Residential exposure to ambient fine particulate matter (PM2.5) and nitrogen dioxide (NO2) and incident breast cancer among young women in Ontario, Canada.

BACKGROUND: Air pollution has been classified as a human carcinogen based largely on findings for respiratory cancers. Emerging, but limited, evidence suggests that it increases the risk of breast cancer, particularly among younger women. We characterized associations between residential exposure to ambient fine particulate matter (PM2.5) and nitrogen dioxide (NO2) and breast cancer. Analyses were performed using data collected in the Ontario Environmental Health Study (OEHS). METHODS: The OEHS, a population-based case-control study, identified incident cases of breast cancer in Ontario, Canada among women aged 18-45 between 2013 and 2015. A total of 465 pathologically confirmed primary breast cancer cases were identified from the Ontario Cancer Registry, while 242 population-based controls were recruited using random-digit dialing. Self-reported questionnaires were used to collect risk factor data and residential histories. Land-use regression and remote-sensing estimates of NO2 and PM2.5, respectively, were assigned to the residential addresses at interview, five years earlier, and at menarche. Logistic regression was used to estimate odds ratios (OR) and their 95 % confidence intervals (CI) in relation to an interquartile range (IQR) increase in air pollution, adjusting for possible confounders. RESULTS: PM2.5 and NO2 were positively correlated with each other (r = 0.57). An IQR increase of PM2.5 (1.9 µg/m3) and NO2 (6.6 ppb) at interview residence were associated with higher odds of breast cancer and the adjusted ORs and 95 % CIs were 1.37 (95 % CI = 0.98-1.91) and 2.33 (95 % CI = 1.53-3.53), respectively. An increased odds of breast cancer was observed with an IQR increase in NO2 at residence five years earlier (OR = 2.16, 95 % CI: 1.41-3.31), while no association was observed with PM2.5 (OR = 0.96, 95 % CI 0.64-1.42). CONCLUSIONS: Our findings support the hypothesis that exposure to ambient air pollution, especially those from traffic sources (i.e., NO2), increases the risk of breast cancer in young women.

A geospatial assessment of industrial releases and pediatric neuroblastic tumours at diagnosis: A retrospective case series.

Environmental risk factors associated with malignancy of pediatric neuroblastic tumours are not well-known and few studies have examined the relationship between industrial emissions and neuroblastic tumour diagnosis. A retrospective case series of 310 patients was evaluated at a tertiary hospital in Toronto, Canada between January 2008, and December 2018. Data from the National Pollutant Release Inventory (NPRI) were used to estimate exposure for a dozen chemicals with known or suspected carcinogenicity or embryotoxicity. Comparative analysis and predictive logistic regression models for malignant versus benign neuroblastic tumours included variables for residential proximity, number, and type of industries, mean total emissions within 2 km, and inverse distance weighted (IDW) quantity of chemical-specific industrial emissions estimated within 10 and 50 km of cases. No significant difference was seen between malignant and benign cases with respect to the mean nearest residential distance to industry, the number or type of industry, or the mean total quantity of industrial emissions within a 2 km radius of residential location of cases. However, there were statistically significant differences in the interpolated IDW emissions of dioxins and furans released between 1993 and 2019 within 10 km. Concentrations were significantly higher in malignant neuroblastic tumours at 1.65 grams (g) toxic equivalent (TEQ) (SD 2.01 g TEQ) compared to benign neuroblastic tumours at 1.13 g TEQ (SD 0.84 g TEQ) (p = 0.05). Within 50 km 3 years prior to diagnosis, malignant cases were exposed to higher levels of aluminum, benzene, and nitrogen dioxide (p = 0.02, p = 0.04, and p = 0.02 respectively). Regression analysis of the IDW emissions within a 50 km radius revealed higher odds of exposure to benzene for malignant neuroblastic tumours (OR = 1.03, CI: 1.01-1.05, p = 0.01). These preliminary findings suggest a potential role of industrial emissions in the development of malignant pediatric neuroblastic tumours and underscore the need for further research to investigate these associations.

Early life exposure to phthalates and the development of childhood asthma among Canadian children.

BACKGROUND: Studies have demonstrated an association between phthalate exposure and childhood asthma, although results have been inconsistent. No epidemiological studies have examined exposure during the first year of life. OBJECTIVE: To investigate the association between phthalate exposures in the home environment during the first year of life, and subsequent development of childhood asthma and related symptoms. METHODS: This study used a case-cohort design including 436 randomly selected children and all additional cases of asthma at 5 years (ntotal = 129) and recurrent wheeze between 2 and 5 years (ntotal = 332) within the CHILD Cohort Study, a general population Canadian birth cohort of 3455 children. Phthalate exposure was assessed using house dust samples collected during a standardized home visit when children were 3-4 months of age. All children were assessed by specialist clinicians for asthma and allergy at 1, 3 and 5 years. Logistic regression was used to assess the association between exposure to five phthalates and asthma diagnosis at 5 years, and recurrent wheeze between 2 and 5 years, with further stratification by wheeze subtypes (late onset, persistent, transient) based on the timing of onset and persistence of wheeze symptoms. RESULTS: Di(2-ethylhexyl) phthalate (DEHP) had the highest concentration in dust (mediansubcohort = 217 µg/g), followed by benzyl butyl phthalate (BzBP) (20 µg/g). A nearly four-fold increase in risk of developing asthma was associated with the highest concentration quartile of DEHP (OR = 3.92, 95% CI: 1.87-8.24) including a positive dose-response relationship. A two-fold increase in risk of recurrent wheeze was observed across all quartiles compared to the lowest quartile of DEHP concentrations. Compared to other wheeze subtypes, stronger associations for DEHP were observed with the late onset wheezing subtype, while stronger associations for di-iso-butyl phthalate (DiBP) and BzBP were observed with the transient subtype. DISCUSSION: DEHP exposure at 3-4 months, at concentrations lower than other studies that reported an association, were associated with increased risks of asthma and recurrent wheeze among children at 5 years. These findings suggest the need to assess whether more stringent regulations are required to protect children's health, which can be informed by future work exploring the main sources of DEHP exposure.

Challenges associated with quantification of selected urinary biomarkers of exposure to tobacco products.

Tobacco use, of which cigarette smoking is the most common, is a global health concern and is directly linked to over 7 million premature deaths annually. Measurement of the levels of tobacco-related biomarkers in biological matrices reflects human exposure to the chemicals in tobacco products. Nicotine, nicotine metabolites, anatabine, and anabasine are specific to tobacco and nicotine containing products. However, as nicotine and its metabolites are ubiquitous in the environment, background contamination during sample preparation can occur, making the quantification of target analytes challenging. The main purpose of the present study was to examine quality control measures needed in the determination of urinary nicotine, nicotine metabolites, anatabine, and anabasine. Urine samples (n = 75) and NIST standard reference materials SRM 3671 and SRM 3672 were analysed. A one-step extraction procedure using cold acetone was used in this study, which involved no additional clean up. The blank matrices investigated included synthetic urine prepared with HPLC-grade water, synthetic urine prepared with Milli-Q water, and bovine urine. By adopting strategies for minimizing the background levels, very low detection limits for all the target analytes ranging from 0.025 ng/mL for 3-hydroxycotinine to 0.634 ng/mL for nicotine, were achieved. Recoveries ranged between 67% and 118% with RSD values below 20%. Intra-day and inter-day precisions were in the range of 1.1-11.7% and 4.8-25.2%, respectively. The levels of all target analytes were higher in daily smokers than in non-smokers, with the largest difference observed for 3-hydroxycotinine. No difference was observed in the levels of target analytes between individuals who were former smokers, who never smoked or who were exposed to environmental tobacco smoke (ETS), except for total nicotine equivalents (TNE), which was significantly higher in non-smokers exposed to environmental tobacco smoke compared with study participants who never smoked. The results obtained from SRM 3671 and SRM 3672 could inform a potential certification of additional biomarkers of exposure to tobacco products in those standard reference materials.

A Selective and Sensitive Gas Chromatography-Tandem Mass Spectrometry Method for Quantitation of Synthetic Musks in Human Serum.

BACKGROUND: Synthetic musk compounds are widely used as fragrances in many consumer products; however, information on human exposure and health effects is limited. Also, analytical methods for their quantification in biological matrices are limited. OBJECTIVE: In this study, an integrated method was developed and validated for the analysis of selected synthetic musk compounds in human serum. METHOD: The method is based on liquid-liquid extraction (LLE), sample clean-up by solid-phase extraction (SPE), and separation and detection by gas chromatography coupled with tandem mass spectrometry (GC-MS/MS). RESULTS: The method demonstrated good recoveries (86-105%) and high sensitivity, with low method detection limits (MDLs) ranging from 0.04 to 0.17 µg/L. The method was applied to the analysis of 10 synthetic musk compounds in 40 serum samples collected from Canadian women aged 20-44 years (20 individual samples collected in 2014 and 20 pooled samples collected in 2006). The most commonly detected compound was Galaxolide (HHCB), with median concentrations of 0.59 µg/L in samples collected in 2006, and 0.34 µg/L for samples collected in 2014. Musk ketone (MK) was not detected in any of the samples collected in 2006, but was detected in 60% of the samples collected in 2014 with a median concentration of 0.29 µg/L. Tonalide (AHTN) was detected in only one sample above its MDL (0.12 µg/L). CONCLUSIONS: This is the first study in Canada to report levels of synthetic musks in human. The data generated from this study has been used in risk screening assessment by Environment and Climate Change Canada and Health Canada.

Insecticide use and risk of non-Hodgkin lymphoma subtypes: A subset meta-analysis of the North American Pooled Project.

Insecticide use has been linked to increased risk of non-Hodgkin lymphoma (NHL), however, findings of epidemiologic studies have been inconsistent, particularly for NHL subtypes. We analyzed 1690 NHL cases and 5131 controls in the North American Pooled Project (NAPP) to investigate self-reported insecticide use and risk of NHL overall and by subtypes: follicular lymphoma (FL), diffuse large B-cell lymphoma (DLBCL) and small lymphocytic lymphoma (SLL). Odds ratios (OR) and 95% confidence intervals for each insecticide were estimated using logistic regression. Subtype-specific associations were evaluated using ASSET (Association analysis for SubSETs). Increased risks of multiple NHL subtypes were observed for lindane (OR = 1.60, 1.20-2.10: FL, DLCBL, SLL), chlordane (OR = 1.59, 1.17-2.16: FL, SLL) and DDT (OR = 1.36, 1.06-1.73: DLBCL, SLL). Positive trends were observed, within the subsets with identified associations, for increasing categories of exposure duration for lindane (Ptrend = 1.7 × 10-4 ), chlordane (Ptrend = 1.0 × 10-3 ) and DDT (Ptrend = 4.2 × 10-3 ), however, the exposure-response relationship was nonlinear. Ever use of pyrethrum was associated with an increased risk of FL (OR = 3.65, 1.45-9.15), and the relationship with duration of use appeared monotonic (OR for >10 years: OR = 5.38, 1.75-16.53; Ptrend = 3.6 × 10-3 ). Our analysis identified several novel associations between insecticide use and specific NHL subtypes, suggesting possible etiologic heterogeneity in the context of pesticide exposure.

Pesticide use and risk of Hodgkin lymphoma: results from the North American Pooled Project (NAPP).

PURPOSE: The purpose of this study was to investigate associations between pesticide exposures and risk of Hodgkin lymphoma (HL) using data from the North American Pooled Project (NAPP). METHODS: Three population-based studies conducted in Kansas, Nebraska, and six Canadian provinces (HL = 507, Controls = 3886) were pooled to estimate odds ratios and 95% confidence intervals for single (never/ever) and multiple (0, 1, 2-4, ≥ 5) pesticides used, duration (years) and, for select pesticides, frequency (days/year) using adjusted logistic regression models. An age-stratified analysis (≤ 40/ > 40 years) was conducted when numbers were sufficient. RESULTS: In an analysis of 26 individual pesticides, ever use of terbufos was significantly associated with HL (OR: 2.53, 95% CI 1.04-6.17). In age-stratified analyses, associations were stronger among those ≤ 40 years of age. No significant associations were noted among those > 40 years old; however, HL cases ≤ 40 were three times more likely to report ever using dimethoate (OR: 3.76 95% CI 1.02-33.84) and almost twice as likely to have ever used malathion (OR: 1.86 95% CI 1.00-3.47). Those ≤ 40 years of age reporting use of 5 + organophosphate insecticides had triple the odds of HL (OR: 3.00 95% CI 1.28-7.03). Longer duration of use of 2,4-D, ≥ 6 vs. 0 years, was associated with elevated odds of HL (OR: 2.59 95% CI 1.34-4.97). CONCLUSION: In the NAPP, insecticide use may increase the risk of HL, but results are based on small numbers.

Silica and asbestos exposure at work and the risk of bladder cancer in Canadian men: a population-based case-control study.

BACKGROUND: Silica and asbestos are recognized lung carcinogens. However, their role in carcinogenesis at other organs is less clear. Clearance of inhaled silica particles and asbestos fibers from the lungs may lead to translocation to sites such as the bladder where they may initiate carcinogenesis. We used data from a Canadian population-based case-control study to evaluate the associations between these workplace exposures and bladder cancer. METHODS: Data from a population-based case-control study were used to characterize associations between workplace exposure to silica and asbestos and bladder cancer among men. Bladder cancer cases (N = 658) and age-frequency matched controls (N = 1360) were recruited within the National Enhanced Cancer Surveillance System from eight Canadian provinces (1994-97). Exposure concentration, frequency and reliability for silica and asbestos were assigned to each job, based on lifetime occupational histories, using a combination of job-exposure profiles and expert review. Exposure was modeled as ever/never, highest attained concentration, duration (years), highest attained frequency (% worktime) and cumulative exposure. Odds ratios (OR) and their 95% confidence intervals (CI) were estimated using adjusted logistic regression. RESULTS: A modest (approximately 20%) increase in bladder cancer risk was found for ever having been exposed to silica, highest attained concentration and frequency of exposure but this increase was not statistically significant. Relative to unexposed, the odds of bladder cancer were 1.41 (95%CI: 1.01-1.98) times higher among men exposed to silica at work for ≥27 years. For asbestos, relative to unexposed, an increased risk of bladder cancer was observed for those first exposed ≥20 years ago (OR:2.04, 95%CI:1.25-3.34), those with a frequency of exposure of 5-30% of worktime (OR:1.45, 95%CI:1.06-1.98), and for those with < 10 years of exposure at low concentrations (OR:1.75, 95%CI:1.10-2.77) and the lower tertile of cumulative exposure (OR:1.69, 95%CI:1.07-2.65). However, no clear exposure-response relationships emerged. CONCLUSIONS: Our results indicate a slight increase in risk of bladder cancer with exposure to silica and asbestos, suggesting that the effects of these agents are broader than currently recognized. The findings from this study inform evidence-based action to enhance cancer prevention efforts, particularly for workers in industries with regular exposure.

Early life exposure to phthalates in the Canadian Healthy Infant Longitudinal Development (CHILD) study: a multi-city birth cohort.

BACKGROUND: Few studies have examined phthalate exposure during infancy and early life, critical windows of development. The Canadian Healthy Infant Longitudinal Development (CHILD) study, a population-based birth cohort, ascertained multiple exposures during early life. OBJECTIVE: To characterize exposure to phthalates during infancy and early childhood. METHODS: Environmental questionnaires were administered, and urine samples collected at 3, 12, and 36 months. In the first 1578 children, urine was analyzed for eight phthalate metabolites: mono-methyl phthalate (MMP), mono-ethyl phthalate (MEP), mono-butyl phthalate (MBP), mono-benzyl phthalate (MBzP), mono-2-ethylhexyl phthalate (MEHP), mono-(2-ethyl-5-oxohexyl) phthalate (MEOHP), mono-(2-ethyl-5-hydroxyhexyl) phthalate (MEHHP), and mono-3-carboxypropyl phthalate (MCPP). Geometric mean (GM) concentrations were calculated by age, together with factors that may influence concentrations. Trends with age were examined using mixed models and differences within factors examined using ANOVA. RESULTS: The highest urinary concentration was for the metabolite MBP at all ages (GM: 15-32 ng/mL). Concentrations of all phthalate metabolites significantly increased with age ranging from GM: 0.5-15.1 ng/mL at 3 months and 1.9-32.1 ng/mL at 36 months. Concentrations of all metabolites were higher in the lowest income categories except for MEHP at 3 months, among children with any breastfeeding at 12 months, and in urine collected on dates with warmer outdoor temperatures (>17 °C), except for MBzP at 3 months and MEHP at 3 and 12 months. No consistent differences were found by gender, study site, or maternal age. CONCLUSIONS: Higher phthalate metabolite concentrations were observed among children in lower income families. Examination of factors associated with income could inform interventions aimed to reduce infant phthalate exposure.

Exposure to crystalline silica in Canadian workplaces and the risk of kidney cancer.

OBJECTIVES: The causes of kidney cancer are not well understood though occupational exposures are thought to play a role. Crystalline silica is a known human carcinogen, and despite previous links with kidney disease, there have been few studies investigating its association with kidney cancer. We addressed this research gap using a population-based case-control study of Canadian men. METHODS: Questionnaire data were obtained from individuals with histologically confirmed kidney cancer, and population-based controls recruited from eight Canadian provinces (1994-1997). An industrial hygienist characterised participants' lifetime occupational exposure, and their confidence in the assessment (possibly, probably or definitely exposed) to silica on three dimensions (intensity, frequency and duration), and cumulative exposure was estimated. Logistic regression was used to estimate ORs and 95% CIs, adjusting for potential confounders. RESULTS: Nearly half of the 689 kidney cancer cases (49%) and 2369 controls (44%) had ever been occupationally exposed to crystalline silica. In a fully adjusted model, workers ever-exposed to silica had a slightly increased risk of kidney cancer relative to those who were unexposed (OR 1.10, 95% CI 0.92 to 1.32). Odds were modestly (and generally not statistically significantly) increased for models with duration of exposure and cumulative exposure, though exposure-response relationships were not evident. CONCLUSIONS: Our findings do not provide evidence that occupational exposure to crystalline silica increases risk of kidney cancer in men.

Glyphosate use and associations with non-Hodgkin lymphoma major histological sub-types: findings from the North American Pooled Project.

Objectives Some epidemiological studies have suggested positive associations between glyphosate use and non-Hodgkin lymphoma (NHL), but evidence is inconsistent and few studies could evaluate histological sub-types. Here, associations between glyphosate use and NHL incidence overall and by histological sub-type were evaluated in a pooled analysis of case-control studies. Methods The analysis included 1690 NHL cases [647 diffuse large B-cell lymphoma (DLBCL), 468 follicular lymphoma (FL), 171 small lymphocytic lymphoma (SLL), and 404 other sub-types] and 5131 controls. Logistic regression was used to estimate adjusted odds ratios (OR) and 95% confidence intervals (CI) for NHL overall and sub-types with self-reported ever/never, duration, frequency, and lifetime-days of glyphosate use. Results Subjects who ever used glyphosate had an excess of NHL overall (OR 1.43, 95% CI 1.11-1.83). After adjustment for other pesticides, the OR for NHL overall with "ever use" was 1.13 (95% CI 0.84-1.51), with a statistically significant association for handling glyphosate >2 days/year (OR 1.73, 95% CI 1.02-2.94, P-trend=0.2). In pesticide-adjusted sub-type analyses, the ordinal measure of lifetime-days was statistically significant (P=0.03) for SLL, and associations were elevated, but not statistically significant, for ever years or days/year of use. Handling glyphosate >2 days/year had an excess of DLBCL (OR 2.14, 95% CI 1.07-4.28; P-trend=0.2). However, as with the other sub-types, consistent patterns of association across different metrics were not observed. Conclusions There was some limited evidence of an association between glyphosate use and NHL in this pooled analysis. Suggestive associations, especially for SLL, deserve additional attention.

Non-Hodgkin lymphoma risk and organophosphate and carbamate insecticide use in the north American pooled project.

Organophosphates and carbamates have been among the most commonly used insecticides, with both agricultural and residential uses. Previous studies have suggested associations of non-Hodgkin lymphoma (NHL) with some of these chemicals; however, many studies have been limited in their ability to evaluate associations with lymphoma subtypes. We evaluated the use of eleven organophosphate and two carbamate insecticides in association with NHL in the North American Pooled Project, which includes data from case-control studies in the United States and Canada (1690 cases/5131 controls). We used unconditional logistic regression adjusting for potential confounders, including use of other pesticides, to estimate odds ratios (OR) and 95% confidence intervals (CI) for associations between these chemicals and NHL overall, and NHL subtypes, i.e., follicular (FL), diffuse large B-cell (DLBCL), small lymphocytic lymphoma (SLL) and others. Ever use of malathion was associated with increased risk of NHL overall (OR = 1.43; 95% CI: 1.14-1.81) compared with never users. Categories using tertiles of duration (<4 yrs., 4-12 yrs., and >12 yrs) also showed a significant exposure-response for increasing years of use of malathion and risk of NHL (OR<4vsUnex = 1.33 (0.88, 2.03), OR4-12vsUnex = 1.42 (1.02, 1.96), OR>12vsUnex = 1.55 (1.05, 2.28, p-trend < 0.01)). In addition, malathion use was statistically significantly associated with FL (OR = 1.58; 95% CI: 1.11-2.27) and DLBCL (OR = 1.61; 95% CI: 1.16-2.22) while there were no apparent associations with SLL or other subtypes, the p-value for heterogeneity across subtypes, however, was not significant. These results support previous studies suggesting an association between insecticide use and NHL overall, and provide new information on associations with NHL subtypes.

Are cell phones an indicator of personal exposure to organophosphate flame retardants and plasticizers?

BACKGROUND: Exposure to organophosphate ester (OPE) flame retardants and plasticizers is widespread and is of concern due to their toxicity. OBJECTIVES: To investigate relationships between and within OPE concentrations in air, dust, hands, electronic product wipes and urinary metabolites with the goal of identifying product sources and exposure pathways. METHODS: Women in Toronto and Ottawa, Canada, provided a urine sample, two sets of hand wipes, access to their homes for air and dust sampling, and completed a questionnaire. OPE concentrations were obtained for air and floor dust in the bedroom (n = 51) and most used room (n = 26), hand wipes (n = 204), and surface wipes of handheld (n = 74) and non-handheld electronic devices (n = 125). All air, dust and wipe samples were analyzed for 23 OPE compounds; urine samples (n = 44) were analyzed for 8 OPE metabolites. RESULTS: Five-8 OPEs were detected in >80% of samples depending on the sample type. OPE median concentrations in hand wipes taken 3 weeks apart were not significantly different. Palms had higher concentrations than the back of hands; both were significantly correlated. Concentrations of 9 OPEs were significantly higher in surface wipes of handheld than non-handheld electronic devices. Six OPEs in hand wipes were significantly correlated with cell phone wipes, with two to four OPEs significantly correlated with tablet, laptop and television wipes. Multiple regression models using hand wipes, cell phone wipes and dust explained 8-33% of the variation in creatinine-adjusted urinary metabolites; air concentrations did not have explanatory power. OPEs in cell phone wipes explained the greatest variation in urinary metabolites. CONCLUSIONS: Handheld electronic devices, notably cell phones, may either be sources or indicators of OPE exposure through hand-to-mouth and/or dermal uptake.

Postdiagnosis Isoflavone and Lignan Intake in Newly Diagnosed Breast Cancer Patients: Cross-Sectional Survey Shows Considerable Intake from Previously Unassessed High-Lignan Foods.

BACKGROUND: Isoflavones and lignans (phytoestrogens) are dietary components with potential anticarcinogenic effects. Although the intake of isoflavones and lignans may affect breast cancer treatment and prognosis-and associations may differ by menopausal status-postdiagnosis intake data are limited. OBJECTIVE: We aimed to describe postdiagnosis isoflavone and lignan intake in newly diagnosed breast cancer patients, examine differences by menopausal status and phytoestrogen type, and inform the assessment of diet and survival in future prognostic studies. METHODS: Our cross-sectional study included 278 women aged 25-74 y, diagnosed with pathologically confirmed breast cancer in April-May 2010 and identified using the Ontario Cancer Registry. Intake in the previous 2 mo was assessed using questionnaires listing 17 soy and 3 high-lignan foods (flaxseed, flaxseed bread, sesame seeds), completed 71 d after breast cancer diagnosis, on average. Food consumption by menopausal status was examined. Geometric mean and median phytoestrogen intakes were estimated among all patients and in consumers only; differences by menopausal status and phytoestrogen type were assessed. RESULTS: Among all patients, foods were similarly consumed by menopausal status and isoflavone intakes were low (median: 56 µg/d). Consumers (n = 219) had higher intakes (median isoflavones: 1808 µg/d); 7% of isoflavone and 21% of lignan consumers had intakes ≥10 mg/d. Intakes were higher in premenopausal than in postmenopausal consumers, particularly for lignans, but were not significantly different (median lignans: 4375 compared with 1863 µg/d; P = 0.07). Lignans were significantly higher than isoflavones among most consumers (postmenopausal means: 746 compared with 100 µg/d; P < 0.0001). CONCLUSIONS: Postdiagnosis lignan intakes from 3 high-content foods may be considerable among newly diagnosed breast cancer patients, yet they have been unassessed in previous prognostic studies. The inclusion of these foods in dietary assessment methods may improve future intake estimates and the distributions on which breast cancer survival analyses are based.

Workplace exposure to asbestos and the risk of kidney cancer in Canadian men.

OBJECTIVE: Previous studies considered the role of occupational causes in kidney cancer but were limited by small sample sizes and imprecise exposure assessment. This study examined the relationship between occupational exposure to asbestos and the risk of kidney cancer across a range of jobs in a large, population-based case-control study in Canada. METHODS: Data were from the case-control component of the National Enhanced Cancer Surveillance System, a study conducted between 1994 and 1997 in eight Canadian provinces. Male kidney cancer cases, histologically confirmed, and controls completed questionnaires on socio-demographics, anthropometry, diet, smoking, secondhand smoke exposure, and physical activity. Occupational histories were also collected, including each job held for at least 1 year since the age of 18. Occupational hygienists, blinded to case status, assigned exposure to asbestos, considering intensity, frequency, and probability of exposure (each 3-point scales). Logistic regression was used to estimate the odds of kidney cancer in exposed participants (defined using three metrics) compared to those without asbestos exposure. RESULTS: There were 712 cases and 2454 controls in these analyses. Ever-exposure to asbestos was associated with 20% increased odds of kidney cancer compared to unexposed workers (OR 1.2, 95% confidence interval 1.0-1.4 when including possibly exposed workers). A small increase in risk was observed with cumulative exposure, while increasing intensity of exposure was related to increased odds of kidney cancer. CONCLUSIONS: This study found some evidence for an association between occupational exposure to asbestos and kidney cancer. Higher intensity of exposure to asbestos had the strongest relationship with kidney cancer risk.

Occupational Exposure to Diesel and Gasoline Engine Exhausts and the Risk of Kidney Cancer in Canadian Men.

Introduction: Kidney cancer is the fifth most common incident cancer in Canadian men. Diesel and gasoline exhausts are common workplace exposures that have been examined as risk factors for non-lung cancer sites, including the kidney, but limitations in exposure assessment methods have contributed to inconsistent findings. The objective of this study was to assess the relationship between occupational gasoline and diesel engine exhausts and the risk of kidney cancer in men. Methods: The National Enhanced Cancer Surveillance System (NECSS) is a Canadian population-based case-control study conducted in 1994-1997. Incident kidney cancer cases were identified using provincial registries, while the control series was identified through random-digit dialing, or provincial administrative databases. Self-reported questionnaires were used to obtain information on lifetime occupational history and cancer risk factors. Two hygienists, blinded to case status, coded occupational histories for diesel and gasoline exhaust exposures using concentration, frequency, duration, and reliability. Logistic regression was used to estimate odds ratios (ORs) and 95% confidence intervals (CIs) separately by exhaust type. The separate and combined impacts of both engine exhausts were also examined. ORs were adjusted for age, province, body mass index, occupational secondhand smoke exposure, and education. Results: Of the kidney cancer cases (n = 712), 372 (52%) had exposure to both exhausts at some point, and 984 (40%) of the controls (n = 2457) were ever exposed. Workers who had ever been exposed to engine exhausts were more likely to have kidney cancer than those who were never exposed (OR diesel = 1.23, 95% CI = 0.99-1.53; OR gasoline = 1.51, 95% CI = 1.23-1.86). Exposure to gasoline exhaust was consistently associated with kidney cancer in a dose-response manner (P value for trends in highest attained and cumulative exposure both <0.0001). Those men with high cumulative exposure to both gasoline and diesel exhaust had a 76% increased odds of kidney cancer (95% CI = 1.27-2.43). Conclusions: This study provides evidence that occupational gasoline, and to a lesser extent, diesel exhaust exposure may increase the risk of kidney cancer.

Passive air sampling of flame retardants and plasticizers in Canadian homes using PDMS, XAD-coated PDMS and PUF samplers.

Passive air samplers (PAS) were evaluated for measuring indoor concentrations of phthalates, novel brominated flame retardants (N-BFRs), polybrominated diphenyl ethers (PBDEs), and organophosphate esters (OPEs). Sampling rates were obtained from a 50-day calibration study for two newly introduced PAS, polydimethylsiloxane (PDMS) or silicone rubber PAS (one with and one without a coating of styrene divinyl benzene co-polymer, XAD) and the commonly used polyurethane foam (PUF) PAS. Average sampling rates normalized to PAS surface area were 1.5 ±â€¯1.1 m3 day-1 dm-2 for both unsheltered PDMS and XAD-PDMS, and 0.90 m3 ±â€¯0.6 day-1dm-2 for partially sheltered PUF. These values were derived based on the compound-specific sampling rates measured here and in the literature for the PAS tested, to reasonably account for site-specific variability of sampling rates. PDMS and PUF were co-deployed for three weeks in 51 homes located in Ottawa and Toronto, Canada. Duplicate PUF and PDMS samplers gave concentrations within 10% of each other. PDMS and PUF-derived air concentrations were not statistically different for gas-phase compounds. PUF had a higher detection of particle-phase compounds such as some OPEs. Phthalate and OPE air concentrations were ∼100 times higher than those of N-BFRs and PBDEs. Concentrations were not systematically related to PM10, temperature or relative humidity. We conclude that both PAS provide replicable estimates of indoor concentrations of these targeted semi-volatile organic compounds (SVOCs) over a three-week deployment period. However, PUF is advantageous for collecting a wider range of compounds including those in the particle phase.

Prostate cancer in firefighting and police work: a systematic review and meta-analysis of epidemiologic studies.

OBJECTIVES: We conducted a systematic review and meta-analysis to evaluate potential associations between firefighting and police occupations, and prostate cancer incidence and mortality. METHODS: Original epidemiological studies published from 1980 to 2017 were identified through PubMed and Web of Science. Studies were included if they contained specific job titles for ever/never firefighting and police work and associated prostate cancer risk estimates with 95% confidence intervals (CI). Study quality was assessed using a 20-point checklist. Prostate cancer meta-risk estimates (mRE) and corresponding 95% CIs were calculated for firefighting and police work separately and by various study characteristics using random effects models. Between-study heterogeneity was evaluated using the I2 score. Publication bias was assessed using Begg's and Egger's tests. RESULTS: A total of 26 firefighter and 12 police studies were included in the meta-analysis, with quality assessment scores ranging from 7 to 19 points. For firefighter studies, the prostate cancer incidence mRE was 1.17 (95% CI = 1.08-1.28, I2 = 72%) and the mortality mRE was 1.12 (95% CI = 0.92-1.36, I2 = 50%). The mRE for police incidence studies was 1.14 (95% CI = 1.02-1.28; I2 = 33%); for mortality studies, the mRE was 1.08 (95% CI = 0.80-1.45; I2 = 0%). By study design, mREs for both firefighter and police studies were similar to estimates of incidence and mortality. CONCLUSION: Small excess risks of prostate cancer were observed from firefighter studies with moderate to substantial heterogeneity and a relatively small number of police studies, respectively. There is a need for further studies to examine police occupations and to assess unique and shared exposures in firefighting and police work.

Occupation and risk of prostate cancer in Canadian men: A case-control study across eight Canadian provinces.

BACKGROUND: The etiology of prostate cancer continues to be poorly understood, including the role of occupation. Past Canadian studies have not been able to thoroughly examine prostate cancer by occupation with detailed information on individual level factors. METHODS: Occupation, industry and prostate cancer were examined using data from the National Enhanced Cancer Surveillance System, a large population-based case-control study conducted across eight Canadian provinces from 1994 to 1997. This analysis included 1737 incident cases and 1803 controls aged 50 to 79 years. Lifetime occupational histories were used to group individuals by occupation and industry employment. Odds ratios and 95% confidence intervals were calculated and adjustments were made for known and possible risk factors. RESULTS: By occupation, elevated risks were observed in farming and farm management (OR=1.37, 95% CI 1.02-1.84), armed forces (OR=1.33, 95% CI 1.06-1.65) and legal work (OR=2.58, 95% CI 1.05-6.35). Elevated risks were also observed in office work (OR=1.20, 95% CI 1.00-1.43) and plumbing (OR=1.77, 95% CI 1.07-2.93) and with ≥10 years duration of employment. Decreased risks were observed in senior management (OR=0.65, 95% CI 0.46-0.91), construction management (OR=0.69, 95% CI 0.50-0.94) and travel work (OR=0.37, 95% CI 0.16-0.88). Industry results were similar to occupation results, except for an elevated risk in forestry/logging (OR=1.54, 95% CI 1.06-2.25) and a decreased risk in primary metal products (OR=0.70, 95% CI 0.51-0.96). CONCLUSION: This study presents associations between occupation, industry and prostate cancer, while accounting for individual level factors. Further research is needed on potential job-specific exposures and screening behaviours.