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Little is known about personal and time-integrated exposure to past and current used pesticides in agricultural areas and within-family exposure similarities. We aimed to assess exposure to pesticides using silicone wristbands in child/guardian pairs living on farms and in villages within two agricultural areas in South Africa. Using silicone wristbands, we quantified 21 pesticides in child/guardian pairs in 38 households over six days in 2018. Levels (in ng/g wristband) of pesticides and their transformation products (12 current-use pesticides and nine organochlorine pesticides) were measured using GC-MS/MS. We assessed the correlation between pesticide levels and between household members using Spearman correlation coefficients (r(s)). Multivariable generalized least squares (GLS) models, using household id as intercept, were used to determine level of agreement between household members, exposure differences between children and guardians and exposure predictors (study area, household location [farm vs. village] and household pesticide use). We detected 16 pesticides with highest detection frequencies for deltamethrin (89%), chlorpyrifos (78%), boscalid (56%), cypermethrin (55%), and p,p'-DDT (48%). Most wristbands (92%) contained two or more pesticides (median seven (range one to 12)). Children had higher concentrations than guardians for four pesticides. Correlation between the pesticide levels were in most cases moderate (rs 0.30-0.68) and stronger in children than in guardians. Five pesticides showed moderate to strong correlation between household members, with the strongest correlation for boscalid (r(s) 0.84). Exposure differences between the two agricultural areas were observed for chlorpyri fas, diazinon, pmthiofos, cypermethrin, boscalid, p,p'-DDT and p,p'-DDE and within areas for cypermethrin. We showed that for several pesticides children had higher exposure levels than guardians. The positive correlations observed for child/guardian pairs living in the same household suggest non-occupational shared exposure pathways in these communities.

Chronic inflammation may be involved in cancer development and progression. Using 28 inflammatory-related proteins collected from prospective blood samples from two case-control studies nested in the Italian component of the European Prospective Investigation into Cancer and nutrition (n = 261) and in the Northern Sweden Health and Disease Study (n = 402), we tested the hypothesis that an inflammatory score is associated with breast cancer (BC) and Β-cell Non-Hodgkin Lymphoma (B-cell NHL, including 68 multiple myeloma cases) onset. We modelled the relationship between this inflammatory score and the two cancers studied: (BC and B-cell NHL) using generalised linear models, and assessed, through adjustments the role of behaviours and lifestyle factors. Analyses were performed by cancer types pooling both populations, and stratified by cohorts, and time to diagnosis. Our results suggested a lower inflammatory score in B-cell NHL cases (β = −1.28, p = 0.012), and, to lesser, extent with BC (β = −0.96, p = 0.33) compared to controls, mainly driven by cancer cases diagnosed less than 6 years after enrolment. These associations were not affected by subsequent adjustments for potential intermediate confounders, notably behaviours. Sensitivity analyses indicated that our findings were not affected by the way the inflammatory score was calculated. These observations call for further studies involving larger populations, larger variety of cancer types and repeated measures of larger panel of inflammatory markers.

Objectives: To characterize the impact of PCB exposure on DNA methylation in peripheral blood leucocytes and to evaluate the corresponding changes in relation to possible health effects, with a focus on B-cell lymphoma. Methods: We conducted an epigenome-wide association study on 611 adults free of diagnosed disease, living in Italy and Sweden, in whom we also measured plasma concentrations of 6 PCB congeners, DDE and hexachlorobenzene. Results: We identified 650 CpG sites whose methylation correlates strongly (FDR

Background: Swimming in a chlorinated pool results in high exposure levels to disinfection by-products (DBPs), which have been associated with an increased risk of bladder cancer. Objectives: By studying molecular responses at the blood transcriptome level we examined the biological processes associated with exposure to these compounds. Methods: Whole-genome gene expression and microRNA analysis was performed on blood samples collected from 43 volunteers before and 2h after 40min swimming in an indoor chlorinated pool (PISCINAII study). Exposure to THMs was measured in exhaled breath. Heart rate and kcal expenditure were measured as proxies for physical activity. Associations between exposure levels and gene expression were assessed using multivariate normal models (MVN), correcting for age, body mass index and sex. A Bonferroni threshold at 5% was applied. Results: MVN-models for the individual exposures identified 1778 genes and 23 microRNAs that were significantly associated with exposure to at least one DBP. Due to co-linearity it was not possible to statistically disentangle responses to DBP exposure from those related to physical activity. However, after eliminating previously reported transcripts associated with physical activity a large number of hits remained associated with DBP exposure. Among those, 9 were linked with bladder and 31 with colon cancer. Concordant microRNA/mRNA expressions were identified in association with DBP exposure for hsa-mir-22-3p and hsa-miR-146a-5p and their targets RCOR1 and TLR4, both related to colon cancer in association with DBP exposure. Conclusions: Short-term exposure to low levels of DBPs shows genomics responses that may be indicative of increased cancer risk. Keywords: Disinfection by-products, Transcriptomics, microRNA, Multivariate normal models

Background: We hypothesize that biological perturbations due to exposure to ambient air pollution are reflected in gene expression levels in peripheral blood mononuclear cells.Methods: We assessed the association between exposure to ambient air pollution and genome-wide gene expression levels in peripheral blood mononuclear cells collected from 550 healthy subjects participating in cohorts from Italy and Sweden. Annual air pollution estimates of nitrogen oxides (NOx) at time of blood collection (1990-2006) were available from the ESCAPE study. In addition to univariate analysis and two variable selection methods to investigate the association between expression and exposure to NOx, we applied gene set enrichment analysis to assess overlap between our most perturbed genes and gene sets hypothesized to be related to air pollution and cigarette smoking. Finally, we assessed associations between NOx and CpG island methylation at the identified genes.Results: Annual average NOx exposure in the Italian and Swedish cohorts was 94.2 and 6.7 mu g/m(3), respectively. Long-term exposure to NOx was associated with seven probes in the Italian cohort and one probe in the Swedish (and combined) cohorts. For genes AHCYL2 and MTMR2, changes were also seen in the methylome. Genes hypothesized to be downregulated due to cigarette smoking were enriched among the most strongly downregulated genes from our study.Conclusion: This study provides evidence of subtle changes in gene expression related to exposure to long-term NOx. On a global level, the observed changes in the transcriptome may indicate similarities between air pollution and tobacco induced changes in the transcriptome.

We recently reported that differential gene expression and DNA methylation profiles in blood leukocytes of apparently healthy smokers predicts with remarkable efficiency diseases and conditions known to be causally associated with smoking, suggesting that blood-based omic profiling of human populations may be useful for linking environmental exposures to potential health effects. Here we report on the sex-specific effects of tobacco smoking on transcriptomic and epigenetic features derived from genome-wide profiling in white blood cells, identifying 26 expression probes and 92 CpG sites, almost all of which are affected only in female smokers. Strikingly, these features relate to numerous genes with a key role in the pathogenesis of cardiovascular disease, especially thrombin signaling, including the thrombin receptors on platelets F2R (coagulation factor II (thrombin) receptor; PAR1) and GP5 (glycoprotein 5), as well as HMOX1 (haem oxygenase 1) and BCL2L1 (BCL2-like 1) which are involved in protection against oxidative stress and apoptosis, respectively. These results are in concordance with epidemiological evidence of higher female susceptibility to tobacco-induced cardiovascular disease and underline the potential of blood-based omic profiling in hazard and risk assessment.

Objective Although poor parental bonding is a known risk factor for suicidality, current literature is inconsistent about the relative role of low parental care and parental overprotection, as well as the combination of the two, termed “affectionless control”. This review presents the current state of knowledge of the relationship between suicidality and these two aspects of parental bonding. Method The computerized databases Medline, PubMed, PsychINFO, PsychLit, and Google Scholar were searched using combinations of the following keywords: suicidality, suicide, suicide attempt, suicidal behavior, parental bonding, and parental bonding instrument. Using the results, we reviewed the reports on the relationship between suicidality and parental bonding as measured by validated parental bonding instruments. Results Twelve papers were analyzed. All of them used the parental bonding instrument (PBI) and one used both the PBI and the object representation inventory (ORI). Most reports agreed that, in mothers, either lack of maternal care and/or overprotection was associated with an increase in suicidal behavior, while in fathers only low care was consistently associated with suicidality. This lack of constancy with regard to the effect of paternal overprotection appears to be due to cultural differences in fathers' role in child rearing. With these differences acknowledged, affectionless control in both parents emerges as the parenting style most strongly associated with suicidal behavior. Common methodological problems included low numbers of subjects, inconsistent control groups, and the lack of a uniform definition of suicidality. Conclusion Despite methodological limitations, current literature consistently indicates that parental affectionless control is associated with suicidal behavior. Recognizing affectionless control as a risk factor for suicide and developing early interventions aimed at modifying affectionless and overprotective parenting style in families with a history of affective disorders may be effective in reducing suicidal risk.

Objectives Vertigo has been reported by people working around magnetic resonance imaging (MRI) scanners and was found to increase with increasing strength of scanner magnets. This suggests an association with exposure to static magnetic fields (SMF) and/or motion-induced time-varying magnetic fields (TVMF). This study assessed the association between various metrics of shift-long exposure to SMF and TVMF and self-reported vertigo among MRI workers. Methods We analysed 358 shifts from 234 employees at 14 MRI facilities in the Netherlands. Participants used logbooks to report vertigo experienced during the work day at the MRI facility. In addition, personal exposure to SMF and TVMF was measured during the same shifts, using portable magnetic field dosimeters. Results Vertigo was reported during 22 shifts by 20 participants and was significantly associated with peak and time-weighted average (TWA) metrics of SMF as well as TVMF exposure. Associations were most evident with full-shift TWA TVMF exposure. The probability of vertigo occurrence during a work shift exceeded 5% at peak exposure levels of 409 mT and 477 mT/s and at full-shift TWA levels of 3 mT and 0.6 mT/s. Conclusions These results confirm the hypothesis that vertigo is associated with exposure to MRI-related SMF and TVMF. Strong correlations between various metrics of shift-long exposure make it difficult to disentangle the effects of SMF and TVMF exposure, or identify the most relevant exposure metric. On the other hand, this also implies that several metrics of shift-long exposure to SMF and TVMF should perform similarly in epidemiological studies on MRI-related vertigo.

Prediagnostic serum/plasma concentrations of B-cell activation markers have been associated with future risk of B-cell lymphomas (BCL) in HIV-infected patients and in the general population. Current evidence for the general population is however limited and relies on relatively small numbers of observations, especially for specific histologies. We carried out a nested case-control study, including 218 BCL and 218 matched controls, within two prospective cohorts, to investigate the association between plasma levels of soluble (s)CD27 and sCD30 and future risk of BCL, and main histologic subtypes separately. To expand the evidence further, we performed meta-analyses of the published data on these associations from prospective studies among the general population. Our study revealed a significant relationship between sCD30 concentration and BCL risk (OR = 0.86, 1.53, 1.76, for the 2nd-4th quartiles respectively, p trend = 0.01). Similar increased risks were observed for diffuse large B-cell lymphoma and follicular lymphoma. Analyses of sCD27 blood concentrations did not show significant associations with BCL, (OR = 0.90, 1.26, 1.65 for the 2nd-4th quartiles, respectively, p trend = 0.17), but significant associations were observed for chronic lymphocytic leukaemia and for the group of "other BCL" subtypes. Our findings involving sCD30 were confirmed within our meta-analyses of five prospective cohorts, while results were more heterogeneous for sCD27 with the exception of CLL which was found consistently in all studies. Data to date suggest that chronic B-cell stimulation might be an important mechanism involved in B-cell lymphomagenesis both in HIV-infected and in the general population.

Benzene exposure has been causally linked with acute myeloid leukemia (AML), but inconsistently associated with other hematopoietic, lymphoproliferative and related disorders (HLD) or solid tumors in humans. Many neoplasms have been described in experimental animals exposed to benzene. We used Poisson regression to estimate adjusted relative risks (RR) and the likelihood ratio statistic to derive confidence intervals for cause-specific mortality and HLD incidence in 73,789 benzene-exposed compared with 34,504 unexposed workers in a retrospective cohort study in 12 cities in China. Follow-up and outcome assessment was based on factory, medical and other records. Benzene-exposed workers experienced increased risks for all-cause mortality (RR = 1.1, 95% CI = 1.1, 1.2) due to excesses of all neoplasms (RR = 1.3, 95% CI = 1.2, 1.4), respiratory diseases (RR = 1.7, 95% CI = 1.2, 2.3) and diseases of blood forming organs (RR = ∞, 95% CI = 3.4, ∞). Lung cancer mortality was significantly elevated (RR = 1.5, 95% CI = 1.2, 1.9) with similar RRs for males and females, based on three-fold more cases than in our previous follow-up. Significantly elevated incidence of all myeloid disorders reflected excesses of myelodysplastic syndrome/acute myeloid leukemia (RR = 2.7, 95% CI = 1.2, 6.6) and chronic myeloid leukemia (RR = 2.5, 95% CI = 0.8, 11), and increases of all lymphoid disorders included excesses of non-Hodgkin lymphoma (RR = 3.9, 95%CI = 1.5, 13) and all lymphoid leukemia (RR = 5.4, 95%CI = 1.0, 99). The 28-year follow-up of Chinese benzene-exposed workers demonstrated increased risks of a broad range of myeloid and lymphoid neoplasms, lung cancer, and respiratory diseases and suggested possible associations with other malignant and non-malignant disorders.

The epidemiologic evidence for the carcinogenicity of lead is inconsistent and requires improved exposure assessment to estimate risk. We evaluated historical occupational lead exposure for a population-based cohort of women (n=74,942) by calibrating a job-exposure matrix (JEM) with lead fume (n=20,084) and lead dust (n=5383) measurements collected over four decades in Shanghai, China. Using mixed-effect models, we calibrated intensity JEM ratings to the measurements using fixed-effects terms for year and JEM rating. We developed job/industry-specific estimates from the random-effects terms for job and industry. The model estimates were applied to subjects' jobs when the JEM probability rating was high for either job or industry; remaining jobs were considered unexposed. The models predicted that exposure increased monotonically with JEM intensity rating and decreased 20-50-fold over time. The cumulative calibrated JEM estimates and job/industry-specific estimates were highly correlated (Pearson correlation=0.79-0.84). Overall, 5% of the person-years and 8% of the women were exposed to lead fume; 2% of the person-years and 4% of the women were exposed to lead dust. The most common lead-exposed jobs were manufacturing electronic equipment. These historical lead estimates should enhance our ability to detect associations between lead exposure and cancer risk in the future epidemiologic analyses.

Crump asserts that we “inappropriately mixed data from exposures lagged 5 years and 15 years” in our study published in Environmental Health Perspectives (Vermeulen et al. 2014). Exposure metrics from different studies available for meta-analysis are rarely, if ever, completely comparable. Therefore, even exposures labeled exactly the same (e.g., “cumulative exposure lagged 15 years”) differ between studies because of differences in exposure assessment (cumulative exposure is accrued in different ways in different populations) and because of differences in age composition and extent of follow-up. As a result, in epidemiological studies, optimal lag times to exclude exposures not affecting risk may be variable across studies. For our meta-regression, we included the exposure–response relationships that were presented as the main analyses in the respective papers. For the two trucking studies (Garshick et al. 2012; Steenland et al. 1998), the exposure metric was lagged 5 years, whereas for the Diesel Exhaust in Miners Study (DEMS; Silverman et al. 2012) it was 15 years. Results for an analysis using a 5-year lag in DEMS were not published, although the 5-year lag had been included in analyses to examine changes in model fit as a function of lag. From those analyses (Silverman et al. 2012, Supplementary Figure 1), it is apparent that a 5-year lag showed the worst model fit of all lags (0–25 years); thus, it does not make sense to use this particular analysis as the primary exposure–response relation simply because the label “5-year lag” coincides with that of the other two studies. We acknowledge that the interpretation of the risk function may be affected by differences in exposure between lag times. For this reason, we performed sensitivity analyses that included different lags from each study; overall results changed only slightly. We extended our earlier sensitivity analyses by including the unpublished 5-year lagged data from Silverman et al. (Silverman DT, personal communication).We note again, however, that these 5-year lagged data from the DEMS do not fit nearly as well as the 15-year lagged data. We stress our belief that they should not be the primary data for use in any risk assessment/meta-regression. Crump argues that his alternative analyses using the 5-year lagged data were more consistent with the underlying DEMS data. Figure 1 includes the individual risk estimates for all three studies, with three alternative lag times for DEMS. It is clear from Figure 1 that the 5-year lagged risk estimates for DEMS selected by Crump for his meta-analysis are considerably lower than those of the two trucking studies and the alternative lag times for DEMS. We also included in the figure three different regression lines based on the two trucking studies and one of three different sets of results for DEMS, obtained using the exposure data lagged 0, 5, and 15 years. All models are fitted using the full estimated covariance matrix to appropriately account for the correlation between categorical point estimates from the same study, a correction ignored by Crump. The lowest meta-regression slope, using the 5-year lagged exposure results from DEMS, a) is higher than that reported by Crump using the variance estimates only; b) is statistically significant (0.00065; 95% CI: 0.00028, 0.0010); and c) falls within our previous sensitivity analyses (Vermeulen et al. 2014). It is also clear that the exposure–response function derived using the 15-year lagged exposure data from DEMS is a much better fit overall. Figure 1 Predicted exposure–response curve of cumulative elemental carbon (EC) and lung cancer risk using different lag-times based on a log-linear regression model using relative risk estimates from the three cohort studies. In summary, we strongly disagree with the assertions made by Crump in his letter that we inappropriately mixed lag times. On his other points, we note that adjustment for employment duration in the trucking industry cohort study was not a second exposure measure, but appropriately reduced bias attributable to a healthy worker survivor effect. Additional analyses presented here confirm that the original findings from the meta-analyses are robust. Therefore, we firmly stand with the conclusions of our original paper.

Exposure to polycyclic aromatic hydrocarbons (PAHs) from burning "smoky" (bituminous) coal has been implicated as a cause of the high lung cancer incidence in the counties of Xuanwei and Fuyuan, China. Little is known about variations in PAH exposure from throughout the region nor how fuel source and stove design affects exposure. Indoor and personal PAH exposure resulting from solid fuel combustion in Xuanwei and Fuyuan was investigated using repeated 24 h particle bound and gas-phase PAH measurements, which were collected from 163 female residents of Xuanwei and Fuyuan. 549 particle bound (283 indoor and 266 personal) and 193 gas phase (all personal) PAH measurements were collected. Mixed effect models indicated that PAH exposure was up to 6 times higher when burning smoky coal than smokeless coal and varied by up to a factor of 3 between different smoky coal geographic sources. PAH measurements from unventilated firepits were up to 5 times that of ventilated stoves. Exposure also varied between different room sizes and season of measurement. These findings indicate that PAH exposure is modulated by a variety of factors, including fuel type, coal source, and stove design. These findings may provide valuable insight into potential causes of lung cancer in the area.

This article presents the theoretical application of Parse's Man-Living-Health theory. The main objective is to offer an interpretation of and to clarify the theory's main principles, themes and concepts in the Swedish language. A hypothetical, and often occurring situation in psychiatric nursing practice has been chosen as an example of how the themes--meaning, rythmicity and co-transcendence could conceivably be applied as a guide for nursing action. It is well known that the patient with the diagnosis, manic depressive disorder, often finds Lithium treatment meaningless. The use of Parse theory may guide the nurse in helping the patient to express his values and beliefs in order to enhance quality of life. One of the emphases and perspectives of the theory is that the patient is the expert in knowing his own needs. The nurse should not impose her own values or make choices for the patient. In order to apply Parse theory, presupposes an understanding of the basic concepts in existentialism and phenomenology as well as a shared psychiatric ideology in the practical setting.