Vehicular traffic exposure to polycyclic aromatic hydrocarbons and breast cancer risk

Polycyclic aromatic hydrocarbons (PAHs) are ubiquitous environmental pollutants, known human lung carcinogens, and potent mammary carcinogens in animal models. However, the association between PAHs and breast cancer in women is unclear. Vehicular traffic is a major source of ambient PAH exposure. This study evaluates the association between residential exposure to vehicular traffic-related PAHs and risk of breast cancer, overall and by tumor subtype, and within strata of nucleotide excision repair and base excision repair genotypes and fruit/vegetable intake. For this population-based study, residential histories, dietary intake, and other factors were assessed in 1996-1997 for 1,508 newly diagnosed breast cancer cases and 1,556 controls. Residential traffic exposure estimates were reconstructed using a validated model for the years 1960 through 1995. The following single nucleotide polymorphisms were genotyped: ERCC1 8092C/A, OGG1 Ser326Cys, XPA -4A/G, XPD Lys751Gln and Asp312Asn, XPF Arg415Gln, XPG Asp1104His, XRCC1 Arg194Trp and Arg399Gln. Medical records and archived tumor tissue were used to determine case tumor subtype. In spline figures, which were used to inform quantile cutpoints for regression models, breast cancer risk was increased among women with the top 1% of traffic PAH exposures. Odds ratios (and 95% confidence intervals) for breast cancer, estimated using unconditional logistic regression, were modestly elevated for the top 5% of long-term 1960-1990 traffic PAH exposure estimates, compared with below the median (1.44 (0.78, 2.68)). Associations between recent traffic exposure in 1995 (top 5% vs. below the median) and breast cancer were attenuated toward the null (1.14 (0.80, 1.64)), but were stronger among women with low fruit/vegetable intake (1.46 (0.89, 2.40)) and hormone-receptor negative tumors (1.67 (0.91, 3.05)). Associations were approximately two- to three-fold stronger among women with variant alleles for XPD (Lys751Gln) and XRCC1 (Arg194Trp), and wild-type alleles for XRCC1 (Arg399Gln) and OGG1 (Ser326Cys), when comparing the upper and lower tertiles of traffic exposure during 1995 or 1960-1990. This study reports positive associations between traffic-related PAH exposure and breast cancer risk among women with comparatively high long-term traffic exposures or among those with certain DNA repair genotypes, low fruit/vegetable intake or hormone receptor negative tumors, although confidence intervals were wide.Doctor of Philosoph

Exposure to sub-chronic and long-term particulate air pollution and heart rate variability in an elderly cohort: the Normative Aging Study

Background: Short-term particulate air pollution exposure is associated with reduced heart rate variability (HRV), a risk factor for cardiovascular morbidity and mortality, in many studies. Associations with sub-chronic or long-term exposures, however, have been sparsely investigated. We evaluated the effect of fine particulate matter (PM2.5) and black carbon (BC) exposures on HRV in an elderly cohort: the Normative Aging Study. Methods: We measured power in high frequency (HF) and low frequency (LF), standard deviation of normal-to-normal intervals (SDNN), and the LF:HF ratio among participants from the Greater Boston area. Residential BC exposures for 540 men (1161 study visits, 2000–2011) were estimated using a spatio-temporal land use regression model, and residential PM2.5 exposures for 475 men (992 visits, 2003–2011) were modeled using a hybrid satellite based and land-use model. We evaluated associations between moving averages of sub-chronic (3–84 day) and long-term (1 year) pollutant exposure estimates and HRV parameters using linear mixed models. Results: One-standard deviation increases in sub-chronic, but not long-term, BC were associated with reduced HF, LF, and SDNN and an increased LF:HF ratio (e.g., 28 day BC: −2.3 % HF [95 % CI:−4.6, −0.02]). Sub-chronic and long-term PM2.5 showed evidence of relations to an increased LF and LF:HF ratio (e.g., 1 year PM: 21.0 % LF:HF [8.6, 34.8]), but not to HF or SDNN, though the effect estimates were very imprecise and mostly spanned the null. Conclusions: We observed some evidence of a relation between longer-term BC and PM2.5 exposures and changes in HRV in an elderly cohort. While previous studies focused on short-term air pollution exposures, our results suggest that longer-term exposures may influence cardiac autonomic function. Electronic supplementary material The online version of this article (doi:10.1186/s12940-015-0074-z) contains supplementary material, which is available to authorized users

A comparison of food sources of nudibranch mollusks at different depths off the Kuril Islands using fatty acid trophic markers

Gastropod molluscs such as nudibranchs are important members of deep-sea benthic ecosystems. However, data on the trophic ecology and feeding specialization of these animals are limited to date. The method of fatty acid trophic markers (FATM) was applied to determine the dietary preferences of nudibranchs off the Kuril Islands. Fatty acid (FA) compositions of Dendronotus sp., Tritonia tetraquetra, and Colga pacifica collected from deep waters were analyzed and compared with those of Aeolidia papillosa and Coryphella verrucosa from the offshore zone. The high level of FATM such as 22:5n-6 and C20 monounsaturated FAs indicated that Dendronotus sp. preys on sea anemones and/or anthoathecates hydroids similarly to that of shallow-water species A. papillosa and C. verrucosa. The high percentage of tetracosapolyenoic acids and the ratio 24:6n-3/24:5n-6 indicated that T. tetraquetra preys on soft corals such as Gersemia and/or Acanella at a depth of 250 m, but soft corals of the family Primnoidae may be the main item in the diet of T. tetraquetra at a depth of 500 m. The high content of Δ 7,13-22:2 and 22:6n-3 shows that C. pacifica can feed on bryozoans. In C. pacifica, 22:5n-6 may be synthesized intrinsically by the mollusks, whereas odd-chain and branched saturated FAs originate from associated bacteria

The Impact of Workplace Harassment on Health in a Working Cohort

Background: Workplace abuse, including sexual harassment, is frequently experienced worldwide and is related to adverse mental health outcomes, and injuries. Flight attendants are an understudied occupational group and are susceptible to harassment due to working in a feminized, client-facing occupation with few protections or sanctioned responses against aggressive behaviors.Objective: We investigated the relationship between workplace abuse and health in a cohort of cabin crew. We also aimed to characterize perpetrator profiles.Methods: We conducted our study among 4,459U.S. and Canada-based participants from the Harvard Flight Attendant Health Study using multivariate logistic regression. Our exposures of interest were episodes of workplace abuse in the past year. We evaluated several mental and physical health outcomes, including depression, fatigue, musculoskeletal injuries, and general workplace injuries.Results: We report that exposures to verbal abuse, sexual harassment, and sexual assault are common among cabin crew, with 63, 26, and 2% of respondents, respectively, reporting harassment in the past year alone. Workplace abuse was associated with depression, sleep disturbances, and musculoskeletal injuries among male and female crew, with a trend toward increasing odds ratios (ORs) given a higher frequency of events. For example, sexual harassment was related to an increased odds for depression (OR = 1.91, 95% confidence interval [CI]: 1.51–2.30), which increased in a dose response-like manner among women reporting harassment once (OR = 1.44, 95% CI: 0.93–1.95), 2–3 times (OR = 1.83, 95% CI: 1.29–2.38), and 4 or more times (OR = 4.12, 95% CI: 3.18–5.06). We found that passengers were the primary perpetrators of abuse.Conclusions: Our study is the first to comprehensively characterize workplace abuse and harassment and its relation to health in a largely female customer-facing workforce. The strong associations with health outcomes observed in our study highlights the question of how workplace policies can be altered to mitigate prevalent abuses. Clinicians could also consider how jobs with high emotional labor demands may predispose people to adverse health outcomes, educate patients regarding their psychological/physical responses and coping strategies, and be aware of signs of distress in patients working in such occupations in order to direct them to the appropriate treatments and therapies

Black Carbon Exposure, Oxidative Stress Genes, and Blood Pressure in a Repeated-measures Study

Background: Particulate matter (PM) air pollution has been associated with cardiovascular morbidity and mortality, and elevated blood pressure (BP) is a known risk factor for cardiovascular disease. A small number of studies have investigated the relationship between PM and BP and found mixed results. Evidence suggests that traffic-related air pollution contributes significantly to PM-related cardiovascular effects. Objectives: We hypothesized that black carbon (BC), a traffic-related combustion by-product, would be more strongly associated with BP than would fine PM [aerodynamic diameter ≤ 2.5 μm (PM$_{2.5}$)], a heterogeneous PM mixture, and that these effects would be larger among participants with genetic variants associated with impaired antioxidative defense. Methods: We performed a repeated-measures analysis in elderly men to analyze associations between PM$_{2.5}$ and BC exposure and BP using mixed-effects models with random intercepts, adjusting for potential confounders. We also examined statistical interaction between BC and genetic variants related to oxidative stress defense: GSTM1, GSTP1, GSTT1, NQO1, catalase, and HMOX-1. Results: A 1-SD increase in BC concentration was associated with a 1.5-mmHg increase in systolic BP [95% confidence interval (CI), 0.1–2.8] and a 0.9-mmHg increase in diastolic BP (95% CI, 0.2–1.6). We observed no evidence of statistical interaction between BC and any of the genetic variants examined and found no association between PM$_{2.5}$ and BP. Conclusions: We observed positive associations between BP and BC, but not between BP and PM$_{2.5}$, and found no evidence of effect modification of the association between BC and BP by gene variants related to antioxidative defense

Imputation method for lifetime exposure assessment in air pollution epidemiologic studies

Background: Environmental epidemiology, when focused on the life course of exposure to a specific pollutant, requires historical exposure estimates that are difficult to obtain for the full time period due to gaps in the historical record, especially in earlier years. We show that these gaps can be filled by applying multiple imputation methods to a formal risk equation that incorporates lifetime exposure. We also address challenges that arise, including choice of imputation method, potential bias in regression coefficients, and uncertainty in age-at-exposure sensitivities. Methods: During time periods when parameters needed in the risk equation are missing for an individual, the parameters are filled by an imputation model using group level information or interpolation. A random component is added to match the variance found in the estimates for study subjects not needing imputation. The process is repeated to obtain multiple data sets, whose regressions against health data can be combined statistically to develop confidence limits using Rubin’s rules to account for the uncertainty introduced by the imputations. To test for possible recall bias between cases and controls, which can occur when historical residence location is obtained by interview, and which can lead to misclassification of imputed exposure by disease status, we introduce an “incompleteness index,” equal to the percentage of dose imputed (PDI) for a subject. “Effective doses” can be computed using different functional dependencies of relative risk on age of exposure, allowing intercomparison of different risk models. To illustrate our approach, we quantify lifetime exposure (dose) from traffic air pollution in an established case–control study on Long Island, New York, where considerable in-migration occurred over a period of many decades. Results: The major result is the described approach to imputation. The illustrative example revealed potential recall bias, suggesting that regressions against health data should be done as a function of PDI to check for consistency of results. The 1% of study subjects who lived for long durations near heavily trafficked intersections, had very high cumulative exposures. Thus, imputation methods must be designed to reproduce non-standard distributions. Conclusions: Our approach meets a number of methodological challenges to extending historical exposure reconstruction over a lifetime and shows promise for environmental epidemiology. Application to assessment of breast cancer risks will be reported in a subsequent manuscript

Black Carbon Exposure, Oxidative Stress Genes, and Blood Pressure in a Repeated Measures Study

BackgroundParticulate matter (PM) air pollution has been associated with cardiovascular morbidity and mortality, and elevated blood pressure (BP) is a known risk factor for cardiovascular disease. A small number of studies have investigated the relationship between PM and BP and found mixed results. Evidence suggests that traffic-related air pollution contributes significantly to PM-related cardiovascular effects.ObjectivesWe hypothesized that black carbon (BC), a traffic-related combustion by-product, would be more strongly associated with BP than would fine PM [aerodynamic diameter ≤ 2.5 μm (PM2.5)], a heterogeneous PM mixture, and that these effects would be larger among participants with genetic variants associated with impaired antioxidative defense.MethodsWe performed a repeated-measures analysis in elderly men to analyze associations between PM2.5 and BC exposure and BP using mixed-effects models with random intercepts, adjusting for potential confounders. We also examined statistical interaction between BC and genetic variants related to oxidative stress defense: GSTM1, GSTP1, GSTT1, NQO1, catalase, and HMOX-1.ResultsA 1-SD increase in BC concentration was associated with a 1.5-mmHg increase in systolic BP [95% confidence interval (CI), 0.1–2.8] and a 0.9-mmHg increase in diastolic BP (95% CI, 0.2–1.6). We observed no evidence of statistical interaction between BC and any of the genetic variants examined and found no association between PM2.5 and BP.ConclusionsWe observed positive associations between BP and BC, but not between BP and PM2.5, and found no evidence of effect modification of the association between BC and BP by gene variants related to antioxidative defense

Black Carbon Exposure, Oxidative Stress Genes, and Blood Pressure in a Repeated-Measures Study

BACKGROUND. Particulate matter (PM) air pollution has been associated with cardiovascular morbidity and mortality, and elevated blood pressure (BP) is a known risk factor for cardiovascular disease. A small number of studies have investigated the relationship between PM and BP and found mixed results. Evidence suggests that traffic-related air pollution contributes significantly to PM-related cardiovascular effects. OBJECTIVES. We hypothesized that black carbon (BC), a traffic-related combustion by-product, would be more strongly associated with BP than would fine PM [aerodynamic diameter ≤ 2.5 μm (PM2.5)], a heterogeneous PM mixture, and that these effects would be larger among participants with genetic variants associated with impaired antioxidative defense. METHODS. We performed a repeated-measures analysis in elderly men to analyze associations between PM2.5 and BC exposure and BP using mixed-effects models with random intercepts, adjusting for potential confounders. We also examined statistical interaction between BC and genetic variants related to oxidative stress defense: GSTM1, GSTP1, GSTT1, NQO1, catalase, and HMOX-1. RESULTS. A 1-SD increase in BC concentration was associated with a 1.5-mmHg increase in systolic BP [95% confidence interval (CI), 0.1-2.8] and a 0.9-mmHg increase in diastolic BP (95% CI, 0.2-1.6). We observed no evidence of statistical interaction between BC and any of the genetic variants examined and found no association between PM2.5 and BP. CONCLUSIONS. We observed positive associations between BP and BC, but not between BP and PM2.5, and found no evidence of effect modification of the association between BC and BP by gene variants related to antioxidative defense.National Institute of Environmental Health Sciences (ES015172, ES014663); National Cancer Institute (2-T32-CA009330); United States Environmental Protection Agency (R832416); United States Deparment of Veterans Affairs; Massachusetts Veterans Epidemiology Research and Information Cente

Association between long-term exposure to traffic particles and blood pressure in the Veterans Administration Normative Aging Study

Particulate air pollution is associated with cardiovascular events, but the mechanisms are not fully understood. The main objective was to assess the relationship between long-term exposure to traffic-related air pollution and blood pressure (BP)

Polycyclic aromatic hydrocarbons and postmenopausal breast cancer: An evaluation of effect measure modification by body mass index and weight change

Polycyclic aromatic hydrocarbons (PAHs) have been linked to breast cancer in many, but not all, previous studies. PAHs are lipophilic and stored in fat tissue, which we hypothesized may result in constant low-dose exposure to these carcinogens. No previous studies have evaluated whether obesity modifies associations between multiple measures of PAHs and breast cancer incidence