in meat industry, such as viruses, nitrosamines, and polycyclic aromatic hydrocarbons, may contribute for elevated cancer risks. Two cohorts have identified increased risks for oral and pharynx cancers in butchers. Johnson et al. [94] in a mortality cohort in the United States found increased risk of oral cavity and pharynx cancer in male meat cutters working in supermarket or grocery store meat departments (SMR 1.8, 95 % CI 1.0–3.0); there was also increased risk for those working as meat cutters in other departments (SMR 1.7, 95 % CI 0.8–3.2). Boffetta et al. [95] in a cohort of butchers and meat workers in Sweden found increased risk for butchers in meat industry (RR 1.6, 95 % 1.0–2.7). Also, a case-control study in Uruguay [96] found increased risk of oral and pharynx cancers in butchers (RR 2.0, 95 % CI 0.4–9.5). In contrast, Coggon and Wield [97] in a cohort study in England and Wales found deficit risks for oral and pharynx cancers in butchers.
Moulin et al. [98] in a cohort study of workers at a man-made mineral fiber (MMMF) factory in France found SIRs of 3.0 for oral and 1.4 for pharynx cancer, both not statistically significant. A Scandinavian cohort of employees in nine factories producing rock-slag wool and glass wool [99] found increased risk of oral cavity and pharynx cancer in those exposed to rock-slag wool (SIR 1.84, 95 % CI 1.22–2.68) but a lower risk for glass wool exposure (SIR 1.31, 95 % CI 0.65–2.34). Two case-control studies reported results for exposure to MMMF; the first [54] found risk deficits for oral or pharynx cancer, and the second [100] reported increased risk for hypopharynx cancer in those ever exposed to mineral wools (RR 1.55, 95 % CI 0.99–2.41).
Marchand et al. [100] found increased risks for those with any exposure to asbestos once (RR 1.80, 95 % CI 1.08–2.99) or cumulative low (RR 1.92, 95 % CI 1.03–3.57) or high exposure (RR 2.14, 95 % CI 1.14–4.01). However, previous case-control studies did not find increased risks of oral and pharynx cancers associated to asbestos [53, 54, 83]. A cohort of Finns born between 1906 and 1945 [69] found increased risks with cumulative asbestos exposure at the lowest (SIR 1.32, 95 % CI 1.08–1.60) and highest levels (SIR 1.26, 1.01–1.55). In a cohort study with construction industry workers [101], an RR of 1.7 was detected (95 % CI 0.9–3.3) for those with moderate exposure to asbestos, but the risk dropped for those with high exposure (RR 0.5, 95 % CI 0.1–5.2).
Several other agents such as chromium, nickel, lead, iron, cadmium, phenoxy acids, solvents, cement dust, asphalt, pesticides, and aliphatic and alicyclic hydrocarbons; occupations such as blacksmiths, bricklayers, drivers, electricians, railway workers, industrial mechanics, painters, metal workers, chemical workers, plumbers and pipe fitters, plastic transformation workers, printers, carpet installers, boiler, furnace and petroleum industry workers, dockers, shoemakers and cobblers, sugarcane farmers, glazers, cutting/sewing workers, hairdressers, dentists, and journalists; and industries such as rubber, paper, pulp, plastics, mining, and building have all been cited as presenting increased risks for oral and pharynx cancers in different cohort and case-control studies. In general, these increased risks were tenuous and imprecise and based in small number of observed cases.
Cooks, waiters, and bartenders, as well as workers at restaurants, bars, and hotels, have shown consistently increased risks of oral and pharynx cancers through some case-control and cohort studies [53, 69, 86]. However, the main hypothesis for these increased risks is the higher prevalence of heavy tobacco smoking and alcohol consumption among these workers.
Nasopharynx Cancer
Tables 4.3 and 4.4 show results of 14 case-control and 7 cohort studies, which examined the association between occupation or exposure to some agents and nasopharynx cancer. Formaldehyde and wood dust showed strong evidence of carcinogenicity to nasopharynx; however, the effect for some other agents and occupations was inconclusive because of results inconsistency among studies.
Formaldehyde
The first epidemiological evidence suggesting an association between exposure to formaldehyde and nasopharynx cancer came in 1986. A mortality cohort study of workers in ten plants producing or using formaldehyde [56] found increased SMRs for different formaldehyde exposure levels. Also a case-control study [52] found increased relative risks for longer exposures. These epidemiological studies were conducted after research with animal models had indicated nasal squamous cell carcinomas occurring in rodents submitted to formaldehyde vapor inhalation [102, 103]. A case-control study in the Philippines [104] has found increased risk for those with long induction period (25 or more years since first exposure). In a cohort study with 14,014 British chemical workers exposed to formaldehyde and followed up for almost 60 years [60], the only death from nasopharynx cancer was of a man whose exposure was classified as low. However, there was evidence of increased death rates from nasopharynx cancer in a cohort of formaldehyde-industry workers by Hauptmann et al. [61], an update of the Blair et al. cohort [56]. This cohort revealed an exposure-response effect for peak and cumulative exposure to formaldehyde, but not for average-intensity exposure or duration.
The study by Hauptmann et al. [61] was a major component in the epidemiological evidence evaluated by the IARC when making their decision on classifying formaldehyde as a definite carcinogen for humans in 2004 [105–107]. Some criticisms on the Haptmann et al.’s [61] cohort study have been addressed, such as the detected association was mainly from one cluster of deaths in a single plant, where five of nine nasopharynx deaths occurred [107]. However, as pointed out by Cogliano et al. [106], in order to classify an agent as carcinogenic, if evidence in humans is insufficient, one should consider that mechanistic evidence and sufficient evidence in experimental animals led to the agent being classified in IARC Group 1. This decision has been upheld in a recent new IARC evaluation [72, 73], and formaldehyde was listed as a known human carcinogen in the 12th Report on Carcinogens of the US National Institute of Environmental Health Sciences [108].
Wood Dust and Wood Industry Work
As well as dust, workers in wood industry may also be exposed to formaldehyde, chlorophenol, and other chemical substances, giving them increased risk of nasopharyngeal cancer. Even so, this increased risk seems to be attributable to wood dust exposure independent to other exposures in the workplace, as the other chemicals do not present relative risks of the magnitude associated to wood dust exposure [77, 109].
In 1983, Armstrong et al. [110] reported increased risk of nasopharynx squamous cell carcinoma in Malaysian Chinese ever exposed to wood dust (RR of 2.2, p = 0.08). Another case-control study in the same population [111] found RR of 2.36 (95 % CI 1.33–4.19) for those exposed once to wood dust and RR of 1.24 (95 % CI 1.07–1.44) for those exposed to a tenfold increased exposure. Almost all other case-control studies that investigated the association between wood-related occupations and nasopharyngeal cancer have found increased risks [22, 79, 112, 113]. However, Vaughan et al. [114] did not find any evidence that exposure to wood dust increased the risk of nasopharyngeal carcinoma, as the modest crude association disappeared after controlling for potential exposure to formaldehyde. Also Siew et al. [115] in a large cohort of Finnish men born from 1906 to 1945 did not find any indication that wood dust and formaldehyde would increase the risk of nasopharyngeal cancer.
In a pooled reanalysis of four American cohorts and one British cohort of wood-related industries [116], excess risks of nasopharynx cancer were found for all combined woodworkers (SMR 2.4, 95 % CI 1.1–4.5), furniture workers (SMR 2.9 95 % CI 1.2–5.9), and plywood workers (SMR 4.6, 95 % CI 0.6–16.4). Mortality risk from nasopharynx cancer was higher in those employed in wood industry prior to 1940 (RR 7.7, 95 % CI 1.6–22.5), but this was restricted to workers from the British cohort as entry into the American cohorts only began in 1946. Increased risks were identified in workers definitively exposed to wood dust from any woodwork (RR 5.3, 95 % CI 1.7–12.4), for furniture workers definitively exposed to wood dust (RR 7.3, 95 % CI 2.4–16.9), and for plywood workers possibly exposed to wood dust (RR 11.8, 95 % CI 1.4–42.5).
The IARC has considered there is sufficient evidence that human exposure to wood dust is carcinogenic to the nasopharynx [109]. This was reaffirmed in a recent revision [77].
Cotton Dust and Textile Work
Several groups of chemicals are found in the textile manufacturing industry; these include flame retardants, textile dyes, solvents, preservatives, and textile prints. Some could be carcinogenic. Also some studies have suggested that cotton dust is a possible carcinogen for the nasopharynx.
In the United States, Roush et al. [117] found a deficit risk for nasopharynx cancer in textile work. In China, Yu et al. [118] also observed decreased risks for those ever exposed to cotton dust at any exposure duration. However, in Malaysia, Armstrong et al. [111] detected RR of 1.77 (95 % CI 0.76–4.11) for those ever exposed to cotton dust and RR of 1.16 (95 % CI 0.94–1.42) for those with a tenfold exposure to cotton dust. Li et al. [119] conducted a case-cohort study in Shanghai and detected increased risks of nasopharyngeal cancer for those exposed to cotton dust: RR of 2.7 (95 % CI 1.2–5.7) for less than 10 years and RR of 1.6 (95 % CI 0.9–2.9) for 10 years or more. An RR of 3.6 (95 % CI 1.8–7.2) was found for those with the highest cumulative exposure to cotton dust category (>143.4 mg/m3 × years). The same study has also found increased risks of nasopharynx cancer for those in the textile industry exposed to acids, bases and caustics, dyes, and inks.
The IARC classifies cotton dust and working in textile industry as possibly carcinogenic to humans (Group 2B) [120]. Results from case-control studies conducted during the last decade of the twentieth century were more incisive on the relationship between cotton dust exposure and nasopharyngeal cancer. Also workers in textile industry have a possible increased risk of nasopharyngeal cancer. Nevertheless, no definite conclusion could be taken at this point on this relationship.
Other Occupations
Evidence linking nasopharynx cancer to other occupational risk factors is less definitive, as the number of studies is limited and results are conflicting. Henderson et al. [121] in a case-control study found increased risks of nasopharynx cancer for fumes, smoke, and chemicals, but not for dusts. Yu et al. [118] found increased risks for smoke and chemical fumes, but not for dusts. Armstrong et al. [111] did not find risks for exposure to chemicals, fumes, or dusts.
Chlorophenols are classified by IARC as possibly carcinogenic to humans – Group 2B [122]. A series of case-control studies have found relationships between exposure to chlorophenols and nasopharynx cancer. Hardell et al. [123] found about a sevenfold risk of nasopharyngeal and nasal cancer analyzed together for exposure to chlorophenols in the wood industry. Mirabelli et al. [124] also found high risks for those classified as ever exposed to high levels of chlorophenols (RR 2.64, 95 % CI 1.10–5.78) and even higher risks for those exposed for less than 10 years (RR 3.52, 95 % CI 1.07–9.73) or 10 years or more (RR 9.07, 95 % CI 1.41–42.9). Zhu et al. [23] found increased risks of nasopharyngeal squamous cell carcinoma in people exposed to chlorophenol (RR 2.2, 95 % CI 1.1–4.3).
Two case-control studies have examined the effect of industrial heat on nasopharynx cancer. Henderson et al. [121] found increased risks, around 1.5, but these were not statistically significant. Armstrong et al. [111] also found increased risks of nasopharynx cancer for heat exposure of RR of 1.23 (p = 0.021), after adjustment for wood dust, diet, and cigarette smoke. Increased risks of nasopharynx cancer were also found for exposure to combustion products in a case-control study in China [118] with RR of 2.7 (p < 0.05) for those with occasional exposure and RR of 10.1 (p < 0.05) for those exposed for 10 years or more. The limited number of studies does not permit definitive conclusions to be made on the effect of industrial heat on nasopharynx cancer.
A case-control study in Taiwan [22] explored the effect of organic solvents on nasopharynx cancer, but risks were low and imprecise, and no dose-response effect was detected.
Zhu et al. [23] found increased risk for all histological types of nasopharyngeal cancer in people working with or around cutting oil (RR 1.9, 95 % CI 1.1–3.1); and increased risk of squamous cell carcinoma was found for occupational exposure to chromium compounds or alloys (RR 2.6, 95 % CI 1.1–6.1). Malker et al. [125] in a cohort study in Sweden found increased SIRs for glassmakers, bookbinders, and cobblers and in shoe repair and fiberboard industries.
Further studies are needed for all these occupational factors in order to have a clearer definition of their carcinogenic role on the nasopharynx.
Conclusion
The efforts to decrease major occupational risk factors for oral, pharyngeal, and nasopharyngeal cancers depend on the knowledge of potential carcinogen agents present in a particular occupation in different industry settings and the effective surveillance and prevention of workers’ exposure to these agents. Table 4.5 shows the carcinogenicity evidence strength of some agents, occupations, or industries on oral cavity, pharyngeal, and nasopharyngeal anatomical sites.
Asbestos, diesel engine exhaust, leather and wood dust, man-made mineral fibers, and welding fumes have a possible association with oral and pharyngeal cancers. Waiters, cooks, and bartenders have a high risk of oral and pharyngeal cancers; however, the prevalence of tobacco smoking and alcohol consumption is higher among these workers than those in other occupations, and this fact could be the straightest explanation for the risk observed. Butchers, vehicle repair mechanics, welders, and woodworkers have showed evidences of possible increased risk of oral and pharyngeal cancers. Regarding the type of industry, jobs in the leather industry, man-made mineral fiber manufacturing, meat industry, vehicle repair service, and wood industry have also presented a possible impact on oral and pharyngeal cancer incidence.
There are convincing documentation on the causal relationship of exposure to chlorophenols, formaldehyde, and wood dust with nasopharyngeal cancer, as well as among woodworkers and in garment manufacturing. The carcinogenicity evidences of cotton dust and heat in the workplace to the nasopharynx are limited.
Additional studies are necessary to confirm the association of many suspicious agents, occupations, and industries with oral cavity, pharyngeal, and nasopharyngeal cancers. Nevertheless, the knowledge accumulated so far enables prevention and safety at work. That can be triggered in the context of surveillance programs, particularly considering exposure to chlorophenols, formaldehyde, and wood dust. For example, a well-oriented control of exposure to dust in the wood industry would prevent not only many cases of nasopharyngeal and sinonasal cancers but also probably some cases of pharyngeal, laryngeal, and lung tumors.
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Filho, V.W. (2014). Cancer of the Oral Cavity, Pharynx, and Nasopharynx. In: Anttila, S., Boffetta, P. (eds) Occupational Cancers. Springer, London. https://doi.org/10.1007/978-1-4471-2825-0_4
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