Exposure to fibres and risk of pleural mesothelioma in the Norwegian Offshore Petroleum Workers cohort.

OBJECTIVES: Pleural mesothelioma is a rare respiratory cancer, mainly caused by inhalation of asbestos fibres. Other inorganic fibres are also suggested risk factors. We aimed to investigate the association between exposure to asbestos or refractory ceramic fibres (RCFs) and pleural mesothelioma among male Norwegian offshore petroleum workers. METHODS: Among 25 347 men in the Norwegian Offshore Petroleum Workers (NOPW) cohort (1965-1998), 43 pleural mesothelioma cases were identified through the Cancer Registry of Norway (1999-2022). A case-cohort study was conducted with 2095 randomly drawn non-cases from the cohort. Asbestos and RCF exposures were assessed with expert-made job-exposure matrices (JEMs). Weighted Cox regression was used to estimate HRs and 95% CIs, adjusted for age at baseline and pre-offshore employment with likely asbestos exposure. RESULTS: An increased risk of pleural mesothelioma was indicated for the highest versus lowest tertile of average intensity of asbestos (HR=1.21, 95% CI: 0.57 to 2.54). Pre-offshore asbestos exposure (vs no such exposure) was associated with increased risk of pleural mesothelioma (HR=2.06, 95% CI: 1.11 to 3.81). For offshore workers with no pre-offshore asbestos exposure, an increased risk of pleural mesothelioma was found for the highest tertile of average intensity of asbestos (HR=4.13, 95% CI: 0.93 to 18), versus the lowest tertile. No associations were found between RCF and pleural mesothelioma. CONCLUSIONS: Associations between JEM-based offshore asbestos exposure and pleural mesothelioma were confirmed in the NOPW cohort. Pleural mesothelioma risk was also associated with asbestos exposure before work in the offshore petroleum industry.

Exposure to benzene and other hydrocarbons and risk of bladder cancer among male offshore petroleum workers.

BACKGROUND: Occupational exposures constitute the second leading cause of urinary bladder cancer after tobacco smoking. Increased risks have been found in the petroleum industry, but high-quality exposure data are needed to explain these observations. METHODS: Using a prospective case-cohort design, we analysed 189 bladder cancer cases (1999-2017) and 2065 randomly drawn non-cases from the Norwegian Offshore Petroleum Workers cohort. Cases were identified in the Cancer Registry of Norway, while work histories (1965-1998) and lifestyle factors were recorded by questionnaire at baseline (1998). Occupational petroleum-related hydrocarbon exposures were assessed by expert-developed job-exposure matrices. Hazard ratios were estimated by weighted Cox-regressions, adjusted for age, tobacco smoking, education, and year of first employment, and with lagged exposures. RESULTS: Increased risks were found in benzene-exposed workers, either long-term exposure (≥18.8 years, HR = 1.89, 95% CI: 1.14-3.13; p-trend = 0.044) or high-level cumulative benzene exposure (HR = 1.60, 95% CI: 0.97-2.63; p-trend = 0.065), compared with the unexposed. Associations persisted with 20-year exposure lag. No associations were found with skin or inhalation exposure to crude oil, mineral oil (lubrication, hydraulics, turbines, drilling), or diesel exhaust. CONCLUSIONS: The results suggest that exposures in the benzene fraction of the petroleum stream may be associated with increased bladder cancer risk.

Lifelong differences in cancer incidence and mortality between subgroups of similar socioeconomic status in the Royal Norwegian Navy.

OBJECTIVES: In a previous cohort study of 28 300 Navy servicemen, vessel crews showed higher cancer incidence and mortality than did land-based personnel. We have extended the follow-up to look for changes in cancer risk, and to explore temporal trends in cancer incidence and cancer mortality during more than six decades of follow-up. METHODS: Cancer incidence and total cancer mortality were compared with the general population by calculating standardised ratios (standardised incidence ratios (SIRs), standardised mortality ratios) for the entire follow-up, with temporal trends through seven consecutive 10-year time spans from individual entry to follow-up. Rates were compared between the subgroups using Poisson regression, expressed as rate ratios (RRs). RESULTS: Cancer incidence in Navy servicemen suggested a healthy soldier effect limited to the first three decades of follow-up and confined to land-based personnel. Overall, vessel crews showed 13% higher cancer incidence and 36% higher cancer mortality than other Navy servicemen. Some of the differences may be explained by a higher risk in vessel crews of cancers known to have less than 25% 5-year relative survival (RR=1.71), such as cancers of the lung, liver, pancreas and mesothelioma. CONCLUSION: Through most of the observation time, vessel crews had an overall cancer SIR that was higher than that of land-based personnel. Much of this excess involved cancers with a generally poor prognosis, linked to lifestyle and work environment. The contrasts in cancer incidence and mortality between the two subgroups of Navy servicemen persisted through more than six decades.

Occupational exposures of firefighting and urinary tract cancer risk among men in the Norwegian Fire Departments Cohort.

OBJECTIVES: Increased risks of bladder cancer and mesothelioma were the strongest evidence for the recent reclassification of firefighting as carcinogenic (Group 1) by the International Agency for Research on Cancer. Our study aim was to develop indicators for specific firefighting exposures and examine associations with urinary tract cancer (UTC), including bladder cancer. METHODS: We developed indicators for exposure from employment at a fire department or in firefighting jobs, to fire and smoke, and to diesel exhaust for men in the Norwegian Fire Departments Cohort (n=4250). Incident UTC cases were obtained from the Cancer Registry of Norway (1960-2021). Poisson regression was used to estimate incidence rate ratios (IRR) with cumulative exposures grouped into tertiles (reference: lowest exposed tertile) with 0-year, 10-year and 15-year lagging of exposures. RESULTS: During 125 090 person-years of follow-up, there were 76 cases of UTC. IRRs were mostly non-significantly increased in the middle tertile and at or below 1 in the highest tertile for total duration of employment, number of fires attended and fire exposure score with and without lags. In the middle tertile for diesel exhaust exposure, UTC risk was elevated over twofold with 10-year (IRR 2.27, 95% CI 1.22 to 4.20) and 15- year (2.21, 1.18 to 4.16) lags, and near 1 in the highest tertile. Findings for bladder cancer were similar to those for UTC. CONCLUSIONS: Dose-response associations between the exposure indicators and UTC were not observed. Future studies using the indicators with more cases are needed.

Benzene exposure and risk of lung cancer in the Norwegian Offshore Petroleum Worker cohort: a prospective case-cohort study.

OBJECTIVE: The objective of our study was to examine whether occupational exposure to benzene is associated with lung cancer among males in the Norwegian Offshore Petroleum Workers cohort. METHODS: Among 25 347 male offshore workers employed during 1965-1998, we conducted a case-cohort study with 399 lung cancer cases diagnosed between 1999 and 2021, and 2035 non-cases sampled randomly by 5-year birth cohorts. Individual work histories were coupled to study-specific job-exposure matrices for benzene and other known lung carcinogens. Weighted Cox regression was used to estimate HRs and 95% CIs for the associations between benzene exposure and lung cancer, by major histological subtypes, adjusted for age, smoking and occupational exposure to welding fumes, asbestos and crystalline silica. Missing data were imputed. RESULTS: For lung cancer (all subtypes combined), HRs (95% CIs) for the highest quartiles of benzene exposure versus unexposed were 1.15 (0.61 to 2.35) for cumulative exposure, 1.43 (0.76 to 2.69) for duration, and 1.22 (0.68 to 2.18) for average intensity (0.280≤P-trend≤0.741). For 152 adenocarcinoma cases, a positive trend was observed for exposure duration (P-trend=0.044). CONCLUSIONS: In this cohort of offshore petroleum workers generally exposed to low average levels of benzene, we did not find an overall clear support for an association with lung cancer (all subtypes combined), although an association was suggested for duration of benzene exposure and adenocarcinoma. The limited evidence might be due to restricted statistical power.

Prospective investigation of herpesvirus infection and risk of glioma.

Glioma is an aggressive neoplasm of the brain with poorly understood etiology. A limited number of pathogens have been examined as glioma risk factors, but data from prospective studies with infection status determined before disease are lacking. Herpesviruses comprise a large family of DNA viruses that infect humans and are linked to a range of chronic diseases. We conducted a prospective evaluation of the association between antibody to six human herpesviruses and glioma risk in the Janus Serum Bank (Janus) and the Cancer Prevention Study-II (CPS-II). In Janus and CPS-II, the risk for glioma was not related to seroprevalence of herpes simplex virus-1, varicella zoster virus, or human herpes viruses 6A or 6B. In Janus, seropositivity to either the Epstein Barr virus (EBV) EA[D] or VCAp18 antigen was associated with a lower risk of glioma (ORs: 0.55 [95% CI 0.32-0.94] and 0.57 [95% CI 0.38-0.85]). This inverse association was consistent by histologic subtype and was observed for gliomas diagnosed up to two decades following antibody measurement. In Janus, seropositivity to at least one of three examined cytomegalovirus (CMV) antigens (pp150, pp52, pp28) was associated with an increased risk of nonglioblastoma (OR: 2.08 [95% CI 1.07-4.03]). This association was limited to tumors diagnosed within 12 years of antibody measurement. In summary, we report evidence of an inverse association between exposure to EBV and glioma. We further report that CMV exposure may be related to a higher likelihood of the nonglioblastoma subtype.

Early detection of prostate cancer in firefighters: a register-based study of prognostic factors and survival.

OBJECTIVES: To examine age at diagnosis, prognostic factors and survival of prostate cancer (PCa) in Norwegian firefighters and three other occupations undergoing occupational health check-ups, and comparing with PCa cases in the general population. METHODS: All PCa cases diagnosed in 1960-2017 were extracted from the Cancer Registry of Norway. Firefighters, military employees, pilots and police officers were identified through occupational data from Statistics Norway. Age at diagnosis, clinical stage, prostate-specific antigen (PSA), Gleason score, performance status and overall survival and PCa-specific survival in cases in these occupations were compared with cases in the general population. RESULTS: Firefighters were significantly younger at PCa diagnosis than cases in the general population in 1960-1993 (mean difference: 2.1 years) and 2007-2017 (mean difference: 4.3 years). At diagnosis, firefighters had significantly lower PSA values, Gleason scores and performance status scores than the general population. Firefighters diagnosed in 2007-2017 had lower risk of all-cause death than the general population (crude HR 0.71 (0.53-0.95)). No difference remained after adjusting for age at diagnosis (HR 1.03 (0.77-1.37)). Firefighters were older at diagnosis in 1994-2006 (mean difference: 3.0 years), but showed no other significant differences in age at diagnosis, PSA values, Gleason scores or performance status compared with military employees, pilots and police officers. CONCLUSIONS: Younger age and better prognostic factors at PCa diagnosis among firefighters and other occupations with requirements for health check-ups than cases in the general population may indicate an increased diagnostic intensity, likely contributing to elevated PCa incidence in such occupations.

Comparison of cancer incidence and mortality in the Norwegian Fire Departments Cohort, 1960-2018.

OBJECTIVES: Elevated risk of cancer at several sites has been reported among firefighters, although with mixed findings. The purpose of this study was to calculate standardised incidence ratios (SIRs) and standardised mortality ratios (SMRs) for cancer and compare them to assess whether use of the different measures could be a source of inconsistencies in findings. METHODS: The Norwegian Fire Departments Cohort, comprising 4295 male employees who worked at 15 fire departments across Norway, was linked to health outcome registries for the period 1960-2018. SIRs and SMRs were derived using national reference rates. RESULTS: Overall, we observed elevated incidence of colon cancer (SIR, 95% CI 1.27, 1.01 to 1.58), mesothelioma (2.59, 1.12 to 5.11), prostate cancer (1.18, 1.03 to 1.34) and all sites combined (1.15, 1.08 to 1.23). Smaller, non-significant elevations were found for mortality of colon cancer (SMR, 95% CI 1.20, 0.84 to 1.67) and mesothelioma (1.66, 0.34 to 4.86), while SMR for prostate cancer was at unity. Potential errors were observed in some of the mortality data, notably for mesothelioma cases. Among those who died of cancer, 3.7% (n=14) did not have a prior diagnosis of malignancy at the same site group. CONCLUSIONS: Assessment of incidence or mortality did not greatly influence the interpretation of results. The most prominent differences in SIR and SMR appeared to be due to inconsistencies between sites of cancer diagnosis and cause of death. The difference in SIR and SMR for prostate cancer suggested a detection bias from differential screening practices.

Toxoplasma gondii infection and the risk of adult glioma in two prospective studies.

Toxoplasma gondii (T gondii) is a common parasite that shows affinity to neural tissue and may lead to the formation of cysts in the brain. Previous epidemiologic studies have suggested an association between glioma and increased prevalence of T gondii infection, but prospective studies are lacking. Therefore, we examined the association between prediagnostic T gondii antibodies and risk of glioma in two prospective cohorts using a nested case-control study design. Cases and matched controls were selected from the American Cancer Society's Cancer Prevention Study-II Nutrition Cohort (CPSII-NC) (n = 37 cases and 74 controls) and the Norwegian Cancer Registry's Janus Serum Bank (Janus) (n = 323 cases and 323 controls). Blood samples collected prior to diagnosis were analyzed for antibodies to two T gondii surface antigens (p22 and sag-1), with individuals considered seropositive if antibodies to either antigen were detected. Conditional logistic regression was used to calculate odds ratios (OR) and 95% confidence intervals (95% CI) for each cohort. In both cohorts, a suggestive increase in glioma risk was observed among those infected with T gondii (OR: 2.70; 95% CI: 0.96-7.62 for CPSII-NC; OR: 1.32, 95% CI: 0.85-2.07 for Janus), particularly among participants with high antibody titers specific to the sag-1 antigen (CPSII-NC OR: 3.35, 95% CI: 0.99-11.38; Janus OR: 1.79, 95% CI: 1.02-3.14). Our findings provide the first prospective evidence of an association between T gondii infection and risk of glioma. Further studies with larger case numbers are needed to confirm a potential etiologic role for T gondii in glioma.

Ultraviolet radiation and risk of cutaneous melanoma and squamous cell carcinoma in males and females in the Norwegian Offshore Petroleum Workers cohort.

BACKGROUND: Increased risk of cutaneous melanoma and squamous cell carcinoma (SCC) has been reported among petroleum workers, but few studies include females, exposure data on ultraviolet radiation (UVR), and potential confounding factors. We aimed to examine UVR exposure in relation to risk of melanoma and SCC among male and female offshore petroleum workers. We also examined the association between UVR exposure and melanoma (Breslow) thickness. METHODS: The Norwegian Offshore Petroleum Workers (NOPW) cohort (n = 27,917) holds information on sunbathing, indoor tanning, sunburns, sunscreen use, and other lifestyle factors recorded in 1998. Linkage to the Cancer Registry of Norway gave information on cancer diagnosis through 2017. We used Cox and logistic regression to estimate hazard ratios (HRs) of skin cancer and odds ratios (OR) of thick (≥1 mm) melanomas, respectively, with 95% confidence intervals (CIs). RESULTS: Melanoma risk increased with increasing frequency of sunbathing after age 20 (ptrend = 0.031), sunburn average intensity (ptrend = 0.028), and sunscreen use (HR = 2.16; 95% CI: 1.42 -3.27 for almost always vs. never/rarely). The risk of thick melanoma was inversely associated with sunbathing frequency after age 20 (OR = 0.38; 95% CI: 0.16 - 0.90 for ≥4 weeks/year vs. 1 week/year). SCC risk increased with increasing frequency of indoor tanning after age 20 (HR = 2.72; 95% CI: 1.22 - 6.05 for ≥3 times/months vs. never), sunburn average intensity (ptrend < 0.001), and sunscreen use (ptrend < 0.001). CONCLUSIONS: Our results support associations between UVR exposure and skin cancer risk in male and female offshore petroleum workers. This occupational group may be especially relevant for targeted sun protection advice.

Prediagnostic serum sCD27 and sCD30 in serial samples and risks of non-Hodgkin lymphoma subtypes.

Elevated prediagnostic serum levels of the immune activation markers sCD27 and sCD30 have been associated with non-Hodgkin lymphoma (NHL). However, the use of a single sample per participant in these studies has limited etiologic inferences. We report findings, overall and by NHL subtype, from a case-control analysis (422 cases, 434 controls) within the Janus Serum Bank with two samples per subject collected on average 5 years apart. Chronic lymphocytic leukemia/small lymphocytic lymphoma (CLL/SLL) was associated with elevated sCD27 in the later, but not earlier, prediagnostic sample (odds ratio [OR] 4.2, 95% confidence interval [CI] 1.5-11.6 and 1.7, 0.7-4.7 per log increase, respectively) in analyses adjusting for both analytes, while follicular lymphoma (FL) was associated with elevated sCD30 in both the later and earlier samples (OR 2.9, 95% CI 1.4-4.4 and 2.3, 1.2-4.4, respectively). CLL/SLL cases were significantly more likely than controls to have higher sCD27 in the later vs. earlier sample (OR 1.4, 95% CI 1.1-1.9 per standard deviation increase); no such difference in sCD30 was apparent for FL. In a joint analysis, NHL cases were more likely than controls to have below-median sCD27 in the earlier sample and above-median sCD27 in the later sample (OR 1.5, 95% CI 1.0-2.3). For sCD30, the association between sCD30 and FL was confined to subjects with above-median analyte levels in both samples (OR 2.5, 95% CI 1.1-5.9). Our findings are compatible with elevated sCD27 representing a disease-induced effect and sCD30 representing a marker of increased FL susceptibility.

Prediagnostic blood levels of organochlorines and risk of non-Hodgkin lymphoma in three prospective cohorts in China and Singapore.

Specific organochlorines (OCs) have been associated with non-Hodgkin lymphoma (NHL) with varying degrees of evidence. These associations have not been evaluated in Asia, where the high exposure and historical environmental contamination of certain OC pesticides (e.g., dichlorodiphenyltrichloroethane [DDT], hexachlorocyclohexane [HCH]) are different from Western populations. We evaluated NHL risk and prediagnostic blood levels of OC pesticides/metabolites and polychlorinated biphenyl congeners in a case-control study of 167 NHL cases and 167 controls nested within three prospective cohorts in Shanghai and Singapore. Conditional logistic regression was used to analyze lipid-adjusted OC levels and NHL risk. Median levels of p,p'-dichlorodiphenyldichloroethylene (p,p'-DDE), the primary DDT metabolite, and ß-HCH were up to 12 and 65 times higher, respectively, in samples from the Asian cohorts compared to several cohorts in the United States and Norway. An increased risk of NHL was observed among those with higher ß-HCH levels both overall (3rd vs. 1st tertile OR = 1.8, 95%CI = 1.0-3.2; ptrend = 0.049) and after excluding cases diagnosed within 2 years of blood collection (3rd vs. 1st tertile OR = 2.0, 95%CI = 1.1-3.9; ptrend = 0.03), and the association was highly consistent across the three cohorts. No significant associations were observed for other OCs, including p,p'-DDE. Our findings provide support for an association between ß-HCH blood levels and NHL risk. This is a concern because substantial quantities of persistent, toxic residues of HCH are present in the environment worldwide. Although there is some evidence that DDT is associated with NHL, our findings for p,p'-DDE do not support an association.

Prediagnostic serum concentrations of organochlorine pesticides and non-Hodgkin lymphoma: A nested case-control study in the Norwegian Janus Serum Bank Cohort.

BACKGROUND: Much of the marked increase in incidence of non-Hodgkin lymphoma (NHL) over the past few decades remains unexplained. Organochlorines, including organochlorine pesticides (OCPs), have been implicated as possible contributors to the increase, but the evidence is inconsistent. OBJECTIVES: To investigate the relation between pre-diagnostic levels of OCPs and risk of NHL in a case-control study nested within the population-based Janus Serum Bank Cohort in Norway. METHODS: Prediagnostic concentrations of 11 OCPs or OCP metabolites were measured in baseline blood samples collected between 1972 and 1978 from 190 cases and 190 controls matched on sex, county, age at blood draw, and date of blood draw. We conducted conditional logistic regression to estimate adjusted odds ratios (ORs) and 95% confidence intervals (95% CIs) for each quartile of lipid-corrected OCP/metabolite relative to the lowest quartile. RESULTS: We observed non-significantly elevated ORs across quartiles of ß-hexachlorocyclohexane compared to the lowest quartile (OR range: 1.40-1.82) although with no apparent monotonic exposure-response relationship. We also found an inverse association between risk of NHL and o,p'-DDT (OR for Q4 vs. Q1 = 0.44, 95% CI: 0.19, 1.01; p-trend = 0.05). In analyses stratified by age at blood collection and duration of follow-up, several other analytes, primarily chlordane-related compounds, showed inverse associations among younger participants or those with longer follow-up time between blood draw and NHL diagnosis. CONCLUSIONS: We found only limited evidence of positive association between selected OCPs and development of NHL.

Prediagnostic serum polychlorinated biphenyl concentrations and primary liver cancer: A case-control study nested within two prospective cohorts.

BACKGROUND: Polychlorinated biphenyls (PCBs) were used in electrical equipment and a range of construction materials. Although banned in the United States and most of Europe in the 1970s, they are highly persistent in the environment and bioaccumulate. Whether PCBs are associated with liver cancer risk at general population levels is unknown. METHODS: This study consisted of 136 incident liver cancer cases and 408 matched controls from the Kaiser Permanente Northern California Multiphasic Health Checkup (MHC) cohort and 84 cases and 252 matched controls from the Norwegian Janus cohort. Sera collected in the 1960s-1980s were measured for 37 PCB congeners and markers of hepatitis B (HBV) and C (HCV) infection. Odds ratios (OR) and 95% confidence intervals (CI) for tertiles of each lipid-adjusted PCB were estimated from conditional logistic regression. We also examined the molar sum of congeners in groups: total PCBs; low, medium, and high chlorination; and Wolff functional groups. RESULTS: Concentrations of individual congeners from the 1960s/1970s sera ranged from 1.3-123.0 and 1.4-116.0 ng/g lipid among MHC cases and controls, respectively, and from 1.9-258.0 and 1.9-271.0 ng/g lipid among Janus cases and controls, respectively. Among MHC participants with sera from the 1960s, collected an average of 27 years before diagnosis among cases, the top tertile of PCBs 151, 170, 172, 177, 178, 180, and 195 was significantly associated with elevated odds of liver cancer (OR range = 2.01-2.38); most of these congeners demonstrated exposure-response trends. For example, ORtertile 3vs1 = 2.38 (95% CI: 1.22-4.64, p-trend = 0.01) for PCB 180. As a group, Wolff group 1b congeners, which are biologically persistent and weak phenobarbital inducers, were associated with increased odds. In MHC participants, ever vs. never HBV or HCV infection modified the PCB-liver cancer associations. There was little evidence of an association between PCBs and odds of liver cancer among the Janus cohort. DISCUSSION: We observed associations between a number of PCB congeners and increased odds of liver cancer among MHC, but not Janus, participants with sera from the 1960s/1970s.

Prediagnostic serum organochlorine insecticide concentrations and primary liver cancer: A case-control study nested within two prospective cohorts.

Although experimental evidence indicates that certain organochlorine insecticides are hepatocarcinogens, epidemiologic evidence for most of these chemicals is very limited. We estimated associations, using prospectively collected sera, between organochlorine insecticide concentrations and cancer registry-identified primary liver cancer in two cohorts, one from the United States and one from Norway. In nested case-control studies, we used sera collected in the 1960s-1980s from 136 cases and 408 matched controls from the Kaiser Permanente Northern California Multiphasic Health Checkup (MHC) cohort and 84 cases and 252 matched controls from the population-based Norwegian Janus cohort. We measured concentrations of nine organochlorine insecticides/metabolites and markers of hepatitis B and C in sera. Adjusted odds ratios (OR) and 95% confidence intervals (CI) for tertiles of lipid-corrected organochlorines were calculated for each cohort using conditional logistic regression. Among MHC participants with sera from the 1960s, there was a suggestive exposure-response trend for trans-nonachlor (second and third tertile of analyte ORs = 1.63 and 1.95, respectively; p-trend = 0.08) and a nonsignificantly elevated risk for the highest tertile of oxychlordane (OR = 1.87). Among Janus participants with sera from the 1970s, we observed an apparent trend for p,p'-DDT (second and third tertile ORs = 1.70 and 2.14, respectively; p-trend = 0.15). We observed little consistency in patterns of association between the cohorts. We found limited evidence that exposure to p,p'-DDT and chlordane-related oxychlordane and trans-nonachlor may be associated with increased risk of primary liver cancer. However, the modest strength of these associations and their lack of concordance between cohorts necessitate caution in their interpretation.

Anthropometric factors and cutaneous melanoma: Prospective data from the population-based Janus Cohort.

The aim of the present study was to prospectively examine risk of cutaneous melanoma (CM) according to measured anthropometric factors, adjusted for exposure to ultraviolet radiation (UVR), in a large population-based cohort in Norway. The Janus Cohort, including 292,851 Norwegians recruited 1972-2003, was linked to the Cancer Registry of Norway and followed for CM through 2014. Cox regression was used to estimate hazard ratios (HRs) of CM with 95% confidence intervals (CIs). Restricted cubic splines were incorporated into the Cox models to assess possible non-linear relationships. All analyses were adjusted for attained age, indicators of UVR exposure, education, and smoking status. During a mean follow-up of 27 years, 3,000 incident CM cases were identified. In men, CM risk was positively associated with body mass index, body surface area (BSA), height and weight (all ptrends < 0.001), and the exposure-response curves indicated an exponential increase in risk for all anthropometric factors. Weight loss of more than 2 kg in men was associated with a 53% lower risk (HR 0.47, 95% CI: 0.39, 0.57). In women, CM risk increased with increasing BSA (ptrend = 0.002) and height (ptrend < 0.001). The shape of the height-CM risk curve indicated an exponential increase. Our study suggests that large body size, in general, is a CM risk factor in men, and is the first to report that weight loss may reduce the risk of CM among men.

A nested case-control study of polychlorinated biphenyls, organochlorine pesticides, and thyroid cancer in the Janus Serum Bank cohort.

BACKGROUND: Polychlorinated biphenyls (PCBs) and organochlorine pesticides have been associated with altered thyroid hormone levels in humans, but their relationship with thyroid cancer is unknown. METHODS: We conducted a nested case-control study of thyroid cancer in the Norwegian Janus Serum Bank cohort using pre-diagnostic blood samples from 1972 to 1985. Incident thyroid cancer (n = 108) was ascertained through 2008. Controls were matched 2:1 by age, date of blood draw, gender, and county. We used gas chromatography/mass spectrometry to quantify 36 PCB congeners and metabolites of pesticides DDT, chlordane, hexachlorocyclohexane, and hexachlorobenzene. PCBs and pesticide metabolites were evaluated individually and summed by degree of chlorination and parent compound, respectively. Odds ratios (OR) and 95% confidence intervals (CI) were computed using conditional logistic regression per specified increase in lipid-adjusted concentration. We additionally stratified analyses by birth cohort (1923-1932, 1933-1942, 1943-1957). RESULTS: Increasing concentration of DDT metabolites (ORper 1000 ng/g = 0.80, 95%CI = 0.66-0.98) was inversely associated with thyroid cancer. Associations for PCBs were null or in inverse direction. We observed interactions for total PCBs, moderately-chlorinated PCBs, and chlordane metabolites with birth cohort (p ≤ 0.04). Among participants born 1943-1957, total PCBs (ORper 100 ng/g = 1.25, 95%CI = 1.00-1.56), moderately-chlorinated PCBs (ORper 100 ng/g = 1.31, 95%CI = 1.01-1.70), and chlordane metabolites (ORper 10 ng/g = 1.78, 95%CI = 1.09-2.93) were positively associated with thyroid cancer. For individuals born before 1943, associations were generally null or in the inverse direction. CONCLUSIONS: Emissions of PCBs and OC pesticides varied over time. Different risk patterns by birth cohort suggest the potential importance of timing of exposure in thyroid cancer risk. Further evaluation of these associations is warranted.

Adjustment for tobacco smoking and alcohol consumption by simultaneous analysis of several types of cancer.

PURPOSE: Tobacco smoking and alcohol consumption are risk factors for several types of cancer and may act as confounders in aetiological studies. Large register-based cohorts often lack data on tobacco and alcohol. We present a method for computing estimates of cancer risk adjusted for tobacco and alcohol without exposure information. METHODS: We propose the use of confirmatory factor analysis models for simultaneous analysis of several cancer sites related to tobacco and alcohol. In the analyses, the unobserved pattern of smoking habits and alcohol drinking is considered latent common factors. The models allow for different effects on each cancer site, and also for appropriate latent site-specific factors for subgroup variation. Results may be used to compute expected numbers of cancer from reference rates, adjusted for tobacco smoking and alcohol consumption. This method was applied to results from a large, published study of work-related cancer based on census data (1970) and 21 years of cancer incidence data from the national cancer registry. RESULTS: The results from our analysis were in accordance with recognised risks in selected occupational groups. The estimated relative effects from tobacco and alcohol on cancer risk were largely in line with results from Nordic reports. For lung cancer, adjustment for tobacco implied relative changes in SIR between a decrease from 1.16 to 0.72 (Fishermen), and an increase from 0.47 to 0.95 (Forestry workers). CONCLUSIONS: We consider the method useful for achieving less confounded estimates of cancer risk in large cohort studies with no available information on smoking and alcohol consumption.

Cause-specific mortality and cancer morbidity in 390 male workers exposed to high purity talc, a six-decade follow-up.

BACKGROUND: This study updates information on mortality and cancer morbidity in a cohort of Norwegian talc workers. METHODS: Follow-up was extended with 24 years, covering 1953-2011. Comparisons were made with the general population and between subgroups within the cohort. RESULTS: Standardized mortality ratio for non-malignant respiratory disease (NMRD) was 0.38 (95%CI: 0.18, 0.69) and for diseases of the circulatory system (CVD) 0.98 (95%CI: 0.82, 1.16). A non-significantly increased NMRD risk was observed at high dust exposures. There were no deaths from pneumoconiosis. CONCLUSIONS: With the clear limitations of a small cohort, our results do hint at an effect of talc dust on mortality from NMRD other than pneumoconiosis, covered by a strong and persisting healthy worker effect. Also, an effect on CVD mortality, masked by a healthy worker selection into the cohort cannot be ruled out. Excess mortality from pneumoconiosis seen in other studies, may reflect exposure to quartz and, possibly, bias due to comparability problems.