Wireless phone use in childhood and adolescence and neuroepithelial brain tumours: Results from the international MOBI-Kids study.

In recent decades, the possibility that use of mobile communicating devices, particularly wireless (mobile and cordless) phones, may increase brain tumour risk, has been a concern, particularly given the considerable increase in their use by young people. MOBI-Kids, a 14-country (Australia, Austria, Canada, France, Germany, Greece, India, Israel, Italy, Japan, Korea, the Netherlands, New Zealand, Spain) case-control study, was conducted to evaluate whether wireless phone use (and particularly resulting exposure to radiofrequency (RF) and extremely low frequency (ELF) electromagnetic fields (EMF)) increases risk of brain tumours in young people. Between 2010 and 2015, the study recruited 899 people with brain tumours aged 10 to 24 years old and 1,910 controls (operated for appendicitis) matched to the cases on date of diagnosis, study region and age. Participation rates were 72% for cases and 54% for controls. The mean ages of cases and controls were 16.5 and 16.6 years, respectively; 57% were males. The vast majority of study participants were wireless phones users, even in the youngest age group, and the study included substantial numbers of long-term (over 10 years) users: 22% overall, 51% in the 20-24-year-olds. Most tumours were of the neuroepithelial type (NBT; n = 671), mainly glioma. The odds ratios (OR) of NBT appeared to decrease with increasing time since start of use of wireless phones, cumulative number of calls and cumulative call time, particularly in the 15-19 years old age group. A decreasing trend in ORs was also observed with increasing estimated cumulative RF specific energy and ELF induced current density at the location of the tumour. Further analyses suggest that the large number of ORs below 1 in this study is unlikely to represent an unknown causal preventive effect of mobile phone exposure: they can be at least partially explained by differential recall by proxies and prodromal symptoms affecting phone use before diagnosis of the cases. We cannot rule out, however, residual confounding from sources we did not measure. Overall, our study provides no evidence of a causal association between wireless phone use and brain tumours in young people. However, the sources of bias summarised above prevent us from ruling out a small increased risk.

Polybrominated diphenyl ethers and perfluorinated alkyl substances in blood serum of New Zealand adults, 2011-2013.

A national survey was conducted in 2011-2013 to assess serum concentrations of brominated flame retardants (BFRs) and perfluorinated alkyl substances (PFASs) in adult New Zealanders. Participants were randomly selected from the 2010 Electoral Roll within 64 demographic strata according to 4 age groups, 4 geographic regions, 2 ethnic groups (Maori/non-Maori) and sex. Eligible participants (n = 734; response rate of contacted individuals = 37%) donated up to 30 mL of blood, after which serum was pooled (49 pools for BFRs, 63 pools for PFASs) according to demographic strata. BFRs were analysed by GC-HRMS and PFASs by LC-MS/MS. Associations between serum BFRs and PFASs and demographic variables (age, region, ethnicity, sex) were assessed using regression analysis. The weighted geometric mean (GM) serum concentrations of BDE47, BDE99, BDE100, and BDE153 were 2.0, 0.66, 0.43, and 1.2 ng/g lipid, respectively. The weighted geometric mean (GM) serum concentrations of PFOS, PFOA, PFHxS, and PFNA were 3.4, 2.4, 1.0, and 0.66 ng/mL, respectively. The majority of BFRs showed higher serum concentrations in younger age groups. Conversely, the four PFASs showed higher serum concentrations in older age groups. Concentrations of BFRs and PFASs were generally lower in females compared to males. In New Zealand, both age and sex are important determinants of BFR and PFAS serum concentrations.

Chlorinated persistent organic pollutants in serum of New Zealand adults, 2011-2013.

A national survey was conducted in 2011-2013 to assess serum concentrations of persistent organic pollutants (POPs) in adult New Zealanders. Participants were randomly selected from the 2010 Electoral Roll within 64 demographic strata according to 4 age groups, 4 regions, 2 ethnic groups (Maori/non-Maori) and gender. Eligible subjects (n=734) donated up to 30ml of blood, after which serum was pooled (n=49) according to demographic strata prior to analysis by GC-HRMS. Associations between demographic variables (age, region, ethnicity, gender) and serum POPs were assessed using linear regression. The weighted geometric mean (GM) of PCDD/Fs was 5.3pg/g lipid toxic equivalents using the WHO 2005 toxic equivalence factors (TEQ05), which increased by age (3.2, 4.4, 4.8, and 8.1pg/g lipid for the 19-24, 25-34, 35-49, and 50-64year age groups, respectively). The weighted GM of dioxin-like PCBs was 1.4pg TEQ05/g lipid which also increased by age (0.82, 0.86, 1.4, and 2.3pg/g lipid for the same age groups, respectively). Of the detected OCPs, the highest concentration was observed for p,p'-DDE (weighted GM, 220ng/g lipid) followed by hexachlorobenzene (HCB; 7.3ng/g lipid), beta-HCH (7.0ng/g lipid), and dieldrin (4.7ng/g lipid). For most Cl-POPs, concentrations were lowest in the youngest age group, and were similar for men and women and Maori and non-Maori. Serum Cl-POPs were, on average, 50% lower than those measured 15years earlier in 1997. This survey provides evidence of declining serum concentrations of chlorinated POPs in the New Zealand adult population. Age was the most important determinant of POPs concentrations. Body burdens of PCDD/Fs and PCBs in New Zealand are relatively low by international comparison, while for OCPs they are similar or lower compared to those reported for other developed countries.

Occupational exposure to trichloroethylene and risk of non-Hodgkin lymphoma and its major subtypes: a pooled InterLymph [correction of IinterLlymph] analysis.

OBJECTIVES: We evaluated the association between occupational exposure to trichloroethylene (TCE) and risk of non-Hodgkin lymphoma (NHL) in a pooled analysis of four international case-control studies. METHODS: Overall, the pooled study population included 3788 NHL cases and 4279 controls. Risk of NHL and its major subtypes associated with TCE exposure was calculated with unconditional logistic regression and polytomous regression analysis, adjusting by age, gender and study. RESULTS: Risk of follicular lymphoma (FL), but not NHL overall or other subtypes, increased by probability (p=0.02) and intensity level (p=0.04), and with the combined analysis of four exposure metrics assumed as independent (p=0.004). After restricting the analysis to the most likely exposed study subjects, risk of NHL overall, FL and chronic lymphocytic leukaemia (CLL) were elevated and increased by duration of exposure (p=0.009, p=0.04 and p=0.01, respectively) and with the combined analysis of duration, frequency and intensity of exposure (p=0.004, p=0.015 and p=0.005, respectively). Although based on small numbers of exposed, risk of all the major NHL subtypes, namely diffuse large B-cell lymphoma, FL and CLL, showed increases in risk ranging 2-3.2-fold in the highest category of exposure intensity. No significant heterogeneity in risk was detected by major NHL subtypes or by study. CONCLUSIONS: Our pooled analysis apparently supports the hypothesis of an increase in risk of specific NHL subtypes associated with occupational exposure to TCE.

Occupational exposure to solvents and risk of lymphoma subtypes: results from the Epilymph case-control study.

BACKGROUND: Several studies have suggested an association between occupational exposure to solvents and lymphoma risk. However, findings are inconsistent and the role of specific chemicals is not known. Objective To investigate the role of occupational exposure to organic solvents in the aetiology of B-cell non-Hodgkin's lymphoma (B-NHL) and its major subtypes, as well as Hodgkin's lymphoma and T-cell lymphoma. METHODS: 2348 lymphoma cases and 2462 controls participated in a case-control study in six European countries. A subset of cases were reviewed by a panel of pathologists to ensure diagnostic consistency. Exposure to solvents was assessed by industrial hygienists and occupational experts based on a detailed occupational questionnaire. RESULTS: Risk of follicular lymphoma significantly increased with three independent metrics of exposure to benzene, toluene and xylene (BTX) (combined p=4 x 10(-7)) and to styrene (p=1 x 10(-5)), and chronic lymphocytic leukaemia (CLL) risk increased with exposure to solvents overall (p=4 x 10(-6)), BTX (p=5 x 10(-5)), gasoline (p=8 x 10(-5)) and other solvents (p=2 x 10(-6)). Risk of B-NHL for ever exposure to solvents was not elevated (OR=1.1, 95% CI 1.0 to 1.3), and that for CLL and follicular lymphoma was 1.3 (95% CI 1.1 to 1.6) and 1.3 (95% CI 1.0 to 1.7), respectively. Exposure to benzene accounted, at least partially, for the association observed with CLL risk. Hodgkin's lymphoma and T-cell lymphoma did not show an association with solvent exposure. CONCLUSION: This analysis of a large European dataset confirms a role of occupational exposure to solvents in the aetiology of B-NHL, and particularly, CLL. It is suggested that benzene is most likely to be implicated, but we cannot exclude the possibility of a role for other solvents in relation to other lymphoma subtypes, such as follicular lymphoma. No association with risk of T-cell lymphoma and Hodgkin's lymphoma was shown.

High risk occupations for non-Hodgkin's lymphoma in New Zealand: case-control study.

OBJECTIVES: Previous studies into occupational risk factors for non-Hodgkin's lymphoma (NHL) in New Zealand have indicated that farmers and meat workers are at increased risk for these neoplasms. A new nationwide case-control study was conducted to assess whether previously observed associations persist and to identify other occupations that may contribute to the risk of NHL in the New Zealand population. METHODS: A total of 291 incident cases of NHL (age 25-70 years) notified to the New Zealand Cancer Registry during 2003 and 2004, and 471 population controls, were interviewed face-to-face. The questionnaire collected demographic information and a full occupational history. The relative risk for NHL associated with ever being employed in particular occupations and industries was calculated by unconditional logistic regression adjusting for age, sex, smoking, ethnicity and socioeconomic status. Estimates were subsequently semi-Bayes adjusted to account for the large number of occupations and industries being considered. RESULTS: An elevated NHL risk was observed for field crop and vegetable growers (OR 2.74, 95% CI 1.04 to 7.25) and horticulture and fruit growing (OR 2.28, 95% CI 1.37 to 3.79), particularly for women (OR 3.44, 95% CI 0.62 to 18.9; OR 3.15, 95% CI 1.50 to 6.61). Sheep and dairy farming was not associated with an increased risk of NHL. Meat processors had an elevated risk (OR 1.97, 95% CI 0.97 to 3.97), as did heavy truck drivers (OR 1.98, 95% CI 0.92 to 4.24), workers employed in metal product manufacturing (OR 1.92, 95% CI 1.12 to 3.28) and cleaners (OR 2.11, 95% CI 1.21 to 3.65). After semi-Bayes adjustment the elevated risks for horticulture and fruit growing, metal product manufacturing and cleaners remained statistically significant, representing the most robust findings of this study. CONCLUSIONS: This study has confirmed that crop farmers and meat workers remain high risk occupations for NHL in New Zealand, and has identified several other occupations and industries of high NHL risk that merit further study.

Mortality in New Zealand workers exposed to phenoxy herbicides and dioxins.

AIMS: To evaluate mortality in New Zealand phenoxy herbicide producers and sprayers exposed to dioxins. METHODS: Phenoxy herbicide producers (n = 1025) and sprayers (n = 703) were followed up from 1 January 1969 and 1 January 1973 respectively to 31 December 2000. A total of 813 producers and 699 sprayers were classified as exposed to dioxin and phenoxy herbicides. Standardised mortality ratios (SMR) were calculated using national mortality rates. RESULTS: At the end of follow up, 164 producers and 91 sprayers had died. Cancer mortality was reduced for sprayers (SMR = 0.82, 95% CI 0.57 to 1.14) and increased in exposed production workers (SMR = 1.24, 95% CI 0.90 to 1.67), especially for synthesis workers (SMR = 1.69), formulation and lab workers (SMR = 1.64), and maintenance/waste treatment/cleaning workers (SMR = 1.46). Lymphohaematopoietic cancer mortality was increased in exposed production workers (SMR = 1.65, 95% CI 0.53 to 3.85), especially for multiple myeloma (SMR = 5.51, 95% CI 1.14 to 16.1). Among sprayers, colon cancer (SMR = 1.94, 95% CI 0.84 to 3.83) showed increased mortality. CONCLUSIONS: Results showed 24% non-significant excess cancer mortality in phenoxy herbicide producers, with a significant excess for multiple myeloma. Associations were stronger for those exposed to multiple agents including dioxin during production. Overall cancer mortality was not increased for producers and sprayers mainly handling final technical products, although they were likely to have been exposed to TCDD levels far higher than those currently in the general New Zealand population.

Mortality and cancer incidence in New Zealand meat workers.

AIMS: To ascertain whether there is an increased risk of cancers of the lung and lymphohaematopoietic tissue in workers employed in the New Zealand meat processing industry, and to identify exposures associated with any increased risks. METHODS: A cohort of 6647 individuals assembled from personnel records from three plants was followed from 1988 until 2000. The observed number of deaths and cancer registrations was compared with expected numbers using five year age and gender specific rates for the New Zealand population. Subgroup analyses evaluated the effect of duration of exposure to selected agents, based on job titles and departments. RESULTS: Vital status was determined for 84% of the cohort, and 92% of the total possible person-years. Mortality from all causes and all cancers was increased, and there was a significant excess of lung cancer. There were significant trends of increasing risk of lung and lymphohaematopoietic cancer with increasing duration of exposure to biological material. CONCLUSIONS: Excess risks were observed for mortality from all causes, all cancers, and lung cancer. Although the increased risk of lung cancer may be partly due to confounding by smoking, it is unlikely to be entirely due to this cause. Furthermore, the dose-response relation observed for lung cancer suggests the effect is related to exposure to biological material contained in animal urine, faeces, and blood. Although numbers were small, the risk of lymphohaematopoietic cancer was also associated with increasing duration and level of exposure to biological material.

Exposure-response analysis and risk assessment for silica and silicosis mortality in a pooled analysis of six cohorts.

AIMS: To study the relation between exposure to crystalline silica and silicosis mortality. Although mortality is an important endpoint for regulators, there have been no exposure-response studies for silicosis mortality, because of the relative rareness of silicosis as an underlying cause of death, and the limited availability of quantitative exposure estimates. METHODS: Data from six occupational cohorts were pooled with good retrospective exposure data in which 170 deaths from silicosis were reported. Standard life table analyses, nested case-control analyses, and risk assessment were performed. RESULTS: The rate of silicosis mortality in the combined data was 28/100 000 py, increasing in nearly monotonic fashion from 4.7/100 000 for exposure of 0-0.99 mg/m(3)-years to 233/100 000 for exposure of >28.1 mg/m(3)-years. The estimated risk of death up to age 65 from silicosis after 45 years of exposure at 0.1 mg/m(3) silica (the current standard in many countries) was 13 per 1000, while the estimated risk at an exposure of 0.05 mg/m(3) was 6 per 1000. Both of these risks are above the risk of 1 per 1000 typically deemed acceptable by the US OSHA. CONCLUSION: The findings from this pooled analysis add further support to the need to control silica exposure and to lower the occupational standards. Our estimates of lifetime silicosis mortality risk are probably underestimates as, in addition to exposure misclassification, our study might have suffered from outcome misclassification in that silicosis deaths might have been coded to other related causes, such as tuberculosis or chronic obstructive pulmonary disease.

Cigarette smoking and bladder cancer in men: a pooled analysis of 11 case-control studies.

The primary risk factor for bladder cancer is cigarette smoking. Using a combined analysis of 11 case-control studies, we have accurately measured the relationship between cigarette smoking and bladder cancer in men. Available smoking information on 2,600 male bladder cancer cases and 5,524 male controls included duration of smoking habit, number of cigarettes smoked per day and time since cessation of smoking habit for ex-smokers. There was a linear increasing risk of bladder cancer with increasing duration of smoking, ranging from an odds ratio (OR) of 1.96 after 20 years of smoking (95% confidence interval [CI] 1.48-2.61) to 5.57 after 60 years (CI 4.18-7.44). A dose relationship was observed between number of cigarettes smoked per day and bladder cancer up to a threshold limit of 15-20 cigarettes per day, OR = 4.50 (CI 3.81-5. 33), after which no increased risk was observed. An immediate decrease in risk of bladder cancer was observed for those who gave up smoking. This decrease was over 30% after 1-4 years, OR = 0.65 (0. 53-0.79), and was over 60% after 25 years of cessation, OR = 0.37 (0. 30-0.45). However, even after 25 years, the decrease in risk did not reach the level of the never-smokers, OR = 0.20. (0.17-0.24). The proportion of bladder cancer cases attributable to ever-smoking was 0.66 (0.61-0.70) for all men and 0.73 (0.66-0.79) for men younger than 60. These estimates are higher than previously calculated.

Bladder cancer in the textile industry.

OBJECTIVES: This study examined the occupations and industries at high risk for bladder cancer in an area where the textile industry is plentiful and the incidence of the disease is very high. METHODS: A case-referent study concerning 218 incident bladder cancer cases diagnosed during 1993-1995 in the county of Vallès Occidental, Barcelona, was carried out. A reference group (N=344) was selected from municipal lists matched to the cases by age, gender, and area of residence. All the subjects were personally interviewed, and a complete occupational history was abstracted together with other sociodemographic and life-style factors. All odds ratios (OR) and 95% confidence intervals (95% CI) were adjusted for age, gender, and smoking. RESULTS: No overall excess risk was found forever having worked in the textile industry (OR 1.13, 95% CI 0.79-1.63) nor for specific sectors of this industry (ie cotton, wool, silk). An excess risk was observed for spinners and winders employed for more than 20 years (OR 3.28, 95% CI 1.08-9.97) and for machine setters employed between 1960 and 1974 (OR 4.26, 95% CI 1.09-16.7). CONCLUSIONS: The results of this study do not support the findings of some earlier studies for an increased bladder cancer risk in the textile industry. However, some elevated risks were observed among the workers with the highest exposures.

Smoking as a confounder in case-control studies of occupational bladder cancer in women.

BACKGROUND: In studies in men, risk estimates on occupation and bladder cancer are distorted by about 10% when not adjusting for smoking. We examined the degree to which occupational risk estimates for bladder cancer in women are confounded by smoking, and the degree of residual confounding by inadequate control of this effect. METHODS: Primary data of 11 case-control studies on occupation and bladder cancer from Denmark, France, Germany, Greece, Italy, and Spain were pooled. Information for smoking and lifetime occupational history for 700 female cases and 2,425 female controls ages 30-79 was abstracted and recoded. Logistic regression was used to calculate odds ratios (OR) by occupation, applying five models which differed in their degree of adjustment for smoking. RESULTS: In major occupational groups, risk estimates were distorted by less than 10% when not adjusting for smoking. A statistically significant excess risk for bladder cancer was found in 13 specific occupations and industries. In most occupations, adjustment for smoking led the ORs towards the null value, but all statistically significant associations were maintained after adjustment. In three occupations (lathe operators, field crop workers, and wood manufacturers), a statistically significant excess risk was masked when not adjusting for smoking. In six occupations, estimates were distorted by more than 10% (-22% up to +40%). In occupations where smoking acted as a positive confounder, the proportion of confounding removed using a dichotomous smoking variable (ever/never) was around 60%. In one occupation (buyers), controlling for smoking status (ever, never) led to over-adjustment, because the percentage of smokers was high but the quantity smoked was low.

Sinonasal cancer, occupation, and tobacco smoking in European women and men.

BACKGROUND: In this analysis of European case-control studies on sinonasal cancer, we examined the risk for occupation and smoking, by gender and histological type. METHODS: The pooled data included 104 female and 451 male cases, and 241 female and 1,464 male controls. Lifetime smoking and occupational history were recoded following uniform criteria, and job-exposure matrices were applied for wood and leather dust. RESULTS: Wood dust exposure was associated with an excess risk in men (OR = 2.36, 95% CI 1.75-3.2) but not in women (OR = 1.17, 95% CI 0.31-4.47). Exposure to leather dust was associated with an excess risk in both genders. Both wood and leather dust were associated with adenocarcinomas rather than squamous cell carcinomas. Excess risks for smoking were higher for squamous cell carcinomas and higher in men than in women. CONCLUSIONS: In these European populations, occupation was associated with about 11% of all sinonasal cancers in women and 39% in men. This difference can, in part, be attributed to variation in exposure patterns between genders.

Tobacco, occupation and non-transitional-cell carcinoma of the bladder: an international case-control study.

Transitional-cell carcinoma is the dominant histological type of malignant tumors of the urinary bladder. There is limited information on risk factors for non-transitional-cell carcinoma (NTCC) of the bladder. We used data from 9 case-control studies on bladder cancer from 6 European countries to examine the association between NTCC, tobacco smoking and occupation. Information on 146 cases diagnosed with NTCC were matched by age, gender and study center to 727 non-cancer population or hospital controls and also with 722 transitional-cell-bladder-cancer controls. Lifetime smoking and occupational history were evaluated. A statistically significant excess risk for NTCC was observed for current smoking [odds ratio (OR) = 3.61, 95% confidence interval (CI) 2.08-6.28]. The risk increased with higher tobacco consumption (OR for highest tertile of pack-years = 7.01, 95% CI 3.60-13.66). The risks were higher for squamous-cell carcinomas than for other types of NTCC. Among major occupational groups, a significant excess risk was seen for field-crop and vegetable-farm workers (OR = 2.06, 95% CI 1.03-4.10). These results indicate that NTCC of the bladder is associated with smoking and specific occupations. The risk pattern seems to differ, in part, from that observed for transitional-cell carcinoma of the bladder.