Formaldehyde and cancer risk: a quantitative review of cohort studies through 2006.

BACKGROUND: Occupational exposure to formaldehyde has been associated with excess risk of nasopharyngeal and selected other cancers. PATIENTS AND METHODS: We reviewed and pooled the results of cohort studies published through February 2007. RESULTS: There were 5651 deaths from all cancers observed in six cohorts of industry workers and six of professionals, with a pooled relative risk (RR) of 0.95 for industry workers and of 0.87 for professionals. Nine deaths from nasopharyngeal cancer in three cohorts of industry workers yielded a pooled RR of 1.33, which declined to 0.49 after excluding six cases from one US plant. The pooled RR for lung cancer was 1.06 in industry workers and 0.63 in professionals. Corresponding values were 1.09 and 0.96 for oral and pharyngeal, 0.92 and 1.56 for brain, 0.85 and 1.31 for all lymphatic and hematopoietic cancers, and 0.90 and 1.39 for leukemia. CONCLUSIONS: Comprehensive review of cancer in industry workers and professionals exposed to formaldehyde shows no appreciable excess risk for oral and pharyngeal, sinonasal or lung cancers. A non-significantly increased RR for nasopharyngeal cancer among industry workers is attributable to a cluster of deaths in a single plant. For brain cancer and lymphohematopoietic neoplasms there were modestly elevated risks in professionals, but not industry workers.     

Cancer among epileptic patients exposed to anticonvulsant drugs

Cancer incidence among 8,004 patients hospitalized for epilepsy between 1933 and 1962 in the Filadelfia treatment community in Denmark was compared to that of the general population. Patients received powerful and prolonged treatment with phenobarbital, phenytoin, and other anticonvulsants. This new survey extends the follow-up from 1976 through 1984. Among 7,864 patients with epilepsy not known to have received radioactive Thorotrast, record linkage with national cancer incidence files identified 789 cancers, compared to 664 expected [relative risk (RR) = 1.19; 95% confidence interval = 1.11-1.27]. Significant risks were found for cancers of the brain and central nervous system (RR = 5.7; n = 118) and the lung (RR = 1.4; n = 106). The excess numbers of brain cancer were concentrated within 10 years of hospitalization (RR = 20.7; n = 80) and decreased significantly over time, which suggests that brain tumors account for the seizure disorder and are not due to phenobarbital exposure as suggested by some epidemiologic studies. No overall risk was apparent when brain cancers were excluded (RR = 1.03). Because bladder cancer was significantly decreased (RR = 0.6; n = 18), the excess risk of lung cancer may not have been related to the "anecdotal" heavy smoking reported among confined groups of epileptic patients in the early years of the study period. The incidence of malignant melanoma was also significantly low (RR = 0.5; n = 7), which suggested limited exposure to sunlight among confined patients. The risk of non-Hodgkin's lymphoma was increased, but not significantly (RR = 1.4; n = 16), which is interesting in view of previous reports suggesting an association with phenytoin. Overall, these data provide little evidence that phenobarbital and phenytoin are carcinogenic to humans, but the excess risks of lung cancer and non-Hodgkin's lymphoma among epileptic patients in our study deserve further evaluation.     

Silica dust and lung cancer: results from the Nordic occupational mortality and cancer incidence registers

Autopsy studies of the relationship between silicosis and lung cancer have been mainly negative; but recent epidemiologic studies have indicated a positive association, and an excess lung cancer risk has been observed in some occupational groups with exposure to silica dust. For the further shedding of light on the possible association between silica dust and lung cancer, analysis was made on mortality and cancer incidence data available in census-based record linkage studies from the Nordic countries for males in occupational groups with potential exposure to silica dust. The study showed an excess lung cancer risk for foundry workers in all the Nordic countries and for miners in Sweden. These results were consistent with findings from previous in-depth epidemiologic studies. The lung cancer risk did not differ significantly from that of the respective national populations for males working in excavation; stone quarries; sand and gravel pits; and glass, porcelain, ceramic, and tile manufacture. Stonecutters, who are probably not exposed to known lung carcinogens at the workplace but in some places to high concentrations of silica dust, showed a significant excess lung cancer risk in both Finland and Denmark. Excess lung cancer risks furthermore were seen for Finish miners, for Finnish males in excavation work, and for Danish glassworkers.     

Herbicides and cancer.

Herbicides are a heterogeneous class of chemicals used in agriculture, forestry, and urban settings to kill weeds, shrubs, and broad-leaved trees. The role of herbicides in the etiology of cancer is controversial. Potential studies for review were identified through a MEDLINE search and from a check of references in related review articles. This review of the literature shows reasonable evidence suggesting that occupational exposure to phenoxy herbicides results in increased risk of developing non-Hodgkin's lymphoma. Several studies have noted large increases in risk of soft-tissue sarcomas with phenoxy herbicide exposure. In contrast, others have failed to observe increased risks, and evidence of an exposure-risk relationship is lacking. Although there have been too few appropriate studies for adequate assessment of risk of cancer at other sites, some findings have linked herbicide exposure with cancers of the colon, lung, nose, prostate, and ovary as well as to leukemia and multiple myeloma. Future studies must better identify and quantify the nature of herbicide exposures. In the interim, it seems only prudent to monitor and promote safety practices among persons occupationally exposed to phenoxy herbicides, particularly farmers and professional sprayers.     

Asbestos cancers as an example of the problem of comparative risks.

Major differences in excess cancer risks have occurred in the asbestos industry in the past; part of this difference is probably related tp dustiness, part to the type of fibre used. In the case of mesotheliomas there is evidence of a major effect of the fibre type in the order of risk, crocidolite greater than amosite greater than chrysotile greater than anthophyllite. Differences of risk within an industry indicate that there is a dose response relation for both bronchial cancers and mesotheliomas. Also that in some instances it has been possible to identify lightly exposed groups in which no excess risks were detectable. As these least exposed groups are likely to have had several orders of magnitude heavier exposure than the general population, the risks to the general public are likely to be negligible. Bronchial cancers in absolute numbers are the major excess risk and are highly smoking-related. Stopping cigarette smoking is likely to be of paramount importance in reducing the excess cancer risks in asbestos-exposed individuals. Cancers in other sites which may possibly be related to asbestos exposure need further study even though the magnitude of the excess risk has been small compared to the lung cancers. In my view it is now possible to use the epidemiological evidence and experimental results to predict with fair confidence the physical and chemical characters and dose of natural and man-made fibres which will not cause a significant hazard in the future.     

Occupational exposure to solvents and bladder cancer: A population‐based case control study in Nordic countries

The objective of the study was to assess the relationship between exposure to selected solvents and the risk of bladder cancer. This study is based on the Nordic Occupational Cancer (NOCCA) database and comprises 113,343 cases of bladder cancer diagnosed in Finland, Iceland, Norway and Sweden between 1961 and 2005 and 566,715 population controls matched according to country, sex and birth year. Census‐based occupational titles of the cases and controls were linked with the job exposure matrix created by the NOCCA project to estimate quantitative cumulative occupational exposures. A conditional logistic regression model was used to estimate hazard ratios (HRs) and their 95% confidence intervals (95% CI). Increased risks were observed for trichloroethylene (HR 1.23, 95% CI 1.12–1.40), toluene (HR 1.20, 95% CI 1.00–1.38), benzene (HR 1.16, 95% CI 1.04–1.31), aromatic hydrocarbon solvents (HR 1.10, 95% CI 0.94–1.30) and aliphatic and alicyclic hydrocarbon solvents (HR 1.08, 95% CI 1.00–1.23) at high exposure level versus no exposure. The highest excess for perchloroethylene was observed at medium exposure level (HR 1.12, 95% CI 1.02–1.23). The study provides evidence of an association of occupational exposure to trichloroethylene, perchloroethylene, aromatic hydrocarbon solvents, benzene and toluene and the risk of bladder cancer.     

Lung cancer mortality among pottery workers in the United States

A proportionate mortality study suggested that members of the International Brotherhood of Potters and Allied Workers in the United States had an elevated frequency of deaths from non-malignant respiratory disease (PMR = 1.54) and lung cancer (PMR = 1.21). The lung cancer excess occurred exclusively among pottery workers employed in the manufacture of plumbing fixtures (PMR = 1.80). A subsequent cohort study examined mortality among 2055 white men employed in three ceramic plumbing fixture factories. There was a significant excess of non-malignant respiratory disease (SMR = 1.73). Lung cancer mortality was also higher than expected (SMR = 1.43) and was highest among workers whose jobs involved simultaneous exposure to silica and non-fibrous talc (SMR = 2.54). Lung cancer mortality risk increased with increasing number of years of exposure to non-fibrous talc and showed no pattern by number of years of exposure to silica. Among men exposed to talc, lung cancer risk increased with years since first non-fibrous talc exposure and decreased with age at first exposure. The data suggested an association between exposure to non-fibrous talc and excess lung cancer risk; however, the role of silica as a co-factor or promoting agent could not be ruled out.     

Pesticides and cancer risks in agriculture

The work environment in agriculture is complex, with many potentially hazardous exposures, but the overall mortality from cancer and other causes is rather low among farmers. However, several studies have consistently indicated an excess of certain cancer forms. Lymphomas, leukemias, multiple myeloma and also malignancies of connective tissue attract special interest, as being possibly associated with the use of pesticides. Phenoxy acid herbicides may play an etiological role, especially for non-Hodgkin's lymphoma, whereas the findings are more ambiguous for Hodgkin's disease and soft-tissue sarcoma, perhaps indicating an interaction with co-factors. The issue has been controversial for many years, however, and one of its aspects involves the use of phenoxy acids in the Vietnam war. Furthermore, DDT has been associated with lung cancer in mixed exposure situations, and with chronic lymphatic leukemia. Arsenical pesticides may have caused skin cancer in vine-growers. Further studies, especially of specific user groups and producers, may avoid the complex exposure situation in agriculture.     

Atributable risk of breast,prostate, and lung cancer in Hawaii due to saturated fat

The dietary data from case-control studies of breast, prostate, and lung cancer in Hawaii revealed that saturated fat was a risk factor for these malignancies. The dietary intakes from the three studies were used to calculate the attributable risk (AR) due to saturated fat. For all ethnic groups combined, the ARs for the highest quartiles of intake were 14.9 percent for female breast cancer, 13.0 percent for prostate cancer, and 23.1 percent for male lung cancer. Our results suggested that a reduction of saturated fat to the lowest quartiles of intake could result in a 10 to 20 percent decrease in risk for these three cancers in Hawaii. We also examined the ethnic-specific risks associated with saturated fat consumption among the Japanese and the Caucasians in the three studies. The ARs for the highest quartiles of intake were notably higher among the Caucasians than the Japanese, primarily due to the difference in their dietary patterns. Although the calculated AR due to saturated fat was higher among the Caucasians than among the Japanese, all persons in the population would derive considerable benefit by reducing their intake of this nutrient.Authors are with the Epidemiology Program, Cancer Research Center of Hawaii, University of Hawaii, 1236 Lauhala Street, Honolulu, HI 96813, USA. Address correspondence to Dr Hankin. This study was supported in part by NIH Grant PO1 CA 33619.     

Skin cancer and non-Hodgkin's lymphoma as second malignancies. markers of impaired immune function?

Successes in cancer therapy have led to increasing numbers of cancer survivors, who are at risk of developing second primary cancers. Therapy- or disease-induced suppression of the immune function may predispose cancer patients to a second malignancy. An excess of squamous cell skin cancers (SCC) and non-Hodgkin's lymphomas has been found in immunosuppressed patients. We used the nationwide Swedish Family-Cancer Database on 10.2 million individuals to calculate the risk of second primary skin cancers and non-Hodgkin's lymphomas following a previous malignancy. A total of 4301 second skin cancers and 1672 non-Hodgkin's lymphomas were identified. Standardised incidence ratios (SIR)s and 95% Confidence Intervals (CIs) were calculated and compared. Among 14 different sites for male or female first primary malignancies, 11 of these sites were followed by an increased risk of skin cancer (SIRs for males for risk of skin cancer as a second primary cancer: 14.1 for SCC; 9.7 for melanoma; 6.1 for leukaemia as the first site; SIRs for females for risk of skin cancer: 14.6 for SCC; 6.8 for larynx; 6.2 for upper aerodigestive tract (UADT) as the first site). The risk of non-Hodgkin's lymphoma was increased after 10 of 14 different male neoplasms and 12 of 17 different female neoplasms. (SIRs for males for risk of non-Hodgkin's lymphoma as a second primary cancer: 6.4 for non-Hodgkin's lymphoma; 3.2 for leukaemias; 3.1 for multiple myeloma as the first site; SIRs for females for risk of non-Hodgkin's lymphoma as a second primary cancer: 12.5 for leukaemias; 7.0 for Hodgkin's disease; 3.6 for UADT as the first site). The high, and after certain sites, very high risks of second skin cancer and non-Hodgkin's lymphoma suggest that immune suppression may be a contributory mechanism.     

Cancer risks in men who had children with different partners from the Swedish Family-Cancer Database.

We used the nation-wide Swedish Family-Cancer Database to analyse cancer risks in men who had had children with more than one woman. Cancer cases were retrieved from the Swedish Cancer Registry from years 1961-1998. A total of 2.9 million men and 298,134 cancer cases were covered. For men having children with two, three or more women, increasing risk trends were shown for upper aerodigestive tract, lung, urinary bladder and oesophageal cancers. Decreasing trends were observed for tumours of the colon, skin (squamous cell and melanoma), nervous system and endocrine glands and against myeloma and non-Hodgkin's lymphoma. The present results indicated that men who had had children with multiple women showed an excess of smoking- and alcohol consumption-related cancers. The decreased risks for colon cancer, non-Hodgkin's lymphoma and melanoma were possibly related to lifestyle factors connected with economic deprivation, less obesity and physical fitness. These ill-defined protected factors may be a challenge to epidemiological studies.     

Occupational groups potentially exposed to silica dust: a comparative analysis of cancer mortality and incidence based on the Nordic occupational mortality and cancer incidence registers

We have analysed mortality and cancer incidence data available in census-based record-linkage studies from the Nordic countries for males in occupational groups with potential exposure to silica dust. The study showed an excess lung cancer risk for foundry workers in all the Nordic countries, and also for miners in Sweden. These results are consistent with the findings of previous in-depth epidemiological studies. The lung cancer risk did not differ significantly from that of the respective national populations for males working in glass, porcelain, ceramics and tile manufacture, in excavation, and in stone quarries, sand and gravel pits. Stone cutters, who are probably not exposed to known lung carcinogens at the workplace but in some places to high concentrations of silica dust, showed a significant excess lung cancer risk in both Finland and Denmark.     

Heterocyclic aromatic amine pesticide use and human cancer risk: Results from the U.S. Agricultural Health Study

Imazethapyr, a heterocyclic aromatic amine, is a widely used crop herbicide first registered for use in the United States in 1989. We evaluated cancer incidence among imazethapyr‐exposed pesticide applicators enrolled in the Agricultural Health Study (AHS). The AHS is a prospective cohort of 57,311 licensed pesticide applicators in the U.S., enrolled from 1993–1997. Among the 49,398 licensed pesticide applicators eligible for analysis, 20,646 applicators reported use of imazethapyr and 2,907 incident cancers developed through 2004. Imazethapyr exposure was classified by intensity‐weighted lifetime exposure days calculated as [years of use × days per year × intensity level]. Poisson regression analysis was used to evaluate the relationship between imazethapyr exposure and cancer incidence. We found significant trends in risk with increasing lifetime exposure for bladder cancer (p for trend 0.01) and colon cancer (p for trend 0.02). Rate ratios (RRs) were increased by 137% for bladder cancer and 78% for colon cancer when the highest exposed were compared to the nonexposed. The excess risk for colon cancer was limited to proximal cancers, (RR = 2.73, 95% confidence intervals 1.42, 5.25, p for trend 0.001). No association was observed for prostate, lung, rectum, kidney, oral, pancreas, lymphohematopoietic cancers or melanoma. These findings provide new evidence that exposure to aromatic amine pesticides may be an overlooked exposure in the etiology of bladder and colon cancer. The use of imazethapyr and other imidazolinone compounds should continue to be evaluated for potential risk to humans. Published 2008 Wiley‐Liss, Inc.     

Carcinogenicity of benzene, toluene and xylene: epidemiological and experimental evidence

Benzene. The evidence for carcinogenicity of benzene in humans was evaluated by the IARC in 1982 as follows: "It is established that human exposure to commercial benzene or benzene-containing mixtures can cause damage to the haematopoietic system, including pancytopenia. The relationship between benzene exposure and the development of acute myelogenous leukaemia has been established in epidemiological studies. "Reports linking exposure to benzene with other malignancies were considered to be inadequate for evaluation. "There is sufficient evidence that benzene is carcinogenic to man." This evaluation now warrants some elaboration and updating. While the epidemiological evidence concerning benzene carcinogenicity is strongest for acute myelocytic leukaemia, there is some limited evidence of increased risks of chronic myeloid and chronic lymphocytic leukaemia. In addition, recent studies have suggested an increased risk of multiple myeloma, while others indicate a dose-related increase for total lymphatic and haematopoietic neoplasms. Corroborative evidence for such a generalized effect comes from experimental studies showing that exposure to benzene depresses all lympho-haematopoietic cell lines. While only limited evidence of benzene carcinogenicity in experimental animals exists, the recent findings of the National Toxicology Program (NTP, 1984) in the U.S.A. and Maltoni et al. (1985) strongly indicate that benzene is an experimental carcinogen. Toluene and xylene. While no direct human evidence is available, there is recent evidence of carcinogenicity of toluene and xylene at high concentrations in experimental animals. It should also be noted that any future epidemiological observations of cancer risks associated with toluene or xylene would have to take account of the suspected effects of benzene impurities.     

Exposure to environmental tobacco smoke and the risk of lung cancer: a meta-analysis

A meta-analysis was carried out to calculate a pooled estimate of relative risk of lung cancer following exposure to environmental tobacco smoke (ETS) and to determine whether there was any heterogeneity in the pooled estimates according to selected characteristics of the studies. A total of 35 case-control and five cohort studies providing quantitative estimates of the association between lung cancer and exposure to ETS published between January 1981 and March 1999 were identified. Using fixed- and random-effects models, we calculated pooled estimates of relative risk for exposure to ETS from subjects' parents (during childhood), spouses, and coworkers. As well, we investigated whether the pooled estimates of relative risk varied by study location, degree of control of potential confounding variables, proportion of cases confirmed histologically, proportion of surrogate respondents, nonresponse rates, and year of publication. The relative risk of lung cancer among non smoking women ever exposed to ETS from their husbands' smoking was 1.20 (95% confidence interval (CI): 1.12-1.29). The pooled relative risk was 1.19 (95% CI: 1.10-1.29) for case-control studies and 1.29 (95% CI: 1.04-1.62) for cohort studies. In various subgroup and meta-regression analyses, we found no statistically significant differences by selected characteristics of the studies. In addition, we found that the risk of lung cancer increased consistently with increasing levels of exposure. The 11 studies reporting relative risks among male non smokers yielded a pooled relative risk of 1.48 (95% CI: 1.13-1.92) for ever exposed to ETS, and the relative risk of lung cancer for ever being exposed to ETS at work was a 1.16 (95% CI: 1.05-1.28). These results are consistent with the hypothesis that exposure to ETS increases the risk of lung cancer. While there may be alternative explanations to the data, it is more likely that the observed association is not an artifact and that ETS causes lung cancer in non smokers.     

Indoor radon and lung cancer in China

Radon has long been known to contribute to risk of lung cancer, especially in undergound miners who are exposed to large amounts of the carcinogen. Recently, however, lower amounts of radon present in living areas have been suggested as an important cause of lung cancer. In an effort to clarify the relationship of low amounts of radon with lung cancer risk, we placed alpha-track radon detectors in the homes of 308 women with newly diagnosed lung cancer and 356 randomly selected female control subjects of similar age. Measurements were taken after 1 year. All study participants were part of the general population of Shenyang, People's Republic of China, an industrial city in the northeast part of the country that has one of the world's highest rates of lung cancer in women. The median time of residence in the homes was 24 years. The median household radon level was 2.3 pCi/L of air; 20% of the levels were greater than 4 pCi/L. Radon levels tended to be higher in single-story houses or on the first floor of multiple-story dwellings, and they were also higher in houses with increased levels of indoor air pollution from coal-burning stoves. However, the levels were not higher in homes of women who developed lung cancer than in homes of controls, nor did lung cancer risk increase with increasing radon level. No association between radon and lung cancer was observed regardless of cigarette-smoking status, except for a nonsignificant trend among heavy smokers. No positive associations of lung cancer cell type with radon were observed, except for a nonsignificant excess risk of small cell cancers among the more heavily exposed residents. Our data suggest that projections from surveys of miners exposed to high radon levels may have overestimated the overall risks of lung cancer associated with levels typically seen in homes in this Chinese city. However, further studies in other population groups are needed to clarify the carcinogenic potential of indoor radon.     

Occupation and larynx and hypopharynx cancer: a job-exposure matrix approach in an international case-control study in France,Italy, Spain and Switzerland

Objective: To investigate the effect of exposure to occupational agents on the risk of hypopharyngeal/laryngeal cancer. Methods: Case-control study conducted during 1979–1982 in six centres in South Europe. An occupational history and information on exposure to non-occupational factors were collected for 1010 male cases of hypopharyngeal/laryngeal cancer as well as for 2176 population controls. The exposure to 10 occupational agents was assessed through a job-exposure matrix. As occupational histories had been collected since 1945 major analyses were restricted to subjects aged less than 55 years (315 cases and 819 controls). Results: Significant elevated risks adjusted for non-occupational variables (smoking, alcohol consumption and diet) and other occupational exposures were consistently found for organic solvents (odds ratio (OR) for ever-exposure: 1.7, 95% confidence interval: 1.1–2.5) and asbestos (OR: 1.6, 1.0–2.5). A significant positive trend for both probability of exposure and duration was found for exposure to solvents. A positive association between exposure to formaldehyde and laryngeal cancer was also suggested. No association was found for exposure to arsenic and compounds, chromium and compounds, and polycyclic aromatic hydrocarbons. Analyses restricted to subjects aged 55 or more did not show elevated risks, with the exception of wood dust (OR: 1.8, 1.3-2.7). Conclusions: In our study occupational exposure to solvents was associated with an increased risk of hypopharyngeal/laryngeal cancer. Results also provide additional evidence of an excess of risk for exposure to asbestos.     

Lung tumors in A/J mice exposed to environmental tobacco smoke: estimated potency and implied human risk

Directly inhaled tobacco smoke is a recognized human lung carcinogen, and epidemiological studies suggest relative risks of about 1.2-1.4 for nonsmoking spouses of smokers typically exposed to environmental tobacco smoke (ETS). While many individual ETS components have been shown experimentally to induce lung tumors, ETS itself was only recently shown to induce lung tumors in a series of studies in which strain A/J mice were exposed to well-defined ETS atmospheres. Data from these studies indicate that ETS exposure clearly can increase combined malignant and benign lung tumors in multiple experiments involving male and female A/J mice, and thus provide convincing evidence that ETS is a positive mouse carcinogen. Tumorigenic potencies estimated from these A/J mouse bioassay data predict a corresponding range of increased human risk (0.2-0.5%) that overlaps that implied by case-control studies showing increased lung cancer risks in lifelong nonsmokers married to smokers. In A/J mice exposed to a significantly tumorigenic ETS concentration, lung tumors were found to be significantly smaller than those in corresponding control mice, and mice so exposed for 9 months had significantly fewer tumors/animal than mice exposed for 5 months followed by 4 months in filtered ETS-free air. These findings support hypotheses that ETS does not promote growth of spontaneous neoplastic foci in A/J mice, and that ETS-induced lung-tumor risk in A/J mice occurs predominantly by genotoxic effects that can be suppressed by reduced cell proliferation associated with chronic, high-level ETS exposure. The results obtained add to evidence that A/J mouse lung tumors induced by ETS provide a relevant biological model of ETS-induced human lung tumors.     

Soft tissue sarcoma and non-Hodgkin's lymphoma in relation to phenoxyherbicide and chlorinated phenol exposure in western Washington

A population-based case-control study was conducted in western Washington State to evaluate the relationship between occupational exposure of men aged 20-79 to phenoxyacetic acid herbicides and chlorinated phenols and the risks of developing soft tissue sarcoma (STS) and non-Hodgkin's lymphoma (NHL). Occupational histories and other data were obtained by personal interviews for 128 STS cases and 576 NHL cases, diagnosed between 1981 and 1984, and for 694 randomly selected controls without cancer. Among the study subjects with any past occupational exposure to phenoxyherbicides, the estimated relative risk and 95% confidence interval of developing STS was 0.80 (0.5-1.2), and of developing NHL, 1.07 (0.8-1.4). Risk estimates of developing STS and NHL associated with past chlorophenol exposure were 0.99 (0.7-1.5) and 0.99 (0.8-1.2), respectively. No increasing risk of either cancer was associated with overall duration or intensity of chemical exposure or with exposure to any specific phenoxyherbicide per se. However, estimated risks of NHL were elevated among men who had been farmers, 1.33 (1.03-1.7), forestry herbicide applicators, 4.80 (1.2-19.4), and for those potentially exposed to phenoxyherbicides in any occupation for 15 years or more during the period prior to 15 years before cancer diagnosis, 1.71 (1.04-2.8). Increased risks of NHL were also observed among those with occupational exposure to organochlorine insecticides, such as DDT [1.82 (1.04-3.2)] and organic solvents [1.35 (1.06-1.7)], and to other chemicals typically encountered in the agricultural, forestry, or wood products industries. These results demonstrate small but significantly increased risks of developing NHL in association with some occupational activities where phenoxyherbicides have been used in combination with other types of chemicals, particularly for prolonged periods. They do not demonstrate a positive association between increased cancer risks and exposure to any specific phenoxyherbicide product alone. Moreover, these findings provide no evidence of increased risks of developing NHL associated with chlorinated phenol exposure or of developing STS associated with exposure to either class of chemical.     

Non-Hodgkin's lymphoma and farming: an expanded case-control study

A previously published case-control study of agricultural risk factors involved male cases of non-Hodgkin's lymphoma registered under code 202 of the International Classification of Diseases (ICD). This study has been expanded with the inclusion of cases registered under ICD code 200, and additional controls. The expanded study comprises 100 ICD 200 cases and 83 ICD 202 cases registered during the period 1977-81, together with 338 controls selected from other cancer registrations during the same period. The largest relative risk for specific farming types was for orchard workers (odds ratio = 3.7, 90% confidence limits 1.1-12.1). No elevated risks were observed for exposure to farm animals, nor for potential exposure to phenoxy herbicides (odds ratio = 1.0, 90% confidence limits 0.7-1.5), or chlorophenols (odds ratio = 1.4, 90% confidence limits 0.8-2.3). The previous finding of an excess risk associated with fencing work was weakly supported by the expanded study (odds ratio = 1.4, 90% confidence limits 1.0-2.0). However, the previous finding of an excess risk associated with meat works employment was more strongly supported (odds ratio = 1.8, 90% confidence limits 1.2-2.6). One relevant risk factor is 2,4,6-TCP which is used in the treatment of pelts, but the excess risks do not appear to be confined to pelt department workers. An alternative hypothesis is that meat workers may be exposed to oncogenic viruses.